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CABS III > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

the hypothalamus produces

A

releasing hormones which stimulate the anterior pituitary to produce stimulating hormones

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2
Q

the anterior pituitary gland produces

A

stimulating hormones which act directly on target organs

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3
Q

endocrine hormones

A

secreted into blood and transported in the blood to distant target cells

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4
Q

neuroendocrine hormones

A

secreted from neurons into the blood or transmitted via gap junctions

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5
Q

paracrine hormones

A

secreted into interstitial fluid and act on target cells adjacent to the secreting cell (within close proximity)

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6
Q

autocrine hormones

A

secreted into interstitial fluid and act on the secreting cell itself

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7
Q

diurnal hormone regulation

A

hormone release is mediated by the circadian clock network which exhibits a 24-hour rhythm where the hormone levels are affected by sleep and circadian rhythm

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8
Q

cyclical hormone regulation

A

hormone release is mediated by the complex interaction of hormones where hormone levels rise and fall during each cycle (example: female menstrual cycle)

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9
Q

negative feedback hormone regulation

A

when the hormone created by the target organ acts as a negative control and will stop the secretion of releasing and/or stimulating hormones from the pituitary and/or hypothalamus to keep hormone levels in check

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10
Q

positive feedback hormone regulation

A

when the hormone created by the target organ acts as a positive control and perpetuates the secretion of the hormone from the pituitary (example: oxytocin)

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11
Q

water-soluble/hydrophilic hormones include

A

amine hormones which are derived from the amino acid tryptophan or tyrosine, peptide hormones which consist of short chains of linked amino acids, and protein hormones which consist of larger chains of linked amino acids which can be larger and contain charge (for example: glucagon, FSH, and insulin)

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12
Q

lipid-soluble/hydrophobic hormones include

A

steroid hormones which are created from the lipid cholesterol and contain charge (for example: cortisol and sex hormones)

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13
Q

location of water-soluble hormone cell receptors

A

receptor is on the cell surface

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14
Q

location of lipid-soluble hormone cell receptors

A

receptor is in the cytoplasm or nucleus

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15
Q

transport of water-soluble hormones in blood

A

do not require a transport protein to travel within the blood, cannot easily cross cell membranes (require a receptor protein)

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16
Q

transport of lipid-soluble hormones in blood

A

require a transport protein to travel within the blood, can easily cross cell membranes (do not require a receptor protein)

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17
Q

water-soluble hormones

A

GH, insulin, PTH, prolactin, FSH, LH, TSH, ACTH, ADH, calcitonin, glucagon, epinephrine, and norepinephrine

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18
Q

lipid-soluble hormones

A

T3, T4, estrogen, steroids including glucocorticoids (cortisol), mineralocorticoids (aldosterone), progestins (progesterone), and testosterone

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19
Q

half-life of water-soluble hormones

A

rapidly broken down with a half-life of minutes

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20
Q

half-life of lipid-soluble hormones

A

bound to a water-soluble transport protein with a much longer half-life

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21
Q

half-life of amine hormones

A

can be fast or slow depending on the specific hormone where some require transport protein and some do not - epinephrine = fast, thyroid hormone = slow

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22
Q

in order to affect a target organ, a hormone must be

A

free or unbound from transport protein (this is also how the hormone is measured in serum)

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23
Q

upregulation/downregulation of hormone target sites can involve

A

a change in the number of binding sites or in the affinity of the binding sites for the specific hormone (can occur within hours)

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24
Q

upregulation of hormone target sites occurs when

A

there is a low level of circulating hormone

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25
Q

downregulation of hormone target sites occurs when

A

there is a high level of circulating hormone

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26
Q

intracellular response to binding of water-soluble hormone

A

hormone binds to a cell surface protein receptor triggering a second messenger response within the cell involving cAMP, cGMP, calcium, and tyrosine kinases which phosphorylate proteins found within the cell causing rapid changes that can change the activity of enzymes, turn on or off cellular membrane proteins for permeability, and upregulate or downregulate protein production

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27
Q

intracellular response to binding of lipid-soluble hormone

A

hormone first diffuses across the cellular membrane and binds to an intracellular receptor which transports it to the nucleus where it modulates gene expression causing a change in protein synthesis and resulting in changes in metabolism, cellular growth, and cellular permeability which is a slower response compared to that triggered by water-soluble hormones

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28
Q

high hormone disease states

A

hormone dysregulation typically due to a primary disorder where the target gland is creating too much hormone resulting in reduced stimulating hormone levels, a secondary disorder where there is inappropriate stimulation from the pituitary or hypothalamus resulting in elevated levels of both stimulating and target hormone, or ectopic production of hormone (hormone-secreting tumor)

