General Principles Week 5 to 7 REV Flashcards
Topic 1 – Prokaryotes (Bacteria)
TLO 1.1 Differences in cell structure between prokaryotic and eukaryotic cells
Prokaryotic and eukaryotic cells differ significantly in their structure
- Nucleus: Prokaryotes lack a membrane-bound nucleus, while eukaryotes have a distinct nucleus enclosed by a nuclear membrane.
- Organelles: Prokaryotes have no membrane-bound organelles, whereas eukaryotes possess various membrane-bound organelles such as mitochondria, endoplasmic reticulum, and Golgi apparatus.
- DNA structure: Prokaryotic DNA is typically circular and located in the nucleoid region of the cytoplasm. Eukaryotic DNA is linear and contained within the nucleus.
- Size: Prokaryotic cells are generally smaller, ranging from 0.1 to 5.0 μm in diameter, while eukaryotic cells are typically 10-100 μm in diameter.
- Ribosomes: Prokaryotes have smaller 70S ribosomes, while eukaryotes have larger 80S ribosomes.
TLO 1.2 Structure and function of bacterial components
Bacterial cells consist of several key components:
- Cell Wall: Provides structural support and protection. It’s composed of peptidoglycan.
- Plasma Membrane: Controls what enters and exits the cell.
- Cytoplasm: Supports and protects cell organelles and contains nutrients.
- Nucleoid: Region where the bacterial chromosome (DNA) is located.
- Plasmid: Extra chromosomal DNA that can confer antibiotic resistance.
- Ribosomes: Responsible for protein synthesis.
- Inclusion/Storage Granules: Store nutrients like sugars and fats.
- Flagella: Aid in bacterial locomotion.
- Pili: Help bacteria attach to surfaces and other cells.
TLO 1.3 Difference between gram-positive and gram-negative bacteria
The main differences between gram-positive and gram-negative bacteria are:
- Cell Wall Structure: Gram-positive bacteria have a thick peptidoglycan layer, while gram-negative bacteria have a thin peptidoglycan layer with an outer membrane.
- Staining: Gram-positive bacteria retain crystal violet stain and appear purple, while gram-negative bacteria lose the stain and appear red.
- Antibiotic Resistance: Gram-negative bacteria are generally more resistant to antibodies due to their impenetrable cell wall.
- Toxin Production: Gram-positive bacteria typically produce exotoxins, while gram-negative bacteria produce endotoxins.
Feature Endotoxins Exotoxins
Origin Part of the outer membrane of Gram-negative bacteria Secreted by bacteria (both Gram-positive and Gram-negative)
Release Released when bacteria die Actively secreted by living bacteria
Potency Generally less potent Highly potent
Effects Can cause fever, inflammation, and septic shock Can damage specific tissues and organs
TLO 1.4 Bacterial growth and division
Bacteria grow and divide through a process called binary fission:
- DNA Replication: The bacterial chromosome is replicated.
- Chromosome Segregation: The replicated chromosomes are separated.
- Septum Formation: A cell wall forms between the two chromosomes, dividing the cell.
- Cell Separation: The two daughter cells split apart.
The time taken for a bacterial population to double is called the generation time, which varies among species but is typically around 20 minutes for many medically significant bacteria.
Topic 2 – Acellular Microbes (Viruses)
TLO 2.1 Structure of the virus
Viruses consist of:
- Genetic Material: Either DNA or RNA, but not both.
- Capsid: A protein coat that protects the genetic material.
- Envelope: Some viruses have an additional lipid membrane surrounding the capsid.
Viruses can have various shapes, including icosahedral, helical, or complex structures.
icosahedral - capsid (capsomere) + genome (cubic symmerty) Example herpesvirus
helical - capsid (capsomere) + genome (helical shape) Example Influenza/Rabies virus
complex structures - capsid (capsomere) + genome (helical shape) example bacteriophage - Poxvirus
Another example - - capsid (capsomere) + genome (circular shape + envelope (Lipid bilayer + gycoprotein)
TLO 2.2 Characteristics of viruses
Key characteristics of viruses include:
- Size: Extremely small, ranging from 20 to 300 nanometers.
- Acellular: Viruses are not cells and lack cellular organelles.
- Obligate Intracellular Parasites: They can only replicate inside host cells.
- Specific Host Range: Each virus can infect only specific types of cells or organisms.
- Genetic Material: Contains either DNA or RNA, but not both.
Feature Bacteria Viruses
Size Larger, usually 1-5 micrometers Smaller, typically 20-300 nanometers
Structure Single-celled organisms with a simple structure Consist of genetic material in a protein coat
Living Status Living organisms Not considered living, need a host to replicate
Reproduction Reproduce on their own through binary fission Require a host cell to replicate
Treatment Treated with antibiotics Treated with antiviral drugs or vaccines
TLO 2.3 Viral growth cycle and replication
The viral replication cycle consists of seven stages:
- Attachment: The virus binds to specific receptors on the host cell.
- Entry: The virus enters the host cell.
- Uncoating: The viral genetic material is released inside the host cell.
- Replication: The viral genome is replicated using host cell machinery.
- Assembly: New viral particles are assembled.
- Maturation: The newly formed viruses undergo final changes to become infectious.
- Release: The new viruses are released from the host cell.
Viruses can undergo either a lytic cycle (where the host cell is destroyed) or a lysogenic cycle (where the viral genome integrates into the host genome).
Stages
Attachment Virus attaches to the host cell surface
Entry Virus enters the host cell, often through endocytosis
Uncoating Viral genetic material is released inside the host cell
Replication Viral genetic material is replicated by the host cell
Assembly New viral particles are assembled from the replicated material
Maturation Viral particles undergo modifications to become fully infectious
Release New viruses are released from the host cell, often causing cell lysis
Topic 3 – Eukaryotic Pathogens (Fungi and Parasites)
TLO 3.1 Structure of eukaryotic microbes (fungi and parasites)
Eukaryotic microbes have a more complex structure compared to prokaryotes:
- Nucleus: Contains the genetic material enclosed by a nuclear membrane.
- Membrane-bound Organelles: Include mitochondria, endoplasmic reticulum, and Golgi apparatus.
- Cell Wall: Fungi have a cell wall made of chitin.
- Cytoskeleton: Provides structure and enables movement.
TLO 3.2 Growth and replication of eukaryotic pathogens
Eukaryotic pathogens grow and replicate through various methods:
- Fungi: Can reproduce sexually or asexually, often through spore formation.
- Parasites: May have complex life cycles involving multiple hosts and stages.
Fungi
- Absorb nutrients from the environment, often through decomposing organic matter
- Reproduce by spore formation (both sexual and asexual reproduction)
Parasites
- Live in or on a host organism, deriving nutrients from the host
- Reproduce through various methods, including binary fission, multiple fission, and sexual reproduction
TLO 3.3 How eukaryotic microbes cause disease and associated challenges
Eukaryotic microbes can cause disease through various mechanisms:
- Tissue Invasion: Direct damage to host tissues.
- Toxin Production: Release of harmful substances.
- Immune Evasion: Ability to avoid or suppress host immune responses.
TLO 4.1 Normal flora (microbiota) associated with body regions
Normal flora, or microbiota, are microorganisms that naturally inhabit various body regions.
They play crucial roles in maintaining health, including:
- Skin: Primarily bacteria that help prevent colonization by harmful microbes.
- Gastrointestinal Tract: Diverse community of bacteria that aid in digestion and immune function.
- Respiratory Tract: Bacteria that help prevent colonization by pathogens.
- Urogenital Tract: Bacteria that maintain pH and prevent infections.
Sometimes Germs Really Upstage
Skin: Staphylococcus epidermidis, Propionibacterium
Gastrointestinal Tract: Gut bacteria (Escherichia coli, Bacteroides)
Respiratory Tract: Respiratory bacteria (Streptococcus pneumoniae, Haemophilus influenzae)
Urogenital Tract: Urinary/Lactobacillus, Candida
Challenges in treating eukaryotic pathogens include:
- Similarity to Host Cells: Makes it difficult to target pathogens without harming host cells.
- Complex Life Cycles: Especially for parasites, making them hard to eliminate completely.
- Drug Resistance: Some fungi and parasites can develop resistance to treatments.
TLO 4.2 Types of symbiotic relationships and examples
Symbiotic relationships include:
- Mutualism: Both organisms benefit (e.g., gut bacteria aiding in digestion).
- Commensalism: One organism benefits while the other is unaffected (e.g., some skin bacteria).
- Parasitism: One organism benefits at the expense of the other (e.g., intestinal worms).
Mutualism Both organisms benefit Gut bacteria and humans (digestive health)
Commensalism One organism benefits, the other is unaffected Staphylococcus on the skin
Parasitism One organism benefits, the other is harmed Malaria parasite in humans
TLO 4.3 Process of infection (bacterial, viral, fungal, helminthic, parasitic)
The process of infection varies slightly depending on the type of pathogen, but generally follows these steps:
- Entry
- Adherence
- Invasion
- Multiplication
- Spread
- Tissue Damage
- Shedding:
Entry All Insects Must Scatter To Survive
TLO 4.3 Process of infection (bacterial, viral, fungal, helminthic, parasitic)
The process of infection varies slightly depending on the type of pathogen, but generally follows these steps:
- Entry: Pathogens enter the host through various routes:
* Bacterial: Through breaks in skin, mucous membranes, or ingestion
* Viral: Similar to bacterial, often through respiratory or mucosal routes
* Fungal: Often through inhalation of spores or skin contact
* Helminthic and Parasitic: Usually through ingestion or skin penetration - Adherence: Pathogens attach to host cells:
* Bacterial: Using pili or adhesins
* Viral: Via specific receptor binding
* Fungal: Through adhesins
* Helminthic and Parasitic: Using hooks, suckers, or other specialized structures - Invasion: Pathogens penetrate host tissues:
* Bacterial: Some remain extracellular, others enter cells
* Viral: Enter host cells for replication
* Fungal: Can invade tissues or remain superficial
* Helminthic and Parasitic: Often migrate through tissues to specific organs - Multiplication:
* Bacterial: Divide by binary fission
* Viral: Replicate using host cell machinery
* Fungal: Grow by extending hyphae or budding
* Helminthic and Parasitic: Often involve complex life cycles with multiple stages - Spread:
* Can occur locally or systemically through blood or lymph - Tissue Damage:
* Direct damage from pathogen activity
* Indirect damage from host immune response - Shedding:
* Release of pathogens from the host to potentially infect others
Topic 5 – Antibiotics
TLO 5.1 Difference between narrow and broad-spectrum antibiotics
- Narrow Spectrum Antibiotics:
- Target specific types of bacteria
- Examples: Penicillin G (effective against gram-positive bacteria), Vancomycin (targets gram-positive bacteria)
- Advantages: Less likely to cause antibiotic resistance, fewer side effects
- Disadvantages: Require accurate diagnosis before prescription
Topic 5 – Antibiotics
TLO 5.1 Difference between narrow and broad-spectrum antibiotics
- Broad Spectrum Antibiotics:
- Effective against a wide range of bacterial types
- Examples: Tetracyclines, Chloramphenicol
- Advantages: Can be used empirically before specific pathogen identification
- Disadvantages: Higher risk of antibiotic resistance, more likely to disrupt normal
Type of Antibiotic Description Examples Pros Cons
Narrow-Spectrum Effective against a specific group of bacteria Penicillin, Erythromycin - Targets specific bacteria effectively - Limited use against a wide range of infections
- Reduces risk of antibiotic resistance - May require precise identification of pathogen
Broad-Spectrum Effective against a wide range of bacteria Tetracycline, Ciprofloxacin - Can treat multiple types of infections - Higher risk of antibiotic resistance
- Useful in situations where the pathogen is unknown - Can disrupt normal flora, leading to side effects like diarrhea
TLO 5.2 Families of antibiotics and their modes of action
- Beta-lactams
- Aminoglycosides
- Tetracyclines
- Macrolides
- Fluoroquinolones
- Sulfonamides
- Glycopeptides
TLO 5.2 Families of antibiotics and their modes of action
- Beta-lactams (e.g., penicillins, cephalosporins):
* Mode of action: Inhibit cell wall synthesis
* Target: Peptidoglycan layer of bacterial cell wall - Aminoglycosides (e.g., streptomycin, gentamicin):
* Mode of action: Inhibit protein synthesis
* Target: 30S ribosomal subunit - Tetracyclines:
* Mode of action: Inhibit protein synthesis
* Target: 30S ribosomal subunit - Macrolides (e.g., erythromycin):
* Mode of action: Inhibit protein synthesis
* Target: 50S ribosomal subunit - Fluoroquinolones (e.g., ciprofloxacin):
* Mode of action: Inhibit DNA replication
* Target: DNA gyrase and topoisomerase IV - Sulfonamides:
* Mode of action: Inhibit folic acid synthesis
* Target: Enzyme involved in folic acid production - Glycopeptides (e.g., vancomycin):
* Mode of action: Inhibit cell wall synthesis
* Target: Peptidoglycan precursors
TLO 5.3 Significance of bacteria producing beta-lactamase
The production of beta-lactamase by bacteria is significant for several reasons:
- Antibiotic Resistance: Beta-lactamase enzymes can hydrolyze the beta-lactam ring of many commonly used antibiotics, rendering them ineffective.
