Brainscape's Knowledge GenomeTM

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


See full index

Endo/Repro > Endocrine Pathology > Flashcards

Endocrine Pathology Flashcards

1
Q

Anterior Pituitary

A

glandular organ –> arises from Rathke’s pouch

  • secretes GH, PRL, FSH, LH, ACTH, TSH
  • all hormones are controlled by hypothalamus (stimulatory except PRL which is inhibited by dopamine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Posterior Pituitary

A

Neural ectoderm -> from diencephalon

  • doesn’t make hormones, it stores hormones (oxytocin and ADH)
  • extension of hypothalamus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Acidophils

A

secretes GH and PRL

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

Basophils

A

secretes FSH, LH, ACTH, TSH

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

Oxytocin

A 
Labor induction
Milk let down
Cuddle hormone
Monogamy
Trust
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Hyperpituitarism

A

too much of one or more anterior pituitary hormones

  • most common cause = pituitary adenoma
  • endocrine abnormalities occur when adenomas secrete hormones, otherwise it can be latent until growth becomes big enough to cause mass effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Mass Effect

A

Visual field abnormalities - bitemporal hemianopsia (optic chiasm)
Symptoms of increased cranial pressure
Compression of pituitary -> HYPOpituitarism

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

Functional vs. Nonfunctional pituitary adenomas

A 
functional = produces pituitary hormone
non-functional = doesn't produce hormone -> becomes really big (mass effect)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Epidemiology of pituitary adenomas

A

occurs most common in adults
3% arise from multiple endocrine neoplasia
- can cause “pituitary apoplexy” –> sudden bleeding that is BAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Microscopic appearance of pituitary adenoma

A

can’t tell type of hormone from histology –> need special stains
- most commonly involve one cell type, can be pleomorphic
MOST COMMON - prolactin-producing
LEAST COMMON - thyroid-stimulating hormone producing

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

Molecular mutations in pituitary adenomas

A

mutated G-proteins -> GNAS1 gene

  • alpha subunit doesn’t turn off -> GTP constantly causing cAMP and PKA pathways
  • some can cause activating mutation of RAS oncogene or overexpression of c-MYC oncogene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Prolactin-producing adenoma

A

MOST COMMON type of pituitary adenoma
- secretes prolactin efficiently -> causes symptoms (amenorrhea, galactorrhea, infertility, loss of libido)
- drugs that interfere with dopamine action can also cause increased prolactin
Tx = bromocriptine (D2 receptor agonist)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Growth hormone producing adenoma

A

Gigantism = GH adenoma BEFORE puberty
Acromegaly = GH adenoma AFTER puberty (changes can happen subtly so that patient doesn’t realize)
Lab - GH unreliable because of pulsatile secretion, check IGF-1
- can also perform glucose test (administer glucose should decrease GH but it won’t)
Tx = get GH back to normal (surgery/radiation)

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

ACTH producing adenoma

A

makes ACTH –> revs up adrenal glands which make cortisol
Cushing Syndrome -> too much cortisol
Cushing Disease -> ACTH producing adenoma that causes cushing syndrome
Nelson Syndrome -> removal of adrenals with cushing syndrome -> BAD (no inhibition of pituitary)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

FSH and LH producing adenomas

A

secrete FSH and LH very inefficiently

- mass effect brings it to attention rather than endocrine abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

TSH-producing adenomas

A

RARE!!!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Non-functioning adenoma

A

secretes no hormones –> gets BIG and causes mass effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Hypopituitarism

A

decreased secretion of pituitary hormones
Causes:
1. Pituitary destruction –> more than 75% (surgery, radiation, tumor compressing it)
2. Ischemic Necrosis -> Sheehan syndrome (pregnancy), pituitary increases in size but not blood supply, hemorrhage of shock during delivery infarcts the pituitary
3. Empty Sella syndrome -> arachnoid membrane and CSF herniate down into sella turcica (more than 75%)
4. Pituitary Apoplexy -> sudden, spontaneous infarct of pituitary (symptoms of severe headache, stiff neck, N/V) -> bad bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Clinical finding of hypopituitarism

A

insidious, chronic onset (need 75% or more of pituitary affected)
Order of Loss of Hormones = GH, FSH/LH, TSH, ACTH
GH -> dwarfism (childhood), muscle atrophy and weakness (adulthood)
FSH/LH -> menstrual abnormalities
PRL -> prevents lactation
TRH -> secondary hypothyroidism
ACTH -> adrenal insufficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Posterior Pituitary Syndromes

A

Diabetes Insipidus and Syndrome of Inappropriate ADH Secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Diabetes Insipidus

A

central or nephrogenic decrease in ADH secretion
- ADH deficiency leads to dilute, massive amounts of urine
- increase in serum osmolality
- head trauma, tumors, or ethanol
Tx = increase water intake and give ADH (vasopressin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

