Quick resp physiology Flashcards
host defence
intrinsic, innate, adaptive
intrinsic defence
always present
4 main ways
- epithelial barrier of respiratory tract secretes anti-fungal and anti-microbial peptides
- mucus
- coughing/ sneezing
- muco-ciliary escalator
innate defences
phagocytosis or inflammation
cell mediated
- neutrophils
- alveolar macrophages
- natural killer cells
which engulf and hydrolyse pathogens
and activate adaptive immune response by presenting the antigen on their surface - APC
non specific
no memory cells
inflammation
- signals and attracts neutrophils and monocytes to an infection site
- how it works:
body tissues release cytokines to activate nearby immune cells
vasodilation occurs to bring more blood cells
swelling and oedema
inflammatory mediators amplify the inflammatory response
adaptive immunity
specific to a pathogen
humoral or cell mediated
humoral - B
cell mediated - T
how it works
- macrophage acts as APC
- T cells differentiate into either one of two types of T helper cells
- Th-1 = cell mediated response
- Th-2 = humoral
Th-1
- activates other cells such as
- macrophages and cytotoxic T cells
- by releasing cytokines (inferferon-gamma)
- pathogens killed by other cells
Th-2
- produces cytokines (interlukin-4)
- activates B lymphocytes
- B lymphocytes produce antibodies which are specific to an antigen
antibody actions
- neutralisation - stops pathogen working
- opsonisation - antibodies make pathogen more visible to macrophages
- complement activation - antibodies activate proteins called complement, which attack pathogens by making holes in them
final stage
- B cells form memory cells so next response is immediate
type 1 hypersensitivity
allergies
IgE produced
bind to mast cells (mature basophils)
when an antigen binds to IgE on mast cell, histamine and cytokines are released
anaphylaxis
type 2 hypersensitivity
IgG or IgM bind to antigens on CSM of self-cells
cells with the antigen are destroyed by antibodies
cytotoxic hypersensitivity
blood transfusion
type 3 hypersensitivity
mediated by antigen-antibody complexes
occurs on exposure to allergen which results in antibody production which will form an antigen-antibody complex
several antigen-antibody complexes hanging around
they are deposited in basement membranes
causes damage to surrounding cells
- the complexes activate the complement cascade
- causes inflammation and histamine release
- attracts macrophages and neutrophils
- called immune-complex hypersensitivity
rheumatoid arthritis
type 4 hypersensitivity
T cells
no antibodies so takes a while to present
delayed type hypersensitivity
CD4+T Helper cells is activated by antigen from APC
cytokines and chemokines released to attract other immune cells
tissue is damaged by inflammation and tissue destruction
contact dermatitis - latex/ poison ivy
same as type 1 but takes longer and with different cell mediators
24-72 h to present
effect of turbinates on nose SA
at least doubles
which nerve supplies frontal sinuses?
opthalmic division of the trigeminal
CN V1
how and where does the maxillary sinuses open into the nose?
middle meatus
hiatus semilunares
innervation of ethmoid sinus
CNV 1
where does the Eustachian tube enter?
nasopharynx
folds of oropharynx
palatoglossal fold attached to tongue
palatopharyngeal fold attached to pharynx
how many cartilages make up larynx?
9
paired larynx cartilages
cuneiform, corniculate and arytenoid
single larynx cartilages
epiglottis
thyroid cartilage
cricoid cartilage below thyroid
cricothyroid membrane
between cricoid and thyroid cartilages
emergency airway
superior laryngeal nerve
sensory innervation to larynx
motor innervation of larynx
RLN
medullary respiratory groups
control inspiration and expiration basic rhythm
pontine groups
rate of breathing
control the transition between inspiration and expiration
DRG
controls inspiration
send impulses to diaphragm and intercostal muscles
phrenic and intercostals
establishes basic breathing rhythm
fires for 2s - inspiration
next 3 seconds, expiration occurs passively
VRG
forced expiration
usually inactive
contracts internal intercostals and rectus abdominis for forced expiration
pneumotaxic
inhibits DRG
shallower and faster breaths
commit ‘tax’ fraud and run away
inhibits apneustic
apneustic
stimulates DRG
prolongs inspiration
longer, deeper breaths
peripheral chemoreceptors
carotid and aortic bodies
sensitive to oxygen and co2
glossopharyngeal and vagus
