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232 Cards in this Set
- Front
- Back
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amine hormones
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hormones derived from tyrosine
-thyroid hormones -catecholamines |
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adrenal glands location
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on top of each kidney
(ad-next to, renal-kidney) |
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adrenal medulla secretes
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amine hormones
mostly epinephrine |
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adrenal cortex secretes
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steroid hormones
1)aldosterone 2)cortisol 3)corticosterone 4)DHEA 5)ancrostenedione |
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what is adrenal medulla evolutionary context
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modified sympathetic ganglion without axons.
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role of nervous system in hormonal control
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1) hypothalamus directly (PP)
2) hypothalamus indirectly (AP)(+/-) 3) ANS directly (adrenal medulla) 4) ANS indirectly (through autonomic ganglion to endocrine gland cell)(+/-) |
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Why does adrenal medulla secrete epinephrine the most?
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because it has PNMT which converts NE into EPI
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peptide hormones
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hormones that are composed of small proteins and sometimes glycoproteins.
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peptide hormone synthesis
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synthesized as preprohormones in ER. they are then cleaved into prohormones and packaged for secretion. During the packaging, they are cleaved again into active hormones.
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steroid hormones
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have 4 carbon rings. synthesized in adrenal cortex (and the gonads).
they are all derived from cholesterol |
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aldosterone
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mineralocorticoid (effects are on mineral regulation)
controlled by angiotensin II. Enters circulation and stimulates water and Na RETENTION and K and H SECRETION in the kidneys. |
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cortisol
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glucocorticoid (effects are on glucose metabolism)
***NOT COMPLETED |
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DHEA and androestendione
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called androgens
similar actions as testosterone |
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3 layers of adrenal gland
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zona glomerulosa (outer cortex) - aldosterone
[have enzymes to convert corticosterone to aldosterone but not to make cortisol] zona fasciculata and reticularis (inner cortex) - cortisol and androgens [have enzymes to convert corticosterone to cortisol but not to make aldosterone] |
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hormonal transport
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peptide and amine hormones are hydrophilic and are transported in blood plasma.
steroid and thyroid hormones are hydrophobic and are bound to plasma proteins |
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total hormone concentration in blood
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the sum of free and bound hormones.
however only the free hormones are biologically important since only they can diffuse out of capillaries |
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what happens after a hormone enters circulation?
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1) excreted through urine/feces
2) inactivated by metabolism 3) activated by metabolism 4) directly binds to target cells for response both 3 and 4 result in a cellular response |
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hormonal plasma concentration depends on:
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rate of secretion
rate of removal (simple enough) |
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how are hormones metabolized
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-liver/kidneys (excretion)
-target cell can metabolize the hormone. [some even digest the hormone intracellularly] -enzymes in blood/tissues |
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why are peptide/amine hormones eliminated from blood stream so fast while steroid/thyroid hormones can remain for much longer?
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amine/peptide hormones are nearly all free and are thus open to enzymatic metabolism
however, steroid/thyroid hormones are mostly bound to proteins and are protected from enzymatic breakdown |
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trends for the enzymatic breakdown of hormones in blood plasma vs binding affinity
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the higher binding affinity a hormone has, the longer it will remain in the blood and be protected from enzymatic digestion
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up-regulation
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increase in the number of hormones receptors.
results from a prolonged exposure to low concentration of hormone |
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down-regulation
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decrease in number of hormones receptors
results from prolonged exposure to high concentrations of the hormone. |
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permissiveness
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one hormone can regulate another hormones effectiveness by regulating it's receptors.
in other words, A must be present (usually in low concentrations) for the full strength of B's effect. |
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example of permissiveness
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thyroid hormones are permissive to the actions of epinephrine.
this is becuase thyroid hormones stimulate synthesis of B receptors and thus allows for EPI to have a greater effect |
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effects of peptide/amine hormones
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bind to plasma membrane receptors.
[cannot cross the bilayer] rapid (non-genomic) response [mostly] delayed (gene transcription) response |
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effects of steroid/thyroid hormones
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receptors are intracellular
[cross bilayer freely] almost always have genetic response as a transcription factor sometimes bind to membrane receptors for fast response |
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what are the inputs that act directly on endocrine cells to regulate secretion of hormones
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-neurotransmitters (CNS)
-other hormones -ions/nutrients -gi tract (not important for now) |
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ion/nutrients role in hormonal control
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the presence of the substance usually triggers hormonal secretion which has a negative-feedback control to decrease the substances plasma concentration
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tropic hormone
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a hormone that stimulates the secretion of another hormone.
