Brainscape's Knowledge GenomeTM

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


See full index

IMMS session 4: introduction to the cardiorespiratory system > cardiovascular respiratory system > Flashcards

cardiovascular respiratory system Flashcards

1
Q

what determines cardiac output?

A
  1. heart rate
  2. stroke volume

stroke volume x heart rate

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

what is the normal range for heart rate?

A

60-100 beats per minute (bpm)

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

what is the heart rate established by?

A

sinoatrial node (SAN)

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

what is the sinoatrial node and where is it found?

A

cluster of pacemaker cells which sits in the right atrium

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

what is the normal SAN pacing rate?

A

100 beats per minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

where does the atrioventricular node (AVN) sit?

A

above the ventricular septum at the junction between the atria and the ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what does the avn do?

A

pass on the impulse from the atria to the ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the delay in AVN conduction and why is this important?

A

delay of about 0.15 seconds, allowing the atria to finish contracting and the atrioventricular valves to close before the ventricles start to contract – this prevents blood from regurgitating back into the atria during ventricular contraction

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

what does the autonomic nervous system do to the heart?

A

induces the force of contraction of the heart and its heart rate, and controls the peripheral resistance of blood vessels

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

what nerve supplies parasympathetic input to the heart?

A

vagus nerves

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

what does a parasympathetic input do to the heart?

A

decrease in heart and contraction force

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

what does sympathetic input do to the heart?

A

increases heart rate and the force of contraction

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

what are baroreceptors?

A

located in the carotid sinus and aortic arch and detect changes in stretch and tension in the arterial wall and changes in arterial pressure

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

what happens if baroreceptors detect an increase in arterial pressure?

A

the parasympathetic pathway is activated, vagus nerves carry impulses so heart rate is reduced, vasodilation occurs to reduce arterial pressure

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

what happens if baroreceptors detect an decrease in arterial pressure?

A

the sympathetic pathway is activated, heart rate is increased and vasoconstriction occurs to increase arterial pressure

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

what does adrenaline do to heart rate and where is it released from?

A

increases heart rate
released from the medulla of adrenal glands

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

what is stroke volume?

A

the difference between the end diastolic volume (EDV), the volume of blood in the heart at the end of diastole, and the end systolic volume (ESV) the volume remaining in the heart at the end of systole ie the amount of blood that is expelled with each heartbeat

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

what can affect stroke volume?

A
  1. central venous pressure (CVP)
  2. Total Peripheral Resistance (TPR)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the central venous pressure?

A

blood pressure in the vena cava as it enters the right atrium

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

what does the central venous pressure reflect?

A

the volume of blood returning to the heart and therefore the volume of blood the heart pumps back into the arteries

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

why does an increase in the CVP increase stroke volume up to a certain point?

A
  1. more blood enters the heart during diastole, leading to an increase in end diastolic volume (EDV)
  2. increased filling of the heart leads to increased ventricular contraction and thus a decrease in end systolic volume (ESV), due to Starling’s Law
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is preload?

A

diastolic filling pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the total peripheral resistance?

A

the pressure in the arteries that blood must overcome as it passes through them, and thus dictates how easy it is for the heart to expel blood (afterload)

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

what is Starling’s Law?

A

the more the heart chambers fill, the stronger the ventricular contraction, and therefore the greater the stroke volume

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

how does an increase in central venous pressure result in an increase in stroke volume?

A

as the heart chamber fills and stretches, it creates more regions of overlap for actin-myosin cross-bridges to form, allowing for a greater force of contraction

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

how is a large concentration gradient maintained in capillaries?

A

via a constant blood flow to allow rapid exchange of molecules with the tissue

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

how is a thin diffusion distance maintained across capillaries?

A

as the endothelium of the capillaries is just one cell thick and measures a few micrometres in diameter

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

what is blood hydrostatic pressure?

A

the pressure exerted by blood in the capillaries against the capillary wall that forces fluid out of the capillary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is the oncotic pressure?

A

the pressure exerted by proteins in the blood, mostly by albumin in the capillaries, that pulls fluid into the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is venous return?

A

the flow of blood back to the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what are veins?

A

low-pressure, low-resistance vessels, which carry blood back to the heart from organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is venous pressure affected by?

A
  1. the rate of blood entering the veins
  2. the rate at which heart pumps out blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

how does cardiac output affect venous pressure?

A

increased cardiac ouput decreases venous pressure as blood is rapidly pumped out of veins, whereas lowered cardiac output backs up the venous system increasing blood volume and venous pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is the skeletal muscle pump?

A

muscles, eg quadriceps, contracting to squeeze veins and therefore increasing venous pressure, forcing the vein’s valves to open, allowing more blood to flow back to the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what are some non-respiratory functions o f the lungs?

A
  1. host defence
  2. speech
  3. vomiting
  4. defecation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what are the types of lung host defences?

A
  1. intrinsic
  2. innate defence
  3. adaptive immunity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is intrinsic defence?

A

always present: physical and chemical. apoptosis, autophagy, RNA silencing, antiviral proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is innate defence?

A

induced by infection (interferon, cytokines, macrophages, NK cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is adaptive immunity?

A

tailored to a pathogen (T cell, B cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

give some examples of chemical epithelial barriers (chemical barriers produced by epithelial cells)?

A
  1. antiproteinases
  2. anti-fungal peptides
  3. anti-microbial peptides
  4. antiviral proteins
  5. opsins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what type of barrier is mucus?

A

physical barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is the purpose of coughing?

A

expulsive reflex action that protects the lungs and respiratory passages from foreign bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what are some causes of coughing?

A
  1. irritants
  2. conditions like COPD
  3. infections like influenza
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is sneezing?

A

involuntary expulsion of air containing irritants from the nose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what are some causes of sneezing?

A
  1. irritation of nasal mucosa
  2. excess fluid in the airway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

can airway epithelium replair?

A

sometimes can completely repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is plasticity in cells?

A

when cells can change cell types

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

how much blood does the heart pump around the body
every minute at rest?

A

around 5L of blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what is the normal pressure in the aorta?

A

120/80 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

when do the ventricles fill with blood?

A
  1. during diastole (heart relaxation)
  2. atrial systole (contraction of the atria)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what happens during the filling phase of the cardiac cycle?

A
  1. blood flows from the vena cava and pulmonary veins into the atria, and passively fill the ventricles.
  2. ventricles fill with blood at a steadily decreasing rate, until the ventricles’ pressure is equal to that in the veins
  3. during atrial systole the atria contract squeezing blood into the ventricles, closing the atrioventricular valves.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what is isovolumetric contraction of the cardiac cycle?

