Bios 355 Exam 3 Flashcards
Systole
Contraction phase
Diastole
Relaxation phase
Cardiac cycle
- Both atria and ventricles are relaxed
- Blood return from venous system enters atria (AV valves between atria & ventricle are open, blood enters ventricle)
- Ventricles expand to accommodate the increase in volume of blood
- SA node initiates AP
- Blood is forced through the AV valves into the ventricles
- AP has progressed through the AV node down the Bundle of his and into Purkinje fibers
- Begin ventricular contraction
- Pressure continues to rise (isovolumetric contraction)
- Ventricular pressure exceeds arterial pressure
- AP is completed
- When ventricular pressure falls below arterial pressure semilunar valves close (2nd heart sound)
- Ventricle replaces isovolumetrically
- When the ventricle pressure falls below the atrial pressure the AV valves will open
Collagen cords (cardiac tendinae)
Tether the valves
End diastolic volume
Max volume in ventricles
Vasculature (flow of blood through the system)
- Blood returns to heart via vena cava
- Through the tricuspid valve to the right ventricle
- Ventricle contracts and pushes blood
- Out of pulmonary circulation
- Coalesce into pulmonary vein
- Pulmonary vein delivery blood to left atria
- Heart contracts
- Aorta > systemic calculation, blood is subdivided to various organs/tissues
- Coalesce into systemic veins
Lungs
Total volume: 5 L/min
% C.O.: 100%
Increase in physical activity: 16 L/min
Brain
Total volume: 0.7 L/min
Weighted volume: 55mL/100g
% C.O.: 14%
Increase in physical activity: 0.7 L/min (no change)
Heart
Total volume: 0.2 L/min
Weighted volume: 70mL/100g
% C.O.: 4%
Increase in physical activity: 0.6L/min
GI tract
Total volume: 1.35L/min
Weighted volume: 100mL/100g
% C.O.: 27%
Increase in physical activity: 0.5L/min
Kidneys
Total volume: 1L/min
Weighed volume: 40mL/100g
% C.O.: 20%
Increase in physical activity: 0.4L/min
Skeletal muscle
Total volume: 1L/min
Weighed volume: 5mL/100g
% C.O.: 21%
Increase in physical activity: 12L/min
Skin
Total volume: 0.25L/min
Weighed volume: 10mL/100g
% C.O.: 5%
Increase in physical activity: 1.5L/min
Characteristics of fluid flow
- Pressure falls as a function of distance (pressure drops due to friction)
- Decrease size of container and the amount of fluid stays the same (pressure increases)
- Blood flows from regions of high to lower pressure
- Resistance opposes flow
Parameters that influence resistance
- Length of the tube (increase length > increase resistance)
- Radius of the tube (decrease radius > increase resistance)
- Viscosity of the fluid (increase viscosity > increase resistance)
Blood vessels
Lined with endothelial cells
Communicate with SM
Low resistance
Arteries
Diameter of 4mm Thick walls 1mm Lots of SM Elastic tissue Fibrous tissue (prevents rupture, strength)
Arterioles
Diameter of 30 micrometers
Walls: 6 micrometers
SM
Little elastic/fibrous tissue
Capillaries
Diameter: 8-9 micrometers
Single layer of endothelial cells
Venules
Diameter: 20-25 micrometers Fibrous tissue Veins Wall: 0.5 mm SM, fibrous and elastic tissue
Blood distribution 1. Pulmonary circulation 2. Heart 3 systemic arteries 4. Systemic capillaries 5. Systemic veins
- 9%
- 7%
- 13%
- 7%
- 64%
Mean pressure
Arteries: 90 mmHg Arterioles: 60 mmHg Capillaries: 25 mmHg Venules: 15 mmHg Veins: 0-10 mmHg
Flow velocity Arteries Arterioles Capillaries Venules Veins
48 cm/s 15 cm/s 1 cm/s 4 cm/s 30 cm/s
Vascular peripheral resistance
Overall resistance to blood flow through the system
Vasoconstriction
Decrease radius Increase resistance Decrease flow 1. NE 2. Serotonin release 3. Endothelin (paracrine)
Vasodilation
Increase radius Decreases resistance Increase flow 1. Epi 2. Nitric oxide 3. Adenosine
Metabolic rate (indicators of high metabolism)
High CO2 Low O2 Low pH High potassium (Increase radius, decrease resistance, increase flow)
Histamine
Local inflammatory molecule
Can cause vascular endothelial cells to contract
Increase in blood flow
Vasodilation
Vasoactive intestinal peptide
Increase blood during digestion
Produce neurons of the enteric nervous system
Capillary exchange
- Single endothelial layer
- Gap between cells that allow fluid out
- Fluid is pushed out of the capillary by the hydrostatic pressure
Fluid bathes cells
Diffusion and transcytosis
Bulk flow
Vascular SM
Regulating the radius of arterioles
Controls blood flow to the capillaries
With histamine
Bigger gaps between endothelial cells Decrease resistance to flow More fluid exits along with proteins Allows WBC to exit Swelling Swelling creates gaps (make it easier for immune cells to get to site of inflammation) Swelling is beneficial at a local level
Cardiac shock
Heart failure
Hypovolumic shock
Blood volume is too low
Blood loss due to hemorrhaging
Septic shock
Bacterial infection
System wide inflammation
Anaphylactic shock
Immune cell over reaction
Miscellaneous agents that influence blood flow
- Inflammation (immune response)
- Malnutrition
- Anemia (low RBC concentration)
Systemic circulation
Left side of heart contracts, pulls blood to periphery
Vasodilate when O2 is low, CO2 is high, pH is low
Pulmonary circulation
Right side of heart contracts, pulls blood to lungs
Vasodilate (SM)
Bloods gains O2
Gets rid of CO2
Angeiogenesis
Growth of blood vessels
Vascularization of a tissue
Exercise promotes angiogenesis in skeletal muscle
Very active during growth and development
Wound healing
Pathologies
Like to promote angiogenesis in coronary heart tissue
Like to prevent angiogenesis in cancer
Blood
5 liters in body
40% blood cells
60% fluid
Erythrocytes
RBC
Gas transport
Leukocytes
WBC
Defense
Immune response
Platelets
Coagulation
Cell fragments
Contain mitochondria, ER, secretory vesicles
Respond to collagen
Proteins in blood
Albumins: transport/attach hydrophobic molecules
Globulins: antibodies
Fibrinogen: blood clotting
Hematocrit
% of RBC in whole blood
Males: 40-52%
Females: 38-48%
Blood cell production
Marrow of bones
RBC > half life of about 4 months
WBC > half life of les than a day (100 billion)
Multipotent progenitor cells
Uncommitted blood stem cell
Lymphocyte stem cell (acquired immune cells, T-cells, B-cells, antibodies)
Uncommitted blood stem cell
Route 1: erythroblast > differentiate > mature RBC
Route 2: megakaryocyte > produce platelets
Route 3: inmate immune cells
RBC production
- Production is regulated by the hormone erythropoietin (EPO)
- EPO is produced by kidney
- EPO target bone marrow (activate the uncommitted blood stem cells)
- Produce erythroblasts (nucleated)
- Nucleus condenses
- Erythroblasts > reticulocyte
- Reticulocytes exit bone marrow (enter circulation)
- 24 hours to mature into adult RBC
(Last about 120 days) - Take on biconcave disk appearance
Reticulocytes
Immature
Migratory
Leave bone marrow and enter circulation
Biconcave disk
Flexible
Increases surface area (more surface area, greater diffusion rate)
Stackable (less adhesion)
Iron transport systems
Intestine
Fe binds to a protein called transferrin
Transferrin: deliver to bone marrow used in Hb synthesis
Thrombopoietin
In liver
Megakaryocytes produce more platelets
Colony-stimulating factor/interleukins
Increase WBC production
Hematopoiesis
Blood cell production
RBC degradation
Damaged RBC are consumed by macrophages Occurs in spleen/liver Digest RBC Bilirubin in the blood Filtered by kidney > excreted in urine
Bilirubin
Incorporated into bile in liver
Excreted
Color feces
Jaundice
Decrease in bilirubin excretion
Increase in bilirubin in blood
Anemia
RBC disorder 1. Blood loss 2. Hemolytic anemia > cytoskeletal defects > hemoglobin defects (sickle cell) > parasitic infection > autoimmune disease > drugs 3. Decrease RBC production > iron deficiency > vitamin deficiency (folic acid, B-12) > certain drugs 4. Kidney problems > decrease EPO production > decrease RBC
Polycythemia Vera
Overproduction of RBC Stem cell dysfunction Hematocrit 60-70% > increase blood velocity > increase flow resistance > decrease O2 delivery > increase pressure (strain on heart)
Secretory vesicles
Contain cytokines (growth-factors)
> stimulate growth to seal the ruptured area
Contain ATP (released into interstitial fluid)
> vasoconstrictor
> decrease blood flow
Serotonin
> vasoconstrictor
Coagulation
Platelets respond to collagen
Collagen wrapped around vessels
Collagen stimulates a receptor on platelets that cause vessels to fuse with PM
Release vasoconstrictor: cytokinesis
Platelets stick to collagen and begin forming a plug
Release thromboxane A2 (induces platelet sticking)
Induces blood clotting
Final stage
Thrombin (enzyme)
Fibrinogen into fibrin
X-link protein is factor 13 (XIII)
Prothrombinase
Factor X and thromboplastin
Can convert prothrombin into thrombin
Antithrombrin III
Prevents clots
Basophils > heparin (anticoagulant)
Thrombmodulin
Promote the breakdown of fibrin
Plasmin > digest clots
Prostaglandins
Required for clot formation
Respiration
- Ventilation of the lungs
- Exchange of gas between the lungs and blood (gas in blood)
- Transport of gas in the blood
- Exchange of gases in the blood and the tissues (gas out of the blood)
Conducting system
- Mouth and nose
- Pharynx and larynx
- Trachea (large pressure changes)
- Primary bronchi (reinforced)
- Secondary bronchi (semi-rigid)
- Bronchioles (wrapped by SM)
> control air flow (regulation) - Terminal bronchioles
- Alveoli (end sack) (gas exchange)
Pressure velocity
High at trachea/bronchi
Low at bronchioles/alveoli
Alveoli
Single cell layer Type I: very abundant Very thin Gas exchange Type II: thicker Secrete surfactants (detergent) Not as abundant
Detergent
Decrease surface tension
Decrease cohesion
Prevents alveoli from sticking and collapsing
Gas laws
- Total pressure of a mixture of gases is the sum pressures of the individual gases (Dalton’s law)
- Gases move from areas of high pressure to areas of low pressure
- Boyle’s law: P1V1 = P2V2
Ideal gas law: PV = nRT
Factors that influence the amount of the gas that can be dissolved in a fluid
- Gas pressure (gradient) (regulate)
- Gas solubility (constant)
- Temperature (constant)
Process the air
- Conducting system has very high surface area
- Bring gas to body temperate (usually warming)
- Bring gas to 100% humidity (saturated with water) > can’t afford to dry out endothelial cells
- Clean the gas > lining of conducting system produces mucus, has cilia that beat in one direction
Create a conveyer belt moving the mucus out of the lungs
Cystic fibrosis
Broken Cl channels
Lungs cannot produce fluid
Mucus gets too thick > cilia can’t move
Mucus builds up in the lungs > decrease gas exchange > pulmonary infection
Lungs (alveoli)
Expand during inspiration (compliance)
Return to resting volume during expiration (elasticity)
Emphysema
Destroys elastic fibers
Lung is compliant but no recoil (difficult to exhale)
Fibrotic lung disease
Loss of compliance
Difficult to inhale
Ventilation
Inspiration > air flow follows the changes in pressure
Rest: atmospheric pressure = intrapulmonary pressure (no air flow)
Muscles in thoracic cage contract > pull on the pleural membrane > force is transmitted to the pleural fluid > pulls on the alveoli
Rapture the pleural membrane > nothing pulling on lung tissue > due to elastic nature it collapses
Increase volume in lungs > decrease pressure in lungs
Atmospheric pressure is greater than the intrapulmonary pressure
Ventilation 2
Airflow from atmosphere > lungs > contraction stops > pressure equilibrates
Expiration
Lack of contraction
Relaxation is passive
Elasticity decreases lung volume > increases lung pressure
Lung intrapulmonary pressure is greater than atmospheric pressure
Regulate frequency and depth
Respiratory control center (medulla)
A. Dorsal respiratory group (DRG)
B. Ventral respiratory group (VRG)
Quiet respiration
DRG controls activity of the intercostal muscles and diaphragm (rhythmic increase in AP frequency) > stimulate skeletal muscle for inspiration
VRG is inactive
Force respiration
DRG AP increases in freq.
stimulates VRG
Increase force of inspiration
Stimulation of VRG provides forced expiration (internal intercostal muscles)
Control of respiratory center
1. Apneustic center (pons) Stimulate DRG 2. Pneumotaxic center (pons) Inhibits Apneustic center These neurons receive sensory info > O2, CO2, pH
Increase activity of pneumotaxic center
Result will be short and shallow ventilation
Decrease activity of pneumotaxic center
Result will be slow deep ventilation
Physical and chemical stimuli in the lungs
Irritants Temperature Pain Water Trigger apnea protective reflexes Coughing/sneezing Reflex ability to stop respiration during swallowing/vomiting
Hering-Brewer reflex
Inflation reflex
Prevents over inflation during forced inhalation
Sensors send AP to both Apneustic center and DRG
AP to VRG > excitatory (promote exhalation)
Increase stretch > increase AP frequently in lungs
> make it increasingly difficult for the DRG to stimulate the muscles
Deflation reflex
Prevent over deflation during forced exhalation
Sensors fire AP to the VRG > inhibitory synapse blocks the VRG > end exhalation
Lung volume capacity
TIDAL volume: normal volume of air exchanged per breath at rest (500 mL)
INSPIRATORY reserve: additional volume during forced inhalation (2500 mL)
EXPIRATORY reserve: additional volume during forced exhalation (1000 mL)
RESIDUAL volume: volume of air remaining in the lungs at the end of max forced exhalation (1000 mL)
VITAL capacity: max total volume that can be exchanged (4800 mL)
TOTAL LUNG capacity: vital capacity + residual volume (6000 mL)
DEAD SPACE: volume of gas residing in the conducting airways (no gas exchange)
Tidal volume must exceed dead space
Chemoreceptors
CO2 + H2O ↔️ H + HCO3
Increase CO2 > increase H (decrease pH)
Bronchiole tubes (air flow)
Increase CO2: dilate
Decrease CO2: constrict
Increase O2: constrict
Decrease O2: dilate
Pulmonary arterioles (blood flow in lungs)
Increase CO2: constrict
Decrease CO2: dilate
Increase O2: dilate
Decrease O2: constrict
Systemic arterioles
Blood flow periphery
Increase CO2: dilate
Decrease CO2: constrict
Increase O2: constrict
Decrease O2: dilate
Chemoreceptors
- CO2/pH sensors
- O2
HO-2 heme oxygenase
Heme oxygenase
Decrease O2 Produces CO Activates qua cyclase GTP > cGMP cGMP > inhibits K channel > depolarize > activate v-gated Ca channel (increase Ca influx, release NT) Fire AP to the respiration control center
Hypoxia-inducible factor
HIF alpha
HIF beta
Both dimer (transcription factor)
Hypoxia stimulate growth of blood vessels
Up regulation of glycolytic enzymes
Stimulate EPO production/increase RBC production
Regulation of respiration
Primary signal is pH (99.99%)
Gas exchange
- Rate of diffusion for a gas is directly proportional to partial pressure concentration gradient
- ” “ directly proportional to the available surface area
- ” “ directly proportional to distance
Total gas pressure
Sea level: 760 mmHg
Atmosphere: 593 mmHg nitrogen
160 mmHg oxygen
0.25 mmHg CO2
O2 transport in blood
Free dissolved O2 (2% total) (usable fraction)
98% of the O2 is carried bound to the Hb inside the RBC
O2 diffuse from the alveoli to the interstitial fluid
O2 diffuse from interstitial fluid to the blood inside the capillary
O2 diffuse from the capillary to inside the RBC (bind to Hb)
Hb is an oxygen buffer (binds O2 when the O2 is high, releases O2 when the O2 is low)
Hemoglobin
4 subunits (centered around an iron)
4 O2 binding sites
Fetal/adult
Factors that influence O2 binding to Hb
- Concentration gradient
- pH (Bohr Effect)
Decrease pH > decrease Hb affinity for O2
Increase pH > increase “ “ - Temperature
Decrease temp > increase “ “
Increase temp > decrease “ “ - Organo-phosphates (glycolytic byproducts)
2,3-diphosphoglycerate
Increase 2,3-DPG > decrease Hb affinity for O2
How does an active tissue induce Hb to release O2?
- Active cell produce a lot of CO2
CO2 + H2O <> H2CO3 <> H + HCO3 (increase CO2 > decrease pH) - Decrease pH will cause a decrease in Hb affinity for O2 > release O2 (Bohr effect)
Bohr Effect
Cells that produce high CO2 levels also consume high levels of O2
CO2/pH as a proxy for O2 demand
Transport of CO2
- Free dissolved CO2 (7%)
- Conversion of CO2 > HCO3
CO2 + H2O <> H2CO3 <> H + HCO3 (70%) - Carbamino linkages
CO2 binding to amine groups > only when the pH decreases
Increase CO2 > decrease pH > induces carbamino linkages
Cl/HCO3 exchanger (band 3 protein) maintains gradient for CO2 diffusion into RBC
Cl maintains electrical neutrality
Unloading of CO2 at lungs
- Alveoli PCO2 is lower than pulmonary blood PCO2 (diffusion of CO2 from blood to alveoli)
- CO2 + H2O <> H2CO3 <> H + HCO3 (decrease CO2)
Converting all the HCO3 back to CO2
CO2 is free to diffuse toward alveoli
Cl shifts in opposite direction as CO2 decreases and pH increases > cause the carbamino linkages to break > release CO2
Hb gains affinity for O2 > Hb binds O2
Pulmonary
Increase pH (decrease CO2)
O2 binds
CO2 is released
Systemic
Increase CO2 (decrease pH)
Release O2
Bind CO2
Ventilation
Maintain PCO2 at the alveoli
pH drives ventilation
Increase activity > increase CO2 production, decrease pH
Respiratory sensors cause ventilation to increase
Hyperventilation
Increase alveoli ventilation above and beyond requirements
Decrease PCO2 beyond normal level
pH increase higher than normal
pH influences Hb O2 binding affinity
Hb binds O2 with greater affinity
Increase in pH Hb does not release O2 (start starving tissue of O2, CNS stutters due to drop in ATP)
Hyperventilation summed up
Decrease lung PCO2 (too far) Decrease blood PCO2 (too far) Increase blood pH (too far) Increase Hb affinity for O2 too much (can't let go) Decrease O2 delivery to tissues
Metabolic acidosis
Respiratory compensation
Decrease PCO2 lower
pH increases
Metabolic alkalosis
Vomiting (loss of acid)
Body fluids pH increases
Respiratory compensation: decrease ventilation, increase PCO2, pH decreases
Asthma
Hypersensitive bronchiole SM Over constricts Increase air flow resistance Decrease ventilation in lungs Inflammatory signals, histamines, leukotrienes, Ach cause bronchiole SM to constrict
Treatment for asthma
Anti histamine
Beta-adrenergic receptor agonists (sympathetic) cause relaxation
Inhalers
Blockers of leukotrienes production
Steroids (anti inflammatory)
Active transcription factors
Produce a protein that blocks phospholipase A2 > makes substrate for leukotriene production
Renal physiology
- Regulate extra cellular fluid volume
- Regulate osmolarity
Increase osmolarity > decrease water conc. (Eat a big of potato chips: increase osmolarity, drink water: decrease osmolarity) - Regulation of ion conc. (Na, K(influence on voltage) Cl, Ca
- Regulate pH (pH changes protein structure)
Excrete excess protons
Conserve protons (add or subtract H protons) - Excretion of waste (or anything foreign)
Urea (nitrogenous waste)
Bilirubin (heme breakdown from RBC)
Creatinine (breakdown of creatine) - Sensory (endocrine gland)
EPO production
Hormones for Ca homeostasis
Deamination
Releases ammonia (NH3) Very toxic (liver) Convert NH3 into urea Urea is less toxic
Uric acid
By product of purine breakdown
Much less soluble
Birds/reptiles > Uric excretion
Uric acid precipitates on shell during development
Renal fascia
Collagen fibers that extend from renal capsule and anchor to the peritoneum
Nephrons
Functional unit of kidney
Glomerulus
Filtration
Fluid out
Modified capillary
Peritubular capillary
Reabsorption occurs
Fluid back in
Coalesce > renal vein > exist kidney
Bowman’s capsule
Surrounds glomerulus and is the collection point for the filtrate
Filtrate is essentially blood minus RBC, WBC, platelets, and big proteins
180 liters/day
Recreate entire fluid phase of blood 60 times a day
Proximal tubule
Nutrient reabsorption
End of proximal tubule: 54 liters/day
Loop of Henle
Create an osmotic gradient (induces osmosis) Promotes retention of water End of loop: 18 liters/day 99% of blood is in the cortex 1% of blood flow to the medulla
Distal tubule
Fine tune urine conc.
K
pH
Ca
Collecting duct
Regulated water permeability
Control the amount of water reabsorbed
Uses gradient created by the loop of Henle
1.5 liters/day (becomes urine)
Kidney process
- Filtration
- Reabsorption (from urine to blood)
- Secretion (from blood to urine)
- Excretion (urination aka micturition)
Filtration route
- In plasma
- Cross the endothelium of the glomerulary capillary
- Cross basement membrane (connective tissue)
- Epithelia of Bowman’s capsule (enters lumen of capsule)
Bowman’s Capsule epithelia
Prodocyte (foot)
Wrap around the capillary
Slits
Gaps between the podocytes
Dictate filtration resistance
Increase size of slits > decrease resistance > more filtrate
Mesangial cells
Contractile
Pull on podocytes
Regulate the slit size and resistance
Phagocytitic >consume clogged debris that gathers in the slits (keep filter clean)
Force driving filtration at the glomerulus
Blood pressure: 50 mmHg + (favors filtration)
Bowman’s capsule: 15 mmHg - (works against filtration)
Osmotic pressure gradient: 25 mmHg -
Total net pressure: 10 mmHg +
Glomerular filtration rate
- Net filtration pressure
- Slit resistance
- Surface area (how much is available)
Average GFR is 125 mL/min
Renal blood flow
Increase flow rate through the glomerulus (no change in blood pressure)
Blood pressure stays at 50 mmHg
Bowman’s capsule stays at 15 mmHg
Increase flow rate > less change in OP > Change in pressure decreases > net pressure increases
Constrict afferent arteriole
Decrease blood pressure at glomerulus
Decrease flow rate
Decrease GFR
Dilate afferent arteriole
Increase blood pressure at glomerulus
Increase flow rate
Increase GFR
Dilate both afferent and efferent arterioles
No change in blood pressure Increase flow (decrease OP) Increase GFR
Regulatory routes
- Auto regulation (myogenic, SM)
- Auto regulation (tubulo glomerular) flow rate of a fluid through the nephron
- Hormonal
- Autonomic nerves
Myogenic auto regulation
Maintain GFR despite changes in local blood pressure/flow
Reflex changes by the vascular SM
Endothelial cells produce paracrine signals
A. Constrict (decrease pressure/flow)
B. Dilate (increase pressure/flow)
Tubuloglomerular auto-regulation
Regulating GFR based on rate of flow through the nephron flow is too fast
Autonomically decrease GFR to slow down the rate the filtrate is entering the nephron
Giving the nephron time to reabsorb all the essential nutrients
Flow is measured by distal tubule
Regulation of GFR
- Myogenic auto regulation
- Tubularglomerular auto regulation
Based on flow rate of fluid through the nephron
Sensor is the macula densa cells of the distal tubule
Example of regulation of GFR
- Increase GFR
- Increase flow rate through the nephrons
- Increase flow at macula densa
- Distal tubule reabsorbs Na
> increase flow > increase Na availability > increase Na transport > cause a voltage change at the macula densa (signal) - Cause the release of a paracrine vasoconstrictor
- Afferent arteriole constricts
> increase flow resistance > decrease glomerular pressure > decrease flow to the glomerulus - Decrease GFR
Autonomic regulation
- Both afferent/efferent arterioles are innervate by sympathetic neurons > release NE > SM - alpha adrenergic receptors
- Activation of receptor causes vasoconstriction
Decrease blood pressure > decrease flow > decrease GFR
GFR issues
Endurance athletes Chronic vasoconstriction at glomerulus Wastes accumulate Low O2 at kidneys Glomerular damage
Liver damage
Decrease plasma protein
Decrease blood OP
Unusually high GFR
Reabsorption at proximal tubules
Excrete 1.5 liters per day
Reabsorb 178.5 liters per day
Anything not selected remains in the nephron and becomes urine (urea, bilirubin, Uric acid, anything not recognized)
Transcytosis
Small proteins can fit through the glomerular slits and enter Bowman’s capsule
P.T. Cells can bind proteins and encapsulate into endocytosis vesicles
Renal physiology
P.T. > reabsorption > Na linked nutrient transport > transcytosis > water by osmosis
Clearance
The ability of the kidneys to clean or clear the plasma (blood) of a certain substance
Clearance of Uric acid should be very high
Clearance of glucose should be very low
Inulin
Modified sugar
Filtered but no reabsorption
Clearance of inulin = GFR
PAH (para amino huyperic acid)
Filtered and totally secreted
No reabsorption
Clearance of PAH = total renal blood flow
If clearance exceeds GFR > substance is secreted
If clearance is less than GFR > substance is reabsorbed
Holding your breath
Increase PCO2
Decrease pH > stimulates ventilation