Week 1 Flashcards
1
Q
Functions of the thorax
A
Protection, Respiration, Conduit (Passageway)
2
Q
What is contained within the thoracic cavity
A
Lungs
Heart
Major blood vessels
Part of the trachea
Oesophagus
3
Q
What forms the thoracic wall
A
Sternum
Thoracic Vertebrae
12 pairs of ribs and costal cartilages
Intercostal muscles fill the intercostal spaces
Arteries and Nerves that supply it
4
Q
What is the latin name for the head of the sternum
A
Manubrium
5
Q
What is the latin name for the tail of the sternum
A
Xiphoid process
6
Q
What are the three layers of the intercostal muscles
A
External intercostal muscle
Internal intercostal muscle
innermost intercostal muscle
7
Q
where are the intercostal arteries, veins and nerves found
A
Between the internal and innermost intercostal musxkss
8
Q
What joints are present in the true ribs
A
Sternocostal joints
9
Q
what joints are present in the false ribs
A
Interchondral joints
10
Q
Which ribs are false ribs
A
8-12
11
Q
Which ribs are floating
A
10-12
12
Q
what kind of joints are the sternocostal
A
Synovial Plane
13
Q
What are the two joints in which thoracic vertebrae and ribs articulate
A
Costovertebral joint
Costotransverse joint
14
Q
Which ribs are atypical
A
1,10,11,12
15
Q
What does the costaovertebral joint articulate
A
The head of the rib
The superior costal facet of the corresponding vertebrae
The inferior costal facet of the vertebrae superior to it
16
Q
What does the costotransverse joint articulate
A
The tubercle of the rib
The transverse process of the corresponding vertebrae
17
Q
What are the two thoracic apertures
A
Superior thoracic aperture
Inferior thoracic aperture
18
Q
What does the superior thoracic aperture act as a passageway between
A
Thoracic cavity
Neck and upper limb
19
Q
What is the function of the inferior thoracic aperture
A
Attachment for diaphragm which separates thoracic and abdominal cavities
20
Q
Boundaries of superior thoracic aperture
A
T1 Vertebrae
First pair of ribs
First costal cartilage pair
Superior border of the sternum
21
Q
Boundaries of the inferior thoracic aperture
A
T12 Veryebrae
The 12th pair of ribs
The costal arch
22
Q
Mean arterial blood pressure for someone with normal 120/80
A
93mmHg
23
Q
What are the attachments of the diaphragm
A
L1-L3 Vertebrae
Inferior costal cartilages and adjacent ribs
Xiphoid Process
24
Q
Where do the left and right domes project towards
A
The level of the 5th rib
25
Which dome of the diaphragm is projected higher up
The right dome, due to the liver
26
What is the Caval opening
Found at level of IV disc between T8-T9
Passage of inferior Vena Cava
27
What is the oesophageal hiatus
Oval opening for the oesophagus
Found at level of thoracic vertebrae 10
28
What is the aortic hiatus
Opening for the aorta and thoracic duct
Located posterior leg in diaphragm
Most posterior and inferior opening
Found at level of T12
29
Describe the external intercostal muscles
Occupy intercostal spaces from posterior to costochondral junction
Muscle fibres run anteroinferiorly
Most active during inspiration
30
Describe the internal intercostal muscles
Occupy intercostal spaces from anterior to angle of ribs
Muscle fibres run anteroposteriorly
Most active during expiration
31
Describe the innermost intercostal muscles
Deep part of internal intercostals
Form an incomplete layer that is most visible laterally
32
What is the intercostal neurovasculsr bundle
Bundle that comprises the intercostal vein, arteries and nerves.
