BIOL intro to mircobiology Flashcards

1
Q

what is a virus?

A

a virus is an nucleic acid (RNA or DNA) surrounded by a coat of protein; it cannot reproduce or carry out metabolic activities outside of a host cell

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2
Q

how do viruses pick their target?

A

by specific receptors that are present of the surface of the target cell; ex. CD4 receptors

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3
Q

host range

A

the number of species that a virus can infect; usually not many but can be

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4
Q

what do viruses bind to host cell by?

A

viral glycoproteins that attach to CD4 receptors

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5
Q

5 steps in viral replication cycle

A

attachment, entry, synthesis, assembly, and release

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6
Q

virus attatchment

A

the virus attaches to a protein on the surface of the host cell

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7
Q

virus entry

A

after attachment, the virus can enter the host cell (either the virus of only the genetic information)

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8
Q

virus synthesis

A

entry of the viral nucleic acid can begin synthesis which causes copies of the viral information and proteins to be made

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9
Q

virus assembly

A

the viral DNA and proteins are packed together to create a new virus (called self-assembly of new virus particles)

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10
Q

virus release

A

the virus exits the cell

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11
Q

what occurs once the viral nucleic acid is inside the cell?

A

transcription and translation and DNA synthesis

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12
Q

forms of viral nucleic acid

A

can be RNA, DNA, and either single or double stranded

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13
Q

what is the result of transcription and translation?

A

capsomeres or other proteins

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14
Q

what is the result of DNA synthesis?

A

more copies of the DNA

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15
Q

what is the result of transcription and translation along with DNA synthesis?

A

causes new viruses to assemble

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16
Q

nucleic acid of HIV

A

two single strands of RNA

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17
Q

capsid

A

a protein shell surrounding the virus; present in HIV virus and is coffin shaped

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18
Q

envelope

A

additional protein coating that occurs when a virus has taken some of the host cell’s plasma membrane, using it for further protection

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19
Q

protease

A

enzyme in HIV virus that helps digest proteins

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20
Q

intergrase

A

enzyme found in HIV virus that helps to insert the viral genome into host cells

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21
Q

proteins found inside HIV virus?

A

gp120 and gp41

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22
Q

gp120

A

glycoprotein in HIV virus that is involved in the attachment of the virus to CD4 receptors to bind to helper T cells

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23
Q

gp41

A

glycoprotein in HIV virus that is required for entry into the cell

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24
Q

reverse transcriptase

A

an enzyme in HIV virus that takes the single strand RNA and converts it to double-stranded DNA

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25
Q

how does attatchment occur for HIV virus?

A

via gp120 and gp41 proteins to CD4 receptors on helper T cells

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26
Q

how does HIV virus enter the host cell?

A

when the viral envelope and the host plasma membrane fuse together, allowing for entry and for the capsid to release RNA into the host cell

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27
Q

what happens when the HIV virus enters the host cell?

A

reverse transcriptase enzyme is activated and this converts ssRNA into dsDNA,; integrase then deposits this into the host cell chromosomes

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28
Q

what releases RNA in the HIV virus?

A

the capsid

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29
Q

how does synthesis occur for the HIV virus?

A

host DNA is made to RNA, then transcription creates new viral proteins (integrase, protease, etc.); DNA synthesis also occurs, making more genome RNA

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30
Q

how does assembly occur for HIV virus?

A

copies of the viral genome (RNA) are packaged with proteins in a vesicle

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31
Q

how do the nucleic acid materials exit in the HIV virus?

A

via getting packaged into a vesicle and sent outside the cell; within the vesicle the proteins develop into functional components, specifically protease

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32
Q

what makes up the vesicle in the HIV virus?

A

RNA and mRNA

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33
Q

transcription

A

produces proteins

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34
Q

translation

A

produces mRNA (or tRNa, rRNA, or non-coding RNA)

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35
Q

why is AIDs recovery not possible?