A

the heart valves are shut as the ventricles contract, causing a build-up of pressure but no change in
volume of blood within the
ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what is the outflow phase of the cardiac cycle?

A

ventricles’ pressure exceeds the pressure in the aorta/pulmonary trunk so the semilunar valves open and blood is pumped from the heart into the great arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what causes the semilunar valves to close?

A

at the end of ventricular systole, the ventricles relax reducing their pressure below the aorta, closing the
valves. backflow of blood also closes the valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what is isovolumetric relaxation?

A

the ventricles relax, ready to re-fill with blood in the next filling phase. the volume of blood within the ventricles remains the same as the atrioventricular valves has not opened yet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what is a “lub” sound from?

A

occurs at the end of the filling phase when the atrioventricular valves snap shut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what is a “dub” sound from?

A

occurs at the end of the outflow phase when the outflow valves snap shut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what is Starling’s law?

A

as the volume of the left ventricle increases (more passive filling, preload), the greater the myocyte stretches and the more forceful the systolic contraction, increasing left ventricular stroke volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what supplies parasympathetic input to the heart?

A

vagus nerve (CNX)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what does parasympathetic innervation do to the heart?

A

slows down heart rate and reduces the force of contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

how do parasympathetic fibres decrease heart rate?

A

releases acetylcholine which binds opens up potassium channels, making it harder to reach the threshold for depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what does sympathetic innervation do to the heart?

A

innervates the SAN and AVN; increasing the heart rate and increasing the force of contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

how do sympathetic fibres increase heart rate?

A

releases noradrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

where are baroreceptors located?

A

aortic arch and carotid sinus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

how do baroreceptors detect a change in blood pressure?

A

they are sensitive to changes in stretch and tension in the arterial wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what nerve carries impulses from the carotid sinus to the CNS?

A

glossopharyngeal nerve (IX)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what nerve carries impulses from the aortic arch to the CNS?

A

vagus (X)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what happens if an increase in arterial pressure is detected by baroreceptors?

A

parasympathetic pathway is activated, impulses are carried to the CNS and back via the
vagus to reduce heart rate and bring on vasodilation to reduce arterial pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

what happens if an decrease in arterial pressure is detected by baroreceptors?

A

sympathetic pathway is activated causing increased heart rate and vasoconstriction to increase blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what is the purpose of the electrocardiogram?

A

trace the electrical activity in cardiac tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what are the most common types of lead ECGs?

A

3 lead and 12 lead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what does a ‘lead’ mean?

A

a view of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

how many physical electrodes are there in a 12 lead ECG?

A

10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

how many chest electrodes are there in a 12 lead ECG?

A

6 chest electrodes (V1-V6)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

how many limb electrodes are there in a 12 lead ECG?

A

4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

why is having many leads beneficial?

A

useful in visualising the electrical activity of the heart from different views, and therefore to localise pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what time frame does a small square on an ECG represent?

A

0.04 secs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what time frame does a large square on an ECG represent?

A

0.2 secs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

how many small squares is in a large square in an ECG?

A

5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

what time frame does 5 large squares on an ECG represent?

A

1 second

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

what time frame does 300 large squares on an ECG represent?

A

1 minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

what does depolarisation towards an electrode give on the ECG race?

A

a positive complex (upwards)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

what does depolarisation away from an electrode give on the ECG race?

A

a negative complex (downwards)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

what does repolarisation towards an electrode give on the ECG race?

A

a negative complex (downwards)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

what does repolarisation away from an electrode give on the ECG race?

A

a positive complex (upwards)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

what does the P wave represent?

A

atrial depolarisation, as a small upwards inflection as the atria and small and depolarisation is moving towards the lead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

what does the QRS complex wave represent?

A

ventricular depolarisation; large upwards inflection and atrial repolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what does the T wave represent?

A

ventricular repolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

what is ST elevation indicative of?

A

myocardial infarction, as the ventricles are not relaxing and therefore filling as much, reducing cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

what is STEMI?

A

ST elevation myocardial infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

what leads to ST elevation?

A

as the tissue dies it becomes leaky to electrolytes, leading to a partial depolarisation during the ventricular repolarisation period (ST segment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

what are gap junctions?

A

clusters of intercellular channels that allow direct diffusion of ions and small molecules between adjacent cells (used in action potentials)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

what is the resting membrane potential (phase 4) and how is it maintained?

A

-70mV
at rest K+ channels are open, therefore resting membrane potential tends towards the equilibrium potential for K+ (EK), which is roughly -70mV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

what is the process of the ventricles getting depolarised (phase 0)?

A

as depolarisation spreads across the cells, voltage-gated Na+ channels open leading to an influx of Na+ (then a greater influx due to increased depolarisation; positive feedback)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

what is phase 1 of
ventricular action potentials?

A

transient K+ channels open and repolarise the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

what is phase 2 of
ventricular action potential?

A

plateau phase
L-type Ca2+ channels open and Ca2+ enters the cell, leading to a plateau balance with the K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

what happens during the plateau phase of ventricular contractions?

A

Ca2+ pass through the L-type Ca2+ channels , triggering the release of Ca2+ from the sarcoplasmic reticulum into the cell, which binds to troponin, which moves tropomyosin away from myosin allowing the actin head to access the myosin head binding site and allowing contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

what happens during phase 3
ventricular contraction?

A

repolarisation
Ca2+ channels close and K+ repolarises the cell. Na+ channels will begin to recover from inactivation as the membrane potential becomes more negative. ATP is needed to break cross bridges so myosin can move along and muscle can relax. Ca++ returns to sarcoplasmic reticulum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

how many phases are there in
ventricular action potentials?

A

(phases 0-4 inclusive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

what enables a refractory period?

A

in phase 0, Na+ channels become inactivated almost immediately after opening and can only recover from inactivation to enter the closed state at very negative membrane potentials (after repolarisation). new action potentials can only be generated after phase 3, but usually during pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

what is the resting membrane potential of the pacemaker cells in the heart and how is this maintained?

A
  1. -55mV
  2. 3Na+/ 2 K+ in, K+ always flowing out through leaky K+ channels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

what causes the membrane potential of the cardiac pacemaker cells to rise?

A

the membrane is also permeable to Ca2+ and Na+ through their leaky channel membranes, which increases the membrane potential?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

what happens when the threshold membrane potential has been reached and what is this threshold?

A
  1. -40mV
  2. voltage-gated calcium channels open, allowing Ca2+ to influx in and depolarise the membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

what happens during pacemaker cell repolarisation?

A
  1. Ca2+ voltage gated inactivate
  2. K+ channels open, there is an efflux of K+ ions out of the cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

what is the impact of parasympathetic activity on cardiac pacemaker cells and how do they work?

