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Disease Mechanisms > Ch 24: Endocrine System > Flashcards

Ch 24: Endocrine System Flashcards

1
Q

what are two main features of endocrine glands

A

ductless
secrete hormones directly into the bloodstream

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2
Q

what are the two main classes of hormones

A

amino-acid hormones
steroid hormones

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3
Q

what are amino-acid hormones

A

one or more amino acids ranging in size
generally are hydrophilic
hydrophilic and must bind to a receptor on the outisde of a cell

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4
Q

what are the three types of amino-acid hormones

A

amines
peptides
proteins

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5
Q

what is a type of amine

A

norepinephrine

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6
Q

what are the two types of negative acting hormones

A

prolactin inhibiting factor (PIF) - dopamine
somatostatin (SST)
their release prevents release of other things

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7
Q

what is a type of peptide

A

oxytocin

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8
Q

what is a type of protein

A

growth hormone

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9
Q

what is a hydrophilic hormone

A

a hormone that loves water and can travel throughout the blood
cannot get into a cell without binding to plasma membrane receptors

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10
Q

what are steroid hormones

A

hormones that are derived from cholesterol
generally hydrophobic and travel unbound

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11
Q

what are three types of steroid hormones

A

cortisol
testosterone
aldosterone

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12
Q

what is a hydrophobic steroid hormone

A

hormones that can cross cell membrane
travels bound to a protein
once inside cell, it binds to receptor in cytosol or on nucleus

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13
Q

what are the four main mechanisms of hormone regulation

A

they have specific rates and rhythms of secretion
they affect only cells with appropriate receptors
they operate within feedback systems
they’re excreted directly by kidneys or metabolized by the liver

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14
Q

how are hormones transported

A

via vessels, specifically the hypothalamic hypophyseal portal system

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15
Q

what is the struture of the hypothalamic hypophyseal portal system

A

vein
capillary
vein
capillary

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16
Q

what is a primary endocrine organ

A

one that has only endocrine functions

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17
Q

what are 5 examples of primary endocrine organs

A

anterior pituitary
thyroid
parathyroid
thymus
adrenal cortex

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18
Q

what is a secondary endocrine organ

A

belongs to another system but produces hormones

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19
Q

what are 7 examples of secondary endocrine organs

A

pancreas
ovaries
testes
hypothalamus
pineal gland
posterior pituitary gland
adrenal medulla

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20
Q

what is a neuroendocrine organ

A

organ made of nervous tissue but secretes chemicals that acts as neurohormones
stimulated by the nervous system

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21
Q

what are the four types of neuroendocrine organs

A

hypothalamus
pineal gland
posterior pituitary gland
adrenal medulla

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22
Q

what is the hypothalamic pituitary axis

A

complex neuroendocrine system that plays a central role in regulating a variety of physiological processes

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23
Q

what are four main functions of the hypothalamus

A

controls all hormones secreted by the pituitary gland
controls ANS
thermoregulation
regulation of feeding and thirst

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24
Q

how does the hypothalamus control hormones secreted by the pituitary gland

A

releases stimulating hormones which stimulate their release
releases inhibiting hormones like prolactin release inhibiting hormone (PRIH) and dopamine

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25
Q

which endocrine organ is the major regulatory of the body

A

hypothalamus

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26
Q

which endocrine gland is the master gland

A

pituitary gland

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27
Q

where is the pituitary gland found and what is it covered with

A

sella turcica of sphenoid bone
covered in diaphragma sella

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28
Q

what is the other name for the anterior pituitary

A

adenohypophysis

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29
Q

what is the other name for the posterior pituitary

A

neurohypophysis

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30
Q

which part of the pituitary gland, anterior or posterior, makes up 80% of the gland

A

anterior pituitary (adenohypophysis)

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31
Q

what are the 6 hormones released by the anterior (adenohypophysis) pituitary

A

growth hormone (GH)
adrenocorticotropic hormone (ACTH)
thyroid-sitmulating hormone (TSH)
gonadotropic hormones (LH and FSH)
melanocyte-stimulating hormone (MSH)
prolactin (PRL)

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32
Q

what are the two hormones released by the posterior (neurohypophysis) pituitary

A

oxytocin (OT)
antidiuretic hormone (ADH)

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33
Q

what is a somatotroph

A

cell of the pituitary stimulated by growth hormone releasing hormone (GHRH) to produce growth hormone (GH)
inhibited by somatostain (SST) to stop releasing growth hormone (GH)

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34
Q

what is a lactotroph

A

cell in pituitary
stimulated by prolactin-releasing hormone (PRH) to release prolactin (PRL)
inhibited by dopamine (PIF) to stop releasing prolactin (PRL)