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29
Q

low hormone disease states

A

hormone dysregulation typically due to a primary disorder where the target organ is not creating enough hormone resulting in increased stimulating hormone levels, a secondary disorder where there is not enough stimulation from the pituitary resulting in reduced levels of both stimulating and target hormone, or a tertiary disorder where there is not enough stimulation from the hypothalamus, the hormone does not work appropriately, or target receptors do not respond appropriately

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30
Q

location of hormone breakdown

A

in the liver and excreted by the kidneys

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31
Q

structure connecting the hypothalamus to the pituitary

A

infundibulum or pituitary stalk

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32
Q

location of hypothalamus within the brain

A

part of the diencephalon at the base of the brain and is considered a major part of the limbic system

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33
Q

function of hypothalamus

A

made up of gray matter nuclei and their tracts and functions to produce, store, and release hormones that act on the pituitary

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34
Q

location of pituitary within the brain

A

measures 1 cm in diameter and sits in the hypophyseal fossa within the sella turcica of the sphenoid bone inferior to the optic chiasm

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35
Q

hypothalamic hypophyseal portal system

A

a group of blood vessels that extend through the pituitary stalk through which the hypothalamus communicates with the anterior pituitary

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36
Q

components of the anterior pituitary/adenohypophysis

A

made up of glandular cuboidal tissue and 7 types of chromophils which are the secretory cells, each of which creates its own specific hormone

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37
Q

components of the posterior pituitary/neurohypophysis

A

made up of neural tissue containing axons that begin within the nuclei of the hypothalamus and extend through the pituitary stalk

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38
Q

hypothalamic hypophyseal tract

A

a bundle of hypothalamic neural axons that extend through the pituitary stalk through which the hypothalamus communicates with the posterior pituitary

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39
Q

major blood supply to the anterior pituitary

A

the hypothalamohypophyseal portal system (flows through hypothalamus first)

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40
Q

major blood supple to the posterior pituitary

A

the inferior hypophyseal arteries which branch off of the internal carotid artery (no blood supply from hypothalamus)

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41
Q

herring bodies

A

terminal ends of nerves extending from the hypothalamus to the posterior pituitary where hormones are stored and released

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42
Q

function of ADH

A

antidiuretic hormone (vasopressin) released by the posterior pituitary that targets the kidneys to increase salt and water retention and smooth muscle to stimulate vasoconstriction, it is stimulated by low blood pressure and high blood osmolality or dehydration and inhibited by alcohol

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43
Q

function of oxytocin

A

released by the posterior pituitary and stimulates uterine contractions and milk ejection in the breast where it is stimulated by positive feedback through uterine stretch and suckling on the nipple by the infant

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44
Q

function of TRH

A

released from the hypothalamus and stimulates the anterior pituitary to release TSH, inhibits prolactin release

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45
Q

function of GnRH

A

released from the hypothalamus and stimulates the anterior pituitary to release FSH and LH

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46
Q

function of somatostatin

A

released from the hypothalamus and inhibits the release of TSH and GH from the anterior pituitary, is also a regulator of many other hormones

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47
Q

function of GHRH

A

released from the hypothalamus and stimulates the anterior pituitary to release GH

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48
Q

function of substance P

A

released by the hypothalamus and stimulates the anterior pituitary to release GH, FSH, LH, and prolactin, inhibits the release of ACTH

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49
Q

function of PRH

A

released by the hypothalamus and stimulates the anterior pituitary to release prolactin

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50
Q

function of LH

A

glycoprotein hormone released by the anterior pituitary that targets the granulosa cells within the ovaries to stimulate ovulation and progesterone production and Leydig cells within the testicles to promote testicular growth and testosterone production

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51
Q

function of FSH

A

released by the anterior pituitary and targets the granulosa cells within the ovaries to stimulate estrogen production and follicular maturation and Sertoli cells within the testicles to stimulate spermatogenesis

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52
Q

function of CRH

A

released by the hypothalamus and stimulates the anterior pituitary to release ACTH

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53
Q

function of ACTH

A

released by the anterior pituitary and regulated by negative feedback, diurnal rhythms, and stress where it targets the adrenal cortex stimulating steroidogenesis (primarily cortisol) and is responsible for the maintenance of the adrenals

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54
Q

function of GH

A

a peptide hormone that is released by the anterior pituitary and targets cells within the bone, adipose tissue, muscle, and liver where it stimulates the production of insulin-like growth factors (which have effects similar to insulin) regulating metabolic growth and adaptation

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55
Q

function of prolactin

A

released by the anterior pituitary and targets breast tissue to induce milk production and secretion and immune response where it is stimulated by estrogens and breastfeeding and inhibited by dopamine