A

acetylcholine acts on the SAN which lengthens the interval between pacemaker potentials, hence slowing heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

what is the impact of sympathetic activity on cardiac pacemaker cells and how do they work?

A

releases noradrenaline which shortens the interval between impulses by making the pacemaker potential steeper, hence increasing the heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

where are calcium ions released from?

A

the sarcoplasmic reticulum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

describe the stages in calcium induced calcium release

A
  1. membrane depolarisation opens voltage-operated calcium channels. releasing calcium ions
  2. calcium bonds to ryanodine receptors on the sarcoplasmic reticulum which induces conformational changes in a Ca2+ channel associated with the ryanodine receptor
  3. ryanodine receptors acre activated which opens them and releases Ca2+ from the SR stores- ‘calcium spark’
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

what happens after calcium induced calcium release?

A

after the calcium spike occurs, calcium binds to troponin-C which moves the tropomyosin away from the actin binding site thus exposing it and initiating cross-bridge binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

describe the process of the sliding filament model of contraction?

A
  1. calcium binds to troponin-C, which moves tropomyosin away from myosin
  2. the actin binds to the myosin head, which releases ADP and an inorganic phosphate
  3. the myosin head pivots and bends, pulling on actin and moving it causing muscle contraction
  4. a new molecule of ATP binds to the myosin head, causing it to detach from the actin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

how is calcium removed after a stimulus is removed?

A

by re-entering the sarcoplasmic reticulum via a SERCA (sarco(endo)plasmic reticulum calcium-ATPase) channel at the expense of an ATP molecule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

what is the lifespan of platelets?

A

7-10 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

what is the normal platelet count?

A

150-400 x 109/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

where are platelets distributed?

A

70% in the blood, 30% in the stream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

what are platelets made from?

A

fragments of megakaryocytes that come off as they travel through the blood vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

what type of granules so platelets contain?

A

alpha-granules and dense granules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

what do alpha granules contain?

A

proteins of high molecular weight, including von Willebrand Factor (vWF), factor V and fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

what do dense granules contain?

A

low molecular weight molecules such as ATP, ADP, serotonin, and calcium ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

what is the function of platelets?

A

formation of blood clots at the site of bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

what are the three main stages in the formation of a blood clot?

A

adhesion, activation and aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

what is the adhesion step in the formation of a blood clot?

A
  1. the injured blood vessel wall exposes its underlying endothelium and collagen fibres.
  2. exposed collagen fibres bind vWF released from the damaged endothelium, which in turn binds to vWF receptors on platelets to promote adhesion.
  3. the exposed collagen itself also promotes platelet binding.
  4. the clotting cascade
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

what is the activation stage of blood clotting?

A

platelet activation results in a morphological change on the membrane surface of the platelet, increasing the surface area and preparing it for aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

what is the aggregation stage of blood clotting?

A

platelets bind to vWF and fibrinogen. fibrinogen facilitates the formation of crosslinks between platelets, aiding platelet aggregation to form a platelet plug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

what type of receptors do platelets have on their surfaces?

A

agonist and adhesion receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

what do agonist receptors do?

A

recognise stimulatory molecules e.g. collagen, thrombin, and ADP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

what do adhesion receptors do?

A

promote the adhesion of platelets to other platelets, the vessel wall or leucocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

what triggers the extrinsic pathway for the coagulation cascade?

A

external trauma which causes blood to escape the circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

what triggers the intrinsic pathway for the coagulation cascade?

A

internal damage to the vessel wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

describe the extrinsic pathway to the coagulation cascade

A
  1. damage to the blood vessel means that factor VII exits the circulation into surrounding tissues
  2. factor VII gets converted to factor VIIa
  3. factor VIIa gets converted to factor X
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

describe the intrinsic pathway of the coagulation cascade?

A
  1. XII turns gets converted to XIIa
  2. XI gets converted to XIa
  3. IX gets converted to IXa
  4. X gets converted to Xa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

what is the common pathway for coagulation?

A

the extrinsic and intrinsic pathways converge, and X
converts prothrombin to thrombin. thrombin con
verts fibrinogen into fibrin which are insoluble and are stabilised by factor XIIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

what is fibrinolysis?

A

fibrin is dissolved leading to the consequent dissolution of the clot, degrading the thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

what type of blood supply reaches the lungs?

A
  1. pulmonary
  2. bronchial
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

what do bronchial arteries do?

A

supply blood to the lung architecture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

what is the difference between the pulmonary and systemic wall?

A

systemic is thicker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

what is the difference between the pulmonary and systemic muscularisation?

A

systemic has more significant muscularisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

how is pulmonary arterial pressure measured?

A

cardiac output x pulmonary
vascular resistance (ohms law)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

how is vascular resistance measured?

A

(8 x L x viscosity)/ (pi r^4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

why does cardiac output increase but pulmonary arterial pressure not increase as much?

A

increased cardiac vessels are recruited which helps to reduce pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

what are the two types of respiratory failure?

A

type I and II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

what is type I respiratory failure?

A

pO2 <8kPA (low) and pCO2 < 6kPA (low-normal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

what is type II respiratory failure?

A

pO2 <8kPA (low) and pCO2 > 6kPA (high)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

what causes type I respiratory failure?

A

embolisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

what causes type II respiratory failure?

A

hypoventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

what causes low oxygen levels?

A
  1. hyperventilation
  2. diffusion impairments
  3. V/Q mismatch
  4. shunt
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

what can cause diffusion impairments?

A
  1. pulmonary oedema
  2. membrane diffusion, interstitial fibrosis
  3. blood diffusion e.g. anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

why is there more perfusion in the alveoli at the bottom of the lung?

A

the alveolar pressure is less than the
venous and arteriole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

what is v/q?

A

ventilation/perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

what is cyanosis?

A

body turning blue as haemoglobin has a low saturation of oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

what is eisenmenger syndrome?

A

the development of pulmonary hypertension (high blood pressure in the lungs) due to an untreated congenital heart defect e.g. ventricular septal defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

where does pulmonary embolism start?

A

in the legs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

what factors increase the likelihood of thrombosis?

A
  1. circulatory statis (not moving)
  2. endothelial injury
  3. hypercoaglable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

what is airway resistance?

A

the degree of resistance to air flow through the respiratory tract during inspiration and expiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

why is the total resistance greater in the trachea and larger bronchi as opposed to bronchioles despite the larger diameter?

A

smaller airways are in larger numbers running in parallel which reduces the total resistance to airflow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

what does sympathetic innervation do to bronchial smooth muscle and airway diameter? and by what mechanism?