SIADH

A

ADH excess causes kidneys to excrete SUPER concentrated urine –> lots of water retention (decrease serum osmolality)
Most common cause -> ectopic ADH producing tumor (small-cell lung cancer)
Tx = restrict water intake

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

Thyroid Embryology

A

thyroid develops from pharyngeal epithelium from back of tongue -> descends anterior portion of neck

  • remnants = thyroglossal duct cyst
  • bilobed structure with isthmus, follicles contain colloid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Thyroid Physiology

A

hypothalamus secretes TRH –> anterior pituitary secretes TSH –> thyroid synthesizes and releases T3 and T4, grows, uptakes iodine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Thyroid Hormone Function

A

increase fat breakdown, decrease carb utilization, stimluate protein synthesis, increased BMR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Thyroid Lab Testing

A

TSH -> amount of TSH in blood, VERY sensitive (even a small fluctuation in T4 causes a rapid, inverse change in TSH)
Free T4 -> tells how much active, free T4 patient has (don’t confuse with total T4 which is bound, inactive)
Free or total T3 -> how much free or total T3 patient is making
TBG - measures thyroglobulin (carrier for thyroid hormone)
Anti-thyroid antibody test - Graves’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Radioiodine thyroid screening

A

123-I radiolabeled is taken up by thyroid
- evaluate thyroid nodules or determine appropriate dosing
Hot -> almost always benign because cancer doesn’t make hormones
Cold -> occasionally malignant because cancer doesn’t make hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Hyperthyroidism

A

HYPERMETABOLIC state caused by increased thyroid hormone levels
Primary -> thyroid over-functioning because of intrinsic problem
Secondary -> thyroid over-functioning because too much TSH (pituitary problem)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Signs and Symptoms of hyperthyroidism

A

Cardiac -> rapid pulse, cardiomegaly, arrhythmias
Neuro -> nervous, tremor, emotional
Eye -> lid lag, wide-staring gaze
Skin -> warm, moist, flushed skin
GI -> diarrhea, weight loss
Skeletal -> osteoporosis
Thyroid Storm –> BAD SHIT -> coma and death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Causes of hyperthyroidism

A

Graves’ disease –> MOST COMMON CAUSE

- goiter, thyroid adenoma, thyroiditis, ingestion of thyroid hormones, pituitary adenoma, struma ovarii, factitious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Diagnosis of hyperthyroidism

A

TSH and free T4
Primary -> high T4 and low TSH
Secondary -> high T4 and high TSH

32
Q

Hypothyroidism

A

HYPOMETABOLIC state by decreased levels of thyroid homrones
Primary -> under-functioning because of intrinsic problem
Secondary -> under-functioning because of low TSH (pituitary problem)

33
Q

Signs and Symptoms of Hypothyroidism

A

Slowing of mind and body -> fatigue, mental slowness, irritability, loss of interest
Myxedema -> accumulation of ground substance in tissues -> not fluid
Cardiac -> slow pulse, diminished contractility
GI - > constipation
Skin -> dry, cool, pale
Cold Intolerance
Delayed deep tendon reflexes
Myxedema Coma -> opposite of thyroid storm

34
Q

Causes of Hypothyroidism

A

Congenital (Cretinism) -> iodine deficiency, developmental or genetic
- symptoms reflect impaired development = short, mental retardation (range of severities)
Acquired (adulthood) -> Hashimoto thyroidits (autoimmune), iatrogenic (surgery or radiation), goiter, amyloidosis, sarcoidosis, thyroiditis

35
Q

Diagnosis of Hypothyroidism

A

TSH and free T4
Primary -> low T4 and high TSH
Secondary -> low T4 and low TSH

36
Q

Thyroiditis

A

inflammation of thyroid gland

  • Hashimoto is most common
  • may be euthyroid, hypothyroid, or hyperthyroid (colloid spilling out)
  • radioactive uptake is decreased (“cold” thyroid tissue)
37
Q

Hashimoto thyroiditis

A

MOST COMMON thyroiditis (F>M)
- Primary Hypothyroidism (T4 low, TSH high)
- enlarged, non-tender thyroid (gradually hypothyroid)
Lab Testing = thyroid tests reflect thyroid status
- anti-peroxidase antibodies (detected by immunofluorescence)
Patho = autoimmune destruction of thyroid gland (T-cells attack thyroid AND stimulate B-cells) –> anti-TSH receptor antibody

38
Q

DeQuervian thyroiditis

A

occurs after upper respiratory infection (viral infection)

  • many patients have HLA-B35 antigen
  • painful, enlarged thyroid (abrupt)
  • self-limiting disease
  • damaged, disrupted follicles and multinucleate giant cells
39
Q

Silent thyroiditis

A

painless, slightly enlarged thyroid (asymptomatic)

