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Year 1 LSS > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

1
Q

Outline the external structure (different layers) of the heart

A

Pericardium: Sack with pericardial fluid between visceral and parietal periacardium

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2
Q

Cardiac anatomy: demonstrate the basic anatomy of the heart, inculding the four chambers and the valves w. its simmilarities and differences

A
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3
Q

Explain different layers of blood vessels and explain their function

A

Tunica externa: collagen, protection and holding blood vessel in place

Tunica media: elastic smooth muscle, collagen and elastin

Tunica intima: vascular endothelium + support

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4
Q

Other name for arteries

A

conduit vessel

carry blood to destination

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5
Q

Ateriole

A

resistance vessel

control flow into capillaries

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6
Q

Other Name for Vein

A

Capacitance vessel

–> store most blood in human body

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7
Q

Explain coronary aterial circulation (3(4)) main arteries

A
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8
Q

Main vein(s) in coronary circulation

A

all blood comes together in coronary sinus

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9
Q

Major arteries in human body

A
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10
Q

Major veins in human ciculation

A

Everything ends in vena cava inferior + superior

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11
Q

Exitation-Contraction Coupling in Heart muscle

A
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12
Q

Length tension relatin in cardiac muscle

A

The more cardia muscle is stretched the higher passive + active force (til a limit)

–> more resistant to stretch and less compliant (nachgiebig) than skeletal muscle

–> due to ECM and cytoskeleton

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13
Q

Explain the two forms of muscle contraciton

A

Isometric: Same lenght, more tension

Isotonic contraction: Same tenstion, length changes

–> both important in cardia muscle contraction

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14
Q

Preload

A

load that stretches muscle in resting state

–> filling of the heart (more blood= more stretched

–> venous return of blood to the heart

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15
Q

Afterload

A

weight that is nor papparent in resting state but after start of contraction

–> load against left ventricle has to pust: Blood pressure

–> more afterload = less isotonic + more isometric contraciton

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16
Q

Frank-Starling-Relationship

A

Increased diastolic fiber length increases ventricular contraction (More preload = more stroke volume)

–> allows input = output

Because

  1. number of myofilament cross-bridges (too short = overlap)
  2. Ca2+ sensitivity increases –> conformational change in Troponin C (theory) increases affinity for Ca2+

Less Ca2+ for same force is needed

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17
Q

Stroke work

A
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18
Q

Law of LaPlace

A

Effect: Left ventricle smaller radius –> more pressure with similar wall stress

–> in failing hearts often hearts get dialated which increases wall stress

Vascular example –> aneurism –> higher radius, higher wall stress

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19
Q

Stroke volume (calculation and normal values)

A

End diastolic volume - End systolic Volume = Stroke Volume

108mL - 36mL = 72 mL

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20
Q

Ejection fraction (definition, calculation, normal ranges)

A

Shows, how much blood is ejected in relation to filling

Normal ; 60 - 70%

Ejection fraction = 100x Stroke Volume / End diastolic volume

67% = 100x 72ml / 108 ml

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21
Q

Cardiac cycle (phases, better overview in written notes)

A

Atrial systole

Isovolumetric contraction (1st heart sound)

Rapid ejection

Reduced ejection

Isovolumetric filling

Rapid passive filling

Reduced passive filling

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22
Q

Expain volume pressure loop and effects of pre and afterload

A

Box-like appearance with top left corner at end-systolic pressure volume relation (ESPVR)

  • Preload: Determines stretching /volume at beginning of stroke –> more preload, shifted to the right

–> increased preload –> increased stroke volume

  • Afterload: Determines pressure –> more after load = hight BP = higher pressure + higher curve

–> increased after load –> decreased stroke volume (less isotonic contraction

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23
Q

cardiac output

A

Blood pumped per minute

Heart rate x stroke volume

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24
Q

Peusoilles equasion

A

Small changes in radius have big effects on flow

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25
Q

Laminar blood flow

A

Straight blood flow without tourbulences

Good –> high shear stress (enlignment of endothelial in vessle wall, vasodialation + anticoagulation)

Velocity here : difference between blood flow in middle of vessle and at sides of vessel

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26
Q

Turbulent flow and shear stress

A

Turbulent flow is bad

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27
Q

Calculate pulse pressure and mean aterial pressure

A
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28
Q

Arterial compliance and pulse pressure

A

Compliance: ability of a vessel to stretch under pressure

Windkessel effect: aorta stretches, more steady blood flow

When arterial compliance decreases (get stiff), pulse pressure increases (pressure difference increases)

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29
Q

General facts about cardia action potential

A
  • very long (200-300ms –> 100x times longer than skeletal muscle)

