POM Flashcards
What are the two possible outcomes when a cell is exposed to a mild injurous agent or stress?
- Reversing the injury if adaptive capacity is exceeded
- Adapting to better be able to deal with the new conditions
What happens if the injurous agent to which the cell is exposed is severe?
The cell suffers irreversible injury and can be:
- Killed via oncosis/necrosis
- Commit suicide via apoptosis
What are the 6 possible causes of cell injury?
- Physical (heat, trauma, radiation etc.)
- Chemical (pH, free radicals, poisons)
- Biological (Micro-organisms, immune responses)
- Nutritional (anorexia, starvation, or excess intake)
- Immunologic (autoimmune reactions)
- Genetic derangements (congenital malformations, predisposing genes)
What are the 4 main ways in which cells are injured?
Decrease in ATP production
Membrane damage
Increase in intracellular Ca2+
Damage due to free radicals
How can ATP production be reduced via cell injury?
Lack of oxygen
Enzyme damage in the cytoplasm
Damage to mitochondria
How does a drop in ATP production harm the cell?
Reduced energy available for DNA and protein repair
Reduced energy available for ATP driven ion pumps (disrupts homeostasis, often causes increase in Na+, H2O and Ca2+ in the cell) Causes cell swelling and activation of damaging enzymes
Reduced protein synthesis, ribosomal detachment from RER
How can the cell membranes be damaged in cell injury?
Free radicals directly harm it Hypoxia (less ATP) Membrane targeting bacterial toxins Failure of membrane Ca2+ pumps Activation of phospholipases during injury, and insufficient ATP for synthesis of new phospholipids
How does plasma membrane damage harm the cell?
Loss of cellular contents, osmotic balance, enzymes, proteins, coenzymes and RNA
Influx of fluid and ions
If lysosomal membranes are burst, the digestive enzymes are released into the cell, and perform autolysis
Mitochondrial membrane damage: high conductance, non-selective channels form, causing a mitochondrial permeability transition. Mitosis cannot occur, and cytochrome c leaks into the cytoplasm, priming the cell for apoptosis.
What can cause increased Ca2+ concentration in the injured cell?
Decreased activity of Ca2+ channels in the membrane
How does increased Ca2+ concentration harm the cell?
Ca2+ dependent destructive enzymes are activated:
ATPase (less ATP)
Phospholipase (destroys membranes)
Proteases (break down membrane and skeleton proteins)
Endonucleases (DNA and chromatin breakdown)
What are free radicals and how do they damage cells?
They are highly reactive species with an unpaired electron. When they collide, they release energy.
They attack the fatty acid double bonds in the membrane, oxidise amino acid side chains in proteins, and react with the T base in DNA.
They are also autocatalytic, so they create more free radicals as they go, furthering the issue.
How does the body defend against free radicals?
We have antioxidants (VA, E etc.), enzymes etc. Oxidative stress occurs when there are more free radicals present than can be coped with.
How can cell proteins be damaged?
Directly (Ca2+ enzymes or free radicals) or having synthesis reduced. Also, glycation.
How is DNA damaged?
UV or Ionizing radiation
Mutagens and Free Radicals
Genetic causes
B12 or folate deficiencies
How does intracellular signalling help in the repair or removal of damaged cells?
- Activate heat shock factors to produce heat shock proteins, which re-fold and hold damaged proteins until they can be repaired
- Stress kinases (P38 MAP kinase, Jun-N terminal kinase) initiate signalling cascades to coordinate repair
- P53 when DNA damage detected. Either stops division for repair or causes cell death
- BMF- damage to cytoskeleton
- Bim- microtubule damage
- Bad- due to inadequate GF stimulation
What are some ways in which cells adapt to mild stressors?
Hypertrophy: Cells grow larger due to increased functional demand or stimulation
Hyperplasia: More cells formed due to division of cells and stem cells (either local or from bone marrow).
Atrophy: Cells shrink due to reduced functional demand, nutrients or stimulation. Involves proteolytic systems using lysosomes and a protein destruction machine known as the uniquitin-proteasome pathway.
