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MBChB 1 > Phase 1 > Flashcards

Phase 1 Flashcards

Biomedical Science

1
Q

Name 4 functions of skin

A
  1. Water Repellent
  2. Immunological Barrier
  3. Mechanical Barrier
  4. Sensation
  5. Synthesis of Vit D
  6. UV Protection
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2
Q

Describe the structure of skin

A

Three Layers; epidermis, dermis, subcutis.

Epidermis (Avascular)

  • Stratum (Keratinocytes)
  • Stratum Lucidum
  • Stratum Granulosum
  • Stratum Spinosum
  • Stratum (Merkel Cells)
  • Basement Membrane (Type IV Collagen)

Dermis
- Papillary Layer
Areolar tissue, connective tissue that contains dermal papilla from epidermis. Meissners Corpuscles - Light Touch.

  • Reticular Layer
    Dense and irregular, contains most accessory structures. Pacinan Corpuscles for deep pressure and vibration.

Subcutis
- Adipocyte rich. Padding. Vascularised.

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3
Q

Describe the main difference between thick and thin skin.

A

Stratum Lucidum exists on palms and soles of the feet. Thin layers do not contain these layers.

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4
Q

Name the cell types found in the epidermis and state their function.

A
  1. Keratinocytes - 95% of cells in the epidermis. Produces keratin.
  2. Melanocytes - produce melanin for UV protection. Transfer via projectins.
  3. Langerhans Cells - DCs, APC.
  4. Merkel Cells - Mechanoreceptors
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5
Q

Name the layers of the epidermis.

A

Epidermis (Strata Corneum, Lucidum, Granulosum,

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6
Q

Describe the role of skin the synthesis of Vit D

A

UVB photons are absorbed to convert 7-dehydrocholesterol to previtamin D3.

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7
Q

Describe the cell junction between the epidermis and the dermis and a pathology associated with it.

A

Epidermis and the dermis is joined at the dermo-epidermo junction by the interactions of Retes Ridges in the papillary layer. Hemi-desmosomes bind intermediate filaments and Focal Adhesions bind Actin Filaments.

Pathology is Epidermolysis Bullosa simplex.

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8
Q

Name the layers of the dermis

A

Papillary (superficial) and reticular (deep)

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9
Q

State 3 types of glands found in the dermis and name their function.

A
  1. Eccrine Glands - produce sweat
  2. Apocrine Glands - Scent
  3. Sebaceous Glands - lubricant of the hair shaft
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10
Q

Describe the accessory structures found in the dermis.

A
  1. Eccrine Glands - produce sweat
  2. Apocrine Glands - Scent
  3. Sebaceous Glands - lubricant of the hair shaft
  4. Meissners Corpuscles - Light Touch
  5. Pacinian Corpuscles - Deep Pressure
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11
Q

State the functions of the subcutaneous layer

A
  1. Fat storage, energy reserve

2. Padding

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12
Q

Name the type of collagen found in the skins and basement membrane

A

Skin - Type I

Basement Membrane - Type IV

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13
Q

Label the diagram (layers of the skin)

A

Epidermis
- Strata Corneum, Lucidum, Granulosum, Spinosum, Basale, Basement Membrane

Dermis

  • Papillary
  • Reticular

Subcutis

Adnexal structures

  • Eccrine, Appocrine, Sebaceous glands
  • Meissner and Pacinian Corpuscles
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14
Q

Describe superficial and deep wound healing

A

Superficial wound healing -

A scrape or graze, no involvement of the basement membrane. Mitotically active keratinocytes in the Basale lose BM adhesions. Migrate in leap frog or train method to form granulation tissue. Epidermal Growth Factor is released.
Basale Layer keratinocytes undergo terminal differentiation to restore lost cells.

Deep

Inflammatory phase
1. Coagulation/ haemostasis
2. Platelets secrete growth factors. WBCs are recruited. Inflammation takes place to allow vasopermeability to increase.
3. Neutrophils and Macrophages phagocytose waste. More growth factors.
(VEG-F, EGF, APF, PDGF, FGF)

Proliferative phase

  1. Basement membrane is reformed and keratinocytes migrate over wound to form granulation tissue (leap frog or train).
  2. Once formed, divide and differentiate. Granulation tissue laid down, mainly Type 3 Collagen.
  3. Neo-vascularisation

Remodelling phase

  1. Granulation tissue tissue matures to scar tissue.
  2. Type 3 collagen is crossed linked, swapped for type 1. More tensile strength.
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15
Q

Name three growth factors secreted by phagocytosis

A
  1. Vascular Endothelial Growth Factor (VEG-F)
  2. Angiogenesis Promoting Factor (APF)
  3. Platelet Derived Growth Factor (PDGF)
  4. Fibroblast Growth Factor (FGF)
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16
Q

Name the two methods by which re-epithelialisation takes place and give a brief description of each.

A
  1. Train method - a lead cell pulls following keratinocytes

2. Leap from - cells leap over one another over the wound base. Much like leap frogging or pepper potting.

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17
Q

Name the cell that produces collagen.

A

Fibroblasts

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18
Q

Give the effects of UV radiation

A
  1. Photoageing
  2. DNA Damage
  3. Carcinogenesis
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19
Q

Name the organelles and state their function

A
  1. Plasma Membrane
    - Barrier to the outside environment, hosts receptors for signalling, mediates diffusion, holds other membrane receptors and channels.
  2. Mitochondrion
    - The power house of the cell (Aerobic Respiration) producing ATP.
  3. Nucleus
    - Contains the genome and is the site of transcription.
  4. Rough Endoplasmic Reticulum.
    - Hosts ribosomes for mRNA translation.
  5. Smooth Endoplasmic Reticulum
    - Calcium Store and lipid synthesis.
  6. Golgi Apparatus
    - “Sorting office” - responsible for post-translational modifications to proteins and packaging.
  7. Lysosomes, Peroxisomes and Proteasomes.

Enzymatic degradation of lipids (L), oxidative reactions/ biosynthesis of bile/ fatty acid metabolism and detox (Perox), protein degradation (Proteasome).

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20
Q 
What pathologies are associated with: 
A. Mitochondrial Damage
B. Defective Lysosomes
C. Microtubule Defects
D. Failure of Cell-ECM junctions
E. Connexin 26 Mutation
A

A. Damage causes the release of cytochrome C, which activate caspases, resulting in a proteolytic cascade activating DNAases, Lamin degradation and cell apoptosis. - Diabetes and Deafness (DaD).
B. Lipid build up. Neural damage. - Tay Sachs Disease.
C. Defects in dyneins in Axonemes. Leads to defunct cilia and flagellum. - Kartageners Syndrome.
D. Loss of Hemidesmosome - Intermediate Filament interaction. - Epidermolysis Bullosa Simplex.
E. Defunct connexins, leads to hearing loss.

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21
Q

Describe the Cell-Cell and Cell-ECM junctions and the cytoskeleton involved.

A

Cell-Cell

  1. Desmosomes - Intermediate Filaments
  2. Adherens - Actin Filaments
  3. Tight Junctions - Actin Filaments
  4. Gap Junctions - Connexin Channels

Cell-ECM

  1. Hemi-Desmosomes - Intermediate Filaments
  2. Focal Adhesions - Actin Filaments
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22
Q

Describe the cytoskeleton

A

A network of proteins, three types.

Microtubules, made of tubulin. Allow for push (kinesins) and pull (dyneins), these Microtubules grow and shrink from centrosomes. Allow for chromosome separation in Mitosis or movement in axonemes (cilia and flagellum).

Microfilaments made up of Actin and Myosin. Dynamic processes, such as cell shape and motility.

Intermediate filaments made up of vimentin and keratin. Provide tensile, rope like strength.

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23
Q

Describe the default secretory pathway.

A

Transcription (Nucleus), Translation (Ribosome).

Signal Recognition Particle on mRNA attaches SRP-Receptor, anchoring it and ribosome to RER. Protein is translated into the ER lumen. Signal pepsidase cleaves the protein. Transportation to the Golgi Apparatus, via the Cis-Cisterna model, is sent to the plasma membrane in vesicles. Where it is modified at the C-Terminus, it is anchored to the plasma membrane.

Proteins for the lysosome are modified with mannose-6-phosphate.

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24
Q

Describe the default cytosolic pathway.

A

Without SRP, the protein is translated into the cytosol.

Here, if destined for the Nucleus, the protein is modified with a Nucleus Translocation Signal (NLS)- moves via importing through the nuclear pore.

Mitochondrion proteins are modified with Mitochondrion Translocation Signal.

Peroxisomal proteins are modified at the C-Terminus with a three amino acid chain.

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25
Q

Describe Lysosomal degradation

A

Cytosolic proteins are taken to the vesicle by autophagy (from the ER - mannose-6-phosphate cleaved at low pH), while extracellular components are taken in by endocytosis (surface proteins) or receptor-mediated endocytosis.

An acidid pH, proteases, lipases and DNAases finish the task.

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26
Q

Describe proteosomal degradation.

A

Proteins for destruction are ubiquitilated. Useful for short-half life proteins, defective proteins and those key in metabolism.

Proteins are then cleaved by proteases and pepsidases.

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27
Q

Define: a. genome b. proteome c. transcriptome

A

a. All genetic material of an organism
b. All proteins translated from the transcriptome
c. All mRNA transcribed from Genome

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28
Q

Why is the proteome larger than the genome?

A
  1. Alternative mRNA splicing
  2. Post translational modification

(Gene splicing and epigenetics?)

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29
Q

Describe translation

A

DNA is transcribed to mRNA in the nucleus. The mRNA attaches to a tRNA via start codon AUG. tRNA anti-codon binds and pre-initiation complex binds small sub unit of the ribosome.

Translation is initiation, working from the 5’ to 3’, cessation at stop codon (varies).

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30
Q

Describe three post-translational modifications

A
  1. Methylation - addition of a methyl group. Example is Histone methylation in gene expression.
  2. Ubiquitination - addition of ubiquitin to a protein. Example is in proteosomal degradation
  3. Phosphorylation - addition of a phosphate. Example is phosphorylation of myosin in muscle contraction.
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31
Q

Outline the functions of blood

A
  1. Transport of gases (o2 and co2), plasma proteins, hormones and of waste such as urea and uric acid.
  2. Homeostasis - buffer of pH, restriction of flui loss.
  3. Immunity by WBCs.
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32
Q

Describe the composition of blood

A
  1. Plasma 55%
    - Plasma Proteins 7% (Albumin, Globulins, Fibrinogens)
    - Solutes 1% (Ions, organic waste such as urea)
    - Organic nutrients like lipids, amino acids.
    - Water 92%
  2. Haematocrit 45%
    - Erythrocytes 99.9%
    - Leukocytes 0.5%
    - Platelets 0.5%
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33
Q

Name the different plasma proteins and their function

A
  1. Albumins
    - Osmotic Pressure
    - Transport protein (such as lipids and billirubin)
  2. Globulins
    - Transport of ions, lipids, hormones
    - Immunoglobulins in immunity
  3. Fibrinogen
    - Coagulation, Haemostasis

Others, such as hormones (insulin), zymogens, coagulation factors.

