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week 17 > the pateint > Flashcards

the pateint Flashcards

1
Q

what is aerobic metabolism?

A

Cells require nutrients and oxygen uptake and the removal of carbon dioxide

Distance and dehydration limits of diffusion rate, and therefore size and habitat

There is the development of specialised, internalised respiratory epithelium

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2
Q

what two regions, can we divide the respitory system into

A

Conducting airways

respiratory airways

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3
Q

What is the conducting zone?

A

there is no gas exchange here

It’s refers to the air passages that lead to site of respiration so gas exchange can occur

The passages external to the lungs are:
Nasal cavities
Larynx and pharynx
Trachea
Primary bronchi

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4
Q

What is the time in a part of the conducting system?

A

bronchioles: bronchi within the lungs, branch extensively to form bronchioles

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5
Q

What is the respiratory zone?

A

it is responsible for gas exchange

It’s refers to the zone that is a part of the respiratory system with gas exchange takes place

This includes:
Respiratory bronchioles
Alveolar ducts
Alveolar sacs
Alveoli

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6
Q

What are the nasal cavities lined with?

A

sweat glands
Sebaceous glands
Hair follicles

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7
Q

what does the olfactory mucosa do

A

this is, what’s the nasal cavity is lined with

It’s provides a sense of smell

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8
Q

what is repiratory mucosa

A

this is what the nasal cavity is also lined with

It secretes an anti-bacterial enzyme and mucus

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9
Q

What is the main purpose of the function of the nasal cavities?

A

to warm, humidify and filter inhaled air

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10
Q

what are the three sections of the pharynx

A

nasaopharynx, oropharynx, laryngopharynx

Part of the digestive system and respiratory system

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11
Q

what is the epiglottis

A

It’s forms an important physical separation

It is a flap that covers the trachea during swallowing, so that food does not enter the lungs

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12
Q

What is the function of the larynx?

A

it is required for speech

It’s contains to vocal folds, which vibrate with breathing

Laryngeal muscles alter tension, positioning of the folds to create different sounds

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13
Q

What is the structure of the trachea?

A

The trachea is slightly flattened, connecting the upper and lower airways (nasal and bronchiole Airways)

It’s has C-shaped cartilage rings which allows flexibility and also prevents the trachea collapsing

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14
Q

What is the function of the bronchi?

A

they help to defended the airways

Goblet cells produce, sticky mucus to trap bacteria

Bronchial epithelial cells produce antimicrobial peptides

Ciliated epithelium cells beat the mucus to the pharynx

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15
Q

what is the mucociliary escalator

A

sticky mucus made of glycoproteins, traps inhaled particles and bacteria

Celia project into the periciliary fluid and a liquid layer secreted by epithelial cells

The action of the ciliary beating the move, the mucus raft to the back of the throat

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16
Q

what are factors that slow mucociliary transport

A

cigarette smoke
Dehydration
Positive pressure ventilation
Endotracheal suctioning
High inspired, oxygen concentrations
Hypoxia
Atmospheric pollutants
General anaesthesia
Parasympatholytic drugs

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17
Q

what are the alveolar ducts and sacs

A

alveolar ducts are tiny ducks, connecting respiratory bronchioles to the alveolar sacs

They are surrounded by smooth muscle, elastin, and collage

Each alveolar sac contains a bunch of alveoli

They are structurally important as a maintains the architecture of the lung to permit gas exchange

Alveolar sacs are collections of alveoli, joined by alveoli docs

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18
Q

what to type of cells are alveoli made up of?

A

type 1
type 2 (replenish damaged type 1 cells)

pneumocytes

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19
Q

What are alveolar macrophages?

A

they are in the alveoli

And they patrol at the tissue for defence. Provide protection.

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20
Q

What is the function of type one cells?

A

They give a thin barrier for gas exchange

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21
Q

What is the function of type two cells?

A

they secrete a surfactant and defend molecules and repair damage

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22
Q

What is cellular respiration?

A

Biochemical reactions that produce ATP

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23
Q

What is external respiration (ventilation)

A

Physiological process for oxygen and carbon dioxide, uptake, transport and elimination

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24
Q

How does external respiration or ventilation occur?

A

it involves transporting oxygen from the atmosphere to cells

And transport and carbon dioxide from cells to the atmosphere

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25
Q

What are the five important factors in the process of breathing?

