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MBBS - Year 2 > Cardiology - Arryhthmias > Flashcards

Cardiology - Arryhthmias Flashcards

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1
Q

Definition of AF

A

SVT
Uncoordinated atrial contraction
Irregular and frequently fast ventricular rate

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2
Q

Epidemiology of AF

A

Commonest cardiac arrhythmia - 1.2%

Prevalence increases with age - 10% > 70yrs, 23% > 80 yrs

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3
Q

ECG appearance in AF

A

No distinct P wave

Irregularly irregular

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4
Q

Classification of AF

A 
First-diagnosed AF 
Paroxysmal AF 
Persistent AF 
Long standing persistent AF 
Permanent AF
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5
Q

First-diagnosed AF

A

AF that hasn’t been diagnosed before

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6
Q

Paroxysmal AF

A

Self-terminating, usually in 48 hrs

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7
Q

Persistent AF

A

AF lasting longer >7 days

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8
Q

Long-standing persistent AF

A

Continuous AF lasting >1 yr when its decided to adopt a rhythm control strategy

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9
Q

Permanent AF

A

AF accepted by pt and Dr

Rhythm control interventions aren’t pursued

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10
Q

AF symptoms

A 
Palpitations 
Dyspnoea 
Chest tightness 
Fatigue/ lethargy 
Sleeping disturbances 
Psychological effects
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11
Q

Modified EHRA symptoms scale

A

1 - 4

No symptoms to disabling symptoms

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12
Q

Aetiological factors of AF

A 
Aging (structural remodelling)
Heart failure 
HTN and DM 
Valvular heart disease (esp mitral)
CAD
Alcohol excess 
Hyperthyroidism (trigger)
Obesity and sleep apnoea 
Autonomic activation
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13
Q

Autonomic activation of AF

A

Sympathetic - increased ectopic activity

Vagal - reduced APD and increased spatial heterogeneity

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14
Q

Target BP for AF pts

A

130/80 mmHg

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15
Q

Mx of wt in AF pts

A

10% reduction in body wt (BMI < 25)
Increased physical activity
Diet (low-calorie food)

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16
Q

Mx of lipids in AF pts

A

Lifestyle measures if LDL >100mg/dL after 2/12 started on statins

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17
Q

Glycaemic control in AF pts

A

HbA1c > 6.5% after 2/12 - metformin

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18
Q

Mx of OSA in AF pts

A

Sleep study

Nocturnal CPAP

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19
Q

OSA

A

Obstructive Sleep Apnoea

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20
Q

Diagnostic workup for AF

A 
12 lead ECG 
BP 
Bloods 
Echo 
Holter monitoring
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21
Q

Bloods for AF

A 
FBC 
U&Es 
LFT 
TFT 
Coagulation
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22
Q

Why do we measure U&Es for AF

A

Abnormal K can ppt AF

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23
Q

Holter monitoring

A

Symptoms/ rhythm correlation
AF burden
Ventricular rate control

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24
Q

Potential consequences of AF

A

Morbidity associated w/ symptoms
AF +/- tachycardia mediated CM
Stroke
Increased mortality

