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Human Physiology > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What is normal plasma pH?

A

7.4

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2
Q

What can disturbance of pH homeostasis cause?

A

-Disturbance of protein shape
-Disturbance of K+ levels
-Effects on excitable tissues

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3
Q

What is the largest determinant of pH?

A

Metabolic production of CO2 is the largest source of excess H+

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4
Q

What is a buffer system?

A

Mixture of 2 compounds that can remove free H+ as needed

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5
Q

What is the most important extracellular buffer?

A

Bicarbonate

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6
Q

What is the most important intracellular buffer?

A

Proteins

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7
Q

What are the 4 buffer systems in our body?

A
  1. Bicarbonate
  2. Proteins
  3. Phosphate
  4. Ammonia
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8
Q

What is the equation for pH?

A

pH = 6.1 + log (HCO3- / CO2)

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9
Q

How does respiratory compensation work as a homeostatic mechanism for pH?

A

Can only fix metabolic pH problems by controlling rate of CO2 removal

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10
Q

How does renal compensation work as a homeostatic mechanism for pH?

A

-Slow but most powerful pH regulator
-Usually secrete H+ to make urine more acidic
-Usually absorb HCO3-

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11
Q

What are intercalated cells?

A

Cells in distal nephron that play key role in renal pH compensation

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12
Q

What are Type A intercalated cells?

A

-Active when in acidosis
-Secretes H+ into filtrate & Absorbs HCO3- into blood

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13
Q

How do Type A intercalated cells secrete H+ into filtrate?

A

Uses H+/K+ exchanger –> acidosis often leaded to hyperkalemia (high K+ in blood)

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14
Q

What are Type B intercalated cells?

A

Active when in alkalosis
-Absorbs H+ into the blood & Secretes HCO3- into filtrate

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15
Q

How do Type B intercalated cells absorb H+ into blood?

A

Uses H+/K+ exchanger –> alkalosis often leads to hypokalemia (low K+ in blood)

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16
Q

What are the types of pH disturbance?

A

-Respiratory acidosis or alkalosis= underlying cause is a change in PCO2
-Any other pH disturbance is referred to as metabolic

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17
Q

What is respiratory acidosis?

A

-Due to hypoventilation
-Respiratory system is the problem, all compensation is renal

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18
Q

What is metabolic acidosis?

A

-Due to addition of acids or removal of HCO3-
-Compensation by lungs (rapid)
-Renal compensation (slow)

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19
Q

What is respiratory alkalosis?

A

-Due to hyperventilation
-Respiratory system is the problem, all compensation is renal

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20
Q

What is metabolic alkalosis?

A

-Due to removal of acids or addition of HCO3-
-Compensation by lungs (rapid)
-Renal compensation (slow)

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21
Q

What are the hypothalamic control centers for food intake?

A
  1. Feeding center: tonically active
  2. Satiety center: inhibits feeding center
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22
Q

What is Neuropeptide Y (NPY)?

A

Neurotransmitter in the brain that is main signal responsible for increased food intake/ hunger

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23
Q

What is Ghrelin?

A

Hormone secreted by stomach when empty to stimulate an increase in food intake

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24
Q

What is leptin?

A

Hormone secreted by adipocytes when fat stores increase in order to decrease food intake

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25
Q

What is CCK & GLP-1?

A

Hormones secreted by the duodenum in response to fats and carbs in chyme to decrease food intake

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26
Q

What is the fed (absorptive) state?

A

Absorbing nutrients at GI tract

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27
Q

What are the characteristics of the fed state?

A

-Mainly anabolic (storage/synthesis)
-Glycolysis is main energy source
-Protein synthesis

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28
Q

What is glycogenesis? What state does this occur in?

A

Glucose is converted to glycogen in liver & muscle; occurs during fed state

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29
Q

What is lipogenesis? What state does this occur in?

A

Fat synthesis in adipocytes; occurs in fed state

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30
Q

What does lipogenesis use?

A

-Glycerol & fatty acids
-Converted excess carbohydrates & amino acids

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31
Q

What is the fasted (post-absorptive) state?