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56
Q

location of pineal gland

A

within the central aspect of the brain posterior to the hypothalamus

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57
Q

function of pineal gland

A

made of photoreceptive cells capable of secreting melatonin where the input of light from the visual center inhibits melatonin secretion and darkness stimulates secretion, functions to regulate our circadian rhythm where melatonin will decrease insulin secretion and also affects the reproductive system increasing GnRH to help trigger puberty

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58
Q

pituitary adenomas

A

typically benign masses that are associated with alterations in the MEN1 gene leading to poor function of tumor suppressor genes, Gs-Alpha mutations, and AIP mutations (familial) that may impinge on the optic chiasm causing bitemporal hemianopia, have hypersecretion cells within the adenoma and decreased secretion from surrounding pituitary cells, and most commonly associated with elevated GH and prolactin (causing altered menstrual cycle and decreased libido)

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59
Q

microadenomas

A

adenomas smaller than 1 cm which are typically asymptomatic and hormonally silent

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60
Q

macroadenomas

A

adenomas larger than 1 cm which alter hormone regulation or impinge on surrounding structures (causing mass effect)

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61
Q

MEN syndrome

A

multiple endocrine neoplasia caused by autosomal dominant disorders that predispose patients to endocrine tumors which includes 4 different subtypes based on the endocrine tissues affected

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62
Q

MEN1

A

associated with pituitary adenomas, parathyroid tumors, gastrinomas, insulinomas, and pancreatic tumors

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63
Q

MEN2A (2)

A

associated with hyperparathyroidism, medullary thyroid carcinoma, and pheochromocytoma

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64
Q

MEN2B (3)

A

associated with mucosal neuromas, marfanoid body habitus, medullary thyroid carcinoma, and pheochromocytoma

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65
Q

causes of hyperprolactinemia

A

most commonly prolactinomas, decreased prolactin excretion (renal failure), primary hypothyroidism (causing increased TRH), antipsychotic medications (dopamine antagonists), and estrogen supplementation inducing hyperplasia of prolactin producing pituitary cells

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66
Q

hyperprolactinemia presentation in females

A

galactorrhea, changes in the menstrual cycle, and after extended exposure can cause low estrogen, hirsutism, and osteopenia

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67
Q

hyperprolactinemia presentation in males

A

gynecomastia, hypogonadism, erectile dysfunction, and after extended exposure can cause low testosterone, hirsutism, and osteopenia

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68
Q

gigantism

A

excessive GH and insulin-like growth factor (IGF-1) during utero, in young childhood, and/or in adolescence while growth plates remain open most commonly associated with excessive GHRH but can also be caused by an ectopic source of hormone or disruption of somatostatin pathway, often associated with other syndromes and not isolated

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69
Q

acromegaly

A

excessive GH during adulthood after growth plate closure most commonly associated with GH-secreting pituitary adenoma and resulting in increased connective tissue development, increased cytoplasm, and proliferation

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70
Q

function of IGF-1

A

manages how GH affects the tissues and stimulates cellular hyperplasia and hypertrophy

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71
Q

acromegaly presentation

A

frontal bossing, enlarged tongue, prognathism, spade-like hands, and enlarged feet and face

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72
Q

gigantism presentation

A

rapid height change, increasing BMI, enlarging hands, and frontal bossing

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73
Q

risk factors for gigantism

A

alteration in the MEN1 gene leading to poor function of tumor suppressor gene, AIP, activation of oncogene gsp, and x-linked duplication error that double codes for G-coupled receptor proteins GPR101

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74
Q

key cation in blood

A

sodium which largely defines the tonicity of intracellular and extracellular space thus maintaining homeostasis (primarily remains extracellular due to Na+/K+ ATPase where K+ primarily remains intracellular)

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75
Q

increased sodium levels cause

A

increased osmolality (total solute concentration) triggering ADH secretion which results in water retention

76
Q

hypertonic solution

A

when solute concentration is higher outside the cell causing water to escape and the cell to shrink

77
Q

isotonic solution

A

when solute concentration is equal both outside and inside the cell

78
Q

hypotonic solution

A

when solute concentration is lower outside the cell causing water to flood into the cell and can cause cells to burst

79
Q

SIADH

A

a posterior pituitary disorder where there is too much ADH caused by infection, ICH, tumor, trauma, or a paraneoplastic syndrome resulting in increased aquaporins within the nephron leading to increased free water reabsorption, increased extracellular fluid, hyponatremia, hypoosmolality, decreased but very concentrated urine output

