Formative Questions EXAM 2 Flashcards
1
Q
What are the main causes of acute inflammation?
A
- Infections (bacterial, viral, fungal, parasitic).
- Tissue necrosis (ischemia, trauma, toxins).
- Foreign bodies (splinters, sutures, dirt).
- Immune reactions (hypersensitivity, autoimmune diseases).
2
Q
What are the four classical signs of inflammation?
A
- Rubor (Redness) – Due to vasodilation.
- Calor (Heat) – Increased blood flow (hyperemia).
- Tumor (Swelling) – Fluid accumulation (edema).
- Dolor (Pain) – Chemical mediators (prostaglandins, bradykinin) stimulate pain receptors.
3
Q
What are the differences between acute and chronic inflammation?
A
Feature Acute Inflammation Chronic Inflammation
Onset Rapid (minutes to hours) Slow (weeks to months)
Duration Short-lived (hours to days) Long-lasting (weeks to years)
Cells Involved Neutrophils Macrophages, lymphocytes, plasma cells
Tissue Damage Mild Severe, fibrosis common
Outcome Resolution, healing, or chronic inflammation Tissue destruction and repair
4
Q
How do neutrophils and macrophages contribute to inflammation?
A
• Neutrophils:
• First responders (within hours).
• Perform phagocytosis, release enzymes, and generate reactive oxygen species (ROS).
• Macrophages:
• Arrive later (24-48 hours).
• Continue phagocytosis, release cytokines (IL-1, TNF-α), and stimulate tissue repair.
• In chronic inflammation, they activate T cells and contribute to granuloma formation.
5
Q
What is granulomatous inflammation, and what conditions cause it?
A
• Granulomatous inflammation is a chronic inflammatory response characterized by activated macrophages (epithelioid cells) surrounded by lymphocytes.
• Causes:
• Infectious:
• Tuberculosis (Mycobacterium tuberculosis).
• Leprosy (Mycobacterium leprae).
• Fungal infections (Histoplasmosis).
• Non-infectious:
• Sarcoidosis.
• Foreign body reactions (sutures, silica).
6
Q
Describe the phases of wound healing.
A
- Inflammation (0-3 days)
• Clot formation.
• Neutrophil infiltration to clear debris. - Proliferation (3-7 days)
• Fibroblast migration, collagen deposition.
• Angiogenesis (new blood vessel formation).
• Formation of granulation tissue. - Remodeling (Weeks to months)
• Collagen type III replaced with type I.
• Wound contraction by myofibroblasts.
• Scar formation.
7
Q
What factors can impair proper wound healing?
A
- Infection – Delays healing, promotes chronic inflammation.
- Poor blood supply (ischemia) – Reduces oxygen & nutrient delivery.
- Malnutrition – Protein & Vitamin C deficiency impair collagen synthesis.
- Diabetes – Delayed wound healing due to poor circulation & high glucose.
- Corticosteroids – Inhibit immune response & collagen synthesis.
- Foreign bodies – Cause persistent inflammation.
8
Q
A
9
Q
What are the main causes of cellular injury?
A
- Hypoxia – Oxygen deprivation.
- Physical agents – Trauma, temperature extremes, radiation.
- Chemical agents & toxins – Poisons, drugs, heavy metals.
- Infectious agents – Bacteria, viruses, fungi, parasites.
- Immunologic reactions – Autoimmune diseases, hypersensitivity.
- Genetic mutations – Defective proteins, accumulation disorders.
- Nutritional imbalances – Deficiencies or excesses of nutrients.
10
Q
How do free radicals damage cells?
A
• Lipid peroxidation → Membrane damage.
• Protein modification → Enzyme dysfunction.
• DNA damage → Mutations, apoptosis.
• Sources: Normal metabolism (ETC), radiation, inflammation.
• Defense mechanisms: Antioxidants (Vitamin C, E), superoxide dismutase (SOD), catalase.
11
Q
Differentiate between hypoxia and ischemia.
A
• Hypoxia: ↓ Oxygen supply but normal blood flow (e.g., anemia, CO poisoning).
• Ischemia: ↓ Blood flow leading to both oxygen & nutrient depletion (e.g., stroke, myocardial infarction).
• Ischemia is more severe because it also blocks waste removal.
12
Q
What are common markers of cell injury?
A
• Cardiac injury → Troponins, CK-MB, LDH1.
• Liver injury → ALT, AST, ALP, Bilirubin.
• Pancreatic injury → Amylase, Lipase.
• Muscle injury → CK (Creatine kinase), Myoglobin.
13
Q
What intracellular accumulations are found in disease states?
A
- Lipids – Fatty liver (steatosis), atherosclerosis.
- Proteins – Misfolded proteins (Alzheimer’s, Parkinson’s).
- Glycogen – Diabetes, glycogen storage diseases.
- Pigments – Hemosiderin (iron overload), Lipofuscin (aging), Bilirubin (jaundice).
- Calcium – Pathologic calcification (dystrophic, metastatic).
14
Q
Describe lipid peroxidation and its role in injury.
A
• Free radicals attack polyunsaturated lipids in membranes → Forms lipid peroxides.
• Leads to membrane damage, increased permeability, and cell death.
• Common in oxidative stress, ischemia-reperfusion injury, and neurodegenerative diseases.
15
Q
What are the consequences of mitochondrial damage?
A
- ↓ ATP production → Cellular energy failure.
- ↑ ROS production → Oxidative stress, DNA damage.
- Release of cytochrome C → Triggers apoptosis.
- Calcium dysregulation → Activates degradative enzymes (proteases, phospholipases).
- Necrosis & apoptosis depending on severity.
16
Q
Compare dystrophic vs. metastatic calcification.
A
Feature Dystrophic Calcification Metastatic Calcification
Cause Local tissue injury/necrosis High serum calcium (hypercalcemia)
Calcium levels Normal serum calcium Elevated serum calcium
Common Sites Atherosclerotic plaques, damaged heart valves Lungs, kidneys, stomach (alkaline tissues)
Examples Aortic stenosis, TB granulomas Hyperparathyroidism, bone metastases
17
Q
What factors influence cellular responses to injury?
A
- Type of injury – Ischemia, toxins, infection.
- Severity & duration – Acute vs. chronic exposure.
- Cell type – Neurons (highly sensitive), skeletal muscle (more resistant).
- Nutritional status – Antioxidants, oxygen supply.
- Genetic factors – Enzyme deficiencies, repair mechanisms.
18
Q
What are the different types of cellular adaptation?
A
- Hypertrophy – ↑ Cell size due to increased workload (e.g., muscle growth).
- Hyperplasia – ↑ Cell number due to growth signals (e.g., liver regeneration).
- Atrophy – ↓ Cell size due to disuse or nutrient deprivation (e.g., muscle wasting).
- Metaplasia – Reversible replacement of one cell type with another (e.g., squamous metaplasia in smokers).
- Dysplasia – Disordered cell growth (potential precursor to cancer).
19
Q
Compare hypertrophy and hyperplasia.
A
see table
20
Q
What is metaplasia, and why can it lead to cancer?
A
• Metaplasia = Reversible change in cell type due to chronic stress.
• Example: Chronic smoking → Columnar epithelium in bronchi → Squamous epithelium (less protective).
• Cancer risk:
• Chronic irritation → Persistent metaplasia → Genetic mutations → Dysplasia → Neoplasia (cancer).
21
Q
Describe the morphological differences between necrosis and apoptosis.
A
see table
22
Q
How does apoptosis help prevent cancer?
A
- Eliminates damaged cells – Prevents mutations from accumulating.
- Removes self-reactive immune cells – Prevents autoimmune diseases.
- Regulates tissue homeostasis – Prevents uncontrolled proliferation.
- p53 activation – If DNA damage is irreparable, p53 triggers apoptosis.
23
Q
What are the clinical consequences of necrosis types (coagulative, liquefactive, etc.)?
A
See table
24
Q
What are the key mechanisms of tissue regeneration?
A
- Stem cells – Self-renew and differentiate into needed cell types.
- Growth factors (EGF, TGF-β, VEGF, FGF) – Stimulate cell proliferation.
- Extracellular matrix (ECM) – Provides structural support for new tissue.
- Angiogenesis – Formation of new blood vessels.
- Cell migration and proliferation – Replaces lost or damaged cells.
25
Compare necroptosis, pyroptosis, and anoikis.
See table
26
What is 16S rRNA sequencing, and why is it useful?
16S rRNA sequencing analyzes the 16S ribosomal RNA gene to identify bacteria.