–> allows enough time for filling + powerful contraction

  • duration of AP controls directly duration of cardiac contraction
  • different parts of heart have different AP patterns (because of different channels that are expressed)
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30
Q

Importance of refractory period

A

very important: allows the heart to fill before the next stroke

–> does not get tetanized production

Refractory period caused by Na+ channel inactivation –> recover while repolirization

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31
Q

Phases of the ventricular AP + ion permeability

A

0: up: PNa+–> Na influx
1: up: PK+ ITO (Transient outwart potassium current)–> K+ eflux

Ca2+ infulx

2: small K+ efflux
3: IK1 receprots open –> highly permeable to K+ –> efflux
4: maintained by IK1 during diastole –> stabelises

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32
Q

Again: Ionic permeability for Ventricular AP

A
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33
Q

Ionic permeability for Sinoaterial AP

A

can be influenced by sympathetic and parasympathetic stimulus ( inhibtion /slow down of rate by parasympathetic)

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34
Q

chronotropy

A

Heart rate affecting

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35
Q

Inotropy

A

heart contractility affecting

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36
Q

Cardiac conduction system

A
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37
Q

Impulse propagation in cardiac cells

A

passive spread of current + cells can get activated via threshold and generating own AP

–> threshold lowered because of gap-junctions –> current easily to neighboring cells (present at intercalated discs)

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38
Q

Mean Aterial Blood Pressure (MAP) equasion

A

Cardiac output (Q) x Total peripheral resistance (TPR)

Diastolic BP + 1/3 Pulse Pressure

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39
Q

Define Autoregulation of vascular system and name the two major hypothesis

A

Autoregulation: vessel radius changes responding to flow

  1. Myogenic mechanism hypothesis = opens in response to movement (fiber tension in vessel walls)
  2. Metabolic mechanism hypothesis = opens in response to accumulation of metabolic products
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40
Q

Name 4 Local hormones/messengers that affect vessel radius

A
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41
Q

Circulating hormones that affect vessel radius

A
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42
Q

Autonomic nervous system: –> two branches, neurotransmitters and length of ganglionic fibres

A
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43
Q

Noradrenaline binding (heart, vessels) and effect

A

Vessels: alpha 1 receptors –> vasoconstriction

Heart beta 1 receptors –> increasing heartbeat + contractive force

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44
Q

Sympathetic control of vessel dilation

A

Signals come from Vasomotor center in Brain (has depressor and pressor signals)

–> SNS always fires some signals (tonic activity –> vascular tonus) but the rate of firing determines radius (low frequency = vasodilation, high frequency = vasoconstriction)

  • No PNS involved
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45
Q

Explain the Effects of the SNS on the Heart

A
  1. increased heart rate ( decreases the threshold for excitation)–> easier excitation
  2. indirect effect via elevating EDV (end diastolic volume) (vasoconstriction, respiratory rate)
  3. Increases force contraction
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46
Q

Baroreceptors

A

Detect changes in pressure in carotid sinus node and aortic arch

–> feeds back on vasomotor center (–> then changes BP)

  • respond to stretch –> the more stretched, the more pressure the more they fire

–> when stretched: increased: vagus nerve firing + less sympathetic NS activation (decrease heart rate) + vasodilation

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47
Q

Blood flow rate equation

A

Blood flow rate (volume of blood through a vessel/minute)= pressure gradient/ resistance

Q=delta P/ R

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48
Q

What is the normal Vascular Tone and why is is kept this way?

A

Arterioles and smooth muscle is always partially constricted to allow adaptation in both directions

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49
Q

Difference between Active Hyperaemia and Myogenic autoregulation

A

Both functions of Arterioles to match blood flow to metabolic needs of the tissue

  1. Active Hyperaemia (mainly chemically driven) built up of metabolic products
  2. Myogenic autoregulation (mainly physically driven) respond to e.g. temperature or stretch (due to BP)
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50
Q

One equation for mean arterial BP

A

MAP = Q x TPR

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51
Q

Arterioles functions

What is meant by intrinsic factors and extrinsic factors?

What are their mechanisms to match tissue needs to perfusion?

A

Intrinsic factors: Match blood flow to needs –>

  1. Active hyperaemia (chemical built up of metabolic products)
  2. Myogenic Autoregulation (physical by body temperature and BP)

Extrinsic factors: to regulate BP (Neural + hormonal)

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52
Q

Differentiate between different types of capillaries

A

Capillaries –> one cell thick, have water-filled gaps between single cells to allow exchange

Different types of capillaries:

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53
Q

Explain the concept of Bulk flow and Starlings force

A

hydrostatic pressure lets plasma leave the capillaries at the gaps between cells –> osmolarity pulls (oncotic force) fluid later back in (when hydrostatic pressure drops later in the vessel

(but not all of it is reabsorbed in the vessels)

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54
Q

List main 5 functions of vascular endothelium

A

Vascular tone (secrete + metabolise vasoactive substances)

Thrombostasis (prevention of clot formation)

Absorption / Secretion (through active/passive transport)

Barrier (pathogens, prevention of plaque formation)

Growth (cell proliferation)

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55
Q

What is Arachidonic acid the precursor for?

