Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

1st year Medicine > Systems- Cardiovascular > Flashcards

Systems- Cardiovascular Flashcards

1
Q

Cardiac output equations

A

Q= change in P/R

Q= MAP(-CVP)/TPR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Poiseulle’s law

A

R= 8 x viscosity x length of tube / pi x radius^4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Overall Q

A

MAP / 8vL/pi(r^4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Starling equation

A

Net volume flow= alpha[(hydrostatic pressure difference) - delta(osmotic difference)]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Hypokalaemia

A

From low dietary K+ or starvation
-> diarrhoea, excess sweating and urinary excretion
ST depression
Extra U wave due to prolonged repolarisation of purkinje fibres
Atrial arrythmias
Ventricular tachycardia or fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Sinus tachycardia

A 
Rate more than 100bpm
Otherwise normal (regular narrow QRS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Ectopic beats

A

Missed beats and extra thumps

Felt most at rest, where there is increased awareness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Supraventricular tachycardia

A

Rate more than 100bpm
No P wave, hidden in QRS
Regular narrow QRS
AVN reentry via slow and fast pathways
Treat with adenosine, valsalver manouver, ablation to cauterise slow pathway
Clearly defined episodes of around 7 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Atrial fibrillation

A

Waves of reentry to atria
Risk of stroke
No P waves, no organised depolarisation
Fluttery, weak and strong beats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Atrial flutter

A

Rate variable- atria around 300bpm, ventricles 150bpm
Regular narrow QRS
Sawtooth atrial ECG
Clockwise impulse wave around right atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Ventricular tachycardia

A

Rate more than 120bpm
Regular broad QRS
P waves variable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Wolff-Parkinson-White syndrome

A

Conduction from atria to ventricles before AVN
In combination with atrial fibrillation can cause death
Short PR interval
Slurred upstroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Sinus bradycardia

A 
Rate less than 60bpm
Otherwise normal (regular narrow QRS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Junctional bradycardia

A

Rate less than 60bpm
No P wave
Regular narrow QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Vasovagal syndrome

A

Vasodilation
Triggered by PPP- posture, prodrome, precipitant, then syncope
Tested in tilt test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Arrythmic syncope

A

Random, any posture

Infrequent- sudden onset and fast recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Sinoatrial disease

A

Malfunction of SAN

Often associated with atrial tachycardias- dangerous as cant slow tachycardia to normal pacemaker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

1st degree heart block

A

Rate variable
Regular narrow QRS and P wave
Slow PR interval
= AVN block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

2nd degree heart block

A

Mobitz- Irregular narrow QRS, not 1:1 with P
Wenckebach- Irregular narrow QRS, not 1:1 with P
- Increasing PR interval, then dropped beat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Complete heart block

A

Regular broad QRS
No conduction though purkinje fibres
No relation between P and QRS
Needs immediate temporary pacing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Inotropy

A

Force of contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Chronotropy

A

Rate of contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Dromotropy

A

Rate of electrical conduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Statins

A

eg Lovarstatin, Atarvastatin
Inhibit enzyme 3-hydroxy-3-glutyl coA reductase which is the rate controlling enzyme of mevalonate pathway producing cholesterol
Used to prevent atherosclerosis
Causes- decreased liver cholesterol synthesis
- increased VLDL and LDL receptor expression, so decreased LDL in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Fibrates

A

Used to prevent atherosclerosis
Ampipathic carboxylic acids, agonists of peroxisome proliferator activated receptor alpha (PPAR-alpha)
-> increased beta oxidation in liver, decreased hepatic triglyceride excretion, increased VLDL clearance by lipoprotein lipase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Bile acid binding agents

A

Used to prevent atherosclerosis

Increase loss of bile acid via gut, so decreased liver cholesterol, increased LDL receptor expression, less LDL in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Nitrates

A

Used to control angina
Increased NO, stimulates guanylate cyclase, activates cGMP-dependent protein kinase, activates myosin light chain phosphorylation, vasodilation
Venous vasodilation-> reduced preload
Arterial vasodilation-> reduced afterload
Side effects- headache
- flushing
- palpitations
- tolerance
- interactions with impotence drugs (viagra) leading to hypotensive crisis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Beta blockers

A

Used to control angina
eg Propanolol, Atenolol, Carvedilol
1st line treatment for chronic stable angina
Reduces myocardial oxygen demand by blocking beta 1 receptors on the heart, slowing heart rate and contractility
Fewer side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Calcium channel blockers

A

Used to control angina and treat hypertension
Less Ca entry to smooth muscle, vasodilation, less heart contraction, less myocardial oxygen demand
Side effects- peripheral vasodilation-> dizziness, headache, erythema, peripheral oedema
- constipation
- HR changes
eg Dihydropiridines (Nifedipine), Phenylalkylamines (Verapamil), Benzothiazepine (Diltiazem)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Aspirin

A

Antiplatelet
Used to treat post MI
NSAID (non steroidal anti inflammatory)
Metabolized to salicylate
Used in low dose long term to prevent MI, strokes, blood clots
Irreversibly inactivates COX in both platelets (making thromboxane A2, increasing clotting) and endothelial cells (making prostaglandins PGI2, inhibiting clotting)
Endothelial cells have nucleus, so can make more prostaglandins almost immediately, platelets can’t make more thromboxane A2 for 7-10 days so overall inhibits platelet aggregation
Low dose of 180mg/day effective in preventing ministroke
335mg/day decreases risk of MI
More than 1000mg/day has no effect, as inhibits endothelial COX also, so cancelling out antiplatelet effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Clopidogrel

A

Antiplatelet
Prodrug that irreversibly blocks ADP receptor on platelet cell membranes
Blocks activation of glycoprotein IIb/IIIa pathway, so prevents amplification of clot formation
Side effects (few)
Decreases risk of stroke, MI, vascular death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Ranolazine

A

Used post MI where there is high risk of electrical disturbances in the heart
Blocks late Na entry, increases QT interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Nitric Oxide

A 
Produced by endothelial cells
Causes VSM relaxation (vasodilation), modulates cardiac contraction, inhibits platelet aggregation
=EDRF (endothelial derived relaxing factor)
ACh-> increase Ca conc in endothelial cell -> endothelial nitric oxide synthase produces NO-> NO to guanylate cyclase of smooth muscle cell-> GTP to cGMP to PKG-> decreased Ca levels-> relaxation
Can be removed by cGMP phosphodiesterase, but NO has short half life and would degrade quickly anyway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Mean arterial pressure

A

MAP= 1/3 pulse pressure + diastolic pressure

MAP= (CO x TPR) + CVP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Thiazides

A

eg Hydrochlorothiazide, Bendroflumethiazide
Treat hypertension via blocking the na/cl symporter in DCT
Mild, so limited use
Also direct vasodilator action, so gives 2 beneficial effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Calcium channel blockers

A

eg Nifedipine
To treat hypertension
Vasodilators, reduce peripheral resistance and reduce filling pressures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

ACE inhibitors

A

eg Captopril and Enlapril
To treat hypertension
Inhibits angiotensin I->II
1) rapid phase due to direct anti ang II effect
2) slow phase due to blood volume effect and control of thirst

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Ang II receptor blockers

A

Eg Losartan
To treat hypertension
Limits blood volume expansion so less water retention, less thirst

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Alpha 1 adrenoreceptor blockers

A

Eg Prazosin, (Doxazosin in emergencies)
To treat hypertension
Block constriction of VSM (so vasodilate) by antagonising noradrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

K+ channel activators

A

Eg Minoxidil, Pinacidil
To treat hypertension
Inhibits calcium entry into cell by blocking k exit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Alpha methyl dopa

A

To treat hypertension
Prodrug, converted to methyl noradrenaline in SNS
Displaces NA but is not metabolised by MAO
Unselective, so only last resort

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Ganglion blockers

A

Eg Guanadrel
In uptake 1, Guanadrel substitutes for NA in secretory granules
So decreases sympathetic effects

Many side effects, so last resort, inhibits all sympathetic ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Quinidine

A

Class 1a antiarrhythmic
Moderate Na channel blocker
Prolongs action potential duration, reduces upstroke
Reduces Na entry to cell
Binds to Na channel (slow)
Slows phase 4 depolarisation, suppresses propagation of automaticity

44
Q

Lignocaine

A

Class 1b antiarrhythmic
Weak Na channel blocker
Decreases action potential disrupt, reduces upstroke
Suppressed automaticity by prolonging the refractory period, decreasing conduction, decreasing Na influx (so Ca influx)
For treatment during and immediately after MI, emergencies only

45
Q

Flecainide

A

Class 1c antiarrhythmic
Strong Na channel blocker
Suppresses automaticity
Increases refractory period
Useful in WPW syndrome, CPVT, recurrent tachyarrhythmias
For post MI to decrease cardiac contractility

46
Q

Atenolol

A 
Class II antiarrhythmic
Beta blockers
Increase action potential duration
Increases refractory period
Decrease SAN/AVN conduction 
Haemodynamic depressant
For supra ventricular tachycardia
47
Q

Amiodrorone

A 
Class III antiarrhythmic
K channel blocker
Increases action potential duration
Increase refractory period
For WPW syndrome, ventricular tachycardias, atrial fibrillation
48
Q

Diltiazem

A

Class IV antiarrhythmic
Ca channel blockers
Difficult to target cardiac not vascular Ca channels
Blocks AVN so good for supra ventricular tachyarrhythmias
Prevent recurrence of paroxysmal supra ventricular tachycardia
Reduce ventricular rate where atrial fibrillation

49
Q

Magnesium

A 
Used as antiarrhythmic
Reduces Ca entry through sarcolemma
Binds ATP and regulates metabolic processes
Depleted in ischaemic cells
Valuable in ventricular arrhythmias

Occasionally genetics- pro arrhythmic

50
Q

Adenosine

A

Antiarrhythmic agent
For supra ventricular tachycardias
Enhances k current in atrial tissues

51
Q

Digitoxin

A

Long duration
Slow onset
Lipophilic- good absorption, strong binding to serum proteins
Act at Na/K ATPase (3 Na out 2 K in) on cardiac glycosides binding sites opposite ATP binding sites on alpha subunit
So decrease Na in cell, some depolarization
Increase Ca in cell via Na/Ca exchange
Increase Ca in cell via sarcoplasmic reticulum pump release
Increase contraction strength (increase force and excitability, decrease A-V conduction and rate)

Not first line but still potent, careful titration needed, used when atrial flutter or fibrillation is present in HF

52
Q

Dobutamine

A

Receptor sympathomimetics
For reversible HF
Beta 1 selective
Given intravenously

53
Q

Milrinone

A

Transduction sympathomimetics
Last line treatment for HF
Increases cAMP by inhibiting cAMP phosphodiesterase, so increasing PKA activity

54
Q

Glyceryl trinitrate (GTN)

A 
Nitrate
For acute hospital cases of HF 
Metabolized to release NO
Decreases preload and afterload
Decreased venous return, so increased CO when decompensated
55
Q

Lowering free cholesterol by decreasing HMG CoA reductase

A

Diet- less saturated fats, increased polyunsaturated fats
Drugs- simvastatin, atorvastatin
1st line (50% decrease in cholesterol possible)

56
Q

Lower free cholesterol by decreasing intestinal uptake of chylomicron remnants

A

Diet- plant stanols, benecol
Drugs- ezetimibe
2nd line (10% decrease in cholesterol possible)

57
Q

Lowering free cholesterol by increasing bile acid excretion

A 
Diet- increase fibre intake
Drugs- cholestyramine
3rd line (bad GI side effects)
58
Q

Furosenide

A 
Loop agent diuretic
Acts at ascending limb of loop of Henle
Inhibits Na/K/Cl transporter
Powerful
Useful for pulmonary and refractory oedema and kidney failure
59
Q

Spironolactone

A 
K sparing diuretic
Acts at convuluted tubule
Antagonises aldosterone
Weak 
Useful for controlling K loss (so used with loop agents)
60
Q

Warfarin

A

Inhibits carboxylation of factors II, VII, IX, X so tissue factors cannot localise to platelets
Oral administration, long term therapy
Slow onset (12+hours), 4-5 day duration
Strongly binds to plasma proteins
Metabolized in liver
Measure prothrombin time (PT) to measure action (clotting time of plasma from patient blood sample following addition of calcium, expressed as ratio, gives INR value, low value is best)
Potentiated by
- drugs displacing it from plasma proteins eg aspirin, so increases its concentration in bloodstream
-drugs interfering with liver function, slowing its breakdown
-drugs which interfere with platelet function
-liver disease
-decreased vitamin k availability
Decreased by
- drugs which induce metabolizing enzymes
-promoted clotting factor synthesis (vitamin k)
-reduced warfarin absorption
Side effects- haemmorhage (stop warfarin until INR below 5.0, give vitamin K)
- tertogenic, affecting foetal development, so not used in pregnancy

61
Q

Heparin

A

Binds antithrombin III, so removes factors IIa and Xa from the bloodstream
LMW heparin inhibits only Xa so less potent
In vivo administration, or injected IV or SC
Complex pharmacokinetics due to plasma protein binding
Initially rapidly removed as it binds to endothelial/macrophage cells
Slower subsequent removal by renal excretion, so give large initial dose then match dosage with renal excretion
lMW has immediate IV effect as doesn’t bind to plasma protein

62
Q

Prasugrel

A

Irreversible ADP receptor antagonist
Antiplatelet
Fast onset
Very effective, so higher risk of bleeding

63
Q

Ticlopidine

A

Irreversible ADP receptor antagonist
Antiplatelet
Slow onset of 3-7 days
Decreases stroke risk

64
Q

Ticagrelor

A

Reversible ADP receptor antagonist
Antiplatelet
Because it is reversible, can be an asset in some clinical scenarios

65
Q

Abciximab

A

IIb/IIIa receptor antagonist
Antiplatelet
Antibody fragment directed against receptor
Used IV in high risk coronary angioplasty with heparin and aspirin
Only single administration, as will become immune

66
Q

Tirofiban

A

IIb/IIIa receptor antagonist
Antiplatelet
Cyclic peptide resembling IIb/IIIa ligands
IV administration

67
Q

Epoprostenol

A

Prostaglandin agonist
Antiplatelet
IV administration
For patients undergoing haemodialysis where they cannot have heparin

68
Q

Dipyridamine

A

Phosphodiesterase inhibitor
Antiplatelet
Increases platelet cAMP levels

69
Q

Streptokinase

A

Fibrinolytic agent
From streptococci bacteria
Blocked by antibodies after 4 days so is then ineffective, limit use to 1x per year

70
Q

Recombinant tPA

A

Fibrinolytic agent
Clot specific, more active at fibrin bound plasminogen
Alteplase- short half life
Reteplase- long half life

71
Q

Contraindications, side effects and uses of Fibrinolytic agents (tPA, SK, UK)

A

Contraindications
- Absolute - active/recent internal bleeding
- recent cerebrovascular accident
- invasive procedures where haemostasis needed
- Relative - pregancy
- cardiopulmonary resuscitation
- trauma
- bacterial endocarditis
Side effects- GI haemmorhage
- allergic reactions
- can generate kinins-> hypotension
Used in acute MI, acute thrombotic stroke, clearing thrombosed shunts, acute arterial thromboembolism

72
Q

Antifibrinolytic drugs

A

Tranexamic acid- inhibits plasminogen activation, used in high bleeding risk
Aprotinin- proteolytic enzyme inhibitor of plasmin, used in high bleeding risk during or after open heart surgery

73
Q

Drugs to treat venous thrombosis

A

Heparin or Warfarin
To reduce effectiveness of clotting cascade
Reduce formation of fibrin

74
Q

Drugs to treat arterial thrombosis

A

Aspirin, Clopidogrel, Abciximab
Reduce platelet activation
Used in acute MI, high risk MI, after coronary bypass, unstable coronary syndromes, after coronary artery angioplasty, thrombotic stroke

75
Q

Drugs to treat life threatening thrombosis

A

Alteplase
Fibrinolytic drug, recombinant tPA
Activates plasminogen, increasing fibrin breakdown

76
Q

Right ventricular failure signs/symptoms

A

Raised CVP (JVP)
Hepatomegaly as congested liver
Peripheral oedema
Parasternal heave (ventricular enlargement)
Murmur of tricuspid regurgitation
Nocturia as fluid from legs returns to circulation
GI organs congested with blood, so abdominal discomfort

77
Q

Left ventricular failure signs/symptoms

A

Symptoms- dyspnoea (breathlessness) as pulmonary venous congestion

  • orthopnoea when lying flat, blood from limbs to lungs
  • fatigue as reduced perfusion of skeletal muscle

Signs

  • cachexia (frail appearance)
  • diaphoresis (excessive sweating)
  • cool peripheries
  • tachycardia
  • tachypnoea
  • murmur of mitral regurgitation
  • crepitations in lungs (congested)
  • cardiac wheeze
78
Q

ANP

A

Atrial natriuretic peptide
Released by atria in response to stretch
Causes more urine excretion to lower blood pressure

79
Q

Preload

A

The load on a myocyte prior to contraction, =filling pressures

80
Q

Afterload

A

The load against which the heart has to work to eject blood

81
Q

Starlings law of the heart

A

The energy of contraction of a cardiac muscle fibre is proportional to the fibre length at rest

82
Q

Adrenaline in high concentration

A

Alpha 1 receptors

Vasoconstriction

83
Q

Adrenaline in low concentration

A

Beta 2 receptors

Vasodilation

84
Q

Investigations- Exercise treadmill test

A 
Cheap
Available in clinic
Instant result
Insight to exercise capacity
but- Low sensitivity and specificity
85
Q

Investigations- CT Calcium scoring

A

Good for ruling out atherosclerosis, not good at ruling in
(Lights up any calcification)
Used in low likelihood of CAD

86
Q

Investigations- Myocardial perfusion scan

A 
(Radionuclide injected, viable tissue takes up, infarcted does not)
Good information given
Lesion specific
but- High radiation dose
- False positives and negatives given
- Time consuming
If intermediate likelihood of CAD
87
Q

Investigations- Stress echo

A

(Stressed via exercise or dobutamine, then look at LV function with ultrasound to see contraction)
No radiation
Equipment readily available
but- Only short time frame available to get images in (90s)
- Not all views of heart possible
- Consultant led
If intermediate likelihood of CAD

88
Q

Investigations- Cardiac MRI

A 
Compare in rest vs stress
Give adenosine for maximal dilation of vessels and then can watch blood travel through heart
Very good definition
No radiation
If intermediate likelihood of CAD
89
Q

Investigations- Coronary angiography

A

BEST
Pass catheter to heart, squirt dye and watch passage of blood through
but- Invasive, risk of MI and death, damage to artery

90
Q

Treating CAD

A 
Lifestyle:
Weight loss
Diet change (even if slim)
Hypertension/cholesterol/diabetes control
Smoking cessation ESSENTIAL
Medication:
Aspirin
Statins
B blockers/ Ca channel blockers
Nitrates (symptomatic relief)

Coronary angioplasty
Coronary artery bypass grafting

91
Q

Pathophysiology of heart failure

A

Inadequate tissue perfusion and volume overload

-> Enlarged ventricles, spherical shape, reduced efficiency

92
Q

Drugs to treat heart failure

A 
Diuretics
Vasodilators (nitrates)
ACE inhibitors
Angiotensin II receptor antagonists
Positive ionotropic drugs- cardiac glycosides and sympathomimetics
93
Q

Myogenic autoregulation

A

Bayliss effect
High bp distends arteries, which respond by contracting (negative feedback)
Stretch-activated ion channels open, depolarisation, voltage-gated ion channels open, Ca enters, VSM contraction
Minimises capillary flow fluctuations and irregular tissue exchange

94
Q

Autoregulation

A

Blood flow remains near constant over a range of pressures by regulating local resistance from signals from blood vessels or surrounding tissue

95
Q

Metabolic autoregulation- active and reactive hyperaemia

A

Local vasodilation caused by CO2, acidosis, lactate, adenosine, K+, hypoxia
Active: increased metabolic activity, decreased O2, increased metabolites, vasodilation, increased flow
Reactive: flow occlusion, accumulation of vasodilating metabolites, rapid and transient increase in flow

96
Q

Metabolic autoregulation- autocoids

A

Vasoactive chemicals,
eg histamine, bradykinin cause vasodilation
endothelin, serotonin cause vasoconstriction
Produced, released and acting locally
For inflammation, trauma and clotting

97
Q

Metabolic autoregulation- eicosanoids

A

Mediate inflammatory responses
Cause vasodilation
eg Prostaglandins, thromboxane

98
Q

Endothelial regulation causing vasodilation

A

Shear stress, ACh, histamine, bradykinin, ATP
Causes endothelial production of EDRF (endothelial derived reacting factor), NO
Stimulates guanylate cyclase in VSM, relaxation

99
Q

Endothelial regulation causing vasoconstriction

A

Circulating factors eg ADH
Cause release of endothelin-1
Opposite effects to NO, increased SR release of Ca, vasoconstriction

100
Q

Nitric oxide synthase (NOS)

A

Only active as dimer
Presence of BH4 necessary for action
Activated by calmodulin and reversible phosphorylation
3 isoforms- eNOS (endothelial) and nNOS (neuronal) are Ca dependant, synthesise NO basally upon stimulation
-iNOS (inducible) is Ca independant, for inflammatory response induced by ischaemia- reperfusion, HF, ageing, septicaemia
Uncoupled in oxidative stress (diabetes, hypertension, atherosclerosis, chronic smoking), where can’t use arginine as a substrate so uses O2 instead which is converted to superoxide

101
Q

Nitric Oxide effects

A 
Inhibits platelet adherence
Inhibits leukocyte chemotaxis
Inhibits smooth muscle cell proliferation and migration
Promotes endothelial regrowth
Vasorelaxation

When combined with superoxide, makes ONOO- and No2 which damage mitochondria, break DNA leading to cell death

102
Q

RAAS effects

A

ADH secretion from posterior pituitary, so H2O absorption from collecting duct
Increased sympathetic activity
Aldosterone secretion from adrenal cortex, so increased tubular Na/Cl reabsorption and K excretion, H2O retention
Arteriolar vasoconstriction, so raise in BP

Overall water and salt retention to increase blood volume, inhibits renin release by Kidney for angiotensin to 1, negative feedback loop

103
Q

Haemostasis

A

Endothelium release inhibiting factors NO and PGI2, these check endothelium for damage
Von Willebrand factor links collagen on damaged vessels to platelets
Activated platelets release ADP and thromboxane A2, amplification
ADP binds to G protein coupled ADP receptor P2Y12
Activation of integrin IIa/IIIb and fibrin binding leading to platelet aggregation

104
Q

Anti-clotting cascade

A

-Antithrombin III
-Proteins C and S
-Thrombomodulin
Cleave Va and VIIIa so they are INactivated, cannot be reactivated

-Lipoprotein tissue factor pathway inhibitor
Endocytosis and degradation of Xa and VIIa so no prothrombin to thrombin

105
Q

Intact endothelium discourage thrombosis by…

A

Express sulphated mucopolysaccharides which activate antithrombotic enzymes
Express tissue plasminogen activator, activating plasminogen, active destruction of thrombus
Synthesise prostacylin, which dilates vessels and disaggregates platelets

106
Q

Platelet Derived Growth Factor

A

Triggers SMCs to change in atherosclerosis, become more like fibroblasts and migrate up to become fibrous cap

1st year Medicine (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions