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Physiology > Final Exam - new material > Flashcards

Final Exam - new material Flashcards

1
Q

what is the normal plasma pH

A

7.4

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2
Q

what does the pH need to be for the person to be in acidosis

A

pH < 7.38
less than

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3
Q

what does the pH need to be for the person to be in alkalosis

A

pH > 7.42
greater than

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4
Q

what is the pH in the alkaline range

A

anything greater than 7

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5
Q

what do disturbances in pH homeostasis cause

A

disruption of protein shape
disturbance of K+ levels
effects on excitable tissues

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6
Q

what is the main problem that causes pH disturbances

A

excess H+

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7
Q

what is the largest source of excess H+

A

metabolic production of CO2 (from respiratory system)

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8
Q

what is the CO2/H+ equilibrium reaction

A

CO2 + H2O –> H+ + HCO3-

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9
Q

what is a buffer system

A

mixture of two compounds that can remove or produce free H+ as needed

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10
Q

what is the fastest response to pH disturbance

A

buffer system
(BUT doesnt remove anything from the body)

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11
Q

what is the most important extracellular buffer

A

bicarbonate

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12
Q

what is the bicarbonate buffering reaction

A

CO2 + H2O –><– H+ + HCO3-
carbonic anhydrase (CA)

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13
Q

what are the main determinants of plasma pH

A

concentrations of CO2 and bicarbonate

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14
Q

what organ is bicarbonate regulated by

A

kidneys

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15
Q

what organ is CO2 regulated by

A

lungs

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16
Q

what is the most important intracellular buffer

A

proteins

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17
Q

what is an example of a protein buffer

A

hemoglobin
H+ + Hb –><– HbH
(absorbs H+ when Co2 is converted to bicarbonate)

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18
Q

what is the urine and intracellular buffer

A

phosphate

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19
Q

what is the urine buffer

A

ammonia

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20
Q

what type of homeostatic pH compensation is slow? fast?

A

slow: renal
fast: respiratory

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21
Q

what type of pH problems can respiratory compensation fix

A

metabolic

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22
Q

how does the respiratory system regulate H+ concentration

A

by controlling rate of CO2 removal
CO2 + H2O –><– H+ + HCO3-

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23
Q

what happens to the respiratory equilibrium equation when the body gets rid of CO2

A

shifts left

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24
Q

what happens to the respiratory equilibrium equation when the body retains CO2

A

shifts right

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25
Q

what is the most powerful pH regulator

A

renal compensation

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26
Q

how does the renal system regulate pH

A

secrete/absorb H+
secrete/absorb HCO3-

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27
Q

what happens to the urine when the renal system secretes H+

A

the urine is acidic

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28
Q

what type of cells play a key role in renal pH compensation

A

intercalated cells in distal nephron

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29
Q

what are the two types of intercalated cells

A

type A
type B

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30
Q

when are type A intercalated cells active

A

when in acidosis (too acidic)

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31
Q

what do type A intercalated cells do

A

secrete H+ into filtrate
absorbs HCO3- into blood

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32
Q

how do type A intercalated cells secrete H+ into the filtrate? what does it often lead to?

A

uses a H+/K+ exchanger
acidosis often leads to hyperkalemia (high K+ in blood) (when H+ is secreted, the body pulls K+ into the blood via the exchanger)

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33
Q

when are type B intercalated cells active

A

when in alkalosis (too basic)

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34
Q

what do type B intercalated cells do

A

absorb H+ into blood
secrete HCO3- into filtrate

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35
Q

how do type B intercalated cells absorb H+ into the blood? what does it often lead to?

A

uses H+/K+ exchanger
alkalosis often leads to hypokalemia (low K+ in blood)
(when H+ is absorbed into the blood, body secretes K+ via the exchanger)

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36
Q

what is the underlying cause of respiratory acidosis or alkalosis

A

a change in PCO2

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37
Q

what is any other pH disturbance (other than respiratory) referred to as

A

metabolic

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38
Q

what is respiratory acidosis due to

A

hypoventilation

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39
Q

what happens to the equilibrium equation (CO2 + H2O –> H+ + HCO3-) due to respiratory acidosis

A

high PCO2 causes high H+ and slightly high HCO3-

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40
Q

if the respiratory system is the problem (like in respiratory acidosis) where does the compensation come from

A

all compensation is renal; secretes H+ and reabsorbs HCO3-

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41
Q

what happens to bicarbonate concentration with renal compensation in respiratory acidosis

A

high bicarbonate which restores the correct [HCO3-]/[CO2]

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42
Q

what is metabolic acidosis due to

A

addition of acids OR removal of HCO3-

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43
Q

what happens to the equilibrium equation (CO2 + H2O –> H+ + HCO3-) due to metabolic acidosis

A

high H+ causes high initial PCO2 and low HCO3-

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44
Q

what two ways does the body compensate for metabolic acidosis

A

compensation by lungs
renal compensation

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45
Q

how do the lungs compensate for metabolic acidosis

A

hyperventilation to lower PCO2 and restore correct [HCO3-]/[CO2]

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46
Q

how does renal compensation compensate for metabolic acidosis

A

secretes H+ and reabsorbs HCO3-

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47
Q

what is respiratory alkalosis due to

A

hyperventilation

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48
Q

what happens to the equilibrium equation (CO2 + H2O –> H+ + HCO3-) due to respiratory alkalosis

A

low PCO2 causes low H+ and slightly low HCO3-

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49
Q

if the respiratory system is the problem (like in respiratory alkalosis) where is all of the compensation coming from

A

renal compensation; absorbs H+ and secretes HCO3-

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50
Q

what happens to the bicarbonate concentration with renal compensation due to respiratory alkalosis

A

low HCO3- restores correct [HCO3-]/[CO2]

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51
Q

what is metabolic alkalosis due to

A

removal or acids OR addition of HCO3-

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52
Q

what happens to the equilibrium equation (CO2 + H2O –> H+ + HCO3-) due to metabolic alkalosis

A

low H+ leads to low initial PCO2 and high HCO3-

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53
Q

what two ways does the body compensate for metabolic alkalosis

A

compensation by lungs
renal compensation

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54
Q

how do the lungs compensate for metabolic alkalosis

A

hypoventilation –> high PCO2 which restores the correct [HCO3-]/[CO2]

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55
Q

how does renal compensation work when compensating for metabolic alkalosis

A

absorbs H+
secrete HCO3-

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56
Q

what are the two competing behavioral states for control of food intake

A

appetite (hunger)
satiety (lack of hunger)

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57
Q

what are the two hypothalamic control centers for control of food intake

A

feeding center: tonically active
satiety center: inhibits feeding center

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58
Q

what is neuropeptide Y (NPY)

A

neurotransmitter in brain responsible for increased food intake (hunger)

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59
Q

what is ghrelin

A

hormone secreted by stomach when empty to increase food intake

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60
Q

what is leptin

A

hormone secreted by adipocytes when fat stores increase to decrease food intake

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61
Q

what are CCK and GLP-1

A

hormones secreted by duodenum (small intestine) in response to fats and carbs in chyme to decrease food intake

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62
Q

what is happening in the GI tract during the fed/absorptive state

A

absorbing nutrients in GI tract

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63
Q

are the pathways in the fed/absorptive state mostly anabolic or catabolic

A

anabolic (building larger molecules)

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64
Q

what is the main energy source in the fed state

A

glycolysis (glucose–>pyruvate)

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65
Q

what happens to amino acids during the fed state

A

protein synthesis

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66
Q

what happens to glucose in the liver and muscle in the fed state

A

glyconeogenesis (glucose –> glycogen) (building up larger molecules)

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67
Q

what happens to lipids in adipocytes in the fed state

A

lipogenesis (fat synthesis)

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68
Q

what do glycerol and fatty acids play a role in (in fed state)

A

lipogenesis

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69
Q

what do converted excess carbohydrates and AAs play a role in (in fed state)

A

lipogenesis

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70
Q

what is happening in the GI tract during the fasted/postabsorptive state)

A

no absorption occurring in GI tract

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71
Q

are the pathways in the fasted state mostly anabolic or catabolic

A

catabolic (breakdown)

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72
Q

what is glycolysis a required energy source for in the fasted state

A

CNS and red blood cells

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73
Q

what is being maintained in the fasted state

A

blood glucose

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74
Q

what happens in the liver during the fasted state

A

glycogenolysis (breaking down glycogen –> glucose) and glucose release

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75
Q

how is glucose being produced in the fasted state

A

gluconeogenesis produces glucose from glycerol (from adipocytes) and pyruvate, lactate, and AA (from skeletal muscle)