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35
Q

what hormone inhibits the production of growth hormone by a somatotroph

A

somatostatin

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36
Q

what hormone inhibits the production of prolactin by a lactotroph

A

dopamine (prolactin inhibiting factor)

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37
Q

what is a corticotroph

A

cell in the pituitary
stimulated by corticotropin-releasing hormone (CRH) to produce adrenocorticotopic hormone (ACTH)
also makes pro-opiomelanocortin (POMC) which eventually leads to melanocyte-stimulating hormone (MSH)

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38
Q

what is a thyrotroph

A

cell of pituitary
stimulated by thyrotropin releasing hormone (TRH) to produce thyroid-stimulating hormone (TSH)

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39
Q

what is a gonadotroph

A

cell of pituitary
stimulated by gonadotropin-releasing hormone (GnRH) to produce follicle stimulating hormone (FSH) and leutinizing hormone (LH)

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40
Q

how is melanocyte-stimulating hormone (MSH) produced

A

corticotrophs produce pro-opiomelanocortin (POMC)
POMC is cleaved into adrenocorticotropic hormone (ACTH)
ACTH is the precursor to melanocyte-stimulating hormone (MSH)

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41
Q

where are antidiuretic hormone (ADH) and ocxytocin (OT) made and stored

A

made by the hypothalamus
stored in synaptic vesicles in axon terminals of hypothalamus
released into blood vessel from posterior pituitary

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42
Q

when is antidiuretic hormone (ADH) released and what does it do

A

released in response to high blood solute concentration or low blood volume
promotes reabsorption of salt and water in the kidney

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43
Q

what stimulates the release of oxytocin (OT) from the posterior pituitary

A

suckling of an infant
stretching of certix or uterus
both tell the hypothalamus to tell the posterior pituitary to release oxytocin

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44
Q

what are the two main posterior pituitary disorders

A

syndrome of inappropriate ADH secretion (SIADH)
diabetes insipidus (DI)

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45
Q

what is syndrome of inappropriate ADH secretion (SIADH) and what are some of its symptoms

A

hypersecretion of ADH from the posterior pituitary
symptoms: headache, seizures, confusion, fatigue, lethargy, and decreased urine output

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46
Q

what are the three main causes of syndrome of inappropriate ADH secretion (SIADH)

A

malignant neoplasms
drug-induced
CNS disorders (infections and trauma)

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47
Q

what type of malignant neoplasm can cause syndrome of inappropriate ADH secretion (SIADH)

A

small cell lung carcinoma

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48
Q

which two types of drugs can cause syndrome of inappropriate ADH secretion (SIADH)

A

carbamazepine
selective serotonin reuptake inhibitors (SSRI)

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49
Q

what is the mechanism of syndrome of inappropriate ADH secretion (SIADH)

A

too much ADH causes reabsorption of water which dilutes sodium levels in the blood (hyponatremia)
diluted blood leads to cerebral edema, neurological dysfunction, and coma

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50
Q

what is hyponatremia

A

low sodium levels in the blood

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51
Q

what are the two types of diabetes insipidus (DI)

A

neurogenic
nephrogenic

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52
Q

what is neurogenic diabetes insipidus

A

most common type of diabetes insipidus
hyposecretion of ADH from posterior pituitary

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53
Q

what are five causes of neurogenic diabetes insipidus (DI)

A

tumors
inflammatory disorders of hypothalamus and pituitary
head trauma
surgical complications of hypothalamus and pituitary
mutation of AVP gene

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54
Q

what is nephrogenic diabetes insipidus (DI)

A

least common type of diabetes insipidus
renal tubule unresponsive to circulating ADH
two types: acquired vs genetic

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55
Q

what are the four causes of aquired nephrogenic diabetes insipidus

A

chronic kidney disorders
lithium carbonate
colchicine
general anesthetics

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56
Q

what are the two causes of genetic nephrogenic diabetes insipidus

A

mutation of AVPR2 gene (V2 receptor protein)
mutation of aquaporin-2 (AQP2)

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57
Q

what is the most common genetic cause (90%) of nephrogenic diabetes insipidus

A

mutation of AVPR2 gene (V2 receptor protein)

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58
Q

what is the mechanism of diabetes insipidus (DI)

A

excretion of large volumes of water dilutes your blood and leads to hypernatremia and hyperosmolality
both cause dehydration

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59
Q

what is hypernatremia

A

excess sodium in the blood

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60
Q

what are the three main symptoms of diabetes insipidus (ID)

