Week 2 CVS Flashcards
1
Q
Define atherosclerosis
A
Formation of focal elevated leisons (in intima of large and medium sized arteries)
2
Q
atheromas
A
In coronary arteries atheromatous plaques narrow lumen leading to ischaemia
Can have serious consequences due to myocardial ischaemia
Complicted by thromboembolism
3
Q
Ateriosclerosis
A
- Not Atheromatous
- Smooth msucle hypertrophy, apparand reduplication of internal elastic laminae, intimal fibrosis decreases vessel diameter
- Contributes to high frequency of cardiac, cerebral, colonic and renal ischaemia in the elderly.
- Clinical effects most apparent when CVS further stressed by haemorrhage, minor sugery, infection or shock
4
Q
What are the 4 different developmental stages of an atheroma?
A
Fatty Streak
Early atheromatous plaque
Fully developed atheromatous plaque
Complicated atheroma
5
Q
Describe a fatty streak atheroma
A
- Earliest significant leisons
- Found in young children
- Yellow linear elevation of intimal lining
- Comprises masses of lipid-laden macrophages
- No clinical significance
- May disappear
6
Q
Describe early atheromatous plaques
A
- Young adults onwards
- Smooth yellow patches in intima
- Lipid laden macrophages
- Progress to established plaques
7
Q
Describe fully developed atheromatous plaques
A
- Central lipid core with fibrous tissue cap, covered by arterial endothelium
- Collagens (produced by smooth muscle cells) in cap provide structural strength
- Inflammatory cells (macrophages, T-Lymphocytes, mast cells) reside in fibrous cap: recruited from arterial endothelium
- Central lipid core rich in cellular lipids/debris derived from macrophages (died in plaque)
- Soft highly thrombogenic, often rim of ‘foamy’ macrophages [foamy due to uptake of oxidised lipoproteins via specialised membrane bound scavenger receptor]
- Dystrophic calcification extensive, occurs in late plaque development [marker for atherosclerosis in angiograms/CT]
- Forms at arterial branching points/bifurcations (turbulent flow)
- Late stage plaques: Confluent, cover large areas
8
Q
Describe a complicated atheroma
A
- Features of established atheromatous plaque (lipid-rich core, fibrous cap) plus
- Haemorrhage into plaque (calcification)
- Plaque rupture/fissuring
- Thrombosis
9
Q
What are the signs of major hyperlipidaemia
A
- Familial/primary vs acquired secondary
- Biochemical evidence: LDL, HDL, total cholesterol, triglycerides
- Premature corneal arcus
- Tendon xanthomata (knuckles, achilles)
- Xanthelasmata
10
Q
Describe the development of atheromatous plaques
A
Two step process:
- Injury to endothelial lining of artery
- Chronic inflammation and healing response of vascular wall to agent causing injury
- Chronic/episodic exposure of arterial wall to these processes -> formation of atheromatous plaques
11
Q
Describe the pathogenesis of atherosclerosis
A
- Endothelial injury and dysfunction
- Accumulation of lipoproteins (LDL) in vessel wall
- Monocyte adhesion to endothelium → migration into intima and transformation to foamy macrophages
- Platelet adhesion
- Factor release from activated platelets, macrophages → smooth muscle cell recruitment
- Smooth muscle cell proliferation, extracellular matrix production and T-cell recruitment
- Lipid accumulation (extracellular and in foamy macrophages)
12
Q
What are the 2 most common causes of endothelial injury?
A
Haemodynamic disturbances (turbulent flow) Hypercholesterolaemia
13
Q
Describe Describe how hypercholesterolaemia can cause injury to the endothelium
A
- Chronic hypercholesterolaemia can directly impair endothelial cell function by increasing local production of reactive oxygen species
- Lipoproteins aggregate in intima and are modified by free radicals produced by inflammatory cells → modified LDL accumulated by macrophages but not completely degraded → foamy macrophages → toxic to endothelial cells plus release of growth factors, cytokines
14
Q
describe how endothelial cells are functionally altered in atherosclerosis
A
- enhanced expression of cell adhesion molecules (ICAM-1, E selectin)
- High permeability for LDL
- Increased thrombogenicity
- Inflammatory cells, lipids -> intimal layer -> plaques
15
Q
Describe advanced plaque formation
A
- Large numbers macrophages, T-Lymphocytes
- Lipid-laden macrophages die through apoptosis -> Lipid into lipid core
- Response to injury = chronic inflammation process
16
Q
What are the consequences of atheroma
A
Many plaques form over lifetime, many clinically unnoticed
Acute changes in plauqes (complicated atheroma) can have serious consequences
17
Q
What does stenosis of 50-75% of vessel lumen lead to?