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76
Q

how does skeletal muscle obtain glucose during the fasted state

A

from its own glycogens stores

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77
Q

do fats or glycogen have a higher energy content

A

fats have higher energy content but are slower to metabolize

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78
Q

what do fats (triglycerides (TGs)) provide

A

major energy source

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79
Q

what is lipolysis

A

TG –> glycerol + free fatty acid (FFA)

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80
Q

what does beta oxidation of fatty acids produce

A

acyl units

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81
Q

what happens to the acyl units that are produced via beta oxidation

A

they enter the krebs cycle (CAC) as acetyl CoA

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82
Q

what is glycerol from lipolysis used for

A

glycolysis

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83
Q

what happens to the body proteins with extended fasting

A

body proteins are used heavily as a source of AA

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84
Q

what does the brain use for energy in extended fasting

A

ketone bodies that are produced from FFA in liver

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85
Q

what ratio regulates metabolism

A

insulin-to-glucagon ratio

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86
Q

what kind of relationship do insulin and glucagon have

A

inverse relationship

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87
Q

is insulin or glucagon dominant in the fed state

A

insulin

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88
Q

what causes pancreatic beta cells to secrete insulin

A

high blood glucose and AA levels

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89
Q

what happens when pancreatic beta cells secrete insulin

A

increased: glucose uptake, glycolysis, glycogenesis (packaging glucose), lipogenesis, protein synthesis

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90
Q

what is the overall result of increased insulin secretion

A

decreased blood glucose

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91
Q

what kind of glucose uptake is insulin-dependent

A

glucose uptake by adipose tissue and resting skeletal muscle

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92
Q

how does glucose get in/out of the cell

A

by transporters being inserted in the membrane

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93
Q

what happens to glucose entry in adipose tissue and resting skeletal muscle in the fasted state

A

no insulin –> no GLUT4 transporters in membrane –> no glucose entry

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94
Q

what happens to glucose entry in adipose tissue and resting skeletal muscle in the fed state

A

insulin binds to receptor –> GLUT4 transporters inserted in membrane –> glucose allowed to enter cell

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95
Q

what does insulin indirectly alter glucose transport in

A

hepatocytes (liver)

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96
Q

what are always present in hepatocyte membrane

A

GLUT2 transporters

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97
Q

what happens to glucose transport in hepatocytes in the fasted state

A

glycogenolysis –> high glucose inside of cell –> glucose diffuses out of the cell

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98
Q

what happens to glucose transport in hepatocytes in the fed state

A

insulin activated glucokinase in cell –> phosphorylated glucose to G6P –> keeps glucose low inside of cell –> glucose diffuses into cell

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99
Q

what are three other factors that influence insulin secretion

A

carbohydrates in gut
distention of gut
sympathetic input

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100
Q

how do carbohydrates in gut affect insulin secretion

A

increased incretions (GIP, GLP-1 (peptides)) lead to increased insulin

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101
Q

how does distention of the gut affect insulin secretion

A

increased parasympathetic input leads to increased insulin

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102
Q

how does sympathetic input affect insulin secretion

A

it decreased insulin secretion because when stressed, hyperglycemia is good

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103
Q

what is dominant in the fasted state

A

glucagon

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104
Q

what kind of cells release glucagon

A

pancreatic alpha cells

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105
Q

what kind of cells release insulin

A

pancreatic beta cells

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106
Q

why is glucagon secreted

A

low blood glucose –> alpha cells secrete glucagaon

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107
Q

what is the target cell of glucagon

A

liver

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108
Q

what two things does the release of glucagon result in? what is the overall effect?

A

increased glycogenolysis
increased gluconeogenesis
overall: increased blood glucose

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109
Q

what are two other hormones that help increase blood glucose

A

cortisol and norepinephrine

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110
Q

what does it mean to say that humans are homeothermic

A

they regulate internal temperature within a narrow range (37 C or 98.6 F)

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111
Q

what happens when temperature is too high

A

hyperthermia
denatures enzymes

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112
Q

what happens when temperature is too low

A

hypothermia
chemical reactions too slow

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113
Q

what is the equation for heat loss

A

external heat input + internal heat production = heat loss

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114
Q

what are the four mechanisms of heat exchange

A

radiation (gain or loss)
conduction (gain or loss)
convection (gain or loss)
evaporative heat loss