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25
Rship between AF and stroke
Blood pools in atria --> blood clot forms --> whole/ part of blood clot breaks off --> travels to brain occluding cerebral artery
26
Mechanisms of AF
``` Ectopic activity (trigger + AF driver) Re-entry - can be single or multiple circuit ```
27
Ectopic activity in AF
Enhances automaticity | Early or delayed after depolarisations
28
What tissue properties are required before re-entry can cause AF
Shortened & heterogenous ARPs Areas of slow conduction - fibrosis Conduction barriers - anatomical vs iatrogenic (scars from catheter ablation/ surgery)
29
AF induced remodelling
Electrical remodelling Contractile remodelling Structural remodelling - irreversible
30
Mx for AF
1. Rhythm control 2. Rate control 3. Anti-coag 4. L atrial ablation and/or ICD placed
31
Rhythm control for AF
Flecanide is 1st line (Class Ic) Amiodarone (class III) w/ structural heart disease Ablation (once drugs have failed)
32
Rate control for AF
BB - LVEF <40% Rate-limiting Ca channel blockers (Class IV) - LVEF > 40% Digoxin (used in combination w/ another drugs as 3rd line) Cardioversion
33
What must be considered before anticoagulating an AF pt
CHADVASC (2 for women and 1 for men) | HASBLED/ORBIT
34
Main anticoagulants given in AF
Apixiban | Dabigatran
35
CHADVASC score
``` Congestive heart failure HTN Age >75yrs - 2 points DM Stroke/ TIA - 2 points Vascular disease (MI. PVD, aortic plaque) Age (65-74 yrs) Sc - sec category (female) ```
36
HASBLED Score
``` HTN Abnormal renal/liver function - 1/2 points Stroke Bleeding tendency Labile INR Age > 65 Drugs - 1/2 points ``` High score is 3/3+
37
Features of L Bundle of His
Large, diffuse structure | Rare to be damaged unless underlying heart disease
38
Features of R Bundle of His
Smaller, discrete structure | More commonly damaged without sig underlying heart disease
39
What part of the cardiac conduction system is supplied by sympathetic nerves
All of it - so drugs that stimulate SNS can increase HR even in heart block
40
What part of the conduction system is supplied by parasympathetic nerves
SAN | AVN
41
Hierarchy of pacemakers
Cardiac cells that polarise fastest will drive HR (60 - 100bpm) SAN is usually fastest then AVN (40-60bpm) then Purkinje network in ventricles (20-40 bpm)
42
Bradycardia definition
HR <60 bpm
43
Physiological causes of bradycardia
High vagal tone (sleep, athletes)
44
Pathogical causes of bradycardia
Fibrosis - occurs in aging IHD - a/c (MI) and c/c Drugs - BB, CCB, digoxin, antiarrhytmics Electrolyte/ metabolic disturbance - esp K Post cardiac surgery (esp aortic valve surgery) Infection e.g. IE
45
What symptoms do pts with bradycardia present with
``` Dizziness Fatigue Difficulty concentrating Exercise intolerance Falls Syncope Breathlessness ```
46
Where is the SAN found
Under epicardium at junction of SVC and RA
47
What are SA nodal cells set in
Dense, fibrous tissue
48
Why is the SAN easily damaged in cardiac surgery
Its superficial location
49
What can go wrong at the sinus node
It can fail to generate an impulse or conduct an impulse at the atrium
50
Sinus bradycardia
Fewer impulses generated than usual | Pts are usually asymptomatic
51
Sinus arrest
No impulse is generated at SAN
52
Sinus arrest on ECG
Period with no wave | Escape rhythm from AVN
53
Types of escape rhythms
Junctional - normal QRS Ventricular - broad QRS Both have no p waves present
54
Sinoatrial block
Impulse generated but not conducted out of SAN to atrium | Pause is longer than P-P interval
55
Tachycardia- bradycardia syndrome
Sick sinus syndorme Alternating bradycardia and tachycardia Usually seen in AF and another bradycardia
56
How many types of AV block are there
3 | 1st to 3rd degree
57
1st degree AV block
PR interval is prolonged, but all impulses are conducted to the ventricle
58
2nd degree AV block
Some (but not all) impulses are conducted to the ventricles | Two types - Mobitz type I, Mobitz type II
59
3rd degree AV block
No impulses are conducted to ventricles | AV dissociation
60
1st degree heart block on ECG
Prolonged PR interval | Rship between every P wave and QRS complex
61
3rd degree heart block on ECG
Rship between QRS complexes Rship between P waves NO rship between p waves and QRS
62
AV dissociation
Any situation in which atria and ventricles beat independently Can be caused by complete heart block
63
Mobitz type I heart block on ECG
PR interval gets more and more prolonged until one P wave isn't followed by QRS complex
64
What is Mobitz type I caused by
Block in AVN
65
Mx for Mobitz type I
No mx required
66
Mobitz Type II heart block on ECG
Sudden loss of AV conduction - one P wave isn't followed by a QRS but PR interval doesn't get progressively more prolonged
67
What is Mobitz type II caused by
Block in His-Purkinje system | Can lead to complete heart block
68
Mx of Mobitz Type II heart block
Mx with pacemaker required even if asymptomatic
69
Symptoms of Mobitz Type I
Lightheadedness/ dizziness | Syncope
70
Symptoms of Mobitz Type II
Chest pain SOB Postural hypotension
71
Symptoms of 3rd degree heart block
Feeling faint SOB Extreme tiredness, sometimes w/ confusion Chest pain
72
2: 1 AV block
Type of 2nd degree AV block | Every other P wave is conducted
73
Treatment of 2:1 AV block
Pacemaker
74
Advanced AV block
AV conduction ratio of 3:1 or higher | Always needs a pacemaker
75
Emergency treatment of bradycardia
ABCDE approach Atropine 500 mcg IV If not responding to atropine, give drugs that stimulate SNS If haemodynamically instable, pace pt
76
Which bradycardia condns have a risk of asystole
Mobitz II AV block | Complete heart block w/ broad QRS
77
What does atropine do
Blocks effect of vagus nerve on heart - increases HR in sinus bradycardia and AVN disease caused by block within AVN
78
What is atropine not effective for
AVN disease caused by block in His-Purkinje
79
Drugs that stimulate SNS
Adrenaline | Isoprenaline
80
Types of temp pacing
Central vein - internal jugular, subclavian, femoral | Transcutaneous
81
Performing transcutaneous pacing w/ defibrillator
Attach pads and connect defibrillator lead Set defibrillator to pacer Set pacer rate and output Conform electrical capture Confirm mechanical capture - feel femoral (R brachial) pulse
82
Cardiac devices
Devices implanted for dx or treatment of cardiac arrhythmias or unexplained syncope
83
Example of a diagnostic cardiac device
Loop recorder
84
Cardiac devices that treat and dx
Pacemaker (low heart rhythm) Defib (treat fast and slow heart rhythm) Cardiac resynchronisation therapy (treat heart failure - either pacemaker or defibrillator)
85
Pacemaker
Electronic device implanted in body that regulates the heartbeat
86
Roles of pacemaker
Detect pts own intrinsic impulses (withhold pacing pulse) - capture Depolarise the heart if there aren't any impulses - capture
87
Limitations of traditional pacemakers
Device can become infected | Leads can fail over time
88
Leadless pacemakers
Only pace RV | Indicated mainly in pts with AF and slow HR
89
ICD
Implantable Cardioverter Defib | Specialised pacemaker that treats life threatening ventricular arrhythmias
90
Who needs an ICD - primary prevention
Severe LV impairment | Inherited cardiac condns
91
Who needs an ICD - secondary prevention
Survivors of a VF/VT cardiac arrest Sustained VT with haemodynamic compromise Sustained VT and severe LV impairment
92
ICD vs anti arrhythmic drugs in SCD
ICD is superior to drugs in preventing Sudden Cardiac Death | Anti-arrhythmics are still important to reduce need for ICD therapies
93
How does an ICD recognise arrhythmias
ICD looks at HR | If above certain threshold, delivers shock
94
What do ICDs do in ventricles
Anti-tachycardia pacing Cardioversion Defib
95
Limitations of conventional ICDs
Leads can become damaged and may not be straightforward to remove
96
What can ICDs NOT do
Treat bradycardia Provide anti-tachycardia pacing Prevent death from progressive heart failure
97
Where are conventional ICDS implanted
Venous system
98
CRT
Treatment for pts with severe systolic heart failure and a broad QRS who remain symptomatic despite medical therapy Also used in CRT Improves symptoms and survival
99
Indications for pacemaker
Either symptomatic bradycardia or high risk e.g. advanced/ complete heart block (but asymptomatic) bradycardia
100
Indications for ICD
Ventricular arrhythmias e.g. VT/ VF | High risk of ventricular arrhythmias e.g. severe LV impairment
101
Indication for CRT
Severe heart failure w/ broad QRS (>120 ms) continuing symptoms despite meds
102
Mx of sick sinus syndrome (tachycardia-bradycardia)
Treat w/ pacemaker for Brady Rate lowering drug (BB) for tachycardia Anticoagulants
103
Types of cardiac cells
Pacemaker cells - conducting cells (SAN) | Non-pacemaker cells - contracting cells
104
What does the resting membrane potential of cardiac cells depend on
K ions as the membrane is semi permeable to K
105
Atrial vs ventricular action potential
Channels in atria are slower and Ca2+ drives depolarisation Channels in ventricles are faster and Na+ drives depolarisation Ventricular ap has plateau phase
106
How many stages does the ventricular ap have
5 | 0 - 4
107
Starting membrane potential of atria
-70 mV
108
Starting membrane potential of ventricles
-85/90 mV
109
Stage 0 of ventricular ap
``` K+ outflux (-ve cell) triggers: Rapid influx Na+ Slow influx of Ca+ Via VG ion channels Causes depolarisation to +20mV ```
110
Stage 1 of ventricular ap
VG Na+ channels close quickly VG K+ channels open for K+ outflux Causes repolarisation
111
Stage 2 of ventricular ap
Ca+ continues influx K+ outflux Membrane potential remains steady = plateau
112
Stage 3 of ventricular ap
VG Ca2+ ion channel closes K+ outflux continues Membrane potential repolarises
113
Stage 4 of ventricular ap
VG K+ channel closes however a steady flux of K+ remains | Resting membrane potential is restored
114
Main methods of pharmacological intervention for arrhythmias
Interfere with ap by blocking certain ion channels | Block sympathetic effects of ANS on heart
115
ERP
Effective Refractive Period Time within which a new ap cannot be released by same cells (stages 0 - 3) Acts as protective mechanism
116
ERP as a protective mechanism
Keeps HR in check Prevents arrhythmias Coordinates muscle contraction
117
Classification of anti arrhythmic agents