A
Critical reduction of blood flow in distal arterial bed -> reversible tissue ischaemia
18
Q
What can very severe stenosis lead to?
A
Ischaemia - pain at rest
[unstable angina, eg ileal popliteal artery stenosis -> intermittent claudication]
19
Q
What can longstanding tissue ischaemia lead to?
A
Atrophy of affected organ eg aterhosclerotic renal artery stenosis -> renal atrophy
20
Q
What does rupture exposing collagen, lipid and debris to the blood stream do?
A
these are all highly thrombogenic plaque contents. Leads to the actiation of coagulation cascade and thrombotic occlusion in very short time
21
Q
What does total occlusion of an artery lead to?
A
Irreversible iscahemia
22
Q
embolisation of the distal arterial bed
A
- Detachment of small thrombus fragments from thrombosed atheromatous arteries -> embolise distal to ruptured plaque
- Embolic occlusion of small vessels -> small infarcts in organs
23
Q
Ruptured atheromatous abdominal aortic aneurysm
A
- Media beneath atheromatous plaques gradually wakened (lipid-related infammatory activity in plaque)
- This leads to gradual dilation of vessle
- Slow but progessive, seen in elderly, often asymptomatic
- Sudden rupture -> massive retroperitoneal haemorrhage
24
Q
What diameter does an aneurism become at risk of rupture?
A
5cm
25
What is a mural thrombuis
Emboli to legs
26
Describe vulnerable atheromatous plaques
- Thin fibrous caps, large lipid core, prominent inflammation
- Proncounced inflammatory activity -> degradation, weakening fo plaque -? increased risk of plaque rupture
- Secretion of proteolytic enzymes, cytokines and reactive oxygen species by plaque inflammatory cells
- Often large fibrocalcific component, little inflammation
27
What is blood flow?
Amount of blood moved per unit time
28
What is stasis?
Stagnation of blood flow
29
What is turbulence?
Forceful, unpredictable flow
30
What do defects in blood flow cause?
- Thromboembolism
- Atheroma
- Hyperviscosity
- Spasm
- External compression
- Vasculitis
- Vascular steal
31
What is virchows triad?
- Changes in the blood vessel wall
- Changges in the blood constituents
- changes in the pattern of blood flow
32
Describe the pathogenesis of thrombosis
1. Atheromatous CA
2. Turbulent blood flow
3. Loss of intimal cells, denuded plaque
4. Collagen exposed to which platelets adhere
5. Fibrin meshwork forms - RBC's trapped
6. Alternating bands: Lines of Zahn
7. Further turbulence and platelet deposition
8. Propagation
9. CONSEQUENCES
33
What do the consequences of thrombosis depend on?
Site
Extend
colalteral circ.
Common clinical scenariosL DVT, Ischaemia limb, MI
34
What is an embolus
Detached intravascular soil, liquid or gaseous mass
35
Where do venous thromboembolus originate from?
Originate from deep venous thromboses (lower limbs)
36
What is the most common thromboembolic disease
Venous thromboembolus
37
What are the types of embolus?
```
Fat
Gas
Air
Tumour
Trophoblast
Septic material
Amniotic fluid embolism
Bone marrow
Foreign bodies
```
38
What is rheumatic fever
- Disease of disordered immunity
39
Where are some inflammatory changes caused by rheumatic fever
- Heart
- Joints
- Sometimes neurological symptoms
40
What is the presentation of someone with RF
Typically present with 'flitting' (painful) polyarthritis of large joints (wrists, elbows, knees, ankles) plus skin rashes and fever
41
What may RF cause in the heart?
Pancarditis (inflammation affecting endocardium, myoicadium in acute phase; heart murmers common)
42
Describe how RF may cause damage to the heart tissue
May be combination of antibody mediated and T cell mediated reactions
43
What is an aschoff body
Focus of chronic inflammatory cells, necrosis and activated macrophages.
Seen in heart in acute rheumatic fever
44
What can pancarditis in acute RF progress to?
Chronic Rheumatic heart disease, mainly manifesting as valvular abnormalities
45
What does inflammation of the endocardium and left sided valves result in?
fibrinoid necrosis of the valve cusps/chordea tendineae over which (and long line of closure) form small vegitations
46
What is rheumatic heart disease characterised by?
Principally by deforming fibrotic valvular disease, particularly involving the mitral valve: Typically leaflet thickening commissural fusion and shortening and thickening and fusion of the chordae tendineae
47
What can RHD cause?
Mitral stenosis
Can cause mitral regurg but now most commonly due to ischaemic heart disease
Potentially still causes an aortic regurg/incompetance
48
What are the 4 types of hypoxia?
Hypoxic
Anaemic
Stagnant
Cytotoxic
49
What is anaemic hypoxia
Normal inspired O2 but blood abnormal
50
What is stagnant hypoxia?
Normal inspitred O2 but abnormal delivery
- Local: occlusion of vessel
- systemic: Shock
51
What is cytotoxic hypoxia?
Normal inspired O2 but abnormal at tissue level
52
What is the functional effect of ischaemia
Blood O2 supply fails to meet demand due to decreased supply; incrased demand or both
53
What are the 2 types of necrosis and where are they seen
Coagulative necrosis - eg heart, lung
| Colliquitive necrosis - brain
54
Describe the appearance of an infarct after less than 24 hours
No change on visual inspection
| A few hours to 12 hours post insult, able to see swollen mitochondria on electon microscopy
55
Describe the appearance of an infarct between 24 and 48 hours
Pale infarct seen in myocardium, spleen, kidney and solid tissue
Red infarct seen in the lung and liver
Microscopically: acute inflammation initially at edge of infarct; loss of specialised cell features
56
Describe the appearance of an infarct after approx 72 hours
Macroscopically:
pale infarct - yellow/white and red periphery
Red infarct - little change
Microscopically: Chronic inflammtion; macrophages remove debir, granulation tissue, fibrosis
57
What is the end result of an infarct?
Scar replaces area of tissue damage
| Shape depends on territory of occluded vessel
58
Describe the presentation of MI 4-12 hours after the initial occlusion
Early coagulation necrosis, oedema, haemorrhage
59
Describe the presentation of MI 12-24 hours after the initial occlusion
Ongoing coagulation necrosis,
myocytes changes
Early neutrophilic infiltrate
60
Describe the presentation of MI 1-3 days after the initial occlusion
Coagulation necrosis
Loss of nuclei and striations
Brisk neutrophilic infiltrate
61
Describe the presentation of MI 7-10 days after the initial occlusion
Well developed phagocytosis
| Granulation tissue at margins
62
Describe the presentation of MI 10-14 days after the initial occlusion
Well established granulation tissue with new blood vessels and collagen deposition
63
Describe the presentation of MI 2-8 weeks after the initial occlusion
Increased collagen deposition, decreased cellularity
64
Describe the presentation of MI >2 months after the initial occlusion
Dense collagenous scar
65
What is a transmural infarction?
When the ischaemic necrosis affects the full thickness of the myocardium
66
What is a subendocardial infarction?
When the ischaemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the chart
67
Describe the histological features of a transmural and subendocardial infarction
Histological features are the same - granulation tissue stage followed by fibrosis - in subendocardial infarct possibly slightly shortened compared to transmural infarct
68
How are acute infarcts classified?
According to whether there is elevation of the ST segment on the ECG
69
What is the classification of a myocardial infarct If there is no ST segment elevation but a significantly elevated serum troponin level
Non STEMI or an NSTEMI
70
What do NSTEMIs tend to correlate with?
Subendocardial infarctions
71
What is angina
A discomfort in the chest and or adjacent area associated with myocardial ischaemia but without myocardial necrosis
72
What is the most common cause of angina?
Obstructive coronary atheroma
73
What features make an angina diagnosis less likely
Sharp/Stabbing pain; pleuritic or pericardial
Associated with body movements or respiration
Very localised: pinpoint site
Superficial with/or without tenderness
No pattern to pain, particularly if often occuring at rest
Begins some time AFTER exercise
Lasting for hours
74
Describe a 1 on the scale of severity of the Canadian classification of angina severity (CCS)
Ordinary physical acticity does not cause angina symptoms, only on significant exertion
75
Describe a 2 on the scale of severity of the Canadian classification of angina severity (CCS)
Slight limitation of ordinary activity, symptoms on walking 2 blocks or >1 flight of stairs
76
Describe a 3 on the scale of severity of the canadian classification of angina severity (CCS)
Marked limitation, symptoms on walking only 1-2 blocks or 1 flight of stairs
77
Describe a 4 on the scale of severity of the canadian classification of angina severity (CCS)
Symptoms on any activity, getting washed/dressed causes symptoms
78
Describe the possible presentation of angina
```
Obesity
Xanthalasma and corneal arcus (hypercholesterolaemia)
Hypertension
Abdominal aortic aneurism
Arterial bruits
Abscent or reduced peripheral pulses
Diabetic retinopathy
Hypertesive retinopathy
Fundoscopy
```
79
What are the signs of exacerbating or associated conditions
Pallor anaemia
Tachycardia: Tremor, hyper-reflexia of hyperthyroidism
Ejection systolic murmur of mitral regurg
Signs of HF such as basal crackles, elevated JVP, peripheral oedma
80
What are the investigations for angina
Bloods
CXR
ECG
ETT
81
What is a diagnostic test for angina
ETT
82
What is seen in an ETT for a positive diagnositc test for angina
commonly ST segment depression is seen
| -'ve ETT doesnt exclude significant coronary atheroma but if negative at high workload overall prognosis is good
83
Describe myocardial perfusion imaging
Superior to ETT in detection of CAD, localisation of ischaemia
Expensive, invovled radioactivity; depending on availability used where ETT no possible/equivacol
Either exercise or pharmacological stress: Adenosine, dipyridamole or dobutamine
Radionulide tracer injected at peak stress on one occasion obtained and at rest on another
Normal myocardium takes up tracer
84
Describe tracer seen at rest but not after stress
= Ischaemia
85
Describe tracer seen seen neither rest or after stress
= Infarction
86
What are the indications invasive angiography
Early or strongly positive ETT (suggests multi-vessel ds)
angina refractory to medical therapy
Diagnosis not clear after non-invasive tests
Young cardiac patients due to work/life effects
Occupation to lifestyle with risk
87
Where are arterial cannulas inserted into
Femoral or radial artery
88
Describe the treatment of angina for influencing disease progression
Statins - consider if total cholesterol >3.5 mmol/L
ACEI - if increased CV risk and atheroma
Aspirin 75mg or clipidrogrel if intolerant of aspirin
89
What is the effect of statins in angina
Reduce LDL-Cholesterol deposition in atheroma dn aslo stabilise atheroma reducing plaque rupture and ACS
90
What is the effect of ACEI in angina
Stabilise endothelium and also reduce plaque rupture
91
What is the effect of aspirin in angina
May not directly affect plaque but does protect endothelium and reduces platelet activation/aggregation
92
What are the possible treatments for relief of anginal symptoms
```
B blockers
Ca Channel Blockers
iK channel blockers
Ca Channel blcokers
Nitrates
K channel blockers
```
93
What is the effect of B blockers in angina
Achieve resint HR < 60bpm
| - Reduced myocardial work and have anti-arrhythmic effects
94
What is the effect of Ca channel blockers in angina
Achieve resting hr <60bpm
| - central acting eg diltiazem/verapamil if beta blockers contraindicated
95
What is the effect of k channel blockers in angina
of k channel blockers in angina
| Ivabridine is a newer medication which reduced sinus node rate
96
What is the effect of ntirates in angina
Produce vasodilation
| - Used as short or prolonged acting tablets, patches or as rapidly actin sublingual GTN spray for immediate use
97
Does stenting approve prognosis
NOPE
98
What is the effect of CABG surgery
Good lasting benefit - 80% symptom free 5 years later
99
Describe the patients who derive prognostic benefit from CABG
70% of left main stem artery
Significant proximal three vessel coronary artery disease
Two vessel coronary artery disease that includes significant stenosis proximal left anterior descending CA and who have ejection fraction <50%
Patients must continue disease modifying medication and predictable dterioration in vein grafts after 10 years
100
Define hypertension
Is that bp at which the benefits of treatment with antihypertensive agnets in reduceing cardiovascular, cerebrovascular and peripheral vascular disease outwight the risks of treatmen
101
Describe Stage 1 hypertension
Clinic 140/90 or higher
| ABPM daytime average 135/85
102
Describe stage 2 hypertension
Clinic 160/100 or higher
| ABPM daytime average 150/95
103
Describe Stage 3 hypertension
Systolic >180
| Diastolic >110
104
When does bp decrease naturally
During the night
105
What are the methods of measuring kidney function
Renal ultrasound
EGFR
Proteinuria = presence of abnormal proteins in urine which may indicate change to the kidneys
106
What is the treatment for reducing LV mass?
