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Cardiorespiratory > :L > Flashcards

:L Flashcards

1
Q

what are major classes of antihypertensive agents? (5)

A

1. angiotension converting enzyme inhibitors (ACE inhbitors): block conversion of angiotension I to II

2. angiotension II receptor blockers

3. dihydropyridine calcium channel blockers:

4. thiazide diuretics: inhibit Na-Cl contransporter in DCT = natriuresis

5. loop diuretics: Inhibit Na-K-Cl cotransporter in loop of Henle = natriuresis

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2
Q

how do loop diuretics work? / mechanism of action?

what does this mean regarding K scerection in urine?

A
  • inhibit the luminal Na-K-2Cl contransporter in thick ascending limb of LoH
  • get increased delivery of Na to distal tubule, enhances K secretion into urine

good for acute response, more research needed for long term reduciton in hypertension

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3
Q

how do calcium channel blockers work?

what are the two major types? & mech of action for each

A
  • block Ca entry to vascualr smooth muscle and myocardial cells: interrupt excitation-contraction coupling

types:

  1. dihydropyridine CCBs: vasodilate dominately. reduced systemic vascular resistance
  2. non dihydropyridine CCBs: reduce HR, contractility, conduction. may worsen heart failure tho
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4
Q

what is angina and how do u treat?

A

angina - restricted blood supply to heart

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5
Q

what is effect of nitroglycerin (and glyceryl trinitrate) in low doses and high doses?

A

low dose:

  • *- decreases preload
  • decrease myocardial o2 demand**

high dose:

  • *- decreases afterload
  • decreaese myocardial o2 demand**
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6
Q

Q

what is MOA for beta blockers for treating angina?

A

Beta Blockers

  • B1 receptor antagonist:
  • causes reduced HR (@ SA node)
  • decrease in o2 demand at SA node
  • negative inotropic effect
  • decrease BP
  • decreased myocardial oxygen demand
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7
Q

what are the two MOA for calcium channgel blockers?

A

- intracellular Ca2+ influx stopped

i) Left ventricle and HR decrease: less o2 consumption in myocardium

_ii) vascular smooth muscle contraction inhibitio_n: coronary artery dilation = coronorary BF increaeed, o2 supply in myocardium increased

decreases angina

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8
Q

what are three types of drugs used for drugs in heart failure?

A
  • positive inotropic drugs
  • vasodilators
  • misceallaneous drugs for chronic failure
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9
Q

what is ejection fraction?

what is normal, borderline and reduced ejection fraction?

A

ejection fraction: compares the measurement of the percentage of blood leaving your heart each time it contracts to the amount of blood pumped oiut

normal ejection fraction: 50-70% (50/70% of blood is pumped out every cardiac cycle)

borderline ejection fraction: 41-49%

reduced ejection fraction: <40%

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10
Q

what 3 movements happen (how) when inhalation occurs?

A
  • *pump handle movement:**
  • during inhalation, get elevation of the ribs: ribs move superior and anterior (increasing diameter)
  • occurs at costal-vertebral joints (ribs & Tvert)
  • *bucket handle movement:**
  • during inhalation: increase lateral diameter of thorax
  • *diaphragm:**
  • during inhalation: flatttens
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11
Q

name 5 chest muscles that involved in inhalation [5]

A

serratus anterior
pectoralis major
pectoralis minor
external intercostal muscles
sternocleidomastoid

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12
Q

describe path of trachea -> alveolar sacs

A

trachea -> main bronchus -> lobar bronchus -> segmental bronchi -> conduncting bronchioles -> terminal bronchioles -> respiratory bronchioles-> Alveolar ducts -> alveolar sacs

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13
Q

where is sensor for the hormonal control of BP?

A

sensor: juxtaglomerular apparatus of the distal tubule of the kidney

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14
Q

which two systems does the juxtaglomerular apparatus of the distal tubule of the kidney control?

A
  • GFR
  • hormonal blood pressure
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15
Q
A
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16
Q

effect of angiotension II on afterload? why?

A
  • angiotension II is a potent vasoconstrictor of smooth muscle of systemic arterioles: raises afterload and therefore BP
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17
Q

what is liddle syndrome / disease?

A
  • enac channels undergo ubiquitination
  • this causes inappropriately elevated sodium reabsorption in the distal nephron
  • this makes have too much water retention and hypertension
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18
Q

what is a different way that renin can be released?

describe how positive feedback can occur because of this alternative renin release xx

A

Renin can also be released by sympathetic stimulation; there are sympathetic nerves to the kidney, and beta receptors on the cells of the juxtaglomerular apparatus.

