Endocrinology Flashcards
1
Q
the hypothalamus produces
A
releasing hormones which stimulate the anterior pituitary to produce stimulating hormones
2
Q
the anterior pituitary gland produces
A
stimulating hormones which act directly on target organs
3
Q
endocrine hormones
A
secreted into blood and transported in the blood to distant target cells
4
Q
neuroendocrine hormones
A
secreted from neurons into the blood or transmitted via gap junctions
5
Q
paracrine hormones
A
secreted into interstitial fluid and act on target cells adjacent to the secreting cell (within close proximity)
6
Q
autocrine hormones
A
secreted into interstitial fluid and act on the secreting cell itself
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
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)
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
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)
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)
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)
13
Q
location of water-soluble hormone cell receptors
A
receptor is on the cell surface
14
Q
location of lipid-soluble hormone cell receptors
A
receptor is in the cytoplasm or nucleus
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)
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)
17
Q
water-soluble hormones
A
GH, insulin, PTH, prolactin, FSH, LH, TSH, ACTH, ADH, calcitonin, glucagon, epinephrine, and norepinephrine
18
Q
lipid-soluble hormones
A
T3, T4, estrogen, steroids including glucocorticoids (cortisol), mineralocorticoids (aldosterone), progestins (progesterone), and testosterone
19
Q
half-life of water-soluble hormones
A
rapidly broken down with a half-life of minutes
20
Q
half-life of lipid-soluble hormones
A
bound to a water-soluble transport protein with a much longer half-life
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
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)
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)
24
Q
upregulation of hormone target sites occurs when
A
there is a low level of circulating hormone
25
downregulation of hormone target sites occurs when
there is a high level of circulating hormone
26
intracellular response to binding of water-soluble hormone
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
27
intracellular response to binding of lipid-soluble hormone
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
28
high hormone disease states
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)
29
low hormone disease states
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
30
location of hormone breakdown
in the liver and excreted by the kidneys
31
structure connecting the hypothalamus to the pituitary
infundibulum or pituitary stalk
32
location of hypothalamus within the brain
part of the diencephalon at the base of the brain and is considered a major part of the limbic system
33
function of hypothalamus
made up of gray matter nuclei and their tracts and functions to produce, store, and release hormones that act on the pituitary
34
location of pituitary within the brain
measures 1 cm in diameter and sits in the hypophyseal fossa within the sella turcica of the sphenoid bone inferior to the optic chiasm
35
hypothalamic hypophyseal portal system
a group of blood vessels that extend through the pituitary stalk through which the hypothalamus communicates with the anterior pituitary
36
components of the anterior pituitary/adenohypophysis
made up of glandular cuboidal tissue and 7 types of chromophils which are the secretory cells, each of which creates its own specific hormone
37
components of the posterior pituitary/neurohypophysis
made up of neural tissue containing axons that begin within the nuclei of the hypothalamus and extend through the pituitary stalk
38
hypothalamic hypophyseal tract
a bundle of hypothalamic neural axons that extend through the pituitary stalk through which the hypothalamus communicates with the posterior pituitary
39
major blood supply to the anterior pituitary
the hypothalamohypophyseal portal system (flows through hypothalamus first)
40
major blood supple to the posterior pituitary
the inferior hypophyseal arteries which branch off of the internal carotid artery (no blood supply from hypothalamus)
41
herring bodies
terminal ends of nerves extending from the hypothalamus to the posterior pituitary where hormones are stored and released
42
function of ADH
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
43
function of oxytocin
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
44
function of TRH
released from the hypothalamus and stimulates the anterior pituitary to release TSH, inhibits prolactin release
45
function of GnRH
released from the hypothalamus and stimulates the anterior pituitary to release FSH and LH
46
function of somatostatin
released from the hypothalamus and inhibits the release of TSH and GH from the anterior pituitary, is also a regulator of many other hormones
47
function of GHRH
released from the hypothalamus and stimulates the anterior pituitary to release GH
48
function of substance P
released by the hypothalamus and stimulates the anterior pituitary to release GH, FSH, LH, and prolactin, inhibits the release of ACTH
49
function of PRH
released by the hypothalamus and stimulates the anterior pituitary to release prolactin
50
function of LH
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
51
function of FSH
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
52
function of CRH
released by the hypothalamus and stimulates the anterior pituitary to release ACTH
53
function of ACTH
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
54
function of GH
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
55
function of prolactin
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
56
location of pineal gland
within the central aspect of the brain posterior to the hypothalamus
57
function of pineal gland
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
58
pituitary adenomas
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)
59
microadenomas
adenomas smaller than 1 cm which are typically asymptomatic and hormonally silent
60
macroadenomas
adenomas larger than 1 cm which alter hormone regulation or impinge on surrounding structures (causing mass effect)
61
MEN syndrome
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
62
MEN1