Metaplasia: under continuous mild damage, cells morph from one type to another type more able to withstand the environment.
What is the point of no return when cells can no longer adapt or repair?
When the membrane and mitochondrial dysfunction becomes irreparable.
What is necrosis? What does it require? Why is it less preferable to apoptosis?
Necrosis involves cells being killed outright by overwhelming damage. It affects large number of cells, and is accompanied by leakage of lysosomes (releasing digestive enzymes) and cytosol (inducing an inflammatory response)
- Requires no energy, but is uncontroled and messy
- Shows featureless cytoplasm, fragmentation and fading of chromatin.
- Debris removed by phagocytosis, but if not removed quickly enough can cause dystrophic calcification (Ca2+ buildup)
What is apoptosis? What does it require? Wy is it preferable to necrosis?
Apoptosis is the controlled suicide of a cell, where cell still have time and energy to execute a suicide. To conserve this energy, most cellular machinery is turned off.
Common after DNA damage, inadequate GF, hypoxia or accumulation of damaged proteins.
Also removes unwanted, wrongly placed, or self-reactive immune or infected cells.
Preferable as can be controlled, cellular cntents do not leak and inflammation is not initiated.
What is the process of apoptosis?
Caspase cascades mediate the events by proteoplytic cleavage. Upstream caspases are turned on first, while downstream caspases do the destroying.
Chromatin is cleaved and condensed (pyknosis) and membrane bound blebs of cytoplasm and organelles are split off and phagocytosed.
What is acute inflammation?
The body’s first response to a tissue injury.
What are the triggers of acute inflammation?
Infection and toxins Trauma Physical and chemical agents Necrosis Foreign bodies Immune reactions (hypersensitivity)
What are the 9 steps of inflammation?
- Pro-inflammatory substances released, activating tissue macrophages and endothelial cells in the blood vessels
- These then produce cytokines, prostaglandins and NO to cause vasodilation and increased blood vessel permeability
- Hyperaemia to affected tissue, increasing flow of protein rich fluid (exudation) to the tissue, which contains fibrinogen (seals damaged vessels, forms dense fibrinoue exudate), antibodies, and cascades. Oedema caused. Increased blood viscosity and slower blood flow (stasis). Leukocytes travel to margins of blood flow (margination), accumulating along endothelium
- Selectin expressed in vessels, causing neutrophils to roll slowly along lumen (attach to glycoprotein receptors) Then, integrin binds to addressins on endothelial cells, causing neutrophils to stop and stick,
- Neutrophils perform diapaedesis, extending a ‘food’ between cells and squeezing through to the extravascular space.
- Neutrophils activated y chemokines, IL-1 and TNF-a. Leukocytes also activated by bacteria bonding their surface toll-like receptors.
- Neutrophils perform chemotaxis towards exogenous and endogenous chemotactic factors. They are promoted by hypoxia.
- Neutrophils attack and and many are killed, releasing vasoactive, chemotactic and damaging substances. They mix with tissue debris & bacteria to form pus.
- Termianation occurs when offeding agent is eliminated and inflammation mediators disappear.
How do X-Rays work?
A high electrical potential is passed from a cathode to tungsten anode across an evacuated tube, bombarding the electrons. As the electrons return to their previous state, they give off energy between .01 and .1 nm in wavelength. These waves can penetrate the body to differing degrees
What are the different densities of X-ray?
Metal is whitest, then bone, soft tissue (water), fat, and air.
What are the positives and negatives of Xray?
Best spatial resolution
Depicts differences in density
Different contrast materials can be added to perform more functions
BUT
Limited contrast resolution
Prolonged exposure is harmful
What are CT scans and their positives and negatives?
CT scans use radiation to form a computer-generated slice of the body in the transverse plane.
They are very expensive and use x rays to work. However, they are very useful for when Ultrasound and X rays won’t give a good picture, and can discriminate between soft tissues due to excellent contrast resolution.
What are MRI scans and their positives and negatives?
