Brainscape's Knowledge GenomeTM

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


See full index

Patho 1 > Chap 24- Endocrine System > Flashcards

Chap 24- Endocrine System Flashcards

1
Q

classifications of hormones

A
  • peptide or AA

- steroid hormones

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

how do AA hormones work?

A

interact with cell surface receptors

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

how do steroid hormones work?

A

diffuse across plasma membranes and interact with intracellular receptors

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

pituitary gland

A
  • made up of anterior and posterior lobes
  • anterior lobe is 80% of gland
  • controlled by hypothalamus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

anterior lobe of pituitary gland

A
  • hormone production controlled by hypothalamus

- carried via portal vascular system

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

posterior lobe of pituitary

A
  • made of modified glial cells and axonal processes extending form hypothalamus
  • oxytocin and ADH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

hormones that come from anterior pituitary

A
  • TSH
  • ACTH
  • FSH
  • LH
  • GH
  • Prolactin
  • Endorphines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

hyperpituitarism

A
  • most commonly anterior pituitary adenoma
  • can be due to:
  • proto-oncogene mutations
  • loss of tumor suppressor genes
  • proliferative pituitary cells
  • epigenetic modifications
  • other promoting factors
  • clinical cours depends on hormones affected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

hypopituitarism

A
  • decreased secretion of pituitary hormones

- due to diseases of hypothalamus or pituitary

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

causes of hypopituitarism

A
  • hypothalamic diseases caused by mass lesions, radiation, infections
  • pituitary diseases caused by mass lesions, pituitary surgery, or pituitary radiation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

clinical features of hypopituitarism

A
  • depends on what hormones are affected
  • growth failure due to GH deficiency
  • LH and FSH can cause amenorrhea, infertility, impotence, decreased libido
  • hypothyroidism and hypoadrenalism
  • failure of postpartum lactation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are the posterior pituitary syndromes?

A
  • central diabetes insipidus

- SIADh

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

central diabetes insipidus

A
  • excessive urination due to inability of kidney to resorb water from urine
  • cause- ADH deficiency
  • mostly idiopathic cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

SIADH

A
  • syndrome of inappropriate ADH
  • increased ADH
  • resorption of too much water, results in hyponatremia
  • Na in blood is “less” due to excessive dilution
  • causes- ADH neoplasms, drugs that increase ADH secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

thyroid gland

A
  • two lobes connected by isthmus
  • two major cell types are follicular cells and C cells
  • hormones cannot be produced without iodine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

thyroid follicular cells

A
  • convert thyroglobulin into thyroxine (T4) and triiodothyronine (T3)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Thyroid C cells

A
  • synthesize and secrete calcitonin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the role of calcitonin?

A
  • promotes absorption of Ca in skeletal muscle

- inhibits resorption of bone by osteoclasts

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

feedback control of thyroid hormones

A
  • homeostasis is disturbed
  • hypothalamus releases TRH
  • pituitary releases TSH
  • TSH effects thyroid and produces T3 and T4
  • T3 and T4 increase basal metabolic rate
  • levels raise is blood and homeostasis is restored
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

hyperthyroidism

A
  • hypermetabolic state due to increased levels of T3 and T4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is radioiodine uptake? (RAIU)

A
  • test to see how reactive thyroid glands/ how much iodine they take
  • active- take more iodine because it is required to produce T3 and T4
  • near absent uptake indicates inflammation and destruction of thyroid tissue or extrathyroidal source of thyroid hormones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

hyperthyroidism with high radioiodine uptake cause

A
  • autoimmune thyroid disease- graves

- autonomous thyroid tissue- multinodular goiter

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

hyperthyroidism with near absent radioiodine uptake cause

A
  • thyroiditis
  • exogenous thyroid hormone intake
  • ectopic hyperthyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

graves disease

A
  • triad: hyperthyroidism, goiter, eye disease (protruded eyes)
  • hyperthyroidism is most common feature of graves
  • cause- autoantibodies TRAb stimulate thyroid hormone production and thyroid growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

types of thyrotropin receptor antibodies (TRAb)

