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119 Cards in this Set
- Front
- Back
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Where are glands located?
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central & peripheral nervous system
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Which endocrine organ has mixed functions?
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pancreas
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hormones
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• secreted into blood stream
• found in either free biologically active form or bound to proteins; only free hormones can bind to receptors • some require metabolism for activation >> intracellular response >> physiological response >> feedback |
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endocrine areas of pathology
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• secretion; hyper or hypo
• elimination rates; if unable to eliminate >> build up of hormones • abnormal second messenger- interrupts ability for receptor to bring about physiological response • receptors over-expression- (+) sensitivity under expression/abnormality- resistance **regardless of origin of pathology >> will affect feedback regulation and hormone levels |
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anterior v. posterior pituitary
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anterior
• mass of pituitary gland • hypothalamus release hypothalamic hormone which acts on cells in anterior pituitary >> stimulates pituitary hormone >> goes into circulation to stimulate third hormone posterior • neurological extension of hypothalamus where neurosecretory cells send axonal projection through connecting stalk and release hormone • oxytocin & vasopressin (ADH) • abnormalities is usually caused by injury to connecting stalk |
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SIADH
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• overproduction of ADH, which causes water retention
• ADH should only be released if plasma osmolarity is elevated • normal osomolarity is 290 milli osmol |
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SIADH causes
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• (+) hypothalamic production, e.g. infections, neoplasms, drug-induced (chemo or antipsychotics)
• pulmonary diseases • severe nausea/pain r/t nervous system • ectopic production of ADH r/t cancer; not under feedback mechanism • drug induced potentiation- ADH levels are normal but its effects are enhanced • idopathic |
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SIADH manifestations
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definitive findings--
• serum hypoosmolarity & hyponatremia • urine hyperosmolarity **whenever serum and urine osmolarity conflict >> something is wrong w/ ADH want to r/o other problems-- • urine sodium excretion that matches sodium intake • normal adrenal & thyroid function • no conditions that can alter volume status, e.g. CHF, renal insufficiency, etc. |
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osmoregulatory defects
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type A- random
• large & unrelated fluctuations in ADH • unrelated to rise in plasma osmolarity • associated w/ tumors type B- reset osmostat • ADH osmolarity threshold is significantly lowered • prompt & parallel rise in ADH w/ plasma osmolarity • associated w/ pulmonary DOs & drug induced SIADH **sensitivity for system is the same but threshold is lowered type C- leak • leaking of vasopressin unrelated to plasma osmolarity • plasma ADH (+) normally above the the threshold for ADH release • associated w/ meningitis or head injuries |
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AVP
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arginine vasopressin; means ADH
thanks sally, that's not confusing |
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What is the normal threshold for ADH?
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**280 milli osmol
normal ADH is 290 milli osmol |
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diabetes insipidus (DI)
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central DI- failure to secrete enough ADH
nephrogenic DI- failure to respond to ADH • excreting of large volumes of dilute urine • partial or total inability to concentrate urine • constantly dehydrated >> polydipsia • urine output can be 4-12 L/day |
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DI causes
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nongenetic--
• injuries, e.g. head trauma, tumor, neurosurgical procedures genetic-- • X-linked NDI- AVPR2 mutation; most common of irish peeps- AVPR2 mutation • autosomal NDI- AQP2 mutation • autosomal CDI can be autosomal dominant (prepro-AVP2) or autosomal recessive r/t DM, optic atrophy, and mental retardation |
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T/F. NDI is more common than CDI.
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False; CDI is more common and is usually caused by head injuries >> damage to connecting stalk >> affects ability to release ADH
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psychogenic polydipsia/polyuria
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accompanies delirium and schizophrenia; ADH system is normal
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lab values for DI
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DI treatment
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CDI--
• desmopressin is synthetic ADH NDI- • vigilant attention to water consumption/loss • paradoxical treatment w/ thiazide diurtetic; patient will have (+) response to ADE >> enhances Na+ and H2O reabsorption in proximal tubule |
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What characterizes anterior pituitary diseases?
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**hyposecretion & hypersecretion of hormones
pituitary tumor is the most common cause in both hyposecretion & hypersecretion-- • small/normal size tumors >> hypersecretion • large tumor crushes the gland >> hyposecretion |
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hypopituitarism causes
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• adenomas
• sheehan syndrome- result of postpartum hemorrhage; anterior pituitary gets larger and O2 demands (+) >> ischemia >> hyposecretion • iatrogenic hypopituitarism • trauma • infiltrative diseases • genetic abnormalities of pituitary development • laron syndrome- growth hormone insensitivity |
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adenoma
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non-cancerous tumors located in anterior pituitary; often derived from the following cell types--
• somatotropes >> GH • lactotropes >> prolactin • gonadotropes >> LH and FSH • thyrotropes >> TSH • corticotropes >> ACTH |
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adenoma classification
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classical--
• acidophil- oversecretion of GH • basophil- oversecretion of ACTH • chromophobe- no endocrine hyper function **now classified based on hormone they secrete microadenomas are < 10 mm macroadenomas are > 10 mm; in addition to over secretion, can cause damage to gland and other neuro symptoms, e.g. blurred vision, headaches, etc. |
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lactotrope adenoma
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**most common
• microadenomas • in females--amenorrhea, galactorhea, infertility • in males--decreased libido, erectile dysfunction |
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nonfunctional pituitary adenomas
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**these adenomas are not secreting hormones; main concern is their size
• null cell adenomas • oncocytoma • silent adenomas |
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somatotrope adenoma
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• 75% are macroadenomas
• oversecretion of GH >> gigantism & acromegaly hypothalamus >> GHRH >> anterior pituitary >> GH GH >> direct & indirect effects 1/ directly acts on target cells directly 2/ acts on liver to stimulate release of IGF (insulin-like growth factor), which acts on target cells • GH has anti-insulin effects, released @ night during non-REM sleep >> GH gets into blood stream and causes rise in blood glucose • (-) uptake of glucose and stimulates liver to put out glucose • second wave of hormone is IGF; IGF brings all the glucose built up into the cell and stimulates growth |
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somatotrope adenoma effects
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acromegaly v. gigantism--
• gigantism- prepuberty; elongation of long bones >> extreme stature b/c epiphyseal plate is not yet solidified • acromegaly- post-puberty; (+) proliferation in connective tissue, cytoplasmic matrix, organ size, & thickening of bones metabolic effects-- • (+) metabolic rate • (+) GH inhibition of glucose uptake • (+) hepatic production of glucose >> (+) risk of DM |
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What is the hormone that inhibits GH?
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somatostatin
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What hormone levels would you expect to observe in patients w/ somatotrope adenoma?
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(+) GH and IGF & low GHRH due to negative feedback @ hypothalamus and anterior pituitary for both GH and IGF
**tumor is ignoring signals |
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somatotrope adenoma manifestations
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• prominent brow ridge & jaw; patients will often look like they are related
• changes in facial features are reversible but tall stature is not • (+) body hair • (+) metabolic rate >> sweat, (+) cardiac demands which lead to cardiovascular problems |
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somatotrope adenoma treatment
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• surgical intervention depending on size of tumor
• octreotride- synthetic somatostatin |
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thyroid hormone system
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hypothalamus >> TRH >> anterior pituitary >> TSH >> thyroid gland >> T3 and T4 >> provides feedback to hypothalamus and anterior pituitary
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thyroid hormone abnormalities
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• hypothyroidism
• hyperthyrodism • euthyroid |
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euthyroid
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**pathology is involved but TH is WNL
non-toxic goiter • problem originates in thyroid gland itself; impaired T3 and T4 production • system compensates by producing more TSH in order to produce normal amounts of T3 and T4 • TSH stimulates hypertrophy & hyperplasia of thyroid gland **can develop into toxic goiter >> hyperthyroidism |
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hypothyroidism causes
