the pateint Flashcards

(210 cards)

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
What are the five important factors in the process of breathing?
inspiration Expiration Compliance alveolar surface tension pulmonary surfactant
26
what is the parietal pleura
lining inside of the throatic cavity
27
what is the visceral pleura
they cover the long in between the pleural space Are they contain? pleural fluid which reduces friction
28
what is negative intrapleural pressure
where interpleural pressure is less than atmospheric pressure
29
what is a pneumothorax
where damage to the pleural cavity that equalises atmospheric and intrapleural pressure results in a pneumothorax
30
what happens in a small pneumothorax
air Collects between the lung and the chest wall
31
what happens in a large pneumothorax
A lot of air collects and pushes on the lung and heart
32
what is the treatment of a large pneumothorax
Trapped air is removed by using a chest tube
33
what is pleural effusion
fluid in the pleural cavity
34
what events occur during inspiration
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
35
What event occurred during expiration
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
36
what are the forces during inspiration
outward recoil of chest wall inward recoil of alveoli air flows in due to pressure gradient
37
describe passive expansion of alevoli
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
38
what is TPD
transmural pressure difference TPD= intrapleural pressure (outside) - alveolar pressure (inside)
39
what are forces at the end of expiration
no airflow atmospheric pressure = alveolar pressure inward elastic recoil of alveoli is balanced by outward recoil of chest wall
40
normal quiet breathing summary inspiration
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
41
normal quiet breathing summary expiration
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
42
what is lung compliance
change in volume divided by change in pressure C=changeV/changeP L/cm^3
43
what does a lower compliance suggest
more intrapleural pressure to change the volume eg in pulmonary fibrosis which has lead to scarring
44
what does a higher compliance suggest
less pressure is needed eg in emphysema due to damaged alveoli
45
what is defined by compliance
the measure of the lungs ability to inflate
46
what affects compliance
many diseases
47
how is compliance measured
changes in pressure and colume
48
how are changes in volume measured
spirometry
49
how are changes in pressure measured
more difficult but a balloon for oesophageal pressure
50
how does emphysema increase compliance
tissue damage less elastin easier to inflate less elastic recoil
51
how does fibrosis reduce compliance
more collagen harder to inflate increases elastic recoil
52
what is elastance
is the inverse of compliance stiff lungs have high elastance and low compliance
53
what is elastin
more compliant easier to inflate
54
what is collagen
less compliant harder to inflate
55
what is alveolar surface tension
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
56
what are two factors that stabilise alveoli
structural independence of alveoli pulmonary surfactant
57
what is alveolar interdependence
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
58
What is a pulmonary surfactant?
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
59
what is produces pulmonary surfactant?
type 2 pneumocytes
60
How does pulmonary surfactant stabilise the lungs?
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
61
how do you use a spirometer
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
62
what is tidal volume
the amount of air moved in and out the lungs during a normal breath
63
what is residual volume
it is the air that remains in the lungs after maximal exhalation
64
what is expiratory reserve volume ERV
is the additional amount of air that can be forcefully exhaled from the lungs after normal exhalation
65
what is inspiratory reserve volume
the additional amount of air that can be forcefully inhaled into the lungs after normal inhalation
66
what is functional residual capacity FRC
is the volume of air that remains in the lungs after normal exhalation, when the muscles of respiration are at rest
67
what is inspiratory capacity IC
is the maximum amount of air that can be inhaled into the lungs after normal exhlation
68
what is total lung capacity TLC
the maximum amount of air the lungs can hold after maximum inhalation
69
what is vital capacity VC
is the maximum amount of air that can be exhaled forcefully after maximum inhalation
70
what is restrictive disease
eg fibrosis reduced compliance and increased elastic recoil increased breathing rate
71
what is obstructive disease
eg emphysema increased compliance/resistance decreased elastic recoil decreased breathing rate
72
what are limitations of spirometry
it can only measure the king volumes exchanged by a conscious con operative subject it cannot measure RV FRC TLC
73
what is nitrogen wash out technique
it is a way of measuring lung volume Nitrogen watch out technique (you breathe 100% oxygen, and measure how much nitrogen is expelled)
74
What is the helium dilution technique?
it is another way of measuring lung volume (Breathe a known volume of helium, and measure the helium left at a steady rate/state)
75
what is body plethysomography
It’s measures the change in pressure in a closed system
76
how to calculate TLC
RV+VC=TLC
77
how to calculate RV
FRC-ERV=RV
78
what is minute volume
is the volume of air entering and leaving the nose every minute
79
what is anatomical dead space
refers to the volume of air that occupies the conducting airways of the respiratory system
80
What is alveolar ventilation?
It’s refers to the volume of air that reaches the alveoli, where the gas exchange occurs per unit of time
81
what is alveolar dead Space
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.
82
what is physiological dead space
anatomical dead space + Alveolar dead space
83
what does Boyles law state?
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
84
What does Boyles law mean?
as you breathe in, the volume of your lungs increases, so the pressure decreases, allowing air to flow into the lungs
85
what does Dalton’s law of partial pressure state?
The total pressure exerted by the mixture of non-reactive gases is equal to the sum of the partial pressures of individual gases
86
what does Dalton’s law mean?
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
what is the calculation for Dalton’s law?
P total = P1+P2+P3 exc
88
What does Henry’s law state?
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
What does Henry’s law mean?
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
what happens during oxygen exchange?
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
What happens during carbon dioxide exchange?
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
What are factors that affect gas exchange?
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
Why is the diffusion coefficient for carbon dioxide greater than oxygen?
Because carbon dioxide is much more soluble in water than oxygen
94
Haemoglobin let us transports the oxygen we need tell me more
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
How do you measure haemoglobin?
using a haematocrit
96
What is a haematocrit?
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
What are factors affecting oxygen Carriage by haemoglobin?
PH Partial pressure of carbon dioxide Temperature
98
what is the bohr effect
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
How does increasing the temperature affect oxygen transport by haemoglobin?
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
factors effecting O2 carriage by Hb 2.3 diphosphoglycerate
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
How is fetal haemoglobin structure any different to normal adult haemoglobin?
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
What is carboxyhaemoglobin?
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
What are the three main ways to transports carbon dioxide?
physically dissolved in the blood (10%) Bound to haemoglobin (30%) As a HCO3 (60%) bicarbonate
104
describe the transport of carbon dioxide by the blood
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
What is the chloride shift?
Movement of bicarbonate ions out of the red blood cell creates proton gradient. Chloride ions are taken into the red blood cell.
106
what is the haldane effect
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
What is the primary function of the respiratory system?
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
What are the three requirements for the respiratory control system?
it must be automatic It must be adaptable It must be subject to voluntary control
109
Why must the respiratory control system be automatic?
maintenance of carbon dioxide and oxygen levels should not depend on levels of consciousness or alertness
110
Why must the respiratory control system be adaptable?
There must be mechanisms to compensate for changes in oxygen uptake or carbon dioxide production
111
Why must the respiratory control system be subject to voluntary control?
there must be mechanisms to voluntarily override, the respiratory control mechanisms, at least for brief periods of time
112
What is the central controller?
The respiratory centre is located in the medulla oblongata. It receives input from the sensors peripheral and central chemoreceptors.
113
Neural control of respiration is involved with three components what are these?
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
What reduces medullary output?
The pneumotaxic centre the apneustic centre
115
what is the primary respiratory control centre?
Medullary respiratory centre
116
What is the dorsal respiratory group (DRG)?
it is mostly inspiratory neurons fire muscles, contract inspiration Stop muscles relax passive expiration
117
what is the ventral respiratory group (VRG)
inspiratory and expiatory neuron’s are in active in normal and quiet breathing active inspiration/expiration activates
118
what generates respiratory rhythm
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
what does the pneumotaxic centre do
it is where the impulses are sent to the DRG It’s switches off Inspiratory neuron’s Its limits inspiration
120
what does the apneustic centre do
It’s prevents inspiratory neurons stopping It’s boosts inspiratory drive
121
what happens when there is no pneumotaxic centre
creates apneustic breathing There is a prolonged inspiration with brief, expiatory, gasps, It is associated with some to severe brain damage
122
Why is cooperation key in the raspatory centres?
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
What does the PRG control?
Timing of inspiration, speech and sleep
124
What is the central pattern generator?
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
What are the overall three phases of the respiratory cycle?
inspiratory phase Post inspiratory phase (expiatory phase 1) Expiatory phase 2
126
What happens in inspiratory phase?
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
What happens in post inspiratory phase (expiatory phase 1)
neuronal activity: reduced discharge from inspiratory, augmenting neurons, expiatory, decrementing, active Muscular effect to function: reduced activity of inspiratory muscles: passive expiration
128
What happens in expiatory, phase 2
neuronal activity: expiatory, augmenting neurones can be activated Muscular effector function: inspiratory muscles are silent; expiatory muscle activity increases gradually.
129
What usually happens in quiet, breathing
Expiration almost completely is passive
130
What happens in active breathing?
Exploration almost is completely active; there is high activity of expiatory augmenting neurons
131
What to do chemoreceptors do?
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
What are the two types of chemoreceptor?
Central and peripheral
133
Where are central chemo receptors found?
in the Medulla
134
What does an increase in partial pressure of carbon dioxide do?
It increases ventilation
135
What do central chemoreceptors respond to?
Partial pressure of carbon dioxide
136
Where are peripheral chemo receptors found?
in the neck and thorax
137
What does the peripheral chemo receptors do?
They detect changes in oxygen and carbon dioxide They respond to partial pressure of oxygen
138
What is hypoventilation?
A reduced breathing rate
139
what does hypo ventilation lead to?
Can produced an increased partial pressure of carbon dioxide and a reduced partial pressure of oxygen
140
what does hyperventilation lead to?
an decrease in ventilation
141
What are the five cardinal signs of inflammation?
Redness (rubor) Swelling (turgor) Heat (calor) Pain (dolor) Loss of function
142
what is the triple response
A model of neurogenic inflammation Whitening, wheal, and flare
143
Under what conditions does inflammation appear
it is a consequence of injury, infection or other disease
144
What is chronic inflammation
present within weeks/months after insult Greater tissue destruction Cellular infiltrate More fibrous tissue present
145
What is acute inflammation?