- Treatment Failure: Infections caused by beta-lactamase-producing bacteria may not respond to first-line antibiotic treatments, leading to prolonged illness and increased healthcare costs.
- Spread of Resistance: Genes encoding beta-lactamase can be transferred between bacteria, potentially leading to widespread antibiotic resistance.
- Need for New Antibiotics: The prevalence of beta-lactamase-producing bacteria has driven the development of new antibiotics and beta-lactamase inhibitors.
- Clinical Implications: Healthcare providers must consider the possibility of beta-lactamase production when selecting antibiotics, often necessitating the use of broader-spectrum or combination therapies.
- Public Health Concern: The spread of beta-lactamase-producing bacteria, especially in healthcare settings, poses a significant challenge to infection control and patient safety.
TLO 5.3 Significance of bacteria producing beta-lactamase
The production of beta-lactamase by bacteria is significant for several reasons:
- Antibiotic Resistance
- Treatment Failure
- Spread of Resistance
- Need for New Antibiotics
- Clinical Implications
- Public Health Concern
Clostridium difficile is a gram-positive bacteria forming one of the large intestine microbiota. However,it can lead to a disease process after antibiotics use especially in elderly. This is mainly due to:
a. Exogenous infection
b. Antibiotics help Clostridia to grow and multiply
c. Mutualistic relationship between the antibiotics and Clostridia difficile bacteria
d. Antibiotic treatment affect the normal population of large intestinal microbiota except for Clostridia due to its ability to form endospores
Antibiotic treatment affect the normal population of large intestinal microbiota except for Clostridia due to its ability to form endospores
The proteins on the external surface of viruses serve several important functions. Regarding these proteins, which one of the following statements is most accurate?
a. They are the antigens against which neutralizing antibodies are formed.
b. They are the proteins that regulate viral transcription.
c. They are the polymerases that synthesize viral messenger RNA.
d. They are the proteases that degrade cellular proteins leading to cell death.
a.
They are the antigens against which neutralizing antibodies are formed.
Which of the following is a dimorphic fungi?
a. Microsporum
b. Blastomyces dermatitidis
c. Candida albicans
d. Trichophyton
b. Blastomyces dermatitidis
Regarding the structure and reproduction of fungi, which one of the following is most accurate?
a.As most fungi are anaerobic, they should be cultured under anaerobic conditions in the clinical laboratory
b.Peptidoglycan is an important component of the cell wall of fungi
c. The fungal cell membrane contains ergosterol, whereas the human cell membrane contains cholesterol
d. Some fungi are dimorphic (i.e., they are yeasts at room temperature and molds at body temperature)
e. Molds are fungi that grow as single cells and reproduce by budding
c. The fungal cell membrane contains ergosterol, whereas the human cell membrane contains cholesterol
The initial step in the process of many bacterial infections is adherence of the organism to mucous membranes. The bacterial component that mediates adherence is the:
a. Peptidoglycan
b. Pilus
c. Plasmid
d. Nucleoid
e. Lipid A
b. Pilus
What kind of spores contain many endospores within tissues?
a. Arthroconidia
b. Conidia
c. Spherules
d. Blastoconidia
c. Spherules
Herpes simplex virus is an enveloped virus. Based on the characteristics you learned about enveloped viruses, which of the following is true?
a. It can survive the GIT environment
b. The lipid component of the membrane will make more easily inactivated by lipid solvents and detergents
c. It can dry out and retain its infectivity
d. The virion structure consists only of proteins
b. The lipid component of the membrane will make more easily inactivated by lipid solvents and detergents
Lysozyme in tears is an effective mechanism for preventing bacterial conjunctivitis. Which one of the following bacterial structures does lysozyme degrade?
a. Endotoxin
b. Peptidoglycan
c. Pilus
d. Plasmid DNA
e. Nucleoid DNA
b. Peptidoglycan
Which of the following are true about sulfonamide/trimethoprim:
a. Narrow spectrum
b. Works as antagonist to folic acid synthesis
c. Works against gram positive only
d. Beta lactam inhibitor
b. Works as antagonist to folic acid synthesis
All Fungal organisms are?
a. Prions
b. Prokaryotic
c. Multicellular
d. Eukaryotic
d. Eukaryotic
You’re watching a television program that is discussing viruses called bacteriophages that can kill bacteria. What’s the difference between viruses and bacteria? Which one of the following would be the most accurate statement to make?
a. Viruses do not have ribosomes, whereas bacteria do.
b. Viruses replicate by binary fission, whereas bacteria replicate by mitosis.
c. Viruses do not have mitochondria, whereas bacteria do.
d. Viruses are prokaryotic, whereas bacteria are eukaryotic.
e. Viruses do not have a nucleolus, whereas bacteria do.
a. Viruses do not have ribosomes, whereas bacteria do.
The purified genome of certain viruses can enter a cell and elicit the production of progeny viruses (i.e.the genome is infectious). Regarding these viruses, which one of the following statements is most accurate?
a. They have a polymerase in the virion
b. Their genome RNA is double-stranded
c. Their genome RNA has positive polarity
d. They have a segmented genome
c. Their genome RNA has positive polarity
Several bacteria that form spores are important human pathogens. Which one of the following is the most accurate statement about bacterial spores?
a. They are produced by anaerobes only in the presence of oxygen.
b. They are metabolically inactive yet can survive for years in that inactive state.
c. They are killed by boiling for 15 minutes.
d. They are formed primarily when the bacterium is exposed to antibiotics.
e. They are produced primarily by gram-negative cocci.
b. They are metabolically inactive yet can survive for years in that inactive state.
Many viruses are highly specific regarding the type of cells they infect. Of the following, which one is the most important determinant of this specificity?
a. The surface glycoprotein
b. The matrix protein
c. The viral mRNA
d. The polymerase in the virion
e. The protease protein
a. The surface glycoprotein
When it comes to fungi, what kind of spores looks like asexual spores formed by a (joint)?
a. Spherules
b. Blastoconidia
c. Conidia
d. Arthroconidia
d. Arthroconidia
What is meant by an extended spectrum penicillin?
a. Bacteriocidal for killing gram positive bacteria
b. Bacteriostatic for killing gram negative bacteria
c. Has an increased half-life in the body
d. Bacteriocidal for both gram negative and gram positive bacteria
d. Bacteriocidal for both gram negative and gram positive bacteria
Which of the following is a beta lactam antibiotic:
a. Clindamycin
b. Penicillin
c. Tetracycline
d. Macrolides
b.Penicillin
In symbiotic association, when an organism is completely dependent on the host to provide their habitat, food, respiratory and other metabolic needs. This type is association is said to be:
a. Parasitism
b. Mutualism
c. Exogenous
d. Opportunistic
e. Commensalism
a.Parasitism
Bacteria that cause nosocomial (hospital-acquired) infections often produce extracellular substances that allow them to stick firmly to medical devices, such as intravenous catheters. Which one of the following is the name of this extracellular substance?
a. Porin
b. Endotoxin
c. Flagella
d. Glycocalyx
e. Axial filament
d. Glycocalyx
Which one of the following contains DNA that is not surrounded by a nuclear membrane?
a. Molds
b. Protozoa
c. Bacteria
d. Yeasts
c. Bacteria
Clostridium difficile is a gram-positive bacteria forming one of the large intestine microbiota. However, it can lead to a disease process after antibiotics use especially in elderly. This is mainly due to:
a. Exogenous infection
b. Antibiotics help Clostridia to grow and multiply
c. Antibiotic treatment affect the normal population of large intestinal microbiota except for Clostridia due to its ability to form endospores
d. Mutualistic relationship between the antibiotics and Clostridia difficile bacteria
c. Antibiotic treatment affect the normal population of large intestinal microbiota except for Clostridia due to its ability to form endospores
Herpes simplex virus is an enveloped virus. Based on the characteristics you learned about enveloped viruses, which of the following is true?
a. The lipid component of the membrane will make more easily inactivated by lipid solvents and detergents
b. It can dry out and retain its infectivity
c. It can survive the GIT environment
d. The virion structure consists only of proteins
a.
The lipid component of the membrane will make more easily inactivated by lipid solvents and detergents
Which of the following are true about sulfonamide/trimethoprim:
a. Works against gram positive only
b. Narrow spectrum
c. Beta lactam inhibitor
d. Works as antagonist to folic acid synthesis
d. Works as antagonist to folic acid synthesis
The initial step in the process of many bacterial infections is adherence of the organism to mucousmembranes. The bacterial component that mediates adherence is the:
a. Lipid A
b. Plasmid
c. Nucleoid
d. Pilus
e. Peptidoglycan
d. Pilus
All Fungal organisms are?
a. Eukaryotic
b. Multicellular
c. Prions
d. Prokaryotic
a. Eukaryotic
Which of the following is a dimorphic fungi?
a. Trichophyton
b. Microsporum
c. Blastomyces dermatitidis
d. Candida albicans
c. Blastomyces dermatitidis
Lysozyme in tears is an effective mechanism for preventing bacterial conjunctivitis. Which one of the following bacterial structures does lysozyme degrade?
a. Nucleoid DNA
b. Endotoxin
c. Plasmid DNA
d. Peptidoglycan
e. Pilus
d. Peptidoglycan
Several bacteria that form spores are important human pathogens. Which one of the following is themost accurate statement about bacterial spores?
a. They are formed primarily when the bacterium is exposed to antibiotics.
b. They are metabolically inactive yet can survive for years in that inactive state.
c. They are produced by anaerobes only in the presence of oxygen.
d.
They are killed by boiling for 15 minutes.
e.
They are produced primarily by gram-negative cocci.
b. They are metabolically inactive yet can survive for years in that inactive state.
The proteins on the external surface of viruses serve several important functions. Regarding these proteins, which one of the following statements is most accurate?
a. They are the antigens against which neutralizing antibodies are formed.
b. They are the proteases that degrade cellular proteins leading to cell death.
c. They are the polymerases that synthesize viral messenger RNA.
d. They are the proteins that regulate viral transcription.
a. They are the antigens against which neutralizing antibodies are formed.
Bacteria Summary
Bacteria are prokaryotes. Their DNA is not contained within a nucleus and there are relatively few cytoplasmic organelles.
The cell wall is a key structure in metabolism, virulence, and immunity. Its staining characteristics define the two major divisions: the Gram-positive and Gram-negative bacteria.
Bacteria may have structures external to the cell wall:
Flagella for motility
Pili for attachment and conjugation
Capsule is antiphagocytic
Slime layer for firm attachment
Bacteria have different shapes: Cocci, Bacilli, and Spiral, and different arrangements: Pairs, Clusters, and Chains.
Bacteria metabolize aerobically and anaerobically and can utilize different substrates.
Certain bacteria can form spores under undesirable environmental circumstances. These spores are medically important because they are heat resistant and cannot be killed by disinfectants.
Bacteria reproduce by binary fission, whereas eukaryotic cells reproduce by mitosis.
Which of the following is considered a prokaryote?
O Protozoa
O Bacteria
O Mammal
O Fungi”
Bacteria
Microbiota Summary
The body is colonized by many organisms (the microbiota), which can be positively beneficial. They live on or within the body without causing disease, and play an important role in protecting the host from pathogenic microbes.
Members of the microbiota can be harmful if they enter previously sterile parts of the body. They can also be causes of hospital-acquired infections.
The usual relationship between the microbiota and the body is an example of beneficial symbiosis; parasitism (in the broad sense, covering all pathogenic microbes) is a harmful symbiosis.
The biological context of host-parasite relationships, and the dynamics of the conflict between two species in this relationship, provide a basis for understanding the causes and control of infectious diseases.
What is the name for a chain of circular shaped bacteria?
Diplobacillus
Streptococci
Streptobacilli
Staphylobacillus
Staphylococcus”
Streptococci
Virus | Target Cell | Receptor
Virus | Target Cell | Receptor — | — | —
Epstein-Barr virus | B cell | C3d complement receptor (CR2, CD21)
HIV | Helper T cell | CD4 molecule and chemokine coreceptor
Rhinovirus | Epithelial cells | ICAM-1 (immunoglobulin superfamily protein)
Poliovirus | Epithelial cells | Immunoglobulin superfamily protein
Herpes simplex virus | Many cells | Herpesvirus entry mediator (HveA), nectin-1
Rabies virus | Neuron | Acetylcholine receptor, NCAM
Influenza A virus | Epithelial cells | Sialic acid
B19 parvovirus | Erythroid precursors | Erythrocyte P antigen (globoside)
Virus Summary
Viruses are obligate intracellular pathogens that range in size from that of large proteins (~20 nm) to that of the smallest cells (~300 nm).
