CV Flashcards
1
Q
Give and explain the risk factors for atherosclerosis?
A
Risk factors for atherosclerosis
- Age - increased time to develop
- Smoking - damage to endothelium
- Diabetes - changes in plaque composition
- Obesity - increased inflammatory cytokines
- Family history
- Increased BP - turbulance
- Increased choloesterol - LDL
2
Q
What does an atherosclerotic plaque contain?
A
Lipids, necrotic core, connective tissue with a fibrous cap
3
Q
When does atherosclerosis occur?
A
Atherosclerosis occurs when there is an injury to the endothelium which leads to endothelium dysfunction.
Injury - cytokines are released - leukocytes are attracted and invade and accumulate in the vessel
4
Q
Give the 4 main stages of the progression of atherosclerosis
A
- Fatty streaks - occur in children
- Intermediate lesion - ‘foam cells, SM cells, T cells, platelets
- Fibrous plaque/advanced lesion - covered by a dense fibrous plaque or collagen and elastin overlying the lipid core with necrotic debris
- Plaque rupture - plaque constantly being resorbed & redeposited. May rupture if balance sways towards inflammatory conditions which makes the cap weaker.
5
Q
Explain how statins work to reduce your cholesterol
A
Statins inhibit HMG-CoA reductase, the enzyme that controls enzyme production in the liver.
Reduced cholesterol synthesis - reduced intracellular cholesterol in hepatocytes -
= Hepatocytes increased the production of LDL receptors
= Increased LDL receptor mediated uptake in the liver (& VLDL)
= Reduced serum conc of LDL
6
Q
What are plaques of clinical relevance?
A
Problems:
Rupture - thrombosis can grow leading too…
Occlusion = Ishaemia
7
Q
Give the 4 clinical manifestations of atherosclerosis
A
- Embolism
- Stenosis (narrowing)
- Occlusion
- Aneuyrism (due to weakend walls)
8
Q
What is angina caused by?
A
Angina is chest pain due to a mismatch of O2 demand and supply
9
Q
Give the exacerbating factors that lead to a reduced supply for angina
A
Reduced supply (blood/O2)
Anaemia
Hypoxemia
Polythemia
Hypothermia
Hypovolaemia
Hypervolaemia
10
Q
Give the exacerbating factors that lead to an increased demand that cause angina
A
Increased demand
Hypertension (high BP)
Tachyarrhythmia (high HR)
Valvular HD
Hyperthyroidism
Hypertrophic cardiomyopathy
11
Q
At which precentage occlusion does ischaemia occur?
a) 5%
b) 25%
c) 55%
d) 75%
A
Ischaemia occurs at about 75% occlusion
12
Q
Explain how as diseased artery can cause SOB on exertion?
A
Stenosed artery cannot relax to reduce resistance
P=QR
High amounts of P needed to increase Q(flow)
Q cannot increase to meet the higher demands
Not enough O2 = drive to breath = SOB
13
Q
What is crescendo angina?
A
Crescendo angina occurs at rest or after minimal exertion
14
Q
Describe the type of pain that is typical of angina
A
Angina pain
= Fist to chest / band around chest
= Heavy / severe
15
Q
What are the cardiac symptoms associated with angina?
A
Chest pain, breathlessness, fluid retention, palpitation, syncope/pre-syncope
16
Q
Which of the following is not included in a typical history for angina
a) Radiates to the shoulder/face
b) Doesn’t stop after rest
c) Starts on exertion
d) Occurs in the middle of the chest
A
b) Doesn’t stop after rest
Typical history:
Onset = exertion,
Position = middle of chest
Quality = tight & heavy
Radiation = arms/shoulders/jaw
Relieving = resting
(OPQRST)
17
Q
What could be a differential diagnosis for chest pain and what are the differences?
A
PE - breathlessness, blood in cough, swollen legs
Pericarditis/myocarditis - pain like a knife
Disection of the aorta - tearing pain going around to the back
Gastro-esophageal reflux - burning and after a meal
MS - take history
Chest infection/pleurisy
18
Q
On exercise testing, what would the ECG show if it was angina?