A

inspiration
Expiration
Compliance
alveolar surface tension
pulmonary surfactant

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26
Q

what is the parietal pleura

A

lining inside of the throatic cavity

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27
Q

what is the visceral pleura

A

they cover the long in between the pleural space

Are they contain? pleural fluid which reduces friction

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28
Q

what is negative intrapleural pressure

A

where interpleural pressure is less than atmospheric pressure

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29
Q

what is a pneumothorax

A

where damage to the pleural cavity that equalises atmospheric and intrapleural pressure results in a pneumothorax

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30
Q

what happens in a small pneumothorax

A

air Collects between the lung and the chest wall

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31
Q

what happens in a large pneumothorax

A

A lot of air collects and pushes on the lung and heart

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32
Q

what is the treatment of a large pneumothorax

A

Trapped air is removed by using a chest tube

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33
Q

what is pleural effusion

A

fluid in the pleural cavity

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34
Q

what events occur during inspiration

A

thoratic cavity lifts upwards and outwards
external inter coastal muscles contract pulling ribs together
internal inter coastal muscles relax

sternocleidomastoids and scale us pulls ribs up

diaphragm contracts and flattens to increase volume

lungs expand

Pulmonary pressure is less than atmospheric pressure which causes air to flow into the lungs

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35
Q

What event occurred during expiration

A

external intercostal muscles relax. Whereas the internal intercostal muscles contract?

throatic cage lift downwards and inwards

The diaphragm relaxes decreasing its volume and the lungs contract

Pulmonary pressure is greater than atmospheric pressure therefore air is forced out of the lungs

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36
Q

what are the forces during inspiration

A

outward recoil of chest wall

inward recoil of alveoli

air flows in due to pressure gradient

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37
Q

describe passive expansion of alevoli

A

alveoli cannot expand by themselves

they respond passively to an increase in pressure across the alveoli wall

Muscles of inspiration contract, which causes intrapleural pressure to become more negative

TPD increases, Alviola pressure decreases, so Alviola volume increases

Air flows into the alveoli

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38
Q

what is TPD

A

transmural pressure difference

TPD= intrapleural pressure (outside) - alveolar pressure (inside)

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39
Q

what are forces at the end of expiration

A

no airflow

atmospheric pressure = alveolar pressure

inward elastic recoil of alveoli is balanced by outward recoil of chest wall

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40
Q

normal quiet breathing summary inspiration

A

diaphragm contracts
chest wall expands
throatic volume increases
intrapleural pressure becomes more negative
alveolar TPD increases
alveoli expand
pressure difference is established
air flows into alveoli until pressures equilibrate

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41
Q

normal quiet breathing summary expiration

A

inspiratory muscles relax
throatic volume decreases
intrapleural pressure becomes less negative
alveolar TPD decreases
drop in TPD allows alveoli elastic recoil to return to pre inspirstory volume
pressure difference established
air flows out of alveoli
until pressures equilibrate

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42
Q

what is lung compliance

A

change in volume divided by change in pressure
C=changeV/changeP

L/cm^3

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43
Q

what does a lower compliance suggest

A

more intrapleural pressure to change the volume

eg in pulmonary fibrosis which has lead to scarring

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44
Q

what does a higher compliance suggest

A

less pressure is needed

eg in emphysema due to damaged alveoli

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45
Q

what is defined by compliance

A

the measure of the lungs ability to inflate

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46
Q

what affects compliance

A

many diseases

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47
Q

how is compliance measured

A

changes in pressure and colume

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48
Q

how are changes in volume measured

A

spirometry

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49
Q

how are changes in pressure measured

A

more difficult but
a balloon for oesophageal pressure

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50
Q

how does emphysema increase compliance

A

tissue damage
less elastin
easier to inflate
less elastic recoil

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51
Q

how does fibrosis reduce compliance

A

more collagen
harder to inflate
increases elastic recoil

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52
Q

what is elastance

A

is the inverse of compliance
stiff lungs have high elastance and low compliance

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53
Q

what is elastin

A

more compliant
easier to inflate

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54
Q

what is collagen

A

less compliant
harder to inflate

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55
Q

what is alveolar surface tension

A

what makes water form droplets

elastic recoil of the lungs is a function of alveolar surface tension

saline filled lungs have a lower elastance than air filled lungs

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56
Q

what are two factors that stabilise alveoli

A

structural independence of alveoli

pulmonary surfactant

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57
Q

what is alveolar interdependence

A

alveoli are not bunches of grapes, or even Sephias structurally alveoli are polygons with shared flat walls

Alveoli are held open by the chest wall, pulling on the outer surface of the lung

Alveoli are dependent on each other

a Collapsing Alveoli increases the stress on adjacent alveoli, these would tend to hold it open

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58
Q

What is a pulmonary surfactant?