## Footnote
Useful because it is highly conserved across bacteria but has variable regions for differentiation, can classify unculturable bacteria, and is used in microbiome studies to analyze bacterial diversity.
27
Describe the structural differences between Gram-positive and Gram-negative bacteria.
See table
28
What is the function of peptidoglycan, and how do antibiotics target its synthesis?
Function: Provides structural integrity and protects against osmotic lysis.
Antibiotic Targets: β-lactams (penicillins, cephalosporins) inhibit penicillin-binding proteins (PBPs); Vancomycin binds D-Ala-D-Ala, preventing cross-linking; Fosfomycin inhibits early steps of peptidoglycan synthesis.
29
What are the steps of Gram staining?
1. Crystal violet → Stains all cells purple.
2. Iodine → Fixes dye into the peptidoglycan.
3. Alcohol (decolorizer) → Removes dye from Gram-negative bacteria.
4. Safranin → Counterstains Gram-negative bacteria red/pink.
30
What is lipopolysaccharide (LPS), and why is it significant in Gram-negative bacteria?
LPS = Endotoxin in Gram-negative outer membrane.
Structure: 1. Lipid A – Toxic component, triggers septic shock; 2. Core polysaccharide – Structural support; 3. O-antigen – Helps evade immune system. Clinical relevance: Causes fever, hypotension, shock; activates TLR4 (Toll-like receptor 4) → Cytokine storm.
31
How do porins contribute to antibiotic resistance?
Porins = Protein channels in Gram-negative outer membrane.
They regulate entry of small molecules (nutrients & antibiotics). Resistance Mechanism: Reduced porin expression → Fewer antibiotics enter; mutation in porins → Alters permeability to drugs.
32
Compare capsules vs. slime layers in bacterial structure and function.
See table
33
What are the roles of pili, fimbriae, and flagella?
Pili → Transfer genetic material (conjugation). Fimbriae → Adhesion to surfaces (e.g., E. coli attachment in UTIs). Flagella → Motility (e.g., Helicobacter pylori movement in mucus).
34
How do fluoroquinolones inhibit bacterial DNA replication?
Fluoroquinolones (Ciprofloxacin, Levofloxacin) inhibit: 1. DNA Gyrase (Topoisomerase II) – Prevents supercoiling relief; 2. Topoisomerase IV – Blocks chromosome separation.
Bactericidal effect → Causes DNA fragmentation.
35
What is the difference between bacterial chromosomes and plasmids?
See table
36
What is the Embden-Meyerhof-Parnas (EMP) pathway, and how do bacteria use it?
EMP pathway = Glycolysis (Glucose → Pyruvate). Used for ATP generation in both aerobic & anaerobic bacteria. Key steps: 1. Glucose → 2 Pyruvate. 2. Produces 2 ATP, 2 NADH. 3. Pyruvate enters fermentation or TCA cycle.
37
How does fermentation recycle NADH+H⁺? What are its end products?
Fermentation regenerates NAD⁺ by reducing pyruvate. End products: Lactic acid (Lactobacillus, Streptococcus mutans). Ethanol + CO₂ (Yeast). Mixed acids (E. coli).
38
How do short-chain fatty acids (SCFAs) influence human metabolism?
Produced by gut bacteria (fermentation of fiber). Functions: Energy source for colonocytes. Regulate immune response. Reduce inflammation (Butyrate). Influence gut-brain axis.
39
What role does S. mutans play in dental caries formation?
Primary cariogenic bacterium. Metabolizes sucrose → Produces lactic acid (lowers pH). Creates glucans → Biofilm formation (dental plaque). Leads to enamel demineralization → Cavities.
40
How does xylitol prevent S. mutans growth?
Xylitol is a sugar alcohol bacteria cannot metabolize. Inhibits glycolysis → Starves S. mutans. Reduces bacterial adhesion to enamel. Promotes remineralization of enamel.
41
What are the acid tolerance mechanisms of S. mutans?
Proton pumps remove H⁺ to maintain pH. Alkali production (arginine metabolism → ammonia). Increased expression of stress proteins (protect enzymes). Altered membrane composition to resist acid damage.
42
What is the role of electron transport in bacterial energy production?
