a "For inquiries, visit www. topnotchboards PHYSIOLOGY Enrico Paolo C. Banzuela, MD UP College of Medicine Class 2005, ‘Approach to Topnotch Physiology é Please buy the following: Physio BRS Sg Bd Canong Physiology 23+ Ed or 25th Ed : + Tobe used as major ks wil help you n + they're very good this subject ‘ + Lecture utizes¥patnly Physio BRS supplemenged bother sources (¢ Guyton, Berne ang bevySGanong); those that you don’t under tbr ned fuer discussion, tlet to Physio’BRS and Ganong + Wewon'gee}taicaver all of physio; wel try to cover: * «What you need asa General Physician (must- Sy knows), uo Mess important tops that has been asked in the past (nlce-to-knows) + Index Student: determines pace ofthe lecture Guided highlighting system: highlight only those that are bold and lealicized + For Topnotch Essentials: we've decided to give you this Physiology handout as a bonus material (originally, you're supposed to receive only the Physiology Pearls Handout). Answer Key tothe questions has been provided at the end ofthis handout. “TOPNGTCH BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C, BANZUELA, For inquiries visit www.topnotchboardprep.com.ph or https: /ww wad facebook. com/topnotchmedicalboardprep/ :om.ph or https://www, facebook, com/tepnotchmedicalbosrderep/ MODULE. PAGE iT. Cell Physiol 1 (Ca Neuro Phystetgg——— a ‘3. Cardiovascular Physiology 22 | 4. Respiratory Physiol 32 $. Renal Physlolog 40 Gastrointestinal Physiology 50 7. Endocrine Physlology 37 Hema and Special Environments Physiology 8 UL Transport Aross Cll Membranes Ul, Osmosis IV, Diffusion Potential, Resting Membrane Pagengigl, Action Potential ey \, Neuromuscular and Synaptic Transmission, ML Seeetal Muscles, x. Vil, Cardiac Muscles ‘VIL Smooth Muscles , 1X. Comparison of Skeletal Muse fh Muscles and Cardiac Muscles ‘1.1 GEL! [BRANES CELL MEMBRANE ‘© The Guardian of isdfvides ‘the body into ECF and ICF compartments + Made up of us f+ (Fluld-Mosale Model) 2558; lip lds Leaflet: Phospatidyicheline, Sphingomyelin, atidylethanolamine jermeability to water-soluble substances 0 49%: Other lipids: glycollpids confer antigentcity 0.3% Carbohydrates fhner Leaflet: Phosphatidylsarine, Phosphatidylinositol 19: Cholesterol: confers membrane fluldity and Pe + sadded wth he allowing proteins: inegra Proteins * Har dghtatchment (needs detergent to remove) Using hydrophobic intractions «span tect cll membrane + Penna on hoes Se corr (L7, part antiport) ATPdependent rs Peripheral roaing TT anPendet Transport "as Tose atacment sing electrostae neracons + Found in th ne eat ote leat « Reaction wt diferent substances Water + Undergoes Osmast va Aquoporins Lipid Scuble(Non pla iyrophobl Substances * Substances underg Slnple Dison 0 Water-Soluble (Polar, Hydrophilic) Substances * Substances underg Carrier medited Tronsport Page 1 of 85TOP IDQUINIGS NISIE weewr topnotchboardorep.com.ph or httpsi//www, facebook, com/topnotchmedicalzoardpren/ TOCATION For tight intercellular adhesion __* Epithelium + Ring-shaped % Epithelial & endothelial cella myocytes 1s Fascia | omuleAdnerens create trtce rea forconact _* teeated dit ofcardae 4 : muscles . t Zonula Oceludens * (+) Reticular pattern; « Leaky: PCT, jejunum T moveren functor «divides cal tuto api . total and bascltera see (abt yunctions) —* Satcateraleide anaceecaoe coe Jrtcalular Transport movement Gap junctior * For rapid intercellular ‘Cardiac and uni gh", Punctional Unit: ConneXON (Its elms sommuntcation muse Subunit: ConnexIN) the spread of acon potentials are {) pp junctions {ej sarcoplnmie ecuug fy ® | (©)sarcoplsmic retical | Ghimerdmddaion sg | @hmitochondia, oy SR __atawe pea i | eye eae: ON TOPNOTCH BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C. BANZUELA, MD For inquiries visit www.topnotchboardprep.com.ph or tas, facebook, com/topnotchmedicalboardpreg/ tt of as1.2 TRANSPORT ACROSS CELL MEMBRANES: eto eas Ton: Carrer MaditedPremspare Reon > 4 Oaygen Miropen CO qsimale Lone 1 © eal lpia narones, Bigulon + (Paeive—_nertale drugs * Divided In Pino: and Propo [cigxscwrasis ___+ Hormonesand Nts | i. Carriersmediated Transport »Lcone> A) Qumosis Heone © Water 7 Heone> ‘BL facLiued Leone) * GLUT transporters, | Dion (amive,* AAwansporers | [Downhity © Na-K-ATPase pump, | “Heatran ee ucone> —_patetaeai amach, «Heatran pimpin Gaiman Hcom) "parent el (ey) Upniy —C#ATPase pumpin che | . cell membrane & SR. s multerugressance anspor + SGLTa nme ST, © SoLT2inehe cr * Leone > NA-K-2Cl in TAL of LH, Denda teatty, + NeCaexhangen amos. Mest Uphill) + Na-H exchange in the PCT (kidneys) ‘SPECIAL NOTES: SIMPLE DIFFUSION “ * Measured using the formule ‘ oJ PA (C1-Cz) : * Where idl J =f Pow (omal/ae, : * P= permeability (cm/sec), c © Azarea (cm2), © CL higher concentration! (mmol/L) * (2 = lower concentration2 (mmol/L) «© P (permeability) in the formula J= PA (Ci-C2) is increased by the following: ‘olncreased Oll/water partition coefficient of solute (increases solubility inthe lipid of the membrane) 0 Decreased Radius of solute ‘Decreased Membrane Thickness + Small Hydrophobic Solutes (Oz, C02): high permeability 2 Hydrophilic Solutes (Na, K): uses aquaporins or transporters to cross cell membrane PHYSIOLOGY HANDOUT BY ENRICO PAOLO C. BANZUELA, MD. TOPNOTCH BOARD PREP com. ph oF http://www. facebook. com, For inquiries visit www. RE scans ieapareesi eect Ta | tiger (A Batman oa | big ts lft pre crore | {© boving th thctnes st ager (0) Doubling the concentration difrence ofthe solute acrovs the : Se seronsthe ‘Solutions A and Bare sgparated by a mambrane thats permeable to ‘rea, Solution A i 10 mM urea, and solution Bis § mM wre. Ith concentration of urea In solution Ats doubled, the fux of urea across the membrane will (A) double SPECIAL NOTES: CARRIER-MEDIATED TRANSPORT * laportan Charatan: tendon Stereos substances may have ° peat, but lfarent “tape jlucos i is fataedion: number stgrungteagh Once all carriers arated up or etratd, aa oppor becomes constant ¢ Maximum) © Competition: different solutesaniay compete for same carrier eee can tae Seg 30 ‘SPECIAL NOTES: ZACILITATED DIFFUSION + Atlow-solute concentration: FD is faster than SD « Athigh-soluta concentration: FD \s slower than SD + GLUT: BBB ,Pancreas, Basement Membrane of SI * GLUT; Muscles, Adipose ‘*-GLUT 5: for fructose transport from S! lumen to SI cell © 0 Og Exractlarspace Sg Sy ° ° oo 6 ° Protein g ° ° : ome no ye: 2 0 "eo © intracellular space SPECIAL NOTES: PRIMARY ACTIVE TRANSPORT + Source of energy: ATP hydrolysis «+ Na-K ATPase Pump © 3 Sodium Out, 2 Potassium In (Mnemonic: “TRINA 70-K- aN’) ‘0 Keeps Na tn the ECF and K in the ICF © Contributes to RMP (-4mav out ofthe -70m¥) ‘© Contributes to Basal Metabolic Rate (BMR) ‘0 Some cardiac Na-K-ATPase pump inhibited by Digoxin © Foundin the basement membrane side except for Choro + Ca-ATPase pump inthe sarcoplasmic reticulum: SERCA + HeK-ATPase pump inthe lumen ofthe parietal cells ofthe stomach: Proton Pump Outside our Page 3 of 85SPECIAL NOTES: SECONDARY ACTIVE TRANSPORT + Source of Energy: downhill ransport of Na (Indirectly relies on ‘Na-K-ATPase pump) + Co-Transport (Symport): solutes move in same direction * Countertransport (Antiport, Exchange): solutes move in ‘opposite directions = + Sodium-Glucose Cotranspore| ‘© Namovea downhill, Glu moves uphill, hath move In the same ‘direction (Cotransport) oe SGLT-1; SI, SGLT-2: Kidneys Na aiucoee ‘° Semevemene. Nar @” zen + Sodium-Colclum Countertransport (Na-Ca Exchange) ‘oNa moves downhill, Ca moves uphill they move in opposite directions © Na-Ca exchange inthe cardiac membrane: decreases intracellular Ca ‘© MOA of Digoxin: inhibits cardiac Na-K-ATPase Pump > {nhibies Na-Ca pump > greater intracellular calelum > renter cardiac contractility Which of the following characteristics is shared by simple and faciliated diflusion of glucose? | (A) Occurs down an electrochemical gradient (8) Is saturable (C) Requirés metabolic energy (0) Is inhibited by the presence of galactose | SESE sei ane geatl |" Transport ofD- and L-plucose proceeds at the fame rate down ag “| x | (A) Simple difuston % (8) Faclitateddifusion (C) Primary active transport (0) Cotransport () Countertransport hich ofthe following would occur as 2 res TPase? processes is involved f transport of slucose from the jumen into # small Intestinal cell is inbbited by abolishing 4° gradient across the cell membrane? : (A) Simple dgiion | () Fact fon (C) Primary acuve transport (0) Cotransport | Adenosine wiphosphate (ATP) i ured inairealy for which ofthe following processes? (A) Atcumulatlon of Ca™by the sarcoplasmic redeulum (SX) j {8) Transport of Na from intracellular to extracellular ld | (© Transport of K from extracellular to ntacalllaruld | (rare rom partum ofc stash | |) abrartion of gun bynes epee eal | Anew drugis developed that blocks the ranaporer for H- secretion in fastrc paretal cell Which of the flowing transport processes being Inhibiea? (A) Simple dtusion | | (8 Facltated auton | (©) Primary active transport i | | (0) cotransport (@) Councertras | © coumertanepor From yi RS From! BRS Ed :3 OSMOSIS 1. OSMOLARITY ‘= Concentration of osmotically active particles Ina solution ‘+ Measured in Osmoles/Liter + "Pogi* polnts of water ‘o The higher the osmolarity ofa solution, the more itattracts nt were as open soe ‘Geir entree rs ol/IeNdmber of partiies/inol + Normal ECF Orel 500 moony Normal ICF Osmolarity: 300 mOsm/L + *ECP and ICP are lsoosmotic relative to each other! ‘* Movement of water across a semipermeable inembrane from a solution with low solute concentration to a solution with high solute concentration + Driving Force: Osmotic Pressure © Osmotic Pressure computed using Van Hoe, ee gx CxRT where: = osmotic pressure (mm Hg or atm) g= number of particles in solution (osm/mol) Cx concentration (mol/L) Rew ges constant (0,082 L—atm/mol—K) Te absolute temperature (0 “nu, EFFECTIVE OSMOTIC PRESSURE “Ss effective Osmotic Pressure = Osmotic Pressure x Reflection Coefficient : + Same effective osmoti pressure: Isétonic + Higher effective osmote pressure: Hypertonic + Lower effective osmotic pressure: lc + Rule: water undergoes osmosis from hypotonic solution to hypertonic solution + Osmotic pressure exerted by proteins: Oncotic Pressure or Colloid Osmotic Pressure REFLECTION COEFFICIENT (OSMOTIC COEFFICIENT) ‘+ Number between zero and one describes ease by which solute ermeates a membrane RC__ DESCRIPTION EXAMPLE NOTES One * No solute * Effective Osmole L. penetration (creates Osm P) Beoween Zero and * Somesolute » Most One Penetration substances | Na inward current + Repolartzation ‘0 Closure of Na-Inactivation Gate (ligate) > stop Na inward o Opening of K gates > K outward current Rev BANZUELA, MD .cebook.com/opnot aa healboar Page 5 of 85— SPECIAL NOTES: ACTION POTENTIAL ata Dl a en eaten laren nara ( Knew developed loc anantheds blocs Ne channels nerves. 1 | Which othe folowing elects onthe action potential would tbe | expected to produce? 1) Decrease the rate of rie of the upstrka ofthe acon potential {6} Shorten the wbroltareractory perioa, | (ChAbolsh the hyperpolarsing aerpotatial (0) Increate the Nar equibrum potential (Decrease the Nav equlllbriam potentiat | me | aaah abel potat onthe selon poeendnT the Kclovestio. | slecrochamical equlorum? aa @2 ses ed 13 | 4 ume @s = store pda negative (B) ther negative | negative (0) there is netinw negative (8) of normal magni (©) of normal magni (€) will nooccur TOPNOTCH BOARD PREP PHYSIOLOGY For inquiries visit www.tor -Egeligeratene cee ciel ae | Age atom ent ene cel rir bce: ne Guy crrent ax the el interor becomes lest | (© theres inward current andthe call icerir becomes mare [negate ica by Daring a nerve scion potehial a wimpulus is delivered as indleated by ae eow shown inthe following figure. In response tothe stimulus, second action potential (A) of smaller magnitude will occur | thus causing Naginactivation gates to igi en “i i 1 ' i yard current and the cell interior becomes less “ From Physilony ORS. 64 | irae will occur tude wil ccur, bt wll be delayed {D) will occur, but will not have an overshoot urna J ae i a HANDOUT BY ENRICO PAOLO C. BANZUELA, MD réprep.com.ph or https://www facebook.com/topnotchmedicalboardprep/ TERM DESCUPTION ce | Depolarization + Make the MP more postive | ce Typerpolarization + Make the MP more neqatv Tle? 7 © Postve charges flow Into the call Inward Gurrent * causing depolartzation oy Josep Be 02 + Poaltve charges Now out ofthe cal —hat Foca Fapanoe ora Ha a mere pote Outward Current * egusing hyperpolarzatn earrbenwnn pit an peau iY ov) © MP where AP Ineviable (A) Movement of Mag the met inward current» net oveward (2) Movement of nang } Threshold current | ieee seca ‘oNa inward current> K outward Hnerruene tet pump - currant from K leak channels | tin nonSiprene-X ump Grershoat TBezursduringan APwhenMP>Onv—| s _ RENE | Terie Songata mambrape penal chat Undershoot (After Sra petbeatpene Sand pein 7 (ee leur above) hyperpolarization) * O&€urs during an AP when MP < RMP er rec aco Ne tof te — ~ Occurs during an AP when no new AP Dorementt ft the cal Absolute eigg_einbeelictednamaver ow argethe | “| “t) Movement eat tary sumulus 11 Aaron tee um \ +a a-Inactvation go |) Inbiden ofthe Na Basis: closed Na-Inactvation gates, Ibi 7 mugen ee | 7 Occurs during an AP after ARP when @ Sara ma wih ara meine ope Tae | Relative new AP canbe elited by required | Catytbeomatty ner abretar valves isan elevated serum Relive period Pretertanusual Neinwardeurrent | | ction Te eae eum ane asc wens Decase aa) + Basis profonged opening of Fy eng mentrae pi gpepltd channels; {B) thee equllrium potenal is hyperpolaraed \ © Occurs when cell mgmibrané is (hie eeu pal zp depolarized busor rapidly enough. chanel tre dosed by depoleation ccommodetios el De eatin {2} channels ore opened by depolarization from Posing Dis, 66} PROPAGATION OF ACTION POTENTIAL + Done through local currents to adjacent areas ofthe membrane + Conduction velocity is increased b ¢ larger the nerve fiber, the smaller the internal resistance, and the faster the conduction velocity ‘oMyelination: myelin acts as insulator. APis regenerated in, ‘Nodes of Ranvier (unmyelinated portions of the axon) “The velocly of conduction of action potentials alonga nerve willbe | increased by | (A) stimulatag the Nasoke pump |G) inhibiting the Nas-ke pump | (0 decreasing the diameter ofthe nerve (0) myeinating the nerve ) lengehenig the ners Ober rom Pilona 95 Page 6 of 851.5 NEUROMUSCULAR AND SYNAPTIC TRANSMISSION PARTS OF THE NEURON toner ‘ Dandrites: where NT receptors are found ‘+ Cell Body (Soma): where organelles, nucleus is seen inital Segment: whore AP starts + Axon: transmitting portion + Nodes of Ranvier: unmyelinated portion of the axon «© Neural Fibril: branches of the axon + Terminal Boutons (End-Feet): distal tips of the axon + Voltage-gated Calcium Channels: stimulated by AP: triggers release of NT into the synapse ‘+ Synapse: space between neurons © NTs: either excitatory (depolarizes) ot inhibitory (hyperpolarizes); binds to post-synaptic receptors SYNAPTIC TRANSMISSION ~ Oneto-ne synapse: one esron.on pas-synep element (eg. NMJ) + Mary-torone snap Many neurons oe postsynaptic Stent (eg spaintarecuons) «+ Excitatory Post-Synaptic Potentials (ERSPH: depolarizes posteyapiec, binges otal Gk, danto Naina ‘ « inttery Poe Synoptic ote BSE: hyperpolsizes postsynaptic cells “Sy Cenauetecinnae « Spt Summation 2 ornate lacy pus he same arc ae ; «Temporal summetig;2o ore excator ips stp ficeson (chad) + Facilieation / Aygméntation / Postetanic Stimulation: brings cell closecsaureshold ‘An inhibitory postsynaptic potential: ; (A) deolartzes the postsynaptic membrane by opening Na channely | {B)depolaraes the postsynaptic membrane by opening K channels {€) hyperpolarizes the postsynaptic membrane by opening C2 channels (0) hyperpolar: channels ines the postsynaptic membrane by opening CI elesnmes rom Poiloay BRS. 6° E4 TOPNOTCH BOARD PREP PI HYSIOLOGY HANDOUT BY ENRICO PAOLO C, BANZUELA, MD NEUROTRANSMITTERS. ‘CHARACTERISTICS * Maybe excitatory or inhibitory + Found inthe NMj,Sympaand Pare | | Preganglionic neurons, Para and some ‘Syma Post-ganglionic neurons, basal sanglla large pyramidal ces ofthe ‘motor cortex, glgantoceliular neurons ofthe REA * Created by: Choline Acetyltransferas {om Acetyl CoA and Choline + Degraded by: Aceylcholinesterase {nto Acetate and Choline (1/2 of which will undergo reuptake) riggers REM sleep : + decreased levee n Huntington’ dementia and Alzheinier's dementia. ‘+ Found in the /ocus ceruleus of pons, Primary NT from post-gangliontc sympa neurons; + for arousal/ wakefulness, Secreted manly by the adrenal madi, « “> | + greater BZ actionthanNE © Secreted in the substantia nigra (fn tunes movement); «Also secreted by the hypo (PIF or PLE) to int pro + Dy Receptor: activ cyclase using Gy prota deny yea ugg protl + Decreased inpoPdnson’s increased ri selena > Foundp*the median raphe of the braly stem, yom exypeophan, “SMowilevels association with depression @.NO synthase converts Arg to citrulline ‘and NO; “| Permeant gas, nhibleory NT, L_ vasodilator ‘Degeneration of dopaminergic neurons has been implicated In REUROTRANSMITTER] | (a) seblzophrenia (©) myasthenia gravis { | (Parkinson's dlaeae (©) crare poisoning | Le rom Ps ota MNEMONICS NEUROTRANSMITTERS “locas Norte 1 locus ceruleus, NE ' “Pare True Love Does Not Exist To Me" | Phenylalanine Derivatives “Trip Mo Sya Noht™ | ‘Tryptophan Derivatives: melatonin, serotonin, nacin Page 7 of 85 " For inquiries visit www. topnotchboardprep.com.ph or https://www. facebook, com/topnotchmedicalboardprJIL ---"™™ gor inquiries, visit www,topnotchbeardprep.c For inquiries, visit rd ‘CHARACTERISTICS TNEUROTRANSMITTER + Spinal cord main inhibitory NT; tne CLinflux com,ph or + Brain main inhibitory NT (eg. splay neurons of the striarum, Purldnje Cells ofthe cerebellum}, « Imereuses Cl influx (GABA‘A) oF K Bix (GABAB) + Brain matn excltatory NT; + 3 Receptor subtypes ionotropic (igand-gated) including NMDA receptors; + 1 subtype metabotrophic(lon- channel-linked) + inhibi neurons in the brain involved in pain perception (eg.enkephalins, endorphins, dynorphins) ~ Involved in Fast Pain and Slow Pain ‘Which ofthe following lv a inilbeory neuroWansmlner Inthe central nervous sya (CNSY? (A) Norepinephrine (8) Gluramate | (© g-Aminobutyric acid (GABA) {D) Serotonin | 1.6 SKELETAL MUSCLES ‘TYPES OF MUS + Skeletal Muscles ‘Intrafual: detects changes In Muscle Length (Innervation: ‘gammarmotorneurons) ‘o Bxtrafuta: for voluntary muscle contéaetion (Innervation: ‘alphasmotorneurons) 1 Type }/Slow-Twitch Muscle Fiber/Red Muscle Fiber/Oxidaive Muscle Fiver: provides Endurance 2, Type 2/Fast-Twitch Muscle Fiber/White Muscle Fiber: provides Power ; * Cardiac Muscies Atrial muscle: (+) gap Junctions, (¢)syncytum 6 Ventricular muscle: (+) gap functions, (+) syncytium 6 Pacemakers (eg. SA Node): (¢) autorhyehmiici’ + Smooth Muscle “ ‘oUnitary smooth muscle (+) gap umetions,() syncytium, forgross motor movements i ‘o Multi-unit smooth muscle: (-) gap jungtio s‘Yor fine motor ‘movements * SARCOMERE aay « Functional and structural unit offs of skeletal and cardiac muscles 4 ‘+ Area between two7Z lings THICK FILAMENTS i "THIN FILAMENTS: ‘© Thick Filaments ‘eqgtalns Thin Filament: contains actin, myosta tropomyosin, woponin iipairStheavy chains, |, 0 Troponin attaches ftsiof light troponin complex to i co Troponin Inhibits acin- myosin bluding (0 Troponin C:caleumm binding protein 02 heads, 1 tall ‘TOPNOTCH BOARD PREP PI #4YSIOLOGY HANDOUT BY ENRICO PAOLO C. BANZUELA, MD FORM myst war topnatehboardprep-com.ph or Ntps//vww,feebeok.com/topn + + Zllnes (Zwischenschelbe"): borders M tine CMicelschelbe'} midline + ABand (“Anisotrophic"): entire length of myosin © HBand (“Heller”): inside A band; purely myosin, no actin Interspersed ~ + Bare Zone: inside H band; no myosin heads ‘+ Tand ("Isotrophic): purely actin, no myosin, pintertpersed a i ann ns of the sarcolemma; contains DHPR = DHPR: jensltive, activates Ryanadine Receptors . te Reticulum (SR): contains Ca needed for muscle traction Ajimodine:Ca-rlease channel nthe SR activated by DHPR Calsequestrin: protein that stores Ca In the SR «SERA pumps Crom C? tothe SR {Tun binds myosin to Zlines, binds Zlnes 0M line + Dystrphin sablizessoreslomma and prevents contraction: induced rupture + Accinin, CapZ Protein: binds Actin to Z lines + Dea: binds nest sarolemma + Nebulinc ats as molecular rulers that sets the length of actin "STEPS IN MUSCLE CONTRACTION Space for Drawing by Srudeats) Page 8 of 85 !—— Fg Me ese! STEPS IN MUSCLE CONTRACTION 4. Action Potential starts a the initiel segment of the motor ‘neuron, spreads through the axon, neural Nbr and then the terminal boutons. 2, Atthe terminal boutons, voltage-gated Ca channels are ‘Activated. Vesicles containing Ach fuses with the nerve membrane and release Ach in the NMI. ‘3. Ach binds with the Ach Receptors (Nw Receptors) at the ‘Muscle End Plate (MEP), This Nu Receptors are ligand-gated fon channels. Once they're activated, they will open Na and K channels. 4. The open Na channels causes Na influx and produces 3 Miniature End Plate Potential (BPP), MEPP summate to produce BPP. This depolarizes the sarcolemma, 8. Depolarization spreads from sarcolemma to T-Tubules. Atthe ‘T-Tubules, DPHR is activated, 6. Once DHPRis activated, Ryanodine Receptors inthe SR are also activated. = 7. Ryanodine Receptors then (Ca from the SR to the ICP. Cabinds with Troponin C, - 8 Binding of Trop C with Ca displaces Tropomyoain. This ‘tropomyosin displacement causes exposure of binding sites in actin for myosin, 9. Myosin heads binds to First Binding Site in Actin. 10, ATP binds to myosin head, This causes myosin to unbind with the Firs Binding Sie in actin, 11. ATP bound to myosin head undergoes partial hydrolysis, producing ADP. This causes: “recockng” ofthe myosin heads. Myosin moves euch that lt now points to the Second Binding Site in Actin and it moves closer to the (+) pole. 12, Myosin binds to Second Binding Sie in actin, 33. ADP bound to myosin unde causes the “power / fore ting stroke” to occur. ‘Myosin heads pull actin towards the M line or the (.) pole. & rose bridge cycle happens. This shores the sarcomere by 10Nm. 14, Do this ain and again to have significant muscle contraction: Steps in Muscle Relaxation i 1. Remove the Ca from Troponin C 2. Tropomyosin the goes back tots original location, coverings, the binding site of actin for myosin. | ae 3, Place the Ca back to the SR using SERCA. A 4. Use Acetylcholinesterase to degrade ACh to Acetate and Choline. Choline may undergo reuptake. BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C. BANZUELA, MD Lewitt sik wwrw.topnotchboatdprep.com.ph or htos://www facebook, com/topnotchmedicalboardpreo/ Y ‘The correct temporal sequen nts a¥ the neuromuscular junetir -narve; Gepolarization of the muscle ve terminal emi end plate, aetyichaine (WG) cause the opening of (a) Ne chanel and depolarteaon toward the Ne eqllbriun vandal en | | (ey Keehannets nd deplariation toward the Kgl event | (Gr channels and deplarzatontowardtheCeequtoriim | potenti | | | (8S mandate a nen tcc Ce ey tioned teen oa : ‘Which of the following temporal sequences is correct for excitation- | cantare ar | |i eal be npn nema cece cee 0 ee eS an epee Sanreehe pnemes rset «fete neem cece nig car | o Memeieet nee | ‘depolarization of the T tubules; Action potential inthe muscle | Ea pommel Tighs a aie Rierngeae eee Suncast hoon moestaonneer ase, sone en 1) Sete ae amen | se) (€) Uptake of a2+ into the SR by Ca%-adenosine triphosphatase (ATPase). | (D) Binding of Ca* to troponin C L_ (2) Binding of actin and myosin From Phyiolopay BRS, 6» £4 | DRUGS THAT AFFECT THE NM 1.Blocks release of Ach from pre-synaptic terminals Competes with Ach for receptors on Motor End Plate Inhibits Acetylcholinesterase —— ‘+ Blocks reuptake of Choline into presynaptic Terminal ‘A. Botulinus Toxin C Hemicholinium Page 9 of 85“pproenge ee Peringuies, va ‘Adz-year-old man with myavihenia gravis notes lncreased muscle] strength whan he is ented with an wea CACHE) hlbleor. The basi for his improvement i Inereased i | "(a) tmoune of acetylcholine (ACK) released from motor nerves « {3} levels Achat he mule endplates | (6) mumber of Ah recaps nth ml ond plan ISOTONIC VS ISOMETRIC CONTRACTION « Isometric Contraction ‘o Length s held constant while muscle contracts ‘0 No muscle sherzening/lengthening © Bags pushing against the wail + Isotonle Contraction ‘Load ls held constant while muscle contracts co with muscle eng (64, lowering weight down) hening: eccentric contraction ‘SPECIAL NOTES ON MUSCLE CONTRACTION + Preload: muscle length + Aftarload: load against which the muscle contracts ‘9 Velacity of muscle shortening decreases as afterload increases # Passive Tension: tension due to muscle stretch 4} Active Tension: tanslon due to muscle contraction; proportional ta number of eross-bridge cycles formed 1 Rigor Morir wsaly oscure 3-6 hours ar death dv to lack of » Tetanus / Tetanle Spasm: happens wher all Ca from the SR has been released; no further Increase in muscle strength following causes rigor inakeletal muscle? 3p potas In motoneurons | i | [a)An crease in itraclular Ca¥avel | (GhAdecrease in intracellular Ca level | (Banincrease in adenosine triphosphate (ATF) evel c (E)Adecreasein ATPlevel From Pyle BS taapeasunaon rtatcaimariclisreoesonaes lS | comacton (tetanus). Accumulation of when seu n intracligg fr” | responsible fr the tetanus? , aye < | @K ca Nee, Liga _____from Piapegans 0s 7 CARDIAC cst ~ CARDIAC MUSCLE + Skeletal Muscle relies purely on intrgeMld Ca (SR Ca) 1 Smooth Muscle relies purely op ca ECF) 1 candiac Musee rells on both AGacallar dnd extracel Ca 1 "Caletum- Induced Calelurm-Rdlease” system ° CARDIAC ACTION POTENTIAL + Phase 0:DuetoNasfik™= 1 Phase 1 Brief pelé@-af repolarization Duet Redux and decrease Nar influx + Phase 2:Plaeaipt AP Dh tint ‘+ Phase 3: Repolarization Decrease Ci? Influx and Increased K° efflux + Phase 4: Resting membrane potential ‘TOPNOTCH B For inquiries ‘TOPNOTCH MEDICAL BOARD'PREP PHYSIOLOGY HANDOUT swine. topnotchbeardorep,com.ch rol ARO PREP PHYSIOLOGY HANDOUT BY'ENRICO PAOLO C, DANZUELA, MD isle ww, topnatchboardprepicer.phof http://www ecebook.com/topnotchmedicalboardprep/ 'BYENRICO PAOLO C. BANZUELA, MD or L La a aT] ie membrane Peto count eth oul pun | (hres 1 | (C) Phase 2 ee | | ~29} i | | | 40) | | 0} \ | 80 i 100! | | ("baring whch pea vance poten | Senduunc Co highest i | “ayrnaseo | grmue Q | | pean . (0) Phase 3 | (ehriues . Which phase ote veneer at (A) Phase 0 © (O)aae tial Is attributable to an Increase In K* conductance (8) an increase in Nz" conductance (6) a decrease in Cr conductance {O)> decease n coconducance {e)simtaneousnressesin and Cr chaos an Plog RS 2B CALCIUM REGULATION OF CARDIAC MUSCLES + Tnereast Intraclilar Cali Type or Slow-Calctum Channel: predominent and voltage-gated 0 T-Type or Fast-Calcium channel + Decreases Intraclislar Calcium siarGo™ Countereransport caraTPase pump SANODE ACTION POTENTIAL + Phase 4: slow Na* Influx towards threshold + Phase 0: Ca Infox (depolarization) + Phase 3: K* Effux (repolarization) Page 10 of 85( 4.8 SMOOTH MUSCLES _ SMOOTH MUSCLE ‘+ NoTroponin, * Contains ‘oMyosin-Light Chain Kinase (MLCK): phosphorylates and activates myosin heads ‘oMyosin-Light Chain Phosphatase (MLCP): dephosphorylates and Inactivates myosin heads © Calmodulta: binds with Ca 1 © Culdesmon and Calpontin; inhibits muscle contraction 0 Dense Bodles: analogous to Z lines ‘Rudimentary SR Rudimentary T-Tubules (Cavooll) ‘TYPES OF SMOOTH MUSCLES (0) Spontaneous depalareton ft ne lik deo cecal cosingheme rt ‘SINGLE-UNIT7 MOLTLUNIT SMOOTH UNITARYSMOOTH MuscLE/ SYNCITIAL SMOOTH MUSCLE NTRACTION VISCERAL SMOOTH MUSCLE STEPS IN SMOOTH MUSCLE CO} m TION OF 1, Hormones, NTs, Stretch triggers increased IC + One nerve, multiple muscle» One nerve, multiple muscle 2. [cP ¢a binds with Calmodulin eae Biece at are meet 3. Calum-Calmodulin Complex acavates aon —____egene _____| 4. MLCK phosphorylates (and activateskityogMyeads ‘© Controlled mainly by nerve * Maybecontrolledby nerve | 5, Activated Myosin Heads: causes sry@Qth Ypusclé contraction s(ACh, NE) signals (ACa, NE), hormones, 6. MLCP dephosphorylates (and inftyvates) Myosin Heads stretch, local factors 7. Inactivated Myosin Heads: joth muscle relaxation + () Gap junctions = (+) Gap junctions | * Rom At oe * Slew when tli posses 1.9 COMPARISI KELETAL MUSCLES, ‘propagation!); s Cle SMOOTH MU: ID CARDIAC MUSCLES + () Spontaneous * May exhit neous CARD! ‘swoore contractions conan uae _wusci * Cillar vuscle,, = ie clowscer rene,» Rage ntdatines ble ducts, a vas deferens: “Ca lnfux: GANode}, Oke of Na tnfux » Na influx (atria, * Ca influx ventricles, Purkinje Fibers) = No(SANode) au ene Yea, — Me ventricles, Me Purkinje Fibers) 150meee (Sh Node, atria) APDuration +1 msec © 250-300sec + 10 msec (Ventricles, Purkinje Fibers) + AP opens all membrane Excitation- —* Use of voltage-gated Crain “USE canduced —Cachannele Coupting”—Cakium — CHfehase + Hormones gated SRCa Channels » (+) only for ee et) = muscles eee eee | 4 [se + Greatest = beast yoain=P +actn * hate * Actin Based Regulation Based using * ACM BSE yn bases + Feet wing Trop, eee |) Thiceand thin laments. a | Tension | @)Tropoaia pene i Freeemaren | (Qerte tine (tr etatan Innon-halry skin + Movement of objects Coy (fingertips and and low-frequency 2) ips) vibration 5 + Bxpanded dp ~ Gives steady-state a a1) * fambinetoform —« Lealizes touch i. sensation and to leceptors determine texture Halrend + Movement object Halrend inharbase ae 7 Hesvyand + Indeep sin, offal prolonged ouch internal Ussues and Corpusctes im (decects pressure) a2) piockcicvery and to sigual deg eneapaulated offoint rot * Onlon-like structure + Detects high Corpuscles insubetaneous frequency vibration x2) sin and deep anc + tapping MerieTand + Zpolnt Meissner discrimination SOMATOSENSORY CORTEX + Primary Somatosensory Area (81) and Secondary Somatosensory ‘Area (S2) has somatotopic organlzation (Sensory Homunculus) © Largest areas are forthe lngers, hands and face * For precise locallzation «+ Sensory Receptors i ‘TYPES OF PAIN foraniea tease FAST / FIRST PAIN SLOW / SECOND PAIN ren Body Dorsal Root or Crantal Nerve Gonglla + afer 04 secof stimulus» After 1c of stimulus eee eee eto ‘0 Cell Body: Spinal Cord or Brainstem + rapid onset and ose destruction, © Axons may decuscate + localized + poorifocallzed Pe cterie heweaa + Stimulated by mechani,» Simulated by mechanieal Nell Body: Relay Nucleus ofthe Thalamus thermal stim thermal chemo remal + Fourth-order Neurons ro * Type A-delta fibers or Type lll « Type Cfibergar Type | Gel Body Sems8 or a ot ils (nervevelocty 620ayie) " (Oscam/ng | Results ‘NT: Ghitamate ‘© NT: Substance P (ralleved by oplods) {YSIOLOGY HANDOUT BY ENRICO PAOLO C. BANZUELA, KD. Torry uaa ey mes oT I ctatenana 4SPECIAL NOTES ON PAIN cle «Receptors: ree-nerve endings that exhibit ittle oF no ber rl ee ise « Tapered y Tin 15 4apCor>43 dg ¢ ; i & hejerred Pat: gy in ‘9 Due to sharing of 2% order neurons in the spinal cord of Eton visceral pan fibers and skin pain fers viaion oolows the Dermateme rule w + Endogenous Analgesia Systam: — toNteinclude Serotndn BpU NE Seg, ‘Blocks pain signal at entry point in the spinal cord r— Suspenton 3 ro snd tocused aon” eo) ‘IMPORTS OINTS: IS10? FAR OBJECTS FOCUS: j | Flat ene | | wean opjecrs Focus: | [Not Fat Spherical) Lens ee REFRACTIVE ERRORS — 7 VE DISORDER DESCRIPTION cence gone ARTA « seonave | (leer “aeeeanoNT tine plcone Sightedness) yretina’ Hyperoplai», ‘short Eyeball" light rays + Convex usiew {Fira Comat anno he retna ante + Refractive Power : 2 ability to bend light a tae Irregular Curvature ofthe ‘o meastired in Diopters |etiomatin Cornea: multiple © Cylindrical * Reciprocal of the focal dstance in meters convergence flghrinche Lenses ‘+ Bye: $9 diopters of refractive power | rece - ‘02/3 by the Cornea | * * Convex '« Fixed refractive power i Presbyopla ° ABt-Related Lass of Lenses if 0.1/3 by the Lens | Accommodation (>40 y. initially with '* Variable refractive power eee eee ee ee 20 * Held by suspensorygament (zm bers) ‘+ When Ciliary Muscles are relaxed ‘o Increased tension from Suspensory Ligaments Lens become Flat . ‘+ When Ciliary Muscles are contracted Decreased tension from Suspensory Ligaments o Lens become Spherical TOPNOTCH BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C. BANZUELA, MD Thnardnran Pritt nh ne htt: Page 16 of 85 Verahanb erm innnntehms ‘arlleathnardineantFrome: For inquiries, visit cme FUNCTION NOTES revert « Involved in macular Tuncelial — seateering) dageneration, toh «Converts 11-cls retinal detachment retinal to alltrans | and albinism |____ rating Receptors « Synapses with . GalinRods* Baal ‘Absent in optic ds ‘Few Cones synapse on single bipolar + Interneuron calle: causes high ‘between Receptor ——_aculty, low Bipolar Calls (Rods, Cones) sensitivity of cones ind Ganglion ells « Many Rods synapse ‘© Contrast Detectors on single bipolar | "lls