final Flashcards
what is blood pressure caused by?
ventricular contraction
how is blood pressure in the blood vessels maintained when the ventricles are in diastole?
the elastic recoil of the arteries
what is systolic blood pressure caused by?
what is diastolic blood pressure caused by?
systolic BP caused by ventricular contraction
diastolic BP caused by elastic recoil of arteries
what is the korotkoff sound?
the pulsating sound arteries produce when BP is being measured
what is pulse pressure?
strength of pressure waves in blood vessels
how do you calculate pulse pressure?
pulse pressure = systolic pressure - diastolic pressure
describe the strength of BP at you go from the left ventricle to the right atrium
left ventricle - syst is full strength dia is very low
arteries - normal BP values ex. 120/80
arterioles - sys and dia BP become progressively lower
capillaries venules, and veins - sys/dia waves disappear and BP becomes progressively less until pressure completely disappears at the right atrium
where can pulse pressure be found?
arteries and arterioles
Pulse pressure drops out in arterioles
what is mean arterial pressure (MAP) and how do you calculate it?
the driving pressure in arteries and arterioles
mean arterial pressure = diastolic pressure + 1/3 of pulse pressure
what is mean arterial pressure determined by?
1) blood volume
2) cardiac output
3) resistance of the system to blood flow
4) relative distribution of blood between arterial and venous blood vessels
what is blood volume determined by?
1) fluid intake
2) fluid loss (which may be passive or regulated at the kidneys)
what is cardiac output determined by?
1) HR
2) stroke volume
what determines the resistance of the circulatory system to blood flow?
diameter of blood vessels
what is relative distribution of blood between arterial and venous blood vessels determined by?
diameter of veins
what is the negative feedback mechanism that regulates high blood pressure?
*HIGH BLOOD PRESSURE DETECTED** (fast response-cardiovascular system) * vasodilation *reduced cardiac output reduced BP
(slow response- compensation by the kidneys)
*excretion of fluid in urine leads to lower blood volume
reduced BP
what is hydrostatic pressure?
what is colloid osmotic pressure?
hydrostatic pressure is the pressure that forces fluid out of a capillary
colloid osmotic pressure is the pressure of proteins within a capillary that pulls fluids into the capillary
how do you calculate net pressure?
net pressure = hydrostatic pressure - colloid osmotic pressure
when the value is a positive number filtration is occurring and fluids are moving out of the capillary
when the value is negative absorption is occurring and fluid is moving into the capillary
which plasma protein is largely responsible for colloid osmotic pressure?
albumin
what is the difference between filtration and absorption in a capillary?
filtration - fluid is moving out of the capillary and into surrounding tissue
absorption - fluid is moving from the tissue surrounding the capillary into the capilarry
what do carotid and aortic baroreceptors detect?
they detect BP by monitoring blood vessel wall stretch
what is aorta and carotid sinus?
they are the location for the carotid and aortic baroreceptors
describe the baroreceptor reflex related to blood pressure
HIGH BLOOD PRESSURE DETECTED
- *INCREASED BP DETECTED BY BARORECEPTORS**
- carotid and aorta baroreceptors fire AP which travels through sensory neurons to the cardiovascular control center in the medulla
- the cardiovascular center increases parasympathetic output while decreasing sympathetic output
- *INCREASED PARASYMPATHETIC OUTPUT**
- more acetylcholine is released on muscarinic cholinergic receptors at the SA node which leads to reduced heart rate> reduced cardiac output>reduced BP
- *DECREASED SYMPATHETIC OUTPUT**
- less norepinephrine is released at BETA 1 adrenergic receptors at the SA node which helps reduce heart rate>reduces cardiac output>reduced BP
- less norepinephrine is released at beta 1 adrenergic receptors on the ventricular contractile cells which leads to reduced contraction force > reduced cardiac output>reduced BP
- less norepinephrine is released at alpha adrenergic receptors on arterial smooth muscle>vasodilation>reduced peripheral resistance>reduced BP
what is orthostatic hypotension?
sudden drop of BP when you go from lying or sitting to a standing position and blood pressure to the brain drops (makes you feel dizzy)
describe the orthostatic hypotension negative feedback mechanism
- mean arterial blood pressure drops upon standing
- carotid and aortic baroreceptors signal cardiovascular center in the medulla
- sympathetic output is increased while parasympathetic output is decreased
- *INCRASED SYMPATHETIC OUTPUT**
- arterioles and veins vasoconstrict = increased peripheral resistance
- ventricular force of contraction increases>increased cardiac output
- heart rate increased at SA node>increased cardiac output
- *DECREASED PARASYMPATHETIC OUTPUT**
- less acetylcholine binding to muscarinic receptors at the SA node increases heart rate > increases cardiac output
BP returns to normal and baroreceptors start firing at a normal rate
describe the effects of vasovagal syncope (emotional fainting)
1) parasympathetic activity increases while sympathetic activity decreases
2) HR and BP drop
3) blood vessels vasodilate
4) cardiac output and peripheral resistance drop
5) insufficient blood flow to the brain causes person to faint
what are the three stages of atherosclerosis?