MRI scans place the patient in a strong magnetic field, causing the H nuclei in the body to align with the field and then return to their original position, emitting signals detected by the machine.
Pros: no radiation, excellent contrast resolution (great for CNS) except for lungs
BUT: Expensive, takes a long time to do
What are US scans and their positives and negatives?
Sends pulses of sound and detects echoes from the body tissue, producing a slice of the body from where the sound began.
Safe, flexible, cheap
BUT: cannot penetrate bone or air-containing structure
What is interventional radiation and how/why is it used?
It involves the use of X rays, US, CTs or MRIs to place needles and catheters in the body in a moving image. US are used for needle/catheter insertion, CT when the lesion is obscured by gas or bone. These are less disturbing to patients than open surgery and can be done outpatient.
What is nuclear medicine?
Radioactive isotopes are injected into a vein, or given orally or anally. They may be taken up by a specific organ or tumour, or respond in an antigen/antibody reaction. The contrast these give can then be observed using Xrays or CTs or be detected by a gamma camera. It cannot precisely define organs, but is good for demonstrating early disease and function, and is safe and cheap.
What are PET scans?
they are a form of nuclear medicine using a chemical with a shorter half life. They are used to show blood flow in the brain, and also for cancers as the chemical is taken up by tumours.
What are the local effects of inflammation?
Redness/rubor (due to protein denaturing)
Swelling/tumor (due to oedema)
Heat/calor
Pain/dolor
Loss of function/functio laesa (due to damage and other local effects)
What are the systemic effects of inflammation?
Pyrexia/fever (mediated by IL-1 and TNF-a released by endothelium and macrophages)
Leukocytosis (increased WBC production)
Acute phase proteins (increased proteins involved with inflam. from liver)
Endocrine changes (more glucocorticoids)
What role do IL-1 and TNF-a play?
Produced by macrophage and endothelial cells.
Cause fever, slepiness, decreased appetite, increased acute phase proteins, haemodynamic shock and neutrophilia.
Increase neutrophil adherence, Increased fibroblast proliferation, collagen synthesis and cytokine secretion from Leukocytes.
How can inflammation lead to harm?
If they are not controlled or occur inappropriately, they can cause disease, hypersensitivity and hyperimmune reactions.
Repair by fibrosis can lead to scars, intestinal obstruction or limited mobility.
What is chronic inflammation>
When the cause is prolonged, and other leukocytes (besides neutrophils) enter the tissue.
Especially monocytes- they are greater killers and transform from into pacrophages as they enter injured tissue
What is granuloma formation?
A focused region of chronic inflammation consisting of a core of necrosis. It involves macrophages fusing into epithelial-esque cells with a collar of lymphocytes surrounding it. This is mainly done to remove foreign bodies.
What is healing?
The body’s attempts to restore original structure and function of injured tissue
What are the 2 parts of healing?
Cleaning up the mess
Rebuilding structure and function
What is involved with cleaning the mess of inflamed tissue?
Ideally, all debris is removed by macrophages
If there is too much, repair is set into motion. This is done by organisation, where macrophages secrete FGF and VEGF. These encourage growth of fibroblasts and blood vessels, and once there are many of these the tissue is termed granulation tissue.
This is then remodeled as the vessels regress and collagen aligns to form a fibrous scar (fibrosis)
However, this may represent loss of functional tissue, and could hinder remaining tissue.
What is involved with rebuilding the structure and function of destroyed tissue?
Attempts to replace parenchymal cells are made. , known as regeneration.
This involves proliferation of stem cells, both locally and from the bone marrow. It is more commonly done in areas of high tissue turnover (skin and gut).
What are the range extremes for the outcome of tissue
Anywhere between fibrous scar (function is lost) and complete resolution.
The longer the tissue damage and inflammation lasts, the less likely resolution will be.
What do X-rays tend to be used for? What contrasts can you add to X rays to make them useful for different purposes?
Mainly used to observe bones
Can add barium for enemas, to look at GI tract
Iodine compounds for angiography, IVUs
Gadolinium to make the pictures useful in MRI scans
What is nuclear medicine used for today?
