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Medicine > CVS > Flashcards

CVS Flashcards

1
Q

What are Fenestrated Capillaries? Where are they found?

A

Small windows bridged by a thin diaphragm exist in thin parts of endothelium
Found in parts of the gut, endocrine glands + Renal glomerus

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2
Q

What are Discontinuous capillaries and where are they found?

A

Larger diameter so have a slower blood flow, have gaps in wall to allow full cells to move between blood and tissue.
Found in Liver, Spleen, + Bone marrow

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3
Q

What is an Atrial Septal Defect? What is the most common site for an Atrial Septal Defect?

A

Opening in septum between two atria that persists after birth
Most commonly seen in foramen ovale, which is open prenatally to permit right to left shunting of oxygenated blood

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4
Q

What is a Patent Foramen Ovale?

A

Foramen Ovale fails to close properly, as left pressure is higher than right sided pressure it normally pushes the flap closed so its clinically silent

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5
Q

What is a Ventricular Septal Defect?

A

Opening in the ventricular septum, Since blood pressure in left ventricle is much higher the blood flow will be left to right

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6
Q

What is the Ductus Arteriosus? What is a Patent Ductus Arteriosus? When can it be heard?

A

Ductus Arteriosus is a vessel in the foetus to shunt blood from the pulmonary artery to the aorta before the lungs are functioning.
Vessel should close after birth due to drop of pressure in pulmonary artery, failure to close is a PDA.
Mechanical murmur can be heard at all times as Aorta is always at a higher pressure

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7
Q

What is Eisenmenger Syndrome?

A

Chronic left to right shunting causes remodeling of the Pulmonary circulation + increase in pulmonary resistance. If resistance of pulmonary circulation increases above systemic circulation then it will reverse the shunt to right to left

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8
Q

What is Coarchtation of the Aorta? How does it present later in life?

A

Narrowing of the aorta at the site of the Ligamentum Arteriosum (former DA). This narrowing increases afterload on the heart leading to left ventricular hypertrophy
Presents with weak + delayed femoral pulse and upper body hypertension

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9
Q

What is the name of heart defects that result in a lower than normal concentration of oxygen in the blood?

A

Cyanotic heart defects

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10
Q

What is Stenosis of the heart valves?

A

Narrowing of the valve

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11
Q

What are the 4 defects of Tetralogy of Fallot? How does it lead to Cyanosis?

A

-VSD
-Overriding Aorta
-Pulmonary Stenosis
-R.Ventricle Hypertrophy
Pulmonary stenosis leads to R.Ventricular hypertrophy as it has to pump harder to get blood into the pulmonary artery, this along with the overriding aorta allows right to left shunting

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12
Q

What is Tricuspid Atresia?

A

Lack of development of the tricuspid valve, leaves no inlet to R.Ventricle. Need to have full right to left shunt of all blood returning to right atrium + a ventricular septal defect or PDA to allow blood flow to the lungs

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13
Q

What is Transposition of Great Arteries? How is it treated?

A

Right ventricle is connected to aorta and left ventricle is connected to pulmonary artery, you have 2 unconnected circuits. The DA can be maintained and/or atrial septal defect formed

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14
Q

What is a Hypoplastic left heart?

A

Left ventricle + ascending aorta fail to develop properly. A Patent foramen ovale or ASD are also present and blood supply to the systemic circulation is via a PDA

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15
Q

What is mostly responsible for the resting membrane potential?

A

The permeability of the cell membrane to K+

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16
Q

Describe the Ventricular Action Potential

A

Depolarisation - Threshold is reached, fast voltage-gated Na+ channels open. Infulx of Na+ causes depolarisation.
Initial Repolarisation - Brief repolarisation due to outflow of K+ and closing of Na+ channels
Plateau - Slow voltage-gated Ca2+ channels open allowing Ca2+ influx, this prevents further repolarisation. Influx of Ca2+ activates Ca induced Ca release causing contraction
Repolarisation - After 280ms Ca2+ channels close and repolarisation is caused by efflux of K+ through K+ voltage-gated channels

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17
Q

What is the membrane potential range for the Ventricular action potential?