A
  • stimulating- majority of pts with graves
  • blocking- results in hypothyroidism
  • neutral
  • some pts have mix of TRAb so clinical presentation depends on balance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

pathogenesis of hyperthyroidism

A
  • thyroid cells turn into antigen presenting cells (MHC Class II) due to insults like inflammation
  • class II molecule expressen presents thyroid antigens to/activates autoreactive T cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

predisposing factors to graves disease

A
  • association with certain alleles of HLA
  • infections of thyroid gland itself
  • stress induced immune suppression and rebound immunologic hyperactivity
  • moderate levels of estrogen
  • post-partum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

clinical manifestations of graves

A
  • eyes protrude outward due to adipogensis and hyaluronic acid production
  • warm and smooth skin
  • increased sweating
  • onycholysis- softening of nails
  • increased HR, contractility, LVEF, CO
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

autonomous thyroid tissues

A
  • benign condition
  • clinically present as single nodule that is hyperfunction or “hot” on scan
  • caused by mutation in TSH
  • most that are “hot” are benign
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

multinodular goiters

A
  • most common benign thyroid tumors

- main issue is whether they are cancerous, whether or not they cause thyroid dysfunction

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

goiter

A
  • abnormal growth of thyroid gland
  • can be diffuse or nodular
  • diffuse- entire gland is big
  • nodular- localized region of thyroid gland is enlarged
  • can be nontoxic or toxic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

etiology of goiter

A
  • iodine deficiency is most common cause worldwide

- mix of genetic and environmental factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

thyroiditis

A
  • transient hyperthyroidism due to inflammation

- can be acute, subacute, or chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

acute thyroiditis cause

A

due to bacterial infection- staph aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

subacute thyroiditis cause

A
  • viral infection of the gland
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

chronic thyroiditis

A
  • usually autoimmune disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

thyroid storm

A
  • rare but life threatening condition
  • extreme/ exaggerated amount of hormones produced
  • usually occurs in untreated thyrotoxosis who experience surgery, infection, or trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

hypothyroidism

A
  • thyroid function at suboptimal level
  • primary- thyroid disease causes decreased T3 and T4, increased levels of TSH
  • secondary- decreased TSH or decreased TRH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

chronic autoimmune thyroiditis/ Hashimoto’s

A
  • most common cause of hypothyroidism in iodine sufficient parts of world
  • caused by cell and antibody mediated destruction of thyroid
40
Q

pathophysiology of hashimoto’s

A
  • compromised function of Treg cells and increased activity of follicular T helper cells
  • DNA fragments and altered miRNA profile
  • cells destroyed via destruction or apoptosis
41
Q

risk factors for Hashimoto’s

A
  • more common in women
  • most common cause of hypothyroidism in children
  • polymorphism in genes for HLA
  • genetic factors
42
Q

graves disease vs. Hashimoto’s

A
  • graves- thryoid cells are overactivated

- hashimoto’s- cell death causes not enough thyroid hormone release

43
Q

types of thyroid carcinomas

A
  • papillary cancer- most common
  • follicular cancer
  • anaplastic (undifferentiated) cancer
44
Q

pathogenesis of thyroid carcinoma

A
  • due to accumulation of multiple genetic factors
  • mutation in oncogenes and tumor suppressor genes -> differentiated thyroid follicle can cause well differentiated papillary or follicular carinomas -> poorly differentiated carinoma -> anaplastic carcinoma
45
Q

papillary carinomas

A
  • biggest risk factor- radiation exposure of thyroid during childhood
  • family history is also cause
  • usually asymptomatic
  • first manifestation may be mass in cervical lymph node
  • clinical features: hoarseness, dysphagia, cough, dyspnea
46
Q

parathyroid glands

A
  • made of two types of cells
  • chief cells- mainly produce PTH
  • oxyphil cells- unknown function
47
Q

selective function of calcium ion

A
  • bone mineralization
  • muscle contraction
  • co-factor for blood coagulation
48
Q

selective function of phosphate ion

A
  • formation of ATP
  • important intracellular anion
  • major components of DNA/ RNA and membrane bilayer
  • bone mineralization
49
Q

how are calcium and phosphate ions related?

A
  • inverse relationship

- Ca goes up and phosphate goes down, vice versa

50
Q

role of vitamin D in Ca and phosphate concentrations

A
  • increases absorption of Ca in gut

- increases release of Ca and phosphate from bones

51
Q

role of PTH in Ca and phosphate concentrations

A
  • increases release of Ca and phosphate from bones
  • increases Ca reabsorption
  • phosphate excretion by kidneys
  • increased production of active vit d can inhibit PTH
52
Q

FGF 23 role in Ca and phosphate concentrations

A
  • increase phosphate excretion by kidneys
53
Q

hyperparathyroidism

A
  • caused be elevated parathyroid hormone (PTH)

- primary, secondary, or tertiary

54
Q

primary hyperparathyroidism

A
  • autonomous overproduction of PTH
  • caused by adenoma in most cases
  • can also be caused by hyperplasia or parathyroid carcinoma
  • important cause of hypercalcemia
55
Q

secondary hyperparathyroidism

A
  • compensatory hypersecretion of PTH in response to prolonged hypocalcemia
  • due to chronic kidney failure
56
Q

tertiary hyperparathyroidism

A
  • persistent hypersecretion of PTH

- happens even after hypocalcemia is corrected i.e. after renal transplant

57
Q

altered calcium sensing on PTH secretion

A
  • determination of serum calcium
  • mutation in calcium receptor- can either activate or inactivate
  • decreased sensitivity to calcium
58
Q

causes of hypercalcemia

A
  • primary hyperparathyroidism *
  • secondary and tertiary hyperparathyroidism
  • hypercalcemia of malignancy
59
Q

hypercalcemia in primary hyperparathyroidism

A
  • PTH mediated activation of osteoclasts -> increased bone resorption
  • intestinal Ca absorption is increased
60
Q

hypercalcemia of malignancy

A
  • most common tumor causes- breast Ca, multiple myeloma, lymphoma, squamous cell cancers
  • tumor secretion of parathyroid hormone related proteins (PTHrP)
  • osteolytic metastases and cytokine release
  • tumor production of 1,25 dihydoxy vit D
61
Q

clinical course of primary hyperparathyroidism

A
  • usually asymptomatic
  • identified on routine blood chemistry profiles
  • painful bones, renal stones, abdominal groans, psych moans
  • excessive resoprtion of Ca -> osteopenia
  • increased excretion of Ca in urine -> kidney stones
62
Q

most common cause of secondary hyperparathyroidism

A
  • renal failure most common cause aka chronic kidney disease- mineral and bone disorder
  • results in chronic hypocalcemia
63
Q

manifestation of secondary hyperparathyroidism

A
  • hypocalcemia
  • phosphate retention
  • increased FGF23 -> increased excretion of phosphate from kidneys
  • decreased vit D
  • abnromal bone turnover, mileralization, growth, strength
  • extraskeletal calficifaction
64
Q

what is extraskeletal calcification?

A
  • calcification of arteries
  • increased levels of phosphate changes SMC to osteoblasts
  • happens in secondary hyperparathyroidism
65
Q

hypoparathyroidism

A
  • PTH not made
  • caused by destruction of gland, abnormal development, or altered regulation of PTH
  • usually is aquired due to surgical or autoimmune damage
66
Q

clinical features of hypoparathyroidism

A
  • related to severity and chronicity of hypocalcemia
  • tetany
  • test with Chvostek sign and trousseau sign
67
Q

Chvostek’s sign

A
  • mechanical stimulation of motor fibers in facial nerve

- tap near PTs ear and they will twitch

68
Q

Trosseau’s sign

A
  • increased excitability of nerves in arm and forearm
  • caused by hypocalcemia
  • occlude brachial artery with pressure cuff -> anaerobic metabolism -> increased excitability
69
Q

components of adrenal glands

A
  • adrenal cortex- outer layer
  • adrenal medulla- middle layer
  • chromaffin cells- produce catecholamines
70
Q

types of steroids synthesized in adrenal cortex

A
  • glucocorticoids- cortisol
  • mineralcoricoids- aldosterone
  • sex setroids- estrogens and androgens
71
Q

feedback in adrenal glands

A

sense glucocorticoids are low -> signal hypothalamus -> release CRH -> goes to adrenal gland -> release glucocorticoids

72
Q

functions of cortisol

A
  • break down of adipose tissue
  • reduces bone formation
  • glucose generation in liver
  • decrease AA uptake in muscles
  • counteracts insulin
73
Q

overproduced hormones in hyperadrenalism

A
  • excess cortisol -> cushing’s syndrome
  • excess aldosterone -> hyperadolsteroneism
  • excess androgens -> adrenogenital syndromes
74
Q

what is the purpose of the circadian clock system?

A
  • regulate glucocorticoid secretion based on environmental changes
75
Q

parts of circadian clock

A
  • central master clock- aka SCN in hypothalamus

- adrenal peripheral clocks in all organs and tissues

76
Q

what does the circadian clock regulate?