1) fatty streak
2) stable fibrous plaque
3) vulnerable plaqu
what are some of the theories behind why people develop primary hypertension?
- increased arterial resistance
- decreased endothelial cell secretion of molecules responsible for vasodilation
- increased endothelin release which causes increased vasoconstriction
- reduced blood vessel compliance (blood vessel wall become rigid and resist vasodilation
- lifestyle, diet, genetics
what are the categories of blood pressure measurements?
normal - less than 120 (sys) 80 (dia)
prehypertension - 120-139 (sys) 80-89 (dia)
hypertension stage 1 - 140-159 (sys) 90-99 (dia)
hypertension stage 2 - >160 (sys) > 100 (dia)
hypertensive crisis - >180 (sys) >110 (dia)
what are some treatments for high BP?
1) Thiazide diuretics
2) beta blockers
3) ACE inhibitors
4) Angiotension 2 antagonists
5) alpha blockers
6) calcium channel blockers
describe thiazide diuretics
cause kidneys to increase urine which removes excess fluid from blood vessels.
diuretics or water pills have minimal side effects
describe beta blockers
make the heart beat slower by blocking nerve stimulating hormones.
describe ace inhibitors
expand blood vessels by blocking certain hormones.
ace inhibitors linked to strokes
describe angiotension 2 antagonists
like ace inhibitors they expand blood vessels by blocking certain hormones but they have fewer major side effects
describe alpha blockers
slows brains action on the nervous system which lowers blood pressure
describe calcium channel blockers
relax blood vessels by interupting the movement of calcium ions into nearby muscles. linked to heart attacks, depression, and suicide
what is the difference between primary hypertension and secondary hypertension?
secondary hypertension is hypertension that is the result of another condition. primary is not due to underlying condition.
what is the respiratory pathway in order?
1) nasal cavity
2) pharynx
3) larynx
4) trachea
5) primary bronchi
6) secondary bronchi
7) bronchioles
8) alveoli
what is included in the respiratory zone?
respiratory bronchioles and alveoli
what is covers the lungs?
pleural membranes
what is the parietal pleura attached to?
the inside of the chest wall
what is the visceral pleura attached to?
the lungs
what does it mean when you say the lungs are compliant?
they are stretchable
what do the elastic fibers in the lungs allow them to do?
it allows them to recoil during exhalation
how is surface tension produced and what can it do to alveoli?
surface tension is produced by hydrogen bonding between water molecules and it will cause alveoli to collapse without intervention from pulmonary surfactant
what does pulmonary surfactant do in alveoli?
it prevents hydrogen bonding which decreases surface tension and keeps alveoli from collapsing
how does the nasal cavity condition inhaled air?
1) humidifies air
2) purifies air
3) warms air
what muscle is the parietal pleura attached to?
the diaphram
what is active inspiration during normal quiet breathing?
inhalation of air to the lungs. it is called active because it relies on muscles to draw air into the lungs
what muscles are involved in active inspiration?
the diaphram and external intercostals/scalenes
describe the air pressure in the lungs when air is being inhaled
when air is inhaled it creates a low pressure condition within the lungs which draws more air in
describe passive expiration during normal quiet breathing
exhalation. it is passive because the cause of exhalation is relaxation of the muscles and the recoiling property of the lungs causes exhalation
describe active expiration
when we force additional air out of our lungs by contracting internal intercostals and abdominal muscles
what is the formula for boyles law?
p1 x v1 = p2 x v2
what happens to alveolar pressure during inhalation and exhalation?
inhalation causes a 1 mmHg pressure drop from atmospheric pressure
exhalation causes 1 mmHg pressure increase compared to atmospheric pressure
in between inhalation and exhalation, alveolar pressure is equal to atmospheric pressure
describe intrapleural pressure during inhalation and expiration
pressure is always less than atmospheric pressure however:
it increases when you exhale and decreases when you inhale
what is pneumothorax?
collapsed lung
what are the different types of pneumothorax?
1) closed- lung is punctured allowing air into the pleural space
2) open- chest wall is punctured allowing air into the pleural space
3) tension- puncture in the chest wall allows air in and then seals to prevent air from escaping which causes air volume to continuously increase within the pleural space. begins to push heart
what is a pulmonary function test?
measures air volume moved with each breath
describe the different air volumes in the lungs
1) tidal volume - air moved in one inspiration or expiration during normal quiet breathing
(approximately 500mL)
2) inspiratory reserve volume (IRV) - the additional air that you can inhale after a normal quiet breathing inhalation
(approximately 3000mL)
3) expiratory reserve volume (ERV) - the air your lungs are capable of forcefully exhaling after a normal quiet breathing exhalation
(approximately 1100mL)
4) residual volume (RV) - the air that remains in the lungs after max exhalation
(approximately 1200mL)
what are lung capacities?