80
Q

diabetes insipidus

A

a posterior pituitary disorder where there is not enough ADH or it is not working appropriately causing excess fluid excretion, dilute urine, hypernatremia, hyperosmolality, polyuria, polydipsia, weight loss, and dehydration

81
Q

central diabetes insipidus

A

when there is not enough (or any) ADH production/secretion from the pituitary (pituitary issue) most commonly idiopathic but may be associated with infiltrative process, infection, surgical changes, or trauma

82
Q

nephrogenic diabetes insipidus

A

when the kidneys are unable to respond appropriately to circulating ADH (kidney issue)

83
Q

central diabetes insipidus presentation

A

polyuria (8-12 L/day - may have bladder enlargement and hydronephrosis), polydipsia, nocturia, and decreased urine osmolality/urine sodium

84
Q

SIADH presentation

A

thirst, anorexia, fatigue, DOE, vomiting, cramping, weight gain, seizures, neurological damage or AMS

85
Q

hypopituitarism

A

lack of one or more hormones typically secreted from the anterior pituitary most commonly associated with a space-occupying lesion such as a pituitary adenoma and can also be associated with large aneurysms, infarction, hypovolemic shock, trauma, infection, and radiation

86
Q

panhypopituitarism

A

when there are no hormones being secreted from the pituitary

87
Q

Sheehan sydnrome

A

ischemia leading to necrosis of the pituitary (which is usually enlarged in pregnancy) due to postpartum hemorrhage

88
Q

pituitary apoplexy

A

hemorrhage into the pituitary

89
Q

Sheehan syndrome presentation

A

amenorrhea, lactation failure, secondary adrenal insufficiency, and hypothyroidism

90
Q

infarction causing hypopituitarism

A

infarction causes edema which leads to increased pressure/space-occupying pressure which results in fibrosis eventually resulting in hypopituitarism

91
Q

ACTH deficiency symptoms

A

decreased cortisol resulting in N/V, fatigue, weakness, hypoglycemia, weight loss, and death

92
Q

TSH deficiency symptoms

A

hypothyroidism, cold intolerance, dry skin, fatigue, low metabolism, and infertility

93
Q

FSH and LH deficiency symptoms

A

amenorrhea, vaginal/breast atrophy, testicular atrophy, and decreased libido

94
Q

GH deficiency symptoms

A

hypopituitary dwarfism (if occurring in children), elevated BMI, osteoporosis, depression, and fatigue in adults

95
Q

pituitary dwarfism

A

associated with growth hormone deficiency which is defined as stature that is in the 3rd percentile for age/sex, may be congenital or develop at a later age, individuals will have normal body proportions

96
Q

TSH is secreted by

A

thyrotropes in the anterior pituitary

97
Q

function of TSH

A

targets the thyroid gland promoting iodide trapping within the follicular cells (uses sodium-iodide transporter) and causing increased production/release of thyroid hormone , inhibited by thyroid hormone through negative feedback

98
Q

blood supply to the thyroid

A

superior thyroid artery which branches off the external carotid and inferior thyroid artery which branches off the thyrocervical trunk from the suprascapular artery

99
Q

the thyroid is innervated by

A

the recurrent laryngeal nerve which is a branch off of the vagus nerve

100
Q

function of the recurrent laryngeal nerve

A

innervates the majority of the muscles of the larynx and provides sensory input for the laryngeal structures inferior to the vocal cords

101
Q

thyroid hormone (T3 and T4) is produced by

A

follicular cells within the thyroid gland which contain binding sites for TSH that triggers the release of stored hormone (can also be triggered by neurotransmitters including acetylcholine and catecholamines)

102
Q

length of time in which the thyroid gland stores hormone

A

2-3 months worth of hormone (colloid is hormone storage site)

103
Q

calcitonin is secreted by

A

parafollicular cells (C cells) within the thyroid

104
Q

function of calcitonin

A

lowers calcium levels in the blood by inhibiting osteoclast activity and promoting osteoblast activity in bone

105
Q

thyroid hormone that makes up the majority of circulating thyroid hormone

A

T4 or thyroxine, a prohormone, that once enters the cell will lose an iodine and be converted to T3 or triiodothyronine, the active form of thyroid hormone

106
Q

production of thyroid hormone process

A

thyroglobulin, which contains a significant amount of tyrosine amino acids, is made within the follicular cells and stored within colloid, when iodide ion is absorbed from the bloodstream it is oxidized by thyroid peroxidase into its active form (iodine) and enters the colloid where it is attached to tyrosine forming iodinated tyrosines which are then linked together forming T3 (3 iodine) and T4 (4 iodine) and packaged into lysosomes to be released into circulation

