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Bioscience 2 > Midterm > Flashcards

Midterm Flashcards

1
Q

Functions of the Conduction Zone

A

warm, humidify and filter air

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2
Q

Types of pnuemocyte

A

Type 1 - squamous epithelium

Type 2 - Produces surfactant

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3
Q

Atmospheric Pressure

Patm

A

-0 mmHg

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4
Q

Alveolar Pressure Palv

A

-must be negative (lower than Patm) during inspiration and higher during expiration

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5
Q

Transmural pressure

A

Palv - Pip

  • the pressure difference across the alveolar wall
  • as this increases alveoli size increases
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6
Q

Intrapleural Pressure Pip

A
  • usually negative and keeps alveoli inflated
  • decreasing this pulls on the alveoli increasing the volume
  • change is generated by muscles
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7
Q

Compliance

A

delta V / delta P

with a lowered compliance you need to muscular work harder to breathe

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8
Q

Elasticity

A

Delta P / Delta V

-if lowered you need to work harder to exhale

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9
Q

What does surfactant do?

A
  • inserts itself between water molecules and reduces surface tension
  • increased lung V, surfactant spreads out and increases surface tension
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10
Q

Dynamic Compression

A

During forced expiration Pip becomes positive

  • if Pip exceeds airway pressure than airways can narrow/collapse
  • Pursed-lip breathing increases Palv to counter act this
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11
Q

What can cause Bronchiolar Smooth Muscle Constriction

A
  • histamine
  • PNS stimulation
  • decreased PCO2
  • expiration
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12
Q

What can cause Bronchiolar Smooth Muscle Relaxation

A
  • epinephrine (Beta2 stim)
  • increased PCO2
  • inspiration
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13
Q

Inspiratory Reserve Volume

A

Top of TV to max inspiratory effort

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14
Q

Inspiratory Capacity

A

TV + IRV

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15
Q

Expiratory Reserve Volume

A

-low point of TV to the most they can expire

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16
Q

Residual volume

A

-gas that is left in the lungs that cannot be exhaled

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17
Q

Total Lung Capacity

A

IRV + TV + ERV + RV

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18
Q

Functional Residual Capacity

A

ERV + RV

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19
Q

FEV1

A

forced expiratory volume in 1 second

-should be 80% of FVC

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20
Q

Minute Ventilation

A

TV x f

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21
Q

Dead Space

A

volume of gas that fills conducting airways and doesn’t do gas exchange

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22
Q

Composition of Alveolar gas and pulmonary veins

A

100 mmHg of O2

40 mmHg of CO2

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23
Q

Composition of gas in pulmonary arteries and peripheral veins

A

40 mmHg of O2

46mmHg of CO2

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24
Q

Intrapulmonary Shunt

A

-perfusion w/o Ventilation

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25
Q

Alveolar Dead space

A

Ventilation without perfusion

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26
Q

Right shift of Oxygen Hemoglobin Dissociation curve

A
  • increased PCO2
  • Increased H+ ion
  • increased Temp.
  • exercise
  • hemoglobin is giving up more O2 more readily
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27
Q

How does anemia affect the O2 hemoglobin dissociation curve

A

-anemia lowers the O2 carrying capacity of the blood and the O2 content, but not the O2 saturation

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28
Q

Buffering of H+ ions in venous blood

A

???

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29
Q

Dorsal Respiratory Group

A
  • connects with skeletal muscle motor neurons
  • active during inspiration
  • sensitive to opiates
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30
Q

Pneumotaxic Center

A
  • provides inhibitory input to the DRG

- active during expiration, allows DRG to shut off Relaxes muscles

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31
Q

Apneustic Center

A
  • signals the DRG to delay the inhibitory input by the PC
  • gives positive impulses to inspiratory neurons
  • prolongs inspiration
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32
Q

Ventral Respiratory Group

A

-active during forced expiratory

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33
Q

Stretch Receptors in the lung

A

-found in airways and responsible for the Hering-Breuer reflex

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34
Q

Hering-Breuer reflex

A

too big of inspiration=too much stretch and inhibits DRG so you don’t continue to inspire

