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746 Cards in this Set

  • Front
  • Back
functions of the nephron
filtration, reabsorption, secretion, excretion
integrated kidney function
-water balance
-Na & ECF balance
-K balance
-Ca balance
-acid-base balance
what is renal function essential for
survival & for maintenance of body homeostasis
where are the kidneys located
in the abdominal cavity, immediately below the diaphram
what do the kidneys do
filter the blood producing urine, which is then excreted out of the body
how do blood enter the each kidney
via ramification of the aorta, called the renal artery
how does cleared blood return in the circulatory system
via two renal veins which end in the inferior vena cava
pathway of urine produced from blood filtration
renal cavity (pelvis)->2 long ducts called ureters->urinary bladder->urethra
functions of the kidneys
-regulation of ECF volume & blood pressure
-regulation of osmolarity
-maintenance of ionic balance
-homeostatic control of pH
-elimination of catabolites & waste
-production of hormones
kidney structure (whats it divided into)
bean-shaped organ, whose tissue can be divided in a peripheral cortex and internal medulla
what departs from the medulla
several funnel-like structures like calyces, sing, calyx
where is the first urine produced by the kidney stored
funnel-like projections of the medulla
what do the calyces form
renal pelvis
where does the renal pelvis deliver urine to
collecting ducts
functional units of the kidney
nephrons
nephron structure
long convoluted tubule
renal corpuscle
the complex of the glomerulus surrounded by the Bowman's capsule
parts of the nephron
-renal corpuscle
-proximal tubule
-loop of henle
-distal tubule
-juxtaglomerular apparatus
-collecting ducts
2 types of nephrons
1.cortical nephrons:almost completely contained in the cortex
2.juxtaglomerular nephrons: that dip deeper into the renal medulla
blood capillary network of the nephron
each nephron has 2 arterioles and 2 sets of capillaries associated with it. from the renal artery, several arterioles depart and one afferent arteriole enters the bowman's capsule in each nephron. there it ramifies into glomerulus and ends in efferent arteriole that leaves the capsule. 2nd set of capillaries (peritubular capillaries) departs, following the course of the renal tubule which end up in the renal vein
what is the main difference in the organization of capillaries in juxtamedullary nephrons
the long peritubular capillaries that dip into the medulla are called vasa recta
what occurs to a substance that enters the renal tubule
1.it's filtered away from plasma in renal corpuscle
2. reabsorption in renal tubule
3. secreted by renal epithelium
4. absorbed from the plasma and released into the renal tubule through the cell apical membrane
what occurs to whatever is left in the tubule after filtration, absorption and secretion
it is excreted in the form of urine
2 layer of the bowman's capsule
1. parietal layer
2. visceral layer
parietal layer
external, forms the surface of the capsule and is constituted by modified renal epithelial cells
visceral layer
internal to the capsule, formed by specialized cells called podocytes
what does each podocyte of the visceral layer have
has several fingerlike processes which interdigitate with one another in the same cell or with neighboring cells to form a sheath that completely surrounds the glomerular capillaries.
filtration slits
spaces between the processes of the podocyte
fenestrae
pores in the endothelium of glomerular capillaries
how do filtered substances pass from the plasma to the bowman's capsule cavity (capsular space)
through the fenestrae and then the filtration slits
forces that cause filtration
hydrostatic blood pressure, colloid osmotic pressure, and hydrostatic (bowman's fluid) pressure
what is necessary for filtration to occur
the net pressure in the renal corpuscle has to exceed the net pressure inside the renal tubule.
equation for net filtration pressure
sum of the pressures in favor of filtration- sum of the pressures opposing filtration
(hydrostatic blood pressure-colloid osmotic pressure-hydrostatic bowman's fluid pressure)
what is filtration fraction
fraction of total plasma volume that is filtered (~20%)
what is glomerular filtration rate (GFR)
the volume of fluid that flows into the bowman's capsule per unit time
what is GFR controlled by
1. net filtration pressure (renal blood flow & bp)
2. filtration coefficient (surface area of the capillaries available for filtration and permeability of capillary- bowman's capsule interface)
what is GFR primarily controlled by
regulation of blood flow through the renal arterioles
autoregulation
maintains a nearly constant GFR when MAP is between 80 and 180mmHg
what is GFR at low bp
it varies proportionally to BP
what do the values in BP mean
arterial systolic pressure (during heartbeat)/ arterial diastolic pressure (during heart relaxation)
BP that signifies hypertension
130/85
how is low blood pressure defined
symptoms of low blood flow
mean arterial pressure formula
MAP= DP+(SP-DP) (~93mmHg for a normal bp of 120/80)
how do mechanisms contribute to GFR autoregulation
by modifying renal blood flow in afferent arterioles
mechanisms of GFR autoregulation (intrinsic regulation)
1.myogenic response :vascular stretch->cell depolarization->contraction->inc vasocons.->dec renal blood flow-> dec GFR
2.tubuloglomerular feedback: exerted by the juxtaglomerular apparatus
where is the juxtaglomerular apparatus
at the region where the ascending limb of the loop of Henle contacts the renal corpuscle
2 cell types of the juxtaglomerular apparatus
1.macula densa cells
2.granular cells
macula densa cells
modified tubular epithelial cells that produce paracrine signals in response to changes in flow through the renal tubule(these paracrines induce contraction of the arteriolar cells and hence vasoconstriction, which reduces renal blood flow and hence GFR-tubuloglomerular feedback)
granular cells
modified smooth muscle cells from the arterial wall. These cells produce renin, an enzyme involved in salt and water balance
tubuloglomerular feedback
GRF inc->flow thru tubule inc->flow past macula densa inc->paracrine diffuses from macula densa to afferent arteriole->afferent arteriole constricts->resistance in afferent arteriole inc->hydrostatic pressure in glomerulus dec->GFR dec
effects of arteriolar resistance on GFR and renal blood flow
1.vasconstriction of the afferent arteriole inc resistance and dec renal blood flow, capillary bp and GFR
2.inc resistance of efferent arteriole dec renal blood flow but inc capillary bp and GFR
neurohormonal control of GFR (extrinsic regulation)
1. sympathetic NS: NE>alpha adrenergic receptor on vascular smooth muscle cells>vasoconstriction of afferent arterioles>dec renal blood flow and GFR
2. hormones/paracrines: ATII-mediated vasoconstriction>constriction of afferent arterioles>dec renal blood flow and GFR
formula for the amount of solute excreted
amount filtered-amount reabsorbed-amount secreted
why is reabsorption important
1. higher GFR allowed
2. easier elimination of non-specific exogenic (toxic) substances (no need for transporters)
3. easier regulation of normal levels of useful substances (thru transport saturation)
what is our GFR
125mL/min
how many times is our blood filtered
~60 times a day
what does renal reabsorption depend on and why?
it depends on active transport of solutes from the tubule to ECF cuz filtrate moving from the bowman's capsule into the tubule has the same solute conc as ECF
principles of renal reabsorption
1.Na is reabsorbed by active transport
2.electrochemical gradient drives anion reabsorption
3.water moves by osmosis, following solute reabsorption
4.conc of other solutes inc as fluid vol in lumen dec. permeable solutes are reabsorbed by diffusion.
pathways of renal reabsorption
1.transepithelial transport: substances cross apical & basolateral membrane
2.paracellular pathway: substances pass thru the junction betw. 2 adjacent cells
3.transcytosis: substances pass thru the cytoplasm via vesicles
mechanisms of renal reabsorption
1.active transport: move substances against conc gradient
2.secondary active transport: move substances across conc gradient
3.passive transport: move substances along conc gradient
ex of active transport
1. Na enters cells thru membrane proteins, moving down its electrochemical gradient
2.Na is pumped out the basolateral side of cell by Na-K-ATPase
ex of secondary active transport
glucose is absorbed against its conc gradient via apical Na-glucose cotransporters. these transporters exploit the Na gradient created by basolateral Na-K ATPase. glucose then follows passively to the interstitial fluid via basolateral glucose transporters (GLUT)
ex of passive transport
urea; since primary and secondary active transport in this tubule cause reabsorption of small solutes and water by osmosis, vol of filtrate dec and urea conc increases.
how is urea produced
by the liver as a product of protein catabolism
what does urea allow
elimination of nitrogen in a neutral form
transport maximum (T_m)
the minimal rate at which saturation occurs
renal threshold
substance plasma concentration at which saturation of transport occur
why is saturation important
it sets the max. plasma conc of a substance
what is filtration of glucose proportional to
plasma concentration
what is reabsorption of glucose proportional to
plasma concentration until the transport maximum is reached
until when is the glucose excretion zero
until the renal threshold is reached
glucosuria
presence of glucose in urine
renal threshold for glucose
300 mg/100mL
what is the main mechanism of renal secretion
secondary active mechanisms
renal secretion
1. enhances the excretion capability of the kidney
2. is an active process since it requires movement of a solute against its conc gradient
3. secretion of K and H is import in homeostatic regulation
4. several organic compounds are secreted by the kidney
what method is used to evaluate renal function
clearance
what is clearance
rate at which a solute disappears from the body by excretion or by metabolism
how is clearance expressed
vol. of plasma (mL) from which a given substance has been cleared/ unit of time (min)
what is the use of clearance
-allows to evaluate renal function
-non-invasive way of measuring GFR
-reveals how kidneys handle a solute
equation for clearance
urine excretion rate of X (mg/min)/
plasma concentration of X (mg/mL plasma)
what is inulin
substance that is neither reabsorbed nor secreted by the nephron
when is there net reabsorption of glucose
at glucose plasma conc of <300mg/100mL
example of substance partially reabsorbed
urea
is inulin practical in a clinical setting, why or why not
no because it has to be administered by continuous intravenous infusion
what is a useful substance in clinical settings in terms of clearance
creatine
what is the patient's GFR equal to
creatine clearance
mincturition
reflex of eliminating urine
what is the bladder and where is it located
it's a large organ lined with smooth muscle tissue and located in the lower pelvic cavity
what is the bladder wall like at rest
it's relaxed, and an internal urinary sphincter is passively contracted to prevent leaking of urine into the urethra.
external urinary sphincter
present in the bladder and is kept tonically contracted by motor neurons under CNS control
mincturition reflex
1.stretch receptors fire
2.parasympathetic neurons fire. motor neurons stop firing.