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primary--
• hashimoto thyroiditis • postradioactive iodine therapy for hyperthyroidism kills off excess thyroid cell; if dosing is not precise >> hypothyroidism • thyroidectomy • radiation for head/neck cancer • iodine deficiency- iodine is needed to synthesize TH • congenital DOs of TH synthesis other causes-- • excessive iodine is toxic to thyroid gland • drugs, i.e. lithium, interferon alpha (antiviral given to hepatitis patients), some anti-epileptic • diseases of hypothalamus |
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hashimoto thyroiditis
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**causes hypothyrodism
immune system attacks thyroid cells-- body produces T cells and B cells that are reactive to thyrocytes >> produce antibodies that will kill off thyroid cells >> reduces hormone production |
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hypothyroidism manifestations
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**manifestation of low metabolism
• pale • cold • constant fatigue • loss/thinning of hair/eyebrows • hoarseness to voice • non-pitting edema >> enlargement of <3 and brain >> chain in neurological function >> AMS and possible coma • amenorrhea/cycle abnormalities |
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hyperthyroidism causes
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• presence of abnormal thyroid stimulator, e.g. grave's disease
• intrinsic disease of thyroid gland, e.g. toxic multinodular goiter, functional adenoma • excess production of TSH by anterior pituitary, e.g. thyrotroph adenoma |
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graves disease
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**most common cause of hyperthyroidism
atypical immune system disorder-- • B cells produce antibodies that attach to TSH receptor which acts as TSH agonist • antibodies are referred to as TSI (thyroid stimulating immunoglobulin) and mimics TSH >> acts on thyroid gland and (+) T3/T4 • not part of (-) feedback; (+) T3/T4 >> (-) TRH & TSH; TSI continues to stimulate thyroid |
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graves disease manifestations
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**effects of (+) metabolism--
• slender, struggle to maintain weight • high strung, can't sit still >> hand tremors • fine hair • goiter • (+) sweating • tachycardia • amenorrhea • bulging eyes due to retro-orbital adema |
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T/F. All types of thyroid problems can lead to goiters.
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true; it is a sign of a thyroid problem, but it does not reveal the TYPE of thyroid problem
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corticotrope adenoma
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• excess ACTH
• cushing syndrome |
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congenital adrenal hyperplasia (CAH)
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hyperplasia of adrenal gland, esp. adrenal cortex
causes-- • result of a number of autosomal recessive enzymatic defects in the biosynthesis of cortisol from cholesterol effects-- • more than 90% of cases of CAH represent a deficiency of 21-hydroxylase >> buildup of intermediates and the increased production of androgens • most common cause of ambiguous genitalia in newborn girls Infant boys may experience sexual precocity and stunted growth |
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addison disease
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**adrenal cortical insufficiency
• autoimmune destruction of adrenal tissue; progressive deficiency of cortisol and aldosterone • lack of aldosterone creates more significant manifestations that lack of cortisol; aldosterone regulates Na+ balance which affects blood volume & BP |
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addison disease manifestations
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• hyperpigmentation- excess ACTH on melanocytes
• weakness, fatigue, anorexia, weight loss r/t BP • dizziness r/t orthostatic hypotension >> syncope due to volume depletion • hyponatremia & hyperkalemia • salt craving • adrenal crisis |
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adrenal crisis
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**patients w/ addison cannot adequately initiate stress response; when faced w/ physical trauma, significant illness, or infection, they decompensate quickly
• @ baseline, have a hard time maintaining BP b/c of (-) cortisol which is needed for vasoconstriction and is necessary for norepinephrine to regulate BP • stress >> hypotension, shock, death; make sure they get supportive steroids |
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cushing syndrome
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**adrenal hyperfunction; chronic elevated glucocorticoids
causes-- • exogenous steroid administration, e.g. s/p organ transplants • endogenous glucocorticoid overproduction, e.g. ACTH-producing pituitary adenoma, certain lung cancers • primary adrenal lesions, e.g. adrenal adenomas/carcinomas • ectopic ACTH production |
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T/F. Women on steroids are more likely than men to develop cushing syndrome.