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115
Q

what is radiation as a heat exchange mechanism

A

warm surfaces emit and absorb electromagnetic waves that travel through space

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116
Q

what is conduction as a heat exchange mechanism

A

heat transmission by contact that is transferred by thermal molecular motion

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117
Q

what is convection as a heat exchange mechanism

A

heat transmission by bulk flow of air or water

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118
Q

what is evaporative heat loss as a heat exchange mechanism

A

from skin to respiratory tract

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119
Q

what two types of heat production are not physiologically regulated

A

normal metabolism
voluntary muscle contractions

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120
Q

how can normal metabolism produce heat

A

~25% of nutrient energy is captured as cellular work and the rest is wasted as heat (can be used to maintain body temp)

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121
Q

what are voluntary muscle contractions used for

A

behavioral thermoregulation

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122
Q

what are the two kinds of physiologically regulated heat production

A

shivering thermogenesis
non-shivering thermogenesis

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123
Q

what is shivering thermogenesis

A

involuntary tremors in skeletal muscles

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124
Q

what is non shivering thermogenesis

A

mitochondrial uncoupling: energy from e transport chain is released as heat instead of ATP

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125
Q

where does non shivering thermogenesis occur

A

in brown adipose tissue where there is a higher density of mitochondria
-important in newborns

126
Q

what two sensors are used for thermoregulation

A

central thermoreceptors (hypothalamus)
peripheral thermoreceptors (skin)

127
Q

what is the integrator in thermoregulation

A

hypothalamus

128
Q

what is the thermoneutral zone in thermoregulation

A

range of environmental temperatures in which thermoregulation requires only vascular adjustments

129
Q

what are the two responses to decreased temperatures

A

sympathetic adrenergic neurons
somatic motor neurons

130
Q

what do sympathetic adrenergic neurons do in response to decreased temperature

A

cutaneous vasoconstriction –> decreased convective flow from interior to skin –> decreased skin temperature –> decreased heat loss at skin

possibly non shivering thermogenesis in infants

131
Q

what do somatic motor neurons do in response to decreased temperature

A

shivering thermogenesis

132
Q

what are the two responses to increased temperatures

A

active cutaneous vasodilation
sweat glands secrete sweat-hyposmotic to blood

133
Q

what is the process of active cutaneous vasodilation when temperatures increase

A

increased heat loss at skin due to sympathetic cholinergic neurons

NOT due to withdraw of adrenergic input
NOT a result of ACh

134
Q

what is the process of sweat glands secreting sweat when temperatures increase

A

sympathetic cholinergic neurons –> ACh –> muscarinic receptor

135
Q

why does sweat secretion increase metabolic rate above thermoneutral zone

A

it is energetically expensive

evaporative cooling = net heat loss

136
Q

where do alterations to the setpoint occur

A

in hypothalamus

137
Q

what causes an increased setpoint

A

fever due to pyrogens from immune cells

138
Q

what causes a decreased set point

A

hot flashes

139
Q

what is the function of the digestive system

A

move materials from external to internal environment

140
Q

what regulates the digestive system

A

enteric nervous system (ENS) - brain of the gut

141
Q

what makes up the enteric nervous system

A

neurons and sensory receptors in GI wall that control motility and secretion

142
Q

what are the two different digestive reflexes

A

short reflex
long reflex

143
Q

where does the short digestive reflex originate and integrate

A

originates within the ENS and is integrated there WITHOUT input from the CNS

144
Q

where is the long digestive reflex integrated? where is the input/output coming from

A

integrated in the CNS
sensory input from ENS (or PNS)
autonomic output to ENS

145
Q

what non-neural component is included in reflex pathways

A

GI peptides: hormones and paracrine signals secreted by gut wall

146
Q

what are the three groups of absorbable units

A

carbohydrates, proteins, lipids

147
Q

where is amylase produced by

A

saliva and pancreas

148
Q

what does amylase do

A

digest polysaccharides to disaccharides

149
Q

where are disaccharides located

A

on membrane of brush border cells of small intestine

150
Q

what digests disaccharides into monosaccharides

A

enzymes located on the brush border of the small intestine

151
Q

how do glucose and galactose first enter the membrane (apical entry)

A

sodium glucose linked transporter (secondary active transport)

152
Q

how do glucose and galactose exit the membrane (basolateral exit)

A

GLUT2 transporter (facilitated diffusion)

153
Q

how does fructose enter the membrane (apical entry)

A

GLUT5 transporter (facilitated diffusion)

154
Q

how does fructose exit the membrane (basolateral exit)

A

GLUT2 transporter (facilitated diffusion)

