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Physiology final > Test 4 > Flashcards

Test 4 Flashcards

1
Q

What hormones are released from the adrenal medulla

A

Epinephrine (80%) and Norepinephrine (20%)

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2
Q

What kinds of hormones are secreted from the adrenal gland

A

steroids from the cortex

catecholamines from the medulla

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3
Q

What is the Adrenal medulla made of, and thereby controlled by

A

post-ganglionic sympathetic neurons

sympathetic nervous system

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4
Q

What affect does Epinephrine have on the pancrease

A

inhibits secretion of Insulin and promotes secretion of glucagon

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5
Q

what affect does epinephrine have on the liver

A

It causes the liver to convert glycogen into glucose

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6
Q

What affect does epinephrine have on skeletal muscle

A

causes the muscle to convert glycogen into lactate, that lactate then gets converted to glucose in the liver

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7
Q

What is the overall affect of epinephrine

A

it increases blood sugar levels

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8
Q

what controls the release of epinephrine

A

the sympathetic nervous system through the neurotransmitter acetocholine

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9
Q

What are the three classes of Corticosteroids

A

Minerolocorticoloids - aldosterone
Glucocorticoroids - Cortisol
Sex Hormones - DHEA

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10
Q

Where do corticosteroids get secreted from

A

the adrenal cortex

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11
Q

What does cortisol do

A
  • increase blood sugar (by increasing glucogenesis in the liver, and decreasing glucose uptake)
  • increases protein degredation (especially in muscle)
  • Increase in lipolysis
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12
Q

What regulates the secretion of Cortisol

A

Stress and circadian rhythm cause
hypothalamus to secrete CRH causes
Ant. Pituitary to secrete ACTH causes
increased cortisol secretion

Increased cortisol negatively feedsback to hypothalamus and Ant. Pituitary

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13
Q

What is Cushings Disease

A

Hypersecretion of cortisol

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14
Q

What can cause cushings disease

A
  • hypersecretion of
    CRH
    ACTH
    and or cortisol
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15
Q

What does Cushings disease cause

A 
increased blood sugar = increased fat deposits (Moon Face)
Weak Muscles
Stretch marks
poor wound healing
Mental retardation in children
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16
Q

What is the common precursor for all steroid hormones

A

Cholesterol

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17
Q

What is 21 hydroxylase

A

The enzyme that helps form cortisol from Pregnenolone

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18
Q

What happens when there is a deficieny of 21 hydroxylase

A

Pregnenolone can’t be turned into cortisol, so most of it is turned into DHEA.
Excessive DHEA leads to excessive Adrenal Androgens.
That leads to early puberty in males and ambiguous sex development in females

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19
Q

What is the disease called when there is a shortage of 21 hydroxylase

A

congenital adrenal Hyperplasia

early puberty in males, ambiguous sex differentiaion in females

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20
Q

What is the exocrine function of the pancreas

A

digestive enzymes

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21
Q

what are the endocrine hormones of the pancreas

A

insulin
glucagon
somatostatin

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22
Q

What cells secrete insulin

A

beta cells

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23
Q

What cells secrete glucagon

A

alpha cells

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24
Q

What cells secrete somatostatin

A

delta cells

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25
Q

What happens with the pancreas and liver when there is low blood sugar

A
  • pancreas secretes glucagon
  • glucagon stimulates the liver
    • increase glycogenolysis
    • increase gluconeogenesis
    • decrease glycogenesis
  • That all increases blood sugar levels
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26
Q

What does glucagon do for carbohydrate metabolism

A

increases blood sugar

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27
Q

what does glucagon do for fat metabolism

A

increases blood fatty acids and ketones

  • decreases triglyceride synthesis from glucose and fatty acids
  • increases lipolysis
  • increases ketogenesis
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28
Q

what does glucagon do for protein metabolism

A

there isn’t a large effect on blood amino acid levels

  • increases gluconeogenesis (uses AA’s)
  • increases protein degredation
  • decreases protein synthesis
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29
Q

