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pop card - NOT COMPLETE Flashcards

1
Q

A diagram of an action potential in a cardiac muscle cell.

a) What causes the peak of depolarisation at the start?

A
  • Influx of Na+
  • T tubule membrane depolarised
  • L-type Ca2+ channel opened (different type of DHPR channel to skeletal – its voltage dependent whereas skeletal isn’t)
  • Ca2+ enters cell
  • Binds to Ryanodine receptor
  • Causes more Ca2+ channels to open
  • Calcium induced calcium release from SR
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2
Q

b) What ion is most important for standing membrane potential?

A

K+

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3
Q

c) What is the main difference between cardiac and skeletal muscle cells’ methods of excitation-contraction?

A
  • In skeletal muscle the dihydropyridine receptor (non-voltage gated sensor), changes conformation in response to Ca2+ which activates the ryanodine receptor and causes Ca2+ to be released from SR.
  • In cardiac cells, the L-type Ca receptor (voltage gated) on t-tubules open Ca channels when depolarised - increase in intracellular Ca causes the ryanodine receptor to be activated and release Ca.
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4
Q

d) What happens to force of contraction when there is Sympathetic stimulation to the heart? Why? (4 marks)

A
  • Force increases
  • CO and SV increase
  • Steeper slope of AP in SAN (reaches threshold potential quicker)
  • NA bind to beta-1 adrenoceptors located on cardiac muscle
  • Activates adenyl cyclase, increase conc cAMP PKA in myocytes
  • Phosphorylation of L type channels which activates them + SR Ca release channels more intracellular Ca more binding sites available (troponin C) more crossbridges stronger contraction
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5
Q

a) Aside from skeletal muscle, name 2 other vascular beds to which vasodilation occurs in exercise

A

Bronchial mucosa (by adrenaline)
Vasodilation in skin vasodilation of heat
Coronary vessels
Metabolic activity increases larger blood supply needed to remove CO2 and supply O2 to muscles.

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6
Q

Why does vasoconstriction occur to other organs’ vascular beds?

A
  • So that blood is diverted towards more metabolically active organs and away from less active ones (more active ones need more O2).
  • Vasoconstriction occurs in GIT + kidney: to increase the TPR, which helps to maintain MABP (despite vasodilation in skin, skeletal muscle) and keep blood flowing to organs.
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7
Q

a) What occurs in exercise to lead to an increase in CO?

A

Activity of skeletal muscles -skeletal muscle and respiratory pumps - increased venous tone, pressure, return - increased EDV -increased preload - increased stroke volume - increased CO

Increased sympathetic activity and adrenaline - increase venoconstriction and HR.

Sympathetic nervous system -increase contractility.

Decrease in PNS activity - increase HR

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8
Q

a) Why does venous return lead to increased CO?

A

Increased venous return - increase in venous pressure, return -increase in EDV - increase preload increase SV - increased CO.

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9
Q

a) Name 2 exercise dependent events that lead to increased venous return

A

Respiratory (reduced intrathoracic pressure increases venous pressure)
Skeletal muscle pumps

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10
Q

Name 2 exercise dependent events that lead to decreased venous return

A

Vasodilation of skin
Plasma vol decreases due to sweating
Vasodilation of the vessels in skeletal muscle + lungs reduced TPR
Increase in capillary pressure across wall hydrostatic pressure increased as MABP increased

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11
Q

a) Name and explain 2 factors in “western culture” that can lead to a predisposition to atherosclerosis

A

Smoking, high blood lipids (diet), blood pressure, diabetes, obesity, lack of exercise.

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12
Q

Name 2 of the 3 cells involved in atherosclerosis

A

Vascular smooth muscle cells, macrophages, vascular endothelial

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13
Q

a) Name two non-modifiable risk factors for atherosclerosis (1)

A

Age, gender, genetic background

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14
Q

a) Name 3 changes to the arterial wall due to atherosclerosis that might lead to clinical complications

A
  1. Endothelial damage leads to macrophage infiltration and release of cytokines
  2. Circulating low density lipoproteins are trapped in the lesion and oxidised
  3. Oxidised LDL is proinflammatory and drives the progression of the atherosclerotic plaque
  4. Smooth muscles cells migrate from the tunica media into the lesion and deposit a collagen-rich matrix that forms a protective fibrous cap
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15
Q

What are the clinical complications that could occur due to atherosclerosis?

A
  • Narrowing of vessel by fibrous plaque: renal artery stenosis, myocardial ischaemia, limb claudication
  • Plaque ulceration or rupture: thrombotic stroke, unstable angina, myocardial infarction
  • Interplaque haemorrhage: thrombotic stroke, unstable angina, myocardial infarction
  • Peripheral emboli: embolic stroke, atheroembolic renal disease
  • Weakening of vessel wall: aneurysms
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16
Q

a) Give 2 ways in which the Vascular Smooth Muscle of the arteries can mediate the stability of plaques

A
  • Smooth muscles cells migrate from the tunica media into the lesion and deposit a collagen-rich matrix that forms a protective fibrous cap
  • Proliferation increases the thickness of the smooth muscle around plaque to prevent rupture.
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17
Q

What organ produces renin? What are the cells in that organ that produce renin?

A

Kidney + juxtaglomerular cells.

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18
Q

a) What does renin do?

A

Enzyme which catalyses the conversion of angiotensinogen angiotensin I.

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19
Q

a) Where does angiotensin come from?

A

Angiotensinogen from liver
Angiotensin from kidneys
ACE from lungs and kidneys

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20
Q

What 2 hormones have an effect on salt and blood pressure in the kidneys.

A

Aldosterone – effect on Na
Angiotensin II – Alice Lee
Vasopressin

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21
Q

a) Which two limbs do Lead II attach to?

A

RA and LF

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22
Q

b) What angle on the hexagonal system does Lead IIs positive end go to, (or something to that effect)

A 
aVL = -30
avR = -150 
avF = 90
Lead I = 0
Lead II = +60
Lead III = +120
23
Q

c) Work out the heart beat per minute, given the R curves of the diagram

A

The rhythm strip is normally 25cm long and covers 10s.
Heart rate/min = number of QRS complexes in 10s * 6

1500/number of small squares between QRS

24
Q

d) Work out how long the PQR interval is

A

1 small square = 0.04s

1 large square = 0.2s

25
Q

e) How long is a normal PR interval?

A

0.12-0.20s

26
Q

a) Given graph of muscle length vs force for cardiac muscle. Label the axis and the lines.

A

Active line - up, curve, then down
passive line - diagonal, goes upwards

  • X – muscle fibre length
  • Y – force
27
Q

b) Draw out the myosin and actin filaments at the start, middle and end.

A
  • Muscle relaxed at A – little overlap of actin and myosin

* Fully contracted at C – maximum overlap

28
Q

c) Which part of the curve is relevant for cardiac muscle in vivo?

A

The ascending part – cardiac muscle is more resistant to stretch due to the pericardial sac

29
Q

c) What does the frank-starling relationship mean?

A

Increased diastolic fibre length increases ventricular contraction (more preload equals greater stroke volume).

30
Q

d) In the cardiac cycle, where is it i) isometric contraction; ii) isotonic contraction?

A

i) Isovolumic contraction

ii) rapid ejection, reduced ejection, atrial systole (ventricular ejection)

31
Q

e) Name two properties of the myofilaments which are responsible for the Frank-Starling laws of the heart (2)

A

Length changing of sarcomere: 1. The number of cross bridges that can form between actin and myosin relative to amount of overlap between the myofilaments (at optimum the actin and myosin filaments are stretched out to form the maximum number of cross bridges).
B) ‘Lattice spacing’ between them: with stretch you increase the probability of creating strong binding between actin and myosin heads so more force for same Ca.

Conformation change in troponin C which means it is more sensitive to Ca therefore less Ca required to produce same force.

32
Q

a) What would be the changes under parasympathetic stimulation to i) airways (2), ii) heart (1), iii) pulmonary vasculature

A

Airways – bronchoconstriction
Reduce heart rate
Vagal stimulation dilates the pulmonary vascular bed

33
Q

a) Name the changes and associated receptors when there is sympathetic stimulation to i) airways (1), ii) heart (2), iii) arterioles (1)

A

Airways – bronchodilation, relax SM beta2
Heart – increase heart rate + force beta1
Arterioles – vasoconstriction alpha1

34
Q

c) What are the effects of NO on i) smooth muscle in the airways, ii) arteriolar smooth muscle (2)

A

Smooth muscle airways = bronchodilation: increase airflow.

Arterioles = relaxation of arterioles causing vasodilation, inhibit growth of smooth muscle.

35
Q

An ECG strip is shown from aVF.

a) Which limb is the positive end of the lead shown attached to?

A

Left foot

36
Q

b) What is the angle of the positive end of Lead III?

A

120

37
Q

How do factor Va and VIIa accelerate blood coagulation?

A
  • 7a catalyses factor 99a (and then 9a catalyses more factor 10a from 10).
  • 7a catalyses 1010a: more 10a means more prothrombinthrombin.
  • 5a is a COFACTOR for Xa which catalyses prothrombinthrombin.
  • [NB: 8a is a COFACTOR for 9a which catalyses 1010a.]
  • Thrombin therefore catalyses the reaction fibrinogenfibrin (fibrin plug formed).
  • Thrombin generates 13a from F13 (cross bridges in fibrin)
  • Thrombin generates more 5a + 8a.
38
Q

How are factors Va and VIIIa activated?