Generates ATP via oxidative phosphorylation. Electron donors: NADH, FADH₂. Electron acceptors: O₂ (aerobic respiration). Nitrate, sulfate (anaerobic respiration). Proton gradient (H⁺ pumps) → ATP synthase produces ATP.
43
Compare aerobic and anaerobic respiration.
See table
44
How do bacteria regulate metabolic pathways?
Gene regulation: Operons control enzyme expression. Allosteric regulation: Feedback inhibition of enzymes. Catabolite repression: Preferential sugar usage (e.g., glucose > lactose). Two-component systems: Sensor-response regulation.
45
What is the function of siderophores in bacterial iron metabolism?
Siderophores = High-affinity iron-chelating molecules. Scavenge Fe³⁺ from host proteins (transferrin, lactoferrin). Essential for bacterial growth & virulence. Example: Pseudomonas aeruginosa produces pyoverdine.
46
Describe the different types of hemolysis and their significance.
See table
47
What is metabolic cooperativity in bacterial biofilms?
Bacteria share metabolic byproducts for mutual benefit. Example: S. mutans ferments sugar → Produces lactic acid → Used by Veillonella. Supports biofilm survival in diverse environments.
48
How do primary and secondary colonizers contribute to dental plaque metabolism?
Primary colonizers: Streptococcus spp. bind salivary pellicle first. Produce glycosidases to free sugars. Secondary colonizers: Fusobacterium nucleatum bridges primary & late colonizers. Consume fermentation byproducts (lactate).
49
What are the different mechanisms of horizontal gene transfer (HGT) in bacteria?
1. Transformation – Uptake of free DNA from the environment.
2. Transduction – DNA transfer via bacteriophages.
3. Conjugation – Direct cell-to-cell transfer using a sex pilus.
50
Compare generalized vs. specialized transduction.
See table
51
What is the role of RecA in bacterial genetic recombination?
• RecA is a DNA-binding protein that promotes homologous recombination.
• Essential for DNA repair and integration of foreign DNA.
• Activated in SOS response when DNA damage occurs.
52
How does conjugation contribute to bacterial evolution?
• Transfers antibiotic resistance genes (R-plasmids).
• Spreads virulence factors (toxins, adhesion genes).
• Increases genetic diversity within populations.
53
What are transposons, and how do they contribute to antibiotic resistance?
• “Jumping genes” that move within the genome.
• Carry antibiotic resistance genes (e.g., Tn3 β-lactamase gene).
• Can integrate into plasmids, spreading resistance between bacteria.
54
How do ICE elements (integrative conjugative elements) function?
• Hybrid between plasmids & transposons.
• Encode their own conjugation machinery.
• Integrate into the chromosome, excise, and transfer via conjugation.
55
What is the CRISPR-Cas system, and how does it protect bacteria?
• Bacterial immune system against phages & plasmids.
• Cas proteins cut invading viral DNA and store fragments as “memory”.
• If reinfected, CRISPR RNA guides Cas to destroy the DNA.
56
Describe the differences between lytic and lysogenic phage cycles.
See table
57
What is an Hfr strain, and how does it differ from standard conjugation?
• Hfr (High-Frequency Recombination) strains have the F plasmid integrated into their chromosome.
• During conjugation, they transfer chromosomal genes, not just plasmids.
• Allows for large-scale gene exchange between bacteria.
58
What is SCCmec, and why is it important in MRSA?
• SCCmec = Staphylococcal Cassette Chromosome mec.
• Carries mecA gene, encoding PBP2a (methicillin resistance).
• Defines MRSA (Methicillin-Resistant Staphylococcus aureus).
59
How can transformation lead to strain diversity in bacteria?
• Uptake of environmental DNA increases genetic variation.
• Can acquire antibiotic resistance or virulence genes.
• Natural competence seen in Streptococcus pneumoniae, Neisseria gonorrhoeae.
60
Why do some bacteria increase mutation rates under stress?
• SOS response activates error-prone DNA polymerases.
• Increases genetic variation to help bacteria survive extreme conditions.
• Example: Antibiotic stress promotes resistance mutations.
61
How do broad-host-range plasmids contribute to gene transfer across species?
• Replicate in multiple bacterial species.
• Facilitate interspecies horizontal gene transfer.
• Spread antibiotic resistance & virulence factors widely.
62
What are the four bacterial growth phases?