A

relaxes bronchial smooth muscle which increases airway diameter to allow more airflow. noradrenaline form adrenal glands act on adrenal medulla to release adrenaline which acts on B2 receptors on airways smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

what does parasympathetic innervation do to bronchial smooth muscle and airway diameter and by what mechanism?

A

increases smooth muscle contraction to reduce diameter (bronchoconstriction) through the vagus nerve where acetyl-choline acts on M3 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

what is radial traction?

A

during expiration, elastic fibres of the surrounding alveoli pull on small airways to hold them open and prevent them from collapsing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

what is laminar flow?

A

the state of flow in which air moves through a tube in parallel layers, with no disruption between the layers, and the central layers flowing with the greatest velocity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

what is turbulent flow?

A

when air is not flowing in parallel layers, and direction, velocity and pressure within the flow of air become chaotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

why do the intercostal muscles and diaphragm would need to work harder to expand and contract the lungs in turbulent flow?

A

turbulence leads to the need for a much greater difference in pressure to move the air

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

what is FEV1?

A

forced expiratory volume in one second

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

what is FVC?

A

forced vital capacity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

what is gas dilution

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

what is plethysmography?

A

measures changes in volume in different parts of the body. the test may be done to check for blood clots in the arms and legs. It is also done to measure how much air you can hold in your lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q
A
163
Q

how are transfer estimates carried out and what do they measure?

A

a person is given some carbon monoxide to breathe in, ad the amount breathed out is measured which allows to estimate the overall function of the lung, eg haemoglobin concentration, alveolar surface area and capillary
volume

164
Q

what is considered normal for forced expiratory volume in one second in litres

A

80% or greater is considered normal

165
Q

what is airways restriction? in what conditions may this happnen?

A

forced vital capacity FVC is less than 80% of predicted. pulmonary fibrosis

166
Q

what is forced vital capacity?

A

the amount of air that can be forcibly exhaled from your lungs after taking the deepest breath possible measured using spiriometry

167
Q

what is airways obstruction and in what conditions will this happen?

A

forced expiratory volume in 1 second (FEV1) to forced vital capacity (FVC) ratio is less than 0.7. asthma and COPD

168
Q

does the urge to breathe come from oxygen or carbon dioxide levels?

A

carbon dioxide levels; when holding breathe oxygen saturation increases and reaches 100%, but the blood pH decreases due to CO2 which gives the urge to breathe in order to remove it

169
Q

what the pons?

A

pneumotaxic and apneustic centre

170
Q

what is the medulla?

A

phasic discharge of action potential

171
Q

when is DRG active?

A

predominately active during inspiration

172
Q

when is VRG active?

A

active in both inspiration and expiration

173
Q

what happens when a diaphragm that is already flat contracts?

A

it shortens

174
Q

what do central chemoreceptors do?

A

detect CO2 concentrations

175
Q

what do peripheral chemoreceptors do?

A

measure CO2 and oxygen and pH

176
Q

where are central chemoreceptors located?

A

in the brainstem, pontomedullary junction, stimulate ventilation

177
Q

what blood vessels supply the pericardium?

A

pericardiacophrenic arteries

178
Q

what blood vessels supply the diaphragm?

A

pericardiacophrenic arteries

179
Q

what do internal jugular veins do?

A

drains the head and the neck

180
Q

what drains the pericardium and the diaphragm?

A

pericardiacophrenic veins

181
Q

what are vagus nerves also known as?

A

cranial nerves X

182
Q

what is the concentration of O2 and CO2 in respiratory failure?

A

PaO2 is low <8kPa
PaCO2 may be elevated >6.8 kPa

183
Q

what is hypoxaemia?

A

a decrease in the partial pressure of oxygen in the blood

184
Q

what is hypoxia?

A

a reduced level of tissue oxygenation

185
Q

what happens to the PaO2 and PaCO2 in type 1 respiratory failure?

A

low PaO2 (hypoxaemia)
low/normal PaCO2 (hypocapnia)

186
Q

what happens to the PaO2 and PaCO2 in type 2 respiratory failure?

A

low PaO2 (hypoxaemia)
high PaCO2 (hypercapnia)

187
Q

is type I or 2 respiratory failure more common?

A

type 1

188
Q

what causes hypoxia in type 1 respiratory failure?

A
  1. mismatching of ventilation and perfusion
  2. shunting
  3. dffusion impairment
  4. alveolar hypoventilation
189
Q

what are some type I respiratory failure treatments?

A
  1. airway patency
  2. oxygen delivery
  3. increasing FiO2
  4. primary cause (e.g. antibiotics for pneumonia)
190
Q

where is type 2 respiratory failure commonly found?

A

COPD

191
Q

what are some symptoms of hypercapnia?

A
  1. rritability
  2. headache
  3. papilloedema
  4. warm skin
  5. pounding pulse
    6.confusion
  6. somnolence
  7. coma
192
Q

what are some type 2 respiratory failure treatments?

A

Airway patency
Oxygen delivery

Primary cause (e.g. antibiotics for pneumonia)

Treatment with O2 may be more difficult
For example; COPD patients rely on hypoxia to
stimulate respiration

assisted ventilation

193
Q

what is a good indicator for eosinophilic respiratory inflammation?

A

exhaled nitric oxide test

194
Q

what percentage of asthma is related to occupation?

A

15%

195
Q

what are some occupational causes of asthma?

A

HMW, Grain, Wood, Animals, fish
Latex, Glutaraldehyde, Isocyanates, Paints, Metal working fluids
Metals

infectious agents, fungi, pets, air pollutants

196
Q

what % of the population have asthma?

A

5-16%

197
Q

is asthma variable amongst countries?

A

yes, as it is influenced by the quality of the air breathed in

198
Q

what metal exposure is associated with emphysema development?

A

cadmium

199
Q

what % of COPD is related to occupation?

A

15%

200
Q

what occupational exposures contribute to COPD?

A

silica, coal, grain, cotton and cadmium

201
Q

what causes asthma?

A

genetic and environmental risks

202
Q

how common is cystic fibrosis?

A

1/2500 have it, 1/25 are carrier

203
Q

where is the genetic defection on cystic fibrosis found?

A

found on the long arm on chromosome 7
F508del most common mutation causing CF

204
Q

how does cystic fibrosis cause symptoms?

A

CTFR protein abnormality (transport protein) leads to dysregulated epithelial fluid transport

205
Q

how is cystic fibrosis diagnosed?

A

immunoreactive trypsinogen test in new-borns

206
Q

how does cystic fibrosis affect the pancreas?

A

blockage of exocrine ducts, early activation of pancreatic enzymes, and eventual auto-destruction of the exocrine pancreas
Most patients require supplemental pancreatic enzymes

207
Q

how does cystic fibrosis affect the intestine?

