GEP (Life Protection) Week 1 Flashcards
What are the 2 main components of the skull
Cranium and mandible
How many types of bones make up the cranium and how many of them are in total
6 types of bones: Occupital, Parietal, Temporal, Frontal, Sphenoid, Ethmoid.
There are 8 bones in total as there are 2 temporal and parietal bones.
What are the joint inbetween these carnial bones called
Sutures
What are fontanelle and how are they formed.
At birth, bones of cranium are incompletely fused.
Soft spots without bone are covered with membrane which ossifies with age.
There are two main fontanelle, the anterior and posterior
What is the timeline of the fontanelle closing
Posterior - usually ossified by 2-3 months
Anterior - usually ossified by 18 months
Identify these anatomical locations
What are mininges
These are 3 layers of membrane the line the skull and vertebral canal and enclose the brain and spinal cord.
What are the layers of the mninges
Dura Mater
-External
-Tougher and thicker
-Vascularised
Subdural Space
Arachnoid Mater
-Thin & delicate
Subarachnoid Space
-Houses CSF, major blood vessels
Pia Mater
-Internal
-Wraps around brain and spinal cord
-Thin & highly vascularised
Dura mater: Dura actually means thick or hard in latin
Subdural space of no note today but this is of note in subdural haemotomas
Arachnoid mater: named after it’s spider like appearance
Pia mater means “tender matter”. Almost like shrink wrap surrounding everything
What is CSF (cerebrospinal fluid)
Cerebrospinal fluid is a clear, colorless body fluid found within the tissue that surrounds the brain and spinal cord
It is an ultrafiltrate of blood plasma
3 main functions:
Protection
Buoyancy
Chemical Stability
Present in the subarachnoid space, ventricular system and spinal cord
How is CSF made
- Originates from filtered plasma
- Made by ependymal cells
- Plasma is pushed across epithelial membranes to create “ultrafiltrate”
- Enters circulation from the choroid plexus in the ventricles through ependymal cells
- At any time, ~125 ml of CSF will be circulating
- Daily turnover of 500 ml
- The choroid plexus are villi
Cuboidal cells will create a polarised electrical charge across the highly specialised membrane to allow ions to cross into the ventricles
The ionic flow then creates an osmotic gradient to allow water across
How is CSF spread around
They are spread mainly through the ventricles in the brain.
From Choroid Plexus to CNS
CSF will exit the 4th ventricle through either the foramen of Lushka (2x lateral apertures) or the foramen of Magendie (median aperture) into the cisterna magna
Cerebral aqueduct is also called aqueduct of sylvius
IV foramen is the foramen of monroe
From central canal, it will coat the spinal cord and brain in the subarachnoid space
How is CSF drained
- Arachnoid granulations in the skull
- These are outpouchings in the top of the skull where a pressure dependent draws it out into the Superior Sagittal Sinus, from there it will re-enter the bloodstream via venous drainage
What are the main changes you see when you go down the spine
- The dura mater around the head is composed of two layers: the periosteal/endosteal layer (superficial) and the meningeal (deep) layer. The dural venous sinuses are between these two layers
- Surrounding the spine, there is just one layer of dura
- CSF, dura & arachnoid mater surrounds the spinal cord up until the filum terminale
- Pia mater becomes filum terminale
Filum terminale both stabilises the spinal cord and connects it to the coccyx
Lumbar cistern is widening of subarachnoid space - accessed in a lumbar puncture
Contains cauda equina and filum terminale
How do you perform a lumbar puncture and what are the spinal ligament you have to go through
- Done to obtain CSF sample
- Taken in L3/4 in adults or L4/5 in children
- Important Precaution: ASSESS FOR Intracranial pressure PRE-PUNCTURE or the brain can be coned
Define these key terminologies:
-Antibody
-Antigen
-Cytokine
-Chemokines
-Cluster of differentiation
Antibody: proteins produced by adaptive immune cells that bind specifically to relatively small parts of foreign molecules known as antigenic determinants or epitopes
-Antigens
Antigen: “anything that can be bound by an antibody“
ANY Toxin, molecule or foreign substance (mainly short peptides or proteins but can be sugars of lipids) that indices an adaptive/acquired immune response
**Cytokine: **small proteins which are produced by cells to regulate the immune system. Often called interleukins.
Chemokines: Subtype of cytokine with chemoattractant properties
**Cluster of Differentiation: **CDs are molecules on cell surfaces which define a cell lineage e.g. CD3 on T-cells or specifically CD4+ and bind to antibodies
IL (interlukins) normally numbered in order of discovery but sometimes have names related to function e.g. TNF-alpha
What is the immune system
- Your immune system is a large network that protect you from germs and other invaders and helps you heal from infections and injuries
Functions include: - Self/non-self discrimination (what happens when this goes wrong?)
