Physiology Exam 2 review

muscle

reflex mechanisms and proprioception (preception/ awareness of position of body parts in space) are crucial for coordinating movement and maintaining balance during physical activities.

gogi tendon organ

• detects changes in tension and prevents tendons from tearing by sending the brain information about heavyiness (preception of work load)

• helps determin te cycling of muscle fibers and how many is eeded moment to moment

muscle spindle

• deteacts muscle strerch, and initiates a reflex that helps regulate muscle length and strech rate, ensuring optimal performance during physical activities.

• more strechn → more AP rate

• triggers muscle strech reflex to maintain length (like the knee jerk test)

  • GTO → tension and heavyness

  • muscle spingler → length and strech reflex

two types of muscle fibers

1. alpha - controls strength of muscle contraction

2. gamma - controls length of muscle contration / senstivity of muscle spindle

muscle types

• smooth muscle - develops tendont slowly (slow contractions) and also involuntary

• types of smooth muscle

  • single unit (myogenic) - depolariazes all at one times (autorhymic), innervated through gap junctions and allows cordinated response,

  • multi unit (neurogenic) - indivualslly innervated, by ANS (autonomic - no control), allows finer control, contraction only from direst nerve stimulation

contraction

calcium binds to calmodulin → activates kinase → stimulates myosin to bind actin → starts contraction

heart

movement of blood

• pulmonary circuit: deoxygenated blood to lungs and back to heart to get oxygenated

• systemic circuit: oxygenated blood to tissues and back to heart

blood moves because of pressule differences

AV - increases pressure during contraction

SV - decreaes pressure during contraction

congestive heart failure

• blood backs up into the system that is failing

  • failure in right → from body so systemic edema (in feet and peripheral body)

  • failure in left → from lungs so pulmonary edema (cough, conjestion into the heart)

cardiac cycle

two types of cardiac muscle

1. contractile - generates force of contractions to pump/ move blood

2. auto rhythmic - generate and conduct AP and do not contract

two phases of the cardiac cycle

1. systole - contration / ejection phase

2. diastole - relaxation phase / filling phase

   ventricle pressure (atrial is top sections, ventricle is bottom)

atrial > ventricle → both close and ventricle fills →

ventricle > atrial → AV value closes

arteries > ventricles → SL valvue closed

ventricles > arteriers → SL valvue opens

early systole = both closed → blood stars to leave from max fill

late systole = AV closed, SL open (LUB sound) → all blood out

early diastole = both closed, SL closes (DUB sound) → starts to fill again

late diastole = AV opens, → max full

filling → end diastolic volume (EDV) → ejections → end systolic volume (ESV)

ventricle volumes

• EDV - when vetnricles are most filled following diasole, constant volume

• ESV - when ventricles are emplied, can change based on strength of contraction

stroke volume = amount of blood ejected per beat

SV= EDV - ESV

cardiac output = amount of blood from heart per min

CO = HR x SV

refactory period: time after inital depolarization when contraction cannot occur

• Na inflows causes rapid depolarization

• plateus when Ca inflows → which opens K channels

• more Ca = stronger contractions

• SNS increases Ca → so it increases contractility

• PNS has no effect

cardiac autorhythmic cells

skelton of the heart, proves support and a nonconducitve barrier between atria and ventricles

• SA node is the pacemaker of the heart → generates AP’s the fastest → where they converge on the AV node

pacemaker activities

• Na responsible for rising phase of AP

• Ca flows into to the threshold then K goes out

heart rate regulation

extrinstic regulation: autonomic regulation

• autonomic stimulation changes ion flow

• sympathic: increase Na, increase Ca influx = increaed depolarization rate = increeased HR (more + moving in)

• parasympatheic: increased K leaving, decrease Ca influc = hyperpolarizes = decrases depolarization = decrease HR

SNS→ up HR, up SV, up contraction → becasue of Ca incrase in cell

PNS → down HR, no effect on SV, and no effect on contractile cells

blood pressure control:

medulla oblongata (cardiovascular center controls blood pressure

factors affecting contractile strength

• stoke volume: whic hdepents on amount of strech on the heart before contraction, depends on venous return to hear

  • venous return is controlled by SNS

• frank starling law : larger the strech, the more forceful the contraction and increased SV

  • up strech → up corss bridges → stronger contraction

  • increased venus retun = greater preload

  • frank starling= mechanical, from strech, relates to preload, and EDV

  • contractality: chemical, influceed by SNS: via altered Ca levels, and ESV

• after load: pressure that venticles must over come to open aortic and pulmonary valvues.