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35
Q

Irritant Receptors in the lungs

A
  • increases rate

- decreases TV

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36
Q

Juxtacapillary Receptors

A
  • in alveolar walls
  • sensitive to excess fluid
  • increased rate and decreased TV
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37
Q

Peripheral Chemoreceptors

what do they monitor and rxn

A

aortic and carotid bodies

  • monitor arterial PO2, H+, and CO2
  • decreased PO2 = increased rate and depth
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38
Q

Central Chemoreceptors

what do they monitor and rxn

A

in respiratory centers in brain stem

  • sensitive to CSF H+
  • increased H+ = increased rate and depth
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39
Q

How does exercise affect PCO2 and PO2

A

doesn’t change during mild to moderate exercise

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40
Q

What happens at anaerobic threshold

A

-arterial PCO2 decreases
-production of lactic acid decreases pH
-

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41
Q

Restrictive Dysfunction = ???

A

Volume Limitation

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42
Q

Obstructive Disease = ????

A

Flow limitation

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43
Q

What is the key method to determine the type of limitation for lung disease?

A

ratio of FEV1 to FVC

  • restrictive disease ratio doesn’t change much
  • obstructive disease the ratio decreases
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44
Q

Flow Volume loops and disease?

A
  • obstructive disease = scooped out shape

- restrictive disease = smaller overall

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45
Q

What does COPD include

A
  • pulmonary emphysema
  • chronic bronchitis
  • asthma
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46
Q

Symptoms of COPD

A
  • chronic cough
  • expectoration of mucus
  • wheezing
  • Dyspnea on exertion
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47
Q

Characteristics of COPD

A
  • inflammation of smaller airways
  • increase mucus production
  • decreased mucous clearance
  • thickened mucous
  • tissue destruction
  • bronchial smooth muscle spasm
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48
Q

Definition of Chronic bronchitis

A

-sputum producing cough on most days for 3 months during 2 consecutive years

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49
Q

Emphysema

A
  • tissue destruction (alveoli and capillaries)
  • decreased elasticity
  • flattening of diaphragm
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50
Q

Cause of alpha 1 antitrypsin deficiency

A

smoking

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51
Q

Asthma

A

reversible airway obstruction caused by smooth muscle spams, inflammation of mucosa and hyper secretion of mucus

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52
Q

Extrinsic asthma?

A
  • most common

- reaction to allergens

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53
Q

Intrinsic asthma

A

-exposure to cold or air pollution

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54
Q

Asthma Mechanism

A

in response to triggers, mast cells, eosinophils, and macrophages release inflammatory mediators

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55
Q

Bonchiectasis

A
  • abnormal dilation of medium sized bronchi

- Obstructive disease

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56
Q

Cystic Fibrosis

A
  • Obstructive Disorder
  • structural damage and increase mucus production
  • liver cirrhosis
  • decreased pancreatic secretions
  • 36.8 median life expectancy
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57
Q

Restrictive Lung Dysfunction

A
  • disorder of Compliance in either the chest wall or the lungs or both
  • decreased TV, increased Rate
  • work of breathing can increase to 25% resting energy
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58
Q

How do corticosteroids work?

A

-blocks release of arachidonic acid from epithelial cells which blocks production of pro-inflammatory agents

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59
Q

What is corticosteroids used for?

A

drug of choice in mild to moderate asthma

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60
Q

Sympathomimetics

A

epinephrine and ephedrine

  • cause peripheral vasoconstriction
  • tachycardia
  • bronchodilation
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61
Q

Parasympatholytics

A
  • anticholinergics that block the binding of acetylcholine to post synaptic membrane
  • spiriva
  • no improvement in survival
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62
Q

Diaphysis

A
  • shaft of the bone
  • compact bone
  • contains marrow cavity
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63
Q

Epiphysis

A
  • head of the bone

- spongy bone

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64
Q

Metaphysis

A
  • area of shaft that widens towards epiphysis

- spongy bone

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65
Q

Compact Bone

A
  • dense and rigid

- functional unit is the osteon

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66
Q

Osteon

A
  • made of osteocytes arranged in concentric layers
  • osteocytes are in extracellular fluid spaces called lacunae
  • 4-20 layers surrounding a Haversian canal
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67
Q

Lacunae

A

osteocytes contained in small extracellular fluid filled spaces

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68
Q

Canaliculi

A

-protrude from lacunae and penetrate the surrounding calcified matrix

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69
Q

Haversian canal

A

contains blood vessels that carry nutrients and wastes to canaliculi

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70
Q

Spongy bone

A
  • primary component of the interior of bones

- made of spicules lined with osteogenic cells

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71
Q

Osteogenic cells

A
  • differentiate into osteoblasts
  • active in growing bone
  • may become activated in adults during fracture or worn out bone
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72
Q

Osteoblasts

A
  • modified fibroblasts
  • make the bone
  • synthesize and secrete organic matrix during ossification
  • calcification of matrix during mineralization
73
Q

Osteocytes

A
  • mature bone cells
  • active in transfer of minerals from interior bone to growth surfaces
  • transfer of Ca and minerals back and forth between blood and organic matrix
74
Q

Osteoclasts

A
  • derived from monocytes
  • break down the organic matrix during bone resorption
  • release calcium from matrix into blood
75
Q

Describe the organic matrix of bones

A
  • synthesized and secreted by osteoblasts
  • made of type 1 collagen, proteoglycans and glycoproteins
  • called osteoid in unmineralized state
76
Q

Describe the inorganic component in matrix

A
  • hydroxyapatites

- calcium phosphates/ flouride/ hydroxide

77
Q

What are the 5 steps of bone growth

A
  1. Bone Collar Forms
  2. Cavitation of hyaline cartilage
  3. Invasion of periosteal bud
  4. Continuation of ossification and medullary cavity
  5. Ossification of epiphysis
78
Q

Bone Collar formation

A
  • periosteum forms, contains osteogenic cells
  • osteogenic cells differentiate into osteoblasts
  • these secrete osteoid against the shaft
79
Q

Cavitation of Hyaline cartilage

A
  • occurs in the middle of the diaphysis
  • chondrocytes stop secreting collagen and mineralization starts
  • chondrocytes die creating cavity
80
Q

Invasion of periosteal bud

A

periosteal bud invades primary ossification center and forms blood/lymphatic vessels and nerves
-brings hematopoietic cells, oblasts, oclasts into cavity

81
Q

Continuation of ossification center

A
  • Oblasts use matrix to lay down osteoid forming bony trabeculae
  • Oclasts break down trabeculae enlarging cavity
  • secondary ossification occurs at epiphysis
82
Q

Ossification at epiphysis

A
  • this is how bones grow

- cartilage continues to proliferate but eventually stops and ossification ocurs

83
Q

Describe the process of epiphyseal plate becoming bone

A
  • chondrocytes increase in number
  • older chondrocytes hypertrophy, the matrix becomes calcified
  • calcification leads to chondrocyte death and matrix deteriorates
  • oblasts secrete osteoid
  • mineralization of osteoid and bone forms
84
Q

Nutrition important for bone growth

A
  • Calcium
  • Vitamin D
  • Vitamin C
85
Q

Hormones for bone growth

A
  • Growth hormone stimulates liver to produce IGF 1 to grow
  • Insulin
  • thyroid hormone
  • testosterone and estrogen
86
Q

Describe the palace of oblasts and oclasts

A
  • osteoclasts express RANK receptor
  • Oblasts secrete protein RANKL
  • Oblasts also secrete osteoprotegerin an inhibitor of RANKL
  • binding of RANKL to RANK activates oclasts and keeps them alive
87
Q

Describe menopause’s effect on osteoclasts

A
  • before=estrogen limits amount of RANKL produced by Oblasts and osteoprotegerin dominates
  • after=RANKL increases which increases osteoclast function
88
Q

What contributes to Ca homeostasis

A
  • PTH
  • calcitonin
  • Vitamin D
  • kidneys
  • GI system
89
Q

Describe Calciums effect on PTH

A
  • there are calcium receptors on the PT gland

- when Ca decreases PTH production increases

90
Q

What does increased PTH do?