Viruses have RNA or DNA but not both and are absolutely dependent on the host to process their genetic information into new virus particles.
The viral genome is covered by a capsid or envelope, which plays a role in host cell specificity for attachment and determines the virus’s capacity to survive outside the host.
The replication of viral RNA or DNA is a complex process, making use of host and/or viral enzymes.
Generally speaking, the size of a virus is:
Smaller than bacteria
The same size as bacteria
Larger than bacteria
Smaller than bacteria
What is the correct sequence of steps in the viral life cycle?
Recognition of target cell
Attachment to target cell
Penetration through endocytosis
Uncoating to release virus
Biosynthesis of viral nucleic acids
Assembly of virus
Release of virus
ANTIBIOTIC CLASSES
AMINOGLYCOSID
CEPHALOSPORINS
PENICILLINS
TETRACYCLINES
QUINOLONES/FLUOROQUINOLONES
MACROLIDE
SULFONAMIDES
GLYCOPEPTIDES
Fungi Summary
Fungi are distinct from plants and animals, have a thick chitin-containing cell wall, and grow as filaments (hyphae) or single-celled yeasts.
Infections may be located superficially, in cutaneous and subcutaneous sites, or in deep tissues.
Fungal infections are most serious in immunocompromised individuals.
Parasites can be either single-celled or multicellular. They can reproduce both sexually and asexually, with complex life cycles.
Some parasites establish a permanent relationship with humans, while others go through a series of developmental stages in a progression of animal hosts.
All parasites reproduce asexually
True
False
False
A symbiotic relationship that is beneficial to both parties and one is completely dependent on the other is called:
Commensalism
Parasitism
Mutualism
Mutualism
Which feature of the influenza virus assists its attachment to host cells?
Exotoxin
Hemagglutinin spikes
Neuroaminidase spikes
Endotoxin
Hemagglutinin spikes
What is the mechanism of action of the antibiotic penicillin?
Inhibit nucleic acid synthesis
Damage cytoplasmic membranes
Inhibit peptidoglycan synthesis
Inhibit cell metabolism
Inhibit protein synthesis
Inhibit peptidoglycan synthesis
What is the term for a single cell fungi?
Pseudohyphae
Hyphae
Yeast
Mycelium
Yeast
ANTIBIOTIC CLASSES
AMINOGLYCOSIDE -VE Streptomycin, Gentamicin Inhibit protein synthesis (30s)
CEPHALOSPORINS +VE/-VE Cefazolin, Cefadroxil Inhibit cell wall synthesis
PENICILLINS +VE/-VE Penicillin G, Ampicillin, Methicillin Inhibit cell wall synthesis
TETRACYCLINES +VE/-VE Tetracycline, Doxycycline Inhibit protein synthesis (30s)
QUINOLONES/FLUOROQUINOLONES +VE/-VE Ciprofloxacin Inhibit DNA replication (topoisomerase I + II)
MACROLIDE +VE Erythromycin Inhibit protein synthesis (50s)
SULFONAMIDES +VE/-VE Sulfamethoxazole Inhibit folate synthesis
GLYCOPEPTIDES +VE Vancomycin Inhibit cell wall synthesis
THE QUEEN’S GUIDANCE COUNSELLOR SAID ANTIBIOTICS CAN PROTECT MANY MOST ROYAL MEMBERS
THE QUEEN’S GUIDANCE COUNSELLOR SAID ANTIBIOTICS CAN PROTECT MANY MOST ROYAL MEMBERS
if not
Tetracycline Quinolone/Fluoroquinolone Glycopeptide Cephalosporin Sulfonamides Aminoglycosides Carbapenem Penicillin Macrolides Monobactam Rifampin Metronidazole
+/-
+/-
+/-
+/-
+/-
+/-
+/-
+/-
+/-
+/-
Tetracycline/Doxycycline Nalidixic acid/Ciprofloxacin Vancomycin Cefdinir Sulfamethoxazole Gentamycin/Streptomycin Meropenem Penicillin/Amoxicillin Erythromycin Aztreonam Rifampin Metronidazole
30s subunit
DNA synthesis II + IV
Cell Wall
Cell Wall
Folic acid synthesis
30s subunit
Cell Wall
Cell Wall
50s subunit
Cell Wall
RNA polymerase
Damage DNA
Difference between virus and bacteria
Aspect Virus Bacteria
Size Smaller (20-300 nm) Larger (0.5-5 micrometers)
Cell Type Not considered cells (acellular) Prokaryotic cells
Genetic Material Either RNA or DNA, but not both Both RNA and DNA
Reproduction Requires a host cell to reproduce Can reproduce independently through binary fission
Structure Consists of genetic material enclosed in a protein coat (capsid); some have lipid envelopes Complex cellular structure with cell wall, membrane, cytoplasm, and organelles
Metabolism No metabolic activity on their own Metabolically active, capable of carrying out various biochemical processes
Living Status Non-living (obligate intracellular parasites) Living organisms
Host Dependency Completely dependent on a host cell for replication Can grow and reproduce in various environments, some are obligate parasites
Treatment Antiviral drugs target specific stages of viral replication Antibiotics target bacterial cell wall, protein synthesis, DNA replication, etc.
Examples Influenza virus, HIV, Rabies virus Streptococcus pneumoniae, Escherichia coli, Mycobacterium tuberculosis
In the process of studying how bacteria cause disease, a rare mutant of a usually pathogenic strain of bacteria was found that failed to form a capsule. Which one of the following statements describes the likely impact of this unencapsulated mutant strain?
A. It was nonpathogenic primarily because it was easily phagocytosed.
B. It was nonpathogenic primarily because it could not invade tissue. C. It was nonpathogenic primarily because it could only grow anaerobically.
D. It was highly pathogenic because it could secrete larger amounts of exotoxin.
E. It was highly pathogenic because it could secrete larger amounts of endotoxin.
A. It was nonpathogenic primarily because it was easily phagocytosed.
Of the following bacterial components, which one exhibits the most antigenic variation?
A. Capsule
B. Lipid A of endotoxin
C. Peptidoglycan
D. Ribosome
E. Spore
A. Capsule
How do prokaryotes replicate?
A. Budding
B. Mitosis
C. Using host enzymes
D. Binary fission
D. Binary fission
Human immunodeficiency virus (HIV) is a retrovirus, its replication occurs via which process?
A. Viral double stranded RNA negative sense strand is transcribed to positive sense DNA and integrated into the host DNA
B. Viral double stranded RNA negative sense strand is transcribed to positive sense RNA and used as mRNA
C. Viral single stranded negative sense RNA is transcribed to positive sense RNA and used as mRNA
D. Viral single stranded positive sense RNA is transcribed into negative sense DNA and integrated into the host DNA
D. Viral single stranded positive sense RNA is transcribed into negative sense DNA and integrated into the host DNA
Blastomyces is a dimorphic fungus that can cause systemic disease. This means that:
A. They convert to yeast in cold conditions
B. They convert to hyphae in cold conditions
C. They convert to bacteria in cold conditions
D. They convert to a parasite in cold conditions
B. They convert to hyphae in cold conditions
A 10-year-old patient presents with stomach cramps, nausea, and watery diarrhea. The unicellular parasite Giardia lamblia is suspected as the cause of the patient’s condition. What type of parasite is Giardia?
A. Protozoa
B. Helminth
C. Arthropod
D. Hyphae
A. Protozoa
What characteristic of bacteria allows gram staining to differentiate between gram-positive and gram-negative bacteria?
A. Thickness of the peptidoglycan cell wall
B. Presence of DNA within the nucleus
C. Thickness of the lipoprotein envelope D. Presence of external cilia or flagella
A. Thickness of the peptidoglycan cell wall
What is a bacteriophage
Type
- Virus
Targets
- Bacteria
Infection Process
1. Attaches to the bacterial cell
2. Injects its genetic material
3. Uses bacterial machinery to replicate
4. Bacterial cell bursts, releasing new bacteriophages
Topic 1 – Pharmacodynamics I
TLO 1.1 Four Molecular Drug Targets and Their Functions
Receptors – These are specialized proteins that bind to endogenous ligands (such as neurotransmitters or hormones) or drugs to initiate a physiological response. They play a key role in signal transduction.
Example: Beta-adrenergic receptors are G-protein coupled receptors (GPCRs) that mediate the effects of epinephrine and norepinephrine. Drugs like propranolol (a beta-blocker) inhibit these receptors to reduce heart rate and blood pressure.
Ion Channels – These are pore-forming proteins in cell membranes that regulate ion flow based on electrochemical gradients. Drugs can either block or modulate ion channels.
Example: Calcium channels allow calcium influx into cells. Nifedipine, a calcium channel blocker, inhibits this process to cause vasodilation, reducing blood pressure.
Enzymes – These biological catalysts facilitate biochemical reactions. Drugs can act as inhibitors (preventing enzyme function) or activators (enhancing enzyme function).
Example: Acetylcholinesterase (AChE) breaks down acetylcholine. Neostigmine, an AChE inhibitor, prolongs acetylcholine activity, improving muscle contraction in myasthenia gravis.
Transporters (Carrier Proteins) – These membrane proteins facilitate the movement of substances across cell membranes, including ions, nutrients, and neurotransmitters.
Example: The serotonin transporter (SERT) is responsible for reuptake of serotonin from the synaptic cleft. Fluoxetine (an SSRI) blocks SERT, increasing serotonin levels and improving mood in depression.
TLO 1.2 Four Receptor Subtypes and Their Signaling Mechanisms
The four primary receptor subtypes, based on their signaling mechanisms, are:
- G protein-coupled receptors (GPCRs),
- ligand-gated ion channels,
- receptor tyrosine kinases (RTKs), and
- intracellular receptors; each activating distinct intracellular pathways upon ligand binding.
Explanation of each receptor subtype and its signaling mechanism:
G protein-coupled receptors (GPCRs):
Structure: A seven-transmembrane domain protein embedded in the cell membrane.
Mechanism: When a ligand binds to the GPCR, it activates a G protein on the cytoplasmic side, which then interacts with downstream effector molecules like enzymes or ion channels, triggering a cellular response.
Example: Adrenaline receptors, which activate the “fight or flight” response.
Ligand-gated ion channels:
Structure: A transmembrane protein with a pore that opens when a specific ligand binds.
Mechanism: Ligand binding directly causes the ion channel to open, allowing ions to flow across the cell membrane, rapidly changing the cell’s membrane potential and triggering a cellular response.
Example: Nicotinic acetylcholine receptors at the neuromuscular junction.
Receptor tyrosine kinases (RTKs):
Structure: A transmembrane protein with an intracellular tyrosine kinase domain.
Mechanism: Upon ligand binding, the receptor dimerizes, activating its intrinsic tyrosine kinase activity which phosphorylates tyrosine residues on target proteins, initiating a signaling cascade.
Example: Insulin receptor.
Intracellular receptors:
Structure: Located within the cytoplasm or nucleus of the cell.
Mechanism: Small, hydrophobic ligands diffuse through the cell membrane and bind to the intracellular receptor, which then translocates to the nucleus to regulate gene expression by binding to DNA.
Example: Steroid hormone receptors like estrogen and testosterone.
Key points to remember:
Different receptor subtypes have different ligand specificities, meaning only certain molecules can bind and activate them.
The downstream signaling pathways activated by each receptor type can vary depending on the cell type and the specific receptor involved.
Many drugs target specific receptor subtypes to modulate cellular processes.
Ligand-Gated Ion Channels (Ionotropic Receptors) – These receptors are directly coupled to ion channels and open upon ligand binding, allowing ions to pass through.
Example: The nicotinic acetylcholine receptor (nAChR) at neuromuscular junctions allows sodium (Na⁺) entry upon acetylcholine binding, triggering muscle contraction.
G-Protein Coupled Receptors (Metabotropic Receptors) – These receptors activate intracellular signaling cascades via G-proteins upon ligand binding. They influence cell function indirectly through second messengers like cyclic AMP (cAMP) or calcium (Ca²⁺).
Example: Beta-adrenergic receptors (Gs-protein coupled) activate adenylate cyclase, increasing cAMP levels, leading to increased cardiac contractility.
Kinase-Linked Receptors – These receptors mediate effects through phosphorylation cascades, leading to gene transcription and protein synthesis.
