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GEM > Module 1 Structure, function & defence > Flashcards

Module 1 Structure, function & defence Flashcards

1
Q

Define the term pharmacodynamics

A

A drug’s mechanism of action

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2
Q

Name the four broad structural types of receptors.

A

Ligand-gated ion channel, G protein coupled (or 7 transmembrane), tyrosine kinase and cytoplasmic/nuclear.

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3
Q

What are the two broad subtypes of receptors for acetylcholine and their different topology

A

Nicotinic - Ion channel
Muscarinic 7TD receptor with intra and extracellular domains

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4
Q

By what characteristics can drugs be classified by?

A

therapeutic use, mode of action, chemical structure

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5
Q

Name two diseases that stem from mutations to one amino acid and how they come about.

A

Cystic Fibrosis - CTFR ion channel structure is changed which controls Na and Cl movement causing excess mucous to gather in the airways
Sickle Cell disease - Point mutation changes the shape of the erythrocytes

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6
Q

What is desensitization and tolerance?

A

Prolonged treatment can reduce the efficacy of a drug due to receptor desensitisation and can eventually lead to total tolerance.

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7
Q

Describe Y linked inheritance and give an example.

A

Male only inheritance due to only males having X Y chromosomes; webbing of the 2nd and 3rd toes.

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8
Q

Are male or females affected predominantly by X linked recessive? Give an example of a X linked recessive disease.

A

Males are, as they only require 1 copy of the gene to express the phenotype. Haemophilia - defective factor VIII gene involved in clotting

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9
Q

Describe Mendelian autosomal dominant, with an example.

A

Disease is expressed with heterozygous and homozygous patients, for example familial hypocholesteraemia - defective LDL receptor gene on chromosome 19.

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10
Q

Describe Mendelian autosomal recessive, with an example.

A

Require two copies of the defective gene to express the condition, for example cystic fibrosis - CPTR gene on C7. Can be a carrier for autosomal recessive conditions

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11
Q

Describe mitochondrial inheritance

A

Circular DNA that is solely maternal - paternal mitochondria excluded during fertilisation. Conditions such as neuropathy. Can be passed on to male and female offspring but only females can pass on the condition.

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12
Q

Inbreeding/consanguinity causes ….., for example……

A

A higher rate of genetic defects, such as ataxia telangiectasia - coordination issues with movement and speech, enlarged vessels in the eye and an increase in alpha fetoprotein in the blood

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13
Q

What causes down syndrome?

A

An extra Chromosome 21.

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14
Q

Define Autocrine, Paracrine, Endocrine, Neurocrine and juxtracrine, with examples.

A

Autocrine signalling acts on the signalling cell itself - IL-4 in monocytes.
Paracrine signalling acts on nearby cells - Thromboxin from platelets to further clotting cells.
Endocrine signalling uses the circulatory system - hormones.
Neurocrine is nerve signalling.
Juxtacrine is physical contact, such as leukocytes using adhesion molecules on EC.

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15
Q

What are the four basic tissue types in the body, and give an example of how they are arranged in tissues.

A

Connective tissue, epithelial tissue, muscle tissue, and nervous tissue. E.g. GI Tract layers involves epithelium around the lumen, multiple layers of differing connective tissue, and muscle; all arranged in a tubular formation.

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16
Q

Name the 3 simple forms of epithelia, their structure (nuclei included) and its function. What does simple mean in this sense?

A

Simple means monolayer structure.

Squamous - Flattened nuclei. Facilitates passive diffusion of gases or fluids. Large protective sheets (mesothelium) lining the body cavities.

Cuboidal - Central nuclei. Usually found lining small ducts and tubules. May have excretory or absorptive functions.

Columnar - Basal stretched nuclei. Most frequently associated with absorption and secretion. May have microvilli on apical surface for increased surface area. Stratified columnar epithelium: rarer several-layered variant e.g. in urethra, anus

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17
Q

What is meant by pseudostratified columnar ciliated and where is it exclusively found?

A

Variant of simple columnar found almost exclusively in the respiratory tract, sometimes referred to as respiratory epithelium.
1 layer appearing as multiple layers; all are attached to the basement membrane.

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18
Q

Describe Stratified squamous keratinizing and non-keratinizing epithelium, and why its structure fits its function.

A

Non-keratinizing - Lots of cell layers: cuboidal in shape near basement membrane, squamous at surface.
Protective function: well adapted to withstand stress and mechanical abrasion
Found at openings to the outside world.

Keratinizing - Adapted to withstand mechanical and chemical damage as well as water loss – epidermis of skin. Keratin: intermediate filament that builds up in the cells

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19
Q

What is urothelium?

A

Only found in ureter and urinary bladder
Adapted to withstand stretch of bladder wall and the toxicity of urine
Umbrella cells: surface cells that can stretch extensively

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20
Q

Name the 5 functions the basement membrane can have

A

Adhesion
Partition
Barrier/permeability
Anchorage for cell organisation
Controlling growth and differentiation

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21
Q

What is the composition of the basement membrane?

A

Composed mainly of type IV collagen, glycoproteins (laminin secreted by epithelial cells, fibronectin from fibroblasts) and glycosaminoglycans (GAGs)

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22
Q

What are the key structural components on the cytoskeleton?

A

Microfilaments: thin strands of the protein actin that determine the shape of the cell membrane e.g. microvilli

Intermediate filaments: thicker strands of protein that provide mechanical strength e.g. keratin in hair

Microtubules: much larger, determine the movement of cell organelles and intracellular vesicles
Made of tubulin
Grow from centrosome and extend to cell periphery, form mitotic spindle for cell division
Form the core of cilia

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23
Q

What are the four cell cell junctions?

A

Tight junctions
Membranes of adjacent cells are sealed together at points to prevent transport of substances between the cells.

Intermediate junctions (adhering junctions)
Connect actin microfilaments in cytoskeletons of adjacent cells to help maintain integrity of epithelium

Desmosomes
Connect intermediate filaments (e.g. keratin) of adjacent cells to maintain integrity of epithelium.
Hemidesmosomes attach to basement membrane

Gap junctions
Communication between adjacent cells e.g. passage of ions, small molecules

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24
Q

How does the structure of Exocrine glands differ to Endocrine?

A

Exocrine glands: hollow duct forms to the epithelial layer, allowing release of secretions e.g. sweat glands, liver

Endocrine glands: connection to epithelium lost, blood vessels form around the secretory portion to allow for release of secretions e.g. pancreatic islets

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25
Q

Exocrine secretion happens in 3 main ways? List them

A

Merocrine (eccrine): cell vesicles release product via exocytosis e.g. sweat glands

Apocrine: vesicles bud off cell with product

Holocrine: entire cell ruptures e.g. sebaceous glands

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26
Q

Name 2 autoimmune conditions caused by cell junction defects.

A

Pemphigus vulgaris: antibodies destroy desmosomes, leading to blisters affecting skin and mucous membranes (e.g. mouth)

Bullous pemphigoid: antibodies attack hemidesmosomes, leading to raised skin rash and large fluid-filled blisters where epidermis and dermis have separated

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27
Q

Connective tissue can have 7 functions. List them?

A

Binding, packing and support
Skeletal framework
Protection
Insulation
Transportation / nourishment
Immunological defence
Repair (scar tissue)

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28
Q

Name the four types of connective tissue cells, and their common name where necessary.

A

Fibroblasts: primary cell types producing ECM in connective tissue

Adipocytes: storage and metabolism of fat, protecting internal organs

Chondroblasts and chondrocytes (cartilage)

Osteoblasts, osteocytes, osteoclasts (bone)

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29
Q

What are Ehlers Danlos syndromes?

A

Reduced tensile strength from collagen disorders causes tissue laxity, joint hyper mobility and susceptibility to injury

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30
Q

There are 3 main types of ordinary connective tissue. Name them and describe their structure/function.

A

Loose, areolar - Widely distributed below epithelia
Forms the lamina propria of a mucosa
Surrounds capillaries

Dense irregular (fibrous) - Found in dermis, submucosa of digestive tract, fibrous capsules surrounding organs etc.
Predominantly collagen fibres, densely packed and irregularly arranged

Dense regular (fibrous) - Predominantly collagen fibres running in parallel. Found in: Ligaments (bone to bone), Tendons (muscle to bone), Aponeuroses (modified flattened tendons found on abdomen and back)

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31
Q

What does a peripheral nerve consist of?

A

Bundles of nerve fibrescalledfascicles

Dense connective tissue covering the nerve fibres and fascicles, binding them together (endoneurium, perineurium and epineurium)

Small blood vessels (vasa nervorum) supplying the nerve tissue

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32
Q

Describe the layers of the GI tract.

A

the mucosa (epithelium, lamina propria, and muscular mucosae), the submucosa, the muscularis propria (inner circular muscle layer, intermuscular space, and outer longitudinal muscle layer), and the serosa.

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33
Q

Describe ion movements involved in a sodium calcium exchanger.

A

Na+ is pumped out in exchange for K+, Na+ comes back across the membrane down its conc. gradient, Ca2+ is exchanged for this Na+ to keep intracellular levels extremely low.

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34
Q

What are the fat soluble vitamins?

A

A, D, E and K (A Dairy Eater Knows) Dairy is fatty

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35
Q

What are the water soluble vitamins?

A

B complex, C

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36
Q

Name the essential compounds, that are not energy yielding.

A

Vitamins, Minerals, Essential fatty acids, Essential amino acids, Ions and cholesterol etc.