lass aculty, reatar sensitivity Amacrine, —¢ Internaurons; fonoow) = eevee Cols, with bipolar cells Tener > Mai ira Mootar "Perec ete «al gle sean '¢ P Calls: Color, Form, © Output cells of the Fine Details: Ganglion Retina © M Calls; Hlumination, Cells © Axons formaptle Movement om «Weal rtoown function a Re atta ol the cones of the Fatna, We ode (Adare more senetve to low intent light (@) adaptto darkness before the cones {Clare mosthighly concentrated on the fovea () are primarily Involved in color vision cone _ Soca ‘tare Rapten, na come tetera rte cawevest ©. thine = oo oT aes 8 S Ess 33 vue uaaennes EQ *mmatmaraasst ao 60 =a ee 6 0) ee seenocn sonno Pep nTSIOLIGY HANDOUT tanya de>" '8Y ENRICO PAOLO C, BANZUELA, MD TCH BOARD PA opnotchbnardPreP. Excitatory inonotrople glutamate receptors in bipolar and hortzontal cells are inhibited. Decreased glutamate > Inhibitory metabotrople glutamate receptors in bipolar and horizontal cells are excited and depolarized, | Which ofthe following ia sap In photoreception inthe rods? | Qa ettconara ata Roden cocoa (6) Metarhodopsin activates tranducln \ (©) Cycle guns ine monophosphate (cGMP) levels increase | (0) Rods depolarza (€)Releaze of neurotransmizer Increnses tr Ploy BS, 8 | RECEPTIVE FIELDS OF THE GANGLION CELLS, LATERAL GENICULATE CELLS, VISUAL CORTEX + Receptor Cells Connected to Ganglion cells via Bipolar Cells: forms Center of Receptive Field of the Ganglion Cells + Receptor Cells connected to Hortzontal Ces: forms Surround of Receptive Pleld ofthe Ganglion Calls + On-Center, Off Surround ls one pattern (center depolarizes, surround hyperpolartzes): apposite Genlculae Ces ofthethalantsreaing patent Page 17 of a5« Inthe Visual Cortex, 3 Cell Types detect shape and orientation of The Internal Ear Agures: ‘0 Simple Cells: have center surround and on-off patteras, ‘elongated rods. Respond to Bars of Light with correct, position and orientation © Complex Cells: respond to Moving Bars or Edges of Light © Hypercomplex: respond to Lines with particular Length and to curves/angles ‘Which typeof eal inthe vinual cortex reuponds | sane |") simple (@) Complex (© Hypercomplex fe) cenaion Prom Hyvlengy BAS bt HEARING * Sound Prequency: measured In Herts (Hs) ‘o Human ear: 20-20,000 Hz + Sound Pressure: measured in Decibels (4B) '° 604B: conversational Speech © 5 dBt limit to pravant Occupational Hearing Loss (05420 dB: causes pain, triggers attenuation reflex (stapedius ‘and tensor tympani contract reflexively) EAR +» Outer Bar ‘© Pinna and external external auditory canal id locallzation and sound collection + Middle Ear teed ‘Tympani membrane, auditory ossicles (maeug cus, stapes) hat nseras no ovel window (agen beeen middle ear and inner ear) o Auditory esiles ampllY sound fro membrane going into smaller oval * For Impedance matching: matched with sound in Wg HEARING * Sound waves causes cochlea to vibrate ~ cilia on hair cells bend by shearing fore since basilar membrane is stifer than tectorial memnbrane + Bended cilia on one direction causes depolzrization, the opposite hyperpolarization as it changes K conductance +> causes oscillating potential called cochlear microphonic potential * Place Theory of Hearing: © Hair Cells near BASE (oval and round windows): respond ‘0 Righ:frequency sound co Halr Cells near Apex (helicotrema): respond to low- Srequency sounds | Woh of the lowing atmans Dat Gece he bala | accede tthe baslar wena] ‘apex responds better to low frequencies | | — ne (Sete evar ton terse i gong labyrinth (semicircular canals, cochlea, vestibule eal | © Membranous labyrinth (series of ducts) (0) High requesles produc maximal dspacementofthe basilar | Sendolymph is seen in the scala media/cochlear duce |p eetbrane near We helieotrema * high in potasstum _ (©) Tapes easly aif eompered tothe base i coperilymph is seen in the scala vestibull and scala tympani Pir Pitney 00,6 £4 | * high in sodium TOPNOTCH BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C, BANZUELA, MD For inquiries visit www.topnotchbaardprep.com.ph or https://www.facebook.com/topnot \medicalboardprey Page 18 of 85+ Central Auditory Pathways * © Fibers ascent through lateral lamnigcus to inferior ealieuius to medial geniculate nucleus of thalamus to audltory cortex © Fibers maybe crossed or uncrossed * Lesions of cochlea of one ear: unilateral deafness + Cental unilateral lesions: may not present with unilateral deafness due to mixture of ascending auditory fNbers from both ears i © (+) tonotrope representation of all requencie central auditory pathway evel of VESTIBULAR SYSTEM « Allows raflex adjustments of the head, eyes and postural muscles to provide stable visual image and steady posture + Consists ‘03 Perpendicular Semieireular Canals: detect angular ‘acceleration etect horizontal (linear) acceleration etect vertical (Unear) acceleration «Receptors: Hair Cells * Cupula: gelatinous structure + Kinocilum: single long cllum of halreel # Stareocita: smaller ella of hal cell + Rule: © Stereocilia bends towards kinoclllum: depolarization © Stereccilia bends away from kinocllium: hyperpolarizes hace vat Lad teen U7 “oor : a | inich ofthe lowing would produce Raion thea {alsin the rghthortzontal semiceuay cgi (i) Hyperpoaraton ofthe halnggl, | (@)Bending he stereoclia away Wart Crefdnotiia | (© Rapid ascent in an elevatgr |L_{BRstaung he head othe right @ From Pinson ons. NYSTAGMUS a + Direction: same ifetion as head rotation « Postrotatory nystagmus: occurs in opposite direction ofthe vl! _{E) nerve deafness or NQUIFIes, Visit www. topnerenboaraprep.COM.pN OF NEEDs:// Wwww.TACSDOOK, com/LOPNOTENMedIcaIDoarapreny, = MOA: ‘© Odorant molecules bind to receptors inthe cla of elfactory receptor calls ‘0 Gayare used as transducers to activate cAMP second ‘messenger systam ‘o Inc cAMP opens Na channels causing depolarizing receptor potential © Action potentials are then generated and propagated once ‘threshold is reached CU Which of folowing ante tbout ean we TT | (A Te reeptar cai are neurone (aye restpnclsere Suge off and are ot replaced | (hasorot eran are oN) eet ors {b} Avon fromrecepareelstyaapee inthe prepiiormcorx | | (©) Fractures ofthe crbriform plate can cause inability to detect =| ae en Page Ste Ae TASTE + Taste Receptors: not true neurons + Ant 2/3 of tongue: CN WH (chorda tympani’ + Posterior 1/3 of tongues CN Zk ‘© Back of throat and epiglottis: CNX cag crea apn nav would none FaTETn——] | ey ied oteany kncton {>(inpted verbal teen | “ABimpared satan tnton 0) impaired te nto From Py ote ‘TASTE PATHWAY ‘+ CHVIL CNX, and CNX-> enter medulla > ascend inthe solitary tract > terminate on second-order taste neurons in the solitary nucleus - ascend ipsilaterally to the ventral posteromedial nucleus ofthe thalamus -> end atthe taste cortex. t 2.3 MOTOR SYSTEMS MOTORUNIT + Singie motoneuron ¢ all the muscle fibers that it innervates ‘0 Small MU (Small Motoneurons):Innervate few muscle fibers Large MU (Large Motoneurons): innervate many muscle rs + Size Principle: Small MU are “recruited frst’ (fire fist) before Big MU to gradually increase muscle tension muscu seNsons Teourowge ws EO NERVE FIBER FUNCTION — > 7 Faicand dynamic Sam DTataT Tamme) |, *Sruplaandll * Sanders Shee tee oven Spindle poranetvocn length (inemonte: 1 ey mens feraucal fibers) aeth | Gea rom Psiclongyaas,eaes | | Golgh ‘+ Group Ib offerents + Muscle Tension | titan Tendon" Gmeelanth (nome Sandon: —— Organ ___ewunfus fibers) Senson) ~ Group aferents . cory Neurons Pacinian ose nly Neurons capable of reproduction (non-permanent Corpuscles (sr are © Vibration cals) «+ Olfactory Epithelium innervated by: Free Nerve. CroupilandIV» Noxious ‘© CN (Olfactory Nerve): cetects scent Endings zs prema Seat Sen v (trigeminal Nerve): detectsmaxlous / painful sumull (eg, ammonia) but not CW V: «+ Cribriform Plate Fracture: damages CN 1 creel anoamla but (+) Fesponse to ammonia -TOPNOTCH BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C. BANZUELA, MD forep.com.phor Mts! /vw facebook, com/topnotchmedicalboardprep/ For inquiries visit www.topnot Landings Teves tat Page 19 of 85MOA OF MUSCLE SPINDLE (INTRAFUSAL FIBERS) 2, When muscle is stretched, muscle spindle also stretched 2, This stimulates Group | and Group ILafterent Fibers of the Muscle Spindle 3. This stimulates Alpha Motoneurons that innervates extrafusal rmuacle fibers-> causes appropriate muscle contraction and shortening 4. Gamma Motoneurons that innervate muscle spindles are also quadriceps ferech > Muscle Spindlegacgivated > Group aatlerent activated > Alpha moraggPons activated > quadriceps contract 2 (ECU ce Petascle stretch leads to a direct Increase In Airing rate of which (ype of ] nerve? (A) a-Motoneurons | (B)-Motoneurons | (©) Group a tbers | o)Group lb bers __om Pier 5.0.54} TOPNOTCH BOARD PREP PHYSIOLOG) FOP eOfetwer tpnatchboardprep.com ph or NDr//www facebook, com/topnotchmedlealboardprep, 5¥ HANDOUT BY ENRICO PAOLO C, BANZUELA, MD | Tee extensors) From Medull «Inhibits both Medullary Reticular Formation Reticulospinal —_to SC interneurons flexors and j Tract Intheintermediate —_Sxtensors (mainly gray area extensors) + Prom Deiters etbuospnat leet tae nb eer Tact PM! motoneurons and Stimulates {interneurons extensors rectospinal _° From Superior Tne Coleulustocervieal * Contols nec sc sus EFFECT OF TRANSECTIONS: AT THE SC 2, + Paraplegia: loss of voluntary movements below level of lesion + Loss of consclous sensation below level of lesion * Spinal Shock ‘Limbs flaccid, reflexes absent immediately after transection, Partial recovery may occur after sometime 07 transection: HR and BP decreases EFFECT OF TRANSECTIONS: ABOVE SC * Lesions above Lateral Vestibular Nucleus: decerebrate rigidity + Lesions between Pontine Reticular Formation and Midbraln: decerebrate rigidity * Lsslons above Red Nucleus: decorate posturing and intact tonic neck reflexes Page 20 of 85Pana es wean riet Pi peace Deermvseare Panta tene Paws prnaled — Exances Acai cerebrate rigidly can be | j Y | A) etmataton of group a afferents {B) cutting the dorsal roous ' (C) wanucionefcreblar connections to thelatravesubuar | nucleus (0) stimulation of «-motoneurons }-gplGlasimulationofy-mosoneurons ____ Pram Photongy O85, | | Regleasraree fessor ereieor i waukinen (A) temporary loss of stretch reflexes below the lesion (B) temporary loss of conscious proprioception below the lesion | (Ghrermazent lous of voluntary contrel of movement above the lesion, Permeein oascne cbr nah fo 1s 084 ‘CEREBELLUM + Functions: © Vertibulocerebellum: for control of balance and eye movements ‘© Pontacerebellum: for planning and initiation of movement © Splnocersbellum: for synergy (controls rate force, ran direction of riovement) 1 + Clinical Conditions associated ~vth cerebellar dysfuncti ‘© Ataxla: lack of muscle coordination that includes delay in Inftation, poor execution of movement sequence and failure to perform rapid alternating movements (dysdiadochokinesia) ontention Tremor: low frequency tremor (<5 H2) who: amplitude of increases as an extremity approaches the ‘endpoint of deliberate and visually guided movement © Absent Rebound Phenomenon: failure of antagonistic ‘muscle to contract after removal of resistance tg limb movement \ A | Which ofthe folowing struciures has pr font ordinate | rate, ange force, and direction of movement. | 1°") Primary motor cortex | (8) Premotor cortex and supplemsatahyatotor cortex (©) Prefrontal cortex “a | | ()Basagangia _{€)Cerebeum “eh ram Psi he iablty to perform ldljalernating movements | (dysdiadochokinesia) Js associated with lesions of the 1 (@) premotor cortex ® ' i (8) motor coréx | | (C)cerebeliim.. | (G)substamua nigra ‘fel meduts sn Positopay 8.6 | +» Layers of the Cerebeliar Cortex (from innermost to outermost) +” Granular Layer: contains granule cells, Golgi Type I cels, jomeruli a. Derknje cu Loyer: contains Purkinje elle ‘0 Only output ofthe cerebellar cortex Outpucare always ahibltory,uslag GABA S Output projects to deep cerebellar nucle and tothe vestibular nucleus Melts urate cerebeun andreas ge id direction of movement (synergy) 4. Molar Layer:contains ele and asks el, dendrites ” of Purkinje and Golgi Type I! cells, parallel fibers (axons of granule cells) TOPNOTCH BOARD PREF + Consists ofstriatum, globus pallidus, subthalamtcnuclel and substantia nigra + Modulate thalamic outflow to motor cortex to plan and execute smooth movemenia ‘Mala NT: GABA + NT between striatum and substantia nigra: Dopamine olnhibies the jathway using Dr receptors © Stimulates the exctatary direct pathway using Di receptors + Lesions: ‘9 Globus Pallidus: inability to matntain posture © Subthalamle Nucleus: wild, falling movements (hemibalismus) Stratum: quick, continuous, uncontrollable movements (€g. In Huntington disease) Substantia nigra: Iremors, cogwinee| Bigdity, reduced valucary movement (Aknei), owurl gies (Mnemonic: T-R-A-P* of Parkinson Disease), % ‘MOTOR CORTEX : + Pre-Motor Cortex and Supplementary (Bas) ‘0 Generates movement plan thal sferred to primary motor cortex for © Supplementary motor co es complex motor sequences ge Marco nue bran movements et ‘ Epllept gpa uses Jacksonian selsures (focal parti at rrr | tgbprdat representation on th prisary motor carter (aren)? ‘sister | fo) ane "(C) Fingers (0) Elbow EL Knee rilopy BS 6 £4 | 2.4 HIGHER FUNCTIONS OF THE CEREBRAL L “ CORTEX BEG WAVES + Made up of alternating excitatory and inhibizory synaptic potentials inthe pyramidal cells ofthe cerebral cortex + Cortical Evoked Potential: changes in the ECG *hat reflect synaptic potentials evoked in large number of neurons aipna WNW beta tomer Mie ees wi Open (13-30 Hi som Lnnyyy Bainssete and Gogenerative brain states (4- sn DS NLL SY Deop sleep, organic brain disease, infants (0.54 Hy Awake; Eyes Closed (8- 13H2) Theta Delta 1p PHYSIOLOGY HANDOUT BY ENRICO PALO C, BANZUELA, MD Forno ot wen opnotenbeurdprep.com. ph Nis /www facebook, com /topnatchmedleatboardprep/ * 2° 8Sih ——" “For inquirtes, visit www. topnorehbosrepre ne —_—————_— SLEEP > Due to an active inhibitory process and not merely due to fatigue of reticular activating systems (Stocaile caureeecreom of Muramy! Peptide REM SLE 1D LEH With Active Dreaming: © occurs avery 90 minutes of slow-wave sleep > brain metabolism, © Ymusele tone, ‘SLOW-WAVE SLEEP si © Urually dreamless or unremembered dreams «+ (+) 10-30% decin BP,HRand + Pupillary constriction, BMR; « Active body movements, # inGl motility + Irregular BP, HR, RR; + Penile erection + Rapid eve movements * Difficult to arouse by sensory , + More dUficult to arouse stimull by sensory stimull + Stages: - 1= Alpha waves Interspersed ‘with Theta waves 2 Theta waves intarruptad by Sloup Spindles (12-44 Hs) and K complexes Cage, slow potentials) 3 ~ Delta waves interrupted by Sleep Spindles 4 = Delta waves alone Beta waves ywhorns: 50% REM Sleep wzodiazepines and age: decreases duration of REM sleep ‘© From NREM to Awake state: Zpl, NE, Histamine, Ach and GABA will all increase 2 LANGUAGE \ * Corpus Gallosum: for interhemspherle communication © RCerebral hemisphere: dominantin facial expression, Intonation, body language, spatial task —_ «© LCerebral hemisphere: usually dominant in language, |esioné here causes aphasia : 0 Wernicke Aphasla receptive aphasia ~“can sy ytean' understand” (Mnemonic: “Wordy Wernlcke7}" ‘0 Broca Aphasia: expressive aphasia ~ “can un cannot say" (Mnemonic: “Broken BLOOD = Mg, Creatinine ‘Which ofthe following has a much lower concentradon in he cerebrospinal Guld (CSF) than in cerebral eapllary blood? (AN (D) Protein | ke. Me | L_(6)0smotariy ram Psilpgy BRS om 2,6 TEMPERATURE REGULATION. REGULATION OF BODY TEMPERATURE ‘+ Mediated by the Hypothalamus © Sensors: Temperature sensors in skin and hypothalamus 0 Detected Temperature compared with Set-point Temperature * Detected Temp Set-Point Temperature: Dead Temp>'s emp Initiate Heat + Heat-Generating Mechanisms o Shivering (most potent), Thyroid Hormone production, decreased sweating, plloerection, skin vasoconstriction (alpha-1), brown fat in babies (beta-3) + Heat Loss Mechanisms © Radiation (most potent), convenction, 3 Vasodllattion, Decreased Heat Productos -TOPNOTCH BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C. BANZUELA, MD For inquiries visit www topnotchboardprep.com.ph or https://www.fac sbook.com/topnotchmedicalboardprep/nn ee EEEEEEeeseeeeee SPECIAL NOTES ON TEMPERATURE REGULATION PEER ee ReXen + Anterior Hypothalamus: for heat loss 1. Gireulery ‘© Posterior Hypothalamus: for heatgaln ie + FO Mod: Pyrogens > it alpha and bata), 