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Flashcards in Final Deck (266):
1

Functions of LI

absorbs remaining water and water soluble vitamins
compaction of feces

2

how is water absorbed by LI

establish ion gradient using Na and then water moves by osmosis

3

what is the main component of feces?

indigestible starch components, we don't have the enzymes to break down cellulose--fiber. Also some metabolic waste

4

role of bacteria in LI

LI is colonized by bacteria.
some breakdown of starch
produce vitamin K
produce gas through cellular respiration

5

defacation

2 anal sphincter. 1 smooth internal, one skeletal external
conscious urge is triggered by stretch of rectum
contract ab muscles to change pressure

6

valsalva maneuver

contraction of ab muscles and increased pressure in thorax assists in defecation. By holding breath you can create a change in pressure to help with defecation

But your heart rate will slow down

7

absorptive state

ingested nutrients are entering the vbloo from the GI tract (in the 4 hours after a meal)
-body wants to absorb more calores thana re required immediatle
some go to blood stream, the remainder are stored.
-total body storage is adequate for the average person to go weekks without food

8

post-absorptive state

GI tract is empt of nutrients fro stored nutrients must be used(in between meals)

9

the role of the liver

most ingested nutrients are carbs and proteins which are absorbed immediately into the blood and transported to the liver in hepatic portal vein
liver can filter/alter nutrients before then tracel to the heart and throughout the body

inactivates and removes toxins using liver enzymes
glucose is taken up

10

absorptive state events carbs

blood glucose levels rise.
is taken up by liver and skeletal muscle which stores it as glycogen
any excess is take up by the liver and converted to fatty acids and triglycerides for storage

11

gucose stoarge as lipids

synthesized lipids in liver are released into the bloodstream bound to protein transport molcules called lipoproteins: FDL, LDL and VLDL

12

What do newly made lipids from glucose travel on?

in blood on VLDLs. These are too big to cross out of capillart. gets to areas of adipose tissue which secrete lipoprotein lipase which seperates the lipid from the liporpotein allowing it to move into the adipose tissue.

13

fate of absorbed carbohydrates

1. directly into blood to boost blood sugar levels
2. stored as glycogen in liver or muscle
3. stored as fat in adipose tissue

14

absorptive state events of lipids

go directly into lymph, then added to the blood in the vena cava.
Travel in aggregates
lipoprotein lipase breaks up aggregates and allows monomers to diffuse out of the bloodstrem to the adipose tissue

15

how are lipids stored?

as triglycerides

16

formation of triglycerides

glycerol head synthesized by glucose in the adipocyte: can be made by 3 sources, glucose from blood thats stored in adipocytes as fatty acids, glucoe from blood can be converted to stored fatty acids in the liver. ingested fatty acids from the blood

17

cholesterol

a type of lipid necessary for plasma membranes, bile salts, hormones.
can't be used to cellular respiration
too much in circulation can contribute to atherosclerosis

18

changes in cholesterol levels

liver can make it
SI can transport some into blood
some passes as feces

liver can also remove colesterol from blood to make bile salts

19

cholesterol set point

liver is primary control
works by negative feedback (if blood cholesterol is to high, the liver cholesterol production will be inhibited and more will be transported to digestive system
set point can change based on diet etc

20

HDLs

remove cholesterol from blood and deliver it to liver or endocrine glands

21

LDLs

supply all cells with cholesterol for membranes

22

What non-diet factors impact HDLs?

smoking decreases HDLs
Exercise increases HDLs
circulating estrogen increases HDLs

23

absorptive state events of proteins

absorbed as AA, which are absorbed by cells for production of new proteins.
If needed for energy some amino acids can be converted to metabolic precursors in the liver-- but the N group must be removed as urea--makes urine

24

Fate of ingested amino acids

1. converted to metabolic precursors for energy
each cell stores the AA for protein synthesis
excess is converted to glycofen or lipids for protein storage

25

post absorptive state

no additional sources of enery
must maintain plasma glucose levels

26

where can glucose come from in the post absorptives tate?

liver glycogen--> glucose
adipose tissue: triglycerides-->glucose
muscle
protein breakdown and conversion to glucose

27

how long can you subside on liver glycogen?