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trophic hormone
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a hormone that stimulates the growth of the stimulated gland
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4 ways to characterize endocrine disorders
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1) hyposecretion
2) hyoersecretion 3) hyporesponsiveness 4) hyperresponsiveness |
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primary hyposecretion
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condition where an endocrine gland secrets too little hormone because it is not functioning normally
-destruction of gland -enzyme deficiency -dietary deficiency |
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secondary hyposecretion
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endocrine gland is not damaged but receives too little tropic hormones.
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how to distinguish between primary and secondary hyposecretion
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administer the tropic hormone
if gland responds then most likely secondary if gland does not respond then most likely primary HOWEVER, sometimes it could be secondary but the gland atrophys and no longer responds to tropic hormone anyway so look out for that! |
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primary hypersecretion
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the endocrine gland secretes too much of the hormone on its own
-commonly caused by a tumor |
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secondary hypersecretion
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excessive stimulation of the gland by its tropic hormone
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how to distinguish between primary and secondary hypersecretion
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measure concentrations of both the hormone and the tropic hormone.
if both concentrations are elevated, it is secondary. if tropic hormone is not elevated, it is primary [the decreased tropic concentration is due to negative feedback] |
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causes of hyporesponsiveness
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-deficiency/abnormal receptors for hormone
-event occuring after hormone binds to receptors may be defective -some hormones are not properly metabolically activated |
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pituitary gland
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aka: hypophysis
lies below the hypothalamus in the sellaturcica of the sphenoid bone |
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sella turcica
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pocket of the sphenoid bone that encases the pituitary gland
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anterior pituitary
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adenohypophysis (hormonal)
arises from invagination of pharynx receives indirect HORMONAL input from hypothalamus via the hypothalamo-pituitary portal vessels hypothalamic neurons terminate on the median eminence where the portal capillaries begin. |
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posterior pituitary
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neurohypophysis (neural)
Gets direct NERUAL projections from the hypothalamus. considered to be an extension of the hypothalamus. Activation causes hormonal exocytosis onto the systemic capillaries. |
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one sign of a pituitary tumor
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visual problems due to pressure on the optic chiasm.
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portal vessels
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blood vessels that pick up hormones in one place (hypothalamus-median eminence) and carry them to a very specific place only (anterior pituitary) as opposed to the general circulation
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where do portal vessels drain?
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They bypass the general circulation. and collect in PORTAL VEINS.
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what is unique about pituitary gland receptors
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they have a ridiculously high affinity to hypothalamic hormones. only very small concentrations are needed.
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short-loop feedback vs long-loop feedback
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short-loop feedback is exerted by the anterior pituitary hormone on the hypothalamus.
long-loop feedback is exerted on the hypothalamus (or a.p.) by the third hormone in the sequence |
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typical flow chart for hormonal release starting with the hypothalamus
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hypothalamus--> A -->anterior pituitary--> B -->Endocrine gland--> C -->target cells
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hormones released by the posterior pituitary
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oxytocin
vasopressin/ADH |
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Oxytocin
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peptide hormone
1) induces the secretion (not production) of milk by contracting muscles in the breasts. [has nothing to do with production] 2) increase contraction of the uterus during labor (an example of a positive feedback loop starting with the stretch receptors lining the uterus) 3) emotional bonding (not enough evidence) |
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can oxytocin induce labor?
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no. it makes contractions stronger but does not stop them. instead, oxytocin is used to help move labor along.
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vasopressin/ADH
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peptide hormone
1) vasoconstrictor (increases blood pressure) 2) anti-diuretic (causes kidneys to retain water) [MOST IMPORTANT] |
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oxytocin levels in male vs female
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in baseline conditions, they are nearly identical. however, in females, the levels go up in certain cases (breastfeeding...)
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diuresis
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Loss of water through excretion
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how do the functions of vasopressin relate?
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by increasing water retention, you are also indirectly helping increase blood pressure
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relation between vasopressin and oxytocin
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both are peptide hormones and are structurally similar
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why is vasoconstriction function of vasopressin not important?
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blood pressure is highly regulated through other pathways. vasopressin really doesn't have that much of an impact.
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what would happen in the absence of vasopressin?
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water would be excreted faster then it could be ingested. would be fatal!
the blood pressure aspect is not as important |
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diabetes mellidius vs diabetes insipidus
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diabetes --> flow of water
mellidius --> sweet tasting insipidius --> sour tasting d.m. --> sweet tasting from too much glucose in urine d.i. --> sour tasting from too much water in urine |
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DDAVP
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chemical vasopressin to healp replenish for those who have small amounts.
helps with bed-wetting! |
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hypophysiotropic hormones
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hormones released by the hyopthalamus that regulate the anterior pituitary
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what do (almost) all hypophysiotropic hormones have in common
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they are all the first in a three-hormone sequence.
exception is dopamine |
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6 classical hormones of the anterior pituitary
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follicle-stimulating hormone - FSH
luteinizing hormone - LH growth hormone (somatotropin)- GH thyroid stimulating hormone (thyrotropin)- TSH prolactin adrenocorticotropic hormone (corticotropin)- ACTH |
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the other 2 hormones of the anterior pituitary (that have no known function)
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beta-lipotropin
beta-endorphin (painkilling?) |
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GH effects
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liver: stimulates IGF-1 secretion and promotes glycogenolysis and gluconeogenesis
inhibits insulin promotes protein synthesis promotes organomegaly (organ growth) |
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what are the 6 hypophysiotropic hormones?
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1) CRH -->stimulates ACTH
2) TRH --> stimulates TSH 3) GHRH --> stimulates GH 4) SS (somatostatin) --> INHIBITS GH 5) GnRH --> stimulates LH and FSH 6) DA (dopamine) --> inhibits prolactin |
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TSH effects
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stimulates thyroid to secrete T3 and T4
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Prolactin effects
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stimulates breast development and milk production
male: reproductive function |
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ACTH effects
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stimulates adrenal glands to secrete cortisol
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thyroid gland
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located anterior to the trachea and the common carotid artery in the neck.
filled with follicles: a sphere of cells filled with gel-like substance (inner part = colloid) contains a reservoir of TH. produces thyroxine (T4) and triiodothyronine (T3). |
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T4 and T3
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both produced in the thyroid gland.
T4 is generally converted to T3 in target cells. so T4 is major secretory product and is in higher concentrations in the blood but T3 is the major thyroid hormone since it elicits the cellular response |
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importance of TH in prenatal life
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TH is needed for CNS development (synapses, myelin, dendritic extensions)
if mother has thyroid deficiency, will not seriously affect the baby since the baby can make its own TH. if mother has iodine deficiency, then it is a problem and can result in cretinism. |
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TH effects
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1) CNS development
2) ANS potentiation 3) Calorigenic regulation |
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TH effect on ANS
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sensitizes target cells by up-regulating the number of EPI and NE receptors.
thus potentiating the ANS response |
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TH effect on metabolism
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TH is the chief factor that controls our basal metabolic rate.
It does so by activating the gene that transcribes the Na/K ATPase! By increasing TH, more ATPases will be produced and the body will work at a higher metabolic rate to keep ATP levels constant. |
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hypothyroidism symptoms
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thyroid gland producing less TH for whatever reason
-decreased ANS (slow pulse and low blood pressure) -decreased metabolism (results in GAINING WEIGHT) -feeling cold -GOITER --> due to the increase in TSH. TSH not only stimulates TH but also stimulates growth of thyroid and it grows too large |
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hashimotos disease
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auto-immune disorder where immune system attacks the thyroid glands resulting in hypothyroidism
mostly females (9:1) |
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what happens to TSH and TRH levels in hypothyroidism
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increase due to the lack of negative feedback!
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Grave's disease
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auto-immune disorder where the immune system ACTIVATES the thyroid gland (becomes TSH agonist) and induces hyperthyroidism
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hyperthyroidism symptoms
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thyroid gland producing excessive TH for whatever reason
-increased ANS activity (high blood pressure, pulse, anxiety) -always feeling warm -increased metabolic rate - LOSE WEIGHT -goiter --> resulting from the immune system acting as TSH agonists. |
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what happens to TSH and TRH levels in hyperthyroidism
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go down from negative feedback. but TSH effects are still potentiated from the immune system!