How are these products generated?

A

phospholipids —(phospholipase A2) —> Arachnidonic acid

—(COX1 + COX2)—> PGH2 (Prostaglandin H2)

PGH2 = precursor

Asperin = blocks Cyclooxygenases

  1. Three different outcomes:
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56
Q

Effect of Prostacyclin (PGI2) on vascular smooth muscle and mechanism of action

A

PGI2 (Prostacyclin) binds to IP receptor (Prostacyclin receptor on vascular smooth muscle)

–>upregulation of Adenylyl cyclase (converts ATP to cAMP)–> up of cAMP

cAMP inhibits Myosin light-chain kinase (forms cross bridges between myosin heads and troponin) –> leads to relaxation and vasodilation

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57
Q

Thromboxane A2 functions and mechanism(s) of action

A
  1. TXA2 binds to TPß receptors on VSM –> activation of Phospholipase C (PLC) –> splits PIP2 into IP3 and DAG

IP3 causes Ca2+ influx –> activation of myosin light chain kinase –> constriction

  1. TXA2 binds to TP alpha receptors on platelets –Y positive feedback activation (more production of TXA2 by platelet) –> aggregation
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58
Q

Nitric oxide mechanism of action on SM cell

A

Endothelial cell:

ACh binds to GPCR –> upregulation Pholohoipase C –> PIP2 into IP3 –> Ca2+ influx –> activation of endothelial Nitric oxide synthase –> production of NO

Muscle cell:

NO migration into SM cell –> (upregulation of cytoplasmic guanuly cyclase which converts GTP into cGMP –> inactivation of Myosin-Light-Chain Kinase —> relaxation

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59
Q

Angiotensin overall all mechanisms to maintain BP

A

Angiotensinogen –> activation to Angiotensin 1 by Renin –> ACE on kidnex and liver —> Angiotensin 2 (has different effects)

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60
Q

Angiotensin effect on Vascular smooth muscle cell + mechanism of action

A

1. Direct contraction of SMC

Angiotensin 1 converted into Angiotensin 2 by Angiotensin-converting enzyme (ACE) on endothelial cells

–> Migration into Smooth muscle cell

activation of PLC –< PIP2 –> IP3 –> Ca2+ influx–> contraction

2. Deactivation of Bradykinin

(gets broken down by ACE) which would cause relaxation (production of NO)

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61
Q

Endothelin 1 mechanism of action

A

Contraciton of SM

  • BIG-ET1 expressed by nucleus–> converted into ET1 (by ECE)

—> ET1 binds to SMC(ETA + ETB receptros) –< activation of Phospholipase C –> IP3 –> Ca2+ influx –> contraction

Relaxation of SM (less important)

  • binds to endothelium –> production of NO –> relaxation (but less important than the constriction part)
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62
Q

Mechanism of action of Aspirin

A

Inhibits COX1+COX2 (Cyclooxygenase)

–< No formation fo precursor of Thromboxane A2,

Prostacyclin still produced bc of site of expression

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63
Q

Pathology and Pathophysiology of atherosclerosis

A

Accumulation of plaque in arteries:

  • Because of activated endothelium ( gets activated by High BP, infections, smoking, inflammation, high glucose, mechanical stress etc.)

Different Mechanism:

  1. Activated endothelium recruits Leukocytes:
    - Normally: good for postcapillary venules but in atherosclerosis: leukocyte recruitment in large arteries causes atherosclerosis (they get trapped)

2. Permeability :

Lipoproteins in blood get into tissue under endothelium –< oxidation –> engulfed by Macrophages–> become Foam cells –< accumulation of fatty streaks

3. Turbulent flow:

promotes: pro-inflammation, pro-apoptosis, coagulation, pro leukocyte adhesion, and reduced NO production (reduced vasodilation)

4. Angiogenesis

good for minimizing damage to ischaemic tissues by formation of new vessels but can influence atherosclerosis in a negative way: contributes to plaque growth (vessels grow under atherosclerotic plaque)

5. Senescence

stops the proliferation of damaged cell (which is a good thing) but cells express pro-inflammatory agents –> bad for atherosclerosis