A

it is a complex mixture of lipids and proteins that lines, the alveoli in the lungs

It acts to reduce the surface tension of the fluid that lines, the alveoli, making it easier for the lungs to inflate and preventing the collapse of the alveoli during exhalation

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59
Q

what is produces pulmonary surfactant?

A

type 2 pneumocytes

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60
Q

How does pulmonary surfactant stabilise the lungs?

A

premature babies without functional surfactant have difficulty in inflating their lungs

there is a tendency for spontaneous alveolar collapse

hypoxia may reduce surfactant production and can lead to acute respiratory distress syndrome

neonates are given exogenous surfactant

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61
Q

how do you use a spirometer

A

inverted canister in a water filled space

inner space is connected to tubing into which the person breathes

breathing pattern is traced on the rotating drum

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62
Q

what is tidal volume

A

the amount of air moved in and out the lungs during a normal breath

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63
Q

what is residual volume

A

it is the air that remains in the lungs after maximal exhalation

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64
Q

what is expiratory reserve volume ERV

A

is the additional amount of air that can be forcefully exhaled from the lungs after normal exhalation

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65
Q

what is inspiratory reserve volume

A

the additional amount of air that can be forcefully inhaled into the lungs after normal inhalation

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66
Q

what is functional residual capacity FRC

A

is the volume of air that remains in the lungs after normal exhalation, when the muscles of respiration are at rest

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67
Q

what is inspiratory capacity IC

A

is the maximum amount of air that can be inhaled into the lungs after normal exhlation

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68
Q

what is total lung capacity TLC

A

the maximum amount of air the lungs can hold after maximum inhalation

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69
Q

what is vital capacity VC

A

is the maximum amount of air that can be exhaled forcefully after maximum inhalation

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70
Q

what is restrictive disease

A

eg fibrosis

reduced compliance and increased elastic recoil
increased breathing rate

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71
Q

what is obstructive disease

A

eg emphysema
increased compliance/resistance
decreased elastic recoil
decreased breathing rate

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72
Q

what are limitations of spirometry

A

it can only measure the king volumes exchanged by a conscious con operative subject

it cannot measure
RV
FRC
TLC

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73
Q

what is nitrogen wash out technique

A

it is a way of measuring lung volume

Nitrogen watch out technique (you breathe 100% oxygen, and measure how much nitrogen is expelled)

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74
Q

What is the helium dilution technique?

A

it is another way of measuring lung volume

(Breathe a known volume of helium, and measure the helium left at a steady rate/state)

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75
Q

what is body plethysomography

A

It’s measures the change in pressure in a closed system

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76
Q

how to calculate TLC

A

RV+VC=TLC

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77
Q

how to calculate RV

A

FRC-ERV=RV

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78
Q

what is minute volume

A

is the volume of air entering and leaving the nose every minute

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79
Q

what is anatomical dead space

A

refers to the volume of air that occupies the conducting airways of the respiratory system

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80
Q

What is alveolar ventilation?

A

It’s refers to the volume of air that reaches the alveoli, where the gas exchange occurs per unit of time

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81
Q

what is alveolar dead Space

A

it refers to the portion of the alveoli volume that is ventilated but not perfused

it occurs when the alveoli are ventilated, but do not receive sufficient blood flow for gas exchange.

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82
Q

what is physiological dead space

A

anatomical dead space + Alveolar dead space

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83
Q

what does Boyles law state?

A

The absolute pressure exerted by a given mass of an ideal gas is inversely proportional to the volume it occupies, If the temperature and amount of gas remain unchanged within a close the system.

P1V1=P2V2

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84
Q

What does Boyles law mean?