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cortisol
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has an effect on almost every cell in the body!
-the chief stress hormone: provides energy while fasting or when in a flight/fight action. -It is the brake on the immune system.Too much cortisol makes you more prone to illness and autoimmune disorders Can be used to prevent immune system from functioning (during a transplant or graft) -Potentiates catecholamines (makes NE more effective) -potentiates certain developmental processes |
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Prednisone
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anti-inflammatory medication that takes advantage of cortisols effect on the immune system
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developmental processes potentiated by cortisol
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produces Surfactant
-surfactants role is to relieve surface tension in parts of lungs that fights every breath. The surface tension is a force that tends to collapse expandable structures that are coated with water but have an interface with air. As soon as a baby is born and it takes a breath, you have air and surface tension. If you cant reduce the surface tension, then you cannot keep the lungs open. Surfactant intercollates into the airways and creates a barrier between the air and the coating water(fluid) First breath is the absolute hardest. The leading cause of morbidity (illness) and mortality (death) in premature infants is insufficient surfactant leading to pulmonary disease. |
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what to do with a mother who is going into early labor?
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give the mother injections of strong cortisol (anti-natal glucocorticoid therapy) that can cross the placenta and the baby will have the lungs of a 9 month old.
Cannot give the mother surfactant because it will not get to the right place. If the birth is not planned generally give synthetic surfactant through the trachea to get to the lungs. |
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addisons disease
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syndrome that occurs during primary adrenal insufficiency.
usually autoimmune but could be from other places. symptoms are: hypotension (due to the lack of aldosterone) [VERY LETHAL] fatigue, hypoglycemia, loss of appetite... (due to cortisol) |
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secondary adrenal insufficiency
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caused by a deficiency in ACTH for any reason.
not as lethal as primary since aldosterone secretion is maintained. |
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Cushings syndrome
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excess cortisol in the blood even in a nonstressed individual.
FOR WHATEVER REASON |
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cushings disease
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cushings syndrome that is manifested through a secondary defect such as an ACTH secreting tumor.
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colors of thyroid gland
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red: capillary bringing blood to the thyroid gland
yellow = follicle cell pink = colloid |
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what happens in deficiency or excess of GH before puberty
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deficiency: dwarfism
excess: giganticism |
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why does GH inhibit insulin?
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- when sleeping, want CNS and heart to have fuel source
- CNS needs glucose available - helps define symptoms of a tumor: chronic hyperglycemia may indicate a GH tumor. |
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erythrocytes
what are there life expectancies |
red blood cells
about as wide as the diameter of a capillary. get very banged up in circulation; have a very short life span of 3-4 months. sent into circulation from bone marrow. removed by the spleen |
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leukocytes
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white blood cells
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hematocrit
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percentage of blood volume that is erythrocytes:
V(erythrocytes) / Total V = Hematocrit -normally 45 in men and 42 in women |
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when you centrifuge blood, how many layers are there?
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3.
top: plasma (55%) middle: leukocytes and platelets (0%) bottom: erythrocytes (45%) |
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pulmonary circulation
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blood pumped from the right ventricle through the lungs back to the left atrium
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systemic circulation
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blood pumped from left ventricle through the body and back into the right atrium
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artery
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any blood vessel that carries blood away from the heart
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veins
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any blood vessel that carries blood to the heart.
Known as capacitance vessels since they can store blood. They are flexible and can be enlarged very easily. they have layers like arteries but not as much so they can accommodate a lot of blood. not all of the blood is pumped, some can be pooled in the veins. |
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in systemic circuit, what are the names of the vessels that the blood leaves/enters the heart
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blood enters through the superior/inferior vena cave
blood exits through the aorta |
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progression of blood flow beginning with the right atrium
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right atrium --> right ventricle --> pulmonary trunk --> pulmonary arteries --> pulmonary capillaries --> pulmonary veins --> left atrium --> left ventricle --> aorta --> arteries --> arterioles --> capillaries --> venules --> veins --> vena cavae --> right atrium
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what are the valves on the right side of the heart
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tricuspid AV valve
pulmonary semi lunar valve |
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what are the valves on the left side of the heart
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bicuspid AV valve (mitral valve)
aorta semi lunar valve |
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open circulatory system
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found in arthropods. contractile elements pump blood into the body cavity.
Doesn’t go through smaller blood vessels that reach into nook and crannies. it is not really blood; rather interstitial fluid. The force of breathing and flying makes this stuff slosh back and forth. This works for very small bodies. |
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closed circulatory system
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more organized.
allows animal to be larger. Doesn’t matter how big you get, as long as you have blood vessels that can carry blood to all ends. There is the ability to redirect blood from place to place as metabolism dictates. considered a "leaky" system due to the capillaries. |
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functions of the circulatory system
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Circulates fluid.
brings nutrients and carries waste away so that they can be eliminated. The cells that comprise the immune system are found in circulation. Thermoregulation. endotherms regulate body temp by shunting blood to/from the body surface. |
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circulatory system's role in thermoregulation
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When it is hot, dilate blood vessels in the skin (there are temp sensors and reflexes involved) and dissipate heat.
when cold, constrict those vessels so that blood going to skin is reduced and heat is not lost. |
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erythropoietin (EPO)
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hormone made by the kidneys to stimulate production rate in marrow.
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When would you want erythrocyte count to increase?
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Anemia--increased EPO levels would be wanted to get more red blood cells.
Increased altitude. at high altitude, the air has less oxygen pressure. this makes it is harder for oxygen to diffuse into blood stream. Oxygen detecting mechanisms stimulate more EPO production. |
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disadvantages to high hematocrit
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blood becomes more viscous. makes the heart work harder due to the increased resistance to flow.
the heart can become hypertrophic and enlarges. gap junctions can break and cause serious electrical disruptions and cause an infarction. |
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advantages to high hematocrit
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can give athletes the edge by elevating oxygenation.
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2 major protein layers surrounding arteries/veins
which are not present in arterioles/venules? which are not present in capillaries? |
elastins and smooth muscles
elastins are not present in arterioles neither are present in capillaries. |
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elastins importance in arteries
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helps maintain blood pressure during the diastole. They stretch back like a rubber band and keep pressure at around 80mmHg until the next systole.
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role of smooth muscle in arteries
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Conributes to squeezing effort of the aorta.
Responsible for shunting blood to/from arterioles |
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blood capillaries
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very very leaky.
most leak out/in by diffusion. only erythrocyes are too big to leak out. everything else: leukocytes, nutrients, blood plasma can all leak out. |
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what is present in the veins below the heart that is absent in the veins above the heart?
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VALVES! you are fighting gravity up!
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how can you tap the reservoir of blood in your veins?
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contract skeletal muscles to compress the veins
use ANS to contract smooth muscles and force blood. |
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pulmonary edema
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fluid buildup in the interstitial space of the pulmonary capillaries.
this pushes the capillary away from the airsac and increases the diffusion distance of Oxygen. Less oxygen comes in. VERY DANGEROUS |
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which side of the heart is stronger, why?
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Left side. want more pressure into the systemic circuit while keeping the pulmonary circuit at a lower pressure to reduce interstitial build up and possible edema.
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which side of the heart are infarctions most likely to occur and why?
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Left side. since it is stronger and demands more nutrients, an interruption in blood flow on the left side would be more devastating
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what happens if left ventricle stops working?
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blood quickly piles up in the pulmonary circuit causing a quick pulmonary edema.
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Congestive heart failure
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This occurs when the cardiac output is too low due to inefficient pumping of the heart.
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what are the first arteries that branch off the aorta?
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coronary arteries that feed the myocardial muscles
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most common sites of heart disease
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coronary arteries
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atherosclerosis
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hardening of myocardial arteries secondary to hypercholesterolemia
-specialized form of arteriosclerosis |
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arteriosclerosis
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hardening of any artery for any reason
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what could cause blockages in arteries?
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-Building up of plaque
-Can be an overgrowth of smooth muscle -a deposit of fat (cholesterol) -Scar tissue due to inflammation |
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stenosis
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abnormal narrowing of a vessel.
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rheumatic fever
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caused by untreated strep infection.
an autoimmune disase where the tissue and valves on the left side of the heart are attacked and become inflammed and scarred. this causes stenosis |
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prolapse
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condition where a valve everts.
i.e. where the AV valves evert into the atrium! |
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what prevents prolapse from occuring?
