8. RESPIRATORY SYSTEM Flashcards
LARGE AND SMALL ANIMALS
gas exhange in lungs because pO2 is higher in
alveolar air that in venous blood that reaches lungs > O2 will diffuse from alveolar air to blood
pCO2 is higher in
blood > diffusion to alveoli
at high altitudes O2 uptake is reduced
due low pO2 inhaled air
transport of O2 in blood
98,5% bound to hemoglobin
>rest dissolved in plasma
binding of O2 to hemoglobin
1 hemoglobin molecule can transport 4 O2 molecules
when all iron atoms in all hemoglobin molecules in blood have bound O2
hemoglobin saturation is 100%
>ocyhemoglobin and deoxyhemoglobin
> saturation is also influenced by pO2
O2 consumption per unit body mass is greater in small animals than in large ones > in small animals
-high density of capillaries
-low affinity of hemoglobin for O2
respiratory tract dfence mechanisms
-coughing
-sneezing
-production of secretion, change in viscosity of secretion
cough 1 protective reflex > role:
to remove secretions and foreign particles from respiratory tract
> coughing is also triggered by irritation of MM due to inflammation, secretions and foreign particles
cough 2: cough receptors
in MM of resp.tract > mainly at back of throat, in throat, trachea, bronchi, as well as pleural mucosa
cough 2: signals from receptors are carried through
vagus nerve to cough centre
cough centre
in medulla oblongata and hypothalamus > controlled by cerebral cortex
cough 2 : as result of reflex irritation-signal is initially carried to
cough center and thereafter from centre to muscles of respiration through motor nerve fibers
types of cough
-productive cough; protective reaction-resp.tract is cleared of secretions
-non-productive cough-produced irritation in resp.tract causes decreased blood flow and disorders of resp.system > pressure in chest may increase, blood flow will accumulate in brain > pain and distress to animal
cough suppression
- direct suppression of cough centre
- reduction of irritation of inflamed MM of resp.tract
substances suppressing cough centre, opioids
-codeine,hydrocodone-opium alkaloids, part of narcotic analgesic group
-butorphanol-narcotic analgesic: also used cough centre suppressant in dogs
suppression of cough centre in
medulla oblongata , indication is dry, non-productive cough
codeine is partially metabolized in organism into
morphine
>effect of codeine itseld on CNS is substantially weaker than morphine
substances suppressing cough centre, non-opioids
- dextromethorphan-part narcotic analgesic group.non-opioid nature
>no analgesic or sedative effect
-causes only depression of CNS in large doses
> effect on cough centre weaker than opioids
>often used together with antihistamines, mucolytic drugs or bronchodilators - diphenhydramine-antihistamine > cough centre suppressant effect unclear, use cough suppressant
expectorants (mucolytics) substances aiding in clearance of
phlegm from airways, mucolytic drugs
> ease excretion of secretions and inflammatory exudate from resp. tract
> incr, motility of ciliated columnar epithelium in bronchial region - thinning secretions, irritating bronchial MM > increase production of thin secretions
expectorants (mucolytics) bromhexine: it makes
secretions thinner
> incr.permeability of alveolar - capillary barrier > ex. ABs can easier penetrate bronchial secretions
acetylcysteine
-mucolytic
-treat paracetamol poisoning dogs, cats
-breaks down disuphide bonds of mucoproteins > sputum becomes thinner
>binds paracetamol metabolites into conjugates
-irritate bronchial MM > bronchial contraction
>not asthmatics!
dembrexine makes
secretions thinner
-horses prep for oral use
not humans
guaifenesin
-mucolytic agent
-horses prep for oral route
bronchodilator agents (4)
- beta (2) adrenomimetics
2.antihistamines - antimuscarinic agents
4- methylxanthines
beta-adrenomimetics (adrenergic agonists)
….-use cautiously for widening bronchi as there are cardiovascular side effects
….-non selective beta agonists
….-selective beta2-agonists used in small animals
…..-selective beta2-agonist, used in horse and cattle
-adrenaline
-isoprenaline, ephedrine
-terbutaline,salbutamol
-clenbuterol
terbutaline produces beta2-receptor-relaxation in
bronchial, vascular and uterine tissues
-used with care: pre-existing cardiac disease, diabetes, hypertension, hyperthyroidism
>salbutamol similar
clenbuterol for treatment of
RAO
antimuscarinis agents :
….in addition to widening of bronchi>large number of side effects exist (tachycardia, decrease GIT motility, urinary tract muscle tone )
-atropine
only used life-threatining bronchospasm
…. antimuscarinic bronchodilators, spasmolytics in small animals, less side - effects
glycopyrrolate, propantheline
methylxanthines: theophylline, euphyllin, aminophylline, theobromine
> relax smooth muscle of bronchi
increase activity of diaphragm
increase cardiac contractility, activity of CNS and diuresis
overdose leads tachycardia, shortness of breath and cramps
effects of theophylline and beta-blockers can be antagonized if administered together
theophylline incr. arrhythmias induced by adrenergic agonists and halothane
theophylline incr, seizures of ketamine
other means of treatments :
-…used in bacterial infections of resp.tract
-…-in case of fever and inflammation
-…-in case of asthma, chronic non-infectious inflammatory diseases
-antibiotics
-NSAIDs
-glycocorticosteroids
respiratory system stimulants; doxapram
-CNS stimulant
-used stimulate breathing during and after anaesthesia in dogs, cats and horses
-occurs via aortic and carotid sinus chemoreceptors
-contraindicated in case of asthma, pulmonary embolism, pulmonary edema and collapsed lung
> side effects incr. BP and cramping
heptaminol+diprophyllin > supportive treatment in case of
acute cardiovascular and/or respiratory insufficiency
>heptaminol-cardiovascular analeptic, effect related to peripheral release of norepinephrine -incr. blood flow in aorta and coronary arteries
>diprophyllin-bronchodilator
asthma 1: bronchoconstriction + inflammation in resp.tract > release of
inflammatory mediators triggers asthma attack
> infl.process trigger permeability of epithelial layer of MM with regard to inflammatory mediators (histamine, cholinergic stimulants)
asthma 2: more permeable epithelial layer of MM enhances mediators reaching
nerve endings located in mucosa, cholinergic bronchoconstriction occurs
> vascular pempeability of BV and production of mucus also increase
> MM sustains damage due to inflammation and MM become extremely sensitive to mediators
treatment of asthma: complex, widening of
bronchi + treatment of inflammation (NSAIDs, glycocorticosteroids, antibiotics) + mucolytic drugs + antihistamines
emphysema: narrowing of
airways, lead to increased resistance of airflow
> expiration is primarily affected > bc. distention of airways is more difficult >increased flow resistance: elevated pressure in lungs
>total area available for diffusion is reduced
>severe deficiency of O2 in tissues
emphysema leads to increased
CO2 supply in body fluids, causing respiratory acidosis
treatment of emphysema
-bronchodilators
-corticosteroids
-NSAIDs