the sum of 2 or more lung volumes
what is vital capacity(VC)?
how do you calculate it?
maximum air moved in and out with one breath
tidal volume + inspiratory reserve volume + expiratory reserve volume
what is total lung capacity?
how do you calculate it?
total air capacity of the lungs
TV + IRV + ERV + RV
how do you calculate inspiratory capacity?
tidal volume + inspiratory reserve volume
how do you calculate functional residual capacity?
expiratory reserve capacity + residual capacity
what lung volumes increase in patients with emphysema?
damage to the lung tissue makes it lose elasticity and residual air volumes increase. patients cant get old air out of lungs
what is total pulmonary ventilation aka and how do you calculate it?
total minute volume - the volume of air move in a minute
total pulmonary ventilation = ventilation rate x tidal volume
what is alveolar ventilation and how do you calculate it?
the total mount of fresh air in alveoli per minute
ventilation rate x (tidal volume - volume of anatomical dead space)
what is anatomical dead space?
the space within the conducting zone of the respiratory tract
what is the approximate volume within the anatomical dead space?
about 150mL
how do you calculate the percentage of fresh air in the alveoli per breath?
(tidal volume - volume in anatomical dead space) / tidal volume
what is eupnea?
normal quiet breathing
what is hyperpnea?
increased respiratory rate and/or volume in response to increased metabolism
ie. exercise
what is hyperventilation?
increased respiratory rate and/or volume without increased metabolism
ie. emotional hyperventilation or blowing up a baloon
what is hypoventilation?
decreased alveolar ventilation
ie. shallow breathing, asthma, restrictive lung disease
what is tachypnea?
rapid breathing. usually increased respiratory rate with decreased depth
ie. panting
what is dyspnea?
difficulty breathing
ie. various pathologies or hard exercise
what is apnea?
cessation of breathing
ie. voluntary breath holding or depression of CNS control centers
what are the three gas exchange locations for CO2 and O2?
exchange 1 = atmosphere-alveoli
exchange 2 = alveoli-blood
exchange 3 = blood-cells/tissue
what are the venous and arterial CO2 and O2 pressures normally?
what is normal venous and arterial blood PH?
VENOUS
Pco2 = 46 mm Hg
Po2 = 40 mm Hg
PH = 7.37
ARTERIAL
Pco2 = 40 mm Hg
Po2 = 95 mm Hg
PH = 7.4
what are normal co2 and o2 pressures in alveoli and tissue cells?
ALVEOLI
Pco2 = 40 mm Hg
Po2 = 100 mm Hg
TISSUE CELLS
Pco2 = 46 mm Hg
Po2 = 40 mm Hg
what is movement of gasses to and from the blood due to?
pressure gradient of the gasses. gasses move diffuse down their concentration gradients to areas of lower concentrations
what determines the PH of the blood?
co2 levels in the blood
what does more co2 in the blood do to PH levels?
more co2 = more acidic
describe conditions that can make it difficult for gasses to diffuse between blood and alveoli
EMPHYSEMA - destruction of alveolar walls reduces surface area of alveoli which reduces gas exchange capability
(Po2 in alveoli = normal or low//Po2 in blood vessels = low)
FIBROTIC LUNG DISEASE - thickened alveolar membranes make it difficult for gas exchange between alveoli and blood vessels. reduced compliance of the lungs may also decrease alveolar ventilation.
(Po2 in alveoli = normal or low//Po2 in blood vessels = low)
PULMONARY EDEMA - fluid in interstitial space between alveoli and capillaries increase the distance gasses need to diffuse across which reduces efficiency. arterial Pco2 levels may be normal due to the solubility of co2 in water.
(Po2 in alveoli = normal// Po2 in capillaries = low)
ASTHMA - constricted bronchioles increases airway resistance and decreases alveolar ventilation
(Po2 in alveoli = low//Po2 in capillaries = low)
what is hypoxia?
when the body (or region of the body) is deprived of o2
what is hypoxic hypoxia and what are some causes?
low arterial Po2 levels
can be due to:
high altitude or alveolar hypoventilation
what is anemic hypoxia and what are some possible causes?
decreased total amount of o2 bound to hemoglobin
can be due to:
blood loss/anemia
carbon monoxide poisoning
what is ischemic hypoxia and what are some possible causes?
reduced blood flow
can be due to:
heart failure (whole body hypoxia)
shock (peripheral hypoxia)
thrombosis (hypoxia in a single organ)
what is histotoxic hypoxia and what are possible causes?
failure of cells to use o2 because they have been poisoned
can be due to:
cyanide or other metabolic poisons
what is hemoglobin that has oxygen bound to it called?
HbO2 or oxyhemoglobin
how do you calculate total blood o2 content?
total blood o2 content = dissolved o2 + o2 bound to hemoglobin
how much O2 can be transported in blood plasma and how much in RBCs?
blood plasma can transport 3mL o2 per liter of blood
RBCs can transport 197mL o2 per liter of blood
what does the % o2 saturation of hemoglobin depend on?
saturation of o2 in the plasma
how do you calculate % o2 saturation?
amount of o2 bound to hemoglobin / maximum o2 that can be bound to hemoglobin x 100
how do you know if you are looking at a tissue cell or alveoli on a graph by looking at o2 content?
Po2 in tissue cell is usually 40 mm Hg
Po2 in alveoli is usually 100 mm Hg
why at rest do hemoglobin only deliver an average on 1 o2 when there are 4 bound to it?
the remaining o2 bound to hemoglobin at rest are reserved for cells at times when o2 demand is higher
how much o2 is dissolved in plasma and how much is bound to hemoglobin after it is diffused into the blood?
<2% dissolved in the blood plasma
>98% bound to hemoglobin
what are the factors that influence dissociation of o2 from oxyhemoglobin so they can be used in tissue cells?
1) pH of the blood
2) temperature of the blood
3) Pco2 of the blood
4) 2,3 DPG
what is increased 2, 3 DPG due to?
chronic hypoxia
what is 2, 3 DPG?
how is 2, 3 DPG produced?
2, 3 diphosphoglycerate
is a a molecule produced in hypoxic conditions from glucose in glycolysis
instead of glucose being converted to 2 pyruvates it is converted into 2, 3 diphosphoglycerate
what effect doe pH level have on oxygen dissociation from oxyhemoglobin near tissue cells?
higher pH levels lead to reduced dissociation and decreased o2 delivery to tissue cells
lower pH levels lead to increased dissociation of o2 from oxyhemoglobin and increased o2 delivery to tissue cells
what is the bohr effect?
the effect pH level has on o2 dissociation from oxyhemoglobin
what effect does temperature have on o2 dissociation from oxyhemoglobin and delivery of o2 to tissue cells?
increased temperatures lead to increased dissociation of o2 from oxyhemoglobin and increased delivery of o2 to tissue cells
decreased temperatures lead to decreased dissociation of o2 from oxyhemoglobin and decreased o2 delivery to tissue cells
what effect does Pco2 have on dissociation of o2 from oxyhemoglobin and o2 delivery to tissue cells?
increased Pco2 leads to increased o2 dissociation from oxyhemoglobin and increased delivery of o2 to tissue cells
decreased Pco2 leads to decreased dissociation of o2 from oxyhemoglobin and decreased delivery of o2 to tissue cells
what effect does 2, 3 diphosphoglycerate concentrations have on dissociation of o2 from oxyhemoglobin and delivery of o2 to tissue cells?
increased levels of 2, 3 DPG leads to increased dissociation of o2 from oxyhemoglobin and increased delivery of o2 to tissue cells
decreased 2, 3 DPG concentrations lead to decreased dissociation of o2 from oxyhemoglobin and decreased delivery of o2 to tissue cells
how is co2 diffused and transported in the blood?
1) co2 diffuses out of cells into systemic capillaries
2) 7% of co2 remains dissolved in blood plasma
3) 23% of co2 binds to hemoglobin and converts it to carbaminohemoglobin
4) 70% of co2 is converted to bicarbonate and hydrogen ions.(hemoglobin buffers hydrogen ions by binding to them).
4a) the enzyme carbonic anhydrase combines co2 with h20 to make carbonic acid which is then converted to bicarbonate.
5) bicarbonate moves into the blood plasma through the chloride shift where chloride is exchanged with bicarbonate (chloride moves into the cell and bicarbonate moves out)
how does co2 exit the circulatory system at the alveoli?
1) co2 that is dissolved in the plasma diffuses out of the blood into the alveoli
2) LAW OF MASS ACTION: co2 unbinds to hemoglobin and diffuses into the plasma and then out of the blood and into the alveoli
3) the reaction that produced bicarbonate is reversed which pulls more bicarbonate into the RBC via chloride shift to be converted back into co2 and water via the enzyme carbonic anhydrase. the co2 is then diffused into the blood plasma and then into the alveoli to be disposed of.
what is hypercapnia and what does it lead to?
hypercapnia is increased Pco2 in the blood and leads to respiratory acidosis
why defines respiratory acidosis?
respiratory acidosis is a acidic blood condition which is the result of co2 being converted into bicarbonate and hydrogen ions. increased hydrogen ions in the blood makes the blood more acidic (acidosis)
since this type of acidosis is brought on by respiratory gasses it is refered to as RESPIRATORY acidosis
where is the central pattern generator and what is its function?
respiratory centers in the pons and the medulla make up the central pattern generator
its function is to generate intrinsic and rhythmic breathing activities (regulate rate and depth of breathing)
what are the components of respiratory regulation?
central pattern generator
peripheral chemoreceptors
central chemoreceptors
where are the peripheral chemoreceptors located?
the aorta and carotid arteries
they are located in the aortic bodies of the aorta and the carotid body of the common carotid artery
what do peripheral chemoreceptors associated with respiratory regulation sense?