Blood

blood is mostly for transport, made of plasma (plasma proteins) and formed elements (RBC, WBC)

there a a few types of WBC

• monocytes: turn into macrophages in tissues, they clean debris

• basophils: realse histamines and help with inflamation

blood proteins: most made by the liver

1. albumin: responsible for blood/ capillary osmotic pressure

   • less albumin → water moves into tissues

   • transports and carries molecules

   • protein starvation → leads to water leaving vessels into tissues → edema

hematocrit: percent of RBC in blood, can affect blood dilution. less hematocrit → anemia (less iron), less blood

hematopoiesis: production of blood cells in the red bone marrow

• pluripotent stem cells → reticulocytes → RBC and megakaryotcytes → platelets

• reticulocytes are immature RBC, old blod cells taken out by spleen

  • more reticulocytes → more rbc production

EPO (erthropoiotin) made in kidney and stimulates production of RBC

• in response to tissues hypoxia (less o2 in tissues)

• hemoglobin bind to O2 for gas transport

abnormalies in EPO

• anemia: not enough RBC or hemoblobin, result of low iron (which is in RBC), not enough oxygen carryig capacity b/c iron is what bind hemoglobin

• negative feed back loop based on O2 supply which regulatees EPO

• tissues hypoxia → body relases EPO → increased RBC production (more iron)→ increaed O2 levels

hemoglobin is broken down by the spleen in to hemo and globin and iron

• globin into AA

• hemo is brokwn down to bilirubin

• is biliruben buils up in tissues (and not poop) it causes jaundice

hemostasis → a sequence of response that stops bleeding

3 mechanisms

1. vascular spasms: occurs when damanged vessels constrict

   • occurs when release of NO and prostacyclin stops, which usally dialate vessels

2. platelet plug formation platelets stick to damaged endothelium to form plug . they are packed full of chemical messagers

   • formed from broken megakaryocyes → platelets relase thromboxane and ADP

   • they regognize breach (exposed collagen) and take action, activating platlets → releases ADP and thoromaxe→ calls more platelets (positive feedback)

3. clotting cascade initiation vs common pathway

intrinsis vs extrinsic initiation

intrinsiic (contact with collagen) → platlet production→ makes chemicals → MANY clotting factors involves → protrombinase → thrombin

extrinsic (noncontact) → tissue damange → produces tissue factor/ thrombinplastin → FEW clotting factors → prothrombinase → thrombin

• initation pathway is an amplifaction proces, where one activated emzyme makes alot fo thrombin which makes the mesh\

common pathway

• prothrombin→ uses prothrombinase to turn into → thrombin, which helps → fibrogen turn into → fibrin, as well as → fibrin mesh

• clotting is supported by Ca and K

  • Ca allows blood clotting to occur, not enough Ca means not enough clotting

cycle of coagulation: fibrinolysis

• plasmingen: a proenzyme present in clots → converted into the enzyme plasmids

  • plasmids action is to break up clot (degrate fibrin mesh)

  • plasmids are made in the liver

• plasmidogen turns into plasmids using tissue plasminogen (tPA)'

• in undamnged vessels clots are called thrombus (embolis if it turns free floating)

  • anti coagulatns can be used to limit thrombus formation

respiratory

pulmonary ventilation pressure changes

inspiration and expiration: mechanical process that depends on volumes in thoratic cavity

• volume changes → pressure chagnes → gas flow

• gas moves from high to low pressure

passive: exhale, and it requires no muscles only uses recoil from lungs

active: inhald uses muscles, and increaes gas exchagne

ventilation

• conducting airways : nose, pharynx, trachea,

• exchagne surface: alveoli

airways resistance

• caused by small airways called broncbiolies (can contract and dialte)

• more dialtion = more flow

ANS intervention

• SNS is not directly inervated but epineferine dialtes airways after beta 2 receptor binds

• PNS directly constris airway

types of reisstance

1. airway resistance

2. mucous blockage: traps particels but can narrow passage if too much is produced

   1. cystic fibrosis is thicken of mucous throughout body

3. alveoli compliance: ease of expansion

respiratory membrane: must be thin and have alot of surface area, but amount of water retention can make it hard to breath (phenmonia)

alveolar surface tension: water molecules along surface of alveoli want to be close to each other, so they have a tendencity to collapse. so the alveoli must resist the pull fo water to keep shape