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37
Q

There are 6 electrolytes. Name them

A

K, Na, Cl, Ca, Mg, P

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38
Q

What are the essential fatty acids? What are they needed for?

A

Omega 3, Omega 6.
Needed for eicosanoids (a class of non-protein bioactive molecule)
Examples of eicosanoids - prostaglandins, thromboxanes, leukotrienes
These signal molecular mediated inflammation, pain and also modulate cell activities including cancer cell production

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39
Q

What is vitamin k key for?

A

It is a blood clotting factor

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40
Q

B6, 12, 7, 9 and 5 are …… vitamins

A

Group transfer agent

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41
Q

Vitamins A and D are precursors for?….

A

Hormones

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42
Q

What are the three psychosocial theories for life development

A

Psychoanalytical, Cognitive and Sociocultural

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43
Q

What are the four attachment stages in child development?

A

Asocial, indiscriminate, specific, multiple
6 weeks 7 months 9 months

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44
Q

What is attachment, in terms of child development?

A

Deep and enduring emotional bond that connects one person to another across time and space

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45
Q

Child development - compare secure attachment to insecure and resistant.

A

Secure = A child can be comforted back to normal after separation.
Insecure/Resistant = Cannot be comforted or shows no anxiety at all

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46
Q

What are the 3 main physical checks are done for children after birth and when?

A

Vision - Within 72 hours of birth
Between 6-8 weeks old
At 1 year or between 2-2.5 years
At 4-5 years (pre-school)

Hearing - Within a few weeks of birth
9 months - 2.5 years: parental concerns
At 4 - 5 years (pre-school)

Walking - Infants walk by 13 months of age
Not walking by 18 months of age is a red flag.
Cases such as down syndrome differ from this - Bottom shuffling ma be utilised by the baby for movement

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47
Q

What is a condition called if it has an unknown cause?

A

Idiopathic

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48
Q

What is a latrogenic condition?

A

A condition caused by medical personnel or procedures (treatment/diagnostic test) or that develops through exposure to the environment of a health care facility.

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49
Q

Contrast hypertrophy and hyperplasia.

A

Hypertrophy
Increase in the size of cells
No new cells - just bigger
Can be physiological or pathological
Cells that don’t divide e.g. cardiac and skeletal muscle
Examples: hypertension - cardiac muscle, exercise

Hyperplasia
Increase in the number of cells
Cells that can divide; For example: breast development at puberty, liver regeneration after resection, wound healing
E.g. psoriasis leads to thickened skin

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50
Q

Name an example in which hyperplasia and hypertrophy occur simultaneously.

A

Uterine enlargement during pregnancy; Smooth muscle.

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51
Q

What is the shrinkage of cell size called due to a loss of cell substance? example?

A

Atrophy
e.g. immobilisation/ageing limb muscle

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52
Q

What is involution? example?

A

Reduction in number of cells - apoptosis. Myometrium of uterus post partum

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53
Q

What is Metaplasia and what can it lead to?

A

Change in type of cell
Reprogramming of stem cells
Survival mechanism in response to injury e.g. Smoking
Specialised function is lost
Can predispose to neoplasia

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54
Q

What is neoplasia?

A

Not an adaptive response

Permanent alteration of normal cellular growth pattern
Abnormal proliferation in the absence/removal of stimulus

Do not respond to normal signals controlling growth
Dysregulated control mechanisms lead to uncontrolled proliferation

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55
Q

What is the normal cell:plasma ratio in blood?

A

cells 45%; plasma 55%

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56
Q

What is serum?

A

Plasma with clotting factors removed

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57
Q

Name 2 components of blood plasma.

A

Albumin - Colloid osmotic pressure (oncotic pressure)
Transporter
Produced in liver
Hypoalbuminemia (low)
Hyperalbuminemia (high)
Marker of inflammation

Fibrinogen - Soluble precursor to Fibrin - clotting factor

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58
Q

5 types of Leucocytes and the 2 categories they fall within? What are their functions?

A

Granulocytes
Neutrophils
Basophils
Eosinophils

Mononuclear leucocytes
Lymphocytes
Monocytes

Neutrophil: leave circulatory system in response to tissue damage. Remove damaged tissue and kill and phagocytose invading organisms. Increased in bacterial infection.

Eosinophil: Phagocytic (anti-body labelled material), elevated in allergic reactions and in parasitic infection

Basophil: Release heparin and histamine that promote inflammation.

Lymphocyte: immunologic response (antibodies). Increased in viral infections (infectious mononucleosis)

Monocyte: Phagocytosis. Rarely elevated. In tissue is called a macrophage

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59
Q

There are 6 blood analysis measurements. Name them.

A

Haematocrit (HCT): The fraction of the blood composed of red blood cells
Erythrocyte sedimentation rate (ESR): The rate at which the red blood cells settle to the bottom of the test tube.
Haemoglobin (Hb): Total amount of haemoglobin in the blood
Mean cell haemoglobin (MCH): calculated using Hb and RBC
Mean cell volume (MCV): average volume of a red blood cell
Mean cell haemoglobin concentration (MCHC): average concentration of Hb in a given volume of packed red blood cells

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60
Q

Discuss Mean Cell Haemoglobin ranges.

A

MCH varies in direct linear relationship with the MCV. Cells with less volume contain less Hb and vice versa

MCH increase: B12 deficiency, folic acid deficiency, haemolytic anaemia
MCH decrease: iron deficiency anaemia, thalassemia

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61
Q

What is the suffix for MCV ranges?

A

-cytic

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62
Q

What is the suffix for MCHC?

A

-chromic

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63
Q

Name the 3 main types of anaemia and how they are caused.

A

microcytic anaemia - Iron deficiency

alpha thalassaemia , beta thalassaemia - Haemoglobinopathies

macrocytic anaemia - B12 / folate deficiency / pernicious anaemia

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64
Q

What are the 5 cardinal signs of inflammation

A

Rubor, Calor, Tumor, Dolor, Functio laesa

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65
Q

Describe the vascular events that occur during the onset of acute inflammation and what it allows.

A

Local blood vessels briefly contract and then dilate to slow the flow of blood to the area; mediated by mast cells (histamine) and endothelial cells (nitric oxide)
Vascular permeability is increased allowing protein –rich plasma to leave the vessels and enter the tissue: the inflammatory exudate
The slowing of flow allows neutrophils to come into contact with the (activated) endothelium

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66
Q

What does inflammatory exudate contain?

A

Plasma and proteins (lots of fibrinogen)
Neutrophils and some macrophages and lymphocytes

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67
Q

Name the cells and proteins involved in inflammation.

A

Main cell is neutrophils but also ECs, macrophages, lymphocytes, platelets, fibroblasts, complement system.

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68
Q

Explain neutrophil extravasation

A

Rolling - Selectins expressed on activated EC surface.
Adhesion - Integrins expressed on neutrophil.
Shape change - CD11 and 18 on EC bind
Extravasation - PECAM1 on both cells facilitates the trans-endothelial emigration.

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69
Q

Name the 4 enzyme cascades of plasma mediators

A

Coagulation system (activated Hageman factor - coagulation factor XII) converts fibrinogen into fibrin, also activates the kinin & fibrinolytic systems

Kinin system e.g. bradykinin – mediates pain

Fibrinolytic system e.g. plasmin – affects fibrin

Complement

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70
Q

Name the mediators of the following inflammatory responses: Vasodilatation

A

Vasodilatation - Histamine, prostaglandins, nitric oxide, bradykinin, PAF

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71
Q

Name the mediators of the following inflammatory responses: Increased vascular permeability

A

Increased permeability -Histamine (transient), C3a, C5a, bradykinin, leukotrienes, PAF, nitric oxide (longer acting)

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72
Q

Name the mediators of the following inflammatory responses:
Neutrophil adhesion

A

Neutrophil adhesion - Adhesion molecules on endothelium are up-regulated by IL-1, IL-8, TNFα, PAF, LeukotrieneB4, C5a, chemokines

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73
Q

Name the mediators of the following inflammatory responses: Neutrophil chemotaxis

A

Neutrophil chemotaxis - C5a, Leukotriene B4, bacterial components, chemokines IL-8

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74
Q

Name the mediators of the following inflammatory responses: Fever

A

IL-1, TNF, prostaglandins

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75
Q

Name the mediators of the following inflammatory responses: Pain

A

Prostaglandins, bradykinin

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76
Q

Name the mediators of the following inflammatory responses: Tissue necrosis

A

Neutrophil lysosomal granule contents, Free radicals generated by neutrophils

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77
Q

What mediators of inflammation are preformed in secretory granules and what cells produce them.

A

Histamine and serotonin - Mast cells, basophils and platelets and in platelets respectfully.

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78
Q

Where are the following inflammatory mediators produced?

• Histamine
• Serotonin
• Prostaglandins
• Leukotrienes
• Platelet-activating factor
• Reactive oxygen species
• Nitric oxide
• Cytokines (e.g. TNF, IL-1)
• Chemokines

A

• Histamine - Mast cells, basophils, platelets
• Serotonin - platelets
• Prostaglandins - Mast cells, leucocytes
• Leukotrienes - Mast cells, leucocytes
• Platelet-activating factor - Leucocytes, ECs
• Reactive oxygen species - Leucocytes
• Nitric oxide - Endothelium, macrophages
• Cytokines (e.g. TNF, IL-1) - Macrophages,
lymphocytes, endothelial cells, mast cells
• Chemokines - Leucocytes, activated macrophages

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79
Q

Most inflammatory mediators are cell derived, which aspects are plasma protein derived?

