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Quick resp physiology Flashcards

(69 cards)

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1
Q

host defence

A

intrinsic, innate, adaptive

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2
Q

intrinsic defence

A

always present
4 main ways
- epithelial barrier of respiratory tract secretes anti-fungal and anti-microbial peptides
- mucus
- coughing/ sneezing
- muco-ciliary escalator

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3
Q

innate defences

A

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

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4
Q

adaptive immunity

A

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

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5
Q

type 1 hypersensitivity

A

allergies
IgE produced
bind to mast cells (mature basophils)
when an antigen binds to IgE on mast cell, histamine and cytokines are released
anaphylaxis

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6
Q

type 2 hypersensitivity

A

IgG or IgM bind to antigens on CSM of self-cells
cells with the antigen are destroyed by antibodies
cytotoxic hypersensitivity
blood transfusion

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7
Q

type 3 hypersensitivity

A

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

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8
Q

type 4 hypersensitivity

A

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

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9
Q

effect of turbinates on nose SA

A

at least doubles

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10
Q

which nerve supplies frontal sinuses?

A

opthalmic division of the trigeminal
CN V1

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11
Q

how and where does the maxillary sinuses open into the nose?

A

middle meatus
hiatus semilunares

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12
Q

innervation of ethmoid sinus

A

CNV 1

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13
Q

where does the Eustachian tube enter?

A

nasopharynx

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14
Q

folds of oropharynx

A

palatoglossal fold attached to tongue
palatopharyngeal fold attached to pharynx

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15
Q

how many cartilages make up larynx?

A

9

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16
Q

paired larynx cartilages

A

cuneiform, corniculate and arytenoid

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17
Q

single larynx cartilages

A

epiglottis
thyroid cartilage
cricoid cartilage below thyroid

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18
Q

cricothyroid membrane

A

between cricoid and thyroid cartilages
emergency airway

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19
Q

superior laryngeal nerve

A

sensory innervation to larynx

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20
Q

motor innervation of larynx

A

RLN

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21
Q

medullary respiratory groups

A

control inspiration and expiration basic rhythm

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22
Q

pontine groups

A

rate of breathing
control the transition between inspiration and expiration

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23
Q

DRG

A

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

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24
Q

VRG

A

forced expiration
usually inactive
contracts internal intercostals and rectus abdominis for forced expiration

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25
pneumotaxic
inhibits DRG shallower and faster breaths commit 'tax' fraud and run away inhibits apneustic
26
apneustic
stimulates DRG prolongs inspiration longer, deeper breaths
27
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
28
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
29
stretch receptors
SASR RASR bronchi and bronchioles visceral pleura detect stretch signals sent to respiratory centres via vagus Hering-Breuer reflex
30
irritant receptors
under pseudostratified ciliated columnar epithelium in large airways respond to irritants signals sent to respiratory centres via vagus cough reflex
31
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
32
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
33
V/Q at apex of lung
3.3
34
V/Q at base
0.63
35
dead space causes and response
pulmonary embolism local bronchoconstriction
36
shunt causes and response
pneumonia hypoxic pulmonary vasoconstriction
37
what shifts curve to left
fall in - H+ - less acidic - temperature - 2-3 BPG (2-3 bisphosphoglycerate) - altitude - HbF
38
Boyle's Law
P1V1 = P2V2
39
Dalton's Law
Ptotal = p1 + p2 + p3...
40
Henry's Law
S1/ P1 = S2/P2
41
Laplace's Law
P = 2T/R
42
alveolar gas equation
pAO2 = piO2 - (paCO2/resp Q) resp q is 0.8
43
causes of hypoxia
hypoventilation blocked airway thoracic cage abnormalities abnormality in respiratory centre V/Q mismatch - shunt diffusion impairment shunt of heart altitude CO
44
causes of hypercapnia
hypoventilation COPD DRG issues V/Q mismatch producing too much in body
45
umbrella causes of respiratory failure
type 1 infective, congenital, airway, parencyma, vasulature type 2 - airway - drugs - metabolic - polyneuropathy
46
ageing lungs
less elasticity less compliant weaker muscles less recoil worsened immune functions decreased response to hypoxia and hypercapnia
47
learn values for volumes and capacities
.
48
functional residual capacity
air left in lungs after non forced exhalation ERV + RV
49
FEV1
volume of air that can be forcible exhaled in 1 second
50
normal FEV1/ FVC
0.8
51
FEV1/FVC for obstructive disease
less than 0.7 FEV1 falls so ratio falls
52
obstructive disease
affect elasticity and compliance of lungs compliance increases elasticity decreases
53
restrictive disease
FVC lowered as lungs can't contain as much air ratio looks fine tuberculosis pulmonary fibrosis compliance decreases elasticity increases
54
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
55
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
56
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
57
parasympathetic airway receptor
Ach to M3 muscarinic receptor
58
sympathetic airway receptor
B2 adrenergic NAD
59
cholinergic receptors
bind to ach muscarinic and nicotinic types whilst adrenergic ones bind to adrenaline
60
where do we find muscarinic receptors?
smooth muscle, cardiac muscle, some glands smooth muscle of bronchi and bronchioles
61
where can we find nicotinic receptors?
autonomic ganglia NMJ and smooth muscle of bronchi and bronchioles
62
normal pH
7.4
63
henderson hasselbach
pH = 6.1 + log10([HCO3-]/ 0.0307 x pCO2) logarithm should be 1.3 so total equals 7.4
64
changing bicarbonate ion concentration
metabolic acidosis/ alkalosis
65
changing co2 conc
respiratory change
66
restore acidosis/ alkalosis
respiratory rate or reabsorbtion or production or bicarbonate ions or hydrogen ions renal compensation
67
respiratory acidosis
high pco2 low ph slight increase in bicarbonate (to compensate for acid)
68
respiratory alkalosis
low pco2 high ph slightly low bicarb
69
physiological dead space
alveolar and anatomical 25 and 150

Phase 1 flashcards (27 decks)

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