A

No absorption occurring at GI tract

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32
Q

What are the characteristics of the fasted state?

A

-Mainly catabolic (breakdown)
-Maintain blood glucose

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33
Q

What is glycogenolysis? What state does it occur in?

A

Glycogen is converted into glucose in the liver and causes glucose release; occurs in fasted state

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34
Q

What is gluconeogenesis? What state does it occur in?

A

Liver produces glucose from glycerol (adipocytes) & pyruvate, lactate, & AAs (skeletal muscle); occurs in fasted state

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35
Q

Why do fats become a major energy source in the fasted state?

A

Fats have higher energy content than glycogen, but are slower to metabolize

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36
Q

What is Lipolysis?

A

Triglycerides are converted into glycerol + free fatty acids
- glycerol used in glycolysis
- fatty acids enters Krebs cycle as acetyl CoA

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37
Q

What happens during extended fasting?

A

-Body proteins used heavily as source of AA
-Brain uses ketone bodies produced from FFA in liver

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38
Q

What ratio regulates metabolism?

A

Inverse ratio of insulin-to-glucagon

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39
Q

Why is insulin dominant in the fed state?

A

High blood glucose stimulates pancreatic beta cells to secrete insulin

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40
Q

What happens when insulin is secreted during the fed state?

A

-Incr. glucose uptake
-Incr. glycolysis
-Incr. glycogenesis
-Incr. lipogenesis
-Incr. protein synthesis
-Decr. blood glucose

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41
Q

What is the mechanism for insulin uptake in the fasted state in adipose tissue and resting skeletal muscle?

A

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

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42
Q

What is the mechanism for insulin uptake in the fed state in adipose tissue and resting skeletal muscle?

A

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

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43
Q

How does insulin indirectly alter glucose transport in the liver?

A

GLUT2 transporters always present in hepatocyte membrane

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44
Q

What is the mechanism for insulin uptake in the fasted state in the liver?

A

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

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45
Q

What is the mechanism for insulin uptake in the fed state in the liver?

A

Insulin activates glucokinase in the cell that phosphorylates glucose to glucose 6-phosphate to keep glucose low inside the cell so that glucose will diffuse into the cell

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46
Q

What are the feedfoward mechanisms influencing insulin secretion?

A

-Carbohydrates in gut stimulate incretins (GIP & GLP-1) to increase insulin
-Stretch of the gut incr. parasympathetic input which incr. insulin

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47
Q

How is glucagon dominant in fasted state?

A

-Low blood glucose stimulates pancreatic alpha cells to secrete glucagon:
- incr. glycogenolysis in liver
- incr. glucogenesis in liver
to incr. blood glucose

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48
Q

What are 2 other hormones that help increase blood glucose?

A

Cortisol & Epinephrine

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49
Q

Why are humans homeothermic?

A

We regulate internal temperature within a narrow range

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50
Q

What happens when our temperature is too high?

A

Hyperthermia = denature enzymes

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51
Q

What happens when our temperature is too low?

A

Hypothermia = chemical reactions too slow

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52
Q

What is the equation for heat gain and loss being balanced at equilibrium?

A

External heat input + internal heat production = heat loss

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53
Q

What are the mechanisms of heat exchange?

A
  1. Radiation (gain or loss)
  2. Conduction (gain or loss)
  3. Convection (gain or loss)
  4. Evaporation (loss)
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54
Q

What is radiation?

A

Warm surfaces emit and absorb electromagnetic waves that travel through space

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55
Q

What is conduction?

A

-Heat transmission by contact
-Transferred by thermal molecular motion

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56
Q

What is convection?

A

Heat transmission by bulk flow of air or water

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57
Q

What is evaporative heat loss?

A

From skin and respiratory tract

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58
Q

How does normal metabolism generate internal heat production?

A

Only ~25% of nutrient energy is captured as cellular work - the rest is “wasted” as heat, but can be used to maintain body temp

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59
Q

How does voluntary muscle contraction generate internal heat production?

A

Can be used for behavioral thermoregulation

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60
Q

What is shivering thermogenesis?