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There are muscles that extend up from the floors of the ventricles and conenct with tendons that attach to the valves (tri/bicuspid) so the valves are linked to the bottom of the heart muscle.
When heart contracts pressure goes up. To prevent AV valves from overshooting and everting these muscles also contract! When they contract they pull on the tendons attached to them and the tendons pull on the valves from the other side. So you have this mechanism where they assist the valves from not everting. |
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chordae tendineae
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papillary myocardial muscles/tendons that prevent prolapse
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oxygenation of venous veins?
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about 70%
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what makes heart muscle action potential different then nervous action potential?
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heart is permeable to Ca.these channels stay open longer and make the depolarization last longer
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where is SA node located
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right atrium where the vena cavae connect
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what makes SA cells spontaneously depolarize?
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F sodium channels (funny) open when cell is polarized and bring the cells to threshold
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where does ANS modulation occur in the heart?
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on the SA node.
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what causes the pause between atrial and ventricular contractions?
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av node is slower to contract. allows for atria to contract
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how does the AV node cause ventricular contraction?
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sends signal to the papillary muscles in the bottom of the ventricle known as the purkinje fibers (an extension of the AV node).
here it extends the action potential out to the entire ventricle. So basically the entire ventricle gets the signal at once and the muscles contract simultaneously. |
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p wave
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atrial depolarization
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qrs complex
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ventricular depolarization (and atrial repolarization)
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t wave
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ventricular repolarization
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systole
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can refer to any contraction but in physiology, always refers to ventricular since ventricles do all the work!
consists of isovolumetric ventricular contraction and ejection |
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diastole
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ventricular relaxation
consists of isovolumetric ventricular relaxation and refilling |
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isovolumetric ventricular contraction
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point during contraction where pressure in ventricle is greater then pressure in atrium so the AV valve is shut. but the pressure is still not greater then the other side of the semilunar valve.
So the volume stays the same until enough pressure is created from the ventricular contraction that would force the semilunar valves to open and complete the diastole |
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isovolumetric ventricular relaxation
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point during diastole where the semilunar valves have closed because the pressure outside became greater.
however, the AV valves are still closed because the pressure in the atrium is still less then the pressure in the ventricle. once the SA fires and the atrium contracts, that provides the kick to force open the AV valves and refill the ventricle. |
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relationship between Cardiac output, resistance and arterial pressure?
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CO x R = P
in a small region, the CO is equal to flow or (F) as resistance increases, pressure increases! |
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homeostasis goal in circulation?
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to maintain a constant pressure so that the needs of all the cells can be met.
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MAP
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mean arterial pressure. not just the average between systolic and diastolic since more time is spent in diastole.
MAP = (Systolic + 2xDiastolic) / 3 |
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what happens when you expand your chest? (with regards to circulation)
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increase volume so create a negative pressure. blood rushes up towards the heart and makes a very large venous return. the EDV becomes much larger leading to larger SV
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EDV
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end-diastolic volume
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SV
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stroke volume (SV = EDV-ESV)
volume of blood pumped out per pump. |
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ESV
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end-systolic volume
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Cardiac output (CO)
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the amount of blood pumped out of the heart per unit of time.
usually in L/min (SV x HR) talking about only the left ventricle |
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difference between SNS and PSNS on myocardial function
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PSNS only synapses on SA node so only decreases HR.
SNS synapses around the entire heart. so the entire heart becomes more excitable and so SNS not only increase HR but also increases ventricular contractility |
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contractility
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the strength of contraction at any given EDV.
meaning independent of starling forces |
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frank-starling mechanism
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if you increase the venous return, you are increasing the EDV and thus the stroke volume.
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how does SNS work on the heart
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NE/EPI activate GPCR --> adenylyl cyclase --> cAMP --> protein kinase --> activates lots of stuff --> increase force and velocity of contraction
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Resistance in circulation is a function of:
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viscosity (usually constant so can be ignored)
length of blood vessel: longer has more resistance (constant length so can be ignored radius: [MOST IMPORTANT] is actually inversely proportional to the fourth power! just a slight change in the radius (from smooth muscles and such) causes a huge change in resistance. |
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what can change SV and what can change HR?