1. Lag phase – No division, bacteria adjust to environment.
2. Log (Exponential) phase – Rapid division, maximum growth rate.
3. Stationary phase – Nutrients deplete, growth rate slows, waste accumulates.
4. Death (Decline) phase – Cell death exceeds growth, population declines.
63
How does quorum sensing regulate bacterial behavior?
• Bacteria release autoinducer molecules (e.g., AHLs in Gram-negative bacteria).
• When threshold is reached, genes are activated for:
• Biofilm formation.
• Virulence factor production.
• Antibiotic resistance.
## Footnote
Example: Pseudomonas aeruginosa uses quorum sensing for biofilm growth.
64
What factors affect bacterial growth?
1. Temperature – Psychrophiles (cold), Mesophiles (body temp.), Thermophiles (hot).
2. pH – Acidophiles (low pH), Neutrophiles (neutral pH), Alkaliphiles (high pH).
3. Oxygen levels – Aerobes, Anaerobes, Facultative anaerobes.
4. Nutrient availability – Carbon, nitrogen, sulfur sources.
5. Water & osmotic pressure – Halophiles thrive in high salt.
65
How do biofilms form, and why are they resistant to antibiotics?
1. Attachment – Bacteria adhere to surface using pili/fimbriae.
2. Microcolony formation – Cells grow, produce extracellular polymeric substances (EPS).
3. Maturation – Complex 3D structure develops, quorum sensing activates.
4. Dispersion – Cells detach and spread.
Why resistant?
• EPS limits antibiotic penetration.
• Persister cells remain dormant and survive.
• Biofilm metabolism differs from planktonic bacteria.
66
What role does S. mutans play in dental caries?
• Primary cariogenic bacterium in plaque.
• Ferments sugars → Produces lactic acid → Lowers pH.
• Acid dissolves enamel → Cavity formation.
• Produces glucans (sticky polymers) to strengthen biofilms.
67
How does xylitol help prevent cavities?
• Non-fermentable sugar alcohol.
• Prevents S. mutans metabolism → No acid production.
• Disrupts bacterial adhesion to enamel.
• Reduces cariogenic biofilm formation.
68
What are persister cells, and how do they promote antibiotic resistance?
• Dormant, metabolically inactive cells within biofilms.
• Survive antibiotic exposure without genetic resistance.
• Repopulate after antibiotic removal → Chronic infections.
• Common in Pseudomonas aeruginosa, E. coli, Mycobacterium tuberculosis.
69
What mechanisms allow biofilms to evade immune responses?
• EPS shields bacteria from phagocytosis.
• Low metabolic activity reduces immune detection.
• Bacteria within biofilms resist complement and antimicrobial peptides.
• Biofilm dispersal releases new bacterial populations.
70
What are the key steps of biofilm formation?
1. Attachment – Bacteria adhere to surfaces using pili/fimbriae.
2. Microcolony Formation – Cells multiply and begin producing EPS (extracellular polymeric substances).
3. Maturation – Biofilm develops a complex 3D structure.
4. Dispersion – Some bacteria detach and spread to new locations.
71
How do primary and secondary colonizers contribute to dental plaque formation?
• Primary colonizers (e.g., Streptococcus spp.) attach to tooth surfaces and form the initial biofilm.
• Secondary colonizers (e.g., Fusobacterium nucleatum) adhere to primary colonizers, facilitating the growth of pathogenic anaerobes.
72
What is metabolic cooperativity in biofilms?
• Bacteria share metabolic byproducts, supporting survival in different niches.
• Example: S. mutans produces lactic acid, which Veillonella uses, reducing acidity and promoting mutual growth.
73
What are corncob and hedgehog structures in biofilms?
• Corncob structures: Rod-shaped bacteria (e.g., Fusobacterium) surrounded by cocci (Streptococcus).
• Hedgehog structures: Layers of diverse bacteria with filamentous bacteria protruding outward.
74
How does Fusobacterium nucleatum act as a bridge in dental biofilms?
• Links early (aerobic) and late (anaerobic) colonizers, stabilizing the biofilm.
• Facilitates the survival of periodontal pathogens.
75
What are the key differences between supragingival and subgingival microbiomes?
See table
76
How do biofilms evade the immune system?
• EPS shields bacteria from phagocytosis.
• Slow metabolism makes them less detectable.
• Antigenic variation helps bacteria avoid recognition.
• Dispersal allows regrowth after immune attack.
77
What mechanisms allow biofilms to resist antibiotics?
• EPS prevents antibiotic penetration.
• Persister cells remain dormant and survive treatment.
• Biofilm bacteria express genes for antibiotic resistance.
78
How does Streptococcus mutans contribute to dental caries?
• Ferments sugars into lactic acid, lowering pH.
• Acid dissolves enamel, leading to cavities.
• Produces glucans to strengthen biofilms and enhance adhesion.
79
How does xylitol help prevent dental cavities?
• Non-fermentable sugar alcohol – S. mutans cannot metabolize it.
• Inhibits bacterial growth and adhesion.
• Stimulates saliva flow, aiding in enamel remineralization.
80
What is selective toxicity in antimicrobial therapy?
• Targets bacterial structures/functions absent in humans.
• Example: Penicillins attack peptidoglycan, which humans lack.
81
Differentiate between bacteriostatic and bactericidal antibiotics.
See table
82
How do β-lactam antibiotics inhibit bacterial growth?
• Bind PBPs (penicillin-binding proteins).
• Inhibit peptidoglycan cross-linking, weakening the cell wall.
• Causes bacterial lysis.
83
What is the significance of MIC and MBC in antibiotic therapy?
• MIC (Minimum Inhibitory Concentration) – Lowest drug concentration that inhibits growth.
• MBC (Minimum Bactericidal Concentration) – Lowest drug concentration that kills bacteria.
• Used to determine effective antibiotic dosing.
84
What are the key mechanisms of antimicrobial resistance?
1. Enzymatic degradation – β-lactamases break down penicillins.
2. Efflux pumps – Pump out antibiotics.
3. Target modification – Alteration of PBPs (MRSA).
4. Biofilm formation – Prevents antibiotic penetration.
85
What is post-antibiotic effect (PAE), and which drug classes exhibit it?
• Persistent bacterial inhibition even after drug removal.
• Seen in aminoglycosides & fluoroquinolones.
86
What is the difference between time-dependent and concentration-dependent killing?
See table
87
How do efflux pumps contribute to antibiotic resistance?
• Actively pump out antibiotics, reducing intracellular drug levels.
• Common in Gram-negative bacteria (e.g., Pseudomonas aeruginosa).
88
How do aminoglycosides differ from other protein synthesis inhibitors?
• Bactericidal (others are bacteriostatic).
• Bind 30S ribosome, causing misreading of mRNA.
89
Why should tetracyclines be avoided in pregnancy and children?
• Crosses placenta, deposits in fetal bones and teeth.
• Causes teeth discoloration in children.
90
What drug causes red-orange body fluids?
• Rifampin – Used for TB, meningococcal prophylaxis.
91
What are the major adverse effects of isoniazid and rifampin?
Drug Major Adverse Effect
Isoniazid Hepatotoxicity, peripheral neuropathy
Rifampin Hepatotoxicity, red-orange secretions
92
How do bacteria resist fluoroquinolones?
1. Mutations in DNA gyrase or topoisomerase IV.
2. Efflux pumps remove drug.
93
How do β-lactams inhibit bacterial cell wall synthesis?
• Bind penicillin-binding proteins (PBPs).
• Inhibit transpeptidation, preventing peptidoglycan cross-linking.
• Causes bacterial lysis due to osmotic pressure.
94
What is the difference between narrow-spectrum and broad-spectrum penicillins?
See table
95
Which β-lactamase inhibitors are commonly used, and how do they work?
• Clavulanic acid, Sulbactam, Tazobactam.
• Bind & inactivate β-lactamases, preventing antibiotic degradation.
• Used in combination with penicillins (e.g., Amoxicillin-Clavulanate).
96
What are the major differences between cephalosporin generations?
Generation Coverage Example
1st Gen Gram-positive Cefazolin
2nd Gen ↑ Gram-negative Cefuroxime
3rd Gen Broad Gram-negative Ceftriaxone
4th Gen Pseudomonas Cefepime
5th Gen MRSA coverage Ceftaroline
97
Which carbapenem requires cilastatin, and why?
• Imipenem requires cilastatin.
• Cilastatin inhibits renal dehydropeptidase, preventing imipenem degradation in the kidneys.
98
How does vancomycin inhibit peptidoglycan synthesis?