A

Involuntary tremors in skeletal muscles

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61
Q

What is non-shivering thermogenesis?

A

-Mitochondrial uncoupling: energy from electron transport system released as heat in brown adipose tissue

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62
Q

Where are the sensors for the homeostatic reflex of temperature regulation?

A

-Central thermoreceptors (hypothalamus)
-Peripheral thermoreceptors (skin)

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63
Q

What is the thermoneutral zone?

A

Range of environmental temperatures in which thermoregulation requires only vascular adjustments

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64
Q

What is the response to decreased temperature by sympathetic adrenergic response?

A

Cutaneous vasoconstriction decreases convective flow from interior to skin to decrease skin temperature to decrease heat loss

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65
Q

What is the response to decreased temperature by somatic motor neurons?

A

Shivering thermogenesis

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66
Q

What is the response to increased temperature through active cutaneous vasodilation?

A

Increase in heat loss at skin due to sympathetic cholinergic neurons

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67
Q

What is the response to increased temperature by sweat glands secreting sweat?

A

-Sympathetic cholinergic neurons
-Energetically expensive: main reason for incr. in metabolic rate above thermoneutral zone
-Evaporative cooling causes incr. net heat loss

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68
Q

What causes an increased set point in the hypothalamus?

A

Fever

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69
Q

What causes a decreased set point in the hypothalamus?

A

Hot flashes

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70
Q

What is the function of the digestive system?

A

Move materials from external to internal environment

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71
Q

What is the enteric nervous system?

A

Neurons in GI wall that control motility & secretion

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72
Q

What is the short reflex in the digestive system?

A

Originates within ENS and is integrated there without input from CNS

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73
Q

What is the long reflex in the digestive system?

A

Integrated in the CNS from sensory input from ENS and Autonomic output to ENS

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74
Q

What is amylase? Where is it found?

A

Amylase is found in saliva and pancreas and digests polysaccharides to disaccharides

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75
Q

What is the disaccharidases? Where is it found?

A

Disaccharidases are found on the membrane of cells in the small intestine and they digest disaccharides to monosaccharides

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76
Q

What kind of energy does a GLUT use?

A

Facilitated diffusion

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77
Q

What kind of energy does a SGLT use?

A

Secondary active transport

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78
Q

How are glucose & galactose absorbed?

A

-Apical entry - SGLT
-Basolateral exit - GLUT2

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79
Q

How is fructose absorbed?

A

-Apical entry - GLUT5
-Basolateral exit - GLUT2

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80
Q

What are endopeptidases?

A

Break peptide bonds in interior or protein/peptide i

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81
Q

What is pepsin & where is it found?

A

Endopeptidase; in stomach

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82
Q

What is trypsin & where is it found?

A

Endopeptidase; in small intestine

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83
Q

What is an exopeptidase?

A

Remove amino acid at the end

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84
Q

What does carboxypeptidase do?

A

Removes from carboxy-terminal end

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85
Q

What does aminopeptidase do?

A

Removes from amino-terminal end

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86
Q

How are free amino acids absorbed?

A

Most by cotransport with Na+

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87
Q

How are di- and tripeptides absorped?

A

-Cotransport with H+
-Most are digested inside the cell to free amino acids

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88
Q

What do bile salts in bile do?

A

Emulsify fats to break into smaller droplets to incr. surface area for enzymatic digestion

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89
Q

What does the lipase do?

A

Digests triglycerides into monoglyceride + 2 free fatty acids

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90
Q

What does the colipase do?

A

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

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91
Q

What do the products of lipid digestion do?

A

Assemble with bile salts & phospholipids into a micelle

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92
Q

What happens in the cephalic phase of digestion?

A

Sight, smell, taste, & thought of food signal the medulla to incr. PSNS input to incr. salivary gland secretion & incr. secretion and motility throughout digestive system

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93
Q

What is the cephalic phase?

A

Feedforward response to anticipation of food

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94
Q

What is the gastric phase?

A

Increase in gastric secretion & motility stimulated by entry into stomach of chyme

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95
Q

What happens during the gastric phase?

A

-Distention & presence of peptides/amino acids in lumen incr. gastrin secretion by G cells, incr. HCl secretion by parietal cells, and incr. pepsinogen secretion by chief cells

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96
Q

What does acid in the lumen during the gastric phase do?

A

Acts as negative feedback to incr. somatostatin from D cells and decr. secretion by G cells, parietal cells, and chief cells

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97
Q

What is the intestinal phase?

A

Changes in secretion & motility stimulated by entry of chyme into duodenum

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98
Q

What does acid do during the intestinal phase?

A

acid incr. secretin secretion that incr., pancreatic bicarbonate secretion

99
Q

What do fat & proteins do during the intestinal phase?

A

fats & proteins incr. CCK which incr. pancreatic enzyme secretion & bile release by gallbladder

100
Q

What do carbohydrates do during the intestinal phase?

A

Carbohydrates incr. incretins which increase insulin secretion

101
Q

What is homeostasis?

A

The ability of the body to maintain a relatively constant internal environment.

102
Q

What are examples of regulated variables?

A

Temperature, pH, ion concentrations, nutrient availability, etc.

103
Q

What are the parts of a control system that maintains homeostasis?

A

Stimulus, Sensor, Integrating center, Target/Effector

104
Q

What is the feedforward control strategy?

A

Occurs in anticipation of change

105
Q

What is the feedback control strategy and what types are there?

A

Feedback occurs in response to change. Negative feedback restores normal value and positive feedback enhances change.

106
Q

Why do compartments maintain different concentrations of each solute?

A

Resulting gradients can be used as energy source.

107
Q

What are the 3 types of transport mechanisms? Describe each and what molecules they transport.

A
  1. Simple Diffusion: diffusion across lipid bilayer (nonpolar molecules: gases, lipids, etc)
  2. Protein-mediated transport: (small polar molecules: glucose, amino acids, water)
  3. Vesicular transport: (very large molecules: proteins)
108
Q

What is a channel protein? What do they transport?

A

Channel proteins form continuous connection between ICF & ECF to transport ions and water.

109
Q

What are the types of channel proteins?

A
  1. Leakage (open)
  2. Gated (closed)
    • Chemically-gated
    • Mechanically- gated
    • Voltage- gated
110
Q

What are the characteristics of channel proteins?

A

-can only mediate passive transport
-rate depends on gradient & number of channels

111
Q

What is a carrier protein?

A

Bind to molecules and change shape to carry them across a membrane.

112
Q

What are the characteristics of carrier proteins?

A

-Never form continuous connection between ICF & ECF (“revolving door”)
-slower than channel proteins
-can move larger molecules
-can use passive or active transport to move across gradients

113
Q

What are the types of carrier proteins?

A
  1. Uniporter: one kind of molecule
  2. Cotransporter: two or more kinds of molecules
    • Symporter: in same direction
    • Antiporter: in opposite direction (exchanger)
114
Q

What is primary active transport? What is an example?

A

Binds ATP directly. Ex: Na/K ATPase

115
Q

What is secondary active transport? What is an example?

A

Uses ATP indirectly. Uses energy stored in a concentration gradient to move something else against its concentration gradient. Ex: Na/glucose-linked transporter

116
Q

What is the electrical potential difference (Vm)?

A

Voltage of stored energy

117
Q

How are ions subject to chemical (diffusional) force?

A

Diffusion down concentration (chemical) gradient

118
Q

How are ions subject to electrical force?

A

From interaction of ionic charge with charge separation across membrane (electrical gradient)
-opposites attract

119
Q

Electrical & chemical forces are _____ & ______

A

equal & opposite

120
Q

What is the membrane potential? What does it arise from?

A

At the resting membrane potential, no ion species is at its equilibrium potential. Membrane potential (Vm) arises from weighted contributions of each ion’s Ex based on:
1. Ion’s concentration gradient
2. Ion’s permeability

121
Q

How are electrical signals produced?

A

Gated channel opens or closes which changes an ion’s membrane permeability and the resting membrane potential.

122
Q

What is tonic control?

