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BI211 > Final > Flashcards

Final Flashcards

1
Q

Functions of LI

A

absorbs remaining water and water soluble vitamins

compaction of feces

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2
Q

how is water absorbed by LI

A

establish ion gradient using Na and then water moves by osmosis

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3
Q

what is the main component of feces?

A

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

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4
Q

role of bacteria in LI

A

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

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5
Q

defacation

A

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

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6
Q

valsalva maneuver

A

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

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7
Q

absorptive state

A

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

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8
Q

post-absorptive state

A

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

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9
Q

the role of the liver

A

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

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10
Q

absorptive state events carbs

A

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

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11
Q

gucose stoarge as lipids

A

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

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12
Q

What do newly made lipids from glucose travel on?

A

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.

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13
Q

fate of absorbed carbohydrates

A
  1. directly into blood to boost blood sugar levels
  2. stored as glycogen in liver or muscle
  3. stored as fat in adipose tissue
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14
Q

absorptive state events of lipids

A

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

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15
Q

how are lipids stored?

A

as triglycerides

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16
Q

formation of triglycerides

A

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

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17
Q

cholesterol

A

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

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18
Q

changes in cholesterol levels

A

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

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19
Q

cholesterol set point

A

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

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20
Q

HDLs

A

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

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21
Q

LDLs

A

supply all cells with cholesterol for membranes

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22
Q

What non-diet factors impact HDLs?

A

smoking decreases HDLs
Exercise increases HDLs
circulating estrogen increases HDLs

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23
Q

absorptive state events of proteins

A

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

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24
Q

Fate of ingested amino acids

A
  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
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25
Q

post absorptive state

A

no additional sources of enery

must maintain plasma glucose levels

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26
Q

where can glucose come from in the post absorptives tate?

A

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

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27
Q

how long can you subside on liver glycogen?

A

~3 hours

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28
Q

using glucose and fats for energy

A

-can provide 720cal/day

organs go into glucose sparing mode where they preferentially use lipids for energy

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29
Q

ketones

A

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

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30
Q

Control of nutrient use:

A

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

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31
Q

insulin

A

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

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32
Q

When does a cell membrane of neuron express glucose transporters?

A

-always expresses glucose transporters

they are insulin independent

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33
Q

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

A
  • have very little body fat but high blood lipids
  • decelop atherosclerosis
  • have endocrine issues
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34
Q

more insulin–> what change in blood glucose production?

A

less glucose in blood

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35
Q

If you accidenly inject excess insulin, what happens?

A

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

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36
Q

Which cells require insulin

A

skeletal and cardiac muscle, and adipose

NOR BRAIN and NS

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37
Q

incretins

A

secreted by enteroendocrin cells in GI tract increase insulin

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

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38
Q

Control over insulin

A

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

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39
Q

diabetes mellitus

A

cells cannot take up glucose from the bloodstream

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40
Q

Cause of Type I

A

auto immune, beta cells are attacked

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41
Q

Type II cause

A

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

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42
Q

gestational diabetes cause

A

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.

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43
Q

Type I Treatment

A

injected insulin at each meal for life

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44
Q

Type2 treatment

A

diet+ exercise, injectable insulin or incretins,

metformin-down reg liver gluconeogenesis, increases insulin sensitivity

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45
Q

gestational diabetes treatment

A

lifestyle, glucose monitoring

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46
Q

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

A
  • 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.
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47
Q

glucagon

A
  • produced by alpha cells of pancreas
  • increase glycogen breakdown and gluconeogenesis in the liver
  • effected by some hormones and sympathetic innervations
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48
Q

gluconeogenesis

A

making of glucose from amino acids or fatty acids

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49
Q

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

A

blood sugar increases

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50
Q

what is energy used for in body?

A

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

excess is stored

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51
Q

basal metabolic rate

A

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

based on body size, typical caloric intake and age

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52
Q

BMR and Body size

A

losing weight slows down metabolism

  • losing 10% body weight–>15% decrease in energy expenditure
  • gaining 10% body weight–>15% increase in energy expenditure.
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53
Q

leptin

A

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
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54
Q

ghrelin

A

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

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55
Q

signals to stop eating

A

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

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56
Q

corticotropin releasing hormone and appetite

A

decreases appetite

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57
Q

leptin source and impact on appetite

A

adipose tissue decrease,

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58
Q

insulinsource and impact on appetite

A

pancrease, decrease

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59
Q

ghrelin source and impact on appetite

A

stomach, increase

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60
Q

CCK source and impact on appetite

A

intestine decrease

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61
Q

peptide YY source and impact on appetite

A

intestine, increase

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62
Q

extreme biggest loser diet

A

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

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63
Q

genetic influece in weightloss

A

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

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64
Q

twin weight study

A

] 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

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65
Q

psychological factors and hunger

A

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

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66
Q

thrifty gene

A

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

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67
Q

adiponectin

A

produced by adipose

decreases inflammation, promites using energy stores

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68
Q

resistin

A

adipose hormone, leads to insulin resistace

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69
Q

visfatin

A

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

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70
Q

adipo-cytokines

A

promote inflammation and mitosis in local areas

adipose hormone

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71
Q

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

A

obesity in adulthood

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72
Q

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

A

high ghrelin levels

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73
Q

would inhibiting glucagon lower blood glucose levels?