A

Complement and Factor XII activation (kinin and coagulation system)

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80
Q

What are the main 4 acute phase proteins? (inflammation) and what are they responsible for?

A

Fibrinogen,
C reactive protein (CRP),
Serum amyloid A (SAA)
Ferritin

Responsible for systemic effects of inflammation

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81
Q

Name 2 systemic effects of inflammation.

A

Mediated by cytokines (mainly from activated macrophages)
act on the brain to increase temperature (fever), reduce appetite and increase fatigue.
act on the bone marrow to increase the production of neutrophils (particularly in bacterial infection)

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82
Q

Contrast tissue resolution and repair

A

Tissue resolution –restitution of normal tissue structure and function. If damage occurred to just the parenchyma.
Repair by fibrosis – scar formation via granulation tissue formation and organisation. Occurs when damage occurs to the stroma as well.

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83
Q

Name the 4 possible outcomes of acute inflammation

A

Tissue resolution
Repair by fibrosis
Abscess formation
Chronic inflammation

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84
Q

Tissue repair can depend on the regenerative capability of the damaged cells. What are the 3 types of regeneration ability/

A

Labile – replicate throughout life; skin and GI epithelium

Stable – Non-dividing in normal circumstances but capable of regeneration – liver/kidney parenchyma

Permanent – non-dividing cells; nerves, cardiac/skeletal muscle

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85
Q

Name the 3 stages of healing by fibrosis.

A

Granulation tissue
Macrophages, fibroblasts and new blood vessels (angiogenesis)

Fibrosis and scar formation - Fibroblasts lay down matrix. Scar is formed as amount of collagen laid down is increased to strengthen the tissue

Remodelling
Over time the number of vessels is reduced and a pale scar remains

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86
Q

Describe the proliferative phase of tissue repair (Skin)

A

Granulation tissue - Building tissue to fill the wound
Fibroblasts secrete: Matrix components, Growth factors to stimulate angiogenesis
Epithelial cells re-grow over the wound

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87
Q

Describe wound contraction and remodelling.

A

Due to the action of fibroblasts laying down collagen and collagenases breaking down collagen to orientate for maximal tensile strength.
Wound contraction
Decreased vascularity

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88
Q

What are the stages of tissue repair in skin?

A

Proliferation > wound contraction > remodelling

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89
Q

Name a model disease regarding chronic inflammation.

A

Gastric Ulcers - Damage and repair occurring simultaneously

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90
Q

What is innate immunity

A

General non specific immunity that does not evolve. e.g. PAMP recognition

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91
Q

What are the primary lymphatic tissues?

A

Bone marrow and the Thymus
Haematopoiesis and T cell maturation respectively

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92
Q

What are the three pathways that activate the complement system?

A

Classical
C1q binds to the Fc regions of these antibodies that are bound to microbial antigens. This activates C1r and C1s that are associated with C1q, leading to the conversion of C4 and C2. The fragments C4b and C2a combine to form C4b2a, which has C3 convertase activity.
Lectin
When mannose binding lectin interacts with microbes, it activates MBL-associated serine proteases that convert C4 and C2, generating C4b2a, aka C3 convertase.
Alternate
Circulating C3b fragments, from the other pathways or spontaneous cleavage of C3, can be stabilised on microbial surfaces with another complement protein to form a version of C3 convertase

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93
Q

Name the 5 antibody isotypes and their abilities.

A

M - first to be expressed, activates complement, pentamer interactions

A - 2nd most abundant found in secretions such as saliva and breast milk, can act as a homodimer.

D - Found on lymphocytes

G - Most abundant, transplacental

E - On basophils, mast cells - involved in allergy response.

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94
Q

Compare and contrast MHCI and II

A

Class I - a1, 2, 3 and B2. CD8+ interaction, on every nucleated cell, endogenous antigens.

Class II - a1, 2, B1, 2, CD4+ interaction, on APCs, exogenous antigens.

Both formed in the endoplasmic reticulum.

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95
Q

Name the major components of the lymphatic system.

A

Thymus, Lymph Nodes, Spleen, Mucosa associated lymphoid tissue, Specialised fixed phagocytes.

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96
Q

Capillaries can be…, …. or ….

A

Continuous – no gaps in wall or basement membrane

Fenestrated - gaps in wall but basement membrane still continuous e.g. small intestine, endocrine organs, kidney

Sinusoidal (gaps in both wall and basement membrane e.g. spleen, liver, bone marrow)

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97
Q

Name the main lymph nodes and where to locate them.

A

Cervical nodes - along internal jugular vein in the neck

Pericranial- base of head

Axillary nodes - in axilla- armpits

Tracheal nodes

Deep nodes - aorta, celiac trunk and mesenteric arteries

Inguinal - pelvic area

Femoral - inside leg in crotch

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98
Q

Describe the draining of lymph into the venous circulation

A

Lymph from right side of head & neck + right upper limb and right thorax will drain into right lymphatic duct and into the junction between the right subclavian vein and right internal jugular vein – right venous angle

Lymph from all other body regions drains into thoracic duct and then into the junction between the left subclavian vein and left internal jugular vein – left venous angle

Lymph from lower half of body initially drains into cisterna chyli

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99
Q

Describe lymph node structure and cell organisation.

A

Small bean-shaped structures that act as filters to trap and phagocytose particulate matter in the lymph.

Macrophages in subcapsular sinus and medulla

Clusters of lymphocytes e.g. B cells in lymphoid follicles, T cells in paracortical area

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100
Q

Why are lymph nodes susceptible to secondary tumours?

A

Flow through lymph nodes is slow, so metastatic cells e.g. from a primary tumour in the breast may lodge in lymph nodes and grow as secondary tumours
Lymph node removal + examination e.g. to assess tumour stage (spread of the cancer

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101
Q

Cancers will spread first to their nearest nodes, name some examples.

A

Testicular cancer = lateral aortic nodes
Breast cancer = axillary nodes (multiple groups)
Genital herpes = superficial inguinal nodes
Bronchitis = cervical lymph nodes

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102
Q

What tests could you order to check for inflammation?

A

Erythrocyte sedimentation rate (ESR)
• This is a separately ordered test from a FBC
• It is a haematological test
• This is a non-specific test for inflammation i.e. it will tell you something is going on but not the diagnosis. However, it can be helpful alongside the history, exam and the results of other tests
• Baseline values tend to be higher in females and it rises with age

Sample normal test
ESR = 2 mm/h (< 12.0)

C-reactive protein (CRP)
• CRP is similar test to ESR though it measures only one acute phase protein rather than several in an ESR making it a more specific test
• Again, it is a test for the presence of inflammation and changes more rapidly than the ESR
• It may help diagnose or monitor activity in conditions such as polymyalgia rheumatica, cranial arteritis, rheumatoid arthritis and Crohn’s disease

Sample normal test
Serum CRP level = <0.5 mg/L (<5.0)

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103
Q

There are 7 main blood tests that can be undertaken. Name them.

A

Full blood count, Erythrocyte sedimentation rate, C reactive protein, Urea and Electrolytes, Liver function, Thyroid function, Gycosylated haemoglobin.

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104
Q

What are Erikson’s 8 stages of psychosocial development?

A

Trust vs mistrust
Autonomy vs shame and doubt
initiative vs guilt
industry vs inferiority
identity vs role confusion
intimacy vs isolation
generativity vs stagnation
integrity vs despair

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105
Q

What are the 3 “health sectors” in relation to psychosocial opinions

A

Professional , folk and popular

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106
Q

The skin has 5 main functions, name them

A

Protection from external damage: UV light, chemical, thermal and mechanical injury and resistance to sheer stress: thick skin
Barrier: waterproof and a barrier to bacteria
Sensation: touch, pressure, pain and temperature
Metabolic: Synthesises vitamin D3, subcutaneous fat is a major energy store
Thermoregulation: Insulation, heat loss by sweat evaporation and vasodilation

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107
Q

Describe the main layers of the skin from bottom to top; and the main structures within them.

A

Hypodermis/subcutis: Adipose tissue and main blood supply.

Dermis: Dense irregular connective tissue: fibroblasts, collagen I, elastin, blood, nerves and receptors. Divided into papillary and reticular dermis

Epidermis: Stratified squamous epithelium (keratinised): keratinocytes

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108
Q

Layers of the epidermis; bottom to top

A

Stratum basale: lowest layer of cells, separated from the dermis by a basement membrane to which they are attached
cuboidal/low columnar shape
attached to the basement membrane by hemidesmosomes and to adjacent basal cell by desmosomes
a layer where mitosis is often observed and is the constant supply of keratinocytes
as keratinocytes divide, new daughter cells migrate upwards forming the stratum spinosum

Stratum spinosum:
Contains so-called prickle cells which are large and polyhedral but flatten towards the junction with the next layer
Cytoplasmic projections containing intracellular fibrils (Tonofibrils) that connect to other cells via desmosomes that look like prickles
Lamellar bodies - secreted fromkeratinocytes, resulting in the formation of an impermeable, lipid-containing membrane that serves as a water barrier and is required for correct skin barrier function.