associated with pituitary adenomas, parathyroid tumors, gastrinomas, insulinomas, and pancreatic tumors
63
MEN2A (2)
associated with hyperparathyroidism, medullary thyroid carcinoma, and pheochromocytoma
64
MEN2B (3)
associated with mucosal neuromas, marfanoid body habitus, medullary thyroid carcinoma, and pheochromocytoma
65
causes of hyperprolactinemia
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
66
hyperprolactinemia presentation in females
galactorrhea, changes in the menstrual cycle, and after extended exposure can cause low estrogen, hirsutism, and osteopenia
67
hyperprolactinemia presentation in males
gynecomastia, hypogonadism, erectile dysfunction, and after extended exposure can cause low testosterone, hirsutism, and osteopenia
68
gigantism
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
69
acromegaly
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
70
function of IGF-1
manages how GH affects the tissues and stimulates cellular hyperplasia and hypertrophy
71
acromegaly presentation
frontal bossing, enlarged tongue, prognathism, spade-like hands, and enlarged feet and face
72
gigantism presentation
rapid height change, increasing BMI, enlarging hands, and frontal bossing
73
risk factors for gigantism
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
74
key cation in blood
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)
75
increased sodium levels cause
increased osmolality (total solute concentration) triggering ADH secretion which results in water retention
76
hypertonic solution
when solute concentration is higher outside the cell causing water to escape and the cell to shrink
77
isotonic solution
when solute concentration is equal both outside and inside the cell
78
hypotonic solution
when solute concentration is lower outside the cell causing water to flood into the cell and can cause cells to burst
79
SIADH
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
diabetes insipidus
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
central diabetes insipidus
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
nephrogenic diabetes insipidus
when the kidneys are unable to respond appropriately to circulating ADH (kidney issue)
83
central diabetes insipidus presentation
polyuria (8-12 L/day - may have bladder enlargement and hydronephrosis), polydipsia, nocturia, and decreased urine osmolality/urine sodium
84
SIADH presentation
thirst, anorexia, fatigue, DOE, vomiting, cramping, weight gain, seizures, neurological damage or AMS
85
hypopituitarism
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
panhypopituitarism
when there are no hormones being secreted from the pituitary
87
Sheehan sydnrome
ischemia leading to necrosis of the pituitary (which is usually enlarged in pregnancy) due to postpartum hemorrhage
88
pituitary apoplexy
hemorrhage into the pituitary
89
Sheehan syndrome presentation
amenorrhea, lactation failure, secondary adrenal insufficiency, and hypothyroidism
90
infarction causing hypopituitarism
infarction causes edema which leads to increased pressure/space-occupying pressure which results in fibrosis eventually resulting in hypopituitarism
91
ACTH deficiency symptoms
decreased cortisol resulting in N/V, fatigue, weakness, hypoglycemia, weight loss, and death
92
TSH deficiency symptoms
hypothyroidism, cold intolerance, dry skin, fatigue, low metabolism, and infertility
93
FSH and LH deficiency symptoms
amenorrhea, vaginal/breast atrophy, testicular atrophy, and decreased libido
94
GH deficiency symptoms
hypopituitary dwarfism (if occurring in children), elevated BMI, osteoporosis, depression, and fatigue in adults
95
pituitary dwarfism
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
TSH is secreted by
thyrotropes in the anterior pituitary
97
function of TSH
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
blood supply to the thyroid
superior thyroid artery which branches off the external carotid and inferior thyroid artery which branches off the thyrocervical trunk from the suprascapular artery
99
the thyroid is innervated by
the recurrent laryngeal nerve which is a branch off of the vagus nerve
100
function of the recurrent laryngeal nerve
innervates the majority of the muscles of the larynx and provides sensory input for the laryngeal structures inferior to the vocal cords
101
thyroid hormone (T3 and T4) is produced by
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
length of time in which the thyroid gland stores hormone
2-3 months worth of hormone (colloid is hormone storage site)
103
calcitonin is secreted by
parafollicular cells (C cells) within the thyroid
104
function of calcitonin
lowers calcium levels in the blood by inhibiting osteoclast activity and promoting osteoblast activity in bone
105
thyroid hormone that makes up the majority of circulating thyroid hormone
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
production of thyroid hormone process
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
thyroid hormone with a longer half-life
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
location of iodide absorption
GI tract (for normal hormone function, we need 1 mg/week)
109
cellular effects of thyroid hormone
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
cardiac effects of thyroid hormone
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
growth effects of thyroid hormone
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
primary hyperthyroidism
elevated T3 and T4 with reduced TSH due to negative feedback response from T3 and T4
113
secondary hyperthyroidism
elevated T3 and T4 with elevated TSH where there is excess TSH being produced/secreted in the pituitary
114
thyrotoxicosis
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
Grave's disease
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
Grave's disease presentation
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
nodular thyroid disease
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
hypothyroidism
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
Sheehan syndrome
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
Hashimoto thyroiditis
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
Hashimoto thyroiditis presentation
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
myxedema coma
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
myxedema coma presentation
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
cretinism
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
thyroid goiter
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
PTH is produced by
chief cells within the parathyroid glands (situated behind the thyroid gland, can be 2-6), parathyroid also contains oxyphil cells with unknown role
127
function of PTH
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
physiologic effects of PTH
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
normal calcium plasma level
8.5 - 10.5 mg/dL
130
processes requiring calcium in the body
cardiac contraction, nerve conduction, cellular growth, enzyme activity, coagulation, and muscle contraction
131
calcitonin is produced by
C cells within the thyroid gland and is a water-soluble hormone
132
function of calcitonin
released from the thyroid in response to high blood calcium levels that inhibits osteoclast activity and stimulates osteoblasts which reduces blood calcium levels
133
primary hyperparathyroidism
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
secondary hyperparathyroidism
elevated PTH due to low calcium typically associated with CKD or vitamin D deficiency, NO hypercalcemia
135
tertiary hyperparathyroidism
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
hyperparathyroidism presentation
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
hypoparathyroidism
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
hypoparathyroidism/hypocalcemia presentation
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
location of pancreas
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
ampulla of Vater
where the pancreatic and bile ducts meet and empty exocrine contents into the duodenum
141
blood supply to the head of the pancreas
superior mesenteric artery (SMA)
142
blood supply to the body/tail of the pancreas
branches off the splenic artery
143
function of the pancreas
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
islets of Langerhans
organized around capillaries within the pancreas which contain 60% beta cells, 25% alpha cells, and 10% delta cells
145
normal glucose range
80-120 mg/dL
146
number of ATP molecules made for every glucose molecule
38 ATP
147
glucose gets into the cell with the help of
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
major storage location for glycogen
in the liver (when glucose is needed, glycogen release is stimulated by epinephrine and glucagon)
149
major fuel source in muscle
fatty acids and glucose where excess is stored as glycogen (broken down to lactic acid)
150
major fuel source in the brain
glucose which is able to pass more readily into these cells (does not require insulin), hypoglycemia = AMS
151
major fuel source in the retina
glucose
152
location of protein breakdown
in the liver which produces ammonia (converted to urea and excreted in urine)
153
function of amylin
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
function of insulin
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
insulin release is triggered by
primarily hyperglycemia, but also elevated levels of circulating amino acids, glucagon, gastrin, cholecystokinin, GH, cortisol, progesterone, estrogen, and autonomic innervation
156
process of insulin release from pancreas
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
effect of insulin on protein metabolism
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
effect of insulin on fat metabolism
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
process of glucagon release from pancreas
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
function of glucagon
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
type 1 diabetes mellitus
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
type 1 diabetes mellitus presentation
most common in children and young adults causing polyuria, polyphagia, weight loss, polydipsia, and blurry vision
163
type 2 diabetes
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
metabolic syndrome
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
amylin is produced by
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
life span of RBCs
120 days
167
hemoglobin A1C diagnostic for diabetes
greater than or equal to 6.5 %
168
diabetic keto acidosis (DKA)
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
DKA presentation
ketonuria, abdominal pain, nausea, vomiting, dehydration, Kussmaul respiration, electrolyte imbalance, ketone breath, weakness, confusion, and possible coma
170
hyperosmolar hyperglycemic state (HHS)
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
blood supply to adrenals
suprarenal arteries which branch off the phrenic artery
172
venous supply from left adrenal
renal vein
173
venous supply from right adrenal
directly to IVC
174
the retroperitoneal space contains
the suprarenal glands, aorta, duodenum, pancreas, ureter, colon, kidneys, esophagus, and rectum
175
the adrenal medulla is innervated by
the celiac plexus and splanchnic nerves
176
effects of aldosterone
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
aldosterone release is stimulated by
angiotensin II and potassium and to a lesser extent, ACTH
178
Addison's disease
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
melanocyte-stimulating hormone (MSH)
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
Addison's diagnosis
ACTH (cosyntropin) stimulation test
180
Addison's presentation
weakness, weight loss, hyperpigmentation, hypotension, and hyponatremia
181
Conn's syndrome (hyperaldosteronism)
increased aldosterone secretion due to tumor of the zona glomerulosa, other causes of hyperaldosteronism are familial hyperaldosteronism, adrenal carcinomas, and paraneoplastic secretion
182
hypoaldosteronism presentation
hypovolemic, hyponatremic, and hyperkalemic which can lead to cardiotoxicity and weakness of contraction and arrhythmias
183
hyperaldosteronism presentation
hypertension, hypokalemia and increased excretion of hydrogen ion leading to increased pH and metabolic alkalosis
184
pheochromocytoma multisystem crisis
blood pressure dysregulation, hyperthermia, AMS, and end-organ damage
185
adrenal crisis
patient with Addison's has increased metabolic demand during disease or stress state and the body is unable to compensate for the demands
186
Cushing's syndrome
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