A

yes,

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74
Q

hypoxia

A

lack of O2

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75
Q

hypercapnia

A

too much CO2

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76
Q

functions of the respiratory system

A

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

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77
Q

cellular respiration

A

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

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78
Q

external respiration

A

movement of gases betwen the environment and th bodys cells

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79
Q

ventilation

A

air exchange between lungs and external air

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80
Q

steps of respiration

A
  • 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
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81
Q

type 1 alceolar cells

A

small thin for gas exchange between alveoli and capillaries

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82
Q

type ii alveolar cells

A

synthesize surfactant

  • lowers surface tension of alceolus, allowing the cells to inflate
  • prevents alveli from collapising alveloi
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83
Q

premature babies and surfactant problems

A

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

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84
Q

is there smooth muscle in lungs?

A

no

elastic fibers cause recoil so that lungs return to resting after the inhale

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85
Q

inflation of lungs

A
  • work of muscles bbetween ribs and diaphram

- widen the thorax and pull the lungs with them by fluid surface tension.

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86
Q

F=

A

change in p/r

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87
Q

boyle’s law of gases

A

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

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88
Q

BOyles law applied

A

inhale, air moves in because pressure is lower inside

exhale- air moves out if pressure is greater outside

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89
Q

If you experience systemic vasodialation, what happens to BP?

A

decreases

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90
Q

pneumothorax

A

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

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91
Q

what happens to flow if you narrow a vessel?

A

flow decreases, due to increase of resistance

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92
Q

asthma

A

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

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93
Q

pulmonary edem

A

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

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94
Q

emphysema

A

decreased alveoli surface area=less diffusion

-treatment is to increased PO2

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95
Q

Daltons Law

A

total pressure=sum of partial pressures

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96
Q

daltons law applied

A

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_

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97
Q

henry’s law

A

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

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98
Q

4 laws of respiration

A

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

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99
Q

PO2 in alveoli=

A

PO2 in arterial blood

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100
Q

PO2 in tissues=

A

between the PO2 in alveoli and the PO2 in venous blood

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101
Q

PCO2 in alveoli=

A

PCO2 in arterial blood

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102
Q

PCO2 in tissues=

A

same as PCO2 in venous blood, or more

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103
Q

hypercapnia

A

elevated PCO2–causes acidosis

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104
Q

control of respiration

A

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

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105
Q

what directs cyclic innate breathin?

A

respiratory center in the medulla oblongata–based on chemoreceptors

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106
Q

peripheral chemoreceptors

A

in aortic and carotid bodies, detect O2 and pH cahngse

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107
Q

central chemoreceptors

A

monitor pH changes in th CSF

108
Q

When will PO2 trigger an increase in ventilation?

A

<60mmHg– the point where Hb dissociation changes

109
Q

COPD

A

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
Q

what normally stimulates an increase in ventilation?

A

high CO2

111
Q

what happens if you give a COPD patient O2?

A

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
Q

Functions of the Urinary System

A
  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
Q

How does the urinary section work, 4 steps

A
  1. Filter
  2. Reabsorb
  3. Secrete
  4. Excete
114
Q

nephron

A

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
Q

portal system

A

when 2 capillary beds meet without first going to the heart

116
Q

Renal Corpuscle

A

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

117
Q

tubule

A

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

118
Q

glomerulus

A

the capillary nest

-fenestrated- but doesn’t allow RBC or plasma proteins out

119
Q

bowmans capsule

A

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
Q

carpuscle

A

bowmans capsule+glomerulus

capillary is fenestrated— leaky

121
Q

nephron

A

corpuscle+ tubule

122
Q

parietal layer

A

the outer layer of bowmans capsule

123
Q

visceral layer

A

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

124
Q

podocytes

A

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
Q

filtration slits

A

spaces between pedicles- line up with fenestrae

126
Q

filtration membrane

A

-endothelium+ podocyte with lined up slits/fenestrae

127
Q

proximal convoluted tubule

A

the tubule as it leaves the glomerular capsule

-reabsorbs stuff that we filtered out of the plasma

128
Q

loop of henle

A

concentrating/diluting urin

-has 3 parts: descending, hairpin turn, ascending

129
Q

distal convoluted tubule

A

name of tubule as it neats the collecting duct

-mostly secretion

130
Q

kidney vasculature

A

efferent arteriole–> peritubular capillaries

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

131
Q

peritubular capillaries

A
  • 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
Q

where does filtration happen?

A

glomerulus

133
Q

where does reabsorption/secretion happen?

A

peritubular capillaries

134
Q

filtration

A

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

135
Q

hydrostatic pressure-

A

higher in capillary, drives fluid out of the capillary

136
Q

osmotic pressure

A

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

137
Q

What happens if you constrict the afferent arteriole?

A

decreased GFR

138
Q

what happens if you dialate the efferet arteriole?

A

decreased GFR

139
Q

what happens if you constrict the efferent arteriole?

A

increased GFR

140
Q

what happens if you dialate the afferent arteriole?

A

increased GFR

141
Q

when do you want to control GFR?

A

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

142
Q

afferent arteriole characteristics

A

has a larger diameter (to increase GFR)

has ha higher density of receptors for sympathetic innervation and hormones

143
Q

efferent arteriole characteristics

A

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

144
Q

glomerular filtrate

A

once it is out of the capillary

145
Q

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

A
  • glomerular capillary endothelium
  • capillary basement membrane
  • epithelium of podocyte- visceral layer of the bowwmans capsule
146
Q

glomerular filtration rate

A

the volume filtered into bowmans capsule per unit of time

147
Q

average GFR=

A

125ml/min

148
Q

what 3 factors determine the GFR?

A
  • 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
Q

how many times is the entire blood volume filtered each day

A

60 times

150
Q

do normal changes in blood pressure alter GFR?

A

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

151
Q

myogenic control of GFR

A

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
Q

juxtaglomerular apparatus

A

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

153
Q

juxtaglomerular cells

A

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
Q

macula densa

A

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

155
Q

juxtaglomerular apparatus and control of GFR

A

-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
Q

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

A

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

157
Q

renin

A

secreted by juxtaglomerular cells to increase solute reabsorption

158
Q

is reabsorption or molecules uder physiological control?

A

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
Q

How is reabsorption accomplished?

A

through active or passive transport—-NOT BY BULK FLOW

160
Q

What 2 surfaces does reabsorption occur across?

A

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

161
Q

transcellular transport

A

from inside the tubular lumen all the way to the capillary

162
Q

what is reabsorbed by passice transport via simple diffusion?

A

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

163
Q

what is rabsorbed cia facillitated diffusion?

A

anything eith a transporter protein down its conc. gradient

164
Q

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

A

Na+/H+ counter transport

countertransport of Na/ glucose or AA

165
Q

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

A

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

166
Q

how does the reabsorbed stuff get back into the blood?

A

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

167
Q

What is secreted?

A

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

168
Q

Renal clearance:

A

how quickly we rid the plasma of a substace.

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

169
Q

What are transporters ruled by?

A

competition, specificity, saturation

170
Q

Diabetes and the kidneys:

A

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
Q

polyuria

A

more water excrete

172
Q

polydipsea

A

excessive dehydration and thirts

173
Q

what secretes vasopressin

A

hypothalamus/posterior pituitary

174
Q

what influencesvasopressin secretion?

A

osmoreceptors in the hypothalamus and baroreceptors in the carotid and aorta

175
Q

what is the action of vasopressin

A

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

176
Q

what inhibits vasopressin?

A

alochol consumption

177
Q

what happens if vasopressin is inhibited

A

water is not reabsorbed, increased urination

178
Q

what does aldosterone do?

A

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
Q

what secretes aldoseterone?

A

adrenal medulla

180
Q

what triggers aldoseterone secretion?

A

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
Q

angiotensinogen

A

is always present and inactive in the blood

is converted to angioteni I by renin (from JG cells in response to decreased BP

182
Q

angiotensi I

A

made by angiotensinogen + renin

is converted to angioteni II by ACE

183
Q

ACE

A

converts angiotensin I to angiotensin II

184
Q

Angiotensin II

A

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

-increases BP

185
Q

how does angiotensin II increase BP?

A
  • increases vasopressin secretion
  • increases thirst
  • potent vasoconstrictor
  • increases sympathetic output to the heart
186
Q

what do ACE inhibitors do?