3.smooth muscle contracts, internal sphincter passively pulled open. external sphincter relaxes.
what happens in a toilet-trained individual
a new reflex acquired with learning superimposes to the basic reflex and is dominant. The learned reflex consists of additional sensory fibers in the bladder wall that signal the degree of fullness to higher brain centers located in the pons.
what do the neural centers in the learned reflex do
1. inhibit parasympathetic neurons that cause contraction of the bladder, thereby overriding the basic reflex
2.trigger voluntary contraction of the external urinary sphincter, hence blocking urine excretion
what can lesions in the pons cause
loss of bladder control (incontinence)
what is renal tissue
a tightly packed ensemble of nephrons
how are the proximal and distal tubules distinguished
on the basis of the presence (proximal) or absence (distal) of a conspicuous sloughed brush border that appears in the lumen of the tubule.
renal medulla
tightly packed ensemble of tubule convolutions
routes of elimination of excess water & electrolytes
kidneys, feces, beathing
sweating
route of LOSS of water and electrolytes, not a way of eliminating excess substrates
necessity for control of body fluid and electrolytes
1.cell volume- shrinkage of swelling can interfered with cell function
2.K balance- excess extracellular K causes cell depolarization. dec. in K conc causes cell hyperpol
3.Ca balance- exocytosis, bone formation, muscle contraction, blood clotting
4.H, HCO3- control of body pH
systems involved in fluid & electrolyte homeostasis
1.kidneys: slow adaptive changes, under endocrine control
2.cardiovascular system: neural control, rapid adaptive changes
3.respiratory system: neural control, rapid adaptive changes
4.behavioral adaptation (thirst, salt appetite)-rapid
what is decreased bp or volume sensed by
volume receptors and baroreceptors in the cardiac atria and carotid arteries and aorta
homeostatic response by the cardiovascular system
generalized vasoconstriction and inc cardiac output, which inc bp
homeostatic response by kidneys
renal water conservation, which minimizes dec in blood vol
homeostatic response: behavioral response
dec blood vol or bp trigger thirst & augment water intake, inc ECF & blood vol & inc bp
2 mechanisms of water conservation by the kidney
1.dec filtration: at low bp, GFR is dec
2.maximize reabsorption
how does transport in kidney occur
it is passive and occurs by osmosis
osmolarity changes of filtrate through the nephron
1.isosmotic fluid leaving the proximal tubule becomes progressively more concentrated in the descending limb
2.removal of solute in the thick ascending limb creates hyposmotic fluid
3.hormones control distal nephron permeability to water and solutes
4.urine osmolarity depends on reabsorption in the collecting duct
what is the filtrate osmolarity at the beginning
300moSm- same as plasma
descending loop of henle permeability
permeable to water but not ions
ascending loop of henle permeability
permeable to ions but not water
if no water is reabsorbed in the collecting duct, what will the urine excreted be
hyposmotic
osmolarity of the most dilute urine
<100mOsm
osmolarity of the most concentrated urine
1200mOsm (equal to ECF)
which hormone controls reabsorption of water
vasopressin (also called antidiuretic hormone)
what is vasopressin produced and released by
hypothalamic neurons from the posterior pituitary lobe
what occurs in the presence of vasopressin
the collecting duct cells of juxtamedullary nephrons are permeable to water. Water leaves the tubule via osmotic diffusion, following the osmotic gradient in the renal medulla, and joins back the plasma in the vasa recta. Blood in the vasa recta returns to the renal cortex and, from there, to the renal vein. Therefore these blood vessels constantly remove the water that has been reabsorbed in the medulla.
what occurs in the absence of vasopressin
, the collecting ducts are impermeable to water, which is “trapped” in the tubule and excreted in the urine.
mechanism of vasopressin action
1.vasopressin binds to membrane receptor
2.receptor activates cAMP second messenger system
3.cell inserts AQP2 water pores into apical membrane
4.water is absorbed by osmosis into the blood
what sense alterations in blood osmolarity, volume, volume and pressure and stimulate the hypothalamic vasopressin producing neurons to release this hormone from the posterior pituitary
Osmolarity receptors in the hypothalamus, stretch receptors in the cardiac atrium and baroceptors in the carotid artery and aorta
what creates the countercurrent system that concentrates solutes in the medulla
the anatomical relationship between the loop of Henle and the vasa recta
what does the countercurrent system produce
hyperosmotic interstitial fluid and hyposmotic filtrate
what does blood in vasa recta do
removes water leaving the loop of henle
what causes reabsorption of urea in the interstitial fluid
facilitated transport and Na+ secondary active cotransport
what happened to if water isnt ingested after NaCl is ingested
Na stays in ECF and draws fluid from cells>>cell shrinkage
what does ingestion of salt cause
no change in volume, inc in osmolarity
what does an inc in osmolarity trigger
secretion of vasopressin by the hypothalamus and also mediates the sensation of thirst.
consequence of quenching thirst
an increase in water intake, which, together with the increased vasopressin, mediate an increased renal reabsorption of water.
what does ECF vol and bp increase trigger
renal and cardiovascular responses
what do the cardiovascular reflexes do in response to salt ingestion
bring the bp back to normal
what do kidneys do in response to salt ingestion
salt and water are excreted to reestablish normal blood volume without altering again the osmolarity
what is Na balance controlled by
hormones
2 hormones that control Na balance
1.aldosterone:produced by adrenal cortex, mediates inc in reabsorption of Na
2.atrial natriuretic peptide (ANP): secreted by endocrine cells in ardiac atrium, promotes Na (and H2O) excretion
action of aldosterone
1.combines with cytoplasmic receptor
2.hormone-receptor complex initiates transcription in the nucleus
3.new protein channels and pumps are made
4.aldosterone-induced proteins modify existing proteins
5.result is inc reabsorption and K secretion
where does aldosterone act
at last third of distal tubule and in cortical portion of the collecting duct
which cells express receptors for aldosterone
principal(P) cells
what kind of hormone is aldosterone
steroid hormone
2 responses to aldosterone entering cytoplasm and activating its receptor
1.rapid response: the Na+ and K+ leak channels located on the apical membrane of the P cell increase their open time.
2.slow response: the hormone-receptor complex is translocated to the nucleus where it initiates transcription of mRNA for production of more leak channels
result of aldosterone
inc in Na reabsorption and K secretion
how is angiotensin II produced
renin cleaves angiotensinogen in the plasma into angiotensin I, an inactive peptide. Then the ACE enzyme converts it into angiotensin II
how does angiotensin II exert its affects
1.in adrenal cortex, it stimulates aldosterone secretion, enhancing Na reabsorption in kidney
2.at hypothalamic level, ATII stimulates release of vasopressin and sensation of thirst, which result in increased water content in blood
3.ATII stimulates cardioavascular control center to activate cardiovascular response to low bp.
4. ATII is potent vasoconstrictor and acts directly on smooth muscle cells contained in arteriolar walls
factors that affect aldosterone release
-increased extracellular K conc (s)
-inc osmolarity (i)
-dec blood pressure (s)
-dec flow past the macula densa (s)
what is atrial natriuretic peptide secreted by and in response to
secreted by atrial myocytes in response to stretch
what does atrial natriuretic peptide cause
Na+ (natriuresis) and water (diuresis) excretion
what does a dec in extracellular K (hypokalemia) cause
excitable cell hyperpolarization
what is the first sign in hypokalemia
muscle weakness
what does sever hypokalemia cause
cardiac and respiratory failure->death
when can massive K loss leading to hypokalemia occur
during diarrhea or kidney disease
what does inc extracellular K (hyperkalemia) cause
cell depolarization; initial inc then dec in cell excitability
what does hyperkalemia cause
life-threatening cardiac arrhythmias
how does reabsorption of K occur
by simple diffusion of K+ through K+ channels in the basolateral membranes of the proximal tubule cells.
what occurs when an excess of K is introduced in the body
plasma potassium concentration rises and this enhances uptake of K+ by the Na/K pump and therefore K+ secretion
what occurs after inc K intake
inc plasma K, inc aldosterone secretion, inc plasma aldosterone, inc K secretion
where does Ca reabsorption occur initially
in proximal tubule
where does Ca reabsorption under hormonal control occur
at the collecting duct
what is calcium balance controlled primarily by
1. 1,25-hydroxy-vitamin d
->promotes Ca absorption in GI tract
2.PTH->stimulates Ca release from bone and reabsorption in the kidney
where are most substance reabsorbed
proximal tubules
where do most hormonally regulated processes occur
in distal tubule and especially in collecting ducts
major functions of glomerulus/bowman's capsule
forms filtrate of plasma
controlling factors of glomerulus/bowman's capsule
starling forces (P_H,p,P_fluid)
major functions of proximal tubule
bulk reabsorption of solutes and water. secretion of solutes (except K) and organic acids and bases
controlling factors of proximal tubule
active transport of solutes with passive water reabsorption
major function of loop of henle
establishes medullary osmotic gradient, secretion of urea
major function of descending limb
bulk reabsorption of water
controlling factors of descending limb
passive water reabsorption
major function of ascending limb
reabsorption of Na
controlling factors of ascending limb
active transport
major functions of distal tubule and cortical collecting ducts
fine-tuning of reabsorption/secretion of small quantities of solute remaining
controlling factors of distal tubule & cortical collecting ducts
-aldosterone stimulates Na reabsorption and K excretion
-parathyroid hormone stimulates Ca reabsorption
major functions of cortical and medullary collecting ducts
fine-tuning of water reabsorption
reabsorption of urea
controlling factors of cortical and medullary collecting ducts
vasopressin inc passive reabsorption of water
behavioral mechanisms in salt and water balance
-control of thirst
-salt appetite
-avoidance behaviors
what is thirst directly stimulated by
inc in ECF osmolarity
thirst response
1.osmoreceptors in hypothalamus are activated when body osmolarity exceeds 280mOsm
2.drinking behavior is triggered
3.oropharynx receptors in mouth & pharynx react to cold water by quenching thirst sensation and sec vasopressin release
salt appetite response
1.angiotensin and aldosterone stimulate hypothalamic receptors
2.craving for salty foods is triggered
avoidance behaviors
help prevent dehydration or dec water intake
examples of avoidance behaviors
1.dec activity during hottest hours
2.avoiding salty foods/water
3.dec physical exercise
disturbances in vol and osmolarity during dehydration
dec vol, inc osmolarity
disturbances in vol and osmolarity during hemorrhage
dec vol, no change in osmo
disturbances in vol and osmolarity during incomplete compensation for dehydration
dec vol, dec osmo
disturbances in vol and osmolarity during replacement of sweat loss with plain water
no vol change, dec osmo
disturbances in vol and osmolarity during eating salt without drinking water
no vol change, inc osmo
disturbances in vol and osmolarity during drinking large amount of water
inc vol dec osmo
disturbances in vol and osmolarity during ingestion of isotonic saline
no vol or osmo change
disturbances in vol and osmolarity during ingestion of hypertonic saline
inc volume, inc osmolarity
what are direct effects
those in which the stimulus acts directly on the organ that will produce the response
what is reflex
when action is indirect and requires activation of specific receptors located in other organs
organs involves in the direct effects of dec bp
granular cells, glomerulus
response of granular cells to dec bp
renin secretion
response of glomerulus in response to dec bp
dec GFR
organs involved in the reflex to dec blood pressure
cardiovascular control center, hypothalamus
stimuli to reflexes to dec bp
carotid & aortic baroreceptors, atrial baroreceptors
organ involved in response to carotid and aortic baroreceptors, response?