A

-90mV - +30mV

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18
Q

Describe the Pacemaker (Sinoatrial Node) action potential

A

Repolarisation activated slow Na+ channels, once cell reaches threshold potential due to funny current voltage-gated Ca2+ channels open depolarising the cell. Once voltage-gated Ca2+ channels close V-gated K+ channels open so K+ leaves cell repolarising it

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19
Q

What effect does increased hyperpolarisation have on pacemaker cells?

A

The more negative the membrane potential the more activated the HCN are (Hyperpolarisation-activated, Cyclic nuclotide-gated channels). This allows more influx of Na+

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20
Q

What features join cardiac muscle cells together?

A
  • Intercalated disks join cells together
  • Gap junctions allow movement of electrical ions between cells + electrically couples them
  • Desmosomes rivet cells together
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21
Q

How are the levels of Calcium in cytoplasm increased?

A
  • Depolarisation opens L-type Ca2+ channels in T tubules.
  • Localised Ca2+ entry opens Ca Induced Ca Released channels in the SR
  • 75% of Ca2+ enters from SR through CICR channels
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22
Q

How are Ca2+ levels returned to normal to relax the cardiac muscle?

A

Most Ca2+ is pumped back into SR by SERCA (raised levels activate the pump), some exits through Ca2+ATPase or Na+/Ca2+ exchanger (NCX)

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23
Q

Describe the mechanism for contraction of smooth muscle fibers

A
  • Depolarisation of cell causes Ca2+ influx, GPCR triggers IP3 which releases Ca2+ from SR
  • Ca2+ binds to Calmodulin (4 per calmodulin)
  • Calmodulin activated Myosin Light Chain Kinase which phosphorylates a light chains on smooth muscle cells causing a conformtational change allowing myosin to bind to actin
  • Myosin Light Chain Phosphotase dephosphorylates the myosin head so it becomes relaxed
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24
Q

What are the features of the Sympathetic nervous system?

A
  • Short pre-ganglionic fibre, long post-ganglionic fibre
  • Pre-ganglionic neurons are cholinergenic
  • Post-ganglionic neurons are noradrenergic
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25
Q

What are the features of the Parasympathetic nervous system?

A
  • Long pre-ganglionic fibre, short post-ganglionic fibre
  • Pre-ganglionic neurons are cholinergenic
  • Post-ganglionic neurons are cholinergenic
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26
Q

What are Chromaffin cells? Where are they located?

A

Specialised post-ganglionic cells that release Adrenaline into bloodstream when stimulated by Ach
Located in the Adrenal Medulla

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27
Q

What is the name of the nerve that provides parasympathetic innervation of the heart? What effect does the parasympathetic innervation have on the heart?

A

Vagus Nerve releases Ach which acts on M2-receptors

Reduces heart rate (negative chronotropic effect)

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28
Q

How does sympathetic innervation effect the heart?

A

Releases NA which acts on B1-adrenoceptors
Increases heart rate (positive Chronotropic effect)
Increases contractility (positive Ionotropic effect)

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29
Q

How does sympathetic innervation speed up heart rate?

A

NA acts on B1 receptors -> Gs G-protein increases cAMP -> Increases open probability of HCN channels -> increases slope (reaches threshold faster)

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30
Q

How does parasympathetic innervation speed up heart rate?

A

Increases open probability of K+ channels, this slows down depolarisation slowing down heart rate

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31
Q

How does sympathetic innervation increase the inotropy in the heart?

A

NA acts on B1 receptors in myocardium, causes increase in cAMP -> activation of PKA.
PKA phosporylates Ca2+ channels increaseing Ca2+ entry during AP.
Increase in Ca2+ increases force of contraction

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32
Q

What is the process of Smooth Muscle Relaxation?

A

Adrenaline stimulate B2 receptors -> increase in cAMP activates PKA -> opens K+ channels + inhibits MLCK -> Relaxatoin of smooth muscle

33
Q

What is the Dicrotic notch caused by?

A

The small amount of back flow caused when blood back flows from the aorta to the left ventricle

34
Q

What is reactive Hyperaemia?

A

When blood flow is cut off to an area vasodilators from metabolising tissues builds up, Arteries dilate maximally. When blood flow returns there is very low resistance so high flow until the vasodilators have been washed away

35
Q

What is Pre-load? Whats it determined by?