``` Class Ia/ Ib/ Ic - Na channel blockers Class II - BB Class III - K blockers Class IV - Ca blockers Class V - misc ``` Anti-arrhythmic drugs have cross-class activity
118
What do Class I anti arrhythmic do
Bind to and block Na channels responsible for depolarisation - Slower depolarisation - Increased ERP - Reduced AV conduction - Reduced automaticity
119
Example of Class Ia anti-arrhythmic
Disopyramide
120
Effects of Class Ia anti-arrhythmic
Prolongs ERP Reduced cardiac excitability Increases AP duration Prolonged repolarisation can increase risk of arrhythmia - torsades de pointes
121
Indications for Class Ia anti-arrhythmic
Maintain sinus rhythm after MI | Prevent and treat ventricular and SV arrhythmias
122
Example of Class Ib anti-arrhythmic
Lidocaine
123
Indication for Class Ib anti-arrhythmic
Cardiopulmonary resuscitation
124
SE of Class Ib anti-arrhythmic
Bradycardia | Convulsion
125
What are Class Ib anti-arrhythmics contraindicated in
AV block
126
Effects of Class Ib anti-arrhythmic
Reduced ERP | Decreases AP duration
127
Example of Class Ic anti-arrhythmic
Flecanide - most potent Na+ channel blocker
128
Effects of Class Ic anti-arrhythmic
Normal ERP Normal AP duration Reduced contractibility
129
Indication of Class Ic anti-arrhythmics
Tachycardia Paroxysmal AF Ventricular tachycardia resistant to other therapy
130
Using Flecanide and amiodarone together
Flecanide dose needs to be halved
131
Examples of Class II anti-arrhythmics
Sotalol Propanolol Atenolol
132
What do Class II anti-arrhythmics do
Block effects of norephedrine and epipharine (SNS) action on SAN
133
Monitoring required for Class II anti-arrhythmic
ECG | U&E
134
What can Class II anti-arrhythmics cause
Prolonged QT interval | AV blocks
135
Examples of Class III anti-arrhythmics
Amiodarone Dronedarone Sotalol
136
What do Class III anti-arrhythmics do
Block K+ channels
137
Effects of Class III anti-arrhythmics
Slow depolarisation Longer ERP Longer AP duration Reduced cardiac excitability
138
Effects of Class II anti-arrhythmics
Slowed pacemaker activity Decrease cardiac conduction and contractibility Increased ERP Increased PR interval
139
Why is there a risk of arrhythmias w/ Class III anti-arrhythmics
Can increase QT interval
140
What do Class IV anti-arrhythmics do
Ca channel blockers
141
Examples of Class IV anti-arrhythmics
Verapamil | Diltiazem
142
Effects of Class IV anti-arrhythmics
Increased PR interval Increased ERP Slow rise of AP and prolonged depolarisation through AVN Reduce contractility
143
Contraindications of Class IV anti-arrhythmics
Pts with heart failure | Pts on BBs
144
Examples of Class V anti-arrhythmics
Digoxin | Adenosine
145
Adenosine as an antiarrhythmic
K+ channel activator = repolarisation Slow pacemaker activity Used in a/c therapy - half life is 10s
146
Digoxin as an anti-arrhythmic
Inhibits Na, K & ATP - +ve inotropic effects Increases myocardial contraction Slows AV conduction and HR
147
What are the main ion channels in cardiomyocytes
K+ Na+ Ca2+
148
What is the funny current in pacemaker activated by
Hyperpolarisation instead of depolarisation | Mainly carried by Na+ channels
149
Example of parasympathetic stimulation on pacemaker cells
Acetylcholine
150
The effects of parasympathetic stimulation on pacemaker potential
Hyperpolarisation | Reduced slope of pacemaker potential
151
The effect of sympathetic stimulation on ventricular action potential and contraction
HR approx doubles Shortening of AP Contraction is stronger, quicker and relaxation more rapid
152
Basic Q's for arrhythmias
Is it brady or tachycardia Are the QRS complexes broad or narrow Is it regular or irregular P waves?
153
Ddx for narrow complex tachycardia
Atrial flutter Atrial tachycardia AVNRT AVRT
154
What does AVNRT stand for
Atrioventricular nodal re-entrant tachycardia
155
What does AVRT stand for
AV re-entrant tachycardia
156
Appearance of atrial flutter on ECG
Saw tooth appearance Narrow complex Irregular
157
What is the usual atrial rate
300 cycles/ min
158
Atrial rate with 2:1 conduction
2 flutter waves: 1 QRS complex | HR is 150 bpm
159
How many bpm with a 4:1 conduction block
75 bpm
160
How many bpm with a 5:1 conduction block
60 bpm
161
Curing atrial flutter
Ablation - breaks spp anatomical short circuit
162
Using adenosine for dx
Increases degree of AV/ AVN block, unmasking flutter waves | Breaks short circuit in AVNRT/ AVRT and returns pt to sinus rhythm
163
Physiology of inverted P waves
Electrical activity starting low in atrium and spreading upwards
164
Retrograde P waves
Inverted P wave is superimposed on the end of the QRS complex Atria and ventricles are depolarising at the same time
165
What do delta waves indicate
Pre-excitation | Seen in extra electrical connection or accessory pathway
166
Tachycardias occurring above AVN
AF Atrial flutter Focal atrial tachycardia
167
Tachycardias occurring below AVN
VT | VF
168
Examples of narrow complex tachycardias
``` Sinus tachycardia AF A flutter Focal atrial tachycardia AVNRT AVRT ```
169
Examples of broad complex tachycardia
VT - suspect until proven otherwise SVT w/ aberration Pre-excited tachycardia Pacemaker associated tachycardia
170
General mx of tachycardia
Mx of thromboembolic risk in AF and AFl Rate control - BB, rate slowing CCB, digoxin Termination of re-entrant arrhythmia Antiarrythmics - Class I, II, III Interventional electrophysiological procedures
171
Indications for interventional electrophysiological procedures
Ablation - AVRT/ AVNRT, A flutter, fibrillation
172
Magnitude of sudden cardiac arrest in UK
~100,000 per yr 1 every 5 mins 20-25% - first px of cardiac disease
173
Possible causes of collapse
``` Cardiac Cardiovascular Catastrophic vascular event Neurological Pyschogenic ```
174
Potential causes of cardiac arrest
Tachycardic - VT - most likely - VF - PMVT/ Torsades Bradycardic - AV block - SA block
175
Underlying causes of cardiac arrest
IHD Cardiomyopathy Structural heart disease Ion channel abnormalities
176
IHD causing cardiac arrest
A/c - ACS/ MI | C/c - ventricular scarring
177
Acquired CM causing cardiac arrest
``` IHD HTN Viral Alcohol Chemo ```
178
Inherited CM causing cardiac arrets
HCM DCM ARVC
179
Relevant hx of cardiac arrest
Hx of event PMH Fhx
180
Relevant tests for cardiac arrest
ECG Echo Monitoring Imaging - angio/ CT/ MRI
181
Treatment of cardiac arrest directly attributable to an ACS
Treatment is of underlying cause | Usual coronary 2' preventative measures
182
When is late arrhythmias in ACS more likely to occur
In setting of impaired LV function | The longer post MI, the more likely they are to be at risk
183
Types of CM
Hypertrophic Dilated Arrhythmogenic (Right ventricular)
184
Causes of acquired long QT
``` Drugs Ischaemia Hypothyroidism Hypothermia Bradycardia ```
185
Triggers of lethal cardiac events in long QT syndrome
Exercise Emotional stress Sleep
186
Where are the leads in transvenous ICDs
Intracardiac
187
Which type of ICD would be used for VT
Transvenous (conventional) ICD
188
Which types of ICD would be used for VF
S/c ICD
189
Mx of A flutter
Ablation | BB
190
Who do SVTs usually present in
Younger pts (150-200 bpm)
191
Vasovagal manoeuvres
Blowing into syringe Blowing on thumb Carotid sinus massage Valsalva manouvre
192
S/e of digoxin
Blurry vison Insomnia Dizziness
193
What can amiodarone be used to treat
``` SVT Paroxysmal SVT AF A flutter VT VF ```
194
Amiodarone and preventing AF
Use after open heart surgery
195
S/e of amiodarone
Thyroid dysfunction Parasthesia May also cause pulmonary fibrosis
196
Which antiarrhythmic can also treat cluster headaches
Verapamil
197
Common causes of atrial flutter
R atrial dilatation - PE, congestive heart failure Ischaemic heart disease Idiopathic
198
For how long should pts not drive after a VT/VF episode
6/12
199
Mx of Torsades de Pointes
IV Magnesium sulfate (slow infusion)
200
What is VF usually a progression from
VT
201
Shockable rhythms
VF | Pulseless VT
202
Px of long QT syndrome
Hx of syncope and blackouts Seizures Heart palpitations
203
Causes of long QT syndrome
``` Hypokalemia Hypomagnesia Hypocalcaemia Hypothermia Congenital long QT syndrome A/c MI Subarachnoid haemorrhage Drugs ```
204
Causes of short QT syndrome
Hypercalcaemia | Congenital short QT syndrome
205
Drugs causing long QT syndrome
AT A CAFE ``` Antihistamines TCAs (tricyclic antidepressants) Anticholinergics/ Antidepressants Chloroquine Antiarrhythmics (esp quinidine and sotalol) Fluoroquinolones Erythromycin ```
206
Mx of long QT syndrome
BB as rate control ICD or pacemaker may be implanted Lifestyle changes - not exercising strenuously, avoiding stressful situations Foods high in K
207
Presentation of cardiorespiratory arrest
Sudden collapse No pulse No breathing
208
Initial ix for cardiac arrest
ABCDE assessment
209
Mx of cardiac arrest
``` CPR and give oxygen Gain IV access Give adrenaline every 3-5 mins Give amiodarone after 3 shocks Defib if pt is in shockable rhythm Treat reversible causes ```
210
Evaluating palpitations
``` Continuous or intermittent? Regular or irregular? Approx HR Associated symptoms Precipitating factors (exercise or alcohol) Structural heart disease ```
211
Discrete attacks of tachycardia
Can happen w/ heart palpitations | >120 bpm
212
Examinations for blackouts and faints
Pulses = problem with BP Lying and standing bp = postural hypotension Murmurs = AS Carotid sinus massage = carotid sinus syndrome (neurocardiogenic cause)
213
Neurocardiogenic mx of blackouts
Reassure Educate about triggers and warning signs Lifestyle changes - increase fluid intake to 3L/ day and increase salt intake Stop BP meds if causing bradycardia
214
Function of cytokines
Mediate communication between cells of immune system and direct cell movement
215
Structure of cytokines
Small proteins/ glycoproteins (<30 kDa) | Generally soluble
216
Examples of biological effects produced by cytokines
Activation Proliferation Differentiation Apoptosis
217
Why is only a low conc of cytokines required
Most cytokines act over short distance
218
Why do cytokines have short half-lives
Ensures localised effect
219
Autocrine action
Cell produces cytokine and receptors
220
Paracrine action
Cytokine acts on nearly cells
221
Endocrine action of cytokines
Circulates in blood stream to reach distant targets cells | Uncommon
222
Different modes of action of cytokines
Pleiotropy Redundnacy Synergy Antagonism
223
Pleiotropy
1 cytokine has several functions e.g. IL4
224
Benefit of cytokines having different modes of action
Antagonism and synergy allows us to modulate immune response
225
What are the majority of cytokines secreted by
Th cells Dendritic cells Macrophages
226
What are cytokines mainly involved in
Cellular and humoral response Infl Haematopoiesis Wound healing
227
Where do cytokines mature in
Thymus
228
Where do cytokines migrate to
2' lymphoid tissue
229
Examples of APC
Macrophages Dendritic cells B cells
230
What do T cells differentiate into
CD4 - Th cells (MHC II) | CD8 - cytotoxic T lymphocytes (MHC I)
231
When are Th1 cells created from CD4 cells
When IL-12 is secreted by APC
232
When are Th2 cells created from CD4+ cells
When IL-4 is secreted by APC
233
What do Th1 cells secrete
IFN gamma
234
What are Th1 cells involved in
Macrophage activation Cellular immunity against intracellular pathogens Autoimmunity Delayed type hypersensitivity
235
What do Th2 cells secrete
IL-4 IL-5 IL-10 IL-13
236
What are Th2 cells involved in
Ig class switching Humoral immunity against extracellular pathogens Allergy
237
When are Treg cells created from CD4
When TGFbeta is secreted by APC
238
What do Treg cells secrete
IL-10
239
What are Treg cells involved in
Inhibition of infl | Immune tolerance
240
Why do cytokines not activate all immune cells
Tightly regulated surface expression of cytokine receptors e.g. only cells activated by spp antigen express certain cytokine receptors Immune synapses
241
Immune synapses
Close cell-cell | Directional cytokine secretion so cytokines restricted to one area
242
Types of cytokines
``` Interleukins (IL) Tumour Necrosis Factors (TNF) Interferons (IFN) Colony Stimulating Factors (CSF) Chemokines ```
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Pro-infl cytokines
IL-1alpha IL-1beta IL-6 TNF-alpha
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Anti-infl cytokines
IL-10 IL-4 TGFbeta
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What does IL-2 cause
T cell proliferation and differentiation into memory and effectors CD4 or CD8 cells in peripheral tissues
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What does IL-4 cause
B cell activation and differentiation into antibody-secreting plasma cells
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What does IL-5 activate
Eosinophils
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Most common TNF
TNF-alpha
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What do TNFs do
Key regulator of infl response produced by activated macrophages
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Levels of TNF in healthy individuals
Undetectable
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When are TNF serum and tissue levels elevated
Infl and infectious condns
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What are anti-TNFs used for
Treatment of infl condns
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Types of IFN
Type 1 | Type 2
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Type 1 IFN
1st line defence in viral infections - IFN alpha and beta
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Mechanisms of Type 1 IFN
Destroys viral RNA --> inhibits protein synthesis Up-regulate MHC Class I presentation Activation of cytotoxic CD8
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Most predominant Type 2 IFN
IFN gamma
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What do Type 2 IFN do
Upregulate MHC expression --> clearance of intracellular pathogen
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TNFalpha in macrophages
Increased infl through pro-infl cytokine and chemokines
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TNFalpha in endothelium
``` Increased cell infiltration Increased angiogenesis (VEGF) ```
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TNFalpha in hepatocytes
Increases CRP in serum
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TNFalpha in synoviocytes
Articular cartilage degradation
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What do CSFs do
Mediate growth and differentiation of immature leukocytes in bone marrow (haematopoiesis)
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Examples of CSFs
M-CSF - macrophage CSF G-CSF - granulocyte CSF GM-CSF - macrophage/granulocyte CSF
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What are chemokines
Small cytokines (7.5 - 12.5 kDa)
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What do chemokines do
Induce movement of leukocytes along conc gradient
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Chemotaxis
Cell movement directed by soluble factors
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Nomenclature of chemokines
According to structure CCL CXCL XCL CX3CL
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Example of chemokine
CXCL8 (IL-8) | Powerful chemo-attractant of neutrophils
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Cytokine-related diseases
Septic shock Cytokine storm T2DM Cancer
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Septic shock caused by cytokines
Release of bacterial products (e.g. lipopolysaccharide) during systemic infections (Staph a, E.coli etc) causes overproduction of pro-infl cytokines