A

bulky stools can lead to intestinal blockage

208
Q

how does cystic fibrosis affect the respiratory system?

A

mucus retention, chronic infection, and inflammation that eventually destroy lung tissue

209
Q

is there a singular cystic fibrosis mutation?

A

no, more than 2000 CFTR cystic fibrosis causing mutations have ben found

210
Q

what is alpha-1 antitrypsin disease?

A

inherited, monogenic condition resulting in early onset emphysema +/- bronchiectasis

211
Q

what initiates parasympathetic innervation of the bronchus?

A

vagus nerve

212
Q

what is ipratropium bromide (atrovent)

A

short term muscarinic (blocks parasympathetic actvity acetyl-choline)

213
Q

how does salbutamol work?

A

activates beta2 receptors onthe airway smooth muscle causes muscle relaxation by activating a

214
Q

whats the relationship between levels and pressure

A

going down 10m increases atmospheric pressure by 1

215
Q

what is boyles law?

A

p1v1=p2v2

216
Q

why is diving hazardous to the lungs?

A
217
Q

what is an apnoea dive?

A

diving whilst holding breath

218
Q

what is the diving reflex?

A

when a human holds their breath and submerges in water, the face and nose become wet which in turn causes bradycardia, apnea, and increased peripheral vascular resistance;

219
Q

what is oxygen toxicity?

A

when people receive high levels of oxygen (for examples as the pressure increases due to diving) leading to shortness of breath, cough and chest pain

220
Q

what is nitrogen narcosis?

A

increased pressure of inspired nitrogen as ambient pressure of air is increasing, increasing coldness and feelings of euphoria

221
Q

what is decompression illness?

A

since nitrogen was delivered under high pressure when diving, because it was purely soluble when the person returns to the surface the nitrogen starts bubbling

222
Q

what is the altitude of the death zone?

A

above 8000m

223
Q
A
224
Q

what is the Aa difference?

A

the difference between the oxygen and arteriole oxygen partial pressure usually 1kPa in healthy individuals but greater in unhealthy

225
Q

what is the treatment of acute mountain sickness or altitude pulmonary oedema?

A

descend immediately

226
Q

when is the pseudoglanders phase?

A

8-17 weeks

227
Q

what is the ductus arteriosus?

A

pulmonary trunk linked to the distal arch of aorta by the ductus arteriosus, permitting blood to bypass pulmonary circulation
muscular wall contracts to close after birth (a process mediated by bradykinin)

228
Q

what is the ductus venosus?

A

oxygenated blood entering the foetus also needs to bypass the primitive liver. This is achieved by passage through the ductus venosus, which is estimated to shunt around 30% of umbilical blood directly to the inferior vena cava

229
Q

what is the foramen ovale?

A

foramen ovale is a passage between the two atria, which is responsible for bypassing the majority of the circulation

230
Q

what are some adaptive changes at birth?

A

Fluid squeezed out of lungs by birth process
Adrenaline stress leads to increased surfactant release.
Gas inhaled
Oxygen vasodilates pulmonary arteries
Pulmonary vascular resistance falls
Right atrial pressure falls, closing foramen ovale

Umbilical arteries constrict

Ductus arteriosus constricts

231
Q

what is pulmonary interstitial emphysema?

A

lung cysts rupturel aveoli

232
Q

how is pulmonary interstitial emphysema treated?

A

Warmth
Surfactant replacement (if intubated)
Oxygen and fluids
Continuous Positive Airway Pressure (maintain lung volumes, reduce work of breathing)
Positive pressure ventilation if needed

233
Q

what are the layer of the heart (outside to inside)?

A

fibrous pericardium, parietal serous pericardium, visceral serous pericardium, myocardium, endocardium

234
Q

how long are systole and diastole?

A

systole 0.3s and diastole 0.5s

235
Q

how much blood is ejected from the ventricles with each contraction?

A

2/3

236
Q

what is diastasis?

A

when the pressure within the atria and ventricles begins to even out and the ventricles no longer passively fill

237
Q

how are blood vessels autoregulated?

A

intrinsically (increasing diameter) and extrinsically (vasodilation and vasoconstriction)

238
Q

does the smooth muscle within the blood vessels ever relax?

A

no

239
Q

what is hyperaemia?

A

increased blood flow

240
Q

what is active hyperaemia?

A

metabolic response that increases blood flow e.g. exercise

241
Q

what is reactive hyperaemia?

A

occluded tissue; after occlusion removed, increased blood flows to it

242
Q

where are peripheral chemoreceptors found, what are they sensitive to and what is their response?

A

aortic arch and carotid sinus. detects an increase in CO2, a decrease in pH and a decrease in oxygen. leads to an increase in blood pressure (sympathetic) impulses to pressor region of medulla

243
Q

where are arterial baroreceptors found, what are they sensitive to and what is their response?

A

aortic arch and carotid sinus. responsa to an increase in blood pressure. when blood pressure increases firing rate also increases more distil to the baroreceptor. the rate of impulses increase to the depressor (centre medulla) to decrease blood pressure parasympathetic

244
Q

where are cardiopulmonary baroreceptors found, what are they sensitive to and what is their response?

A

found in atria, ventricles and pul. artery. responds to an increase in blood volume. when blood volume increases the baroreceptor gets distorted more so more impulses are sent to depressor region of medulla to decrease blood pressure parasympathetic

245
Q

how is cardiac output calculated?

A

stroke volume x heart rate

246
Q

how is blood pressure calculated?

A

cardiac output x total peripheral resistance

247
Q

how is pulse pressure calculated?

A

systolic pressure - diastolic pressure

248
Q

how is mean arteriole pressure calculated?

A

diastolic pressure + 1/3 pulse pressure

249
Q

what is Poiseuille’s law?

A

flow - (pi x r^4)/ (8 x length x viscosity)

250
Q

how is flow (I) calculated?

A

pressure (v)/ resistance (r)

251
Q

what is Frank Starlings law?

A

the greater the end diastolic volume (or
ventricular filling) the harder the contraction as the myocytes stretch more to accommodate the greater filling, which increases contraction strength. stroke volume increases and therefore so does cardiac output

252
Q

what pressure keeps blood in vessels and how?

A

oncotic pressure, albumin presses on vessel walls and keeps fluid in

253
Q

what force squeezes blood out of vessels?

A

hydrostatic pressure (increased pressure within the vessel forces blood out)

254
Q

how can failing hearts be treated and why?

A

failing hearts have a decreased cardiac output, can be treated by increasing stroke volume by increasing the volume of extracellular fluid via injections

255
Q

what are vasodilators?