A

Signal is always present, but changes in intenstiy

123
Q

What is antagonistic control?

A

Opposing signals send parameter in opposite directions

124
Q

What is the HPG axis? What is an example?

A

Hypothalamic-pituitary-gonadal axis
GnRH (hypothalamic) –> LH/FSH (pituitary) –> sex hormones (gonads)

125
Q

What is the HPT axis? What is an example?

A

Hypothalmic-pituitary-thyroid axis
TRH (hypothalamic) –> TSH (pituitary) –> thyroid hormones (thryoid)

126
Q

What is the HPA axis? What is an example?

A

Hypothalamic-pituitary-adrenal axis
CRH (hypothalamic) –> ACTH (pituitary) –> cortisol (adrenal cortex)

127
Q

What is long-loop feedback?

A

Peripheral gland secretion inhibits secretion by hypothalamus & anterior pituitary

128
Q

What is short-loop feedback?

A

Anterior pituitary secretion inhibits secretion by hypothalamus

129
Q

What is a primary pathology?

A

Dysfunction of peripheral endocrine gland

130
Q

What is secondary pathology?

A

Dysfunction of pituitary gland

131
Q

What is tertiary pathology?

A

Dysfunction of hypothalamus

132
Q

What are the functional regions of a neuron?

A

Input region: dendrites & soma
Integrative/trigger zone: Initial segment of axon
Conductive region: Axon body
Output region: axon terminal

133
Q

What are the 2 types of electrical signals?

A
  1. Graded potentials
  2. Action potentials
134
Q

What is the purpose of a graded signal?

A

Local signals to carry information from input region to trigger zone.

135
Q

What is the purpose of an action potential?

A

Used for long-distance signals to carry information from trigger zone to axon terminal.

136
Q

What are the characteristics of graded potentials?

A

-Originate in input region due to opening of gated channels
-Decrease in amplitude as they travel
-Carry information to integrative zone
-Can be excitatory or inhibitory

137
Q

What does an excitatory signal do?

A

Depolarize the cell to make it easier to produce an action potential.

138
Q

What does an inhibitory signal do?

A

Hyperpolarize the cell to make it harder to produce an action potential.

139
Q

What is a receptor potential? Is it excitatory or inhibitory?

A

A receptor potential is a graded potential in the input region of a sensory neuron.
-Always excitatory

140
Q

What is an EPSP?

A

An excitatory postsynaptic potential is a graded potential in the input region of an interneuron and motor neuron.

141
Q

What is an IPSP?

A

An inhibitory postsynaptic potential is a graded potential in the input region of an interneuron or motor neuron.

142
Q

What is an EPP? Is it excitatory or inhibitory?

A

An end-plate potential is an excitatory graded potential in the input region of a skeletal muscle.

143
Q

How are amplitude & duration graded in a graded potential?

A

-Directly proportional to triggering stimulus
-Conveys information about stimulus amplitude (intensity) & duration

144
Q

Why do neurons summate graded potentials?

A

A typical neuron receives many inputs which it integrates at the trigger zone to determine whether an action potential is produced.

145
Q

What is temporal summation?

A

Summation of graded potentials from the same source at different times.

146
Q

What is spatial summation?

A

Summation of graded potentials from two or more sources

147
Q

What kind of potenial(s) occur at the trigger zone?

A

Both graded & action

148
Q

What are the characteristics of action potentials?

A

-Long-distance signals
-Rapid depolarization followed by repolarization
-Don’t decrease in amplitude as they travel
-All or none
-Don’t summate
-Regenerated

149
Q

What is a measure of intensity in action potentials?

A

Frequency

150
Q

What is a neuromuscular junction?

A

Synapse between axon terminal of somatic motor neuron & motor end plate of skeletal muscle fiber

151
Q

What occurs at the neuromuscular junction?

A

Neuronal action potential opens voltage-gated Ca2+ channels and allows exocytosis of Acetylcholine from axon terminal

152
Q

Where can nicotinic acetylcholine receptors be found at the neuromuscular junction?

A

Skeletal muscle fiber membrane (sarcolemma)

153
Q

What is the response from Ach release at the neuromuscular junction?