A

The end diastolic stretch of the myocardium, determined by venous pressure

36
Q

What is After-load?

A

The force necessary to expel blood into the arteries

37
Q

Explain Starling’s Law

A

The more the heart fills the harder it contracts so the bigger the stroke volume. When it gets to a certain point it begins to become over stretched and contractility reduces as there is less overlap between actin + myosin

38
Q

How does the CVS respond to standing up?

A
  1. Blood pools in superficial veins of the leg
  2. Central venous pressure falls
  3. Cardiac output and Arterial pressure falls
  4. Baroreceptors detect fall in arterial pressure + increase HR
  5. Arterial pressure still low so body increases total peripheral resistance to protect arterial pressure
39
Q

How does the CVS respond to exercise?

A
  1. Muscle pumping forces extra blood back to the heart
  2. Causes increase in venous pressure and fall in arterial pressure
  3. Baroreceptors detect fall in arterial pressure and increases HR
40
Q

What is the response of the CVS to Haemorrhage?

A
  1. Reduction in blood lowers venous pressure, causing a fall in CO and arterial pressure
  2. Baroreceptors detect fall in arterial pressure and HR + TPR is increased
  3. This further lowers venous pressure making the problem worse
  4. To fix the problem venous pressure needs to be increased
41
Q

What is the response of the CVS to long term increase in blood volume?

A
  1. Increase in venous pressure causes rise in CO
  2. This causes a rise in arterial pressure
  3. Increase in arterial pressure causes more blood to perfuse the tissues which autoregulate and increase TPR
  4. Arterial pressure increases again and stays up
42
Q

What do the PQRST waves correspond to in an ECG?

A

P wave - Atrial depolarisation
Q wave - Septal depolarisation spreading to ventricle
R wave - Main ventricular depolarisation
S wave - End ventricular depolarisation
T wave - Ventricular repolarisation

43
Q

How do you work out HR from an ECG?

A

ECG’s run at 300 squares per minute

44
Q

What is a Ventricular Ectopic Beat? How does it show on an ECG?

A
  1. Ventricular cells gain pacemaker activity causing contraction in addition to normal depolarisation
  2. Ventricular beat may occur every few beats. Beat is often wider and taller than a normal rhythm
45
Q

What is Atrial Fibrillation? How does it show on an ECG?

A
  1. The muscles of the atria aren’t contracting in a coordinated way
  2. P-wave is absent and in its place is irregular fibrillation waves, as there is no regular stimulus reaching the AV node other pacemakers generate rhythm
46
Q

What is Ventricular Fibrillation? How does it show on an ECG?

A
  1. Uncoordinated contraction of the Ventricles, causes a quiver rather than a contraction. Can quickly lead to death
  2. Wavy line rather than clear QRS complex
47
Q

What is Heart Block?

A

A communication problem between the atria and the ventricles

48
Q

What is First Degree Heart Block and how does it present on an ECG?

A
  1. P-R interval is elongated from its normal 200ms as there is a conduction delay through the AV node, but all signals reach the ventricles.
  2. Elongated P-R Interval
49
Q

What is Type I Second Degree Heart Block and how does it present on an ECG?

A
  1. P-R interval elongates until a QRS complex is dropped and the system resets, some but not all atrial beats get through to the ventricles
  2. Elongation of P-R interval then a missing QRS complex
50
Q

What is Type II Second Degree Heart Block and how does it present on an ECG?

A
  1. Electrical excitation sometimes fails to get through the Av node
  2. Normal constant P-R interval but not all P waves are followed by QRS complexes
51
Q

What is Third Degree Heart Block and how does it present on an ECG?

A
  1. There is no electrical conduction conveyed to the ventricles. Atrial contraction is normal, ventricles produce their own signal through an ectopic pacemaker
  2. P-wave present and rhythmic, QRS complex also present but in different slower rhythm than P-waves
52
Q

How does bundle branch block appear on an ECG?

A

Lengthens + changes the shape of the QRS complex

53
Q

What is the Ventilation-Refusion ratio? Whats the optimum ratio? What insures the optimal ratio?

A
  1. For efficient oxygenation of the blood the ventilation of the alveoli needs to match the perfusion of the alveoli
  2. Optimum ratio is 0.8, to maintain this alveoli that are not well ventilated have less blood supply
  3. Hypoxic Pulmonary Vasoconstriction - Alveolar hypoxia results in vasoconstriction of pulmonary vessels
54
Q

How is Blood flow to the brain regulated?

A
  1. Blood pressure - an increase causes vasoconstriction, decrease causes vasodilation
  2. Metabolic regulation - Hypercapinia (high CO2) causes vasodilation, Hypocapinia (low CO2) causes vasoconstriction
55
Q

What is Cushing’s Reflex?

A

Increase in intracranial pressure an impair cerebral blood flow (e.g. Cerbral tumour or haemorrhage). Impaired blood flow to vasomotor controls of brainstem leads to increased Sympathetic activity. This causes increased BP + Bradycardia, common signs of space occupying lesion

56
Q

How is the Skin used to regulate body temperature?

A
  1. Arteriovenous Anastomoses are used to control the amount of blood flow to the skin
  2. Reduction in core temp. -> Increased Sympathetic tone to AVA’s -> Vasoconstriction to reduce blood supply to skin
  3. Increase in core temp. -> Reduced vasomotor tone to AVA’s -> Dilation to increase blood flow to AVA’s
57
Q

What are common causes of Atrial Fibrillation? What is a serious concern of Atrial Fibrillation?

A
  1. Damage to the atria can cause several short re-entrant loops so excitation doesn’t spread normally through the atria.
  2. Can be caused by an ectopic focal point of excitation
  3. Major concern of Atrial Fibrillation is the risk of thrombus formation
58
Q

What can cause Ventricular Tachycardia? What is a risk of Ventricular Tachycardia?

A
  1. Following an MI damaged myocardium can cause an ectopic pacemaker
  2. Can lead to Ventricular fibrillation
59
Q

What are the 4 classes of antiarrythmic drugs, an example of each and how they work

A
  1. Class I - (Lidocaine) Block voltage sensitive Na+ channels, Blocks Na+ channels in the open + inactive states preventing automatic firing of the depolarised ventricle in damaged areas of myocardium
  2. Class II - (Propanolol) β-blockers, block sympathetic activity to the heart, decreases the slope of the pacemaker cells + reduce demand for O2. Slow conduction of AVN so prevent supraventricular tachycardias
  3. Class III - Prolong AP by blocking K+ channels lengthening the absolut refractory period
  4. Class IV - (Verapamil) Blocks Ca2+ channels, decreases slope of pacemaker, AVN conduction + inotropy
60
Q

Which drugs are used to increase Cardiac output and decrease the workload of the heart in Heart Failure?

A
  1. Digoxin - Blocks Na+/K+ ATPase so increase in [Na+], Na+/Ca2+ exchanger increases so increase in [Ca2+] increasing inotropy
  2. Dobutamine - β-adrenoceptor antagonist
  3. ACE Inhibitors - Inhibits the action of Angiotensin Converting Enzyme, prevents the conversion of Angiotensin I -> II, Angiotensin II acts on the Kidney to increase Na+ and water absorption + act as vasoconstrictor. So reduces BP
61
Q

What is Angina? What causes it?

A

Ischemia of the heart muscle causes chest pain, due to narrowing of the coronary arteries

62
Q

Organic Nitrates are used to treat Angina, how do they work? Whats an example of Organic Nitrates?

A
  1. React with Thiols in vascular smooth muscle, causing NO2- to be released, this is reduced to NO. NO activates cGMP which lowers intracellular [Ca2+] causing relaxation of smooth muscles. Causes venodilation and reduction of preload + O2 demand.
  2. Examples are Glyceryl trinitrite
63
Q

What are the two types of Antithrombotic drugs and examples of each?

A
  1. Anticoagulants - Heparin - Inhibits thrombin, used acutely for short term action
    - Warfarin - Antagonises action of Vit. K
  2. Antiplatelet - Asprin - Following acute MI or high risk of MI
64
Q

Name some causes of chest pain that are not caused by the CVS

A
  • Pneumonia
  • Pulmonary Embolism
  • Pneumothroax
  • Oesophogeal Reflux
  • Gastric, Pancratic disease
65
Q

What is a Coronary Atheroma?

A

Atheromatous plaque has a necrotic centre and a fibrous cap, stable plaques have a small core and a thick cap where as venerable plaques have the opposite meaning its more likely to rupture

66
Q

What is looked for in an exercise stress test to diagnose Angina?

A

Transient sub-endocardial ischemia with exercise shows as ST depression on ECG, when rested ST returns to normal

67
Q

How is Angina treated?

A
  1. Nitrates, Calcium channel blockers (Peripheral vasodilation), β-blockers used to reduce workload
  2. Protection of the atheroma by; Asprin (reduced platelet aggregation so reduced thrombus formation), Statins (reduced cholesterol + LDLs so reduced plaque progression)
68
Q

What causes a STEMI? What area of myocardium is injured? How does it present on an ECG?

A
  1. Complete + persistent occlusion of the artery
  2. Full thickness injury of myocardium
  3. ST elevation, Q-wave develops, T-wave inversion (2-5 days)
69
Q

What Biochemical markers will be in the blood following a STEMI?

A

Cardiac Troponin I + T

Creatine Kinase

70
Q

What is the difference between NSTEMI’s and Unstable Angina?

A

There is no necrosis or Biomarkers present in Unstable Angina

71
Q

How are STEMI’s treated?

A
  1. Re-establish perfusion, Angioplasty + stenting. If this isn’t possible in 90-120 minutes the thrombolysis with fibrinolytic drugs
  2. Antiplatelet drugs (Asprin), Anti-coagulents (Heparin), Anti-ischeamic therapy (Nitrates + β-blockers), ACE Inhibitors, Statins
72
Q

Describe the Renin-Angiotensin-Aldosterone system

A
  1. Reduction in BP stimulates release of Renin from kidneys
  2. Renin converts Angiotensin -> Angiotensin I, ACE converts Angiotensin I -> Angiotensin II
  3. Angiotensin II is a powerful vasoconstrictor, promotes release of Aldosterone from Kidneys
  4. Aldosterone causes salt + water retention in the Kidney increasing blood volume
73
Q

Which drugs are used to treat Heart Failure?

A
  1. Diuretics
  2. ACE Inhibitors
  3. Organic Nitrates
  4. Digoxin (used to treat atrial fibrillation)
  5. β-Blockers
74
Q

What is Cardiogenic shock? What can it be caused by?

A

Pump failure - Heart fills but fails to pump properly leading to raised venous pressure and dramatic drop in arterial BP, Tissues poorly perfused (worsens due to weakened contraction)
Caused by post MI-damage, Serious arrhythmias or acute worsening of heart failure

75
Q

What is Mechanical Shock? What is it caused by?

A

Inability to fill properly - Cardiac Tamponarde restricts filling of the heart and limits end diastolic volume. Leads to increased central venous pressure + reduced arterial BP
Massive Pulmonary Embolism Increases pulmonary artery pressure + CVP, reduces return to L.ventricle so reduced arterial BP

76
Q

What is Hypovolaemic Shock? Describe how it occurs

A

Reduced blood volume

  1. Venous pressure falls, CO + arterial pressure also fall
  2. Baroreceptors detect fall, causes Tachycardia, +ve inotropy, peripheral Veno/vasoconstriction
  3. Reduced BP causes internal transfusion so net movement of fluid into capillaries
  4. Decompensation - Increased peripheral vasoconstriction causes tissue damage due to hypoxia, tissues release vasodilators -> TPR + BP falls dramatically
  5. Vital organs no longer perfused leading to multi-system failure
77
Q

What causes Toxic Shock? Describe how it occurs

A

Caused by Septicaemia

  1. Bacteria release endotoxins causing vasodilation, this reduces TPR + BP, Capillaries become leaky reducing blood volume
  2. Vital organs have impaired infusion
  3. Baroreceptors detect change and increase sympathetic output, vasoconstrictor effect is overridden by vasodilator
78
Q

What causes Anaphylactic Shock? Describe how it occurs

A

Caused by sever allergic reaction

  1. Release of Histamines from most cells along with other mediators
  2. Powerful vasodilator effect causes fall in TPR + BP
  3. Sympathetic output increased but cant overcome vasodilation, causes impaired perfusion to vital organs
  4. Mediators also cause bronchoconstriction + laryngeal oedema -> difficulty breathing
  5. Treated with insulin

Medicine (10 decks)

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