107
Q

thyroid hormone with a longer half-life

A

T4 or thyroxine which accounts for 93% of thyroid hormone produced is released into the bloodstream and binds to thyroxine-binding globulin where it must be deiodinated by deiodinase into T3 to become active upon reaching target tissues

108
Q

location of iodide absorption

A

GI tract (for normal hormone function, we need 1 mg/week)

109
Q

cellular effects of thyroid hormone

A

upon entering a target cell, thyroid hormone either moves into the nucleus and upregulates specific protein production thereby increasing metabolism, or can have nongenomic effects including changing ion channel regulation, increasing protein and fat catabolism, increasing the number and size of mitochondria, increasing metabolic rate through increased glucose/carbohydrate metabolism, and increasing thermogenesis

110
Q

cardiac effects of thyroid hormone

A

increased metabolic rate will increase oxygen demand and lead to increased blood flow, increased cardiac contractability and output, increased sensitivity of HR to catecholamines, increased nervous system excitability, and increased heat production

111
Q

growth effects of thyroid hormone

A

required for normal growth and development affecting cellular metabolism of protein, fat, and glucose resulting in increased sodium-potassium ATPase activity, increased oxygen demand and metabolic rate, and increased thermogenesis (over time, thyroid hormone will cause an increase in the number of mitochondria intracellularly), also needed to other hormone function

112
Q

primary hyperthyroidism

A

elevated T3 and T4 with reduced TSH due to negative feedback response from T3 and T4

113
Q

secondary hyperthyroidism

A

elevated T3 and T4 with elevated TSH where there is excess TSH being produced/secreted in the pituitary

114
Q

thyrotoxicosis

A

symptomatic elevation in circulating thyroid hormone due to primary (most commonly Grave’s), secondary, ectopic production of TSH (TSH pituitary adenoma), or excess exogenous intake

115
Q

Grave’s disease

A

an autoimmune disorder that causes 50-80% of cases of hyperthyroidism that is thought to have a genetic predisposition with an environmental trigger caused by a type II hypersensitivity reaction resulting in tissue-specific antigens and TSH receptor agonist autoantibodies causing increased thyroid hormone production and cellular hyperplasia (goiter)

116
Q

Grave’s disease presentation

A

protein depositions causing infiltrative changes to the ocular muscles causing inflammation, edema, too much content in the orbit, exophthalmos which can weaken the ocular muscle leading to diplopia, lid lag, pretibial myxedema due to increased hyaluronic acid production, swelling, induration, and erythema to anterior lower extremities

117
Q

nodular thyroid disease

A

thyroid cellular hypertrophy caused by high thyroid hormone demand or inadequate production (typically after stressor) which can result in toxic adenoma or toxic multinodular goiter if these cells continue to make excess thyroid hormone

118
Q

hypothyroidism

A

most common disorder of the thyroid where the most common cause is autoimmune Hashimoto thyroiditis due to medications, iatrogenic causes, and iodine deficiency worldwide, or tumor that is limiting thyrotrope’s ability to secrete hormone, TBI, hemorrhage, or CVA (central cause)

119
Q

Sheehan syndrome

A

lack of blood flow or ischemia of the pituitary associated with increased size of the pituitary during pregnancy and postpartum hemorrhage resulting in reduced pituitary secretion or panhypopituitarism

120
Q

Hashimoto thyroiditis

A

autoimmune thyroiditis that is the most common cause of hypothyroidism in areas that have sufficient iodine characterized by antagonist autoantibodies to receptors on follicular cells, thyroglobulin, thyroid peroxidase, and TSH receptors within the thyroid causing infiltration, fibrosis, and apoptosis (by B and T lymphocytes) that has a genetic predisposition and epigenetic trigger including exposure to a mimicking molecule (virus that is similar to proteins being destroyed), radiation, medications, stress, pregnancy, iodine, chronic disease states, also closely linked with Grave’s

121
Q

Hashimoto thyroiditis presentation

A

progressive or insidious onset of cold intolerance, fatigue, low body temperature, bradycardia, constipation, dry skin, hoarse speech, narrowed pulse pressure, delayed relaxation of reflexes, increased total cholesterol circulating in blood, and transient hyperthyroidism symptoms (Hashitoxicosis) which is a transient surge of hyperthyroid symptoms due to the release of stored thyroid hormone within dead thyroid cells

122
Q

myxedema coma

A

a rare and often fatal condition associated with untreated, longstanding hypothyroidism where the body is unable to compensate due to increased demand for thyroid hormone due to infection, trauma, or other physiological stressor where decreased metabolic rate and cellular metabolism will result in decreased mentation or AMS

