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MD1 > Cardiology Week 1-2 > Flashcards

Cardiology Week 1-2 Flashcards

1
Q

Does symp or parasym have greater influence on HR at rest

A

Parasymp

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2
Q

What happens to HR if block symp and parasymp

A

heart keeps beating - because intrinsic pacemaker cells

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3
Q

describe phases of SA node pacemaker cell AP

A

phases:
4 - unstable membrane potential -60mV, spontaneous depolarisation - Ifunny (mostly Na, Ca)

0 - depolarisation Ca in

3 - repolarisation K out

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4
Q

Phases of ventricle AP

A 
phases:
4 - stable membrane -90mV
0 - rapid depolarisaiton Na in Ca in (some)
1 - rapid repolarisation Kout
2 - plateau Ca in 
3 - repolarisation K out
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5
Q

how does parasym lower HR

A

M2 receptors coupled to Gi to cause decrease in cAMP and opening of K+ channels –> K efflux causes hyperpolarisation, slowed Na and Ca fluxes, longer to reach threshold

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6
Q

How does symp increase HR

A

NA and A through B1 coupled to Gs to increase cAMP cause opening of Ca channels –> causes increased slope of phase 4, increase SA firing rate, and more rapid conduction (AV node)

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7
Q

intrinsic factors leading to dysrhythmias

A

changes to cardiac tissue structure and function - ischaemia, infarction, fibrosis, cardiomyopathy

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8
Q

extrinsic factors leading to dysrhythmias

A

hypo/hyperthermia, neural syndromes, jaundice, raised intracranial pressure, stress, smoking, caffeine, drugs

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9
Q

3 mechanisms underlying dysrhythmias

A

altered impulse formation
altered impulse conduction
triggered activity (early or late after-depolarisations)

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10
Q

early afterdepolarisation

A

excitation during plateau or rapid repolarisaiton phase - aberrant Ca or Na channel opening

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11
Q

delayed afterdepolarisation

A

excitation on completion of repolarisation - Ca overload activation of 3Na/Ca exchange

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12
Q

4 major classes of antidysrhythmias

A
  1. Na channel blockers - 1a moderate 1b weak 1c strong
  2. Badrenoceptor antagonism
  3. K channel blockade
  4. Ca channel blockade
    (SOME BLOCK POTASSIUM CHANNELS)
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13
Q

action of Na channel blockers

A

RHYTHM

reduce phase 0 slope and peak of ventricular AP

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14
Q

action of Badrenoceptor antagonists

A

RATE

decrease rate and conduction, membrane stabilising effects on purkinje fibres

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15
Q

action of K channel blockade

A

RHYTHM

delay phase 3 of ventricular AP, prolong ADP

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16
Q

action of Ca channel blockade

A

RATE

most effective at SA and AV nodes - reduce rate and conduction

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17
Q

lignocaine

A

class 1b Na channel blocker - mild Na block, shorten repolarisation, decrease ERP

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18
Q

lignocaine taken at home?

A

no - only hospital - concentration dependent side effects

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19
Q

adverse effects of Badrenoceptor antagonists

A

bradycardia, reduced exercise capacity, hypotension, AV conduction block, bronchoconstriction, ANXIETY

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20
Q

amiodarone

A

K channel inhibitor, also Na and Ca and Badrenoceptor blocker

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21
Q

Verapamil

A

cardioselective Ca channel blocker- acts preferentially on SA and AV nodal tissue

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22
Q

drug types effecting rhythm

A

Na and K channel blockers

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23
Q

drugs types effecting rate

A

Ca channel blockers, Badrenoceptor antagonists

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24
Q

what is considered HIGH BP

A

> 140/90

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25
Q

risk factors for hypertension

A

smoking, diet, weight, stress

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26
Q

antihypertensive drugs ABCD

A

a - angiotensin system inhibitors
b - Badrenoceptor antagonists
c - calcium channel blockers
d - diuretics

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27
Q

renin-angiotensin system

A

antiotensiogen converted to angiotensin I by Renin

angiotensin I to II by angiotensin converting enzyme

converted then to aldosterone

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28
Q

actions of angiotensin II

A

cell growth, vasoconstriction

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29
Q

how symp effects renin system

A

NA acts on B1adrenoceptors on kidney - promote renin release

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30
Q

ACE inhibtors actions

A

reduce vascular tone
reduce aldosterone production
reduce cardiac hypertrophy

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31
Q

Prils

A

ACE inhibitors

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32
Q

Problem with ACE inhibitors

A

ACE = kinninase II - stops bradykinin breakdown - dry cough etc.

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33
Q

“sartans”

A

angiotensin R antagonists

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34
Q

clinically useful to block which AT receptor

A

AT1

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35
Q

actions of angiotensin R antagonists

A

same as ACE inhibitors except at receptor level

not as bad side effects

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36
Q

“olols”

A

Badrenoceptor antagonists

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37
Q

actions of Badrenoceptor antagonists

A

reduce CO (rate, contractility), reduce renin release (blood volume, TPR)

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38
Q

side effects of Badrenoceptor antagonists

A

symp blockade - cold extremities etc.
fatigue, dreams, insomnia
bronchoconstriction

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39
Q

Calcium channel blockers action

A

block L-type Ca channels in myocardium and vasculature

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40
Q

dihydropyridines

A

Calcium channel blocker - vascular selective

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41
Q

calcium channel blocker adverse effects

A

verapamil - oedema, headache, bradycardia,

dihydropyridines - oedema, headache, reflex tachycardia

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42
Q

Hydrochlorothiazide

A

diuretic - reduce blood volume for hypertension

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43
Q

why do we need oxygen carrier in blood

A
  1. cant carry enough to meet demands
  2. oxygen diffuses slowly
  3. oxygen v reactive - oxidation
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44
Q

heme structure

A

Fe(II) - 6 coordinating bond positions:
4 bonds to N
5th to histidine F8
6th bond to O in oxygenated Hb

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45
Q

colour of haem group for - Hb02, Hbde02, HbCO

A

Hb02 - scarlet
Hbde02 - dark
HbCO - cherry (CO binds 200x more strongly to Hb)

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46
Q

myoglobin or haemoglobin monomeric or tetrameric

A

myoglobin - monomeric

haemoglobin - tetrameric

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47
Q

what allows o2 access to heme in buried hydrphobic pocket in myoglobin

A

transient “breathing” of alpha helices

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48
Q

myoglobin - does O2 affinity change with O concentration

A

NO - myoglobin is saturated at low pressures of O2

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49
Q

structure of haemogloibn

A

2 alpha and 2 beta chains

alpha and beta subunits associate more strongly with each other than with the same subunits

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50
Q

T and R state haemoglobin

A

T - deoxy

R - oxy

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51
Q

curves of myoglobin vs haemoglobin binding

A

myoglobin - hyperbolic

haemoglobin - sigmoidal

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52
Q

23-BPG acts as a

A

heterotropic allosteric modulator (external ligand that modulates function)

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53
Q

what does 23-BPG do

A

binds to cavity of positve amino acids, decrease Hb affinity for O keeps haem in deoxy state to help Hb release O in tissues
(forced to unbind at high O2)

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54
Q

how CO2 transported in blood

A

1 - carried by Hb on amino terminal groups of deoxy-Hb as carbamate

2 - CO2 converted to HCO3- by carbonic anhydrase - soluble in plasma

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55
Q

Bohr effect

A

binding of H+ to Hb lowers affinity for O2

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56
Q

in absence of effectors (H, 23-BPG) what happens to curve

A

approaches Mb-like properties

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57
Q

foetal Hb

A

Hb-F - binds O with higher affinity than mothers HbA - gives foetus access to O carried by mothers HbA

also less able to bind 23-BPG - so not locked into deoxy state

gamma subunits instead of Beta

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58
Q

HbS

A

sickle cell anaemia Hb - abnormal beta chain

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59
Q

HbC

A

mutation in beta gene

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60
Q

HbE

A

mutation in beta gene

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61
Q

HbS mutation

A

HbS has val instead of Glu in beta globulin

Val is hydrophobic, Hb shouldnt have hydrophobic residues on surface because they sticky - subunits stick to each other

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62
Q

pancytopenia

A

not enough blood cells

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63
Q

leukopenia
neutropenia
lymphopenia

A

not enough white BCs

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64
Q

thrombocytopenia

A

not enough platelets

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65
Q

polycythaemia

A

too many red cells

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66
Q

leukocytosis

A

too many white BCs

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67
Q

thrombocytosis

A

too many platelets

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68
Q

dyserythropoiesis

A

RBCs not working properly

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69
Q

anaemia defined as

A

a Hb level below that which is normal for age and gender

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70
Q

tissue oxygen delivery equation

IMPORTANT

A

tissue oxygen delivery = CO x Hb x %Satn x 1.34

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71
Q

%Satn

A

oxygen saturation

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72
Q

ability of body to compensate due to anaemia

A

anaemia from chronic blood loss (slow) - over months compensate by increasing SV

acute - cant increase SV immediately

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73
Q

clinical signs of anaemia

A

pale, lethargic, failure to thrive, hypoxic (confused), ischaemia, tachycardia

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74
Q

sign used to monitor if anaemia getting better

A

tachycardia/ HR - because consistent sign for anaemia

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75
Q

causes of anaemia

A

failure of production
increased destruction/loss
inappropriate production

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76
Q

Hct

A

fraction of cells vs plasma (haematocrit)

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77
Q

MCV

A

mean cell volume

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78
Q

MCH

A

mean cell haemoglobin

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79
Q

blood film

A

morphology of red cells, white cells and plts

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80
Q

words denoting size of RBCs

A

normocytic, microcytic, macrocytic

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81
Q

words denoting colour of RBC

A

normochromic
hypochromic
polychromasia (blue - probably still have some RNA in them - fresh out of bone marrow - means marrow working overtime to get cells out)

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82
Q

classifications of anaemia

A
  1. regenerative (bone marrow working) vs aregenerative (not working)
  2. RBC size
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83
Q

signs of increased RBC production

A

reticulocytes, polychromasia

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84
Q

signs of increased destruction

A

jaundice (increased serum bilirubin - byproduct of RBC breakdown), haptoglobins, LHD (storage proteins in blood - if hap low and LHD high - evidence of RBC destruction

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85
Q

is increased destruction of RBC more dangerous than failure of production

A

YES - capacity for rapid reduction in Hb

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86
Q

how much blood is good, when replaced

A

RBCs - 3-5x10^12/L, replaced 120 days
WBCs - 2-6 x10^9/L (less than RBCs), replaced every 3-5 days
Platelets - 150-400 x10^9/L, replaced every 10 days

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87
Q

site of haemopoiesis

A

yolk sac - first few weeks
liver and spleen - 6weeks-7months
bone marrow - 7months - life

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88
Q

50% of marrow consists of

A

fat spaces (even in active haemopoietic areas)

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89
Q

haemopoiesis

A

pluripotent stem cell differentiates into all haemopoietic cell lines (also lymphocytes and osteoclasts)
capable of self renewal

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90
Q

bone marrow stroma

A

microenironment for bone marrow to grow

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91
Q

bone marrow communication with blood

A

bone marrow in constant communication with blood - circulates through v quickly

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92
Q

why progenitors dont leave bone marrow until mature

A

progenitor cells held with adhesion molecules onto stroma, changes in expression of adhesion molecules driven by GFs determines when cells leave marrow

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93
Q

bone marrow aspirate

A

needle into bone marrow, suck out, put on slide - no achitecture of marrow

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94
Q

do you see precursors in peripheral blood?

A

NOT USUALLY
if you do, not good for one of two reasons:
1. overwhelming infection - bone marrow throws out WBCs even when not ready cos need lots of them
2. leukaemia - no room for normal cells in marrow

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95
Q

bone marrow transplant

A

iv - cells know where to go - attach straight to stroma

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96
Q

haemopoietic growth factors

A

glycoprotein hormones, local and circulating action

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97
Q

do haemopoietic GFs act across multiple cell linages?

A

some do, some only on specific linages

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98
Q

redundancy in H GFs?

A

YES LOTS - lots of overlap

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99
Q

granulocyte colony stimulating factor

A

reduce amount of time cancer patients are neutropanic - reduce life threatening infections, enables more aggressive chemotherapy

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100
Q

do Haemopoietic GFs cause same thing in all cells?

A

NO
cause different things depending on what cell (i.e. what R they activate)
if early cell - stimulates proliferation
if late cell - activation

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101
Q

haematinics

A

nutrients required for formation and development of blood cells
iron
vitamin B12
folate

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102
Q

iron deficiency as a toddler

A

may or may not become anaemic but will lose IQ points

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103
Q

vitamin B12 sources, important for what

A

animal products only, important for all blood cell production

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104
Q

folate sources, important for what

A

green leafy vegies, important for all blood cell production and all cells

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105
Q

haemostasis

A

coagulation

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106
Q

fibrinolytic process

A

fibrinolysis - dissolving clot to get back to laminar flow

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107
Q

primary secondary haemostasis

A

primary - vasoconstrictin, platelet adhesion and aggregation

secondary - activation of coagulation factors, formation of fibrin

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108
Q

virchow’s triad

A

vessel wall, blood composition, blood flow

all lead to thrombosis if small abnormality in any one of these

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109
Q

role of vessel wall in clotting

A

can be antithrombotic or prothrombotic depending on expression of surface molecules and secretion of proteins

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110
Q

coagulation system

A

tissue factor - starter motor
complex system of positive and negative feedback
key enzyme=thrombin
all proteins in system work in other regulatory systems as well
individual interactions between protiens happen on cell surfaces

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111
Q

3 phases of coagulation

A

initiation - kick start
activation - produce lots of thrombin
propagation - clot inreases in size, plugging with fibrin

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112
Q

action of thrombin

A

converts fibrinogen to fibrin

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113
Q

inactivation of thrombin

A

at least 3-4 mechanisms

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114
Q

thrombin actions outside of coagulation pathway

A

activation of PAR’s (protease-activated receptors)

embryonic growth, tumour spread, vascular disease

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115
Q

coagulation system tests for risk of bleeding, risk of clotting, monitor anticoagulant drugs - types of tests

A

risk of bleeding - global tests, specific assays, genotype for specific disorders

risk of clotting - NO global tests, yes to other two

monitor anticoag- all three

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116
Q

important principles of coagulation tests

A

sample integrity - CRUCIAL

multiple consistent tests before diagnosis

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117
Q

global tests for bleeding

A

ACT (activated clotting time)
APTT (Activated Partial Thromboplastin time)
thrombin generation

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118
Q

specific assays for bleeding

A

factor assays
collagen binding assays
fibrinogen

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119
Q

chromogenic assays

A

type of specific assay
have chromogenic substrate taht protein can cleave to cause light emission
tells you how much function that protein has
(but problem - sometimes can cleave chromogenic substrate but not physiological one)

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120
Q

global functional assay

A

PT (prothrombin time)
PT ratio
INR =(patient PT/mean normal PT)^ISI

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121
Q

ISI

A

international sensitivity index - reflects sensitivity of reagent to reduction in Vit K dependent factors

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122
Q

APTT

can you cross compare between labs?

A

activated partial thromboplastin time
cant cross compare between labs

tells us: factor deficiency, lupus anticoagulant (an Ab), heparin monitoring

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123
Q

epithelium of epicardium

A

simple squamous epithelium

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124
Q

myocardiocytes

A

cardiac muscle cells

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125
Q

intercalated discs consist of what

vertical and horizontal parts

A

consist of adhernes junctions, desmosomes and gap junctions
vertical - adherens junctions
horizontal - gap junctions

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126
Q

why cardiac cells have gap junctions

A

electrically couple cells and coordinate APs

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127
Q

purkinje fibres - contractile?, intercalated discs?, glycogen?, bundles?

A

modified cardiac muscle cells - larger, irregular, limited contractile machinery, NO intercalated discs, FULL of glycogen, form bundles in subendocardium, terminate on cardiac msucle fibres

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128
Q

3 layers of blood vessel

A

tunica intima, tunica media, tunica adventitia/externa

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129
Q

structure of tunica intima

A

simple squamous epithelium (often aligned in direction of blood flow), with basal lamina
supported by thin subendothelial connective tissue layer
elastic lamina - part of connective tissue, boundary between intima and media

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130
Q

3 roles of endothelium

A

barrier
blood clotting
release vasoactive substances - endothelin (constrictor), NO (dilator)

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131
Q

tunica media function, what do they secrete

A

luminal diameter

smooth muscle cells secrete the connective tissue in which embedded (collage type III, elastin, ground substance)

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132
Q

tunica adventita structure, blood supply

A

connective tissue comprises: collagen type I, elastin, ground substance, embedded fibroblasts
anchors vessel to tissue
has its own blood supply - vasa vasorum IN LARGER VESSELS

133
Q

two types of arteries

A
  1. elastic - close to heart - dampen large fluctuations in BP while maintaining BP, elastin, pulsatile
  2. muscular - further from heart, distributing arteries, little elastin - concentrated in internal elastic laminae
134
Q

vessle that has greatest contribution to BP

resistance equation

A

arterioles - theres heaps of them (massive length), resistance proportional to inverse of radius ^4

so if small radius, more able to control resistance

135
Q

metaarteriole

A

intermediate between arterioles and capillaries incomplete smooth muscle coat

136
Q

3 structure types of capillaries

A

fenestrated
sinusoidal - large spaces that can accomodate more than one RBC - particularly in areas where need to exchange cells
continous

137
Q

structure of capillary endothelial cell

A

single endothelial cell rolled into tube, tight junction, basal lamina, v little cytoplasm, sometimes pericyte (modified smooth muscle cell), surrounded by only few collagen fibres (adventitia)

138
Q

where fenestrated capillaries found

A

pancreas, intestines, endocrine glands

139
Q

fenestrated capillaries structure

A

continuous basal lamina, pores spanned by diaphragm (contain 8 wedge shaped channels and radially oriented fibrils)
sometimes diaphragm missing- kidneys

140
Q

sinusoidal capillaries where are they found

A

liver, lymphoid tissue, endocrine organs, bone marrow, spleen

141
Q

Structure of sinusoidal capillaries

A

discontinous basal lamina, larger pores, +-diaphragm , endothelial cells may lack tight junctions

142
Q

layers of veins

A

same as arteries BUT thinner media, thicker adventita

143
Q

preferred site of diapedesis of leukocytes

A

venules

144
Q

characteristics of medium to large veins

A

subendothelial connective tissue well developed

adventitia enlarged, often at expense of media

145
Q

embolism

A

when a thrombus travels somewhere it shouldnt

146
Q

muscular arteries elastin

A

internal and external elastic lamina

147
Q

arteriosclerosis

A

hardening of arteries/thickening of intima (healing but with fibrosis)

148
Q

hyaline arteriolosclerosis

A

smooth muscle cells produec too much matrix, proteins from blood leak across damaged endothelium into arteriole wall

149
Q

3 sequelae of arteriolosclerosis

A

1 - cerebral haemorrhage
2 - benign nephrosclerosis - ischaemia from narrowed arterioles
3 - hypertensive retinopathy

150
Q

consequences of arteriosclerosis

A

arteries lose elasticity, become narrowed
impairs artery’s role in BP
impair blood supply to downstream tissues

151
Q

atherosclerosis

A

build-up of inflammatory, fibrotic, necrotic and fatty material in intima of arteries
fibrosis outside, necrotic tissue inside

152
Q

fibroinflammatory lipid plaque (atheroma)

A

fibrous cap, necrotic lipid core

153
Q

formation of atherosclerosis

A
  1. fatty streaks
  2. stable atherosclerotic plaque
  3. unstable atherosclerotic plaque
154
Q

fatty streaks

A

collections of foam cells in intima - macrophages (and smooth muscle cells) that have phagocytosed lipid

155
Q

unstable (vulnerable plaques)

A

prone to rupture leading to ‘acute plaque events’

thinner fibrous cap, more necrotic core, more inflammatory cells, less stenosed lumen (than stable)

156
Q

main complication of atherosclerosis

A

acute plaque events

157
Q

acute plaque events - whats wrong

what leads to

A

something wrong in plaque- rupture, haemorrhage into plaque, erosion of endothelium

leads to thrombosis, thromboembolism, atheroembolism,

158
Q

aneurysm

A

stretching of artery due to weakness in media- weak so easily ruptures

159
Q

claudication

A

crushing central leg pain

result of chronic ischaemia

160
Q

how are risk factors for atherosclerosis linked to endothelim

A

hypertension - low-grade shear effect
smoking - toxic and pro-inflammatory
high blood sugar and lipids - damage endothelium

161
Q

LDL

A

bad cholesterol, taken up into intima, oxidised - becomes pro-inflammatory
taken up by macrophages and smooth muscle cells - they become foam cells

162
Q

how activated endothelium act differently

A
  1. adhesion molecule expression
  2. produces cytokines and GFs
  3. change from anti-coagulant to pro-coagulant
  4. becomes leaky - macrophage entry into intima
163
Q

HDL

A

circulating HDL absorbs lipids from plaques

164
Q

role of inflammation in atherosclerosis

A

perpetuates endothelial dysfunction, attracts more infalmmatory cells - vicious cycle

165
Q

role fo smooth muscle cells in atherosclerosis

A

GOOD
migrate into intima, change phenotype, proliferate adn produce ECM - collagen
gives thicker fibrous cap - more stable atheroma

166
Q

10 morphological features of atherosclerosis

A

narrowed lumen, thickened intima, thinned media, fibrous cap, necrotic core, foam cells, cholesterole clefts, inflammatory cells (monocelular), clacification, neovascularisation

167
Q

two ways pathological calcification arises

A
  1. dystrophic calcification - appears in areas of cell degeneration
  2. metastatic calcification - serum calcium adn phosphate levels too high - fall out of solution
168
Q

AAA (abdominal aortic aneurysm) – associated with what, often contain what

A

associated with atherosclerosis, often contain thrombus

169
Q

berry aneurysm, where, weakening of what, major cause of

A

in cerebral circulation, weakening of a congenital defect, major cause of subarachnoid haemorrhage

170
Q

cardiac tamponade

A

compression of heart by fluid (or blood) accumulation in pericardium

171
Q

exsanguination

A

blood loss to a degree that causes death

can be caused by ruptured aneurysm into thorax

172
Q

causes of ventricular hypertrophy

A

hypertension, aortic stenosis, genetic

173
Q

childhood growth of ventricles

A

ventricles start out v similar - right ventricle pumping into lower pressure system so doesnt hypertrophy as much

174
Q

normal heart size depends on

A

body size, genetics, athletic, BP, angiotensin II and catecholamiens

175
Q

mean left ventricular mass

A

160g

176
Q

relative wall thickness =

A

LV wall thickness/LV chamber size

177
Q

cardiac remodeling

A

changes in size, shape and function of heart after cardiac injury - more general -includes hypertrophy among other things

178
Q

causes of cardiac remodeling

A

MI, cardiac damage (e.g. myocarditis), volume or pressure overload

179
Q

concentric hypertrophy

A

increase LV mass

increase relative wall thickness

180
Q

eccentric hypertrophy

A

increase LV mass

normal relative wall thickness

181
Q

remodeling

A

normal LV mass

increase relative wall thickenss

182
Q

concentric hypertrophy often due to, more sarcomeres in …

A 
pressure overload (high afterload) - hypertension, aortic stenosis 
more sarcomeres in parallel
183
Q

eccentric hypertrophy often due to

more sarcomeres in…

A 
volume overload (high preload) - mitral and aortic regurgitaiton, ventricular septal defect 
myocyte stretching - more sarcomeres in series
184
Q

hypertrophy increased myocardial cell size or number??

A

SIZE

also increased fibroendothelil cell numbers, interstitial matrix

185
Q

eccentric hypertorphy maintains SV by

A

increasing LVEDV and EF (ejection fraction)

186
Q

long term decompensations of hypertrophy

A

LV dilation, increased LDEDV, LVESV and decreased EF
reduced systolic functiona nd CO
increased LVEDP

187
Q

identification of LVH

A

clinical - forceful apex beat, S4, S3
ECG - tall voltages, T wave inversion
CXR - large hart in ecentric, may be normal size in concentric

188
Q

diastolic dysfunction

A 
thick muscle is stiff
increased LVEDP
increased LA adn pulmonary vein pressure 
pulmonary congestion
atrial kick more important
189
Q

LV remodeling
causes
what happens

A

following MI

increase LV volume and spherical shape, myocyte hypertrophy and apoptosis\, interstital fibrosis

190
Q

LV remodeling reduced by

A

angiotensin blocking, Badrenoceptor blocking

191
Q

causes of RV hypertrophy

A

congenital (transposition of great arteries), pulmonary hypertension, right heart valves regurgitation or stenosis

192
Q

hypertrophic cardiomyopathy

A

autosomal dominant, mutations in genes for sarcomere proteins
increased LV wall thickness (esp septum), cellular hypertrophy, myocyte disarray

most common cause of cardiac death in young people

193
Q

phenotype of hypertrophic cardiomyopathy

A

heterogeneous phenotype - same mutation may cause differnet phenotypes

194
Q

dilated cardiomyopathy

A

proteins taht hod muscle cells together weaken - most common cardiomyopathy

195
Q

athlete’s heart

A

eccentric hypertrophy, cardiac function normal

196
Q

how can you measure RVEDP

A

JVP

197
Q

how can you measure LVEDP

A

catheter inserted via artery across aortic valve - measure left atrial pressure because at end of diastole atrial pressure =ventricular pressure =pulmonary artery wedge pressure (pumonary venous pressure)

198
Q

capillary pressure more like venous pressure or arteriole pressure

A

venous pressure

199
Q

starling forces

A

forces across capillaries

200
Q

what causes oedema

A

increase in venous pressure - heart failure
decreased osmotic pressure - plasma protein loss (renal or liver failure)
blocked lymphatics - cancer

201
Q

two uses of EDP

A

1 measure of filling of ventricles

2 measure of venous pressure driving fluid out of capillaries

202
Q

LVEDP =

A

=preload:LV function

= LAP=PVP: lung capillaries

203
Q

RVEDP =

A

=preload: RV function

= RAP = JVP: peripheral capillaries

204
Q

how does body compensate for heart failure and decreased CO

problem?

A

fluid retention

problem - oedema in legs and lungs

205
Q

clinical features of left and right heart failure

A

left - shortness of breath, fatigue, tachycardia, lung reps

right - oedema

206
Q

cardiac failure inappropriate adaptations

A

Na and water retaition
K loss
vasoconstriction
these three by renin system

also symp activation

207
Q

mechanisms and consequences of fluid retention

A

decreased CO - decreased renal blood flow - activation of renin system - fluid and NA retention, K loss (arrythmias) vasoconstriction

208
Q

mechanisms and consequences of symp NS activation

A

increased NA - initial increased contractility - long term deleterious effect (vasoconstriction, ventricular arrhythmias, direct toxic effect)

209
Q

3 right heart failure mechanisms

A

global heart disease - cardiomyopathy
2 specific right heart disease
3 - left heart failure

210
Q

cardiac failure treatment

A

diuretics, aldsterone antagonists, ACE inhibitors, AT R antagonists
digoxin (mild positive ionotropic effect), beta blockers

211
Q

escape rhythm

A

rhythm not caused by SA node

212
Q

leads of ECG

A

lead 1 - right arm to left arm
lead 2 - right arm to left leg
lead 3 - left arm to left leg

213
Q

current moving away from lead

A

negative deflection on ECG

214
Q

current moving towards lead

A

positive deflection on ECG

215
Q

current moving perpendicular to lead

A

zero on ECG

216
Q

P wave - maximal in leads

A

II and V1

217
Q

ectopic beat

A

extra beat coming from ventricle

218
Q

result of beat coming from ectopic pacemaker cell on ECG

A

wider QRS - because signal goes from cell to cell rather than through conduction system - takes longer

219
Q

sinus bradycardia: junctional escape

A

no P wave - SA node stopped firing

get junctional escape beat - AV takes over for a beat

220
Q

retrograde P wave

A

if get beat coming from AV - can go backwards up into atria

atria contrac same time as ventricle

221
Q

sinus pause and junctional escape

A

SA node stops - no P wave

then get junctional escape rhythm (may take several seconds)

222
Q

escape beats vs ectopic beats

A

escape - late, after sinus bradycardia or pause, pacemaker cell at normal rate (slower than SA)

ectopic - early, after a normal beat, pacemaker cell firing early (faster than SA)

223
Q

1st degree AV block

A

prolonged P-R

224
Q

2nd degree AV block

A

some beats not conducted

wenckebach block/mobitz 1 block -progressively prolonged PR until dropped beat - block at level of AV node

Mobitz 2 block - constant PR interval with dropped beat - block at level of HIs bundle

225
Q

3rd degree AV block

A

no beats conducted
junctional escape rhythm
complete disconnection between atria and ventricle

226
Q

atrial fibrillation characteristics

A

fast rate, irregular rhythm, no P waves, impulse conducted irregularly through av node due to chaos in atrium - av node hit with irregular rhythm
fast rate decreases LV filing time so increased LA pressure - pulmonary congestion

227
Q

2 mechanisms of tachycardias

A

1 automatic focus

2 reentry

228
Q

reentry tachycardia

A

transient conduction block in one limb of circuit

if timing right tissue no longer in refractory so impulse can reenter circuit

229
Q

3 re-entry tachycardias

A

1 - atrial flutter - re-entry circuit in right atrium
2 - AV nodal re-entry tachycardia
3 - ventricular tachycarida - reentry circuit in ventricle around scar

230
Q

where does atrial fibrillation originate

A

left atrium at entry of pulmonary veins

231
Q

what structure determines the ventricular pulse rate in atrial fibrillation

A

av node

232
Q

management of AF

A

1 slow ventricular rate - digoxin, B blocker, Ca Blocker

2 revert to sinus rhythm - antiarrhythmics, DC shock

233
Q

autotransfusion

A

transfusion of blood from venous side to arterial side

234
Q

arterial or venous pressure more sensitive to changes in volume

A

arterial pressure

235
Q

mean circulatory filling pressure

A

pressure when heart stops - depends on volume of blood and compliance of vessles
=7mmHg

236
Q

venous function curve

A

describes what happens to venous pressure as Co increases

237
Q

what happens to venous function curve with Increased blood volume
decreased TPR

A

curve moves up - increased blood volume

curve moves up but maintains x axis - decreased TPR

238
Q

central venous pressure

assessed by what

A

pressure in SVC/IVC just outside of heart

JVP

239
Q

cardiac function curve

A

describes what happens to CO as venous pressure increases

240
Q

what substances does endothelium produce

A

NO - vasodilation
endothelin - vasoconstriction (potent - irreversible binder)
PGs (both depending on PG)

241
Q

WBCs release

A

NO
histamine
cytokines

242
Q

platelets release

A

thrombin - clotting and vasoconstriciton
ADP-clotting and vasoconstriction
thromboxane A2

243
Q

for any given volume of blood, pressure depends on

A 
compliance
active tension (of the wall)
244
Q

ESV

A

75mL

245
Q

LV pressure volume curve in diastole and systole

A

see curves

246
Q

frank-starling relationship

A

more stretch = more tension

more EDV = more SV

247
Q

contractility increases due to

A

acidosis, symp, caffeine, adrenaline, hypercapnia (high Co2)

248
Q

ABCD points of LV volume pressure circuit

A

B - EDV

D - ESV

249
Q

what happens to graph when :
increase contractility
decrease compliance
increase aortic pressure

A

up and back
loop right border to the left
up and forwards

250
Q

afterload

A

load encountered by ventricle as commences contraction

251
Q

preload

A

stretch on monocyte fibres before they commence contraction

252
Q

why do local mediators act locally

A

labile OR rapidly metabolised OR diluted beyond biologically active range close to site of release

253
Q

local mediators mostly what response

A

inflammatory response

254
Q

stimuli inducing histamine relase

A 
antigen via IgE
complement C3a/C5a
neuropeptides
cytokines and chemokines
bacterial components
physical trauma
255
Q

Histamine receptors and where located

A

H1 2
H3 - CNS
H4 - immunomodulation

256
Q

histamine triple response

A

reddening
wheal (increase vascular permeability causing swelling)
flare (spreading response through sensory nerve fibres

257
Q

3 types of H1R antagonists

A

1 sedative - chlorpheniramine, promethazine
2 non-sedative - terfenadine, astemizole
3 - new non-sedative - cetrizine, loratidine

258
Q

H2R antagonist uses

A

peptic ulcer treatment - decreases stomach acid production (but not used anymore)

259
Q

gastric acid secretion

A

ach acts on enterochromaffin-like cell to release Histamine
acts on H2R on parietal cell
causes increase in cAMP
activates H+/K+ exchanger

260
Q

bradykinin production

A

prekallikrein (inactive plasma protien) converted to kallikrein by Factor XII
kallikrein converts HMW kinninogen into bradykinin

261
Q

actions of bradykinin

A 
vasodilation 
increase permeability
stimulates seonsory nerve endings - pain
contract uterus, airways, gut
epithelial secretions in airways and gut
262
Q

breakdown of bradykinin

A

kinninase I and II (kinninase II=ACE)

263
Q

hereditary angioedema

A

C1 esterase inhibitor deficiency

kallikreins are C1 esterases. if C1 esterase inhibitors deficient, get overactivity of these proteases
- defects in coagulation
angioedema (plasma exudation from deeper blood vessels)

264
Q

icatibant

A

B2 R antagonist for hereditary angioedema

265
Q

why ach sometimes vasoconstrictor and sometimes vasodilator in vitro

A

endothelium removed - helical strip - vasoconstriction with ach
endothelium intact - transverse ring - vasodiation with ach - ach acts on endothelium to release NO
(if increase ach concentration eventually get constriction as acting on smooth muscle)

266
Q

endothelium derived vasoactive factors

A

prostacyclin (PGI2)
NO = endothelium-derived relaxing factor (EDRF)

(endothelin - constriction)

267
Q

how does ach cause NO release

A 
ach acts on MRs on endothelial cells
causes increase in intracellular calcium
activates NO synthase
converts arginine to NO
NO converts GTP to cGMP - relaxation
268
Q

basal release of what regulates vascular tone

A

NO

269
Q

NO synthase isoforms and where located

A

nNOS - nerves, epithelial cells
iNOS - inducible - macrophages, smooht muscle
eNOS - endothelial

270
Q

NOS inhibitors

A

L-arginine analogues - cause vasoconstriction

271
Q

NO physiological roles

A

flow dependent vasodilation
inhibits platelet adhesion and aggregation
NT

272
Q

20:4

A

arachidonic acid, an omega 6 fatty acid

273
Q

dietary sources of PUFAs

A

indirectly as linoleic acid(converted to arachidonic acid in body)
directly as arachidonic acid

274
Q

PLA2 activated by

A

increased intracellular ca

275
Q

eicosanoids

A

biologically active metabolites of arachidonic acid

276
Q

lipoxygenase

A

first step in metabolism of arachidonic acid to leukotrienes

277
Q

cyclic endoperoxides

A

unstable PGs

278
Q

why do PGs have a local action

A

metabolised by endothelial cells of pulmonary capillaries

279
Q

PGE2

A

vasodilator/natriuretic
hyperalgesic
pyrogenic
angiogenic

280
Q

PGF2alpha and PGD2

A

bronchoconstrictors

281
Q

how does PGE2 enhance pain

A

acts before bradykinin - get prolonged and increased pain response compared to BK alone

282
Q

IL-1B induces

A

increase BK1 R

increase COX-2 adn PLA2

283
Q

fever production

A

peripheral inflammation causes macrophages activation
they release cytokines which circulate to hypothalamus (outside BBB)
induce COX2 production - produces PGE2
increases cAMP - raises temperature

284
Q

PGE2 good role

A

gastro-protective - increases mucous secretion, decrease gastric acid secretion

promotes blood flow, promotes angiogenesis

285
Q

prostacyclin or thromboxane more unstable

A

thromboxane (30s) vs prostacyclin (3mins)

286
Q

action of aspirin on Cox

A

acetylates serine in active site of COX1 and 2

287
Q

action of aspirin acetlyated COX2

A

retains some activity - produces epi-lipoxins from arachadonic acid
epi-lipoxins bind to formyl peptide R2 (FPR2) which actively suppresses neutrophil recruitment

288
Q

advantage of omega 3 fatty acids

A

replace omega 6 fatty acids in membrane - their metabolism produces larger amount of prostacyclin than thromboxane due to substrate preference of thromboxane synthase

289
Q

ach biosynthesis

A

choline + acetyl coa –> Ach + CoA

ach carrier into vesicle

290
Q

NA/A biosynthesis

A

tyrosine to L-Dopa by tyrosine hydroxylase
L-DOPA to dopamine by DOPA decarboxylase
DA to NA by dopamine B-hydroxylase
NA to A by PNMT

291
Q

NA uptake

A

neuronal - high affinity uptake 1

extraneuronal - low affinity uptake 2

292
Q

atropine

A

M R antagonist

293
Q

d-tubocurarine

A

NiR antagonist

294
Q

alpha-bungarotoxin

A

NiR antagonist

295
Q

phenylepherine

A

alpha 1 agonist

296
Q

isoprenaline

A

beta agonist

297
Q

endrophonium

A

short duration anticholinesterase - diagnosis of MG

298
Q

neostigmine

A

reverse effect of non-depolarising neuromuscular blockers, MG treatment

299
Q

donepezil

A

enters CNS, alzheimers treatment

300
Q

myasthenia gravis

A

autoimmune - Abs against AchR

301
Q

NiRs on skeletal muscle and gangion in ANs

A

Nm type - skeletal

Nn type - ganglion

302
Q

Ni antagonists

A

pre-surgical skeletal muscle relaxant =non-depolarising

303
Q

pilocarpine

A

MR agonist for glaucoma

304
Q

hyoscine

A

MR antagonist - motion sickness

305
Q

ipratropium

A

MR antagonist - chronic obstructive pulmonary disease

306
Q

beta agonist

A

isoprenaline

307
Q

beta antagonist

A

propranolol

308
Q

beta 1 agonist

A

dobutamine

309
Q

beta 1 antagonist

A

atenolol

310
Q

beta 2 agonist

A

salbutamol

311
Q

alpha antagonist

A

phentolamine

312
Q

alpha 1 agonist

A

phenylepherine

313
Q

alpha 1 antagonist

A

prazosin

314
Q

body usually uses what type of antagonism

A

functional

315
Q

verapamil

A

L-type Ca channel blocker - inhibits cardiac function

316
Q

allosteric modulators modulate

A

orthosteric ligand affinity
orthosteric ligand efficacy
receptor activation level

317
Q

advantages of allosteric

A

selectivity between receptor subtypes
incomplete activation/inactivation possible
physiological modulation can continue

318
Q

are drugs that are surmountable in vitro always surmountable in vivo

A

NO- limit of endogenous agonist

319
Q

factors effecting rout of administration

A

patient convenience
cost
bioavailabilty
local vs systemic

320
Q

elimination rate proportional to

A

concentration in plasma

321
Q

drug distribution affected by

A

molecular size
plasma protein binding
lipid solubility

322
Q

drug resevoirs can

A

prolong action
quickly terminate action
lead to slow distribution

323
Q

Vd =

A

X/C

apparent volume of body water drug appears to be dissolved in after distribution

324
Q

GFR =

A

120mL/min

325
Q

renal clearance

A

amount of blood from which drug removed by kindeys per unit time

326
Q

CLrenal =

A

GRF +TS-TR

327
Q

CL =

A

rate of elimination/C

328
Q

cytochrome p450 which phase of metabolism

A

1

329
Q

tubular reabsorption dependent on

A

pH

MD1 (5 decks)

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