-cardiovascular control center; inc sympathetic output, dec parasym output
-hypothalamas; thirst stimulation, vasopressin secretion
organ involved in response to atrial baroreceptors, response?
hypothalamus; thirst stimulation, vasopressin secretion
organs involved in direct effect of inc bp
glomerulus and myocardial cells
response to glomerulus after inc bp
inc GFR
response to myocardial cells after inc bp
natriuretic peptide secretion
stimulus involved in reflex to inc bp
carotid and aortic baroreceptors, atrial baroreceptors
organs involved in carotid and aortic baroreceptors stimulus after dec bp and response
-cardiovascular control center, dec symp output, inc parasymp output
-hypothalamus, thirst inhibition and vasopressin inhibition
organs involved in atrial baroreceptors stimulus after dec bp and response
hypothalamus, thirst inhibition
stimulus at inc osmolarity (direct effects), organ involved and response
pathological dehydration, adrenal cortex, dec aldosterone secretion
stimulus at inc osmolarity (reflexes), organ involved and response
osmoreceptors, hypothalamus, thirst stimulation and vasopressin secretion
stimulus at dec osmolarity (direct effects), organ involved and response
pathological hyponatremia, adrenal cortex, inc aldosterone secretion
stimulus at dec osmolarity (reflex), organ involved and response
osmoreceptors, hypothalamus, dec vasopresin secretion
what cardiovascular adjustments occur after a decrease in blood vol/pressure
baroreceptors in carotid arteries and aorta are activated and transmitted to the cardiovascular control center in the medulla oblongata. The neurons integrate the sensory input from the receptors with nervous autonomic responses (parasym/symp. increased sympathetic and decreased parasympathetic output to the heart and vessels.
effect of cardiovascular adjustment in the heart after dec blood vol/pressure
an increase in rate and contractility and results ultimately in an increased cardiac output.
effect of cardiovascular adjustment in the vessels after dec blood vol/pressure
inc sympathetic action causes vasoconstriction
what does a dec in bp cause in the renal front
1. dec GFR, conserves blood vol
2.activation of granular cells by paracrines released by macula densa and production of renin, hence angiotensinII
what does angiotensin II stimulate
the CVCC, arteriolar vasoconstriction and adrenal gland
what prevents aldosterone production and Na reabsorption during dehydration
integration of the high osmolarity signal at the adrenal level
how does ATII inc water content in blood during dehydration
it stimulates vasopressin release and thirst in hypothalamus
anuria
no urine excretion
what does low bp and high osmolarity cause at the hypothalamic level
inc release of vasopressin and stimulates thirst, inc water reabsorption
formula for pH
pH=-log_10[H+]
plasma (ECF) pH
7.38-7.42
acidosis
plasma pH<7.38
alkalosis
plasma pH>7.42
gastric pH
as low as 1
urine pH
4.5-8.5
what does pH influence
protein structure
what occurs in acidosis
dec neuronal excitability, CNS depression, coma, respiratory arrest
what occurs in alkalosis
inc neuronal excitability, numbness/tingling, muscle twitches, tetanus, respiratory muscle paralysis
what does pH imbalance alter
K+ balance (renal H+/K+-ATPase)->cardiac adverse effects
sources of acids
1. acidic foods: HA->A- + H+
2. cellular respiration: glucose +O2-> CO2 + H20
CO2+ H2O -> H+ + HCO3-
sources of bases
basic foods, ammonia
control of pH homeostasis
pH buffers, lungs, kidneys
pH buffer
substance which moderates changes in pH without preventing them by binding or releasing H+
intracellular pH buffers
-cellular proteins
-phosphate ions
-hemoglobin
extracellular pH buffers
-plasma HCO3- (from hemoglobin)
what enzyme converts CO2 into carbonic acid
carbonic anhydrase
what does an inc in ventilation cause
inc in amount of CO2 (acid) eliminated from body and pH elevation
what does a dec in ventilation cause
accumulation of CO2 and lowered pH
what is the main mechanism that controls pH homeostasis
ventilation
what is the slowest mechanism involved in regulation of pH homeostasis
renal handling of H+ and HCO3-
2 levels of nephron where renal handling of H+ and HCO3- occur
1. proximal tubule (where absorption of bicarbonate and secretion of H+ occur)
2. fine tuning of pH balance by the kidney occurs in collecting ducts
2 mechanisms for pH homeostasis in proximal tubule
1. Na-H antiport secretes H, H in filtrate combines with filtered HCO3 to form CO2, CO2 diffuses into cell and combines with water to form H and HCO3, H is secreted again and excreted, HCO3 is reabsorbed
2. glutamine is metabolized to ammonium ion and HCO3, NH4 is secreted and excreted, HCO3 is reabsorbed
2 types of cells that respond to acidosis and alkalosis in the collecting ducts
1. type a intercalated cells
2. type b intercalated cells
type a intercalated cells
active during acidosis and secrete H+ while reabsorbing HCO3 and K
type b intercalated cells
active during alkalosis and exrete HCO3 and K, while reabsorbing H
frontal lobe
motor
parietal lobe
sensory integration
what happens after a major stroke in the right parietal cortex
contralateral neglect syndrome: neglected left visual field
direction of left field visual info to occipital lobe
thalamus->visual cortex in occipital lobe
what is the problem in visual neglect
inability to integrate visual information of a scene
where does left visual field get info from
both retinas
wheres does the info from the left visual field go
right occipital cortex (crossed system b4 it gets to cortex)
parietal lobe
sensory integration
temporal lobe
receptive region, cortical region for audition, learning, memory, facial recognition, language
hippocampus
part of temporal lobe, memory + learning
Agnosia
temporal lobe phenomenon; difficulty recognizing, identifying and naming categories of objects
Prosopagnosia
right temporal lobe damage; inability to recognize and identify faces
describe motor & sensory function
it is crossed so that the right hemisphere is involved in assessing sensory input from the left side of the body and providing motor output to the left side of the body
occipital lobe
vision
lateralization
2 hemispheres need to talk to each other but when you separate them, there's a theory that each hemisphere is a brain within itself
Left brain-right brain (dominance)
left brain does one thing and right brain does something totally different
handedness (very poor predictor of hemispheric dominance)
someone that is left handed thinks that the right hemisphere is dominant
Wada procedure
-injection of fast-acting barbiturate into the right or left artery in order to assess the function of a single hemisphere (puts the hemisphere to sleep)
-if the anesthesized hemisphere is dominant for speech, then the person will not be able to talk
what did the Wada procedure find
that language is localized to the left hemisphere in 93% individuals
3 areas involved in language
broca's area, angular gyrus, wernicke's area
where is broca's area located
frontal cortex (involved in motor aspect of speech)
where is wernicke's area located
temporal lobe
where is angular gyrus located
temporal/parietal region
direction of sensory integration when repeating a spoken word
into wernicke's area->up to arcuate fasciculus->left to broca's area
direction of sensory integration when repeating a written word
primary visual cortex->thru angular gyrus->into wernicke's area, to broca's area
corpus collosum
fiber tract that lets 2 hemispheres talk to eachother
stereognosis
ability to recognize an object by feel
direction of sensory info. from right hand
left cortex->communicated with circuitry involved in speech so they can tell you they had ball in their hand
person with split brain
-objects in left hand cant be named, objects in right hand can be named
broca's aphasia
-can understand spoken and visual info but cant express self. (broca's area is in frontal cortex=motor!)
-called expressive aphasia
wernicke's aphasia
-cant understand spoken or visual info
-fluent & nonsensical speech
-called receptive aphasia
criteria for brain death
-nature & duration of the coma must be known
-cerebral and brainstem function are absent
explain how the nature and duration of coma must be known
-known structural damage to brain or irreversible systemic metabolic disease
-no chance of drug intoxication (from paralyzing or sedative drugs)
-no severe electrolyte, acid-base, or endocrine disorder that can be reversible
-patient isnt suffering from hypothermia
explain how the cerebral and brainstem function are absent
-no response to painful stimuli other than spinal cord reflexes
-pupils unresponsive to light
-no eye movement in response to stimulation of vestibular reflex or corneal touch
-apnea (no spontaneous breathing) for 8 min when ventilator is removed, CO2 over 60 mmHg
-systemic circulation may be intact
-purely spinal reflexes may be retained
-confirmatory neurological exam after 6 hrs
brainstem structures: role in definition of brain death
1.midbrain:pupillary light reflexes
2.pons:eye movements with vestibular stimulation
3.medulla: apnea
4.spinal cord: spinal reflexes intact
vestibular stimulation
tested by asking individual to lie on his side and put cold water in his ear->his eyes will move toward the water
if brainstem, is dead, eyes dont move
hormone
chemical messenger secreted by a cell or group of cells into the blood for transport to a distant target, where it exerts its effects in very LOW concentrations
how do hormones exert their effects
by acting through various classes of ligand-gated receptors
mechanisms of hormone action on target cells
-activate genes for transcription
-alter membrane permeability and/or electrical state by activating 2nd messenger systems
-regulate transport of molecules across membranes
-induce endocytosis (secretory activity)
chemical classes of hormones
-peptides:largest class, derived from amino acids, include insulin, glucagon, vasopressin (AVP), ANF, ACTH, TRH, TSH
-amines: derived from tyrosine and include E, NE, thyroid hormones
-steroids: derivatives of cholesterol, include cortisol and aldosterone
what are thyroid hormones similar to, how
steroid and peptides. thyroid gland stores precursor for hormone but once the precursor comes off, it has all the properties of steroid hormone (lipophillic)
synthesis & storage of peptide hormones
made in advance; stored in secretory vesicles
synthesis & storage of steroid hormones
synthesized on demand from precursors
steroid & thyroid hormone release from parent cell
simple diffusion
steroid & thyroid hormone half life
long
steroid & thyroid hormone location of receptor
nucleus
steroid & thyroid hormone response to receptor-ligand binding
activation of genes for transcription and translation
steroid & thyroid hormone general target response
introduction of new protein synthesis
examples of peptide hormones
ACTH, TRH, TSH
examples of steroid hormones
cortisol, aldosterone, estrogens, androgens
examples of catecholamines (amines)
epinephrine, norepinephrine
examples of thyroid hormones
T3 & T4
which thyroid hormone is more biologically active
T3
major function of thyroid hormones in fetus & infant, effect of deficiency
normal maturation of nervous system.