A
  • central clock controls HPA axis
  • creates diurnal oscillation of hormones and cortisol
  • HPA axis adjusts daily rhythms of glucocorticoids
  • synchronizes other peripheral clocks
77
Q

functions of glucocortioids

A
  • synchronization of circadian clocks
  • decrease immune and inflammation
  • congition
  • increase depression and anxiety
  • decrease growth and reproduction
  • increase CV tone
  • increase gluconeogensis, lipolysis, and proteolysis
78
Q

Cushing’s syndrome

A
  • hypercortisolism

- either endogenous or exogenous

79
Q

types of endogenous cushing’s syndrome

A
  • ACTH dependent

- ACTH independent

80
Q

ACTH- dependent Cushing’s syndrome

A
  • no up and down of cortisol levels, remains high
  • usually due to pituitary adenoma
  • ACTH secretion not regulated by hypothalamus
  • increased ACTH -> hyperplasia and hypersecretion of cortisol -> normal circadian rhythm lost
81
Q

possible mechanism of Cushing’s disease

A
  • abnormalities in gluccocorticoid receptor
  • abnormal expression of enzyme that converts cortisol to cortisone
  • inappropriate repression/ expression of certain genes i.e. POMC gene
82
Q

what is the most common cause of hypercortisolism?

A

ingestion of prednisone, usually for non-endocrine reasons

83
Q

clinical features of Cushing’s syndrome

A
  • weight gain
  • moon face
  • buffalo hump
  • stretch marks on skin due to inhibition of collagen synthesis
  • neuroskeletal defects
  • neuropsych abnormalities
84
Q

Cushing’s syndrome and diabetes

A
  • glucoccorticoids effect insulin sensitivity
  • tissues become unresponsive to insulin
  • insulin secretion also impaired
  • causes hyperglycemia
85
Q

primary aldosteronism

A
  • type of hyperadrenalinism
  • caused by too much aldosterone
  • too much aldosterone -> Na retention -> HTN
  • cause is usually idiopathic, adenoma, or increased sensitivity of aldosterone in kidney
86
Q

adrenal insufficiency

A
  • destruction of adrenal cortex and reduction of adrenal hormones
  • primary insufficiency- Addison’s autoimmune disease
  • Secondary insufficiency- inadequate pituitary or hypothalamic stimulation of adrenal glands
87
Q

pathogenesis of adrenal insufficiency

A
  • humoral immunity: presence of antibodies in serum
  • cellular immunity: T cells produce interferon gamma, cytotoxic T cells and activated macrophages cause destruction of adrenal cortex
  • genetic susceptibility strongly associated with HLA
88
Q

Symptoms of Addison’s disease

A
  • hyper pigmentation due to excess ACTH secretion which stimulates melanocytes
  • hypotension due to volume depletion from aldosterone deficiencty
89
Q

adrenal crisis

A
  • sudden worsening of adrenal insufficiency sx
  • main feature- shock
  • can be caused by infection, major stress, after bilateral adrenal infarction, pt who abruptly stop doses of glucocorticoids
90
Q

pheochromocytoma

A
  • excess catecholamines due to tumor
  • neoplasm of chromaffin cells
  • concentration of DA, NE, and E varies based on tumor
91
Q

clinical features of pheochromocytoma

A
  • triad:
  • headaches
  • palpitations
  • sweating
  • results in life threatening hypertensive emergencies
92
Q

Sustained hypertension in pheochromocytoma

A
  • continuous release of NE -> constant vasoconstriction

- pts experience orthostatic hypotension

93
Q

paroxysmal hypertension in pheochromocytoma

A
  • sporadic, sudden release of E that is unpredictable

- can happen due to physical stress, emotional stress, smoking, etc.

94
Q

pineal gland

A
  • made of pineocytes
  • photosensory and neuroendocrine fns
  • main product- melatonin
95
Q

melatonin

A
  • made from AA tryptophan
  • serotonin is intermediate between tryptophan and melatonin
  • secreted into blood and cerebrospinal fluid
  • transfers signals to the brain about sleep and circadian rhythms
96
Q

melatonin physiology

A
  • daylight- serotonin is stored
  • darkness- release NE and causes stored serotonin to become accessible
  • NE activates enzyme that converts serotonin to melatonin
  • melatonin levels rise in blood and diffuse across BBB
  • shows circadian rhytm

Patho 1 (12 decks)

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