155
Q

how are most enzymes for protein digestion secreted

A

in inactive form

156
Q

what do endopeptidases/proteases do

A

break peptide bonds in interior of protein/peptide

157
Q

what are three examples of endopeptidases/proteases

A

pepsin
trypsin
chymotrypsin

158
Q

where is pepsin located

A

in stomach

159
Q

when are endopeptidases/proteases activated

A

once they are in the lumen

160
Q

where are trypsin and chymotrypsin located

A

in small intestine (come from the pancreas)

161
Q

what do exopeptidases do

A

remove AA at end

162
Q

what are two examples of exopeptidases

A

carboxypeptidase
aminopeptidase

163
Q

where does carboxypeptidase remove from

A

removes from carboxy-terminal end

164
Q

where does aminopeptidase remove from

A

removes from amino-terminal end

165
Q

how are free AA absorbed

A

most by cotransport with Na+

166
Q

how are di and tripeptides absorbed

A

cotransport with H+

167
Q

where are most di and tri peptides digested

A

inside the cell to free AA

168
Q

how are some larger (small) peptides (~3AA) absorbed

A

by transcytosis
(gets endocytosed, then exocytosed)

169
Q

what are most lipids

A

triglycerides (fats)

170
Q

are lipids water soluble

A

no

171
Q

where are bile salts secreted and stored

A

secreted by liver
stored in gallbladder

172
Q

what do bile salts do

A

emulsify fats (break into smaller droplets) to increase surface area for enzymatic digestion
- speeds up digestion

173
Q

where does lipase come from

A

pancreas

174
Q

what does lipase do

A

digests triglycerides into monoglyceride and 2 free fatty acids (FFA)

175
Q

where does colipase come from

A

pancreas

176
Q

what is colipase

A

protein cofactor that displaces part of the bile salt coating to give lipase access to fats inside

177
Q

what are the 3 enzymes (lipases) that help digest lipids

A

bile salts
lipase
colipase

178
Q

what do products of lipid digestion assemble with and into after digested

A

assemble with bile salts and phospholipids into a micelle

179
Q

where do free fatty acids (FFA) and monoglycerides enter after digestion? how?

A

enter enterocytes (brush border cells) by simple diffusion

180
Q

what happens to FFA and monoglycerides after the enter enterocytes

A

the smooth ER reassembles them into triglycerides

181
Q

how is cholesterol absorbed

A

actively via carrier protein

182
Q

what are triglycerides and cholesterol coated with to form chylomicrons

A

lipoprotein

183
Q

where do triglycerides and cholesterol chylomicrons go after they are coated with lipoprotein

A

exocytosed to interstitial fluid

184
Q

how do chylomicrons get into the blood

A

they cannot cross basement membrane of blood capillaries so they enter lacteals (small lymphatic vessels) instead

185
Q

what are the three phases of digestion

A

cephalic phase
gastric phase
intestinal phase

186
Q

what kind of response is the cephalic phase

A

feedforward response to anticipation of food

187
Q

what kind of reflex happens in the cephalic phase

A

long reflex

188
Q

what is the pathway in the cephalic phase that ends in physiological responses

A

sight, smell, taste, thought of food –> medulla oblongata –> parasympathetic NS

189
Q

what are the parasympathetic responses from the pathway in the cephalic phase

A

increase salivary gland secretion
increased secretion and motility throughout most of digestive system (stomach, intestines, pancreas, liver)

190
Q

what nerve / nervous system is used to get physiological results in the cephalic phase

A

vagus nerve and ENS

191
Q

what happens in the gastric phase

A

increase in gastric secretion and motility stimulated by entry of chyme into the stomach

192
Q

what kind of reflexes does the gastric phase involve

A

short reflexes in addition to hormones/paracrines

193
Q

what causes physiological responses in the gastric phase

A

distention and presence of peptides/AA in lumen

194
Q

what are the results of distention and presence of peptides/AA in lumen in the gastric phase

A

increased gastrin (hormone) secretion by G cells
increased HCl (acid) secretion by parietal cells
increased pepsinogen secretion by chief cells (activated to pepsin by acid)

195
Q

what kind of feedback occurs when there is acid in the lumen

A

negative feedback

196
Q

what does the negative feedback due to acid in the lumen cause

A

increased somatostatin (paracrine) from D cells
decreased secretion by G cells, parietal cells, and chief cells