mental retardation (cretinism)
major function of thyroid hormones in children, effect of deficiency
normal bodily growth because they facilitate the secretion of and response to growth hormone.
deficient growth in children
major function of thyroid hormones in all ages, effect of deficiency
normal alertness and reflexes
restlessness, irritable, anxious, wakeful, hyper-reflexic
major function of thyroid hormones in basal metabolic rate, deficiency and excess?
major determinant of the rate at which the body produces heat during the BMR
deficiency: low BMR, cold intolerance, dec food appetite
excess: high BMR, heat intolerance, inc food appetite, inc catabolism of nutrients
major function of thyroid hormones in sympathetic NS, effect of excess?
facilitates the activity of sympathetic NS by stimulating the synthesis of 1 class of receptors (beta receptors) for epinephrine and NE
excess: symptoms similar to those observed with activation of the sympathetic NS (inc HR)
what is the thyroid gland associated with
follicular cells
thyroid gland, location
butterfly0shaped gland, located just below the larynx
control pathways for release of thyroid hormones
1.ions or nutrients
2.neurotransmitters
3.hormones (hormones release hormones)
hormone release of hormones pathway
TRH manufactured in the hypothalamic neurons stimulates secretion of TSH in the anterior pituitary
pathway of TRH
from the hypothalamic neuron thru arterial inflow from heart to capillaries in median eminence and anterior pituitary (2 capillary bed connected-portal circulation), to venous outflow to heart
effect of TRH
activates G protein>inc activity phospholipase C>release IP3 and DAG>activate IP3 (Ca channel)>elevates intracellular Ca>release of secretory vesicles>release of TSH>enters systemic circulation>affects follicular cells of thyroid gland
multiple roles in the TSH release of T3 and T4
1.trapping:TSH inc activity of Na/I cotransporter>inc iodine trapping>ratio of follicular cell iodine to plasma iodine inc with high TSH
2. iodide leaves cell and enters lumen. follicular cells also secretes thyroglobulin. thyroid peroxidase, on the luminal surface of secretory vesicle, oxidizes I- to I^o
3.iodination:TSH stimulates iodination of thyroglobulin in follicular lumen
4.conjugation: TSH stimulates the conjugation of iodinated tyrosines to form T4 and T3 linked to thryglobulin
5.endocytosis: TSH stimulates endocytosis of iodinated thyroglobulin into follicular cells
6.proteolysis: TSH stimulates proteolysis of iodinated thyroglobulin, forming T4 &T3
7.secretion: TSH stimulates T4 & T3 secretion
8.hyperplasia: TSH exerts a growth factor effect
how are T3 and T4 transported through blood
via protein
thyroid hormones cell of origin
thyroid follicle cells
chemical nature of thyroid hormones
iodinated amine
biosynthesis of thyroid hormone
from iodine and tyrosine; formed and stored on parent protein thyroglobulin in follicle colloid
thyroid hormone transport in the circulation
bound to thyroxine-binding globulin and albumins
thyroid hormones half-life
6-7 days for thyroxine (T4) and 1 day for T3
factors affecting thyroid hormones release
tonic release
control pathway for thyroid hormone
TRH (hypothalamus)>TSH (anterior pituitary)>T3+T4 (thyroid)>T4 deiodinates in tissues to form more T3
target cells of thyroid hormones
most cells of body
target receptor of thyroid hormones
nuclear receptor
whole body or tissue action of thyroid hormones
inc oxygen consumption(thermogenesis); protein catabolism in adults but anabolism in children; normal development of NS
thyroid hormone action at cellular level
inc activity of metabolic enzymes and Na-K ATPase
thyroid hormone action at molecular level
production of new enzymes
thyroid hormone feedback regulation
T3 has neg feedback effect on anterior pituitary and hypothalamus
goiters
overstimulation of thyroid glands
what is the primary effect of hypothyroidism (involved endocrine organ itself)
dec T3, T4, inc TSH->goiter (hyperplasia)
secondary hypothyroidism (s/t external to thyroid is downgrading release of T3/T4)
dec TRH, dec TSH, dec T3, T4, no goiter
Hashimoto's disease
autoimmune disease, hypothyroidism
primary hyperthyroidism(grave's disease)
inc T3,T4, dec TSH, inc TSI->goiter
secondary hyperthyroidism
dec TRH, dec TSH, dec T3,T4->no goiter
symptoms of hyposecretion
low BMR, listlessness, no energy, feeling cold, lethargy, sleepiness, mental sluggishness, impaired memory, slowed speech, slowed reflexes
primary hyperthyroidism (tumor)
inc T3, T4, dec TSH, no goiter
thyroid stimulating immunoglobulin (TSI)
TSH receptor antibodies that stimulate the TSH receptor and cause goiter
what occurs in grave's disease
body doesn't recognize the follicular cell as "self" so it generates antibody to receptors
symptoms of hypertension
high BMR, restlessness, hyperexcitable, sweating, weight loss despite ample food, inc HR, heart pounding, exaggerated response to stimuli in environment, nervousness, irritability
glucose stimulus for the release of hormones
eat meal>inc plasma glucose>inc insulin secretion of pancreatic islet beta cells>inc plasma insulin>glucose uptake in adipocytes and muscle, cessation of glucose output in liver>restoration of plasma glucose to normal
describe calcium induced calcium release by glucose
glucose enters via GLUT2 transporter>glucose influx stimulates glucose metabolism leading to inc ATP>inhibits ATP sensitive K channel>depolarization>opens Ca channel>Ca influx>ca induced ca release>release of insulin into blood
insulin receptor
tyrosine kinase receptor (monomer)
where is tyosine kinase receptor located
in adipose tissue or muscle
what occurs to tyrosine kinase receptor when insulin binds
the monomer dimerizes and autophosphorylates tyrosine residues intracellularly>provides substrate for phosphorylation of intracellular proteins
goal of glucose entering
to use it, store it, and form free fatty acids and proteins
what does glucose entering do
inc glucose utilization
inc glycogen synthesis
inc lipid synthesis
inc protein synthesis
muscle response to inc in plasma insulin
in glucose uptake and utilization
net glycogen synthesis
net aa uptake
net protein synthesis
adipocytes response to inc in plasma insulin
inc glucose uptake and utilization
net triglycerides synthesis
liver response to inc plasma insulin
inc glucose uptake
net glycogen synthesis
net triglyceride synthesis
insulin cell of origin
beta cells of pancreas
chemical nature of insulin
51-amino acid peptide
biosynthesis of insulin
typical peptide
insulin transport in circulation
dissolved in plasma
insulin half-life
5 min
factors affecting insulin release
when plasma glucose >100mg/dL
insulin target cells or tissues
liver, muscle, and adipose tissue primarily.
brain, kidney, intestine not insulin dependant
insulin target receptor
membrane receptor with tyrosine kinase activity, pathway with insulin-receptor substrates
insulin whole body or tissue action
dec plasma glucose by inc transport into cells or inc metabolic use of glucose
insulin action at cellular level
inc glycogen synthesis, inc aerobic metabolism of glucose, inc protein and triglyceride synthesis
insulin action at molecular level
inserts GLUT4 transporters in muscle & adipose cells; alters enzyme activity. complex signal transduction involved
insulin feedback regulation
dec plasma glucose shuts off insulin release
glucose tolerance test: ingest glucose orally
fast for 24 hours and drink glucose drink, blood is drawn periodically
normal subject result for receiving glucose orally
within 1-2 hrs insulin & glucose peak then come down.
3-4 hours later you're back to baseline
diabetic subject result for receiving glucose orally
high resting glucose conc
1-2 hrs, glucose inc but close to peak levels and dont come down
3-4 hours, glucose still elevated and no insulin
diabetes mellitus (type 1DM)
insulin hyposecretion or hypoactivity (insulin dependent)
10% of all diabetics
commonly an autoimmune disease, destruction of beta cells in the pancreas
result of diabetes mellitus (type 1DM)
-hyperglycemia: inc plasma glucose
-glucosuria: inc renal filtration of glucose and ketones
-polyuria: inc Na & H2O excretion
-polydipsia: dec plasma vol
-polyphagia: inc appetite
-metabolic ketoacidosis
-tissue loss: blood vessels. eyes, kidneys, CNS
why do diabetes mellitus patients have ketoacidosis
go to other sources or energy like free fatty acids which are converted into ketones (acidic)
hypoglycemia (insulin shock)
insulin excess- result of insulin injection in excess of an individual's caloric intake and exercise level
result of hypoglycemia
circulating glucose taken up in excess by insulin-dependent mechanisms, depriving the brain of a sufficient supply of glucose->depressed brain function, coma, death
treatment for hypoglycemia
eat or drink something sugary
glucose tolerance test: receive glucose through IV: results for type 1 and type 2 diabetics
Type 1: since beta cell isnt there, theres no source of insulin
Type 2: beta cells release insulin, something is wrong with its release or how its used peripherally
1st phase of normal subject in response to intravenous glucose
release of stored glucose
2nd phase of normal subject in response to intravenous glucose
continued release of stored insulin and release of newly synthesized insulin
type 2 diabetes (T2DM)
-principally caused by being overweight
-90% of all diabetics
-insulin resistance, defects in beta-cell's ability to secrete insulin in response to inc plasma glucose
-hyperglycemia
treatment for type 2 diabetes
-diet & exercise
-oral drugs to treat hyperglycemia, which stimulate beta cells to release insulin
result of type 2 diabetes
atherosclerosis (closing of arteries)
renal failure
blindness
neurological damage
gestational diabetes
-associated with ~4% pregnancies
-hyperglycemia due to maternal insulin resistance
what does untreated gestational diabetes lead to
fetal hyperglycemia, hyperinsulinemia, macrosomia (fat babies)
systemic circulation pressure
93mmHg
pulmonary circulation pressure
12mmHg
directional blood flow through the heart
right atrium>(right AV valve)right ventricle>(pulmonary semilunar valve) pulmonary circulation>left atrium>(micral valve) left ventricle>aortic semilunar valave
how do the 4 valves set directionality
they open & close in a distinct pattern: AV vales open & close together, and semilunar valves open & close together.