Example: The insulin receptor is a tyrosine kinase receptor that, upon insulin binding, triggers glucose uptake via GLUT4 translocation in muscle and fat cells.
Nuclear Receptors – These receptors are intracellular and function as transcription factors when activated.
Example: The glucocorticoid receptor binds cortisol, moves to the nucleus, and modulates gene expression, reducing inflammation.
TLO 1.3 Gating Properties of Ion Channels
Ion channel gating refers to the opening and closing of ion channels, which is controlled by stimuli like voltage, ligands, or mechanical forces. Gating is a conformational change in the protein that makes up the channel.
Types of gated ion channels
Voltage-gated ion channels: Open and close in response to changes in the voltage across the cell membrane
Ligand-gated ion channels: Open and close in response to binding of ligands to the channel
Mechanosensitive channels: Open and close in response to physical deformation of the cell membrane
Phosphorylation-gated ion channels: Change their structure and permeability by phosphorylation
Leakage ion channels: Are constantly activated
Ion channel gating mechanisms
Activation: The transition from the resting state to the open state
Inactivation: A self-restraint mechanism to limit ion conduction
Ion channel function
Ion channels are responsible for the electrical excitability of muscle cells, and they mediate most forms of electrical signaling in the nervous system
Types of Gating:
Voltage-gated: Open or close in response to changes in membrane potential (e.g., voltage-gated Na⁺ channels in neurons).
Ligand-gated: Open when a specific molecule binds (e.g., GABA-A receptor allowing Cl⁻ influx).
Mechanically gated: Respond to physical forces like stretch (e.g., mechanoreceptors in touch-sensitive neurons).
Modulation Mechanisms:
Phosphorylation: Addition of a phosphate group can enhance or inhibit channel activity.
Ligand Binding: Agonists/antagonists can modulate ion flow.
Voltage Changes: Ion channels respond to depolarization/hyperpolarization.
Selectivity Mechanisms:
Determined by pore size, charge distribution, and amino acid composition, allowing selective ion passage.
Topic 2 – Pharmacodynamics II
TLO 2.1 Drug Action Properties
Selectivity: A drug’s ability to preferentially bind to a specific target (e.g., atenolol selectively blocks beta-1 receptors, sparing beta-2 receptors).
Affinity: Strength of drug binding to its receptor, measured by dissociation constant (Kd).
Potency: The drug concentration required to elicit 50% of its maximal effect (EC₅₀).
Efficacy: The maximum effect a drug can produce, regardless of dose.
TLO 2.2 Types of Agonists
Full Agonist: Produces maximal receptor activation (e.g., morphine at opioid receptors).
Partial Agonist: Produces a submaximal response even at high concentrations (e.g., buprenorphine).
Inverse Agonist: Produces the opposite effect of an agonist by stabilizing the inactive receptor conformation (e.g., propranolol at beta receptors).
TLO 2.4 Orthosteric vs. Allosteric Modulation
Orthosteric: Binds at the receptor’s active site (e.g., atropine at muscarinic receptors).
Allosteric: Binds at a separate site, modifying receptor activity (e.g., benzodiazepines enhance GABA-A receptor function).
TLO 2.3 Competitive Antagonists
Reversible: Compete with agonists but can be displaced by increasing agonist concentration (e.g., naloxone for opioid overdose).
Irreversible: Bind covalently, permanently blocking receptor activity (e.g., phenoxybenzamine, an alpha-blocker for pheochromocytoma).
Topic 3 – Pharmacokinetics I
TLO 3.1 Drug Absorption Factors
Drug ab- sorption involves the movement of the drug across a cell membrane and is largely dependent on diffusion. The absorption rate is deter- mined by the preparation of the drug, route of administration, size of the molecule, concentration gradient, degree of protein binding and lipid solubility of the drug
The first-pass metabolism of a drug that mainly takes place in the gastrointestinal tract (GIT) and liver greatly reduces the systemic bioavailability as well as the efficacy of an orally administered drug as compared to the parenteral drugs
Lipid Solubility: Lipophilic drugs cross membranes more easily.
pH & Ionization: Weak acids (e.g., aspirin) absorb better in acidic environments (stomach), while weak bases (e.g., morphine) absorb in alkaline environments (intestine).
First-Pass Metabolism: Hepatic metabolism before systemic circulation reduces bioavailability.
TLO 3.2 Routes of Administration
Oral: Most convenient but undergoes first-pass metabolism.
Intravenous (IV): Immediate effect, 100% bioavailability.
Intramuscular (IM)/Subcutaneous (SC): Slower, sustained absorption.
Other information
Drugs are introduced into the body by several routes. They may be
Taken by mouth (orally)
Given by injection into a vein (intravenously, IV), into a muscle (intramuscularly, IM), into the space around the spinal cord (intrathecally), or beneath the skin (subcutaneously, sc)
Placed under the tongue (sublingually) or between the gums and cheek (buccally)
Inserted in the rectum (rectally) or vagina (vaginally)
Placed in the eye (by the ocular route) or the ear (by the otic route)
Sprayed into the nose and absorbed through the nasal membranes (nasally)
Breathed into the lungs, usually through the mouth (by inhalation) or mouth and nose (by nebulization)
Applied to the skin (cutaneously) for a local (topical) or bodywide (systemic) effect
Delivered through the skin by a patch (transdermally) for a systemic effect
TLO 3.3 Drug Bioavailability
The fraction of the administered dose reaching systemic circulation unchanged.
IV = 100%, oral varies due to first-pass metabolism and solubility.
Absolute bioavailability is defined as 100% of the substance reaching the bloodstream, which can only be achieved through an intravenous (IV) means. Relative bioavailability is the amount of the substance that reaches the bloodstream through other means of administration, like oral and sublingual.
TLO 3.5 Drug Distribution
Factors Affecting Distribution:
Blood flow (high in liver, kidneys, brain; low in fat, bone).
Plasma protein binding (e.g., albumin).
Tissue permeability (lipophilic drugs distribute widely).
Absorption, distribution, metabolism, and excretion
TLO 3.6 Two-Compartment Model
Central compartment: Rapidly perfused organs (heart, liver, kidney, blood).
Peripheral compartment: Less-perfused tissues (fat, muscle).
The two-compartment pharmacokinetic model describes the evolution of drug levels in the organism by depicting the body as two pharmacokinetic compartments (the central and the peripheral compartments, also commonly referred to as compartment 1 and compartment 2, in that order).
Topic 4 – Pharmacokinetics II
TLO 4.1 First-Pass Metabolism
Hepatic metabolism before reaching systemic circulation.
Reduces oral drug bioavailability (e.g., nitroglycerin).
The first-pass metabolism or the first-pass effect or presystemic metabolism is the phenomenon which occurs whenever the drug is administered orally, enters the liver, and suffers extensive biotransformation to such an extent that the bioavailability is drastically reduced, thus showing subtherapeutic action
TLO 4.2 Phase 1 & 2 Biotransformation
Phase 1: Oxidation, reduction, hydrolysis (CYP enzymes).
Phase 2: Conjugation (glucuronidation, sulfation).
Phase I reactions involve formation of a new or modified functional group or cleavage (oxidation, reduction, hydrolysis); these reactions are nonsynthetic. Phase II reactions involve conjugation with an endogenous substance (eg, glucuronic acid, sulfate, glycine); these reactions are synthetic.
TLO 4.3 CYP Enzymes in Drug Interactions
CYP3A4: Metabolizes many drugs; inhibitors (e.g., ketoconazole) and inducers (e.g., rifampin) alter metabolism.
An overly active CYP enzyme will render the drug ineffective. However, if these enzymes are not active enough, the drug can stay in the body for a prolonged duration leading to toxicity. Of all the different CYP proteins that are present in the human body, six of them are involved in the metabolism of 90% of drugs.
Cytochrome P-450 (CYP) enzymes are a family of enzymes that metabolize many drugs. They are often involved in drug interactions, which can lead to adverse reactions or therapeutic failures.
How do CYP enzymes cause drug interactions?
Inhibition
Drugs can inhibit CYP enzymes, which can increase the amount of a drug that is absorbed and increase its bioavailability.
Induction
Drugs can induce CYP enzymes, which can reduce the amount of a drug that is absorbed and reduce its bioavailability.
Genetic variability
Genetic differences in CYP enzymes can affect how a patient responds to certain drugs.
Examples of drugs that interact with CYP enzymes warfarin, antidepressants, antiepileptic drugs, and statins.
How can clinicians use this information?
Clinicians can use knowledge of CYP enzyme substrates, inducers, and inhibitors to help determine therapeutic strategies and doses for drugs.
Clinicians can ask patients about their use of complementary and alternative medicines when considering the use of a medicine that is altered by CYP3A4
TLO 4.4 Drug Excretion
Renal: Filtration, secretion, reabsorption.
Biliary: Liver to bile, excreted in feces.
Pulmonary: Volatile drugs via respiration.
Renal, biliary, and pulmonary excretion are all ways that drugs are eliminated from the body.
Renal excretion
The primary way that drugs are eliminated from the body
The kidneys filter drugs from the bloodstream, and some are reabsorbed back into the bloodstream, while the rest are excreted in the urine
The kidneys are the main organs responsible for excreting water-soluble substances
Biliary excretion
The liver excretes waste and byproducts into the bile
Some drugs and their metabolites are excreted in the bile
Pulmonary excretion
The lungs eliminate drugs like alcohol and anesthetic gases
Pulmonary excretion is important for gaseous lipophilic substances
Drugs diffuse from the plasma into the alveolar space and are excreted during expiration
Other routes of excretion transcutaneous loss, saliva, sweat, and breast milk.
Drug elimination is the irreversible removal of a drug from the body. The process of drug elimination is characterized by pharmacokinetic parameters, such as clearance.
Topic 5 – Applied Principles of Pharmacokinetics
TLO 5.1 Therapeutic Index (TI)
Definition: The ratio of the toxic dose (TD₅₀) to the effective dose (ED₅₀). A higher TI indicates a safer drug.
Formula:TI=TD50ED50TI=ED50TD50
Example: Warfarin has a low TI, meaning small dosing errors can lead to toxicity. Penicillin has a high TI, making overdoses less dangerous.
TLO 5.2 Renal Clearance
Definition: The volume of plasma cleared of a drug per unit time, usually in mL/min.
Factors influencing renal clearance:
Glomerular filtration (small, unbound drugs pass into urine).
Tubular secretion (active transport of drugs into urine).
Reabsorption (lipophilic drugs may diffuse back into blood).
Example: Creatinine clearance is used to estimate renal function.
TLO 5.3 Plasma Half-Life (t1/2t1/2)
Definition: The time required for the plasma concentration of a drug to decrease by 50%.
Formula (First-Order Kinetics):t1/2=0.693×VdCLt1/2=CL0.693×Vd where VdVd is the volume of distribution, and CLCL is clearance.
Clinical Importance: Determines dosing intervals. Drugs with short half-lives require frequent dosing.
Plasma half-life (t1/2) is the time it takes for the concentration of a substance in the plasma to decrease by half. It is an important pharmacokinetic parameter that helps determine the dosing interval of a drug.
Here are some examples of plasma half-lives for different substances:
Caffeine: 5 hours
Alcohol: 4-5 hours
Nicotine: 2 hours
THC: 30 hours
Water: 7-14 days
The plasma half-life of a substance can be affected by a number of factors, including age, weight, liver function, and kidney function.
For example, the plasma half-life of caffeine is shorter in smokers than in non-smokers.
TLO 5.4 First-Order vs. Zero-Order Kinetics
First-Order Kinetics: A constant fraction of drug is eliminated per unit time (most drugs follow this).
Zero-Order Kinetics: A constant amount of drug is eliminated per unit time (seen with saturation of enzymes).
Example: Ethanol follows zero-order kinetics at high doses because alcohol dehydrogenase becomes saturated.
TLO 5.5 Drug Interactions in ADME (Absorption, Distribution, Metabolism, and Excretion)
Drug interactions occur when two or more drugs (including prescription medications, over-the-counter drugs, herbal supplements, or even certain foods) interact with each other in ways that can affect their intended effects, metabolism, or safety. These interactions can lead to various outcomes, such as increased or decreased drug effectiveness, enhanced side effects, or even new adverse reactions that wouldn’t have occurred if the drugs were taken separately.
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📍 Drug interactions occur when two or more medications or substances interact with each other in a way that affects their efficacy, safety, or both. These interactions can lead to changes in the way drugs are absorbed, metabolized, distributed, or eliminated from the body.
📍 There are several types of drug interactions:
* Pharmacokinetic Interactions
* Pharmacodynamics Interactions
* Synergistic Effects
* Antagonistic Effects
* Food and Drug Interactions
* Drug-Disease Interactions:
* Herb-Drug Interactions
* Drug-Laboratory Test Interactions
📍 It’s important to note that not all drug interactions are harmful. Some interactions are intended and can be beneficial, such as combining medications to enhance their therapeutic effects. However, others can lead to adverse effects or reduced treatment efficacy.
Absorption: Chelation (e.g., tetracyclines + calcium) reduces drug absorption.
Distribution: Plasma protein displacement (e.g., warfarin + aspirin increases free warfarin).
Metabolism: CYP inhibition (e.g., grapefruit juice + statins increases statin levels).
Excretion: Probenecid inhibits penicillin renal clearance, prolonging its effect.
There are several types of drug interactions:
- Pharmacokinetic Interactions: These interactions involve changes in the absorption, distribution, metabolism, or elimination of a drug. They can affect how the body processes a drug, potentially leading to changes in its effectiveness or toxicity. For example, one drug might inhibit the enzymes responsible for breaking down another drug, leading to higher levels of the second drug in the body.
- Pharmacodynamic Interactions: These interactions occur when two drugs with similar or opposing effects are taken together. For instance, taking two drugs that lower blood pressure can cause excessive lowering, leading to dizziness or fainting.
- Combined Toxicity: Some drugs can cause toxic effects when taken together, even if they wouldn’t cause harm when taken individually.
- Additive Effects: When two drugs with similar effects are taken together, their combined effect might be stronger than expected. This can be desirable in some cases, but it can also lead to overmedication.
- Antagonistic Effects: Drugs that work against each other can lead to reduced therapeutic effects. For instance, an antacid taken with an antibiotic might interfere with the antibiotic’s absorption.
- Food-Drug Interactions: Certain foods can interact with drugs, affecting their absorption or metabolism. For example, grapefruit juice can inhibit the activity of enzymes responsible for breaking down certain drugs, leading to higher drug levels in the body.
- Herb-Drug Interactions: Herbal supplements and alternative medicines can also interact with conventional medications, leading to unpredictable effects.
It’s important to note that drug interactions can occur with both prescription and over-the-counter medications, and even with supplements. To minimize the risk of potential interactions:
Communication: Keep your healthcare provider informed about all the medications you are taking, including prescription drugs, over-the-counter medications, supplements, and herbal remedies.
Pharmacist Consultation: When picking up a new prescription, talk to your pharmacist about potential interactions with your current medications.
Read Labels: Always read labels and package inserts to identify potential interactions and contraindications.
Patient Education: Educate yourself about your medications and their potential interactions. Many drug interaction resources are available online and in various medical references.
Personal History: Your age, gender, genetics, and overall health can influence how your body metabolizes drugs, so consider these factors when discussing medications with your healthcare provider.
Timing: Taking medications at specific times of day or with or without food as directed by your healthcare provider can help minimize interactions.
Remember, healthcare professionals are your best resource for understanding and managing potential drug interactions. Always consult them before making any changes to your medication regimen or starting new medications or supplements.
Topic 6 – Autonomic Nervous System (ANS) Pharmacology
TLO 6.1 Sympathetic vs. Parasympathetic Nervous System
*Sympathetic (“Fight or Flight”)
Neurotransmitter: Norepinephrine (NE)
Effects: ↑ Heart rate (HR), ↑ Blood pressure (BP), bronchodilation, pupil dilation (mydriasis)
Key receptors: Alpha (α) and Beta (β) adrenergic receptors
Example Drug: Albuterol (β₂ agonist) for asthma
*Parasympathetic (“Rest and Digest”)
Neurotransmitter: Acetylcholine (ACh)
Effects: ↓ HR, ↑ digestion, pupil constriction (miosis), bronchoconstriction
Key receptors: Nicotinic & Muscarinic (M) receptors
Example Drug: Bethanechol (M agonist) for urinary retention
TLO 6.2 ANS Neurotransmitters
*Preganglionic Neurons
Release ACh (both sympathetic & parasympathetic systems).
Bind to nicotinic receptors in ganglia.
*Postganglionic Neurons
Sympathetic: Release norepinephrine (NE) (except sweat glands, which release ACh).
Parasympathetic: Release ACh onto muscarinic receptors.
TLO 6.3 Cholinergic and Adrenergic Receptors
Cholinergic Receptors (Bind ACh):
Nicotinic (N): Fast ligand-gated ion channels (e.g., NMJ, ganglia).
Muscarinic (M): GPCRs (e.g., M2 in heart ↓ HR, M3 in glands ↑ secretions).
TLO 6.3 Cholinergic and Adrenergic Receptors
Adrenergic Receptors (Bind NE/Epi):
Adrenergic Receptors (Bind NE/Epi):
Alpha-1 (α1): Vasoconstriction (e.g., phenylephrine).
Alpha-2 (α2): Decrease NE release (e.g., clonidine).
Beta-1 (β1): Increases heart rate & contractility (e.g., dobutamine).
Beta-2 (β2): Bronchodilation & vasodilation (e.g., albuterol).
TLO 6.4 Neurotransmission Modulation
Blocking Receptors:
Beta-blockers (e.g., metoprolol) → ↓ HR.
Muscarinic blockers (e.g., atropine) → ↓ secretions.
Enzyme Inhibitors:
Acetylcholinesterase (AChE) inhibitors (e.g., neostigmine) → ↑ ACh levels.
TLO 6.5 Other ANS Neurotransmitters
Dopamine (DA): Modulates blood pressure & renal function.
Serotonin (5-HT): Affects mood, gut motility.
Nitric Oxide (NO): Vasodilator, relaxes smooth muscle.
Topic 1: Basic Components of the Immune System
TLO 1.1: List the main characteristics of the innate and adaptive immune systems
- Innate Immunity:
o Speed of Response: Immediate (minutes to hours) upon infection.
o Specificity: Recognizes broad pathogen-associated molecular patterns (PAMPs); not highly specific to a single epitope.
o Memory: No immunologic memory; repeated exposures to the same pathogen do not generally enhance the response.
o Primary Components:
* Physical barriers: Skin, mucosal membranes.
* Cellular components: Neutrophils, macrophages, dendritic cells (DCs), natural killer (NK) cells, mast cells, eosinophils.
* Soluble factors: Complement proteins, cytokines, acute-phase proteins.
o Function: Provides an immediate line of defense; activates and shapes the adaptive immune system.
Topic 1: Basic Components of the Immune System
TLO 1.1: List the main characteristics of the innate and adaptive immune systems
- Adaptive Immunity:
o Speed of Response: Slower on first exposure (days to weeks), but quicker on subsequent exposures.
o Specificity: Highly specific to individual antigens and epitopes.
o Memory: Long-lasting immunologic memory ensures faster and more robust responses on re-exposure.
o Primary Components:
* Cellular components: B and T lymphocytes (Helper T cells, Cytotoxic T cells, Regulatory T cells).
* Humoral components: Antibodies (immunoglobulins).
o Function: Eliminates or neutralizes specific pathogens, provides long-term protection.
TLO 1.2: Contrast the differences between passive and active immunity, using examples
- Active Immunity:
o Definition: Immunity generated by the individual’s own immune system in response to exposure to an antigen.
o Mechanism: Involves B-cell and T-cell activation, clonal expansion, and formation of memory cells.
o Duration: Often long-lasting (years to lifelong).
o Examples:
* Natural: Infection with a pathogen (e.g., recovery from measles confers immunity).
* Artificial: Vaccination (e.g., administration of an inactivated or attenuated pathogen).
TLO 1.2: Contrast the differences between passive and active immunity, using examples
- Passive Immunity:
o Definition: Immunity conferred by transferring antibodies or immune cells from an immune individual to a non-immune individual.
o Mechanism: Does not require the recipient’s immune system to mount its own response; relies on exogenous antibodies/cells.
o Duration: Temporary; protection wanes as transferred antibodies degrade (weeks to a few months).
o Examples:
* Natural: Maternal IgG crossing the placenta or IgA in breast milk.
* Artificial: Administration of intravenous immunoglobulins (IVIG) or monoclonal antibodies.
TLO 1.3: Compare the primary and the secondary immune response to an antigen
- Primary Immune Response:
o Exposure: Occurs upon the first contact with a particular antigen.
o Lag Phase: Longer delay before a detectable immune response (often 5–7 days or more).
o Peak Response: Generally lower magnitude of antibody titer and effector cell function.
o Isotypes: Initial antibody is typically IgM, followed by class switching to other isotypes (IgG, IgA, etc.).
o Memory: Priming of memory B and T cells occurs.
TLO 1.3: Compare the primary and the secondary immune response to an antigen
- Secondary (or Anamnestic) Immune Response:
o Exposure: Occurs upon subsequent contacts with the same antigen.
o Lag Phase: Much shorter due to presence of memory cells.
o Peak Response: Higher and more rapid production of antibodies (often dominated by IgG, especially in serum).
o Higher Affinity: Antibodies have undergone affinity maturation, leading to stronger binding and greater efficacy.
o Clinical Relevance: Underpins the principle of booster vaccinations.
TLO 1.4: List several important morphologic features and functional activities of cells involved in the innate and adaptive immune response: B and T lymphocytes, natural killer cells, neutrophils, mast cells, eosinophils, monocytes, macrophages, and dendritic cells
- B Lymphocytes:
- B Lymphocytes:
o Morphology: Small lymphocytes with large nucleus, sparse cytoplasm; have surface immunoglobulin (B-cell receptor).
o Function: Produce antibodies, present antigen to helper T cells, differentiate into plasma cells (antibody-secreting) and memory B cells
TLO 1.4: List several important morphologic features and functional activities of cells involved in the innate and adaptive immune response: B and T lymphocytes, natural killer cells, neutrophils, mast cells, eosinophils, monocytes, macrophages, and dendritic cells
- T Lymphocytes (T cells):
- T Lymphocytes (T cells):
o Morphology: Similar to B cells in appearance but with T-cell receptors (TCRs).
o Subsets:
* Helper T Cells (CD4⁺): Coordinate immune response via cytokine secretion.
* Cytotoxic T Cells (CD8⁺): Kill virus-infected or tumor cells.
* Regulatory T Cells: Modulate and suppress excessive immune responses to maintain tolerance.
TLO 1.4: List several important morphologic features and functional activities of cells involved in the innate and adaptive immune response: B and T lymphocytes, natural killer cells, neutrophils, mast cells, eosinophils, monocytes, macrophages, and dendritic cells
- Natural Killer (NK) Cells:
- Natural Killer (NK) Cells:
o Morphology: Larger granular lymphocytes with cytotoxic granules.
o Function: Kill virus-infected cells and tumor cells without prior sensitization; recognize “missing-self” (lack of MHC I) or stressed cells.
TLO 1.4: List several important morphologic features and functional activities of cells involved in the innate and adaptive immune response: B and T lymphocytes, natural killer cells, neutrophils, mast cells, eosinophils, monocytes, macrophages, and dendritic cells
Neutrophils
- Neutrophils:
o Morphology: Granulocytes with multilobed nucleus and abundant cytoplasmic granules.
o Function: First responders to acute bacterial infection; phagocytic; release reactive oxygen species and granule enzymes to kill pathogens.
TLO 1.4: List several important morphologic features and functional activities of cells involved in the innate and adaptive immune response: B and T lymphocytes, natural killer cells, neutrophils, mast cells, eosinophils, monocytes, macrophages, and dendritic cells
- Mast Cells:
- Mast Cells:
o Morphology: Tissue-resident cells with abundant granules containing histamine and other mediators.
o Function: Crucial in allergic reactions (Type I hypersensitivity); degranulation triggered by cross-linking of surface-bound IgE.
TLO 1.4: List several important morphologic features and functional activities of cells involved in the innate and adaptive immune response: B and T lymphocytes, natural killer cells, neutrophils, mast cells, eosinophils, monocytes, macrophages, and dendritic cells
Monocytes
- Monocytes:
o Morphology: Large leukocytes in circulation with kidney-shaped nucleus.
o Function: Differentiate into macrophages or dendritic cells upon entering tissues; phagocytic and cytokine-producing.
TLO 1.4: List several important morphologic features and functional activities of cells involved in the innate and adaptive immune response: B and T lymphocytes, natural killer cells, neutrophils, mast cells, eosinophils, monocytes, macrophages, and dendritic cells
Macrophages
- Macrophages:
o Morphology: Tissue-resident phagocytes derived from monocytes; have pseudopods and large vacuoles.
o Function: Phagocytosis and digestion of pathogens, antigen presentation to T cells, release of inflammatory cytokines.
TLO 1.4: List several important morphologic features and functional activities of cells involved in the innate and adaptive immune response: B and T lymphocytes, natural killer cells, neutrophils, mast cells, eosinophils, monocytes, macrophages, and dendritic cells
- Dendritic Cells (DCs):
- Dendritic Cells (DCs):
o Morphology: “Stellate” cells with dendritic processes; found in tissues interfacing with the external environment.
o Function: Professional antigen-presenting cells (APCs); capture antigen in periphery and migrate to lymph nodes to activate T cells.