Po2
Pco2
pH
while they sense all three of these, Pco2 and pH have a bigger influence on regulation than Po2
how do respiratory chemoreceptors communicate with central pattern generator?
use low Po2 as example
low Po2 is detected by chemoreceptor
cell depolarizes and leads to exocytosis of neurotransmitters
neurotransmitters cause sensory neuron to fire AP
AP travels to central pattern generator
respiratory centers in pons and medulla process incoming AP and cause increased ventilation
where are respiratory central chemoreceptors located and what do they detect?
located in the medulla, they detect Pco2 indirectly
how do central chemoreceptors associated with the respiratory system detect Pco2?
1) when Pco2 in the blood is high, more diffuses into the CSF.
2) some of the co2 binds directly to central chemoreceptors while others are converted into carbonic acid via carbonic anhydrase
3) when carbonic acid breaks down into hydrogen ions and bicarbonate, the hydrogen ions also bind to central chemoreceptors
4) central chemoreceptors are able to use co2 and H+ concentrations to detect levels of co2.
5) if high levels of co2 are present they signal respiratory centers in pons and medulla to increase ventilation in order to reduced Pco2
what is respiratory acidosis and respiratory alkalosis?
respiratory acidosis - increased co2 retention due to hypoventilation, which can result in the accumulation of carbonic acid and thus a fall in pH to below normal
respiratory alkalosis - a rise in blood pH due to loss of co2 and carbonic acid through hyperventilation
what are the three functions of the nephron?
1) filtration (glomerulus)
2) reabsorption (PCT, loop of henle, DCT)
3) secretion (PCT, loop of henle, DCT)
NEPHRON
what is the definition of filtration?
fluid/molecules move from glomerulus to the PCT
what type of capillaries are the glomerulus made of?
fenestrated
are proteins normally filtered out of the blood through the glomerulus?
no they are too large to pass through the fenestrations of the capillaries and the space between podocytes
what is GFR?
glomerular filtration rate. this is measured to determine kidney efficiency
what is the normal GFR?
125mL/min
describe the pressures that determine net filtration pressure at the glomerulus and the formula used to calculate it
hydrostatic pressure(blood pressure) - pressure within the capillary that forces filtrate from the glomerulus to the glomerular capsule
colloid osmotic pressure - osmotic pressure due to proteins in the plasma draw fluids back into the glomerulus
fluid pressure - pressure within the glomerular capsule
hydrostatic pressure - colloid osmotic pressure - fluid pressure = net filtration pressure
(if the calculated number is positive there is a net movement of of fluid into the bowmans capsule (filtration).)
(if number is negative then fluids are traveling backwards from the capsule into the glomerulus)
what is glomerular autoregulation?
the ability of the glomerulus to maintain a constant GFR within a wide range of BP
what is a normal GFR?
PER DAY
180 L/day
between what MAP values can glomeruli maintain a 180 L/day GFR?
80-180 mm Hg
what are methods of glomerular autoregulation?
1) myogenic response
2) tubuloglomerular feedback
describe glomerular myogenic responses in high and low BP situations?
HIGH MAP
afferent arteriole constricts and reduces pressure in the glomerulus
LOW MAP
efferent arteriole constricts and increases pressure in the glomerulus
describe the tubuloglomerular feedback via juxtaglomerular apparatus
the macula densa cells sense flow in the distal tubule and secrete paracrine signals that affect the afferent and efferent arteriole diameter
what cells are involved with the juxtaglomerular apparatus ?
1) macula densa
2) granular cells
describe the tubuloglomerular feedback mechanism in times of increased GFR
1) GFR increases
2) flow through tubule increases
3) flow passed macula densa increases
4) macula densa release paracrine signal to afferent arteriole
5) afferent arteriole constricts
6) resistance in afferent arteriole increases which decreases pressure in the glomerulus
7) GFR decreases
how much filtrate is reabsorbed?
99% of filtrate is reabsorbed into peritubular capillaries
what are the capillaries called that are intertwined with the PCT and DCT?
1) capillaries surrounding the cortical nephrons are called peritubular capillaries
2) capillaries surrounding the medullary nephrons are called vasa recta
what is reabsorption driven by?
pi pressure (colloid osmotic pressure)
how do molecules travel across epithelial cells in reabsorption?
epithelial transport - molecules can travel between epithelial cells
transcellular pathway - molecules can travel through cells
how does sodium get through epithelial cells during reabsorption?
sodium travels through epithelial cells by transcellular pathway (active transport)
how do anions get through epithelial cells during reabsorption?
they can either travel through cells by transcellular pathway or travel between cells by epithelial transport
how does water travel across epithelial cells during reabsorption?
they can travel by transcellular pathway or epithelial transport via osmosis
how does potassium, calcium, and urea travel across epithelial cells during reabsorption?
they can either travel across epithelial cells via transcellular pathway or epithelial transport
how specifically does sodium get across epithelial cells during reabsorption?