Stratum Granulosum: contain many keratohyalin granules and tonofibrils
These are combined together to form the mature keratin complex

Stratum lucidum: appears clear by light microscope, hence name – sometimes not visible
A layer of dead cells between the granulosum and corneum
Lysosomal enzymes in the cell burst and break down the cell organelles and nuclei

Stratum corneum: a layer of flattened, dead cells containing only mature keratin
Dying cells release a hydrophobic glyophopholipid which renders the skin surface waterproof

These cells constantly need replacing and this comes from the lower layers – turnover depends on the skin site ie higher trauma, faster turnover

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109
Q

What are the layers of the basement membrane zone

A

Lamina lucida –contains adherence proteins to cells above
Lamina densa - principally type IV collagen
Anchoring fibrils – arrays of type VII collagen – extend into papillary dermis

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110
Q

Name a defect caused by the separation of the epidermis from the dermis with minimal shearing forces

A

Epidermolysis bullosa

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111
Q

Epidermolysis bullosa can occur at three different locations in the basement membrane, name them and their consequences.

A

EB simplex: defective cytoskeleton - Good healing
Junctional EB: defective hemidesmosomes - fatal
Dystrophic EB: defective BM collagen - scarring

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112
Q

There are 4 main skin cell types…

A

Keratinocytes: 95% of cells
Stratified squamous keratinising epithelial cells
Produce keratin – structural protein

Melanocytes
Pigment synthesising cells responsible for skin and hair colour
Neural crest derived cells lying
in the stratum basale
Melanosomes in cytoplasm contain melanin and are passed to keratinocytes – scattering of UV light

Langerhans cells:
All layers and upper dermis-prominent in spinosum. Bone marrow derived. Dendritic, antigen presenting cells-migrate to regional lymph nodes and communicate with the immune system.

Merkel cells:
Clear cells in SB. Plentiful in touch areas. Connected to keratinocytes and afferent nerves.
Neuroendocrine function

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113
Q

What are the 2 layers of the dermis, top to bottom

A

Papillary dermis: a narrow zone just below BMZ of epidermis. conical papillae (rete ridges), richly vascularised (capillaries), lymph and nerve

Reticular: Contains most of the dermal collagen. Horizontal collagen and elastin fibres
Contains hair and gland structures

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114
Q

What are rete ridges?

A

Downgrowths from the epidermis
Found where there are more shearing forces e.g. palms of hands and soles of feet

115
Q

Describe hair follicles

A

Produce hair shafts (keratin) for thermoregulation and display.
Growth from a hair bulb at the base
Arrector pili muscle
Sebaceous glands
Majority associated with hair follicles.
Secrete lipid mixture: sebum into hair follicle (waterproofing)

116
Q

Describe the two types of sweat gland

A

Eccrine: dermal-subcutaneous junction of all skin, produce sweat. Ducts open onto skin surface (thermoregulation)

Apocrine: Localised (axilla/groin) scent production. Open into hair follicles above sebaceous duct. Functional at puberty

117
Q

Name and describe 3 cells that innervate the skin

A

Pacinian corpuscle (modified Schwann cells): subcutis, deep pressure and vibration

Meissners corpuscle: papillary dermis, rapidly adapting mechanoreceptors - light touch/pressure sensation

Ruffini corpuscle: mechanoreceptors, stretching of skin

118
Q

Name 2 bacterial infections of the skin

A

Impetigo: Staphylococcus/streptococcus
Subcorneal blisters +/- pus
Burst and spread: yellow crusting
Highly contagious, children

Cellulitis: Strep pyogenes/staph
Superficial dermis, spreading factor
Can lead to necrotising fasciitis
Limbs – penetrating injury/bite

119
Q

Lifecycle of a virus

A

Attachment, entry, uncoating, macromolecular synthesis, assembly, and release.

120
Q

RNA must be …. polarised to be for translation to occur (viruses)

A

positively

121
Q

Name the two main virus capsid symmetries

A

Icosahedral, helical

122
Q

Viruses can have 4 different effects on cells

A

Acute cell death

Chronic (a.k.a. persistent) infection - Continuous viral replication within cell, but cell survives.

Latency- No virus replication, Viral genome present, but no production of viral proteins, Once infected, always infected, e.g. herpesvirus
Virus replication can be reactivated
Primary and secondary infections

Transformation – immortalisation of the cell
Eg Epstein-Barr virus (EBV) - cancer potential

123
Q

3 effects of antibody binding to viruses and infected cells

A

Antibody
- blocks binding and entry to cells (neutralization)
- activates intracellular degradation via TRIM21

Antibody + complement
- damage to enveloped viruses
- opsonisation for phagocytosis

Antibody bound to infected cells
- antibody-dependent cellular cytotoxicity

124
Q

What is antibody neutralisation

A

Block attachment through steric interference, capsid stabilisation, structural changes.

125
Q

Intracellular degradation facilitated by TRIM21

A

Antibody recognition > TRIM recruitment > ubiquitination > proteasome degradation

126
Q

Antigenic shift vs drift

A

Shift is mixing of 2 separate viruses RNA/DNA, Drift is accumulation of mutations over time.

127
Q

what are and what is the Action of interferons in viral infections

A

Signals to neighbouring cells to undergo apoptosis, destroy RNA and reduce protein synthesis and activate immune cells

128
Q

How is HLA1 involved in immune recognition

A

HLA I expression is lowered in some virally infected cells so natural killer cells can recognise it as abnormal and needs killing

129
Q

Killer cells kill cells via …., …. and …..

A

Perforins (osmotic lysis), granzymes and the Fas ligand (apoptosis via caspase and endonucleases)

130
Q

On which side of the neuronal membrane are Na+ ions more abundant?

A

: The neuronal membrane potential depends on the ionic concentrations on either side of the membrane. K + is more concentrated on the inside of the neuronal membrane, whereas Na+ and Ca2+ are more concentrated on the outside

131
Q

There is a much greater potassium K+ concentration inside the cell than outside. Why, then, is the resting membrane potential negative?

A

The resting membrane potential is negative because the neuron is filled with negatively charged molecules, such as proteins, that do not traverse the cell membrane through channels the way ions do.

132
Q

Which ions carry the early inward and late outward currents during the action potential?

A

During the early part of the action potential, the influx of sodium ions across the membrane briefly depolarizes the membrane. The brief inward sodium current is a consequence of opening the voltage-gated sodium channels for only 1 msec. Membrane repolarization is the result of potassium efflux, which is the outward potassium current because of opening voltage-gated potassium channels after a delay of 1 msec.

133
Q

How does the conduction velocity of action potential vary with axonal diameter? Why?

A

The speed of action potential depends on how far depolarization spreads ahead of action potential. This, in turn, depends on the physical characteristics of axons. The two paths that a positive charge can take are inside an axon and across the axonal membrane. When the axon is narrow with many open pores, more of the current flows across the axonal membrane and is lost. When the axon is wide with a few open pores, the current flows inside the axon. The farther down the axon the current flows, the farther ahead of the action potential the membrane will be depolarized and the faster the action potential will propagate. As a result, the conduction velocity of axons increases with the diameter of axons.

134
Q

Voltage-gated Na+ channels can be in 4 states

A

Resting (inactivated)
Open (activated)
Inactivated
Closed and inactivated - absolute refractory period

135
Q

Absolute vs relative refractory period

A

Absolute is all gates inactivated, prevents refiring. Relative is a few are inactivated so a big stimulus could produce an action potential.

136
Q

Multiple sclerosis

A

Autoimmune, attacks and hardens myelin sheath > slows nerve conduction > weakness, coordination, vision and speech issues.

137
Q

Name the 3 main glial cells

A

Microglia - Remove debris from dead or degenerating glia

Astrocytes - Regulate the chemical content of the extracellular space. e.g. neurotransmitter removal

Oligodendrocytes (Scwann cells in the PNS)

138
Q

4 lobes of the brain

A

From front to back and around
Frontal - cognition and motor control
Parietal - Sensory
Occipital - vision
Temporal - auditory and memory

139
Q

How many cranial nerves are there?

A

12

140
Q

How many pairs of spinal nerves are there?

A

31:
8 cervical (C)
12 thoracic (T)
5 lumbar (L)
5 sacral (S)
1 coccygeal (Co)

141
Q

When looking at a thoracic X-Ray, what is ABCDE

A

Airways
Bones
Cardiac region
Diaphragm
Everything else

142
Q

What are the colours on X-Rays of Bone, Fat, Soft tissue, Air and Man made items

A

Bone = White
Soft tissue = Grey
Fat = Dark grey
Air = Black
Manmade = Bright White

143
Q

Is posterior anterior or AP preferred?

A

PA is preferred - less magnification

144
Q

Weak acid drug - stomach and intestine absorption?

A

A- + H+ -> AH

Stomach
At low pH, [H+] is high, equilibrium goes towards HA
Very little ionised > lots absorbed

Intestine
At high pH, [H+] is low,
More ionised > little absorbed
Less absorbed

145
Q

Weak base - stomach and intestine absorption

A

B + H+ -> BH+

Stomach
At low pH, [H+] is high,
Equilibrium goes towards BH+
Lots ionised
Little absorbed

Intestine
At high pH, [H+] is low,
Less ionised
More absorbed

146
Q

Bioavailability

A

Amount of drug that reaches systemic circulation with respect to the amount administered

147
Q

What is first pass metabolism

A

Many drugs are metabolised by enzymes in the gut wall or the liver.