A
ST depression
19
Q
Name the drugs which are suitable to treat angina
A
Aspirin
B-Blockers
Nitrates - GTN & LA
Statins
ACE inhibitors
Ca2+ channel blockers
K+ channel openers
Drugs that stop the plaque growing (antiplatelet) and stop the heart working as hard)
20
Q
Explain how beta blockers work to stop angina
A
B1 blockers:
- ve choronotrophic = reduce HR
- ve inotrophic = reduce LV contraction
= Less work & less O2 demand
B2 blockers: peripheral vasoconstriction & broncospasm
21
Q
Give 2 examples of beta blockers
A
Propranol = non-selective
Bisopranol = B1 selective
22
Q
How do nitrate drugs work to reduce angina?
A
Nitrates GTN & LA
LA - metabolised in liver to NO3
NO3 = endothelial relaxant
= vasodilation of veins and large arteries
= reduced pre-load & work the heart has to do
23
Q
What are the 4 features of aspirin which are desirable when using it to treat angina?
A
Anti-platelet - decrease platelet aggregation
Antipyretic
Anti-inflammatory
Analgesic
24
Q
What does hypertension increase your risk of?
A
Hypertension increases your risk of:
Stroke
MI
HF
Chronic renal disease (CRD)
Atrial fibrillation
25
Define stage 1 and 2 hypertension
Stage 1:
Clinical BP = 140/90mmHg AMBP = 135/80 mmHg
Stage 2:
Clinical BP = 160/100mmHg AMBP = 150/95mmHg
26
When do you treat stage 1 and stage 2 hypertension with antihypertensives?
Hypertension
Stage 1: \<80 with one of the following -
Organ damage, renal disease, cardiac problems, diabetes & 10 year CV risk of 20%/\<
Stage 2: treat at any age
27
List the drug types which can be used to treat hypertension
Drugs that can be used to treat hypertension:
## Footnote
ACE-I
Beta-blockers
CCB
A1- blockers
ARD
Aldosterone antagonists
Renin inhibitors
Centrally acting
28
Which of the following is an ACE-I that could be used to treat hypertension
## Footnote
a) Enalapril
b) Valsartan
c) Verapamil
d) Furosemide
These are all drugs which can be used to treat hypertension but there is only one ACE-I
**Enalapril = ACE-I**
Valsartan = ARB
Verapamil = Phenylalkylamine CCB
Furosemide = Diuretic
29
Explain the ways that angiotensin II can be used to prevent hypertension
Angiotensin II normally causes:
1. Aldosterone release - increases Na+ and H20 retention leading to increased blood volume
2. Peripheral resistance (increased TPR)
3. Vascular growth - hyperplasia and hypertrophy of SM cells
Less angiotensin II = Reduced blood volume + reduced peripheral resistance
30
What are the main AE from ACE-I
ACE-I AE:
ACE-I main effect significantly reduces the amount of AII
Due to reduced angiotensin II = hypotension, actute renal failure, hyperkalaemia, teratogenic effects in pregnancy.
AII inactivates chemical medicators - if lower there is an increase in kinins
AE due to kinin increase = cough, rash, anaphalactoid reactions
31
Which of the following are not treated with calcium channel blockers?
## Footnote
a) Hypertension
b) Isheamic heart disease
c) HF
d) Arrhythmia
CCB are used to treat hypertension, IHD & arrhythmias
They are not used to treat HF - verapamil can make it worse and increase the systolic dysfunction
32
What are the main AE of calcium channel blockers?
AE of CCB:
Due to periferal vasodilation = headaches, flushing, oedema, palpations
Due to -ve choronotrophic effects = bradycardia, AV block
33
What are the main AE from beta blockers?
AE due to BB:
Bradycardia, tiredness/nightmares, erectile dysfunction, cold hands and feet
Severe broncospasms in people with asthma + heart block
34
What are the main AE due to statins
AE due to statins:
Muscle ache and abdominal discomfort
35
Give the possible causes for acute coronary syndrome
ACS
## Footnote
Rupture of atherosclerotic plaque + thrombosis
Coronary vasospasm
Disection of the coronary artery
36
What is the marker for cardiac muscle injury and give examples when this is raised?
**Troponin** = selective marker for cardiac tissue injury
## Footnote
Raised in MI... + PE, HF, myocarditis & arrhythmias
37
a) What is the role of P2Y12 inhibitors?
b) Give examples of P2Y12 inhibitors with a brief explanation of them
c) Give the main AE for P2Y12 inhibitors
a) P2Y12 inhibitors are type of antiplatelet drug which are used to reduce platelet activation amplication
b) Clopidogrel, prasugrel + triagrelor
c) Bleeds, rash & GI problems
Clopidogrel = prodrug that is activated by CYP450 enzymes in the liver. 1/3rd of people have reduced activity of these enzymes.
Interactions between genetics, diseases - diabtetes/kidneys, drug-drug - omeprazole (inhibit CYP450 3A enzymes)
Prasugrel = pro drug with only one step so is more efficient that clopidogrel - increased risk of major bleeds
Ticagrelor - inhibits adenosine uptake - more adenosine in circulation = vasodilation, antiplatelet, cardioprotection & immunomodulation
38
A patients has just been in a car accident and has now got very cold, pale and sweaty skin. On checking their pulse you notice that it is rapid and weak with a slow capillary refil. They have become very confused and weak.
What could this be?
**Circulatory shock**
A patients has just been in a car accident and has now got very **cold, pale and sweaty skin**. On checking their **pulse** you notice that it is **rapid and weak** with a **slow capillary refil**. They have become very **confused and weak**.
CV system is unable to provide adequate substrate for aerobic respiration
39
Give the 3 main reasons that circulatory shock may occur with examples of each
Circulatory shock
## Footnote
(Inadequate CO)
**Hypovolaemic -** bleeding (trauma), Fluid loss (burns)
**Cardiogenic -** ACS, arrhythmias, aortic disection, acute valvular failure
(Peripheral circulatory failure)
**Distributive -** sepsis, anaphalaxis, neurogenic ( SC injury, epidural, spinal anaesthia), endocrine failure (Addison's), drugs (anaesthetics, antihypertensives & cyanide)
40
What are the following describing?
a) 15% blood loss - \<100 bpm - normal BP - RR 15-25
b) 15-30% blood loss - \>100 bpm - normal BP - RR 30-40 - decreased urine
c) 30-40% blood loss - \>120 bpm - decreased BP - RR \>30-40 - decreased urine (5-15ml/hr) & confused mental state
Classification of haemorrhagic shock 1 - 4 with increasing severity.
a) **1 =** 15% blood loss - \<100 bpm - normal BP - RR 15-25
b) **2 =** 15-30% blood loss - \>100 bpm - normal BP - RR 30-40 - decreased urine
c) **3 =** 30-40% blood loss - \>120 bpm - decreased BP - RR \>30-40 - decreased urine (5-15ml/hr) & confused mental state
Think tennis numbers - 15, 30, 40
41
How does shock result in death?
Most people die from shock a few days after the acute event due to coagulopathy, hypothermia or metabolic acidosis
42
What is the most improtant thing to do for a patient in septic shock and why?
Give **antimicrobials ASAP** - aim to decrease microbial load which in turn decreases toxic burden, inflammation, cellular dysfunction and tissue injury.
Septic shock = when sepsis is complicated by persistant hypotension unresponsive to fluid resucitation
43
Explain how haemorrhage and shock can affect the following organs?
## Footnote
a) Kindeys
b) Brain
c) Lungs
d) Heart
Explain how haemorrhage and shock can affect the following organs?
## Footnote
a) Kindeys = acute tubular necrosis
b) Brain = confusion, irritability, coma, stokes
c) Lungs = ARDS
d) Heart = MI/ishaemia
MI & stokes are common if you already have a damaged vessel
44
a) What is anaphalactic shock?
b) Give the signs and symptoms of an anaphalactic shock
Anaphalactic shock is a massive allergic reaction. Type 1, IgE mediated hypersensitivity reaction that results in a huge release of histmaine. This causes capillary leak, wheeze, cyanosis, oedema & urticaria
b) S&S = itching, sweating, diarrhoea & vomiting, erythema, urticaria, oedema. Wheeze, laryngeal obstruction, cyanosis. Tachycardia & hypotension
45
Which causes hypertrophic cardiomyopathies?
## Footnote
a) Sarcomic protein gene mutations
b) Cytoskeletal gene mutations
c) Desmosome gene mutations
d) Ion channel protein gene mutations
Hypertrophic cardiomyopathies are caused by **s****arcomic protein gene mutations**
HCM may cause angina, dyspnoea, palpitations, dizzy spells or syncope
46
Which causes dilated cardiomyopathies?
a) Sarcomic protein gene mutations
b) Cytoskeletal gene mutations
c) Desmosome gene mutations
d) Ion channel protein gene mutations
Dilated cardiomyopathies are caused by **cytoskeletal gene mutations.**
Usually present with HF symptoms
LV/RV/4 chamber dilation/dysfunction
47
Which causes arrhythmogenic cardiomyopathies?
a) Sarcomic protein gene mutations
b) Cytoskeletal gene mutations
c) Desmosome gene mutations
d) Ion channel protein gene mutations
Arrhythmiogenic cardiomyopathies are caused by **desmosome gene mutations**
(singals need to be transfered through the desmosomes)
48
Which causes inherited arrhythmia (channelopathy)?
a) Sarcomic protein gene mutations
b) Cytoskeletal gene mutations
c) Desmosome gene mutations
d) Ion channel protein gene mutations
Inherited arrhythmia (channelopathy) is causes by **ion channel protein gene mutations**
K/Na/Cl
Include long QT, short QT, brugada and CPVT
The heart is structurally normal - may present with reccurent syncope
49
What is familial hypercholesterolaemia?
Familial hypercholesterolaemia is an inherited abnormality of cholesterol metabolism - increased amounts of LDL that leads to premature coronary and vascular disease
50
Explain what a dissecting aneurysm is.
A dissecting aneurysm (aortic disection) occurs when a tear in the intima causes causing blood to force the layers of the aortic wall apart.
This is a medical emergency.
Tearing pain which may radiate to the back.
51
What is the difference between an aneurysm and a false aneurysm?
Aneurysm = localised permenant dilation of a vessel due to the wall becoming weaker. Involve all layers of the arterial wall
False aneurysm = a blood-filled space that forms around a vessel usually as a result of truamatic injury or perforating injury. Outer layer (adventitia) only
52
What are the typical causes of aneurysms?
Causes of aneurysms:
## Footnote
Atheroma
Trauma
Infection - mycotic aneurysm in endocarditis, teritary syphilis
Connective tissue disorders - Marfan's
Inflammatory - Takayasu's aortitis
53
Where do Berry aneurysms occur?
Berry aneurysms occur in the circle of Willis. They occur when the normal muscular arterial wall is replaced by fibrous tissue.
More common in young hypertensive patients.
Subarachnoid haemorrhage = the most important complication
54
What are capillary mico-aneurysms associated with?
Capillary micro-aneurysms are associated with hypertension and diabetic vascular disease.
They occur in intracerebral capillaries.
55
What are mycotic aneurysm due to?
Mycotic aneurysm are the weakening of the arterial wall as a result of a bacterial or fungal infection.
56
Describe dilated (congestive) cardiomyopathy
Dilated (congestive) cardiomyopathy
## Footnote
Thin walls with dialted cavities = too little contraction
Cytoskeletal and sarcomeric protein gene mutations
Appears as HF in young people.
Poor prognosis - 40% mortality after 2 years
57
Describe hypertrophic (obstructive) cardiomyopathy
Hypertrophic (obstructive) cardiomyopathy
## Footnote
Thickening of heart muscles
Disarray affects mechanical and electrical conduction
Too much conduction
AF, VF & sudden deaths are the most important complications - leading cause of sudden death in young people
Sarcomeric protein gene mutations (B myosin, a tropomyosin, troponin T)
58
Describe arrhythmogenic cardiomyopathy
Arrhythmogenic cardiomyopathy
## Footnote
Death of muscle - inflammatory response - fibrofatty replacement - fibrosis = insulator
Desmosomal gene mutations
59
Give the 4 ion channelopathies
All detected on ECG
1. Long QT - triggered by accustic, shocks & drugs
2. Short QT
3. Brugada - death by VF - Ajmaline test exaggerates ECG
4. CPVT (catecholaminergic polymorphic ventricular tachycardia) - triggered by exersice and stress
60
What is a D-dimer test used for?
D-dimer test is a negative predictive test to estabilish a DVT.
Normal = _not_ DVT
High = not diagnostic of DVT (surgery, pregnancy, malignancy)
Tests for breakdown products of blood.
61
A patient presents with a problem of their lower leg. Their calf is warm, tender & swollen. It is red showing signs of pitting oedema - they have a temp of 38 degrees
What could be the possible diagnosis?
**DVT -** clot between groin and knee
A patient presents with a problem of their lower leg. Their calf is warm, tender & swollen. It is red showing signs of pitting oedema - they have a temp of 38 degrees
62
What increases your risk of DVT?