1-6-> PGE: cardia Racrephyloy SB peacpoine temperature n hypothalamus > causes V,caris utp eabgenarating mechanisms VI, Regulation of BP ‘ASA: inhibit COX > YPGE: > set-point temp VII. Microcirculation and Lymph ‘0 Steroids: inhibits release of arachidonic acid from brain Vill, Special Clreulation «op itemholbs > VPGEs» Varepoactemp 1 ray Bere Hamorroge bn increases setpoint temp. = euLRRY OF THE CARDIOVASCULAR | ‘* Mnemonic: PGE1 - "PGE:: £2 mong bukas ang ductus 3.4 CIRCUITRY OF THE CARDIOVASCULAR ‘arteriosus. PGEx: E2 ang para sa fever!” SYSTEM. IMPORTANT PRINGIPLES * Cardiac Output (CO), Pugin ht produce fer cure — om aRxSV=VR tn dnrasedproaceo fata (3) oe er Ih cnrund panne netpan | Pry ieee {G}vodlationoftoed vss inthe sin j * CO R Heart: Pulmonary Blood Flow & From Phvaiolopay ORS, 64 Ed | At rost: SL/min - Man CO (NoneAthet}: 201/min + Heat Exhaustion: excessive sweating that decreases BP and © Max CO (Athlete): $0L/min . causes syncope + Heat Stroke: high body temperature that causes tissue damage: sweating is impaired which further increases temperature; maybe lethal + Hypothermia: when ambient temperature i so low, that core temperature cannot be maintained at set-point + Malignant hyperthermia: overexcltation of akelotal muscles ddue to defective ryanodine receptors i response to halotha and suecinylcholine ‘Treatment: Dantrolene, a Ca-channel blocker and muscle relaxant Cardiac ouput of tha rigitae a Cardiac ouput the ld o (a) 25% 1) 100% | me (0) Alby Regen ventricular shunt ilar failure | a ‘COMPONENTS OF THE CIRCULATION + Latass roseactonal aren; DESCRIPTION. | + has endothelial cells oily; slowest blood flow velocity; * Control Conduits; | pre-cay i oe green reson «= (4) site of greatest resistance,A1- | vhs tapecioner nee Vosoconstriets; B2-Vasodilates | ee eae Q * 644 of ood found here with one way valves © Drals proteins and lds from the interstitium, carries chylomicrons and involved in mmunly and cancer ‘TOPNOTCH BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C, BANZUELA, MD sop wOTires wait wn. topnetehboardprep.com.ph or hits: /‘ww. facebook, com /topnotehmedicaboardprep/ te” 22°" 8 | + Contains stressed volume: | sh pressure| Muti oe ue bos perire iot ~] mot ‘aorea Right atrium | : {2} cena vein {aan arery | we : (€)Pumonery arcery | [Nes Reynolds number | Fav gem peared ton ocr erent 32 Bieter od ant arariles because = Veodly of blood dow |" (A) ey have te grncent surface area 1s Viseoaty of blood (B) thay have the gretest cronstectional area {(C) the velocity of blood flow through them is the highest + Anemia: Vblood viscosity > Turbulent BF {) the veloc of blood flow through ther iste lowest + Atherosclarotic blood vessel > ‘blood velocity > Turbulent BF (2) they have the greatest resistance ram Phila BS, tendancy for blood flow tobe turbulent a icreaned By 3.2 HEMODYNAMICS ered cay BLOOD FLOW VELOCITY anal opine sarks (©) partial occlusion of blood vessel en + Slowest: capillaries (because of large total cross-sectional ord) SHEAR « Astrain n the structure ofa substance prod when ts layers are laterally shifted in rela ee « Mphere athe walls of Bloed Vessels (ue Pogiforance in blood flow (mL/min) Hod veloc) s, ‘Ax cross-sectional area (cm?) . ase atthe cecer of Blood Vessel it blood stoop iow caracrtace/conuanes, + Directly proportional tc Pressure Difference +» Distensibitity of blood vessel} + Inversely proportional to resistance * Inversel el sce (stiffness) + beam anise | qeahit — ne emp lt rca puri tl pre Cordie orpat rote C= capacitance or compllange (mL/mm Hg) = Vevolume (ml) o Jow ur cardiac output (mL/min) P= pressure (mm Hg) P=) gradient (mum Hy r! rep sane nnumtiin | ane en rain TE whe we dete res 1 Bynes wth [An increase in arteriolar resistance, without change In any othgy | component ofthe cardiovascular system, will produce a | (A) adecrease in total peripheral resistance (TPR) =, | (B)anincreasein capillary filtration | (Ganinerease in arterial pressure {10} decrease in afteroad ram Pugs BRS, £4 | i. RESISTANCE TO BLOOD FLOW + Based on Poiseuille's Law (pronounceditssPua"zweeh") ne where Re Resistance 11 = Viscosity of blood |= Length of blood vessel + Radius of blood vessel raised to the fourth power ARTERIAL PRESSURES: - - 1 Highest Arterial Blood Pressure ‘* Rememben,plgod viscosity = hematocrit — 2 lowest prea Blood Pressure ‘o Polycythidmla: increased resistance, 2 SytolePresture~ Dial Pressure © Ifa vessel radius decreases: highly increases resistance Tsu S maporatretaieeatae olm unt when it es to the control conduits arterioles: —— 3 Most ‘of Pulse Pressure me 6 =2/3 (Diastole} + 1/3 (Systale) = Diastole + 1/3 PP H 7. Synonym: Right Atrial Pressure = 8. Estimates Left Atrial Pressure blood | *PPincreases wich age due to arterial compliance (eapacitance) 53-year-old woman s found, by arteriography @have SO% farrowing o her lft renal artery. What ls the expected change in ve throug he stenotic artery? Migybecesets if (O)Decrasero1/16 & Baer E Riera] (8) Decrease t0 1/4 {E) No change Central Venous Pressure . Pulmonary opr Wedge | (CLDecreaseto 16 Pram igen S68 Ed) LAMINAR VS. TURBULENT BLOOD FLOW Viaminar Blood flow. Streamline blood flow, with blood velocity D, Mean Areral Pressure ffstest inthe center and slowest near the vessel walls : « Turbulent Blood Flow: irregular, disorderly blood Now ~ cee minced with high Reynold's Number (+2000) & brults : py (audible vibrations) > ; RD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C, BANZUELA, ‘TOPNOTCH BOAR is ts seen rene sit www topnotchboardprep,com.ph or http://www facebook com/topnotchmedicaboardprepdPraee remus a prauuremaanured nh erie (B) the lowest pressure measured in the arteries: ee durng cane | SS) tected Sate etme (2) decreased when the capacitance ofthe arteries docret rom Paolo BRS 2 Et ‘3.3 CARDIAC ELECTROPHYSIOLOGY ECG ‘© Pwave: Atrial Depolarization © QRS Complex: Vent Depolarization © T Wave: Vent Repolarizarion + PR Incervali depends on Conduction Velocity through AV Node ‘+ QT Interval Period of Vent Depolarization + Repolarization ‘© PR Segment: AV Node Conduction Jeetrle: correlates wit sk Tot leery of Von AP Ele : Tian * Can decrease AV Node Cofdu Heart Block > Conduction Vel Hypokalemia Hyperkalemia = Low | Hypocalcemia Fi OE neem | [Q-Wave infarct /. | Transmural Infarct ‘Segment Elevation _| ‘Non-Q-Wave Infai 3 = boa | Subendocardial- ‘ST Segment Depression an venticlest completely depolarized during which wceletic | portion ofthe electrocardiogram (ECG)? | © (A) PRinterval (Oy st segmens {B) QRS complex wave (eiariwerat am inlay 5,6 CG) has noP wave, buthas a normal “A person's electrocardiogram (EC : QRS complex and a normal T wave. Therefore his pacemaker Is located inthe (A) sinoatrial (SA) node (0) Purine system. | (Byatrioventricular (AV) node (E) veatriculay ao |_ CC. bundie or is ta Selpoarold female pauenté elecrocardiogram (ECG) shows (wo P ae are rea QRS comple The nerpretaion of 8 parent | want Feseased ring rate ofthe pacemaker nthe sioatia (SA) 0006, | oo decreaged pring rate ofthe pacemaker inthe atriovenrclas (AV) ial Jp the SA node | iereated firing rate ofthe pacemaker 10 | (Doaecested conduction arough ihe AV nde | | febinereased conduction through te HICPHTADI ns ay) r iY HANOI TOPNOTCH BOARD PREP PHYSIOLOG\ For inquiries visit www topnatchboarder SPECIAL NOTES ON THE ECG — : ECG CHANGES * Stimulates AV Node > Ay Sympathetic NS ‘+nConduction Velocity -> b Interval UT BY ENRICO PAOLO C, BANZUELA, MD om, ph or https://www facebook. com/topnotchmedicalboardprep/ CARDIAC ACTION POTENTIAL + Stable RMP: -90mY (almost simliar to K equilibrium potential) + Cardlacal 0,1,2,3.4 CARDIAC PACEMAKERS + SA Node: Master Pacemaker (exerts overdrive suppression of ‘other pacemakers) + AV Node, Bundle of His, Purkinje: Latent Pacemakers © When latont pacemakers assume pacemaking activity: Sctople Pacemaker + Intrinsic rate of Phase 4 Depolarization (and Hoart Rate): ‘SA Node > AV Node > His-Purkinje ‘0 SA Node: 70-80 beats/min AV Node: 40-60 beats/min (slowest conduction velocity at 0.01-0.05 m/sec) Bundle of His: 40 beats/min (o Purkinje Fibers: 15-20 beats/min (astest conduction velocity at 2-4 m/sec) SANODE AP ‘» Has unstable RMP (Phase 4) ‘* No sustained Plateau, no Phase 1, no Phase 2 + Contains Phase 4,0, 3 more Ca available for release to the sarcomere + Cardiac Glycosides (digitalls) i ‘Inhibition of some cardiac Na-K-ATPase pump > activity of Na-Ca pump > Tintracellular Ca Pancras following agens ar changer basa najavenatopiceica | | onthe ce | (a) Increased heart rate Beirne | @)symonteversmuaton —— sis sey (C) Norepinephrine ws 6 [Vin electrocardlogram (ECG) on a peraqn Hows ventricular | | cxtrasystoles, The excrasystolic beat wOUld produce (G)Inreaved pus prseygbenure eat rates intend (©) decreased pulse press wengrieula filing time is Increased | (0) decreased palvagetiure because stroke volume is decreased {E) decreased pulse pressure becouse the PA intervals increased a Prom Physiology BRS. 6 Bd Thaws ventricular | fpextrnormar ventricular (a) increased pulse pressuxg because contraciliy i increased | | “ha electrocardiogram (ECO) on pe ‘extrasytoles. After an extrasystole, contraction produces (A) increased pulse pressure {is increased (8) Increased pulse pressure because (TPR) is decreased (Cy increased pulse pressure because coniplance ofthe veins is decreased (0) decreased pulse isincressed ae eincared pulse pressure because TPR|s decreas 2S coal From Physiolopgy ORS, 6" Ed | qameense a contac is domonstaedona Frank-storing | Amimerease in comtracilisy ‘because the contractilty of the ventricle we peipbericessones | | | | i | pressure because the contraciliy ofthe ventricle | i | ciagram by i! Oy eacarlacouputforagivenend-dasiatcvolume || Ay 68 ef "Gteecartacesferageenenssjicvcne || (ah 438 a | (Cj deereased cardiac output for agiven dda ns 1) @so0tymin - 8.00 L/min ‘even volume Ph | decenad cara ou or? Phrsiloar BBS 6ske| | CCnlocoupuso = 200 PRT AS 6 i (G24mLO, fk - 0.16 MLO, mL TOPNOTCH a peer et eee ee ee BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C. BANZUELA, MD ——____2 860i /min or 826\/min For Inquires vist woew.topnotchboardorep.com.ph or https //www facebook, com/topnotehmedlcalbaar dre poms es AUTONOMIC EFFECTS ON HEART AND BLOOD VESSELS + Sympathetic NS ‘0 HR, Conduction Velocity (AV Node) and Cardiac Contractility: ‘via BI © Skin and splanchnic arterioles, velns: vasoconstrict via AZ Skeletal muscle arterioles: vasodilate via £2 + Parasympathette Ns ‘© HR, Conduction Velocity (AV Node) and Atrial Contractility: via M2 Little to no effect on blood vessels ‘Which receptor mediates constriction of artariolst 6 (A) ai Receptors (©) 2 Receptors i (8) 1 Receptors (0) Muscarinic receptors | from Poaclongy BRS 66 3.4 CARDIAC OUTPUT TENGTH-TENGION RELATION IN THE VENTRICUIRS + Preload: End-Diastoltc Volume (EDV), which in turns influenced by R Atrial Pressure te, ‘oNPreload-> ‘Cardiac Output (by increasing SV) «+ Afterload: Aortic Pressure for the L vanezicle, aig Pulmonary ‘Artery Pressure for the R ventricle 7% © Inversely proportional to velocityof tentraction at fixed | rmuscle length : opAfterload > VCardlacOusait py Increasing resistance toventricular outflow); | '» Frank-Starling Mech, venous Re pp R Atel Pressure > ‘PEDV (Preload) > PStretch ‘sarcomeres (‘ventricular Aber Nength) 1 grenter folgg gf contraction (due to greater tension) > PSY 3 eo ' + at ° turn (VR) > ‘PR Atrial Pressure > stimulates wulmonary baroreceptars (law-pressure receptors) “> agin 00 ats MNEMONICS FRANK STARLING MECHANISM VS. BAINBROGE REFLEX Frank-Starling Mechanism | Bainbridge Reflex AVR ASV-> PCO AVR HR 1CO i IMPORTANT CARDIO CONCEPTS + Stroke Volume : © Blood ejected by the ventricle per heart beat © Equal to EDV- ESV © Normal Value: 70mL + Bjection Fraction ‘ Percenitage of EDV that is actually ejected by the ventricle co Equal to SV/EDV Normal value: 55% + Cardiac Output ‘Total blood volume ejected per unit oftime Equal to HRxSV ‘© Normal value: SL/min (restin carta ouput arg yas —— we 102 pnoesry ery | Atarpateed patent an ejection fraction of 0.4, a heart rate of 5 -ats/min, anda cardiac output of 3.5 L/min, What is the patient's end ; diastolic volume? ie ee ae i i (A) t4mL A (@)37 mL ian | telssmc (40m. 1 LSS From? ens eo ed_| | The following measurements were obtained in a male patient; 1 Central venous pressure: 10 mm Hig | | Meartrate: 70 beats/min | Pulmonary ven (02) = 024 mL 02/mi, “ulmonary artery [02] = 0.16 mL 02/mL ‘Whole body 07 consumption: 500 mL/min What is this patient's cardiae output?Ifthe ejection tration lncFoases, there wil bm Gecrense in al (A) eardic ourput (0) pulee pressure i LSeninaotevsume (©) rola volume A pcoerscey $C eg a ony «Stroke work ovEsy ‘0 Work heart performs on each beat © Main Energy for Stroke Work: Patty Acids + Cardiac O2 consumption | (Directly related to amount of tension developed by ventricles 6 Increased by an Increase in the following: afterioad, sizeof ‘the heart, contractility, heart rate ‘On the graph showing left ventricular volume and pressure, H . Isovolumatrie contraction occurs from polat ERO MeNevetine ling cange cause aninerane myocardial ae | Super? oped Ci Beeet ores (ea L~ rene | deeredcoaracaliy Uoee 5 | | (ep inereasedintux of Nav during the upstroke ofthe action potential er iin 2 | VENTRICULAR PRESSURE-VOLUME LOOPS + From 1-> 2: lsovolumetric Contraction ohVent Pressure (but Aor Pressure) no change in Vent lume (0) Increased size of the heart | | | | oll heartvalves are closed tha aor valve dara pot * AV valves close (causes $1) eee (a oe a a se Presue 9 Veneer an Bi Ejection |_frem Phusiolonay BRS. € b¢__| + 29.3: Ventricular Ejection re tathear Te pai © Width: stroke volume mo 93 i © AtPoint 3: volume is ESV @2 ©) | +39 4: Lsovolumetric Relaxation [fe a Sets Ws ha aac output of evant oUvent Pressure (but> Atrial Pressure Pressure),no change | ise 7 ieee a | cnllheur valves are closed vimin bs | * ab vaves ore (causes St) (plese reste | ‘© At Point 4: Atrial Pressure > Ventricular Pressure -> Vent Filling SS 3.5 CARDIAC CYCLE © 44: Ventrieular Filling» ‘= Cardiac events that occur ina single heartbeat Iilustrated In the ‘oAt Point 1: volume is EDV (approx 140m) ae Wigger Diagram em," Wigger Diagram has the following components: ‘o Heart Sounds (Phonocardiogram) ECG ‘0 Ventricular Volume Curve 0 Ventricular Pressure Curve o Atrial Pressure Curve o Aortic Pressure Curve © Preload ‘o-fVenous Return = EDV a asv + afterload ‘0 Aortic Pressure “us = NESV Oe Ep PHYSIOLOGY HANDOUT BY ENRICO PAOLO C. BANZUELA, MD YARD PRE TOPNOTCH BO: ‘opnotchboardprep.com.ph or https: //www. facebook, com/topnotchmedt. For inquiries visit www. Pag cardores tm 27 8S17 PHASES OF THE CARDIAC CYCLE 1. Atal Contraction/ Systole (occurs during distal third of diastole) 2; Isovolumic Contractic 3. Rapid Ventricular Ejection 4. Slow/Reduced Ventricular Bjection §. Inovolumle Relaxation 6. Rapid Ventricul Piling (occurs during early third of diastole) 7. Slow/Reduced Ventricular Filling (occurs during middle third of diastole) © NOT essential for ver ECG: preceded by p + Ventricular Volume «Atrial Pr tricular Alling ‘wave «Atrial Pressure: Increases slightly ‘© Ventricular Pressure: Increases slightly Increases slightly sure curve: a-wave seen « Heart Sounds: 44 heart sound maybe heard dus to atria ‘contracting agains se aeifvantrictes (eg, In LV hypertrophy) ‘+ BCG: preceded by QRS complex * ari + Ventricular Press Prassure Curve: e wave ls seen re: Increases but Ventricular Pressures still ¢ Aortic Preszure ‘0 Semilunar valves are still dosed * Blood will NOT flow from LV ti Aorta ‘¢ Ventricular Volume: remains the same ‘© Ventricular Pressure > Atrial Pressure AV valves will close ‘© Heart Sounds: S1 will be heard ‘Atrial fling begins * Ventricular Pressure: rapidly Increases to a point that it ls now greater than Aortic Pressure © Semilunar valves open «+ Ventricular Volume: rapidly decreases Blood will low from LV to aorta ‘Aortic pressure: decreases because of runoff of blood from large arteries to smaller arteries S.lspvolumic Relaxation + ECG: preceded by t-wave + Atrial Pressure Curve: v wave seen + Ventrlcular Pressure: rapidly decreases but Ventricular Pressure > Atrial Pressure ‘AV valves are stil closes ‘No blood flow from Atria to Ventricles + Ventricular Volume: remains the same + Ventricular Pressure < Aortic Pressure © Seinllunar valves will close + Heart Sounds: $2 ls heard (phystologte split $2; occurs during inspiration) te + Aortic Pressure Curve: netsure / Droge ji en ‘$.Bapld Ventricular Pilling *% * Ventricular Pressure: rapidly fo aoine that itis ‘now less than Atrial Pressure os ‘© Opening of the AV valves", ° * Blood rapidly flows fromiiA®rium to Ventricles * Heart Sounds: 3-4 Heart sound may be heard (due to rapid ventricular filing) “nu + Ventricular Volupeiryppidly increases 2 neta vic oe aca) + Longest pt 0 ardlac cycle ‘o Bapengly on haart rate + Vengfela} Volume! Reduced incrause TINENONICS CARDIAC CYCLE w», | [Uistances when Atrial Pressure Increase: | a'wave: atrial Contraction ‘wave: contraction of Ventricle ' | vwave: venous blood golng to atria | ve | w g fon awave ” a atnat — 3 s4 | compliant rE ne vente depolarization) |? ‘aasconpiar | —ewave 2, wovalumle ose ot | ves! ss conn Contraction St] avvaes |? sailed ae] o fapid Wo hor +— Ventiuter opening of St lee 3 | section aves & [esiow Twave | Ventricular (ventricular + ‘ eation sesolartiton) %. lovelumie Teareot | wreage oy Waa Relaxation _| ** |_stvaives vena iacwens nan wi! raid vecae sa | vertncuter | opening of 1 og | AV valves olor DASTASIE (atria vertices) oncestpnane | 9 | 7 nd DEPENDENT ! on Moris Vania proce Ws vendor vole Sorat peture far shoe pesere {oes machi TOPNOTCH BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C. BANZUELA, MD. For inquiries visit www. "sopnatenboardprep.com.ph or https: tw facebook, com/tepnatchmedicalboardprep/ tt 22% 8SInspiration splits the sacond heat sound because Ti seneerenine {A the aor valve closes before the pulmonic valve | (@) ventricular pressure (8) the pulmonic valve closes befor the ari valve | (Gard prasssre {G)themtral valve ona befor the trcuspé valve Comal | {6} hetrcuspa valve closes before th ral valve : {E) lingo the vents hus fast tnd slow components rom Plena BS, £4) | j ope vooat OR SF | Tortie Valve. 