A

because the helper T cells are being destroyed

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36
Q

primary infection or first phase of HIV

A

flu like symptoms including fever, fatigue, weight loss, diarrhea, aches, and headaches; during this phase HIV and antibody concentration is increasing in the blood, but helper T cell population is declining

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37
Q

second stage of HIV

A

immune system starts to kick in, so there is an increase in antibodies and a slight decrease in viral cells; this stage can occur for years

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38
Q

third stage of HIV

A

HIV virus is increasing in the blood while T cells and antibody levels are decreasing

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39
Q

fourth stage of HIV

A

AIDS is present; the beginning of the decline and T cells and antibody levels are declining rapidly

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40
Q

fifth stage of HIV

A

AIDS is present, virus continues to increase and there is no immune response; due to this opportunistic infections will persist eventually causing death

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41
Q

AIDS definition (4 criteria)

A

the presence of several opportunistic infections; the presence of interferon induced by HIV virus; severely low numbers of helper T cells and CD4 cells; and a positive test for HIV virus

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42
Q

what is the extended stage of HIV called?

A

clinical latency

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43
Q

how does penicillin act?

A

it destroys the cell wall, allowing the bacteria to become susceptible to osmosis drives, causing the cell to shrivel or burst

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44
Q

what drugs inhibit cell protein synthesis?

A

aminoglycerdies, tetracyclines or macrolides

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45
Q

common mechanisms of antimicrobial action (6)

A

inhibition of cell wall synthesis, inhibition of protein synthesis, disruption of cytoplasmic membrane, inhibition of general metabolic pathway, inhibition of DNA or RNA synthesis, and inhibition of pathogen attachment to the host cell

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46
Q

what drug disrupts cytoplasmic membrane?

A

polymyxins or polyenes

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47
Q

what drugs inhibit the general metabolic pathway?

A

sulfonamides, trimethoprim, or dapsone

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48
Q

what drugs inhibit DNA or RNA synthesis?

A

actinomycin or nucleotide analogs

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49
Q

what drugs inhibit the pathogen to attach to the host cell?

A

arildone or pleconaril

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50
Q

what mechanisms of antimicrobial action can be dangerous to humans

A

inhibition of protein synthesis, inhibition of RNA/DNA synthesis, inhibition of general metabolic pathway, and disruption of cell membrane; this is because humans share all these characteristics with microorganisms

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51
Q

spectrum of action

A

the range of organisms a particular antimicrobial drug can affect; can be narrow-spectrum drugs or broad spectrum drugs

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52
Q

narrow spectrum drugs

A

will only affect a small or single amount of species

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53
Q

example of narrow spectrum drugs

A

penicillin or polymyxin

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54
Q

what type of bacteria does penicillin target?

A

gram-positive

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55
Q

what type of bacteria does polymyxin target?

A

gram-negative

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56
Q

super infectious

A

reinfection or second infection caused by a microorganism when it is resistant to treatment

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57
Q

broad-spectrum drugs

A

can affect a wide range of species, however can be dangerous as they can harm the natural flora and make you vulnerable to opportunistic infections

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58
Q

example of broad spectrum drugs

A

sulfonamides or erythromycin

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59
Q

antibiotic resistance

A

occurs when some bacteria mutate during replication, making them resistant to the drug; the result of this is that the non-mutated bacteria will die but the mutated ones will not and replicate, making them harder to fight in the future

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60
Q

where are antibiotic resistance bacteria often found?

A

in hospitals

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61
Q

3 levels of defence

A

intrinsic, innate, and acquired

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62
Q

intrinsic defence

A

natural barriers of the body like the skin and the mucous membranes

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63
Q

innate immunity

A

general immune response that will attack all infectious agents through mechanisms like macrophages, cytokines, and the complement cascade

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64
Q

acquired response

A

aka adaptive response; specific response that will use T and B cells, or memory cells as an immune response

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65
Q

what produce the innate response?

A

cytokines

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66
Q

what triggers the adaptive response?