A

Trace amounts of thrombin activate Xa and XIIIa from their zymogen precursors.

39
Q

How are factors Va and VIIIa inactivated?

A

DIRECT: Antithrombin breaks down cofactors.
INDIRECT: Thrombin binds to thrombomodulin. Complexes with protein C and protein S (cofactor). This complex breaks down factor Va and XIIIa. (Therefore no more thrombin can be generated as Va is cofactor for Xa which catalyses prothrombin thrombin. XIIIa is a cofactor for IXa which catalyses XXa).

40
Q

What are the consequences for impaired activation of Va?

A

Disturbs haemostatic balance.
Va is not broken downstill active.
Va continues to act as cofactor for IXa which catalyses XXa.
Therefore excessive thrombin is formed (catalysed by Xa).
Thrombosis leading to venous thromboembolism. E.g. factor V lieden.
Fibrinogenfibrin. Blood is more likely to clot excessively/without need/without endothelial damage.
Blood clots may lead to thrombosismay embolise causing PE or may lodge in arteries causing an infarction (myocardial, brain).

41
Q

Write down the anatomical positions of the ECG chest electrodes as placed on the body.

A 
V1: Right 4th ics next to sternum
V2: Left 4th ics next to sternum
V3: Left 5th ics between V2 and V4
V4: Left 5th ics at mid clavicular lin
V5: Left 5th ics at anterior-axilliary line
V6: Left 5th ics mid axillary line
42
Q

Name and briefly explain both of the mechanisms that are believed to be responsible for the phenomenon of autoregulation.

A
  1. Myogenic - where the vascular smooth muscle of the arterioles contracts in response to being stretched. The vascular smooth muscle closest to the capillaries are the most sensitive. This mechanism is important for autoregulation in the kidney and skin
  2. Metabolic - where a vasodilator substance is produced in the tissues and cleared by the blood. Higher blood flow lowers the concentration of the vasodilator in the tissue leading to increased resistance. The rate of production of the vasodilator is directly proportional to metabolism. This mechanism is important for autoregulation in the heart and skeletal muscle.
43
Q

Which of these statements about capillaries is true:
• Capillaries often contain smooth muscle
• Metabolically active tissues do not have many capillaries
• The kidneys contain only continuous capillaries
• Fenestrated capillaries are highly impermeable
• Discontinuous capillaries often allow proteins to cross the capillary wall.

A

Discontinuous capillaries often allow proteins to cross the capillary wall.

44
Q 
Which of the following is NOT a mechanism by which capillaries optimise exchange:
•	Thin endothelium
•	Extensive capillary branching
•	High resistance
•	Dense networks in skeletal muscle
•	They have 80nM gaps throughout
A

• They have 80nM gaps throughout

45
Q

Atrial fibrillation:

a. is usually life-threatening
b. the atrial impulses often occur at 500 per minute or faster
c. becomes more common with increasing age
d. nearly always causes symptoms
e. increases the risk of stroke

A

increases the risk of stroke

46
Q

Valvular heart disease
the most important symptoms of aortic stenosis is palpitations (irregular heart beats)
mitral stenosis is often complicated by atrial fibrillation
atrial fibrillation increase the risk of systemic embolism
tricuspid regurgitation cause backpressure in the left atrium
the leaking mitral valve always needs to be replaced since it cannot be repaired

A

atrial fibrillation increase the risk of systemic embolism

47
Q

In the cardiac cycle, the period of isovolumic contraction:

a. starts with the first heart sound
b. produces an increase in pressure in the left ventricle that approaches aortic pressure
c. commences with the end of the QRS complex
d. forces blood into the aorta
e. follows the period of atrial systole

A

a. follows the period of atrial systole

48
Q

Describe the distribution of hypertension.

A

shape of curve of systolic BP of population – uniform distribution

49
Q

Name 2 causes of secondary hypertension:

A
  • Renal artery stenosis
  • Conn’s syndrome: excess production of aldosteroneby theadrenal glandsresulting in lowreninlevels.
  • Oral contraceptive pill
  • Liddle’s syndrome: excess reabsorption ofsodiumand loss ofpotassiumfrom therenal tubule.
  • Pre-eclampsia
50
Q
  1. Name 4 fatal diseases caused by hypertension:
A
  • MI
  • Heart Failure
  • Stroke,
  • Peripheral vascular disease
  • Retinopathy
  • Renal failure
  • Atrial fibrillation
  • Dementia
51
Q

What is the normal PR interval?

A

: 0.12-0.20s

52
Q

What is normal QT?

A

0.38-0.42s

53
Q

What is normal mean frontal plain axis?

A

-30 to 90

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