197
Q

what starts the intestinal phase

A

entry of chyme into duodenum

198
Q

what kind of reflexes are involved in the intestinal phase

A

short reflexes

199
Q

what happens when acid enters the duodenum (intestinal phase)

A

increased secretin (hormone) –> increased pancreatic bicarbonate secretion (neutralizes the acid)

200
Q

what happens when fats and proteins enter the duodenum (intestinal phase)

A

increased CCK (hormone) –> increased pancreatic enzyme secretion and bile released from gallbladder (bile emulsifies fats)

201
Q

what happens when carbohydrates enter the duodenum (intestinal phase)

A

increased incretins (GIP and GLP-1 (hormones)) –> increased insulin secretion (feedforward effect)

202
Q

what are gastric motility and acid secretion by the stomach inhibited by (in intestinal phase)

A

ENS, secretin, CCK, incretins (GIP, GLP-1)

203
Q

what will increase acid

A

gastrin (gastric phase)

204
Q

what will decrease acid

A

somatostatin (gastric phase)
secretin (increases pancreatic bicarbonate secretion in intestinal phase)
secretin, CCK, incretins, ENS (decreases stomach HCl secretion in intestinal phase)

205
Q

what does it mean to say that embryonic structures are bipotential

A

they can develop into either female or male form

206
Q

what sex develops if there is no Y chromosome

A

develop as female

207
Q

what gene is on the Y chromosome that makes the embryo develop as male

A

SRY gene

208
Q

what does the SRY gene cause

A

testis develop and secrete:
- anti-mullerian hormone
- testosterone –> dihydrotestosterone (DHT) (converted in peripheral tissues)

209
Q

how can sexual genotypes (XX or XY) differ from sexual phenotype

A

if signals or receptors for signals are missing

210
Q

what does the hypothalamus secrete in the HPG axis

A

GnRH (gonadotropin releasing hormone)

211
Q

what does the anterior pituitary secrete in the HPG axis

A

gonadotropins
- FSH (follicle stimulating hormone)
- LH ( luteinizing hormone)

212
Q

what does LH stimulate in the HPG axis

A

sex steroid hormone secretion by gonads

213
Q

what does FSH stimulate in the HPG axis

A

gametogenesis (gamete production)
(sex steroids also play role in this)

214
Q

where do the sex steroids feedback (neg or pos) to

A

hypothalamus or anterior pituitary

215
Q

what three groups of steroids do both sexes produce

A

androgens: T and DHT
estrogens: estradiol (E)
progestins: progesterone (P)

216
Q

what enzyme do both ovaries and testes have? what does it do?

A

aromatase
- converts T to E

217
Q

what do the testes (gonads) produce after LH and FSH are released by GnRH

A

sperm and hormones

218
Q

what does LH do in male hormonal regulation

A

secretes testosterone from Leydig cells

219
Q

what does FSH (and testosterone) do in male hormonal regulation

A

secretes paracrines from sertoli cells which increase spermatogenesis

220
Q

what two things do sertoli cells secrete

A

paracrines to increase spermatogenesis
androgen binding protein (ABP) to keep T from diffusing away

221
Q

what does testosterone do in male hormonal regulation

A

decrease GnRH, LH, and FSH
- engage in negative feedback

222
Q

what are the two cycles in the menstrual cycle

A

ovarian cycle: changes in follicles of ovary
uterine cycle: changes in uterine lining

223
Q

what are the three phases of the uterine cycle

A
  1. menses
  2. proliferative phase
  3. secretory phase
224
Q

what is the menses phase of the uterine cycle

A
  1. menses: if pregnancy not achieved, shed endometrium - bleeding from uterus
225
Q

what is the proliferative phase of the uterine cycle

A
  1. proliferative phase: endometrium thickens in preparation for pregnancy
226
Q

what is the secretory phase of the uterine cycle

A
  1. secretory phase: endometrial secretions promote implantation
227
Q

what are the three phases of the ovarian cycle

A
  1. follicular phase
  2. ovulation
  3. luteal phase
228
Q

what happens in the follicular phase of the ovarian cycle

A

development of follicle
- granulosa cells proliferate and secrete estrogen
- maturation of oocyte

229
Q

what happens during ovulation of the ovarian cycle

A

mature follicle bursts, releasing the oocyte

230
Q

what happens during the luteal phase of the ovarian cycle

A

ruptured follicle develops into corpus luteum
- secretes progesterone and some estrogen to prepare from pregnancy