148
Q

Name two routes of administration that avoid first pass metabolism

A

Mouth - Sub-lingual, Buccal
Rectal

149
Q

Routes of administration and advantages

A

Sub-lingual – glyceryl trinitrate
Undergoes first pass metabolism
Need quick response

Sub-cutaneous – local anaesthetics
Acting locally
Can be given with vasoconstrictor to delay systemic absorption

Intra-muscular depot preparations – contraceptives
Gradual release  sustained concentrations
Convenience

Rectal – anti-epileptic drugs
Diazepam for epilepsy when patient is fitting continuously

Topical – anti-inflammatories
Ibuprofen, avoids irritation to stomach
Corticosteroids, to avoid systemic side effects

Inhalation – asthma COPD drugs
Direct to target, minimises side effects

Intra-articular – anti-inflammatories
Corticosteroids, direct to target, avoids systemic side effects

150
Q

Factors that affect absorption from the gut

A

Gastric emptying
Gastrointestinal motility
Blood flow
Particle size and formulation
Extended-release formulations
Enteric coatings
Physicochemical factors e.g. solubility, molecular weight, binding to calcium (esp. in milk) or fat in food
Metabolism (enzyme-catalysed reactions)

151
Q

Volume of distribution

A

volume of plasma that would contain the total body content of the drug at a concentration equal to that in the plasma.

152
Q

Describe drug solubility in Blood > interstitial > inside cells with respect to Vd

A

Hydrophilic > very lipid soluble
3.5 L/70kg > 14 > 40 > 40<

153
Q

Phases of drug metabolism

A

Phase 1 reactions often catalysed by cytochrome P450 enzymes (CYP).
Important for non-polar drugs e.g. CYP1A2 - caffeine, paracetamol

Phase 2: Conjugation - Increases solubility in water and therefore excretion in the kidney

154
Q

Drug metabolism in the liver depdnds on

A

Perfusion
Plasma protein binding
Secretion into bile
Presence and activity of transporters and enzymes

155
Q

Clearance (drug)

A

the volume of plasma from which all the drug molecules would need to be removed per unit time to achieve the overall rate of elimination of drug from the body

156
Q

Name the stages of cell growth

A

GO – No cellular activities regarding cell growth

G1 – Cell grows to full size

S – DNA synthesis for doubling genome (chromosome)

G2 – Rapid cell contents production. Final Check for errors

Mitosis – Cell divides

Cytokinesis – Cell separates into daughter cells

157
Q

Describe a regulatory pathway regarding the cell cycle

A

E2F – S phase gene transcription factor - normally bound by retinoblastoma protein (Rb) rendering E2F inactive

Under favourable conditions, Cyclins will be produced and bind to CDK

Cyclin / CDK complex phosphorylates Rb

Phosphorylated Rb changes conformation and uncouples from E2F

E2F is free to act as transcription factor for S phase gene transcription

158
Q

Name example enzymes involved in S phase initiation in the cell cycle

A

Critical initiation of S phase by retinoblastoma protein phosphorylation regulated by Cyclin D / CDK4/6 and Cyclin E / CDK2 complexes

159
Q

What are the stages of mitosis?

A

Prophase – Chromosomes start condensing and organised. Spindle fibres formed. Nuclear membrane resolves

Prometaphase – Chromosomes attached to spindle fibres. Chromosomes further condense

Metaphase – Chromosomes start aligning in centre. Sister chromatids facing opposite poles

Anaphase - Separation of sister chromatids then migrate to opposite poles

Telophase - Chromatids in positions and start decondensing, Formation of nuclear membrane, Spindle fibres resolve

Cytokinesis - Cytoplasm divides
Completion of cell division
Two identical cells formed

160
Q

Two types of microtubules projecting from the microtubule organising centres

A

Polar microtubules and the kinetochore microtubules (K fibres)

161
Q

Cell cycle checkpoints

A

Each stage of cell cycle cannot progress without checking for:
DNA damage
DNA replication error
Spindle fibre assembly and chromosome alignment

162
Q

Affinity

A

Affinity: how tightly the drug binds its receptor.
the concentration required to occupy the receptor

163
Q

Efficacy

A

maximum response

164
Q

Potency

A

Concentration required
to give half the maximum
response (EC50).

165
Q

Allosteric antagonists are as good as competitive antagonisits. T/F?

A

False, may not be able to reduce response totally.

166
Q

Ligand gated ion channel example

A

Nicotinic Acetylcholine, GABA, Glutamate
Small molecules
Fast neurotransmission e.g. nerve to muscle (nicotinic), nerve to nerve.
Movement of ions through channel  electrical activity

167
Q

GPCR Example

A

Muscarinic ACh, dopamine, adrenaline, noradrenaline, serotonin, opiods,
Small molecules and peptides
Neurotransmission, modulation of neurotransmission,
Activation of enzymes and modulation of ion channels  signalling cascades

168
Q

Tyrosine Kinase example

A

EGF, VEGF, PDGF, TNFa, Interleukins, Interferons
Peptides and proteins
Regulate cell growth, proliferation, death
Activation of protein signalling cascades leading to change in gene transcription

169
Q

Nuclear receptor example

A

Corticosteroids (e.g. cortisol)
Sex steroids (e.g. oestrogen and testosterone)
Thyroid hormone
Steroids and thyroid hormone
Regulate gene transcription
Gene transcription  synthesis of mRNA and protein

170
Q

Consequentialism

A

Judge action by its outcome
e.g. move carriage to kill1 instead of 5 is good.

171
Q

Deontology

A

Moral of the action itself - independent of the outcome
e.g. dont move the carriage as you will actively be killing the 1 person

172
Q

Virtue ethics

A

What would a good person do

173
Q

Autonomy

A

Patient has ultimate decision making responsibility.

174
Q

Beneficence

A

Best interest of the patient

175
Q

Non-malifecence

A

Do not harm

176
Q

Justice

A

Act on Legality, rights, and distributive care

177
Q

Describe serous membranes

A

line the inside of the body wall and cover many organs
Formed from embryonic mesoderm
Mesothelium: simple squamous epithelium + thin layer of connective tissue with blood vessels

Inner visceral layer, outer parietal layer

178
Q

What is superficial fascia

A

Deep to skin: loose connective tissue and fat (adipose)
Variable thickness
Contains collagen, fat cells & elastic tissue

179
Q

What is deep fascia

A

Surrounds muscles
Fibrous, strong and tough sheet
Forms routes for infection spread
Forms compartments: can have consequences during a bleed

180
Q

What is fascia

A

Connective tissue layers which can be thin, thick, fatty or loose

181
Q

Name examples of anatomical variation

A

Differences in build and shape (body habitus)
Palmaris longus muscle
Situs inversus and dextrocardia
Renal agenesis: one kidney at birth instead of two

182
Q

What are the vertebral levels

A

7 Cervical
12 Thoracic
5 Lumbar
Sacrum (5 fused)
Coccyx (3/4 fused)

183
Q

Distinguishing features of the vertebrae

A

Spinous processes point inferiorly

Heart-shaped vertebral bodies

Vertebral bodies have costal facets for articulating with head of rib

T1 – T10 transverse processes have transverse costal facets for articulating with tubercle of the corresponding rib

184
Q

How many ribs and which are true, false or floating

A

12
Ribs 1-7 = true ribs
Articulate with the sternum via their own costal cartilage

Ribs 8-10 = false ribs
Articulate with the sternum via shared costal cartilage

Ribs 11 & 12 = floating ribs
Do not articulate with sternum

185
Q

Describe the anatomy of a typical rib

A

Ribs 3-9

Head: articulates with vertebral body at same level plus the vertebral body above
Neck
Tubercle: articulates with transverse process of vertebra at same level
Costal angle
Body or shaft with costal groove running inferiorly

186
Q

Describe the 1st rib

A

Flat, sickle-shaped appearance
Single facet on head for articulation with T1 vertebral body only
Subclavian grooves
Scalene tubercle (anterior scalene muscle)

187
Q

Describe the 2nd rib

A

Longer than first rib
Has two facets on head – articulates with T1 and T2 vertebral bodies
Tuberosity for serratus anterior muscle

188
Q

Describe the 10th-12th ribs

A

10th – 12th ribs
Single facet on head for articulation with one vertebral body e.g. T10 for 10th rib

189
Q

What are real spaces?

A

keep their structure when empty e.g. trachea (airway)

190
Q

What are potential spaces?

A

small, flattened spaces that have the potential to become much larger:
Serous membrane cavities e.g. pleural cavity
Fascial planes

191
Q

Name the 3 structures of the sternum

A

Manubrium, body and xiphoid process

192
Q

Describe features of the sternum and where they lie in relation to the rest of the body

A

Manubrium has attachments for the clavicles and first costal cartilages (for first ribs)

Suprasternal (jugular) notch is at T2 vertebral level

Sternal angle (manubriosternal joint) is at the level of the intervertebral disc between the T4 and T5 vertebrae
Attachments for second costal cartilages

Body of the sternum is between T5-T9 vertebral levels

Xiphoid process is at T10 vertebral level

193
Q

What does the thoracic plane at the sternal angle signify in the mediastinum

A

The start and end of the arch of the aorta
The site where the superior vena cava enters the heart
The pulmonary trunk
The bifurcation of the trachea into the left and right main bronchi

194
Q

Describe the formation of the morula

A

After 3 days of cell division, 12-16 cells are evident. The embryo is now called a morula, because it looks like a mulberry.

The inner cells of the morula are called the inner cell mass, and the surrounding cells are referred to as the outer cell mass.

195
Q

Describe the formation of the blastocyst

A

Blastocyst forms an inner fluid filled cavity called the blastocele. Inner cells form the embryoblast at one pole, outer cell mass flattens and forms the trophoblast as a sphere around the whole thing.

196
Q

What is a teratogen?

