Etp Physio Exam Iii

Front 1

layers of digestive tract

Back 1

mucosa
submucosa
muscularis externa
serosa

Front 2

digestive tract mucosa

Back 2

mucous membrane- epithelial barrier w/ mucus producing cells

lamina propria- acellular connective tissue
"basement membrane"

muscularis mucosa- smooth muscle

>> tube runs down from mouth to anus; basic components remain the same but certain layers will be emphasized depending on the area/function
1/ esophagus- transport; thick muscularis, minimal mucosa
2/ small intestine- thin muscularis, elaborate mucosa layer for max absorption

Front 3

muscularis externa

Back 3

outer longitudinal muscle
contraction >> shortens tube

inner circular muscle
contraction >> decreases tube diameter

Front 4

epithelial tissue

Back 4

made of epithelial cells that are specialized for selective transport across membranes; *very tight junctions

Front 5

apical v. basal v. lateral surfaces

Back 5

apical- faces anterior lumen
basal- faces underlying vascular tissue
lateral- faces neighboring epithelial cells

Front 6

goblet cells

Back 6

produce mucus

Front 7

exocrine v. endocrine cells

Back 7

exocrine- secretes/releases digestive enzymes & juices into anterior of GI

endocrine- produce/releases GI specific hormone into blood stream; designed to regulate and coordinate GI function

Front 8

serous membrane

Back 8

visceral peritoneum- covers organ
parietal peritoneum- lines inside the organs

*continuous w/ one another

Front 9

mesentery

Back 9

double layer of peritoneum that connects the visceral and parietal portion

serves as a conduit for blood vessels, nerves, and lymphatic vessels

Front 10

digestive processes

Back 10

1/ motility
2/ secretion
3/ digestion
4/ absorption

Front 11

motility // mechanism rules
& their exceptions

Back 11

propulsive movements // peristalsis
wave of muscle contraction that moves down GI tract
*accomplish both movements in stomach

mixing // segmentation contraction
primarily circular muscle contraction that moves around the tube
*accomplish both movements in small intestine

Front 12

secretion

Back 12

mucus is secreted throughout the gut, product is dependent on location within tract/accessory gland(s)

HCl-, digestive enzymes, & bile salts

Front 13

digestion

Back 13

carbohydrates--
polysaccharides uses amylase >> maltose >> monosaccharides
disaccharides (e.g. sucrose and lactose) can be broken down by the tongue

proteins >> polypeptide fragmins >> amino acids

fats--
triglyceride (3 fatty acid chains attached to glycerol backbone) uses lipase >> monoglyceride & two free fatty acid chains

Front 14

absorption

Back 14

*most important

small intestine has specific mechanism for transporting water, monosaccharides, fatty acids, and AA across mucosal wall and into blood vessels

Front 15

non-digestive functions of GI tract

Back 15

excretion

fluid/electrolyte balance- small intestine reabsorbes up to 9-11 L/day

immunity- large barrier for pathogens; lymphocytes and mast cells are located in b/w epithelial and lamina propria
GALT

Front 16

What happens if pathogen is able to cross GI and get into the blood stream?

Back 16

hepatic phagocytic system!

Kupffer cells can endocytose pathogen and initiate immune response.

Front 17

short loop v. long loop regulation

Back 17

short loop- local, gut can regulate digestive function autonomously w/o input from brain

long loop- brain can influence or override short loop

Front 18

enteric nervous system (ENS)

Back 18

short loop, part of PNS
*intrinsic

has two major neural networks--
1/ myenteric plexus
2/ submucosal plexus

Front 19

myenteric plexus

Back 19

located between longitudinal and circular muscle layers
>>regulates motility

Front 20

submucosal plexus

Back 20

receives information r/t composition inside GI tract (e.g. distention, fat content, osmolarity, pH, bacteria content)
>> directly controls secretion
>> indirectly influences gut motility by communicating w/ myenteric plexus
>> indirectly influences absorption depending on what secretions it stimulates and its effect on motility

Front 21

How does the submucosal plexus influence absorption?

Back 21

It can enhance digestive enzymes and slow down motility, resulting in (+) absorption. It can decrease digestive enzymes and have the opposite effect.

Toxins in the GI tract will cause increased water/mucus secretion and gut motility, (-) absorption. The net effect is the removal of the toxin.

Front 22

extrinsic control of gut

Back 22

controlled by sympathetic stimulation and vagus nerve input (which is part of PNS but not part of the enteric system)

Front 23

control and regulation of GI

Back 23

endocrine cells release hormones via

1/ directly senses change in gut
2/ instructed by enteric submucosa plexus
3/ brain triggers release via vagus n.
4/ different GI hormone

Front 24

stomach

Back 24

fundus
body
antrum

>>has two types of motility
>>physically uniformed across the three portions w/ secretory cells @ bottom of gastric pits

Front 25

receptive relaxation

Back 25

gastric filling

volume of stomach when empty- 50 mL
>> can increase 20x when ruggae stretches before distention @ stomach wall

Front 26

peristalsis

Back 26

pace setter cells are located along the fundus and are spontaneously active; depolarization only reaches threshold while consuming food

>> peristalsis will move down from fundus
before reaching pyloris sphincter, chyme is able to get into duodenum || once it reaches sphincter, it will close, rebounding the chyme up the stomach to be mixed again

Front 27

oxyntic mucosa

Back 27

*in body & fundus of stomach

mucosa cells--
produce thick alkaline mucus that acts as a protective coating against acidity of stomach

chief cells--
produce pepsinogen >> pepsin, which breaks down proteins

parietal cells--
HCL and intrinsic factor
intrinsic factor binds to vit B12, it is necessary for the uptake of B12 in the terminal portion of the small intestine

enterochomaffin-like cells--
acts like chief and parietal cells

Front 28

pyloric gland area (PGA)

Back 28

only found in antrum

gastrin aka G-cells
stimulates gastric secretion and motility by (+) chief & parietal cells and peristalsis

somatostatin aka D-cells
decreases gastric secretion and motility

Front 29

phases of gastric secretion

Back 29

1/ interdigestive
2/ cephalic
3/ gastric
4/ intestinal

Front 30

interdigestive phase

Back 30

not thinking about or eating food

gastric secretion is lowest in AM and highest in PM

Front 31

cephalic phase

Back 31

cues are anticipatory; food has not entered stomach
*control is from long loop; (+) secretion & motility

Front 32

gastric phase

Back 32

food enters stomach
*short and long loop; (+) secretion and motility

Front 33

intestinal phase

Back 33

food leaving stomach & entering duodenum
*short and long loop; (-) secretion and motility

predominately sensed by D-cells
protein withdrawal & drop in pH >> (+) somatostatin

Front 34

What are three strong stimulus for the intestinal phase?

Back 34

1/ low pH
2/ protein
3/ fat

other factors include hypertonicity, distension

when mucosa of duodenum sense these changes >>
1/ enterogastric reflex- slows gastric emptying
2/ enterogastrones- triggers 2 hormones responsible for pancreas and liver secretions

Front 35

What is the purpose of inhibiting motility?

Back 35

slows gastric emptying so that duodenum can stimulate pancreas and liver for secretions

pancreas- digestive enzymes & NaHCO3 neutralizes acid
liver- bile salts help w/ fat digestion

>> fat slows down gastric emptying the most b/c its digestion starts and ends in duodenum

Front 36

enterogastrones

Back 36

cholecytokinin (CCK)
(-) gastric emptying
(+) pancreatic secretion
(+) bile secretion

secretin--
(-) gastric emptying
(-) gastric acid secretion
(+) NaHCO3

Front 37

acinar cells v. duct cells

Back 37

acinar cells- stimulated by CCK, releases digestive enzymes

duct cells- stimulated by secretin, releases NaHCO3

both pancreatic cells, digestive enzymes and NaHCO3 are secreted together

Front 38

pancreatic enzymes

Back 38

1/ proteolytic
trypsin- first to be activated by amino peptidase
>> will activate the rest- chymotrypsin, carboxypeptidase

2/ pancreatic amylase

3/ pancreatic lipase; the only source of lipase! therefore, if you eliminate pancreas function, fat digestion will be affected the most

Front 39

How are carbohydrates digested?

Back 39

salivary amylase, start at the mouth

Front 40

bile

Back 40

composed of bile salts, cholesterol, lecithin, & bilirubin suspended in aqueous alkaline fluid

amphipathic and creates emulsification droplets when interacting w/ fat so that they cannot reform
>> increases SA that lipase can act on

Front 41

CCK action

Back 41

-secretes bile
-opens sphincter of odii
-gall bladder contraction

>> bile will emulsify
>> 50% will get reabsorbed, when bile is reabsorbed back into liver, it is a strong stimulus for more bile secretion
>> this system will only shut down when fat digestion is complete and CCK is no longer secreted

Front 42

small intestine

Back 42

*where all food digestion and absorption will be completed

divided into duodenum, jejunum, & ileum

primary motility is segmentation; responsible for mixing and propulsive actions

Front 43

segmentation

Back 43

-a response to distention in the duodenum
-increases surface area of absorption w/ food
-slow frequency at earlier, lower parts of intestine; higher frequency of segmentation in upper areas >> slow propulsive movements

Front 44

mucosal membrane of small intestine

Back 44

brush border- membrane bound digestive enzymes
1/ enterokinases
2/ disaccharidases
3/ aminopeptidase

arranged in villi and microvilli which increases SA available for digestion by 600x

Front 45

central lacteal of villas

Back 45

fat that gets absorbed enters here, and eventually gets drained into the liver

Front 46

disaccharides >> enzymes >> monosaccharides

Back 46

maltose >> maltase >> glucose
sucrose >> sucrase >> fructose
lactose >> lactase >> galactose

amino fragments >> amino peptidase >> AA

Front 47

fat digestion/absorption

Back 47

lipid emulsion droplets- triglyceride surrounded w/ bile salt

pancreatic lipase breaks down triglycerides to form micelles- fatty acid and monoglyceride surrounded by bile salts

micelle is absorbable form of digestive fat, gets into brush border

Front 48

large intestine

Back 48

no more food; if food gets into colon, bacteria will go into fermentation reactions >> gas

feces w/ H20, electrolyses, and mineral that we want back; moves from terminal ilium through iliocecal valve into cecum >> ascending colon >> transverse colon >> descending colon >> sigmoid colon >> rectum, etc.

Front 49

motility in colon

Back 49

haustral contractions--
type of segmentation, mixes feces, increases contact w/ colon wall to (+) absorption

mass movements--
propulsion, drives feces 3/4 or whole length of colon
stimulated by gastrin
if pushed into rectum, distention will stimulate defecation reflex

Front 50

defecation reflex

Back 50

stretch receptors of rectal wall will cause relaxation of internal anal sphincter (smooth muscles, involuntary)

external anal sphincter- skeletal muscles, voluntary

if defecation is delayed for too long, mass movement will move feces back into rectum >> the longer it stays in colon, the more water is absorbed >> stool will get hard >> constipation

Front 51

causes of diarrhea

Back 51

1/ colonic motility is too fast, not enough time to absorb water

2/ osmotic- osmolarity of feces is elevated esp. undigested material in colon (usually caused by enzyme deficiency e.g. lactose, fiber)

we cannot digest fiber and it is used as stool softener

Front 52

kidneys

Back 52

-perfused by renal arteries
-filters blood and forms urine
-filtered blood returns to heart via renal vein
-urine goes through ureter >> bladder >> urethra

two major zones--
1/ cortex- outer, lighter in color
2/ renal medulla- organized into renal pyramids where urine collects before it is drained into renal pelvis >> ureters >> bladder

Front 53

How many nephrons does each kidneys have?

Back 53

1 million; a healthy adult has a total of 2 million nephrons

each nephron has vascular and tubular component

Front 54

renal vascular blood flow

Back 54

>> afferent arterioles- renal arteries form arterioles right before it enters kidneys
>> glomerulus (capillaries)
>> efferent arteriole
>> peritubular- network of of capillaries wrapped around tubule portion of nephron
>> out of kidneys via renal veins

Front 55

exchange @ capillaries

Back 55

1/ glomerulus 20%
2/ peritubular capillaries 80%

Front 56

glomerulus exchange

Back 56

bowman's capsule >> proximal tubule >> descending loop of henle >> ascending loop of henle >> distal tubule >> urine is emptied into collecting duct

has same composition as plasma excluding particles that could not cross bowman's capsule (WBC, RBC, plasma proteins)

as it moves down the nephron, there is opportunity for exchange (reabsorption) but once it leaves collecting duct into renal pelvis, there is no more modification in the composition of that urine

Front 57

nephron's regional differences

Back 57

all originate in the cortex of the kidney, difference lies in the proximity to the glomeruli

cortical nephrons (80%)
-outer cortex
-short loop of henle that only enters superficial portion of medulla
-peritubule capillaries wrapped around the entire tubule

juxtamedullar nephrons (20%)
-inner cortex
-long loop of henle
-peritubule capillaries wrapped only around tubule found only in cortex
-vasa recta runs along the loop of henle
-important in producing urine @ various concentrations

Front 58

formation of urine

Back 58

1/ glomerular filtration
2/ tubular reabsorption
3/ tubular secretion

if you knock out glomerular filtration, will be unable to form urine

Front 59

renal corpuscle

Back 59

refers to glomerulus and bowman's capsule

Front 60

glomerular membrane

Back 60

barrier b/w glomerular capillaries and interior of bowman's capsule; composed of three layers

1/ capillary walls are composed of endothelial cells w/ pores
**glomerulus' pores are significantly more leaky and allow small plasma proteins to pass endothelial layers

2/ basement membrane; acellular connective tissue
**charge filter; glycoprotein has net (-) charge that repels plasma proteins that are also (-)

3/ inner membrane of bowman's
**size filter; pedocytes have projections that wraps around glomerular capillaries--they inter digit, creating a very small slit

Front 61

forces in glomerular filtration

Back 61

1/ capillary blood pressure
pushing of blood against capillary wall, wants to push fluid out into bowman's >> filtration
55 mmHg

2/ plasma colloid osmotic pressure
pulling exerted by plasma protein, wants fluid in >> opposes filtration
30 mmHg

3/ bowman's hydrostatic pressure
pushing, water pushes against its container >> opposes filtration
15 mmHg

**capillary BP > colloid and hydrostatic pressure for normal filtration to occur
net filtration pressure: 10 mmHg

Front 62

glomerular filtration rate (GFR)

Back 62

depends on
-net filtration pressure
-surface area available
-permeability of glomerular membrane

GFR = Kf x net filtration pressure, where Kf = SA x permeability

Variation of GFR- gender and age
Men has bigger kidneys >> more SA
Decline of healthy nephron mass as people age >> less SA

Front 63

control of GFR

Back 63

1/ autoregulation- maintain GFR w/ normal fluctuations in BP w/o regard to systematic BP; kidneys able to maintain independently via vasoconstriction and vasodilation

2/ extrinsic- alter GFR inorder to control blood volume and BP; stress response, emergency goal

Front 64

tubuloglomerular feedback mechanism

Back 64

mediates autoregulation @ juxtaglomerular apparatus- part of distal tubule where afferent and efferent arteriole bifurcates

macula densa- tubule cells monitor the rate of fluid flow; indirectly measures GFR--(+) GFR will (+) fluid rate

granular cells- vascular cells sense BP @ afferent arteriole; indirectly monitors systemic BP

>> rise in either component will trigger vasoconstriction
>> drop in either component will trigger vasodilation

Front 65

extrinsic control of GFR

Back 65

sympathetic input can override autoregulatory responses

smooth muscle cells of afferent and efferent arterioles contain many a-adrenergic receptors (epinephrine and norepinephrine) >> stimulation will cause vasoconstriction

afferent arterioles constrict >> (-) glomerular BP >> (-) GFR

efferent arterioles constrict >> (+) filtration fraction

**reduce GFR to lose less volume

Front 66

tubular reabsorption

Back 66

100% of glucose is reabsorbed
99.5% of salt filtered in reabsorbed
99% of water filtered is reabsorbed

>> has to cross laminal membrane, interior of cell, basolateral membrane, interstitial fluid, and endothelial of peritubular capillary

Front 67

reabsorption of Na+

Back 67

80% of energy requirements of kidneys is used for Na+; usually coupled to reabsorb other solutes and perform other tasks

passively crosses luminal membrane // Na/ATP pump @ basolateral membrane

reabsorbed @ every portion of nephron EXCEPT the descending loop of henle

Front 68

locations of Na+ reabsorption

Back 68

proximal tubule- crucial role in reabsorption of glucose, AA, water, and urea

ascending loop of henle- important role in urine concentration

distal tubule and collecting duct- under hormonal, regulates ECF volume and BP

Front 69

Na+ reabsorption in proximal tubule

Back 69

*major adjustments to urine composition will occur in proximal tubule

Na+ is a cotransporter; sneaks in glucose, AA, water-soluble vitamins

Front 70

How does glucose end up in urine?

Back 70

tubular max (TM)- maximal rate of transport, limited by # of cotransporters

renal threshold- max plasma concentration @ which you reach TM

high concentration of glucose will overwhelm and saturate cotransporters; TM for glucose is 375 mg/min

Front 71

Na+ reabsorption in ascending loop

Back 71

symports K+ and Cl- at laminal membrane
K+ and Cl- passively cross basolateral membrane

Front 72

Na+ reabsorption in distal tubule

Back 72

symports Cl- at laminal membrane
Cl- passively cross basolateral membrane

Front 73

Na+ reabsorption in collecting duct

Back 73

Na+ is alone, passive channel only @ laminal membrane

Front 74

H2O reabsorption

Back 74

80% of H2O is reabsorbed in the proximal tubule and loop of henle

usually follows Na+ reabsorption; however, H2O reabsorption is independent in distal tubule and collecting duct

two mechanisms--
paracellular route- between epithelial cells
transcellular route- through epithelial cells