Topic 2: Antigen and Antibody
TLO 2.1: List the origins of antigens to which the immune system may respond
1. Exogenous Antigens
- Endogenous Antigens
- Autoantigens
- Alloantigens
- Xenoantigens
- Exogenous Antigens: Enter the body from outside (bacteria, viruses, fungi, allergens, toxins).
- Endogenous Antigens: Generated within cells due to infection (intracellular pathogens) or abnormal cellular proteins (tumor antigens).
- Autoantigens: The body’s own molecules that can trigger autoimmunity under certain conditions.
- Alloantigens: Antigens from other members of the same species (e.g., blood group antigens, transplanted organ antigens).
- Xenoantigens: Antigens from different species (e.g., pig heart valves in xenotransplantation).
TLO 2.2: Name the structural features and biologic properties of the different immunoglobulin classes
1. IgG:
2. IgA:
3. IgM:
4. IgE:
5. IgD:
- IgG:
o Structure: Monomer; four subclasses (IgG1–IgG4).
o Properties: Crosses the placenta (maternal-fetal immunity), opsonization, complement activation, neutralization of toxins/viruses. - IgM:
o Structure: Pentamer (5 monomers linked by J chain).
o Properties: First antibody produced during primary response; highly efficient in complement activation and agglutination. - IgA:
o Structure: Monomer in serum; dimer in secretions (linked by J chain and secretory component).
o Properties: Found in mucosal areas (GI tract, respiratory tract), breast milk; protects mucosal surfaces by neutralizing pathogens. - IgE:
o Structure: Monomer.
o Properties: Binds to mast cells and basophils; involved in Type I hypersensitivity and defense against parasites. - IgD:
o Structure: Monomer.
o Properties: Primarily membrane-bound on naive B cells; role in B-cell activation is less well-defined compared to other isotypes.
What cells produce IL-10 to induce peripheral tolerance of T and B cells? (Single choice)
Th1
Th2
CTLs
Treg
NK
I don’t know
Treg
TLO 2.3: Describe a range of diagnostic tests based on antigen-antibody interaction, indicating the general principle of each test
- ELISA (Enzyme-Linked Immunosorbent Assay):
- Western Blot:
- Immunofluorescence (Direct and Indirect):
- Flow Cytometry:
- Agglutination Tests (Latex Agglutination, Hemagglutination):
- ELISA (Enzyme-Linked Immunosorbent Assay):
o Principle: Detects antigen or antibody via enzyme-labeled secondary antibody and a colorimetric reaction.
o Applications: Quantification of hormones, antibodies (e.g., HIV test), detection of specific proteins in serum. - Western Blot:
o Principle: Proteins separated by electrophoresis, transferred to a membrane, and probed with specific antibodies; visualization by enzyme or chemiluminescence.
o Applications: Confirmatory test for HIV, detection of specific protein expression. - Immunofluorescence (Direct and Indirect):
o Principle: Fluorescently labeled antibodies bind to specific antigens in tissues or cells and are visualized under a fluorescence microscope.
o Applications: Autoantibody detection (e.g., in lupus), viral antigen detection, research staining. - Flow Cytometry:
o Principle: Cells are tagged with fluorescent antibodies to cell-surface or intracellular antigens, then passed through a laser beam for analysis of fluorescence.
o Applications: Immunophenotyping (CD4 counts in HIV), identification of abnormal cell populations in leukemia/lymphoma. - Agglutination Tests (Latex Agglutination, Hemagglutination):
o Principle: Visible clumping occurs when particulate antigen binds to specific antibodies.
Antibodies
Antibodies
Attach to antigens → Antibody-antigen complex
Attach to toxins (antigens) → Neutralise toxins
Attach to receptors → Disrupt the function
Attach to pathogens → Clump together → “Agglutination”
Act as opsonins → Present to phagocytes
Antibody-dependent cell-mediated cytotoxicityAttach to antigens → Antibody-antigen complex
Attach to toxins (antigens) → Neutralise toxins
Attach to receptors → Disrupt the function
Attach to pathogens → Clump together → “Agglutination”
Act as opsonins → Present to phagocytes
Antibody-dependent cell-mediated cytotoxicity
TLO 2.4: Explain the terms monoclonal antibodies (mAbs), hybridoma, fully human, humanized, and chimeric
Monoclonal Antibodies (mAbs) Antibodies produced by a single clone of cells, designed to target a specific antigen with high specificity and uniformity.
Hybridoma A cell line created by fusing an antibody-producing B cell with a myeloma (cancer) cell, allowing for the continuous production of monoclonal antibodies.
Fully Human Antibodies made entirely from human genetic material, reducing the risk of immune reactions when used in humans.
Humanized Antibodies that are mostly human, but contain small parts derived from non-human sources (e.g., mouse), engineered to reduce immune reactions.
Chimeric Antibodies that are part human and part non-human (e.g., mouse), with the variable regions from the non-human source and constant regions from humans.
1. Monoclonal Antibodies (mAbs): o Definition: Uniform antibodies derived from a single B-cell clone, each recognizing the same epitope. o Advantages: High specificity, consistent batch-to-batch reactivity. 2. Hybridoma: o Definition: A cell line produced by the fusion of an antibody-producing B lymphocyte with a myeloma cell, creating an immortalized cell line that secretes monoclonal antibodies. 3. Fully Human Antibodies: o Definition: Antibodies with both variable and constant regions derived entirely from human immunoglobulin sequences (generated via transgenic mice or phage display). 4. Humanized Antibodies: o Definition: Mostly human antibody framework with complementarity-determining regions (CDRs) from a non-human (e.g., mouse) source. 5. Chimeric Antibodies: o Definition: Antibodies where the variable regions (heavy and light) are from one species (often mouse) and the constant region from another (human).
TLO 2.5: List several examples of mAbs application in clinical medicine
- Cancer Therapy:
- Autoimmune Diseases:
- Transplant Rejection Prevention:
- Infectious Diseases:
- Cancer Therapy:
o Rituximab (anti-CD20) for certain B-cell malignancies (e.g., non-Hodgkin lymphoma).
o Trastuzumab (anti-HER2) for HER2-positive breast cancer. - Autoimmune Diseases:
o Infliximab (anti-TNF-α) for rheumatoid arthritis, Crohn’s disease.
o Natalizumab (anti-integrin) for multiple sclerosis. - Transplant Rejection Prevention:
o Basiliximab (anti-IL-2 receptor) used to prevent acute rejection. - Infectious Diseases:
o Palivizumab (anti-RSV F protein) for high-risk infants against respiratory syncytial virus.
Topic 3: Antigen Presentation and Recognition; Cytokines
TLO 3.1: Describe the main structural features of the class I and class II MHC gene products
- Class I MHC (HLA-A, -B, -C in humans):
- Class II MHC (HLA-DP, -DQ, -DR in humans):
Topic 3: Antigen Presentation and Recognition; Cytokines
TLO 3.1: Describe the main structural features of the class I and class II MHC gene products
1. Class I MHC (HLA-A, -B, -C in humans):
o Structure: Consists of a heavy α chain (three domains: α1, α2, α3) non-covalently associated with β2-microglobulin.
o Peptide-Binding Groove: Formed by α1 and α2 domains.
o Expression: All nucleated cells (and platelets).
o Presentation: Presents endogenous (intracellular) peptides to CD8⁺ T cells.
2. Class II MHC (HLA-DP, -DQ, -DR in humans):
o Structure: Composed of two chains (α and β), each with two domains (α1, α2 and β1, β2).
o Peptide-Binding Groove: Formed by α1 and β1 domains.
o Expression: Primarily on professional antigen-presenting cells (APCs) like dendritic cells, macrophages, B cells.
o Presentation: Presents exogenous (extracellular) peptides to CD4⁺ T cells.
TLO 3.2: Explain the genetic basis of MHC polymorphism and polygeny, and their significance for the functioning of the immune system
- Polymorphism:
pathogens.
2. Polygeny:
- Significance:
TLO 3.2: Explain the genetic basis of MHC polymorphism and polygeny, and their significance for the functioning of the immune system
1. Polymorphism:
o Definition: Multiple variants (alleles) of each MHC gene in a population.
o Result: Increases the range of peptides that can be presented by the population as a whole; enhances survival against diverse pathogens.
2. Polygeny:
o Definition: Multiple MHC genes encoding different class I and class II molecules in each individual (e.g., HLA-A, -B, -C for class I and HLA-DP, -DQ, -DR for class II).
o Result: Each individual co-expresses several MHC molecules, broadening peptide presentation.
3. Significance:
o Immune Defense: High MHC diversity makes it less likely that a single pathogen can evade the entire human population.
o Transplantation: MHC polymorphisms contribute to graft rejection.
TLO 3.3: Describe the concept of MHC restriction
The principle that T cells recognize antigens only when they are presented by the host’s own MHC molecules.
- Definition: T cells recognize antigenic peptides only when presented on self-MHC molecules.
- CD8⁺ T cells: Require peptide presented on class I MHC of the host.
- CD4⁺ T cells: Require peptide presented on class II MHC of the host.
- Clinical Implication: T cells generally do not respond to peptide antigens presented by non-self MHC, complicating allograft acceptance.
TLO 3.4: Compare peptide antigen binding to class I and class II molecules
1. Class I MHC:
- Class II MHC:
o Peptide Origin: Extracellular proteins taken up via endocytosis.
o Processing Pathway: Antigen is degraded in endosomal/lysosomal compartments; class II is assembled in ER with invariant chain → invariant chain is removed in endosome → peptide loaded.
o Peptide Length: Longer (usually 13–25 amino acids).
TLO 3.4: Compare peptide antigen binding to class I and class II molecules
1. Class I MHC:
o Peptide Origin: Intracellular proteins (viral, cytosolic).
o Processing Pathway: Proteasome degrades proteins → peptides transported into ER via TAP → loaded onto class I.
o Peptide Length: Typically 8–10 amino acids in length.
2. Class II MHC:
o Peptide Origin: Extracellular proteins taken up via endocytosis.
o Processing Pathway: Antigen is degraded in endosomal/lysosomal compartments; class II is assembled in ER with invariant chain → invariant chain is removed in endosome → peptide loaded.
o Peptide Length: Longer (usually 13–25 amino acids).
TLO 3.5: List the main categories of antigen recognition molecules, including coreceptor complexes
1. T-Cell Receptors (TCRs):
- Immunoglobulins (Surface B-cell Receptors):
- CD4 and CD8 Coreceptors:
- Pattern Recognition Receptors (PRRs) in Innate Immunity:
TLO 3.5: List the main categories of antigen recognition molecules, including coreceptor complexes
1. T-Cell Receptors (TCRs):
o Heterodimer of α and β chains (or γ and δ in fewer T cells).
o Recognize peptide bound to MHC.
2. Immunoglobulins (Surface B-cell Receptors):
o Membrane-bound form of antibodies on B cells.
3. CD4 and CD8 Coreceptors:
o CD4 binds MHC II, CD8 binds MHC I; stabilize TCR-MHC interaction and facilitate signaling.
4. Pattern Recognition Receptors (PRRs) in Innate Immunity:
o Toll-like receptors, NOD-like receptors, RIG-I-like receptors, etc.; recognize PAMPs.
TLO 3.6: Give two classifications of cytokines
1. By Function:
- By Structure/Family:
TLO 3.6: Give two classifications of cytokines
1. By Function:
o Pro-inflammatory: e.g., IL-1, IL-6, TNF-α.
o Anti-inflammatory: e.g., IL-10, TGF-β.
o Hematopoietic growth factors: e.g., GM-CSF.
o Antiviral: e.g., IFN-α, IFN-β.
2. By Structure/Family:
o Interleukins (IL-1, IL-2, etc.)
o Interferons (Type I: IFN-α/β; Type II: IFN-γ)
o Tumor Necrosis Factors (TNF family)
o Chemokines (CC, CXC families)
TLO 3.7: List main functions and properties of cytokines
1. Main Functions:
TLO 3.7: List main functions and properties of cytokines
1. Main Functions:
o Regulate immune cell activation, proliferation, and differentiation: IL-2 drives T-cell proliferation, IL-4 drives Th2 responses, etc.
o Mediate inflammation: TNF-α and IL-1 induce endothelial activation and recruit inflammatory cells.
o Influence hematopoiesis: Factors like G-CSF and M-CSF stimulate granulocyte or macrophage lineage expansion.
o Antiviral defense: Type I interferons (IFN-α, IFN-β) inhibit viral replication.