Lies between internal and innermost intercostals
33
34
What is the order of the intercostal neurovasculsr bundle
V
A
N
35
What forms the intercostal nerves
Anterior Rami of T1-T11 spinal nerves = intercostal nerves
Anterior ramus of T12 = sub costal nerve
36
How many intercostal veins are there
11 posterior intercostal veins and 1 subcostal vein on each side
AND
9 pairs of anterior intercostal veins
37
Where does the posterior intercostal artery originate from
The aorta
38
Where does the anterior intercostal artery originate from
Internal thoracic cavity (branch of the subclavian artery)
39
Where does the internal thoracic artery travel
Along the inner surface of the anterior chest wall on both sides of
40
Where does the internal thoracic artery travel
Along the inner surface of the anterior chest wall on both sides
41
What happens if there is a stricture of the proximal aorta
The internal thoracic arteries and the anterior intercostal arteries can actually expand to maintain the blood supply
42
43
44
What are the thoracic cavity subdivisions
Pulmonary Cavity
Mediastinum
Pulmonary Cavity
45
What are the three layers of the pericardium
Visceral layer serous pericardium
Parietal layer serous pericardium
Fibrous pericardium
46
What is the pericardium
Fluid filled sac that encapsulates and protects the heart and the roots of the s main vessels
47
Describe the fibrous pericardium
Tough layer of connective tissue
Attaches to central tendon of the diaphragm inferiorly
Attaches to great vessels at the top of the heart
48
Describe the serous pericardium
Produces pericardial fluid to lubricate the heart as it beats
Two layers: Parietal and Visceral
Parietal is firmly attached to fibrous pericardium
Visceral is innermost layer
49
Name of the space between two layers of serous pericardium
Pericardial cavity
50
Describe the pleura
Parietal pleura: Lines the thoracic wall, mediastinum and the diaphragm
Visceral: Covers the external surface of the kung
51
Describe the pleura
Parietal pleura: Lines the thoracic wall, mediastinum and the diaphragm
Visceral: Covers the external surface of the lung
52
What lies between the two types of pleura
the Pleural cavity containing a film of fluid called serous pleural fluid. Lubricates the pleural surfaces and this is important to avoid friction of the two layers during respiration
53
latin name for the root of the lung
The hilum of the lung
54
Subdivisions of the parietal pleura
Costal pleura
Diaphragmatic pleura
Mediastinal pleura
Cervical pleura
55
Name of the spaces when the lung doesn’t fill the pleural cavity during expiration
The pleural recesses
Provide additional space for the lungs to expand
56
Largest pleural recess
Diaphragmatic pleural recess
57
What is a thoracentesis
The procedure by which a hypodermic needle is inserted through an intercostal space into a pleural cavity to remove blood or fluid from that level
58
What is the best space for a thoracentesis
Space 9
Between ribs 9 and 10
Mid axillary line
59
Which side of the heart collects deoxygenated blood
The right side
60
Where is the tricuspid valve
Between the right atria and right ventricle
61
Where is the mitral valve
Between the Left atria and left ventricle
62
How many cusps do the outflow valves have (semilunar)
Three each
63
How to calculate cardiac output
CO = SV x HR
64
65
How to calculate blood pressure
BP = CO x PVR (peripheral vascular resistance)
66
What is preload
how much blood you prime the chamber with
67
What is positive inotropy
When the body responds with a greater amount of contraction/stroke volume
68
Define inotropy
Contractile capability of the heart muscle aside from pre-load etc
69
Describe the positive relation of cardiac haemodynamics
As you increase the volume of blood that you’re priming in the ventricles, the ventricle responds by ejecting more. Adapting to the needs of the body by increasing stroke volume
70
Describe the contractile unit of cardiac muscle cell
Large, long, thin cells
Striated
Lots of mitochondria for energy
Cells are arranged linearly
Contractile filaments (actin and myosin)
Specialised junctions called intercalated discs
71
Define membrane potential
Term which describes the fact that there is a potential difference across the cell membrane of cardiac cells
72
What is the resting potential of a cardiac cell
-80 mV
More negatively charged ions on the inside of the cell
When the electrical gradient equals the concentration gradient
73
What cause depolarisation
If positive charges move inside the cell
Na+ and Ca2+ moving into the cell
74
What causes repolarisation
When the positive charges move back outside the cell
K+ moving outside the cell
75
What causes an action potential
Sequential activation and inactivation of inward Na and Ca currents and outward K currents
76
What is the plateau phase
Where depolarisation and repolarisation and balanced
77
Describe phase 0 of action potential
Upstroke
Opening of voltage gates Na+ channels allows inward Na+
Depolarisation
78
Describe phase 1
Notch
Rapid voltage dependent inactivation of the sodium current.