signals travel from nerve to medulla/ pons
low oxygen
- increase respiratory rate and tidal volume
- direct blood to where needed
- increase cardiac output
central chemoreceptors
medulla
sensitive to pH/ carbon dioxide
H+ conc of CSF
most of respiratory control here
increased carbon dioxide
- more ventilation
or other way around
stretch receptors
SASR
RASR
bronchi and bronchioles
visceral pleura
detect stretch
signals sent to respiratory centres via vagus
Hering-Breuer reflex
irritant receptors
under pseudostratified ciliated columnar epithelium in large airways
respond to irritants
signals sent to respiratory centres via vagus
cough reflex
Juxtacapillary receptors
J fiber or C fiber
in alveoli and pulmonary capillaries
stimulated by fluid build up in lungs and between alveoli and capillary
signals sent to respiratory centres via vagus (again)
rapid, shallow breathing helps oxygen intake
7 layers for gas exhange
alveolar epitheelium
interstitial fluid
capillary endothelium
plasma layer
RBC membrane
RBC cytoplasm
Hb binding site
apes in capes protect red riding hood
V/Q at apex of lung
3.3
V/Q at base
0.63
dead space causes and response
pulmonary embolism
local bronchoconstriction
shunt causes and response
pneumonia
hypoxic pulmonary vasoconstriction
what shifts curve to left
fall in
- H+ - less acidic
- temperature
- 2-3 BPG (2-3 bisphosphoglycerate)
- altitude
- HbF
Boyle’s Law
P1V1 = P2V2
Dalton’s Law
Ptotal = p1 + p2 + p3…
Henry’s Law
S1/ P1 = S2/P2
Laplace’s Law
P = 2T/R
alveolar gas equation
pAO2 = piO2 - (paCO2/resp Q)
resp q is 0.8
causes of hypoxia
hypoventilation
blocked airway
thoracic cage abnormalities
abnormality in respiratory centre
V/Q mismatch - shunt
diffusion impairment
shunt of heart
altitude
CO
causes of hypercapnia
hypoventilation
COPD
DRG issues
V/Q mismatch
producing too much in body
umbrella causes of respiratory failure
type 1
infective, congenital, airway, parencyma, vasulature
type 2
- airway
- drugs
- metabolic
- polyneuropathy
ageing lungs
less elasticity
less compliant
weaker muscles
less recoil
worsened immune functions
decreased response to hypoxia and hypercapnia
learn values for volumes and capacities
.
functional residual capacity
air left in lungs after non forced exhalation
ERV + RV
FEV1
volume of air that can be forcible exhaled in 1 second
normal FEV1/ FVC
0.8
FEV1/FVC for obstructive disease
less than 0.7
FEV1 falls so ratio falls
obstructive disease
affect elasticity and compliance of lungs
compliance increases
elasticity decreases
restrictive disease
FVC lowered as lungs can’t contain as much air
ratio looks fine
tuberculosis
pulmonary fibrosis
compliance decreases
elasticity increases
flow volume curves
look at pictures
positive y axis is expiration
negative y axis is inspiration
sharp point is peak expiratory flow rate
Restrictive is shifted to the Right
altitude
pio2 falls
fio2 same
high altitude pulmonary oedema - pulmonary capillaries leak fluid into air spaces and alveolar walls
due to vasoconstriction
hypertension and overperfusion so capillaries leak
cerebral oedema can also occur
curve shifts right
respiratory alkalosis due to hyperventilation
depth
pressure increases
gas solubility increases - henry
more gas dissolves into tissues
oxygen toxicity as partial pressure of oxygen increases
inert gas narcosis - nitrogen
coming up
- decompression sickness
- pressure rapidly decreases
- air bubbles in circulation
- arterial gas embolism
- pulmonary barotrauma
parasympathetic airway receptor
Ach
to M3 muscarinic receptor
sympathetic airway receptor
B2 adrenergic
NAD
cholinergic receptors
bind to ach
muscarinic and nicotinic types
whilst adrenergic ones bind to adrenaline
where do we find muscarinic receptors?
smooth muscle, cardiac muscle, some glands
smooth muscle of bronchi and bronchioles
where can we find nicotinic receptors?
autonomic ganglia
NMJ
and smooth muscle of bronchi and bronchioles
normal pH
7.4
henderson hasselbach
pH = 6.1 + log10([HCO3-]/ 0.0307 x pCO2)
logarithm should be 1.3 so total equals 7.4
changing bicarbonate ion concentration
metabolic acidosis/ alkalosis
changing co2 conc
respiratory change
restore acidosis/ alkalosis
respiratory rate or reabsorbtion or production or bicarbonate ions or hydrogen ions
renal compensation
respiratory acidosis
high pco2
low ph
slight increase in bicarbonate (to compensate for acid)
respiratory alkalosis
low pco2
high ph
slightly low bicarb
physiological dead space
alveolar and anatomical
25 and 150