A

Always excitatory - tonic control = signal always “on” with no possibility of inhibition

154
Q

What kind of receptor is nAChR?

A

Ionotropic: binding of ACh allows ion flow to depolarize the sarcolemma

155
Q

What kind of potential is an end-plate potential (EPP)?

A

A graded potential - always excitatory

156
Q

How does EPP potential produce muscle contraction?

A

EPP opens voltage-gated Na+ channels which always produces a sarcolemmal action potential that causes muscle contraction

157
Q

What NT is secreted by the pre-ganglionic neuron in both the SNS & PSNS?

A

Acetylcholine

158
Q

What is the type of receptor found on post-ganglionic neurons in both the SNS & PSNS?

A

Nicotinic AChR

159
Q

What NT does the post-ganglionic neuron of the PSNS secrete?

A

Acetylcholine

160
Q

What NT does the post-ganglionic neuron of the SNS secrete?

A

Norepinephrine

161
Q

What is the type of receptor found on target cells of the SNS?

A

Adrenergic receptors

162
Q

What is the type of receptor found on target cells of the PSNS?

A

Muscarinic

163
Q

What is the relationship between cardiac output and MAP?

A

Incr. CO = Incr. MAP

164
Q

What is the relationship between diameter of arterioles and MAP?

A

Decr. diameter = increase TRP = incr. MAP

165
Q

How does NE change the diameter of arterioles?

A

Most systemic arterioles innervated by SNS neurons which release NE to incr. vasoconstriction through:
-alpha adrenergic receptors
-tonic control

166
Q

What is the relationship between blood volume and MAP?

A

Incr. Blood Volume = Incr. MAP

167
Q

What happens when Epi acts on alpha-adrenergic receptors?

A

Vasoconstriction

168
Q

What are the responses to changes in blood volume in the cardiovascular system and kidneys?

A

Cardiovascular system = rapid
Kidneys = slow

169
Q

What are baroreceptors?

A

Stretch-sensitive, respond to pressure

170
Q

What occurs in the baroreceptor reflex when MAP is too high?

A

An incr. of baroreceptor firing toCVCC due to increase stretch of aorta:
-incr. PSNS to decr. HR
-decr. SNS to cause vasodilation
-overall decrease in CO & MAP

171
Q

What is the intestinal phase?

A

Changes in secretion & motility stimulated by entry of chyme into duodenum

172
Q

What does the presence of fats & proteins do during the intestinal phase?

A

fats & proteins stimulate CCK to stimulate pancreatic enzyme secretion &bile release by gallbladder

173
Q

What is the role of acid in the intestinal phase?

A

Acid incr. secretin to stimulate bicarbonate secretion

174
Q

What do carbohydrates do in the intestinal phase?

A

Carbohydrates stimulate incretins to stimulate insulin secretion

175
Q

What happens to the activity of the stomach during the intestinal phase?

A

Gastric motility & acid secretion inhibited by ENS, secretin, CCK, and incretins

176
Q

What does it mean that embryonic structures are bipotential?

A

Can develop into either female or male form

177
Q

What determines if our embryonic structures are female vs. male?

A

-If no Y chromosome, then develop as female
-If Y chromosome, the presence of SRY gene causes development of testis

178
Q

What do the testis secrete in embryonic structures?

A

-Anti-Mullerian hormone
-Testosterone (from DHT)

179
Q

What happens in the HPG axis in both males and females?

A

Hypothalamus secretes GnRH which stimulates anterior pituitary to secrete the gonadotropins FSH & LH

180
Q

What does LH (luteinizing hormone) do?

A

Sex steroid hormone secretion by gonads

181
Q

What does FSH (follicle stimulating hormone) do?

A

Gametogenesis

182
Q

What sex steroids do both sexes produce?

A

-Androgens: Testosterone & DHT
-Estrogens: Estradiol (E)
-Progestins: Progesterone (P)

183
Q

What is aromatase?

A

Both ovaries and testes have aromatase which is an enzyme that converts T to E

184
Q

What does LH do in the male gonads?