Activation of outward K+
Repolarisation
79
Describe phase 2 of action potential
Plateau
Balance of inwards Ca2+ and outward K+
80
Describe phase 3 of action potential
Repolarisation
Inward currents are inactivated and outward K+ predominates
81
82
Describe phase 4 of action potential
Resting
Whole cell is reprimed for the action potential to happen again
Sitting at -80mV
83
What mediates normal heart rhythm
Complex series of specialised Action Potentials
84
Bpm of SAN
70bpm
85
bpm of AVN
50bpm
86
bpm of purkinje cells
30bpm
87
where do the coronary arteries arise from
Right and left sides of the aorta right above the valve
88
What does the left coronary artery divide into
L Circumflex artery
L Anterior descending
89
what does the right coronary artery divide into
R posterior descending artery
90
Where do the coronary veins drain into
The coronary sinus then the right atrium
91
How is coronary arterial flow different o regular arteries
It’s diastolic
92
What is the first heart sound
Closure of AV valves
93
What is the second heart sound
Closure of the SL valves
94
When do you feel the radial pulse
in between heart sounds 1 and 2
NOT 2 and 1
95
where do you listen for the aortic valve
2nd-3rd right interspace
96
where do you listen for the pulmonic valve
2nd -3rd left interspace
97
where do you listen for the tricuspid valve
left sternal border
98
where do you listen for the mitral valve
apex
99
Equation for mean arterial blood pressure
MABP = CO x TPR
100
101
why are there holes in the internal lamina
allow direct communication between endothelial cells of intima and circumferential cells of media (blood to muscle)
102
proportion of scots with hypertension
a third
33% of men
28% of women
103
what has a larger effect on flow rate, length or diameter
diameter
104
what blood pressure values highlight the start of hypertension
140-159
90-99
105
what are the bp values fro grade 2 hypertension
160-179
100-109
106
what are the bp values for grade 3 hypertension
>180
>110
107
what percentage of the hypertensive population have primary hypertension
90%
108
outline risks for primary hypertension
lifestyle; smoking, obesity, high salt, excessive alcohol, lack of exercise
genetic
age
anxiety and emotional stress
109
example of a cause of secondary hypertension
renal disease or endocrine disorders (hyperaldosteronism)
110
results of chronic hypertension
vascular remodelling and end-organ damage
damaged endothelium
impaired endothelium function
decrease in blood flow to organs
increase in vessel stiffness, leakiness, thrombosis risk, TPR
111
examples of what chronic hypertension can increase the risk of
coronary artery disease
chronic kidney disease
peripheral arterial disease
vascular dementia
112
statistics of effects of antihypertensive therapy
40% reduction in stroke
25% reduction in MI
>50% reduction in heart failure
113
effects of beta 1 blockers on bp control
reduce cardiac output
reduce renin release from kidney
114
effects of alpha 1 blockers on bp control
reduce effects on blood vessels
115
effects of ACE inhibitors and angiotensin receptor blockers on bp control
inhibition of renin-angiotensin-aldosterone system
(control blood pressure)
116
effects of Ca2+ channel blockers on bp control
induce vasodilation which reduces peripheral resistance
117
effects of diuretics on bp control
increase sodium and water excretion to reduce blood volume
118
role of renin in RAAS
converts angiotensinogen to angiotensin 1
119
role of ACE inhibitors
inhibits conversion of angiotensin 1 to angiotensin 2
- angiotensin 2 is a vasoconstrictor
- reduces blood volume
120
role of angiotensin 2 in RAAS
can be converted into aldosterone
increases Na reabsorption and H2O retention
increases ADH release, Na+ appetite, thirst
Arteriolar constriction
121
role of aldosterone in RAAS
increase K= urinary secretion, Na+ reabsorption, H2O retention
decreases serum potassium
122
role of angiotensin receptor blockers
inhibits effects of angiotensin 2
123
compare captopril to other ACE inhibitors (enalapril, ramipril, trandolapril)
captopril - active compound and active metabolites
the others have a longer half-life; prodrugs converted to active metabolite by liver
124
side effects of ACE inhibitors
sudden fall in BP on 1st dose
persistent irritant cough
hyperkalaemia
In pregnancy DON'T USE: retard foetal growth, renovascular disease
125
what does the AT1 receptor mediate
vasoconstrictor and aldosterone releasing actions of angiotensin 2
126
examples of AT1 blockers
Losartan, valsartan, candesartan
127
key difference in side effects of Angiotensin 2 receptor blockers and ACE inhibitors
ARBs do not affect bradykinin levels, hence no irritant cough
128
describe mechanism of Ca2+ channel blockers
Bind to and block L-type voltage Ca2+ channels
Decrease Ca2+ entry in response to membrane depolarisation
resting membrane potential determines tissue selectivity
vasodilation
Decrease in bp
decrease in force of contraction + HR = reduced CO
129
describe Dihydropyridines
Calcium channel blocker
Allosteric modulators
Highest affinity in an inactivated state
smooth muscle is sensitive to them due to less negative Em
first line treatments for hypertension
- small effect on cardiac muscle is counteracted by baroreceptor reflex
130
describe Non-DHPs
interacts directly with Ca channel
highest affinity when channel is in an active state
both vascular and cardiac channels are blocked
causes vasodilation, decreased inotropy and HR
131
side effects of Ca2+ channel blocks
headache and dizziness
flushing
peripheral oedema
abdominal pain and constipation
132
describe mechanism of thiazide diuretics
reduced renal reabsorption of NA+ and water in the distal tubule
`lowers blood pressure by reducing blood volume
133
side effects of thiazide diuretics
decrease in plasma K+
Gi disturbances, fatigue, dizziness, headache
134