A

as you breathe in, the volume of your lungs increases, so the pressure decreases, allowing air to flow into the lungs

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85
Q

what does Dalton’s law of partial pressure state?

A

The total pressure exerted by the mixture of non-reactive gases is equal to the sum of the partial pressures of individual gases

86
Q

what does Dalton’s law mean?

A

Changes in the percentage of gas in the lung create a driving force (pressure differential) to move the gases into and out of the lungs

87
Q

what is the calculation for Dalton’s law?

A

P total = P1+P2+P3 exc

88
Q

What does Henry’s law state?

A

at a constant temperature, the amount of a given gas that dissolves in a given to type and volume of liquid is directly proportional to the partial pressure of the gas in the equilibrium with that liquid.

89
Q

What does Henry’s law mean?

A

That’s the amount of oxygen transported into the blood depends on partial pressure. Oxygen has to be transported in the blood as a dissolved gas

90
Q

what happens during oxygen exchange?

A

oxygen is carried physically dissolved in the blood and chemically combined to haemoglobin

Oxygen enters the blood in the lungs down it’s partial pressure gradient

Oxygen leave the blood in the tissues down it’s partial pressure gradient

91
Q

What happens during carbon dioxide exchange?

A

carbon dioxide enters the blood in the tissues down. It’s partial pressure gradient

Carbon dioxide, leave the blood in the lungs down its partial pressure gradient

92
Q

What are factors that affect gas exchange?

A

The rate of gas exchange will be reduced if:

Partial pressure gradient is reduced
Surface area for exchange is reduced
The distance for transfer is increased
The solubility of gases reduced (temperature dependent)

93
Q

Why is the diffusion coefficient for carbon dioxide greater than oxygen?

A

Because carbon dioxide is much more soluble in water than oxygen

94
Q

Haemoglobin let us transports the oxygen we need tell me more

A

4 polypeptide chains to our four and two beta subunits

there is one haem group per polypeptide

One iron group per haem

One oxygen molecule per iron

Each molecule of haemoglobin can carry up to 4 molecules of oxygen

This increases oxygen carrying capacity

95
Q

How do you measure haemoglobin?

A

using a haematocrit

96
Q

What is a haematocrit?

A

It’s measures the percentage of red blood cells in a total volume of blood

It is also sometimes referred to as a packed cell volume (PCV)

It’s usually lies between 37 and 54%

97
Q

What are factors affecting oxygen Carriage by haemoglobin?

A

PH
Partial pressure of carbon dioxide
Temperature

98
Q

what is the bohr effect

A

increase in carbon dioxide, concentration, lowest blood pH. Resulting in the ability of haemoglobin to transport oxygen.

The lower pH causes haemoglobin to release more oxygen

A higher pH causes haemoglobin to hold onto more oxygen

Lactic acid is produced, the pH is a reduced, therefore more oxygen is released at the site of muscle activity . The curve shift to the right.

99
Q

How does increasing the temperature affect oxygen transport by haemoglobin?

A

A small increase in temperature also shift the curve to the right

Blood temperature is higher than metabolically, active tissues

This affect helps to unload oxygen from haemoglobin

At low blood temperature haemoglobin will not release oxygen, and there is a very high affinity for the binding of oxygen in the lungs

100
Q

factors effecting O2 carriage by Hb

2.3 diphosphoglycerate

A

it is produced by red blood cells during normal glycolysis

However, this chemical binds to haemoglobin and reduces the affinity for oxygen

An increase in this chemical will shift the curve to the right

101
Q

How is fetal haemoglobin structure any different to normal adult haemoglobin?

A

Fetal haemoglobin has a higher affinity for oxygen

The curve is shifted to the left

Fetal blood can acquire oxygen from maternal, placental blood

102
Q

What is carboxyhaemoglobin?

A

haemoglobin has a 240 times higher affinity for carbon monoxide than oxygen

Haemoglobin plus carbon monoxide formed carboxyhaemoglobin

This reaction is less reversible and it’s shift the curve to the left

Carbon monoxide prevents oxygen loading into the lungs and oxygen unloading in the tissues

Smoking/urban pollution can increase carboxyhaemoglobin concentration

103
Q

What are the three main ways to transports carbon dioxide?