Front 75

paracellular route

Back 75

H2O moves through leaky tight junctions

lateral membranes are packed w/ K+/Na+ pump, causing an extremely high osmolarity @ tight junctions >> sucks H20 into interstitial space

Front 76

transcellular route

Back 76

H20 has to move through cell via aquaporins
>> always present @ basolateral membrane
>> varies @ luminal membrane

H2O is NEVER reabsorbed @ ascending loop of henle

Front 77

chloride reabsorption

Back 77

*electrical gradient
Na+ in the lateral membranes attracts Cl- across

Front 78

What follows H2O reabsorption?

Back 78

H2O creates a concentration gradient by leaving; the solutes left behind (urea, Cl-, K+) will also move down its gradient through leaky tight junction

most commonly seen @ proximal tubule

Front 79

reabsorption of PO4- and Ca+

Back 79

reabsorption of some substances helps regulate plasma levels of those substances

renal threshold = normal plasma levels
>> if plasma level increases, only "X" amount will get reabsorbed and excess is secreted through urine

*glucose is not apart of this system b/c its renal threshold is 3x normal

Front 80

What does not get reabsorbed?

Back 80

waste products (except urea)
1/2 N+ gets recycled to make AA

Front 81

tubular secretion

Back 81

movement of substances from peritubular capillaries into tubular lumen for elimination

Front 82

H+ ion secretion

Back 82

plays an important role in acid/base balance

acid ionizes in blood stream, H+ >> actively pumped through basement membrane >> exits laminal membrane via

Na+/H+ antiporter @ proximal tubule
facilitated diffusion @ collecting duct & loop of henle

Front 83

K+ secretion

Back 83

K+ reabsorption is unregulated; it's passive and proportional to Na+ and H2O reabsorption @ proximal tubule

K+ secretion is regulated
*only occurs in collecting duct and distal tubule where K+ channels are on the luminal membrane

Aldosterone opens luminal Na+ channels and increases Na+/K+ ATPase expression

Front 84

anion/cation secretion

Back 84

these organic ions can be endogenous or exogenous (e.g. food additives, pollutants, drugs); their excretion involves energy, and Na+ reabsorption

reasons why proximal tubules contains two secretory pathways for organic ions
1/ some are bound to plasma proteins and is never filtered by the glomeruli >> this is a second opportunity to get rid of them
2/ increase the speed of elimination

Front 85

urine concentration

Back 85

100 mOsm to 1200 mOsm
body is in perfect balance when it produces 300 mOsm, which is isotonic

[urine] increases as it gets closer to the renal pelvis

Front 86

obligatory water loss

Back 86

we have to lose water, cannot stop producing urine--therefore, body is better dealing w/ persistant overhydration than persistant dehydration

Front 87

loop of henle permeability

Back 87

descending
permeable to H2O, impermeable to Na+

ascending
permeable to Na+, impermeable to H2O

>> urine that leaves loop of hence will have low osmolarity (after losing Na+); 100 mOsm
>> sets up absorption gradient for collecting duct

Front 88

medullary countercurrent system

Back 88

nephron structures working together to vary [urine]
-loop of henle of juxtamedullary nephrons are responsible for creating gradient
-collecting duct uses this gradient

water gets reabsorbed at collecting duct and will increase [urine]

Front 89

vasopressin (ADH)

Back 89

determines how much water is reabsorbed by determining the permeability of H2O

>> binds to tubular epithelial cell, increases cyclic AMP to increase aquaporins on laminal surface

@ distal tubule and collecting duct

Front 90

ECF volume

Back 90

helps maintain blood pressure and blood supply to tissue

Front 91

ECF osmolarity

Back 91

helps maintain cell volume

regulated by maintaining water balance; assuming body has fixed # of solute, you want to maintain water to keep osmolarity @ isotonic concentration

total body osmolarity is defined as the ratio of total-body osmoles to total-body water, where body osmoles is primarily determined by ECF sodium content

regulation involves the detection of plasma osmolarity

Front 92

Na+ balance

Back 92

gains- ingested Na+ absorbed through GI tract

losses- renal excretion & nonrenal loss (sweat, feces)