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64
Q

Three main classifications of Arrhythmias

A
  1. Supraventricular = SN (Sinus bradycardia, Sinus tachycardia, Sinus Arrhythmia)
  2. Junctional arrythmia= at AV node (Atrial fibrillation, Atrial flutter, 1st. degree heart block, 2nd, 3rd degree)
  3. Ventricular arrythmias= potentially deadly, not ventricular impacted ( ventricular tachycardia, ventricular fibrillation, St depression/elevation)
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65
Q

Sinus bradycardia

A

slow, regular rhythm,

otherwise normal

(might be due to normal, medication, vagus nerve)

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66
Q

Sinus tachycardia

A

regular, fast rhythm

often physiological response

67
Q

Sinus arrhythmia

A

normal conduction, but at an irregular rate

68
Q

Atrial fibrillation

A

oscillating baseline –> atria not properly contacting –> turbulent flow —> clotting

rate may be slow, irregular

69
Q

What is Atrial flutter ? How does the ECG look like?

A

Atrial flutter results from an abnormal circuit inside the right atrium, or upper chamber of your heart

regular slow-tooth pattern (2,3, aVF)

P waves may be hidden

70
Q

1st-degree heart block

A

Prolonged P-R interval

but: regular still functioning –> sign of aging

71
Q

2nd-degree heart block (Mobitz 1)

A

Gradual prolongation of PR interval until a beat is skipped

regularly irregular (disease of AV node)

also called Weckenbach

72
Q

2nd-degree heart block (Mobitz 2)

A

regular skipping of a heartbeat –> not all P waves follow by QRS

No P-R prolongation

regularly irregular

–> can easily change into 3rd degree

73
Q

3rd-degree heart block

A

P waves regular, QRS regular but no relationship

P waves might be hidden

non-sinus rhythm –> backup pacemakers take over (Slower QRS)

74
Q

Ventricular tachycardia

A

hidden P waves, regular but fast ( 100-200 bpm)

high risk of cardiac arrest but shockable

75
Q

Ventricular fibrillation

A

cardiac arrest

irregular

very fast (250bpm or faster) —> ventricles don’t have enough time to fill

shockable

76
Q

ST elevation/depression

A

> 2mm in deviation

depression: myocardial ichaemia
elevation: infarction

Example: ST elevation

78
Q

ambulatory BP

A

preferred way of measuring BP now –> electronic devices at home, 5-10 mmHg lower than in surgery

79
Q

Isolated systolic hypertension

A

often in people over 60 –> isolated systolic hypertension due to stiffening of vessels

80
Q

Associated factors with Established hypertension

A

Increased TPR

  • Active narrowing in arteries ( short term vasoconstriction)
  • Structural narrowing in arteries ( changes in arteries e.g. wall thickening)
  • Capillary loss (same amount of blood in fewer vessels –> adaptive? damage?

Decreased arterial compliance

  • –> often in people over 60 –> isolated systolic hypertension due to stiffening of vessels

Normal Cardiac output

Normal blood volume

BUT: shift in blood volume (more in the arterial system)

  • –> secondary to reduce venous compliance
81
Q

Which organ plays a key role in hypertension?

A

Kidney? –> Major role in BP regulation + hypertension is transplantable with kidney

Endocrine factors

Sympathetic nervous system

–> environmental factors+ genetic factors

82
Q

Treatment of hypertension

A

Lifestyle changes:

Weight loss, healthy diet, exercise, less alcohol

Medication:

  • ACE inhibitors + Angiotensin receptor blockers –> would inhibit upregulating effects of Renin-Angiotensin system
  • Diuretics (Loop –> only used in hypertensive crisis + thiazide –> concrete mechanism still unknown
  • ß- blockers –> reduce CO + renin secretion (rarely used anymore to just treat hypertension)
  • Calcium channel blockers
83
Q

Explain Primary hemostasis and all factors involved

A

included molecules

  • Von-Willebrand Factor (large protein with many binding sites)
  • Platelets (also many binding sites (GP1b for Van Willebrand receptor)
  • Collagen

Mechanism

  1. Tissue damage –> Collagen release
  2. Von-Willebrand factor binds to collagen
  3. Platelets bind to Von Willebrand-factor and therefore slow down –> with lower speed can now bind to Collagen as well –> Platelet activation
84
Q

Platelet activation (triggers and changes)

A

e.g because of binding to VWF and Collagen

change in shape

degranulation : release of many factors (Thromboxane A, Von Willebrand factor, Fibrinogen –> connects platelets, ADP (recruits more platelets)

85
Q

Explain secondary haemostasis (coagulation cascade)

A

Stabilisation of platelet clot in larger arteries

  1. Tissue Factor (III) + Factor VII (in circulation) activate Factor X
  2. Factor X activates Factor IX and catalyzes activation of Factor II into active form –> Thrombonin
  3. Thrombin binds to platelets and induces the release of factor XI, Factor VIII, and V
  4. Factor VIII and IX together cause strong activation of factor X
  5. Factor X and V together form complex that is even more powerful in activating Thrombin
  6. Thrombin activates Fibrinogen into Fibrin –> formation of mash

–> amplification of system

86
Q

Indirect inhibition of coagulation

A

downregulation of thrombin by inactivating VIII and V via Protein C

87
Q

Regulation of coagulation: which pathways directly inhibit coagulation?