how does blood always flow
from atria to ventricles or ventricles to pulmonary or systemic circulation
cardiac conduction system
set of cells that are non-contractile (don't develop forces)
where does the cardiac conduction system start
in pacemaker cell->drive cells in AV node which connect with fivers in the bundle of his which branches, the branches fuse with the purkinje fibers which spread excitation to ventricular muscle >SA node firing, atrial muscle fibers contract>ventricular muscle contracts
sequence of depolarization of cardiac muscle tissue
depolarize atria>depolarize septum from left to right>depolarize anteroseptal region of myocardium toward the apex>depolarize bulk of ventricular myocardium, from endocardium to pericardium (outward)> depolarize posterior portion of base of the left ventricle>ventricles are now depolarized
what does ECG record
electrical events which correlate with contractions
which lead is preferred, why
lead II cuz its the closest to being the axis of depolarization
why is there a delay in AV nodal cells
to give time for the atria to contract so blood can get to ventricle
what does lengthening of PR interval indicate
1st degree AV conduction block
what does loss of QRS waves indicate
2nd degree AV conduction block
what is lengthening of QT interval indicative of
congenital defects in cardiac voltage gated Na or voltage gated K channels
3rd degree AV block
ventricle contracts completely out of sync with atria
ventricular fibrillation
ventricle isnt pumping blood (not enough force)
what is a singularly important function of the cardiovascular system
to ensure continuous adequate blood flow through capillaries
poiseulle's law
delta P= F*R
delta P=pressure gradient along the length of a rigid tube
F= flow of fluid
R=resistance to fluid flow
what does poiseulle's law describe
what happens to fluid as it passes rigid tubes
equation for MAP
MAP= CO * R
MAP= mean arterial pressure (delta P)
MAP= mean pressure in aorta-mean pressure in vena cava at junction with right atrium
CO= cardiac output= HR*SV
R=peripheral resistance
pacemaker cells
SA nodal cells
how do SA node cells generate AP
dec in membrane voltage opens HCN, Na comes in and depolarized the membrane, opens Ca channel, get threshold for AP
what do nodal cells lack which cardiac muscle cells have
voltage-gated Na channels
what is the upstroke of AP due to
opening of voltage-gated Ca (L) type channel
what is repolarization of SA node cells due to
delayed opening of K channels
AV nodal cells
slower pacemakers (~40-60bpm)
normal resting HR
70-80bpm
what dec HR
ACh activation of muscarinic receptors in SA nodal cells
what nerve innervates the SA node
cranial nerve 10 (vagus nerve) in the parasympathetic division of the ANS
what occurs when ACh binds to muscarinic receptor
ACh binds to G-protein coupled receptor>it dissociated into alpha and beta-gamma, the beta-gamma is the active moidy and it binds to the Ca channel>hyperpolarize membrane of SA node cell (dec slope of pacemaker potential)>slows HR
which 2 areas of the heart are affected by the autonomic nerves
SA node (chronotropic effect)
AV node (dromotropic effect)
parasympathetic effect on the SA node (chronotropic effect)
decreased HR
parasympathetic effect on the AV node (dromotropic effect)
decreased conduction rate
what inc HR
NE, E activation of beta1-adrenergic receptors in SA nodal cells
effect of NE/E
sympathetic neurons (NE)>beta1 receptors of autorhythmic cells>inc Na and Ca influx>inc rate of depolarization>inc HR
effect of sympathetic nerves on SA node (chronotropic effect)
inc HR
effect of sympathetic nerves on AV node (dromotropic effect)
inc conduction rate
mechanical events in cardiac cycle
systole:contraction
diastole:relaxation
stroke volume
EDV-ESV (blood that the ventricle forces into the aorta, into systemic circulation)
EDV
blood in ventricle at the end of diastole
ESV
blood in ventricle at end of systole
isovolumetric contraction
volume of blood in the left ventricle isn't changing but the ventricle is contracting
what happens when pressure in aorta<pressure in ventricle
aortic semilunar valve opens
what happens when pressure in aorta>pressure in ventricle
closing of aortic semilunar valve
Frank Starling Mechanism (starling's law of the heart)
increasing sarcomere length of cardiac muscle fibers increases stroke volume
where does majority of blood reside
venous side of circulation (60%)
what is the venous side talked about in terms of
capacitance
what is a pure inc in venomotor tone equivalent to
a transient transfusion
what happens when u inc sympathetic nerve activity on capacitance vessels
venoconstriction>inc venous return
pathway of inc skeletal muscle pump
inc inspiration movements>inc venous pressure>inc venous return>inc atrial pressure>inc EDV>inc stroke vol
effect of increased preload
inc EDV>inc amount of blood in ventricle>shifts pressure-vol curve>frank starling law of the heart
what kind of properties does frank starling's law of the heart represent
properties that are extrinsicly generated
physical regulation of stoke volume
-inc length of cardiac muscle fibers: Frank starling mechanism (starling's law of the heart)
-frank starling property represents extrinsically generated changes in cardiac muscle performance
-inc contractility
what does increased contractility mean in cardiac muscle
an inc in developed tension without a concomitant change in resting muscle length
describe the response of beta receptors to the release of NE or E
the receptor (g protein linked pathway) activates adenylyl cyclase>2nd messenger for the pathway is CAMP>can expect mult. cellular responses cuz of phosphorylation of many proteins
modulation of cardiac contractility by NE and E
epinephrine from adrenal medulla, NE from sympathetic neurons>beta receptors on myocardial contractile cell>activate 2nd messenger system>phosphorylation of phospholamban and voltage gated Ca channels
what happens after phosphorylation of voltage gated Ca channels by E or NE
open time inc, inc of Ca entry from ECF>inc Ca released thru Ca induce Ca release>more forceful contraction>shorter duration of contraction
what happens after phosphorylation of phospholamban
inc Ca-ATPase activity of sarcoplasmic reticulum>inc Ca stores in SR. Ca removed from cytosol faster>time of Ca troponin binding shorter
what happens when u inc amount of Ca stored in SR
get more forceful contraction
ejection fraction (EF)
ratio of stroke volume to end diastolic volume (EDV)
what is EF typically
50-75%
how does inc contractility affect EF
inc EF
how does sympathetic stimulation affect the cardiac function curve
the curve moves up and to the left
what do changes in contractility represent
intrinsic alterations in cardiac muscle performance
effect of inc EDV
inc SV>inc CO
effect of inc activity of sympathetic nerves to heart
inc stroke vol>inc CO
effect of inc plasma epinephrine
inc SV & inc HR>inc CO
effect of dec in activity of parasympathetic nerves to heart
inc HR>inc CO
formula for resistance
R=8Ln/pi*r^4
L=length of tube (constant except in obesity)
n=viscosity of blood (hematocrit)
r=radius of tube (arteriolar radius)
smooth muscle
-not striated (no sarcomere)
-innervated by the ANS
-vascular smooth muscle is innervated only by sympathetic NS
-contains actin, myosin, tropomyosin, NOT troponin
-conc of myosin=1/2 of striated muscle, 2X actin content
-can develop comparable max tension/unit area as striated muscle
properties of smooth muscle
-generates tension differently
-contraction of smooth muscle follows release of neurotransmitters
-smooth muscle can be relaxed by released neurotransmitter
-contraction or relaxation of smooth muscle can be initiated by hormones
-smooth muscle can be initiated by mechanical stretch stimuli
-smooth muscle lacks a specialized end plate region associated with the release of neurotransmitter
what is different in organization of contractile proteins in smooth muscles
-myosin is diff isoform
-cross bridge recycling much slower (takes longer to develop tension)
G protein linked pathway associated with alpha receptor
E or NE bind to alpha receptor>phospholipase C cleaves lipoprotein into DAG & IP3>IP3 breaks off, diffuses & binds to the Ca receptor in SR membrane>Ca comes out, binds to Ca receptor (rianidine receptor) and opens the channel
pathway for smooth muscle contraction
-intracellular Ca concentrations inc when Ca enters cell and is released from SR
-Ca binds to calmodulin
-Ca-calmodulin activates myosin light chain kinase (MLCK)
-MLCK phosphorylates light chains in myosin heads and inc myosin ATPase activity
-active myosin crossbridges slide along actin and create muscle tension
what is calmodulin
Ca binding protein
smooth muscle relaxation
-free Ca in cytosol dec when Ca is pumped out of the cell or back into SR
-Ca unbinds from calmodulin
-myosin phosphatase removes phosphate from myosin, which decreases myosin ATPase activity
-less myosin ATPase results in dec muscle tension
pathway of Ca in in smooth muscle
inc cytosolic Ca>Ca binds to calmodulin in cytosol>Ca-calmodulin complex binds to myosin light chain kinase>myosin light chain kinase uses ATP to phosphorylate cross bridges>phosphorylated cross bridges bind to actin filaments>cross bridge cycle produces tension & shortening
what receptors sense changes in pressure and where are they located
baroreceptors: carotid sinus baroreceptor & aortic arch baroreceptor
pathway of baroreceptors
they receive sensory info about pressure, send it to dorsal part of medulla where its integrated into output pathway to generate a consolidated response to reverse the change its sensing
response pathway of baroreceptors after inc bp
inc bp>inc firing of baroreceptors in carotid arteries and aorta>sensory neurons>cardiovascular control center in medulla oblongata>dec sympathetic output and inc parasympathetic output
effect of dec sympathetic output in response to high bp
less NE released:
-alpha receptor>arteriolar smooth muscle>vasodilation>dec peripheral resistance>dec bp,
-beta2 receptor>ventricular myocardium?dec force of contraction>dec cardiac output>dec bp
-beta1 receptor>SA node>dec HR>dec CO>dec BP
effect of inc parasympathetic output in response to high bp
more ACh on muscarinic receptor>SA node>dec HR>dec CO>dec bp
what 2 types of regulation of arterial bp exist
short term & long term
2 mechanisms for long term regulation of arterial bp
1.dec activity of renin-angiotensin-aldosterone system->inc Na excretion
2.dec kidney tubular reabsorption of Na (pressure natriuresis)
what does inc plasma vol mean
inc blood volume, inc arterial pressure
3 responses to inc arterial pressure in kidney
1.inc activity of "low pressure" baroreceptors
2.dec AVP secretion due to atrial stretch (dec insertion of aquaporin channels)
3.inc secretion of ANP (atrial natriuretic peptide)
where is the atrial natriuretic peptide (ANP) stored and when is it released into circulation
stored in the atrial myocytes, and when atria are stretched cuz of expansion of blood volume, this hormone is released into circulation
effect of inc blood volume on arterial pressure
inc blood volume>inc venous pressure>inc venous return>inc EDV>inc SV>inc CO>inc arterial pressure>inc urinary loss of NA and H2O>dec plasma vol
atrial natriutetic peptide pathways
inc plasma vol>inc distention>inc ANP secretion>inc plasma ANP>inc plasma aldosterone and >kidneys>arterioles (afferent dilation, efferent constriction, inc GFR) & tubules (dec NA reabsorption) >inc Na excretion
hypovalemic shock