A

hypoxia, low pH high CO2, bradykinin, NO, prostacyclin, high K+, acetyl choline, atrial natriuretic peptide

256
Q

what are vasoconstrictors?

A

endothelium 1, angiotensin II, ADH, noradrenalin

257
Q

define stroke volume

A

ventricular ejection at systole

258
Q

define cardiac output

A

ventricular ejection/ unit time

259
Q

define total peripheral resistance

A

total peripheral systemic resistance. arterioles (highest)

260
Q

define preload

A

amount of myocyte stretch in ventricular filling. a
volume

261
Q

define afterload

A

resistance myocytes contract against in
ventricular systole. a resistance

262
Q

define contractility

A

how hard the heart beats

263
Q

define compliance

A

how easy heart fills in diastole

264
Q

define frank starlings law

A

higher EDV leads to harder vent. contraction

265
Q

define diastolic distensibility

A

pressure to fill ventricles a diastole to EDV

266
Q

how are parasympathetic effects carried out on the CVD?

A

acetyl choline acts on M2 receptors, to decrease heart rate and decrease the force of contraction. less Ca2+ ions enter myocyte, triggering less action potentials decreasing contractility and cardiac output

267
Q

how are sympathetic effects carried out on the CVD?

A

noradrenaline acts on B1 receptors to increase heart rate and increase the force of contraction. more Ca2+ ions enter myocyte, triggering more action potentials increasing contractility and cardiac output

268
Q

what are the two different types of arteries and where are they found?

A
  1. elastic: aortic, closer to the heart have more elastic tissue in tunica media, larger lumen as need to withstand greater pressures and maintain constant pressure by quick elastic recoil
  2. muscular: distil to heart. more muscle in tunica media, smaller lumen. more muscle for vasodilation and vasoconstriction
269
Q

what are arterioles?

A

arteries with 3 or less muscle layers in tunica media. where arteries transition towards capillaries. site of most resistance

270
Q

what is responsible for end diastolic volume?

A

veins

270
Q

how do veins return blood to the heart?

A
  1. skeletal muscle contractions
  2. resp muscles need blood so increase venous return
  3. peristalsis (smooth muscle contraction in HI track neds blood)
271
Q

what regulates entry of blood into the capillaries?

A

precapillary sphincters

272
Q

what are the three types of capillaries?

A

continuous: fully intact endothelium + basement membrane - tiny molecules pass through
fenestrated: endothelial gaps, basement membrane intact. allows glucose and aa through
discontinuous: huge endo gaps, incomplete basement membrane, whole RBC can fit through

273
Q

what are the normal pressures in systemic and diastolic vessels? and what happens to the vessels where there is lots of and a lack of oxygen?

A

pulmonary 25/8 (lower pressure prevents oedma), systemic 120/80. systemic thicker walls. pul, hypoxia is vasoconstriction, systemic hypoxia is
vasodialation

274
Q

how long do RBCs last for, what hormone stimulates their production and where from, what is their structure and what are young RBCs called?

A

120 days, erythropoietin (kidney), 2 alpha and 2 beta chains (gamma in foetus), reticulocyte

275
Q

how long do white blood cells last for, what hormone stimulates their production?

A

6-10 hours, granulocyte macrophage colary stimulating factor

276
Q

how long do platelets last for, what hormone stimulates their production?

A

7-10 days, thrombopoietin

277
Q

what is serum?

A

plasma without clotting factors

278
Q

what is blood made from?

A

plasma and blood cells (red, white and platelets)

279
Q

what is haematocrit?

A

a measurement of the the percentage by volume of red cells in your blood. ~0.45

280
Q

what is the precursor to all blood cells?

A

hemocytoblast (pluripotent). the formation of blood cells are haematopoiesis

281
Q

what is the main function of neutrophils as well as their appearance?

A

inflammatory response. granulocytes (release primary and secondary granules), multilobed

282
Q

what is the main function of monocytes as well as their appearance?

A

immature cells, become macrophages and antigen presenting cells. kidney bean looking nucleus, also large

283
Q

what is the main function of eosinophils as well as their appearance?

A

fights parasitic worms. antihistamines (reduce allergic response). pink granules with IgE receptors

284
Q

what is the main function of basophils as well as their appearance?

A

produces histamine (increase allergic response). dark blue granules with IgE receptors

285
Q

what is the main function of lymphocytes as well as their appearance?

A

cell mediated + innate response. very little cytoplasm, mostly nucleus

286
Q

what is the precursor cell to platelets?

A

megakaryocytes

287
Q

what is endomitosis?

A

the formation of platelets, where the DNA doubles but the cell does not divide

288
Q

what do inactive platelets look like?

A

smooth and discoid

289
Q

what do active platelets look like?

A

increased surface area and pseudopoid

290
Q

what granules does platelets release?

A

electron dense granules (for energy, ADP, ATP, Ca++, serotonin) and alpha dense granules (mediate scaffolding VWF. fibrinogen, platelet derived growth factor)

291
Q

what is having too much platelets called and what is the risk?

A

thrombocytosis, increased risk of spontaneous clots

292
Q

what is having too little platelets called and what is the risk?

A

thrombocytopenia (cuts can cause increased bleeding)

293
Q

what is the first stage to the coagulation cascade?

A

vascular constriction; endothelium 1 is released from damaged endothelium which causes constriction

294
Q

what keeps healthy blood vessels open?

A

prostacyclin and NO

295
Q

describe the formation of the platelet plug

A

factor 8 VWF binds to exposed collagen at injured endothelium using GP 1b. platelets adhere to
VWF on collagen via GP IIa/IIIb and become activated. alpha and electron granules are released and more platelets become activated by positive feedback to form a primary platelet plug

296
Q

what hydrolyses the platelet plug?

A

tissue plasminogen activator converts plasminogen to plasmin. plasmin eats fibrin and converts it to fibrinogen

297
Q

what clotting factors are produced in the liver?

A

all bar VWF

298
Q

what blood type is the universal acceptor?

A

AB+

299
Q

what blood type is the universal donor?

A

O-

300
Q

where are ABO antigens produced and can they cross the placenta?

A

produced in spleen cannot cross

301
Q

can rhesus antigens cross the placenta?

A

yes

302
Q

what is the most immunogenic rhesus and how will you have the antibodies?

A

D, if DD or Dd will have antibodies therefore no immune response

303
Q

what is haemolytic disease of the foetus and new-born?

A

mother has a child with a DD or Dd man. child is born as Dd, mother makes RhD antibodies against babies antigens but baby is fine. when second baby is born, mothers RhD antibodies attack foetus leading to anaemia and death

304
Q

how does the AVN delay signals?