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34
Q

Name the cell types found in blood and state their function.

A
  1. Erythrocytes
    - Carriage of o2 and co2.
  2. Leukocytes
    - Innate and Adaptive Immunity
  3. Platelets
    - Not technically cells. Coagulation, haemostasis.
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35
Q

Describe a RBC

A
  1. Also called erythrocytes
  2. Biconcave in shape, allows flexibility
  3. Anucleated with no organelles, allowing extra capacity for haemoglobin
  4. Life span of 120 days
  5. Contains molecules of haemoglobin, accounts for red colour
  6. Low energy demand
  7. Carriage of o2 and co2 (Binds haemoglobin)
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36
Q

Describe the platelet

A
  1. Not a cell
  2. Cell fragments (Megakaryocyte)
  3. Small
  4. Principle role in coagulation/ haemostasis
  5. Short life span 9-12 days
  6. Anucleated, no organelles
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37
Q

Describe the different WBCs and state whether their origin is lymphoid or myeloid.

A
  1. Neutrophil - Myeloid
    - Most common at 65%
    - Multi-lobed nucleus
    - granule rich
    - Innate
  2. Lymphocytes - Lymphoid
    - 2nd most common at 30%
    - Large nucleus occupies most of the cytoplasm
    - Differentiates into, T, B and NK types for adaptive immunity.
  3. Monocyte - Myeloid
    - Differentiates to Macrophage
    - Kidney shaped nucleus (bilobe)
    - 3rd most common - 8%
  4. Eosinophils - Myeloid
    - Red in colour, acidophillic.
    - Bilobed nucleus
    - Granule rich, cytotoxic.
    - Fight parasites - Innate
    - 4th most common, 4.5%
  5. Basophils
    - Blue, basic.
    - Highly granulated
    - Role in allergy
    - less that 1%
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38
Q

List the WBCs in order of abundance

A
  1. Neutrophil
  2. Lymphocyte
  3. Monocyte
  4. Eosinophil
  5. Basophil
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39
Q

Describe the triage system and the role of the triage nurse

A

Triage, french for “sieve”, is a system used to prioritise patients for treatment based on medical urgency. It is commonly used in pre-hospital, A&E and military settings. It is dynamic and changes with assessment.

Multiple systems exist. In the UK, A&E’s commonly use the Manchester System defining categories as:

  1. Immediate (, MI)
  2. Very Urgent, 10 mins (Chest pain)
  3. Urgent, 1 hour (poison)
  4. Standard, 2 hours (minor injury)
  5. Non-urgent, 4 hours (non-acute)

The triage nurse will monitor patients, carry out obs, bloods, ECGs and aid the the triage picture. Dependant on Trust.

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40
Q

Define shock and list five types.

A

Shock is the loss of circulating blood, causing inadequate perfusion of body tissue impairing metabolic function.

  1. Hypovolemic
    - A bleed
    - Loss of sodium causing dehydration
  2. Cardiogenic
    - Acute M.I reduced cardiac output
  3. Septic
    - Systemic inflammation causing vessels to become “leaky”. Fluid migrates to tissues.
  4. Anaphylactic
    - Allergy, inappropriate inflammation causing leakage.
  5. Spinal
    - Injury causing loss of sympathetic innervation and decrease in vasomotor tone leading to hypotension (C.O cannot match compliance).
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41
Q

Define differentiation

A

The process by which a cell matures and specialises through regulated gene expression.

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42
Q

Define the terms:

  1. Totipotent
  2. Pluripotent
  3. Multipotent
  4. Unipotent
A

Totipotent - can differentiate into all cell types. Zygote.

Pluripotent - can differentiate into most cell types - blastocyst.

Multipotent - progenitor cell able to differentiate into many cell types.

Unipotent - able to mature into one cell type, such as erythroblasts.

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43
Q

Describe haematopoeisis and discuss it’s regulation.

A
  1. Is the production of blood cells from Haematopoeitic Stem Cells (HSCs) in the bone marrow.
  2. HSCs can differentiate into Myeloid and Lymphoid stem cells.
  3. Lymphoid Stem Cells are directed by normal control originating in the Thymus. Pre-T-Cells migrate to the Thymus to undergo selection, while Pre-B/ NK cells remain in the Bone Marrow these are acted upon by IL-7.
  4. Common Myeloid Progenitor cells give rise to erythroblasts (stimulated by EPO), megakaryocytes (TPO) and select leukocytes (IL-3, IL-6m GM-CSF). GM-CSF plays a large role in all cell types of Myeloid lineage.
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44
Q

Outline the possible fates of a stem cell.

A
  1. Self Renewal
  2. Quiescence
  3. Apoptosis
  4. Differentiation
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45
Q

Compare adult and embryonic stems cells.

A

(You’ll have to touch on ethics here, too)

Adult Stem Cells

  • Less ethical issues
  • Difficult to culture
  • Less potent
  • Useful for transplants
  • Multipotent at best

Embryonic

  • Highly emotive topic, ethical maze
  • Easy to culture
  • High potency
  • Risk of rejection
  • Pluripotent
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46
Q

Describe the process of haemostasis and coagulation

A
  1. The arrest of blood loss.
  2. Vascular phase
    - local vasospasm reduces blood flow.
    - Basement membrane collagen is exposed.
    - Damaged endothelial cells release Endothelins (promotes growth and repair and vasoconstriction).
    - Tissue Factor to initiate Extrinsic Coagulation.
    - NO balance is upset with tissue damage, prostacyclin released.
  • Endothelial cells become “sticky”
  1. Platelet phase
    - Platelets stick to exposed collagen and endothelial cells.
    - Platelets release granules on binding. vWF facilitates early binding and aggregation. Released in granules are: ADP, TxA2 and serotonin.
    - Bound platelets express Glycoproteins II/IIb
    - Prostacyclins keep this +be feedback loop in check.
    - This primary haemostasis plug is formed.
  2. Coagulation
    - Initiated at the extrinsic pathway (tissue factor - PT time assesses this).
    - Tissue Factor III(3) activates VII (7) to VIIa (7a).
    - These combine to form TF-VIIa (3-7a).
    - This in turn activates X to Xa (10 - 10a)
  • Concomitant with the intrinsic pathway (contact activation).
  • XII (12) is activated to XIIa (12a).
  • XI (11)is activated to (11a)
  • IX (9) is activated to IXa (9a)
  • X is activated to Xa (10 - 10a)

Xa marks the convergence to the Common Coagulation Pathway. Xa is activated in the presence of Ca and Pl.

  • Prothrombin II (2) is activated to Thrombin IIa (2a) by Va and Xa.
  • IIa activates V (5) to Va (5a) and Fibrinogen I (1) to Fibrin Ia (1a).

XIIIa (Fibrin stabilising) helps cross link Ia. The stable Fibrin Clot is formed.

  1. Clot lysis
  • by Plasmin
  • TF is inhibited by TFPI
  • Protein C inhibits lots of Fs.
  • Antithrombin. Think.
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47
Q

Describe the basic structure of bacteria and their function.

A
  1. Cell Wall - A polysaccharide layer, protective.
  2. Plasma Membrane - phospholipids. Boundary of the cytosol.
  3. Plasmids - Short fragments of DNA that can be exchanged. With other CFUs.
  4. Mesosomes - Folded invagination of the cell wall, increasing surface area.
  5. Chromosomes - Genetic material, as with eukaryotic cells.
  6. Ribosomes - for protein translation
  7. Flagellum - for motility
  8. Pili - Hairlike appendages. Allow for adherence, can also be used in conjugation (sex pili).
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48
Q

State the different shapes of bacteria

A
  1. Cocci
    - Single (Coccus), double (diplococci) or bunched (cocci)
  2. Bacilli
    - Rod like
  3. Coccobacilli
    - Round rod, like a rugby ball.
  4. Spirochetes
    - Spiral in structure.
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49
Q

Define the terms Gram Positive and Gram Negative in microbiology.

A

Gram Positive (Gram +ve). - Stains well in “Gram Stain”. Due to a thick peptidoglycan wall.

Gram Negative (Gram -ve)
Stains poorly due to a thinner peptidoglycan wall. Usually has outer layer/ capsule holding LPS and endotoxins. Bad times.
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50
Q

Describe two key differences between gram +ve / -ve

A

+ve stains rich in Gram Stain, think peptidoglycan wall.

-ve stains poorly, thin peptidoglycan wall and hosts outer layer rich in LPS and Endotoxins.

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51
Q

Name two of each:

  1. Gram -ve Bacilli
  2. Gram -ve Cocci
  3. Gram +ve Bacilli
  4. Gram +ve Cocci
A
  1. E.coli and S.enterrica
  2. N.meningitidis and H.Influenzae
  3. C.Dificile and L.monocytogenes
  4. Staph.aureus and Strep.aureus
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52
Q

Define:

  1. Endotoxin

2. Exotoxin

A
  1. Endotoxins: a bad time. Structures found on the outer layer of gram -ve bacteria. Can be shed. Common example is LPS.
  2. Secreted (not shed) by bacteria, disrupting cellular metabolism
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53
Q

Describe basic viral structure.

A
  1. Genetic material that comes in a variety of flavours.
    - Double or Single stranded DNA (dsDNA/ssDNA)
    - Double or Single stranded RNA (dsRNA/ssRNA)
  2. Capsid. Viral protein coat made up of capsomeres.
  3. Some contain basic enzymes, such as reverse transcriptase.
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54
Q

Describe the shapes of nucleocapsids

A

Viral.

Icosahedral. 20 triangular shapes organised to form a coat.

Helical. Rod shaped and filamentous.

Prolate. Sophisticated is shape. A cylinder flanked by two caps. Bacteriophages.

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55
Q

Describe the process of viral replication

A
  1. Absorption. The virus binds to a specific receptor. Such as HIV binding CD4 CCR5.
  2. Penetration. The viral coat fuses with the cell or is endocytosed.
  3. Uncoating. The viral capsid is lost, free nucleic acid is in host cytosol.
  4. The coup etat. Host cell metabolism halts. Viral nucleic acid is transcribed and translated using host cell organelles.
  5. Synthesis. Viral genome is replicated.
  6. Assembly. Viral products are assembled, capsomeres self-assemble around viral genome to form new virions.
  7. Release. Virions either bud from the host cell, or cause cell lysis.
  8. The virus spreads.
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56
Q

State the primary and secondary lymphoid glands.