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True
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cushing syndrome manifestations
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effects of cortisol...on crack
• (+) blood glucose >> hyperglycemic, signs of DM; if pancreas is in good shape, can maintain normal glucose levels • skin breakdown b/c body cannot mobilize acute inflammatory response, e.g. ulcers, poor wound healing • immunocompromised • (+) subcutaneous fat on face >> red face, chipmunk cheeks aka "moon face" • (-) subcutaneous fat everywhere else >> slender limbs • (+) central adiposity >> abdominal & back fat aka "buffalo hump" • (+) vasoconstriction & BP >> HTN & LV hypertrophy • cortisol demineralize bones >> early osteoporosis • amenorrhea & decreased fertility in women |
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diabetes mellitus (DM)
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disturbance of glucose homeostasis; characterized by chronic hyperglycemia and other disturbances in carbohydrate and fat metabolism
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regulation of glucose homeostasis
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1/ glucose production in liver & sometimes kidneys
--energy substrate (lactate acid and AA) are sent to liver & kidneys >> gluconeogenesis >> blood stream 2/ glucose storage in skeletal muscle & liver --glycogen synthesis, glycogenolysis 3/ glucose uptake by peripheral tissue, esp. skeletal muscle, liver, & fat **insulin-mediated; uptake by peripheral tissue is regulated b/c they can derive energy by other means; when glucose is low, uptake can be limited & redirected to tissues that cannot make their own energy, e.g. neuro tissues |
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normal fluctuations in plasma glucose
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• absorptive- actively consuming food; priority is to (-) plasma glucose to prevent marked elevation
• post-absorptive- fasting; priority is to (+/maintain) plasma glucose to prevent marked drop |
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absorptive state
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**limit use of fat as primary energy source, (+) fat storage
(-) gluconeogenosis and gluconeolysis (+) tissue permeability to glucose (+) glucose storage- glycogen synthesis |
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post-absorptive state
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**use of fat as primary energy source
• release of glucose from stores • gluconeogenesis • limit access to glucose to only tissues that absolutely need it by dropping insulin levels |
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How does glucose get in and out of cells?
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glucose enters & exits via facilitated diffusion--transporter binds and carry glucose across a concentration gradient
glut-1 transporter-- • constitutively expressed by all cells and is responsible for low levels of basal glucose uptake • expression is increased with prolonged fasting and decreased by persistent exposure to excessive glucose glut-4 transporter-- • not constitutively expressed, availability is dependent on insulin • expressed in cardiac, skeletal, adipose, and liver tissues |
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insulin and glut-4 interaction
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PI-3K pathway--
• glut-4 found inside cell on plasma membrane of intracellular vesicle • insulin binds to receptor >> signals PI-3K >> stimulates exocytosis of glut-4 into plasma membrane so glucose can be taken up PI-3K also stimulates-- • cell survival/proliferation • lipid, protein, & glycogen synthesis MAPK signaling pathway-- • cell growth/proliferation |
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pancreas
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**has both endocrine & exocrine component
endocrine portion aka islet of langerhans-- • secretes both insulin and glucagon, which are antagonists for one another exocrine portion-- • duct cells secrete aqueous NaHCO3 solution • acinar cells secrete digestive enzymes >> both are mixed w/ bile and secreted into duodenum and are critical for digestion |
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What is the islet of langerhans composed of?
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a-cells secrete glucagon
b-cells secrete insulin |
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actions of insulin
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**absorptive state; promotes lipogenesis, inhibits lipolysis
(-) gluconeogenosis & glycogenolysis (+) tissue permeability to glucose by affecting glut-4 transporters (+) glycogen systhesis any significant concentration of insulin is a strong signal for adipose tissue to maintain its density; if there's no insulin in bloodstream >> adipose tissue breakdown |
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actions of glucagon
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**postabsorptive state; promotes lipolysis, inhibits lipogenesis
• release of glucose from storage • gluconeogenesis • limit access to glucose; presence of glucagon decreases >> decreases insulin >> glut-4 retracts limiting permeability to glucose stimulates enzymes needed for glycogenolysis & gluconeogenesis |
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insulin & glucagon diagram
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insulin release
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1st peak is associated w/ cephalic phase of digestion; has nothing to do w/ plasma glucose
**is critical 2nd peak is triggered by rise in blood glucose |
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DM classifications
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primary forms--
• DMI- autoimmunity that causes B-cell destruction >> absolute insulin deficiency; idiopatic • DMII- insulin resistance w/ relative insulin deficiency • genetic defects of B-cell function- e.g. maturity-onset diabetes of the young (MODY) is caused by mutations in several autosomal genes producing defects in insulin production; mild version of DMI secondary forms-- • exocrine pancreatic defects, e.g. chronic pancreatitis, pancreatectomy, neoplasia, & cystic fibrosis • endocrinopathies, e.g. acromegaly, cushing syndrome, hyperthyrodism • infections, e.g. CMV, coxsackie virus • drugs, e.g. glucocoritcoids, thyroid hormones, a-interferon, b-adrenergic agonists, protease inhibitors, thiazides; **any steroids will elevate glucose levels • genetic syndromes- down, turner, & kleinfelter • gestational diabetes- temporary diabetes that affect women during pregnancy |
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T/F.
DMI- insulin-dependent, juvenile onset DMII- non-insulin dependent, adult onset |
False;
DMI- increasing cases of adult onset DMII- increasing childhood cases due to environmental lifestyle factors; treated w/ insulin earlier and become independent |
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"pre-diabetic" condition
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• impaired glucose tolerance (IGT)- rise of blood glucose is not adequately responded to by the body
• impaired fasting glucose (IFG)- persistent elevation |
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DM screening tools
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• oral glucose tolerance test (OGTT)- challenge test to person's system
• fasting plasma glucose (FPG)- finger stick for capillary blood s/p 12-hrs fast; slight underestimation of plasma glucose • HbA1C- hemoglobin in blood stream that attaches to glucose; reflects 2-3 mos of average blood glucose; heavily weighted to most recent 2 weeks |
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glucose and HbA1C values
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glucose--
normal < 100 mg/dl IFG 100-126 mg/dl DM > 126 mg/dl HbA1C-- normal < 5.7 IGT 5.7-6.4 DM > 6.5 |
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oral glucose tolerance test
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1/ fast prior to test
2/ fasting level is obtained 3/ drink high concentration of glucose; ~75 g for avg person, ~100 for pregnant • not the standard; don't want to give diabetics a shot of glucose; FPG is standard for diagnosis • useful in detecting early signs of diabetes |
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Why use oral glucose v. bolus of glucose for OGTT?
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giving bolus will skip cephalic peak
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DMI
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**absolute insulin deficiency & exceedingly high levels of glucagon
two major types-- • immune type 1 • idiopathic type 1 |
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DMI pathogenesis
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absolute insulin deficiency >> glucose cannot be taken up by cells; liver cannot take up glucose >> will think it is in a post-absorptive state and (+) glucose
• clinical onset is abrupt but autoimmune attack is chronic and usually starts years before • clinical manifestations occur at >90% B-cell destruction mechanisms for B-cell destruction-- • T-cell mediated immune attack against poorly defined B-cell antigens • cytokine induced B-cell damage • autoantibodies against islet cells or insulin; in 70-80% of patients; usually accompanied by autoantibodies against B-cell antigens genetic susceptibility-- • MHC locus- presence of certain MHC II alleles, which affects T cell antigen presentation • non-MHC genes- tandem repeats polymorphs of insulin gene, which turns off insulin reactive T-cells environmental factors-- • infections, e.g. MMR |
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DMII
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genetics & environmental factors--
• concordance rate b/w identical twins is 50-90% and 20-40% b/w first degree relatives v. 5-7% in general population • activity level, diet • most powerful risk is obesity, esp. high abdominal adiposity ( >1 waist-to-hip ratio), increased visceral adiposity; fat underneath abdominal muscle is worst b/c it surrounds the organs |
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DMII pathogenesis
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metabolic defects--
• insulin resistance; (-) sensitivity to insulin by peripheral tissue • B-cell dysfunction >> unable to produce enough insulin to overcome resistance • insulin resistance is usually primary even, B-cell dysfunction is secondary |
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What causes insulin resistance?
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**abnormalities of insulin signaling pathway
• down-regulation of insulin receptors • (-) insulin receptor-initiated kinase activity • reduced levels of insulin receptor signaling intermediates • impaired docking & fusion of GLUT4-containing vesicles w/ plasma membrane |
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B-cell dysfunction
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1/ initially >> hyperinsulinemic state can maintain maintain normal plasma glucose
2/ early B-cell failure-- • loss of normal pulsatile/oscillating pattern of insulin secretion • loss of "rapid phase" insulin secretion triggered by elevation of plasma glucose • secretory defects affect all phases; some basal secretion persists 3/ late B-cell failure-- • (-) B-cell mass • islet cell degeneration • amyloid islet deposition >> scar tissue **beginning of absolute insulin deficiency >> DMII will start to look like DMI |
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Why is catching DMII early so important?
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By catching DMII early & making necessary lifestyle changes, patients will reduce insulin resistance >> gives B-cells time to heal and reduce chronic inflammation.
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obesity and DM
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• link b/w obesity & DM is mediated through insulin resistance; esp. central adiposity b/c it is close to liver >> insulin resistance is more directed to liver and can cause DM to precipitate more quickly
• prolonged caloric overload and hypertrophied state causes derangement of normal adipocyte endocrine function recent hypotheses-- 1/ elevated circulation FFA interferes w/ insulin's ability to bind w/ receptors 2/ adipocyte hypertrophy stimulates release of cytokines that attract microphages 3/ chronic inflammation causes (+) lipolysis which elevates FFAs; back to numero uno |
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T/F. Fat can also act as an endocrine tissue.
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True; in addition to storage, fat also contributes to overall energy balance and releases hormones (adipokines) to help regulate food intake & energy balance
• adiponectin- enhances insulin sensitivity, inversely related to body fat • resistin- reduces sensitivity; directly proportional to body fat • leptin- acts on brain, inhibitory effect on appetite and food intake; ideally correlated to overall fat mass |
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gestational DM
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• hPL ensures that fetus has enough glucose to support growth and development of brain during last
stages; does this by antagonizing insulin stores (decreases sensitivity) • mom responds by increasing plasma insulin -------- • GDM women cannot produce insulin levels high enough to overcome pregnancy induced insulin resistance • hPL levels drop and insulin resistance goes away s/p delivery • GDM moms have increased risk of DMII; pancreas may not be able to meet increased demands |
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DM manifestations
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appears in all forms of DMs in this order--
1/ hyperglycemia 2/ glucosuria 3/ polyuria 4/ polydipsia complications-- • hypoglycemia • hyperglycemia coma • diabetic ketoacidosis • hyperosmolar hyperglycemic nonketotic snydrome |
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hypoglycemia symptoms
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autonomic--
**first set of response >> strong cue to eat something • adrenergic- tremors, anxiety, palpitations, tachycardia • cholinergic- sweating, hunger neurologic-- • weak, fatigued, drowsy • headache • AMS, confusion • diplopia • difficulty speaking, slurring • seizures, coma **hypoglycemic unawareness w/ repeated episodes; loss of autonomic signals >> first clues are neurologic |
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glucose counter regulation
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T/F. Activation of sympathetic nervous system is solely make person aware of low blood glucose.
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False; it also stimulates glycogenolysis and gluconeogenesis
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T/F. Glucagon response to hypoglycemia goes away and normal counter-regulation decreases for people w/ chronic diabetes for many years.
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True; their onset and progression is rapid and quick >> HbA1C value is higher than normal to balance (+) risk of hypoglycemia
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diabetic ketoacidosis (DKA)
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**absolute deficiency of insulin or an increase in counter-regulatory hormone, e.g. catecholamines or glucagon >> (+) fat metabolism, causing (+) production of keto-acids
• occurs w/ increased frequency w/ infection, trauma, surgery, MI, or (+) stress occurs in following conditions-- plasma glucose 250 mg/dcL pH < 7.3 |
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DKA manifestations
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• kussmaul respirations- hyperventilate to compensate for acidosis
• postural dizziness • CNS depression • nausea • abdominal pain • polydipsia, polyuria • ketouria >> dehydration >> hypotensive, tachycardia |
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What is the main difficulty of treating DKA?
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**managing hyperkalemia while patients are vulnerable to hypokalemia
• K+ is vulnerable to changes in acidosis; K+ will shift out of cells in exchange of H+ going into cells >> patient can appear hyperkalemic • BUT they are actually hypokalemic b/c K+ is pushed out of cell and is being excreted via urine • insulin brings K+ into cells >> can (+) risk of hypokalemia |
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T/F. DKA is seen exclusively in DMII.