TLO 3.7: List main functions and properties of cytokines
- Properties:
o Pleiotropy: One cytokine can have different effects on different cell types.
o Redundancy: Different cytokines can exert similar biological effects.
o Synergy and Antagonism: Cytokines can work together or counteract each other.
o Local and Systemic Effects: Can act paracrine, autocrine, or endocrine.
- Properties:
o Pleiotropy: One cytokine can have different effects on different cell types.
o Redundancy: Different cytokines can exert similar biological effects.
o Synergy and Antagonism: Cytokines can work together or counteract each other.
o Local and Systemic Effects: Can act paracrine, autocrine, or endocrine.
Topic 4: T and B Lymphocytes
TLO 4.1: Name the major steps in the pathway of T-cell development; give definition to double-positive and single-positive thymocytes
- Location: T-cell precursors originate in the bone marrow and migrate to the thymus.
- Major Stages:
o Double-Negative (DN) Stage: T-cell progenitors do not express CD4 or CD8.
o Double-Positive (DP) Stage: Thymocytes express both CD4 and CD8 co-receptors (CD4⁺CD8⁺).
o Single-Positive (SP) Stage: Thymocytes differentiate into either CD4⁺ or CD8⁺ T cells, depending on TCR specificity for MHC II or MHC I, respectively.
TLO 4.2: Compare positive and negative selection of T lymphocytes in thymus
1. Positive Selection (occurs in the cortex):
- Negative Selection (occurs in the medulla):
TLO 4.2: Compare positive and negative selection of T lymphocytes in thymus
1. Positive Selection (occurs in the cortex):
o Mechanism: DP thymocytes that can weakly recognize self-MHC I or II survive.
o Outcome: Ensures T cells can interact with self-MHC (MHC restriction).
o Failure: Cells that do not recognize MHC at all undergo apoptosis.
2. Negative Selection (occurs in the medulla):
o Mechanism: T cells that strongly bind self-antigen presented on MHC undergo apoptosis.
o Outcome: Removal of autoreactive T cells; induces self-tolerance.
o Failure: Autoimmune pathology if highly self-reactive T cells escape deletion.
TLO 4.3: Draw the events involved in naive T-cell activation
(Conceptual description)
TLO 4.3: Draw the events involved in naive T-cell activation
(Conceptual description)
1. Antigen Recognition: Naive T cells bind specific peptide-MHC complexes on APCs via the TCR.
2. Co-stimulation: Additional signals needed, such as CD28 (on T cell) binding to B7-1/B7-2 (CD80/CD86 on APC).
3. Cytokine Environment: APC-derived cytokines (e.g., IL-12) influence T-cell differentiation.
4. Clonal Expansion: Activated T cells proliferate and differentiate into effector (e.g., Th1, Th2, Th17, CTLs) and memory cells.
TLO 4.4: Outline the differences between TH1, TH2, TH17, and CTL responses
TLO 4.4: Outline the differences between TH1, TH2, TH17, and CTL responses
1. TH1 Cells:
o Cytokines Produced: IFN-γ, IL-2, TNF-β.
o Function: Activate macrophages, support cell-mediated immunity against intracellular pathogens.
o Key Transcription Factor: T-bet.
2. TH2 Cells:
o Cytokines Produced: IL-4, IL-5, IL-13.
o Function: Help B cells produce antibodies (especially IgE), support eosinophil activation, involved in defense against parasites and allergic responses.
o Key Transcription Factor: GATA-3.
3. TH17 Cells:
o Cytokines Produced: IL-17, IL-22.
o Function: Recruit neutrophils, combat extracellular bacteria/fungi, involved in some autoimmune pathologies.
o Key Transcription Factor: RORγt.
4. Cytotoxic T Lymphocytes (CTLs, CD8⁺):
o Cytokines Produced: IFN-γ (some), also use perforin and granzymes.
o Function: Direct killing of virus-infected cells or tumor cells.
TLO 4.5: Recall changes in cell surface molecules during the B-cell development pathway
TLO 4.5: Recall changes in cell surface molecules during the B-cell development pathway
1. Pro-B Cell: Begins rearrangement of immunoglobulin heavy chain; no surface immunoglobulin.
2. Pre-B Cell: Expression of μ heavy chain with surrogate light chain on surface (Pre-BCR).
3. Immature B Cell: Expression of complete IgM on surface.
4. Mature (Naive) B Cell: Co-expression of IgM and IgD on surface.
5. Activated B Cell (After antigen encounter): Undergoes class switching (IgG, IgA, or IgE), affinity maturation, and differentiation into plasma or memory B cells.
TLO 4.6: Compare positive and negative selection of B lymphocytes in bone marrow
1. Positive Selection:
o Less pronounced in B cells than T cells.
o B cells that successfully rearrange and express functional BCR move to the next stage.
TLO 4.6: Compare positive and negative selection of B lymphocytes in bone marrow
- Negative Selection:
o Immature B cells that bind self-antigens strongly (in bone marrow) either undergo apoptosis or receptor editing (light chain gene rearrangement to reduce self-reactivity).
o Ensures central tolerance.
- Negative Selection:
o Immature B cells that bind self-antigens strongly (in bone marrow) either undergo apoptosis or receptor editing (light chain gene rearrangement to reduce self-reactivity).
o Ensures central tolerance.
TLO 4.7: Describe how naïve B and T cells are primed by cell-cell interactions with antigen-presenting cells
- Naive T Cells: Require APCs (e.g., dendritic cells) presenting antigen on MHC molecules along with co-stimulatory signals (CD80/CD86 → CD28).
- Naive B Cells: Can bind antigen via BCR directly, but often require T-cell help (for T-dependent antigens). Helper T cells recognize peptides from the same antigen presented on MHC II of the B cell, then provide signals (CD40L on T cell binds CD40 on B cell) plus cytokines that drive B-cell activation, class switching, and affinity maturation.
TLO 4.8: Compare T-dependent and T-independent B-cell activation
- T-Dependent Antigens:
o Composition: Typically proteins.
o Mechanism: B cell presents processed peptide on MHC II to helper T cell → receives help (CD40-CD40L interaction + cytokines).
o Outcome: Isotype switching, affinity maturation, robust memory response. - T-Independent Antigens:
o Composition: Often polysaccharides or repeating epitopes.
o Mechanism: Cross-linking of multiple BCRs → direct activation without T-cell help.
o Outcome: Mainly IgM response, limited immunologic memory, little or no class switching or affinity maturation.
Topic 5: Hypersensitivity
TLO 5.1: Explain the Gell and Coombs classification of hypersensitivity reactions
- Type I (Immediate):
o Mechanism: IgE-mediated mast cell degranulation.
o Examples: Allergic rhinitis, anaphylaxis, asthma. - Type II (Antibody-Mediated Cytotoxic):
o Mechanism: IgG or IgM antibodies directed against cell-surface or extracellular matrix antigens → complement activation or opsonization.
o Examples: Hemolytic anemia, Goodpasture’s syndrome, myasthenia gravis (some forms). - Type III (Immune Complex-Mediated):
o Mechanism: Antigen-antibody (IgG) complexes deposit in tissues → complement activation and inflammation.
o Examples: Serum sickness, Arthus reaction, certain forms of vasculitis. - Type IV (Delayed-Type or Cell-Mediated):
o Mechanism: T-cell mediated; either CD4⁺ T helper cells (Th1) activate macrophages or CD8⁺ cytotoxic T cells kill target cells.
o Examples: Contact dermatitis (e.g., poison ivy), tuberculin skin test, type 1 diabetes (β-cell destruction).
Hypersensitivity Reactions
Type Immune Response Immunoglobulin/Cells Response Time Mechanism Examples
Type I Antibody mediated immunity IgE Fast response (minutes) Allergic reactions Asthma, Allergic rhinitis
Type II Antibody mediated immunity IgG, IgM Intermediate Body cells directly attacked by antibodies Rheumatic heart disease, Autoimmune haemolytic anaemia
Type III Antibody mediated immunity IgG Intermediate Complex accumulation and destruction Rheumatoid arthritis, Poststreptococcal glomerulonephritis
Type IV Cell mediated immunity T helper cells (Th1) Late response (48-72 hours) Cell mediated cytotoxicity Transplant rejection, Contact dermatitis
If you need any more help or have further questions, feel free to ask!
TLO 5.2: Describe the immunologic factors that predispose to allergy and explain how these may be increasing allergy at a population level
- Genetic Factors:
o Atopic individuals have a predisposition (often multiple genes) leading to higher IgE production and increased Th2 responses.
o Polymorphisms in cytokines (IL-4, IL-13) or their receptors can enhance IgE class switching. - Environmental Factors:
o Hygiene Hypothesis: Reduced childhood infections may lead to an under-stimulated Th1 response, skewing toward Th2 and atopy.
o Exposure to pollutants, diet changes, antibiotic overuse can alter gut and skin microbiome, affecting immune tolerance. - Increasing Prevalence of Allergy:
o Urbanization, decreased exposure to farm animals or soil microbes, and other lifestyle changes may account for rising allergy rates.
TLO 5.3: Describe the techniques used to identify allergens involved in immediate hypersensitivity
- Skin Prick Test (SPT):
o Allergen extracts placed on skin → pricked → wheal-and-flare response indicates sensitization. - Serologic Tests:
o Specific IgE Measurement (e.g., RAST, ImmunoCAP): Detect allergen-specific IgE in patient serum. - Elimination/Challenge Testing:
o For food allergies, removing suspect foods from the diet and then reintroducing under controlled conditions.
TLO 5.4: Describe anaphylaxis and its immediate treatment
- Anaphylaxis:
o Definition: Severe, systemic allergic reaction triggered by widespread mast cell and basophil degranulation.
o Clinical Features: Hypotension (shock), bronchoconstriction (wheezing), laryngeal edema, urticaria, GI symptoms. - Immediate Treatment:
o Epinephrine (adrenaline) IM injection is the first-line therapy; stabilizes mast cells, reverses bronchospasm, and supports blood pressure.
o Additional treatments: Antihistamines, corticosteroids, IV fluids, and oxygen support as needed.
TLO 5.5: List the modes of action of drugs used to treat allergy
- Antihistamines (H1 blockers): Block histamine receptors (e.g., diphenhydramine, cetirizine).
- Mast Cell Stabilizers: Prevent degranulation (e.g., cromolyn sodium).
- Leukotriene Receptor Antagonists: (e.g., montelukast) reduce leukotriene-mediated inflammation.
- Corticosteroids: Suppress inflammatory gene expression (e.g., prednisone, fluticasone).
- Anti-IgE Antibodies (e.g., omalizumab): Binds circulating IgE, preventing its interaction with mast cells/basophils.
Topic 6: Autoimmune Diseases
TLO 6.1: List what evidence there is for autoimmunity in normal, healthy individuals
- Natural Autoantibodies: Low affinity, polyreactive antibodies often present at low levels.
- Autoreactive T Cells: Low-level autoreactive T cells can exist but are kept in check by regulatory mechanisms.
- Fas-Fas Mechanisms: Continuous peripheral deletion of self-reactive lymphocytes.
TLO 6.2: Describe how the immune system tolerates most autoantigens and how tolerance can break down
- Central Tolerance:
- Central Tolerance:
o T cells in the thymus (negative selection) and B cells in bone marrow (clonal deletion or receptor editing).
TLO 6.2: Describe how the immune system tolerates most autoantigens and how tolerance can break down
- Peripheral Tolerance:
- Peripheral Tolerance:
o Anergy: Lack of co-stimulatory signals leads to non-responsiveness.
o Regulatory T Cells: Secrete immunosuppressive cytokines (IL-10, TGF-β) to maintain tolerance.
o Ignorance: Self-antigens may be sequestered in immune-privileged sites (brain, eye, testes).
TLO 6.2: Describe how the immune system tolerates most autoantigens and how tolerance can break down
- Breakdown of Tolerance:
- Breakdown of Tolerance:
o Molecular Mimicry: Infectious agents share epitopes with self-antigens → cross-reactivity.
o Epitope Spreading: Tissue damage exposes hidden self-epitopes.
o Genetic Susceptibility: Certain MHC alleles predispose to autoimmunity.
TLO 6.3: Using the examples of type 1 diabetes, celiac disease, and systemic lupus erythematosus, describe how genes and environmental factors work together to cause autoimmune disease
- Type 1 Diabetes (T1D):
o Genetic Factors: Strong association with certain HLA class II alleles (e.g., HLA-DR3, DR4).
o Environmental Triggers: Viral infections (coxsackie virus), gut microbiome factors.
o Mechanism: Autoreactive T cells attack pancreatic β-cells → insulin deficiency.