Front 93

baroreceptors

Back 93

changes in plasma volume are sensed by monitoring blood pressure

short term- aortic arch & carotid sinus
long term- renal

Front 94

angiotensin II actions

Back 94

these are long term regulations; sensed by JGA granular cell receptors; "renin, aldosterone, angiotensin"

increases sodium (and water) reabsorption
1/ stimulates aldosterone release @ distal tubule and collecting duct (indirect)
2/ stimulates Na+/H+ exchanger in proximal tubule (direct)

decreases GFR
3/ direct vasoconstriction of afferent arterioles, elevating BP
4/ enhances tubuloglomerular feedback

increased water consumption and reabsorption
5/ stimulates thirst and ADH secretion

Front 95

non-renal baroreceptors

Back 95

any decrease in BP sent to brain >> increases sympathetic activity

1/ increase norepinephrine from renal nerve onto renal arterioles >> vasoconstriction to afferent arteriole

2/ renal nerves innervate JGA, stimulates granular cells >> increase renin >> angiotensin II

3/ increases ADH secretions

Front 96

summary control of plasma volume

Back 96

Front 97

water balance

Back 97

gains- water consumed & water liberated from metabolic processes

losses- through urine, feces, sweat

Front 98

effector mechanisms for water/osmolarity balance

Back 98

1/ diuresis
2/ thirst

both part of negative feedback loop that starts in hypothalamus

Front 99

central osmoreceptors

Back 99

circumventricular organs (CVOs)
SFO & OVLT

senses the change in osmolarity >> releases ADH

Front 100

sensitivity of ADH release

Back 100

plamsa osmolarity is 290 mOsm in healthy adults

threshold for ADH release is ~280 mOsm; that means any lower will shut down ADH release

increases by as little as 1% in plasma osmolarity can produce a large increase in plasma ADH

Front 101

Where does angiotensin II intersect w/ the osmolarity system?

Back 101

There are angiotensin II receptors on SFO and OVLT; brainstem is increasing sympathetic activity while simultaneously stimulating thirst and ADH

>> plasma osmolarity rises, plasma volume/BP drops

Front 102

inappropriate ADH release

Back 102

rate of ADH breakdown--
e.g. when liver function declines, (+) plasma ADH

pain, fear, trauma--
increases sympathetic activation, (+) ADH

alcohol, (-) ADH

Front 103

CV blood flow

Back 103

Front 104

AV valves

Back 104

right <3 is tricuspid
L <3 is mitral

-ensures unidirectional flow
-strong cartilage to prevent collapse
-leaflets are anchored by cordinae tendinae

Front 105

semi-lunar valves

Back 105

shaped more like cusp; blood fills these cusp and helps seal this valve to prevent back flow of blood

Front 106

pericardial sac

Back 106

reduces frictional forces during contraction

Front 107

cardiac muscle

Back 107

-striated
-branching pattern

*intercalated discs attach cardiac muscle cells to one another; at this junction; there are--
1/ desmosome- protein anchors that physically attach one cardiac cell to the next
2/ gap junction- allows the 2 cells to be coupled electrically so that simultaneous contractions can occur

Front 108

cardiac cells

Back 108

contractile muscle cells 99%
autorhythmic cells 1%

Front 109

contractile cells AP

Back 109

4/ resting membrane potential

0/ rapid depolarization; Na+ in

1/ closure of Na+ channel

2/ plateau; sustained by balance of Ca+ in and K+ out
*AP is wider, plateau allows it to spend more time @ depolarization so that they can fire and contract muscles @ same time

3/ repolarization; Ca+begins to close while K+ continues to go out

Front 110

autorhythmic cells AP

Back 110

*never sustains a membrane potential

@ -60 mV, no gated channels are open but there is a leakage in Na+ channels >> causes slow depolarization

transient Ca+ channel opens up enough for Ca+ to go in and reach threshold

long type Ca+ channel opens, cell depolarizes

Ca+ closes, K+ channel opens and K+ goes out

Front 111

autorhythmic cells

Back 111

70-80 APs/min SA
40-60 APs/min AV
20-40 APs/min bundle of his & perkinje fibers

SA node fires >> interatrial pathway to L atrium and internodal pathway to AV node
*AV nodal delay (100 msec) maximizes ventricular filling; want this delay so that AV will cause R and L bundle of his to fire @ same time

Front 112

EKG

Back 112

records all the cells in the heart

1/ P wave- depolarization of atria once SA node fires
2/ PR- represents AV nodal delay
3/ QRS- depolarization of both ventricles
4/ ST- ejection of blood from ventricles
5/ T- repolarization of both ventricles
6/ TP- diastolic time

