exam 4 Flashcards
components of the urinary system
kidneys
ureters
bladder
urethra
function of the kidneys
filter blood
remove waste products and convert filtrate into urine
ureters
transport urine
from kidneys to urinary bladder
bladder
expandable sac
stores as much as 1L urine
urethra
eliminates urine from body
right kidney is slightly _______
inferior to larger liver lobe
other functions of kidney
-regulation of ion levels and acid-base balance
- production and release of erythropoietin
- regulation of blood pressure
regulation of ion levels and acid-base balance
helps control blood’s inorganic ion balance
e.g., Na+, K+, Ca2+
aids in maintaining acid-bas balance
production and release of erythropoietin
indirectly measures oxygen level of blood
secretes erythropoietin (EPO) in response to low blood oxygen
- stimulates red bone marrow to increase rate of erythrocyte production
- erythrocytes transport oxygen from lungs
regulation of blood pressure
alters amount of fluid lost in urine (helps regulate blood volume)
releases renin enzyme (required for production of angiotensin II, hormone results in increased blood pressure)
the kidney is responsible for
healthy blood
characteristics of the kidney
kidneys are two symmetrical, bean-shaped organs
size of hand to second knuckle
concave medial border, hilum
lateral border convex
adrenal gland rests on superior aspect of kidney
hilum
where vessels, nerves, and ureter connect to kidney
medullary area
contains renal columns that help anchor medullary tissue as well as subdivide into renal pyramids
renal sinuses
minor and major calyx
minor calyx
first region that is closest to the renal pyramid and runs into major calyx
major calyx
has connection between minor calyx and renal pelvis
striations are presented as a result of
how collecting ducts and nephron limbs are located and sown on kidneys
structures of the kidney
nephrons
collecting tubules
collecting ducts
nephron
- microscopic functional filtration unit of kidney
- consists of renal corpuscle and renal tubule
- all of corpuscle and most of tubules reside in cortex
glomerular capsule contains visceral and parietal layer but is not a…
serous membrane
fluid and solutes within the kidney are going to
pass through glomerulus and connect in capsular space
glomerular capsule
Bowman’s capsule
nephron loop
“Loop of Henle”
tubular fluid descends down into medullary region where it turns around and goes back into cortex
main components of nephron loop
renal corpuscle
proximal convoluted tubule (PCT)
nephron loop
distal convoluted tubule (DCT)
renal corpuscle is composed of
glomerulus
capsular space
two types of nephron
cortical nephron
juxtamedullary nephron
nephron loop causes
high salt concentration in medullary tissue which serves osmotic draw to send it into the body
nephron drainage
- nephrons drain into a collecting tubule (each kidney contains thousands, cuboidal-shaped cells)
- then empties into larger collecting ducts (tall columnar cells)
- empty into papillary duct
- both collecting tubules and collecting ducts project towards renal papilla
juxtaglomerular apparatus (JG)
- helps regulate blood filtrate formation, systemic blood pressure
- primary components: granular cells, macula densa cells
granular cells
- modified smooth muscle cells of afferent arteriole
- located near entrance to renal corpuscle
- contract when stimulated by stretch sympathetic stimulation
- synthesize, store, and release renin
macula densa
- modified epithelial cells in wall of DCT
- located on tubule side next to afferent arteriole
- detect changes in NaCl (salt) concentration of fluid in lumen of DCT
- signal granular cells to release renin through paracrine stimulation
granular cells are responsible for
stretching of afferent arteriole increasing or decreasing blood flow
blood flow through kidneys
- 20%-25% of resting cardiac output
- filtrate formed when blood flows through glomerulus
- some components of plasma enter capsular space
two parents of flow in kidneys
flow of blood into and out of the kidney
flow of filtrate, tubular fluid, urine through the nephron and other urinary structures
blood supply to kidney flow
renal artery
segmental artery
interlobar artery
arcuate artery
interlobular artery
afferent arteriole
glomerulus
efferent arteriole
peritubular capillaries and vasa recta
interlobular vein
arcuate vein
interlobar vein
renal vein
peritubular capillaries are associated with
convoluted tubules
vasa recta is associated with
nephron loop
filtrate
- blood flows through glomerulus where water and solutes are filtered from blood plasma
- moves across wall of glomerular capillaries and into capsular space
forms filtrate
substances that transport fluid through urinary system
filtrate
1. capsular space
tubular fluid
2. proximal convoluted tubule (PCT)
3. descending limb of nephron loop
4. ascending limb of nephron loop
5. distal convoluted tubule (DCT)
6. collecting tubules
7. collecting duct
urine
8. papillary duct
9. minor calyx
10. major calyx
11. renal pelivs
12. ureter
13. bladder
14. urethra
glomerular filtration
the movement of substances from the blood within the glomerulus into the capsular space
tubular reabsorption
the movement of substances from the tubular fluid back into the blood
tubular secretion
the movement of substances from the blood into the tubular space
active transport
process of urine formation
- glomerular filtration
- tubular reabsorption
- tubular secretion
filtration membrane
refers to the structures that materials need to pass through
filtration membrane is composed of
endothelium of fenestrated capillary
basement membrane (thin layer of glycoproteins)
filtration slits between adjacent podocytes
components of visceral layer of glomerular capsule
pedicels
filtration slits (have openings in addition to normal routes)
podocytes (have slits between adjacent podocytes)
filtrate includes
water, glucose, amino acids, ions, urea, some hormones, vitamins B and C, ketones, and very small amounts of protein
what stays in the blood when becoming filtrate
formed elements and proteins
- endothelium blocks formed elements
- basement membrane blocks large proteins
- filtration slits block small proteins
net filtration pressure
hydrostatic pressure of blood in glomerulus
opposing pressure
- blood osmotic pressure (oncotic pressure)
- fluid pressure in capsular space of renal corpuscle
values in net filtration pressure in glomerular filtration
HPg - (OP +HPc) = NFP
60 mm Hg - (32 mmHg + 18mmHg) = NFP
60mmHg - 50mmHg = 10 mmHg
typical numbers
glomerular filtration rate (GFR)
- GFR is the volume of fluid filtered from the glomerular capillaries into the capsular space per unit time (typically one minute)
- tightly regulared
- helps kidney control urine production based on physiologic conditions (hydration status)
- influenced by changing lumen diameter of afferent arteriole and altering surface area of filtration membrane
- process within kidney (intrinsic controls) external to kidney (extrinsic controls)
what effect would dehydration have on GFR and urine production
GFR would decrease if dehydrated therefore decreasing urine output
change in luminal diameter of afferent arteriole and GFR
if arteriole dilates (widens) GFR increases
if arteriole compresses (shrinks) GFR decreases
alteration of surface area and GFR
increase in surface area of filtration membrane increases GFR
decrease in surface area of filtration membrane decreases GFR
intrinsic controls of kidney
self regulating mechanisms
extrinsic controls of kidney
influence GFR but not in kidney
endocrine and nervous system influence
renal autoregulation
intrinsic controls
intrinsic ability of kidney to maintain constant glomerular blood pressure an thus GFR despite changes in systemic arterial pressure
renal autoregulation serves to
maintain a stable and constant glomerular BP and filtration rate
if something causes BP to elevate you would expect
glomerular in BP to elevate as well but renal autoregulation prevents this from happening
myogenic response
reflex response of afferent arteriole in response to changes in blood pressure (contraction or relaxation of smooth muscle of afferent arteriole)
decreased BP, less stretch of smooth muscle in arteriole causes
smooth muscle cells to relax and vessels to dilate which allows for
- more blood into glomerulus
- compensates for lower systemic pressure
GFR remains normal
increased BP, more stretch of smooth muscle in arteriole causes
smooth muscle cells to contract, vessels to constrict which allows for
- less blood into glomerulus
which compensates for greater systemic pressure and GFR remaining normal
decreasing GFR through sympathetic stimulation
- stimulus: stressor/emergency
- sympathetic stimulation of kidneys
- vasoconstriction of afferent and efferent arterioles resulting in decreased blood flow to glomerulus
- granular cells of JG apparatus release renin which causes an increase in angiotensin II production leading to contraction of mesangeal cells resulting in decreased filtration rate at glomerulus - overall:
- decrease in GFR
- decrease in urine production
- retain fluid
maintain blood volume
goal is not to maintain but change
GFR depending on physiological needs
increasing GFR through atrial natriuretic peptide
- stimulus: increase in blood volume or blood pressure
- atrial wall stretches
- ANP released by heart
- vasodilation of afferent arteriole resulting in increased blood flow to glomerulus
- renin release from granular cells of JG apparatus is inhibited causing a decrease in angiotensin II production leading to relaxation of mesangial cells causing an increased filtration rate at glomerulus - overall:
- increase in GFR
- increase in urine production
- loss of additional fluid
- decrease in blood volume
maintaining GFR
renal auto regulation maintains GFR despite changes in systemic BP:
- decreased systemic BP results in vasodilation of afferent arteriole
- increased systemic BP results in vasoconstriction of afferent arteriole
decreasing GFR
sympathetic division decreases GFR by
- afferent arteriole vasoconstriction
- triggering mesangial cells to contract, which decreases filtration surface area
urine production is decreased which helps maintain blood volume
increasing GFR
ANP increases GFR by
- afferent arteriole vasodilation
- triggering mesangial cells to relax which increases filtration surface area
urine production is increased which decreases blood volume
nutrient reabsorption
some substances 100% reabsorbed
two major classes: nutrients and filtered plasma proteins
nutrients are normally completely reabsorbed in
proximal convoluted tubule
- each nutrient has its own specific transport proteins
glucose reabsorption
- glucose is transported from tubular fluid into tubule cell of PCT by secondary active transport UP its concentration gradient
- levels of Na+ much higher than glucose levels so active transport is needed
- sodium moves down into the tubular fluid as glucose enters into the tubular cell - glucose diffuses down its concentration gradient by facilitated diffusion
- high concentration for glucose into the cell and low glucose in interstitial fluid allows for passive movement of glucose out of the cell with aid of transport protein (facilitated diffusion) - glucose is reabsorbed into the blood
- once glucose is in interstitial fluid, it is 100% reabsorbed as it continues along the length of PCT
most transport proteins are
not freely filtered due to size and charge
some small and medium sized proteins may appear in filtrate
small amounts of large proteins
proteins are transported from
tubular fluid in PCT back into blood
protein moves across the luminal membrane of cell by:
- pinocytosis
- receptor-mediated endocytosis
pinocytosis
protein enters into divots in plasma membrane which closes off and forms a vesicle
receptor mediated endocytosis
specific receptors on given proteins bind to sepcific receptor and pinch off as vesicle having proteins within the vesicle where they dissolve within
sodium reabsorption is regulated by
hormones near end of tubule
- aldosterone and ANP
- dietary intake of Na+ varies
Na+/K+ pumps are embedded in
the basolateral membrane
Na+/K+ pumps help
keep Na+ relatively low within tubule cells
pumps require substantial energy
aldosterone and Na+ reabsorption
- steroid hormone produced by adrenal cortex
- stimulates protein synthesis of Na+ channels and Na+/K+ pumps
- embedded in plasma membranes of principal cells
- increase in Na+ reabsorption
- water follows by osmosis
atrial natriuretic peptide and Na+ reabsorption
- inhibits reabsorption of Na+ primarily in the collecting ducts
- inhibits release of aldosterone
- more Na+ and water excreted in urine
- increases GFR
if there is less aldosterone, in turn there will be
less Na+ channels and pumps causing less Na+ to be reabsorbed
sodium reabsorption of Na+ in PCT
- Na+ diffuses down concentration gradient by facilitated diffusion from tubular fluid into tubule cells
- Na+ transport protein allows Na+ to move down concentration gradient - Na+ is moved up its concentration gradient by active transport from tubule cell into interstitial fluid
- from interstitial fluid about 65% of Na+ is reabsorbed into the blood
- process continues as fluid proceeds through nephron loop
35% of Na+ remains in
tubular fluid
sodium reabsorption in lumen of DCT, CT, or CD
WHERE FINE TUNING OCCURS
- when tubular fluid reaches this part, 98% of Na+ will be absorbed
- tubular fluid flows down
1. High concentration of Na+ in tubular fluid is passively diffused down concentration gradient into principal cells through Na+ channels
2. Na+/K+ pumps lining the principal cells move K+ up its concentration gradient into the principal cells from interstitial fluid while moving the low Na+ from principal cells into interstitial fluid
principal cells
have receptors for aldosterone which is released from adrenal cortex which is stimulated by low blood Na+
the effect of binding of aldosterone on Na+ reabsorption
both the number of Na+ channels and Na+/K+ pumps resulting in an increase in Na+ reabsorption
water reabsorption
- 180L filtered daily; all but 1.5 L reabsorbed
- tubule permeability varies along its length
- 65% reabsorbed in PCT
- aquaporins constant number
- water follows Na+ by osmosis, obligatory water reabsorption
10% of filtered water is reabsorbed in the
nephron loop
water reabsorption within distal convoluted tubule, collecting tubules, and ducts
- water reabsorption controlled by aldosterone and antidiuretic hormone
- aldosterone increases Na+/K+ pumps and Na+ channels
- therefore, increases water reabsorption
antidiuretic hormone and water reabsorption
ADH binds to principal cells which
- increases migration of vesicles containing aquaporins to membrane
- adds channels to increase water reabsorption
concentration gradient within interstitial fluid
- independent of Na+ reabsorption
- water reabsorption regulated by ADH near end of tubule
- tubular reabsorption = facultative water reabsorption (dependent on hydration status)
water reabsorption steps
- ADH causes principal cells to increase number of aquaporins allowing for more passageways to get water out of tubule and into blood
- the driving force for this is high concentration of salts in interstitial fluid to draw water down its concentration gradient
- serves to raise BP
antidiuretic hormone and water reabsorption
- increases water reabsorption from tubular fluid into blood
- results in smaller volume of more concentrated urine
- elevated levels during dehydration (urine noticeably darker)
- with decrease, urine is less concentrated
- urine range 1200 mOsm to 50 mOsm
which hormone contributes to concentration of urine
antidiuretic hormone (ADH)
movement of potassium
- almost all of potassium is reaborbed
- both reabsorbed and secreted
- under the influence of aldosterone (increases the secretion of K+ into the tubular fluid
low sodium triggers
aldosterone release
dehydration releases
aldosterone
60-80% of K+ is reabsorbed in the
PCT
10-20% of K+ is reabsorbed in th
nephron loop
regulated K+ reabsorption and secretion occurs in
collecting tubules
type A intercalated cells (of collecting duct)
cells are interspersed around other cells in collecting duct
reabsorb K+ continuously
whatever K+ that enters collecting duct is reabsorbed by type A intercalated cells
principal cells of collecting duct
vary K+ secretion depending upon aldosterone levels
parathyroid hormone (PTH)
- regulates excretion of calcium(Ca2+) and phosphate (PO43-)
- inhibits phosphate reabsorption in PCT
- stimulates calcium reabsorption in DCT
- less phosphate available to form calcium phosphate
- calcium deposition in bone decreased
- calcium blood levels increased
calcium ion and phosphate ion reabsorption
- PTH inhibits reabsorption of PO43- in PCT
- PTH stimulates reabsorption of Ca2+ in DCT
- Result: increased PO43- lost in urine
PTH acts in DCT to
bring more calcium to blood
- corrects hypercalcemia
pH of urine and blood is regulated in
collecting tubules
if acidic blood, then
synthesized HCO3- (bicarbonate) reabsorbed into the blood
- H+ excreted within filtrate by type A intercalated cells
- increased blood pH and decrease urine pH
goal is to reabsorb bicarbonate ions into blood and give off H+ to lower the pH into the tubular fluid
if alkaline blood, then
- type B intercalated cells are active
- secrete HCO3- and reabsorb H+
- lower blood pH and increase urine pH
goal is to get rid of bicarbonate into tubular fluid and reabsorb H+ into blood
80-90% of HCO3- is reclaimed in
PCT
10-20% of HCO3- is reclaimed in
nephron loop
regulation of HCO3- and H+ reabsorption and secretion occurs in
collecting tubules
urinary system prevents accumulation of
1) metabolic waste
2) various hormones and metabolites
3) foreign substances
main nitrogenous waste products
urea
uric acid
creatinine
urea
molecule produced from protein breakdown
uric acid
produced from nucleic acid breakdown in liver
creatinine
produced from creatine metabolism in muscle
establishing concentration gradient
- present in interstitial fluid surrounding nephron
- established by various solutes (Na+ Cl-, progressive increase in concentration from cortex into medulla)
- exerts osmotic pull to move water into interstitial fluid (when ADH is present)
countercurrent multiplier
- establishes high solute concentration in interstitial fluid
- thick region of nephron loop is impermeable to water but actively transports NaCl out of the tubular fluid into the interstitial space so there is now an increase in salt concentration in interstitial fluid
- tubular fluid enters into PCT starts at 300 mOsm and as it descends this area is permeable to water but not to salt so water is going to be osmotically drawn into interstitial fluid from tubular fluid due to high salt concentration
countercurrent exchange
- MAITAINS concentration gradient
- involves vasa recta
- capillary walls are permeable so as blood flow descends down solute concentration is increasing in blood
- osmotic flow of water out of the cell
- NaCl is going to flow into capillaries
- as vasa recta is moving up there is a lesser concentration of salt in blood as it is drawn out and water is drawn back into the blood which brings us back to regular plasma concentration
countercurrent multiplier vs countercurrent exchange
multiplier establishs the gradients and the exchanges maintains the gradient
urea recycling
- help concentrating process in interstitial fluid
- recycled urea (1/2 of solutes of interstitial fluid gradient)
- urea removed from tubular fluid in collecting duct by uniporters
- diffuses back into tubular fluid in thin segment of ascending limb
- remains within tubular fluid until it reaches collecting duct
- urea cycled between collecting duct and nephron loop
proximal convoluted tubule
- site for majority of reabsorption
1. reabsorption: the following move from PCT into blood - 100% of nutrients
- majority of water
- majority of ions
- PO43- reabsorption is inhibited by PTH
2. secretion: the following move from blood into PCT - some drugs
- nitrogenous wastes
nephron loop and vasa recta
- site of countercurrent multiplier and countercurrent exchange
- continues reabsorption of water and ions that begins in PCT
- nephron loops of juxtamedullary nephrons establish interstitial fluid concentration gradient (along w/ urea recycling) for reabsorption of water induced by ADH
distal convoluted tubule, collecting tubule, and collecting duct are sites of
regulation!
- Na+ reabsorption is regulated by aldosterone and ANP
- water reabsorption is regulated by aldosterone and ADH
- amount of K+ secreted into the tubular fluid is dependent upon both intercalated cells and principal cells
- Ca2+ reabsorption is increased by PTH
- pH is regulated by intercalated cells
(type A cells secrete H+ (acid) and retain base (HCO3-) while type B cells secrete base and retain acid)
renal plasma clearance test
- a means of assessing kidney function
- measures volume of plasma cleared of substance in given time (typically one minute)
RPC with substance neither absorbed or secreted
clearance would = GFR (125 ml/min)
e.g., inulin
RPC with reabsorbed substance
clearance is lower than GFR
glucose (0ml/min)
if substance filtered and secreted
clearance is higher than GFR
creatinine (140ml/min)
urine
product of filtered and processed blood plasma
sterile unless contaminated with microbes in kidney or urinary tract
urinalysis is common diagnostic test
composition of urine
95% water
solutes only make 5% of urine
volume of urine
inverse relationship between urine volume and concentration
if patient says they are urinating too often, can lead to inability for kidneys concentrating urine
specific gravity of urine
diluted and watery - dark highly concentrated
1.005-1.030
no units because they are relative numbers
pH of urine
most humans urine is about pH of 6
related to diet
most of us have high protein diet that renders urine around pH 6
vegetarians usually have a more alkaline urine
UTI can cause decrease in H+ in urine
color of urine
indicative of health issues
red brown - myoglobin in urine
turbidity of urine
cloudiness
should be clear
bacterial organisms, WBCs, persent in urine
smell
ketones insert fruity odor to urine
ureters
- long epithelial lined fibromuscular tubes
- conduct urine from kidneys to urinary bladder
- originate from renal pelvis as it exits hilum of kidney
- enter wall of base of urinary bladder
ureter walls composed of 3 tunics
1 mucosa
2 muscularis
3 adventita
muscosal folds on mucosal layer of ureters allow for
expansion to accomodate urine flow
muscularis
muscle tissue of ureter
ability to distend to accommodate increase urine flow
adventita
layer of protective CT
trigone
boundaries are indicated by imaginary lines between ureter openings and internal urethral sphincter
internal urethral sphincter
smooth
involuntary control
circular arangment of muscle fibers it closes off of so urine cannot be expelled
detrusor muscle encompasses
all 3 layers in wall of bladder
external urethral sphincter in female urethra
embedded within urogenital diaphragm which is a span of muscle that lies against pelvis
EUS is under conscious control to allow or not allow urine flow
male urethra
longer as it extends length of penis
prostatic, membranous, and spongy urethra
micturition
expulsion of urine from bladder
associated with 2 reflexes
- storage reflex and micturition reflex
- regulated by sympathetic and parasympathetic divisions of the autonomic nervous system
storage reflex
- continuous sympathetic stimulation
- causes relaxation of detrusor to accomodate urine
- stimulates contraction of internal urethral sphincter
- so urine retained in bladder
external urethral sphincter and storage reflex
continuously stimulated by pudendal nerve to remain contracted
micturition reflex
1) volume of urine in bladder about 200-300mL
- bladder distended and baroreceptors activated in bladder wall
2) visceral sensory neurons signaled by baroreceptors
- stimulate micturition center in pons
3) micturition center
- increases nerve signals down spinal cord through pelvic splanchnic nerves
4) parasympathetic stimulation
- causes detrusor muscles to contract
- causes internal urethral sphincter to relax
conscious control of urination
initiated from cerebral cortex through reduced stimulation by pudendal nerve
- causes relaxation of external urethral sphincter
- facilitated by voluntary contraction of abdominal and expiratory muscles (Valsalva maneuver)
can empty bladder prior to micturition reflex
- contract abdominal muscles to compress bladder
- initiates micturition reflex by stimulating stretch receptors
fluid in our body =
intracellular and extracellular
intracellular fluid (ICF)
fluid within our cells
two-thirds of total body fluid
enclosed by plasma membrane (allows passage of some, but not all substances through it)
extracellular fluid (ECF)
fluid outside our cells
includes interstitial fluid and blood plasma
interstitial fluid composes
2/3 of ECF
blood plasma
extracellular fluid within blood vessels
separated from interstitial fluid by capillary vessel wall (more permeable than plasma membrane)
when drinking water
the blood plasma within capillary becomes hypotonic causing water to move out of capillary into interstitial fluid and into hypertonic intracellular fluid from original hypotonic blood plasma
when dehydrated
solutes within blood plasma is increased so capillary is hypertonic causing the hypotonic intracellular fluid to push water outward by osmosis into interstitial fluid and into blood capillary
metabolic water is generated in the body as a result of
metabolic processes
200 mL of total intake of water
fluid intake includes
- preformed water (drinking and food)
- metabolic water
fluid output includes
- expired air
- sweat
- cutaneous transpiration
- feces
- urine (obligatory and facultative)
obligatory loses include
expired air, sweat, cutaneous transpiration, feces, obligatory urine (must happen to dilute solutes in urine)
facultative losses
facultative urine loss (according to circumstances)
insensible losses
cant quantify (expired air, sweat, cutaneous transpiration)
sensible losses
include feces and urine losses
sodium balance
- 135-145 mEq/L
- get Na+ from diet
- release Na+ from urine, feces, and sweat
- hormones regulating Na+ concentration by altering loss of both Na+ and H2O in urine (aldosterone, ADH, ANP)
sodium balance: aldosterone
retains Na+ and water
- maintains Na+ blood plasma concentration
sodium balance: ADH
retains water
- decreases Na+ blood plasma concentration
sodium balance: ANP
increases excretion of Na+ and H2O
- decreases Na+ blood plasma concentration
increased sodium or decreased H2O effect on blood
- most Na+ is found in ECF
- decreased H2O or increased Na+ concentration would cause blood to be hypertonic causing water to osmotically flow into the blood from ICF
decreased sodium or increased H2O effect on blood
increased H2O or decreased Na+ concentration causes solute concentration in the cells to be higher then in blood so water osmotically flows into the ICF from blood
potassium balance
- most important ion in ICF
- 3.5-5.0 mEq/L
- K+ intake from diet
- K+ output from urine, feces, sweat
- aldosterone helps regulate K+ blood plasma concentration by altering loss of K+ in urine
aldosterone on K+ balance
causes K+ secretion by kidneys (and excretion in urine)
decreases K+ blood plasma concentration
K+ distribution is dependent upon
K+ levels, H+ levels, and insulin
maintaining normal K+ blood levels
if K+ in blood increases, K+ enters cells
if K+ in blood decreases, K+ exits cells and enters blood
maintaining blood pH
if blood H+ ion increases, H+ enters cells and K+ exits cells
if blood H+ ion decreases, H+ exits cells and K+ enters cells
maintaining normal blood K+ following a meal
insulin increases movement of both glucose and K+ into cells
chloride ion (Cl-)
- associated with Na+
- follows Na+ by electrostatic interactions
- regulated by same mechanisms
- amount lost in urine dependent upon blood plasma Na+
- most abundant anion in ECF
- found in lumen of stomach as HCl
- participates in chloride sift within erythrocytse
- obtained in diet from table salt and processed foods
- lost in sweat, stomach secretions, and urine
calcium ion (Ca2+)
- most abundant electrolyte in bone and teeth (99% of Ca2+ stored here)
- moved by pumps out of cells into sarcoplasmic reticulum
- prevents binding phosphate within cells and hardening
- needed for muscle contraction and neurotransmitter release
- participates in blood clotting
- obtained from yogurt, milk, soy, cheese, sardines, green leafy vegetables
- lost in urine, feces, and sweat
calcium is regulated by
parathyroid hormone
- increases secretion of calcium
phosphate ion (PO43-)
- most abundant anion in ICF
- 85% stored in bone and teeth as calcium phosphate
- component of DNA, RNA, and phospholipids
- intracellular buffer and urine buffer
- most ionized (90%) in blood plasma, rest bound to proteins
- regulated by many of same mechanisms as Ca2+
most abundant anion in extracellular fluid
chloride
most abundant electrolyte in bone and teeth
calcium
most abundant anion in intracellular fluid
phosphate
renin-angitensin system
- Stimulus:
- Low blood pressure (detected by JG apparatus)
- sympathetic division stimulation - Receptor:
- The JG apparatus responds to stimuli - Control Center:
- The JG apparatus releases renin enzyme into the blood - Renin converts angiotensinogen to angiotensin I, and angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II.
- Effectors: angiotensin II binds to effectors to cause-
- vasoconstriction
- decreased GFR
- activation of thirst center
- release fo ADH from posterior pituitary gland
- release of aldosterone from adrenal cortex - Net effect: blood pressure increases
angiotensin II on systemic blood vessels
vasoconstriction in systemic blood vessels causing increase in BP
angiotensin II on kidneys
decreased GFR leading to a decrease in urine output to maintain blood volume and blood pressure
angiotensin II on hypothalamus
- activation of thirst center to increase fluid intake causing a rise in BP and blood volume
- release fo ADH from posterior pituitary gland which decreases urine output to maintain blood volume
angiotensin II on adrenal cortex
release of aldosterone from adrenal cortex to maintain blood volume with decreased urine output
Antidiuretic Hormone
- Stimulus
- angiotensin II (produced with a decrease in BP)
- sensory input from baroreceptors in heart and vessels detect low blood volume
- chemoreceptors within hypothalamus detect increased blood osmolarity - Recptor
- the hypothalamus responds to stimuli - Control Center
- the hypothalamus stimulates the posterior pituitary gland to release ADH into the blood - Effectors: ADH binds to effectors to cause-
- activation of thirst center
- increased water reabsorption
- vasoconstriction - Net Effect: Increased BP (with fluid intake); blood volume increases (with fluid intake); blood osmolarity decreases
ADH effect on hypothalamus
activates thirst center causing increased fluid intake which increases blood volume and blood pressure
ADH effect on kidneys
increases water reabsorption; decreases water lost in kidney to maintain blood volume and decreases blood osmolarity
ADH effect on blood vessels
vasoconstriction occurs in high does of ADH
increases peripheral resistance and BP
aldosterone
- Stimulus
- angiotensin II (produced with a decrease in BP)
- decreased Na+ blood plasma levels
- increased K+ blood plasma levels - Receptor
- adrenal cortex responds to stimuli - Control Center
- the adrenal cortex releases aldosterone into the blood - Effector
- increases K+ secretion into tubular fluid (H+ can be substituted for K+ in condition of low pH) - Net Effect: blood plasma Na+ maintained; blood plasma K+ decreases. blood volume and BP maintained by decreasing urine output)
atrial natriuretic peptide
- Stimulus: increased stretch of baroreceptors in atria
- Receptor: Atria responds to stimuli
- Control Center: Atria releases ANP into the blood
- Effectors: ANP binds to effectors to cause
- vasodilation
- increased GFR
- increased loss of Na+
- decreased release of renin - Net effect: peripheral resistance decreases; blood volume decreases, BP decreases
ANP on systemic blood vessels
vasodilation occurs, decreasing peripheral resistance and decreasing BP
ANP on kidneys
- increases GFR which increases urine output to decrease blood volume and BP
- increased loss of Na+ and water in urine; decreases blood volume and BP
- decreased release of renin (and interferes with action of angiotensin II); decreased release of aldosterone and ADH
Acid-Base Balance
- also called pH balance
- normal pH; 7.35 - 7.45 (slightly alkaline)
- proper pH balance critical
- pH inversely related to H+ concentration
(adding an acid increases H+, base reduces it)
increased blood H+ concentration (decrease in pH)
- Contributing Factors
- acid is added to the blood from the GI tract and cell metabolic waste
- H+ increases in blood plasma making blood more alkaline - balance mechanism
- excess H+ is excreted in urine and HCO3- is added to blood through type A intercalated cells
loss of HCO3- causes
diarrhea
decreased blood H+ concentration (increased pH)
- contributing factors
- base is added to the blood form the GI tract
- pH decreases in blood making blood acidic - balance mechanism
- excess HCO3- is excreted in the urine and H+ is added to the blood through type B intercalated cells
loss of H+ in blood causes
vomitting
type B intercalated cells add
HCO3- ions
type A intercalated cells add
HCO3- ions
abnormal increase in respiratory rate
- causes elevated levels of CO2 to be expired
- decreases blood CO2 concentration
- blood h+ concentration decreases
- blood pH increases
- decrease in partial pressure of CO2
equation driven to the left: - CO2 + H2O - H2CO3 - H+ HCO3-
abnormal decreases in respiratory rate
- increases amount of CO2 retained, elevating blood CO2
- blood H+ concentration increases
- blood pH decreases
equation driven to the right - CO2 + H2O - H2CO3 - H+ HCO3-
acid-base disturbance / acid-base imbalance
- persistent pH change
- life threatening for any extended period of time
four categories of acid-base disturbances
- respiratory acidosis
- respiratory alkalosis
- metabolic acidosis
- metabolic alkalosis
respiratory acidosis
most common acid-base disturbance
due to impaired elimination of CO2 by respiratory system
PCO2 in arterial blood is above 45 mm Hg (n=38-42)
Accumulation of CO2 and subsequent increase in H+ concentration
possible causes of respiratory acidosis
- injury to respiratory center by trauma or infection
- disorders of muscles or nerves involved with breathing
- airway obstruction
- decreased gas exchange (due to reduced respiratory surface area or thickened respiratory membrane)
respiratory alkalosis
- PCO2 below 35 mm Hg due to increase in respiration
- decrease of CO2 and subsequent lower H+ concentration
- possible causes of hyperventilation (severe anxiety, condition in which individual isn’t receiving sufficient oxygen like high altitude, heart failure, severe anemia)
metabolic acidosis
- may occur from loss of HCO3- or gain of H+ (more commonly due to gain of H+)
- H+ binding to HCO3-, decreasing levels
- occurs when HCO3- levels drop below 22 mEq/L (n=22-26 mEq/L)
possible causes of metabolic acidosis
increased production of metabolic acids
e.g.:
- ketoacidosis from diabetes
- lactic acid from glycolysis
- acetic acid from excessive alcohol intake
- decreased acid elimination due to renal dysfunction
- increased elimination of HCO3- due to severe diarrhea
metabolic alkalosis
arterial blood levels of HCO3- above 26 mEq/L
from loss of H+ or increase of HCO3-
possible causes:
- vomiting (most common)
- large amounts of antacids
- increased loss of acids by kidney with diuretic overuse
renal compenstation
occurs in response to elevated or decreased blood H+ (due to a cause other than renal dysfunction)
type A intercalated cells
excrete H+ and reabsorb HCO3-
occurs at a greater degree than normal during compensation
blood levels HCO3- high in compensation
during renal compensation urine pH with elevated levels of H+ levels are
lower than normal
urine levels of H+ high in compensation
renal compensation in response to decreased blood H+
type B intercalated cells reabsorb H+ and excrete HCO3-
occurs to a greater degree than normal during compensation
blood levels of HCO3- are low in compensation
urine pH is higher than normal
respiratory compensation
- attempts to compensate for metabolic imbalances
- less effective than renal compensation
respiratory compensation from increased H+ concentration
respiratory rate increases as a result and causes
- higher amounts of CO2 expired
- lower blood PCO2 value
respiratory compensation from decreased H+ concentration
respiratory rate decreases and as a result
- lower than normal amounts of CO2 expired
- higher than normal blood CO2 value
- limited by development of hypoxia