A

polyuria
thirst
polydipsia

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61
Q

what is polyuria

A

excess dilute urine output

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62
Q

what is polydipsia

A

excess thirst

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63
Q

what is hypopituitarism

A

deficiency of anterior pituitary hormones

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64
Q

what is hyperpituitarism

A

overproduction of anterior pituitary hormones

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65
Q

what is the most common cause of hypopituitarism

A

traumatic brain injury leading to a subarachnoid hemorrhage

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66
Q

what is Sheehan syndrome

A

cause of hypopituitarism
pituitary loses blood supply during a post-birth hemorrhage
leads to ischemic necrosis of gland

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67
Q

what is pituitary apoplexy

A

cause of hypopituitarism
acute hemorrhage due to rapidly growing pituitary adenoma

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68
Q

what is a rathke cleft cyst

A

cause of hypopituitarism
pituitary cyst that accumulates proteinaceous fluid and explands

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69
Q

what are hypothalamic lesions and what do they cause

A

benign or malignant tumors of the hypothalamus
affect the entire pituitary gland and lead to hypopituitarism

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70
Q

metastases to the hypothalamus of which two malignant tumors leads to hypopituitarism

A

metastases of breast and lung carcinomas

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71
Q

which type of infection can cause hypopituitarism

A

tuberculous meningitis

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72
Q

which rare genetic defect can cause hypopituitarism

A

mutation of PIT1 gene which leads to a decrease in GH, PRL, and TSH production

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73
Q

what is empty sella syndrome

A

iatrogenic cause (surgery or radiation) casues damage to the pituitary gland which leads to hypopituitarism

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74
Q

what is the mechanism of primary empty sella syndrome

A

cause of hypopituitarism
defected in diaphragma sella (dura covering) allows arachnoid mater and CSF to herniate
herniation leads to expansion of sella and compression of gland

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75
Q

who is most at risk for primary empty sella syndrome

A

obsese women with history of multiple pregnancies

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76
Q

what is the mechanism of secondary empty sella syndrome

A

cause of hypopituitarism
after a sella mass is removed, pituitary gland undergoes sponatenous necrosis

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77
Q

what is panhypopituitarism

A

absense of all pituitary hormone production

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78
Q

what percentage of lost pituitary parenchyma is considered hypofunction

A

75%

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79
Q

what does a deficiency in growth hormone lead to

A

dwarfism in children

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80
Q

a gonadotropin deficiency leads to which four things

A

amenorrhea (loss of period)
infertility
impotence (inability to get an erection)
loss of pubic and armpit hair in men

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81
Q

what does a thyroid stimulating hormone (TSH) deficiency lead to

A

hypothyroidism which leads to things like tiredness, coldness, weight gain, and depression

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82
Q

what does a deficiency in prolactin lead to

A

failure to lactate after birth

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83
Q

what does an adrenocorticotropin hormone deficiency lead to

A

hypoadrenalism which leads to weakness, fatigue, low blood pressure, and pallor
lack of cortisol and aldosterone production as well as deficient melanocyte function

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84
Q

what is cortisol important for

A

cellular metabolism

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85
Q

what 3 things happen when you have a cortisol deficiency due to an adrenocorticotropic hormone deficieny

A

hypoglycemia
depletion of glycogen stores
decreased gluconeogenesis

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86
Q

what is hyperpituitarism

A

over production of anterior pituitary hormone

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87
Q

what is the most common cause of hyperpituitarism and what does it cause

A

pituitary adenoma on the anterior lobe which causes excess hormone secretion

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88
Q

adenomatous tumors secrete how many hormones and which is the most common type of hormone

A

usually just two hormones
most commonly, prolactin
secrete hormones from cell type they arised from

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89
Q

what is acromegaly

A

a type of hyperpituitarism
large stature due to a somatotroph adenoma that releases excessive levels of growth hormone
elevation of insulin-like growth factor 1 (IGF-1)
exposure to these excessive levels comes after the epiphyseal plates close

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90
Q

what is giantism

A

somatotroph adenoma causes excessive production of growth hormone and elevated levels of IGF-1
exposure to these excessive levels comes before the epiphyseal plates close

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91
Q

who is more at risk, men or women, for acromegaly

A

females
tend to get diagnosed later in life

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92
Q

what are six clinical features of acromegaly

A

bony proliferation (hands, feet, and face)
hyperglycemia (insulin resistance)
arthritis
thick skin (skin tags)
congestive heart failure
increased risk of GI tumors

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93
Q

how is acromegaly treated

A

tumor in anterior pituitary is removed

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94
Q

what is a prolactinoma

A

benign, anterior pituitary lactotroph adenoma that secretes prolactin

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95
Q

what are the four signs of a prolactinoma in women

A

amenorrhea (lack of period)
infertility
galactorrhea
osteopenia (loss of bone mass)