What is the overall action of glucagon

A

promotes hepatic glucose production and secretion

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30
Q

What are the steps of glucagon signaling

A
  • glucagon binds to the receptor
  • g protein moves over to adenylate cyclase and activates it
  • that turns atp into cAMP
  • cAMP activates PKA
  • PKA phosphorylates other proteins
  • This initiates a cellular response
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31
Q

What is the primary action of insulin

A

decrease blood glucose (makes cells absorb it better)

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32
Q

What does insulin do for carbohydrate metabolism

A
  • increases glucose uptake into most cells
  • increases glycogenesis in skeletal muscle and liver
  • decreases glycogenolysis in skeletal muscle and liver
  • decreases gluconeogenesis in liver
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33
Q

What does insulin do for fat metablolism

A
  • increase triglyceride synthesis from glucose and fatty acids
  • decreases lipolysis
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34
Q

What does insulin do for protein metabolism

A
  • increases amino acid transport into cells
  • increases protein synthesis
  • decreases protein degredation
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35
Q

What does insulin do for
adipose tissue
liver
muscle

A
  • increases glucose uptake and storage as fat
  • increases glucose uptake and storage as glycogen and fat
  • increases glucose uptake and storage as glycogen
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36
Q

how exactly does insulin cause increased glucose uptake into cells

A
  • Insulin binds to IR (insulin receptor)
  • This causes IRS1 to be activated
  • this causes translocation of the GLUT 4 in microvesicles to the sarcolemna
  • The GLUT 4 molecules are the glucose channels that allow Glucose to enter the cell
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37
Q

What are the different methods of control for insulin release

A

Food intake

  • increase gastrointestinal hormones stimulate insulin release
  • parasympathetic situation causes insulin to release
High blood amino acid concentration stimulates insulin release
sympathetic stimulation (epinephrine) decreases insulin release

Blood glucose levels

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38
Q

What is the major control of insulin release

A

blood glucose levels

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39
Q

What does Diabetes Mellitus mean

A

increased urine output, sweet tasting

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40
Q

what is diabetes mellitus

A

a group of diseases characterized by elevated blood glucose levels

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41
Q

What is Type 1 Diabetes mellitus

A

Caused by an autoimmune destruction of the beta cells of the pancreatic islets
This causes insulin deficiency
patients must take insulin to survive

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42
Q

What is Type 2 Diabetes mellitus

A

An increase in insulin resistance
90% of all diabetics
early on the insensitivity is compensated for by increased insulin secretion
when insulin defiecieny occurs then you have hyperglycemia

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43
Q

What is the average age of onset for type 2

A

35

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44
Q

what are the 6 problems created by an insulin deficiency

A
  • polyuria
  • polyphagia
  • polydipsia
  • muscle wasting
  • ketosis
  • peripheral circulatory failure
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45
Q

What are the short term complications for Diabetes

A
  • hyperglycemia
  • glycosuria (dehydration due to osmotic diuresis)
  • Ketoacidosis
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46
Q

What are the long term complications for diabetes

A
  • Atherosclerosis
  • renal failure
  • retinopathy
  • neuropathy
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47
Q

how prevelent is diabetes

A

8% of people in the us

25% for people over 60

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48
Q

what are the treatments for diabetes

A 
lifestyle changes
- exercise
- diet changes
Medication
- insulin sensitizers
- insulin
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49
Q

What are the treaments for major medial complicatoins from diabetes

A

dialysis
amputation
not much for retinopathy and neuropathy

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50
Q

what caused the sharp rise in diabetes in kids

A

fatter from the diets,. and less exercise due to video games

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51
Q

How does exercising help prevent diabetes

A

Muscle contractions also stimulate the GLUT 4 to move to the sarcolemma increasing glucose uptake by the cells

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52
Q

How does muscle contraction act like insulin and increase glucose uptake

A

it stimulates the activation of AMPK which helps in the translocation of GLUT 4 to the sarcolemma