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False; seen exclusively in DMI--there is adequate level of insulin to maintain fat stores in DMII
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hyperosmolar hyperglycemic nonketotic syndrome (HHNK)
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**similar to DKA minus ketoacidosis
insulin levels high enough to suppress lipolysis but not high enough to facilitate glucose entry to skeletal muscle & fat tissue occurs in following conditions-- glucose > 600 plasma osmolarity ~310 (high) • usually seen in DMII; is a complication of insulin resistance & relative deficiency |
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HHNK manifestations
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• hyperglycemia
• glucouria • polyuria • polydipsia |
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DM chronic complications
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**extreme variability among patients
macrovascular-- • coronary artery disease, e.g. ischemic heart disease, MI, heart failure • cerebrovascular disease, e.g. CVA • peripheral vascular disease; plaques >> poor circulation to legs >> diameter gangrene, ulcers, lower limb amupation microvascular-- • diabetic nephropathy • diabetic retinopathy neuropathy-- • autonomic • sensory |
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diabetic nephropathy
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• endothelial cells in glomerular capillary are esp. vulnerable; 1/3 of renal failure in due to hyperglycemia
• glomerular membrane thickens >> sclerosis (scarring of capillary) >> progressive damage >> cascade of compensatory of hypertrophy, etc. • nephrons cannot keep up >> renal insufficiency >> renal failure |
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diabetic retinopathy
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retina of eyes are thin neuronal cells @ back of eye; delicate & highly vascularized // higher incidence w/ HTN
phase one-- • non-proliferative- vision is not impaired unless it occurs @ macula • aneurysm, hemorrhage, exudate due to capillary damage phase two-- • proliferative- capillaries die and retina become hypoxic >>growth of abnormal vessels >>hemorrhage & bleed gets into vitruous and impairs vision • as new vessels are forming, can pull on retina and cause detachment >> loss of vision |
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T/F. Autonomic neuropathy occurs prior to sensory neuropathy.
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False; sensory occurs prior to autonomic neuropathy
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sensory neuropathy
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**dulled perception of esp. vibrant vibration & temperature for most patients
--can be very painful to some >> aledenia- enhanced perception of light touch • most noticeable in extremity, esp. in lower limbs • usually bilaterally & symmetrical |
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autonomic neuropathy
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** reflexes/autonomic functions are dulled
can affect-- • GI- n/v/anorexia • erectile dysfunction • cardiovascular baro-reflex maintains perfusion to brain >> loss will cause orthostatic hypertension; this is called autonomic dysreflexia |
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peptic ulcer disease (PUD)
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• break in protective mucosal lining of lower esophagus, stomach, or duodenum >> exposes submucosa to gastric secretions >> causes autodigestion
• ulcers can be acute or chronic, superficial or deep |
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locations of peptic ulcers
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• lower esophageal; gastric acid from stomach can cause reflux into lower esophagus
• antrum of stomach; cells that produce HCl are found in antrum • duodenum; most common--does not have thick alkaline mucus covering but receives acidic contents from stomach making it extremely vulnerable |
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erosion
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• superficial ulcer
• mucosal lining is thin or broken; underlying blood vessels/muscle layers are intact & unaffected • asymptomatic- gastric acid is not interacting w/ nervous tissue |
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acute ulcer
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• true, deep ulcer
• penetrates through submucosal layer and penetrates into muscle layers • becomes painful; gastric acid interacts w/ nerves within walls of stomach or GI tract |
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perforating ulcer
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• penetrates through layers of GI tract
• exposes body cavities to contents of tracts • dangerous |
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PUD risks
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**anything that (+) gastric acid production >> (+) irritation of mucosal lining, OR (+) inflammation >> damage to mucosal lining
• smoking • H. pylori infection • NSAIDs • alcohol • high psychological stress • emphysema • rheumatoid arthritis • cirrhosis |
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H. pylori
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• found in 50% of stomachs; can trigger ulcers in 10-15%
• bacteria is thought to cause > 90% of duodenal ulcers & 80% of gastric ulcers • contributes to stress/injury to mucosal lining how does it cause peptic ulcers? • stimulates acid production • releases toxins >> mucosal irritation • (+) inflammatory response if detected by immune system |
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T/F. Duodenum depends on NaCHO3 to prevent ulcers.
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True
food moves from stomach to duodenum; presence of food/acid triggers duodenum to release CCK and secretin >> which triggers liver and pancreas to release bile and digestive juices into the duodenum secretin acts on exocrine portion of pancreas and binds to duct cells >> releases NaCHO3 (alkaline) >> enters duodenum and is designed to neutralize acid from stomach |
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duodenal ulcer causes
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• hypersection of gastric acid and pepsin, e.g. smoking, H. pylori infection, excess parietal cells (which produces HCl)
• elevated plasma gastrin- stimulates gastric acid & pepsin • inadequate secretion of pancreatic NaCHO3; mechanism for neutralizing acid is impaired • excessive rapid gastric emptying does not give duodenum enough time to neutralize acid • immune reaction to H. pylori can cause damage to duodenal lining |
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duodenal ulcer
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**manifestation is chronic intermittent pain in epigastric region; heals spontaneously but reoccur within months
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T/F. Gastric ulcers are acute and do not heal on its own.