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96
Q

what is galactorrhea

A

milky white discharge from breasts seen in those with prolactinomas

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97
Q

what are the two signs of a prolactinoma in men

A

hypogonadism
erectile dysfunction

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98
Q

what are the four roles of prolactin

A

mammary gland growth
initation of milk production
maintenance of milk production
shuts down gonadotropin-releasing hormone pathway

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99
Q

what are the 3-5 parathyroid glands derived from

A

pharyngeal pouches

100
Q

what are the two types of cells of the parathyroid glands

A

chief cells
oxyphil (transitional) cells

101
Q

what hormone is secreted from the chief cells of the parathyroid

A

parathyroid hormone (PTH)

102
Q

how much do the parathyroid glands weigh in total

A

25-40 mg

103
Q

what is the main function of parathyroid hormone (PTH) that is realased from the chief cells of the parathyroid glands

A

regulates calcium levels by raising them if they’re too low

104
Q

what are the four effects of parathyroid hormone (PTH)

A

increases release of calcium ions from bone
causes kidneys to convert vitamin D into its active form
increases renal tubuluar reabsorption of calcium
increases urinary phosphate excretion

105
Q

what is the active form of vitamin D

A

calcitriol (vitamin D3)

106
Q

what does calcitriol do

A

increases absorption of dietary calcium from small intestine

107
Q

what is primary hyperparathyroidism

A

overproduction of parathyroid hormone usually due to an adenoma

108
Q

what are the three causes of primary hyperparathyroidism

A

adenoma that secretes parathyroid hormone (most common 85-85% of cases)
hyerplasia of parathyroid cells
parathyroid carcinoma (least common <1%)

109
Q

who is most at risk for primary hyperparathyroidism

A

older women (4:1)

110
Q

what is the most common clinical feature of primary hyperparathyroidism

A

hypercalcemia (too much calcium in blood)
body is responding to excessive PTH by releasing excessive amounts of calcium

111
Q

what is secondary hyperparathyroidism

A

prolonged deficiency in calcium causes a hypersecretion of parathyroid hormone
seen mostly in cases of chronic renal failure

112
Q

what is tertiary hyperparathyroidism

A

patient experiences prolonged calcium deficiency and are given a renal transplant
hypersecretion of parathyroid hormone (PTH) despite having the renal transplant

113
Q

what is the saying for symptoms of primary hyperparathyroidism

A

painful bones, renal stones, abdominal groans, and psychic moans

114
Q

what are six symptoms of primary hyperparathyroidism

A

bone disease, pain, and fractures due to demineralization
nephrolithiasis (kidney stones) which can cause obstruction
GI disturbances like constipation
CNS alterations like confusion and memory loss
neuromuscular issues like weakness and fatigue
aortic or mitral valve calcification

115
Q

what is the mechanism of secondary hyperparathyroidism

A

chronic disease state like chronic renal failure leads to chronic hypocalcemia (decreased calcium levels)
hypocalcemia leads to hyperplasia of parathyroid
excess of parathyroid cells leads to increase in parathyroid hormone (PTH) secretion

116
Q

what are the four causes of secondary hyperparathyroidism

A

chronic renal failure (most common)
intestinal malabsorption
vitamin D deficiency
paraneoplastic syndrome

117
Q

what are paraneoplastic syndromes

A

tumors that ectopically produce parathyroid related protein (PTHrP)
cause of secondary hyperparathyroidism

118
Q

what are the three ways to treat secondary hyperparathyroidism

A

treat underlying cause
increase calcium levels with calcium and vitamin D replacements
phosphate binders

119
Q

what is the main cause of hypoparathyroidism

A

rare but usually caused by unintentional removal of parathyroid glands during thyroid or neck surgery

120
Q

what are four lesser common causes of hypoparathyroidism

A

congenital absence of thyroid
familial isolated (inherited)
dominant mutation in CASR gene
autoimmune (body attacks endocrine organs)

121
Q

in which syndrome is there a congenital absence of the thyroid leading to hypoparathyroidism

A

DiGeorge syndrome

122
Q

what happens in a mutation of the CASR gene

A

calcium-sensing receptor is mutated and has a gain of function
your body thinks you have enough calcium so it supresses PTH, eventually leading to hypocalacemia

123
Q

what are two conditions caused by hypoparathyroidism

A

hypocalacemia
hyperphosphatemia

124
Q

what are four symptoms of hypoparathyroidism

A

cardiac issues (tetany)
dental abnormalities (enamel)
basal ganglia calcification
mental status change