A

Activates Leydig cells to secrete testosterone

185
Q

What does FSH do in the male gonads?

A

Activates Sertoli cells to secrete paracrines that increase spermatogenesis & secrete ABP to keep T from diffusing away

186
Q

What is the negative feedback loop present in the male gonads?

A

Incr. Testosterone decreases GnRH, LH, and FSH

187
Q

What does the menstrual cycle include?

A
  1. Ovarian cycle = changes in follicles of ovary
  2. Uterine cycle = changes in uterine lining
188
Q

What is the menses phase of the uterine cycle?

A

If pregnancy is not achieved, shed endometrium which causes bleeding from uterus

189
Q

What is the proliferative phase of the uterine cylce?

A

Endometrium thickens in preparation for pregnancy

190
Q

What is the secretory phase of the uterine cycle?

A

Endometrial secretions promote implantation

191
Q

What happens during the follicular phase of the ovarian cycle?

A

-Development of follicle cells
-Granulose cells proliferate and secrete estrogen
-Maturation of oocyte

192
Q

What happens during the ovulation phase of the ovarian cycle?

A

Mature follicle bursts releasing oocyte

193
Q

What happens during the luteal phase of the ovarian cycle?

A

-Ruptured follicle develops into corpus luteum
-Secretes progesterone & some estrogen to prepare for pregnancy

194
Q

What does LH do in the female gonads?

A

LH tells thecal cells to secrete androgens that diffuses into granulosa cells, where aromatase converts into estrogen

195
Q

What does FSH do in the female gonads?

A

FSh increases follicular development with help from the granulosa cells producing estrogen

196
Q

What does the corpus leuteum do?

A

Secretes progesterone & some estrogen

197
Q

What is the negative feedback loop in the female gonads?

A

An increase in E&P causes a decrease in GnRH, LH, and FSH

198
Q

What does persistent high estrogen cause?

A

Switches to positive feedback and causes ovulation

199
Q

What occurs during days 0-7 of the menstural cycle?

A

-Ovarian cycle: early follicular phase
-Uterine cycle: menses
-Hormones:
- FSH & LH increase
- Estrogen = low GnRH, LH, FSH

200
Q

What occurs during days 7-14 of the menstural cycle?

A

-Ovarian cycle: Late follicular phase (follicular matures)
-Uterine cycle: Proliferative phase
-Hormones:
- Increased E changes to positive feedback to cause LH surge to trigger ovulation

201
Q

What happens on day 14 of the menstrual cycle?

A

-Follicle ruptures and releases oocyte
-Thecal & granulosa cells start to become luteal cells

202
Q

What happens days 14-21 of the menstural cycle?

A

-Ovarian Cycle: early luteal phase - corpus luteum develops
-Uterine cycle: secretory phase
-Hormones:
- Corpus luteum secretes P & E which decreases GnRH, LH, & FSH

203
Q

What happens days 21-28 of the menstrual cycle if no pregnancy?

A

-Ovarian Cycle: late luteal phase - corpus luteum degenerates & ceases hormone production
-Uterine cycle: secretory phase
-Hormones:
- lack of P from corpus luteum = death of endometrium
- FSH & LH secretion resume

204
Q

What happens if fertilization occurs?

A

-Fertilized egg implants in endometrium
-Placenta develops & secretes hCG to maintain corpus luteum

205
Q

Why must the corpus luteum be maintained in the beginning of pregnancy?

A

Corpus luteum continues secretion of progesterone & estrogen - critical for maintaining pregnancy, but placenta eventually takes over progesterone production

206
Q

What are oral contraceptives & what they do?

A

Synthetic estrogen & progesterone to decr. GnRH, LH, and FSH to prevent follicle maturation & ovulation

207
Q

What is the function of the immune system?

A

-Protect body from pathogens
-Remove dead & damaged cells
-Remove “abnormal self” cells

208
Q

What are the immune cells?

A

Leukocytes (white blood cells)

209
Q

What are immunogens?

A

Anything that triggers immune response

210
Q

What is an allergy?

A

Overeactive immune response

211
Q

What is an autoimmune disease?

