Physiology Flashcards
How do pancreatic fluid secretions change with flow rate? What controls / secretes this?
Fluid is isotonic and secreted by pancreatic ductal (NOT acinar cells, which are in control of enzymes)
Low flow rates -> High Cl- levels (in the absence of secretin), low HCO3- levels
High flow rates -> High HCO3- levels, low Cl- levels (stimulated by secretin)
Na+ is high and K+ is low (like plasma ultrafiltrate), and this remains constant. #6574
How are salivary gland secretions affected by flow rate?
Low flow rates -> more contact with acinar cells, Na/Cl is resorbed, K+ is secreted more
High flow rates -> saliva becomes more like an ultrafiltrate of plasma because there’s no time.
What does CO * TPR =
Change in P = MAP - RAP
Where Mean arterial pressure = 1/3 systolic + 2/3 diastolic, since diastole is usually 2x as long as systole.
What happens to the pulse pressure in the elderly and why?
Increased arterial stiffness -> decrease compliance -> decreased ability to smooth out the systolic / diastolic BP differential -> increased pulse pressure (greater difference between systolic / diastolic pressure)
What determines afterload?
DIASTOLIC BP -> the force that the heart must push against
How do Beta1 receptors improve cardiac output?
Via action of Protein Kinase A
-> phosphorylation of L-type calcium channel -> improved Ca+2 entry -> improved contractility
-> phosphorylation of phospholamban -> increases active SERCA activity -> faster relaxation to improve diastolic filling
What is the formula for wall stress? What increases / decreases it?
Wall stress = (Pressure x Radius) / 2(wall thickness)
-> force with cardiomyocytes must push against
Increased by greater radius from center to wall of ventricle, and systolic pressure (afterload)
Stress is decreased via increasing wall thickness
Why is afterload approximated by mean arterial pressure?
Afterload is actually wall stress -> Force per unit area the heart must push against
However, we assume that ventricular radius and wall thickness are pretty much constant, so pressure (in the numerator of wall stress equation) is a pretty good proxy.
Pressure = Force per area
Radius = length (i.e. cm)
Wall thickness = length (i.e. cm)
(F/A * cm) / cm = F/A, Laplace’s law
How does wall stress change during ejection?
It decreases because
- The size of the LV cavity decreases -> Radius decreases
- LV wall thickness increases -> more sarcomeres pushed together (think of flexing your bicep)
What is wall tension? How does it relate to oxygen demand?
Pressure (MAP) * radius
-> it’s the numerator of the wall stress equation
Force you’re pushing against * the radius of the circular ventricle cavity
Increasing wall tension will increase oxygen demand (related to afterload)
How does blood velocity relate to cross-sectional area?
Remember P = CO*TPR
CO = Q
Q = flow rate
Volumetric flow rate (m^3/s) = flow velocity (m/s) * cross-sectional area (m^2)
Increasing the cross-sectional area for a given flow rate / cardiac output will decrease the flow velocity.
Thus, blood travels fastest in the aorta and slowest in the capillaries (largest total cross-sectional area)
How is resistance dependent on hematocrit?
Resistance = 8viscositylength / (pi* r^4)
Viscosity is mostly dependent on hematocrit
- > viscosity increased in polycythemia
- > viscosity also increase in hyperproteinemia state
Viscosity decreased in anemia (lower hematocrit)
What should you think of Total Peripheral Resistance as in order to get questions right? How will it affect cardiac output and venous return?
Arteriolar resistance -> since most of the resistance is at the level of the arterioles
Decreasing TPR -> decreases arteriolar resistance
- > more blood reaches veins = increased venous return
- > less pressure to push against = decreased afterload -> increased cardiac output
What is the median systemic pressure? What changes the x-intercept of the venous return vs right atrial pressure graph?
X intercept represents the median systemic pressure -> pressure in veins / arteries if there was no cardiac output
Increasing volume or venous tone -> increased RA pressure at 0 cardiac output (X-intercept)
Decreasing volume or venous tone -> decreased RA pressure at 0 cardiac output
Remember that venous tone is what maintains venous return and RA pressure (prevents pooling of blood in veins due to too much compliance)
How does an AV fistula affect TPR and what will it do to median systemic pressure overtime?
Lowers TPR -> increased cardiac output and venous return, since you have a low resistance system to push thru
Despite increased CO, most CO is going thru fistula -> decreased systemic perfusion -> decreased kidney perfusion
Activation of RAA system by kidney -> fluid retention, increasing median systemic pressure over time (X-intercept)
Waves of jugular venous pulsation:
a wave -> Atrial contraction, corresponds with s4
c wave -> RV Contraction, with tricuspid valve bulging into right atrium, corresponds to just after s1
x descent -> downward displacement of closed tricuspid valve during rapid ventricular ejection
v wave -> “villing” of right atrium against closed tricuspid valve
y descent -> RA emptYing into RV before next cardiac cycle (absent in cardiac tamponade -> cannot fill, prominent in constrictive pericarditis, with abrupt stop)
When does the physiologic delay in splitting happen?
Inspiration -> P2 happens even later due to increased venous return. It is normally after A2 anyway, just becomes more prominent.
What causes wide split vs paradoxical split heart sounds?
Wide split - right BBB, pulmonic stenosis -> delayed RV ejection, slow P2 closure
Paradoxical split - splitting on expiration, none or smaller on inspiration - left BBB, aortic stenosis -> delayed LV ejection, slow A2 closure
What causes fixed splitting / why does it happen?
Equalization of left and right atrial pressures with an atrial septal defect
-> elimination of respiratory variation in splitting.
How does increasing afterload affect an aortic stenosis murmur?
Decreases it
-> will decrease the transvalvular gradient, lessening the murmur
How does a Valsalva manuever destroy a supraventricular tachycardia?
Inhale / strain -> preload is reduced as blood is held in lungs -> reflex tachycardia
Release -> massive rush of blood from lungs to heart -> increased preload / contractility -> reflex bradycardia
-> massive parasympathetic input terminates the SVT
How does squatting affect preload / afterload?
Increases preload -> you get closer to the ground and also use muscles to force blood back into your heart
Increases afterload -> much like a handgrip, muscle contraction increases load you must push against.
How does squatting affect aortic stenosis murmur?
Increase in preload is more significant than the increase in afterload
-> increases aortic stenosis murmur
Remember that preload is necessary to maintain perfusion in patients with aortic stenosis -> cardiovert if they have AFib
When is a PDA the loudest?
At S2
-> highest blood flow at end of systole
What channel in cardiac pacemakers do ACh / adenosine and symphathetic nervous system modify?
I-funny channel, nonselective Na/K channel
- > ACh / adenosine decreases firing
- > Ne / E increases firing
-> affect the phase 4 slow diastolic depolarization
Normal times for PR interval, QRS compelx, and QT interval?
PR interval: <200 ms (1 big box)
QRS complex: <120 msec (3 small boxes)
QT interval: <450 ms
What’s the J point?
Junction of the end of the QRS (ventricular depolarization) and start of ST segment (sustained ventricular depolarization)
What electrolyte imbalances can precipitate torsades?
Hypokalemia (impaired repolarization), hypomagnesiemia (explains why Mg+2 can treat the arrhythmia)
What does WPW syndrome do to the QRS and PR intervals? What is the tachycardia which can result?
QRS - widens it (delta wave via bundle of kent)
PR - shortens it (Due to premature appearance of delta wave before Q wave)
Tachycardia - atrioventricular re-entrant tachycardia
How can you tell if the pace of the ventricles in 3rd degree heart block is set by the AV node or the His Purkinje system?
AV node - pace is 45-55 bpm with narrow QRS
Purkinje system - pace is <40 bpm with wide QRS
What is the mechanism of the natriuretic peptides?
Signal by increasing cGMP levels -> vasodilation
Also dilate the afferent arteriole of the kidney and constrict the efferent arteriole -> increase GFR
What drug is a recombinant natriuretic peptide?
Nesiritide -> BuMP the GruMP, it is necessary to turn the tide
What nerves transmit blood pressure information to the brain, and where do they signal to?
Aortic arch - via vagus nerve (X) -> nucleus solitarius of medulla
Carotid sinus - via glossopharyngeal nerve (IX) -> nucleus solitarius of medulla
What is the mechanism of the Cushing reflex?
Increased ICP -> poor perfusion adn increase pCO2 with decrease pH. Body senses the need to increase cerebral perfusion
Increase SANS -> hypertension + tachycardia (phase 1)
Phase 2 -> hypertension sensed by peripheral baroreceptors -> induce increased parasymphatetic tone
-> bradycardia with hypertension (sympathetic mediated vasoconstriction with vagal bradycardia)
Phase 3 -> increased pressure on medulla induces irregular respirations
Where are the peripheral chemoreceptors located? Do they respond to O2?
Located in carotid / aortic bodies (With barorceptors)
Peripheral ones respond to O2 and CO2.
Oxygen response is really only important in COPD where hypoxemia drives respirations. Correction of hypoxemia -> decreased respiratory drive in these patients, as they become desensitized to hypercapnia.
Central = Co2 only = located in the medulla.
What is the rule for remembering total body water, intracellular and extracellular volume?
60-40-20 rule
60% of total body weight = water
40% of total body weight = ICV
20% of total body weight = ECV
i.e. Intracellular volume is twice the extracellular volume
Extracellular volume = plasma volume (~5 L) + interstitial fluid (~10 L)
What would be the approximate volume of distribution of a drug that distributes to total body water? How can it be higher than this?
70 kg (average person) * 0.6 (60% = TBW) = 42 L
Around 42L is a hydrophilic molecule which is uncharged and can spread out.
Can be higher than this if lots of drug is administered and it collects in tissues, with a low measured plasma concentration (highly lipophilic)
What is the mechanism of pulsus paradoxus in cardiac tamponade?
Decreased area for RV to fill up in inspiration (increased venous return) leads to an exaggerated bowing of IV septum into the LVOT -> limiting stroke volume / CO of LV.
> 10 mmHg drop during inspiration #1782
How do you tell apart LV enlargement from mitral regurg vs hypertension?
Mitral regurg - will be ECCENTRIC hypertrophy (to accommodate volume overload) -> no increased thickness of wall, just increased chamber volume
Hypertension - CONCENTRIC hypertrophy to deal with greater afterload -> increased wall thickness #181
How does left heart failure lead to right heart failure?
Back of blood in the lungs actually leads to leakage of proteins into interstitium / endothelial dysfunction -> decreased NO, increased endothelin -> development of pulmonary hypertension -> RV failure #198
Does insulin cross the placenta?
NO!
Fetal macrosomia is due to endogenous production of insulin in response to maternal high blood sugar
What does GLUT5 transport?
Fructose
What two signalling pathways are utilized by insulin and which one is unaffected in Type 2 diabetes, mediating increased cell growth?
- PI3K/Akt/mTOR pathway, also known as PKB pathway -> controls GLUT4 / anabolic effects
- RAS/MAPK pathway -> responsible for cell growth, DNA synthesis. Unaffected in Type 2 diabetes -> accounts for how diabetes is associated with cancer.
How does glucagon affect insulin levels?
Glucagon STIMULATES insulin release -> to allow target tissues to take up sugar.
What cancer types release PTHrP?
Q + urinary tract + BRCA
Women and men have similar levels of testosterone in circulation. Why don’t women have hirsutism?
Women have increased SHBG relative to men.
What stimulates secretin, what releases it, and what are its actions?
Acidic chyme in duodenum stimulates release by S cells
Actions - increase pancreatic and Brunner’s glands bicarbonate secretions, decrease gastric acid secretion
How does bilirubin get made and transported to the liver?
Made in reticuloendothelial system (i.e. spleen)
Heme -> biliverdin = open chain form of heme porphyrin ring. (Via heme oxidase)
Unconjugated bilirubin made from biliverdin, and transported via albumin in blood (UCB is water insoluble, needs to be conjugated)
What is the fate of bilirubin once it enters the intestine?
Bacteria in the gut deconjugate it to urobilinogen.
Urobilinogen can be excreted in stool after being made into stercobilin -> gives the stool its brown color.
Some urobilinogen is reabsorbed -> can be excreted again in bile, or transported to kidneys where it is oxidized to urobilin -> gives the urine its yellow color.
What are the embryonic globins?
Zeta and Eta chains -> produced in fetal yolk sac
Who is the universal donor and recipient of plasma?
Universal donor -> AB (no anti-RBC antibodies in plasma)
Universal recipient -> O (can handle any anti-RBC antibodies in donor plasma)
Order of migration distance in hemoglobin electrophoresis?
Accelerates - farthest - HbA
Fast
Slow
Crawls
What effect does estrogen have on the myometrium?
Increases endometrial excitability via upregulation of gap junctions -> ripens it for labor during pregnancy
What type of estrogen has the greatest increase in pregnancy?
Estriol -> indicator of fetal well-being