~3 hours

28

using glucose and fats for energy

-can provide 720cal/day
organs go into glucose sparing mode where they preferentially use lipids for energy

29

ketones

form when the liver breaks down fats for energy, leads to ketosis

30

Control of nutrient use:

endocrine pancrease (insulin and glucagon)
epinepherine and cortisol
sympathetic innervation to liver and adipose

31

insulin

storage hormone
secreted by beta cells of pancreas
controls cell-expresion of glucose receptors
-promotes glycogen production in the liver and inhibits glucose secretion by the liver


glucose present, results in insulin release--binds to insulin receptors which results in expression of glucose receptor to bind glucose and transfer it into the cells

32

When does a cell membrane of neuron express glucose transporters?

-always expresses glucose transporters
they are insulin independent

33

if you had a mutation so you didn't express lipoprotein lipase you would

-have very little body fat but high blood lipids
-decelop atherosclerosis
-have endocrine issues

34

more insulin--> what change in blood glucose production?

less glucose in blood

35

If you accidenly inject excess insulin, what happens?

blood flucose is absorbed by the cells, not enough is left for the brain

36

Which cells require insulin

skeletal and cardiac muscle, and adipose
NOR BRAIN and NS

37

incretins

secreted by enteroendocrin cells in GI tract increase insulin

ie sense candy bar in your stomach, so increase insulin to deal wiht it

38

Control over insulin

glucose level in blood
incretins
hormones that inhibit insulin
sympathetic neurons-- fight or flight inhibts insulin secretion

39

diabetes mellitus

cells cannot take up glucose from the bloodstream

40

Cause of Type I

auto immune, beta cells are attacked

41

Type II cause

genetics and lifestyle
cells become insulin resistant, later beta cells slow insulin production
glucose receptors internalize after excessive stimulation.

42

gestational diabetes cause

idiopathic, probably genetic or tendency toward insulin insensitivity
are then more likely to develop type II

if mom has high glucose levels--baby gets high glucose, and baby doesn't have diabetes so gets it all.

43

Type I Treatment

injected insulin at each meal for life

44

Type2 treatment

diet+ exercise, injectable insulin or incretins,

metformin-down reg liver gluconeogenesis, increases insulin sensitivity

45

gestational diabetes treatment

lifestyle, glucose monitoring

46

what would be one of the first signs of type Ii diabetes?

- high blood bressure, b/c excess sugar as a solute in the blood, will drive water in
-increased frequency of infections-high glucose levels in tissues too, feeds more bacteria/yeast to grow.

47

glucagon

-produced by alpha cells of pancreas
-increase glycogen breakdown and gluconeogenesis in the liver
-effected by some hormones and sympathetic innervations

48

gluconeogenesis

making of glucose from amino acids or fatty acids

49

what would the effect of the fight or flight response be on blood sugar?

blood sugar increases

50

what is energy used for in body?

protein synthesis, ion pumps, cellular transport, muscle contraction, heat

excess is stored

51

basal metabolic rate

amount of energy to fuel basic properties without exercise or other increase in metabolism

based on body size, typical caloric intake and age

52

BMR and Body size

losing weight slows down metabolism
-losing 10% body weight-->15% decrease in energy expenditure
-gaining 10% body weight-->15% increase in energy expenditure.

53

leptin

inhibits appetite. Mice withour leptin voaraciously eat and become obese
-made by adipocytes and released in proportion to the amount ot fat in adipose cells
-stimulates metabolism
-says that you have enough energy, don't need to eat as much

54

ghrelin

made by somach lining cells
stimulates appetite
lack of stretch of stomach results in release (empty somach

55

signals to stop eating

leptin
insulin release
-increase in body temperature
-stretch receptors and hormones in stomach, SI, LI

56

corticotropin releasing hormone and appetite

decreases appetite

57

leptin source and impact on appetite

adipose tissue decrease,

58

insulinsource and impact on appetite

pancrease, decrease

59

ghrelin source and impact on appetite

stomach, increase

60

CCK source and impact on appetite

intestine decrease

61

peptide YY source and impact on appetite

intestine, increase

62

extreme biggest loser diet

ghrelin soar, leptin levels sink, body thinks you're starving, these changes remain for 6 years

63

genetic influece in weightloss

hormone levels, BMR, food preference may be genetically driven, tendency to gain/lose weigjt

64

twin weight study

] increased calorie intake, decreased exercise

all twins gained the same amount of weight and in the same places, some sets of twins gained 10, some gained 30. l

65

psychological factors and hunger

stress adrenaline and cortisol-decrease appetite and GI motility
-serotonin is released by intestines in response to food- might change depression