A

An agent or factor which causes malformation of an embryo or disruption to a normal developmental process or deformation of a part of the body or dysplasia/abnormal organisation of cells in tissues resulting in a congenital abnormality/birth defect:

197
Q

What can prevent neural tube defects?

A

by taking 0.4 milligramsof folic acid daily

198
Q

Name different types of teratogens with examples

A

Infections
Sexually transmitted e.g. chlamydia – premature rupture of membranes, preterm labour
Non-sexual infections e.g. rubella (German measles) – heart defects
Zika virus infection - microcephaly

Maternal diet
Lack of folic acid – neural tube defects (e.g. spina bifida)

Maternal drugs
Methotrexate (immunosuppressant used in rheumatoid arthritis): skeletal defects involving the face, cranium, limbs and vertebral column

Environment
Ionising radiation e.g. X-rays: microcephaly, mental deficiency, skeletal anomalies, delayed growth, cataracts

Maternal health
Alcohol: fetal alcohol syndrome: IUGR, mental deficiency, microcephaly, ocular anomalies, joint abnormalities, short palpebral fissures

199
Q

When are teratogens most likely to cause defects?

A

Embryonic weeks 3 to 8 are when teratogens are most likely to cause defects, as this is when organogenesis

200
Q

When are teratogens most likely to affect organ size?

A

After week 9

201
Q

Describe implantation of the blastocyst into the endometrium.

A
202
Q

Describe bilaminar embryonic disc formation

A

Embryoblast forms two layers; epiblast and the hypoblast.

203
Q

Describe amniotic cavity formation

A

Cells from the epiblast layer form the lining (amnion) of the amniotic cavity

204
Q

Describe primary and secondary umbilical vesicle formation

A

Blastocele becomes the primary umbilical vesicle upon implantation. Splits into the primary remnant and the secondary by the extra embryonic coelom

205
Q

Describe trilaminar embryonic disc formation

A

The process begins with formation of the primitive streak on the surface of the epiblast
Cells of the epiblast migrate toward the primitive streak
They then slip beneath it in a process called invagination
Some invaginating cells displace the hypoblast, creating the endoderm.
Other cells come to lie between the epiblast and newly created endoderm to form mesoderm
Cells remaining in the epiblast form ectoderm

206
Q

What does the endo, meso and ectoderm give rise to?

A

The ectoderm gives rise to the nervous system (neuroectoderm) and the epidermis of the skin (surface ectoderm).

The mesoderm gives rise to the muscle cells and connective tissue in the body, the dermis of the skin and linings of the body cavities (serous membranes e.g. pleura, pericardium, peritoneum).

The endoderm gives rise to the epithelial lining of the digestive and respiratory systems and many internal organs (eg liver, pancreas, thyroid gland).

207
Q

Describe embryo neuralation

A

The notochord induces the overlying ectoderm to thicken and form the neural plate.
The neural plate lengthens and the lateral edges elevate to form the neural folds with the neural groove lying in the midline.
The neural folds approach each other in the midline and begin to fuse.
The folds fuse in a cranial and caudal direction from the cervical (neck) region
The neural tube is formed.
The two ends of the neural tube eventually close
The rudimentary central nervous system (brain and spinal cord) is formed

208
Q

What do neural crest cells give rise to?

A

Neural crest cells from the trunk region migrate to form melanocytes in the skin, sympathetic neurons and ganglia of the autonomic and enteric nervous system, Schwann cells and cells of the adrenal medulla.

Neural crest cells from the cranial end form glial nerve cells, parts of the connective tissues of the face and skull and neurons of cranial ganglia.

209
Q

Describe the changes that the mesodermal layer undergoes after gastrulation.

A

The mesodermal germ layer comes to form either side of the developing notochord (day 17)

The mesoderm begins to thicken to form the paraxial mesoderm.
Laterally, the mesoderm remains thinner and forms the lateral plate mesoderm
The lateral plate mesoderm begins to break down and divide into two layers (20 days)
The 2 layers are called the somatic or parietal mesoderm and the visceral or splanchnic mesoderm

: The splitting of the lateral plate mesoderm (together with folding of the embryo) will eventually create the intraembryonic coelom or cavity

210
Q

What do the somites form?

A

The sclerotome – which forms the vertebrae and ribs
The myotome – which forms the skeletal muscles of the back and limbs
The dermatome – which ultimately forms the dermis for the skin of the back and body wall

211
Q

Describe embryo lateral folding.

A

The lateral body walls come together anteriorly in the midline and pinch the yolk sac as they do so.

Eventually the lateral body walls close completely:
The only area of the embryo where the lateral walls don’t completely close is at the umbilical cord
Part of the endoderm is incorporated into the body of the embryo and forms the primitive gut tube
The intraembryonic coelom/cavity has been formed) – this single cavity will eventually divide to form the pericardial, pleural and peritoneal cavities.

212
Q

What mesoderm covers the intraembryonic cavity wall and the gut tube

A

The intraembryonic cavity wall is lined with parietal mesoderm and the gut tube (and eventually other organs) is lined with visceral mesoderm.

213
Q

Describe longitudinal folding

A

At the same time as lateral folding, lengthening of the neural tube causes the embryo to curve into the foetal position as the head and tail regions move ventrally and longitudinal folding of the embryo occurs

As the head and tail longitudinal folding occurs, the amnion is pulled down to surround the embryo which then comes to lie within the amniotic cavity:
As folding continues the heart and the oropharyngeal membrane (where the mouth will form) turn under onto the ventral surface of the embryo

As longitudinal folding continues, the yolk sac is ‘pinched’ until the connection with the gut tube is narrowed to form the omphaloenteric (or vitelline) duct

214
Q

Outline organogenesis in weeks

A

4 - the neural tube continues to close; somites continue to develop (21-29 by now); 1-3rd pharyngeal arches have developed (form the head and neck); the heart, liver and early limb buds have begun to form, the tongue has begun to form, the heart tubes have looped (and beats); the early lung buds develop.

Week 5: 30 somites are present; the developing eye and ear are visible; the early nose and face has started to form; the stomodeum (the future mouth) is evident, the early heart chambers are forming; the liver is expanding; paddle-shaped limb buds are evident.

Week 6: further development of the limbs showing hand buds and digital rays; the elbow joint forms; parts of the face have developed (oral and nasal cavities); the early inner and middle ear structures are forming; the gut tube is elongating and looping (normal herniation of the gut is evident due to the rapidly growing intestines).

Week 7: the eyelids have formed; the external ear is evident; partial separation of the digital rays is evident but the hand plates are still webbed; the foot plate is present; the trunk has straightened; further genital development is evident; palate formation has started.

Week 8: the head is more rounded, the hands and feet come closer together and touch each other; coordinated limb movements are seen; gut herniation is still evident (they return to the abdominal cavity during the 10th week); accurate sex identification is not possible yet.

215
Q

Describe the location of parasympathetic ganglia

A

Preganglionic neurones are in grey matter of brainstem ( midbrain, pons, medulla) OR lateral horn of spinal cord grey matter from S2-4 (hence craniosacral)
Long, synapse with postganglionic neurones at or near organ

Cell bodies are in distinct ganglia near or on their final target organ
Short, synapse on target organ

216
Q

Describe the location of sympathetic ganglia

A

Pre-ganglionic cell bodies are in the lateral horn of spinal grey matter from T1-L2 (hence thoracolumbar)
Short, synapse with postganglionic neurones near spinal cord

Cell bodies are in the sympathetic chain or other named ganglia
Long, synapse on the target organ

217
Q

Which part of para and sympathetic neurones are myelinated?

A

preganglionic neurones

218
Q

Describe nerve routes in the sympathetic chain

A

Pre-ganglionic fibres pass into the chain via the white ramus communicans (white because fibres are myelinated)

Fibres concerned with head and thorax terminate with post-synaptic cell bodies in sympathetic chain. These return to spinal nerve via grey ramus communicans (grey because unmyelinated)

Pre-ganglionic fibres concerned with pelvic and abdominal viscera pass uninterrupted through chain to the plexuses - to the corresponding post-ganglionic neurones

219
Q

Name the midbrain ps nuclei

A

Edinger-Westphal nucleus of the oculomotor nerve (CN III)
Provides parasympathetic innervation to iris & muscles of ciliary body (constricts pupils and change shape of lense)

220
Q

Name the PS nuclei of the Pons

A

Superior salivatory nucleus of the facial nerve (CN VII)
Provides parasympathetic innervation to lacrimal glands (to produce tears) and sublingual and submandibular salivary glands (to produce saliva)

221
Q

Name the medulla nuclei

A

Inferior salivatory nucleus of glossopharyngeal nerve (CN IX)
Provides parasympathetic innervation to parotid salivary gland (to produce saliva)

Nucleus ambiguus (axons travel in CN X)
Provides parasympathetic innervation to larynx, pharynx & heart

Dorsal motor nucleus of vagus nerve (CN X)
Provides parasympathetic innervation to lungs, pancreas, GI tract & heart

222
Q

What brain structure regulates the ANS?

A

Hypothalamus via the Dorsal Longitudinal Fasciculus being the principle tract.

223
Q

Name two disorders of the ANS

A

Postural hypotension - Dizziness, damage to sympathetic nerves supplying blood vessels due to diabetes or syphilis e.g..

Horners syndrome - Drooping of upper eyelid, miosis, anhidrosis, interuption of s nerve to eye. CAUSED BY BRAIN LESIONS OR LUNG cancer (affects ganglia)

224
Q

Diagnostic test specificity

A

the ability of the test to correctly identify people without the disease; i.e., the percentage of individuals without the disease who have negative test results.