• surfactant: is a detergent like lipid protin made by type II alveolar cells which reduces surface tenion by breaking bonds between water molecuels, helping to not collapse the alveoli

atelectasis (lung collapse): can occur from a variety of things

1. plugged bronchioles → lead to collapse of surface tension

2. puncture of lung breaks lung adherance to pleural cavity

3. past surgury

ventilation/ perfusion matching

• v ( ventilation)= amount of gas getting to alveoli

• q (perfusion)= pulmonary capillary flow (amount of blood reaching alveoli to be oxygenated)

mismatch leads to perfusion of blood without gas exhagne and ventilation of alveioli with no blood to exchange

• O2 high → arterioles dialate

• O2 low → arterioles constrict

• there is more perfusion (passage of blood across capilaries) lower in the lungs where blood pools

perfusion source of mismatch: from decreaed blood to alveoli from diversion of injury (pulmonary embolism)

• pulmonary embolism: type of perfusion source when pulomonary arterial flow to lungs is blocked = blood cannot get oxygenated

ventilation source of mismatch: from poorly ventilated alveioli (cystic fibrosis)

• COPD: damange to alveioli= no perfusion, gas exhagne occurs at alvioli without damagne

gas exchange and transport:

paricle pressure of gas → pressure exherted by gas in mixture

• liquid pressure of gas pushes gas molecules into water → diffusion

• equilibrium when pressures are equal, but push determins how much gas is desolves

• so no pressure gradient so difussion

factors taht affect diffusion across membrane

rate = surface area x concentration gradient / ressistance x thickness

gas exchange

• o2 diffusion into blood b/c of PO2 (oxygen pressure gradient)

• to mainthain PO2 gradient and keep O2 moving in, O2 must bind to Hemoglobin

• hemoglobin creates the gadient by decreasing PO2

• there is a resever of 100% PO2 that can be used during excersize to keep muscels oxygenated

oxygen affinisty = how strongly hemoglobin hold on O2

• higher affinity → stronger binding in lungs

• lower affinity → weaker binding in tissues

condistions in lungs vs tissues that affect affinity

1. inceaed in O2 affindity: conditions in lungs

   1. lower timp

   2. higher pH less acidic

   3. lower CO2 particle pressure

2. decrease O2 affindity: condistions in tissues

   1. higher temp

   2. lower pH more acidic

   3. higher CO2 particle pressure

PCO2> PCO2 venous blood > PCO2 alveoli

• only 25% of bound PO2 is unloaded during one systemic cycle

CO2 also difuses across respiratory membrane and tissues

• CO2 concentration gradient created by tissues through metabolism

• transported into blood via 1. plasma 2. bound to hemaglobin 3. 70% is turned into bicarbonate via enzyme called carbonic anhydrase in RBC

• CO2 acts like acid to control blood pH

Buffering acid: as tisseus produce acids there is a build up

1. hemoglobin buffer Hb combinds with H to regualte pH

2. HCO3 in plasma acts as bicarbonate buffer

   • if H increase → H + HCO3 decrease in concentriom → decresing pH

regulation of breathing

• regualtion of respiratory function → by neurons

• breathing is automatic and intrinsially reguated (w/o) external input

control of respiration: by respiratory center of medulla oblongata

• controls pace and depth

1. ventral respiratory group (VRG) → has pacemaker activity → generates pattern (rate and depth of respiration)

2. dorsal respiratory group (DRG) → receives chemical information

   • modififed rate of VRG

   • integrates sensory information from chemoreceptors

chemoreceptors: regulating breathing patterns by detecting CO2, H and O2 in blood

• central → via the medulla

• peripheral → via carotid body and aortic arch

CO2 is the primary drive for respiratory rate

Hypoxia → not enough oxygen getting difussed into blood

ventilation chagnes gas levels in blood

• hyperventilation = faster RR → more gas exchange, lower PCO2, higher pH (less acidic) → more O2 in blood

• hypoventilation = slower RR → less gas exchange, high PCO2, lower pH → less O2 in blood

urinary

kidneys manage water balance by adjusting filteration and reabsorption

they also manger

1. blood pressure: short term through hormones

2. RBC production: erythropoietin (which stimultes RBC production)\

3. calcaoim homeostasis (vit d → Ca)

nephron: functional unit of the kidney

• contain a glomerus (ball of capillaires to make filterate), and renal capsule which collects the filterat

urine formation: depends on amount 1. fitered 2. reabsorbed 3. secreated

regulation of glomerulat filtertaion rate (GFR)