A

Antithrombin –> inhibits thrombin (+ other factors IX, X, XI, heparin binds Antithrombin and Thrombin together

TFPI in the initial phase (inactivates TF, VII, X)

88
Q

Fibrinolysis

A

break down of a blood clot

  1. tissue plasminogen activation + Plasminogen together release Plasmin

Plasmin breaks down Fibrin –> production of degradation products

Plasmin: regulated by anti-plasmin

89
Q

Problem with bleeding in Primary Haemostasis

A
  1. Collagen abnormalities
  • Age
  • Steroid treatment
  • Scurvy
  • —> all three: less collagen available, less initiation of VWF collection
  1. Von-Willebrand
    * von-Willebrand disease (genetic mutation)
  2. Platelet
  • Aspirin
  • Thrombocytopaenia –> too little number of platelets

Characteristic: never really stops bleeding because coagulation never starts

90
Q

Possible problems in secondary haemostasis : Bleeding

A
  1. Genetic reasons
    * Hemophilia –> no Factor VIII or IX —> barely any thromboxane activation
  2. Acquired
  • Liver disease (no coagulation factors anymore produced)
  • Drugs (e.g. warfarin –> antithrombotic drug)
  • Dilution by volume replacement (no replacement of plasma after trauma)
  • DIC –> Disseminated Intravascular Coagulation: inflammation expresses Tissue Factor in Blood vessels –> activation of coagulation everywhere within blood vessel –> all coagulation factors are used up and are not available anymore

Characteristics: delayed bleeding because clot can’t be stabilized, not in small vessels (primary is enough) Haemathorisis –> bleeding into joints

91
Q

Bleeding: Problem in Fibrinolysis

A
  1. Excess fibrinolytic
  • used as therapeutics e.g. in stroke
  • sometimes expressed by tumor
  1. Deficient in antifibrin
92
Q

Another cause for bleeding: Excess antithrombotic agents

A

Excess antithrombotic agents

often therapeutic

93
Q

Treatment of throbisis

A
  1. Lyse clot
    e. g. tPa –> only as an acute treatment because of a high risk of bleeding
  2. Limit reoccurring of emboli or extension

increase anticoagulant activity

inhibit coagulant pathways

94
Q

Virchow’s triad

A

There are three factors possibly contributing to thrombosis:

1. Blood (higher influence in venous thrombosis)

  • –> factors in the blood (e.g. deficiency in anticoagulant factors etc.)–> hypercoagulation

2. Vessel wall injury (more important in arterial thrombosis)

3. Flow (stasis)

  • –> reduced flow = accumulation of blood, easier clot formation
95
Q

Heart failure most important feature

A

Cardiac output is inadequate (often measured by Echocardiogram)

96
Q

Types of heart failure classification

A
  1. Left vs right
  2. Chronic vs acute
  3. Reduced Ejection Fraction vs Preserved EF
97
Q

Left heart failure

A

left ventricle

ejection or filling issue

congestion in lungs –> respiratory symptoms, might lead to dizziness and cyanosis

98
Q

Right heart failure

A

Right ventricle

ejection or filling issue

congestion in systemic circulation

often 2ndary to left heart failure –> due to increased afterload because of pulmonary hypertension

99
Q

Chronic heart failure

A

slow onset

due to e.g. MI, pulmonary embolism, surgery, infection etc.

100
Q

Acute Heart failure

A

rapid onset

as chronic but quicker and often more severe than chronic

101
Q

Reduced Ejection Fraction Heart failure

A

abnormal systole

impaired contraction –> due to damage to cardiac myocytes

–> end systolic volume is too high

higher diastolic pressure

102
Q

Preserved EF heart failure

A

abnormal diastole

normal contraction but

impaired filling (often due to stiffness of ventricle or lack of relaxation) (e.g. thickening of wall with increased afterload)

103
Q

Orthopnoea

A

difficulties to breath when lying down

104
Q

Causes of heart failure

A

Ischaemic heart disease

Hypertension

MI

Valve disease

Cardiomyopathy (dialated or hypertrophic)