123
Q

myxedema coma presentation

A

AMS, HTN, dry, cool skin, hypothermia, constipation, distention, ileus, fecal impaction, hypoventilation, arrhythmia, heart block, facial changes including macroglossia, ptosis, and sparse hair, nonpitting edema, and acquired Von Willebrand syndrome = increased bleeding risk

124
Q

cretinism

A

occurs due to profoundly low thyroid hormone during development, infancy, or early childhood which can be associated with agenesis, underdevelopment, and/or mental decline, is more so associated with decreased skeletal growth that causes the child to be disproportionate and have enlarged soft tissues (microglossia)

125
Q

thyroid goiter

A

abnormal cellular growth that may be diffuse throughout the gland or more localized to a nodule where elevated TSH will cause increased demand for thyroid hormone in the follicular cells which causes hyperplasia, may be associated with the inability to trap iodide, insufficient peroxidase enzyme to convert iodide into iodine, lack of or defective thyroid peroxidase, or iodide deficiency, may have normal or low thyroid hormone levels (can also be associated with Hashimoto’s, Grave’s, tumors, and infiltrative processes)

126
Q

PTH is produced by

A

chief cells within the parathyroid glands (situated behind the thyroid gland, can be 2-6), parathyroid also contains oxyphil cells with unknown role

127
Q

function of PTH

A

lipid soluble hormone that is stored within vesicles in the parathyroid gland that is profoundly sensitive to low calcium (hypocalcemia) which will result in secretion into the bloodstream, with high or normal calcium levels, calcium is bound to cellular g-protein calcium receptors on chief cells inhibiting the release of PTH

128
Q

physiologic effects of PTH

A

PTH first triggers the inhibition of osteoblasts and increases osteoclast activity causing bone degradation and increased calcium and phosphate release into the blood (can occur within minutes), it also binds to cells in the distal collecting duct to increase calcium reabsorption from the urine and phosphate excretion in the urine, and works to activate vitamin D in the kidneys to increase absorption of calcium from the small intestine

129
Q

normal calcium plasma level

A

8.5 - 10.5 mg/dL

130
Q

processes requiring calcium in the body

A

cardiac contraction, nerve conduction, cellular growth, enzyme activity, coagulation, and muscle contraction

131
Q

calcitonin is produced by

A

C cells within the thyroid gland and is a water-soluble hormone

132
Q

function of calcitonin

A

released from the thyroid in response to high blood calcium levels that inhibits osteoclast activity and stimulates osteoblasts which reduces blood calcium levels

133
Q

primary hyperparathyroidism

A

elevated PTH because of a gland issue most commonly associated with solitary parathyroid adenoma, can also be associated with MEN syndrome, hyperplasia, and cancer

134
Q

secondary hyperparathyroidism

A

elevated PTH due to low calcium typically associated with CKD or vitamin D deficiency, NO hypercalcemia

135
Q

tertiary hyperparathyroidism

A

long-standing hyperparathyroidism for whatever reason, where once the underlying cause is corrected, PTH continues to be elevated - often noted after kidney transplant or can be associated with paraneoplastic syndrome

136
Q

hyperparathyroidism presentation

A

fatigue, nephrolithiasis (calcium phosphate stones), polydipsia, polyuria, N/V/D, abdominal discomfort, arrhythmia, fractures (osteoporosis), neurologic symptoms (memory, depression, decreased cognition, confusion), may also have hypoglycemia and hypertension (stones, bones, abdominal groans, and psychiatric overtones)

137
Q

hypoparathyroidism

A

damage to to the parathyroid most commonly due to accidental removal with thyroidectomy, neck radiation, or purposeful removal, may be associated with DiGeorge syndrome, autoimmune disorders, pseudohypoparathyroidism (target organs are resistant to PTH), or infiltrative disorders such as hemochromatosis, sarcoidosis, and Wilson’s disease

138
Q

hypoparathyroidism/hypocalcemia presentation

A

hypocalcemia, hyperphosphatemia, and decreased activation of vitamin D leading to muscular tetani, seizures, extrapyramidal symptoms, prolonged QT, positive Chvostek sign (tap on facial nerve anterior to ear resulting in facial twitch), and positive Trousseau sign (BP cuff causes carpal spasm)

139
Q

location of pancreas

A

retroperitoneal behind the stomach, medial to the spleen, and abutting the duodenum where the head attaches to the duodenum, the Uncate process extends inferiorly, the neck lies next to the stomach, and the tail is anterior to the kidney

140
Q

ampulla of Vater

A

where the pancreatic and bile ducts meet and empty exocrine contents into the duodenum

141
Q

blood supply to the head of the pancreas

A

superior mesenteric artery (SMA)

142
Q

blood supply to the body/tail of the pancreas

A

branches off the splenic artery

143
Q

function of the pancreas

A

a heterocrine organ that has both endocrine and exocrine functions and contains alpha (produce glucagon), beta (produce insulin and amylin), delta (produce gastrin and somatostatin), F cells (produce pancreatic polypeptide), and acinar cells (exocrine and make up the majority of parenchyma)

144
Q

islets of Langerhans

A

organized around capillaries within the pancreas which contain 60% beta cells, 25% alpha cells, and 10% delta cells

145
Q

normal glucose range

A

80-120 mg/dL

146
Q

number of ATP molecules made for every glucose molecule

A

38 ATP

147
Q

glucose gets into the cell with the help of

A

sodium-glucose co-transport carrier molecules which are stored intracellularly in vesicles and are placed into the cell wall/membrane when signaled by insulin binding to its receptor (remain for about 3-5 minutes and then go back into cell for storage)

148
Q

major storage location for glycogen

A

in the liver (when glucose is needed, glycogen release is stimulated by epinephrine and glucagon)

149
Q

major fuel source in muscle

A

fatty acids and glucose where excess is stored as glycogen (broken down to lactic acid)

150
Q

major fuel source in the brain

A

glucose which is able to pass more readily into these cells (does not require insulin), hypoglycemia = AMS

151
Q

major fuel source in the retina

A

glucose

152
Q

location of protein breakdown

A

in the liver which produces ammonia (converted to urea and excreted in urine)

153
Q

function of amylin

A

a peptide hormone that is released with insulin in response to eating and helps trigger satiety, slows gastric emptying, suppresses glucagon, and prevents hyperglycemia with insulin (can lead to amyloid deposits seen in type 2 Diabetes)

154
Q

function of insulin

A

an unbound hormone with a half-life of 6 minutes that travels to the liver and stimulates glycolysis and glycogenesis, travels to the muscle and increases the influx of glucose and amino acids into myocytes inducing glycolysis, glycogenesis, and protein synthesis, and travels to adipose tissue and increases the influx of glucose into cells which induces formation of triglycerides (broken down by insulinases in the liver, kidneys, and muscle)

155
Q

insulin release is triggered by

A

primarily hyperglycemia, but also elevated levels of circulating amino acids, glucagon, gastrin, cholecystokinin, GH, cortisol, progesterone, estrogen, and autonomic innervation

156
Q

process of insulin release from pancreas

A

beta cells of islets of Langerhans have glucose transporters embedded in the cell wall that do not require insulin resulting in glucose freely entering the cell, is broken down increasing ATP which alters cellular membrane proteins changing the intracellular voltage and opening calcium-gated channels leading to increased intracellular calcium, this triggers the release of insulin vesicles into circulation

157
Q

effect of insulin on protein metabolism

A

insulin increases cells’ ability to intake free amino acids which can be used as building blocks for proteins, increases mRNA thus increasing the act of protein building, and inhibits protein catabolism, when no insulin or deficiency, there will be reduced protein synthesis and unopposed catabolism resulting in increased levels of circulating amino acid levels

158
Q

effect of insulin on fat metabolism

A

once the liver has reached its maximal glycogen storage capacity, it will store the remaining glucose at fat under the direction of insulin which the liver releases in the form of triglycerides which enter adipose tissue, if there is no insulin - triglycerides will continue to circulate in the blood leading to atherosclerosis

159
Q

process of glucagon release from pancreas

A

low glucose causes decreased ATP in the alpha of the islet of Langerhans which causes membrane channels to become sensitive causing an influx of calcium, this results in the fusion of vesicles containing glucagon to the cell wall followed by release into circulation

160
Q

function of glucagon

A

after being released into circulation, it goes to the liver and stimulates the breakdown of glycogen into glucose, stimulates gluconeogenesis, activates adipose cell lipase enzyme which breaks down triglycerides into fatty acids and glycerol, increases cardiac contraction, renal blood flow, and bile excretion (increases during exercise)

161
Q

type 1 diabetes mellitus

A

autoimmune disease characterized by autoantibodies that degrade beta cells islets, glutamic acid decarboxylase (GAD65), and insulin itself leading to absolute insulin insufficiency that is thought to have a genetic disposition with epigenetic trigger HLA gene that can occur at any age but most commonly children < 14 years old

162
Q

type 1 diabetes mellitus presentation

A

most common in children and young adults causing polyuria, polyphagia, weight loss, polydipsia, and blurry vision