  • middle age or after pregnancy
  • transient and self-limiting
  • abundant lymphocytes (like Hashimoto but none of the features of Hashimoto)
40
Q

Reidel’s thyroiditis

A

Rock-hard, woody neck mass –> fibrosis

- fibrosis may progress and put pressure on trachea

41
Q

Graves’ Disease

A

MOST COMMON cause of hyperthyroidism (F>M)
- Classic Triad = hyperthyroidism, ophthalmopathy, dermopathy
Labs = high T4, low TSH, high uptake of iodine
- Autoimmune disease with anti-TSH receptor antibodies (opposite effect of Hashimoto)
- eye muscles and skin has TSH receptors –> that’s how those symptoms occur

42
Q

Treatment of Graves’

A

decrease symptoms of hyperthyroidism (beta-blocker)

decrease synthesis of thyroid hormones = PTU, radioiodine ablation

43
Q

Goiters

A

big thyroid gland
low T4 –> high TSH –> BIG THYROID
Simple –> first stage (smooth)
Multinodular –> second stage (bumpy and big)
Labs = euthyroid
Histo –> hyperplastic cells, then cells become exhausted and involute (oversized colloid)

44
Q

Cause and Treatment of Goiters

A

Lack of iodine, diet rich in goitrogen
Tx = levothyroxine –> suppress TSH and shrink goiter
- be careful of Jod-Basedow phenomena –> giving iodine to patient –> acute hyperthyroidism

45
Q

Neoplastic thyroid disease

A

most thyroid bumps are non-neoplastic –> but need to aspirate/biopsy to make sure

46
Q

Thyroid Adenoma

A

euthyroid patients, commoner in adults
- Labs = normal T4 and TSH, cold thyroids
Solitary nodules, encapsulated, and generally not invasive
Tx = surgical removal
- need to look at capsule to see if there is tumor cells –> that means it’s invasive

47
Q

Papillary Adenocarcinoma

A

most common cause of thyroid carcinoma (best prognosis too)

  • papillary growth pattern
  • nuclei look empty (Orphan Annie’s eyes), nucelar pseudoinclusions, psammoma body
48
Q

Follicular Adenocarcinoma

A

follicular growth pattern, well-differentiated
Hard to identify from thyroid adenoma
- look for vascular invasion and tumor cells extending into thyroid capsule
Tx = surgical excision, look for metastasis

49
Q

Medullary Carcinoma

A

endocrine tumor
- thyroid C-cells –> makes calcitonin -> creates amyloid deposits (congo red stain)
- vague nests
Tx = anyone suspected of MEN II or familial thyroid

50
Q

Anaplastic thyroid carcinoma

A

rapidly-enlarging bulky neck mass –> often metastasized already upon presentation
Anaplastic cells –> VERY undifferentiated = bad prognosis

51
Q

Parathyroid Gland

A 
4 glands in 2 pairs
Upper lobes -> 4th pharyngeal pouch
Lower lobes -> 3rd pharyngeal pouch
- chief cells -> PTH
- oxyphil cells -> unknown function
52
Q

Parathyroid Physiology

A

Chief cells secrete proparathyroid -> cleaved to PTH -> binds to PTH receptors -> stimulate AC -> PLC -> IP3 and DAG

53
Q

PTH Actions

A
  1. Stimulate osteoblasts -> stimulate osteoclasts -> increase blood calcium
  2. Increase renal absorption of calcium
  3. Increase renal conversion of Vit D to active form
  4. Increase urinary excretion of phosphate
  5. Absorb gut calcium
54
Q

What controls PTH release?

A

serum calcium –> NOT pituitary
serum calcium increases -> PTH decreases
serum calcium decreases -> PTH increases

55
Q

Hypercalcemia

A 
Lots of things can cause it:
M alignancy
D iuretics
P arathyroid
I diopathic
M egadose of Vit D
P aget's disease
S arcoidosis
M ilk-alkali syndrome
E ndocrine
56
Q

Hyperparathyhroidism

A

Primary -> over-functioning because of intrinsic problem
Secondary -> over-functioning because of something else causing chronic hypocalcemia
Pseudohyperparathyroidism -> hypercalcemia caused by production of PTH related protein by cancers (squamous cell lung carcinoma)

57
Q

Primary Hyperparathyroidism

A

Stone -> kidney stones (hypercalcemia)
Bone -> bone pain (osteoclasts erode bone)
- brown tumors -> microfractures and hemorrhage
Groan -> GI problems (constipation, ulcers, nausea)
Moan -> mental changes (depression, lethargy)
Labs = increased PTH, increased Ca, decreased PO4, increased 24-hr urine Ca, increased urine cAMP