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SV: SNS activation or a change in EDV (frank starling)
HR: PSNS or SNS activation |
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total periphery resistance (TPR)
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Resistance for the entire systemic circulation
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angiotensin II
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large vasoconstrictor which increases blood pressure
also activates release of NO from surrounding area |
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how is angiotensin II made?
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the liver makes angiotensinogen (precursor to angiotensin)
this is secreted into blood and acted on by Renin (made in kindeys) Renin clips a piece of the precursor off and makes an inactive angiotensin I Angiotensin I is then acted on by ACE (on epithelial cells. Poking out of membrane) and converted to Angiotensin II the active molecule. |
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ACE
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angiotensin converting enzyme
ACE inhibitors are potent vasodilators |
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Renin
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proteolytic enzyme that cuts angiotensinogen into angiotensin I (inactive).
produced in the kidneys |
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why would angiotensin II release NO?
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they are contradictory (vasodilator vs vasoconstrictor)
but the NO is like a safety switch so that the angiotensin doesnt constrict the vessels too much! this shows how serious adjusting the radius of the vessel is |
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local metabolic control over vasodilation/constriction
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the more CO2 produced dilates the vessels.
this is example of how the body knows exactly how much it needs by using metabolic end products as signals to adjust its need. |
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2 main locations of baroreceptors
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The large arteries of the neck and the aorta. they are respectively called the carotid sinus baroreceptor and the aortic arch baroreceptor.
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carotid sinus baroreceptor
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There are 2 common carotid arteries, each split into 2 other arteries. At the point where the bifurcate is known as the carotid sinus.
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Sinus
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sinus is a dilation of blood vessel.
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aortic arch baroreceptor
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At that spot and the arch of aorta are the nerve endings. The baroreceptors there are lodged into the opening of the blood vessel.
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where do baroreceptors terminate?
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at the medulla - the cardiovascular control center
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circulatory shock
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a state at which pressure is too low to make a profusion of the vital organs like the heart and brain. Consequently the organs start to die.
If it goes really low, can never get back out. Called irreversible shock. |
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what causes the medullas set point for circulatory blood pressure to change?
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-age (increases)
-diet (high salt—increases) -obesity (increases). |
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main difference between venous constriction and arteriole constriction
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venous: constriction increases flow of blood (by depleting reserves)
arterial: constriction decreases flow of blood |
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how can you change MAP?
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change CO or TPR
MAP = CO x TPR |
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how to regulate SV?
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SNS (NE or EPI) or increase EDV (frank starling)
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how to regulate heart rate?
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PSNS or SNS
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how to regulate TPR
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change arteriolar radii
change blood viscosity |
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how to regulate arteriolar radii
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hormonal: epi(both), angio II(cons), ADH (cons)
neural: NO(dil), SNS (cons) local: CO2 (dil), O2 (dil), H(dil), NO(dil) |
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pulse pressure
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the difference between systolic pressure and diastolic pressure
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air consists of:
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misxture of gases mostly N(79%) and O(21%)
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amount of pressure contributed by oxygen in the air
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take percentages: 760 x .21 = 160mmHg
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difference between active breathing and passive breathing
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active: force air into lungs
passive: use pressures to bring air passively into the lungs |
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at rest what is the hydrostatic pressure of the pleural space (Pip)
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-4 (when compared with Patm)
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transmural pressure
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the pressure gradient across any wall.
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Ptp
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transpulmonary pressure. it is the difference between the alveoli pressure and the intrapleural pressure.
It is the pressure difference that opposes the inward elastic recoil of the lung Ptp = Palv - Pip usually +4 mmHg |
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Pcw
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chest wall pressure. it is the difference between the intrapleural pressure and atmospheric pressure.
it is the pressure difference that opposes the outward elastic recoil of the chest wall Pcw = Pip - Patm usually -4 mmHg |
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what direction does the chest wall want to go?
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wants to go outward but the pressure difference between the Pip and Patm keeps it from doing so.
