Methods of transmission of infectious agents and virulence mechanisms of human pathogens Flashcards
(361 cards)
1
Q
- What are the different portals of entry for microorganisms?
A
A: Mucous membranes (respiratory, gastrointestinal, conjunctiva), skin, and parenteral route.
2
Q
How do microorganisms move within the body?
A
They move by invading host cells, using adhesins, or being aided by running on motile organs.
3
Q
What are the various stages of infection?
A
Entry of microorganisms, portal of entry, penetration or evasion of host defenses, damage to the host cells, and multiplication of bacteria.
4
Q
How does the immune system respond to infection?
A
It tries to fight back and eliminate the pathogen.
5
Q
What mechanisms help microorganisms evade the immune system?
A
Capsule formation, cell wall components, antigenic variation, siderophores, and cytoskeleton modifications.
6
Q
What are some ways in which microorganisms damage host cells?
A
They produce toxins (exotoxins, endotoxins), lysogenic conversion, and direct damage to tissues.
7
Q
What happens if the immune system fails to eliminate the pathogen?
A
The microorganism can establish infection and cause disease.
8
Q
What is the role of adhesins in infection?
A
Adhesins help microorganisms attach to host cells and tissues.
9
Q
How do microorganisms protect themselves from host defenses?
A
They use capsules, antigenic variation, and other mechanisms to evade the immune response.
10
Q
What are the major types of mucous membranes that serve as portals of entry for microorganisms?
A
Respiratory tract, gastrointestinal tract, genitourinary tract, and conjunctiva.
11
Q
How does the skin act as a portal of entry for microorganisms?
A
It provides a barrier, but microorganisms can enter through cuts, wounds, or hair follicles.
12
Q
What is the parenteral route of microorganism entry?
A
It involves direct entry into tissues through injections, bites, cuts, or punctures.
13
Q
What is the function of capsules in bacterial infections?
A
Capsules prevent phagocytosis by immune cells, helping bacteria evade destruction.
14
Q
How does antigenic variation help pathogens evade the immune system?
A
Pathogens alter their surface proteins to avoid detection by immune cells.
14
Q
What are siderophores, and how do they help bacteria?
A
Siderophores are molecules that bacteria produce to steal iron from the host, which is essential for their growth.
15
Q
What are the two main types of bacterial toxins?
A
Exotoxins and endotoxins.
16
Q
How do exotoxins differ from endotoxins?
A
Exotoxins are proteins secreted by bacteria, while endotoxins are part of the outer membrane of Gram-negative bacteria.
17
Q
What is lysogenic conversion, and how does it contribute to bacterial virulence?
A
It occurs when a bacteriophage transfers new genes to bacteria, increasing their ability to cause disease.
18
Q
What happens when the immune system successfully fights off an infection?
A
The pathogen is eliminated, and the body may develop immunity
18
Q
What are the six components of the chain of infection?
A
Infectious agent
Reservoir
Portal of Exit
Mode of Transmission
Portal of Entry
Susceptible Host.
19
Q
What are some ways the immune system fights infections?
A
Producing antibodies, activating white blood cells, and initiating inflammatory responses
20
Q
What is an infectious agent?
A
A microorganism that can cause disease, such as bacteria, viruses, fungi, or parasites.
21
Q
Give two examples of reservoirs in the chain of infection.
A
People, water, food.
22
Q
What is a portal of exit?
A
The route through which an infectious agent leaves the reservoir, such as blood, excretion, or skin.
23
Name two modes of transmission.
Physical contact and airborne transmission.
24
What are the common portals of entry for infections?
Mucous membranes, respiratory system, digestive system, broken skin.
25
Who is considered a susceptible host?
A person with a weakened immune system due to age, disease, or medical treatments.
26
How can the chain of infection be broken?
By controlling reservoirs, blocking portals of entry/exit, maintaining hygiene, and improving immunity.
27
Why is hand hygiene important in preventing infections?
It helps break the chain of infection by preventing the spread of microorganisms.
28
What factors can make someone more susceptible to infections?
Weakened immune system, chronic disease, poor nutrition, stress, or age.
28
What type of fimbriae in Escherichia coli binds to mannose-containing receptors?
Type I fimbriae
29
What type of receptors do P fimbriae of Escherichia coli bind to?
Galactose and glycoproteins present on epithelial cells
30
Which bacterial genera possess Type IV pili?
Pseudomonas vibrio and Neisseria
30
What are examples of glycolipids mentioned in the image?
cerebrosides
31
What is the role of Type IV pili in Pseudomonas aeruginosa?
It affects the lung in cystic fibrosis patient
32
How does Vibrio cholerae use Type IV pili?
It attaches to the Gastrointestinal epithelium
33
What is the significance of fimbriae in bacterial adhesion?
Bind to host cells
Biofilm formation by protecting the bacteria from immune system and antibiotics
34
How do glycolipids contribute to bacterial attachment?
It serves as receptors to establish infection
It strengthens the attachment between the host and bacterial cell
It helps to determine the site of infections
It helps in the formation of biofilm to protect the bacteria from antibiotics and immune response
It helps the bacteria to camouflage and evade immune detection increasing their survival
35
Why are Type IV pili considered virulence determinants? use example
Play roles in pathogenesis by aiding in adhesion
motility
immune evasion
genetic exchange
pseudomonas aeruginosa cause lung infection
vibrio cholera use type pilli to attach to GI epithelium
36
How does bacterial adhesion contribute to infections?
pseudomonas aeruginosa cause lung infection in cystic fibrosis patients
37
What is the significance of E. coli binding to the surface of macrophages?
Binding to macrophages can help E. coli evade the immune response, survive within immune cells, trigger inflammation, and contribute to systemic infections.
38
How do E. coli bacteria damage urinary tract cells?
E. coli mediates an increased inflammatory response, leading to tissue damage in the urinary tract.
39
What role does inflammation play in urinary tract infections?
Inflammation is a defense mechanism triggered by bacterial invasion, but excessive inflammation can damage urinary tract cells, causing pain, discomfort, and infection symptoms.
40
How do E. coli fimbriae stabilize attachment to different types of urinary tract cells?
Fimbriae help E. coli adhere to various urinary tract structures, including the proximal tubules, vessel walls, bladder, and distal tubules, ensuring bacterial persistence.
41
Which specific urinary tract structures are targeted by E. coli?
E. coli binds to proximal tubules, vessel walls, bladder (muscular layers and vessel walls), distal tubules, and collecting ducts.
42
What is uroplakin, and why is it important in bacterial adhesion?
Uroplakin is a protein found on bladder epithelial cells that E. coli recognizes and binds to, promoting bacterial attachment and infection.
42
How do E. coli recognize mannose-containing host proteins?
E. coli fimbriae contain adhesins that specifically bind to mannose-containing receptors on host cells, facilitating adhesion and infection.
42
Why is type 1 fimbriae-mediated attachment considered a crucial stage for cystitis?
The attachment of E. coli via type 1 fimbriae to bladder cells is a key step in cystitis (bladder infection) because it enables bacterial colonization, persistence, and subsequent inflammation leading to infection symptoms.
42
How are P fimbriae organized?
They are highly organized and composed of at least six subunits.
42
What structure do P-fimbriated E. coli attach to?
The carbohydrate structure alpha-D-Galp-(1-4)-beta-D-Galp.
42
Which kidney structures do P-fimbriated E. coli bind to?
Bowman’s capsule, glomerulus, and endothelial cells of vessel walls.
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What happens when P-fimbriated E. coli enter the urinary tract?
They establish bacteriuria (bacteria in urine).
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What effect do P fimbriae have on red blood cells?
It causes hemaglutination of erythrocytes
42
How can P-fimbriated E. coli contribute to systemic infection?
By crossing the epithelial barrier to enter the bloodstream
42
Which gene cluster encodes P fimbriae?
The pap gene cluster
42
How do pap+ E. coli strains differ from pap- strains in intestinal flora?
pap+ strains persist longer in the intestinal flora than pap- strains.
42
What role do bacterial toxins play in invasiveness?
Toxins help bacteria damage host tissues and spread beyond the initial infection site.
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What is invasiveness in the context of bacterial infections?
The ability of bacteria to spread in host tissues after establishing an infection.
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What is an example of a non-invasive bacterial infection?
Tetanus, since Clostridium tetani does not spread in tissues but releases toxins.
42
Where are P antigens expressed in the human body?
On the surface of red blood cells and cells lining the urinary tract.
42
Which bacterial infection spreads via toxins from a wound?
Tetanus, caused by Clostridium tetani.
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Which bacterial infection can lead to septicemia from a wound infection that is cause bloodstream infection?
Streptococcal septicemia caused by Streptococcus species.
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Why is Clostridium tetani considered invasive despite not spreading through tissues?
Because its toxin spreads and causes systemic effects.
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What is septicemia, and how can it result from a wound infection?
Septicemia is a life-threatening bloodstream infection that can occur when bacteria spread from a wound.
43
Name three bacteria that produce exotoxins.
Vibrio cholerae, Enterotoxigenic E. coli, Shigella dysenteriae
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What type of environment favors the growth of Clostridium tetani?
Anaerobic (low-oxygen) environments, such as deep puncture wounds.
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What is a major virulence factor of Streptococcus species in septicemia?
Enzymes and toxins that help bacteria evade the immune system and spread in the bloodstream.
43
What are the two main types of bacterial toxins?
Exotoxins and Endotoxins
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How is toxin production encoded in bacteria?
Through plasmids and bacteriophage genes
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What is an example of an exotoxin affecting normal cellular processes?
Diphtheria toxin or Cholera toxin
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Which bacterial groups produce exotoxins?
Both Gram-positive and Gram-negative bacteria
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What are the properties of exotoxins?
Secreted by living cells, protein-based, heat-labile, highly antigenic, enzymatic action, specific effects, can be converted into toxoids for vaccines
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Which exotoxins help bacteria spread in tissues?
DNAse, hyaluronidase, collagenase
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Which type of toxin is heat-stable?
Endotoxins
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Which exotoxins cause cell lysis?
Hemolysins and leucocidins
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What is an example of an exotoxin that affects the nervous system?
Tetanus toxin
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Which bacterial group produces endotoxins?
Gram-negative bacteria
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What is the main endotoxin component?
Lipopolysaccharide (LPS), specifically Lipid A
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When are endotoxins released?
Upon bacterial death or disruption of the cell
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List three bacteria that produce endotoxins.
Salmonella species, Shigella species, E. coli
(SSE)
43
What are the properties of endotoxins?
Part of the cell wall, heat-stable, poorly antigenic, non-specific action, no enzymatic activity, cannot be converted into toxoids
43
Which type of toxin is highly antigenic and can be used to make vaccines?
Exotoxins
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Which type of toxin is released only when bacterial cells die?
Endotoxins
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Which type of toxin has specific targets, such as the CNS or intestines?
Exotoxins
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Why can exotoxins be used in vaccine production but endotoxins cannot?
Exotoxins can be converted into toxoids, while endotoxins cannot be neutralized in this way
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How do toxins cause harm to human?
Breaking down tissues for bacterial spread
Killing host cells, weakening immunity
Disrupting essential cellular functions
Triggering systemic inflammation and shock
Targeting specific organs with deadly effects
47
What exotoxin is produced by Corynebacterium diphtheriae?
Diphtheria toxin
48
What is the mechanism of action of diphtheria toxin?
Inhibits protein synthesis by inhibiting Elongation Factor-2 (EF-2)
49
Which bacterium produces alpha-toxin, and what is its effect?
Clostridium perfringens; it has lecithinase and phospholipase activity, causing myonecrosis.
50
How does tetanus toxin (Clostridium tetani) affect the nervous system?
It decreases the release of inhibitory neurotransmitters (glycine & GABA), leading to muscle spasms.
51
What neurotransmitter does botulinum toxin (Clostridium botulinum) affect?
Acetylcholine (it decreases its release, causing flaccid paralysis).
52
What are the two exotoxins produced by diarrheagenic E. coli?
Heat-labile toxin and heat-stable toxin
52
Which two bacteria produce exotoxins that increase cAMP in target cells, leading to diarrhea?
Escherichia coli (diarrheagenic) and Vibrio cholerae
53
How does the shiga toxin (Shigella dysenteriae type 1) cause damage?
Inhibits protein synthesis by inhibiting ribosomes.
54
Which bacterium produces an exotoxin that inhibits Elongation Factor-2, similar to diphtheria toxin?
Pseudomonas
55
What is the mechanism of action of verocytotoxic exotoxin in E. coli?
Inhibits protein synthesis by inhibiting ribosomes.
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Which exotoxins inhibit protein synthesis by inhibiting ribosomes?
Shiga toxin and verocytotoxic toxin.
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Which exotoxins work by increasing cAMP levels in target cells?