A

physically dissolved in the blood (10%)
Bound to haemoglobin (30%)
As a HCO3 (60%) bicarbonate

104
Q

describe the transport of carbon dioxide by the blood

A

Carbon dioxide combines with water to form carbonic acid than this disassociates to hydrogen ions and bicarbonate ions

Carbonic anhydrase catalyses this reaction. This is an enzyme that is present at high concentration in red blood cells.

105
Q

What is the chloride shift?

A

Movement of bicarbonate ions out of the red blood cell creates proton gradient. Chloride ions are taken into the red blood cell.

106
Q

what is the haldane effect

A

This allows the blood to load more carbon dioxide at the tissues. Where there is more deoxyhemoglobin and unload more carbon dioxide at the lungs by there is more Oxy haemoglobin.

an increase of oxygen in the blood displaces carbon dioxide from haemoglobin

Therefore, the tendency of haemoglobin to combined with carbon dioxide is decreased. Therefore carbon dioxide is released on return to the alveoli.

This is the opposite of the bohr effect

107
Q

What is the primary function of the respiratory system?

A

It is to take oxygen and to remove carbon dioxide in order to maintain normal levels of partial pressure of oxygen and carbon dioxide

108
Q

What are the three requirements for the respiratory control system?

A

it must be automatic
It must be adaptable
It must be subject to voluntary control

109
Q

Why must the respiratory control system be automatic?

A

maintenance of carbon dioxide and oxygen levels should not depend on levels of consciousness or alertness

110
Q

Why must the respiratory control system be adaptable?

A

There must be mechanisms to compensate for changes in oxygen uptake or carbon dioxide production

111
Q

Why must the respiratory control system be subject to voluntary control?

A

there must be mechanisms to voluntarily override, the respiratory control mechanisms, at least for brief periods of time

112
Q

What is the central controller?

A

The respiratory centre is located in the medulla oblongata. It receives input from the sensors peripheral and central chemoreceptors.

113
Q

Neural control of respiration is involved with three components what are these?

A

factors that generate inspiration and an expiration rhythm

Factors that to generate magnitude of breathing (depth and rate)

Factors that modify, respiration for other purposes (speaking and coughing)

114
Q

What reduces medullary output?

A

The pneumotaxic centre
the apneustic centre

115
Q

what is the primary respiratory control centre?

A

Medullary respiratory centre

116
Q

What is the dorsal respiratory group (DRG)?

A

it is mostly inspiratory neurons
fire muscles, contract inspiration
Stop muscles relax passive expiration

117
Q

what is the ventral respiratory group (VRG)

A

inspiratory and expiatory neuron’s are in active in normal and quiet breathing

active inspiration/expiration activates

118
Q

what generates respiratory rhythm

A

pre-botzinger complex in the medullary respiratory centre

A network of neurons here display a pacemaker activity

The rate of DRG firing is driven by this complex

119
Q

what does the pneumotaxic centre do

A

it is where the impulses are sent to the DRG

It’s switches off Inspiratory neuron’s

Its limits inspiration

120
Q

what does the apneustic centre do

A

It’s prevents inspiratory neurons stopping

It’s boosts inspiratory drive

121
Q

what happens when there is no pneumotaxic centre

A

creates apneustic breathing

There is a prolonged inspiration with brief, expiatory, gasps,

It is associated with some to severe brain damage

122
Q

Why is cooperation key in the raspatory centres?

A

they cooperate to regulate the rate and depth of breathing as an involuntary unconsciousness activity

respiratory centre responds to the physiological needs of the body for oxygen and carbon dioxide, exchange and for blood acid-base balance 

123
Q

What does the PRG control?

A

Timing of inspiration, speech and sleep

124
Q

What is the central pattern generator?

A

there is no single pacemaker in your own responsible for initiating, breathing, groups of neurons generate bursts of activity

Breathing requires a complex interaction of at least six groups of neurons

There is three phases to the respiratory cycle

125
Q

What are the overall three phases of the respiratory cycle?

A

inspiratory phase
Post inspiratory phase (expiatory phase 1)
Expiatory phase 2

126
Q

What happens in inspiratory phase?