ACEI or ARB
107
What is the target BP
135/80-85
108
When do you commence with hypertension treatment?
When 10% chance of CVD within 10 years
| [treatment reduces MI by 16-30% and cerebrovascular disease 40-50%]
109
Describe the approach to medication for hypertension
Stepped approach for treatment of hypertensives
| Use low dose of several drugs as this minimises adverse effects and maximises patient compiance
110
Describe renin concentrations over the ages
Young people = high renin
| Old people = low renin
111
What antihypertensive drugs would you prescribe in a patiennt <55
ACEI/ARB
112
What antihypertensive drugs would you prescribe in a patiennt >55
CCB/Thiazide type diuretic
113
Are ACEI teratogenic?
YEP - they change the babies, dont change the babies man
114
Whwn would you start treating patients >80-y/o
```
ABPM 85/135
Established CVD
Diabetes
10 year risk of CVD 20% or greateer
Evidence of target organ damage
Renal disease
```
115
Anithypertensive drugs are offered to anyone after they are on what stage hypertension?
Stage 2
116
Describe the first step of hypertensive treatment
Prescribe a CCB or thiazide type diuretic
| [in patients under 55 offere CCB or ACEI]
117
Describe the second step of hypertensive treatment
Add thiazide type diretic such as indapamide to CCB or ACEI/ARB
118
Describe the third step of hypertensive treatment
Add CCB, ACEI and diuretic together
119
Describe the third step of hypertensive treatment
- Consider compliance issues
- Consider higher-dose thiazide-like diuretic treatment if the blood K level is higher than 4.5 mmol/l
- Consider further diuretic therapy with low dose spironolactone (25 mg once daily) if the blood K level is <4.5 mmol/l
- Caution in people with a reduced EGFR because they have an increased risk of hyperkalaemia
120
Describe the mechanism of thiazide type diuretics
Increase Na exretion + urine volume.
Reduction in blood volume
Long term: reduction in the TPR due to suble alterations in the contractile responses of vascular smooth muscle
121
Describe the mechanism of ACE inhibitors and give some examples
Rampril + perindopril
- competitively inhibits actions of angiotensin converting enzyme
- Has cough as common side effect
122
What are the ACEI contraindications?
renal artery stenosis
Renal failure
Hyperkalaemia
123
What are the relevant drug to drug interations concerning ACEI
NSAIDS - prepitate acute renal failure
K suppliments = hyperkalaemia
K sparing diruetics = Hyperkalaemia
124
What is Conns syndrome
too much aldosterone - renin levels reduced
125
Conns syndrome
Hypertension is symptom
Causes are increased size of adrenal glands where aldosterone is produced or adenoma
Uncommon causes: adrenal cancer or familial hyperaldosteronism
126
give examples of ARBS
Losartan
Valsartan
Candesartan
Irbesartin
127
What are the 2 types of CCB?
Vasodilator or rate limiting
128
Give examples of vasodilating CCBs
Amlodipine
| Felodipine
129
Give some examples of rate limitng CCBs
Verapamil
| Diltiazem
130
Describe the mechanism of CCBs
- Block L type ca Channels (voltage type)
- Selectively between vascular and cardiac L type channels
Relaxing large + small arteries -> reducing peripheral resistance
131
What are the contraindications for CCBs
Acute MI
HF
Bradycardia
132
What are the ADRS for CCBs
Flushing
headache
Ankle oedema
Indigestion and reflux oesophagitis
133
What are common side effects for CCBs
Bradycardia
| Constipation
134
hiazide type diuretics
Indapamide
Clortidladone
- Proven benifit in stokre and MI reduction
- ADRs not common but are gout and impotence
135
What are the less commonly used antihypertensive agents?
Alpha-adrenorecepor antagonists: doxozosin
Centrally acting agents: Methycdopamonoxnidne
Vasodilators: Hyralazine, monoxidil
136
What is ACS?