125
Q

what two hormones are secreted by the thyroid gland

A

thyroid hormone (T4 and T3)
calcitonin

126
Q

what are the three main stimuli that trigger the release of thyrotropin releasing hormone (TRH) from the hypothalamus

A

decreased levels of thyroid hormone (T3 and T4) in blood
exposure to cold
rapid growth and development

127
Q

what is the weight of a thyroid gland in an adult

A

10-30g

128
Q

which cells of the thyroid gland secrete thyroid hormone (T4 and T3)

A

follicular cells

129
Q

which cells of the thyroid gland secretes calcitonin

A

parafollicular cells

130
Q

what is the thyroid hormone T4 (90%)

A

thyroxine

131
Q

what is the thyroid hormone T3 (10%)

A

triiodothyronine (active derivative)

132
Q

what two things does calcitonin do

A

lowers calcium levels if they’re too high
prevent bone breakdown

133
Q

how do T4 and T3 work

A

T4 is converted to T3
T4 and T3 act on nulcear receptors to increase metabolism up to 100%

134
Q

what are the three types of thyroid disorders

A

hyperthyroidism
hypothyroidism
lesions of thyroid

135
Q

what is thyrotoxicosis

A

hypermetabolic state caused by excess thyroid hormones (T3 and T4)
associated with hyperthyroidism
can be primary or secondary

136
Q

what is an example of secondary hyperthyroidism

A

pituitary tumor that secretes TSH

137
Q

what are the three main causes of primary hyperthyroidism

A

diffuse hyperplasia
hyperfunctioning (toxic) multinodular goiter
hyperfunctioning (toxin) adenoma

138
Q

what is an example of diffuse hyperplasia

A

graves disease

139
Q

how does toxic multinodular goiter appear under a radioactive iodine uptake test

A

thyroid is enlarged with areas of darkly staining nodules

140
Q

how does a thyroid with graves disease appear under a radioactive iodine uptake test

A

thyroid is homogenously darkened minus the periphery

141
Q

how does a toxic adenoma appear under a radioactive iodine uptake test

A

thyroid has one singular darkly staining nodule

142
Q

what do the dark areas in a radioactive iodine uptake test indicate

A

area of hormone hypersecretion

143
Q

what are the four systemic clincial manifestations of someone with hyperthyroidism

A

warm skin
heat intolerance
sweating
weight loss

144
Q

what is the GI clinical manifestation of hyperthyroidism

A

hypermobility which leads to malabsorption, steatorrhea (fat in stool), and hepatomegaly

145
Q

what is a cardiac clincial manifestation of hyperthyroidism

A

tachycardia with palpatations

146
Q

who with hyperthyroidism is most at risk for cardiac clinical manifestations

A

older individuals with A. fib and congestive heart failure

147
Q

what are four neuromuscular clincial manifestations of hyperthyroidism

A

tremor
anxiety
proximal muscle weakness
loss of muscle mass

148
Q

what are the two, ocular clinical manifestations of hyperthyroidism

A

wide staring gaze
lid lag (lids cannot close all the way)

149
Q

what is the main skeletal clinical manifestation of hyperthyroidism

A

bone reabsorption which leads to osteoporosis (more fractures and muscle atrophy)

150
Q

what are 6 general clincial manifestations of hyperthyroidism

A

pretibial myxedema
oligomenorrhea (irregular periods)
goiter
emotional issues
insomnia
fine hair

151
Q

what is a thyrotoxic crisis (storm)

A

abrupt onset of severe hyperthyroidism due to some stressor that is most common in graves disease
can be fatal if not treated quickly

152
Q

what are three stressors that can cause a thyrotoxic crisis (storm) and how does it happen

A

infection
surgery
cessation of antithyroid medication
all cause acute elevation of catecholamines and lead to the storm

153
Q

what are the two main symptoms of a thyrotoxic crisis (storm)

A

tachycardia
fever out of proportion

154
Q

what is graves disease

A

diffuse hyperplasia that causes primary hyperthyroidism
autoimmune disease that invovles over active thyroid (hyperthyroidism)
usually occurs in women and those 20-40 years old

155
Q

what is the pathogenesis of graves disease

A

autoimmunity causes stimulation of thyroid stimulating immunoglobin autoantibodies
TSI autoantibodies bind to TSH receptor on thyroid follicular cells
binding causes uncontrolled production of T4 and T4
no negative feedback to pituitary

156
Q

what are the lab findings in someone with graves disease

A

increased free T3 and T4 in serum
decreased TSH in serum

157
Q

what are the three main clinical findings of graves disease

A

diffuse enlargement of thyroid gland
infiltrative ophthalmopathy
localized, infiltrative dermopathy (pretibial myxdema)