Bone scans
V/Q scans for pulmonary emboli
Thyroid, white cell, liver, renal and brain scans
What are ultrasounds used for?
Examining pain, swelling, mass. Screening for renal dysfunction, cancer.
Checking vasculation and abnormal liver function
What are CT scans used for?
Head scans
Abdominal pain, trauma, cancer, bowel obstruction, vascular imaging
What are MRIs used for?
mainly brain, but can also look at abdominal structures
What are PET scans used for?
Cancer staging mainly
What are the types of microbes able to be recognized by our immune system?
Viruses: - Particle capsid shapes' antigens - Cells damaged by infection (due to the changes at their surfaces) - Virus-infected cells Bacteria and Fungi: - Bacterial surface antigens - Bacterial/fungal metabolites - Cells damaged by infection Parasites: - Surface shapes - Cells damaged by infection - Life cycle changes within a parasite- as the shapes of the parasites change over their life cycles.
What is the process of phagocytosis, and what cell types perform this?
Foreign microbe adheres to phagocyte
Membrane of phagocyte activated
Ridges of cytoplasm extend around microbe, leading to phagosome formation as the microbe is engulfed
Fusion and digestion of microbe
Release of degraded products
Granulocytes (neutrophils, short lived) and monocytes (longer lived)
Describe the components and uses of the complement system
Complement system stimulates and enhances the processes of inflammation and phagocytosis. This is done by the release of a cascade of blood-derived proteins.
- First complement components are able to bind with the membrane antigens of the agents involved, having evolved to recognize most common shapes. When a group of them congregate and form enzymes, they activate other components of the system
- Some increase vascular permeability
- Some attract granulocytes into tissues by helping with chemotaxis
- Some perform opsonisation, where the target is coated with molecule with a high affinity for the phagocyte.
Briefly describe the reticuloendothelial system
Derived of different macrophage-like cells from the stem cells of bone marrow.
These are strategically placed where they will most likely encounter harmful agents.
How does the lymphatic system work?
Fluid drains into the thin-walled vessels perforating the interstitial fluid, and is pumped up the branches by the movement of muscles, held where it is pumped by leaf valves.
Afferent vessels take fluid from tissues to lymph nodes
Efferent vessels take fluid from the nodes to the thoracic duct, where it is emptied into the bloodstream
What is the function of the lymph system?
Prevent oedema
Recycle components of ECM
Carry information about infection from the tissues to the lymph nodes
What are primary vs. secondary lymphoid organs?
Primary: Lymphocyte formation site. Includes bone marrow, thymus, fetal liver
Secondary: Residence of mature lymphocytes. Includes lymph nodes, tonsils, adenoids, peyer’s patches, skin.
What are the 3 categories of innate immunity?
Physical- mucus, skin
Microgial- organisms living on/in us that make it hard for invaders to proliferate
Humoral factors: Chemicals (eg. in sweat)
Microbe
Microscopic entity
Pathogen
Thing capable of generating a disease
Endemic
Thing found in a place or population
Epidemic
More cases of a thing than you would expect to see
Pandemic
Epidemic spread across a wide area
Infection
New presence of a microbe
Infectious disease
Symptomatic illness caused by pathogens
Endogenous
Originating within an organism
Exogenous
Present but originated outside an organism
Subclinical
Infectious disease triggering the immune system, but not causing symptoms
Transmission
Manner of spread of a microbe (can be direct or indirect)
Autopoiesis
Dynamic process of self-production (ie making your own new cells)
Adaptation
Maintenance of a mutually satisfactory relationship between organism and environment
Why is it important that organisms are able to distinguish self from non-self?
- To protect against infection
- To recover from infection and damage
- To maintain the relationship with the environment
What shapes does the lymphatic system respond to?
Unusual shapes
Familiar shapes in unusual contexts
What secondary organs do different infected tissue types bring infectious particles to?
Blood takes them to spleen
Tissues to lymph nodes
Gut to peyer’s patches
What is innate immunity?
The first line of defense to antigen exposure
Includes physical microbial and chemical factors
They are effective at preventing invasion or growth of invasion, and act early.
Includes lysozyme in secretions from the skin, like tears, sweat and saliva. These break down the cell membranes of some bacteria
Also commensal organisms which compete with pathogens for survival
How are white blood cells formed?
Pluripotent haemopoietic stem cells found in bone marrow
- Some mature directly into B lymphocytes
- Some migrate to the thymus to become T lymphocytes
- Some develop into megakaryocytes and are broken into platelets
- Some develop into monocytes and are then converted to macrophages in the tissues
- Some develop into basophils, eosinophils, neutrophils or erythrocytes
What can happen if the maturation of WBCs is prevented?
Susceptibility to infection
Low blood counts
Inability to clot blood, leading to petechial haemorrhages
Large numbers of immature WBCs in the blood due to their overcrowding the RBM
What are the two types of receptors able to recognize antigens of infectious agents?
Antibodies- secreted by B-lymphocytes, recognize foreign antigens
Cell surface receptors- Attached to lympocyte surface, recognize changes in our own cells that appear on the cell surface.
What are the two types of receptors that can bind to angigens?
- Antibodies (soluble, secreted by B cells) Prevent binding of virus to other cells
- Cell surface receptors- attached to surfaces of cells, act as hands. See changes in our own cells
What is cross-reactivity?
Some antibodies may bind to many things with a similar shape- perhaps with low affinity, but enough to bind. This means a single antibody can help to defend against many pathogens
What are the 6 qualities of the specific immune system?
Defence
Specificity- response directed against only the agent stimulating disease
Diversity- responds to a wide range of substances
Adaptivity- unexpected stimuli response provides rapid appropriate response
Self/nonself- discrimination between own and foreign antigens
Memory- system remembers responding to respond more vigorously next time
How does the immune system know self from not-self?
Early in development, the immune cells become ‘used’ to whatever antigens are preexisting within the body- called acquired immunological tolerance
How are foreign antigens delivered to the immune system?
Meet dendritic cells, which collect antigenic information. These then migrate into the lymphatic system, entering the nearest lymph node while presenting the antigen on their surface
T Cells cluster around them when they arrive, and those with an appropriate receptor are activated
When it comes to lymphocytes, what are effectors vs. regulators?
Effectors: - B Cells (produce antibodies) - Cytototoxic T cells (actively kill cells) - NK and K cells (kill cells) Regulators: - CD4 T cells - Helper T cells - Regulatory T cells
What can be recognized by B vs T cells?
B cells recognize a wide range, T cells only recognize short antigens
What is the general structure of T vs B cells?
B cell: CD79 transduction molecules, Surface Ig receptor with binding sites
T Cell: CD3 signal molecules, TCR
What is the structure of an antibody?
Made of 2 light chains and 2 heavy chains.
Heavy chains have CH1,2,3 parts and a Variable part at the end Between CH1 and 2 there is a hinge region, which allows the antibody to flex between a T and a Y shape
Light chains have a hypervariable area and a constant area.
The CH2 and 3 areas are able to be crystallized, and can be sensed by neutrophils, improving their phagocytosis
The chains are held together by disulphide bonds
What is the difference between primary and secondary antibody responses?
Primary responses occur when we respond to something we had not previously encountered. There is a lag of a few days, and then a small rise in specific antbodies, before decaying to low levels.
A secondary response occurs subsequent times we are exposed to things, and consists of a vigorous and lengthy reaction to the pathogen
How do B cells react when activated?
An antigen matches with a specific receptor of a virgin B cell, causing it do express new receptors which match with signals sent from helper T cells. It does this to determine if the related pathogen is dangerous or not. If dangerous, the B cells proliferate, forming plasma cells which form antibodies, and replacement B cells called memory cells. These are longer lived, there are more of them, they circulate to all nodes rather than staying in one, and react without the help of T helper cells.
What happens to B cells in leukemia?
B cells’ development isn’t controlled and they spill over into the blood, as well as their precursors. These precursors smudge due to their fragility when put under the microscope slide, leading to their being named smudge cells
What are the 4 ways in which antibodies operate?
- Direct neutralization: Antibodies block the virus from being able to bind to and infect other cells
- Opsonisation: The antibodies bind to the virus, exposing their Fc region, which neutrophils have high adherence for. This increases the efficiency of phagocytosis
- ADCC: K cells rely on Fc areas to bind to and kill bacteria using short-range cytotoxicity
- Complement activation: Forming an antibody-antigen complex activates the first components of the complement zone.
How do antibodies change their shape?
They bind to the antigen, changing to a Y shape.
What are the pathways of the complement system?
Activated by: Antigen-antibody complexes
First components recognize the surface of the pathogen
Presence of bacterial sugars bind to proteins
Enzymes formed convert C3 to C3a and C3b
Effects:
C3a causes vasodilation and chemotaxis
C3b causes vasodilation
C3b also forms a focus for late component assembly, which punch holes into the membranes of pathogens to cause cell lysis.
Colonisation
Infection with microbe for varying period. Host immune response, but no symptoms. Potentially infectious
Infectious disease
Interaction with microbe causing damage to the host
Zoonosis
Infectious disease transmitted by a non-human animal host
What factors increase susceptibility to infection?
Immune deficiency (age related, treatment related etc.), other illnesses, risk behaviours
What are endogenous vs. exogenous infections?
Endogenous are those arising from our own bacteria, microbes and other flora
Exogenous are infections coming from animals, the environment (uncommon) and human to human transmission
What are some common settings for infection to occur in?
Community onset/acquired (most common, GP visit)
Hospital onset/acquired/nosocomial (reduced by handwashing)
What are the 2 requirements of a pathogen for it to cause damage, and what are virulence factors?
It must interact with the host cells
It must damage or incite an immune response within the host
Virulence factors include the avoidance of the immune system, improved adherence, damage and invasion
What is pyogenic invasion?
Tissue invasion, involving multiplication and causing an acute immune response
What is intoxication, immune mediation and carcinogenism, in terms of infection?
pathogens may use toxins to change the host physiology or to physically damage tissue
They may mimic the antigens on other cells
They may also cause the formation of cancerous cells
What is antibody mediated/humoral immunity?
Uses B lymphocytes to produce antibodies
Effective against extracellular antigens including:
Viruses & toxins (stop attachment)
Extracellular bacteria (enhance phagocytosis)
What is cell-mediated immunity?
Uses T lymphocytes, but no antibodies Effective against intracellular antigens, including: Virus-infected cells tumour cells Transplanted organs
Compare and contrast the different T cells
Both:
- Contain CD3
- Have T cell receptors (TCRs)
- Originate in the thymus
- Can bind only to antigens presented to them by MHC determinants on APCs
T-Helpers
- Contain CD4
- Produce cytokines
Cytotoxic T Cells
- Contain CD8
- Kill cells outright
What are differences between T and B cells?
T cells made in thymus, B in bone marrow
T cells do not make antibodies
T cells can only react to antigens presented to them by APCs
What are MHCs?
Genes coding for surface structures on cells to present antigens to T lymphocytes
Class 1: Produces double chained structures, found on all nucleated cells. Expressed co-dominantly, polymorphic (HLA-DP/DQ/DR all code for them) and present only to cytotoxic T cells
Class II: Code for structures found only on APCs and B cells. Expressed co-dominantly, polymorphic (HLA-A/B/C all code for them) and present only to helper T cells
How do antigens become presented on cells?
Way 1: Virus infects cell and replicates, changing the physiology of the cell and the composition of its proteins. A sample of these proteins are expressed on the MHC structures, so the immune system notices any changes Way 2: If the pathogen is phagocytosed, it is broken into small fragments, some of which are presented on MHC class II.
What is the process for the activation of cytotoxic T cells?
Precursors with TCRs matching the antigens on class 1 MHC structures are activated and receive helper signals to divide them into effector cells and memory cells
What is the process for the activation of helper T cells?