- Destroys faulty cells (e.g. cancer)
- Destroy & protect against pathogens (bacteria, parasites, viruses, fungi)
- Basically keep you good
Easy way to remember the role of immune system
Immunological Recognition
Immune Effector Function
Immune Regulation
Immunological Memory
OR
Recognise
Remove
Regulate
Remember
what is the Immune system mainly split into
- The immune system is split into the adaptive and the innate systems
- The innate is the first response
- Works within the first 96 hours
- The adaptive is what takes over as it is the more specialised response
What is the innate Immune system
Non-specific means it will do the same thing to all pathogens to try and destroy it
What is the adaptive immune system
- Slower but specific
- Has memory of previous pathogens
- Catches pathogens that evade the innate immune system
- The more the adaptive system is stimulated, the better the response
- Mainly uses B & T lymphocytes
- Recognises pathogens using T cell receptors
Not a question but a summary
Summary of the main differences in Innate and Adaptive immmune system
What are the organs of the immune system and difference between primary and secondary lymphoid organs
Primary Lymphoid organs - forming and maturation of lymphocytes
-Bone Marrow
-Thymus
Secondary Lymphoid organs - regulation of contents
- Spleen
- Lymph nodes
- MALT/GALT
Immune cells are spread between both
How do the innate and adaptive immune system come together
In infection:
One comes after the other to destroy pathogen
Helps to remember pathogens which reduces rate of re-infection
Pathogen recognition by cells of the innate immune system, with cytokine release, complement activation and phagocytosis of antigens
The innate immune system triggers an acute inflammatory response to contain the infection
Meanwhile, antigen presentation takes place with the activation of specific T helper cells
CD4 helper T cells then coordinate a targeted antigen-specific immune response involving two adaptive cell systems: humoral immunity from B cells and antibodies, and cell-mediated immunity from cytotoxic CD8 T cells
-You can’t live without both
What are main catogeries of white blood cells
Granulocytes:
Neutrophils 40-75% of all WBCs, 1st line, phagocytose, segmented nuclei & intracellular granules
Eosinophils: 1-6%, act on multicellular parasites, involved in IgE allergic disorders, bilobed nuclei, granules
Basophils: -1% mast cells, bilobed nuclei intracellular granules
Monocytes & macrophages
Monocyte: 2-10%, become macrophages, phagocytose APC and cytokine production, large cells with fine “ground glass” granules and horseshoe shaped nuclei
Tissue macrophages: same but in tissues, create the pagolysosome, many different specialised ones
DCs: main professional APC
Lymphocytes
B: 20,45% of all WBC, 25% of total lymphocyteEssential for humoral immunity, plasma cells and memory B cells
T: 70% of total, various subtypes, helper CD4, cytotoxic CD8, regulatory and memory
NK: 5%, larger, in both adaptive and innate, viral immunity and tumour rejection
How are white blood cells made from Stem cells
Explain further the timeline and the roles of White blood cells during the cellular component of inflammation
- Day 1 (0-24 hours): Neutrophils
-Arrive during hours 6-24, die after 24-48 hours
-Generate ROS and nitrogenous species, releasing it with granules
-Phagocytose
-NETosis - Day 2 (24-48 hours): Macrophages
-After arriving will survive and proliferate
-Start to regulate the immune response
-Begin tissue repair
-Phagocytosis
Phagocytosis helps with dead cell clearance and tissue repair
What are pro-inflammatory cytokines
Proinflammatory cytokines are produced predominantly by activated macrophages and are involved in the up-regulation of inflammatory reactions. There is abundant evidence that certain pro-inflammatory cytokines such as IL-1(β), IL-6, IL-12 and TNF-α are involved in the process of pathological pain
What is the process of Phagocytosis and NETosis in the process of destroying pathogens
- Phagocytosis
-Chemotaxis
-Recognition
-Ingestion
-Phagosome (early and late)
-Degradation (phagolysosome)
-Exocytosis - NETosis
-Neutrophil kills itself, releasing chromatin
-Chromatin is sticky, and binds to other neutrophils to for a net
-Chromatin has antimicrobial properties, so pathogens are caught and killed
What are the main outcomes of acute inflammation
What is Fever
- Fever (pyrexia) is an elevation of body temperature above the anterior hypothalamic set point.
- This set point is different for everyone, and changes throughout the day.
- Thermoreceptors detect central and peripheral changes in temperature and feed back to the anterior hypothalamus.
- When temperature is above or below the set point, the hypothalamus sends out signals that act on effector systems leading to both physiological and behavioural changes in order to restore homeostasis.
What is the pathogenesis of Pyrexia
- As mentioned, pyrexia is elevation of body temperature above set point.
WITHOUT CLEAR CAUSE - Clinically, pyrexia is a temperature >38°C
- If set point is raised, body will perceive self to be cold -> shivering, vasoconstriction, metabolic heat generated to increase body temperature.
- This is driven by the release of PGE2, therefore inhibition of PGE2 release can lower hypothalamic set point in cases of fever.
- Cytokines that drive pyrexia - IL-1, IL-6, IL-8, TNF-α, INF-γ
What is the process of checking for infection
- Start with an ABCDE assessment (airway, breathing, circulation, disability, exposure)
- Record and repeat:
-HR
-RR
-Temperature
-CRT (capillary refill time) - Assess for signs of dehydration.
- Assess for any red flag symptoms using the NHS Traffic Light Tool.
What is the NHS traffic light tool
Colour
Activity
Respiratory
Circulation and hydration
Other
What is the childhood vaccination schedule
2 main method
What are the classification of bacteria
Shape
Gram staining
What is the process of Gram Staining
There are 5 main ones
What are the antibiotics mechanism of action
Antibiotic spectrum
-mycin – gram positive
-micin (-cin without my) – gram negative
What is antibiotic stewardship
Antibiotic stewardship is key to minimising the risk of bacteria developing resistance.
There is both a personal (patient) and institutional (NHS) duty:
-Personal - take antibiotics as prescribed, for full course.
-Institutional - have policies in place (and follow them) that aim to reduce antibiotic resistance.
What is antibiotic resistance and how can it present
- Bacteria develop genetic mutations to improve survival. There are many strains of antibiotic-resistant bacteria, which is why identification of causative organism plus stewardship is so important.
- Mechanism of mutations:
1)Spontaneous
2)Transferred
-Conjugation from another bacterium
-Transduction via bacteriophage
-Transformation via uptake of nucleic acid
What are the clinical features of Meningitis
- Non-specific -> suspect infection:
-Fever
-Vomiting and nausea
-Lethargy
-Irritability
-Anorexia
-Headache
-Muscle and joint pain
-Respiratory difficulty
-ENT pain
-Diarrhoea - Specific -> suspect meningitis:
-Non-blanching rash
-Stiff neck
->2 seconds CRT
-Unusual skin colour
-Bulging fontanelle
-Photophobia
-Kernig’s sign
-Brudzinski’s sign
-Loss of consciousness
-Focal neurological deficit
What are the causative Bacteria
Note that streptococcus is common at all ages.
Fungi, Bacteria etc
What are the main difference between lumbar puncture results with the microorganisms that can cause it.
Name some other non bacterial causes of Meningitis
Normally at the start of admission
What other further investigation is crutial with Meningitis
- Most importantly: should be conducted within 1 hour of admission (but can be done up to 24 hours)
- Features of a bacterial diagnosis:
-Cloudy/turbid CSF
-Evidence of bacterial culture in microscopy (80% sensitivity reduced to 60-70% if antibiotics started)
-CSF leukocytosis
-High protein content
-Low glucose
What is the treatment of Meningitis
Make sure to notify public health
How would you treat emergency meningitis
- ABCDE
- If away from hospital give IM benzylpenicillin stat if patient septic or >1hr away from hospital
- Transfer to hospital immediately for antibiotic therapy
- Support patient through
-Shock, elevated ICP, seizures and coagulopathy complications
-Electrolyte imbalances (glycaemia, acidosis, biochemical)
This is a not a question
This is a summary of meningitis