A

neuronal activity: there is a sudden onset by early inspirtory neutrons this is followed by a ramp increase in inspiratory augmenting neurons

Muscular effector function: inspiratory muscle contraction

127
Q

What happens in post inspiratory phase (expiatory phase 1)

A

neuronal activity: reduced discharge from inspiratory, augmenting neurons, expiatory, decrementing, active

Muscular effect to function: reduced activity of inspiratory muscles: passive expiration

128
Q

What happens in expiatory, phase 2

A

neuronal activity: expiatory, augmenting neurones can be activated

Muscular effector function: inspiratory muscles are silent; expiatory muscle activity increases gradually.

129
Q

What usually happens in quiet, breathing

A

Expiration almost completely is passive

130
Q

What happens in active breathing?

A

Exploration almost is completely active; there is high activity of expiatory augmenting neurons

131
Q

What to do chemoreceptors do?

A

They determine partial pressure of oxygen and carbon dioxide and hydrogen ions and provide feedback to the breathing centres of the brain to modify rate and tidal volume

132
Q

What are the two types of chemoreceptor?

A

Central and peripheral

133
Q

Where are central chemo receptors found?

A

in the Medulla

134
Q

What does an increase in partial pressure of carbon dioxide do?

A

It increases ventilation

135
Q

What do central chemoreceptors respond to?

A

Partial pressure of carbon dioxide

136
Q

Where are peripheral chemo receptors found?

A

in the neck and thorax

137
Q

What does the peripheral chemo receptors do?

A

They detect changes in oxygen and carbon dioxide

They respond to partial pressure of oxygen

138
Q

What is hypoventilation?

A

A reduced breathing rate

139
Q

what does hypo ventilation lead to?

A

Can produced an increased partial pressure of carbon dioxide and a reduced partial pressure of oxygen

140
Q

what does hyperventilation lead to?

A

an decrease in ventilation

141
Q

What are the five cardinal signs of inflammation?

A

Redness (rubor)
Swelling (turgor)
Heat (calor)
Pain (dolor)
Loss of function

142
Q

what is the triple response

A

A model of neurogenic inflammation

Whitening, wheal, and flare

143
Q

Under what conditions does inflammation appear

A

it is a consequence of injury, infection or other disease

144
Q

What is chronic inflammation

A

present within weeks/months after insult

Greater tissue destruction

Cellular infiltrate

More fibrous tissue present

145
Q

What is acute inflammation?

A

rapid in onset

Duration is day is two weeks

Changes in blood flow

An increase in vascular permeability

Accumulation of protein, rich oedema fluid (white blood cells)

146
Q

What are the possible outcomes of acute inflammation?

A

resolution

Abscess formation (suppuration)

Healing (scar)

Chronic inflammation

147
Q

What is the stereotypical response in acute inflammation?

A

local changes to their microcirculation

Increased blood flow to the capillaries

Increased permeability

Escape of plasma and plasma proteins to form serous exudate

Escape of white blood cells

148
Q

What does changes in vasculature blood flow mean?

A

that is a possible smooth muscle response

Widespread dilation of arterioles, and venules
hyperaemia 10x more blood flow

Construction of veins, leading to the local increase in pressure

Leakage of plasma leads to slowing of blood flow in vessels (stasis) encouraging cell, adhesion and clotting

149
Q

What does vascular permeability lead to?

A

an increase in pressure which causes increased

exudate carrying foreign matter carried to lymph glands, where immune response is initiated

150
Q

What does white blood cell recruitment entail?

A

expression of adhesion molecules

emigration of neutrophils

Directed to the site of injury/infection by chemo, taxis

Neutrophils are predominant in the first 24 hours

151
Q

What is the role of neutrophils?

A

they live for 3 to 4 days

They die at the inflammatory site

The phagocytose and engulf and remove agent

Microbial killing is achieved by lysosomal enzymes and free radicals generated in the respiratory burst

152
Q

what are morphological features

A

Cardinal signs

Severe skin injury (blisters)

Epithelial injury

Boil (collection of neutrophils and debris is pus)

153
Q

What are the advantages of the effects of acute inflammation?

A

Dilution of toxins

plasma protein, release (antibodies)

Fibrin formation

cell nutrition

plasma mediator system, activated

Promotes immunity

154
Q

What are the harmful effects of acute inflammation?

A

swelling (obstruction of breathing)

Interference with blood flow (meningitis)

Inappropriate inflammation

155
Q

What are the resolutions of acute inflammation?