A

Incorrect immune response

212
Q

What is immunodeficiency?

A

Lack of immune response

213
Q

How do cells distinguish self vs. non-self cells?

A

Cell surface molecules

214
Q

What are self-markers?

A

-Major histocompatibility complex on nucleated cells
-ABO & Rh blood types on RBCs

215
Q

What are non-self markers?

A

Antigens are molecules that trigger immune response that bind to pattern recognition receptors on leukocytes

216
Q

What antibodies do we have in our plasma for blood typing?

A

Have antibodies in plasma to any antigen that is not on our RBCs

217
Q

What antigens does someone with type O blood have?

A

O antigens (recessive)

218
Q

What happens if matching antigens & antibodies mix?

A

Blood cells clump

219
Q

When considering blood transfusions, what do you need to know about the recepient?

A

What antibodies they have in plasma

220
Q

When considering blood transfusions, what do you need to know about the donor?

A

Antigens on donor RBCs

221
Q

What are the 3 lines of defense against pathogens?

A
  1. Barriers
  2. Innate immune response
  3. Adaptive Immune response
222
Q

What is the barriers line of defense?

A

skin, mucous membranes

223
Q

What is the innate immune response?

A

-non, specific & rapid

224
Q

What is the adaptive immune response?

A

-B cells & T cells
-Slow
-Specificity: recognize & react to one antigen only

225
Q

What is immunological memory?

A

For stronger & quicker response (acquired immunity) to subsequent exposures

226
Q

How does the innate immune response remove dead & damaged cells?

A

Macrophages = primary scavenger

227
Q

How does the innate immune response kill cells?

A

create pores in target cell membrane to kill it

228
Q

How does the innate immune response use phagocytosis?

A

-Requires receptor binding
-may be assisted by antibodies
-target ingested and destroyed with lysosomal enzymes
-by phagocytes

229
Q

What is inflammation?

A

Nonspecific reaction of immune system to foreign invader, part of innate immune response

230
Q

How does inflammation occur?

A

-Mast cells secrete histamine which causes vasodilation to incr. blood flow causing redness & heat
-an incr. in capillary permeability allows proteins to enter the ISF causing edema & pain
-macrophages secrete cytokines which attract neutrophils

231
Q

How does the innate immune response activate T cells?

A

-Antigen fragment is presented within self marker
-Performed by antigen-presenting cells

232
Q

What do the the antigen-presenting cells (APC) do in the innate immune response?

A

-Dendritic cells = most important APC for initiating adaptive immune response

233
Q

What cells are involved. inthe adaptive immune response?

A

-B cells, cytotoxic T cells, helper T cells

234
Q

What does a correct match between antigen & receptor of the adaptive immune system do?

A

Activated cell to divide rapidly = clonal expansion

235
Q

What are the cells that emerge from clonal expansion?

A

Effector cells (plasma cells) & memory cells

236
Q

What is the primary response (first exposure to antigen) from the adaptive immune response?

A

-Initial response is slow
-Clonal expansion produces effector & memory cells

237
Q

What is the secondary immune response (subsequent exposure) from the adaptive immune response?

A

-Due to memory cells, clonal expansion is more rapid allowing for a quicker, stronger response

238
Q

What do B-cells do?

A

-Provides antibody-mediated immunity
-extracellular pathogens

239
Q

What does activation of B cells require?

A

-binding to antigen
-cytokines from helper T cell

240
Q

What do plasma cells do?

A

Secrete antibodies that attack to pathogen to tag them for phagocytosis

241
Q

What do cytotoxic T cells do?

A

-Provides cell-mediated immunity
-Intracellular pathogens
-attack abnormal cells by creating membrane pores in target cell

242
Q

What does activation of cytotoxic T cells require?

A

-Binding to matching antigen on APC
-Cytokines from helper T cell

243
Q

What do Helper T cells do?

A

-Secrete cytokines
-Crucial in activating B cells and cytotoxic T cells

244
Q

What does activation of helper T Cells require?

A

-Binding to matching antigen on APC

Human Physiology (10 decks)

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