True Negative/ (True Negative+ False Positive)

225
Q

Diagnostic test sensitivity

A

the ability of the test to correctly identify people with the disease; i.e., the percentage of individuals with the disease who have positive test results.

True Positive/ (True Positive+ False negative)

226
Q

When is high sensitivity good and when is high specificity

A

High sensitivity useful (e.g., screening breast cancer, HIV)
Life-threatening diseases (if untreated)
Improvement in survival rate with early treatment
Is ok to “over diagnose” (more false positives) as all positives will have further testing – screening

High specificity useful (e.g. Down syndrome during pregnancy)
Not life-threatening if untreated
Subsequent tests/treatments are too invasive or have serious side effects
High cost of treatment
Low pre-test probability (prevalence)

227
Q

Positive predictive value

A

True positive/(True Positive + False Positive)

228
Q

Prevalance =

A

(TP + FN)/ (TP + FN + FP + TN)

229
Q

What is the kappa ratio

A

Measuring the extent to which agreement exceeds that expected by chance requires a measurement statistic called the kappa.

230
Q

Apoptosis as a physiological event

A

Embryological development (GI lumen, digits)
Involution of hormone dependant tissues (breast/uterus)
Maintenance of cell number in tissues with high cell turnover (intestinal epithelium)
Elimination of unwanted individual cells (neutrophils /lymphocytes after inflammation/immune response)

231
Q

Apoptosis as a pathological event

A

DNA damage (eg radiation, cytotoxicity, viral infection. p53)
Misfolded proteins: due to intrinsic or extrinsic mechanisms accumulate in RER and cause stress (eg death of nerve cells in neurodegenerative conditions)
Growth factor deprivation

232
Q

Morphology of apoptosis

A

Degradation of cytoskeletal framework
Fragmentation of DNA
Loss of mitochondrial function
Nucleus shrinks (pyknosis) and fragments (karyorrhexis)
Cell shrinks
Cell fragments: apoptotic bodies
Membrane intact but attracts phagocytes – secondary necrosis

233
Q

Intrinsic pathway of apoptosis

A

Cell injury detected by Bcl-2 sensors.

The Bcl-2 family - apoptotic regulators
B-cell lymphoma gene 2 (Bcl-2) – controls the permeability of mitochondria

Anti-apoptotic members e.g. Bcl-2, Bcl-XL
Pro-apoptotic members e.g. Bax, Bak, Bok

Balance of pro- and anti- apoptosis proteins determine mitochondrial membrane permeability
Increased permeability = cytochrome C release
Cytochrome C activates caspases > endonucleases >cytoskeleton breakdown

234
Q

Extrinisic pathway of apoptosis

A

The Fas family - cell death receptors
Part of the Tumour Necrosis Factor (TNF) and Neuronal Growth Factor (NGF) receptor family

Cell death receptors differ from the rest of the family by the presence of the intracellular Death Domain (DD): Fas, TNFR1

Fas Ligand (FasL) - membrane protein expressed on activated T lymphocytes.
Ligands bind to Fas or TNF receptor.
Cluster and activate caspases via adapter proteins.

235
Q

Morphology and mechanism of reversible injury

A

Swelling - hydropic change
Earliest manifestation of almost all forms of cell injury
As a result of sodium and water influx into cell
Membrane damage rendering it more permeable to sodium
Membrane sodium pump damaged
Membrane sodium pump deprived of ATP

Fatty change
Organs actively involved in lipid metabolism e.g. liver (steatosis)
Accumulation of triglyceride-filled vacuoles due to disruption of metabolic pathways – toxic injury e.g. alcoholism

236
Q

Pathological apoptosis examples

A

Bcl-2 overexpressed in many cancers: lymphomas, small lung cell carcinoma, chronic lymphocytic leukaemia, melanoma

Apoptosis deregulated: prostate, ovarian, cervical, bladder, breast, colorectal, pancreatic and gastric cancers

Too little apoptosis: autoimmune diseases, cancer, chronic inflammatory diseases
Too much apoptosis: immunodeficiency (e.g. AIDS), neurodegenerative diseases

237
Q

What is necrosis

A

Continuation of reversible injury: severe swelling of mitochondria, lysosomes and membrane damage
Lysosomal enzymes are released and the organelles are destroyed (autolysis)
Necrosis is followed by inflammation

238
Q

Coagulative necrosis

A

Most common
Due to interruption of vascular supply (ischaemia) - infarction
Common in solid organs e.g. heart and kidney
Denaturation of protein
Gross appearance: firm, dry and slightly swollen (cooked)
Histology appearance: pale staining with loss of nuclei and cellular components but retention of tissue architecture

239
Q

Liquefactive/colliquative necrosis

A

Seen in the brain (primary event) and in infections (secondary to infection of necrotic tissue with pyogenic organisms: abscess)
Due to hydrolytic lysosomal enzymes.
Neutrophils contributing to the liquefaction (from hydrolases)
Gross appearance: local accumulation of protein-rich, semifluid material.
Histology: No architecture, proteins and phagocytes

240
Q

Caseous necrosis

A

Seen in tuberculosis
Combination of coagulative and liquefactive necrosis
Gross appearance: yellow-white cheese-like
Histology: amorphous proteinaceous mass, lysed cells with no cell outlines/architecture. Surrounded by a granulomatous inflammation

241
Q

Gummatous necrosis

A

Gross: Firm and rubbery dead tissue
Histology: no architecture, amorphous proteinaceous mass-like caseous
Only referred to in the context of syphilis infection

242
Q

Gangrene

A

Necrosis of all tissue in an area
Wet gangrene-coagulative necrosis from lost blood supply + liquefactive from infection (often bacterial)
Dry gangrene- coagulative necrosis from anoxia (diabetes mellitus/atherosclerosis)

243
Q

Fibrinoid necrosis

A

Seen in blood vessels in the case of immune reactions e.g. arteries in the case of vasculitis/malignant hypertension
Necrotic area of smooth muscle layer in the artery is filled with fibrin leaked from vessels
Histological only

244
Q

Fat necrosis

A

Necrosis of adipose tissue
Due to trauma (breast) or lipolytic enzymes (pancreas).
Gross: foci of hard, yellow material
Histology: Necrotic fat cells and inflammation

245
Q

Haemorrhagic necrosis

A

Blockage of venous drainage - leads to congestion and failure of arterial perfusion.
Gross: dead tissues infiltrated by large numbers of extravasated red cells.
Histology: congested tissues with abundant RBCs

246
Q

What is ischaemia?

A

Impaired vascular perfusion, depriving the affected tissue of vital nutrients, especially oxygen
Tissue effects can be reversible, but is dependent on:
duration of the ischaemic period-brief ischaemic episodes may be recoverable
metabolic demands of the tissue-cardiac myocytes and cerebral neurones are the most vulnerable

247
Q

What is infarction?

A

Death (necrosis) of tissue as a result of ischaemia

248
Q

Cellular events in ischaemia

A

Reduction or loss of O2 - ATP production reduced - failure of energy-dependent processes
Membrane pumps fail (require energy) - Na+ and H2O influx – swelling
Anaerobic glycolysis – increased lactic acid – decreased pH – compromised enzyme environment
ER swelling – ribosome detachment – decreased protein synthesis
Organelle membrane damage:
Increased cytosolic Ca2+ (from mitochondria and ER)
Lysosomal breakdown releases enzymes (proteases etc.) - digestion of cell components

249
Q

Reperfusion injury

A

Further effects of ischaemia when perfusion is re-established
Oxygen free radicals built up
Depletion of scavengers (antioxidants e.g. vitamin E)
Excess generation (e.g. mitochondria, neutrophils)

Build-up of metabolic by-products (ATP use) – O2 influx – conversion to reactive oxidants
DNA, protein and lipid damage

Additional tissue damage due to increased numbers of inflammatory cells – increased secondary inflammation

250
Q

Tissue susceptibility to infarction

A

Availability of blood supply
Anastomosis – collateral blood supply
Watershed area – vulnerable in hypotension
Infarct shape dependent on perfusion territory of the occluded blood supply e.g. wedge-shaped

Metabolic activity of tissue
Neurones and cardiac myocytes are most vulnerable to ischaemia - high metabolic demand

Regenerative ability
Tissues which can regenerate (labile, stable) can recover, non-dividing tissue (permanent) will have scar tissue

251
Q

What are the main energy sources for the heart when:
1 Immediately after a meal?
2 Between meals in a steady state?
3 During starvation or prolonged exercising?

A

1 = glucose (glycolysis)
2 = Fatty acids (β-oxidation)
3 = Ketone bodies and fatty acids

252
Q

What are the fates of pyruvate in both aerobic and anaerobic respiration?

A

In aerobic respiration it is converted into acetyl-CoA which enters the citric acid cycle to make NADH and ATP
In anaerobic respiration it can be used to regenerate NAD+ which can be used to make small numbers of ATP. This requires the enzyme lactate dehydrogenase which produces lactate and NAD+ from pyruvate and NADH. This has the effect of lowering the pH

253
Q

What are the clinical signs of cardiac ischemia?

A

Chest pain (angina)
Shortness of breath
Fast heartbeat
Shoulder or back pain
Neck, jaw, or arm pain
Sweating/clamminess
Nausea/vomiting
Fatigue
Dizziness or light-headedness
Myocardial infarction (heart attack)

254
Q

What are the main biomarkers for cardiac ischemia and why do we need more than one?