Heat-labile toxin, heat-stable toxin, and cholera toxin.
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Which exotoxin leads to spastic paralysis by blocking inhibitory neurotransmitters?
Tetanus toxin.
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Which exotoxin leads to flaccid paralysis by blocking acetylcholine release?
Botulinum toxin.
60
What are the main components of a Gram-negative bacterial outer membrane?
The outer membrane consists of lipopolysaccharides (LPS), phospholipids, proteins, and lipoproteins.
61
What is an endotoxin, and where is it found?
An endotoxin is a toxic component of the outer membrane of Gram-negative bacteria, primarily found in the lipopolysaccharide (LPS) layer
62
Which part of bacteria is responsible for endotoxin production?
The outer membrane of Gram-negative bacteria, specifically the lipid A component of LPS, is responsible for endotoxin production.
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What is the primary component of endotoxins?
The primary component of endotoxins is lipid A, which is embedded in the bacterial outer membrane and triggers immune responses.
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Which types of bacteria produce endotoxins?
Gram-negative bacteria, such as Escherichia coli, Salmonella, Pseudomonas, and Neisseria, produce endotoxins.
64
What is the primary function of endotoxins in bacterial infections?
Endotoxins help bacteria evade the immune system by triggering inflammation, fever, and immune responses that may lead to septic shock.
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What immune cells do endotoxins activate first?
Endotoxins first activate macrophages and dendritic cells, which initiate the immune response.
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Which cytokines are released in response to endotoxin exposure?
Endotoxin exposure leads to the release of IL-1, TNF-α, and IL-6.
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How does IL-1 contribute to fever?
IL-1 stimulates the hypothalamus to increase prostaglandin production, which raises the body’s temperature, leading to fever.
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What role does TNF-α play in endotoxin response?
TNF-α promotes inflammation, increases vascular permeability, and contributes to hypotension and septic shock.
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What happens when nitric oxide is released due to endotoxin exposure?
Nitric oxide causes vasodilation, leading to hypotension and decreased organ perfusion, which may contribute to septic shock.
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How do endotoxins contribute to hypotension?
Endotoxins induce the release of TNF-α and nitric oxide, which dilate blood vessels and reduce blood pressure, leading to hypotension.
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Which complement system components are activated by endotoxins?
Endotoxins activate C3a and C5a, leading to inflammation, increased vascular permeability, and neutrophil recruitment.
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What causes neutrophil chemotaxis during endotoxin response?
C5a, a complement protein activated by endotoxins, attracts neutrophils to the site of infection to enhance immune defense.
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How does endotoxin exposure lead to disseminated intravascular coagulation (DIC)?
Endotoxins trigger excessive coagulation factor activation, leading to widespread microclot formation and subsequent depletion of clotting factors, causing bleeding disorders.
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How do cytokines affect the hypothalamus in fever development?
Cytokines like IL-1 and TNF-α stimulate the hypothalamus to release prostaglandins, which reset the body’s temperature, leading to fever.
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How do endotoxins contribute to septic shock?
Endotoxins cause widespread vasodilation, hypotension, and inflammation, leading to organ failure and septic shock.
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How does the hypothalamus regulate body temperature in response to endotoxins?
The hypothalamus increases body temperature through vasoconstriction, muscle contractions (shivering), and behavioral changes to conserve heat.
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What role do prostaglandins play in the pyrogenic response?
Prostaglandins (especially PGE2) increase the hypothalamic temperature set point, causing fever as a defense mechanism.
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Why do endotoxins lead to widespread inflammation?
Endotoxins trigger massive cytokine release, leading to inflammation, tissue damage, and immune system overactivation.
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What is the feedback loop in the pyrogenic response?
The feedback loop involves cytokine release stimulating prostaglandin production, which raises body temperature; once the infection is controlled, anti-inflammatory signals restore normal temperature.
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Where is the endotoxin located in Salmonella bacteria?
The endotoxin is located in the lipopolysaccharide (LPS) layer of the outer membrane of Salmonella bacteria.
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What effect does the endotoxin in the LPS layer cause in the human body?
The endotoxin triggers fever, inflammation, and septic shock by activating the immune system and releasing cytokines like TNF-α and IL-1.
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What is the function of O antigen in Salmonella?
The O antigen inhibits phagocytosis, helping the bacteria evade immune detection and destruction.
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How do anti-phagocytic proteins benefit Salmonella?
These proteins prevent phagocyte recognition and killing, enhancing bacterial survival within the host.
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What role does the virulence plasmid play in Salmonella infections?
The virulence plasmid carries genes that enhance bacterial survival and pathogenicity, making the infection more severe.
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How do type 1 fimbriae contribute to Salmonella infection?
Type 1 fimbriae help in adherence to host cells, allowing the bacteria to colonize and establish infection.
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What is the function of siderophores in Salmonella?
Siderophores scavenge iron from the host, which is essential for bacterial growth and survival.
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How does cytotoxin affect host cells in Salmonella infections?
The cytotoxin inhibits protein synthesis in host cells and disrupts calcium balance, leading to cell damage and death.
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What are the roles of H antigen and flagella in Salmonella?
The H antigen helps in adherence and flagella provide motility, allowing the bacteria to move and invade host tissues.
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What is the causative agent of cholera?
Vibrio cholerae, a Gram-negative bacterium, causes cholera.
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How does the Vi capsule antigen help Salmonella evade the immune system?
The Vi capsule inhibits complement binding, reducing immune recognition and preventing bacterial destruction.
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How is Vibrio cholerae transmitted?
It is transmitted through contaminated food or water, often due to poor sanitation.
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How many binding and active units does cholera toxin have?
Cholera toxin has 6 binding units (B subunits) and 2 active units (A subunits).
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What is the function of the binding unit in cholera toxin?
The binding unit attaches the toxin to the ganglioside receptor (GM1) on intestinal epithelial cells, allowing entry into the cell.
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What happens once the cholera toxin is internalized in the host cell?
The A subunit is released inside the cell, where it activates adenylate cyclase, increasing cAMP production.
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How does cholera toxin affect adenylate cyclase?
It continuously activates adenylate cyclase, leading to excessive cAMP production.
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What is the role of cyclic AMP (cAMP) in cholera toxin action?
High cAMP levels cause ion channels to remain open, leading to massive ion and water loss.
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Which receptor does cholera toxin bind to on the host cell?
It binds to the GM1 ganglioside receptor on the intestinal epithelium.
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What happens to ion channels in intestinal epithelial cells when cAMP levels increase?
Chloride channels open, leading to an outflow of Cl⁻, Na⁺, and water, causing diarrhea.
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How does cholera toxin lead to severe diarrhea?
By disrupting ion transport, cholera toxin causes excessive water loss into the intestines, leading to severe dehydration and diarrhea.
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What is the role of G-protein in cell signaling?
G-proteins act as molecular switches that transmit signals from receptors to intracellular pathways, activating enzymes or ion channels.
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How does a signal molecule activate a receptor?
A signal molecule (ligand) binds to a G-protein-coupled receptor (GPCR) on the cell membrane, inducing a conformational change that activates the associated G-protein.
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What enzyme does the G-protein activate?
The G-protein activates adenylate cyclase, an enzyme responsible for converting ATP into cyclic AMP (cAMP).
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What is the function of adenylate cyclase in the signaling pathway?
Adenylate cyclase catalyzes the conversion of ATP to cAMP, which acts as a second messenger to propagate the signal within the cell.
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How does cAMP act as a second messenger in the cell?
cAMP activates protein kinase A (PKA), leading to the phosphorylation of target proteins that regulate various cellular functions.
81
What happens when cAMP levels increase in the cell?
Increased cAMP levels activate PKA, which can alter gene expression, enzyme activity, and ion channel function.
81
What is the role of protein kinase in cAMP-mediated signaling?
Protein kinase A (PKA) phosphorylates target proteins, leading to changes in metabolism, gene transcription, and cellular activity.
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How does the activation of ion channels influence cellular functions?
Ion channels regulate membrane potential, neurotransmission, muscle contraction, and cellular signaling when activated.
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What happens to the signaling process when the first messenger is removed?
The receptor returns to its inactive state, the G-protein deactivates, cAMP levels drop, and the signal transduction stops.
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How does cAMP help in ion exchange across the membrane?
cAMP opens ion channels, allowing ions like Na⁺, Cl⁻, and Ca²⁺ to flow in or out of the cell, influencing electrical and chemical gradients.
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What are ion channels, and why are they important?
Ion channels are protein structures in the cell membrane that regulate the movement of ions across the membrane, crucial for nerve signaling, muscle contraction, and homeostasis.