sever hemorrhage or excessive vomiting, diarrhea, polyuria>loss of blood vol>dec CO>dec MAP
what occurs in response to inc Na and H2O loss due to diarrhea
inc RAAS activity and inc AVP secetion
RAAS activity in response to inc Na and H2O loss due to diarrhea
reflexes mediated by venous, atrial, and arterial baroreceptors & inc activity of renal sympathetic nerves
inc AVP secretion in response to inc Na and H2O loss due to diarrhea
dec Na and H2O excreted
what is the RAAS system activated by
dec MAP and dec GFR
what does RAAS activity do
activates renal sympathetic nerves that innervate granular cells that surround afferent arterial to the glomerulus> granular cells synthesize and release renin, which enters circulation and chops up peptide angiotensinogen into angiotensin I (inactive)>ACE converts it into angiotensin II with synthesizes & releases aldosterone>inc # Na retained (reabsorbed), then water follows (get max reabsorption)
hemorrhage
10-20% rapid loss of blood volume
effect of hemorrhage on arterial blood pressure
dec blood vol>dec venous pressure>dec venous return>dec atrial pressure>dec ventricular EDV>dec SV>dec CO>dec arterial bp
reflex compensations that occur immediately after hemorrhage
-inc SV
-inc HR & CO
-inc total peripheral resistance and MAP
what returns HR back to normal after hemorrhage
inc in contractility & SV
myogenic autoregulation
maintains a nearly constant GFR when MAP is betw 80 and 180 mmHg
compensation for blood loss after hemorrhage (slow responsE)
dec arterial pressure>dec capillary hydrostatic pressure>inc fluid absorption from interstitial compartment>inc plasma vol>restoration of arterial pressure towards normal
effect of starling forces after hemorrhage
they will favor reabsorption (NFP>0) and fluid will move from the interstitial space into the vascular space
bulk flow
mechanism to redistribute ECF vol (determines distribution betw interstitial space & plasma space)
compensation for blood loss (rapid response)
inc constriction in arterioles>dec hydrostatic pressure>inc fluid absorption from interstitial compartment>inc plasma vol>restoration of arterial pressure towards normal
what does autotransfusion represent
redistribution NO replacement
what changes in volume between time immediately after hemorrhage to 18H after hemorrhage
total blood vol and plasma vol
what doesn't change in volume between time immediately after hemorrhage to 18H after hemorrhage
erythrocyte volume
what does fluid replacement after hemorrhage involve
inc fluid intake and minimization of fluid loss via kidneys
what does replacement of rbc (erythrocytes) require
release of the hormone erythropoietin by kidneys to stimulate erythropoiesis and/or whole blood transfusions
cardiogenic shock
-congestive heart failure
-heart fails to pump an adequate cardiac output
-consequence of inc in afterload as occurs in prolonged hypertension (elevated MAP):diastolic dusfunction
hypertrophic heart
muscle fiber is wider, shorter, and stiffer because the heart pumped against high bp for a long time
physiological hypertrophy
long distance runner get; inc in muscle mass cuz of inc length of muscle fiber (reversible)
which ventricle is larger why
left ventricle is largest ventricular muscle mass cuz it must pump against higher pressure
what can heart failure result from
damage to cardiac ventricular tissue resulting from dec coronary blood flow: systolic dysfunction
cardiovascular responses to cardiac failure due to systolic dysfunction
-dec CO triggers baroreceptor reflex->inc HR,SV,R, restores CO and MAP
-longer term leads to massive expansion of extracellular fluid vol: inc aldosterone, inc Na reabsorption, inc AVP, H2O retention->this inc plasma vol, inc venous return, inc EDV, inc SV
cardiac function curve of failing heart
shifts down and right: inc SV and contractility, at one point u fill ventricle with so much blood that its torn apart
what problems exist due to cardiovascular responses to cardiac failure due to systolic dysfunction
1.ventricles become engorged with blood, SV dec
2.edema (inc venous pressure, inc interstitial fluid due to inc NFP)
3. pulmonary edema
4.chronic inc TPR forces failing heart to work harder
starling forces in heart failure
expansion of plasma vol cuz ure excreting less, thats redistributed via bulk flow from vascular system to interstitial space
pulmonary edema
left ventricle fails to pump the same amount of blood as the right ventricle, resulting in an inc in pulmonary capillary hydrostatic pressure on the venous end of capillaries: NFP inc
why is pulmonary edema so bad
it inc the distance for diffusion in a medium that oxygen doesnt want to be in
what are cardiac failure responses similar to
those invoked during hemorrhage, but sustained for longer periods of time resulting in chronic hypervolemia (inc afterload)
treatments for cardiac failure
1.diuretics (inc urinary excretion of Na and H2O)
2.cardiac inotropic drugs (inc contractility)
3.inhibit AVP binding to receptors in kidney and vascular smooth muscle
4.inhibit RAAS
5.vasodilator drugs (dec R):organic nitrate
how to cardiac inotropic drugs work (like digitalis)
poison Na-K ATPase pump>u dont extrude the extracellular Ca and inc intracellular Ca>inc contractility
problem with digitalis (cardiac inotropic drugs)
it alters extracellular concentrations of Na K throughout entire body
what is inhibiting AVP binding to receptors & inhibiting RAAS similar to, why
inducing diuresis cuz it prevents insertion of aquaporin channels- lowers plasma vol
what do vasodilator drugs do
prevent effect of epinephrine and NE on alpha receptors peripherally, lead to dilation of peripheral vasculature->dec in total peripheral resistance
what does inhibiting RAAS do
inhibits formation of angII: inc Na excretion>inc urination>polyuric state (losing plasma vol by diuresis)
anaphylaxis
-allergic response classified as immediate hypersensitivity
-rapid onset
-mediated predominantly by IgE immunoglobulins, mast cells, basophils
2 immune responses
humoral & cell-mediated
what do B cells do
recognize antigen, bind to its receptor, differentiates into memory cells then plasma cells that synthesize antibodies
memory helper T cells
upregulate normal cytotoxic T cell response or humoral immune response by accelerating proliferation of B lymphocytes
pathway after allergen exposure
first exposure>allergen ingested and processed by antigen-presenting cell>APC activates helper T cell>activates B lymphocyte>becomes plasma cell that secretes antibodies
what does the T cell recognize
complex of the antigenic fragment + MHCII
early allergic reactions
-bronchial smooth muscle contraction
-vascular leakage (swelling)
-hypotension (shock)
what is mast cell filled with
granules
where do IgE antibodies fix to
membrane of mast cells
what occurs open 2nd exposure to allergen
all receptors are already fixed on mast cells so when allergen comes in, mast cells degranulate (release inflammatory mediators)
smooth muscle
muscle that lines outer portion of brachea, upper respiratory systems, makes up bladder
vascular smooth muscle
arterioles
what do u use with person during allergic reaction, why
epipen: epinephrine is agonist on alpha & beta receptors and it activates those receptors causing vascular smooth muscle contraction & bronchiolar dilation
hypertension
-chronically inc MAP (140/90)
-major abnormality is inc peripheral resistance due to dec arteriolar radius of unknown etiology
-baroreceptors reset
what is the cause of hypertension in a minority of ppl
kidney dysfunction
organ most affected by hypertension
heart (left ventricular hypertrophy)
what does hypertension inc chances of
having a stroke
which value in bp would be most dangerous if elevated, why
diastolic cuz thats the force the ventricle needs to open aortic valve
treatments for hypertensive disease
-diuretics (dec blood vol, dec CO)
-beta1 adrenergic blockers: dec CO by dec HR & SV
-alpha1 adrenergic blockers: dec total peripheral resistance by inc arteriolar radius
-Ca channel blockers: dec total peripheral resistance, may inc risk of heart attack
-ACE inhibitors
what does ACE inhibitor do
prevents formation of angiotensin II, potent vasoconstrictor, inhibits release of aldosterone
vasovagal syncope (emotional fainting)
emotional stress>cortex>hypothalamus> medulla>inc vagal output & dec sympathetic output>dec arterial pressure>dec cerebral blood flow>loss of consciousness
effect of dec sympathetic output
dec total peripheral resistance
effect of inc vagal output
dec cardiac output, dec venous return
conditions that generate emotional fainting
Bezold-Jarish Reflex
what occurs to CO during exercise, why
inc, HR and SV inc
what occurs to HR during exercise, why
inc, sympathetic nerve activity to SA node inc, parasympathetic nerve activity dec
what occurs to SV during exercise, why
inc, contractility inc due to inc sympathetic nerve activity to the ventricular myocardium; inc ventricular end-diastolic vol also contributes to inc SV by Frank-Starling mechanism
what occurs to total peripheral resistance during exercise, why
dec, resistance in heart and skeletal muscles decreases more than resistance in other vascular bed inc
what occurs to MAP during exercise, why
inc, CO inc more than total peipheral resistance dec
what occurs to pulse pressure during exercise, why
inc,SV and velocity of ejection of SV inc
what occurs to EDV during exercise, why
inc, filling time is dec by the high HR, but the factors favoring venous return-venoconstriction, skeletal muscle pump, and inc inspiratory movements-more than compensate for it
what occurs to blood flow to heart & skeletal muscle during exercise, why
inc, active hyperemia occurs in both vascular beds, mediated by local metabolic factors
what occurs to blood flow to skin during exercise, why
inc, sympathetic nerves to skin vessels are inhibited reflexly by the inc in body temp
what occurs to blood flow to viscera during exercise, why
dec, sympathetic nerves to blood vessels in the abdominal organs and kidneys are stimulated
what occurs to blood flow to brain during exercise, why
inc slightly, autoregulation of brain arterioles maintains constant flow despite the inc mean arterial pressure
what occurs to blood during exercise
blood volume (5L) stays fixed but it goes to diff places rapidly
flow autoregulation
flow from brain
vasodilation due to local autoregulation
flow from skeletal muscle and skin
vasodilation due to sympathetic nerve inhibition inc temp
flow from skin
vasoconstriction from flow
flow from skin, kidney, abdominal organs, other
aspects of reproduction in mammals
1.sexual (vs asexual)
2.separation of sexes (hermaphroditism)
3.sexual dimorphism
where is sex determination in humans
in genes
chromosome
single molecule of DNA that contains thousands of genes
number of chromosomes in human species
46
2 types of sex chromosomes
x & y
karyotype
organized array of chromosomes
cause of karyotype abnormalities, ex?
gross physiological/anatomical abnormalities
ex: down's syndrome (extra chromosome 21)
turners syndrome
45 chromosomes, XO
turners syndrome symptoms
-sexual infantilism
-ovarian failure (infertilitY)
-short stature
-webbed neck
-low posterior hairline
-shield-like chest
-cardiovascular malformations
-hypothyroidism
klinefelter syndrome
47, XXY
klinefelter syndrome symptoms
-infertility
-sparse hair
-dec muscle mass & strength
-feminine distribution of adipose tissue
-gynecomastia
-small testes & penis
what is the determinant of sex in human species
presence/absence of chromosome Y
when can we tell the sex of the fetus? why?
