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EOYS > CR EOYS3 > Flashcards

CR EOYS3 Flashcards

1
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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2
Q

what is the green?

A

costodiaphragmatic recess :)

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3
Q

what is the nerve supply to the

i) diaphragmatic pleura? [2]
ii) mediastinal pleura? [1]

A

i) diaphragmatic pleura: intercostal and phrenic nerves
ii) mediastinal pleura: phrenic nerve

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4
Q

what is the nerve supply to the

i) diaphragmatic pleura? [2]
ii) mediastinal pleura? [1]

A

i) diaphragmatic pleura: intercostal and phrenic nerves
ii) mediastinal pleura: phrenic nerve

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5
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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6
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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7
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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8
Q

where is sensor for the hormonal control of BP?

A

JG cells

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9
Q

what is angina and how do u treat?

A

angina - restricted blood supply to heart

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10
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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11
Q

how can sympathetic action of JGA cause a positive feedback of reninn release?

A

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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12
Q

which gland in olfactory cavity produces mucous? [1]

A

Bowmans glands

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13
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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14
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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15
Q

why does changing resp. rate impact the excretion of co2 but not o2? [1]

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

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16
Q

Q

what are the nasopharynx, oropharynx and laryngopharynx innervated by? [3] (theyre different)

A

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

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17
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.

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18
Q
A
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19
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

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20
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
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21
Q

draw a graph of ventilation / perfusion of lungs

A
22
Q

Q

what 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

23
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.

24
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

25
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)
26
Q

define inspirtary and expiratory 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

27
Q

how do you calculate alveolar ventilation? [1]
whats the unit?[1]

work out alveolar ventilation from information below

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,

A

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

alveolar ventilation is 12 x 350 = 4200 ml per minute. This is the effective ventilation that brings abut the exchange of O2 and CO2.

28
Q

what is the equation to work out o2 or co2 exchange in lung? [1]

A

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

29
Q

calculate the o2 and co2 exchanges for the below values. assume alveolar ventilation is 4.2 l/min

Room o2 = 21%
alveolar o2 = 14%

Room Co2 = 0.04%
alveolar Co2 = 5.5%

A

Co2 output = 4.2 X (5.5 - 0.04 / 100) = 0.231 L/min

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

30
Q

what is intrapleural pressure a balance of? [2]

what is intrapleural pressure normally? [1]

A
  • 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 = PPl

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

31
Q

how do you calculate compliance in respiratory physiology?

A

compliance = change in volume / change in pressure

32
Q

which two factors cause an increase in resp workload? [2]

A

compliance
airway resistance

33
Q

what do u add to blood sample to measure hematocrit? [1]

what method is used to display blood cells? (which stain?) [1]

A

what do u add to blood sample to measure hematocrit? [1]
anticoagulant, e.g. heparin

what method is used to display blood cells? (which stain?) [1]
wrights stain

34
Q

name 3 types of cells that monocytes can differentiate into [3]

A

monocytes:
- differentiate into macrophages & phagocytose stuff, Kupffer cells, Langerhan cells, alveolar marcophages

35
Q

label these parts of thymus histology :)

A
36
Q

label this bit of spleen :)

A
37
Q

label this bit of spleen :)

A
38
Q

what are the two branches found in palmar arches?
where do they come from?^

A

superficial & deep palmar arches

  • Branches of both radial and ulnar arteries
    i) Superficial arch mainly from ulnar artery.
    ii) Deep arch mainly from radial artery.
39
Q

what is allen test?

how do you perform?

A

allen test: assess hand vascularisation and impaired blood flo

  • compress both ulnar and radial arteries supplying wrist, then make a fist.
  • open hand, should look pale / white (keep compression).
  • Pressure released of either radial or ulnar arteries individually
  • capillary refill of entire hand indicates patent artery and palmar arches
40
Q
A
41
Q
A
42
Q
A
43
Q

at what point does external iliac artery –> femoral artery? [1]

A

as soon it passes under the inguinal ligament

44
Q

where is the location you palpate for the femoral pulse? [1]

A

below inguinal ligament and mid-ingual point. This is half way between pubic symphysis and anterior superior iliac spine

45
Q
A
46
Q

describe the arterial supply to the nasal cavities [3]

A

Arterial supply to the nasal cavities:

  • from both the external and internal carotid arteries:
    i) branches from the external carotid artery via the maxillary and facial arteries
    ii) branches from the internal carotid artery via the ophthalmic artery

venous drainage:

i) branches to the maxillary and facial veins then drains to external jugular vein
ii) branches to the opthalmic vein into the cavernous sinus

47
Q
A
48
Q

label A-C

A

A: omohyoid
B: SCM
C: sternohyoid

49
Q
A

Vestibular Folds – Mucous membranes encasing vestibular ligaments. Protective function.

Rima Vestibuli – Space between vestibular ligaments

Vocal Folds (Vocal Cords) – Mucous membranes encasing vocal ligaments

Rima Glottidis - Space between vocal ligaments

Glottis – Vocal apparatus of larynx including vocal folds, ligaments and Rima Glottidis

50
Q

which is the main cartilage that move for phonation? [1]

which intrinisc muscle is not involved in movement of cartialge to produce phonation? [1]

A

The main cartilages that move for phonation are the arytenoid cartilages

All of the intrinsic muscles, other than the cricothyroid, are involved in movement of cartilage to produce phonation.

51
Q
A

EOYS (39 decks)

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