A

the innate response; cytokines, natural killer cells, and dendritic cells

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67
Q

macrophages

A

wandering cells that digest foreign materials via phagocytosis and bring them back to the immune system

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68
Q

what attracts the macrophage to the site of infection

A

chemotaxis

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69
Q

phagosome

A

a vesicle creating by macrophages that stores the infectious agent

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70
Q

how does the macrophage engulf the material?

A

phagocytosis

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71
Q

phagolysosome

A

occurs when a phagosome and a lysosome fuse, in which digestive enzymes will digest the foreign material to destroy the pathogen

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72
Q

what does a phagolysosome do after digesting material?

A

with fuse with the cell membrane and release its contents by exocytosis

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73
Q

residual body

A

the remaining vesicle of debris of the pathogen after phagocytosis

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74
Q

how does the pathogen leave the cell after phagocytosis

A

the residual body will fuse will the plasma membrane and spill out the debris into the interstitial fluid

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75
Q

chemotaxis

A

the movement of the phagocyte toward the pathogen due to the secretions of complement proteins, normal microbial components, damaged tissues, and defensins

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76
Q

interferons

A

unaffected neighbouring cells will produce these to cause antiviral cells to be attracted to the site

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77
Q

how was interferon discovered?

A

in 1957 by chicken cells

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78
Q

two major interferon molecules

A

interferon alpha and interferon beta (gamma also exists but no need to know this)

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79
Q

how are interferons produced?

A

affected cells by viruses release viral nucleic acids and interferons and these interferons will bind to receptors on neighbouring unaffected cells, causing them to transcript and translate inactive antiviral proteins, and these degrade mRNA and bind to ribosomes, stopping viral replication

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80
Q

what are interferons produced by?

A

the host cell when it is invaded by a virus

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80
Q

how are interferons released from the host cell?

A

exocytosis

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81
Q

what activates antiviral proteins during interferon process?

A

double stranded RNA of the viral material

82
Q

what do interferons cause?

A

flulike symptoms that make us sick

83
Q

what is the primary purpose of interferons?

A

to save neighbouring cells from the virus

84
Q

what response are interferons involved in?

A

innate response

85
Q

what microbe are interferons involved with?

A

viruses

86
Q

3 types of complement activating pathways

A

classic pathway, alternative pathway, and lectin pathway

87
Q

classic activating complement pathway

A

when antigens bind to antibodies

88
Q

alternative complement pathway

A

pathogens produce endotoxins and glycoproteins

89
Q

lectin complement pathway

A

microbial polysaccharides bind to activating molecules; lectin is a molecule found in microorganisms

90
Q

what is the result of the complement cascade?

A

the membrane attack complex and lysis of cells

91
Q

functions of complement cascade (5)

A

cytolysis, activation of inflammation, production of cytokines, opsonization, and solubilization of immune complexes

92
Q

cytolysis

A

bursting of bacteria cells

93
Q

opsonization

A

causes pathogens to clump together, making it easier for immune cells to find them

94
Q

cytokines

A

signalling molecules of the immune system

95
Q

solubilization

A

breaks up antigen-antibody complexes that can damage organs

96
Q

how can a microbiota become an opportunistic pathogen?

A

by being introduced into an unusual site in the body or to changes in populations; ex. E coli are mutualistic in the colon but can cause diseases in other areas of the body

97
Q

what do E coli produce?

A

vitamin K

98
Q

what bacteria often replace E coli in the gut, causing infection

A

C. Diff; this is commonly caught in hospitals

99
Q

how do yeast infections develop?

A

when fungi move into the vagina following the destroying of bacteria from antibiotics

100
Q

what are yeast infections treated with?

A

erythromycin

101
Q

what type of microbe is often treated with narrow-spectrum drug?