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
What are the possible outcomes of acute inflammation?
resolution Abscess formation (suppuration) Healing (scar) Chronic inflammation
147
What is the stereotypical response in acute inflammation?
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
What does changes in vasculature blood flow mean?
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
What does vascular permeability lead to?
an increase in pressure which causes increased exudate carrying foreign matter carried to lymph glands, where immune response is initiated
150
What does white blood cell recruitment entail?
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
What is the role of neutrophils?
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
what are morphological features
Cardinal signs Severe skin injury (blisters) Epithelial injury Boil (collection of neutrophils and debris is pus)
153
What are the advantages of the effects of acute inflammation?
Dilution of toxins plasma protein, release (antibodies) Fibrin formation cell nutrition plasma mediator system, activated Promotes immunity
154
What are the harmful effects of acute inflammation?
swelling (obstruction of breathing) Interference with blood flow (meningitis) Inappropriate inflammation
155
What are the resolutions of acute inflammation?
removal of stimulus No permanent loss of function Associated with healing Excessive scarring
156
What happens in chronic inflammation
main white blood cell is macro phage Healing and repair coexists with inflammation Fibrosis is main cause of loss of function
157
what are eicosanoids
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
what is PGE2 in inflammation?
It’s causes pain It enhances bone turnover and cartilage degradation in arthritis It acts on called sensitive neurons in the hypothalamus (fever)
159
what does LTB4 do
Neutrophil activation
160
what does LTC4 and LTD4 do
They increase vasodilation
161
what does LTC4, D4 and E4 do
The increase mucus secretion (asthma)
162
What is histamine?
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
Tell me more about histamine
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
describe the pathophysiology of the H1 Receptor
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
what is the bradykinin cascade
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
what is substance P
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
opioid peptides
endorphins and enkaphalins block pain transmission at the spinal cord stimulate pathways in the brain to block pain transmission and perception
168
what are similarities between T and B cells
they are lymphocytes they develop in the bone marrow they have diverse AG receptors on their surface
169
why are T cells unlike B cells
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
what does the Fc region of an antibody do
talks to the rest of the immune system
171
what does the Fab region of the antibody do
binds to Ag
172
what is the TCR
the T cell receptor antigen receptor of T cells resembles a membrane associated Fab fragment of immunoglobulin
173
describe the structure of the TCR
membrane bound glycoprotein (heterodimer) one Ag binding site Ag binding at the top surface two transmembrane domains per chain short cytoplasmic tail
174
what does the one Ag binding site in the TCR consist of
one alpha chain TCR alpha one beta chain TCR beta
175
what are the hyper variable regions on a TCR molecule
Complimentary determining regions (CDRs) On loops at tip
176
how does TCR diversity effect gene arrangement
happens pre-antigen gene segment recombine for each chain (DNA rearrangement) Essentially, using the same mechanisms as for B cells
177
what is different with TCR and B cells
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
what consists of the alpha chain
V&J regions only 1C region
179
what consists of the beta chain
V,D and J regions 2C regions but there is no functional difference
180
what do alpha chains like
light chain (V-J)
181
what do beta chains like
heavy chains (D-J) then (V-DJ)
182
why is RAG important (RAG1 and RAG2)
recombination activating gene
183
what is RSS
Recombination signal sequences
184
what is SCID
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
list ways in which there could be TCR diversity
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)
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explain how extra proteins are needed for TCR expression
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
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what are the two classes of T cell population
a chain & b chain y chain and sigma chain 1-5% less frequent Less studied Less variable
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how do T cells recognise Ag
though TCR
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what is the TCR complex required for
Required for trafficking and signalling
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why are there two different classes of MHC and T cell
to deal with different pathogens (intracellular/extracellular) To interact with different T cells
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How do T cells help?
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
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how do T cells kill
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
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what does MHC do
allows CD4/CD8 to bind
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what does the MHC bind to
CD8/CD4 and TCR + (co-receptor)
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what are the 2 major compartments of a cell
cytosol vesicular system
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what is the cytosol
peptides from intracellular pathogens
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what is the vesicular system
peptides from extracellular pathogens
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What is the class one pathway?
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
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what can class 1 not do
leave the ER without a peptide
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what happens in Bare lymphocyte syndrome
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
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what else do MHC class 1 do
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)
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what is the MHC class 11 (2) pathway
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
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MHC 1 expression profile
most human cells
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MHC class 11 expression profiles
professional (APC) thymic epithelium for T cell testing
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what are MHC molecules
polygenic enclosed by different gene families different classes clustered in chromosomal region MHC are polymorphic
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another word for different variants
isotypes
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another word for different alleles
allotypes
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how many MHC class 1 does each human cell contain
3 class 1 from each parent 6 class 1 per cell
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how does MHC prevent a population being susceptible to a single infection?
Permits lots of different peptide presentations
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what is MHC a primary reason for
it is the major reason for transplant rejection, so a perfect match is needed (twins or clones)