2 ICSR Smee | ae a (B) vencclar presur | Prrieuspid Valve 48-50 ICS L Parasteraal| | ate pressore | [ialtrat Valve SP ICSLMCL AS |_ (0 venerealrvelume Fron Pilggy BS, 64 "During which phase ofthe cardac eye does the mitral valve open? | (yatta yaote | (e)tnovoumete venice contraction | (Glave act, (0) Reduced ventricular ction {E.leovolometteventrcur relation Frm Pyeng BR 064 3.6 REGULATION OF BLOO! RE ring whieh phase ofthe cardiac eye i abre pressure highest? EP CONTROL (a) ai ayaa + Vasomotor Area ofthe Medulla (Serene omrcin | Ee eta ar Seomatenelr ane Found nthe Medule | SY un 37) | ELlsovolumetric ventricular relaxation _from Phwsilopy 985 6+ 64 | a ana During which pate ofthe caring ela volume lowes? + Medial Portion: nk{blioyy Area (VAR & BP) | Oar gmcte nearer evened velune lowes Contralled by the us and ater higher nervous | ()sovolumetre vetielar contraction centers * } (C)Rapié venrctar ejection + Acute Control (0) Reduce verter election ANS Cont rs, Chersoracaptors, Low-Pressure ° su Recepta heme Response + Longgte CE n= ° fotensin-Aldosterone-System (RAS) st + isovolumic thee» Parasympathetle Contraction Increase BP via ANS: $2 (eplitduring > Closure of 7 Hovolumle * Arteriolar Vasoconstriction -> (\TPR > VBP inspiration) ___Semilunar Valves “Relaxation | S + Venous Vasoconstriction > 4VR > %CO-> BP 5 + UR & SV via By Receptors ofthe Heart -> ‘CO -> TBP jag * Atrial Contra ANS EFFECT ON THE HEART AND BLOOD VESSELS a ones Systole SYMPATHETIC PARASYMPATHETIC x { fect tur Bffect Receptor PHYSIOLOGICALLY SPLIT S2_. om Heart tate £ Bs Ma [conduction Velocity(AV B ¥ Ma Node) coon ea contcity ne pi Pees (avi only scular Smooth Muscle 1 Eres my a Dilation Br Veins ‘Constricion At penn cone —, __| Wien receptor medias owing ofthe ean?) DESCRIPTION aS Ce Recep ee Reaors | ms * Split appears (@)pt Receptors (O) Muscarinic receptors yslologic SP APPCRS al —_ Pom Pier BBS 6+ Split s2 . ‘Propranolol bas which of the folowing effects? 7 Insplration lowing efecs? et a beled Onsetaf (9 Decent barre i dyralrteSunleSranh| | S)StMEIdenredrgecton acn | « spicappears oe (LBBB) Right (D) Decreases splanchnic vascular resistance i psn “gape, PROGR || Split s2 Os 2) Prolongation of LV een BRS, 60 4 | Expiration —Sycole dortic Stenosis, | When proprasolaliesdminiared Boclade fetch eospaetne Weaeane "etgonsble forthe deceaseincardlacoutputtiatoccus | Cardiomyopathy (A) at Receptors (©) Moscarinte receptors | Ty Deed Onsecotay ——) | SLRs (Nici receptors | | persistent + Splitappears Systole:Right Bundle | TERReceptors ____Fram Phsbopgy BRS, 68 £¢_ Spllting of throughout Branch Block (RBBB) : 2 Respiration 2) Prolongation of RV Systole CEE {ASD Pulmonic Stenosis ‘TOPNOTCH BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO-PAOLO C, BANZUELA, MO Fer ngs vst wor. topnoteboarépep.com. her Miso. iaebek con/tepnathmedeabearorep/ 8°29 © 85 Fore SE eee EE+ Baroreceptors: arAet fast; Buffers minute-to-minute changes In BP Stretch Recoptors on the Carodid Sinus and Aortic Arch TEpBP > BStretch > ‘Firing of CN IX to NTS > trigger parasympathetic response «Yap vestretch > VFlring of CN IX to NTS > trigger sympathetic response co Hering’s nerve! branch of CN IX that carries signals from carotid sinus to NTS Carotid Baroreceptors: respond increase/decrease in pressures from SOmmbig-180 mmHg co Aortic Baroreceptors: respond to Increase in pressure >80mmHg ‘Set Point for MAP in Vasomotor Center: 100mmitg 20 r wt sem ralowinga synpathectony a Gb eared man experiences iesaic hypotension, The explanation for this currence 6 Pan eggersted response ofthe rein-anglotensi-aldoserone nem (e) Leappressed responie ofthe renin-angotenin-alostrore system i (c)anexaggerated response ofthe baroreceptor mechs | (Hy itppeesed response ofthe baroreceptor mechan | ram Prt B85. 66 | ‘a acuta decrease arava bod pressure ets which of = folowing compensatory changes? {ay Dressed tring rae of the caro sinks nerve i (a aces parasympathetic quo to he heat {cj Decrestedhearerate (0) Decreased contracuiy ‘ ased mean systemic pressure {E) Decreased mean systemic el TOPNOTCH BOARD PREF PHYSIOLOGY HANDOUT BY ENRICO PAOLO C, BANZUELA, MD soeer oot wr. tepnatchboardPrep.Om.Ph or hitp/w facebook com topnetchmedlcalboardprep/ rep! + Valsalva Maneuver ‘> Expiring against closed Glottis > ‘Pintrathoracic Pressure > YWR-> VCO and BP -> sensed by BR> THR ‘0 Once you stup Valsalva Maneuver - sudden rebound * in ‘VR, CO and BP? sensed by BR-> VHR + Chemoreceptors ‘o could also induce changes in BP ‘© Responds to low O2, high COs concentration whenaver BP ‘TPR? DBP « Lowpressure Receptors (Cardlopulmonary Baroreceptors) ‘on the atria and pulmonary arteries aetna fullness” of vascular system (intravascular volume) ‘ln response to increased intravascular volume: . seuerlal Natriuretic Peptide (ANP): “)Na* & HiO excretion + Vane Dluretc Hormone (ADH): urkyg puput 1 Renal Vasodllation: urine output 1 Ateart Rate (Bainbridge Reflex): vRw/CO + CNS Ischemic Response a ‘The vasomotor center itself respoyay gee {ischemia during low BP co Surtsat BPc6ommHg and opting] ara BP+15-20mmHg ‘The “last-ditch” stand: * all systemic arte strict severely EXCEPT for Vessels lex eased Intracranial Pressure (€.¢- le, Irregular Resplrations {tenstin-Aldostarone-System (R-A~A’S) 23 20 minutes to take effect advwinen faster mechanisms (eg. baroreceptors) fail late BP 0 responsible for maintaining normal BP despite wide arlation in sal intake on ~ NorRENIN. ANGIONTENSION-ALDOSTERONE SYSTEM (RAAS) «Activated first before RAAS: Baroreceptor Reflex « Senses BP Changes: Macula Densa «+ Macula Densa: stimulates Juxtaglomerular (1G) Cells (Granular Cells) to release Renin «+ Renin > converts Liver Angiotensinogen to Angiotensin | + Lung ACE: converts Angiotensin I to Angiotensin I! «+ Angiotensin Il Effects: obiinains PRESERVE) normal GPR (vasoconstricts Efferent > Afferent) ‘0 Vasoconstricts systemic arterioles -> ‘NTPR ‘ Stimulates Aldosterone secretion by zona glomerulosa adrenal cortex ‘o‘NNa+H exchange In the PCT “> contraction alkalosis ‘ot thirst and ADH secretion -> ‘intravascular volume ‘0% Epi, NE, Cortisol secretion -> vasoconstricts arterioles + Aldosterone Effects on the KIDNEYS: ‘oNa reabsorption ‘oKsecretion ‘oH secretion (GUDRUN [ wwnten team renal roemeeni balan’ cae (hAssaetchrone 01) | | Sacer Biiteretereeg | Sige ee | 60-year-old businessinan is evaluated by is phy 1 amare a ees am ae re i en eae ee ream real icv Hirght 6 ‘vein renin level is deere , What is the most caus | Patient's hypertension? 2 | aa rune | eee (Ginnie | piteracr From Py ow | 30of85‘3.7 MICROCIRCULATION AND LYMPH EXCHANGE OF SUBSTANCES ACROSS CAPILLARIES « Lipld-Soluble Substances ‘oSimple difusion across capillary endothelial cells Bg. Ozand CO: ‘« Small Water-Soluble Substances. (0 Uses clefts (pores) between endothalial cells Bg. water, glucose, amino acids Tight clefts: BBB; Wide clefts: Liver Sinusolds «Large Water-Soluble Substances ‘0 Uses pinocytosis eg, Proteins "Which o 1 | Shrough waters | | ayaa : | (econ (0) Glucose | Fram Physlolopay BRS. 6 £6 STARLING FORCES + Describes uid movement into (absorption) or out of (eration) the capillary ‘rpceaat Pressure. STARLING EQUATION + Fluid Movement (:) © if Positive, promotes ftration (uid moves out of the capillary) olf Negative, promotes absorption (uid moves into the capillary) = Kil —PI-(Re= mI) where 4, = Fluid movement (ml/min) (= Hydraulle conductance (ml/min + mm #8) P,= Capillary hydrostatic pressure (mun Hg) POP INGUIIGE ) NISIE SEEPS SRT RTER COMLPE OF ites: Uwwiw.fecebook.com/topnotchmedicalboardprep/ FLUID FLOW 1. Capillary Hydrostatic Pressure increases ——2. Capillary Hydrostatic Pressure Decreases 53. Capillary Oncotie Pressure Increases 4 Capillary Oncotic Pressure Decreases 5 Interstitial Hydrostatic Pressure Increases 6 interstitial Hydrostatic Pressure Decreases 7, Interstitial Oncote Pressure Increases 4 Imtermttial Oncotic Pressure Decreases Ts xrincreases “A. Filtration (iuld moves out ofthe capillary) B._Reabsorption (iuld moves into the capillary) inecapllary, Pele 30 mmilg PI -Rms Hg welv 8 AE and wD tmmilg What the dreeton of fuld mavernantand the net driving | free? (A) Absorption: 6mm Hg (3) Asorpion; 9mm HE | (©) Fieration; 6 mm Hg (0) Fain; 9 mm Hg (G) Thee eno nat ald movern Notpressure =(P, -F)~ (x, -®) | «= [20 =(-2)~(28-2)] mmtig | = 3zmmHg ~ 23 mmHg ommig [iavcapiiny Peso mpg Fipvamm ewan 2s mei, | Ome aTiGs ng ober of owe SBeeaplary wall Me, (Aj o0smt/ming” 5 | Ghoasmurmie (C) 450 ft | or'gotmp sin Li uyfingAtic system 2-8, of lymph produced per day ++ Ras one-way valves, flow is unidirectional + Functions ‘2 Reabsorbs proteins and excess fluid back tthe circulatory system absorbs fat (using lacteas) Contains mph nodes aes, S. EDEMA + Excess flu inthe interstitial spaces beyond the capability ofthe Iymphatic system to return in to the blood vessels ‘P= Interatital hydrostade pressure (mm Hg) e-= Capillary oncole pressure (mm Hg) ‘m= Interstiial oncotic pressure (mun Hg) esi aa STARLING FORCES Rie STARLING caiimrrion NORMAL FORCES aS VALUE Capillary + Fa¥vpe filtration; Hydrostatic « determined by pressure & + 25miniig | Pressure 1», yesistance inarteres & veins | + Opposes filtration (favors | Capillary absorption): _ os = increased by increases in ree plasma protein concentration ~ Opposes filtration (favors Interstitial * OPPO = ie ¢ « anmie Hydrostatle sighy negative due to | ae jymphatic pump Tnterstidal + Favors firation: | Oncotic + determined by interstita! + Gmmiig Pressure protein concentration m 7 Hydraulic conductance of Filtration capillary wall (capillary Coefficient permeability: | + promotes filtration | Normal Net * 2rnb/min | | siitration ‘TOPNOTCH BOARD PRI For inquiries visit wwwstor onotchHAArAArAR Frm nh ne hi IEP PHYSIOLOGY HANDOUT BY ENRICO FAOLC C. BANZUELA, MD CAUSES OF EDEMA EXAMPLES, “Arterolar dilatation venous constriction capil Mpanoweatle © venous pressure Pressure, * heart allure ‘+ ECF volume expansion + standing ‘+ Vplasma protein concentration cay ei Tae” severe liver disease, Pressure * Protein malnutrition, + nephrotic syndrome ‘Filtration Coefficient histamine, cytokines) [Te tendency for eens Gear wi be nceaedby | (A) artertolar constriction | | Gl incrases venus pense | | {Chinereaed plasma protein concentration |L_f) museular activin From Phsologgy BES 6 Page 31 of 85 4 Carahrnl enmiiannntchmndicstneedam 3.8 SPECIAL CIRCULATIONS: ‘CONTROL OF BLOOD FLOW =S=* For inquiries, visit www, topnotchboardpres.<: ‘© Maybe Intrinsle (Local) or Extrinsic (Hormonal/Humeral) [REASONS FOR LOCAL CONTROL OF BLOOD FLOW ‘© For the tissues to get thelr proper amounts of oxygen and ‘nutrients and to remove wastes ++ For thermoregulation (en the skin) For homeostasis (eg, kidneys) Blood Flow to Diteren Organs and Tissues Under Basal Conditions Percent = mimin = mV/min“100 9 Bria “4 700 0 Heart 4 200 0 Broneht a 100 2 Kidaoys 2 100 360 Liver n 1380 9s Por! a 1050 “Arterial ¢ 300 Musele (Inactive state) is 750 4 Bone $ 250 3 $80 (cl wenn) 6 300 3 1 0 160 ‘Adrenal pance as % Ey Other tues 33 15 13 Tout 1009 = $000 ‘sed cuialy on da compled by Dr. A. Saplela, ‘MECHANISMS FOR LOCAL BLOOD FLOW CONTROL © Acute Control ‘Decreased tissue oxygenation will increase blood flow ‘© Mechanisms for Acute Control of Local Blood Flow * Myogente Theory: when vascular smooth muscle are stretched, there's reflex contraction and vice versa ~ May explain autoregulation, but not active or reactive hyperemia * Metabolic Theory: vasodilator metabolites (Aden ae (COz, H,K, lactate) are produced as a result of od activity Increasing blood flow during hypoxia, ; os + Acute Control: amples 0fvatabolie Thea 0 Reactive Hyperemia opal ** Nin blood flow in response to fod of Vblood flow + Eg. if vessels blocked fora toan hour > blood flow increases 4 Active Hyperemia * Blow flow increases Gu. glands during « Acute Contrgy nseguaton of oo ow Cn et heelack \ereased metabolic riod, brain during rapid mental activity + Maculatdensa in the distal tubule detects fluid levels + Afferent arteriole constriction/dilation occurs to ‘maintain appropriate renal blood flow and GFR Brain: C02 and H ‘an increase will cause vasodilation to wash out excess COz o Heart: Perfusion Pressure 1 If perfusion pressure to the hearts suddenly decreased, ‘compensatory vasodllation of arterioles would occur to maintain constant flow + Long-term Control ‘0 Via Angiogenesis : *» Due to VEGF, FGF, Anglogenin * Occurs in response to hypoxia co Vascularity is determined by Maximum Blood Flow Need, not by average need oh ot of capillary beds are closed most of the time, and only open needed ‘TOPNOTCH ‘or hitas://www. facebook, com/tepnotchmedicslboardorep/ EXTRINSIC CONTROL OF BLOOD FLOW = Through ‘oSympathetic NS ‘Vasoactive Hormones HORMONAL/HUMORAL MECHANISMS FOR BLOOD FLOW CONTROL ‘* Vasoconstrictors © Vasopressin: most potent vasoconstrictor ‘0 Serotonin: release as a result of blood vessel damage; ‘causes arteriolar vasoconstriction; implicated in migraine © Endothelin: released by damaged endothelium ‘PGP and TXAx: vasoconstrictors ONE Ep co Angiotensin IL + Vasodlaer an) ‘9 Prostacylin (Ply): counteracts TXAz co Nlerle Oxide (NO): vasodilates upstream blocd vessels * MOA: guanylate cyclase and cGMP * Acetylcholine causes vasodlladion by in production of NO in vascular amo ‘© PGE: vasodilators Lactate, Adenosine: found in mi 3 © Bradykinin & Histamine: ca i afation & venous constriction leading to IncreaggiQt*htion (local edema) off,COx and K OS ‘OANP o imal | (Carbon doxlde (COs) regulates blood Now to which one of he following |) organs? | "Witeare (D) Skeletal muscle at rest (stun () Skeletal muscle during exercise C1 Brain Fron BRS. 6 Ed Biot owt ih orga a contaled paar by teste | mreus stem rater tna poe meson? (A) Skin (©) Brain | Bien {Dstt muscle doing eerse ro Priinar 85o84 3.9 GRAVITY, EXERCISE AND HEMORRHAGE STANDING + Blood pools in the veins > WVR-> Wc > VBP * YBaroreceptor suetch-> fring rate of CW IX Sympathetic + BHR TSV-> 2CO> TEP + Vasoconstriction of systemic arterioles > ‘TPR-> NEP + Vasoconstriction of Veins > VR > CO-> SBP BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C. BANZUELA, MD JoPNO ies vsit wevw.topnotchboardprep.com.ph or DitEi//ww. facebook, com Iboardpreoy NP 2 9 85Mire perarees ong RoE which se wing cmpentinnchangesoceurt? Ma) Decreased bent | | (incase contacty | | {eh Decree at prpheral reine CR) (5) Deersoedeardae opt | (Binteet eRineste | | Ate-yeairoid woman present to the emergency department with ‘severe dlarrhea, When sels supine (lying down), her blood pressure Is | 90/60 mm Hg and her heart rate i 100 beats/i | (inereaued). When she is moved to a standing position, he | | further Increases to 120 beats/nuin. Which of the