231
Q

what do the ovaries (gonads) produce in response to LH and FSH release from GnRH

A

estrogen and some progesterone

232
Q

what does LH cause in female hormonal regulation

A

androgens secreted by thecal cells, which diffuses into granulosa cells

233
Q

what happens after androgens diffuse into granulosa cells

A

aromatase converts it into estrogen

234
Q

what does FSH cause in female hormonal regulation

A

granulosa cells produce estrogen which increases follicular development

235
Q

what does the corpus luteum secrete after ovulation

A

progesterone and some estrogen

236
Q

generally, what are the results of estrogen and progesterone

A

decreased GnRH, LH, FSH
(negative feedback)

237
Q

what is caused by persistent high estrogen

A

switches to positive feedback –> ovulation

238
Q

what is the ovarian cycle phase called in days 0-7

A

early follicular phase

239
Q

what is the uterine cycle phase in days 0-7

A

menses (no pregnancy - shedding of endometrium)

240
Q

what hormones are being released during days 0-7 and what do they cause

A

FSH and LH: follicular development and estrogen
estrogen: decreases GnRH, LH, FSH

241
Q

what is the phase of the ovarian cycle during days 7-14

A

late follicular phase (follicle matures)

242
Q

what is the phase of the uterine phase during days 7-14

A

proliferative phase
- estrogen causes the endometrium to grow in preparation for pregnancy

243
Q

what hormones are being released during days 7-14 and what do they cause

A

increased estrogen
- estrogen changes from negative to positive feedback on LH
LH surge triggers ovulation

244
Q

what day does ovulation occur

A

day 14

245
Q

what happens during ovulation

A

follicle ruptures, releasing oocyte
thecal and granulosa cells start to become luteal cells

246
Q

what phase of the ovarian cycle occurs during days 14-21

A

early luteal phase
- corpus luteum develops from follicle

247
Q

what phase of the uterine cycle occurs during days 14-21

A

secretory phase
- endometrial secretions promote implantation of fertilized oocyte

248
Q

what hormones are secreted during days 14-21

A

corpus luteum secretes P (and E)

249
Q

what does P promote in days 14-21

A

decreases GnRH, LH, FSH (negative feedback)
increased endometrial development

250
Q

what phase of the ovarian cycle occurs during days 21-28 if no pregnancy

A

late luteal phase
- corpus luteum degenerates and ceases hormone production

251
Q

what phase of the uterine cycle occurs during days 21-28 if no pregnancy

A

secretory phase

252
Q

what hormones are secreted during days 21-28 if no pregnancy

A

LACK of P from corpus luteum leads to death of endometrium –> menses (day 0)

FSH and LH secretion resume for next cycle

253
Q

what happens 5-7 days later if fertilization occurs

A

fertilized egg implants in endometrium

254
Q

what is secreted as the placenta develops

A

human chorionic gonadotropin (hCG)

255
Q

what does hCG maintain

A

corpus luteum

256
Q

what does the corpus luteum secrete that is critical to maintain a pregnancy

A

progesterone and estrogen

257
Q

what later takes over progesterone production later in pregnancy

A

placenta
- corpus luteum degenerates

258
Q

what are oral contraceptives made of

A

progesterone and estrogen

259
Q

what does synthetic estrogen and progesterone lead to

A

decreased GnRH, LH, FSH –> prevents follicle maturation and ovulation

progesterone thickens cervical mucus –> barrier to sperm

260
Q

what are the three functions of the immune system

A

protect body from pathogens
remove dead and damaged cells
remove “abnormal self” cells (cancerous)

261
Q

what are leukocytes

A

white blood cells / immune cells

262
Q

what are immunogens

A

anything that triggers an immune response
pathogens
allergens: cause allergic response

263
Q

what are the differences between an overactive response. incorrect response, and lack of response

A

overactive: allergy
incorrect: autoimmune disease
lack: immunodeficiency

264
Q

what are the different cell surface markers/molecular markers

A

self markers
non self markers

265
Q

what are the two different self markers

A

major histocompatibility complex (MHC) - on nucleated cells

ABO and Rh blood types - on non nucleated cells (RBCs)

266
Q

what is the non self marker

A

antigens - molecules that trigger immune response
(pathogen-associated molecular patterns (PAMPs))

