General Physiology Flashcards
Intracellular component consists of
- Water
- K+
- Acidic
- intracellular organs
Extracellular component consists of
- Na+
- blood plasma/interstitial fluid
What’s the membrane potential of a cell? (NO NET MVMT)
(-) 90mV
- leaky K+ (flowing in and out of the cell) but exist mostly INSIDE the cell
-Na/K ATPase pump
Resting membrane potential
-70mV
- Na+ can slowly diffuse through the cell membrane causing resting membrane potential
- Na/K ATPase
Na+/K+ pumps
3 Na+ OUT
2 K+ IN
Depolarization
inside cell becomes more positive due to influx of Na+
Hyperpolarization
Inside cell becomes more negative due to efflux of Na+
Action potential
when membrane is depolarize beyond a certain threshold
2 directions for cellular transport
- Uphill/against graident (requires ATP)
- Primary active tranpsport: directly uses ATP
- Secondary active transport: indirectly uses ATP (Na+/K+ pump) - Downhill/w/ gradient (does not require ATP)
- Simple: non-electrolytes (no charge) diffuse across membrane
- Carrier-Mediated transport: integral membrane proteins to move charged molecules across the membrane facilitated diffusion
2 types of secondary active transport
- Cotransport: ions move SAME direction (ex. Na+/AA in PCT kidneys, Na+/K+/2Cl- in ascending loop of henlen)
- Counter-tranpsort: ions move in OPPOSITE direction (Ex. Na+/Ca2+ transport in muscles)
passage of glucose, AA, and other polar molecules are mediated by..?
carrier protein
- maximum rate = transport maximum (carriers are saturated)
Which adrenoreceptors inhibits adenylyl cyclase = decr cAMP?
a2
“a2 is different from you”
B-blockers side effects
act on B1 and B2 receptors
- bronchoconstriction, bradycardia
ask about pulmonary sx before prescribing!
Which receptors are the only receptors that can open Na+ and K+ channels? Where are they located?
Nicotinic, other receptors alter either calcium concentration or cAMP
- causes depolarization
- located in the motor end plates of skeletal muscles on postganglionic neuron cell bodies within the ganglion of the sympathetic and parasympathetic nervous system, and adrenal medulla
these are unique
Muscarinic receptors Which recpetors increase intracellular Ca2+
alpha 1 and muscarinic
Which receptors increase cAMP?
B1 and B2
Where are muscarinic receptors located?
PNS effector organs, vascular SM, sweat glands.
Calculate Intracellular volume
Intracellular volume = Total volume - extracellular volume
- ICF is slightly more acidic
- ECF and ICF has the same osmolality
Diffusion
- passive transport (high to low)
- uses thermal energy, not ATP
- stops when concentration of molecules are equal on both sides of the membrane
rate of diffusion increases under which condtions?
- decr membrane thickness
- incr temp
- incr membrane permeability
Simple diffusion
- passive transport involving mvmt of small molecules and inorganic ions
- Na+ and K+ pass thru specific channels
- steroids and hormones pass directly through the phospholipid bilayer
Osmosis
- simple diffusion of water across a semipermeable membrane
- low to high solute
- solution with higher osmolality (more solutes) = higher osmotic pressure
the right and left lungs have how man lobes?
3 right lobes (larger and wider)
2 left lobes
3 surfaces of the lung
- Coastal = faces sternum, costal cartilage, and ribs
- Mediastinal = faces hilum of lungs and medial to the mediastinum
- Dipaphragm = rest on the dome of the diaphragm
Each lung has 2 zones:
- Conducting zone = upper airways, trachea, bronchi, bronchioles.
- warms and humidifies air before reaching respiratory zone
- innervated by SNS via B2 receptor causing relaxation of smooth muscle, bronchodilation, inward flow of air - Respiratory zone
- includes respiratory bronchioles, alveolar ducts, alveolar sacs, alveoli
- allow blood and air to interfuse
Inspiration
- active process
- diaphragm contracts (lowers and flattens, incr throacic volume)
- Parasternal and external intercostal muscles contract
- scalenes lift rib cage in ant-post position
incr thoracic volume and intrapulmonary pressure
Expiration
- Passive process
- diaphragm relaxes
- decr lung volume = incr alveoli to incr above atmospheric pressure causing air to be pushed out from lungs
- forced expiration, the internal intercostal muscles contract and squeeze rib cage and abdominal muscles force organs up against the diaphragm
decr volume of thorax
Tidal volume
air volume inspired or expired after each normal breath
Inspiratory Reserve Volume (IR)
max volume inspiration after a tidal volume (normal) inspiration
Expiratory Reserve Volume (ER)
max volume of expiration that can be pushed out after tidal volume (normal) expiration
Inspiratory capacity
total amount of air you can breathe in after taking a normal breath without straining.