1) sodium potassium pumps on the basal side of the cell ( side of cell closest to capillary) pumps sodium out into the ECF near capillary keeping concentrations of sodium low in the epithelial cell (primary active transport)
2) sodium diffuses through sodium linked symporters on the apical side of the cell following the concentration gradient established by the sodium potassium pump (secondary active transport). other molecules such as amino acids, some ions, and vitamins hitch a ride with sodium through the sodium linked transporter.
how specifically does glucose travel across epithelial cells during reabsorption?
1) SGLT (sodium linked glucose transporters) on the apical side of the tubular epithelial cells transport glucose against its concentration gradient by using the kinetic energy of sodium transport down its concentration gradient.
2) glucose is transported out of the basal side of the cell via GLUT transport protein
3) sodium is transported out of the basal side of the cell via sodium potassium pump (ATPase)
what percentage of glucose is normally reabsorbed?
100%
describe renal threshold
renal threshold is when transporters become saturated and transport rate is maximum
describe filtration rate of glucose
filtration of glucose is proportional to the plasma concentration. filtration does not saturate
describe glucose reabsorption rate
glucose reabsorption rate is proportional to plasma concentration until transport maximum is reached (renal threshold)
what is the renal threshold for glucose?
about 300 mg/ 100mL plasma
describe excretion of glucose
glucose excretion is zero until renal threshold is reached.
what is the clinical term for glucose present in the urine?
glucosuria
define nephron secretion
molecules move from peritubular capillaries into the kidney tubules
what is excretion KIDNEYS
elimination of waste from the body
how do you calculate amount excreted from kidneys?
amount excreted = amount filtered - amount reabsorbed + amount secreted
RENAL
what is clearance?
the rate a solute is cleared from the plasma
what is inulin?
a protein used to check kidney function
the body doesnt utilize inulin thus does not reabsorb it in the tubules. the clearance of the substance should be equal to GFR
what should inulin clearance be if GFR is 100mL/min?
100mL/min
what should the clearance of glucose be if GFR is 100mL/min?
0mL/min
why is penicillin clearance higher than GFR?
because none is reabsorbed and additional penicillin is secreted
why is the clearance rate of urea 50mL/min when GFR is 100mL/min?
because half is reabsorbed
describe what happens in the fatty streak stage of atherosclerosis
fatty streak -
a) LDL cholesterol accumulates between endothelium and connective tissue and is oxidized
b) macrophages ingest cholesterol and become foam cells
c) smooth muscle cells are attracted by macrophages and begin to divide and take up cholesterol
describe what happens in the stable fibrous plaque stage of atherosclerosis
stable fibrous plaque -
a) lipid core developes
b) fibrous scar tissue forms
c) smooth muscle cells divide and contribute to the thickening of intima
d) calcifications are deposited within the plaque
describe what happens in the vulnerable plaque stage of atherosclerosis
vulnerable plaque-
a) macrophages release enzymes that dissolve collagen and convert stable plaques to unstable plaques
b) platelets come into contact with exposed collagen and activate and initiate blood clot formation
what is counter current exchange?
2 parallel capillaries or tubules that exchange concentration or temperature gradients
what is a counter current flow vs. concurrent flow?
countercurrent flow - parallel tubules or capillaries with opposite flows.
(small gradients are maintained throughout the vessels)
concurrent flow - parallel tubules or capillaries that have flows in the same direction
(large gradients disappear quickly)
what is the multiplier system?
the multiplier system refers to the concentration increase that coincides with the depth of the kidney
(cortex is 300mOsm and the deepest part of the cortex is 1200mOsm)
describe the concentrations of the loop of henle and how they are achieved
concentrations of the loop of henle coincide with the concentration of the surrounding tissue.
* the top of the descending limb is 300mOsm and gets more concentrated until it reaches the bottom of the loop at which point it is 1200mOsm.
this concentration is achieved by the removal of H20 from the tubule
- concentrations become more dilute as filtrate travels up the ascending limb until it reaches 100mOsm at the top of the ascending limb
this is due to sodium and chloride being reabsorbed out of the loop of henle.
what happens to water once it diffuses out of the descending limb of the loop of henle?
it travels through the tissue and is absorbed back into the vasa recta due to the high sodium/chloride concentrations within the vasa recta
how does the vasa recta become so concentrated with sodium?
sodium and chloride molecules diffuse into these capillaries from the surrounding tissue. their concentrations coincide with the concentrations of the medulla
what is is the medulla of the kidney, loop of henle, and vasa recta concentrated with?
sodium chloride (salt)
what affects vasopressin release and what part of the kidney does it act on?
blood osmolarity affects its release and it acts on the collecting ducts of the kidneys
how does vasopressin function?
vasopressin diffuses out of capillaries near the collecting duct and bind to vasopressin receptor on CD cells
this activates cAMP second messenger that signals the release of vesicles containing aquaporin (water pores) to the plasma membrane (apical side)
once aquaporin is integrated into the plasma membrane, water from the collecting duct travels through into the cell and is absorbed through osmosis out of the basal side and back into capillaries.
what is the vasopressin pathway for low blood pressure?
- decreased BP
- carotid and aortic baroreceptors detect decreased wall stretch
- signals travel through sensory neurons to hypothalamus
- hypothalamic neurons synthesize vasopressin
- posterior pituitary releases vasopressin
- vasopressin acts on collecting ducts to retain water
what is the vasopressin pathway for high blood concentrations?
- increased blood concentration
- hypothalamic osmoreceptors in the hypothalamus detect high blood concentration and send signals through interneurons to hypothalamic neurons to make vasopressin
- vasopressin is released from posterior pituitary which acts on collecting ducts to retain water
what is the highest concentration urine can be in the human body?
why?
1200mOsm because thats the highest concentration found in the kidneys
what is the concentration of urine when vasopressin is not present?
100mOsm
what happens to your body when you ingest salt?
- no change in blood volume but blood osmolarity climbs
- thirst sensation occurs and vasopressin secretion increases
- drinking occurs due to thirst and water retention at the kidneys occurs due to vasopressin release
- blood volume and BP increase
- fast (cardiovascular) and slow (renal) responses occur to reduce blood pressure
- blood osmolarity and volume return to normal
what are the three methods of activation used to release renin and start the Renin Angiotensin Aldosterone Pathway?
1) decreased blood pressure directly acts on granular cells of the afferent arteriole and stimulates the release of renin
2) decreased GFR initiates the tubuloglomerular pathway. macula densa releases paracrine which travels to the granular cells and stimulates the release of renin
3) decreased BP is sensed by the cardiovascular center in the medulla which signals an increase of sympathetic activity. this stimulates granular cells in the afferent arteriole to release renin
how is aldosterone created?
- angiotesinogen which is constantly produced in the liver is also always floating around in blood plasma
- once it comes into contact with renin it is converted into angiotensin 1
- ACE (angiotensin converting enzyme) is produced by the endothelial cells of blood vessels and contacts angiotensin 1 once it is produced
- when ACE comes into contact with angiotensin 1, angiotensin 1 is converted to angiotensin 2
- angiotensin 2 travels to the zona glomerulosa in the adrenal cortex and stimulates the production and release of aldosterone
how does aldosterone regulate potassium and sodium?
- aldosterone combines with cytoplasmic receptor
- the hormone receptor complex initiates transcription in the nucleus
- causes protein synthesis that makes new protein channels and pumps
- aldosterone induced proteins modulate existing channels and pumps
- this process results in the secretion of potassium and the reabsorption of sodium
what is renin?
an enzyme
what cells in the kidneys does aldosterone act on?
p cells of the collecting duct
when aldosterone stimulates the creation of pumps and channels in P cells, where do they position themselves?
pumps become part of the basil membrane and channels become part of the apical membrane
describe atrial natriuretic peptide function
- *HELPS REGULATE SODIUM**
- increased blood volume causes atrial walls to stretch
- myocardial cells in the atrium stretch and release natriuretic peptide
- natriuretic peptide acts on the hypothalamus, kidneys, adrenal cortex, and the medulla
describe the effect natriuretic peptide has on the hypothalamus
causes the hypothalamus to produce and release less vasopressin which increases NaCl and H20 excretion
this reduces blood volume and thus blood pressure
describe the effects atrial natriuretic peptide has on the kidneys
**it acts on the tubules to reduce sodium reabsorption which increases sodium and water excretion.
this reduces blood volume and thus blood pressure
**it acts on afferent arterioles to decrease renin secretion and dilate arteriole which increases GFR
this helps to increase sodium and water excretion which lowers blood volume and pressure
describe the effect of atrial natriuretic peptide on the adrenal cortex
it decreases aldosterone production and secretion which helps to excrete more sodium and water which lowers blood volume and pressure
describe the effects of atrial natriuretic peptide on the medulla oblongata during high bp conditions
decreases sympathetic output which reduces bp
in people with respiratory and metabolic acidosis, what are the: Pco2 H+ pH HCO3 levels?
respiratory acidosis: Pco2 - elevated H+ - elevated pH - decreased HCO3 - elevated
metabolic acidosis: Pco2 - normal or decreased H+ - elevated pH - decreased HCO3 - decreased
in people respiratory and metabolic alkalosis what are these levels: Pco2 H+ pH HCO3
respiratory alkalosis: Pco2 - decreased H+ - decreased pH - elevated HCO3 - decreased
metabolic alkalosis: Pco2 - Normal or elevated H+ - decreased pH - elevated HCO3 - elevated
what are buffers the body uses to compensate for pH disturbances?
- HCO3 in ECF
- proteins, hemoglobin, and phosphates in cells
- phosphates and ammonia in urine
how does H+ come into the body and how does the body dispose of it?
input - diet and metabolism
output - ventilation and renal
what is the feedback pathways for increased plasma H+ concentration and Pco2?
high plasma Pco2 = high plasma H+ concentration
- *increased H+ concentration is detected by carotid and aortic chemoreceptors while increased Pco2 is detected by central chemoreceptors
- *peripheral and central chemoreceptors send signals to the respiratory control centers in medulla
- *the respiratory control centers send signals that stimulate increased ventilation rate and depth
Pco2 and H+ concentrations drop which acts on central and peripheral chemoreceptors and tells them to stop sending signals to the medulla
how does the kidneys secrete H+?
WITHING CUBOIDAL CELLS OF TUBULE
CO2 + H2O—carbonic anhydrase–>H2CO3———>H+ + HCO3
H+ is then diffused out of the cell into the filtrate to be excreted in urine
what is the cephalic phase of the digestive system?
the sight, smell, and thought of food
it initiates the digestive process
what is mastication?
chewing
what is salivary amylase?
what is its function?
an enzyme that is responsible for chemical digestion in the oral cavity.
it breaks polysaccharides into disaccharides
what is salivary lipase and what is its function?
it is an enzyme that is responsible for breaking lipids down in the oral cavity
what is lysozyme and what is its function?
it is an enzyme in the oral cavity that is responsible for destroying bacteria that is ingested
what are the components of saliva?
amylase
lipase
lysozyme
immunoglobulin
what is food called when it is chewed and mixed with saliva?
bolus
what is deglutition and how does it occur?
the act of swallowing bolus
1) tongue pushes bolus against the soft palate and back of mouth, triggering the swallowing reflex
2) breathing is inhibited as bolus travels passed the closed airway
3) bolus moves downward into the esophagus propelled by peristaltic waves and aided by gravity
describe mucus neck cell secretions and their functions
- *mucus - physical barrier between lumen and epithelium
* *bicarbonate - buffers gastric acid to prevent damage to the epithelium
describe parietal cell secretions and their functions
gastric acid (HCl) - activates pepsin; kills bacteria
intrinsic factor - complexes with vitamin B12 to permit absorption
how are hydrogen ions and chloride transported into the stomach
water is broken down into H+ and OH-
H+ is transported out by a hydrogen pump that exchanges hydrogen for potassium
OH combines with CO2 to form HCO3 via carbonic anhydrase
HCO3 is transported out of the basal side of the parietal cell via chloride shift where it is exchanged for chloride
chloride travels into the stomach via protein channel where it combines with H+ to form HCl (gastric acid)
describe enterochromaffin-like cell secretions and their functions
they secrete histamines that stimulate gastric acid secretion
describe chief cell secretions and their functions
Pepsin(ogen) - digests proteins
gastric lipase - digests fats
describe D cell secretions and their functions
somatostatin - inhibits gastric acid secretion
describe G cell secretions and their functions
gastrin - stimulates gastric acid secretion
what are the cells that make up the gastric pits?
Mucus neck cells
parietal cells
chief cells
D cells
G cells
how is pepsinogen activated?
when it comes in contact with hydrogen ions it is activated into pepsin
what is bolus ground down and mixed with stomach acids called?
chyme?
describe stomach secretion regulation
1) vagus nerve and food stimulates G cells to secrete gastrin
2) gastrin and vagus nerve stimulates ECL cells to secrete histamine
3) histamine stimulates parietal cells to secrete HCl
4) HCl stimulates chief cells to secrete pepsinogen
5) pepsinogen is secreted and comes into contact with hydrogen ions and is activated to pepsin
6) HCl provides a negative feedback signal that acts on D cells and stimulates them to release somatostatin which inhibits ECL cells
7) HCl also inhibits G cells and parietal cells
what is Zollinger Ellison syndrome?
pancreatic tumor that increases gastrin release
the increased gastrin secretion causes increased HCl secretion. this causes dyspepsia and peptic ulcers
what are some causes of stomach ulcers?
Zollinger Ellison syndrome
NSAIDS (nonsteroidal anti-inflammatory drugs)
helicobacter pylori (bacteria)
why do NSAIDS cause stomach ulcers?
NSAIDS block cyclooxygenase (COX1) which is responsible for converting arachidonic acid to prostaglandin
prostaglandin protects stomach lining from stomach acids so without it stomach acid eats away at the stomach lining and eventually forms ulcers
what are some cures for stomach ulcers?
how do they cure it?
1) histamine antagonists - counter acts histamine which inhibits parietal cell HCL secretion
2) proton pump inhibitors - inhibits proton pumps in parietal cells responsible for H+ secretion
3) antibiotics - if ulcers are caused by bacteria, antibiotics will kill the bacteria that is eating away the stomach lining
what is tagamet?
histamine antagonist
what is prilosec otc?
a proton pump inhibitor
what is nexium?
a proton pump inhibitor