58
Q

Causes of primary hyperparathyroidism

A
  1. Parathyroid Adenoma -> most common
    - composed mostly of chief cells
    PRAD1 -> genetic alterations in sporadic cases
    MEN1 or RET -> genetic alterations in familial cases
  2. Parathyroid Hyperplasia -> normal looking cells, just a lot of them, some MEN1 syndromes
  3. Parathyroid Carcinoma -> abrupt onset of pain bain, usually just one gland affecteed, tumors are well-differentiated
59
Q

Secondary Hyperparathyroidism

A

Due to chronic hypocalcemia -> renal failure, poor calcium, Vit D deficiency
Pathophysiology = chronic renal failure -> phosphate not excreted -> Ca goes down -> stimulates PTH to be secreted
Symptoms overshadowed by chronic renal failure

60
Q

Hypoparathyroidism

A

Iatrogenic, congenital (DiGeorge’s -> thymic aplasia, absence of parathyroids), familial

61
Q

Signs and Symptoms of Hypoparathyroidism

A

TETANY -> tingling around mouth/extremities
- Chvostek’s sign -> stroking/tapping cheeck induces eye, mouth, and nose contraction
- Trousseau’s sign -> occluding forearm circulation induces carpal contraction
Mental Status changes
CV disease
Dental Abnormalities

62
Q

Adrenal Anatomy and Histology

A

paired gland at top of kidneys, cortex has 3 zones, medulla has chromaffin cells

63
Q

Adrenal Cortex and Medulla and hormones

A

Zona glomerulosa -> mineralocorticoids
Zona fasciculata -> glucocorticoids
Zona reticularis -> sex steroids
Medulla -> Catecholamines

64
Q

Cushing Syndrome

A 
increased glucocorticoids (cortisol) in blood
- stable BP, decreased Bone, decreased inflammation, decreased immunity, increased gluconeogenesis
65
Q

Signs of Cushings

A 
HTN and weight gain
adipose tissue distributed truncally, moon facies, buffalo hump
- weakness
- glucose intolerance
- thin fragile skin
- infections
66
Q

Labs for Cushing

A

24 hr urine free cortisol –> diagnosis

ACTH level, dexamethasone test –> cause

67
Q

Causes of Cushing

A

Iatrogenic -> drug ingestion (low ACTH, dex doesn’t suppress cortisol)
Pituitary adenoma -> ACTH high, dex suppresses cortisol
Adrenal lesion -> ACTH low, dex doesn’t suppress cortisol
Ectopic ACTH production -> ACTH high, dex doesn’t suppress cortisol

68
Q

Hyperaldosteronism

A

High Aldosterone, high Na/low K
Primary - high aldosterone -> low renin
- HTN, weakness, fatigue
- Labs = high aldosterone, low renin, high Na/low K, metabolic alkalosis
Secondary - high renin -> high aldosterone
- symptoms same
- Labs = high aldosterone, high renin, high Na/low K, metabolic alkalosis

69
Q

Adrenogenital syndromes

A

VIRILIZATION

Primary gonadal disorders, primary adrenal disorders

70
Q

Congenital Adrenal Hyperplasia

A

enzyme block in cortisol pathway (21-hydroxylase MOST COMMON)
- precursors are shunted to other pathways –> mostly to sex steroids (testosterone) –> turns females to have male features

71
Q

Addison disease

A

Primary CHRONIC adrenal insufficiency -> intrinsic adrenal cortex problem leading to decreased cortisol and mineralocorticoids
Causes -> autoimmune, infections, metastatic carcinoma
Features -> chronic (takes a while for symptoms to appear), hypoglycemia, metabolic acidosis, skin hyperpigmentation from POMC -> makes both ACTH and MSH

72
Q

Primary Acute adrenal insufficiency

A

adrenal SUDDENLY aren’t releasing their stuff

Addisonian crisis, steroid withdrawal, massive adrenal hemorrhage

73
Q

Massive Adrenal Hemorrhage

A

newborns following difficult delivery
anticoagulated patients
DIC
following bacterial infection (WFS)

74
Q

Waterhouse-Friderichsen syndrome

A

overwhelming bacterial infection (N. meningitidis)
hypotension and shock
DIC
rapidly progressive massive adrenal hemorrhage

75
Q

Secondary Adrenal Insufficiency

A

low ACTH -> low adrenal products
Causes = pituitary insufficiency, hypothalamic insufficiency
Features = symptoms of low cortisol and low sex steroids

76
Q

Pheochromocytoma

A

Neoplasm of catecholamine producing cells derived from neural crest
Pressure (BP), Pain, perspiration, palpitations, pallor
10% tumor = extra-adrenal, bilateral, familial, malignant, don’t have HTN

77
Q

Neuroblastoma

A

neoplasm derived from neural crest cells -> common childhood tumor

  • round, blue rosette cells
  • N-myc amplification associated with bad prognosis

Endo/Repro (34 decks)

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