- Vol is approx 3L
Vital capacity
the maximum amount of air a person can exhale forcefully after taking the deepest breath possible.
- volume is approx 4.5L
Residual volume
volume of air that remains in the lungs even after a maximal exhalation
RV = Functional residual capacity (FRC) - Expiratory reserve (ER)
FRC = it’s the amount of air left in your lungs after you’ve exhaled normally
ER = additional amount of air that you can forcibly exhale from your lungs after a normal, passive exhalation
Functional residual capacity
it’s the amount of air left in your lungs after you’ve exhaled normally
FRC = ER + RV
Total lung capacity
maximum volume of air that the lungs can hold at the end of a maximal inhalation
TLC = VC + RV
Forced Vital capacity
measure of the maximum amount of air that a person can forcefully exhale after taking the deepest breath possible
It’s similar to vital capacity (VC), but in FVC, the exhalation is done as forcefully and rapidly as possible, whereas VC can be exhaled at a more relaxed pace.
Forced expiratory volume (FEV1)
measure of the amount of air that a person can forcefully exhale in one second (FEV1)
Respiratory rate
number of breaths per min
Normal = 12 breaths per min
Minute ventilation
Tidal volume x breaths/min (TV x RR)
Spirogram
clinically used to measure lung function and dz
- ratio <80% = obstructive lung dz (COPD, chronic bronchitis, emphysema, asthma)
– reduced FEV1/FVC ratio
Restrictive lung dz
- poor expansion of lungs with a decr in lung volume and normal to elevated FEV1/FVC ratio
- ex. toxoplasmosis, histoplasmosis, sarcoidosis
Anatomic dead space
portion of the respiratory system where no gas exchange occurs during breathing.
- conducting zone (bronchi and bronchioles, trachea)
Where does gas exchange occur?
alveoli
- O2 and CO2 diffuse across the alveolar and capillary walls to and from blood stream
functional dead space
- specifically refers to alveoli
- occurs when there is ventilation of lung areas that are not effectively perfused with blood, such as areas with reduced or absent blood flow due to conditions like pulmonary embolism or areas affected by lung disease. As a result, the air that reaches these alveoli during inhalation does not participate in gas exchange with the blood.
Physiologic dead space
- includes airways and non-functional alveoli within the lungs. This space represents the portion of each breath that doesn’t contribute to the exchange of oxygen and carbon dioxide in the blood.
- combination of functional and anatomic dead space
Which part of the lung has the highest blood flow?
base of the lung, greatest exchange of O2
Hemoglobin
- 98% of O2 is bound to Hb, remaining 2% dissolved in plasma
- 4 peptide subunits
- each subunits contains a heme group with a reduced iron core that shares elctrons with an O2 molecule
- considered oxygenated when saturated with 4 O2 molecules
- Hb carrying less than 4 O2 is considered deoxygenated
CO2
- concentration is 20X greater compared to O2 in the blood stream
- 90% of CO2 is transported to lungs in form of bicarbonate. Carbonic anhydrase (found in RBC) catalyze reversible conversion of CO2 and H2O: CO2 + H2O ⇌ H2CO3
CO2 + H2O ↔ H2CO3↔ H+ + HCO3-
- reaction occurs rapidly and facilitates transport of CO2 from tissues to lungs for elimination
In the lungs, process is reversed
- carbonic anhydrase to bicarb to CO2 and water
Transport of CO2
- CO2 to RBC = simple diffusion
- CO2 is hydrated to H2CO3 within RBCs
- H2CO3 is broken down into HCO3- and H+ by carbonic anhydrase
- Deoxyhemoglobin acts as a buffer within the bloodstream to counteract released H+ ions from the breakdown of H2CO3
- Cl- and HCO3 are exchanged across RBC membrane. HCO3- within the plasma is then taken to the lungs
- After reaching the lungs, Cl- and HCO3 are exchanged across the RBC membrane in the veins of the lungs. HCO3 then combines with H+ to form H2CO3
- H2CO3 dissociates into CO2 and H2O which are expired by the lungs
Atmospheric pressure
760mmHg
Partial pressure of O2 (PO2)
160 mmHg
Partial pressure of CO2
0
What happens to PO2 when air enters the trachea/lungs?
Decr b/c of vaporization of water as it travels into the blood stream
What happens to PCO2 within the lungs
incr as CO2 diffuses from bloodstream into the alveoli
What conditions decr the surface area of the lungs?
emphysema, causing decr exchange of CO2 and O2
Which one is more soluble CO2 or O2?
CO2 20x more soluble than O2
Partial pressure will always flow from
high to low pressure
How will thickness and SA affect diffusion rate?
increase thickness = decr diffusion rate, they are inversely proportional
incr SA = incr diffusion rate
Oxygen dissociation curve
The oxygen dissociation curve shows how easily hemoglobin in red blood cells binds to and releases oxygen molecules depending on the partial pressure of oxygen in the blood
- the higher the PO2 = the higher the O2, vice versa
- sigmoid shape curve
Imagine the oxygen dissociation curve as a rollercoaster ride. The x-axis represents the partial pressure of oxygen (how much oxygen is available), and the y-axis represents the saturation of hemoglobin with oxygen (how much oxygen hemoglobin is carrying).
At lower partial pressures of oxygen, like what we have in tissues where oxygen is needed, the rollercoaster is steep. This means that even small changes in oxygen levels lead to significant changes in how much oxygen hemoglobin carries. This steep part of the curve indicates that hemoglobin eagerly grabs onto oxygen when it’s available.
At higher partial pressures of oxygen, like what we have in the lungs, the rollercoaster levels off. This means that even when there’s a lot of oxygen around, hemoglobin doesn’t hold onto it tightly. Instead, it releases oxygen more readily, making it available for tissues that need it.
So, the oxygen dissociation curve helps us understand how efficiently hemoglobin picks up oxygen in the lungs and delivers it to tissues throughout the body.
Oxygen dissociation curve
- Right shift indicates?
- Left shift indicates?
Right = decr affinity for O2
- Increased acidity (decreased pH)
- Increased temperature
- incr CO2
Left = incr affinity for O2
- decr acidity
- decr temp
- decr CO2
Carbon monoxide
- binds to hb more readily than CO2
- decr ability of hb to release O2 into the bloodstream
Respiration is controlled through..
Neural and chemical regulators
Part of the brain that activates neurons that control respiratory muscles to produce an automatic breathing cycle? What is it influenced by?
Medulla oblongata
- influenced by apneustic and pneumotaxic centers of the pons in pons, as well as feedback info
- pulmonary stretch receptors in the bronchioles leads to negative inhibition, helping to prevent lung over-inflation
- conscious breathing includes direct control by cerebral cortex via the corticospinal tracts
Chemical control
- Peripheral chemoreceptors
- Central receptors
Peripheral chemoreceptors
- located within the walls of the carotid and aorta, sensitive to CO2 changes
- Monitor O2 and CO2 levels within arterial blood and provide feedback to the medullary centers
- they detect CO2 changes via increase acidity in the plasma and incr levels of carbonic anhydrase
- decr O2 = incr CO2 (affect sensitivity or carotid and aortic bodies)
Central receptors
- sensitive to H+ changes
- H+ CANNOT enter BBB but CO2 can
- High CO2 = High H+ = increase acidity and ventilation
- buffering ability of CSF is very limited, so it is very sensitive to changes in CO2 and H+
Ex. Change in PCO2 from 40 to 44 within the bloodstream cause respiration rate to double
Increased acidity in the blood leads to ….
increased ventilation
Respiratory acidosis
“Problem with breathing”
- caused by hypoventilation
- incr CO2 = incr H+ = incr acidity
- Kidneys compensate by holding HCO3 - incr HCO3 in the plasma
Respiratory alkalosis
“excessive breathing”
- hyperventilation
- decrease CO2 = decr H+ = increase alkaline
- kidneys compensate by increasing HCO3 excretion which incr CO2 and returns pH to normal
Metabolic acidosis
- LOSE HCO3 = increase H+ and incr acidity
- diarrhea
- Compensate by hyperventilation, decr CO2, incr alkalinity, kidneys excrete H+
Metabolic alkalosis
- incr HCO3, lose H+
- vomiting
- Compensate: hypoventilation, kidney excrete HCO3 (increase H+ and CO2), incr acidity
Atrium
recieves venous blood from the body
Right ventricle
Largest part of the anterior and inferior surface of the heart
- goes through the pulmonary valve > pulmonary artery > lungs
Left atrium
- forms the base of the heart
- site for the four pulmonary veins
Left ventricle
- forms apex of the heart
- blood from this area is pumped to the aorta
What supplies the heart muscle/myocardium
left and right coronary arteries
Deoxygenated blood comes through the body through ____ to reach the atrium.
vena cava
Blood flow to the heart
vena cava > tricuspid > right ventrical > pulmonary valve > pulmonary artery > left atrium > left ventricle > aorta (to the rest of the body)
Systole
Contraction of the heart
- first lub sound
What makes the lub sound?