A
  • differentiates Oblasts to Oclasts
  • increases Oclast activity
  • Ca reabsorption in kidney and decreased Ca excretion in urine
  • GI absorbs more Ca
91
Q

What are the effects of calcitonin on Ca

A
  • calcitonin is secreted by parafollicular cells of the thyroid
  • the stimulus is high Ca concentration
  • inhibits the release of Ca from bone
  • decreases renal reabsorption of Ca
92
Q

Vitamin D

A

-very high levels in fish liver oil
-fatty fish
-eggs
beef liver

93
Q

Hypocalcemia

A
  • increased neuronal excitability
  • Trousseaus and Chvosteks sign
  • neuromuscular instability
  • death
  • fatigue
  • anxiety
  • dental problems
94
Q

Hypercalcemia

A
  • depressed neuronal excitability
  • decreased reflexes
  • brady cardia
  • most common cause is PTH dyfunction
95
Q

Treatment of a fracture

A
  • reduction
  • immobilization
  • restoration of function
96
Q

What are the 4 stages of fracture healing

A
  • hematoma formation
  • Fibrocartilaginous callus formation
  • Bony Callus Formation
  • Remodeling
97
Q

Describe the Hematoma Formatoin

A
  • starts first 1-2 days
  • hematoma develops from injured blood vessels
  • a large clot forms days 2-5
  • invasion of new blood vessels and early fibrosis begins
98
Q

Describe the Fibrocartilaginous Callus formation

A
  • soft tissue callus
  • fibroblasts and osteoblasts go into fracture and secrete collage
  • osteoblasts deposit osteoid
  • collar forms around fracture site
  • reaches max girth 2-3 weeks
  • stable fracture but not load bearing
99
Q

Describe the bony callus formation

A
  • ossification of matrix 3-4 weeks
  • spongy bone initially forms
  • radiographic union cast can be removed sometimes
100
Q

Describe the remodeling phase

A
  • osteoclasts resorb dead and excess bone
  • reestablish medullary canal
  • compact bone replaces spongy bone
101
Q

Timeline for fracture healing

A

kids 4-6 weeks
adolescents 6-8 weeks
adults 10-18 weeks

102
Q

Osteomyelitis

A

-bacterial infection of bone

103
Q

Routes of infection for osteomyelitis

A
  • hematogenous = blood borne
  • contiguous = infection that spread from adjacent tissues
  • exogenous = direct traumatic intro from external environment
104
Q

Hematogenous osteomyelitis

A
  • more likely in children and sick adults

- staphylococcus aureus

105
Q

Sequelae

A

pus limits blood flow to bone and starts necrosis

-fragmentation occurs separating from blood supply

106
Q

Sequestra

A

devascularized necrotic bone fragments

107
Q

Involcrum

A

new bone that forms around sequestra

108
Q

Tuberculosis

A

infects bone from lungs or lymph

-most common in vertebrae and long bones

109
Q

Osteonecrosis

A

-bone death from fracture, thrombus, embolism, infection, vascular compression

110
Q

What is the most common consequence of metastatic bone disease

A

-hypercalcemia - decreased excitability

111
Q

DXA scan and values

A

comapres BMD to BMD of 30 y/o
> 1 SD below = osteopenia
>2-2.5 = osteoporosis

112
Q

Type 1 osteoporosis

A

caused by menopausal estrogen deficiency

  • primarily spongy bone
  • vertebrae and radial fractures
113
Q

Type 2 Osteoprosis

A
  • senile, occurs with aging
  • both spongy and cortical bone lost
  • hip, long bone, and vertebrae
114
Q

Biphosphonates

A

-inhibit osteoclast activity

115
Q

Selective estrogen receptor modulators

A

-raloxifene

116
Q

Antigen

A

substance foreign to the host which can stimulate an immune response
-bacteria, pollen

117
Q

Epitope

A

the immunologically active sites on antigens

-the portion of the antigen that interacts with the antibody

118
Q

Major Histocompatibility Complex Molecules

A

-self recognition molecules on the surface of nucleated cells

119
Q

Cytokines

A

proteins made during an immune response that regulate leukocytes

120
Q

What is the second line of defense mechanism

A

inflammatory response initiated by tissue injury

121
Q

How does vasodilation help with inflammatory response

A

-enhances delivery of neutrophils and monocytes

122
Q

How does chemotaxis help with inflammatory response

A

WBCs are attracted to injured tissues

123
Q

What happens when complement is activated?

A
  • 5 complement proteins form a complex called the (MAC) that inserts itself into membrane of bacteria and creates a pore that causes cell lysis and death
  • enhances other inflammatory responses
  • can act as opsonizing agent enhancing phagocytosis
124
Q

Specific Immune Defense

A

-typically against bacteria, viruses, and non-microbials

125
Q

Antibodies

A

proteins in the serum

-contain a Y shaped variable that determine specificity to antigen

126
Q

Where are antibodies found?

A
  • surface of lymphocytes

- soluble antibodies are produced by plasma cells

127
Q

IgA

A
  • 15% of antibodies
  • found in body secretions
  • protect against microbes
128
Q

IgD

A
  • .2%

- found on surface of immature B lymphocytes

129
Q

IgE

A
  • capable of triggering the most powerful immune response

- binds to mast cells

130
Q

IgG

A
  • 75%
  • most abundant
  • can cross placenta
  • activates complement
131
Q

IgM

A
  • 10%

- potent complement activator

132
Q

Describe the antibody mediated immune response

A
  • antigen enters blood
  • recognized by B lymphocyte, and antigen binds to antibody
  • antigen encounters macrophages and processes and is presented on the surface of the macrophage in a complex with class 2 MHC proteins
  • macrophage presents antigen complex to CD4+ Cell
  • antigen presenting cell and helped T cell triggers release of cytokines which trigger
133
Q

Memory cells

A

ensure a more rapid response when re-exposed to antigen

134
Q

What happens when a soluble antibody binds to an antigen?

A
  • the antibody acts as a opsonizing agent to link phagocytes to antigen
  • activates complement and MAC kills cells to which antibody is attached
135
Q

Active immunity

A
  • due to formation of memory cells
  • developed by natural infection
  • vaccination
136
Q

Passive Immunity

A

-due to direct transfer of antibodies by
injection
placenta
breast milk

137
Q

What mediates the Cell Mediated Immune Response?

A
  • CD8+ or Cytoxic T cells in the lymphoid tissues

- they respond to virus and cancer cells

138
Q

Immunodeficiencey

A

abnormality in the immune system that makes a person susceptible to disease that are normally preventable

139
Q

Hypersensitivity/Allergic Disorders

A

an immune system in which responses to an environmental antigen causes inflammation and tissue damage

140
Q

Acquired Immunodeficiency Syndrome

A

-Human immunodeficiency virus selectively attacks CD4+ lymphocytes and macrophages

141
Q

IgE mediated disorder (type 1 hypersensitivity)

A
  • immediate response within 5 mins

- allergic reaction

142
Q

Antibody Mediated Disorder (type 2 hypersensitivity)

A

-ABO or Rh

143
Q

Immune Complex Allergic Disorder (type 3 hypersensitivity)

A

-soluble antibody binds to antigen forming insoluble complex

144
Q

Cell Mediated Hypersensitivity Disorder (Type 4)

A
  • delayed hypersensitivity

- against TB or viruses

145
Q

NRTI

A
  • zidovudine or Retrovir

- can cause myopathy

146
Q

NNRTIs

A
  • Sustiva

- nausea and skin reactions

147
Q

Protease inhibitors

A
  • Invirase

- hyperglycemia, thrombophlebitis

148
Q

Fusion inhibitors

A

Fuzeon

149
Q

Where is the liver located?