66

thrifty gene

if poor nutrition at young age, your genome encourages the storage of more energy

67

adiponectin

produced by adipose
decreases inflammation, promites using energy stores

68

resistin

adipose hormone, leads to insulin resistace

69

visfatin

agonist to insulin receptor, increases glucose uptake from the blood, mimics insulin
adipose hormone

70

adipo-cytokines

promote inflammation and mitosis in local areas
adipose hormone

71

according to the thrifty gene hypothesis, poor nutrition in infancy would result in

obesity in adulthood

72

what kind of ghrulin levels would you expect in a person who recently lost weight?

high ghrelin levels

73

would inhibiting glucagon lower blood glucose levels?

yes,

74

hypoxia

lack of O2

75

hypercapnia

too much CO2

76

functions of the respiratory system

gas exchange, acid-base balance, vocalization, immunity, waterloss and heat loss

77

cellular respiration

intracellular reaction that uses O2 and glucose to make Co2, h20 and ATP

78

external respiration

movement of gases betwen the environment and th bodys cells

79

ventilation

air exchange between lungs and external air

80

steps of respiration

-ventilation
-exchange of O2 and CO2 between alveoli and capillary
-transport of O2 and CO2 in blood
-exchange of O2 and Co2 betwee blood and tissues
-cellular utilization of O2 and production of Co2

81

type 1 alceolar cells

small thin for gas exchange between alveoli and capillaries

82

type ii alveolar cells

synthesize surfactant
-lowers surface tension of alceolus, allowing the cells to inflate
-prevents alveli from collapising alveloi

83

premature babies and surfactant problems

get respiratory distress because type 2 alveolar cells ar one of the last cell types to develop

84

is there smooth muscle in lungs?

no
elastic fibers cause recoil so that lungs return to resting after the inhale

85

inflation of lungs

-work of muscles bbetween ribs and diaphram
-widen the thorax and pull the lungs with them by fluid surface tension.

86

F=

change in p/r

87

boyle's law of gases

if temp is constant:
pressure in inversely proportional to volume

if you increase volume, you decrease pressure`

we must icrease the volume of our lungs (And thus decrease the pressure) to sufficienctly form a pressure gradient with atmospheric pressure and allow for flow

88

BOyles law applied

inhale, air moves in because pressure is lower inside
exhale- air moves out if pressure is greater outside

89

If you experience systemic vasodialation, what happens to BP?

decreases

90

pneumothorax

air gets between the peural layers and the lung is no longer held t othe thorax by surface tension

91

what happens to flow if you narrow a vessel?

flow decreases, due to increase of resistance

92

asthma

inflammation and swelling of bronchiole walles
decreased diameter of bronciole- bronchoconstriction
less O2 air to alveloi
CO2 build up in alveoli
increased resistance lowers air flow

93

pulmonary edem

increased blood pressure, increased pressure, fluid leaves lungs and increases diffusion distance.

94

emphysema

decreased alveoli surface area=less diffusion
-treatment is to increased PO2

95

Daltons Law

total pressure=sum of partial pressures

96

daltons law applied

chemoreceptors in the blood are sensitive to hypoxia-- you can increase or decrease the conc. of O2 by changing partial pressure (administering O2) or changing total pressure (changes with altitude_

97

henry's law

states that the partial pressure of a liquid will equilibrate to that of a gas--- means the partial pressure of a liquid will equilibrate to that of a gas

PO2 in air=PO2 in alveoli=PO2 in blood

98

4 laws of respiration

boyle-pressure and volume
fick-diffusion
dalton-gasses and proportional pressure
Henry-liquids and gases

99

PO2 in alveoli=

PO2 in arterial blood

100

PO2 in tissues=

between the PO2 in alveoli and the PO2 in venous blood

101

PCO2 in alveoli=

PCO2 in arterial blood

102

PCO2 in tissues=

same as PCO2 in venous blood, or more

103

hypercapnia

elevated PCO2--causes acidosis

104

control of respiration

diaphragm and intercostal muscles
- dont need to think about it, but can change it if you want
-

105

what directs cyclic innate breathin?

respiratory center in the medulla oblongata--based on chemoreceptors

106

peripheral chemoreceptors

in aortic and carotid bodies, detect O2 and pH cahngse

107

central chemoreceptors

monitor pH changes in th CSF

108

When will PO2 trigger an increase in ventilation?

<60mmHg-- the point where Hb dissociation changes

109

COPD

narrowing, hardening and mucus build up in the bronchioles.
leads to chronic hypoxia and hypercapniia (low O2, high CO2)
-over time the chemoreceptors adapt, which means that the stimulus for increasing ventilation switches from high PCO2 to low PO2,

110

what normally stimulates an increase in ventilation?

high CO2

111

what happens if you give a COPD patient O2?

they stop breathing, because they have adapted to low O2 being a trigger to breath, so now having excess O2 they are not prompted to breath

112

Functions of the Urinary System

1. Regulate extracellular volume and BP
2. Regulation of osmolarity
3. Maintainance of ion balance
4. Regulation of pH--kidneys selectively secrete H of HCO3
5. Excretion of waste and foreign chemicals
6. Priduction of hormones

113

How does the urinary section work, 4 steps

1. Filter
2. Reabsorb
3. Secrete
4. Excete

114

nephron

the functional unit of the kidney
-blood processing unit
-work with capillaries to monitor and filter plasma
has 2 functional sections: renal corpuscle, tubule

115

portal system

when 2 capillary beds meet without first going to the heart

116

Renal Corpuscle

a capillary nest and cup around it that filters the plasma--filtration

117

tubule

long pipes, secretes and reabsorbs- fine tunes what leaves the body and what stays

118

glomerulus

the capillary nest
-fenestrated- but doesn't allow RBC or plasma proteins out

119

bowmans capsule

the surrounding capsule

catches filtrate and directs it through the tubules
Has 2 walls: parietal and visceral, with a lumen space between these 2 layers

120

carpuscle

bowmans capsule+glomerulus
capillary is fenestrated--- leaky

121

nephron

corpuscle+ tubule

122

parietal layer

the outer layer of bowmans capsule

123

visceral layer

the inner layer of the bowmans capsule- has epithelial cells called podocytes that cover the glomerular surface

124

podocytes

part of vsceral wall
have branching pedicles that wrap around the capillary and intertwine with each other
-connect to the basement mmbrane of the capillary endothelium

125

filtration slits

spaces between pedicles- line up with fenestrae

126

filtration membrane

-endothelium+ podocyte with lined up slits/fenestrae

127

proximal convoluted tubule

the tubule as it leaves the glomerular capsule
-reabsorbs stuff that we filtered out of the plasma

128

loop of henle

concentrating/diluting urin
-has 3 parts: descending, hairpin turn, ascending

129

distal convoluted tubule

name of tubule as it neats the collecting duct
-mostly secretion

130

kidney vasculature

efferent arteriole--> peritubular capillaries
as materials are reabsorbed from the tubule they enter back into the blood flowing through the peritubular capillaries

131

peritubular capillaries

-arise from efferent arteriole and drain into venules to return blood to the heart
-supply glucose, O2 to the nephron
-reabsorbed materials return to the blood here
-secreted substances are moved from the blood to the tubule here

132

where does filtration happen?

glomerulus

133

where does reabsorption/secretion happen?

peritubular capillaries

134

filtration

the bulk flow of plasma out of capillaries into vowmans capillary- affected by osmotic pressure and hydrostatic pressure

135

hydrostatic pressure-

higher in capillary, drives fluid out of the capillary

136

osmotic pressure

is higher inside the capillary, draws fluid In to the capillary

137

What happens if you constrict the afferent arteriole?

decreased GFR

138

what happens if you dialate the efferet arteriole?

decreased GFR

139

what happens if you constrict the efferent arteriole?

increased GFR

140

what happens if you dialate the afferent arteriole?

increased GFR

141

when do you want to control GFR?

high/low BP, increase/decrease blood solutes, stress

142

afferent arteriole characteristics

has a larger diameter (to increase GFR)
has ha higher density of receptors for sympathetic innervation and hormones

143

efferent arteriole characteristics

smaller diameter
exits the glomerular capsule and brings blood to the peritubular capillaries
-blood here has low pressure and is very concentrated

144

glomerular filtrate

once it is out of the capillary

145

what 3 barriers does filtrate pass through before getting to the lumen of the tubule?

-glomerular capillary endothelium
-capillary basement membrane
-epithelium of podocyte- visceral layer of the bowwmans capsule

146

glomerular filtration rate

the volume filtered into bowmans capsule per unit of time

147

average GFR=

125ml/min

148

what 3 factors determine the GFR?

-hyrostatic pressure-- higher in drives fluid out
-osmotic pressure-higher in, drives water IN
-hydrostatic pressure of the capsule-- since it is an enclsed space, the pressure can drive fluid back into the capilary

149

how many times is the entire blood volume filtered each day

60 times

150

do normal changes in blood pressure alter GFR?

between 80-120 has no difference, because the afferent arteriole can change its diameter to maintain a constant GFR

151

myogenic control of GFR

when stretch receptors are activated in the affterent arteriole due to an increase in BP, smooth muscle cells constrict, decreasing flow into the glomerulus

increase in pressure-->decrease rate of flow--> maintained GR

152

juxtaglomerular apparatus

an anatomical site here the afferent arteriole and DCT are adjacent to each other.

153

juxtaglomerular cells

the smooth muscle cells of the afferent arteriole-- these are mechanoreceptors that sense blood pressure in the afferent arteriole

sense stretch and then can contract or relax in response

secrete renin

154

macula densa

the enlarged epithelial cells in the DCT
these are osmoreceptors, chemoreceptors and mechanoreceptors. They detect solute concentration changes in the tubular lumen

155

juxtaglomerular apparatus and control of GFR

-when more solutes are detected in the DCT, the macula densa cells in the DCT send a paracrine message to the juxtaglomerular cells in the A.A. to constrict and decrease GFR

156

what does to many solutes at the end of the tubule indicate?

hat the filtration/reabsorption/secretin is going to fast and needs to slow down, will signal constrivtion of A.A.

157

renin

secreted by juxtaglomerular cells to increase solute reabsorption

158

is reabsorption or molecules uder physiological control?

Some yes. ie we can alter how much water we reabsorbed based on need

some no-- ie we always reabsorb as much glucose as possible

159

How is reabsorption accomplished?

through active or passive transport----NOT BY BULK FLOW

160

What 2 surfaces does reabsorption occur across?

luminal membrane of the tubular cells, the blood facing side of the tubular cells

161

transcellular transport

from inside the tubular lumen all the way to the capillary

162

what is reabsorbed by passice transport via simple diffusion?

anything small, non-polar, lipid soluble down its conc. gradient

163

what is rabsorbed cia facillitated diffusion?

anything eith a transporter protein down its conc. gradient

164

how are Na and glucose/AA transported into the proximal tubule celles from tubular lumen?

Na+/H+ counter transport
countertransport of Na/ glucose or AA

165

How are glucose/K/Na transported from the proximal tubule cells out into the intersticial fluid?

down their conc. with simple diffusion, or via active transport Na/K pump

166

how does the reabsorbed stuff get back into the blood?

peritubular capillaries are very low in pressure, so it flows in via bulk flow and diffusion

167

What is secreted?

organic ions, metabolic waste, drugs, some H_, J

168

Renal clearance:

how quickly we rid the plasma of a substace.

Mas od S excreted per unit time/ Plasma [S]

169

What are transporters ruled by?

competition, specificity, saturation

170

Diabetes and the kidneys:

increased plasma [glucose]
increased BP
Increase GFR
increased urine volume

since glucose transporters are sturated, the glucose remains in the rubule, which results i more water remaining in the tubule.

171

polyuria

more water excrete

172

polydipsea

excessive dehydration and thirts

173

what secretes vasopressin

hypothalamus/posterior pituitary

174

what influencesvasopressin secretion?

osmoreceptors in the hypothalamus and baroreceptors in the carotid and aorta

175

what is the action of vasopressin

opens aquaporins in collecting duct, water is free to leave followig osmotic gradient

176

what inhibits vasopressin?

alochol consumption

177

what happens if vasopressin is inhibited

water is not reabsorbed, increased urination

178

what does aldosterone do?

increases reabsorption of Na in DCT
-also controls K secretion because some Na transporters are Na/K pumps
IF VASOPRESSIN Is present-- H20 follows the Na reabsorption via osmotic gradient

179

what secretes aldoseterone?

adrenal medulla

180

what triggers aldoseterone secretion?

decreased BP-- JG cells secrete renin
angiotensinogen is converted to angiotensin I by renin
Angiotensin I is concerted to angiotensin II by ACE
Angiotensin II trigers release of aldosterone

181

angiotensinogen

is always present and inactive in the blood
is converted to angioteni I by renin (from JG cells in response to decreased BP

182

angiotensi I

made by angiotensinogen + renin

is converted to angioteni II by ACE

183

ACE

converts angiotensin I to angiotensin II

184

Angiotensin II

travels in blood to adrenal medulla and triggers the release of aldosterone

-increases BP

185

how does angiotensin II increase BP?

-increases vasopressin secretion
-increases thirst
-potent vasoconstrictor
-increases sympathetic output to the heart

186

what do ACE inhibitors do?

prohibits formation of angiotensin I-- act as ablood pressure drug

187

atrial natriuretic peptide

produced in myocardial cells of the right atrium in response to stretch
increase GFR, decrease Na reabsorptoin

188

mechanisms for increasing BP

aldosterone, vasopressin, thirst

189

mechanisms for decreasing BP

atrial natiuretic peptide

190

skeletal muscle

long, multinucleated, myofibrils, striated, voluntary contraction

191

smooth muscle

no banding, not voluntary contraction, spindle shaped, contract as a sheet, can divide

192

smooth muscle contraction

-don't have tropoin or sarcomere
thin filaments are anchored to membrane or dense bodies. Contraction pulls the ends of the cell closer together and widens the middle

Ca binds to Calmodulin, which activates a kinase that phosphorylates myosin, activating it and allowing for cross bridge cycling

Ca comes from sarcoplasmic reticulum and the extracellular flud

No Na

193

Cardiac Muscle

striated, troponin and tropomyosin, single nucleated, forked. Fused ends called intercalated disks

194

Cardiac muscle contraction

Na procivide intiail depolarization, which then opens the Ca channels

195

tropic hormone

stimulate other glands to make and release hormones

196

humoral stimulus

endocrine glands monitor the blood and release hormoes in response to a change in the blood

197

hypothalamus

influences hormone secretion from the anterior pituitary, produces hormones itself. Oversees hormone secreting by the adrenal medulla

198

posterior pituitary

stores hypotalamic hormones

199

anterior pituitary hormones:

thyroid stimulaing hormone, prolactin, adrenocorticotropic hormone, growth hormone, follicle stimulting hormone and luteinizing hormone

200

posterior pituitary hormones

oxytocin and vasopressin

201

oxytocin

cervical opening in labor, milk let down in lactatione, role in bonding with baby

202

vasopressin

constricts smooth muscles around blood vessels increasing blood pressure and decreasing urine output

203

calcitonin

encourages calcium deposition intot he brain from the blood "calcium to the bone"

204

parathyroid hormones

opposes calcionin, stimulates vit D formation,

205

growth hormone

stimulates maturation and mitosis of chondrocytes, triggers release of insulin like growth factors from the liver and osteoprogenitor cells

206

cortisol

stunts growth

207

interstitial/leydig cells

in seminiferous tubule-- secrete testosteron

triggered by LH

208

sertoli cells

make up the seminiferous tubules, aid in spermatogenesis
filter nutrients for developing sperm, transport testosterone to the lumen.

Trigered by FSH

209

production of testosterone

endocrine cells in the testes
cholesterol--> androstenedione (also made in adrenal cortex)-->testosterone

testosterone is also converted to estradiol via aromatase

210

egg production

egg matures in follicle.
After ovulation the follicle remains in the ovary and is called the corpus luteum (this time after ovulation is the luteal phase

211

theca sells

stimilated by LH, make androgens

212

granulosa cells

stimulated by FSH, convert androgens to estrogen

213

progesterone

made by corpus luteum and placentaa, also by adrenal cortex.

Maintain uterine lining, water and ion balance, regulation of synaptic activity associated with mood, memory and immune functions

also in kidney.

214

ovarian cycle

estrogen peaks, triggeres LH secretion LH triggers ovulation (secretion of LH by anterior pituitary is controlled by estrongen

menstruation occur when progesterone levels fall (corpus luteum that had been secreting progesteron dies)

215

FSH

stimulates development of follicles

216

LH

trigger ovulation

217

estrogen

prepares uterine lining,

the surge in estrogen is what triggers LG secrection.

218

progesteron

maintains uterine lining (Secreted by corpus luteum) and inhibits secretion of FSH and LH-- so you don't keep ovulating while pregnane

219

Prostaglandin

increases with decrease of estrogen and progesterone, , this trigers vasoconstriction and uterine contractions

220

adrenal glands

-cortex-secretes aldosterone+ cortisol+androgens

medulla--> epinephrine

Salt, sugar and sex

221

epinephrine

increases breathing rate, increases heart rate, breaks down glycogen and fat for more glucose in the blood, decreased appetitei

222

cortisol

shifts blood flow to skeletal muscles
breakdown protien and fat for more glucose in the blood. decrease sex drive, decreased inflammtion and immunity, decrease bone growth etx increases need to eat to replenish glucose stores

223

what does cortisol do to blood pressure?

causes ssystemic blood presure which increases bloodpressure

224

what does stress do to ADH and vasopressing,

have decreased need to pee, so increases ADH and vasopressin

225

adreal insufficienct: hyposecretion

weakness, fatigue, decresed appetite, decreased BP, decreased glucose. caused by decreased cort.

226

hypersecretion/cushings sydrome

due to increased cort. leads to osteoporosis, hypertension, hyperglycemia, immunosuppression

227

albumin

in blood plasma-- is an osmotic regulator to reduce edema and increase viscosity

228

tramsferrin

plasma protein tha inds iron

229

ferritin

liver protein what stores iron

230

RBC production

triggered by erythropoietin which is a hormone released by the kidneys when O2 delivery to the kidneys falls below a certain level
testosterone also triggers erythroopoitin

231

anemia

reduced O2 capacity
pernicious-lack of b12
iron deficiendy

232

polycythemia

too many RBCs

233

clot formation

platelets gather, exposed to collagen, leads to platelet activation.
prothrombin (plasma prot.) is cleaved into thrombin
thrombin cleaves fibrinogen to fibrin monomers
fibrin monomers polymerize into fibrin net

234

bacteria

single celled, reproduce on their own, can share DNA via proximity

235

virus

can't reproduce on own, insert their DNA into ours, we reproduce them.

236

fungus

reproduce on their own, have nucleuys

237

parasites

must be transmitted from host to host, can reproduce on their own

238

b cells

antibody production

239

helper t cells

recruit other cells to sites of infection

240

killer t cells

kill infected cells

241

macrophages

clean up waste and extracellular pathogens-- activate b and t cells

242

neutrophils

engulf and kill pathogen

243

eosinophils, basophils, mast cells

inflammation

244

•  Ventricular muscle cell contracAon must be

Rapid
– have a long absolute refractory period
– Have a short relaAve refractory period to be ready
for next impulse

245

ventriculat muscle cell depolarization

-has leaky k to begin with
Na enters,
Ca enters, later than Na but for longer (long absolute fractory period
K exits (short relative refractory period)

246

nodal cell decpolarization

spontaneous (a few Na and Ca channels open when voltage is negative, more Ca open when threshold is reached
rapid
long absolute
short relative does not depolarize all the way to 30, stops at zero

247

How does the parasympathetic nervous system impact heart rate?

increases k permeability, decreases Ca permeability

248

how does sympathetic nervous system impact heart rate?

increases ca and na permeability

249

p wave

atria depolarizing

250

qrs

ventricle depolarizing

251

t wave

ventricle repolarizing

252

systole

contraction- blood is ejected

253

diastole

relaxation, blood filld

254

cardiac output

HR*stroke volume

255

portal systems

1.  Hepa7c Portal Vein: delivers nutrients to liver
from intesAnes, low O2
2.  Hypothalamus-Pituitary Portal system: brings tropichormones from hypothalamus to pituitary
3.  Kidneys: delivers plasma to be filtered for
urinaAon, connects arterial capillary to arterial
capillary

256

angiogenesis

making new blood vessels

257

blood pressure in veins

pulmonary pump and skeltal muscle pump

258

pulse pressure

systolic-diastolic

259

Mean arterial pressure

avg blood pressure in the vessels over time. Diastole lasts longer than systole so the mean pressure is closer to diastollic

260

MAP

HR*SV*TPR

heart rate, stroke volume, total peripheral resistance

261

how tp change bblood flow?

change resistance or change pressure (voume or HR)

262

myogenic mechanism

increased blood flow, results in hincreased diameter and your body decreases diameter as a responese to limit blood flow

263

CCk

from SI, stimulates bile release, inhibits gastric emptying

264

secretein

from SI, inhibits acid and motility in stomach, stimulates HCO3 release

265

cephalic phase

sight smell taste etx

266

gastric phase

stretch, acidity, contents of stomach