Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y2 Patho > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Causes/origins of hyperpituitarism:

A
  1. Adenoma of the pituitary gland-> overproduction of hormones
  2. Carcinoma (rare)
  3. Hyperplasia (rare)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Types of pituitary tumours:

A
  1. Adenoma (benign) (usually this)
  2. Carcinoma (rare)
  3. Craniopharyngioma: cystic tumour derived from embryonal remnants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What hormones do the pituitary gland secrete?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Effects of hypopituitarism:

A

Decreased GH-> pituitary dwarfism (failure of growth)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is the thyroid gland regulated?

A
  1. Regulated by TSH produced by the pituitary gland.
  2. -ve feedback: thru Ca2+ levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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+)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Name the primary causes of hyperthyroidism:

A
  1. Graves disease (diffuse)
  2. Toxic multinodular goitre (localised nodules)
  3. Toxic neoplasm (tumour)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name a secondary cause of hyperthyroidism:

A

Pituitary hyperfunction.

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Name a secondary cause of hypothyroidism:

A

Pituitary failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is opthalmopathy?

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:

A
  1. Hyperthyroidism (go back to the signs and symptoms)
  2. Thyrotoxicosis
  3. Opthalmopathy
  4. Diffuse goitre
25
Q

Pathogenesis of Graves disease:

A
  • 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
Q

The most common cause of hypothyroidism in SG is…

A

Hashimoto’s thyroiditis

27
Q

Hashimoto’s thyroiditis is more common in..?

A

Females, familial clustering

28
Q

Pathogenesis of Hashimoto’s thyroiditis:

A
  • 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
Q

Lymphoma of the thyroid gland is related to..

A

Hashimoto’s thyroiditis

30
Q

What are hurthle cells?

A

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
Q

Gross features of hashimoto’s thyroiditis:

A

Histology:
- lymphoid follicles
- hurthle cell changes

32
Q

Subacute (granulamatous) thyroiditis/ DeQuervain thyroiditis

A

-post-viral inflammatory process
- self-limiting
- short history
- more common in females
- linked to viral, bacterial & autoimmune etiologies

33
Q

Symptoms of Subacute (granulamatous) thyroiditis/ DeQuervain thyroiditis

A
  • flu-like
  • inflammation of thyroid gland
  • painful goitre (other goitre conditions dont result in pain)
34
Q

Histology of Subacute (granulamatous) thyroiditis/ DeQuervain thyroiditis

A
  • granulomatous
  • acute & chronic inflammation in thyroid
35
Q

Gross features of follicular adenoma:

A
  • rounded, encapsulated well-demarcated nodule
  • bulging from cut surface
36
Q

Histology of follicular adenoma:

A
  • completely surrounded by intact capsule
  • follicles
  • resembles normal thyroid
37
Q

Types of thyroid carcinomas:

A

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
Q

Characteristics of follicular thyroid carcinomas (well-differentiated):

A
  • 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
Q

Characteristics of papillary thyroid carcinomas (well-differentiated):

A
  • 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
Q

Papillary thyroid carcinomas metastasise to?

A

Lymph nodes

41
Q

Follicular thyroid carcinomas metastasise to?

A

Organs via bloodstream e.g. lungs, bone, liver

42
Q

Characteristics of anaplastic thyroid carcinomas:

A
  • rapidly enlarged
  • undifferentiated
  • more common in elderly
  • poor prognosis (months)
43
Q

Effects of anaplastic thyroid carcinomas

A
  • compressive symptoms (squeezes trachea)
  • often spread beyond thyroid
  • metastasises to lungs
44
Q

Characteristics of medullary thyroid carcinoma:

A
  • 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
Q

What does the parathyroid gland do?

A

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
Q

Causes of hyperparathyroidism:

A

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
Q

Causes of hypoparathyroidism:

A
  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
Q

Complications from hyperthyroidism:

A
  1. Renal & urinary calculi, nephrocalcinosis
  2. Osteitis fibrous cystica (skeletal disorder)
  3. Hypertension
  4. Pancreatitis
  5. Peptic ulcers
  6. Metastatic calcification
49
Q

Complications from hypoparathyroidism:

A
  • 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
Q

What are the adrenal glands regulated by?

A

ACTH released by pituitary glands
-> stimulates release of adrenal cortical hormones

51
Q

What does the cortex of the adrenal glands produce?

A
  1. Aldosterone
    - regulates bp, Na+/water retention, K+ excretion
  2. Cortisol
    - maintain homeostasis
  3. Androgens
    - for sexual development & function
52
Q

What does the medulla of the adrenal glands produce?

A

Catecholamines (adrenaline, noradrenaline)

53
Q

Name the causes of adrenal hyperfunction:

A

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
Q

Increased aldosterone levels lead to:

A

Conn’s syndrome

55
Q

Increased cortisol levels lead to:

A

Cushing’s syndrome

56
Q

What syndromes can adrenal hyperfunction lead to?

A
  1. Conn’s syndrome (elevated aldosterone)
  2. Cushing’s (elevated cortisol)
57
Q

List the clinical features of Cushing’s syndrome:

A
  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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions