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FBS2 > PPoP > Flashcards

PPoP Flashcards

1
Q

What are the fractions of blood?

A

Plasma - 50%
Haematocrit - 40-45%
White blood cells & platelets - 1-5%

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2
Q

What are the sites of haematopoesis?

A

In foetus:
spleen, bone marrow, liver, yolk sac, lymph nodes

In adults:
bone marrow and lymph nodes

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3
Q

What are the features of red blood cells?

A

Biconcave
no nucleus, golgi body or mitochondria
120 day life span

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4
Q

What are the precursors of RBCs?

A

Normoblast in bone marrow
nucleus removed and moves to blood = reticulocyte
reticulocyte matures and loses organelles

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5
Q

What are some features of platelets?

A 
produced in bone marrow from megakaryocytes
discoid 
anuclear
8-12 day life span
increase surface area when activated
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6
Q

What are some features of megakaryocytes?

A

giant cells

large irregular nucleus

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7
Q

What are some features of neutrophils

A

most common, make up 60% of leukocytes
polymorphonuclear
rapidly respond to chemotactic substances
first cell type recruited to inflammation sites

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8
Q

What are some features of eosinophils

A 
rare 
pholymorphonucleus
involved in parasite healing 
can live several days
cytotoxic secretory substances
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9
Q

What are some features of monocytes?

A

mononuclear
highly phagocytic and motile
mature into macrophages

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10
Q

What is the process leading to platelet plug formation?

A

Damage to blood vessel -> platelets exposed to collagen, vWF and thrombin -> platelets adhere and activate -> release mediators -> vasoconstriction and aggregation of platelets -> soft platelet plug formation

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11
Q

What are the 3 stages of clotting?

A

initiation, amplification and propagation

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12
Q

What activates initiation of clotting

A

Tissue factor expressed on cells

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13
Q

What activates amplification and propagation of clotting?

A

Thrombin (FIIa) on activated platelets

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14
Q

What cofactors are required for initation clotting?

A

calcium ions and phospholipid

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15
Q

What are the features of a plaque

A

fibrous cap and lipid rich core

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16
Q

What are the features of an arterial plaque?

A

white
platelets are the major component
treated with anti-platelet drugs
caused by MI and stroke

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17
Q

What are the features of a venous plaque?

A

red
fibrin and RBCs are major component
treated with anti-coagulants
caused by trauma and surgery

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18
Q

What are the 3 components of Virchow’s triad?

A

blood flow
endothelial injury
hypercoagulability of blood

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19
Q

What are the 3 types of anti-platelet drugs?

A

Aspirin - COX inhibition -> no TXA2 production
P2Y12 antagonists -> receptor on platelet for aggregation
GPIs -> compete with fibrinogen and vWF

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20
Q

What is the main anticoagulant drug?

A

Heparin

  • inhibits factors in clotting pathway
  • for prevention and rapid treatment
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21
Q

What are the pros and cons of unfractioned heparin

A

Pros:
cheap, effective, short half life

Cons:
variable bioavailability, risk of HIT and haemorrhage

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22
Q

What are the pros and cons of low molecular weight heparin (LMWH)?

A

Pros:

  • increased bioavailability and half life
  • less risk of HIT

Cons:

  • expensive
  • risk of haemorrhage
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23
Q

What is heparin induced thrombocytopenia (HIT)?

A

When heparin binds to PF4 and an antibody is produced

2nd exposure of heparin leads to immune-mediated platelet activation

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24
Q

What is pharmacodynamics?

A

The actions of a drug on the body

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25
Q

What is pharmacokinetics?

A

The actions of an organism on a drug

Includes absorption, distribution, metabolism and excretion

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26
Q

What are the 3 types of names a drug is given?

A

Proprietary (brand), common and chemical names

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27
Q

What is Emax?

A

the maximum effect of a drug (max heigh of log dose-response graph)

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28
Q

What is LogEC50?

A

The concentration of a drug that gives 50% of the maximum response
- value on x axis at 50% of y axis

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29
Q

What is KD?

A

The molar concentration of a drug needed to occupy 50% of receptors at equilibrium
measures affinity of a drug - high KD = low affinity

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30
Q

What do agonists need to be effective?