A

a. Primary. Where lymphocytes are produced and mature; Bone marrow and Thymus.
b. Secondary. Where lymphocytes migrate to undergo clonal expansion. Lymph nodes.

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57
Q

Describe how lymph is formed.

A

Blood arrives to the capillary bed at high hydrostatic pressure.

Fluid, minus haematocrit is force through capillary gaps. As blood moves along the capillary, fluid returns due to osmotic pressure. Remaining fluid in the tissues is the lymph. It is returned to circulation via the right and left venous angle.

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58
Q

State 4 functions of Lymph

A
  1. Transport of lipids, fat and chyle
  2. Removal of excess fluid, preventing oedema
  3. Transport of APCs and Antigens to initiate the adaptive immune response
  4. Maintenance and distribution of lymphocytes.
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59
Q

Describe lymphopoeisis

A

Haematopoeitic Stem Cell, which is multipotent differentiates into either Myeloid or Lymphoid Stem Cells. Lymphoid Cells remain in the bone marrow, or migrate to the Thymus. Thymus cells undergo selection, and can be induced by APCs, while B and NK cells are influence into growth by IL-7.

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60
Q

Describe Lymph flow through a lymph node.

A
  1. Afferent lymphatic
  2. Subscapular space and cortical sinus
  3. Through the deep cortex and germinal centres.
  4. Through the paracortical area
  5. Through medullary cords in the medulla and out via the efferent lymphatic.
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61
Q

List (label) the parts of the lymph node, and the cell type prominent in each zone.

A
  1. Afferent Lymphatics
  2. Germinal Centres - B CELLS (proliferate and mature)
  3. Cortex - B CELLS
  4. Paracortical area - T Cells
  5. Medulla - Macrophages and Plasma Cells.
  6. Afferent Lymphatics
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62
Q

Describe Innate Immunity

A
  1. Physical Barriers
    - The skin, and other epithelial linings.
    - Secretions can support these barriers, such as sweat on the skin or secretion of mucus in the airways. A variable pH in the alimentary tract also acts to eliminate microbes.
    - Immunoglobulins in secretions (IgA in saliva)
  2. Associated Lymphoid Tissues
    - around epithelial linings, such as the Peyers patches (GALT). Rich in immunoglobulins.
  3. Innate line leukocytes
  • Monocytes, Neutrophils, Dendritic Cells (phagocytic)
    • These act as APCs, presenting to T Helper Cells.
  • Recognise Pathogen Associated Molecular Patterns (PAMPs) and Damage AMPs via Toll Like Receptors (TLRs). Eg. TLR-4 Recognises -ve LPS.
  1. Immune surveillance
    - Natural Killer Cells “ID Check” via MHC-I. Kill any self-cells that have gone awry (viral or cancerous).
  2. Interleukins and Interferons (Cytokines)
    - Soluble proteins. Broad usage. Such as IL-6, pyrogenic or IFN-Y, increases MHC-II expression and M.O recruitment.
  3. Complement
    - Opsonisation, Inflammation, Lysis. A cascade of proteins. Three pathways. Classical, Alternative and Lectin. C3a kick starts it all (such as by binding Fc Ab).
  4. Inflammation

Palor, Rubor, Dolor, Tumor, Functio Laesa

  1. Fever

IL-1 and IL-6 encourage the release of prostaglandins in the hypothalamus, increasing core body temperature, off setting ideal growth environment for pathogens.

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63
Q

Explain the concept of PAMPs and TLRs

A

PAMPs, Pathogen Associated Molecular Patterns, are highly conserved components of pathogens. These components are fundamental to the pathogens function, so is usually expressed. They are detected by Toll Like Receptors (TLRs) on host Leukocytes. Example: Lipopolysaccharide (LPS) on -ve bacteria are detected by TLR-4.

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64
Q

Name five pro-inflammatory cytokines

A
  1. IL-1 - pyrogen
  2. IL-6 Pyrogen
  3. TNF-A - Vasopermability
  4. IL-8 - Chemoattractant of neutrophils
  5. IFN-Y - stimulates Macrophages

(IL-12 - Activates NK Cells)

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65
Q

Describe the physical barriers of the body

A
  1. Epithelium
  2. Mucous Membranes
  3. Secretions
  4. Ear wax
  5. Hair in the nose and ears
  6. Tears
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66
Q

Describe the MHC and which cells they are found on.

A

MHC Class I, found on all nucleases cells. Present self antigen to NK Cells and Tc Cells. Made of three alpha and 1 beta2 chains.

MHC Class II - Found on Antigen Presenting Cells (in abundance on professional APCs). Present ingested, non-self antigen to Th Cells. 2 alpha and 2 beta chains.

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67
Q

Name the three pathways of the complement system.

A
  1. Classical Pathway (Adaptive, C3a is activated by Ab Fc)
  2. Alternative Pathway (C3 binds the pathogen)
  3. Lectin Pathway (fungi and parasites)
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68
Q

Give three functions of the complement system

A
  1. Inflammation. Anaphylatoxins formed during cleavage are responsible.
  2. Opsonisation, another component of cleaved proteins. “Tag” microbes for more effective killing.
  3. Lysis. The terminal sequence of complement by the formation of the Membrane Attack Complex (MAC).
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69
Q

What is the equation for the activation of C3a?

A

C3 ——- C3a via C3 Convertase (C3bBb or C4bC2a)

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70
Q

Explain how NK Cells kill.

A

Natural position is to kill other cells, bind MHC-I. If non-self/ aberrant/ absent antigen is presented, the cell is killed by performing and granzymes.

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71
Q

State the functions of the Interferons

A

Alpha - produced by infected cells. Chemoattractant for NK Cells and phagocytes.

Beta - Produced by infected cells to stimulate anti-viral proteins in non-infected cells.

Gamma - Produced by T Cells to stimulate macrophages. (Also expression of MHC-II).

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72
Q

State the cardinal signs of inflammation, and how they are produced.

A

Rubor - Redness. Increased vasodilation
Tumor - Growth. Increased vasopermeability.
Dolor - Pain. Stretching of tissue.
Calor - Heat. Fever and blood flow.
Functio Laesa - Loss of Function, due to swelling. Restrictive and protective.

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73
Q

Describe the process of leukocyte extravasation.

A
  1. Chemoattraction - cytokines cause endothelial cells to express selectins. Leukocytes slow down due to vasodilation.
  2. Margination and Rolling Adhesion - Leukocytes bind selectins via integrins. Rolling and slowing.
  3. Tight Binding.
  4. Diapedesis. “Foot through” of Leukocyte through junctions between endothelial cells.
  5. The cell fully migrates.
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74
Q

Describe Adaptive Immunity

A

Active:
- Natural (Infection) or Artificial (Vaccine).

Passive:

  • Natural (gaining Abs from mother breastmilk or across the placenta.)
  • Active (vaccine).

Antigen Presentation.
More traditional.

  1. Carried out by Professional Antigen Presenting Cells (APCs) or standard APCs via Major Histocompatibility Complex Class II (MHC-II)
  2. APCs or free antigen travel to the lymph nodes via the afferent Lymphatics.
  3. Antigen is presented to CD4+ Lymphocytes (Th Cells).
  4. Th Cells are co-stimulated by adnexal receptors and activated. (B7 APC - CD28 ThC)
  5. Cytokines IL-2, IL-6 facilitate this.
  6. Cells undergo Clonal Expansion. The differentiation of cells to target the same epitope.
  7. T Cells act similarly, but react via MHC-I.
  8. B Cells mediate the humoral (antibody) response while T Cells either help, or facilitate the cell mediate response (cytotoxicity.)
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75
Q

Describe the five classes of antibody.

A

IgM - A pentamer. Binds a broad range of epitopes.
IgA - Dimer, found often at Lymphoid Associated Tissues.
IgD - Membrane bound, used as a receptor.
IgG - Highly specific binding.
IgE - Role not really known, targets parasites and helminths. Role in allergy.

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76
Q

Draw and label an IgG molecule.

A
  1. Two long chains
  2. Two short chains
  3. Joined by disulphides bonds.
  4. Variable, antigen binding site/ region. “Fab”
  5. Constant region “Fc”.
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77
Q

What is the function of IgE?

A

Allergy. Mast Cell degranulation.

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78
Q

Give five functions of antibodies.

A
  1. Opsonisation
  2. Complement Activation
  3. Neutralisation
  4. Agglutination
  5. Attract phagocytes
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79
Q

Define the term Neoplasia

A

A new abnormal growth, occurs due to unregulated cell proliferation.

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80
Q

Define the term Tumour

A

A growth of the same neoplasm.

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81
Q

Define the term Cancer

A

A neoplasia that has metastasised.

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82
Q

Define the term Cell proliferation

A

Cell division and reproduction

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83
Q

Define the term Apoptosis

A

Programmed cell death

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84
Q

Define the term hyperplasia

A

Increase in cell number, causing an increase in tissue size. Often early sign of neoplasia.

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85
Q

Define the term dysplasia

A

Abnormal growth/ organisation of a tissue

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86
Q

Define the term metaplasia

A

A tissue has differentiated into another tissue type/ mimics another tissue type.

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87
Q

Define the term Benign

A

A tumour that does not metastasise.

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88
Q

Define the term Malignant

A

A tumour which has invaded or metastasised. Gives rise to secondary tumours.

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89
Q

Define the term hypertrophy

A

Increase in cell size, causing increased tissue size.

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90
Q

Define the term labile

A

Not stable. Rapid cell turnover

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91
Q

Define the term stable

A

Not labile. Slow cell turn over.

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92
Q

Define the term permanent (cells)

A

No cell turn over

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93
Q

Define the term cell cycle

A

The interval between two mitotic divisions resulting in two daughter cells.

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94
Q

Describe the four phases of the cell cycle.

A

“Interphase”

  • G1 phase. Mitogen dependant. The cell grows in size, proteins are synthesised.
  • S phase. DNA is synthesised.
  • G2 phase. Cell grows, organelles are replicated.

Mitosis/ M Phase.
Prophase, (Pro)metaphase, Metaphase, Anasphase, Telophase, cytokinesis.

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95
Q

Describe regulation of the cell cycle.

A

The four checkpoints to be revised in MBChB 1 are:

Restriction Point
G1/S Checkpoint
G2/M Checkpoint
Metaphase Checkpoint

The restriction point:

  1. Most important apparently.
  2. A mitogen stimulates a Receptor Tyrosine Kinase, which activated the Ras pathway. (The phosphorylation of Rb, unblocking E2F.)
  3. Without this, the cell will Diverge to G0 (quiescence).

G1/S and G2/M Checkpoints.
1. Checks for DNA damage. P53 is active where DNA damage is detected. This activates P21, which prevents Cyclin E and A binding CDK 2.