A

removal of stimulus
No permanent loss of function
Associated with healing

Excessive scarring

156
Q

What happens in chronic inflammation

A

main white blood cell is macro phage

Healing and repair coexists with inflammation

Fibrosis is main cause of loss of function

157
Q

what are eicosanoids

A

they are a group of signalling molecules that are derived from poly unsaturated fatty acids

They are produced locally in response to stimuli, such as injury or infection

They are 20 carbon fatty acids from membrane phospholipids, which are oxygenated and poly unsaturated

158
Q

what is PGE2 in inflammation?

A

It’s causes pain

It enhances bone turnover and cartilage degradation in arthritis

It acts on called sensitive neurons in the hypothalamus (fever)

159
Q

what does LTB4 do

A

Neutrophil activation

160
Q

what does LTC4 and LTD4 do

A

They increase vasodilation

161
Q

what does LTC4, D4 and E4 do

A

The increase mucus secretion (asthma)

162
Q

What is histamine?

A

it is an amine that has many actions in both the periphery, and in the central nervous system

It is released in type, one hypersensitivity. Common in allergies and allergens, including contact, dermatitis, eczema, hayfever, food allergy

163
Q

Tell me more about histamine

A

it is a basic amine

It is actively taken up by platelets

It is found in mast cells and other white blood cells, some nerves and specialised cells in the gut

H1 is involved in inflammation
H2 is released in the acid in the stomach

H1-H3 are GPCR receptors

164
Q

describe the pathophysiology of the H1 Receptor

A

It’s causes muscle contraction and increases post capillaries venule permeability

It’s a decrease in blood pressure, mainly by receptors on the arterioles, but constrict blood blood vessels

H1 receptors on nerve endings cause itch

They have a role in allergy and hayfever due to an increase in vascular permeability

165
Q

what is the bradykinin cascade

A

tissue injury and collagen exposure
Leads to activation of clotting cascade

kallikrein and kinases

Activation of sensory nerve endings an increase in vascular permeability

166
Q

what is substance P

A

it has 11 amino acid nuclear found in sensory nerves

a member of the neurons in family of peptides

pain transmitter in the spinal cord

releases histamine and other inflammatory mediators

mediator of neurogenic inflammation

167
Q

opioid peptides

A

endorphins and enkaphalins

block pain transmission at the spinal cord

stimulate pathways in the brain to block pain transmission and perception

168
Q

what are similarities between T and B cells

A

they are lymphocytes

they develop in the bone marrow

they have diverse AG receptors on their surface

169
Q

why are T cells unlike B cells

A

they mature in the thymus

exert their functions by interacting with other cells of the immune system

they recognise different Ag (peptides, processed, presented with MHC)

they never release a soluble Ag receptor

their receptor doesn’t change on Ag recognition

170
Q

what does the Fc region of an antibody do

A

talks to the rest of the immune system

171
Q

what does the Fab region of the antibody do

A

binds to Ag

172
Q

what is the TCR

A

the T cell receptor

antigen receptor of T cells

resembles a membrane associated Fab fragment of immunoglobulin

173
Q

describe the structure of the TCR

A

membrane bound glycoprotein
(heterodimer)

one Ag binding site

Ag binding at the top surface

two transmembrane domains per chain

short cytoplasmic tail

174
Q

what does the one Ag binding site in the TCR
consist of

A

one alpha chain TCR alpha
one beta chain TCR beta

175
Q

what are the hyper variable regions on a TCR molecule

A

Complimentary determining regions (CDRs)

On loops at tip

176
Q

how does TCR diversity effect gene arrangement

A

happens pre-antigen
gene segment recombine for each chain (DNA rearrangement)

Essentially, using the same mechanisms as for B cells

177
Q

what is different with TCR and B cells

A

in B cells, after Ag binding, heavy chain, constant regions could change (class, switching of Ab)

This doesn’t ever happen with the TCR

178
Q

what consists of the alpha chain

A

V&J regions
only 1C region

179
Q

what consists of the beta chain

A

V,D and J regions
2C regions but there is no functional difference

180
Q

what do alpha chains like

A

light chain (V-J)

181
Q

what do beta chains like

A

heavy chains

(D-J) then (V-DJ)

182
Q

why is RAG important (RAG1 and RAG2)