• Binds D-Ala-D-Ala terminus, preventing cross-linking.
• Blocks transglycosylation & transpeptidation.
• Effective against Gram-positive bacteria (MRSA, C. difficile).
99
What are the main side effects of aminoglycosides?
• Nephrotoxicity (kidney damage).
• Ototoxicity (hearing loss, vestibular damage).
• Neuromuscular blockade (rare).
100
Why should tetracyclines be avoided in pregnant women and children?
• Crosses placenta & deposits in fetal bones and teeth.
• Causes teeth discoloration & enamel hypoplasia in children.
101
Which antibiotics are used for MRSA?
• Vancomycin (IV, severe cases).
• Daptomycin.
• Linezolid.
• Ceftaroline (5th-gen cephalosporin).
102
How do polymyxins disrupt bacterial membranes?
• Bind LPS (lipopolysaccharide) in Gram-negative bacteria.
• Disrupts outer & inner membrane integrity.
• Leads to leakage of cell contents & bacterial death.
103
How do aminoglycosides differ from other protein synthesis inhibitors?
• Bactericidal (most others are bacteriostatic).
• Bind 30S ribosome, causing misreading of mRNA.
104
What is the mechanism of fluoroquinolones, and what are their contraindications?
• Inhibit DNA gyrase (Topoisomerase II) & Topoisomerase IV.
• Prevent DNA replication & transcription.
• Contraindications:
• Avoid in pregnancy & children (cartilage damage).
• Can cause tendon rupture (Achilles tendonitis).
105
Why should tetracyclines be avoided in pregnancy and children?
• Causes permanent tooth discoloration.
• Delays bone growth in fetuses and young children.
106
What are the major adverse effects of isoniazid and rifampin?
Drug Major Adverse Effect
Isoniazid Hepatotoxicity, peripheral neuropathy
Rifampin Hepatotoxicity, red-orange secretions
107
Which drug causes red-orange body fluids?
• Rifampin – Used for TB, meningococcal prophylaxis.
108
What is the treatment for Pneumocystis jirovecii pneumonia?
• Trimethoprim-Sulfamethoxazole (TMP-SMX) (1st-line treatment).
• Pentamidine (if TMP-SMX is contraindicated).
109
What are the three possible bacterial responses to antibiotics?
1. Susceptible (killed by antibiotic).
2. Intermediate (higher dose required for effect).
3. Resistant (not affected by antibiotic at normal doses).
110
What is the difference between MIC and MBC?
• MIC (Minimum Inhibitory Concentration) – Lowest concentration that inhibits bacterial growth.
• MBC (Minimum Bactericidal Concentration) – Lowest concentration that kills bacteria.
111
How does the Kirby-Bauer disk diffusion test determine resistance?
• Antibiotic-impregnated disks placed on bacterial culture.
• Zone of inhibition (clear area) indicates susceptibility.
• Larger zone = More effective antibiotic.
112
What are the major categories of antibiotic resistance mechanisms?
1. Enzymatic inactivation (e.g., β-lactamases).
2. Efflux pumps (pump out drugs).
3. Target modification (alter PBPs, ribosomes).
4. Biofilm formation (prevents penetration).
113
How do efflux pumps contribute to antibiotic resistance?
• Actively expel antibiotics from bacterial cells.
• Reduce intracellular drug concentration.
• Common in Gram-negative bacteria (e.g., Pseudomonas aeruginosa).
114
What is the function of β-lactamases, and how are they inhibited?
• Enzymes that break down β-lactam antibiotics.
• Inhibited by β-lactamase inhibitors (Clavulanic acid, Sulbactam, Tazobactam).
115
How does MRSA resist β-lactams?
• Alters penicillin-binding protein (PBP2a), reducing β-lactam binding.
• Encoded by mecA gene.
116
What is the mechanism of vancomycin resistance in VRE?
• D-Ala-D-Ala replaced by D-Ala-D-Lac, reducing vancomycin binding.
• Encoded by vanA gene.
117
How do bacteria resist fluoroquinolones?
1. Mutations in DNA gyrase or topoisomerase IV.
2. Efflux pumps remove drug.
118
What are the mechanisms of aminoglycoside resistance?
1. Aminoglycoside-modifying enzymes inactivate drug.
2. Ribosomal mutations reduce binding.
3. Efflux pumps remove drug from cell.