A

there are less gap junctions to allow the electrical signal to pass and the fibre has a smaller diameter

305
Q

what are the three binding sites on troponin?

A

myosin, actin and tropomyosin

306
Q

how do nodal cells become depolarised?

A

t-type Ca++ allow influx into the cell till threshold of -40mV is met where L type Ca++ open till +10 is reached. VG K+ open and K+ leaves the cell

307
Q

what is bradycardia?

A

low heart rate <60bpm

308
Q

what is tachycardia?

A

high heart rate >100bpm

309
Q

what does the right coronary artery supply?

A

SAN, AVN and post IV septum

310
Q

what does the right marginal artery supply?

A

RV, apex

311
Q

what does the posterior descending artery supply?

A

RV, LV. post 1/3 IV septum

312
Q

what does the left coronary artery supply?

A

left atrium, left ventricle, septum, AV bundle of His

313
Q

what does the left anterior descending artery supply?

A

anterior 2/3 IV septum, RV, LV

314
Q

what does the left marginal artery supply?

A

left ventricle

315
Q

what does the circumflex artery supply?

A

left atrium and left ventricle

316
Q

what is systolic heart failure?

A

heart does not pump hard enough

317
Q

what is diastolic heart failure?

A

heart doesn’t fill to full
volume

318
Q

what is left sided heart failure and what does it cause?

A

blood backs up into the lungs causing pulmonary oedma fluid build up in lungs

319
Q

what is right sided heart failure and what does it cause?

A

blood backs up in the rest of the body causing peripheral oedma, mostly in the legs

320
Q

embryology of the heart

A
321
Q

at what level does the trachea bifurcate?

A

t4

322
Q

what is the respiratory tree?

A

trachea to right and left lobar bronchi, to segmental bronchi, terminal bronchioles, respiratory bronchioles, alveolar ducts and sacs

323
Q

what does the upper airway consist of? conducts air

A

nasopharynx to terminal bronchioles

324
Q

what does the lower airway consist of? gas exchange

A

respiratory bronchioles to alveolar sacs

325
Q

what is respiratory epithelium?

A

pseudostratified ciliated columnar epithelium with interspersed goblet cells

326
Q

what are the accessory muscles that aid in active inspiration?

A

sternocleidomastoid, serratus anterior, latissimus dorsi

327
Q

what are the accessory muscles that aid in active expiration?

A

internal intercostal muscles, abdominal muscles

328
Q

why is the interpleural space important?

A

the chest wall has a natural tendency to pull out, and the alveoli a natural tendency to pull in. during inspiration, pathology of the space pre
vents the alveoli from moving out

329
Q

what is the transpulmonary pressure and its value?

A

alveolar pressure- interpleural pressure. alveolar pressure is 0, IP pressure is -4 so transpulmonary pressure is 4mmHg

330
Q

what happens if the transpulmonary pressure decreases?

A

the lungs move more naturally inwards, parietal pleura remains stuck to chest wall. air flows into interpleural space causing pneumothorax

331
Q

pontine and medullary centers

A
332
Q

what are slow acting stretch receptors?

A

found in the smooth muscle of the airway, respond to distension. activated at the starts the process of expiration and ends inspiration (myelinated)

333
Q

what are the three types of lung receptors?

A
334
Q

what are rapid acting stretch receptors?

A

found between airway epithelium, responds to irritants and activated leads to bronchoconstriction (myelinated)

335
Q

what are j receptors?

A

found across capillary walls, respond to increased lung pressure due to fluid (embolisms). leads to increased respiration (unmyelinated)

336
Q

describe peripheral chemoreceptors

A

found in aortic arch and carotid sinus. sensitive to changes in ppO2 and activated when ppO2<60%. fast response

337
Q

describe central chemoreceptors

A

found in medullary and detect changes in ppCO2. constitutes respiratory drive as mixes w water by crossing the blood brain barrier lowering pH. slow response

338
Q

what is V/Q?

A

ventilation/perfusion. should be equal. if not hypoxia

339
Q

what happens when the V/Q
value is high?

A

areas are ventilated but not perfused well, which is called dead space. can be cause by an embolism (blood clot)

340
Q

what happens when the V/Q
value is low?

A

areas are well perfused but not ventilated. can be caused by pulmonary oedma as alveoli are collapsed which leads to blood being shunted

341
Q

what does the body do when the V/Q value is high?

A

local bronchoconstriction, where air is diverted to better perfused areas

342
Q

what does the body do when the V/Q value is low?

A

hypoxic pulmonary vasoconstriction as blood is diverted to better
ventilated areas

343
Q

what factors shift the oxygen dissociation curve to the left?

A

high pH, low CO2, low O2, low DPG

344
Q

what factors shift the oxygen dissociation curve to the right?

A

low pH, high CO2, high O2, high DPG

345
Q

in what ways and proportions is carbon dioxide transported in teh blood?

A
  1. dissolved in plasma (10%)
  2. bound to Hb carbaminohaemoglobin (23%)
  3. as HCO3- (65%)
346
Q

normal blood pH?

A

7.35-7.45

347
Q

what does hypoventilation cause?

A

resp acidosis

348
Q

what does hyperventilation cause?

A

resp alkalosis

349
Q

hendson hasselback equation (pH of buffers)

A

pH = pKa + log10 ([A–]/[HA])

350
Q

what is Dalton’s law?

A

total pressure = ppA + ppB +….

351
Q

what is Boyle’s law?

A

P1V1=P2V2

352
Q

what is Henry’s law?

A

volume of gas dissolved in liquid depends on pp and solubility of it.
conc gradient = solubility coefficient x pp

353
Q

what is the alveolar gas equation?

A

PAO2 (alveolar) = PiO2 (inspired oxygen) − (PaCO2÷R). R= 0.8 usually

354
Q

what is Laplace’s law?

A

alveolar pressure depends on surface tension and radius
P = 2T/ r

355
Q

what secretes surfactant?

A

type ii pneumocytes

356
Q

what does greater lung compliance mean?

A

the lungs more readily expand

357
Q

what determines lung compliance?

A

surface tension and elasticity of lung tissue

358
Q

what is hypoxia most commonly caused by?

A

hypoxaemia (lowered paO2)

359
Q

what are four causes of hypoxaemia?

A
  1. hypoventilation (increased PaCO2)
  2. diff. impairment (thickening of membrane)
  3. shunt (septal defect, perfusing unventilated alveoli)
  4. V/Q mismatch
360
Q

what is hypercapnia?

A

increased CO2 levels; caused by hypoventilation and
V/Q mismatch

361
Q

what is important to consider when giving an asthmatic with type ii respiratory failure oxygen?