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True
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food-pain relief pattern
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**consuming food triggers acid production by stomach >> pain BUT additional consumption can alleviate pain b/c it gets b/w acid and ulcer
gastric ulcers-- • food immediately enters stomach >> no immediate pain • pain after 20-30 mins • keep consuming to automatically relieve pain duodenal ulcers-- • food moves out of duodenum after an hour >> starts to feel pain • consume food 20-30 mins after initial consumption >> relief |
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PUD treatment
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• antacids, i.e. histamine blocker >> decreases acid production
• proton pump inhibitor, e.g. omeprazole; is an antacid proton pump moves H+ out of parietal cell into stomach >> will bind w/ chloride to make HCl • antibiotic to treat H. pylori infection reduces damage to duodenum and stomach lining • anti-cholinergic drugs inhibit secretion, suppresses gastric motility, and delays gastric emptying |
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stress ulcer
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• acute form of PUD that accompanies severe illness, systemic trauma, or neural injury
• ischemic • involves multiple sites distributed throughout stomach & duodenum **triggers of stress response changes perfusion to GI tract |
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cushing ulcer
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• type of stress ulcer
• particularly severe, involves trauma and activation to stress response; normal pathology + increase acid production trauma is to part of brain where vagal nerve originate >> stress response and intense activation of vagus nerve stimulating gastric acid production |
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maldigestion v. malabsorption
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maldigestion >> malabsorption
however, there are primary malabsorptive disorders--anything that affects absorptive surface area of small intestine, e.g. anything that kills mucosal cells that affects villi/microvilli of small intestine |
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pancreatic insufficiency
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**occur when both endocrine and exocrine pancreas is effected, e.g. pancreatitis, pancreatic carcinoma, or cystic fibrosis
deficient production of pancreatic enzymes; very devastating when exocrine pancreas is affected b/c it is necessary to digest all types of food • lipase- fat • amylase- carbs • trypin & chymotrypsin- protein |
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T/F. Amylase insufficiency is the most devastating part of pancreatic insufficiency.
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False; lipase insufficiency
• pancreas is the only source of lipase • fat is the most caloric dense form of food >> w/o it, unable to maintain weight >> body wasting |
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What is the clearest sign of pancreatic insufficiency?
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• weight loss
• steatorrhea- fat in stool; oily, smelly, yellow, & can float! |
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bile salt deficiency
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• caused by cirrhosis, obstruction of bile ducts, anything that can decrease bile production
• bile emulsifies fat so that it cannot re-form; fat-soluble vitamins get trapped in big glob of fat clinical manifestations r/t poor intestinal absorption of fat and fat-soluble vitamins >> deficiencies in-- • A- night blindness • D- decreased calcium absorption >> bone demineralization (osteoporosis), bone pain, & fractures • K- prolonged prothrombin time >> bleeding & spontaneous bruising • E- neurological effects, esp. in children as their nervous system is maturing |
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T/F. Bile salt deficiency will not have same effect on fat digestion as pancreatic deficiency.
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True
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What color stool do you expect from a patient w/ bile salt deficiency?
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bilirubin in bile is what colors feces brown; in absence of bile >> stool will be gray or clay-colored
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disaccharides
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maltose = glucose + glucose
sucrose = glucose + fructose lactose = glucose + galactose |
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lactose deficiency
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aka lactose intolerance
• disacchridases are found on plasma membrane of mucosal cell in small intestine within microvilli; they are bound to the brush border • lactase is a recessive trait; dominant trait is the progressive decline of lactase formation as we age (no longer need breast milk) • inability to lactase is esp. common in african or middle eastern descent lactose moves through small intestine >> large intestine undigested; gets consumed by bacteria of the colon and goes through fermentation >> • gas is one of the byproduct >> painful gas cramps • severe flatulence • presence of lactose in colon (+) osmolarity of feces and draws water into colon >> causes osmotic diarrhea |
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T/F. Cheese and yogurt is easier for lactose intolerant patients to digest than milk.
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True; the milk in these products have been incorporated w/ non-harmful bacteria and fermentation process has already started
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