During systole, closing of mitral and tricuspid valves
on the EKG where is systole located?
Q-T
Diastole
- relaxation of the ventricles
- second dub sound
- aortic and pulmonary valves close
- contraction of the atria forces tricuspid and mitral valves open
- ventricles relax and atria contracts
Where is Diastole located on the EKG complex?
T-R
Mechanical events of the heart
Isovolumic contraction
- Ventricular contraction (after mitral valve closure, before aortic valve opens)
- doesn’t force blood out of the heart so volume stays the same
Ventrical (Systolic) Ejection:
- pressure in the ventricles exceeds the aorta, the aortic valve opens
Isovolumic Relaxation
- ventricles relax
Ventricular filling
- immediately after the mitral valve opens, ventricles fill with blood
- during diastole
- NO change in pressure in ventricles
Systole vs Diastole
systole is the contraction phase of the heartbeat, where blood is pumped out of the heart, while diastole is the relaxation phase, where the heart fills with blood.
Lub dub sound
(S1) lub = closing of the tricuspid and mitral valves/bicuspid
(S2)dub = closing of the aortic and pulmonary valves
Electrical cycle of the heart
SA node > AV node > Purkinje of HIS
**spread of depolarization through atria and ventricles **
pacemaker of the heart
SA node, self generates action potentials and spread to other cells
Arrhythmias
- abnormal electrical depolarization in the heart
- abnormal stimuli of action potential or abnormal (drug-induced or myocardial cell death) conduction pathways( Ex. A-fib or heart block)
Describe this EKG complex
P = atrial depolarization
QRS = ventricular depolarization, atrial repolarization
T = ventricular repolarization
QT = systole
T-R = diastole
Fast myocardial AP
Phase 0
Phase 1
Phase 2
Phase 3
Phase 4
Phase 0 = Depolarization/AP causes Na+ channels to open
Phase 1 = K+ channels open
Phase 2 = Ca2+ channels open
Phase 3 = K+ cells open further, allowing K+ to leave the cell
Phase 4 = returns to resting membrane potential via Na/K pump
important for generating impulses that coordinate contraction of the heart
Slow myocardial Action potentials: SA and AV nodes
Phase 0
Phase 1 and 2: absent
Phase 3
Phase 4
- so slow they do not have phase 1 or 2
Phase 0 = depolarization, Ca2+ channels open cause Ca2+ influx (THEY DO NOT HAVE Na+ channels)
- slow conduction from AV node (allow time for ventricles to fill)
Phase 3: Repolarization, Ca2+ leaves the cell
Phase 4: slow diastolic depolarization. membrane potential spontaneously depolarizes as Na+ conductance incr. This causes SA and AV nodes to fire spontaneously
- When the heart is resting, its cells slowly start to become more positively charged inside, mainly because sodium ions start to flow in more. This makes the SA and AV nodes in the heart start firing on their own
What determines the heart rate?
speed of SA node
Blood flow through a vessel is determined by what 2 factors?
- resistance to blood flow through the vessel
- The pressure differences at the beginning and end of the vessels
Arterioles have high or low resistance to blood flow?
high resistance due to smaller diameter
While veins have a larger diameter = low resistant to blood flow
Poiseuille’s Law
Rate of blood flow
Flow (Q) = r^4/nL
nL = vessel length and vessel viscosity
Change in pressure
Flow (Q) = change in pressure/ resistance
Total peripheral resistance
- Sum of all vascular resistances within the systemic circulation is the total peripheral resistance
- Vasodilation can decr the total peripheral resistance
Starling forces
Starling forces refer to the balance between hydrostatic pressure and oncotic pressure across the walls of capillaries.
Hydrostatic Pressure (Outward Force): Pushes fluid out of the capillaries into the surrounding tissues.
Oncotic Pressure (Inward Force): Pulls fluid back into the capillaries from the surrounding tissues.
These forces regulate the movement of fluids across capillary walls, maintaining a balance between fluid inside and outside the blood vessels.
Starlings equation
0 = no fluid mvmt
+10 = vessel to tissue
-10 = tissue to vessel
Oncotic vs hydrostatic pressure
Oncotic = dependent on protein content
Hydrostatic = fluid pressure that is generated from the heart
Where are Baroreceptors found and what is their function?
- These are found in the walls of carotid artery (neck) and Aortic arch
- SNS
- Senses blood pressure changes
Where does baroreceptors send their signal?
medulla oblongata (where the cardiovascular control center is located) via vagus (CN X) and glossopharyngeal nerve (CN IX)
What hormones elevate BP?
ADH (released by posterior pit)
Angiotensin 2 (potent vasoconstrictor)
Aldosterone (released by adrenal glands)
Epinephrine/Norepinephrine
ejection fraction (EF)
amt of blood pumped out of a ventricle with each heart beat
end-diastolic volume
blood within ventricles before it contracts
end-systolic volume
blood left in ventricle after it contracts
Stroke volume
Stroke volume = end-diastolic - end-systolic
What’s a normal ejection refraction?
normal EF is 50% or greater
less than this means the pt has heart damage from heart attack or congestive heart failure
A healthy man with a SV of 72 ml and EDV of 120 ml, what’s the ejection fraction EF?
60% (normal EF)
Cardiac output (CO)
- how much blood the heart pumps in a minute
- incr as a result of increase stroke volume
- heart rate is too high = diastolic filling is incomplete (not enough time to fill the ventricles) = decr CO
Cardiac output equation
CO = heart rate x stroke volume
stroke volume increases when..
- preload increases
- after load decrease (less pressure needed to pump blood out, making it easier)
- contractility incr
Factors that increase stroke volume and contractility
- increased intracellular Ca2+
- Decreased extracellular Na+
- Digitalis (incr intracellular Na+)
- sympathetic stimulus
Factors that decrease stroke volume and contractility
- Heart failure
- Loss of heart cells due to infarction
- Acidosis and hypoxia
How does the sympathetic system affect the kidney?
- decr GFR and urine production
- increase blood volume
- increase cardiac output and total peripheral resistance so blood flow can be direct toward the heart and muscles
Angiotensin 2
potent vasoconstrictor
induces the following mechanisms
- incr ADH levels
- incr aldosterone levels
- incr Na+ levels
- incr water reabsorption in the collecting duct of kidneys
ADH (Vasopressin)
- regulates reabsorption of water
- incr osmolality due to dehydration or salt intake
- released in the posterior pituitary
- works in the collecting duct to reabsorb water
Aldosterone
- decr blood volume
- decr blood flow to kidneys and incr K+ concentration cause the juxtaglomerular cells to release renin ( converts angiotensinogen to angiotensin I)
- acts on kidneys to increase salt and water retention
Renin
- converts angiotensinogen and angiotensin I
- the ACE enzyme then converts angiotensin I to angiotensin II which stimulates the adrenal cortex to release aldosterone
ACE enzyme
- the ACE enzyme then converts angiotensin I to angiotensin II which stimulates the adrenal cortex to release aldosterone
Function of the kidney
- eliminates drugs (along with liver)
- Excretes waste products and toxic materials from protein metabolism
- Maintains extracellular volume and ionic concentration
- Maintains blood plasma volume
- Regulates BP
- Produces and secretes erythropoietin
Hilum
where renal artery enters and retinal vein and ureter exits
Describe the blood flow of kidneys
How many nephrons are in a one kidney?
1 million
2 types of nephron based on location:
- Cortical nephron (80%): outer 2/3 of renal cortex (MOST COMMON)
- juxtamedullary (20%): inner 2/3 next to the medulla (long loops)
Which kidney is lower and why? Where is the kidney located?
Retroperitoneal
- right kidney lower due to liver
Bowman’s capsule
Bowman’s capsule, also known as the renal corpuscular capsule, is a cup-shaped structure located at the beginning of each nephron in the kidney. It is part of the renal corpuscle, which is the initial site of blood filtration in the process of urine formation.
- afferent and efferent arteriole
- vascular pole and urinary pole
- parietal layer and inner visceral layer
Glomerular filtrate
fluid that filters through the glomerular membrane
Glomerular Filtration Rate
- how much blood is filtered per minute in both kidneys
- want hydrostatic pressure to be high so that it filters more
