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Phase 2 AR > CV > Flashcards

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
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2
Q

What does an atherosclerotic plaque contain?

A

Lipids, necrotic core, connective tissue with a fibrous cap

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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

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4
Q

Give the 4 main stages of the progression of atherosclerosis

A
  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.
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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

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6
Q

What are plaques of clinical relevance?

A

Problems:

Rupture - thrombosis can grow leading too…

Occlusion = Ishaemia

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7
Q

Give the 4 clinical manifestations of atherosclerosis

A
  1. Embolism
  2. Stenosis (narrowing)
  3. Occlusion
  4. Aneuyrism (due to weakend walls)
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8
Q

What is angina caused by?

A

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

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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

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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

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11
Q

At which precentage occlusion does ischaemia occur?

a) 5%
b) 25%
c) 55%
d) 75%

A

Ischaemia occurs at about 75% occlusion

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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

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13
Q

What is crescendo angina?

A

Crescendo angina occurs at rest or after minimal exertion

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14
Q

Describe the type of pain that is typical of angina

A

Angina pain

= Fist to chest / band around chest

= Heavy / severe

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15
Q

What are the cardiac symptoms associated with angina?

A

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

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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)

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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

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18
Q

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

A

ST depression

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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)

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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

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21
Q

Give 2 examples of beta blockers

A

Propranol = non-selective

Bisopranol = B1 selective

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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

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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

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24
Q

What does hypertension increase your risk of?

A

Hypertension increases your risk of:

Stroke

MI

HF

Chronic renal disease (CRD)

Atrial fibrillation

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25
Q

Define stage 1 and 2 hypertension

A

Stage 1:

Clinical BP = 140/90mmHg AMBP = 135/80 mmHg

Stage 2:

Clinical BP = 160/100mmHg AMBP = 150/95mmHg

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26
Q

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

A

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

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27
Q

List the drug types which can be used to treat hypertension

A

Drugs that can be used to treat hypertension:

ACE-I

Beta-blockers

CCB

A1- blockers

ARD

Aldosterone antagonists

Renin inhibitors

Centrally acting

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28
Q

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

a) Enalapril
b) Valsartan
c) Verapamil
d) Furosemide

A

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

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29
Q

Explain the ways that angiotensin II can be used to prevent hypertension

A

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

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30
Q

What are the main AE from ACE-I

A

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

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31
Q

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

a) Hypertension
b) Isheamic heart disease
c) HF
d) Arrhythmia

A

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
Q

What are the main AE of calcium channel blockers?

A

AE of CCB:

Due to periferal vasodilation = headaches, flushing, oedema, palpations

Due to -ve choronotrophic effects = bradycardia, AV block

33
Q

What are the main AE from beta blockers?

A

AE due to BB:

Bradycardia, tiredness/nightmares, erectile dysfunction, cold hands and feet

Severe broncospasms in people with asthma + heart block

34
Q

What are the main AE due to statins

A

AE due to statins:

Muscle ache and abdominal discomfort

35
Q

Give the possible causes for acute coronary syndrome

A

ACS

Rupture of atherosclerotic plaque + thrombosis

Coronary vasospasm

Disection of the coronary artery

36
Q

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

A

Troponin = selective marker for cardiac tissue injury

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

37
Q

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

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
Q

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?

A

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
Q

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

A

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)

40
Q

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

A

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
Q

How does shock result in death?

A

Most people die from shock a few days after the acute event due to coagulopathy, hypothermia or metabolic acidosis

42
Q

What is the most improtant thing to do for a patient in septic shock and why?

A

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
Q

Explain how haemorrhage and shock can affect the following organs?

a) Kindeys
b) Brain
c) Lungs
d) Heart

A

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

44
Q

a) What is anaphalactic shock?
b) Give the signs and symptoms of an anaphalactic shock

A

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
Q

Which causes hypertrophic cardiomyopathies?

a) Sarcomic protein gene mutations
b) Cytoskeletal gene mutations
c) Desmosome gene mutations
d) Ion channel protein gene mutations

A

Hypertrophic cardiomyopathies are caused by sarcomic protein gene mutations

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

46
Q

Which causes dilated cardiomyopathies?

a) Sarcomic protein gene mutations
b) Cytoskeletal gene mutations
c) Desmosome gene mutations
d) Ion channel protein gene mutations

A

Dilated cardiomyopathies are caused by cytoskeletal gene mutations.

Usually present with HF symptoms

LV/RV/4 chamber dilation/dysfunction

47
Q

Which causes arrhythmogenic cardiomyopathies?

a) Sarcomic protein gene mutations
b) Cytoskeletal gene mutations
c) Desmosome gene mutations
d) Ion channel protein gene mutations

A

Arrhythmiogenic cardiomyopathies are caused by desmosome gene mutations

(singals need to be transfered through the desmosomes)

48
Q

Which causes inherited arrhythmia (channelopathy)?

a) Sarcomic protein gene mutations
b) Cytoskeletal gene mutations
c) Desmosome gene mutations
d) Ion channel protein gene mutations

A

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
Q

What is familial hypercholesterolaemia?

A

Familial hypercholesterolaemia is an inherited abnormality of cholesterol metabolism - increased amounts of LDL that leads to premature coronary and vascular disease

50
Q

Explain what a dissecting aneurysm is.

A

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
Q

What is the difference between an aneurysm and a false aneurysm?

A

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
Q

What are the typical causes of aneurysms?

A

Causes of aneurysms:

Atheroma

Trauma

Infection - mycotic aneurysm in endocarditis, teritary syphilis

Connective tissue disorders - Marfan’s

Inflammatory - Takayasu’s aortitis

53
Q

Where do Berry aneurysms occur?

A

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
Q

What are capillary mico-aneurysms associated with?

A

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

They occur in intracerebral capillaries.

55
Q

What are mycotic aneurysm due to?

A

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

56
Q

Describe dilated (congestive) cardiomyopathy

A

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

57
Q

Describe hypertrophic (obstructive) cardiomyopathy

A

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)

58
Q

Describe arrhythmogenic cardiomyopathy

A

Arrhythmogenic cardiomyopathy

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

Desmosomal gene mutations

59
Q

Give the 4 ion channelopathies

A

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
Q

What is a D-dimer test used for?

A

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
Q

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?

A

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
Q

What increases your risk of DVT?

A

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

(high oestrogen = prothrombotic)

63
Q

A pateint presents with chest pain & SOB. You think it is due to a PE, what could be included in the differential diagnosis?

A

Chest pain & SOB

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

64
Q

What is the nerve supply to the heart giving the appropriate receptors & their location

A

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
Q

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

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
Q

How can left ventricular failure cause dyspnoea?

A

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
Q

What is orthopnoea?

A

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
Q

What are the two subdivisions of tachycardias?

Explain the difference

A

Supraventricular tachycardia = arise from atria/AVN

Ventricular tachycardias = arise from ventricles

69
Q

What are the treatment aims for managing chronic AF?

A

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
Q

What are the main causes for aortic stenosis?

A

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
Q

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?

A

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

72
Q

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

a) Heart failure
b) Angina
c) Syncope

A

50% survival in those with aortic stenosis and…

a) HF = <2 years
b) Angina = 5 years
c) Syncope = 3 years

73
Q

Aortic stenosis:

Which has the following values?

AVA <1.0cm2 and velocity >4.0m/s

a) Mild AS
b) Moderate AS
c) Severe AS

A

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

74
Q

Give the management for aortic stenosis

A

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
Q

What can cause mirtal regurgitation?

A

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

Phase 2 AR (6 decks)

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