A

prohibits formation of angiotensin I– act as ablood pressure drug

187
Q

atrial natriuretic peptide

A

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

188
Q

mechanisms for increasing BP

A

aldosterone, vasopressin, thirst

189
Q

mechanisms for decreasing BP

A

atrial natiuretic peptide

190
Q

skeletal muscle

A

long, multinucleated, myofibrils, striated, voluntary contraction

191
Q

smooth muscle

A

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

192
Q

smooth muscle contraction

A

-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
Q

Cardiac Muscle

A

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

194
Q

Cardiac muscle contraction

A

Na procivide intiail depolarization, which then opens the Ca channels

195
Q

tropic hormone

A

stimulate other glands to make and release hormones

196
Q

humoral stimulus

A

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

197
Q

hypothalamus

A

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

198
Q

posterior pituitary

A

stores hypotalamic hormones

199
Q

anterior pituitary hormones:

A

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

200
Q

posterior pituitary hormones

A

oxytocin and vasopressin

201
Q

oxytocin

A

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

202
Q

vasopressin

A

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

203
Q

calcitonin

A

encourages calcium deposition intot he brain from the blood “calcium to the bone”

204
Q

parathyroid hormones

A

opposes calcionin, stimulates vit D formation,

205
Q

growth hormone

A

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

206
Q

cortisol

A

stunts growth

207
Q

interstitial/leydig cells

A

in seminiferous tubule– secrete testosteron

triggered by LH

208
Q

sertoli cells

A

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

Trigered by FSH

209
Q

production of testosterone

A

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

testosterone is also converted to estradiol via aromatase

210
Q

egg production

A

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
Q

theca sells

A

stimilated by LH, make androgens

212
Q

granulosa cells

A

stimulated by FSH, convert androgens to estrogen

213
Q

progesterone

A

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
Q

ovarian cycle

A

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
Q

FSH

A

stimulates development of follicles

216
Q

LH

A

trigger ovulation

217
Q

estrogen

A

prepares uterine lining,

the surge in estrogen is what triggers LG secrection.

218
Q

progesteron

A

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

219
Q

Prostaglandin

A

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

220
Q

adrenal glands

A

-cortex-secretes aldosterone+ cortisol+androgens

medulla–> epinephrine

Salt, sugar and sex

221
Q

epinephrine

A

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

222
Q

cortisol

A

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
Q

what does cortisol do to blood pressure?

A

causes ssystemic blood presure which increases bloodpressure

224
Q

what does stress do to ADH and vasopressing,

A

have decreased need to pee, so increases ADH and vasopressin

225
Q

adreal insufficienct: hyposecretion

A

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

226
Q

hypersecretion/cushings sydrome

A

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

227
Q

albumin

A

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

228
Q

tramsferrin

A

plasma protein tha inds iron

229
Q

ferritin

A

liver protein what stores iron

230
Q

RBC production

A

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
Q

anemia

A

reduced O2 capacity
pernicious-lack of b12
iron deficiendy

232
Q

polycythemia

A

too many RBCs

233
Q

clot formation

A

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
Q

bacteria

A

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

235
Q

virus

A

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

236
Q

fungus

A

reproduce on their own, have nucleuys

237
Q

parasites

A

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

238
Q

b cells

A

antibody production

239
Q

helper t cells

A

recruit other cells to sites of infection

240
Q

killer t cells

A

kill infected cells

241
Q

macrophages

A

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

242
Q

neutrophils

A

engulf and kill pathogen

243
Q

eosinophils, basophils, mast cells

A

inflammation

244
Q

•  Ventricular muscle cell contracAon must be

A

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

245
Q

ventriculat muscle cell depolarization

A

-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
Q

nodal cell decpolarization

A

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
Q

How does the parasympathetic nervous system impact heart rate?

A

increases k permeability, decreases Ca permeability

248
Q

how does sympathetic nervous system impact heart rate?

A

increases ca and na permeability

249
Q

p wave

A

atria depolarizing

250
Q

qrs

A

ventricle depolarizing

251
Q

t wave

A

ventricle repolarizing

252
Q

systole

A

contraction- blood is ejected

253
Q

diastole

A

relaxation, blood filld

254
Q

cardiac output

A

HR*stroke volume

255
Q

portal systems

A

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
Q

angiogenesis

A

making new blood vessels

257
Q

blood pressure in veins

A

pulmonary pump and skeltal muscle pump

258
Q

pulse pressure

A

systolic-diastolic

259
Q

Mean arterial pressure

A

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

260
Q

MAP

A

HRSVTPR

heart rate, stroke volume, total peripheral resistance

261
Q

how tp change bblood flow?

A

change resistance or change pressure (voume or HR)

262
Q

myogenic mechanism

A

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

263
Q

CCk

A

from SI, stimulates bile release, inhibits gastric emptying

264
Q

secretein

A

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

265
Q

cephalic phase

A

sight smell taste etx

266
Q

gastric phase

A

stretch, acidity, contents of stomach

BI211 (11 decks)

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