describe the mechanism of Beta-adrenoceptor blockers
competitive reversible antagonists
block beta1 sympathetic tone in the heart
- decreases HR, SV, CO, renin release, blood volume
reduces bp and unloads heart
135
side effects of beta-adrenoceptor blockers
intolerance to exercise, fatigue
bradycardia and dizziness
depression and confusion
sleep disturbances and nightmares
exacerbation of asthma and bronchospasm
136
describe the mechanism of alpha1-adrenoceptor blockers
competitive reversible antagonists
block alpha1 adrenoceptors in arterioles to reduce effect of sympathetic tone
decreased TPR and hence BP
137
describe the side effects of alpha1-adrenoceptor blockers
postural hypotension
reflex tachycardia
138
function of excitatory post-synaptic potential
depolarises the target neuron
139
function of inhibitory post-synaptic potential
hyperpolarizes the target neuron
140
describe the sympathetic pathway in heart rate regulation
response to stimulation begins slowly as;
- nerve terminals slowly release Norepinephrine
- downstream effects mediated by relatively slow second messenger system involving cAMP production
141
describe the parasympathetic heart rate pathway
rapid response to stimulation as;
- nerve terminlas rapidly releases acetylcholine
- downstream effects mediated by specialised acetylcholine-regulated k+ channels directly couples to muscarinic receptors to which acetylcholine binds
142
sympathetic activity on stroke volume
increases stroke volume by increasing magnitude and rate of force generation
143
where are arterial baroreceptors located
carotid sinuses and aortic arch
144
how do baroreceptors work
stretch increases receptor firing, inhibiting sympathetic outflow from pressor organ (depressor effect)
decreases sympathetic outflow to heart and vessels
increases parasympathetic outflow to the heart
145
describe the intima layer
single layer of endothelial cells acting as a metabolically active barrier between blood and vessel wall
146
describe the media layer
thickest layer, composed of elastin, collagen, and vascular smooth muscle
147
describe the adventitia layer
layer of connective tissue containing nerves, lymphatics and blood supply to the vessel wall
148
describe the composition of arterioles
composed of endothelium and smooth muscle, arranged in rings around the vessel, allowing large channels in vessel diameter
149
what is intrinsic control
local conditions surrounding the blood vessels
150
what is extrinsic control
nervous system input
151
two sources of extrinsic control of flow
sympathetic regulation
hormonal regulation
152
describe sympathetic regulation of blood flow
stimulation of pressor region causes sympathetic outflow, resulting in vasoconstriction
stimulation of depressor region causes inhibition of pressor region, resulting in vasodilation
153
what controls the extrinsic control of blood flow
regions in cerebral medulla that influence muscle tone
influenced by neural impulses and by blood concentrations of CO2 and O2
154
signalling molecules that cause vasoconstriction
norepinephrine
ATP
Neuropeptide Y
155
signalling molecules that cause vasodilation
Vasoactive intestinal peptide
Nitric oxide
156
which (intrinsic or extrinsic) mechanisms are dominant in brain and heart
intrinsic
157
which (intrinsic or extrinsic) mechanisms are dominant in skin
extrinsic
158
which (intrinsic or extrinsic) mechanisms are dominant in skeletal muscle
both interact, allowing tuned response to changes in activity
resting - extrinsic
exercise - intrinsic
159
160
What is atherosclerosis
the build up of fatty deposits in the vessel wall, which ultimately restricts blood flow
161
Describe the beginning of atherosclerosis
Adhérons is initiated by Endothelial dysfunction or injury
eg, due to smoking, infection, diabetes
These cause a reduction in endothelial protective factors such as nitric oxide
Plaques form in areas of variable shear stress
162
Describe the first step in initiation of atherosclerotic lesion
Due to endothelial damage it becomes more leaky. This allows LDL particles to cross the endothelium into the intima where they become oxidised and promote the expression of adhesion molecules Circulating
163
Describe the second step in initiation of atherosclerotic lesion
Circulating monocytes adhere and migrate, then mature into macrophages
164
Describe the third step in atherosclerotic lesion initiation
Macrophages take up oxidised LDL via scavenger receptors to become large lipid filled foam cells that form the fatty streak
165
Describe the last step in initiation of atherosclerotic lesion
Release of PDGF attracts SMC migration into intima
166
Describe the first step in advanced lesion formation in atherosclerosis
SMCs secrète fibrous matrix (eg collagen) that form a protective cap
167
Describe the second step in advanced lesion formation in atherosclerosis
Over time, SMCs and macrophages divide and undergo cell death
168
Describe the third step in advanced lesion formation in atherosclerosis
Cellular debris accumulates forming the necrotic lipid-rich core
169
Describe the fourth step in advanced lesion formation in atherosclerosis
The ability of SMC to synthesise collagen is impaired by INFy from T cells
170
Describe the fifth step in advanced lesion formation in atherosclerosis
MMPs from macrophages degrade collagen
171
Describe the last step in advanced lesion formation in atherosclerosis
Thinning and weakening of the fibrous cap increase the susceptibility of the plaque to rupture
172
Describe the problems associated with an unstable fibrous plaque
Fibrous cap can rupture leading to coagulation in and around plaque
Thrombus formation can occlude the vessel or cause an embolism downstream triggering an acute ischaemic event
Thrombus may also be absorbed to form a healed plaque
173
Describe vulnerable plaques
Highest risk of rupture!!