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airway branching
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trachea --> 2 bronchi --> bronchioles --> alveolar ducts --> alveolar sacs
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where do alveoli first appear
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the walls of the respiratory bronchioles
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conducting zone
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from top of trachea to the beginning of the respiratory bronchioles.
gases do not exchange with the blood. |
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respiratory zone
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from respiratory bronchioles downward.
this is the region where gases exchange with the blood |
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cystic fibrosis
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genetic disease where airway epithelium can no longer secrete watery fluid and mucous hardens and obstructs the airway.
due to a defect in chloride channels. |
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thorax
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synonymous to chest. located between the neck and abdomen.
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what encases each lung
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pleura and the pleural sac.
they are like a water balloon but very thin |
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visceral pleura
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the inner layer of the pleural sac that is firmly attached to the lung by connective tissue
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parietal pleura
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outer layer of pleura that is firmly attached to the interior thoracic wall and diaphragm
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ventilation
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the exchange of air between atmosphere and aveoli
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equation to describe bulk flow
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F = change of pressure / R
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at what point during the respiratory cycle is the Ptp the greatest?
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at the point right before exhalation. where the chest wall is outward the most and there is the greatest amount of recoil force on the lungs to go inward.
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2 msucles that inspire?
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intercostal muscles pull anteriorly and superiorly
diaphragm muscles pull inferiorly |
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baroreceptors
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monitor blood pressure
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chemoreceptors
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monitor H and CO2 and O2 concentrations in blood (O2 the least)
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how far do oxygen levels have to decrease before being registered?
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35%
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carbonic anhydrase
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enzyme that breaks down CO2 and H20 into bicarbonate
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what percentage of co2 is bicarbonate?
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70%
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hypoventilation
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not breathing enough causes a buildup of co2 in the body and a lower pH
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hyperventilation
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breathe too much, the co2 output is greater then input (from the cells) so the pH in the blood increases!
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why are you not hyperventilating during exercise?
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Because more co2 is bering produced so you need to breathe faster to match input with output
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why are there chemoreceptors for both H and co2?
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because you can get H in different ways other then co2...such as lactic acid
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metabolic acidosis
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a serious decrease in pH brought about by increased metabolism and more H ions
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respiratory compensation
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adjusting breathing to match the input of co2 with output.
to adjust acidosis breathe more to adjust alkylosis breathe less |
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respiratory acidosis
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not breathing enough leading to the buildup of co2 and decrease in pH
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metabolic compensation
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body adjusts metabolism to match the output of co2.
it is adjusted through the kidneys and how mcuh H+ is excreted. to adjust acidosis, metabolism decreases to adjust alkylosis, metabolism increases |
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emphysema
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the inability to breathe properly.
this is primarily due to a loss of elastic fibers in the respiratory system. you don’t have recoil ability to exhale this leads to COPD (chronic obstructive pulmonary disorder) Pco2 goes up! but kidneys prevent the change in pH so Pco2 is chronically elevated. eventually the chemoreceptors desensitize and you lose the drive to breathe so you need very low o2 levels to keep the reason to breathe. |
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where is respiration controlled
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respiratory center in the medulla and pons
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what are the nerves that project to respiratory muscles
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Intercostal nerve: intercostal muscles
Phrenic nerve: diaphragm muscles |
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exercises affect on respiration
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increase. even if you physically manipulate the muscles, respiration increases
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progesterones effect on respiration
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increases
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stretch receptors (in the lungs) effect on respiration
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decreases (prevents you from breathing too hard)
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sleeps effect on respiration
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decrease
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stress's effect on respiration
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increases
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barbiturates effect on respiration
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decreases
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where are chemoreceptors located
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by the baroreceptors. in the carotid arch (called the carotid bodies)
and the aortic arch (aortic bodies) |
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type 1 alveolar cells
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where exchange occurs. small, thin, flat and make up the alveoli
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type 2 alveolar cell
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what secretes surfactant. globular and bigger
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drugs to treat hypertension
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diuretics: increase excretion of water and lower CO (no change in TPR)
beta blockers: lower CO Ca blockers: lower muscle activity and decrease TPR ACE inhibitors: stop a very potent vasocontrictor to decrease TPR |
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drugs to treat CHF
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diuretics: eliminate fluids and decrease CO
vasodilators: ace inhibitors beta blockers |
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chf vs mi
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chf: condition where heart fails to pump adequate CO. could be due to hypertension or starved myocardial msucles
mi: coronary artey blockage and myocardial muscles do not work effectively |