A

Upper right Quadrant

-not palpable

150
Q

Describe the lobule of the liver

A
  • functional unit of the liver
  • a branch of the hepatic vein is at the center of each lobule
  • at each corner is bile duct, hepatic artery and portal vein
151
Q

Kuppfer cells

A
  • macrophagges in sinusoid

- consume RBC, bacteria

152
Q

Stellate cells

A
  • fat storing cells in the perisinusoidal space
  • storage of Vitamin A
  • regeneration after injury, deposit collagen and can cause cirrhosis
153
Q

In the liver cells farthest from the central vein…

A

are most oxygenated

-involved in AA, gluconeogensis, and bile formation

154
Q

In the liver cells closest to the central vein…

A
  • least oxygenated,

- involved in glycolysis, lipogenesis, and drug metabolism

155
Q

What supplies blood to the liver?

A

hepatic portal vein (60-70%)

-hepatic artery

156
Q

Biotransformation

A

-modification of substances from the blood to return to circulation or excrete to bile

157
Q

Filtration

A

-done by kuppfer cells

158
Q

The liver and CHO metabolism (2)

A
  • the liver stores glucose as glycogen, and can then break down to maintain blood sugar.
  • Converts CHO to triglycerides for storage in tissues
159
Q

What does the Liver do during fasting?

A

-synthesizes glucose from AA or LA (gluconeogenesis)

160
Q

The liver and lipid metabolism

A
  • almost all fat synthesis from CHO and protein occurs in liver
  • synthesis of cholesterol, phospholipids occurs in liver
161
Q

The liver exports cholesterol in what 2 forms?

A
  • used to synthesize bile acids

- enters the blood as VLDL

162
Q

Transamination

A
  • how the liver metabolizes proteins

- transfer amino group to an ketoacid which allows AA to gluconeogenesis, and lipid synthesis

163
Q

Bilirubin

A

-a product of breakdown of RBC

164
Q

Describe the process of the breakdown of bilirubin

A
  1. hemoglobin is broken down into biliverdin and then converted to free bilirubin and binds with albumin
  2. converted to conjugated bilirubin in liver
  3. exported to bile (soluble)
165
Q

Jaundice

A
  • yellow discoloration of skin and sclera of eye

- excess plasma bilirubin

166
Q

What can cause Jaundice

A
  • excessive RBC lysis
  • decreased hepatic BF
  • limited conjugation of bilirubin
  • obstruction of bile ducts
167
Q

What does bile do?

A

-excretion of bilirubin and cholesterol
-promotes digestion and absorption of lipids
-emulsify lipids to be absorbed
-

168
Q

What does the gallbladder do?

A

concentrates bile salts, bilirubin, and cholesterol by as much as 10-20 X

169
Q

What is cholestasis

A
  • the suppression of bile secretion backed up into the systemic circulation
  • caused by cirrhosis
170
Q

Cholecystitis

A
  • inflammation of the gallbladder

- partial or complete obstruction of cystic or common duct

171
Q

Signs of cholecystitis

A
  • RUQ pain, muscle spasm and vomiting after a meal

- Jaundice 25%

172
Q

Cholelithiasis

A
  • too much cholesterol with too little bile salts

- leads to bile stasis and formation of stones

173
Q

Hepatitis that are fecal-oral transmission

A

A, E

174
Q

Hep A

A
  • young children

- RNA virus

175
Q

Hep B

A
  • DNA virus

- transmitted through body fluids

176
Q

Hep C

A
  • most common cause of liver disease, cirrhosis

- usually asymptomatic

177
Q

Pancreatitis

A
  • release of enzymes into pancreas and tissues

- usually caused by alcohol abuse

178
Q

Where are antibodies found?

A
  • surfaces of B lymphocytes (receptors)

- circulate in plasma

Bioscience 2 (2 decks)

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