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53
Q

What is AMPK

A

an energy sensing enzyme that counteracts impending ATP depletion

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54
Q

How does AMPK fight impending ATP depletion

A
  • acutely activates fatty acid oxidation and glucose uptake (sources of energy for ATP synthesis)
  • Increases capacity for ATP synthesis (GLUT 4 and mitochondrial enzymes) in response to endurance training
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55
Q

what are the benefits of running for diabetes

A

muscle contraction has an insulin like effect
inactivity decreases insulin sensitivity of muscle
endurance training increases insulin activity in muscle
- wears off after 40 hours

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56
Q

What are other health reasons to run

A
  • reduces the risk of premature death
  • reduces the risk of heart disease
  • reduces the risk of hypertension
  • reduces the risk of colon cancer
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57
Q

What are the two hormones secreted by adipose tissue

A
  • Adiponectin

- Leptin

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58
Q

What does adiponectin do

A

increased glucose uptake and decrease glucose formation in liver

decreases caloric intake and increases BMR in hypothalamus

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59
Q

What Leptin do

A

decreases caloric intake and increases BMR in hypothalamus

increases fatty acid oxidation in muscle

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60
Q

What is a virus

A

DNA/RNA in a protein coat

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61
Q

What is a bacteria

A

single celled living microorganism

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62
Q

What are the functions of the immune system

A
  1. defend against invading pathogens (major targets are viruses and bacteria)
  2. Remove worn out cells and tissue damaged by trauma
  3. identifies and destroys abnormal or mutant cells that originated inside the body
  4. Mounts innappropriate immune responses that lead either to allergies or to autoimmune diseases
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63
Q

How do Bacteria attack cells

A

they shoot them with toxins

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64
Q

how do viruses attack cells

A

they invade and take over the cell, which can transform the cell, starve it, and cause it to shoot out toxins

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65
Q

What are the 5 types of leukocytes

A
  1. Neutrophils
  2. Eosinophils
    3, Basophils
  3. Monocytes
  4. Lymphocytes
    - B cells
    - T cells
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66
Q

What do Neutrophils do

A

Phagocytosis

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67
Q

What do Eosinophils do

A

Parasitic destruction and allergic reactions

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68
Q

What do basophils do

A

histamine and heparin release, allergic reactions

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69
Q

What do monocytes do

A

transform into macrophages (phagocytosis)

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70
Q

What do lymphocytes do

A

B cells - Secrete antibodies (antibody mediated immunity)

T cells - destory virus infected and mutant cells (Cell-mediated immunity)

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71
Q

What are the two categories of immune defense

A

Innate (nonspecific) immunity

Adaptive (specific) immunity

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72
Q

What is innate immunity

A

inherited as part of the organism
nonselectively fights against forein invaders
first line of defense
rapid but limited response

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73
Q

What is adaptive immunity

A

organism adapts to defend against specific invaders

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74
Q

What are the defenses of the innate immunity

A
  1. Inflammation
  2. Interferon
  3. Natural Killer Cells
  4. Complement system
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75
Q

What is inflammation

A

an innate non specific series of events that occur in response to an injury or infection of a tissue

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76
Q

What is the goal of inflammation

A

bring phagocytotic cells, fluid, and plasma proteins (clotting factors and compliment proteins) to the affected area to

  1. kill microorganisms
  2. Remove debris
  3. prepare the tissue for healing
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77
Q

What are the steps of the inflammatory response

A
  1. Activation of Macrophages - phagocytosis (this makes cytokines)
  2. Histamines released from the mast cells- vasodilation
  3. cytokines and histamine increase capillary permeability
  4. Leukocytes migrate out into tissue
  5. the Debris and bacteria are phagocytized
78
Q

What are mast cells

A

tissue bound basophils

79
Q

What are phagocytic secretions and what do they do

A

They are secretions from the phagocytes that become important when there are lots of phagocytes in the tissues.
Those secretions secretes Endogenous Pyrogen

