Exam 3 Flashcards
What affects % saturation of Hb
Composition of inspired air
Alveolar vent. rate
efficiency of gas exchange
What affects amount of Hb binding sites
Hb content per RBC and number of RBCs
Oxyhemoglobin Saturation curves
Show the physical relationship between PO2 and Hb saturation
Shift right/left on a Oxyhemoglobin curve
Right: Decreased affinity for O2 –> release more O2 to tissues, more significant
Left: Increased affinity for O2 –> more O2 stays bound to Hb
Normal numbers for Hb saturation at 100 and 40 mmHg PO2
@ 100 (arteries): 98%
@ 40 (resting cell/venous): 75%
Why is only ~25% of available O2 used at rest
Allows for a reservoir of O2 to accumulate on Hb incase metabolism increases or demand increases in another way.
Hb saturation of skeletal muscle
PO2 = 20 mm Hg
Hb 30%
–> Body using 70% of O2
Fetal Hb Oxyhemoglobin curve
left shift –> increased affinity
Need to get O2 from mom’s blood
Factors that cause a Change in Hb shape
Plasma pH, temp, PCO2, 2,3-BPG
Effect of plasma pH on Oxyhemoglobin
Drop in pH (more acidic) –> right shift, more O2 released
Effect of temp on Oxyhemoglobin
Increase temp –> right shift
Effect of 2,3-BGP on Oxyhemoglobin
Increase in the intermediate means increase in glycolysis which is increase of metabolism which causes a right shift and greater O2 release.
effect of high CO2
Lowers plasma pH (acidic)
CNS depressant (inhibits/slows neural function)
Ways Co2 is transported in blood
7% dissolved in plasma
23% Bound to Hb
70% Dissolved as bicarbonate ions which act as mode of transport, buffer in plasma, and relies on carbonic anhydrase
Go over transport pathway on slide 28
Regulation of ventilation
depends on skeletal muscle and somatic motor neurons
3 factors that influence rate of vent
CO2 receptors in medulla Oblongata (central chemo)
O2/pH receptors in carotid/aortic bodies (peripheral chemo)
Emotional and voluntary control
*Control still not totally understood
Neural control of breathing
- Resp. neurons in medulla control inspiratory and expiratory muscles
- Neurons in Pons integrate sensory info and interact with medullary neurons to influence ventilation
- The rhythmic pattern of breathing arises from a brainstem neural network with spontaneously discharging neurons
- Ventilation is subject to continuous modulation by chemo/mechano receptor linked reflexes and higher brain centers (emotional)
Dorsal Respiratory group (DRG)
Medulla Oblongata
Receives sensory input from CN IX and X and Chemoreceptors monitoring CO2
Controls muscles of inspiration
Ventral Respiratory Group (VRG)
Medulla Oblongata
Pre-botzinger complex
Controls active expiration and greater than normal inspiration
Controls muscles of larynx, pharynx, and tongue (vocalization)
Pre-Botzinger Complex
Spontaneously firing neurons
Pacemaker of breathing
Pontine Respiratory group (PRG)
Pons
Receives sensory input from DRG
Influence initiation and termination of breathing rate
Provides tonic input to medullary groups
Central Chemoreceptors
Primary stim for changes in vent. rate
CO2 receptors in ventral medulla
Detect CO2 in CSF
See diagram slide 37
Functions of the kidney
- Regulation of Extracellular fluid volume and blood pressure
- Regulation of osmolarity
- Maintenance of ion balance
- Homeostatic regulation of pH
- Excretion of wastes
- Production of hormones
Regulation of Extracellular fluid volume and blood pressure
Work with CVS to maintain ECF volume
Regulation of osmolarity
Tied to behavior drives like thirst
Plasma osmolarity = ~290 mOsM
Maintenance of ion balance
Balance dietary intake with urinary loss
Homeostatic regulation of pH
Excretes H+ or HCO3- to maintain plasma pH
Excretion of wastes
Excrete metabolic wastes or foreign substance
Creatine, urea, uric acid
Production of hormones
Synthesizes erythropoietin (RBC production), renin (RAAS System aka BP), vitamin D conversion
Urinary system components
Kidneys, ureters, bladder, urethra
Kidney location
Retroparitaneal cavity, dorsal side, 11/12th rib
Kidney blood volume
Receives 25% of CO despite being only 0.4% of body weight
Structures of the kidney
Cortex, medulla, renal pelvis, Nephrons…
see slide 10
Nephron
Functional unit of the kidney; smallest structure that can perform all the functions of an organ
1 million/kidney
Types and amount of nephrons
Cortical- 80% within cortex
Juxtamedullary- 20% extend down into medulla
Structures of nephron
Glomerulus, afferent/efferent arteriole, bowman’s capsule, proximal tube, descending/ascending loop, descending/ascending limb, loop of Henle, collecting duct
See slide 12
Vasculation of kidney
Arrives via renal artery
Highest perfused organ in our body
Contains portal system
Renal portal system
Afferent arteriole
Glomerulus (1st cap bed)
Efferent arteriole
Peritubular capillary (2nd bed)
See diagram slide 14
Tubular elements of kidney
Single layer of epithelial cells, apical/basal sides, connected by tight junctions
Renal tubule consists of:
Bowman’s capsule, proximal tubule, loop of henle, distal tubule, collecting duct
Bowman’s capsule
Fused to glomerulus, filtration
Not regulated
Proximal tubule
Isosmotic reabsorption of nutrients, ions, and water
Some secretion of metabolites and xenobiotics
Not regulated
Loop of henle
Reabsorption of ions
Primary site for creating dilute urine
More solute reabsorbed than water so filtrate becomes hyposmotic to plasma
Start 54 L/day end 18 L/day
Not regulated
Distal tubule
Regulated reabsorption of ions and water
Collecting duct
Regulated reabsorption of ions and water
Amount of fluid filtered per day
180 L/day
Only 1.5 L/day excreted
Four major processes of a Nephron
Filtration, reabsorption, secretion, excretion
Filtration of nephron
Movement of fluid from blood into nephron, only occurs in Bowman’s capsule, creates filtrate
Reabsorption of nephron
Moving substances from tubule back into blood
Secretion of nephron
Selectively removes molecules from the blood and moves them into the filtrate;
more selective than filtration, requires membrane proteins
Excretion of nephron
Removal of substance from body; not technically a nephron process
Renal Corpuscle
Glomerulus and Bowmans Capsule
20% of plasma enters BC
Creates the filtrate (180 L/day)
Filtrate (contains and lacks)
Contains ions, nutrients, metabolic wastes
Lacks RBCs, WBCs, large proteins
Descending loop
Reabsorbs mostly water
Ascending loop
Reabsorbs mostly ions
Distal Nephron
DT and CD (Regulated)
Final volume falls to 1.5 L/day (urine)
Hormones regulate water and salt movement
Why filter 180 L/day just to reabsorb 99%
Protective mechanism
Three barriers to filtration
Glomerular capillary endothelium
Basal Lamina
Epithelium of Bowman’s capsule
See diagram
Glomerular Capillary endothelium
Fenestrated capillaries (more leak)
Blood cells not filtered
Negatively charged surface repels most proteins
Basal Lamina
Netting
ECM that acts as net
Blocks proteins
Epithelium of Bowman’s Cap
Podocytes wrap around G. Capillaries
Creates additional filter slits
3 forces that determine filtration amount
Capillary BP (hydrostatic)
Colloid osmotic P
Capsule fluid P
Capillary BP (hydrostatic)
55 mm Hg
Forces fluid through leaky endothelium –> favors filtration
Colloid osmotic P
30 mm Hg
Proteins in plasma promote reabsorption
Capsule fluid pressure
15 mm Hg
Bowman’s cap has fluid that opposes movement into capsule (favor reabs.)
Net driving pressure of Capillary
10 mm Hg in filtration direction
Glomerular Filtration Rate (GFR)
Volume of fluid that filters into the Bowman’s capsule per unit time
Avg: 125 mL/min (180 L/day)
Indicator of kidney function!
2 factors that influence GFR
Net capillary filt. pressure (change in BP or plasma protein)
Filtration coefficient (SA of glomerular caps & permeability of caps)
GFR relatively constant
How does GFR remain constant across wide range of MAPs
Myogenic autoregulation
Tubuloglomerular feedback
Afferent arteriole vasoconstriction
Less blood entering renal corpuscle
GFR decreases
Efferent arteriole vasoconstriction
Blood “dams up” in front of constriction
GFR increases
Myogenic autoregulation
Local control
Stretch receptors, increase P causes constriction
Maintain constant flow to renal corpuscle
Why does GFR fall when MAP is <80 mm Hg
Stop excretion of any fluid volume when blood volume is super low
Ex: Major blood loss
Tubuloglomerular Feedback
Local control
Juxtaglomerular apparatus:
Macula densa cells detect increase in filtration which release paracrine to constrict afferent and reduce GFR
Granular cells secrete renin to regulate salt/water
See diagram
ANS filtration control
Sympathetic neurons innervate afferent and efferent arterioles
NE binds a-receptors –> constriction
Drop in MAP will trigger strong SNS constriction of afferent
Why is SNS control dominant during exercise
Retain fluid and redirect blood to muscles
Reabsorption
From tubule to blood
99% filtrate reabs.
Active OR passive
Trans OR para cellular
Active transport of Na+
Primary driving force for most renal reabsorption
Basolateral membrane (closer to BV) NaK pump
Passive Na+ transport
Apical membrane
Na-H exchanger from tubule lumen to tubule cell
Symport with Na+
Glucose, AAs, ions, organic metabolites
Passive transport of urea
Urea at high [] is toxic
Moves paracellulary (no proteins needed)
Follows movement of Na and water
Removal of proteins from tubule
If protein gets into filtrate somehow, it can get transported by: Receptor-mediated endocytosis (active)
AA move into blood
Protein mediated transport characteristics
Saturation
Specificity
Competition
Saturation of Renal transport
Max transport rate when all carrier are occupied by substrate
(Tm: transport max)
Why glucose found in blood in Type 1 diabetes
100% gluc is filtered and normally 100% reabs.
BUT
Lack insulin = high [gluc] in blood = high [gluc] in filtrate
Glut transporters get saturated and glucose excreted in urine
Difference between filtration and secretion
Secretion is specific and filtration is not
Secretion
Movement from blood to tubule
Protective way to get things out of the body
Why is very little Na+ secreted
Water would move with the Na and we would become dehydrated
Endogenous Organic anions
Naturally produced by body
Bile salts
Dicarboxylates (CAC)
Exogenous Organic anions
Not naturally from body
Benzoate, salicylate, saccharine
Organic Anion Transporters (OATs)
Non-specific transporters
Tertiary active transport
Move OAs from blood to urine
Excretion
Out of body
E = filt - reabs + secretion
Substances NOT normal in urine
Glucose
AAs
Useful metabolites
Substances normally found in urine
Water
Ions (include H+)
Urea
Organic wastes and anions
Renal clearance
If a substance is freely filtered (100%) and neither reabsorbed nor secreted then it can be used to estimate GFR
ex: Creatinine or Inulin
Micturition
Peeing (voiding)
Filtrate leave collecting duct, can no longer be modified
Bladder
Layers of smooth muscle
Holds ~ 500 mL
Stretch receptors in walls to give urge to pee
2 bladder sphincters
Internal sphincter (involuntary control)
External sphincter (skeletal muscle so controlled voluntarily)
Process of Micturition
Stretch receptors fire
Parasymph neurons fire, motor neuron keeping external contracted stop firing
Smooth muscle contracts, internal sphincter pulled open
*See diagram
Elements in the fluid we consume
Sodium, Potassium, Calcium, Hydrogen, Bicarbonate
Physiological mechanisms to maintain mass balance
Kidneys remove water and ions
Water and ions lost in feces and sweat
Excrete water and CO2 through breathing
Behavioral mechanisms to maintain mass balance
Thirst drive via osmolarity receptors in hypothalamus
Salt appetite
Why is the regulation of ECF critical to cells?
Depending on enviro, the cell will be hyper or hypo tonic and gain or lose water
Water intake
Food and drink 2.2 L/day
metabolic reactions 0.3 L/day
Water loss
Urine (1.5 L/day)
Feces (0.1 L/day)
Insensible (0.9 L/day)- skin and lungs
Conditions that impact water balance
Excessive sweating, diarrhea, abnormal water intake, blood loss, composition of fluid matters
Why is excessive water intake a problem
Hypotonic ECF causes cells to fill and burst, effects nervous system due to decrease plasma osmolarity messing up retsing Vm
Role of kidneys
Kidneys can remove excess water but cannon replenish lost water, only conserve it
Loop of Henle in urine regulation
Descending loop permeable to water, ascending to solutes
Movement is passively regulated
Diagram slide 15
Collecting duct in urine regulation
Water and solutes movement is actively regulated by hormones
Water reabsorption is dependent on conc. of renal medulla interstitium
Diagram slide 15
Countercurrent multipliers
Renal medulla ECF is hyperosmotic
Loop of Henle and vasa recta (BV) move in opposite direction
Ends in dilute urine (hyposmotic)
SEE SLIDE 19!
Transporters in countercurrent multiplier
NKCC (Sodium, potassium, Cl cotransporter)
KCl transporter
Leak channels
vasa recta
Absorbs water leaving LoH
Prevents edema, high osmolarity of medullary intersitium is needed for water to move out of CD
Urea
Contributes to medullary interstitium, gets transported out of LoH and CD
Vasopressin
Regulates aquaporin expression in CD
More water reabsorbed (urine concentrated) when vasopressin is present
Anti-diuretic
Conserve water
3 factors that stimulate vasopressin release
High plasma osmolarity-
[plasma] high, hypothalmus release VP due to osmoreceptors
Blood volume- Dec. BV –> increase VP
Blood pressure- Dec. BP –> increase VP
Vasopressin at night
Follows a circadian rhythm pattern which is good because that means we conserve water and don’t urinate at night
