2024 Exam GIL Flashcards
Innate Vs Acquired Immunity (9 comparisons)
Innate immune responses are fast and constantly active, relying on general recognition of pathogens through pathogen-associated molecular patterns (PAMPs) or microbe-associated molecular patterns (MAMPs). These responses lack specificity and memory, utilizing physical and chemical barriers, the complement system, and cells of innate immunity like macrophages to provide broad protection.
In contrast, acquired immunity is slower during the first exposure to a pathogen but becomes faster and more effective in subsequent encounters. It is highly specific, using MHC class I and II receptors to recognize antigens on pathogen surfaces. This system involves both humoral immunity (B-cells and plasma cells) and cell-mediated immunity (T-cells), and it retains memory of previous infections to enhance future responses.
What are the 4 Cardinal Signs of Innate Inflammation?
- Oedema
- Redness
- Heat
- Pain / sensitivity
Explain the physiological basis for the oedema in detail.
Proinflammatory cytokines released by local macrophages / monocytes / neutrophils lead to increased vasodilation and increased localised blood flow and vascular permeability -> increases in vascular permeability leads to the leakage of plasma proteins from the blood vessels into the extracellular space -> increased protein concentration in extracellular space causes a change in the osmotic potential of the extracellular space, where water/fluid “follows” the proteins into the extracellular space -> causing oedema.
Explain the physiological basis for the redness in detail.
As a result of increased vasodilation brough about by pro-inflammatory cytokines, the diameter of blood vessels increases, and as a result,t ehy are more proximally located to the surface epithelium. As a result, the colour of the blood within the blood vessels is more visible through the more translucent epithelium, this colour is red, as the haem component within the haemoglobin within red blood cells is red in colour.
Explain the physiological basis for the heat in detail.
As a result of an increase in blood flow and vasodilation to the area due to pro-inflammatory cytokines, there is an increase in blood flow into the localised area. This causes an increase in heat as blood is composed in large part by water, which has a relatively high heat capacity and is able to transport heat effectively.
Explain the physiological basis for the pain/sensitivity in detail.
2 actions - firstly, pro-inflammatory cytokines act directly on local free-nerve endings to lower the threshold required to fire an AP (e.g., pain signal). Secondly, due to the increased oedema and pressure buildup in the extracellular space, there is pressure applied on free endings which is enough to stimulate the generation of AP, i.e., feeling pain/sensitivity.
Immunology in Perio - PMNs
Critical component of periodontal immunity, polymorphonuclear neutrophils; 3 key actions:
1. Degranulation: PMNs are able to degranulate and release soluble antimicrobial agents (e.g., defensins, lysozymes, cytokines), which are then able to attach to and directly kill bacteria within the sulcus, as well as mediate inflammatory processes.
2. Phagocytosis: PMNs are able to engulf and phagocytose bacteria, and then further act as antigen-presenting cells to activate the acquired immune system if needed.
3. NETosis: PMNs can unwind their DNA, and then bind them back together to form NETs (Neutrophil extracellular traps). When within range of a microbial target, they rapidly open their pasma membranes, and release the NETs to catch the microbe, either directly killing it or trapping it for other immune cells to kill the microbe. The PMN can (not always) die by forming using NETs.
Immunology in allergic reactions (T1 hypersensitivity)
Sensitisation phase:
1. allergen enters the body, where a dendritic cell will phagocytose, process and present it via an MHC class II receptor.
2. Naive T helper cell read the presented allergen protein and becomes activated, leading to the activation of nearby naive B cells via cytokines, into allergen-specific plasma cells.
3. These plasma cells produce and release specific IgE antibodiees for the allergen, which then go on to bind ot mast cells’ surface (variable numbers in different people, absed on level of activation), sensitising them for future exposures.
Then upon subsequent exposures to the specific allergen:
allergens bind to the specific IgE molecules on the surface of sensitised mast cells -> cross-linking of IgE and allergens. -> cross-linking leads to the degranulation of mast cells, releasng soluble factors (histamine, cytokines).
Severity of symptoms is determined by the number of mast cells that degranulate…
few mast cells -> less severe symptoms (swelling, itching, vomiting)
more mast cells -> more severe symptoms (hives, arrhythmias, anaphylaxis).
What are the structures within the respiratory tract?
two major parts: conducting and respiratory zone.
Conducting zone: nose, nasopharynx, larynx, trachea, bronchi, bronchioles -> ends at terminal bronchiole.
Respiratory zone: starts at the respiratory bronchioles, then goes to alveolar ducts, sacs and alveoli.
What are the condition requirements for air intake? What are the 4 functions of the conducting zone?
3 Ws: warm, wet and wash.
- filtration - traps dust / allergens via mucus and vibrissa in nose.
- cleansing - moves trapped particles within mucus to the pharynx through the actions of muco-ciliary elevator.
- moisten - moistens and humidifies the air via serous and mucous secretions.
- heat exchange - Warms / cools the air via vasculature (blood vessels).
What are the functions of the respiratory zone?
- site of external respiration - exchange of O2 and CO2 between the atmosphere and cells of the body.
- Facilitates oxygenation of blood and release of O2 into the environment.
What are the 8 cell types within the respiratory tract?
- pseudo-stratified columnar ciliated epithelium
- brush cells
- goblet cells
- basal cells
- alveolar type 1
- alveolar type 2
- club cells
- small granule cells
Describe the location and function of the pseudo-stratified columnar ciliated epithelium.
pseudostratified ciliated epithelium is located throughout the respiratory tract except larynx and pharynx.
- It moistens and protects the airways.
- Physical barrier against pathogens.
- Contain mitochondria which help to facilitate mucus production as well as the muco-ciliary elevator.
Describe the location and function of the Brush cell.
Brush cells, also known as airway tuft cells, are found interspersed within the respiratory epithelium. These columnar cells have a microvillous apex containing 120-140 apical microvilli and are connected to afferent sensory nerve endings at their base.
Their primary function is chemosensory, allowing them to detect harmful substances, such as bacterial pneumonia, airborne allergens, and fungi. In response to these threats, brush cells release acetylcholine, which stimulates neighboring cells with motile cilia, increasing their beating. This defensive mechanism enhances the clearance of harmful particles from the airways, contributing to the body’s protective response against respiratory threats.
Describe the location and function of the Goblet cells.
Goblet cells are located within the conducting zone of the respiratory system. They produce mucus, which contains mucin and glycoproteins, playing a key role in trapping particles and pathogens, thereby protecting the respiratory tract from harmful substances.
Describe the location and function of the Basal (short) cells.
Basal cells are located in the respiratory epithelium and function as stem cells. They have the ability to self-renew and differentiate into various cell types within the respiratory epithelium. In response to injury, basal cells increase their proliferation rate, contributing to the repair and regeneration of the epithelial lining.
Type 1 pneumocyte
they are located with in the alveolus with large cells with dense nucleus-large surface area which allows it to facilitate exchange. Makes up most of alveolar lining.
Type 2 pneumocyte
They are located within the alveolus, they produce pulmonary surfactant which is largely lipid content (90 % lipid, 10 % proteins), preventing collapse of the lungs after expiration. It reduces surface tension to prevent collapse.
What is COPD? what are it symptoms?
Chronic obstructive pulmonary disease (COPD) is a progressive respiratory condition characterized by several key symptoms. One common symptom is the activation of accessory muscles during breathing, indicating increased effort to breathe. Dyspnoea, or labored and difficult breathing, often causes mental distress due to the inability to ventilate enough to meet the body’s demand for air. Another notable symptom is wheezing, a continuous whistling noise caused by airway narrowing, most pronounced during expiration, which is often prolonged.
Cyanosis, a late-stage symptom, manifests as a blue discoloration of the nail beds, mucous membranes, or skin. It occurs when deoxyhaemoglobin levels exceed 5 g/100 mL of blood. Importantly, cyanosis may not appear in anaemic patients with hypoxia due to low haemoglobin levels, while patients with polycythemia (increased red blood cells) can exhibit cyanosis despite having normal oxygen levels (HbO2).
What are the causes of dyspoea?
Causes of dyspnoea (difficulty or labored breathing) include several physiological and psychological factors. One key cause is the presence of abnormal respiratory gases in the blood, particularly elevated levels of carbon dioxide (CO₂). Another factor is sensations arising from the respiratory muscles, where the body becomes aware that an abnormally high amount of effort is required to maintain adequate ventilation. Additionally, neurogenic and emotional factors, such as anxiety or claustrophobia, can also contribute to the sensation of dyspnoea.
Describe the causes and effects of asthma.
Asthma is a chronic condition characterized by inflammation of the airways. Symptoms can be triggered by various factors, including allergens, respiratory infections, or physical exercise. The effects of asthma include the secretion of excessive amounts of thick mucus and smooth muscle spasms, both of which lead to the narrowing of the airways, making it difficult to breathe. These airway obstructions contribute to the hallmark symptoms of asthma, such as wheezing, shortness of breath, and chest tightness.
Describe the causes and effects of chronic bronchitis
Chronic bronchitis is caused by the inhalation of cigarette smoke, polluted air, or other irritants. These irritants trigger an inflammatory response in the airways, leading to the over-secretion of mucus by goblet cells. Additionally, the function of cialia is impaired, reducing the clearance of mucus from the airways. Therefore, more of the microbes and foreign bodies are trapped within the respiratory zone and cannot be removed. This causes frequent and repeated infections in this lung -> chronic bronchitis. As a result, the airways becomes restricted, contributing to symptoms such as persistent coughing, difficulty breathing, and increased mucus production.
Describe the causes and effects of emphysema.
Emphysema is caused by the inhalation of irritants, such as cigarette smoke, which triggers an autoimmune response. Alveolar macrophages release enzymes that damage the alveolar walls. It can also have a genetic cause, such as antitrypsin deficiency, which leads to insufficient protection of the lungs from enzyme damage.
The effects of emphysema include the breakdown of alveolar walls, reducing the surface area available for gas exchange. Additionally, the degradation of elastin impairs the lungs’ elastic recoil, making it more difficult for the lungs to exhale air. As a result, respiration becomes impaired and breathing more laborious.
Describe PEP-PTS.