A

CK-MB (mass), Cardiac Troponins (I or T) and Myoglobin. More are in development.
We need more than one marker as none of the markers we have are ideal, so a multiple approach give a more accurate picture of what is happening. Also, each of the markers are useful on different time scales allowing the diagnosis of an MI from 1 hr to 15 days

255
Q

What time frames do we see biomarkers appear after a myocardial infarction (heart attack) and how long are they a useful tool as a marker of a past cardiac event?

A

Myoglobin is released withing 1-4 hr but gone in 24hr
CK-MB is released in 3-12 hr and is around for 2-3 days
Troponin T is released from 4-12 hr and is around for up to 15 days

256
Q

What are free radicals? What can they do

A

Single unpaired electron in outer orbit
Superoxide (O2-) hydroxyl radical (·OH)

Normally generated during
oxidative phosphorylation and
Mopped up by antioxidants:
e.g. vitamins A, C and E
Or neutralised by enzymes e.g. catalase

This is an increased problem when cellular homeostasis is lost
(particularly when mitochondria are disrupted)

Can result in lipid peroxidation and protein damage thus increasing cellular dysfunction

257
Q

Temporal aspect of cell damage

A

Ion leakage, metabolite accumulation, membrane rupture - macromolecules

258
Q

Describe the structure and function of smooth muscle

A

A single nucleus present in the central thick portion.
Cytoplasm appears homogenous without striations.
Fewer mitochondria as compared to the skeletal muscle.
Metabolism mostly glycolytic.
Actin, Myosin & Tropomyosin but NO Troponin
Dense bodies serve the same purpose as the Z-discs
Attached to the dense bodies are numerous numbers of Actin filaments
Interspersed between the actin filaments are Myosin filaments

In the walls of hollow organs, blood vessels, eye, glands, uterus, skin.
Some functions: propel urine, mix food in digestive tract, dilating/constricting pupils, regulating blood flow,
In some locations, autorhythmic
Controlled involuntarily by endocrine and autonomic nervous systems

259
Q

Cardiac muscle structure and function

A

Striated, Actin and myosin, Epinephrine, Ca2+ from ECF and SR, Troponin as ca2+ regulatory protein, Gap junctions.

Heart: major source of movement of blood
Autorhythmic
Controlled involuntarily by endocrine and autonomic nervous systems

260
Q

Skeletal muscle structure and function

A

Striated, Actin and myosin, No homrmonal contril, Ca2+ from SR, Troponin as ca2+ regulatory protein.

Attached to bones
Makes up 40% of body weight
Responsible for locomotion, facial expressions, posture, respiratory movements, other types of body movement
Voluntary in action; controlled by somatic motor neurons

261
Q

How is smooth muscle organised

A

Grouped into sheets in walls of hollow organs
Longitudinal layer – muscle fibers run parallel to organ’s long axis
Circular layer – muscle fibers run around circumference of the organ
Both layers participate in peristalsis

262
Q

Single unit Smooth muscle

A

Muscles of visceral organs .e.g. GIT, uterus, ureters & some of the smaller blood vessels.
Form a sheet or bundles of tissue.
Cell membranes show gap junctions that allows AP to pass rapidly from cell to cell.
AP spreads rapidly throughout the sheet of cells – cells contract as a single unit.

263
Q

Multi-unit smooth muscle

A

Iris & Ciliary body of the eye, large arteries, Piloerector muscles
Showing discrete, individual smooth muscle fibers.
Smooth muscle cells not electrically linked. Each muscle fiber innervated by a single nerve ending. NT itself can spread and lead to an AP.
Selective activation of each muscle fiber that can then contract independently of each other.

264
Q

Smooth muscle contraction mechanism

A

Ca2+ binds calmodulin > Calmodulin binds myosin light chain kinase > MLCK phosphorylates light chain in myosin heads > ATPase activity increases > Actin slides along myosin to create tension.

265
Q

How does epinephrine work

A

Causes hyperpolarization which causes a reduced amount of cytosolic Ca2+ and thus relaxes the muscle cell

266
Q

Ach vs norepinephrine

A

ACh & norepinephrine are never secreted by the same nerve fiber

ACh can be excitatory or inhibitory - determined by the type of receptor expressed by the target cell

ACh and NE usually cause the opposite reaction at a target cell (If Ach is stimulatory then NE will most likely be inhibitory)

Depending on the type of receptor norepinephrine and epinephrine can have different results on the smooth muscle cell

Epinephrine bound to beta-adrenergic receptors on smooth muscle cells of the intestine causes them to relax

Epinephrine also binds to the alpha2-adrenergic receptor found on smooth muscle cells lining the blood vessels in the intestinal tract, skin, and kidneys

Epinephrine bound to alpha2 receptors causes the arteries to contract (constrict), reducing circulation to these organs

267
Q

Describe the relative nutritional value of the following nutrients: Carbohydrates, Proteins, Fats, Alcohol

A

More ATP comes from fat than alcohol than carbohydrate or protein

268
Q

Glycolysis

A

1 Glucose goes through a series of linked enzymatic reactions and is split into:

2 Pyruvate
4 ATP (but 2 were used)
2 NADH
269
Q

How is pyruvate turned into Acetyl CoA?

A

Transported into mitochondria

Oxidatively decarboxylated to acetyl-CoA

Pyruvate dehydrogenase (enzyme complex- 3 enzymes multiple copies)
Irreversible reaction

This reaction mainly takes place in tissues with high oxidative capacity- e.g. cardiac

270
Q

What is the TCA cycle?

A

For every 1 glucose
(2 acetyl CoA)
the cycle generates:

4 CO2
6 NADH
2 FADH2
2 ATP

De na de na a fa na

271
Q

What is oxidative phosphorylation

A

The transfer of electrons from organic compounds through a series of electron carriers to O2 (or other inorganic or organic molecules (via oxidization)- keep in mind for free radicals)

The transfer of electrons
from one carrier to the next
generates energy which is
used to make ATP from
ADP by chemiosmosis

272
Q

What has a higher energy yield? fat or glucose

A

Fat

273
Q

How is fat stored

A

As Triacylglycerols

274
Q

How is energy derived from fats?

A

Free Fatty acids converted to acetyl CoA for the TCA cycle. 131 ATP from whole process

275
Q

Why make glycogen?

A

Glycogen mobilized faster than fat
1% - 2% of mass in rested skeletal muscle
Glycogen  Glucose-6-Phosphate
G-6-P enters glycolytic pathway

Glucose metabolism is both aerobic and anaerobic (in part)
Fat metabolism is only aerobic

Muscle lacks G-6-phosphatase
Glucose cannot be exported

Liver has G-6-phosphatase
Glucose can be exported
Liver provides body’s glucose

276
Q

What are ketone bodies?

A

During excessive fatty acid mobilisation:
examples: b-oxidation, fasting, type I diabetes

acetyl CoA production in liver is very high

mitochondria oxidation of acetyl CoA cannot match production

acetoacetate accumulates

acetoacetate (~75%) is reduced to  b-hydrobutyrate

ketone bodies  (acetoacetate, acetone & b-hydroxybutyrate)  enter circulation

	ketone bodies can be used for energy in heart and brain  (converted back to acetyl CoA)
277
Q

vDefinition of an Adverse Drug Reaction:

A

An unwanted or harmful reaction experienced following the administration of a drug or combination of drugs under normal conditions of use and which is suspected to be related to the drug

278
Q

ADRs: top five examples

A

NSAIDS (29.6%) e.g. aspirin, ibuprofen GI bleeding, CV haemorrhage, renal impairment
Diuretics (27.3%) for high blood pressure Renal impairment, hypotension, electrolyte disturbance
Warfarin (10.5%) To prevent clotting GI bleeding, haematuria, prolonged INR
ACE-I/ARB (7.7%) for high blood pressure Renal impairment, hypotension, electrolyte disturbance
Antidepressants (7.1%) Confusion, hypotension, constipation, hyponatraemia

279
Q

On target ADRs

A

Exaggeration of the drug’s normal effect
E.g. excessive bleeding with warfarin
Generally dose-dependent and can be reversed by lowering dose

Why?
Genetic factors
Age
Concurrent disease (esp liver or kidney disease)

280
Q

Off-target ADRs (4)

A

Idiosyncratic, not pharmacologically predictable e.g. allergic response to penicillins
May be chronic - persisting for a relatively long time e.g. benzodiazepine dependence; analgesic nephropathy
Delayed reactions - become apparent some time after the use of a medicine e.g. carcinogenic and teratogenic effects
End of use reactions - Associated with withdrawal of a medicine e.g. insomnia, anxiety and perceptual disturbances following withdrawal of benzodiazepines such as midazolam

281
Q

Example of pharmacovigilance: (2)

A

UK Yellow Card scheme
https://yellowcard.mhra.gov.uk/
Started in 1964 in response to thalidomide.
Can lead to…
Additional information in product leaflet
Change in dosage
Warnings to particular patient groups
Withdrawal from market

Black triangle scheme
New medicines and vaccines that are under additional monitoring have an inverted black triangle symbol (▼) displayed in their package leaflet and in the British National Formulary (BNF)
You should report all suspected ADRs for these products.

282
Q

Polar uncharged amino acids

A

Serine, Threonine, Cystine, Asparagine Glutamine, Tyrosine

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283
Q

Polar acidic amino acids

A

Aspartate, Glutamate

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284
Q

Polar basic amino acids

A

Lysine, Arginine, Histidine

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