105
Q

Cardiomyopathy

A

Abnormal organisation or cardiac myocytes

Dialated vs Hypertrophy

106
Q

Clinical features of heart failure

107
Q

Natriuresis

A

sodium excretion

108
Q

B-type natriuretic peptide

A

hormone secreted by cardiac myocytes in response to stress

–> sodium excretion : inhibits renin + aldosterone secretion, vasodilation –> reduced pressure

109
Q

Treatment of heart failure

A
  1. Lifestyle
  2. Medication: ACE inhibitors, ß-Blockers, diuretic
  3. Surgical: fluid control, aortic balloon pump, VAT, transplantation, valve replacement
110
Q

Modifiable and non-modifiable risk factors of Coronary heart disease

A

Non-Modifiable

  • genetics
  • sex
  • age

Modifiable:

  • alcohol
  • smoking
  • obesity
  • lack of exercise
  • lipid intake
  • high BP
111
Q

Atherosclerosis mechanism

A

Mechanism

  1. Location: when turbulent flow —> low shear stress: endothelial gets leaky
  2. LDL can get under the endothelium

–> binds to proteoglycans + gets oxidised

  1. this attracts Macrophages (activation regulated by Nuclear Factor Kappa B)

—> engulf LDL and form Foam Cells

  1. secrete free radicals (NADPH oxidase, Myeloperoxidase) –> + feedback on 2 (oxidise LDL)
  2. Cytokines –> increased expression of endothelial cell adhesion molecules) –> +ve feedback on 3
  3. Chemokines –> attract Macrophages
  4. Wound healing – the> proliferation of SM cells+, they make more collagen (is good) but: break down of collagen in fibrous cap + increased platelet growth factors
  5. —>>> Chronic Inflammation
  6. Apoptosis of Macrophages –> release of LDL and formation of Plaque
112
Q

Explain the concept of active hyperemia

A

Chemical Way to match blood perfusion to metabolic needs:

When cells increase metabolism, they also increase possibly vasodilatory byproducts

–> accumulation of these products vasodilation and thereby an increased blood perfustion

113
Q

What is the difference between Phospholipase C to Adenylyl Cyclase?

What does each of them cause?

A

Phospholipase C normally converts PIP2 into

  • IP3 –> normally increases intracellular Ca2+ –> often increasing muscular contraction
  • DAG activates e.g. protein kinase C, often leading to muscle contraction

Adenylyl Cyclase

  • Turns ATP into cAMP –> Many physiological actions, normally leading to smooth muscle relaxation but also increased intracellular Ca2+
114
Q

How do cardiac and sceletal muscle differ looking at compliance and resistance?

What does this differnce lead to?

A

Cardiac muscle more resistant to stretch and less compliant than skeletal muscle

—> Stretches less than skeletal muscle + returns quicker to old form

Cardiac muscle can contract stronger when it is stretched more

115
Q

Explain the structure and the different layers of a blood vessel

116
Q

What are endothelial stimmuli for atheogeneisis?

A
  • High LDL
  • Hypertension
  • High glucose
  • Oxidative stress
  • Inflmmation
  • Viruses
  • Mechanical damage
  • Smoking
  • Sex hormone imbalance
  • Toxins
  • Altered blood flow (e.g. turbulent flow)
117
Q

How does activated endothelia differ from normal, non-activated endothelium?

A

It turn to

  • Pro-inflammators
  • Pro- thrompotic
  • And pro-angiogentic
118
Q

Name the 5 steps following endothelial activation that lead to the formation of atherosclerosis

A
  1. Leukocyte recruitement
  2. Increased permeability
  3. Turbulent flow
  4. Angiogenesis
  5. Senescence
119
Q

Explain the step of Leukocyte-recruitment in normal physiology and in the formation of Atherosclerosis.

A

Normally: Adhere to post-capillary venules in times of inflammation to migrate into tissues

  • leukocytes adhere to activated endothelium of large arteries get stuck in the subendothelial space

—> different target site

–> Monocytes adhere, migrate into tissues and become macrophages

120
Q

Explain the structure of post-capillary venules

121
Q

Explain the concept and consequence of increased vascular epithelial permeability in the formation of Atherosclerotic plaques

A

Permeability is increased (inflammation) to normally allow leukocyte recruitment But:

  • Also, Lipoproteins can migrate into tissue
  • Get oxidised (–> attracts more leukocytes)
  • Phagocyted by Macrophages
  • Become Foam cells

Accumulate into tissues and form fatty streaks

122
Q

Explain the role of turbulent flow in the formation of Atherosclerosis (endothelium)

A

Atherosclerosis occurs most of the time at sites of turbulent flow :

Disturbed blood flow promotes

  • coagulation,
  • leukocyte adhesion,
  • SMC proliferation,
  • endothelial apoptosis and
  • reduced nitric oxide production
123
Q

Explain the role of Epigenetics in the formation of atherosclerosis

A

A: Stable flow (s-flow)

  • downregulates the expression of DNA methyltransferases (DNMTs), which allows the promoter of antiatherogenic genes, such as Klf4and HoxA5, to remain demethylated, enabling their expression.

B: Disturbed flow (d-flow)

  • upregulates DNMT expression —> hypermethylation of the promoter of antiatherogenic genes, such as Klf4and HoxA5, repressing their expression.
124
Q

Explain the (two-sided) role of Angiogenesis in plaque formation

A
  1. Contributes to plaque growth —> When they grow under plaque
  2. But can also limit damage of ischaemia as providing alternative route
125
Q

Explain the role of senescent cells in atherosclerotic plaque formation

A
  • Damaged cells that spüe to proliferate to not havint limited daughter cells BUT
  • These cells are pro-inflammtory and pro-thromboitic making atherosclerotic plaque worse
126
Q

What happens to the permeability of the endothelium with reduced shear stress?

A

It gets more permeable and “leaky” allowing LDL + leukocyte recruition

127
Q

Which Substances are being produced by foam cells that influence atherosclerosis formation?

A
  1. Chemicals like NADPH oxidate + Metalloprotein
    * That are free radicals that oxidise LDL (+ve feedback)
  2. Cytokines
    * Recruit Macrphages (by increasing endotheilal cell adhesion molecules)
  3. Chemokines
    * Increased signals for macrophage attraction
128
Q

Explain the role of wound healing in the formation of atherosclerosis

A

Wound Healing–> promoted by recruited macrophages

Promote Atherosclerosis:

  • Increase chemotaxis,
  • the proliferation of muscle cells
  • platelet growth factors

Beneficial:

  • Collagen synthesis provides a fibrous cap to stabilize plaque from rupturing
129
Q

Which effects does apoptosis of macrophages in the formation of plaques play?

A
  • Killed macrophages release fat to accumulate in plaque
  • Modify SM cells which leads to a degradation of collagen and thereby making the plaque more instable
130
Q

Which role does the Nuclear Factor Kappa B (NfKB) play in the formation of atherosclerotic plaque?

A

Activated by numerous inflammatory stimuli

  • •Scavenger receptors
  • •Toll-like receptors
  • •Cytokine receptors

Switches on numerous inflammatory genes

  • •Matrix metalloproteinases
  • •Inducible nitric oxide synthase

–> indirectly activates macrophages

131
Q

Which transcription factor plays a big role in atherosclerotic plaque formation by upregulating pro-inflammatory genes like

  • Matrix metalloproteinases
  • Inducible nitric oxide synthase?
A

Nuclear Factor kappa B (NFkB)

132
Q

What is cardiomyopathy?

A
  • a general term for diseases of the heart muscle, where the walls of the heart chambers have become stretched, thickened or stiff

Dilated cardiomyopathy:

  • Muscle = stretched + thin: can’ contract anymore

Hypertrophic

  • Hypertrophy of muscle
133
Q

WHat is the relevance of TFPI and what does it stand for in Haemostasis?

A

TFPI= Tissue factor pathway inhibition

–> binds III, VIIa and Xa to inhibit intiation of coagulation

BUT if Thrombin is already made, it will amply the reaction anyway —> ,,Thrombin Funke”

134
Q

Which role do NO and Prostacycline play in the regulation of thrombostasis?

What else is contributes to this which is derived from the endothelium?

A

Both are endothelial-derived substances that inhibit platelet activation

ADPase on the epithelial surface will break down ADP and will attract less Platelets

135
Q

Name the Three pathways that can coagulation be limited/inhibited?

A
  1. Indirect Pathway
  2. Direct pathway
  3. Fibrinolysis
136
Q

How does the direct pathway inhibit coagulation?

A

Antithrombin is present on the endothelial surface

–> When it meets thrombin: it inhibits it (this reaction is amplified by Heparin)

It Also deactivates Factor IX, X, XI

137
Q

How can coagulation be regulated by the indirect pathway?

A

Via indirect inactivation of the Co-Factors (Factor VIII and V)

By binding to Thrombomodulin (on the endothelial surface)

–> Thrombomodulin modifies Thrombin so that is activates Protein C

Protein C inactivates Factor VIII and V

138
Q

How is a clot broken down? (Explain the concept of Fibrinolysis)

A
  1. The clot breaks itself down after some time via Plasminogen and tissue plasminogen activator
  2. These two things have to be brought together (Plasminogen would otherwise not be activated) –> On Fibrin
  3. On Fibrin tPa turns Plasminogen into Plasmin
  4. Plasmin breaks down Fibrin into Fibrin degeneration product
  5. Antiplasmin regulates Plasmin activity –> Localised mechanism
139
Q

Differnetiate between the activation and action of phospholipase C and Protein Kinase C

A

Phospholipase C

  • A G-Protein coupled receptor
  • that cleaves IP3 into PIP2 and DAG

Protien Kinase C

  • Kinase that is activated via the products of Phospholipase C (DAG and increased Ca2+) that cleaves
140
Q

What is a normal duration for an RR interval?

141
Q

What is the normal duration of a P wave?

142
Q

What is the normal duration fo a QRS complex?

143
Q

What is the normal duration of a QT interval?

144
Q

What is the normal duration of a T-Wave?

145
Q

What is the normal range of the QRS axis?

A

Between -30 and 90°

146
Q

How do you calculate the cardiac axis?

A

Look at deflections from two leads which are 90° apart from another

–> Then via trigonominy:

tan(a)= gegenkathete/ ankathete

147
Q

What lines the inner pericardium?

A

The pericardium is lined by a single layer of cells called mesothelial cells with surrounding fibroconnective tissue rich in blood vessels and nerves.

148
Q

The supraventricular crest is an expanse of muscle which separates two valves from each other. Which two valves does it separate?

A

The supraventricular crest is a circular muscular ridge on the inner wall of the right ventricle, separating its inflow and the outflow aspects (i.e. the tricuspid and pulmonary valves.

149
Q

How do venous and arterial cloths differ in appearance of the clot itself?

A

The venous thrombosis normally is read –> including erythrocytes+ fibrin rich

The arterial thrombosis normally white –> platelets

150
Q

When does a third heard sound normally occur?

When does this occur?

A

It normally occurs in early diastole (rapid ventricular filling), immediately after S2 –>

Sudden deceleration of blood when the ventricle reaches its elastic limit

Physiological:

young individuals (< 40 years) or pregnant women

Pathological

  • Chronic mitral regurgitation
  • Heart failure (dilated ventricles)
  • Dilated cardiomyopathy
151
Q

If a 4th heart sound is present, in which heart phase can it be heart?

Which underlying reasons might be?

A

Ventricular filling sound:

  • late diastolic contraction of the atria (“atrial kick”) against a high ventricular pressure
  • Immediately before S1

Atrial gallop: Ten-nes-see pattern (S4-S1-S2)

Physiological: advanced age

Pathological:

  • atrial gallop
  • Ventricular hypertrophy (e.g., hypertension, aortic stenosis, cor pulmonale)
  • Ischemic cardiomyopathy
  • Acute myocardial infarction
152
Q

What is a bundle branch block?

A

It is a block in the bundle branches (down the septal wall) –> failed conduction on one sides leads to slower propagation of electrical signal on that side

153
Q

What is aortic stenosis?

Which heart sounds can you hear at auscultation?

A

It is a hardening and narrowing of the aortic valve

  • Murmor in systole
  • 4th heart sound before S1 (due to left ventricular hypertrophy and hardening)
154
Q

What is aortic Regurgitation?

Which heart sounds can you hear?

A

Aortic valve not completely leak-free

Murmor in diastole –> Turbulent blood flow from the aorta into the left ventricle creates a murmur during early diastole

155
Q

At which angles would Lead I, II, III, and aVL be in a standard hexagonal reference system?

156
Q

When do L-type Ca+ channels and when do T-type calcium channels play a role in a cardiac action potential?

A

L-type Ca2+ channels: cardiac muscle contraction

T-type Ca2+ channels: in exitable cells –> pacemaker cells

157
Q

What is a ventricular ectopic beat?

How does a ventricular ectopic beat look like in an ECG?

A

It is a bigger, premature ventricular contraction –> big beat in ECG

158
Q

What is mitral stenosis?

How does is present during auscultation?

A

Stiffening of the mitral valve

diastolic decrescendo murmur occurring after an opening snap

–> Enlarged left atrium

Turbulent blood flow from the left atrium into the left ventricle is responsible for the murmur

159
Q

Where are the positive and negative ends of lead I, II and III attached to?

A

From negative to positive

Lead I : Right arm to left arm

Lead II: Right arm to left leg

Lead III, Left leg to right arm

160
Q

What are the positive and negative attachments of leads aVF, aVL and aVR?

161
Q

Which chest leads show a inferior view of the heart?

A

II, III, aVF

162
Q

Which leads show a lateral view of the heart?

A

I, aVL, V5, V6

163
Q

Which leads show an anterior view of the heart?

164
Q

Which leads show a septal view of the heart?

Year 1 LSS (12 decks)

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