Metaphase Checkpoint.

  1. Check for spindle attachment to chromatids. If improper attachment is detected, CDK 1 remains phosphorylated.
  2. If all is well, CDK 1 binds Cyclin B.

*Cyclin B awaits CDK 1 to bind.

Cyclin B is present from G2 in anticipation. CDK1/CYCB is named in some papers as Maturation Promoting Factor (MPF). Allows for destructed of the nuclear envelope, chromatin condensation, spindle formation.

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96
Q

Explain Hydrophobic Cell Signalling and examples of hormones involved.

A

The signal passes through the plasma membrane, acting on cytosolic receptors. Receptor-signal complex forms the transcription factor. Gene expression is altered, protein is translated and the effect is achieved. Example: testosterone.

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97
Q

Give three reasons why cell signalling should be studied

A
  1. It forms the basis of pharmacology.
  2. Elucidates cellular pathways and processes.
  3. Allows for the study and understanding on key hallmarks of disease.
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98
Q

Explain the problems hydrophilic signalling molecules face and how this is overcome.

A

These signal molecules cannot cross the plasma membrane.

Instead they bind cell surface receptors and activate a signal transduction pathway/ cascade. This then leads to an inter-cellular response.

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99
Q

Describe G-Protein Coupled Receptors.

A
  1. Serpentine in shape, with 7 transmembrane domains, starting at an extracellular binding site.
  2. Ligation causes a conformational change at the intracellular domain, where a G-Protein binds.
  3. GDP is swapped for GTP on the G-Protein.
  4. The G-Protein splits into alpha and beta subunits.
  5. Beta affects ion channels, Alpha has three principle targets.
    - Adenylyl Cyclase which increases the production of Cyclic AMP from ATP. Binds Protein Kinase A (PKA). PKA moves to phosphorylation L-Type Calcium Channels, CREB and Phosphorylase Kinase.
    - Phospholipase C. Acts on IP3 and DAG. IP3 acts on the ER. DAG on Protein Kinase C.
    - Other G-Proteins

An example is Adrenaline and Cyclic AMP.

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100
Q

Describe enzyme linked receptors.

A

Principle steps. Example with Receptor Tyrosine Kinase.

  1. Ligand binds with two monomers, causing dimerisation.
  2. The dimer is autophosphorylated.
  3. Phospho-tyrosine residues in the cytosol act as binding sites for intracellular proteins.
  4. The signal is transduced.

Example is FGFR3

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101
Q

Describe Ion Channels.

A

Five principle steps.

  1. Ligation at one of several binding sites, as the channel is multimeric.
  2. Conformational change takes place. Classic.
  3. Central pore is now open.
  4. Ions passively diffuse.
  5. Shape is maintained when ligand is bound.

Example is ACH-R.

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102
Q

Name two signalling molecules that bind GPCRs, RTKs and Ion Channels.

A
  1. Adrenaline and Glucagon
  2. PDGF and FGF
  3. GABA and ACH
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103
Q

Define the term Tumour Suppressor Gene.

A

A gene which, when transcribed, produces a protein that inhibits tumour growth by suppressing the cell cycle until repair or apoptosis can take place.

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104
Q

Define the term Proto-Oncogene.

A

A normal functional gene that translates to a protein in normal metabolism, regulating cell cycle and differentiation.

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105
Q

Define the term oncogene

A

A mutated Proto-oncogene, which is now abberantly expressed. This causes inappropriate expression of a protein and cell behaviour (malignancy).

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106
Q

Describe the term mutation.

A

A change in genetic mutation.

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107
Q

Describe the term activating mutation.

A

A mutation that activates an established oncogene.

108
Q

Give examples of mutations.

A

Deletion - deletion of nucleotides from a sequence, can cause a frame shift.

Point Mutation - A mutation of a single base pair.

Substitution - A base pair is swapped for another

Chromosomal Rearrangement - portion of a chromosome swaps with another. Such as Philadelphia Chromosome (BCR-ABL).

Over expression of proteins, such as in BCR-ABL, causing over signalling. Another example is where TKR is formed as a dimer, in achondroplasia. Look this up.

109
Q

Give an example of a tumour suppressor gene and explain how it works.

A

“Brakes on the cell cycle”

  1. Retinoblastoma. Binds and inhibits E2F, halting the cell cycle at the restriction point.
  2. P53. Activated when DNA damage is detected. Will induce apoptosis in high concentrations, in low concentrations will activate P21, which inhibits CDK2 binding Cyclin A and E, so repair can take place.
110
Q

Describe how telomeres prevent over proliferation of cells.

A

Chromosomes/ DNA have a tail of telomere, which is added by the enzyme telomerase. Typically, at each cell division this tail shortens, indicating life expectancy of the cell. When the tail is depleted, the chromosomes inappropriately fuse. This is detected as an aberrant genome and the cell is killed.

Mutations in telomerases can result in immortal cells, as the tail is constantly renewed.

111
Q

Describe the Philadelphia translocation.

A

Occurs in a reciprocal translocation between Chromosome 22 and 9. The breakpoint is part way through the BCR gene on C22, fusing with (part) of the ABL gene on C9, forming the “always on” BCR-ABL gene. The product is a RTK that is active without ligation. Found commonly in Chronic Myeloid Leukaemia.

112
Q

Describe loss of TSG function.

A

It is the loss of the “brakes” of the cell cycle. Without these genes and their proteins, such as P53, DNA damage goes unrepaired and accumulates. This contributes to the multi-hit model of Carcinogenesis.

113
Q

Explain the constraints faced but tumours and how they are overcome.

A

A. Neoplastic growth can often outgrow existing vascular supply, so must increase it’s angiogenic potential to perfume it’s growth. This is facilitated with mutation and the over expression of growth factors such as vascular endothelial growth factor. This is a hallmark of cancer.

B. Tumours can be confined to their original tissue, but can invade with the expression of matrix metallo proteases, breaking through basement membranes and penetrating adnexal tissues. This facilitates metastasis.

C. Metastatic cancer cells can express E-Catherin, allowing them to move within tissues.

Other hall marks of cancer.

114
Q

Describe Magnetic Resonance Imaging.

A
  1. Protons align with or against a really big magnet.
  2. Protons that align against the magnet have a higher energy level, creating an energy difference.
  3. Radio waves are fired at low energy protons which excites them to a high energy state.
  4. As they return to a low energy state, they will emit radio waves at the same wavelength as absorbed.
  5. This is detected and data is plotted into an image.
  6. Dyes and contrast can be used.
  7. Well expensive
  8. Low radiation though.
  9. Always in high demand.
  10. Good for soft tissue.
  11. Great detail.
115
Q

Describe X-Rays

A
  1. Electrons are emitted from a heated cathode to an anode.
  2. These elections “knock” electrons in the anodes a high energy state. As they lower, they emit X-Ray radiation.
  3. This is detected in a black and white image. Black representing air, white is bone while soft tissues appear a light grey.
  4. Quick and inexpensive.
  5. Easy
  6. Good for bones, chest exams.
  7. Easy to access. Dyes can be used.
  8. High radiation.
116
Q

Describe CT scans

A

Circular X-Ray. Multiple X-Rays are taken, and constructed into a 3D image. Computer Tomography. High radiation.

117
Q

Describe the pathophysiology of Osteoarthritis (OA).

A

A degenerative disease of the bones and joints.

  1. Can have a gradual onset by the gradual loss of articular cartilage at synovial joints, or can be the result of trauma.
  2. Initially, an increase in water content is seen.
  3. Proteoglycan synthesis drops
  4. Aggregate, hyaluronic acid lowers in concentration.
  5. Cytokines IL-1 and TNF are released in response to tissue damage.
  6. Synovium inflames.
  7. Neutrophils migrate to the joint and release matrix metallo proteases and collagenases. The articular cartilage is damage further.
  8. Joint space reduces.
  9. Subchondral sclrerosis occurs.
  10. Wearing of the bone forms subchondral cysts (fluid filled sacs).
  11. Osteophyte formation.
118
Q

Define Osteoarthritis

A

A progressive, degenerative disorder of the joints caused by a loss of articular cartilage and subsequent damage to joint tissues.

119
Q

Describe common joints affected by Osteoarthritis

A
  1. Weight bearing joints (knees)
  2. Carpometacarpal joint.
  3. DIP and PIP
120
Q

Describe common changes seems in Osteoarthritis

A
  1. Loss of joint space
  2. Subchondral sclerosis
  3. Subchondral cysts
  4. Osteophytes
  5. Trendelenberg sign.
121
Q

Give diagnostic techniques and symptoms of Osteoarthritis

A 
A. X-Ray to asses bone health, joint space, osteophytes.
B. Local Pain
C. Joint Mobilisation
D. Trendelenburg Sign.
E. Occupational History
F. Morning Sickness
G. Crepitations
122
Q

Describe the Aetiology of Osteoarthritis

A
  1. Primary (idiopathic). - Degenerative.
  2. Secondary (of other disease)

Trauma, hip dysplasia, inflammation.

123
Q

Give the risk factors and treatments of Osteoarthritis

A

Risk factors

  • Modifiable
    1. Nutrition
    2. Weight (obesity)
    3. Exercise
    4. Muscle Weakness
  • Non modifiable
    1. Age

Gender - men under 50, women over 50 (genetics?).

Treatments

  • surgical
    1. Arthroplasty
    2. Arthroscopic repair
    3. Microfracturing of subchondral bone to promote healing
    4. Cartilage transplant

Non-surgical

  1. Walking aids
  2. NSAIDS
  3. Corticosteroids
  4. Analgesics
  5. Physio
  6. Weight loss
124
Q

Describe the Skeletal Muscle

A
  1. Multinucleated
  2. Striated
  3. Contractions are voluntary.
  4. Variable speeds of contraction, fast.
  5. Regenerative potential if damaged.
125
Q

Describe Smooth Muscle

A
  1. Mononuclear
  2. Non-striated
  3. Mostly involuntary contractions - hormones and the ANS.
  4. Organised around organs or vessel walls.
  5. Slow contractions.
126
Q

Describe Cardiac Muscle

A
  1. 1-5 nuclei
  2. Semi-striated, Y-Shaped organisation.
  3. Involuntary contractions
  4. Connected by inter-calated discs for conductivity.
  5. Medium contraction speed.
  6. Independent pace set.
127
Q

Define the term Excitable Cell

A

A cell with a resting membrane potential and are electrically excitable.

128
Q

Define the term Resting Potential

A

The potential difference in charge across a plasma membrane.

129
Q

Describe the displacement of ions across the membrane.

A

Generally, there are more sodium ions on the outside of the cell, while the cytosol is rich in potassium ions.

130
Q

Describe excitation of a neurone and skeletal muscle cell.