Antigen binding to TCRs on T lymphocytes cause the cell to express cytokine receptors. A second activation signal from helper cells cause differentiation into cytokine secreting cells or memory cells.
What are cytokines and what do they do?
Cytokines are low weight glycoproteins secreted mainly by CD4 T cells
They are produced locally and transiently, and are responsible for regulating the quality, amplitude, duration of immune reactions
Their action differs depending on concentration, other cytokines, target cell and history of cell
They also affect other systems- eg. control sickness behaviour through nervous system
What are some problems with the immune system?
Overreaction to innocuous substances- generate strong IGe antibody responses to harmless things (eg. pollen, fur etc.) This causes hypersensitivity where the substance touches you, or in bad cases, systemic reactions (anyphrylactic) can occur.
Immune mediated tissue damage- strength of immune/inflammatory response is so great it can damage other tissues. Eg. immune complexes produced in such high numbers that they lodge in capillaries, activating complement system and starting vasculitis
The system can also be destroyed from within, eg. when T helper cells are infected with HIV and cytotoxic T cells kill the majority of them
Autoimmunity- results in chronic illnesses as the body treats self-cells like non-self cells
Immune system can get confused- eg. strep. Some people have heart antigens similar to strep antigens, so immune responses to this damage heart valves too
What are 3 examples of autoimmunity?
Hashimoto’s thyroiditis: Antibodies/Cytotoxic T cells against thyroid antigens, destroying thyroid gland
Pernicious Anaemia: Immune system targets parietal stomach cells, impacting B12 absorption
Systemic Lupus Erythematosus: Antibodies made against DNA from cell nuclei, binding to broken cells throughout the body, activating the complement and damaging tissues throughout the body (particularly kidneys and skin due to immune complexes clogging)
What is streptococcus pyogenes and what does it do/can it do?
It is a virus that lives in the pharynx, commonly causing pharyngitis and skin infection. Firstly, the immune system is activated as S. Pyogenes colonizes the pharynx and irritates the tissue. Then, the pharynx becomes inflamed, causing pain, swelling, redness and pus. They contain M proteins which the body forms antibodies against, although the M proteins are similar in shape to the cells in other locations. If the antibodies bind to our own proteins, they will form a response against them in places not colonized by the bacteria. This can then cause rheumatic fever, with fever, painful joints, inflammed connective tissue of the heart, rash and chorea (strange movement)
How does penicillin work and what is the problem with it?
It works by targeting the enzyme responsible for linking the peptide chains within the bacteria’s cell wall.
If this enzyme is inhibited, cracks in the cell wall can’t be repaired and the bacteria explodes.
There are different types of penicillin, some administered intravenously and some orally depending on whether they get dissolved in the stomach or not
However, the issue is that penicillin (and other antibiotics) are being used for viruses etc. which they have no effect on, which results in bacteria gaining resistance to the drugs
What are the different types of disease transmission and some precautions against them?
- Direct (sexual, faecal-oral, droplet, airborne)
- Indirect (contact, vector borne, healthcare worker, transfusion, airborne)
Universal protections (always done): Glove/gown, decontamination of waste, disposal or sharps, waste management, clean environment, hand hygiene Contact precautions (GI infections): Gloves, gowns, eyeware Droplet precautions (flu etc.) masks Airborne precautions (TB, chickenpox): Respiratory masks for patients and staff
What is a virus?
Viruses are nucleic acid that aims to replicate, enclosed within a caspid. Some have an envelope formed from the host cell
How can we classify viruses?
Can be classed by their genetic content- RNA, DNA etec.
OR what they cause- hepatitis vs. resp. (this down’t predict structure
OR how they are transmitted- arbovirus (arthopod borne), enterovirus (faecal-oral) or respiratory virus (droplet/contact)
What are the steps of a viral infection?
- virus attaches to cell
- Virus enters the cell, host enzymes dissolve the capsid and release the RNA
- mRNA from the virus is formed, and 4. protein synthesis occurs
- Genome replicates to 6. form a new clone of the virus so that it can be 7. released from the cell