80
Q

What Does Endogenous Pyrogen do

A

Pyrogen enters the blood and travels up to the hypothalamus, where it stimulates the release of prostoglandin, which increases the body’s thermostat

81
Q

How Do NAIDS affect inflammation

A

not sure

82
Q

What are interferons

A

an innate non specific defense mechanism

83
Q

what do interferons do

A

Interfere with viral replicatoin

84
Q

How do interferons interfere with viral replication

A
  1. a cell affected with a virus produces interferons
  2. These interferons travel to nearby cells
  3. at the other cells they bind and trigger the production of enzymes
    4,. these enzymes prevent viral replication and break down the viral RNA

Virus’ can still invade the cell, but they can’t control it

85
Q

What are natural killer cells

A

Non specific, they attack any virus infected or cancerous cell
They are rapidly activated
They are limited in their response

86
Q

What is the compliment system

A
  • produced by the liver
  • Non specific defense mechanism
  • COmplements the actions of antibodies
  • made up of 9 proteins (usually inactive)
87
Q

What are the two pathways of the compliment system

A

alternate pathway and classical pathway

88
Q

what is the alternate pathway of compliment system

A

C1 non specifically binds to bacteria

89
Q

What is the classic pathway of the compliment system

A

C1 binds to antibodies specific to the bacteria

90
Q

What are the actions of the compliment system

A 
Augmentation of inflammation
- Chemotaxis
- Opsonization (better phagocytosis)
- Mast cell activation
- vasodilation
MAC formation
91
Q

What is MAC

A

The membrane attack complex

92
Q

How does MAC destroy bacteria

A

the long skinny proteins dive into the membrane creating a pore that leads to lysis of the bacteria.
Activating C1 starts it all, then one C5 dives in, C6 dives in next to it C7 and C8 do the same. Then A bunch of C9’s join in to finish the pore

93
Q

What is adaptive immunity

A

organism adapts to defend against specific invaders

94
Q

What are the two classes of adaptive immunity

A

Antibody mediated immunity

Cell mediated immunity

95
Q

what are the two players in antibody mediated immunity

A

Antigen and Antibody

96
Q

What is an antigen

A

Any foreign protein that is unique from body proteins

97
Q

What is an antibody

A

protein molecules produced by B lymphocytes in response to the introduction of an antigen

98
Q

What is the process of antibody synthesis

A
  1. Millions of different clones of B cells are developed as a fetus
  2. Each clone of a B cell has surface receptors for a specific antigen
  3. The B clone cells are inactive until activated by an antigen
  4. once they are activated by the antigen, the cells differentiate into plasma cells and memory cells
99
Q

What do plasma cells do in antigen mediated immunity

A

They create the antibodies needed to fight the antigens

100
Q

What do Memory cells do in antigen mediated immunity

A

They are just copies of the original clone, but now there are many so that if the antigen returns again the body will be way more prepared

101
Q

What is an antibody shaped like

A

a y, with the antigen receptors at the top points

102
Q

What kind of feedback is the anitgen/antibody mediated immune system

A

Negative

103
Q

What can antibodies do

A
  1. Agglutination (clumping of cells)
  2. Opsonization (bacteria/virus made prone to phagocytosis)(phagocyte encircles the bacteria)
  3. Neutralization (poisons are made non toxic)
  4. Activation of a compliment system Antibody binds to bacteria and C1
  5. Stimulation of Natural Killer cells (antibody binds to bacteria and natural killer cells)
104
Q

What is the difference between primary and secondary immune responses

A

secondary immune response is about 3 times as strong, and twice as fast.

105
Q

How do vaccinations work

A
  1. a Dead or attenuated pathogen is injected
  2. The body mounts an attack against the antigen and makes memory cells
  3. Then when the real pathogen comes, the immune response is fast and powerful so that no or few symptoms show.
106
Q

What is cell mediated immunity

A

involves the production of activated T lymphocytes

- Directly attack unwanted cells

107
Q

What are the three types of T lymphocytes

A

Cytotoxic T cells
Helper T cells
Suppressor T cells

108
Q

What do cytotoxic T cells do

A

destroy cancer cells and virus infected cells

109
Q

How do Cytotoxis T cells work

A
  • Cytotoxic T cells have an antigen receptor on them that are very specific like cloned b cells
  • When the antigen is bound by a class 1 MHC the Cytotoxic t cells recognize the antigen
  • this activates the Cytotoxic T cell and causes it to replicate creating an army of specific cells
  • Then the Cytotoxic T cells kill the infected cell by secreting perforin molecules (like natural killer cells)
  • once the cell is destroyed the virus gets out and is destroyed by macrophages, antibodies, and the compliment system
110
Q

What do helper t cells do

A

secrete cytokines to enhance the activity of cytotoxic t cells, b cells, and macrophages

111
Q

What do suppressor t cells do

A

supress b cell, cytotoxic t cell, and helper t cell activity.

112
Q

What is AIDS

A

Acquired Immune Deficiency Syndrome
Caused by HIV
HIV attacks helper T cells
patient dies from infections and cancers that would normally be easily handled

113
Q

What is immune tolerance

A

normally the immune system doesn’t form antibodies against proteins from your body

114
Q

What are the Two Immune diseases

A

Autoimmunity - the immune system creates antibodies against ones own tissues or proteins

Allergy - Inappropriate immune attacks against harmless environmental substances

115
Q

What determines the genetic Sex of the individual

A

Whether the individual is XX or XY

116
Q

How does male development occur

A
  1. SRY stimulates the creation of TDF
  2. TDF directs differentiation into Testes
  3. The Testis secrete testosterone and MIH
  4. Testosterone causes Wolfiann ducts to develop
  5. MIH inhibits the growth of the Mullerian duct
  6. Testosterone is converted into DHT
  7. DHT promotes the development of penis and scrotum
117
Q

What is Gonadal Sex

A

whether you have ovaries, or testes

118
Q

What is phenotypic sex

A 
internal = mullerian or wolfiann ducts
External = penis or vagina
119
Q

How does female development occur

A
  1. No SRY = no TDF
  2. Lack of TDF leads to development of ovaries
  3. Ovaries don’t secrete Testosterone or MIH
  4. No testosterone = wolfian ducts don’t develop
  5. No MIH = Mullerian ducts develop
  6. N testosterone = no DHT
  7. No DHT = no penis (clitoris and labia)
120
Q

what does the genital tubercle turn into for males and females

A

Penis and clitoris

121
Q

What does the urogenital folds turn into for males and females

A

penis and labia minora

122
Q

What does the labioscrotal swellings become for males and females

A

scrotum and labia majora

123
Q

What are some errors in sexual differentiation

A

Hermaphroditism
pseudohermaphroditism
female hermaphroditism
male hermaphroditism

124
Q

What is hermaphroditism

A

Ovarian and testicular tissue is present

125
Q

what is a probable cause of hermaphroditism

A

some cells may be lacking the short arm of the Y chromosome with the SRY gene

126
Q

What is pseudohermaphroditism

A

Individual has either testes and ovaries, but accessory sex organs, or external genetilia are not appropriate for thier chromosomal sex

127
Q

what is female hermaphroditism

A

chromosomal female/male external genetilia

128
Q

What is a possible cause of female hermaphroditism

A

congenital adrenal hyperplasia

129
Q

What is male hermaphroditism

A

Chromosomal male/female external genetalia

130
Q

What are the possible causes of male hermaphroditism

A

5 alpha reductase deficiency

testicular feminization syndrome or lack of testosterone receptors

131
Q

What is congenital adrenal hyperplasia

A

lack of 21 hydroxylase leads to extra DHEA production, which leads to excess adrenal androgens. This leads to early puberty in males, and wrong sex development in females

132
Q

What does 5 alpha reductase do

A

convert testosterone to DHT

133
Q

What would happen if you didn’t have enough 5 alpha reductase

A

you would have testis, and internal male phenotypic sex, but you would not have male external phenotypic sex

134
Q

What happens if a man doesn’t have testosterone receptors

A

They dont have either internal phenotypic sex and they have female external phenotype

135
Q

What are the parts of the testis

A

ductus deferens
epidydimis
seminiferous tubules
leydig cells

136
Q

What do the leydig cells do

A

secrete testosterone

137
Q

How are leydig cells stimulated in development

A

Plancental HCG stimulates them to make testosterone which leads to male development

138
Q

How is testosterone controlled at puberty

A

GnRH released from Hypothalamus
stimulates Lh release from ant pit
Lh causes leydig cells to secrete testosterone
that leads to pubertal growth and maturation

INcreased testosterone goes back and does negative feedback on the hypothalamus and the ant pit

139
Q

Where do the sperm develop in the testis

A

between the sertoli cells

140
Q

where are the sertoli cells

A

in the seminiferous tubules

141
Q

How do sperm develop

A

they start out on the edge of the seminiferous tubules and slowely work toward the lumen of the seminiferous tubules as they develop

142
Q

How is spermatogenesis controlled

A
  1. Hypothalamus secretes GnRH
  2. that causes Ant. Pit to secrete FSH and LH
  3. FSH directly causes sertoli cells to do spermatogenesis
  4. Lh causes leydig cells to produce Testosterone
  5. Testosterone causes sertoli cells to do spermatogeneis too.

Testosterone the does negative feedback on the Hypothalamus and the Ant. Pit (LH)

Sertoli cells secrete inhibin as they make sperm, this goes back and does negative feedback on the Ant Pit (FSH)

143
Q

What is the function of the ovaries

A

Produce ova

secrete estrogen and progesterone

144
Q

What is the function of the ovaducts

A

transport ova

site of fertalization

145
Q

What is the function of the uterus

A

maintain fetus during pregnancy

expels fetus during childbirth

146
Q

what is the function of the vagina

A

site of sperm deposition during sex

passageway for delivery of the baby

147
Q

What are the functions of estrogen

A
  1. essential for ova maturation and release
  2. Establishes 2ndary female sexual charateristics
  3. essential for transport of sperm from vagina to oviduct
  4. contributes to breast development in anticipation of lactation
148
Q

What are the functions of progesterone

A
  1. important for preparing a suitable environment in the uterus for nourishing a developing baby
  2. Contributes to breasts’ ability to produce milk
149
Q

What is the menstual cycle

A

repeated changes in the ovary and uterus

150
Q

What are the two parts of the menstrual cycle

A
  1. Ovarian cycle

2. Uterine cycle

151
Q

What causes the menstual cycle

A

changes in estrogen and progesterone concentrations

152
Q

what are the parts of the ovarian cycle

A
  • follicular phase

- luteal phase

153
Q

What is the follicular phase

A

phase during which the follicle matures

154
Q

what is a follicle

A

developing ovum and surrounding granulosa cells

155
Q

What is the luteal phase

A

marked by the presence of the corpus luteum

156
Q

what is the corpus luteum

A

developes from the ruptured follicle

157
Q

What do the granulosa cells do

A

secretes estrogen and inhibin

nourish the ovum

158
Q

What does FSH do during the follicular phase

A

induces antrum formation

stimulates proliferation of granulosa cells

159
Q

What does estrogen do during the follicular phase

A

stimulates proliferation of the granulosa cells

160
Q

what does LH do during follicular phase

A

stimulates estrogen secretion

161
Q

What hormone dominates during the follicular phase

A

estrogen

162
Q

the thecal and follicular cells start to secrete estrogen from the follicle during the follicular phase

A

kj

163
Q

what causes the estrogen levels to continually rise during the follicular phase

A

rising LH levels

164
Q

how is ovulation controlled

A

It is triggered by a surge in LH, it occurs when estrogen reaches high enough levels that it switches from an inhibitor of LH to a stimulator

165
Q

What happens in the luteal phase

A
  1. After egg is pushed out Corpus luteum forms
  2. This secretes progesterone and estrogen
  3. progesterone inhibits FSH and LH secretion
  4. This prepares the uterus for implantation
  5. if no fertalization occurs then the corpus luteum degenerates ending the luteal phase
166
Q

What are the phases of the uterine cycle

A

Proliferative phase
Secretory phase
Menstrual phase

167
Q

What is the proliferative phase

A
  • starts at the end of the ovarian follicular phase
  • Estrogen stimulates thickening of the endometrium
  • from end of menstruation to ovulation
168
Q

What is the secretory phase

A

starts at ovulation and ends when the corpus luteum degenerates
converts estrogen primed endometrium to be highly vascularized

169
Q

What is the menstrual phase

A

first day of menstruation stars a new cycle
starts at the end of the ovarian luteal phase
discharge of blood and endometrial debris
lasts up to 5 to 7 days

170
Q

What affect does the sympathetic NS have on erections

A

it kills them, the norepinephrine causes vasoconstriction

171
Q

What happens to form an erection

A
  1. Stimulus increases parasympathetic and decreases sympathetic
  2. this causes the arterioles to dialate, and it causes the bulbourethral and urethral galnds to secrete mucus
  3. arteriole dialation leads to an erection
  4. the erection compresses veins leading to even more erection
172
Q

What is the chemical happenings during an erection

A
  1. NO is released from the parasympathetic neuron
  2. this activates guanylyl cyclase
  3. this converts GTP to cGMP
  4. this causes relaxation and dialation
  5. PDE-5 gets rid of cGMP and gets rid of the erection
173
Q

What does viagra do

A

if blocks PDE-5 making easier to get and sustain an erection

174
Q

What are the steps of ejaculation

A

emission

expulsion

175
Q

What happens during emission

A

continual stimulation causes spinal reflex activation of sympathetic nerves to the prostate seminal vesicles and reproductive ducts, this causes them to deliver semen to urethra

176
Q

What happens during expulsion

A

semen in the urethra triggers sysmpathetic reflex, skeletal muscle contractions at the base of the penis

177
Q

How does fertalization occur

A

Estrogen helps carry sperm into the oviduct where it will meet the ova
many sperm use thier acrosome to try to break through the corona radiata
once one gets through its head pops off inside with the DNA and fertalization has occured

178
Q

Where does fertalization occur

A

oviduct

179
Q

what happens when the acrosome touches the corona radiata

A

it releases enzymes to break down the corona radiata and the zona pelucida

180
Q

What happens when one sperm reaches the plasma membrane

A

a change in the membrane is triggered and no more spermies can get in

181
Q

what happens after fertalization (when the egg and sperm fuse)

A

The zygote mitotically divides over and over again forming a blastocyst

182
Q

what does the blastocyst do

A

migrates to the uterus where it implants on the endometrium

183
Q

What is the placenta

A

the inner most lining of the endometrium, a temprorary endocrine organ

184
Q

What does the placenta do

A

its the organ of exchange between maternal and fetal blood

185
Q

What are the hormones that change during pregnancy released from the placenta

A

hCG - spikes a lot right after fertalization and then drops quickly
Estrogen - steadily increases from day 1 to delivery
Progesterone - steadily increases from day 1 to delivery but not as much as estrogen

186
Q

What is hCG

A

Human chorionic gonadotropin

187
Q

when is hCG produced and by what

A

the firts trimester of pregnancy, by the placenta

188
Q

what does hCG do

A

maintains the corpus luteum (which secretes estrogen and progesterone) until the placenta takes over in the 2nd trimester

189
Q

What does estrogen do in pregnancy

A

Maintains endometrium

stimulates growth of myometrium

190
Q

where does estrogen come from in pregnancy

A

1st trimester the corpus luteum, after that the placenta

191
Q

where does progesterone come from in pregnancy

A

1st trimester the corpus luteum, after that the placenta

192
Q

What does progesterone do in pregnancy

A

Maintains endometrium
supresses uterine contractions
uterine plug formation

Physiology final (10 decks)

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