The PEP-PTS (Phosphoenolpyruvate-Phosphotransferase System) is a high-affinity transport system that functions as an efficient mechanism for transporting mono- and disaccharides. It acts like a “teaspoon,” ensuring precise uptake of sugars. This system is constitutively active for glucose and sucrose but inducible for other sugars.
PEP-PTS operates optimally in famine conditions, such as environments with neutral pH and limited carbohydrate availability. However, it is repressed in feast conditions, when there is a low pH and an abundance of sugars.
Describe Permease Transport.
Glucose permease is a lower-affinity, high-capacity transport system, acting like a “shovel” to move large volumes of glucose across the membrane. It operates optimally in feast conditions, such as environments with low pH and high sugar concentrations, facilitating efficient glucose uptake. In contrast, glucose permease is repressed under famine conditions, where the pH is neutral, and carbohydrate availability is limited.
When is most effective to have fluoride?
Fluoride is an inhibitor of enolase, reducing PEP production (which is required for glucose transport in the PEP-PTS system). Therefore, fluoride would be more effective in famine environments, when the PEP-PTS system is most active.
Describe the Metabolic Effects of Fluoride
Fluoride inhibits enolase, an enzyme in the glycolytic pathway, which reduces the production of phosphoenolpyruvate (PEP). Since PEP is required for glucose transport via the PEP-PTS system, this inhibition directly affects glucose uptake under glucose-limiting conditions. As a result, the organism’s ability to grow is reduced due to the low levels of PEP available for transport.
In glucose excess conditions, the effect of fluoride on bacteria is minimized because the PEP-PTS system is repressed. In these conditions, glucose uptake is carried out by glucose permease, which does not depend on PEP. Thus, fluoride’s inhibitory effect is less impactful when sugar is abundant.
Glucose uptake system presents in acidogenic bacteria. Play a role in the pathogenesis of caries.
Feast and Famine Regulation Systems
In glucose-limited (famine) conditions, the reduced availability of glucose decreases pyruvate kinase (PK) activity. This reduction allows phosphoenolpyruvate (PEP) to accumulate, which is crucial for glucose transport via the PEP-PTS system. The accumulation of PEP favors the PFL pathway, ensuring the organism maximizes the efficiency of glucose uptake in these conditions.
In contrast, during feast conditions with an excess of glucose, high concentrations of glycolytic intermediates, particularly fructose-1,6-diphosphate (FDP), are produced. This abundance shifts the metabolic balance towards the LDH pathway, favoring the use of the glucose permease system for glucose uptake, which is independent of PEP and operates efficiently under high glucose availability.
Anatomy
Describe the swallowing processes
Swallowing / Deglutition:
- Buccal Phase (Voluntary) – This phase involves the oral cavity and oropharynx. The bolus is compressed against the hard palate by the tongue. The tongue then retracts, forcing the bolus into the oropharynx while the soft palate elevates to seal off the nasopharynx, preventing food from entering the nasal passages. The bolus contacts the oropharynx, triggering a reflex to continue the swallowing process.
- Pharyngeal Phase (Involuntary) – This phase also involves the oral cavity and oropharynx. Two actions occur simultaneously: first, tactile receptors in the palatal arch and uvula are stimulated, prompting a coordinated muscle contraction pattern in the pharyngeal muscles, initiated by the swallowing center in the medulla oblongata, to push the bolus down into the esophagus. Secondly, the larynx elevates and the epiglottis folds over, preventing the bolus from entering the respiratory tract.
- Esophageal Phase (Involuntary) – This phase involves the esophagus and stomach. The pharyngeal muscles contract, pushing the bolus through the relaxed upper esophageal sphincter into the esophagus. Peristaltic waves then move the bolus down the esophagus. As the bolus reaches the stomach, the lower esophageal sphincter relaxes, allowing food to enter the stomach.
Which nerve is responsible for taste?
More information about fluorosis
Pathogenesis of caries
- White Spot Lesions (WSL): These non-cavitated lesions can be treated with topical fluoride. They may or may not be visible on radiographs. Acidic metabolites from bacteria cause surface demineralization of the enamel, leading to the appearance of white spots.
- Progression: As demineralization continues, the enamel becomes more porous, allowing acid to permeate through the lamellar pores. A triangular pattern of demineralization develops, following the arrangement of enamel rods and extending toward the dentinoenamel junction (DEJ). At this stage, lesions are more likely to be detected radiographically. The surface enamel remains intact, with a subsurface lesion forming beneath.
- Caries Spread into Dentine: The decay follows the path of least resistance along the DEJ, initially causing the formation of affected dentine. The lesion spreads along the DEJ, often exhibiting a ballooning pattern and triangular shape due to the porous structure of the dentine.
- Formation of Infected Dentine: As the decay progresses, increased bacterial ingress occurs due to the porosity of the dentine. This results in the development of both an affected and infected zone as bacteria penetrate deeper.
- Advanced Progression and Cavitation: Further progression leads to the breakdown of the collagen structure in the dentine, compromising its integrity. This deterioration often results in cavitation, as the enamel above cannot support tensile loads effectively once the underlying dentine structure is compromised.