following accounts for | | the further Increase in heart rate upon standing | 1 | (A) Decreased total peripheral resistance (B) Increased venoconstriction | {C)nereased contractyy (0) Increased afterload (E) Decreased venous return ‘Prom Philongy BRS 60 £4 EXERCISE # Sympathetic outflow > THR, PSV > NCO Mblood flow to skalotal muscles + Vasoconstriction of splanchnic and renal arterioles > blood Mow to skelital muscles, + Vasoconstriction of veins > VR ->,®CO-> ‘blood flow to skeletal muscles ‘+ ‘vasodilator metabolites -> vasodilation of skeletal muscle arterioles -> VTPR-> ‘blood flow to skeletal muscles During exercise total peripheral reisance ‘CTPR) decreases because of | 8 affect of (A) the sympathee nervous rystem on splanchnic arterioles (G) the pararympathetic nervous system on shalatal muscle arterioles (©) local metabolites on skeletal muscle artarioles | (@) local metabolites on cerebral arterioles (8) hitamine on skeletal muscle arterioles Wkomall as uung Volumes and Capacities U, Mechanics of Breathing IL Gas Exchange IV, Oxygen Transport V. CO: Transport VI. Pulinonary Circulation VIL. V/Q Defects VIIL. Control of Breathing 1X, Integrated Responses to the Respiratory System (41 LUNG VOLUMES AND CAPACITIES} PECIAL NOTES ON RESPIRATORY PHYSIOLOGY ‘TERM DESCRIPTION ‘© Air from the Nose to Terminal ‘Anatomic (conducting rone) that does Dead Space gas exchange: a, # (Normal Value: 150mL} | Ee aera NOT thdergo Alveolar Dead tratory zone N Space gas exchange dustp V/Q inismiatch . yrmial Val ye a 3 “ Piyeitagle « anata iglvaplar Dead space ane fnonary Segments (segmental Asatomicumie * eee ‘Respiratory er [ratory bronchiole, alveolar ducts, Unit of he Lu ‘walveolar sacs Typed af'"*,"¥+ For gas exchange, Paw « larges than Type It Tad” + For surfactant production; L po. |éteumocyte + smaller than Type | ‘Which fe ewig parameters Gaceated sing moderate a ~ Produces mucus for lubrication Inthe | exeretset : ‘acbte cots some | (A) Arteriovenous 02 difference ty, bck | (8) Heart rate a Clara Cells / * Produces protective GAGs and metabolize | Oeeiatetpue and | cubes” —_" aivborne toxins | (huts pressure [teat perteracesiane (7m) DustCells Alveolar Macrophages HEMORRHAGE ‘© MBRR> THR, PSV, PTPR, Pvasoconst BP . ‘© (PRAAS activation > PNa reabsorptiog’# itravascular volume > BP a ‘+ WSystemic Capillary sacral “2 uid absorption abi 9 > intravascular volume > Loe ol Payatolegic Dead Space Vr = Tidal volume (mL) Paco, = Poo, of arterial blood (mm Hg) Pico, = Poo, of mixed expired air (mm Hg) Minute Ventilation: Minute ventilation = Vrx Breaths/min + Alveolar Ventilation: Va=(Vt—Vo)x Breaths/min where Va = Alveolar ventilati i Vr= Tidal volume (ry) = Vo = Physiologic dead space (mL) | Abealthy 65-year-old man with a dal volume 145 Las | breahing frequency of 16 breathe/min Hlssrey oo Goan and the PCO ois expire areal PCO 641 mim He | rontladog? 6AM #35 mmHg What hisalveotar | (9) 0.066 47min + (9)0381/min (0) 61¢1/min (ON tee tt ‘TOPNOTCH BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C, BANZUELA, MD Fram Phyriolopgy BRS» 64 For inquiries visit www.topnotchboardoreD.com.dh or httos://www. faceticok. -com/toonatchmadicathaarenean st 23 of 8 | t 1eee ee ‘LUNG VOLUMES AND CAPACITIES ‘= Air in lungs Is divided into: ‘o Lung Volumes: /RY, TV, ERV, RV © Lung Capacities: Sum of 2 or more lung volumes: IC, FRG, VC, Tue + Lung volumes and Capacities: 20-25% lower in females ed angen LUNG VOLUMES AND CAPACITIES (SPACE FOR DRAWING BY STUDENTS) Cave normal value 0096 ROOM ine eth folowing lng vole oF apace canbe meray rome (A) Functional residual capacity (8) Physiologic dead space. Ler] {C) Residual volume (RV) | (D) Total lung capacity (TLC) ) Vial capaciey (Ve) From Pgtlpay BAS. Et ‘Which volume remains in Whe Tongs Rar dal volume V7) expired? (A) Tidal volume (1V) (8) Vita capaciey (VO) | (C) Expiratocy reserve volume (ERV) | (©) Residual volume (RV) | {5 ineonal raul capac (7) | Tnapira (pearance fea 1 3Seyear ld man has vial apa (VG) af atidl volume (TV) of | O13 Lam inepratary eapacty of 3. anda funcional residual eapaty (Gre or 2s Whatis his expratary revere volume (ENV)? (A)4SL. (D)3.0L (15k Ss omar ea ; Sete 8 | eee eer er aa Y roan oe eee ae A 10'S alr expired after one second of forced maximal tal volume of alr expired of forced maximal exhalation ‘00fnL divided into: space (450mL) unit of the lung (350mL) > Albus of alr exhaled after expiration of tidal ald lume sng arin tholngrafer mana ees + maintains oxygenation in between breaths: * cannot be measured by spirometry ie TVeikv | + ERV RI | © equillbrium/resting volume of the lung; | sacs marker for lung junclon; | eo © during this time, alveolar pressure = atmospherte pressure; 1 » cannot be measured by spirometry T IRV TV + ERV veor RY Mivolune ofairthateanbeinhaled or | FVC exhaled | IRV + TV > ERV + RV: TLC 5 cannot be measured by spirometry a ESTRICTIVELD —— RESTRICTIVELD pale? (ex. COPD) fibrosis . ao Fav i G °| VC v vw | Ke FEVi/FVC v Normal or 4 | | Ge * z TERM. DESCRI | 4.2 MECHANICS OF BREATHING 7 dal volume; ‘MUSCLES INVOLVED IN PULMONARY VENTILATION + Inspiration aca garnets ‘© Normal inspiration: Active (main muscle: Diaphragm) Forced Inspiration: External Intercostals, Accessory 7 Muscles: SCM, Anterior Serrat, Scalene, Alae Nasi, Genloglossus, Arytenold ‘Ribs move upward and outward; abdominal contents move downward + Expiration ‘© Normal Expiration: Passive ‘Forced Expiration: Internal intercostals, Abdominal muscles (Rectus Abdominis, Internal and External Oblique, ‘Transversus Abdominis) ‘© Ribs move downward and inward; abdominal contents move upward COMPLIANCE OF THE LUNGS ¢ Distensibllty of he ngs anid chest wall ‘+ Change in voluine for a given change in capacitance of vessels) alr aeeaaled + Inversely related to elastance + Slope ofthe press-volume curve © Inspiration has a different curve than expiration due to need to overcome surface tension forces du noes ‘during inspiration © Highest compliance: at middle: range of © Lowest compliance: mge of pressures ‘at high pressures (curve flattens here) TOPNOTCH BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C. BANZUELA, MD For inquiries visit www.topnotchboardprep.com.ph or httos://www. facebook. com/to {tev sacebool.cam/topnotchmedlealboardprep/ Page 34 of 85Inspiration Roprauregye «nga: has natural tendoncyt9 collapse ‘Chest wall: has a natural tendency to expand « AtPRC: lungs and chest wall are at equilibrium ‘o Intrapleural pressure Is negative + Preumothorax "intrapleural pressure = atmosphere pressure Lungs collapse, chest wall expands CLINICAL CONDITIONS + Emphysema ‘Lung compliance is increased -> new, higher FRC will be ‘seen to balance tendency of chest wall to expand vs tendency ‘of lungs to collapse -> patient becomes barrel-chested + Fibrosis ‘o Lung compliance is decreased -> new, lower FRC will be seen to maintain balance ng (A) The slope of each ofthe curves i resis (8) The compllance ofthe lungs alone Is ess than the compliance of the lungs plus chest wall | wall (0) When airway pressure ls zero (atmospherl), the volume ofthe | “3 combined system isthe functional residual capacity (FRC);.."=,, {(€) When airway pressure is ero (atmospheric), intrapleural pressure is zero ie ofthe lungs plus ch cheat wat ony. tel nga Ll 4s es, 6 Ed | ‘SURFACE TENSION «+ Force caused by water molecules at the air-liquid interface that tends to minimize surface ares (6) The compliance ofthe chest wall alone isles than the complance | {y LUNG SURFACTANT il that produces surfactant 2’ main component of Surfactant = SActive component of Surfactant 4 Mechaniams for DPPC reducing wurtace DEN TS effect of Surfactant on i) . —" T= 6 start of Surfactant production 7. Maturation of Surfactant pee ieee Fe tia SY Teens ~Kgiampnipate ware 3. Decres 3" (Hydrophobic and C typetPn Xeww# Hydrophilic) . Type | Preumocytes, D. Type It Pneumo E, Dipalmitoyl- 4H. Amniotic L:S Ratio I. Sterolds, Surfactant PPC) J. 24t week AOG K, 35™ week AOG. pal weak 25 has neonatal leh ofthe following would be Hal PO2 of 100 mm Hg. | §f8) collapse ofthe small alveolt (0) Increased lung compliance (0) Normal breathing rate {2} Lecthinsphingomyelin ratio of greater than 2:1 in amniotic Mule ee from trio BB. AIRWAY RESISTANCE + Described by Polseuille Law Velength of the airway reradius of the airway «+ Major site of airway resistance: medlum-sized bronchi + Factors affecting Airway Resista © Bronchal Smooth Muscle Conraction/Relsaton duet * alters radius of airways tung Volume * due to radial traction exerted on alrways by surrounding, lng tissue + High lung volumes ~> greater traction, decreased airway + Law of Laplace of Laplace resistance (asthmatic patients learn to breathe at higher volumes to ofset airway resistance) © Viscosty/Density of inspired gas where * Low-density gas (eg, hellum) reduces resistance to = Collapsing pressure on alveolus (ynes/em') o Pressure required to keep alveolus open | Which ofthe folowing isthe ste of highest airway resistance? (ynes/co) | (A) Trachea () Smallest bronchi ‘T= Surface tension (dynes/exn) | Warestoenat Baveat ‘r= Radius ofthe alveolus (=m) | (c)Mediumszed brome From Phyology BRS. 6 « pre-Term Bables: high collapsing pressure due to: “smaller alveolar radius (50 mlcrometers) compared to adults o Lack mar sar pHYSIOLOGY HANDOUT BY ENRICO PAOLO C PPI BANZUELA, 'CH BOARD PRET MD Page 35 of 85 For inquiries visit www. topnotchboardprep, .com.ph or http://www facebook, com/topnotchmedicalboardotep/+ ALS" For inquirled) Viele wa, topnotchbearderep.comi Sh or htt PARTIAL PRESSURES OF Oz AND CO7 BREATHING CYCLE + Remember: lung pressures are expressed relative to atmospheric pressure ‘© ACPRC, alveolar pressure = 0 «Before Inspiration: ‘0 Intrapleural pressure is negative, alveolar pressure = 0 150 * During inepiration ro, 160 Watton Toe ce St ‘o Intrapleural pressure becomes more negative, alveolar eulbraion tev | pressure becomes more negative sey seyetne Siinnete secreing | + During expiration: Ea 'o Alveolar pressure Increases and becomes greater than. wo 40 6 atmospheric pressure Ones i oem, ated om 0 Deed acded eaulbration awe | Increasing win slvecter Poo) an See o Intrapleural pressure increases back to its resting value PCO, [iranares of the lung is not vandlaiad because of branchial obstruction, pulmonary caplary bloed serving that area wl that (A) equal to atmospheric POs (@) equal to mixed venous POs {¢) equal to normal systamic arterial POs (0) higher than inspired POs a [_ teeter an ne eo Pn | a ons. ee | ALVEOLAR-BLOOD GAS: «+ Parfuslonslimited Gas © Gas equillbvates with jonary capillary near the start of the pulmonai © Diffusion of ‘only by increasing blood flow jormal conditions Which of the following struedurig inapiraion? | (a) tntrapeural pressures postive |The volume i he longs less than the functional residug! | Or Gpaaty Re) (c) Aiveolt pressure equals atmosphere pressure {b) alveolar pressure is igher than tmospherle pressure {@)Intrepleural pressure ls more negative than Ils durlgEtygtion ee EEL 43 GAS aa PERTINENT LAWS OF PHYSICS FoR nuprta¥ony prvsio.os PHYSICS FOR RESEIOATORY PHYSIC : oust REBT REIOMGY | oo tad a tng Px = PBXF Lung Volume | 0 Gas Does NOT equilibrate even until the end of the : roe es eg retcoes nrc and ves sites orPordial Toul preenurex ta for tend (emphysema, fibrosis) Pressure, Fractional gas concentration Henry's L (x = Px x Solubility a vrs Faw eros Lec caent ceemnsamene * ee of Dissolved nehralpmretpe tae solution efoto ete ty DAAP inceil | Pesta of ee eee | Diffusion cana diffusion: Partial ST RAS ae meron Presture | * difference (NOT concentration of | uses -TOPNOTCH BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C, BAN Horio eles walt www topnotchboardprep.com.ph or Ntps// www facebook cont notchmedicalboay Page 36 of 85 : lcalboardprep/ olay“4-4 OXYGEN TRANSPORT. = HEMOGLOBIN + 0x ‘0.9096: transported via HgD, (0.296: transported freely dissolved in plasma ‘+ Hemoglobin can bind with oxygen (oxyhemoglobin), carbon monoxide (carboxyhemoglobin) or carbon dloxide (carbaminohemoglobin) + Oxygen normally binds wich Fei and not Fe? HbA: aap + HOF: cays + Hemoglobin s: “8 + 2,3 BPG binds more to HbA and binds less with HOF . "0.02 affinity is higher in HBF than HBA (shift co the left of he (02-HgB dissociation curve) Facil ‘of Oa from mother to fetus + Onbinding capacity ‘© Maximum amount of Os that ean be bound to gS o Measured at 100% saturation ‘Expressed in mL, O2/gram of hemoglobin ‘© Normal value: 1.36 ** Orcontent of the blood ‘Total amount of 02 carried in blood, Including bound and dissolved 02 ©, content= ( jobin concentration O,-bindlng capacity x % saturation) + Dszolved O; (0s-HgB DISSOCIATION CURVE + Sigmoldal in shape (© POs of 25 mmHg: $0% saturated (Pao) (© PO2 of 40 mmHg: 75% saturated (mixed venous blood) ‘© POs of 100 mmHg: almost 100% saturated (arteria/ blood) ‘+ Exhibits Positive Cooperativity ‘0 Binding of first 0: molecule increases affinity for second Or ‘molecule and so forth ‘Or HEMOGLOBIN DISSOCIATION CURVE. ee Or-HigB DISSOCIATION CURVE A (SPACE FOR DRAWING BY STUDENTS) __ TOPNOTCH BOARD PREP PHYSIOLOGY HANDOUT 87 Eh (OLO ¢, BANZUELA, MD For inquiries vislt www.topnotchboardprep.com.ph oF hntps://wwy.facebook,com/topnotchmedicalboardorap/ * Shift to the RIGHT: ‘o Increased UNLOADING of O2 from HgB o Increased Poo © Due to increased Carbon DIOXIDE, Acidosis (Bohr Effect), 2,3 BPG, Exercise & Temperature Shift to the LEFT ‘o {ncreased BINDING of Oz to HgB © Decreased Pso ‘Due to Increased Carbon MONOXIDE, HoF © "CO; binds 250x better to Hg than Os, decreases Ox content of blood and causes shift to the left of Ox-HigB dissociation curve ¥ we Poin 2s MNEMONICS ‘Or Hig DISSOCIATION CURVE “GABET/Go the RIGHT thing, LET GO" | ox | Acidosis P BPG (2.3 BPG) | Exercise \ ‘Temperature CUE /"in the hemoglobin-02 dissodation curves shown above, the shift from | curve Ato cuve B could be caused by (A) increased pt 1 (8) decreased 2.3-diphosphoglycerate (DPG) concentration () strenuous exercise (0) fetal hemoglobin (HOF) | | i i | {E)etbon menace (C0) potolng 100 \ z | 5 | § By | i j ft \ i i | | | | co 50 ss 100 | i oa (mm Hg) | __ rom Pla BS, | The shift from curve.A to curye B is associated ae naam (A) increased #30 (B) increased affity ofhemoglobin fr 02 | Gye ty ied ote un rested O2-carrying capac {e} encased O2- carping capac ofhemseoen "rom Pitolena 05 64 Page 37 of 85HYPOXEMIA VS. HYPOXIA + Hypoxemia ‘9 Decreased areartal PO? ‘oWill lead to hypoxia °° radlent used to differentiate between causes of hypoxemia Not always caused by hypoxernia Triggers: EPO production (through Increased production of hypoxla-inducible factor 1) ‘Ava GRADIENT * Difference between Alveolar POz and Arterial POs ay Ara gredieat where: dea gradient «difference between alveolar Poy and arterial Poy Pio, = alveolar Po, (calculated from the alveclar gas equation) P al Po; (maasured in arterial blood) I ma" For inquiries, visit www, topnetshbearderes. com. ph or Dita ee eearentee 4.5 COz TRANSPORT. ‘© Transported in Forms: 19 70%: HCOs" 0 2346: CarbaminolgB 0 796: freely-dissolved in plasma jemoglobin buffers He inside RECS Poy Plog = Inspired Po, Peay = alveolar Poo, = arterial Pc, (measured In arterial blood) = respiratory exchange ratio or respiratory quotient {00g production/O, consumption) MRR Gis sirens = : cou ‘ asin Ta a pecs Nar nite BE a en. NE oie en acne ins i cE AE AAD ei 8 ee 3 a baer ara nee See a ara ag Fer PL Fh Pay att og We elope . ‘ eee Mechanimt ‘cardia euput 1 load tow ‘ol a iio IETS Anemie 4 Hemoglobin concentration eausus 4 0, content of iene og A SE BED cuore iit 1 “nh as Toma tir ae ie ee tea eran ‘uocatntn ae hut oa | Gheommaereehe ene De ae “on +A AS att gt 1 ar carpanecy fe | ape who iyporenlatngévetomorhineoveriose | {(C) Person at 12,000 feet above se level {0) Person with normal lungs breathing S0% 03 {Ee} Person with normal lungs brething OOO. nani ir fe ' aaa gem aoe {ellowing occurs in venous blood? (4) Conversion of CO, and| HDs in the red blood cals ty Ueoute ote ip eater eerie ae {Mie denyenegbinn vous od | AGG cxytsmopobin ra beter butler fr Hethans deoxjhemoglobin ‘ * 2 : ry ‘HALDANE: LUNGS BOHR: Booy Tissues LUNGS e Jarbonic anhydrase in venous blood from COs and 0 i buffered by HCOs" in venous ©, TISSUES $ Va Soe (“4.6 PULMONARY CIRCULATION] PULMONARY CIRCULATION 1. Pulmonary Circulation: PRESSURE. cet meee Goan ean 3. Pulmonary Circulation: CARDIAC OUTPUT _——~4 Pulmonary Blood Flow: SUPINE ig | ee ee Ge rai STANDING pa ‘Hypoxia (low PAQz) on Pulmonary Arterioles _—— 7. Causes of Pulmonary Global Hypoxie Vasoconstriction cocertang oseae nese _—— 9. Causes Bronchoconstriction [A> Systemic Cireslation tricia RV: ] B. < Systemic Circulation © Bronchoconstteton | | ©. = Systemle Circulation High alude Fee | D.Lowestat the Apex Highest st Circulation. | the Base E.Samethrough heentrelung ft Hucrehe a ~—— co, o2—> 3e— <——n* in which vascular bed d063 Bypoaa Uma : Wow tc a (@) Pulmonary e ©) Sian C) cerebral “Compared with the systemie From Physiolopgy BRS. 6 £d (A) higher blood flow 0) ‘circulation has a = : enn ONpartcnee i Pom Png ans be! IOTCH BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C. BANZI : TOPNOTCH BOARD Pi toprotenboa’ Alveolar Air {rPretad with supplemental Oh appley@agl 6: Pressure during systole but less than that during diastole helpful ifthe person's predominant V/Q, * Zones a eeoaicnee “rtocl Alveolar Capllay Pressure» Alveolar Alr Pressure Getta throughout the cycle ——ppen otto Langs x Ene ‘one eee eetaptestontnn | SHB? a 4 Entire lungs During exercise eee 5 Pulmonary Hemorrhage and Positive Pressure Ventilation * Cerebral Co + Control ine Midbrain and Po: 1 Ghemorecaptors shunts rs + Right-to-Left Shunts cles {Normal ta smal exten since 296 of cardiac output bypasses lungs 1 CORTEX © Abnormal conditions (eg. TOR) results in hypoxemia veag {gil overtde the autonomic brainstem centers + Leftcto-Right Shunts some out Voluntary Hyperventiaton sirjorecommon than rightto-leftshunts (eg.PDA) —“S/"5**" oVPaCO2> pH > LOC S does not cause hypoxemia; PO2 will be elevated on the Pa, “zr + Voluntary Hypoventilation (breath-holding) side of the heart = 0 Pas, *PaCOz > YpH > LOC Fe” ‘CONTROL CENTERS IN THE MIDBRAIN, PONS £7 V/Q DEFECTS a ae Came #2 Creates the Basic Resplratory Rhythm Reticular formation of medulla contains the Dorsal Ventilation (Alveolar Ventilation) “~ “Resp i ratory Group (DRG), Ventral Respiratory Gi + @ Perfusion (Pulmonary Blood Flow) (vRe) canteen Caamsecreaees ee Soe 1 Normal V/Q Ratio: 08 + Pons o Results in: 2, = Loommng BSS 0 Modifies the Basic Respiratory Rhythm a “Vwi Pos Peas ‘contains the Apneustic and Pneumotaxic centers «* High V/Q: high PO:, low PCOz (eg. lung apex) Ww PO:, high PCOz(eg. lung base) + ¥/Q=2er0 ‘Shunt (e.g, RL shunt, airway obstructions) + ¥/Q=tnfiniee | : 'o Dead Space (e.. pulmonary emoolism) TOPNOTCH BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C. BANZUELA, MD JOP MOTs vst www topnotchboardprep.cOM.Ph oF hits: / www. facebook, com/topnete oardorens tt‘MECHANORECEPTORS. Leen ee =a [eee DESCRIPTION NOREEN TRUTHS Vian Respiratory Center + stimuleted by Ling Dstnsion or baste yeh fr breathing: ung Stresch — Inkates Hering Brover Reflex that 1 Ethormal Resting Inspiration Rechptons— Sacroues Respiratory Rate by prolonging ore “pee Gr peroneal chmerecnors expineey me and CN X (peripheral chemoreceptors an: . lmb M¢ t dung mechanoreceptors) Joint& Muscle cere aepanry ineaas “4 Respiratory ; Si : eee Suze on exercise ies Rave during Exercise Supplements effect of DRG during exerdae, > al vee * for forced Inspiration and expiration Ireteant cee eee eaprcien sod wrronet ~teseihemtcenim Recpeore —* runes bconcbocees Pneumotaxic * Location: Upper Pons ne rn il ‘* Found in “juxtacapillary” areas Center + Shortens time or nsplration > RR See waueoary onlay, T Leraion: Lower Pons engorgement Apneustie —_* Prolangs time for inspiration > VRR TReceptors —_, Causes rapid shallow breathing and Center * Causes deep and prolonged inspiratory gesp responsible for the fe ing ageree (es. fapnewsls) site| Intesided heart allure) “%of™y_ CENTRAL AND PERIPHERAL CHEMORECEPTORS + Central Chemoroceprors ‘© Location: ventral medulla (© Respond directly to CSFH* o Causes PRR oes weg Hypoxemla produces hyperventiadon Oy» juget ofeCiph the rors any {A parenienerve (0) edu se ore (8) j receptors (B) caroudartigertic body (lung stretch receptors + Peripheral Chemoreceptors ‘e Losation: Carotid and Aortis Bodies . ‘© Responds MAINLY to PaO2 <60mmHig * Possibly due to excitable Giomus Cells (also seen'in central chemoreceptors) = Glomus Cell Action Potential: PCO2/YP02.2,, potassium efflux > opening of voltgge-say calcium channels ~ Calcium Influx ~ Secretion of NTS (eg. Ach, NE, dopamine, Substaga®-?, met- enkephalin) a 0 Causes RE gs 2 Also respond thigh PaCOs, high arta H+ s TMNEMONICS CHEMORECEPTORS T Central Cheers, AE H+ (comes from plasma C02) | Peripheral Chemorgcéptotd= Pang Low Oxygen (2) J |) As2-year-old Wegman with severe pulmonary brosis is evaluated by] her physic the following arterial blpod gases: pH = 7.48, Pa02 1258 mm Hg. and PaCOs = 32 mm Hg, Which stateruent best explains the ‘observed value of PaCOs? I (A) The increased pH stimulates breathing ia peripheral chemoreceptors | (8) The increased pit stimulates breathing via central chemoreceptors (©) The decreased Pa0s inhibits breathing via peripheral chemoreceptors ! (0) The decreased Pa0s stimulates breathing via peripheral chemoreceptors (€) The decreased Pa02 stimulates breathing via central chemoreceptors From Phyilopy ‘TOPNOTCH BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C. BANZUELA, KD For inquirles visit www.topnotchboardprep.com.ph or https://www. facebook. com/topnotchmedicalboardprap/ 4.9 INTEGRATED RESPONSES OF THE RESPIRATORY SYSTEM RESPIRATORY RESPONSES TO EXERCISE {INCREASES (%) DECREASES (V) NO CHANGE * 02 Consumption cos Rraiean Arterial POz and. © Arterial pH Pcor + Respiratory Rate (strenuous * Venous PCO: exercise dueto —* Artes) PH + Pulmonary Blood lacticacidosis) «(moderate exercise) Flow | Which ofthe following changes occurs during streaunus exercise? (A) Ventilation rate and 02 consumption increase tothe same extent | (@) Systemic arterial PO2 decreases to about 70 mm Hg | (©) Systemic arterial PCO? increases to about 60 mm Hg (0) Systemic venous PCO? decreases to about 20 mm Hg (2) Pulmonary bod Now dereases athe expense of systemic blood RESPIRATORY RESPONSES TO HIGH ALTITUDE INCREASES (4) DECREASES (V) | Respiratory Rate «Arterial pH ‘+ HgB Concentration ' Alveolar POz +23 BPC ‘= Arterial POz | + Pulmonary Vascular Resistance | (Hypoxic vasoconstriction] lve to Leadvle Colorado (10200 fet bore ex cosy ince following will occur as a result of residing at alti nde bleed fvig wi oar oredr high se (area en 0 creased 2 cphasphop eras (DP) concentra {0)shinwuueripvottbehemogebn-Or sorte coe |_(8)Pulmonaryvatodiation Frum Phaangy BRS, 6» 60 | Page 40 of 85 | A38-ear-lé woman maves with ber family rom New York Gly (sea | i("Kiayearcld boy has a severe sathmatle attack with wheeting. He | expertences rapid breathing and becomes cyanotic His arterial PO2 Is | Simm Hig andhis Peo? is 30mm hg, Which afte folowing ‘atument about this pallets mont kayo bev? A Pore exiaoy volume /frced wal expacy (FEVS/EVC) x increased (2) Venton persion (V/Q rato is tncresed nthe fected areas othis ngs (cp Minar! PCO hghar than normal because of adequate xchange (0) His areal PCO lower tan norma because hypoxemia causing him to hypervenlate (E) His residual volume (RV) ls decreased sooner en ANNAN — trom Ebanar BS | To reat patient. he phyla should adinater | (A) anat-adrenergic antagonist | (C) a Ba-adrenergic agonist: | (hamuscaratcagonst (8) Bi-adrenergic antagonist (@)anleotinieagonist Ni jody Flulds AL The Nephron, Renal Clearance, Renal Blood Flow (RBF) and Glomerular Filtration Rate (GFR) UL, Reabsorption and Secretion IV, NaCl Regulation V. K Regulation, VL. Renal Regulation of Urea, Phosphate, Calcium and Magnesium Vil. Concentration and Dilution of Urine Vill. Renal Hormones 1X Acid-Base Balance X. Diurettes XI. Integrative Examples 5.1 BODY FLUIDS MNEMONICS "60-40-20" RULE 60% of BW: Water | fom eraser | oe raw Ecr [COMPART-% OF ins MAJOR) MENT BODY WT. ATION: + Tritiated Total Body water | Water + 60%, BO AS crew) ntipyrine Extracellula i -_ of wy he Compare! . ns = ‘ment (ECF) = aibactive jotinated : enum Na Plasma ‘Albumin t (REA) | Ard + Evans Blue 7 + ECF 715% in a Interstitial (7595 of PMS NaS icon Fluid (F) ECF) ‘indirect + Organic Tntra- + TBW-ECF Prosphates| cellular + 40% =” Uindirecsy) °K te calla (indirect) + Protein RD a ajced nia a worsen Aer eqalbraon a | ore te mplhad a annie concentration of 008 During te car io pred, Z0wol the njected manaltl wa xreted nthe gp eral fsa (CP) volume 3 ela ul (ECF) volume 3 (9 react ua (Ic) volumeis {ehecrvlume e101 {D)tcr volumes 10 2) interstitial volume is 12.5 Fram Pryslopay BRS BOARD HYSIOLOGY HANDOUT BY ENRICO Pat yaw opnetchboar prep.cOM.ph or Ny TOPMOTCH For inquiries visit worw.toP" { Which ofthe folowing substances or combina bbe used to mearure nterstital Muld volume? (0) Inulin ang 2:0 lone of subitanear could | (4) Mannitol (8) DiO alone Ch Ev L blue | Subjecs A and Bare 70ckg men. Subject A dg 2 and subject B drinks 2 of lotonte ot fubjecB will ave (A) greater change in intracal volume (B) higher postive eeowaty (C20) (©) greater change in recs (0) higur urine oemolarcy Poa = plasma osmolarity (mOsm/L) ‘Na’ = plasma Na* concentration (mEq/L) Glucose = plasma glucose concentration (mg/dL) BUN = blood ures nitrogen concentration (mg/dL) [ 5.2 NEPHRON, RENAL CLEARANCE, RENAL | BLOOD FLOW (RBF), GLOMERULAR, | FILTRATION RATE (GFR) NEPHRON + Structural and Functional Unit of the Kidneys = Two Types: © Cortical Nephron: 75% of nephrons, located In renal cortex, with shorter Loops of Henle and with peritubular capillaries Juxtamedullary Nephrons: 25% of nephrons, located in the corticomedullary junction, longer Loops of Henle and with Vasa Recta ‘+ Two Major Parts: ‘Renal or Malphigian Corpuscle: Afferent arterioles, ‘glomerular capillaries, efferent arteriole, podocytes, mesangial cells, ]G apparatus, Bowman's Space, Bowman's Capsule o enol Tubular sya: PET, DT, RENAL conPUsCLE~3 cuaRce, ass OF THE GLOMERULUS a 7 * Capiliary Endothelium Chlgitnesned oSerte NO ana TT + Basement Memrene own pe cagen Main charge bron «Destroyed in glee eases + Pedsyes ‘© Contains foot processes and filtration slits ith pores 8 nm in diameter ‘OLO C. BANZUELA, MD www facebook.com/topnotchmedi Page 41 of 85 TEDL, facebook com/topnotchmedlealboardorap/*f* *t °t ®RENAL CORPUSCLE- OTHER CELLS + Mesanglal Cells ‘olntraglomerular: modified smooth muscles capable of Phagocytosis 0 Extraglomerular aka Lacis Cells: may play role tn renal autoregulation, RAAS and EPO secretion + Juxtaglomuerutar JG) Cells OAC the walls of afferent arterioles co Secrete renin + Macuta Denso on oT ‘© Monitor Na concentration inthe lumen of DT (and consequenty, Blood Pressure) ruowanserrm See ee | eee : Sree ri + Distal Tubule (DT) ft © Second Part: Late Di. lile/Connecting Tubule, Cortical Collecting Pubple o Medullary’ Seihg rubute 0 Collecting Duct Proximal ube Contax Loop ef Hen 2 Madu “Thick segment of | ascending imp: ‘Tn sogeni ct —— = ecanding im Descending ib — ue TOPNOTCH BOAI .RD PREP PHYSIOLOGY HANDOUT BY ENRICO Pao} For Inquiries visit wwwtopnotchboardprep.com.ph or https! //www.fae tDs://www. For inquiries, visit www, sopnotchboerderen . K> inulin > urea > Na > glucose, amino acids and Cor + Highest Clearance: PAH ‘Reason: Filtered and Secreted, not reabsorbed © Used to estimate for Renal Blood Flow (RBF) and Renal Plasma Flow (RPF) * Lowest Clearance: Proteln, Na, Glucose, amino Aclds, HCOs can F ‘© Reason: Not filtered (protein) or filtered but mostly reabsorbed (everything else listed above) ‘© Normally not found or found in small amounts in the urine + Clearance equal to GFR: (nulin, creatinine ‘© Reason: filtered but not secreted not reabsorbed © Marker for Kidney function (glomerular marker} | Whe (te owing abxancar tare igh eal Wea | “Gi Parwaminchpuneadd ran) wae ene | inate Be \ | toh coe rom yong Bn. 6 | Te Yolowingnformatn war aiadin 20yearaldcaoge ste | | stowaspartpatnginareeaehsadyln ie Cte Aeseeeh Uni | | ae te Bd 2me/at | : Urine ain) 150 = 00 g/m Urine dow t= imigai P2200 me | Assuming that Xs freely tered, which fhe following statements (A) There is net secretion oft | (0) Theres net reabsorption oft {© There bth reabarton nd seredion of i clearance of could be used treasure the glomerular | | etrmmenme ter) Soneeeere: (€) The clearance os greater than the clearance of inulin $$ rom rttoay Bas, 60 | RENAL BLOOD FLOW (RBI + 25% of Cardiac Output ” * Directly proportional to pressure difference between renal artery and renal vein; inversel sry anda ly Proportional to resistance of LO C, BANZUELA, MD book com/topnotchmedlealboardorep/ e 42 of 85,ToPNgIgH TOPNOTCH MEDICAL BOARD PREP PHY: Tecate erinquiren, ie ‘0 Vasodilation of Renal Arterioles: Increases REP een prep.cs Tene nn or htpsi// te ‘SPECIAL NOTES ON GLOMERULAR CAPILLARY STARLING + Bg. PGBs Ph, bradykinin, NO, doparaine FORCES © Vasoconstriction of Renal Artarioles: Decreases ROP ‘STARLING VEE Sympcthete ns and Angiotensin If (pretrentily roRce DESCRIPTION constrlets efferent arterioles) + "Water pressure” atthe GC. «© "ANP: vasodllates Afferent Arterfoles and to a lesser extent Gc * Promotes GFR. vacoconstricts Efferent Arterioles. Net effect: increases REF Hydrostatic» increased by vasodilation of afferent arteriole « Renal Plasma Flow (RPF) Pressure or moderate vasoconstriction of afferent ‘Estimated by PAH Clearance arteriole © PAH Clearance underestimates true RPF by 10% duetoRPF [Bg + "Water pressure? atthe BS that opposes GC to kidney regions that do not ler and secrete PAH hydrostate Pressure and GFR. + Renal Blood Flow | Pressure» Increased by ureteral obstruction ‘+ “Proteins attracting water” atthe GC. ppp=—_E__ Gconcoue | QceR 1-Hematocrit Pressure « increased by plasma protein concentration, un \orad”. asoncole > Normal ue (oa promis namaly ‘Apatiants infused with para-arainobippuric add (PAH) to measure ‘renal bled flow (RBF).She kag a urine low rate of 5 m/min, «plasms Pressure ‘Altered to BS) iy 7 Nota Starling Force. %y ~ + Hydraule conductnce/fueaianyedeMclent (PAH) of § mg/ml. a uriz Paid of 600 mpi and &heosemetof 45%. What is her “effects | 600 mL/mi 1091 mL/min Lf describes capillary per comtfain {31855 m/min | + Promotes GFR Inergafed hy hlstsinine an #. (e.g., In burns) fe orm es ar raiin= Taahi + Amount fltered in the glomerular capillaries per unit time ‘0 Normal Value: 425mL/min or 180L/day ‘0 Determined by Starling Forces atthe level ofthe glomerular capillary (glomerulus) + BUN and Creatinine increase when GFR decreases In pre-renal azotemia (eg. Hypovolemia), BUN increases more than creatinine and BUN/Crea ratio > 20:1 0 GER decreases with age, but Creatinine remains constant cue to decreased muscle mass, STARLING FORCES + Describes fluld movement into (absorption) or out of (Aeration) the capillary . + GLOMERULAR FILTRATION RATE + GFA = Kil(PexPes)~ (Oar On] iltration coefficient of pe Glomt atic Pressure (Pec Glomerular Capillary H} (0 Pas Bowman's Space ijulrogatic Pressure ‘© Oct= Glomerular Capifiym} Oncotic Pressure (mmig) 0 Oss= Bowman's Space’Gncotie Pressure (mmHg) *s euler Cpilares Lace — /SIOLOGY HANDOUT BY EN! fphaardnren crm nh nr ‘TOPNOTCH BOARD PREP PHY’ Far Ineuirles vill wrsew tannin RICO PAOLO C. BAN; space hydrostatle praagyre » 10mmHg acne pegs Om ‘Atwhat value of glome lary oneeti pressure would | at te (0)0 mmHg | dlomerular Mating mm Hg vm Hi geet a tcets | Bowman’ (A) 57 mm Ha 6, “4, orn, , — Se icaMled anavicle Vesodtans | A tnereases, 3 . Afferent Arteriole: Vasoconstricts c Release oat 3 Eferent Arteriole: Vasodilates ic i374. Efferent Arteriole: Moderate vasoconstriction por 'S. Efferent Artertole: Severe Vasoconstriction y 6. GC Hydrostatic Pressure: Increases 7.GC Hydrostatic Pressure: Decreases '8, GC Oncotic Pressure: Increases 9.GC Oncotic Pressure: Decreases 10. Ke Increases FILTRATION FRACTION (FF) + Fraction of rena plasma flow that ls filtered + Normal Filtration Fraction: 20% © Miltration Fraction > ‘peritubular capil Concentration reabsorption Inthe tates” GFR, RPP, FE f "EFFECT EFFECT OF EFFECT ON + _ONGER _RPF FF asoconsticton of AfferentArteriole * NoGene Vasoconstriction of Efferent Arteriole ie Y a ‘Plasma Protein VY _No change v Ureteral Stone We Change: z | Which ofthe following would produc | ‘Sasmotic fluid in the proximal bute? oa (W increased traton fnton (8) Ercalar ul (ECF) volume expansion (C) Decreased peritubular (0) Increaed peritubular oon Pratel concentration ee ee hich he lowing weld From lpg BS 62 | atone (GF) heal la ow ery oe iyperprte ? | Asrertsone (emma arent arere mothe cen (he erent arerle {101 Dilation ofthe afferent irs (ZUELA, MI ore haat nm ttannntatenndtncttarccinenn abe 43 of BS leAUTOREGULATION OF RENAL BLOOD FLOW « helps maintain constant GFR ‘0 Occurs at BP 80-200mmHg (In other textbooks ‘160mmHlg), renal blood flow remalns constant via * Myogenlc mechanism = renal afferent arterioles reflexively responses to stretch by contracting ‘« Tubuloglomerular Feedback / Macula Densa Feedback ~ Remember: this is not the same as glomerulotubular balance BP 75- Scenario iif BP islow (og. 80mmig) ‘* VBP > VGC Hydrostatic Pressure -> VGFR (<125ml/min) > Detected by Macula Densa ‘+ Macula Densa increases secretion of: ‘© Anglotensin It (via RAAS stimulation) Vasoconstriets EFFERENT Arteriole > “GPR back to normal (125ml/min) Nitric Oxide * Vasodllates AFFERENT Arteriole > YGPR back to ‘normal (125ml/min) Scenario 2iiCAP ishigh (2.g.200mmHg) + BP > NGC Hydrostatic Pressure > NGFR (>125ml/min) > Detected by Macula Dens ‘+ Macula Densa increases secretion off. ‘Adenosine * Vasoconstrlets APFERENT arteriole -> GFR back to normal (125ml/min) REMEMBER AUTOREGULATION OF RENAL BLOOD FLOW. "TUBULOGLOMERULAR TEEDBACK Macula Densa Feedback; For Autoregulation of GFR GLOMERULOTUBULAR BALANCE Percentage of salute reubsorbed is held constant; Buffers effect of drustle GFR changes on urine output j 5.3 REABSORPTION AND SECRETION, #" BASIC MOVEMENTS INVOLVED IN URINE FORMATION, SS ‘5 * (Glomerular) Filtration ‘2 Movement from Glomerular Capillaries to Bowman’ « (Tubutar) Reabsorpion CN! ‘© Movement from Tubules to interstitium to Ps 7 Capillaries a3 + (Tubular) Secrecion ‘0 Movement from Peritubular Capillagigg Wa intérstitium to ‘Tebules: ~ oa AN von Bet some * See — i ‘Glomentar. +4, Excretion. Lsnary excretion Excretion = Fltraton - Reabeorpin + Secretion PREP PHYSIOLOGY HANDOUT BY ENRICC PAOL( TOPNOTCH BOARD eytlh Henechtye. For inquiries visit www.top IMPORTANT FORMULAS Filtered load = GFRx[plaama] Excretion rate « V x{urine] Reabsorption rate « Filired load ~ Excretion rate Secretion rate » Excretion rate~Filtered load ‘+ Where V = urine flow rate of substance (a mL/min) ‘o Plasma Plasma concentration of substance (In mg/dL) ‘Urine » urine concentration of substance (in mg/dL) + lffllered load > excretion rate: net reabsorption + If filtered load « excretion rate; net secretion BASIC PRINCIPLES IN TUBULAR PROCESSING + Most solutes (e.g, glucose) actively reabsorbed or secresed exhibtt: ‘Renal Threshold * Substance start to appear In the urine + Some nephrons exhibit saturation ‘Renal Transport Maximum * Al exces batanze appear n che uray * All nephrons exhibit saturation ‘180 200 360 «00 800 060 700 #t0 Pum otucone oncanraton SSrean.noresonnacunve + Tm Curve of Glucose o Normal: Filtered, 100% reabsorbed 6 Fllmation properdonal ta plasma glucose concentration Reaborpton: occurs sing SOLT- In PCT 6 Renal Tareholé: plasma gluone 200mg (some nephrons fatrated) cen Transpore Masimum; plasma glucose > 375mg/dL (al nephrons tured) me snare © Splay: between 200mg/dL.~37Smg/db (glucose excretion before complete saturation of all nephrons) + Tm Curve of PAH ‘© Normal: Filtered, Secreted, Not reabsorbed © Secretion of PAH occurs using carriers in the PCT. ‘Filtration load proportional to plasma PAH secretion ‘© Secretion: also exhibits saturation SSS Ga ae Seni amipien eter iter al Seuhnce furore | (mn eet pe ee ee | Ar planed can am noBIppOSICSELE TPR Pen Poon BRS t+ Ba | ‘plasma pars-minohippai ad ons Tapert cere ene (PAH) concentrations below the (A) reabsorption snot eturated (@) clearance equastnulin dearance (© secrecon rate equals PAH exertion rate (©) concentration nthe renal vine ote to zero (©)canenraton he renal vin egls Pl concentration inthe rom Pyle BRS. Eé 0 C. BANZUELA, MD "tbs: ltwwwSecebook.com/topnotchmedicalboardprep/ ** 4 oeIg TOPNOTCH MEDICAL BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C: BANZUELA, MD") For inquiries, visit www, topnetchbcardprep.com.ph or https://www.facebook.com/topnotchmedicalbosrdprep/ NONIONIC DIFFUSION excretion increased by’ of weak bases alkalinizing urine) tient produces «change n rin that alc ci What wae change urine what she mechanism of neeased salle ei etretion? a) Aidan, whic conver salle ais HA form |, {B)Alainistion which onver sll eof frm | (C) Acidification, which converts salicylic acid to its A~ form (G) Alalnizaion, which conve elec acl toe HA orm WEAr AIDS WERK BAS TA Form (pie + Bie For watow Forme" ohbleJing Form anise) and Frm (water-soluble) | (lipid-soluble) + Ble Form predominaces es + HaForm 2 ; "back diffusion”, Inacie ROMINA MOTE ocean xeon Urine pH diet (WB) thlazide diuretic administration i from BRS 6460 | 5.6 RENAL REGULATION OF UREA, ‘Which curve describes th S_ From Physiolengy B Gilead ms. e084 | Wie carve Sm arnohippuric aid (PAH) profile along the nephron? | curve, eames | (cur @cure -_ 5.5 K REGULATION REGULATION OF POTASSIUM ; + Plasma K* = 4.2 mEq/l and tlghth-regulated + I Line of defense oMovement of K+ across. ane SAN Ot Cal fpeatonia ‘and. Caen of it nt Calapan SESS Ee TOPNOTCH BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAOLO C, hts f For inquiries visit www.tcpnotchboardprep.com.ph or httas: PHOSPHATE, CALCIUM AND MAGNESIUM. REGULATION OF UREA * PCT: reabsorbs 50% of filtered Urea via simple diffusion * Thin Descending Limb of LH: secretes urea via simple diffusion + DT, Cortical Collecting Ducts and Outer Medullary Collecting Ducts: Impermeable to Uren * Inner Medullary Collecting Ducts: ADH increases permeability of these ducts to via facilitated difusiontransporter for ree wr. ‘© Contributes to urea recycling and development of ofRibiretwtan > heer aN se yater AND Urea Low Urine Flow Rate ae REGULATIONOF CALCIUM * Plastaa Ca?* = 2-4mBg/L + Hypercalcemia: can cause arrhythmias + Hypocalcemia: can cause + Calbindin: Stimulated by vit D; Intestines + 60% of plasma Ca2+ is Mltered + PCT and Li reabsorbs 90% of fite + DT and CD reabsorbs 896 of filter * PTH, Thlazides increases Ca + Loop Diuretics decreases Ca BANZUELA, MD facebook.com/topnetchmadieathaurdnean ‘binds with calclum in the red Calcium red Calelum Reabsorption fon Page 46 of 85(Ce KANDUNG IN THE NEPHRON REGULATION OF PHOSPHATE ‘Transport Maximum » C.1mM/min fen exceeded in diets with milk and meat CT: reabsorbs 85% of Mltered Phosphate via Na-PO« cotransport other parts to do not reabsorb POs © remaining 15% is excretec.in the urine © Resbsorption inhibited by PTH (adenylate cyclase and cAMP Inhibition ofthe Na-POs cotransport) * Causes Phosphaturta (Increased urinary PO4) and Increased urinary cAMP ‘0 Unreabsorbed POs serve as urinary buffer for H* REGULATION OF MAGNESIUM Plasma Mgi* = 1.8mEq/L + 50% stored in the bones ‘+ Only 10% of plasma Mg excreted daily ‘0 PCT -25% reabsorption © TAL of LH - 65% reabsorption “ ‘Inthe TAL of LH, Ca?* and Mg?* compete for reabsorption ~ Hypercalcemia causes hypomagnesemia = Hypocalcemia causes hypermagnesernia /Atwhich nephron sit des the amouni of Re tn wuld eee the _ ole thered fins panama pl | aysten ik | @stes . i ()Sitec | (o)sned (Skee t From Physiolopay BRS, {__ss__ ns “Ar whigh nephron sites the tubular Muld/plasma (TF/?) osmolarity | Towest in a person who has been deprived of water? (a) site (0) Sted | | sues (e)snee sc) site Fro Phylolopay BRS. 6° Ed _ | which nephron sites the bular Auld Inulin concentration highest during ancidiuresis? | (A) Site A (oy sted | sie E Dswse CSN am Pyslny BS. s_| chick nephron site ste tabula Mud Tnlin concentration lowest? —| (a) Site A (0) Site D | (@) site )suee i e)sitec From Ptpgy BRS, at Te apron ws i ular pone oneenraton ihe | (Aa) site (0) Site D wise FE me tion {sue lon BAS. 6 bd_| TOPNOTCH BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO Pa‘ 5.7 CONCENTRATION & DILUTION OF URINE WATER DEPRIVATION VS. WATER INTAKE WATER WATER DEPRIVATION | INTAKE Immediate affect on F v Plasma Osmolarity : Effect on Osmoreceptors in iaorbeijeetatan Stimulates Inhibits "ADH Secretion from a + Posterior Pituitary a effect on water * v permeability in DT & CD Bffect on Urine Osmolarity * v Effect on Urine Volume v * Vrain Taare Final Reault on Plasma ommolarty _pémplarty back Garachariey back to normali|”%, te normal PRODUCTION OF CONCENTRATED URINE, ©” + Concentrated urine / Hypercsmotiglitings Urine osmolarity > blood + Mechanisms: ‘© Cordleopapillary Osmotlt the Renal Interatttum Yeap} * Created by it Multiplier: Loop of Henle * Supplem Recycling: increases maximum \mOsm/L to 1200m08m/L tarcurrent Exchanger: Vasa Recta ‘(water channels) inthe LOT and CD to reabsorption > “rurine osmolarity and Vurine jent / Graded Osmotarity in Inserts UTY to *Urea recycling and WaK2Cl activity in TAL LH to osmolarity of the corticopapiilary osmotic ou Se" gradient PRODUCTION OF HYPEROSMOTIC URINE High ADH PRODUCTION OF DILUTE URINE * Dilute urine / Hypoosmotic Urine: ‘0 Urine osmolarity < blood osmolarity * ADH levels are low or Ineffective Less countercurrent ‘multiplication, urea recycling and Insertion of AQP-2 ‘+ Urine: high volume, low concentration ‘OLO C; BANZUELA, MD Tor inquiries visit www.topnatchboardprep,com,ph or https: wi Page 47 of 85, ‘aw fasshonh sam/tennotchmedicalboardpreote USER organ, ae FREE WATER CLEARANCE (Cxz0) ‘© Free Water (Solute Fre © Produced by diluting: ‘but not water ‘o Estimates ability to concentrate or llute the urine *"If() ADH: Frea Water excreted and Cia ‘IF (+) ADH: Free Water is NOT excreted a TOPNOTCH MEDICAL BOARD PREP PHYSIOLOGY HANI iDOUT BY ENRICO PAOLO C. BANZUELA, MD or bet (__S.SRENAL HORMONES) jorMoNE —SITEOF EFFECTS RNa &H20 Reabsorption Aldosterone» DT © MK Secretion 2TH Secretion + tNa Reabsorption + SH20 Reabsorption Angiotensin» PCT, TALLH, | 1 or «© *NNa-H antiport and HCO3- (8) Urire osmolarity | {(@)Plasma osmolarity | (D) Circulating levels of antidiuretic hormone (ADH) | “negative ee-watecerance (-Cns) wl acura person wi, ~ A) drinks 2 Lof dated water in 30 minutos a {G}btpnegrrng ge vumes are wines cooley oft saban/Laferssrvere head ny | (©)tr receiving lithium treatment for depression, ang-nag polyuria | Susunfegeeietsoeeimmccectigges | Sormene (OH) s Oar enone of he lung ang rer urne witha | | Oana eae Afecg te | Compared with person who ingests C water, a person a | with water deprivation willhavea (anger estar eeaane roe sone a tr uaredchormone (ADH) | Oe eg nacr/) ool nie poxina! we cer mt Ngabaron nthe caecng a |Awoman ar apm Smelt oT900 mOsn/t and urine Meng of Haimoen/ithe correc canons | a ot Reprapaat andaureae hormone (D1) | (8) water deprivation (©) central dlabetes insipidus t | (0) nephrogenic dlabetes insipidus darinkingtarge volumes ofdstlled water see oxy {OTCH BOARD PREP PHYSIOLOGY HANDOUT BY ENRICO PAQLO C. sorte uiries visit www.topnotchboatdprep.com,ph or httpst/rwm. reabsorption inthe PCT. Cy ™ free-water clearance (mL/min) Gatechol- PCT, TALE, , water, Na Reabsorption “AY murine flow rate (mL/min) amines Dr,cD Cog O8mOLAE clonraINCE (VsunV/ Pou) (raL/ min) = BT, CD (MOAT : ANP, Guanylate » Na Resbsorption Cyclase, GMP) CONDITIONS INVOLVING ADR. —— . ~ GRRE eee ara © PCT,CD ‘¢ YWater, Na Bapsorption SERUM SERUM OSM URINE 5 ; 5 ADH /SERUMNA ‘OSM RATE ClO Dopamine + FCT Pag Bespin youume + PCT.TALLH ¢ Sevarabsciption Primary , mn _ (Mon: ‘Alpha Fipipea YY Hmenmnte 06 | frm et PM Central Div‘ __Wypoommetic 4% (1) faction [Peripheral + TALLH, DT, Peri * ‘> — Hypoosmotic «= (+) Tad a remen Wak ae ADH receBigr,»— )Reabsorption an a oe ieee uae ‘SIADH Atv _Wyperometie YO) seca) Ing an aio of parathyroid harmcne (PTH) on the Whiehf the following would best dlaunguish an otherwicebelihy dperaielerns Pert person with savere water froma person withthe syndrome Stinappropriateansiduretichrmone (SIADH)? fs (A) Frap-watar clearance (CH20) “p(chinbibion of eal bul Cae reabsorption (E)cordopaplonyoamotle qradent rom Pte an ag ae iniulation of presimal tubular phesphate reabsorption inhibition of production of 1,25-dihydroxycholecalcferol 5.9 ACID-BASE BALANCE ASIC REDHASE PAVRIOLDY «Almost all enzyme systems are influenced by H'levels and must be regulated ‘0 Normal Plasma H+ # 0.00004 mEq/L sumbersome! *# Reason for using pH system ‘© Normal Plasma pH = «log [H*] « 7.4 + pH=6.8-8.0 ‘0 Compatible with life pH and HY Concentra eH Ear tnt serial Blood {teow Sees %s Interstitial fie 138 Intracellular uid 1x10? tod x 105 601074 Urine 3x10 01x 10% 451089 Gastric HO. 160 os ‘To maintain normal He balance, tal dally cretion aT ‘the dally dally ‘of He should equal (A) fied ai pred : | (B) Hoo: ove ee | (C) HCO3- fitered load | | Sa | |. (2) ered tad ote [iat tt concen eae | 1/0 tat orae TA = 84+ 109 AY Geunmmmer — dong awa MA (0) 10umes tnacor- fae | (]@)100times thatofA- 100 = A’/HA pr HAYA" Is 100 | ie) BANZUELA, MD facebook, ¢om/toprotchmedicalboardorepy Page 48 of a5BASIC ACID-BASE PHYSIOLOGY ‘+ Systems that regulate H+ Concentrations © Body Fluid Buffer Systems © COz + H20 = HiCOs = H+ + HCOa- * Phosphate Buffer System (HaPO« and HPO«) = Intracellular Proteins © Respiratory Center * Controls PCOa (Respiratory Acidosis/Alkalosis) 0 Kidneys * Controls HCOa (Metabolic Acidosis/Alkalosis) RESPIRATORY REGULATION OF ACID-BASE BALANCE * Responds to Hr lavals ‘OMH! > PRR Vplasma PCO? oH > URR> Nplasma PCOz * 50-75% effective in returning pH back to normal within 3-12 minutes RENAL REGULATION OF ACID-BASE BALANCE + Mechanisms ‘9 Secretion of excess H + Nav Countertransport in the PCT. LH, DT ‘« HATPase pump {n the Distal Tubules and CD © Reabsorption of filtered HCOs"If warranted * Coupled to He Secretion © Production of New HCOs"if warranted * Use of Ammonia (Wi) and Phosphate(NaHPOe) butters ~ These buffers also help excrete titratable acids | The reabsorption of filtered HCO. (A) results in reabsorption of less than 50% of the itered load When |) TReplasma concentration of HCOsis24 mEG/L ! (w)aciaines tubular uid toa pit of 4.4 (C)is directly linked to excretion of Has NH | (D)isinhibited by decreases in arterial PCO: {(E) can proceed normaly in the presence ofa ‘anhydrase inhibitor ei lS tassbeeh som/tepnotchmedicatboardprep/ RESPIRATORY AciDOSIS + Due co condltions resulting In Decreased Ventlation (RR) + Ea Ones Sedative Anette Gulab Sadr, lio, Amyotrophic ater Sleoeis Multpe Sclerosis Ai Obstruction, ARDS, COPD ' a. RESPIRATORY ALKALOSIS Due to conditions resulting in Increased Vantifation (RR) , Pheumonia, Pulmonary embolus, High Altitude, Psychogenic, Salicylate Intoxication ‘ANION QAP OF PLABUA Pro rap ‘ran oa METABOLIC ACIDOSIS + Due to conditions resulting in excess acid or loss of base + Bg, Ketoacldosis, Lactic ‘Acidosis, Salicylate Intoxication, Methanol/Formaldehyde Intoxication, Ethylene ‘lyeol intoxication, Diarrhea ‘+ Anion Gap (AG) used to help diagnose cause of metabolic acidosis Plasma enion gap [Na*]~((HOOs]+(CI"D) where Plasma anion gap = Unmseasured anions (mBa/L) Ma") = Measured extlon (g/L) HCO; and {Cr} = Measured anions (mEq/L) (eg. ketoacids, salicylate) to maintain: ty iloride to maintain electroneutrality iso called Hyperchloremic Metabolic Acidosis with ‘Normal Anion Gap MNEMONICS METABOLIC AC:DOSIS. — HAGMA. Methanol, Uremia, DKA, Paraldehyde.Propylene Glycol, ron | Isoniazid, idiopathic Acidosis, Lactic Acidosis(in Sepsis, Shock), | Ethylene Glycol, Ethanol, Salicylic Acid HARD-UP: NAGMA Hyperalimentation, Acetazolamide, RTA, Diarrhea, Uertoroenteric fistula, Pacreaticoduodenal Fistula 1 Ties ACID-BASEABRORNALITIES 7 rh 40 24 ~ Normal | 74 | atere| mmbted meas . + PH Excretion | vempao|y | aches | 9]: Set Acidosis IA J Reabsorption | rie © UitExcretion Respiratory |“ | we | | + vHCos Alkalosis 2. “*{>", Reabsorption te © Hyper- [Morabote [yp] » | % | SY | Pettisnon | Acidosts —— ‘Metabolic 7 v ? oF, ventilation Alkalosis REME-IBER ‘TRIO OF ELECTROLYTES ' He, cam, Ke | Pie levels > Hypercalcemia Hope Kalernie TOPNOTCH BOARD PRE! For inqul -p PHYSIOLOGY HANDOUT BY ENRICO PAOLO C. BANZUELA, MD cH BOAT www .topnotchboardprep.com.ph or http://www, facebook, com/topnotehmedicalboardprep/ METABOLIC ALKALOSIS * Due to conditions resulting in loss of acid or gain of base ‘+ Eg, Loop Diuretics, Thiazide Diureties, Vomiting, Hyperaldosteronism, Ingestion of Alkaline Drugs (Sodium Bicarbonate) ‘Which ofthe following ia cause of metabolic alkalosis? ] | (A) Diarshea (0) Treatment with acetazolamide | (@) Chronicrenal falluré —_(€) Hyperaldosteronism (C) Ethylene glycol ingestion bk From Physiolopay BRS £6 | |" Xa:yearia woman develops tevere darthea while on vacation She | haste faliowing arterial blood values: [aa 7as PcO2 = 24mm Hg : [HCO3-] = 10 mEq/L | ‘Venous blood samples show decreased blood [K+] and anormal anion | shen eet pets | ic Se a as Gaaiccae, eminent, | acidos From BRS 6 E4_| L_( respira Page 49 of 85,