267
Q

what do antigens bind to

A

pattern recognition receptors (PRR) on leukocytes

268
Q

what are the two antigens expressed on RBCs

A

A and B

269
Q

what leads to an O blood type

A

A and B both absent
- is recessive

270
Q

what are the 4 possible blood types

A

A B AB O

271
Q

which antibodies are in blood plasma

A

antibodies to any antigen that is not on RBC
(anti-A, anti-B, both, or neither)

272
Q

what happens if matching antigens and antibodies mix

A

blood agglutinates (clumps)

273
Q

when considering blood transfusions, what do you need to know

A

what antibodies the recipient has
what antigens are on the donors RBCs

274
Q

what are the three lines of defense against pathogens

A

barriers
innate immune response
adaptive immune response

275
Q

what are examples of the barriers

A

skin
mucous membranes

276
Q

are innate immune responses
specific/nonspecific
rapid/slow

A

nonspecific
rapid (hours)

277
Q

what kind of cells are involved in adaptive immune response

A

B cells
T cells
(lymphocytes)

278
Q

what does it mean to say that the adaptive immune response has specificity

A

recognize and react to one antigen only

279
Q

what is immunological memory

A

for stronger and quicker response (acquired immunity) to subsequent exposures

280
Q

what is the main function of the innate immune response

A

removes dead and damaged cells

281
Q

how does the innate immune response remove dead and damaged cells

A

creates pores in targer cell membrane to kill it
phagocytosis

282
Q

how are abnormal self (cancer cells) killed

A

innate immune response created pores in the target cell membrane and natural killer cells kill them

283
Q

what are the three types of phagocytes

A

macrophages, neutrophils, dendritic cells

284
Q

what can phagocytosis be assisted by

A

antibodies

285
Q

how is the target ingested in phagocytosis

A

destroyed with lysosomal enzymes

286
Q

what kind of immune response is inflammation and what is it

A

innate immune response
- nonspecific reaction of immune system to foreign invader

287
Q

what do mast cells secrete in response to inflammation

A

histamine

288
Q

what is the affect of histamine

A

vasodilation –> increased blood flow –> redness and heat

289
Q

what does increased capillary permeability in response to inflammation cause

A

increased capillary permeability –> proteins enter interstitial fluid –> edema –> pain

290
Q

what do macrophages attract

A

neutrophils

291
Q

what is a cytokine

A

peptide signals among leukocytes

292
Q

where are neutrophils found

A

circulate in blood until attracted to site of infection

293
Q

how are T cells activated

A

antigen fragment is presented within MHC self marker by antigen presenting cells (APC)

294
Q

what are the three types of antigen presenting cells

A

dendritic cells
macrophages
B cells

295
Q

what do dendritic cells intiate

A

adaptive immune response
(most important APC)

296
Q

what kind of cells are involved in the adaptive immune system

A

B cells
cytotoxic T cells
helper T cells
(all are lymphocytes)

297
Q

what does each cell of the adaptive immune system have its surface

A

antigen receptors for a specific antigen
- all cells in a clone have same antigen receptor

298
Q

what is clonal expansion

A

correct match between antigen and receptor activated cell to divide rapidly which produces effector cells and memory cells

299
Q

what are the effector and memory cells of B cells

A

effector: plasma cells
memory: memory B cells

300
Q

what is the primary immune response

A

initial slow response
- clonal expansion produces effector and memory cells

301
Q

what is the secondary immune response

A

quicker stronger response due to memory cells making clonal expansion faster
- basis for vaccines

302
Q

what do B cells provide

A

antibody-mediated (humoral) immunity to extracellular pathogens

303
Q

what two things does activation of B cells require

A

binding to antigen
cytokines from helper T cell

304
Q

what do plasma cells secrete and what do they do

A

plasms cells secrete antibodies that attach to a pathogen to tag it for phagocytosis

305
Q

what do cytotoxic T cells provide

A

cell-mediated immunity to intracellular pathogens

306
Q

what two things does activation of cytotoxic T cells require

A

binding to matching antigen on APC
cytokines from helper T cell

307
Q

what do cytotoxic T cells attack

A

abnormal cells

308
Q

what does the cytotoxic part of cytotoxic T cells mean

A

they create pores in target cells, like NK (natural killer cells) but are antigen-specific

309
Q

what do helper T cells secrete

A

cytokines

310
Q

what are cytokines crucial for

A

activating B cells and cytotoxic T cells

311
Q

what does activation of helper T cells require

A

binding to matching antigen on APC

Physiology (5 decks)

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