A

recombination activating gene

183
Q

what is RSS

A

Recombination signal sequences

184
Q

what is SCID

A

severe combined immunodeficiency

Happens when there is a lack of functional B and T cells

opportunistic infections

lethal during infancy unless treated or BM transplant

various mutations can cause this including RAG defects

185
Q

list ways in which there could be TCR diversity

A

rearrangement of the gene segment (DNA)

Transcription (RNA)

Splicing (mRNA)

Translation (rough endoplasmic reticulum)

Endoplasmic reticulum (Association of alpha and beta chains, transport to T cell serface)

186
Q

explain how extra proteins are needed for TCR expression

A

TCR complex is required for exit from ER

4 invariant chains are required

held together with strong electrostatic interactions

Signalling components of TCR

Defects here lead to immuno deficiency

187
Q

what are the two classes of T cell population

A

a chain & b chain
y chain and sigma chain 1-5%
less frequent
Less studied
Less variable

188
Q

how do T cells recognise Ag

A

though TCR

189
Q

what is the TCR complex required for

A

Required for trafficking and signalling

190
Q

why are there two different classes of MHC and T cell

A

to deal with different pathogens (intracellular/extracellular)

To interact with different T cells

191
Q

How do T cells help?

A

defined to an antigen on either a macro phage or B cell (MHC)

Cytokines, then destroy this antigen

Correct antibodies are now formed from the plasma cell, or there is an activated macro phage

CD4

192
Q

how do T cells kill

A

CD8 T cell binds to a virus, infected cell

There is a cell contact

Lysozymes are released and a dead virus infected cell is produced

193
Q

what does MHC do

A

allows CD4/CD8 to bind

194
Q

what does the MHC bind to

A

CD8/CD4 and TCR + (co-receptor)

195
Q

what are the 2 major compartments of a cell

A

cytosol
vesicular system

196
Q

what is the cytosol

A

peptides from intracellular pathogens

197
Q

what is the vesicular system

A

peptides from extracellular pathogens

198
Q

What is the class one pathway?

A

cytosolic proteins are degraded
This generates peptides
Which are transported into the endoplasmic reticulum lumen
TAP (transporter of antigenic, peptides), transport class, one type, peptides
chaperone holds MHC1 til it binds
Peptide loading complex is formed
TAP delivers the peptide
The complex disassociates, and it is loaded to the surface
MHC1 is loaded with a peptide that is too long at the N-terminus
ERAP removes terminal amino acids to give a peptide of 8 to 10 residues
MHC class 1 molecule travels to the cell surface

199
Q

what can class 1 not do

A

leave the ER without a peptide

200
Q

what happens in Bare lymphocyte syndrome

A

non functional TAP
peptides cannot enter the endoplasmic reticulum
That is very low levels of surface MHC class 1

That is a low cytotoxic, T cell response (CD8)

Chronic respiratory infections, poor response to viruses

201
Q

what else do MHC class 1 do

A

display self antigens too

displays peptides derived from normal self proteins

there is no immune response to these, unless self reactive T cells have been allowed to leave the thymus (autoimmunity)

202
Q

what is the MHC class 11 (2) pathway

A

phagocytosis
Phagosome
Lysosome function
Peptide formation

Vesicular fusion
Peptide loading

binding of peptides to MHC class 11 molecules in the ER
in vesicles invariant chain is cleaved leaving the CLIP fragment bound
CLIP blocks binding of peptides to MHC class 11 in vesicles
HLA-DM facilitate the release of CLIP
Allowing peptides to bind

203
Q

MHC 1 expression profile

A

most human cells

204
Q

MHC class 11 expression profiles

A

professional (APC)
thymic epithelium for T cell testing

205
Q

what are MHC molecules

A

polygenic
enclosed by different gene families
different classes
clustered in chromosomal region MHC
are polymorphic

206
Q

another word for different variants

A

isotypes

207
Q

another word for different alleles

A

allotypes

208
Q

how many MHC class 1 does each human cell contain

A

3 class 1 from each parent
6 class 1 per cell

209
Q

how does MHC prevent a population being susceptible to a single infection?

A

Permits lots of different peptide presentations

210
Q

what is MHC a primary reason for

A

it is the major reason for transplant rejection, so a perfect match is needed (twins or clones)

week 17 (3 decks)

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