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Symptoms of cytokine storm
Pyrexia Circulatory collapse Diffuse intravascular coagulation Haemorrhagic necrosis All these lead to multiple organ failure
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What can cause cytokine storms
``` Dilation of blood vessels Leakage of fluid into body tissues Pertubation of blood supply Tissue injury Widespread blood clotting Organ failure ```
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Infections inducing cytokine storms
Viral e.g Spanish influenza, SARS, bird flu, COVID-19
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T2DM and cytokines
Constitutive expression of TNF-alpha by adipose tissue of obese individuals --> decreased cellular response to insulin and glucose uptake
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Cancer and cytokines
IL-6 overexpression in most types of tumours --> enhanced proliferation, angiogenesis, invasiveness, and metastasis ---> increased metabolism --> cachexia
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Cytokine-based therapies
Modulation of immune response by purified cytokines, soluble cytokine receptors and monoclonal antibodies against cytokines
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Main applications of cytokine-based therapies
Blocking of TNF-alpha, IL-1 or IL-2 signalling - dampening of immune response in autoimmune disease (RhA, Crohn’s) or after transplantation Recombinant interferons - activation of immune reponse against cancers and c/c viral infections (Hep B & C) Recombinant haemopoietic cytokines (CSFs, IL-11) – stimulate haematopoiesis during immunodeficiency, chemotherapy or certain types of anaemia
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Risks of cytokine-based therapies
Reduces cytokine activity ---> increased risk of infection and malignancy Targeted delivery (paracrine actions) vs systemic admin V short t1/2 (mins) --> freq admin Pleiotropic action of cytokines --> unpredictable and severe s/e
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How are AV valves reinforced
Chordae tendinae attached to papillary muscles | They contract & 'brace' during ventricular systole
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Why do SL valves not need to be reinforced
Blood they're stopping is at a much lower pressure - passive back flow from arteries rather than high pressure being pushed out by ventricles
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Function of aortic sinus
Allows blood to pool after ventricular systole and from there flow into coronary sinus Stops cusps from sticking to aortic walls when fully opens
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Why is the LV wall thicker than the RV wall
LV has to pump blood further so generates greater force in systole
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Blood flow over cusps in bicuspid valve
Blood flows over both in atrial and ventricular systole | Clinical relevance - more likely to wear down than other valves
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Cusps of pulmonary valve
Anterior Left Right
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Cusps of aortic valve
Left (coronary) Right (coronary) Posterior (non-coronary)
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Cusps of mitral valve
Anterior | Posterior
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Cusps of tricuspid valve
Anterior Posterior Septal
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Function of moderator bands
Conduct impulse from Bundle of His to base of anterior papillary muscle Ensures impulse reaches papillary muscle at same time as apex of heart Allows papillary muscle to contract, 'bracing' AV valves in advance of ventricular systole
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Starting point of ventricular contraction
Apex of heart
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Clinical significance of moderator bands
Assist in stopping the valves everting, preventing back flow of blood into atrium during systole
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Why is jugular distension and RV heave seen in MS
MS decreases blood flow into LV | As LA pressure increases, flow is decreased in pulmonary vessels so RV distends and JVP rises
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Why is cardiomegaly a complication of MS
Heart attempting to decrease pressure
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Why is blood clot formation a complication of MS
Blood stuck behind stenotic cusp can clot
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What is fossa ovale an embryological remnant of
Foramen ovale
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What is the right auricle an embryological remnant of
Primitive atrium
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What is crista terminalis an embryological remnant of
Junction between sinus venosus and auricle
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What is Ligamentum venosum an embryological remnant of
Ductus venosum
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What is the smooth wall of atria an embryological remnant of
Sinus venosus
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What is Ligamentum arteriosum an embryological remnant of
Ductus arteriosum
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Which foetal structure acts as a shunt between pulmonary artery and aorta
Ductus arteriousm
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Which foetal structure acts as a shunt allowing blood to bypass liver
Ductus venosum
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Which foetal structures act as precursor of atrium
Junction between sinus venous and auricle Sinus venosus Primitive atrium
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Which foetal structure acts as a shunt between L and R atria
Foramen ovale
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How do oxygenated blood bypass the foetal lungs
Foramen ovale acts as shunt, thereby bypassing pulmonary circulation Ductus arteriosus diverts blood from pulmonary trunk to arch of aorta, thus bypassing lungs
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Main processes occurring to facilitate change from foetal to postnatal circulation
Closure of umbilical arteries Closure of umbilical veins & ductus venous - blood is now passing through liver Closure of ductus arteriosus Closure of foramen ovale
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Key factor in closure and fusion of septum premium and septum secundum
A relative increase within LA forces septum primum against the septum secundum associated with the first breath
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Cardioversion vs defibrillation
Cardioversion - one or more SMALL electrical shocks to restore rhythm Defibrillation - one or more LARGE electrical shocks to restore rhythm
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Treatment of fast AF - acute px
Go trough ABCDE | Cardiovert electrically
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What can cause sinus bradycardia
``` Hypothermia Hypothyroidism Vagal stimulation Drugs (e.g BB) Raised ICP MI ```
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Infections causing sinus bradycardia
Legionnaires disease Typhoid fever Lyme disease
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Rhythm abnormalities seen in cardiac arrest
Pulseless VT VF PEA Asystole
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PEA
Pulseless electrical activity | Organised electrical activity on ECG w/ no pulse or demonstrable BP
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Reversible causes of cardiac arrest
4 H'S & 4 T's Hypokalaemia Hypothermia Hypovolaemia Hypoxia Tamponade Tension pneumothorax Toxins Thromboembolism
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What risk increases when the QT interval > 500ms
Ventricular arrythmias
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When do we see absent A wave in JVP
AF
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When do we see a canon wave in JVP
Heart block
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Xanthopsia
Yellow vision | Can be caused by digoxin poisoning
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Which drugs reduce clearance of digoxin
CCBs and NSAIDs
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Inotropy
Looks at drug effect on cardiac contractility
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Chronotropy
Looks at drugs effect on HR
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What metabolic disturbance can hypothyroidism cause
Hyperkalaemia
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What type of heart block can an inferior MI cause
3rd degree Can also be caused by combo of rate-limiting CCBs and BBs
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What can sudden cardiac death in the young be caused by
VT | HOCM
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Why can you not take verapamil or diltiazem with BB
Rate-limiting CCBs and BBs both reduce contractility and are -vely inotropic Will cause slow conduction at AVN too much
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Inotropic vs chronotropic
+vely inotropic - increases contractility | +ve chronotropic - increases HR
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MOA of atropine
Vagus nerve inhibitor so increases HR
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Mx of sick sinus syndrome
BB DOACs Pacemaker
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Features of haemodynamic instability
HF IHD Shock Syncope Abnormal BP, HR etc
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How can an overdose of BB or CCBs be reversed
IV glucagon
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Synchronised vs unsynchronised shocks
Synchronised happens at certain point in cardiac cycle for haemodynamically compromised pts Unsynchronised is used when contraction is random - defibrillator
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Digoxin effects on ECG
Widespread down sloping ST segment T wave inversion Flattened and shortened QT interval Prominent U waves

MBBS - Year 2 (20 decks)

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