A

affinity and efficacy

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31
Q

What is the difference between full and partial agonists?

A

full agonists have high efficacy, partial agonists have low efficacy

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32
Q

What are the properties of reversible antagonists?

A

affinity but no efficacy
surmountable (effects can be overcome)
shifts dose-response graph to the right

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33
Q

What is pA2?

A

affinity of an agonist (extent of shift in curve)

-log[antagonist] that requires 2x[agonist] to get the same response

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34
Q

`What is a key properties of irreversible antagonists?

A

The effects are not summountable

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35
Q

What type of kinetics are most drugs?

A

first order kinetics

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36
Q

how do you calculate the half life of drugs?

A

Ln(A0) / K

A0 = initial concentration
K = elimination rate constant
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37
Q

How do you calculate the volume of distribution?

A

Dose A/AO

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38
Q

What limits clearance of drugs?

A

organ blood flow

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39
Q

How do you calculate clearance?

A

Cl = K x Vd
or
Cl = dose/AUC

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40
Q

How do you calculate hepatic clearance?

A

liver blood flow (Q) x extraction ration (Eh)

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41
Q

How do you calculate bioavailability (F) ?

A

For IV = 100%

For oral administraton = AUC (oral)/ AUC (IV)

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42
Q

What is the funny current?

A

mixed Na+ and K+ current in pacemaker cells
causes unstable resting membrane potential
triggers contraction

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43
Q

Which ion channels are involved in pacemaker cell contraction?

A

Ca2+ influx -> K+ loss -> If triggers next contraction

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44
Q

What ion channels are involved in cardiac cell contraction?

A

Fast Na+ influx -> Ca2+ entry through L-type channels -> K+ lost

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45
Q

What are the 7 stages of the cardiac cycle?

A
  1. atrial systole
  2. isovolumetric ventricular systole
  3. ventricular ejection
  4. reduced ventricular contraction
  5. isovolumetric ventricular relaxation
  6. rapid ventricular filling
  7. reduced ventricular filling
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46
Q

What 3 factor regulate cardiac pumping?

A

preload
afterload
autonomic nervous system (SNS increases, PNS decreases)

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47
Q

What is preload?

A

End diastolic pressure

stretch in ventricles prior to contraction

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48
Q

What is afterload?

A

The resistance the heart needs to overcome to eject blood into the systemic circulation

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49
Q

Why does pulmonary circulation have low resistance?

A

the arteries are short and wide

allows low pulmonary artery pressure generated by the RV

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50
Q

What is pulse pressure?

A

systolic-diastolic

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51
Q

How do you calculate mean arterial pressure?

A

MAP = diastolic + (systolic - diastolic)/3

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52
Q

how is change in pressure calculated?

A

CO x TPR

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53
Q

What are some features of the venous system?

A

Low resistance
skeletal muscle pump
respiratory pump

54
Q

What factors can change CVP?

A

blood volume
venous constriction
posture/orthostasis

55
Q

How do you calculate stroke work from a pressure-volume loop?

A

area inside the loop

56
Q

How do you calculate stroke volume from a pressure-volume loop?

A

End-diastolic volume - end-systolic volume

max vol on graph - min volume on graph

57
Q

What are the features of the jugular venous pressure wave?

A

biphasic
low pressure
affected by bulging, stenosis and regurgitation of tricuspid valve

58
Q

What are the components of the jugular venous wave?

A 
a wave = atrial contraction
c wave = carotid pulse 
x descent = atrial relaxation
v wave = atrial filling
y descent = passive atrial emptying
59
Q

What are the features of the peripheral arterial pressure wave?

A

Monophasic

influenced by reflected waves, compliance, resonance, interference and damping

60
Q

How is CVP measured?

A

From the internal jugular vein pulse

  • needs to be at 45 degrees to see pulse and avoid collapse
  • measures height of pulse above the manubriosternal angle
61
Q

Why is the internal rather than external jugular vein used to measure CVP?

A

closer to RA
valveless
visible
external is superficial and prone to kinks

62
Q

How does the shape of the JVP wave change in tricuspid stenosis?

A

A wave is enhanced

V wave is diminished

63
Q

How does the shape of the JVP wave change in tricuspid regurgitation

A

A wave is diminished

V wave is enhanced

64
Q

What are the features of the arterial pressure pulse wave?

A
  • big pulse followed by a reflected wave
  • elastic in arteries maintains pressure
  • shape is affected by aging, hypertnesion, drugs etc
65
Q

What are the primary heart sounds?

A 
s1 = AV valve closure
s2 = semilunar valve closure
66
Q

What are the additional heart sounds?

A 
s3 = av valve opening
s4 = atrial systole
67
Q

What is gallop rhythm and when is it heard?

A

When additional heart sounds are heard

occurs when end-diastolic pressure is raised

68
Q

What are murmurs?

A

Sounds heard due to turbulence of blood

occur in valve stenosis or regurgitation

69
Q

What kind of murmur is heard in mitral stenosis?

A

diastolic

70
Q

what kind of murmur is heard in aortic incompetence?

A

early diastolic murmur

71
Q

what kind of murmur is heard in aortic stenosis?

A

systolic murmur

72
Q

what kind of murmur is heard in mitral incompetence?

A

pan systolic lush

73
Q

When is jugular venous pressure considered pathological?

A

if it is more than 3cm above the manubriosternal angle

74
Q

Why is jugular venous pressure important?

A

indicates right atrium pressure
can indicate cardiac or pulmonary disease
e.g. congestive heart failure or pulmonary embolism

75
Q

What determines preload?

A

central venous pressure (CVP)

  • vasconstriction (e.g. excercise) increases
  • blood loss decreases
76
Q

What factors influence afterload?

A

TPR and aortic stiffness

77
Q

what are the 4 factors that directly influence Cardiac output?

A
  • afterload
  • preload
  • contractility
  • heart rate
78
Q

What is Starling’s law?

A

Stroke volume increases with volume due to stretch

79
Q

Why is cardiac muscle more sensitive to starling’s law than skeletal?

A

It becomes more sensitive to calcium with stretch

- steeper graph

80
Q

What are the consequences of starling’s law?

A
  • stroke volume of LV and RV are matched
  • CVP (and therefore preload) determines CO
  • CO is maintained in increased afterload or decreased contractility
81
Q

What happens to the frank-starling curve in heart failure?

A

becomes lower

  • decreased bp -> less water and salt excretion -> increased blood volume
  • activation of SNS and RAAS increase HR = compensated heart failure
82
Q

What is the effect of afterload on `CO

A

No real effect, as it causes a reduction in stroke volume, but this is overcome by secondary effects:

  • increased blood in heart = increased SV (frank-starling)
  • ANREP effect
  • depression of CO by barroceptor reflex
83
Q

What is the main regulator of contractility?

A

intracellular calcium concentration

84
Q

What is the effect of the ANS on the funny current?

A

SNS increases If to increase heart rate

PNS decreases current

85
Q

What are the features of a cardiac action potential?

A 
long duration
long refractory period
short relative refractory period
RMP is very permeable to K+ 
AP duration changes with HR
86
Q

How are SAN cells adapted for pacemaker activity?

A

lots of membrane and little cytoplasm

87
Q

What are the 2 theories for the unstable RMP in cardiac pacemaker cells?

A
  • membrane clock (funny current)

- calcium clock (cyclic release of Ca2+ from intracellular stores)

88
Q

What allows fast ventricular conduction?

A 
interdigitated junctions
(fast along fibre, slower across fibre as less connexons)
89
Q

What direction is the cardiac dipole in?

A

depolarisation spreads from base (top right) to apex (bottom left) of the heart

90
Q

What are the 2 electrodes in ecg called?

A

Recording and reference

91
Q

What are the 3 standard limb leads?

A

limb lead I - LA-RA
limb lead II - LF-RA
limb lead III - LF-LA

92
Q

Which limb lead gives the standard ECG?

A

limb lead II

93
Q

What do the different stages of the ECG indicate?

A 
p = atrial depolarisation
q = septum depolarisation 
r = depolarisation of ventricles towards apex
s = depolarisation of ventricles towards atria 
t = ventricle repolarisation
94
Q

What happens during the P-Q interval, and name a pathology this affects?

A

atrial conduction & AV delay

AV block

95
Q

What happens during the QRS interval, and name a pathology this affects?

A

ventricular conduction

bundle branch block

96
Q

What happens during the S-T interval, and name a pathology this affects?

A

ventricle depolarisation

myocardial infarction

97
Q

What happens during the Q-T interval, and name a pathology this affects?

A

action potential duration

long QT syndrome

98
Q

What is excitation-contraction coupling?

A
  • in contraction of cardiac cells
  • action potential opens L-type calcium channels in membrane -> rise in Ca2+
  • Ca2+ bind RyR receptors on sarcoplasmic reticulum to induce more calcium release
99
Q

How does relaxation occur in cardiac myocytes?

A

SERCA takes Ca2+ up into SR

Na+/Ca2+ exchanger on membrane removes Ca from cell

100
Q

What do chronotropic agents affect?

A

heart rate

101
Q

what do inotropic agents affect?

A

strength of contraction

102
Q

what do lusitropic agents affect?

A

rate of relaxation

103
Q

what are some chronotropic agents?

A 
Positive = SNS e.g. adrenaline and noradrenaline
Negative = PNS e.g. Ach
104
Q

what is vascular tone?

A

balance between constriction and dilation

105
Q

what are some constricting factors?

A

noradrenaline (main), angiotensin II, adrenaline

106
Q

what is the myogenic response?

A

increased pressure causes vasoconstriction

107
Q

What factors cause dilation?

A

NO and EDH released from endothelial cells

108
Q

How does oxidative stress affect endothelial function of blood vessels?

A

superoxide binds NO, preventing it from mediating dilation

109
Q

What are the 2 main types of vasodilation?

A

No-mediated and hyperpolarisation

110
Q

what is autoregulation of blood vessels?

A

constant maintenance of blood flow to important vascular beds over a wide range of pressures

111
Q

What is the main mediator of autoregulation?

A

myogenic resposne

112
Q

What is the effect of tissue metabolites on vasculature?

A

cause vasodilation

113
Q

what is metabolic hyperaemia?

A

increased metabolism in excercise, get build up of metabolites causing vasodilation
increases blood flow

114
Q

what is reactive hyperaemia

A

cutting off local blood flow e.g. in isometric exercise

metabolites accumulate to cause vasodilation

115
Q

what types of endothelium are in capillaries?

A

continuous
fenestrated (kidneys, joints, intestinal mucosa)
sinusoidal (liver, bone marrow, spleen)

116
Q

What are the pressure gradients driving fluid movement in capillaries?

A

hydrostatic pressure and osmotic pressure

117
Q

What are the units between valves in lymphatics called?

A

lymphangion

118
Q

what is the baroreceptor reflex

A

rapidly limits changes to blood pressure

119
Q

where are the baroreceptors?

A

carotid sinus and aortic arch

120
Q

what regulates long term control of blood pressure?

A

blood volume

- mainly determine salt intake

121
Q

what is pressure natriuresis?

A

when high blood pressure increases perfusion to kidneys, so there is increased Na+ excretion

122
Q

What stimulates the RAAS system?

A

decreased blood volume, Na+ conc or blood pressure

123
Q

What is the neurogenic model of BP control?

A

that the SNS can contribute to long term control of BP as well as the kidneys

124
Q

Permeability of which ion determines the resting membrane potential in the heart?

A

potassium

125
Q

does a positive charge moving into a cell generate an inward or outward current?

A

inward

126
Q

does a negative charge moving into a cell generate an inward or outward current?

A

outward

127
Q

why is the ventricular action potential long?

A

to prevent tetany and arrhythmias

128
Q

What formula is used to calucate a corrected QT interval and normalise the AP duration?

A

Bazett or Fredericia’s formula

129
Q

What is the bradycardic agent that blocks the funny current?

A

Ivabradine

130
Q

What are the common forms of connexons in the heart?

A

connexin 43
connexin 45
connexin 40

131
Q

What does anisotropic mean?

A

a substance that has different properties when measured in different directions
- e.g. in heart fibre orientation

132
Q

list the major E-C coupling proteins phosphorylated by PKA?

A 
L-type Ca channels
RyRs 
PLB
PLB 
Myofilament proteins (troponin I and myosin binding protein C).

FBS2 (3 decks)

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