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Flashcards in CV Deck (76):

Give and explain the risk factors for atherosclerosis?

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 


What does an atherosclerotic plaque contain?

Lipids, necrotic core, connective tissue with a fibrous cap 


When does atherosclerosis occur?

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 


Give the 4 main stages of the progression of atherosclerosis

  1. Fatty streaks - occur in children
  2. Intermediate lesion - 'foam cells, SM cells, T cells, platelets
  3. Fibrous plaque/advanced lesion - covered by a dense fibrous plaque or collagen and elastin overlying the lipid core with necrotic debris 
  4. Plaque rupture - plaque constantly being resorbed & redeposited. May rupture if balance sways towards inflammatory conditions which makes the cap weaker. 


Explain how statins work to reduce your cholesterol

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 



What are plaques of clinical relevance?


Rupture - thrombosis can grow leading too... 

Occlusion = Ishaemia 


Give the 4 clinical manifestations of atherosclerosis 

  1. Embolism 
  2. Stenosis (narrowing)  
  3. Occlusion 
  4. Aneuyrism (due to weakend walls) 


What is angina caused by?

Angina is chest pain due to a mismatch of O2 demand and supply 


Give the exacerbating factors that lead to a reduced supply for angina

Reduced supply (blood/O2) 








Give the exacerbating factors that lead to an increased demand that cause angina

Increased demand 

Hypertension (high BP) 

Tachyarrhythmia (high HR) 

Valvular HD 


Hypertrophic cardiomyopathy 


At which precentage occlusion does ischaemia occur?

a) 5% 

b) 25% 

c) 55% 

d) 75% 

Ischaemia occurs at about 75% occlusion 


Explain how as diseased artery can cause SOB on exertion?

Stenosed artery cannot relax to reduce resistance 


High amounts of P needed to increase Q(flow) 

Q cannot increase to meet the higher demands 

Not enough O2 = drive to breath = SOB 


What is crescendo angina?

Crescendo angina occurs at rest or after minimal exertion


Describe the type of pain that is typical of angina

Angina pain  

= Fist to chest / band around chest 

= Heavy / severe 


What are the cardiac symptoms associated with angina?

Chest pain, breathlessness, fluid retention, palpitation, syncope/pre-syncope 


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 

b) Doesn't stop after rest

Typical history: 

Onset = exertion, 

Position = middle of chest 

Quality = tight & heavy 

Radiation = arms/shoulders/jaw 

Relieving = resting 



What could be a differential diagnosis for chest pain and what are the differences?

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 


On exercise testing, what would the ECG show if it was angina?

ST depression 


Name the drugs which are suitable to treat angina



Nitrates - GTN & LA 


ACE inhibitors 

Ca2+ channel blockers 

K+ channel openers 

Drugs that stop the plaque growing (antiplatelet) and stop the heart working as hard) 



Explain how beta blockers work to stop angina

B1 blockers:

 -ve choronotrophic = reduce HR 

-ve inotrophic = reduce LV contraction 

= Less work & less O2 demand 

B2 blockers: peripheral vasoconstriction & broncospasm 


Give 2 examples of beta blockers

Propranol = non-selective 

Bisopranol = B1 selective 


How do nitrate drugs work to reduce angina?

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



What are the 4 features of aspirin which are desirable when using it to treat angina?

Anti-platelet - decrease platelet aggregation 





What does hypertension increase your risk of?

Hypertension increases your risk of: 




Chronic renal disease (CRD) 

Atrial fibrillation 


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


When do you treat stage 1 and stage 2 hypertension with antihypertensives?


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 


List the drug types which can be used to treat hypertension

Drugs that can be used to treat hypertension: 




A1- blockers 


Aldosterone antagonists 

Renin inhibitors 

Centrally acting 


Which of the following is an ACE-I that could be used to treat hypertension 

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


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 


What are the main AE from ACE-I 


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 


Which of the following are not treated with calcium channel blockers?

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 


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 



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 



What are the main AE due to statins 

AE due to statins: 

Muscle ache and abdominal discomfort 


Give the possible causes for acute coronary syndrome 


Rupture of atherosclerotic plaque + thrombosis 

Coronary vasospasm 

Disection of the coronary artery 


What is the marker for cardiac muscle injury and give examples when this is raised?

Troponin = selective marker for cardiac tissue injury 

Raised in MI... + PE, HF, myocarditis & arrhythmias 


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 


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 


Give the 3 main reasons that circulatory shock may occur with examples of each 

Circulatory shock

(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) 


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 




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 


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 



Explain how haemorrhage and shock can affect the following organs?

a) Kindeys 

b) Brain 

c) Lungs 

d) Heart 

Explain how haemorrhage and shock can affect the following organs?

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 


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 


Which causes hypertrophic cardiomyopathies?

a) Sarcomic protein gene mutations

b) Cytoskeletal gene mutations 

c) Desmosome gene mutations 

d) Ion channel protein gene mutations 

Hypertrophic cardiomyopathies are caused by sarcomic protein gene mutations

HCM may cause angina, dyspnoea, palpitations, dizzy spells or syncope 


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 


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) 



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 


Include long QT, short QT, brugada and CPVT 

The heart is structurally normal - may present with reccurent syncope 


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 


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. 



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 



What are the typical causes of aneurysms?

Causes of aneurysms: 



Infection - mycotic aneurysm in endocarditis, teritary syphilis 

Connective tissue disorders - Marfan's 

Inflammatory - Takayasu's aortitis 


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 


What are capillary mico-aneurysms associated with?

Capillary micro-aneurysms are associated with hypertension and diabetic vascular disease. 

They occur in intracerebral capillaries. 


What are mycotic aneurysm due to?

Mycotic aneurysm are the weakening of the arterial wall as a result of a bacterial or fungal infection. 


Describe dilated (congestive) cardiomyopathy

Dilated (congestive) cardiomyopathy

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 



Describe hypertrophic (obstructive) cardiomyopathy

Hypertrophic (obstructive) cardiomyopathy

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) 


Describe arrhythmogenic cardiomyopathy 

Arrhythmogenic cardiomyopathy 

Death of muscle - inflammatory response - fibrofatty replacement - fibrosis = insulator

Desmosomal gene mutations 



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


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. 



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 


What increases your risk of DVT?

Immobility, surgery, leg fracture, OC pill, HRT, pregnancy 


(high oestrogen = prothrombotic) 


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 

MI, infection, malignancy, pneumothorax, cardio/gastirc causes 


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 


Name the coronary artery that supplies the following parts of the heart

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 


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 


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 


What are the two subdivisions of tachycardias? 

Explain the difference 

Supraventricular tachycardia = arise from atria/AVN 

Ventricular tachycardias = arise from ventricles


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 


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 


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 

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 


Prognosis of aortic stenosis is poor. Give how many years have a 50% survival with: 

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 


Aortic stenosis: 

Which has the following values?

AVA <1.0cmand velocity >4.0m/s

a) Mild AS 

b) Moderate AS 

c) Severe AS 

Aortic stenosis: 

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 


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


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