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How do ion channels regulate the movement of Na⁺, K⁺, Cl⁻, and Ca²⁺?
Ion channels allow specific ions to pass through the membrane, maintaining the cell’s electrochemical balance and enabling signal transmission.
84
What triggers ion channels to open or close?
Ion channels open or close in response to ligand binding, voltage changes, mechanical forces, or secondary messengers like cAMP.
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What is the function of HCO₃⁻/Cl⁻ exchangers in cells?
These exchangers regulate pH balance and chloride transport, crucial for maintaining homeostasis in epithelial and nerve cells.
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How does ATPase help in ion transport across the membrane?
ATPase enzymes, like the Na⁺/K⁺ pump, actively transport ions against their concentration gradient using ATP energy.
87
What is the role of charge separation in ion movement across membranes?
Charge separation creates a membrane potential, which drives ion movement and enables electrical signaling in neurons and muscles.
88
How does the extracellular and intracellular ion concentration affect cell function?
Ion concentration differences regulate osmotic balance, nerve signaling, muscle contractions, and enzyme activity.
89
What happens to ion movement when cAMP activates channels?
cAMP activates channels, leading to ion influx or efflux, affecting cellular signaling, water balance, and neurotransmission.
90
What is the role of cyclic nucleotide-gated channels in cellular signaling?
These channels respond to cAMP or cGMP, controlling ion flow and influencing vision, olfaction, and neurotransmission.
91
Why is the regulation of ion exchange crucial for normal cellular function?
Proper ion exchange maintains cell volume, electrical excitability, metabolic function, and signal transduction in various physiological processes.
92
How does Vibrio cholerae cause diarrhea?
Vibrio cholerae produces cholera toxin, which activates chloride channels (Cl⁻ channels or CFTR) in intestinal epithelial cells, causing excessive loss of Cl⁻, Na⁺, K⁺, and water into the lumen, leading to diarrhea.
93
What happens to ion movement when cAMP levels increase in intestinal epithelial cells?
Increased cAMP opens Cl⁻ channels, leading to the loss of Cl⁻, Na⁺, and K⁺ from the cells into the intestinal lumen, drawing water with them and causing severe dehydration.
94
Why does dehydration occur in cholera infections?
Excessive ion loss into the lumen causes an osmotic imbalance, drawing water out of the cells and into the intestines, leading to dehydration.
95
What is the role of CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) in cholera-induced diarrhea?
CFTR is a chloride ion channel that becomes hyperactivated by cholera toxin, causing an excessive outflow of Cl⁻ and water into the intestines.
96
How does the loss of Na⁺ and Cl⁻ contribute to water loss from the body?
The loss of Na⁺ and Cl⁻ increases osmolarity in the intestinal lumen, pulling water out of epithelial cells via osmosis, leading to watery diarrhea.
97
Why does oral rehydration therapy (ORT) help treat cholera?
ORT contains glucose and electrolytes, which help reabsorb Na⁺ and water through sodium-glucose cotransporters, reversing dehydration.
98
What is the function of SNARE proteins in neurotransmitter release?
SNARE proteins help synaptic vesicles fuse with the neuron membrane, allowing the release of neurotransmitters like acetylcholine.
98
How does botulinum toxin affect neurotransmitter release?
Botulinum toxin cleaves SNARE proteins, preventing vesicle fusion and blocking acetylcholine release, leading to muscle paralysis.
98
What are the symptoms of botulinum toxin poisoning?
Symptoms include muscle weakness, paralysis, difficulty breathing, and potentially fatal respiratory failure.
98
Why is botulinum toxin considered one of the most potent biological toxins?
It can block neurotransmission completely, leading to paralysis and death even in tiny amounts.
98
How is botulinum toxin transmitted?
It is transmitted through contaminated food, wounds, or inhalation, often found in improperly preserved foods.
99
How does botulinum toxin differ from tetanus toxin in its mechanism?
Botulinum toxin blocks excitatory neurotransmitters (acetylcholine), causing paralysis, whereas tetanus toxin blocks inhibitory neurotransmitters, causing muscle spasms.
99
What is the medical use of botulinum toxin?
It is used in Botox treatments for reducing wrinkles, treating muscle spasms, and medical conditions like chronic migraines.
100
Why does botulinum toxin cause flaccid paralysis?
Without acetylcholine release, muscles cannot contract, leading to flaccid (loose) paralysis.
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