Immobility, surgery, leg fracture, OC pill, HRT, pregnancy
(high oestrogen = prothrombotic)
63
A pateint presents with chest pain & SOB. You think it is due to a PE, what could be included in the differential diagnosis?
Chest pain & SOB
## Footnote
MI, infection, malignancy, pneumothorax, cardio/gastirc causes
64
What is the nerve supply to the heart giving the appropriate receptors & their location
**Adrenergic nerve** supply to the A & V muscle fibres and the conduction system.
Beta 1 predominate - respond to both adrenaline and noradrenaline with +ve inotrophic and choronotrophic effects
**Cholinergic nerves** from vagus nerve supply the SAN & AVN via M2 muscarinic receptors
65
Name the coronary artery that supplies the following parts of the heart
## Footnote
a) Posterior part of the interventricular septum
b) Anterior left ventricular wall
c) Right atrium
d) SAN & AVN in 60&90% of people respectively
a) Posterior part of the interventricular septum = posterior descending coronary artery
b) Anterior left ventricular wall = LAD
c) Right atrium = Right coronary artery
d) SAN & AVN in 60&90% of people respectively = Right coronary artery
66
How can left ventricular failure cause dyspnoea?
LVF can cause dyspnoea due to oedema of the pulmonary interstitium and alveoli. This makes lungs less compliant and increases the respiratory effort required to ventilate the lungs
67
What is orthopnoea?
Orthopnoea = breathlessness while lying flat
Blood is re-distributed from legs to torso, increasing pulmonary and central BV
Patients used more pillows to sleep
68
What are the two subdivisions of tachycardias?
Explain the difference
**Supraventricular tachycardia =** arise from atria/AVN
**Ventricular tachycardias =** arise from ventricles
69
What are the treatment aims for managing chronic AF?
Treatment of AF
Anticoagulation - heparin/warfarin if risk of emboli is high
Rate contorl - BB or rate limiting calcium channel blocker (Non-dihydropyradines)
Rhythem control - sotalol/amiodarone
70
What are the main causes for aortic stenosis?
Aortic stenosis
Congenital aortic stenosis
**Congenital bicuspid valve** - (1% of the population have this) - associated with aortic coaraction, disection or aneurysm
Aquired - **degenerative calcification**
71
A 66 yo presents with heavy chest pain, history of recent faints and signs of heart failure. On examination you find a slowly rising pulse with narrow pulse pressure, a softer 2nd heart sound, ejection systolic murmur and the presence of a 4th heart sound.
What is the possible diagnosis?
Aortic stenosis
## Footnote
Angina, syncope & heart failure
Slowly rising pulse with narrow pulse pressure
Softer 2nd heart sound - less powerfully closing valve
Ejection systolic murmur - loudness not indicative of severity
The presence of a 4th heart sound
72
Prognosis of aortic stenosis is poor. Give how many years have a 50% survival with:
## Footnote
a) Heart failure
b) Angina
c) Syncope
50% survival in those with aortic stenosis and...
a) HF = \<2 years
b) Angina = 5 years
c) Syncope = 3 years
73
Aortic stenosis:
## Footnote
Which has the following values?
AVA \<1.0cm2 and velocity \>4.0m/s
a) Mild AS
b) Moderate AS
c) Severe AS
Aortic stenosis:
## Footnote
AVA = aortic valve area normally 3-4cm
AVA(cm2) Velocity(m/s)
Mild: \>1.5 2.6-3.0
Moderate: 1.0-1.5 3.0-4.0
Severe: \<1.0 \>4.0
74
Give the management for aortic stenosis
Management for aortic stenosis
Reduce risk of **infective endocarditis** - good dental hygiene - IE prophalaxis for procedures
Surgical replacement - any symptomatic patient, decreased EF or if they are under going CABG
**Transcutaneous aortic valve replacement TAVI** (if not fit for surgery - good for comorbidities) - balloon cracks open the AOV, a catheter & cage like structure is places above the origional valve and takes over its funtion
75
What can cause mirtal regurgitation?
Mitral regurgitation = the back flow of blood from the LV to the LA during systole
Could be due to:
* Myoxmatous degeneration (weakening of connective tissue)
* Isheamic MR
* Rheumatic HD
* IE
76