  • flash card answer is poor.
A
  1. Neutron resting potential sits at -70Mv, while Skeletal Muscle is around -85Mv.
  2. A neurotransmitter binds and opens a Ligand Gated Sodium Channel causing Depolarisation.
  3. Depolarisation must reach threshold (-55 in neurones and -60 in skeletal muscles) for an Action Potential to be created.
  4. The cell then hyperpolarises returning to resting potential, enforcing a unidirectional AP.
131
Q

Describe the structure of skeletal muscle

A

Micro anatomy -

  1. Epimysium surrounds the perimysium.
  2. Perimysium is contains fascicles, blood vessels and nerves.
  3. Fascicles contain individual muscle fibres, lower muscle neurones, myosatellite cells and the endomysium. This is best learnt by looking at a diagram.
  4. Highly vascularised. The muscle fibre found in fascicles is made up of Actin (thing) and Myosin (Thick filaments).

Organised into sarcomeres -

  1. I Band -a region containing only thin filaments. Bisected by the Z Line and spans between the A bands.
  2. Z Line - the boundary of the sarcomere. Titin extends from the top of the actin filament to the Z- Line to anchor.
  3. A Band - the region of overlap between thin and thick filaments
  4. M Line - the centre of the A band. Central to the thick filaments.
  5. H Band - thick filaments, no thin.
132
Q

Describe the mechanism by which muscle contraction occurs.

A
  1. The action potential arrives at the axonal terminal.
  2. Calcium ions diffuse into the axonal terminal. The terminal releases vesicles of Acetylcholine (ACh).
  3. ACh diffuses across the Neuromuscular Cleft and ligates with ACh-Receptor (nicotinic cholinergic). Ion channels open, sodium diffuses into the Sarcoplasm.
  4. Acetylcholinesterase breaks down ACh.
  5. Influx of sodium propagates down the Sarcolemma to the T-Tubules.
  6. This causes L-Type Calcium Channels of the Sarcoplasmis Reticulum to release Calcium.
    1. Calcium binds Troponin
      1. Troponin denatures and moves, exposing actin binding sites to myosin
      2. The myosin head binds. ADP is swapped for ATP.
      3. Power stroke, the muscle contracts.
      4. Myosin head cocks back, hydrolysing ATP to ADP + H. Myosin detaches.
      5. Tropomyosin covers the binding site and the muscle relaxes.
      6. Calcium is pumped back into the Sarcoplasmic Reticulum.
133
Q

Define the term ECM

A

Extracellular Matrix is a network of proteins and polysaccharides secreted by cells to provide structural support and create a supportive extracellular environment.

134
Q

State the function of ECM.

A
  1. Structural Support
  2. Tensile Strength
  3. Sequester Growth Factors
  4. Provide a route for cellular migration
  5. Transmission of force
  6. Anchors cells (structure)
135
Q

Describe the composition and components of ECM.

A
  1. Collagen
    - Provides tensile strength
    - Helical structure
    - Gly-X-Y repeating units
  2. Elastin
    - Elastic properties, allows the structure to retain its shape after change.
  3. Ground Substance
    - Water
    - Proteoglycans
    - Aggrecan
    - Glycosaminoglycans
    - Glycoproteins
136
Q

Name four different types of Collagen and where they are found.

A
  1. Type I - tendons, skin, bone, ligaments
  2. Type II - Cartilage
  3. Type III - with Type I, especially in wound healing.
  4. Type IV - Basement Membrane
137
Q

Describe the Basement Membrane

A

Three layers.

Lamina Lucida
Lamina Densa
Lamina Fibrireticularis

Rich in Type IV Collagen.

5 Functions:

  • Support
  • Allows for nutrient diffusion
  • Binds epithelium of underlying tissue
  • Path for migration in wound healing (re-epithelialisation)
  • Barrier preventing down growth
138
Q

Give examples of fibrous joints

A

Suture joints in the skull, gomphosis in teeth.

139
Q

Give examples of cartilaginous joints.

A

Pubic symphysis and joints between intervertebral discs.

140
Q

Give types of synovial joints

A
  1. Plane
  2. Pivot
  3. Hinge
  4. Condyloid
  5. Saddle
  6. Ball and Socket
141
Q

Describe the cells of the nervous system and their functions

A

A. Neurones - transmission of action potentials.
1. Uni, bi and multipolar.

B. Glia (support) Cells.

  1. Schwann Cells - support and form myelin sheaths over PNS neurones
  2. Oligodendrocytes - support and form myelin sheaths over CNS neurones.
  3. Microglia - Phagocytic cells
  4. Ependyma Cell - Secretes CSF
  5. Astrocytes - Nutritional Support of the CNS
142
Q

What cells secrete Cerebrospinal Fluid?

A

Ependyma Cells

143
Q

Describe the organisation of the nervous system.

A

Central Nervous System

  • The Brain
  • The Brain Stem
  • Spinal Cord
Peripheral Nervous System
 - Spinal Nerves
A. 8 Cervical 
B. 12 Thoracic 
C. 5 Lumbar
D. 5 Sacral
E. 1 Coccygeal
F. 12 pairs
144
Q

What is the function of the Frontal Lobe of the brain?

A

Higher order thinking, conscious though and memory

145
Q

What is the function of the Occipital Lobe?

A

Visual data processing

146
Q

What is the function of the Parietal Lobe?

A

Integration of sensory input

147
Q

What is the function of the Temporal Lobe?

A

Primary auditory cortex.

148
Q

Name the 12 cranial nerves

A
  1. Olfactory
  2. Optic
  3. Oculomotor
  4. Trochlear
  5. Trigeminal
  6. Abducens
  7. Facial
  8. Vestibulocochlear
  9. Glossopharyngeal
  10. Vagus
  11. (Spinal) Accessory
  12. Hypoglossal
149
Q

What are the types of hypersensitivity?

A

Type I - Allergy/ Immediate - Asthma
Type II - Cytotoxic/ Antibody Dependant - Thrombocytopenia
Type III - Immune Complex Disease - Rheumatoid Arthritis
Type IV - Delayed type. Cell mediated. - Coeliac Disease
Type V - Autoimmune - Grave’s Disease

150
Q

Briefly DASPITE Asthma

A

Definition: a Type I hypersensitivity disorder causing chronic inflammation and reversible restriction of the airway.

Aetiology:
Extrinsic/ Atopic - genetic/ environmental. Allergy, IgE mediated. FHx.
Intrinsic - adult onset/ occupational. Cold weather, bronchitis. Medications such as B Blockers.

Signs and Symptoms:

  1. Wheezing
  2. S.O.B
  3. Tight chest

Pathophysiology:

  1. Inappropriate response to a stimuli such as allergen.
  2. IgE recognise the allergen.
  3. Bound IgE ligates with Mast Cells via their Fc portion.
  4. Mast Cells degranulate.
    • Histamine increases vascular permeability. (Oedema)
      - Leukotrienes cause smooth muscle contraction (constriction)
      - Prostaglandins increase vasodilation
      - Proteases damage and irritate tissues. (Remodelling)
  6. Extravasation of WBCs
    - CD4+, Eosinophils, Macrophages.
  7. Hypertrophy of smooth muscle cells, angiogenesis and collagen deposits.
  8. Necrosis occurs where angiogenesis is insufficient.

Investigations:

  1. FHx
  2. FEV1
  3. S&S

Treatments:
1. Bronchodilators
- Adrenoreceptor Agonists
A. Short Acting B2 Agonists (SABAS) binds B2-RSIGS and upregulates Cyclic AMP. - bronchodilation. Salbutamol
B. Long Acting B2 Agonists (LABAs). - As SABAs. Salmetrol.
2. Anti-Muscarinic.
A- Short Acting. Block cholinergic receptors (parasympathetic) to inhibit contractions. Ipratropium.
B. Long Acting. As above. - Tiotropium.
3. Glucocorticoids
- antagonists of Leukotrienes. Xanthines.
4. Theophylline
- reduces airway responsiveness to histamines.

Order of use: 
SABA
SABA + Steroids
SABA + LABA + Steroids
SABA + LABA + Steroids +/-Xanthine

Epidemiology:

Increasing worldwide. Hygiene hypothesis has been suggested. 1/11 children and 1/12 adults in UK.

151
Q

Describe the Autonomic Nervous System.

A

Control of smooth muscle, physiological homeostasis, efferent fibres of the visceral NS.

Split into two divisions.

Sympathetic-
1. T1-L2, following the ventral spinal route.

Principle Neurotransmitters: Adrenaline (Beta and Alpha), Noradrenaline (Alpha and Beta).

Receptors:
Beta 1: Heart, Renal, Adrenal Glands
Beta 2: Airways and Lungs
Alpha 1: Arteries
Alpha 2: Veins, coronary vasculature.

Variations:
ACh in peripheral vessels and sweat glands.
Nitrous Oxide works as a vasodilator.

Functions: Fight or Flight.

Parasympathetic.
Carniosacral route.

Cranial Nerves:
CNIII -Oculomotor
CNVII -Facial
CNIX -Glossopharyngeal
CNX -Vagus

Sacral S2-S4.

Receptors
Muscarinic: smooth muscle cells and salivary glands

Nicotinic: Skeletal muscle.

Functions: Rest and Digest.

Sexual arousal.

152
Q

Describe the cough reflex.

A

Innate autonomic reflex to expel irritants or clear the airway.

Afferent nerve fibres from the vagus nerve provides sensory input to the medulla oblongata.

Efferent signals sent via the lower motor neurones of the respiratory muscles. Phrenic - diagphragm. Laryngeal - larynx.

Production of the cough.

  1. Efferent nerves to the diaphragm and internal intercostals undergo a deep contraction, drawing air in.
  2. Laryngeal nerve closes the glottis. Expiratory muscles contract.
  3. High intrathoracic pressure and a rapid opening of the glottis causes a violent expiration.
153
Q

Describe vasovagal syncope and the first aid response.

A

A faint caused by a sudden drop of blood pressure caused by inappropriate peripheral vasodilation.

Loss of sympathetic inner vat ion/ increase in parasympathetic.

Contractility, heart rate and cardiac output decrease, peripheral compliance increase.

Aetiology/ risk factors.

  1. Stress
  2. Intense pain
  3. Heat injury
  4. Dehydration

Symptoms:

  1. Light headedness.
  2. Loss of sight
  3. Tinnitus
  4. Nausea
  5. Sweating
  6. Pale/ cold skin
  7. Slow pulse

First aid:

  1. Secure the area
  2. Lie the patient down
  3. Treat bleeds
  4. Elevate the legs
  5. Recovery position if required.
154
Q

Describe the histology of the GI tract.

A

Starts at the mouth stops at the butthole

Histology of the GI tract. So many. 
- 4 layers
1. Mucosa 
 A. Epithelium. Squamous.
 B. Lamina. Areolar connective tissue,
 C. Muscularis mucosa. Smooth muscle.
  1. Submucosa. Areolar tissue that binds the mucosa. Vascular. Secretions.
  2. Muscularis propria. Skeletal muscle and under voluntary control. Not continuous. Lower portions contain smooth muscle.
  3. Serosa. Simple squamous epithelium. Superficial
155
Q

Describe the mouth (GI Tract Organ).

A
  1. Mouth
    - the opening of the G.I tract.
    - buccal cavity at cheeks. Hard palate, soft palate, tongue.
    - mastication and digestion with saliva.
156
Q

Describe the pharynx (GI Tract Organ)

  • this one is very short.
A
  1. Pharynx
    - skeletal muscle.
    - pass into oesophagus.
157
Q

Describe the oesophagus (GI Tract Organ)

A
  1. Oesophagus.
    - muscular tube.
    - movement by peristalsis.
    - non-keratinised squamous epithelium.
    - passes oesophageal hiatus of the diaphragm at T10.
    - top third - striated
    - mid third - mix
    - lower third smooth.
    - two sphincters. Upper (pharynx) and lower (gastro-oesophageal. Prevents acid reflux).
158
Q

Describe the stomach (GI Tract organ)

A
  1. Stomach.
    - major digestive organ
    - J shaped.
    - mix food and gastric secretions
    - anatomically found in the epigastric/ left hypochondriac regions.

Four sections - fungus, cardia, body and pylorus.

Cells

  1. Endocrine cells - gastrin
  2. Chief cells - pepsinogen and gastric lipase
  3. Parietal cells - HCL and intrinsic factor
  4. Mucous neck cells - mucous
159
Q

Describe the duodenum (GI Tract organ)

A

Small intestine.

Four parts

  1. Superior - joined by the hepatoduedenal ligament.
    - relieves chyme
  2. Descending - major duodenal papilla. Surrounded by sphincter of oddi.
  3. Inferior - travels laterally to the aorta and IVC.
  4. Ascending - duodenaljejunal flexure.

Brunners glands secrete alkaline mucous.

Pancreatic and hepatic secretions are received here.

Ampulla of Vater - pancreatic and common bile duct.

Cells:
- absorptive cells. Brush border

  • goblet cells. Produce mucous.
  • granular cells. Produce enzymes
  • endocrine cells. Produce hormones.
160
Q

Describe the Jejunum (GI Tract organ)

A

Digestion and absorption

161
Q

Describe the Ileum (GI Tract organ)

A

Absorption of bile salts, Vit B12.

162
Q

Describe the colon (GI Tract organ)

A

5 parts.

  1. Caecum and appendix.
  2. Ascending
  3. Transverse
  4. Descending
  5. Sigmoid

Absorbs water, electrolytes, vitamin K. Stores and transports faecal matters.

Gut flora. Aids in immunity, digestion and production of vitamins.

Taenia coli - incomplete layer of longtitudal muscle

Haustrations - ring like circular muscles.

163
Q

Describe the rectum (GI Tract organ).

A

Starts after the sigmoid colon.

Five parts.

  1. Sacral flexure
  2. Anorectal flexure
  3. Superior flexure
  4. Intermediate
  5. Inferior
164
Q

Describe the anal canal (GI Tract organ)

A

Two sphincters.

Internal (upper 2/3), smooth muscle

External (lower 1/3), striated.

165
Q

Describe the salivary glands of the GI Tract

A

Salivary glands.

Submandibular - sublingual - parotid.

  • induction of thirst
  • stores fats and digests carbohydrates (alpha amylase and lingual lipases)
166
Q

Describe the pancreas

A

Digestive (exocrine) and hormonal (endocrine) functions. Retroperitoneal.

Secretions out of the pancreatic duct.

99% of secretions are exocrine. Contain:
(Pancreatic)
1. Amylase
2. Lipase
3. Digestive enzymes
4. DNAases
5. Salts
6. Sodium bicarbonate
7. Water

Endocrine secretions -

  1. Alpha Cells: glucagon
  2. Beta Cells: Insulin
  3. Delta Cells: Somatostatin
167
Q

Describe the liver (GI Tract organ)

A

Four lobes-

  1. Left
  2. Right
  3. Quadrate
  4. Caudate

Functions:

  1. metabolism such as conjugation of proteins
  2. storage of glucagon
  3. inactivation of drugs (P450)
  4. production of clotting factors
  5. cholesterol storage
  6. production of bile
168
Q

Describe the gall bladder (GI Tract organ)

A

Location: peritoneal cavity. Right hypochondrium. Posterior to the liver.

Functions-

  1. Stores bile
  2. Release of bile

Via the common bile duct, merges with the pancreatic duct and secretes through the sphincter of oddi.

169
Q

Name the functions of the alimentary canal

A
  1. Take in
  2. Digest
  3. Absorb
  4. Expel
170
Q

Name the three salivary glands

A
  1. Sublingual
  2. Submandibular
  3. Parotid
171
Q

Name five functions of saliva

A
  1. Carbohydrate and fat digestion
  2. Induction of thirst
  3. Lubrication
  4. Hosts IgA.
  5. Moistens mouth for speech
172
Q

What region of the abdomen is the liver found?

A

Right hypochondrium and epigastrum.

173
Q

What region of the abdomen is the caecum found?

A

Right Iliac fossa.

174
Q

Name the parts of the stomach.

A
  1. Fundus
  2. Cardia
  3. Body
  4. Pylorus
175
Q

Name the cell types found in the stomach.

A
  1. Endocrine cell - gastrin
  2. Chief cells - pepsinogen
  3. Parietal cells - intrinsic factor and HCL
  4. Mucous neck cells - mucous
176
Q

List the structures that make up the small and large intestine.

A
  1. Duodenum
    - superior
    - descending
    - inferior
    - ascending
  2. Jejunum
  3. Ileum
  4. Colon
    - caecum
    - ascending
    - hepatic flexure
    - transverse
    - splenic flexure
    - descending
    - sigmoid

(Haustrations and taenia coli)

177
Q

Describe Binary fission

A
  1. Replicate the genome
  2. Chromosomal segregation
  3. Cytokinesis
178
Q

What are the immune privileged sites?

A
  1. Eyes (not conjunctiva)
  2. Blood
  3. CNS
  4. Inner ear
  5. Middle ear
  6. Sinuses
179
Q

Name the functions of the pancreas

A 
Exocrine:
(Pancreatic) 
1. Amylase
2. Lipase
3. Digestive enzymes
4. DNAases 
5. Salts (bicarbonate, makes it alkaline)
6. Water

Endocrine (langerhans cells):

  1. Alpha: glucagon
  2. Beta: insulin
  3. Delta: somatostatin
180
Q

Name the functions of the liver

A
  1. Inactivation of drugs and hormones.
  2. Metabolism and conjugation of wast
  3. Storage of glycogen and release of glucose
  4. Platelet production
  5. Production of clotting factors
  6. Storage of cholesterol
  7. Production of bile acid and alkaline fluid
181
Q

Describe the digestion of carbohydrates.

A
  1. Begins in the mouth
  2. Salivary alpha amylase produced acini cells digests 1-4 glycosidic bonds.
  3. Glycogen —-> maltose
  4. Bolus enters the stomach, chyme enters the duodenum
  5. Pancreatic amylase in the duodenum breaks 1-4 G bonds again.

Brush border enzymes:

  • lactase - lactose= glucose and galactose
  • Maltase - maltose= glucose
  • sucrase - sucrose= glucose
182
Q

Describe digestion of proteins.

A
  1. Starts in the stomach
  2. HCL from parietal cells cleaves pepsinogen to pepsin.
  3. Pepsin converts proteins into polypeptides.
  4. HCL works to break peptide bonds
  5. In the duodenum - pancreatic and bile secretions contain proteolytic enzymes.
  • trypsin (first enzyme, starts cascade)
  • elastase
  • chymotrypsin
  • carboxypeptidase
183
Q

Describe the digestion of fats.

A
  1. Begins in the mouth
  2. Salivary lipase.
  3. Moves as bolus to stomach - gastric lipase.
  4. Most takes place in the duodenum.
  5. Bile emulsifies the fat. Triglycerides become monoglycerides.
  6. Fats are packaged into micelles
  7. Fats are absorbed by microvilli.
  8. Fats are converted back into triglycerides and aggregate with cholesterol, proteins and phosphopholipids to form chylomicrons.
  9. Chylomicrons are taken up by the lymph.
184
Q

Describe the absorption of carbohydrates

A

Happens along the brush border. Can be passive, facilitated or active.

Glucose and galactose - facilitated diffusion with Na co transporters

Fructose - facilitated diffusion

185
Q

Describe the absorption of amino acids

A

Along the brush border.

Active transport

Facilitated diffusion with Na co transporters

186
Q

Describe the absorption of peptides

A

Along the brush border.

Facilitated diffusion with H+ co transporter.

187
Q

Describe the absorption of fatty acids

A

Along the diffusion.

Short chain - simple diffusion

Long chain and 2-monoglyceride -
1. Simple diffusion in micelles (converted to chylomicrons).

188
Q

Define metabolism

A

The sum of all reactions in the body that produce energy, and where energy is then used.

189
Q

What is “energy” needed for in the body?

A
  1. Maintenance of membrane potentials
  2. Muscle contraction
  3. Movement
  4. Active processes
  5. Disposal of wastage
  6. Generation of heat
  7. Biosynthesis

Energy is stored as ATP and hydrolysed to ADP + Pi.

190
Q

Name the methods by which ATP is produced.

A
  1. Creatine phosphate
  2. Anaerobic respiration
  3. Aerobic respiration
  4. Lipolysis
191
Q

What are the outputs of the Kreb Cycle?

A
  1. Two ATP
  2. 6 NADH
  3. 2 FADH2
192
Q

Describe the electron transport chain.

A

In the cristae of the mitochondria. The site of oxidative phosphorylation.

  1. Redox of NADH+H+ at Complex I - electrons to Complex I. Four protons pumped from matrix to inter-membrane space.
  2. Redox of FADH2 at Complex II. Coenzyme Q moves electron to Complex III.
  3. Redox of Complex III. Four protons move from the matrix to inter-membrane space. Carrier C moves electron to Complex IV.
  4. Redox of Complex IV. Two protons are pumped from matrix to inter-membrane space. H20 is formed.
  5. ATP Synthase action. Protons pumped to the matrix, ATP is formed.
193
Q

Define pharmacokinetics

A

The movement of drugs in the body.

194
Q

Name the four stages pharmacokinetics

A
  1. Absorption
  2. Distribution
  3. Metabolism
  4. Excretion
195
Q

Describe the routes of drug administration.

A

A. Paternal routes:

  1. Intramuscular injections.
    - must have blood to the muscle
    - avoids first pass metabolism
    - rapid onset
    - poor usage in shock.
  2. . Subcutaneous injections.
    - slower onset
    - avoids first pass metabolism
    - poor use in shock
  3. Intravenous injections.
    - rapid onset
    - avoid first pass metabolism
    - more specific, titration of drug dose.
    - use can be poor in severe shock.

Enteral routes:

  1. Oral
  2. Rectal
  3. Lingual
    - safe
    - non invasive
    - subject to first pass metabolism
    - delayed onset
    - patient compliance can be low

Other routes:

Pulmonary
- inhaled, absorption is poor.

Topical
- onto the skin. Sublingual sprays. Buccal.

196
Q

Define the term bioavailability.

A

The fraction of administered drug that reaches circulation to have an active effect.

197
Q

Name four factors that affect the bioavailability of drugs.

A
  1. Hepatic first pass
  2. Molecular weight
  3. Gastric health
  4. Ingestion of other foods and drugs
198
Q

Define the term loading dose.

A

The amount of drug administered to achieve target concentration.

199
Q

Define the term half-life (pharmacology)

A

The time taken for the plasma concentration to decrease by half.

200
Q

Define the term clearance.

A

The theoretical volume of plasma cleared of the drug per unit of time.

201
Q

Define the term steady state.

A

Where the drug administered is equal to the amount of drug cleared.

202
Q

Define pharmacodynamics.

A

The biochemical and physiological mechanisms that underpin drug action.

203
Q

Describe targets for drugs.

A

Drugs target receptors.

Usually proteins, receptors affect:

  1. Regulation of metabolism
  2. Enzymes
  3. Transport of proteins
  4. Structure of proteins.
204
Q

Define the term affinity.

A

A measure of the ability of a drug to bind a receptor.

205
Q

Define the term efficacy.

A

The ability of a bound drug to produce it’s intended effect.

206
Q

Define the term agonist.

A

A molecule that binds to a receptor, mimicking it’s biological ligand, producing the same/ similar effect.

Can be full or partial.

207
Q

Define the term antagonist.

A

A molecule that binds to it’s receptor and inhibits a biological response.

It can be competitive or non-competitive.

208
Q

Define the term ED50.

A

Effective dose. The dose at which 50% of the population tested exhibit the desired effect.

209
Q

Define the term TD50.

A

Toxic dose. The dose at which 50% of the population tested exhibit toxic effects.

210
Q

Define the term LD50.

A

Lethal dose. The dose at which 50% of the population tested exhibit lethal effects.

211
Q

Describe the basic anatomy of the kidneys.

A

With the ureters, form the upper urinary tract.

  1. Retroperitoneal, found at T12-L3 (left kidney is higher).
  2. Four layers of fascia and fat.
    - Pararenal Fat
    - Renal Fascia
    - Perirenal Fat
    - Renal Capsule (fibrous)

Structure of the kidney.

  1. Cortex - outer
  2. Medulla - inner.
    - divided into renal pyramids by renal columns.
    - drains into the renal papilla.
    - papilla drains to the minor calyx.
    - merge to form the major calyx.
    - drain to the renal pelvis
    - drains to the ureter. Through the hilum, formed by the renal fissures.
  • enter the bladder at the ureteral opening. Peristaltic, wave like contractions fill the bladder. Hydrostatic pressure and gravity aid this.
212
Q

List the functions of the upper urinary tract.

A

Kidneys and ureter.

  1. Produce and transport urine
  2. Filtration of blood
  3. Maintenance of blood volume and pressure.
  4. Acid-base buffering.
213
Q

Describe the arterial supply of the kidneys.

A

Served by renal arteries, which are branches of the abdominal aorta.

Branch into suprarenal arteries (but can also arise independently from the Abdominal Aorta). Nephrons attach at the arcuate or cortical vessels.

Renal veins drain into the Inferior Vena Cava.

214
Q

Describe the histology of the ureters.

A
  1. Mucosa - mucous membrane with transitional epithelium. Goblet cells secrete mucous.
  2. Lamina propria - areolar connective tissue with Lymphatics and blood vessels.
  3. Muscularis - inner and outer longitudinal layers.
  4. Adventitia - superficial fascia. Vascular access, Lymphatics, nerves. Structure.
215
Q

What organs contribute to the lower urinary tract?

A

Urinary bladder and urethra.

216
Q

What are the functions of the bladder?

A
  1. Storage of urine
  2. Capacity of around 500mls of urine.
  3. Expulsion of urine (detruser muscle and two sphincters)
217
Q

Describe the anatomy of the bladder.

A

Overview:

  1. Hollow and distensible organ.
  2. Found in the anterior pelvic cavity.
  3. Urine enters via the ureters at the trigone.
  4. Folded with riggae.
218
Q

Describe the histology of the bladder.

A

Four layers. Similar to the ureters.

  1. Mucosa - mucous membrane. With transitional epithelium. Goblet cells secrete urine.
  2. Lamina propria - Areolar tissue, vascular, lymphatics.
  3. Muscularis - three layers
    - inner, middle (circular) and outer. Form the detrusor muscle.
  4. Adventitia - superficial fascia. Vascular, lymphatics and nerves.
219
Q

Describe the urethra in males and females.

A

Males:

  1. 18-20cm
  2. Carries urine and semen.
  3. Three portions. Prostatic (prostate), membranous (pelvic floor. external sphincter is here) and spongy (penile).

Females:

  1. 3-5cm
  2. Bladder - external urethral orifice.
  3. Only urine.

Sphincters:
Internal:
Males: circular smooth muscle at the neck to prevent premature ejaculation.

Females: formed by the neck of the bladder.

External:

The same in both.
- skeletal muscle. Voluntary.

220
Q

Briefly describe the gonads and the differences between male and female.

A

Males:

Urinary and reproductive exocrine duct share the urethra. Genitalia are external. Penis and scrotum. Prostate is internal.

Two membranes; (tunica) vaginalis (visceral and parietal layers) and albuginea (lobules and seminiferous tubules).

Sperm: Produced in seminiferous tubules, travel to epididymis. Leave via ductus deferens/ vas deferens- enters prostatic urethra.

Female:

Internal. Separate from urethra.

Ovaries, no direct contact with the tract. Uterine tubules provide transport for eggs.

Produce: oestrogen and progesterone.

221
Q

Watch an Armando video on the kidneys.

Describe the microscopic structure and physiology of their kidneys.

222
Q

Describe the prostate gland.

A
  1. . Located inferior to the neck of the bladder and superior to the external urethral sphincter.
  2. Secretes proteolytic factors that prevent coagulation of semen. Prostate Specific Antigen.
  3. Four regions.
    - Peripheral zone, contributes 7080% of Prostatic Ca.
    - central zone, very invasive if Ca.
    - Transitional zone - BPH.
    - Anterior zone - connective tissue.
223
Q

What is Benign Prostatic Hyperplasia?

A

The benign growth of the transitional zone of the prostate, causing organ enlargement.

High levels of DHT are thought to contribute.

224
Q

What are the signs and symptoms of BPH?

A
  1. Difficulty peeing
  2. Incomplete urination
  3. Frequent urination
  4. Stop-start-slow stream.
  5. Urgency to pee
225
Q

Describe the production and maturation of sperm in males.

A
  1. Immature sperm produced in the seminiferous tubules. Travel to rete testes via straight tubules.
  2. Travel to epididymis via efferent ductules. Mature here.
  3. Ejected via the ductus deferens - vas deferens - prostatic urethra.
226
Q

Watch an Armandoh video on nephrology.

Describe filtration of the kidneys

A

Just do it.

227
Q

Describe renal flow.

There’s 13 steps.

A
  1. Renal artery
  2. Segmental artery
  3. Interlobar artery
  4. Arcuate artery
  5. Interlobular artery
  6. Afferent arteriolar
  7. Glomerular capillaries
  8. Efferent capillaries
  9. Peritubular capillary.
  10. Interlobular vein
  11. Arcuate vein
  12. Interlobar vein
  13. Renal vein
228
Q

Describe normal bladder function.

A

Influence by Anti Diuretic Hormone.
Max ADH: 1mL/min
Min ADH: 20mL/min

Micturition:

Three phases.

  1. Storage phase.
    - passive filling.
    - Stretch sensation is received by the Sacral Spine S2-24.
    - hypogastric nerve at T12-L2 causes relaxation of the detrusor muscle (BA-R) and constriction of the internal sphincter (AC-R).
    - Pudental nerve is stimulated - external sphincter constricts (N-R).
    - pressure builds up.
  2. Voiding phase
    - desire to urinate around 300mLs.
    - stretch receptors detect filling.
    - micturition centre inhibit hypogastric nerve.
    - parasympathetic fibres cause contraction of the detrusor muscles.
    - desire reduces once voiding begins.
  3. Reflex phase
    - parasympathetic nerve is innervated to keep bladder contraction until urine is voided.
229
Q

Define screening

A

Screening is a Public Health Service which tests a defined population for risk of a certain disease.

It is not diagnostic.

230
Q

State 10 criteria of screening.

Past question asks for six

A
  1. The condition must be important to the population and the individual.
  2. There should be an accepted treatment for those diagnosed.
  3. There should be facilities for diagnosis treatment.
  4. There should be a recognisable early/ asymptomatic stage.
  5. There should be a suitable test
  6. Test should be acceptable to the target population
  7. The disease pathology should be adequately understood.
  8. There should be agreed policy of who to treat.
  9. Cost to benefit ratio acceptable.
  10. Should have follow up.
231
Q

Name three screening programmes and their target age range.

A
  1. Cervical Cancer.
    - smear test
    - Women 25-65
    - 25-49 every 3 years
    - 50-65 every 5 years.
  2. Breast Cancer.
    - mammogram
    - women 50-70
    - every 3 years.
  3. Bowel Cancer
    - two samples from bowel movements.
    - men and women 50-74
    - every two years.

Additional -

  1. Abdominal Aortic Aneurysm.
    - ultrasound
    - men over 65.
  2. New born screening
    - new borns
    - physical
    - hearing
    - blood spot
232
Q

Describe thermoregulation.

A

The maintenance of core body temperature at 37c (+/- 0.5)

Two thermoreceptors:

  1. Hypothalamic
    - arterial flow through the brain.
    - also acts as the control centre.
  2. Peripheral
    - the external environment.

Involuntary responses (in heat)

  1. Vasodilation
  2. Sweat
  3. Hairs relax

Visa versa in cold - with shivers, adrenaline and increased metabolism.

Voluntary behaviour:

Heat

  • doth clothing
  • find shade
  • take on fluids

Cold

  • don clothing
  • seek shelter
  • huddle
  • try not to die
233
Q

Describe the physiology of fever.

A

Elevation of core body temperature at the “thermostat” in the hypothalamic temperature control centre.

  1. Response to infection. IL-1 is released. Pyrogenic.
  2. Prostaglandins secreted in the brain. The thermostat is reset.
  3. Heat increase is promoted. Vasoconstriction.
  4. Adrenaline and thyroxine increase metabolism.
  5. Shivers generate heat.
  6. Erector pili contract. “Chill phase” - cold sensation on skin.
  7. Pyrogens decrease, and the hypothalamus resets. Heat loss is then promoted.
  8. Sweating and peripheral vasodilation.
  9. Erector pili relax - crisis phase.
  10. Antipyretics, such as paracetamol, inhibit COX enzymes in the CNS to prevent prostaglandin production. Analgesic.
234
Q

Describe the anatomy of the ear.

A

Three regions.

Outer

  • pinna/ auricle.
  • sebeceous and ceramenious glands. - external auditory meatus

Middle

  • tympanic membrane
  • auditory ossicles (malleus, Incas, stapes)

Inner

  • vestibule
  • cochlea
  • round and oval windows.
  • semi-circular canals
  • vestibular nerve (balance)
  • auditory nerve (hearing)
235
Q

Describe the physiology of hearing

A
  1. Sound (changes in air pressure). Travel down auricle and external auditory meatus.
  2. Sound is received by the tympanic membrane.
  3. Sound is transferred (back and forth) Malleus - Incas - stapes (amplified by x22)
  4. These auditory ossicles concentrate movement . Stampeding-vestibular joint transfers sound through the oval window.
  5. Oval window moves back and forth - fluid pressure waves in the peri lymph of the scala vestibuli.
  6. Travels to the scala tympani (tympanic duct).
  7. Travels to the round window - relieves pressure.
  8. This pressure wave moves end of lucid in the scala media (cochlear duct) against the organ of corti via the basilar membrane.
  9. Hairs of the organ of corti brush against the tectorial membrane, which stimulates stereocilia to stimulate CNVIII. Higher pitch - low pitch.
236
Q

Describe the RAA system

A

Aims is to raise blood pressure.

Three mechanisms from the junta-medullary apparatus.

  1. Baroreceptors (- BP in the kidneys in the afferent arterioles)
  2. Sympathetic nerve stimulation (B1-AN)
  3. Macula densa mechanism (DCT detects NaCl. Low? = Renin.

Renin (an enzyme) converts angiotensinogen to angiotensin I. Travels to the lung, and is converted by Angiotensin Converting Enzyme (ACE) to Angiotensin II.

Angiotension II works on the Pituitary Gland (ADH) and the Adrenal Gland (Aldosterone) to raise blood pressure. Auto regulated loop.

237
Q

Describe eye anatomy.

A

Three layers.

  1. Fibrous layer(s)
    - cornea (central passage for light)
    - sclera (white of eye)
  2. Vascular layer
    - Iris (colour)
    - Pupil (light into eye)
    - Lens (focuses light)
    - ciliary body (controls lens shape)
    - chloroid (dark pigment, limits reflection)
  3. Retina
    - neural portion
    - pigmented part (rod cells and cone cells)

Cavities:

  1. Anterior - two. Anterior, posterior. Aqueous humour.
  2. Posterior - behind iris. Virtuous humour.

Optic nerve, CNII.

Orbital stuff:

Superior rectus - CNII

Inferior rectus - CNII

Lateral rectus - CNVI

Medial rectus - CNII

Superior oblique - CNIV

Inferior oblique - CNII

238
Q

What cranial nerve is responsible for vision?

A

CNII - Optic.

239
Q

Name the eye muscles and then nerve that innervates each.

There are six.

A
  1. Superior rectus - CNII (Oculomotor)
  2. Inferior rectus - CNII (Oculomotor)
  3. Lateral rectus - CNVI (Abducens)
  4. Medial rectus - CNII (Oculomotor)
  5. Superior oblique - CNIV (Trochlear)
  6. Inferior oblique - CNII (Oculomotor)
240
Q

Describe tear production and drainage.

A
  1. Produced by the lacrimal glands. Superior and lateral to the orbit.
  2. Secreted onto the eye and drains lateral to medial and superior to inferior.
  3. Drains to the lacrimal sac via the nasolacrimal gland.

Functions: Lubricates the eye and removes dirt// washes the eye.

241
Q

Name the bones of the orbit and the borders.

A

Apparently we should patch the borders.

Bones:

  1. Maxilla
  2. Zygomatic
  3. Frontal
  4. Palatine
  5. Ethmoid
  6. Sphenoid
  7. Lacrimal
242
Q

Name the three cavities and four sinuses found in the skull.

A

3 cavities:

  1. Nasal cavity
  2. Oral cavity
  3. Orbit

4 Sinuses:

  1. Frontal
  2. Maxillary
  3. Sphenoid
  4. Ethmoid
243
Q

Describe the structure of the nose.

A

Structure:

  1. External nares
  2. Conchae (superior, middle, inferior)
  3. Internal nares
  4. Nasopharynx
  5. Nasolacrimal glands.
  6. Pseudostratified ciliated columnar epithelium, goblet cells.
  7. Olfactory epithelium at the posterior wall. CNI (Olfactory)

Functions in breathing:

  1. Filters air
  2. Warms and humidifies air.
244
Q

Describe the innervation of the tongue.

A
  1. Anterior 2/3
    - Lingual branch of the mandibular division of the trigeminal nerve (CNIII)
    - taste - CNIII and facial nerve - CNCVII.
  2. Posterior 1/3
    - glossopharangeal (CNIX)
  3. Movement
    - hypoglossal - CNXII
245
Q

Name the cranial nerves and their function.

A
  1. CNI Olfactory - Smell
  2. CNII Optic - Sight
  3. CNIII Oculomotor - Movement of the eye
  4. CNIV Trochlear - Superior oblique
  5. CNV Trigeminal - taste, hearing.
  6. CNVI Abducens - Stapedius muscle
  7. CNVII Facial - tears and taste.
  8. CNVIII Vestibulocochlear - Hearing and balance
  9. CNIX Glosspharyngeal - Posterior 1/3 of the tongue
  10. CNX Vagus - Heart, bronchi and lungs
  11. CNXI (Spinal) Accessory - Trapezius
  12. CNXII Hypoglossal - Movement of the tongue.
246
Q

Define the term Bacteriocidal

A

An agent that kills bacteria

  • Penicillin
247
Q

Define the term Bacteriostatic

A

An agent that inhibits bacterial growth

  • Trimethoprim
248
Q

Give examples of antibiotics and their mechanism of action.

A
  1. Cell Wall Synthesis
    - Glycoproteins (Vancomycin)
    - Beta-Lactams (Pennicillins)
  2. Protein Synthesis
    - Macrolides (Azithromycin)
    - Tetracylins (Tetracycline)
  3. DNA Synthesis
    - Quinolones (Ciprofloxacin)
  4. Metabolism
    - (Trimethoprim)
249
Q

In the brain, what is the Frontal Lobe responsible for?

A

Movement, co-ordination. Executive function. Higher thinking (reasoning, planning). Memory.

250
Q

In the brain, what is the Parietal Lobe responsible for?

A

Sensation and sensory information.

251
Q

In the brain, what is the Occipital Lobe responsible for?

A

Interpretation of visual data.

252
Q

In the brain, what is the Temporal Lobe responsible for?

253
Q

In the brain, what is the Broca Area responsible for?

A

Speech.

Frontal Lobe

  • clinically, if this is damaged, the patient can understand conversation but not speak.
254
Q

In the brain, what is the Wernicke Area responsible for?

A

Language and reading.

Parietal/ temporal lobe.

  • clinically, if this is damage, the patient is able to speak however the words will amount to nonsense.
255
Q

What are the deep structures of the brain?

A

Four main structures.

  1. The Limbic System
    - emotion, behaviour, learning and memory (via the hippocampus)
  2. Basal Ganglia
    - control of movement and reward centre.
  3. Hypothalamus
    - homeostasis
  4. Thalamus
    - relays sensory information between the spinal cord and cerebral cortex.
256
Q

What are the layers of the meninges (superficial - deep).

A
  1. Dura Mater
  2. Arachnoid Mater
  3. Pia Mater - this is where the CSF is found.
257
Q

What are the functions of CSF?

A
  1. Nutritional support
  2. Clearance of metabolites
  3. Maintains intracranial pressure/ brain density
  4. Bouyancy
  5. Protect: shock transmission
  6. Prevent: ischaemia
  7. Homeostasis
258
Q

What are the three basic mechanisms by which bacteria are awarded resistance to antibiotics?

A
  1. Mutation of the target
  2. Expression of inactivating enzymes
  3. Reduced access. (Expression of efflux pumps, lack of transport channels)
    - an example is B-Lactams resistance is conferred by altered porins (reduced uptake)
    - expression of B-Lactamases. (Can be countered by anti-enzymes like Tazocin)
259
Q

What are the three methods of antibiotic usage?

A

Guided: ideal, specific. Investigation dependant.

Prophylactic: prevention. Targeted at high-risk groups.

Empiric: based on clinical judgement. The best guess, with broad spectrum abx.

260
Q

What are the four allergic reaction types to antibiotics?

A

Type I - Anaphylaxis
Type II - Haemolytic Anaemiaa
Type III - Vasculitis
Type IV - Delayed

  • non allergic reactions exist. D&V, seizures, bone marrow dysfunction.
261
Q

What are the three germ layers Post gastrulation?

What example tissues arise from each?

A
  1. Ectoderm
    - the skin, epithelial layers of the mouth and anus..
  2. Mesoderm
    - skeletal system, muscular system, dermis.
  3. Endoderm
    - epithelial layers of the intestinal tract, liver, thymus.
262
Q

What does PICO stand for?

A

P: Population, problem or patient.
I: Intervention
C: Comparator, control
O: Outcome

263
Q

What is Binge Eating Disorder?

A

Frequent or recurrent episodes of binge eating with compensatory behaviour.

  • eating very quickly
  • eating until uncomfortable full
  • eating lots when not hungry
  • eating alone due to embarrassment
  • feeling extreme guilt after eating
264
Q

What is Anorexia Nervosa?

A

A significant deficit in weight for the patients age, height and developmental stage, with persistent patterns that block restoration of normal body weight.

Clinical criteria: BMI <18.5. Under 5th percentile in adults and children.

265
Q

What is Bulimia Nervosa?

A

Recurrent episodes of overeating, accompanied with inappropriate compensatory behaviour. Patients may make an effort to block wright gain.

S/S - eroded teeth, Russell’s sign (purging, scratches on the back of the hand).

May be within normal BMI, which separates it from Anorexia Nervosa.

Can lead to G.I complications, cardiac arrhythmia and kidney damage.

MBChB 1 (3 decks)

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