A

giving them O2 causes hyperventilation, which reduces PaCO2, reducing ability to breathe. alveoli collapse breathing ceases leading to death

362
Q

what is pulse pressure?

A

the difference between systolic and diastolic pressure

363
Q

what is Poiseuille law?

A

small changes in radius leads to a greater change in vascular resistance
8xLxviscosity / πxr4

364
Q

how can Ohm’s law be translated to arteriole pressure?

A

mean pulmonary arteriole pressure - mean arteriole wedge pressure = CO x peripheral vascular resistance

365
Q

what is the normal FEV1/FVC ratio?

A

0.75

366
Q

what is the inspiratory reserve volume?

A

max inhalation in excess of tidal (normal) volume ~2000ml

367
Q

what is exhalatory reserve volume?

A

max exhalation excess of normal exhalation ~1250ml

368
Q

what is tidal volume?

A

tidal normal breathing ~500ml

369
Q

what is residual volume?

A

air in lungs left after max expiration ~1250ml

370
Q

lung capacity

A
371
Q

why does lung compliance decrease with age?

A

costal cartilages become more stiff and lung elasticity decreases

372
Q

what is prone with ageing lungs?

A

V/Q mismatch, lower compliance, weaker immune response, delayed hypercapnia/hypoxia response. lower FEV1 an FVC that could falsely show obstruction

373
Q

what are some features of the innate immune system?

A

non specific, inherited and immediate

374
Q

how do neutrophils kill bacteria?

A

identify threat. becomes activated by cytokines, adhesion to the site of infection, diaphoresis (neutrophil-neutrophil adhesion) via chemotaxis where the neutrophils move in response to a chemical stimulus, phagocytosis, bacterial killing

375
Q

what is adaptive immunity?

A

specific, uses APCs. T+B cells

376
Q

what do T cells do and what are the types?

A

directly kills pathogen. cytotoxic t cells bind to CD8 receptors and puncture holes in cell membrane by releasing perforin which empties cell contents. t helper cells induces other cell activation through CD4 receptors

377
Q

what is the function of B cells?

A

secrete antibodies to kill pathogen through humoral action

378
Q

what are the different classes of antibodies Ig’s?

A

GAMED, G (most abundant), A (breast milk and mucosa) ,M ( first found in infection),E (allergens), D (unknown, may be a B cell activator)

379
Q

what are the broad classifications of host defences within the lungs?

A

immune and non immune barriers

380
Q

what are examples of non immune barriers within the lungs and how do these act as barriers ?

A
  1. respiratory epithelium (barrier, antipathogen, mucus).
  2. mucus (mucos-cillary escalator to be coughed up and swallowed and general protection/ lubrication)
  3. coughing (air is forced out by a pressure gradient created by the epiglottis closing and thoracic pressure increasing)
381
Q

what are examples of immune barriers within the lungs and how do these act as barriers ?

A

alveolar macrophages which represent 95% of all macrophages within the lung that act on a regular basis with minor disturbances. neutrophils are involved in larger response leading to inflammation

382
Q

what is hypersensitivity?

A

allergic hyper-response, inflammation of self cells

383
Q

what is type I hypersensitivity with examples?

A

IgE receptors bind to basophils which secrete histamine and PGs leading to bronchoconstriction and
vasodilation and inflammation. e.g. asthma and hayfever

384
Q

what is type II hypersensitivity with examples?

A

IgM and IgG leads to a cytotoxic response and tissue damage/altered receptors e.g. autoimmune responses

385
Q

what is type III hypersensitivity with examples?

A

IgG immune complex formation and deposition e.g. pigeon fancier lung and malt worker’s

386
Q

what is type IV hypersensitivity with examples?

A

T cell mediated, delayed response

387
Q

where are beta type 1 and 2 receptors found?

A

2 in the lungs (2 lungs) and 1 in the heart (1 heart)

388
Q

how are respiratory issues treated?

A

bronchodilation. B2 agonists (salbutamol) and M3 antagonists (ipa/trospium)

389
Q

how to calculate pressure of inspired gas?

A

atmospheric gas x fraction of inspired gas

390
Q

how to calculate partial pressure of arteriole oxygen?

A

partial pressure of alveolar oxygen - (alveolar/arterial concentration gradient, typically 1)

391
Q

how to calculate partial pressure of arteriole carbon dioxide?

A

constant of ventilation of carbon dioxide x alveolar
ventilation

392
Q

what physiological responses occur with increased altitude?

A

hypoxia due to less oxygen leading to hyperventilation. lower PaCO2, increase heart rate and increase blood pH (temp alkalosis)

393
Q

what pathology occurs with increased altitude and what are the symptoms and treatment?

A

acute mountain sickness (headaches, treated with descent). high altitude pulmonary oedema (oxygen and descent)

394
Q

what pathology occurs with decreased altitude and what are the symptoms and treatment?

A

depression sickness (N2 can not be excreted properly leading to bubbles in tissue), inert gas narcosis (N2), CNS oxygen toxicity (too much oxygen), arterial gas embolism (presents 15min after surfacing), pulmonary barotrauma

395
Q

what is the foramen ovale?

A

a hole between the left and right atria (upper chambers) of the heart to allow blood to bypass lungs as it is already oxygenated

396
Q

what is the ductus venosus?

A

a shunt that allows oxygenated blood in the umbilical vein to bypass the liver and is essential for normal fetal circulation. blood becomes oxygenated in the placenta and travels to the right atrium via umbilical veins through the ductus venosus, then to the inferior vena cava

397
Q

what is the ductus arteriosus?

A
398
Q

embryology of the lungs

A

a blood vessel that connects the pulmonary artery (main vessel supplying the blood to the lungs) to the aorta (main vessel supplying the blood to the body) to bypass lungs

399
Q

what do umbilical arteries do and how many are there?

A

2, carry deoxygenated blood from foetus to the mother

400
Q

what do umbilical veins do and how many are there?

A

1, supplies oxygenated blood from the mother to the foetus

401
Q

what happens during the first breath?

A

fluid is squeezed out of the lungs and surfactant is produced. air is inhaled and the pul arteries vasodilate

402
Q

what does the umbilical
vein become?

A

ligamentum teres

403
Q

what does the ductus venous become?

A

ligamentum venosus

404
Q

what does the ductus arteriosus become?

A

ligamentum venosus arteriosus

405
Q

what does the foramen ovale become?

A

fossa ovale

406
Q

what are the aortic arches?

A

a series of six arches that develop consecutively to connect the aortic sac with the paired dorsal aorta

407
Q
A

IMMS session 4: introduction to the cardiorespiratory system (11 decks)

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