Physio Flashcards
Cardiac Pressures
sys + dias for 4 chambers, pulmonary artery + aorta
RA - <5 mmHg RV - 25/5 PA - 25/10 LA - <10 LV - 120/10 Aorta - 120/80
Renal Excretion Rate calculation
what is used to estimate GFR and how?
Inulin clearance estimates GFR (freely filtered + not secreted or reabs. in tubules)
RER = total filtration rate - total tubular reabsorption rate
total filtration rate = GFR x plasma conc. of substance in question
Fluid Balance Changes in…
Diabetes Insipidus
Hyperosmotic volume contraction…
loss of HYPOtonic urine causes overall volume loss (ECF and ICF) with HYPERosmotic blood
Fluid Balance changes in…
GI hemorrhage or diarrhea
Isotonic ECF loss
blood is ECF and is obviously isotonic with blood…
no changes in ICF or blood osmolarity
Fluid balance changes in…
adrenal insufficiency
Hyposmotic volume contraction (with ICF gain)
no aldo > NaCl and ECF loss > hypoosmotic plasma > fluid shift to IC space
Fluid balance changes in…
hypertonic saline infusion
Hypertonic volume expansion (with IFC loss)
hypertonic fluid addition to ECF (plasma) > water drawn out of ICF > further ECF expansion
Fluid balance changes in…
primary polydipsia -or- SIADH
Hyposmotic volume expansion (clinical euvolemia)
hyposmotic intake > fluid shifts into cells > both ICF and ECF increase + osmolarity decreases
ECF increases less due to normalization via ANP/aldo balance
High Altitude Sickness
initial ABG?
compensated ABG (when?) ?
“Hypobaric Hypoxia” - % of air that is O2 is same, but lower barometric pressure means decreased pO2
Initial - pH is significantly high (7.5+); pCO2 is low (hyperventilation) and pO2 is low
Compensated WITHIN 48 HOURS - bicarb excretion leaves pH NEAR-NORMAL, while pCO2 and pO2 are still low
Vessel with lowest PO2
Coronary sinus
Myocardial oxygen extraction is the highest in the body (60-75%)
Formula for expected CO2 level during respiratory compensation of metabolic acid-base disorder
Winter formula
PaCO2 = [1.5 x HCO3] + 8 +/- 2
gives a range of 4 mmHg, if the CO2 falls below that range = additional respiratory alkalosis
if above that range = additional respiratory acidosis
Which substance can be used to estimate renal blood or plasma flow? Why?
PAH
it is filtered AND actively secreted, so the rate at which the kidneys clear PAH reflects RPF.
Must use both urinary and plasma concentrations to calculate, plus urine flow rate.
(remember PAH for Plasma!)
How can RPF be calculated with PAH?
RPF = [urine PAH] x urine flow / [plasma PAH]
What affects filtration fraction?
FF is decreased by DECREASED GFR or INCREASED RPF
Functions of DAG and IP3 in the Gq > PLC > Ca release pathway?
PLC hydrolyzes PIP2 into DAG and PIP, then…
DAG - direct PKC STIMULATION
IP3 - mediates Ca release from ER > major stimulator of PKC
effect of ADH other than vasoconstriction + water reabsorption
increases urea reabsorption in the INNER MEDULLARY COLLECTING DUCT
this accentuates the medullary concentration gradient > maximizes free water reabsorption
large releases of ADH as in hypovolemic shock can thus result in ELEVATED SERUM UREA and a BUN:CREAT RATIO >20:1
what 2 molecules are FREELY FILTERED by the glomerulus and NOT REABSORBED / SECRETED by the tubules?
INULIN
MANNITOL
what 3 substances are FREELY FILTERED by the glomerulus and REABSORBED by the tubules?
there are many more like this, but these are some classic examples
SODIUM - heavily reabsorbed, FENa normally <1%
UREA - passive resorption in pct and inner medullary collecting duct; passive secretion in thin parts of Henle loop; regulated by ADH (increases inner medullary collecting duct resorption + thus water resorption)
GLUCOSE
What 2 substances are FREELY FILTERED by the glomerulus and actively SECRETED by the tubules?
PAH
CREATININE (is secreted somewhat, but no nearly as much as pah)
PTH kidney effects
increased Ca resorption
decreased Pi resorption
PTH bone effects
indirect osteoclast activation by…
osteoblast activation > RANKL secretion
decreased OPG secretion > higher RANKL activity
What is the “Haldane effect”? (2 effects, really)
In the lungs, at high pO2, hemoglobin will have…
1) DECREASED CO2 AFFINITY - unloads CO2 carried from tissues (off carbamino terminals of alpha/beta subunits); abt 10% CO2 carried to lungs in this form
2) INCREASED ACIDITY OF Hb MOLECULE - stabilization in the “T” tense state > release of H+ from histidine side chains; most CO2 is carried to lungs in HCO3- > H+ ions combine with bicarb to form carbonic acid, then water and CO2 for further co2 release
What is the “Bohr effect”?
more specifically, what happens to O2 and CO2 during the Bohr effect?
in peripheral tissues, HIGH pCO2 causes an INCREASED AMBIENT ACIDITY (H+ conc.) that shifts Hb dissociation curve RIGHTWARD > unloading of O2
abt 10% of CO2 forms “carbamino adducts” with Hb molecule itself
the rest forms H+ and HCO3- via RBC carbonic anhydrase > H+ binds Hb to stabilize deoxygenated form
HCO3- is exchanged (out to plasma) for chloride (into RBC) via the “chloride shift”
Proximal convoluted tubule
handling of water? solutes? relationship of tubular fluid to plasma?
water and solutes BOTH reabsorbed
tubular fluid is ISOTONIC (300 mOSm/L) to blood
Descending limb of loop of Henle
handling of water? solutes? relationship of tubular fluid to plasma?
ONLY WATER is reabsorbed, not solutes
tubular fluid becomes HYPERTONIC (> 300 mOSm/L, and up to 1200 in the medulla)
Ascending limb of loop of Henle
handling of water? solutes? relationship of tubular fluid to plasma?
ONLY SOLUTES are reabsorbed, not water
tubular fluid becomes HYPOTONIC (< 300 mOSm/L)
(thick + thin ascending limbs are the main region of urine dilution, mainly via NaCl resorption)
Distal convoluted tubule
handling of water? solutes? relationship of tubular fluid to plasma?
is relatively impermeable to water + SOLUTES ARE STILL REABSORBED, so…
tubular fluid is the MOST HYPOTONIC of all segments in the DCT (about 100 mOsm/L)
Collecting Duct
handling of water? solutes? regulation?
primary region of urine concentration via ADH-mediated water resorption
ADH mediates aquaporin translocation (V2 > Gs > cAMP > Aq-2) and the high medullary interstitial osmolarity drives diffusion of water through the aquaporins out of the tubules
Hepcidin
what stimulates/inhibits its release?
it’s an ACUTE PHASE REACTANT
stimulated by - HIGH IRON and INFLAMMATION
inhibited by - HYPOXIA and ERYTHROPOIESIS
How does HEPCIDIN influence body iron stores?
Hepcidin binds the FERROPORTIN on enterocytes and macrophages > causes INTERNALIZATION of ferroportin and less release of iron from GI into circ or from macrophages
Baroreceptor firing rate
how does hypotension affect it?
hypertension?
hypotension - firing rate DECREASES and baroreceptor reflex helps restore bp via increased HR
hypertension - firing rate INCREASES and baroreceptor reflex lowers bp via decreased HR
what changes are detected by CAROTID baroreceptors? and by AORTIC baroreceptors?
carotid detects BOTH increase and decrease in BP
aortic detects ONLY increases
What are the signaling mechanisms and functions of the V1 and V2 receptors for vasopressin?