New onset of a collection of symptoms related to a problem with the coronary arteries
137
What do the CA supply?
Myocardial cells
138
What does ACS cause?
Myocardial ischaemia
139
What is stable angina caused by?
'Stable' Coronary leison
140
What are acute coronary syndromes caused by?
Unstable coronary leison
141
How do you diagnose ACS?
Detection of cardiac cell death (troponin) AND: symptoms of ischaemia
- New ECG changes
- Evidence of coronary problem on coronary angiogram or autopsy
- Evidence of new cardiac damage on another test
142
What is a type 1 MI?
Spontaneous MI associated with iscahemia and due to a primary coronary event such as plaque erosion, rupture, fissuring or dissection
143
What is a type 2 MI?
Due to imbalance in suppply and demand of oxygen. Result of ischaemia but not ischaemia from thrombosis of CA
144
What is a type 3 MI?
Sudden Cardiac death, including cardiac arrest, with symptoms of ischaemia, accompanied by new ST elevation of LBBB. Verified coronary thrombus by angiography or autopsy but death occurring before blood samples could be obtained or before biomarkers appear in the blood
145
What is a type 4a MI?
MI associated with PCI. PCI related crease of biomarkers greater than X 99th percentile of the upper reference limit is by convention defined as MI
146
What is a type 4b MI?
MI assocaited with verified statment stent thrombosis via angiography or autopsy
147
What is a type 5 MI?
MI Assocaiteed with CABG, >5x99th percentile upper reference limit plus new Q waves or LBB or imaging of new loss
148
What does LBBB stand for?
Left bundle branch block
[ A cardiac conduction abnormality seen on the ECG. In this condition, activation of the left V of the heart is delayed, which causes the LV to contract later than the RV]
149
What type of MI would be a vasospasm or endothelial dysfunction be?
MI type 2
150
What type of MI would be a fixed atherosclerosis and supply-demand imbalance by?
MI type 2
151
What type of MI would a plaque rupture with a thrombus be?
MI type 1
152
What type of MI would be a supply demand imbalance alone?
MI type 2
153
Describe the typical presentation of a patient with STEMI
- Ischaemic sounding heart pain
- May radiate to neck/arm
- Often deny it is a 'pain', more of a 'discomfort, weight or tightening'
- May be associated with nausea, sweating and breathlesness
154
What does the initial ECG of a person with a complete coronary occlusion show?
ST elevation
155
What does the ECG at 3 days show after a complete coronary occlusion
Q waves
156
What does the initial ECG of a partial coronary occlusion show?
ST depression
T wave inversion
May still be normal
157
What does the ECG of a partial coronary occlusion at 3 days show?
No Q waves
158
What may show/not be shown on an ECG of a posterior MI
As the posterior wall supplied by the let circumflex artery may not see any ST elevation anywhere, even if LCx is completley blocked
159
If a posterior MI is suspected what investigation is reccomended?
Put ECG leads on back of chest - will see opposite changes in leads however
160
What is a mechanical reperfusion therapy?
PCI
161
What is a pharmacological reperfusion therapy?
Thrombolysis
162
When would you not give thrombolysis
- If recent stroke, or ever had a previous intercranial bleed
- Caution if had recent surgery, on warfarin, or has severe hypertension
163
How do you decide whether to treat with thrombolysis or cath lab
If you can get to cath lab within 2 hours, then dont give thrombolysis
164
What are the investigations for a NSTEMI
```
Serial ECG's
- As to not miss an evolving STEMI or a posterior STEMI
Blood tests
- Troponin
- Cholesterol levels
```
165
What are the possible treatment options for an ACS with no ST elevation
```
GTN
Opiates
Antithrombotic drugs with a P2Y12 antagonists
Anticoagulant drugs
B blockers
Statins
ACEI
```
166
What are the effects of GTN?
Vasodilator - opens up CA - wont help if artery is completely blocked
167
How can GTN be given?
Sub-lingual or as IV
168
What are the effects of morphine
Help relieve anxiety
| Helps venodilate which may have haemodynamic effects
169
Describe the procedure of dual anti-platelet therapy for an NSTEMI
Aspirin plus one of the P2y12 receptor antagonists:
- Clopidogrel
- Tricagrelor
- Prasugrel
170
Describe the dosing of:
- Aspirin
- Clopidogrel
- Tricagrelor
- Prasugrel
Aspirin: 300mg loading dose, then 75mg
Clopidogrel: 300mg loading dose, then 75mg
Tricagrelor: 180mg loading dose, then 90mg
Prasugrel: 60mg loading dose, then 10mg
171
What procedure is given to those with NSTEMI unless frail/elderly?
Coronary angiogram
172
What is the management for someone with an NSTEMI
- Keep attached to cardiac monitor for first 24-48 hours
- Listen to new murmers and signs of heart failure every day
- Start 'secondary prevention' medication
- Do an Echo
173
What 2 conditions would be classes as ACS
MI (STEMI or NSTEMI)
| Unstable angina pectoralis (UAP)
174
What 2 conditions would be classes as stable coronary heart disease
```
Angina pectoralis (stable)
Silent ischaemia
```
175
List 8 classes of drugs used to treat stable CAD
```
B blockers
CCBs
Ivabradine
Nitrates
K Channel activators
Na current inhibitor
Aspirin/clopidogrel/ticagrelor
Cholesterol lowering agents
```
176
What is the main action of B blockers
Lower HR
Lower force of contraction
Lower systolic wall tension
177
Name 2 examples of B blockers
Bisoprolol
| Atenolol
178
Describe how B-blockers function?
Antagonists of B1 and B2 receptors
| i.e block sympathetic system
179
Name 2 rate limiting CCBs
Diltiazem
| Verapamil
180
Name a vasodilating CCB
Amlodipin
181
Describe how CCBs function
Prevent Ca influx into myocytes + smooth muscle lining of arteries/arterioles
Via blocking L-type Ca2 channels
182
What is important to remember when prescribing Nifedipine?
Never use Nifedipine immediate release (could cause MI/stroke) --> use delayed/sustained release
183
What is the main action of nitrovasodilators/ntirates
Vasodilation (arterioles + peripheral)
184
Name 3 vasodilators
GTN
Isosorbide mononitrate
Isosorbide dinitrate
185
Describe how nitrovasodilators function
- Relax almost all smoth muscle via NO release
- This stimulates cGMP production -> smooth muscle relaxation
- Decreases preload and afterload
- Thus decreases myocardial O2 consumption
186
What is the main action of potassium channel activators?
Coronary vasodilator properties
187
Name a pottasium channel activator
Nicorandil
188
Describe how potassium channel activators function
Activates ATP sensitive K channels which allow K entry into myoccytes
This inhibits Ca influx
This then induces relaxation of smooth muscle + vasodilatiom
189
What is the main action of a Sinus node inhibitor?
Decreases HR and therefore myocardial demand
190
Name a sinus node inhibitor
Ivabradine
191
When should ivabradine be used?
For symptomatic treatment of chroncic stable angina in adults with normal sinus rhythm + HR >70bpm
192
What is the main action of late Na current inhibitors
Decreases heart wall tension causing decreased O2 requirement
193
Name a late Na current inhibitor
Ranolazine
194
Describe how late Na current inhibitors function
- Inhibits presistent or late inwardd Na current in heart muscle
- Leads to decrease in intracellular Ca levels
Leads to reduced heart wall tension
195
What does NICE reccomend as second line drugs for angina
Ranolazine
196
What medications are used for anti-platelet therapy?
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Aspirin
P2Y12 inhibitors (eg clopidogrel, icagrelor, prasugrel)
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197
Describe how anti-platlet agents function
Prevent formation of pletlet aggregates which are important in the pathogenesis of angina
198
how does aspirin inhibit platelet aggregation?
Is a potent inhibitor of platelet thromboxane production (thromboxane stimulates platelet aggregation)
199
How do P2Y12 inhibitors work?
Block pletlet P2Y receptor, which plays a key role in platelet activation + amplification of arterial thrombus formation
200
When should you use dual anti-platlet therapy
In patients with high/moderate risk of ischaemic evetns who do not have a high bleeding risk
201
What is the main action of cholesterol lowering agents?
Lower LDL cholesterol level
202
Name 2 cholesterol lowering agents
Atorvastatin
| Simvastitin
203
How can you identify a cholesterol lowering agent from the name
End in statin (as they are statins)
204
Describe how cholesterol lowering agents
Are HMG CoA reductase inhibitors