Front 113

P wave

Back 113

before--
atrial pressure > ventricular pressure allowing for passive filling >> ventricular volume increases

during--
contraction
(+) atrial pressure (green line exceeds red)
(+) ventricular volume

Front 114

QRS complex

Back 114

ventricular pressure exceeds atrial pressure (red line shoots up)

AV valve shuts causing
-first heart sound
-flat line of ventricular volume "end diastolic volume"

isovolumetric contraction- time it takes for ventricle to create enough pressure to open aortic valve; must overcome aortic pressure

Front 115

ST

Back 115

ventricular ejection

aortic valve opens;
(+) in both aortic & ventricular pressure but ventricular pressure stays slightly higher than aortic
(-) ventricular volume >> end systolic volume s/p ejection

SV= EDV-ESV

Front 116

T wave

Back 116

isometric ventricular relaxation

ventricular pressure falls below aortic pressure >> closure of aortic and pulmonic valves; causes 2nd heart sound and will continue to resting

*dicrotic notch- when aortic valve closes, there is a bump in aortic pressure

Front 117

TP

Back 117

passive filling

cardiac suction- dip in atrial pressure so that draws blood into atria; occurs during ejection phase while ventricles are contracting

when ventricular pressure falls below atrial pressure, valves will open again
>> passive rush of blood into ventricles
*most of filling of ventricle is done passively during diastole

Front 118

CO

Back 118

*primary measure of cardiac performance

CO = HR x SV

cardiac reserve = max CO - reserve CO
-max CO is affected by age; 220-age
-exercise increases max SV, making the heart more efficient
-heart failure will cause reserve to narrow >> activity intolerance

Front 119

<3 parasympathetic pathway

Back 119

decreases heart rate
R and L vagus n. stimulate both SA and AV nodes

SA receives more R vagus n. stimulation- releases acetylcholine and (-) firing rate

AV receives more L vagus n. stimulation and (+) AV nodal delay

Front 120

<3 sympathetic pathway

Back 120

releases norepinephrine

(+) firing rate @ SA
(-) nodal delay @ AV; normally does not reduce ventricular filling unless you are very tachy

Front 121

T/F. Athletes have lower firing rate @ SA node.

Back 121

False; natural firing rate remains the same--they have a higher vagal tone @ rest, which is why their HR is usually much lower

Front 122

ejection fraction

Back 122

healthy person should be able to eject ~55% w/ every beat

Front 123

control of SV

Back 123

SV is a function of contractility

1/ intrinsic control- increased filling
*frank starling- more filling >> more stretch >> more force in contraction
*length-tension relationship; changing length can change its potential tension
-positional changes can enhance filling (if you feet are above your heart >> increase venous return to heart)

2/ extrinsic control- sympathetic stimulation to <3, directly creates stronger muscle contractions

Front 124

frank-starling graph

Back 124

green- normal frank-starling
purple- frank-starling on sympathetic stimulation

Front 125

flow dynamics

Back 125

F = pressure gradient / resistance

resistance
-viscosity (ratio of plasma to RBC is stable)
-radius of blood vessels (causes dramatic change)

Front 126

arterial BP

Back 126

arteries
1/ transport from heart to tissues
2/ store pressure and provide driving force for flow when heart is resting

BP- force of blood against vessel wall

<3 contracts and empties
>> stretch in arteries, registers as systolic BP

<3 relaxes and fills
>> arteries rebound, registers as diastolic BP

Front 127

mean arterial pressure (MAP)

Back 127

MAP = diastolic pressure + 1/3 pulse pressure

average BP at anytime in artery; represents perfusion pressure @ all times
-----------
How does arteriole diameter relate to BP?
MAP = CO x TPR
TPR is most influenced by arteriolar resistance

Front 128

measuring BP

Back 128

korotkoff sounds--

(1) when radial pulse is no longer palpable >> above systolic pressure

(2) cuff is just below systolic pressure; first sound is an estimate of systolic

every subsequent tap is when BP exceeds cuff pressure

sounds get more muffled as cuff pressure gets closer to resting pressure >> (5) no longer hear sound, cuff pressure is below diastolic; blood flow is no longer forceful and does not generate sound

Front 129

<3 intrinsic control

Back 129

chemical--
local metabolic changes
histamine release >> vasodilation

physical--
temperature
myogenic response to stretch >> momentary vasoconstriction

Front 130

What local metabolic changes will lead to vasoconstriction/vasodilation?