• interinsic: within kidneys

• extrinsic: ans, endocrine

• filteration depends on pressure gradient and surface area as passive process

hydrostatic → favors filteration outer push

osmotic pressure → opposes filteration ( proteins/ albumin) as it favros reabsorption

• pressure if directly associated with blood flow / filteration through glomeruli more pressure → higher GFR

podocytes help reguate surface areas for filteration with filteration slits

interinsic vs extrinsic regulation: afferetn arteriuloees (primary controller of GFR, reulates blood flow through glomrtulos)

interinsisc: happens in tisseus of kidneys

• myogenic strech: negative feedback loop dialtion → causes refelx contration → leads to dialtion

• macula densa cells: inside distal convoluted tubule

  • detects osmolarity and signals afferent arterial to dialte when flow is too slow, using paracrine signalling

• endothelial cells also relase prostagladins (hormone that controls bodyily functions) to dialate afferent arterioles (primary controller of GFR)

• prostaglins → made by COX → COX is inhibited by NSAIDS (aspirin/ advil)→ lead to kidney failure in patietns

extrinsic regulation: by SNS

1. decrease blood pressure: response to preserve blood volume

   • decrease filteration by rerouting blood → constrict afferent arterial

2. increse blood pressure: reponse to long term decrease in volume

rein-angiotension-aldosterone system: long term control of BP

• granular cells release the enzyme renin which triggers cascase to increase BP

• low systemic BP→ angiotensin uses renin → angiotensin I uses ACE → angiotensin II which can vasoconstrict, and trigger kidneys to release aldosterone

aldosterone: hormone that acts on kidneys to influene BV, in the nephron it incraes Na/K pumps to retain BV (water follows Na)

• acts on sodium → which water follows→ doesnt directly influence water absorption

anti-diuretic hormone: decreaes urine output, increases BP and BV

• allows water to osmotically follow Na

• enables Aldosterone to work to help reabsorb water

• powerful vasocontrister, increases BP in short term

Blood Pressure meds: diuretics

• diuretics increase volume of urine (so decrease BV)

• pee more → solute concentrion does down in blood → decrease blood volume → decrease blood pressure

• inhibition of angiotenion II with diuretics → less NA pumps → down BP

• ACE inhibitors → preventions Angiotension I into angiotension II → reduces vasoconstriction → longer decrease in BV

extrinsic endocrine regulation helps regulate GFR by regulting water balance

naturietic peptide system

• ANP atrial naturetuc peptide, stimulates muscle strech → increases venous return

  1. inhibits RAAS

  2. inhibits intrinsic mechanism to increase GFR

• ANP is a very imporant controller as it

  • anti ADH, anti RAAS (decreases renin), anti aldosterone (decrease sodium reabsorption), intrinsic regulator, inhibits thrist (anti angiotension II)

  • directly increaes GFR

transporter mechanismsm

• tubular reabsorption: seconard active transport Na/K is primary source of most tubular reuptake

• water reabsroption follows NA uptake (thanks to aldosterone)

1. obligatory reabsorption: kidneys have no choice

2. facultative: controlled hormonally via ADH, which opens aqua porins and aldosterone creates osmotic gradient

renal theshold: amounf os substance that can be absorbed

• with diabetes this is very low for glusose so much glucuse gets wasted out in pee

reabsorption in proximal convulutes tubule

• drier by Na/K pump, all glucose, AA and vitamins are uptaken

water and ion reabsorption in loop of henle

• desending: concentrated, water can leave, ions cannot

• ascending: dilutes, water cant leave, Na/K, 2Cl pump allow ions to leave

  • active transport keeps hypertonic enviornment which maintains osmotic pull of water to be absorbed

  • ADH aka vasopressin allows water to leave collecting duct, concentrating a small amount of urine

  • low ADH leads to large around o dilutes in urine

alchol can lead to dehydration as it inhibits aDH release → minics dibetics → increases water loss through urine

Acid / base balance

• acid produciton: most H made by metabolism in muscles

  • lactic acid: from anaerobe repiration of glucose

  • fatty acids and ketone bodies from fat metabolism

    • diabetic ketoacidosis is hwere fats are used instead of glucose

• respiratory pH balance: controls pH by conrolled CO2 exceration, which thus controls amount of H in body

• urinary: controls reabsroption of filtered bicarbonate and gets rid of daily acid load