This raises the possibility of positive feedback; sympathetic stimulation increases renin release, angiotensin then increases noradrenaline release which in turn increases renin release leading to hypertension

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19
Q

what does activation of AT1 receptors cause to occur? [3]

A

AT1:

i) GCPR which increases Ca entry into smooth muscle & constriction to occur
ii) stimualtes noradrenaline release from sympathetic nerve terminlas (can increase BP via SNS too)
iii) found in cells of adrenal cortex: secretes aldosterone

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20
Q

what is bradykinin & how do ACE inhibitors interact with them?

A
  • bradykinin: 9 amino acid peptire
  • ACE inhibitors: increase bradykinin levels by inhibiting its degradation
  • causes a dry cough in patients who take ACE inhibitors (why people often stop taking them)
  • can cause angioedema - occurs 5x higher in African descent: which is why ACE inhibitors are not the first line of drugs for treating hypertension
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21
Q

the airway tree divides how many times? into what two subparts?

A

The airway tree divides 23 times:

  • first 16 divisions make up the conduction airways
  • the last 7 are the respiratory zone
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22
Q

which gland in olfactory cavity produces mucous? [1]

A

Bowmans glands

23
Q

what happens in mucous with cystic fibrosis

A

CF:

  • *- mucous is abnormally thick**
  • difficult for cilia to move it
  • require regular physio to cough up and remove it so it doesnt become infected with pathogens
24
Q

why does changing resp. rate for excreting co2 and incoming o2 mean with regards to each other?

A

pressure gradient for co2 is much less than for 02 (6 mmHg vs 60 mmHg) changing resp. rate can alter excretion of CO2 without significantly affecting uptake of O

25
Q

what is the name for blockage of the eustachian tube ?

A

otitis media - causes build up of mucous / fluid. can be due to inflammation or infection

26
Q

what are the nasopharynx, oropharynx and laryngopharynx innervated by?

A

nasopharynx: CN V2
oropharynx: CN IX
laryngopharynx: CN X

27
Q

how many cartilages are there in the larynx?

which are the paired
which are the unpaired?

A

9 cartilages

three unpaired cartilages: epiglottis, thyroid and cricoid cartilage

three paired cartilages: arytenoid, corniculate and cuneiform

28
Q

at which structure does ithe internal laryngeal nerve and superior laryngeal artery enter larnyx?

A

Internal laryngeal nerve and superior laryngeal artery come through thyrohyoid membrane.

29
Q
A
30
Q

how does right cardiac output match the left cardiac output, but the pulmonary circulation has less pressure? :)

A

Then pulmonary vascular resistance R needs to be much lower than systemic vascular resistance for the cardiac output to be same on both sides of heart.

31
Q

sympathetic innervation to the lungs - where does the action work? which receptors?

A
  • The sympathetic fibres innervate: smooth muscle within the walls of bronchi and small pulmonary vessels –> form plexi around the BV
  • Activation: bronchodilation via beta 2 receptors.

Bronchial muscle relaxation due to sympathetic nerves is greatly augmented by circulating adrenaline

32
Q

what are J receptors?
where found?
stimulated by?
causes?

A

J receptors:

  • location: alveolar walls
  • stimulated by: enlargement of pulmonary capillaries / pulm. oedema
  • causes: brachycardia, hypotension
33
Q

parasympathetic post-ganglionic nerve fibres on airway smooth muscle and mucous glands: ? (NT and receptor)

A

parasympathetic post-ganglionic nerve fibres on airway smooth muscle and mucous glands: Ach & M3 (muscarinic receptors)

34
Q

hat is ventilation AND blood flow (perfusion) like in base v apex?

which (ventilation or blood flow) shows a steeper decline with height of lung?

A
  • blood flow and ventilation are higher at the base of the lungs c.f apex
  • blood flow (Q on graph) shows a steeper decline with height than ventilation

At the base, blood flow is greater than ventilation yet at the apex, blood flow is worse than ventilation

35
Q

what is the V/Q (ventilation: perfusion ratio) like at the

a) base of the lung
b) apex of the lung?

A

what is the V/Q (ventilation: perfusion ratio) like at the

a) base of the lung: less than 1 - around 0.6
b) apex of the lung: more than 1

36
Q

In conditions of airway obstruction V/Q ratio is ?? than normal

In conditions of blood flow obstruction (eg from an embolus) V/Q ratio is ?? than normal.

A

In conditions of airway obstruction V/Q ratio is LOWER than normal

In conditions of blood flow obstruction (eg from an embolus) V/Q ratio is HIGHER than normal.

37
Q

what does hypoxia cause to occur to local blood vessels in alveoli?

A

hypoxia: causes vasoconstriction of the local blood vessels

If ventilation is reduced in one alveolus, then the capillaries around it constrict, and blood is redirected to better ventilated alveoli.

38
Q

which, out of ventilation or perfusion, regulates the other? what does this mean, if have hypoxia?