158
Q

what are the 2 mechanisms of infiltrative ophthalmopathy of graves disease

A

T helper cells cause fibroblast proliferation and synthesis of ECM protein
leads to progressive infiltration of retroorbital space

accumulation of loose CT behind the eye causes protuberant appearence

159
Q

what is localized, infiltrative dermopathy (pretibial myxedema)

A

symptom of graves disease
scaly thickening on shins

160
Q

what are the three primary causes of hypothyroidism

A

autoimmune thyroid disease
congenital defects
iatrogenic (surgery, drugs, radiation)

161
Q

what is the most common cause of primary hypothyroidism

A

hashimoto thyroiditis - an autoimmune thyroid

162
Q

what does a primary thyroid malfunction lead to

A

low levels of thyroid hormone and high levels of thyroid stimulating hormone (TSH) and thyroid releasing hormone (TRH)

thyroid not making T3 and T4 so hypothalamus keeps trying to stimulate it
hypothyroidism

163
Q

what does a pituitary malfunction lead to

A

low levels of thyroid stimulating hormone (TSH) and thyroid hormone (TH) and high levels of thyroid releasing hormone (TRH)

hypothalamus is trying to stimulate pituitary but it’s not working so thyroid isn’t getting stimulated
hypothyroidism

164
Q

what does a hypothalamic malfunction lead to

A

low levels of thyroid releasing hormone (TRH), thyroid stimulating hormone (TSH), and thyroid hormone (TH)

if the main factor is low, everything down stream of it is low too
hypothyroidism

165
Q

what are five clinical manifestations of hypothyroidism

A

weight gain
bradycardia
coarse hair
large tongue
menorrhagia (heavy bleeding)

166
Q

what is cretinism

A

a symptom of hypothyroidism in developing children or infants

167
Q

what are the two causes of cretinism

A

dietary iodine deficiency
genetic defects

168
Q

what are some clinical features of cretinism

A

impaired development of skeletal system and CNS
intellectual disability
short
coarse facial features
protruding tongue
umbilical hernia

169
Q

what is myxedema and what does it causes

A

a symptom of hypothyroidism in older children and adults
causes slowing of mental and physical activity

170
Q

what causes the symptoms of myxedema

A

extracellular matrix protein accumulation in skin, subcutaenous tissue, and visceral sites

171
Q

what are four symptoms of myxedema

A

non-pitting edema
deep voice
constipation
weight gain

172
Q

what is hashimoto thyroiditis (chronic lymphocytic thyroiditis)

A

autoimmune disorder that causes decreased thyroid hormone secretion and fibrosis of thyroid gland (hypothyroidism)

173
Q

what is the pathogenesis of hashimoto thyroiditis

A

helper T cells, cytotoxic T cells, and antibodies cause inflammatory disease and destruction of follicular cells of thyroid gland
causes decrease of thyroid hormone secretion

174
Q

what are the two antigens involved in hashimoto thyroiditis

A

thyroglobulin (TGB)
thyroid peroxidase (TPO)

175
Q

what is a goiter

A

enlargement of thyroid gland
two types: diffuse nontoxic (simple)(colloid goiter) and multinodular

176
Q

what is the pathogenesis of a goiter

A

dietary iodine deficiency leads to production of impaired T3 and T4
leads to increase in thyroid stimulating hormone which causes hypertrophy and hyperplasic of thyroid follicular cells

177
Q

what is a diffuse nontoxic (simple or colloid) goiter

A

enlargement of thyroid gland without nodules
two types: endemic and sporadic

178
Q

what is an endemic diffuse nontoxic (simple or colloid) goiter

A

goiter caused by dietary iodine deficiency (10% of population)
most commonly seen in underdeveloped countries with low levels of salt (ex. south america)

179
Q

what is a sporadic diffuse nontoxic (simple or colloid) goiter and who does it most commonly affect

A

goiter caused by ingestion of substances that interfere with thyroid hormone synthesis or enzymatic defect
most commonly affects women in puberty and young adulthood

180
Q

what is a multinodular goiter

A

an advanced form of a simple goiter
irregular, nodulated enlargement of thyroid due to varied responses of thyroid follicular cells to external stimuli

181
Q

what are the four main types of thyroid tumors

A

papillary (most common)
follicular
medullary
anaplastic

182
Q

which type of thyroid carcinoma has the worst prognosis

A

anaplastic carcinoma

183
Q

what does the zona glomerulosa of the adrenal cortex produce

A

mineralcorticoids

184
Q

what is an example of a mineralcorticoid

A

aldosterone

185
Q

what does the zona fasiculata of the adrenal cortex make

A

glucocorticoids

186
Q

what is an example of a glucocorticoid

A

cortisol

187
Q

what does the zona reticularis of the adrenal cortex make

A

androgens

188
Q

what are two examples of androgens

A

testosterone
dehydroepiandrosterone (DHEA)

189
Q

what are the three stimuli of adrenal glands

A

morning hours
stress
sympathetic nervous system

190
Q

what are the three stimulatory effects of cortisol

A

gluconeogenesis in liver
release of amino acids from muscle tissue
release of fatty acids from adipose tissue
all provide more fuel sources for metabolism

191
Q

what are the three types of adrenal cortical steroid hormones and what are they all derived from

A

mineralcorticoids
glucocorticoids
sex hormones
all derived from cholesterol

192
Q

how does the endocrine system handle short-term stress

A

SNS stimulates adrenal gland to produce amino acid hormones like catecholamines (NE and EPI)

193
Q

how does the endocrine system handle long-term stress

A

hypothalamus stimulates the pituitary to stimulate the adrenal glands to produce steroid hormones like mineralcorticoid and glucocorticoids

194
Q

what are the three types of adrenocortical hyperfunction (hyperadrenalism)

A

cushing syndrome
hyperaldosteronism
androgenital or virilizing syndromes

195
Q

what is cushing syndrome (hypercortisolism)

A

a type of hyperadrenalism
excess cortisol levels because of increased levels of glucocorticoids

196
Q

what is the most common cause of cushing syndrome

A

administration of steroids to treat inflammatory diseases
cortisol is a steroid, so taking it causes too much in your system (hyperadrenalism)

197
Q

what is a cause of cushing syndrome (not the most common)

A

adrenal tumor directly secretes cortisol
high cortisol despite low ACTH levels

198
Q

what are two secondary causes of cushing syndrome

A

pituitary adenoma causes excessive ACTH secretion (causes Cushing disease)
ACTH-producing tumor elsewhere in the body

199
Q

what are some clincal features of cushing syndrome

A

moon face
buffalo hump
glucose intolerance
thin skin
abdominal stretch marks

200
Q

what is Conn syndrome

A

a type of hyperaldosteronism
solitary adenoma of adrenal gland causes secretion of aldosterone which leads to hypertension

201
Q

what is the primary cause of adrenocortical insufficiency (hypoadrenalism)

A

adrenal disease

202
Q

what is the secondary cause of adrenocortical insufficiency

A

deficiency of ACTH causes decreased adrenal stimulation

203
Q

what are the three types of adrenocortical insufficiency

A

primary acute
primary chronic
secondary

204
Q

what are the three caues of primary acute adrenocortical insufficiency (adrenal crisis)

A

stress requiring increase of steroid output from glands that can’t respond

rapid withdrawl of steroid in patient dependent on exogenous corticosteroids

massive adrenal hemorrhage

205
Q

what is the most common cause of acute adrenocortical insufficiency (adrenal crisis)

A

massive adrenal hemorrhage

206
Q

what is addison disease

A

aka chronic primary adrenosortical insufficiency
body destroys adrenal cortex which leads to deficiency in multiple hormones
90% of gland must be destroyed to show symptoms

207
Q

what are some clincial manifestations of addison disease

A

hyperpigmentation (tanness) due to high ACTH
low blood volume
adrenal atrophy
weight loss

208
Q

what is secondary adrenal cortical insufficiency (hypoadrenalism)

A

decreased pituitary secretion of ACTH or decreased hypothalamic secretion of CRH

209
Q

what are the four causes of secondary adrenal cortical insufficiency

A

metastatic cancer
infection
infarction
irradiation

210
Q

what are the two most common primary tumors that affect the adrenal medulla

A

pheochromocytoma
neuroblastoma

211
Q

what is a pheochromocytoma

A

chromaffin cell tumor arising in the adrenal medulla
causes hypersecretion of catecholamines into blood

212
Q

what three gene mutations cause pheochyromocytoma

A

mutations in RET, NF1, and VHL

213
Q

what is the rule of 10 of adrenal medulla disorders

A

10% extra adrenal
10% bilateral
10% malignant
10% not HTN related
25% from oncogenic germline mutation

214
Q

what are some clinical manifestations of adrenal medulla disorders

A

hypertension (90%)
headache
tachycardia
diaphoresis (excessive sweating)
tremors
catecholamine cardiomyopathy

215
Q

what are the three types of hypertension

A

abrupt
precipitous (high all of the sudden)
episodic (comes and goes)

216
Q

what are three things catecholamine cardiomyopathy can lead to

A

heart failure
myocardial infarction
ventricular fibrillation

217
Q

what do the exocrine acinar cells of the pancreas do

A

secrete digestive enzymes

218
Q

what do the endocrine pancreatic islets (islets of Langerhans) do

A

secrete hormones directly into blood stream

219
Q

what are the three types of cells in a pancreatic islet (islet of langerhans)

A

alpha
beta
delta

220
Q

what do alpha cells in the pancreas secrete

A

peptide hormone glucagon

221
Q

what do the beta cells of the pancreas secrete

A

protein hormone insulin

222
Q

what do the delta cells of the pancreas secrete

A

peptide hormone somatostatin

223
Q

how does glucagon from the pancreas regulate glucose in the blood

A

releases it in response to low blood
stimulates breakdown of glycogen to glucose in the liver to raise blood glucose

224
Q

how does insulin from the pancreas affect blood glucose levels

A

released in response to high blood sugar
stimulates glycogen formation in the liver
also stimualtes glucose uptake from blood so it can be stored in muscle, kidney, and fat tissue
both lower blood sugar

225
Q

what happens when your blood glucose level decreases

A

alpha receptors in pancreas increase glucagon secretion
glucagon stimulates glycogen to be broken back down into glucose in the liver

226
Q

what does insulin do

A

increases the rate of glucose transport mostly into muscle
reduces production of glucose from glycogen in the liver

227
Q

what is the mechanism of insulin

A

insulin binds to receptor which activates it
AKT is produced which causes a GLUT-4 vesicle to be made
vesicle is released from cell which causes protein increase, decrease in glu synthesis, and increase glycogen synthesis

228
Q

how does insulin affect adipose tissue

A

increases glucose uptake
increases lipogenesis
decreases lipolysis

229
Q

how does insulin affect the striated muscle

A

increases glucose uptake, glycogen synthesis, and protein synthesis

230
Q

how does insulin affect the liver

A

decreases gluconeogenesis
increases glycogen synthesis
increases lipogenesis

231
Q

what happens when blood glucose levels increase

A

beta cells of the pancreas increase insulin secretion
this causes increased glucose uptake by cells as well as storage of glucose, amino acids, and fats

232
Q

what is the mechanism of diabetes mellitus (DM)

A

defective insulin production or inadequate action of insulin leads to hyperglycemia

233
Q

what are the two major forms of diabetes mellitus (DM)

A

type 1 diabetes (T1D) - insulin deficiency
type 2 diabetes (T2D) - insulin resistant

234
Q

what is the most common type of diabetes mellitus (DM)

A

type 2 diabetes (T2D) - insulin resistant

235
Q

in the US, what is the leading cause of ESRD, adult-onset blindness, and lower extremity amputation

A

diabetes mellitus (DM)

236
Q

what is the mechanism of type 1 diabetes (T1D)

A

autoimmune
T helper cells release cytokines which causes inflamation
cytotoxic T cells destroy beta cells in pancreas
leads to a deficiency of insulin

237
Q

when are those with type 1 diabetes (T1D) most commonly diagnosed

A

younger than 20 years old

238
Q

what are the two abnormalities of type 2 diabetes (T2D)

A

insulin resistance in peripheral tissues (skeletal muscle, adipose tissue, and liver)
beta cell dysfunction due to insulin resistance and hyperglycemia

239
Q

what is the major risk factor of type 2 diabetes

A

central or visceral obesity

240
Q

when are those with type 2 diabetes (T2D) most commonly diagnosed

A

patients over 45 years of age

241
Q

how does obesity cause type 2 diabetes (T2D)

A

increased adipokines, FFAs, and inflammation from fatty tissue leads to insulin resistance
this makes the beta cells compensate by making more insulin
eventually, beta cells fail and don’t secrete insulin, leading to type 2 diabetes

242
Q

what are the clinical manifestations of type 1 diabetes (DI)

A

polyuria
polydipsia (excessive thirst)
polyphagia (extreme hunger)
ketoacidosis
(after 90% or more beta cells are destroyed)

243
Q

what are the clincial manifestations of type 2 diabetes (T2D)

A

starts off asymptomatic but is found on blood testing
eventually:
polyuria
polydipsia (excessive thirst)
polyphagia (extreme hunger)
ketoacidosis

244
Q

what are some complications of diabetes

A

damage to arteries
atherosclerosis - gangrene and necrosis of legs
diabetic neuropathy/nephropathy/retinopathy
coma

245
Q

what are the three most common causes of mortality in diabetics

A

MI
renal vascular insufficiency
cerebrovascular accidents

Disease Mechanisms (19 decks)

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