Easy to detect in pathological samples but more difficult in clinic
Can occur in arteries even without significant stenosis
174
Warning signs for vulnerable plaques
Large lipid core (>40% of area)
Thin fibrous cap
Abundance of inflammatory cells
Low level of SMCs
Microscopic or spotty calcification
175
Describe the consequences of atherosclerosis
Symptom free until blockage of vessels, plaque rupture or thrombosis
Can affect any tissue
Pulmonary embolism
Erectile dysfunction
176
Describe obesity as a risk factor for atherosclerosis
Adipose tissue is not just a depot for fat storage but also synthesises inflammatory cytokines and hormones
Perivascular adipose tissue around blood vessels can also affect function and includes immune cells
Hence, obesity can generate system inflammation
177
What is cholesterol essential for
Incorporating into cell membranes
Maintaining membrane fluidity and permeability
Production of steroid and fat-soluble vitamins
178
Role of the liver in cholesterol
Monitors levels
Regulates cholesterol via synthesis, absorption and secretion of bile
179
describe function lipoproteins
Macromolecular complexes that transport lipids
180
describe structure of lipoproteins
Core: Cholesteryl ester, Triglycerides
Coat of: Phospholipids, Free cholesterol
181
role of apoproteins
One or more per lipoprotein
Stabilises lipoproteins and it recognised by specific cells
eg, Apo B-100 is a ligand for the LDL receptor
182
Role of chylomicron lipoproteins
Carry Triglycerides from intestines to liver, muscle, and adipose
183
Role of very low density lipoproteins
carry newly synthesis triglycerides from liver to adipose tissue
184
role of intermediate density lipoproteins
an intermediate between VLDL and LDL
185
role of low density lipoproteins
major reservoir of cholesterol; taken up by LDL receptors via endocytosis
186
role of high density lipoproteins
adsorb cholesterol released by dying cells: also act as « reverse transport » to take cholesterol to live
187
what is exogenous cholesterol transport
the absorption of lipids from the diet and transport to tissues and the liver
188
what is endogenous cholesterol transport
the cycling of lipids from the liver to the tissue
189
How much cholesterol in blood is biosynthesised
75%
190
Describe familial hypercholesterolaemia
Affects 1/250 people
Most common mutation in LDL receptor gene
Risk of coronary artery disease is 13x higher if untreated
191
Signs of familial hypercholesterolaemia
Xanthomas- fatty cholesterol rich deposits in the skin often found around the elbows, knees, knuckles and achilles tendon
Xanthelasmas - fatty deposits in and around the eyelids
Arcus senilis - a white ring around the cornea
192
Describe secondary hyperlipidaemia
Less severe but much more common
High circulating levels of free and bound cholesterol and triglycerides
Cause: Diabetes mellitus, alcoholism, hyperthyroidism, liver disease, drugs, diet
193
Side effects of statins
GI disturbances, hepatotoxicity (rare), myalgia is commonly reported by true muscle toxicity is rare
194
Describe HMG-CoA reductase i inhibitors (statins)
Competitive inhibitors of rate-limiting step in cholesterol biosynthesis
Decrease in cholesterol levels causes up-regulation of hepatic receptors for ApoB and ApoE = increase clearance of LDL, IDL, and VLDL from plasma
can stabilise and even reduce plaque size
195
196
Describe Pectus Excavatum
Concaved chest
Chest wall indents into thoracic space
197
Describe pectus carinatum
Convex chest
Sternum is more protuberant than normal
« Birds chest »
198
what is a pneumothorax
When the lung gets punctured and air leaks into the pleural cavity
199
What is a pleural effusion
Collapse of the lung due to water in the thoracic cavity
200
what is the innervation of the diaphragm
C3, C4, C5
201