V1 - Gq > VASOCONSTRICTION, myocardial hypertrophy, platelet agg, GLYCOGENOLYSIS and uterine contraction
V2 - Gs > insertion of Aquaporin-2 into apical membrane of collecting duct cells; release of vWF and FACTOR VIII; plus VASODILATION
What is the LENGTH CONSTANT in nerve conduction physiology?
aka?
how does myelination affect it?
aka SPACE CONSTANT
the DISTANCE an AP can propagate along an axon WITHOUT ACTIVE REGENERATION BY ION CHANNELS
myelination INCREASES length constant
What TWO RESISTANCES does the LENGTH CONSTANT of a nerve depend on and how?
AXOPLASMIC resistance and MEMBRANE resistance
when axoplasmic R is lower than membrane R, the AP will propagate forward along the axon rather than dissipating out through the membrane
MYELINATION increases membrane R > aids axonal propagation
what is TIME CONSTANT in nerve conduction physiology?
is based on what?
time it takes for membrane potential to respond to a change in permeability
based on membrane RESISTANCE and CAPACITANCE
How does myelination affect the time constant?
it decreases capacitance and increases resistance of the membrane, resulting in a LOWER TIME CONSTANT
meaning the membrane potential can CHANGE FASTER when nerve is myelinated
How is bicarbonate dealt with along the PCT?
it is ACTIVELY REABSORBED due to CARBONIC ANHYDRASE activity (inhibition > excretion of bicarb > metabolic acidosis; eg, acetazolamide)
so on a chart of solute conc. along PCT, bicarb is hyperbolically decreasing
Differential handling of PAH, inulin and creatinine in the PCT
PAH - freely filtered and then 90% of remainder is secreted in PCT
Creatinine - freely filtered and then only 20% of remainder is secreted in PCT
Inulin - freely filtered and then NONE is secreted
(but conc. of all three increases along length of PCT because water is reabsorbed and they are not)
How does Ca++ promote muscle contraction?
(2 molecule names)
(within the muscle cell, not referring to presynaptic Ca++ influx that stimulates ACh release)
Binds to TROPONIN C and then TROPOMYOSIN is displaced from actin so that myosin can bind
How does muscle cell action potential result in Ca++ release from the SR?
2 components
causes a conformational change in the cell membrane 1) DHPR (dihydropyridine receptor) which is mechanically coupled to the sarcoplasmic reticulum-surface 2) RYR that releases Ca++
After Troponin C binds Ca++ and tropomyosin displacement frees up myosin binding sites…
what 2 steps occur before myosin release?
and what is the status of myosin-ADP/ATP binding during this?
- CROSSBRIDGE formation - myosin binds actin with its attached ADP + Pi
- POWER STROKE - myosin head cocks back, pulling actin with it, which occurs via the RELEASE OF Pi from ADP
What happens between the power stroke and myosin detachment from actin?
(2 steps)
- ADP IS RELEASED from myosin
2. ATP BINDS to myosin > myosin head releases actin (and Ca++ is resequestered in SR)
What causes the myosin head to return from the detached-from-actin-but-still-bent state to the “cocked” high energy (90 deg angle) state?
ATP hydrolysis to ADP + Pi
What is a miniature end plate potential in NMJ physio?
the EPP produced by a SINGLE ACh vesicle
the smallest possible depolarization that can be induced in a muscle
usually around 0.4 mV - would NOT be reduced in response to something like botulism because botulism just inhibits vesicle release, but if a vesicle is released it will still have an effect and make an mEPP
How do the oxygen dissociation curves of MYOGLOBIN and HEMOGLOBIN differ?
Hemoglobin - has a SIGMOIDAL curve with a “P50” of 26 mmHg (meaning 50% saturation at pO2 26); due to increasing affinity as O2 binds each of 4 heme grps
Myoglobin - has a HYPERBOLIC curve with a P50 of 1 mmHg; is monomeric with a single heme group and higher affinity than Hb
What is the relationship of structure + function between single hemoglobin subunits and myoglobin?
both alpha and beta subunits of hemoglobin are very similar in secondary/tertiary structure to myoglobin so…
they bind O2 with similar affinity (high) when in monomeric form (a HYPERBOLIC o2 dissociation curve, ie left-shifted)