Back 130

vasoconstriction
*endothelin released when endothelium senses (-) metabolic rate
(+) O2
(-) CO2
(-) acidity, rise in pH
(-) adenosine

vasodilation
*EDRD identified as nitric oxide is released
(-) O2
(+) CO2
(+) acidity, rise in pH
(+) adenosine

Front 131

<3 extrinsic control

Back 131

sympathetic nerve fibers supply arteriole smooth muscle everywhere but the brain

releases norepinephrine which binds to
1/ beta receptors are found on smooth muscles that perfuse skeletal muscles >> vasodilation
2/ alpha receptors are found everywhere else >> vasoconstriction

generally speaking--
(+) sympathetic >> vasoconstriction
(-) sympathetic >> vasodilation

Front 132

@ rest v. exercise

Back 132

@ rest-- total CO = 5,000
27% digestion
20% kidney
9% skin
13% brain

exercise-- CO = 12,500
64% skeletal muscle
4.8% digestion
4.4% kidneys

*no change in blood flow

Front 133

hormonal influence on arteriolar diameter

Back 133

sympathetic activity releases epinephrine and norepinephrine--
-epinephrine has stronger affinity for beta receptors >> vasodilation
-norepinephrine binds to alpha receptors >> vasoconstriction

vasopressin (ADH) and angiotensin II >> vasoconstriction

Front 134

How are capillaries are highly adapted for diffusion?

Back 134

1/ diffusion distance is minimized
2/ thickness of diffusion barrier is minimized
3/ surface area is maximized
4/ blood velocity slows down through capillary beds, maximizing the opportunity for diffusion

Front 135

How does blood flow rate remain constant if blood velocity slows down @ the capillary beds?

Back 135

The increase in cross-sectional area compensates for the decrease in velocity.

Front 136

transport across capillary wall

Back 136

Front 137

Explain why diameter of capillary is usually equal the diameter of RBC.

Back 137

It is designed to minimize diffusion difference.

Front 138

metarteriole v. capillary bed

Back 138

*precapillary sphincter determines whether blood will diffuse into capillary bed or if it will be diverted into metarteriole

> high metabolic activity relaxes sphincter >> capillary beds for more exchange, greater SA

> low metabolic activity constricts sphincter >> metarterioles for less exchange, smaller SA
*metarterioles are like shortcuts, moves quickly from arteries straight into venules

Front 139

bulk flow

Back 139

-movement of ECF between plasma and interstitial fluid
-determined by passive forces >> ultrafiltration & reabsorption
-will affect BP

Front 140

bulk flow forces

Back 140

1/ capillary BP "pushing" >> ultrafiltration
2/ capillary oncontic "pulling" caused by plasma that cannot leave capillary >> reabsorption

3/ interstitial hydrostatic pressure "pushing" >> reabsorption
4/ interstitial oncotic pressure "pulling" >> ultrafiltration
*minimal; this is theoretical--if protein is able to escape capillary

Front 141

reabsorption v. filtration

Back 141

reabsorption--
capillary oncotic pressure & interstitial hydrostatic pressure is fixed in healthy adult; capillary oncotic pressure will decrease in ill patients w/ low albumin count

filtration--
capillary BP is variable and will be greater than capillary oncotic and interstitial hydrostatic pressures if
1/ capillary sphincter is relaxed
2/ (+) plasma volume, (+) BP; will increase capillary BP pressure regardless of action @ sphincter site

Front 142

veins

Back 142

-high capacitance vessel capable of holding large volume of blood
-vasoconstriction of veins means decreasing compliance and not allowing them to expand; this will cause (+) venous return to the heart

Front 143

increasing venous return

Back 143

1/ sympathetic stimulation >> vasoconstriction >> (-) compliance >> (+) return

2/ skeletal muscles contract >> milk veins and encourages blood flow back to <3

3/ venous valves >> open and (+) venous return; close to prevent backflow

4/ thoracic cavity is 5 mmHg less than atm >> sucking pressure (+) return

5/ cardiac suction; ventricles contract >> atrial volume increases >> negative pressure >> (+) return

Front 144

orthostatic hypotension

Back 144

blood starts to poll to leg after standing upright for a long period of time >> syncope

(-) venous return
(-) CO
(-) MAP

Front 145

baroreceptor reflex

Back 145

short term regulation- carotid sinus baroreceptor & aortic arch baroreceptor respond to BP changes by altering their firing rates
**will eventually adapt to persistent change in BP and return to normal firing rate

(+) BP >> (+) firing rate
(-) BP >> (-) firing rate

act by stimulating CV center in medulla >> (+) vagus n. >> (-) HR >> (-) CO >> (-) MAP