3 months because that is when the sex glands (gonads) develop
gonadogenesis
formation of gonads
SRY gene
sex-determining region on the Y chromosome
whats the product of the SRY gene
a transcription factor
what do the proteins activated by SRY gene drive
the transformation of the indifferent gonad into a testis
what hormones do the testis produce
hormones that guide the development of a male genital apparatus
leydig cells
secrete testosterone, which is responsible for the development of both male internal and external genitalia
sertoli cells
produce a substance called the antimüllerian hormone, which causes regression of those embryonic structures that could potentially give rise to feminine genitalia.
internal genitalia
gonads and accessory structures
what drives the external genitalia
development of the gonads
active metabolite in testosterone
dihydrotestosterone (DHT)
what does it mean that the female and male external genitalia are "homologs"
they derive from the same primordial structures
example of homologs in female & male external genitalia
-labia majora in female derive from same tissue that gives rise to scrotum
-labia minora are homologs to the shaft of penis
-clitoris to glans
main control center of reproduction
superior centers in the brain cortex collect and integrate endogenous and exogenous stimuli and convey this information to the hypothalamus
neuroendocrine cells
is cells that are both neurons, capable of detecting electric signals, and endocrine cells capable of producing and secreting hormones
2 types of hypothalamic hormones
1.hormones that go directly to bloodstream and reach target organs in various parts of the body
2.hormones secreted in a local venous circuit that delivers them to the pituitary gland.
2 types of hypothalamic secretions
1. directly into the bloodstream
2.indirectly through the median eminence, into the vasculature of the adenohypophysis
first and primary reproductive hypothalamic hormone
gonadotropin releasing hormone (GnRH)
biochemical nature of GnRH
peptide
pituitary hormone from GnRH
FSH, LH
effector organ of GnRH
testes, ovaries
importance of gonads in males
produce steroid and peptidic hormones that produce gametes
importance of gonads in females
to sustain the development of the new individual in case of fertilization.
3 main actors in the hormonal control of reproduction
brain, hypothalamo-pituitary pathway, gonads
feedback mechanisms important in hormonal control of reproduction
1.short loop neg feedback from pituitary to hypothalamus. pituitary hormones can inhibit hypothalamic secretion of their respective stimulating hormones
2.long loop feedback from gonads to hypothalamus and pituitary (can be pos or neg)
2 types of cells in humans
somatic cells & germ cells
zygote
first cell of the new individual
result of mitosis
2 daughter cells that are identical to the mother cell
result of meiosis
4 daughter cells with half as much DNA as the mother cell
when does crossing over occur
in prophase I or meiosis I
main advantage of sex
genetic variability
meiosis process
paternal + maternal homologs>DNA duplication>pairing of duplicated homologous chromosomes>bivalents line up on the spindle>cell division I>cell division II>gametes
spermatogonia
most immature germ cell in males
when is replication of spermatogonia enhanced
at puberty
2 types of cells that result from replication of spermatogonia
1.immature spermatogonia
2.spermatogonia that slightly differ from their progenitors, will differentiate into primary spermatocytes
what is a primary spermatocyte committed to
differentiation into a sperm
secondary spermatocytes
form from meiotic division of primary spermatocytes, have diploid # of DNA
what do the 4 haploid spermatids become
mature sperm cells
immature germ cells in females
oogonium
when does proliferation of immature germ cells occur in women?
during fetal life
why cant women produce gametes their entire life?
primary oocytes start to degenerate well before birth
when do primary oocytes undergo meiosis
when menstrual cycle starts
when does formation of secondary oocyte occur
during expulsion of an ovarian follicle from the female gonad (ovary), in a process known as ovulation
what happens to the other primary oocytes that didnt undergo ovulation
theyre frozen in prophase
what does the secondary oocyte yield
1 mature egg (functional female gamete) & 2nd polar body
differences in gamete production betw female & male
1.time scale (limited gamete production in female, unlimited in male)
2.only 1 type of gamete produced in female, two in male
3.meiotic division if symmetric in male, in female it only yields 1 mature gamete & 2 polar bodies that degenerate
4.in the female, only 1 mature gamete is produced at a time and released by ovaries, but in male gamete production is continuous and yields millions of gametes
functions of male sex apparatus
1.production of sperm
2.delivery of sperm into the female reproductive apparatus for fertilization
where is sperm produces
testes
testes
male gonads; located external to the body just b4 birth where the descend from the abdominal cavity into a skin structure called the scrotum
cryptorchidism
"hidden gonads"- condition where the testes dont descend to the scrotum
what is the external location of the testes essential for
correct spermatogenesis to occur
pathway of sperm from the testes
epididymus>vas derens>bladder>urethra>penis
accessory glands of male reproductive system
seminal vesicles, prostate, bulbourethral glands
main function of accessory glands of male reproductive system
produce the fluid portion of the semen which preserves, nourishes and vehicles the sperms.
what is the penis formed by
shaft (long portion) and glans (shorter head) covered by the prepuce
what is the urethra surrounded by
corpus spongiosum
what forms the erectile tissue of the penis
corpus spongiosum and corpora cavernosa
what are the testis formed by
seminiferous tubules
what is the thick wall of the seminiferous tubules formed by
sertoli cells
what do sertoli cells do
surround and sustain a heterogeneous population of cells consisting of germ cells at all stages of development
what does environment surrounding tubules contain
leydig cells
functions of testis
1.production of male gametes
2.production of testosterone, which sustains spermatogenesis and triggers the development of the male secondary sexual characteristics
2 important cell types in testis
sertoli cells and leydig cells
sertoli cells
-produce & secrete hormones, growth factors, androgen-binding proteins.
-promote and sustain sperm development
leydig cells
-produce and secrete testosterone
-active in fetal life>gonadogenesis
-quiescent after birth
-active at puberty and on (sexual maturity/function
how does FSH stimulate spermatogenesis
by activating sertoli cells which produce substances that stimulate and sustain division & differentiation of spermatogonia
what do sertoli cells also produce
-peptide hormone inhibin; inhibits via a feedback mechanism secretion of FSH
-androgen binding protein (ABP) which tenders lypophillic steroid hormones like testosterone
what does LH target
Leydig cells and activates their production of testosterone
what 2 levels does testosterone act in
1.stimulates the Sertoli cells to produce more substances necessary for spermatogenesis
2.secreted into bloodstream by ABP, where it affects all organs & mediates development of secondary sex characteristics
secondary sex characteristics
sex-essential features that are part of sexual phenotype
prostaglandins
local mediators that act mainly in smooth muscle structures surrounding female & male genital canals, , inducing local rhythmic contractions that are thought to play a role in sperm transport.
function & source of sperm
gamete, seminiferous tubules
function & source of mucus
lubricant, bulbourethral glands
function & source of water in semen
provides liquid medium, all accesory glands
function & source of buffers in semen
neutralize acidic environment of vagina, prostate, bulborethral glands
function & source of nutrients in semen
nourish sperm, seminal vesicles prostate epididymus
function & source of enzymes in semen
clot semen in vagina then liquefy the clot, seminal vesicles and prostate
function & source of zinc in semen
unknown
function & source of prostaglandins in semen
smooth muscle contraction;may aid sperm transport, seminal vesicles
male sexual act
erection & ejaculation
2 pathways that erection occurs via
1.tactile stimuli collected by mechanoreceptors in penis transmitted thru terminals of nerve neurons to the spinal cord
2.exogenous and endogenous stimuli can trigger erection even in absence of mechanical stimulation (brain can control autonimic neurons via descending pathway)
erection reflex
-exogenous and endogenous stimuli activate a spinal reflex via higher brain centers
-tactile stimuli activate directly the spinal reflex centers
-activation of spinal reflex center inhibits vasoconstriction and stimulates vasodilation
-blood fills corpora cavernosa & corpus spongiosum & erection occurs
2 phases of ejaculation
emission & ejaculation
emission
sperm moves out of vas deferens into urethra, where its joined by gland secretions and forms semen
ejaculation
series of rapid involuntary muscular contraction expel the semen from urethra
-about 3ml of semen containing 200 millions of spermatozoa are expelles
main differences betw male & female reproductive systems
-gonads are internal
-urethra isnt part of sex apparatus
-no accessory glands (have mammary glands)
-can sustain development of new individual
-reproductive activity is limited and lost
-reproductive activity is cyclic
external genitalia of the female sex organs
-involved in female sex act
-possible role in promoting fertility (climax)
-passive involvement in parturition
where a female external genitalia located
ventrally to the mons pubis, an elevation of tissue located over the pubic bone
vagina
opening of birth canal
what is vagina partially occluded by
membrane called hymen
anatomy of the female sexual organs internal genitalia
-active role in sperm transport
-support fertilization
-support embryo implantation and development
-active role in parturition
uterus
large, triangular hollow organ located in the lower abdominal cavity of the woman.
what projects laterally from the uterus
2 narrow canals; fallopian tubules and oviducts
mullerian structures
the tubes, the uterus and the upper portion of the vagina (no male homologs)
2 levels involved in menstrual cycle
1.ovarian cycle (ovulation)
2.endometrial cycle (embryo development/ menstruation)
ovulation
maturation & expulsion of a mature gamete (egg/ovum)
endometrium
internal uterine wall
2 outcomes of endometrial cycle
-periodic and dramatic destruction of the endometrial epithelium, with emission of blood and tissue debris from the vagina (menstruation)
-If the egg is fertilized by a sperm and the resulting embryo implants successfully in the uterus, though, there is no menstruation and the endometrium is deeply modified to host embryo development
hormonal control of female reproductive function
1.GnRH and gonadotropin production follows a characteristic cyclic pattern
2.LH plays essential role in gamete production
3.long-loop feedback action exerted by the ovaries on the hypothalamo-pituitary axis is not only inhibitory but also stimulatory
pituitary gonadotropins (LH, FSH)
-glycoproteic hormones
-very specific action on the gonads
-cyclic patterns of secretion, shaped by GnRH pulses and feedback mechanisms
-stimulate production of estrogens and progesterone in the ovaries
extraovarian functions of estrogens
-development of female secondary sexual characteristics
-skeletal growth (inc osteoblastic activity, fusion of epiphyses)
-metabolic effects (subcutanous fat accumulation, inc in total body proteins)
extraovarian functions of progesterone
-promotes uterine secretion and decrease uterine contractility
-promotes secretion by tubal epithelium
-involved in milk production
-thermogenic effect
parts of ovarian cycle
1.follicular phase
2.ovulation
3.luteal phase
follicular phase
progressive growth of ovarian follicles. results in the outgrowth of only 1 of them which buds on the ovarian surface
ovulation
dominant follicle bursts and the oocyte is expelled into the abdominal cavity
luteal phase
most of the cells that formed the follicle wall will remain in the ovary and give rise to a secretary structure called corpus luteum. this structure generates spontaneously if pregnancy doesnt occur
ovarian follicle
complex formed by the oocycte and the surrounding granulosa cells
ovarian cycle
growth & development of ovarian follicles under the influence of gonadotropins and steroid hormones
level of steroid hormones at beg of follicular phase, why?