A

local ventilation regulates local perfusion

39
Q

what is the difference to pulmonary arterial presure and pulmonary arterial resistnace when exercise is undertaken? [2]

A

- pulmonary arterial pressure: increases only slightly during exercise.
- pulmonary arterial resistance: greatly decreasing during exercise (by dilating)

40
Q

what is inspiratory and expiatory reserve volume

A

Inspiratory reserve volume is the volume of air you can draw into your lungs

Expiratory reserve volume is the volume of air you can expel from your lungs

41
Q

how do you calculate forced vital capacity? (2)

A

1) forced vital capacity = Inspiratory reserved volume + tidal volume + expiratory reserve volume
2) forced vital capacity = Inspiratory capacity + expiratory reserve volume

42
Q

what is FEV1?

A
  • FEV1 = volume of air exhaled in in first second of forced exhalation
43
Q

what is normal FEVi/FVC?
where might you see abnormal FEVi/FVC?

A

normal FEVi/FVC: 70-80%
abnormal FEVi/FVC: due to airflow limitation, for example asthma1

44
Q

which accessory muscles are used in forced inhalation? [3]

A

pectoralis major and minor, and the serratus anterior

45
Q

how do you calculate alveolar ventilation?

A

alveolar ventilation: (tidal volume - dead space) x resp rate (breaths per minute)

Tidal volume is 500ml, and anatomic dead space is 150ml. If fresh air entering the lungs is therefore 350 ml, and resp rate is 12 breaths per minute, then alveolar ventilation is 12 x 350 = 4200 ml per minute. This is the effective ventilation that brings abut the exchange of O2 and CO2.

46
Q
A

flow volume loop: measures flow (L/s) (y axis) versus volume (L) (x axis)

  • subject fills lungs to maximum, place tight seal around spirometry mouth piece
  • subject exhales as much as possible: progesses along x axis
  • for every volume air exhaled out, the device measures the corresponding airflow of y axis

force vital capacity: volume measure alonged x axis / the volume exhaled !

47
Q

how do you calculate co2 and o2 exchange?

Room o2 = 21%
alveolar o2 = 14%

Room Co2 = 0.04%
alveolar Co2 = 5.5%

A

o2/ co2 exhancge = volume of alveolar ventilation X (room co2 / o2 - alveoli co2/ o2 / 100)

Room Co2 = 0.04%
alveolar Co2 = 5.5%

Co2 output = 4.2 (volume of alveolar ventilation) X (5.5 - 0.04 / 100) = 0.231 L/min

Room o2 = 21%
alveolar o2 = 14%

O2 input: 4.2 (volume of alveolar ventilation) X (21 - 14 / 100) = 0.294 L/min

48
Q

what is intrapleural pressure a balance between?

what normally like?

A

intrapleural pressure (Ppl)

  • the chest wall and lungs are locked together by the intrapleural fluid in the intrapleural space
  • at the end of exipration get opposing forces:
    a**) lungs: elasticity is causing them to collapse
    b) chest wall: elasticity is causing to spring outwards
  • generates a pressure = P**Pl

intrapleural pressure usually negative with respect to the atmosphere and the air pressure in the alveoli

49
Q

what are the changes that occur in intrapulmonary (pressure in lungs) and intrapleural pressure during inspiratio and expiration?2

A

during each breath, get about 500ml of air in/out of lungs

inspiration:
i_ntrapulmonary pressure:_ becomes more negative / decreases (lung volume increases)
intrapleural pressure: becomes more negative / decreases

expiration:
intrapulmonary pressure: becomes more positive / increase (lung volume decrease)
i_ntrapleural pressure:_ returns to inital value as chest wall recoils

50
Q

how do you calculate compliance in respiratory physiology?

A

compliance = change in volume / change in pressure

51
Q

explain how emphysema’s effect on lung compliance (2)

A

desctruction of the alveoli: elastic fibres and collagen lost

  • causes impaired elastic recoil
  • lung is more easily distended and compliance increases
52
Q

what is infant respiratory distress syndome:

a) caused by?
b) results

A

infant respiratory distress syndome:

cause: premature babies havent produced enough surfactant to breathe properly (start produce it during week 24-28 pregnancy, by week 34 is enough to breath on own)

results in: lungs collapsing

53
Q

which are most important sites of aiway resistance? (2) why ? (2)

A

sites of airway resistance: small bronchi and bronchiole - cross sectional area is relatively small here (1) and increase in no. of airways hasnt exerted its effect yet (1)

which are most important sites of aiway resistance? (2) why ? (2)

54
Q

changes in WHAT cause an increase in workload for respiration (2)

A

changes in compliance & airway resistance

Cardiorespiratory (41 decks)

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