A

viruses; ex. acyclovir

102
Q

contamination

A

the presence of microbes in or on the body

103
Q

infection

A

successful invasion of the body following contamination; requires a microbe to successful reproduce in the host body and for the host to initiate an immune response

104
Q

3 major portals of entry in the body

A

skin, mucous membranes, and placental (parenteral sometime considered a fourth; bite or contaminated needle)

105
Q

other portals of entry into the body

A

the ear, conjunctiva, nose, mouth, penis, vagina, urethra, and anus

106
Q

why is the skin an inhospitable enviornment?

A

because sebum is produced by sebaceous glands increasing pliability, sweat kills bacteria by osmosis, and the shedding of skin also sheds microorganisms

107
Q

openings in the skin that microbes may enter in

A

sweat glands, sebaceous glands, or cuts

108
Q

mucous membranes

A

most common portals of entry and include the respiratory tract, the GI tract (intestines), and the conjunctiva; are epithelial cells that secrete a mucous fluid

109
Q

pathogenicity

A

the ability of a microorganism to cause disease; is yes or no

110
Q

virulence

A

the degree of pathogenicity to infect a host and cause disease; it determined by virulence factors

111
Q

virulence factors (5)

A

traits of the pathogen that interact with the host and determine how it enters the host, adhere to host cells, gains access to nutrients from host, escapes the host’s immune system, and prevents removal from host by immune system

112
Q

why is virulence not a measure of the severity of the disease

A

to infect a host does not always cause severity of the disease; ex. rabbit fever is very virulent but not severe

113
Q

three types of virulence factors

A

enzymes, toxins, and antiphagocytic factors

114
Q

two examples of enzyme complexes

A

hyaluronidase and collagenase, and coagulase and kinase

115
Q

enzymes and pathogens

A

enzymes are secreted proteins that help the pathogen to dissolve chemicals of structures in the body; ex. hyaluronidase and collagenase

116
Q

coagulase and kinase

A

coagulase causes blood proteins to clot, providing a hiding place for bacteria within the clot; when the immune system stops looking for it, kinase will then digest the clot, allowing it to circulate in the bloodstream

117
Q

toxemia

A

when toxins enter bloodstream and affect many sites in the body

118
Q

enzyme and toxin relationship

A

enzymes can be toxins

119
Q

toxins

A

chemicals that harm tissues or trigger host immune responses and cause damage

120
Q

2 types of toxins

A

exotoxins and endotoxins

121
Q

exotoxins

A

produced by living bacteria and destroy host cells or interfere with host cell metabolism; are more common is gram-positive bacteria

122
Q

example of a exotonin

A

cytotoxin

123
Q

cell wall of gram-negative bacteria

A

rich in lipopolysaccharide, particularly lipid A

124
Q

why are antibiotics bad for gram-negative bacteria?

A

can cause endotoxins to be released when the bacteria dies

125
Q

antiphagocytic factors

A

block phagocytosis through 2 ways: incomplete phagocytosis or blocked by the capsule

126
Q

incomplete phagocytosis

A

the pathogen can survive and live inside the phagocyte, causing it to reproduce within the cell and be protected by the immune system, it can also release lipid A, causing toxemia

127
Q

mother stem cell for all blood cells

A

pluripotent stem cell

128
Q

what two cells arise from pluripotent stem cells?

A

myeloid stem cells and lymphoid stem cells

129
Q

what do myeloid stem cells develop into?

A

RBCs, platelets, mast cells, granulocytes, and monocytes

130
Q

what do lymphoid stem cells develop into?

A

T lymphocytes, B lymphocytes, or natural killer cells

131
Q

granulocytes

A

neutrophils, eosinophils, and basophils

132
Q

neutrophils

A

most abundant WBC; are granular and multilobed; function for phagocytosis and chemical destruction of microbes

133
Q

eosinophils

A

granular and biloped cells; function to combat the effects of histamine in allergic reactions like antihistamines; also destroy parasitic worms and phagocytosis antigen-antibody complexes

134
Q

basophils

A

function to release inflammatory chemicals like histamine

135
Q

rubor

A

inflammatory property referring to redness

136
Q

calor

A

inflammatory property referring to heat

137
Q

tumor

A

inflammatory property referring to swelling

138
Q

dolar

A

inflammatory property referring to loss of function or pain

139
Q

agranulocytes

A

monocytes and lymphocytes

140
Q

monocytes

A

agranular and have a horseshoe shaped nucleus; migrate from the bloodstream to be phagocytes

141
Q

lymphocytes

A

agranular and second most abundant WBC; round nucleus with a little indent; consists of T and B cells which are active in the adaptive immune response

142
Q

anatomy of lymphoid tissue

A

reticular fibres which are a loose CT; these create a filter for microbes and damaged cells passing through the lymphatic system

143
Q

how is lymph created?

A

it is filtered from the interstitial fluid to return proteins to the bloodstream

144
Q

3 functions of the lymphatic system

A

drains excess interstitial fluid, transports dietary lipids and lipid soluble vitamins (A, D, E, and K), and carries out the immune response

145
Q

how are dietary lipids absorbed into the lymphatic system?

A

they are wrapped in a micelle in the small intestine, diffuse into the blood by then being wrapped in a chylomicron, and then are absorbed into a lacteal through a villus

146
Q

anatomy of lymphatic vessels

A

are similar to venules but have thinner walls and more valves

147
Q

lymph nodes

A

bean shaped organs with masses of B and T cells

148
Q

lymphatic vessels in the skin

A

lie in the subcutaneous tissue and follow the same route as veins

149
Q

lymphatic vessels of the viscera

A

follow the arteries, forming plexuses around them

150
Q

what tissues lack lymphatic vessels?

A

avascular tissues like cartilage or epidermis, the CNS, some of the spleen, and the red bone marrow

151
Q

what do lymphatic vessels start as?

A

lymphatic capillaries

152
Q

lymphatic capillaries compared to blood capillaries

A

lymphatic capillaries are more permeable, can absorb large molecules like proteins and lipids, are larger in diameter, and have a one way flow structure

153
Q

permeability of lymphatic capillaries

A

when pressure is greater it the ISF, the overlapping endothelial cells will separate slightly, allowing for fluid to enter

154
Q

anchoring filaments

A

part of lymphatic system and are filaments of elastic fibres; when there is excess ISF, the anchoring filaments are pulled on by the surrounding tissues, making the opening between the endothelial cells larger

155
Q

how are lymphatic vessels unidirectional?

A

the endothelial cells will not move apart when the pressure is greater in the lymphatic vessels relative to the ISF

156
Q

how are minivalves formed in lymphatic vessels?

A

the adjacent endothelial cells overlap loosely enough that they create mini valves

157
Q

lacteals

A

specialized lymphatic capillaries found in the small intestine which carry dietary lipids

158
Q

chyle

A

lymph contains lipids from the small intestine

159
Q

flow of lymph

A

lymphatic capillaries > collecting vessels > trunks > ducts

160
Q

where does the lumbar trunk drain lymph from?

A

the lower limbs, the walls and viscera of the pelvis, the kidneys, the adrenal glands, and the abdominal wall

161
Q

where does the bronchomediastinal trunk drain lymph from?

A

the thoracic wall, the lungs, and the heart

162
Q

where do the subclavian trunks drain lymph from?

A

the upper limbs

163
Q

where do the jugular trunks drain lymph from?

A

the head and the neck

164
Q

where does the intestinal trunk drain lymph from?

A

the stomach, intestines, pancreas, spleen, and some of the liver

165
Q

2 main channels for lymph

A

the thoracic duct and the right lymphatic duct

166
Q

cisterna chyli

A

where the thoracic duct begins; anterior the the second lumbar vertebrae

167
Q

where does the cisternal chyli receive lymph from?

A

R and L lumbar trunks and the intestinal trunk

168
Q

where does the thoracic duct receive lymph from?

A

the left jugular vein, left subclavian vein, and left bronchomediastinal trunk

169
Q

what does the thoracic duct drain into?

A

the junction between the left internal jugular vein and the left subclavian vein

170
Q

where does the right lymphatic duct drain into?

A

the junction between the right internal jugular vein and the right subclavian vein

171
Q

skeletal muscle pump for lymph

A

the contraction of skeletal muscles compresses the lymph vessels to force the lymph up towards the subclavian/jugular intersect

172
Q

respiratory pump

A

decreases in pressure in the thoracic cavity due to breathing causes lymph to move up from the abdominal region into the thoracic region

173
Q

what cell does HIV target

A

helper T cells

174
Q

how does protein synthesis occur?

A

nucleic acid is transcribed into mRNA to make proteins such as capsids

175
Q

tRNA

A

found in HIV virus capsid which helps with translation of RNA sequence

176
Q

criteria for infection

A

for the microbe to successfully reproduce in the host body and for the host to initiate an immune response

177
Q

endotoxin

A

associated with gram-negative bacteria and when they die, they release stored products from their cell wall (lipid A), causing toxic effects in hosts

178
Q

toxic effects of endotoxins

A

shock, fever, inflammation, diarrhea, and abnormal blood clotting)

179
Q

3 reasons why antibiotics can be harmful

A

they have cause bacteria to release endotoxins, they can disrupt the normal flora, and they can create antibiotic resistance

180
Q

hyaluronidase and collagenase

A

hyaluronidase dissolves hyaluronic acid to digest tight junctions between cells, then collagenase digests the collagen in the basement membrane to reach underlying CT’s or bloodstream

181
Q

what is key to the process of viruses picking their targets

A

viral glycoproteins

182
Q

what must occur for the viral genome once it enters the host cell?

A

it must become uncoated and separated from the protein

183
Q

self-assembly of new virus

A

the viral DNA and proteins are assembled together to create a new virus

184
Q

how does the host machinery copy viral DNA?

A

via ex. DNA polymerase III or ligases

185
Q

what does the host machinery transform viral DNA into?

A

capsomeres

186
Q

what HIV component becomes active only after release from the host cell?

A

protease

187
Q

what happens to gp 41 and gp 120 proteins after the virus enters the host?

A

they remain part of the cell wall

188
Q

function of ribosomes in HIV virus replication

A

they translate mRNA into viral polypeptides

189
Q

what is the host DNA broken up into for the HIV virus?

A

genome RNA and mRNA

190
Q

pseudopod

A

arm-like extensions that are made of cytoplasm; found in macrophages and these are used for phagocytosis

191
Q

what do active antiviral proteins bind to?

A

ribosomes

192
Q

5 major lymph nodes

A

submaxillary group, cervical group, axillary group, subtrochlear group, and inguinal group

193
Q

submaxillary lymph node group

A

found in the floor of the mouth

194
Q

cervical lymph node group

A

near the sternocleidomastoid muscle

195
Q

axillary lymph node group

A

underarm and upper chest

196
Q

supratrochlear lymph node group

A

above the bend in the elbow

197
Q

inguinal lymph node group

A

found in the groin

198
Q

anatomy of neutrophils

A

granular, are multilobed (2-5), cytoplasm is light purple, and nucleus is dark purple

199
Q

anatomy of eosinophils

A

granular, are biloped, nucleus is dark purple, and cytoplasm is stained red/orange

200
Q

anatomy of basophils

A

are granular, cytoplasm is dark blue/purple, and nucleus is dark purple (bilobed); hard to see because it is very granular

201
Q

anatomy of lymphocytes

A

are agranular, have a large nucleus with a small indent, and are dark purple (but not as dark as basophils), and cytoplasm is sky blue but hard to see

202
Q

anatomy of monocytes

A

are agranular and have a kidney shaped nucleus (dark purple); cytoplasm is grey-blue and looks foamy

203
Q

anatomy of platelets

A

much smaller than cells and have no nucleus