• acidosis: low blood pH, too acidic becuase too much H

  • leads to renal failure and diarea

  • to fix: add HCO3 to blood, and H to tubule

  • H is able to leave tubule with help of limited PO4

• alkadosis: high blood pH, too basic not enough H

  • vomiting

  • to fix: alkadosis: add H to blood/ add HCO3 to tubule

digestive system

salavia: defense, digestion, mucous electrolytes

• intrinsic: glands, keeps mouth moist

• extrinsic: glands make secretions when we injest foodsalvaotry galnds send implues along para sympathic fibers

strong sns inhibts salavation → dry mouth

pns stimution → increases secretion and motility

funcstions of the digestive system

1. injestion : take in food

2. digestion: break down

3. absorption: water soluable vs fat soluable (moving through cell wall)

4. motility: mixing (segmentation), vs propelling (peristalsis)

   • mechanical: chewing/ segmentation, chemical: HCl, enzymes

small intestine

• absorptive cells (enterocytes) in the epithelium digest and absorb nutruents in the intestinal chyme

• goblet cells secrete mucus (which can protect stomach lining)

• intestinal glands secrete intestinal juice , enzymes and bicarbonate

surface area is increased by

1. pilea cirularuis→ ridgies and folds within intestine

2. villi → little brushes that stick out and increase surface area

3. microvilli → little brissles on top of villi that explain surface area even more

amylase→ digestive starch

lipase→ digestive lipid

gastric secretion is regualted by

1. neutral and hormonal mechanisms

2. stimulatory and inhibitatory events in 3 phases

   1. cephalis (relaxation phase): PNS prepare as brain thinks of food

      • brain activates vagus nerve and makes more digestive juices to prepare

   2. gastric phase: 3-4 hours after food enters

      • chemoreceptors monior pH of stomach chyme and release HCl to increase stomach acid, strech activates PNS and waves of peristalsis being, protein trigger relase of gastrin

   3. intestinal phase: food leaves stomach in little sections into intestines which sense food and trigger endo. and sns

      • once food enteres the small intestine the enterogastic reflez is triggered by stomach receptors, which limit motility from stomach as to not fill it up too much

stomach

• lower esophagus sphicter protects esophagus from stomach acid

• doesnt absorb much, there is a variety of exocrine and endocrine in the mucosal cells

• parietal cells make interinsic factor and HCl

  • HCl kills microbes, denatures proteains and turns pepsinogen to peptides

  • HCl is nessesary to absorb vitamin b12

• cheilf cells secrete pepsinogen (inactive enzyme), only activaited when needed by HCl)

  • pensinogen with HCl → pepsin → breaks down proteins

GURD: when lower spinchter doesnt close and stomach acid moves to esophagus

Ulsers: mucus degrades exposing tissue to acid

the stomach uses peristaltic movement (mixing around) to amcerate food→ turn it into chyme

HCl regulation in stomach

• stimulated by ACh, histamin and gastric through 2nd messenger systems

vomiting: loss of K and H, loss of K → possible hypokalima (low k in blood)

diarrhea: loss of HCO3 → makes H when HCO3 is replaced →metabolic ketoacidosis

g cells in stomach secrete the hormone gastrin into the blood

gastrin:

• makes parietial cells, secrete HCl, increaes motility (mixing), and stimulating cheilf cells to make pepsinogin

• gastrin makes → parietial cells and cheif cells → which make pepsinogin

somatostatin: inhibits gastric activity → release triggered by low pH (negative feedback) (high acidity

chrones disease: affects absorptive surface by shortening or removing microvilli

lipid droplets are osmotic particles in intestines whichincrease osmotic pressure

peristalsis requres cordinated contraction in two layers of smooth muscles: longitudinal and circular

3 main fucntions of the small intestine

1. movement, peristalsis (moves chyme) abd segmentation (mixing) and complete digestions of marcomolicues into monomers, absorb 90% of nutrients

acessory organs secretions

• liver/gall bladder → bile → breaking down lipids relased by CCK

• pancreas → digestive enzymes and buffer to counter acid

• GIP glucose causes insulin to increase

• CCK, affects gall bladder making it contract and digest cuases pancrease to release digestive enzyme

• carbohydrates must be hydrolyzed into sugars in intesinal epithelium

bile

• dark pigment is created by biliruben (from catabolized RBCs)

• live disease, too much biliruben build up in body leaves skin yellow and white poop

cystic fibrosis - thickening of mucous in digestive system

hepatic portal system: any part of cirulation whre blood is drained from capillaries to another strucutre

gastroileal: intensifies peristalsis (chyme into cecum)

gastrocolic: quickly drive from colon → rectum

as bacterium digest they relase vitamin k and b and amino acids