163
Q

type 2 diabetes

A

a disease characterized by target cell resistance to insulin and progressive beta cell dysfunction leading to less and less of a stimulus on the target cells, elevated circulating glucose which triggers more insulin secretion from beta cells (hyperinsulinemia), and decreased beta cell activity over time, much more common than type 1 diabetes, associated with genetic predisposition and likely multifactorial risk factors including sedentary lifestyle, obesity, smoking, heavy alcohol consumption, PCOS, Cushing’s syndrome, acromegaly

164
Q

metabolic syndrome

A

contributes to insulin insensitivity in target cells leading to decreased intracellular shift of glucose, hyperglycemia, elevated triglycerides, low HDL, elevated BMI, and release of adipokines from adipose tissue which may also increase insulin resistance

165
Q

amylin is produced by

A

beta cells within the pancreas where increased insulin production causes increased amylin production (can decrease the effect of glucose on beta cells and lead to amyloid deposits)

166
Q

life span of RBCs

A

120 days

167
Q

hemoglobin A1C diagnostic for diabetes

A

greater than or equal to 6.5 %

168
Q

diabetic keto acidosis (DKA)

A

occurs most commonly in type 1 diabetics when there is increased demand for insulin due to infection or other stress but no insulin is produced or administered, cells become starved for glucose because it cannot enter the cell and this triggers the release of catabolic hormones like glucagon, epinephrine, cortisol, and GH which increase glucose production in the liver and the breakdown of fatty acids into ketones for energy (only energy besides glucose the brain can use) which creates ketone bodies which consume carbonate and lead to metabolic acidosis and protein catabolism resulting in muscle wasting

169
Q

DKA presentation

A

ketonuria, abdominal pain, nausea, vomiting, dehydration, Kussmaul respiration, electrolyte imbalance, ketone breath, weakness, confusion, and possible coma

170
Q

hyperosmolar hyperglycemic state (HHS)

A

occurs only in type 2 diabetes when stress increases insulin demand causing a relative insulin deficit which results in glucosuria, polyuria, dehydration, polydipsia, neural damage, and renal failure of untreated (does not lead to ketone production)

171
Q

blood supply to adrenals

A

suprarenal arteries which branch off the phrenic artery

172
Q

venous supply from left adrenal

A

renal vein

173
Q

venous supply from right adrenal

A

directly to IVC

174
Q

the retroperitoneal space contains

A

the suprarenal glands, aorta, duodenum, pancreas, ureter, colon, kidneys, esophagus, and rectum

175
Q

the adrenal medulla is innervated by

A

the celiac plexus and splanchnic nerves

176
Q

effects of aldosterone

A

regulated by the RAAS, released from the zona glomerulosa, and causes increased sodium retention and potassium and hydrogen excretion, increases BP (takes 90 minutes - 6 hours to reach full effect)

177
Q

aldosterone release is stimulated by

A

angiotensin II and potassium and to a lesser extent, ACTH

178
Q

Addison’s disease

A

insufficient adrenal hormones including cortisol and aldosterone primary causes most commonly associated with autoimmune disorders leading to atrophy of the cortices and secondary causes associated with insufficient stimulation of ACTH

179
Q

melanocyte-stimulating hormone (MSH)

A

a prohormone that is formed during production of ACTH so when there is increased ACTH production, there is also increased MSH (acts on melanocytes of the dermis to stimulate melanin)

180
Q

Addison’s diagnosis

A

ACTH (cosyntropin) stimulation test

180
Q

Addison’s presentation

A

weakness, weight loss, hyperpigmentation, hypotension, and hyponatremia

181
Q

Conn’s syndrome (hyperaldosteronism)

A

increased aldosterone secretion due to tumor of the zona glomerulosa, other causes of hyperaldosteronism are familial hyperaldosteronism, adrenal carcinomas, and paraneoplastic secretion

182
Q

hypoaldosteronism presentation

A

hypovolemic, hyponatremic, and hyperkalemic which can lead to cardiotoxicity and weakness of contraction and arrhythmias

183
Q

hyperaldosteronism presentation

A

hypertension, hypokalemia and increased excretion of hydrogen ion leading to increased pH and metabolic alkalosis

184
Q

pheochromocytoma multisystem crisis

A

blood pressure dysregulation, hyperthermia, AMS, and end-organ damage

185
Q

adrenal crisis

A

patient with Addison’s has increased metabolic demand during disease or stress state and the body is unable to compensate for the demands

186
Q

Cushing’s syndrome

A

excess cortisol that causes increased gluconeogenesis, increased catabolism of proteins, easy tissue damage, and mobilization of fat from the lower extremities to the thorax, upper abdomen, and face most commonly caused by exogenous steroid use, can also be caused by pituitary adenoma, hypothalamic dysfunction with increased CRH, and paraneoplastic syndrome secreting ACTH

CABS III (5 decks)

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