TLO 6.3: Using the examples of type 1 diabetes, celiac disease, and systemic lupus erythematosus, describe how genes and environmental factors work together to cause autoimmune disease
- Type 1 Diabetes (T1D):
o Genetic Factors: Strong association with certain HLA class II alleles (e.g., HLA-DR3, DR4).
o Environmental Triggers: Viral infections (coxsackie virus), gut microbiome factors.
o Mechanism: Autoreactive T cells attack pancreatic β-cells → insulin deficiency.
TLO 6.3: Using the examples of type 1 diabetes, celiac disease, and systemic lupus erythematosus, describe how genes and environmental factors work together to cause autoimmune disease
- Celiac Disease:
o Genetic Factors: Predominantly HLA-DQ2 or DQ8 haplotypes.
o Environmental Trigger: Dietary gluten (gliadin component).
o Mechanism: Immune-mediated damage to small intestinal villi.
TLO 6.3: Using the examples of type 1 diabetes, celiac disease, and systemic lupus erythematosus, describe how genes and environmental factors work together to cause autoimmune disease
- Systemic Lupus Erythematosus (SLE):
o Genetic Factors: Multiple genes (HLA-DR2/DR3); complement deficiencies (C1q, C2, C4).
o Environmental Factors: UV light, sex hormones (estrogen), infections can exacerbate.
o Mechanism: Loss of tolerance leads to autoantibody production (especially anti-nuclear antibodies) and immune complex deposition.
TLO 6.4: Describe how immunofluorescence tests and ELISAs are used to detect autoantibodies
- Immunofluorescence Tests (Indirect):
o Patient serum applied to substrate tissue (e.g., HEp-2 cells), autoantibodies bind, then detected by fluorescently labeled anti-human Ig. - ELISA:
o Antigens (specific autoantigens, e.g., dsDNA, tissue transglutaminase) coated on a plate → patient serum added → enzyme-labeled anti-human IgG → colorimetric readout.
Topic 7: Immunodeficiencies
TLO 7.1: Explain differences between primary and secondary immunodeficiencies
- Primary (Congenital):
o Definition: Genetic or developmental defects resulting in defective immune function (e.g., SCID, DiGeorge syndrome, Bruton’s agammaglobulinemia).
o Onset: Often in early childhood with recurrent, severe infections. - Secondary (Acquired):
o Definition: Result from external factors (e.g., HIV infection, chemotherapy, malnutrition).
o Onset: Can occur at any age depending on exposure or underlying disease.
TLO 7.2: Construct lists of the types of infections that affect patients with T- and B-cell disorders
- T-Cell Disorders:
o More susceptible to intracellular pathogens (viruses, fungi, opportunistic organisms like Pneumocystis jirovecii), and certain intracellular bacteria (mycobacteria). - B-Cell (Humoral) Disorders:
o Recurrent pyogenic bacterial infections (e.g., Streptococcus pneumoniae, Haemophilus influenzae), especially encapsulated organisms; can also struggle with some viruses that rely on neutralizing antibodies (e.g., enteroviruses).
TLO 7.3: List the cells affected by HIV infection and briefly describe their functions and roles in HIV infection
- CD4⁺ T Cells (Helper T cells):
o Function: Orchestrate immune responses via cytokine secretion; essential for B-cell antibody production and macrophage activation.
o Role in HIV: Main target for HIV binding via gp120 → progressive depletion leads to immunodeficiency (AIDS). - Macrophages and Dendritic Cells:
o Function: Antigen presentation, phagocytosis, and immunoregulation.
o Role in HIV: Act as reservoirs; HIV can infect these cells (via CCR5 co-receptor), allowing for persistent infection and spread.
TLO 7.4: Describe how you would monitor a patient with HIV infection
- CD4⁺ T-Cell Count:
o Critical for determining degree of immunosuppression and opportunistic infection risk. - Viral Load (HIV RNA PCR):
o Indicates level of active viral replication; used to monitor response to antiretroviral therapy (ART). - Clinical Monitoring:
o Track opportunistic infections, overall health, and medication side effects. - Other Laboratory Tests:
o Complete blood counts, liver and renal function tests to monitor ART toxicity or comorbidities.
TLO 7.5: List host factors that affect the course of HIV infection
- Genetic Factors:
o CCR5∆32 mutation confers resistance or slower disease progression.
o HLA types can influence immune response effectiveness. - Co-infections and Comorbidities:
o Certain infections (e.g., TB, hepatitis) can exacerbate or accelerate progression. - Immune Status and Nutrition:
o Malnutrition or other immunocompromising conditions worsen outcomes. - Adherence to ART:
o Poor adherence → higher viral loads → more rapid disease progression.
Topic 8: Immunity in Malignancy
TLO 8.1: Describe the different types of tumor antigen and explain how tumors evade the immune response
- Types of Tumor Antigens:
o Tumor-Specific Antigens (TSAs): Unique to tumor cells (e.g., mutated oncogenes or viral antigens).
o Tumor-Associated Antigens (TAAs): Overexpressed or re-expressed normal proteins (e.g., prostate-specific antigen). - Evasion Strategies:
o Reduced MHC Expression: Tumor cells downregulate MHC I to avoid CTL recognition.
o Immunosuppressive Molecules: Secretion of TGF-β, IL-10 to inhibit T-cell function.
o Immune Checkpoints: Upregulation of PD-L1 or CTLA-4 pathways to dampen T-cell activity.
TLO 8.2: Explain how host and viral oncogenes interact to cause cancer
- Host Oncogenes (Proto-oncogenes):
o Mutations or overexpression convert them into oncogenes → uncontrolled cell proliferation. - Viral Oncogenes:
o Some viruses (e.g., HPV, EBV, HTLV-1) introduce or activate oncogenes or inactivate tumor suppressor genes (e.g., p53, Rb). - Interaction:
o Viral infection can initiate or promote oncogenic processes in a genetically susceptible host, leading to malignant transformation.
TLO 8.3: List several approaches to cancer immunotherapy
- Checkpoint Inhibitors
- CAR T-Cell Therapy:
- Cancer Vaccines:
- Monoclonal Antibodies:
- Adoptive Cell Transfer (ACT):
- Checkpoint Inhibitors:
o Antibodies blocking PD-1/PD-L1 or CTLA-4, reactivating T cells against tumors (e.g., nivolumab, pembrolizumab). - CAR T-Cell Therapy:
o Engineering patient T cells with chimeric antigen receptors targeting tumor-specific antigens (e.g., CD19 in B-cell malignancies). - Cancer Vaccines:
o Prophylactic (e.g., HPV vaccine) or therapeutic vaccines to elicit antitumor immunity. - Monoclonal Antibodies:
o Direct tumor targeting (e.g., rituximab, trastuzumab) or immune modulation (e.g., anti-CD40). - Adoptive Cell Transfer (ACT):
o Expansion of tumor-infiltrating lymphocytes (TILs) ex vivo and re-infusion to the patient.
Topic 9: Transplantation
TLO 9.1: List the different types of transplants and the organs transplanted
- Autograft: Transplant from one site to another on the same individual (e.g., skin graft).
- Isograft (Syngeneic Graft): Between genetically identical individuals (e.g., identical twins).
- Allograft: Between different individuals of the same species.
- Xenograft: Between different species (e.g., pig to human).
* Commonly Transplanted Organs: Kidney, liver, heart, lung, pancreas, cornea, bone marrow/stem cells.
TLO 9.2: Describe the three phases of rejection of solid organs
TLO 9.2: Describe the three phases of rejection of solid organs
1. Hyperacute Rejection:
o Timing: Minutes to hours after transplant.
o Mechanism: Pre-formed antibodies against donor ABO blood group or HLA antigens → complement activation → rapid thrombosis and necrosis.
2. Acute Rejection:
o Timing: Days to weeks (or months) post-transplant.
o Mechanism: T-cell mediated (cellular) or antibody-mediated (humoral) attack on donor tissue.
3. Chronic Rejection:
o Timing: Months to years post-transplant.
o Mechanism: Low-level immune response leading to vascular damage (intimal thickening, fibrosis), gradual organ failure.
TLO 9.3: Explain how stem cell transplantation differs from solid organ transplant
- Stem Cell (Bone Marrow) Transplant:
o Replacing Hematopoietic and Immune System: Infusion of donor stem cells repopulates recipient’s bone marrow.
o Graft-versus-Host Disease (GVHD): Donor T cells can attack recipient’s tissues (skin, liver, gut); a major complication unique to stem cell transplants.
o Immunologic Reconstitution: Takes months to fully recover an immune system; prophylaxis against infections is critical. - Solid Organ Transplant:
o Replacing a Specific Organ: Donor organ must be matched for ABO compatibility and partially for HLA.
o Host-versus-Graft Reactions: Predominant concern. The recipient’s immune system can reject the donor organ.
TLO 9.4: List the problems that need to be overcome to make xenotransplantation safe
- Hyperacute Rejection: Pre-existing natural antibodies to animal epitopes (e.g., alpha-gal).
- Zoonotic Infections: Potential cross-species transmission of viruses (porcine endogenous retroviruses).
- Physiological and Size Mismatch: Ensuring transplanted organ functions adequately in a human environment.
- Ethical/Regulatory Concerns: Pathogen control, public health risk, and acceptance.
Topic 10: Vaccination
TLO 10.1: Explain the mechanism of action of vaccines
- Mechanism:
o Vaccines introduce antigens (live attenuated, killed, subunit, etc.) that mimic infection, prompting the immune system to generate a protective adaptive response (antibody production, memory B/T cells) without causing the full-blown disease. - Immunologic Memory:
o Upon real exposure to the pathogen, the immune response is rapid and prevents clinical disease.
TLO 10.2: Give classification of vaccines
- Live Attenuated:
o Weakened form of the pathogen (e.g., measles, mumps, rubella, varicella).
o Induce robust immunity; can be contraindicated in immunocompromised individuals. - Inactivated (Killed):
o Pathogen killed by chemicals/heat (e.g., inactivated polio, hepatitis A).
o Generally safer; often require boosters. - Subunit/Conjugate:
o Contain only essential antigens (e.g., hepatitis B surface antigen, pneumococcal conjugate).
o Reduced risk of adverse effects; may need adjuvants. - Toxoid:
o Inactivated bacterial toxins (e.g., tetanus, diphtheria).
o Elicit neutralizing antibodies against the toxin. - mRNA Vaccines:
o Encode antigenic proteins (e.g., COVID-19 vaccines).
o Stimulate robust B- and T-cell responses.
TLO 10.3: Describe three different types of vaccine currently in use and how these vary in their safety and efficacy
- Live Attenuated Vaccine (e.g., MMR):
o Safety: Risk of reversion to virulence is extremely low but possible; contraindicated in immunosuppression or pregnancy.
o Efficacy: Induces strong, long-lasting immunity, often with a single dose. - Inactivated Vaccine (e.g., Inactivated Poliovirus Vaccine, IPV):
o Safety: Cannot replicate; minimal risk even in immunocompromised.
o Efficacy: Often requires multiple doses and boosters; immunity may be less robust compared to live vaccines. - Subunit/Conjugate Vaccines (e.g., Hepatitis B, Pneumococcal Conjugate):
o Safety: Extremely safe due to containing only specific antigens.
o Efficacy: Generally good; immunogenicity can be enhanced by conjugating the antigen to a carrier protein and/or adding adjuvants. Often require booster doses.
What type of vaccine is CONTRAindicated for patients with severe immunodeficient states?” is:
- Live attenuated
Contraindicated means that a specific procedure or treatment is advised against due to potential harm or adverse effects. It is a medical term used to indicate that certain actions should be avoided because they could be dangerous or inappropriate for a particular patient.
Type of Immunity
Innate Immunity Physical barriers (skin, mucous membranes), chemical barriers (stomach acid, enzymes), cellular components (phagocytes, NK cells)
Humoral Immunity B cells, antibodies, memory B cells
Cellular Immunity T cells (helper, cytotoxic, regulatory)
different types of vaccines:
Type of Vaccine Description
Live Attenuated Contains weakened form of the pathogen.
Inactivated (Killed) Contains killed pathogen that cannot cause disease.
Subunit, Recombinant, Conjugate Contains pieces of the pathogen (like protein or sugar), not the whole microbe.
In which of the following is GVHR (graft vs host reaction) seen?” The options are:
* Stem cell transplantation
* Kidney transplantation
* Heart transplantation
* Liver transplantation
* Skin transplantation
* I don’t know
Stem cell transplantation.
Graft-versus-host reaction (GVHR) typically occurs in stem cell or bone marrow transplants. In this condition, the donated cells (graft) recognize the recipient’s body (host) as foreign and attack it.
“HIV infection belongs to which type of immunodeficient state according to the classification of immunodeficiencies?”
The options are:
* Stimulated
* Primary
* Spontaneous
* Induced
* Acquired
* I don’t know
Acquired