low because these hormones ar produced by cells that surround oocyte in the follicle that arent numerous now
what does the low level of steroid tells the hypothalamus & pituitary
that the ovaries need stimulation
what causes growth of primary oocytes
high level of gonadotropins
what does the progressive growth of the follicle cause
the follicular cells (granulosa and theca cells) to produce more steroid hormones
what does an inc production of steroid hormones result in
neg long-loop feedback action on the hypothalamo-pituitary axis that causes a dec of gonadotropin secretion
what do high estrogen levels in bloodstream result in
positive feedback; GnRH and gonadotropin secretion is increased
LH surge
blood conc of gonadotropins (LH) peaks
what does the LH surge mark
end of follicular phase and triggers ovulation
how does LH surge cause ovulation
high amount of LH causes follicular cells to swell and accumulate fluid in the follicular cavity. enzymes destroy ovarian stroma. follicle bursts and oocyte is released from ovary
during which period of menstrual cycle does ovulation occur
middle
corpus luteum
cells that were part of follicular walls that are left in ovary after ovulation
what occurs to level of steroid hormones during luteal phase of ovarian cycle
it grows
feedback action of estrogen after corpus luteum is formed
negative, inhibition of gonadotropin secretion causes regression of corpus luteum which is replaced by corpus albicans
uterine (endometrial cycle)
1.proliferative (estrogen) phase
2.secretory (progestational) phase
3. menstruation
what is the uterine cycle caused by
cyclic fluctuations in hormone production by the ovaries
endometrium
internal layer of the uterine wall
where is uterus
female lower abdominal cavity, its enclosed by an outer capsule of connective tissue.
what is most of the uterine wall thickness given by
a layer of strong muscular tissue called myometrium
functions of endometrium
1.support implantation of the fertilized egg
2.support early stages of embryonic development
product of endometrial glands
cervical mucus
cervical mucus
fluid composed of electrolytes & small molecules that function as nutrients & osmolites like sugars and small proteins & by larger molecules like polysaccharides, glycoproteins and proteoglycans that function as "Water traps"
composition of cervical mucus during first (proliferative) phase of uterine cycle
watery & thin
composition of cervical mucus during secretory phase of uterine cycle, in particular if pregnancy occurs
thick & rich of nutrient substances
main function of cervical mucus if pregnancy occurs
nourish embryo during 1st stages of development, when placenta is poorly developed
purpose of water & thin cervical mucus
facilitates sperm cell transport during proliferative phase; import in female fertility
composition and pH of cervical mucus
varies throughout diff phases of menstrual cycle
what is the proliferative phase of menstrual cycle (day 4-14) driven by
inc amount of estrogens produced by developing follicles
what occurs during proliferative phase of menstrual cycle (day 4-14)
re-epithelialization of endometrium, a new functional layer forms
what is the secretory phase of menstrual cycle driven by
estrogens and progesterone produced by corpus luteum after ovulation
what occurs during secretory phase (day 4-28)
glands and blood vessels develop enormously & secreted mucus becomes thicker & rich of proteins (uterine milk)
menstruation
involution of the corpus luteum, endometrial glandular structure involutes, involution blood vessels cause massive tissue necrosis and release of blood and tissue debris into uterine cavity
what does degeneration of corpus luteum cause
hormone (especially progesterone) withdrawal
what occurs after fertilization
the embryo implants in the uterine wall and starts producing hormone called chorionic gonadotropin (similar to LH) and prevents degeneration of corpus luteum
what do hormones produced by corpus luteum sustain
endometrial structure and further promote its growth
where does egg go after ovulation
peritoneal cavity
what is the egg surrounded by
capsule called zona pellucida & layer of follicular cells (corona radiata)
where does fertilization occur
in fallopian tubes (central portion called ampulla)
where does implantation occur
uterine cavity
implantation
nesting of the zygote into the uterine wall, which will provide support to its growth & development until birth
when does implantation occur
5-9 days after ovulation
what is the zygote called during implantation
blastocyte
what does pregnancy officially start
after implantation
4 components of cumulus oophorus
-secondary oocyte
-perivitelline space
-zona pellucida
-corona radiata
6 steps of fertilization
-sperm capacitation
-acrosome reaction
-sperm penetration in the perivitelline space
-cell membrane fusion
-cortical reaction
-fusion of pronuclei
3 portions of mature sperm
-sperm head (acrosome) that contains nucleus & vesicle full of enzymes
-narrow neck separates heads from 2nd portion of sperm, the middle piece
-long tail
what does the middle piece of sperm contain
structures responsible 4 sperm movement & its energy supply (spirals of mitochondria)
what is the long tail of sperm used for
propulsion
what does the sperm cell membrane fuse with during sperm penetration
oocyte membrane
what does the fusion of sperm cell with oocyte membrane trigger
completion of meiosis in oocyte; mature haploid egg has formed and a 2nd polar body is extruded
events in sperm penetration
1.sperm capacitation
2.acrosome reaction
3.cortical reaction
sperm capacitation
"Capacitating factor" present in cervical mucus inactivates an inhibiting factor on sperm and prevents it from fertilizing the egg
acrosome reaction
-acrosome membrane fuses with sperm cell membrane
-hydrolytic enzymes are released that loosens the corona radiata, so that they are destroyed and the sperm contacts zona pellucida
-release of acrosomal enzymes
-zona pellucida is locally destroyed and sperm cell reaches egg cell membrane and starts fusing with it
-this contact triggers cortical reaction
what does cortical reaction prevent
penetration of other sperm cells in fertilized egg, avoiding the formation of a polyploid prganism
cortical reaction
-oocyte membrane depolarizes and voltage gated calcium channels open
-Ca enters cytoplasm and trigger exocytotic release of cortical granules
-enzymes contained in cortical granules modify zona pellucida, making it inaccessible to other sperm cells
what does fusion of female & male pronuclei result in
fertilized egg with diploid # of chromosomes which then divides by mitosis, yielding 2 diploid cells
fertilization facts
-completed within 24 hrs of ovulation
-about 200 mill. sperms are deposited at cervical opening during ejaculation
-only about 200 sperms reach fertilization site, most degenerate and are absorbed by female genital tract
what is the epithelium that forms the internal cavity of zona pellucida & corona radiata covered by, why
microcilia, it creates neg pressure that sucks egg into tubes
where are major hormones involved in pregnancy produced by
placenta
placenta
organ formed by maternal & fetal tissues
how is placenta formed
-after implantation, most external cells in blastocyte form fingerlike structures that extend in the endometrium (chorionic villi)
-empty spaces (lacunae) open betw villi & endometrium and are filled w/blood
-embryonic blood vessels extend into chorionic villi
-placenta (villi,lacunae,maternal & embryonic blood vessels) is formed
functions of placenta
-gas exchange (fetal lung)
-nutrient absorption (fetal gut)
-fluid vol. control/elimination of catabolites (fetal kidney)
-secretion of hormones to sustain pregnancy
placental hormones
-chorionic gonadotropin (hCG)
-progesterone
-estrogens
chorionic gonadotropin (hCG)
-similar structure and physiological function to LH
-produced early by embryonic portion of placenta (used in pregnancy tests)
-prolongs life of & stimulates secretion by corpus luteum
-stimulates secretion of steroid by corpus luteum, in absence of GT secretion
progesterone
-increasing level of production
-increases secretion by endometrium
-contributes to breast maturation and lactation
estrogens
-necessary for enlargement of uterus during gestation
-contribute to mammary gland development
-produce enlargement of female external genitalia in preparation for parturition
how long does normal pregnancy last
38-42 weeks
how does corpus luteum keep GT levels low
via negative feedback
why is progesterone needed in early phases of pregnancy
to sustain embryo development
what happens to corpus luteum when the placenta has fully developed
it degenerates
duration of pregnancy
1.limit of viability:23 weeks
2.pre-term:23-37 weeks (premature baby)
3.full term:38-42 weeks
4.post-term:later than 42nd week (post-mature baby)
parturition
1.at the end of the term, weal & periodic uterine contractions present during last period of development become increasingly intense & frequent (labor)
2.onset of mechanical and hormonal positive feedback loop results in expulsion of fetus out of maternal body
pos feedback loop of parturition
fetus drops lower in uterus>cervical stretch>oxytocin from posterior pituitary>prostaglandins from uterine wall>uterine contractions>cervical stretch & cycle repeats
when does cesarean section occur
when fetus isnt positioned head-first
what is the last phase of parturition
expulsion of placenta
how does newborn receive nourishment in form of essential nutrients
milk from female's mammary glands
when does mammary gland development start
in puberty, under effect of estrogens
what occurs to mammary glands during pregnancy
estrogens & progesterone further stimulate mammary gland growth & maturation
what does milk secretion require
-pituitary secretion of prolactin (enhanced during pregnancy by dec in hypothalamic hormone that inhibits prolactin release (PIH)
-release from inhibitory action of placental steroids (which occurs with expulsion of placenta at birth)
composition of human milk
water, carbs, proteins, milk lipids, vitamins, minerals
PIH
prolactin-inhibiting hormone, this hypothalamic hormone turned out to be the neurotransmitter dopamine
PRL
prolactin
OT
oxytocin
what does baby suckling stimulate
mechanosensors in nipple>further inhibition of PIH secretion (inc PRL) and release of OT from hypothalamus>OT induces contraction of smooth muscle cells that surround ducts and alveoli>milk is ejected in ducts
galactorrhea
discharge of milk or a milk-like secretion from breast in men or in non-breastfeeding woman in absence of pregnancy, parturition of beyond 6 months postpartum
most common causes of galactorrhea
hyperprolactinemia; primary tumors, hypothalamic and pituitary stalk lesions, medications, primary hypothyroidism, chronic renal failure, neurogenic causes, neonatal galactorrhea, idiopathic
how do medications cause galactorrhea
reduce dopamine
how does renal failure cause galactorrhea
reduced renal clearance of PRL>elevated serum PRL
neurogenic causes of galactorrhea
prolonged, intensive breast stimulation, such as from suckling, self-manipulation, or stimulation during sexual activity
examples of neurogenic causes of galactorrhea
chest surgery, burns, and herpes zoster that affects the chest wall. Stimuli are thought to pass along the intercostal nerves to the posterior column of the spinal cord, to the mesencephalon, and finally to the hypothalamus, where the secretion of prolactin inhibitory factor is reduced.
neonatal causes of galactorrhea
high levels of estrogens in placental-fetal circulation can result in gynecomastia in newborn infants
idiopathic causes for galactorrhea
diagnosed by exclusion