Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 1 flashcards > Quick resp physiology > Flashcards

Quick resp physiology Flashcards

1
Q

host defence

A

intrinsic, innate, adaptive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

effect of turbinates on nose SA

A

at least doubles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

which nerve supplies frontal sinuses?

A

opthalmic division of the trigeminal
CN V1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

middle meatus
hiatus semilunares

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

innervation of ethmoid sinus

A

CNV 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

where does the Eustachian tube enter?

A

nasopharynx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

folds of oropharynx

A

palatoglossal fold attached to tongue
palatopharyngeal fold attached to pharynx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how many cartilages make up larynx?

A

9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

paired larynx cartilages

A

cuneiform, corniculate and arytenoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

single larynx cartilages

A

epiglottis
thyroid cartilage
cricoid cartilage below thyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

cricothyroid membrane

A

between cricoid and thyroid cartilages
emergency airway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

superior laryngeal nerve

A

sensory innervation to larynx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

motor innervation of larynx

A

RLN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

medullary respiratory groups

A

control inspiration and expiration basic rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

pontine groups

A

rate of breathing
control the transition between inspiration and expiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

VRG

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

pneumotaxic

A

inhibits DRG
shallower and faster breaths
commit ‘tax’ fraud and run away
inhibits apneustic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

apneustic

A

stimulates DRG
prolongs inspiration
longer, deeper breaths

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

peripheral chemoreceptors

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

central chemoreceptors

A

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
Q

stretch receptors

A

SASR
RASR
bronchi and bronchioles
visceral pleura
detect stretch
signals sent to respiratory centres via vagus
Hering-Breuer reflex

30
Q

irritant receptors

A

under pseudostratified ciliated columnar epithelium in large airways
respond to irritants
signals sent to respiratory centres via vagus
cough reflex

31
Q

Juxtacapillary receptors

A

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
Q

7 layers for gas exhange

A

alveolar epitheelium
interstitial fluid
capillary endothelium
plasma layer
RBC membrane
RBC cytoplasm
Hb binding site
apes in capes protect red riding hood

33
Q

V/Q at apex of lung

A

3.3

34
Q

V/Q at base

A

0.63

35
Q

dead space causes and response

A

pulmonary embolism
local bronchoconstriction

36
Q

shunt causes and response

A

pneumonia
hypoxic pulmonary vasoconstriction

37
Q

what shifts curve to left

A

fall in
- H+ - less acidic
- temperature
- 2-3 BPG (2-3 bisphosphoglycerate)
- altitude
- HbF

38
Q

Boyle’s Law

A

P1V1 = P2V2

39
Q

Dalton’s Law

A

Ptotal = p1 + p2 + p3…

40
Q

Henry’s Law

A

S1/ P1 = S2/P2

41
Q

Laplace’s Law

A

P = 2T/R

42
Q

alveolar gas equation

A

pAO2 = piO2 - (paCO2/resp Q)
resp q is 0.8

43
Q

causes of hypoxia

A

hypoventilation
blocked airway
thoracic cage abnormalities
abnormality in respiratory centre
V/Q mismatch - shunt
diffusion impairment
shunt of heart
altitude
CO

44
Q

causes of hypercapnia

A

hypoventilation
COPD
DRG issues
V/Q mismatch
producing too much in body

45
Q

umbrella causes of respiratory failure

A

type 1
infective, congenital, airway, parencyma, vasulature
type 2
- airway
- drugs
- metabolic
- polyneuropathy

46
Q

ageing lungs

A

less elasticity
less compliant
weaker muscles
less recoil
worsened immune functions
decreased response to hypoxia and hypercapnia

47
Q

learn values for volumes and capacities

A

.

48
Q

functional residual capacity

A

air left in lungs after non forced exhalation
ERV + RV

49
Q

FEV1

A

volume of air that can be forcible exhaled in 1 second

50
Q

normal FEV1/ FVC

A

0.8

51
Q

FEV1/FVC for obstructive disease

A

less than 0.7
FEV1 falls so ratio falls

52
Q

obstructive disease

A

affect elasticity and compliance of lungs
compliance increases
elasticity decreases

53
Q

restrictive disease

A

FVC lowered as lungs can’t contain as much air
ratio looks fine
tuberculosis
pulmonary fibrosis
compliance decreases
elasticity increases

54
Q

flow volume curves

A

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
Q

altitude

A

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
Q

depth

A

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
Q

parasympathetic airway receptor

A

Ach
to M3 muscarinic receptor

58
Q

sympathetic airway receptor

A

B2 adrenergic
NAD

59
Q

cholinergic receptors

A

bind to ach
muscarinic and nicotinic types
whilst adrenergic ones bind to adrenaline

60
Q

where do we find muscarinic receptors?

A

smooth muscle, cardiac muscle, some glands
smooth muscle of bronchi and bronchioles

61
Q

where can we find nicotinic receptors?

A

autonomic ganglia
NMJ
and smooth muscle of bronchi and bronchioles

62
Q

normal pH

A

7.4

63
Q

henderson hasselbach

A

pH = 6.1 + log10([HCO3-]/ 0.0307 x pCO2)
logarithm should be 1.3 so total equals 7.4

64
Q

changing bicarbonate ion concentration

A

metabolic acidosis/ alkalosis

65
Q

changing co2 conc

A

respiratory change

66
Q

restore acidosis/ alkalosis

A

respiratory rate or reabsorbtion or production or bicarbonate ions or hydrogen ions
renal compensation

67
Q

respiratory acidosis

A

high pco2
low ph
slight increase in bicarbonate (to compensate for acid)

68
Q

respiratory alkalosis

A

low pco2
high ph
slightly low bicarb

69
Q

physiological dead space

A

alveolar and anatomical
25 and 150

Phase 1 flashcards (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions