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Pathology > Cardio > Flashcards

Cardio Flashcards

1
Q

What is an aneurysm and how are they categorised

A

A localised permanent abnormal dilation of a blood vessel

Catergories:
True- due to weak vessel wall
False- Caused by trauma- haematoma mainly in femoral artery

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2
Q

What are the different types of true aneurysms

A
  1. Saccular and diffuse- atherosclerosis and inflammatory- aorta & cerebral artery
  2. Dissecting aneurysm- Marfans- Aorta and branches
  3. Capillary micro- HTN, diabetes- Cerebral and retinal capillaries
  4. Mycotic- Infection and sepsis- anywhere
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3
Q

What is myocarditis ?

What is it caused by

A

Inflammation of the myocardium

Caused by infection
Viral- Coxsaxkie, adenoids, ECHO, chicken pox, influenza 
Bacterial- Diptheria, menuungococcus 
Parasites 
ionising radiation 
Drugs- adriamycin
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4
Q

What is pericarditis and what causes it?

A

An inflammatory reaction involving the visceral or parietal layers of the pericardium

Causes -Non specific -viral -bacterial -TB -Post MI -Post surgery
-Dressler’s syndrome -Carcinomatous -Uraemic

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5
Q

Name the different types of shock

A
  • End results = hypotension, impaired tissue perfusion and cell hypoxia
    1. Cardiogenic - acute HF
    2. Hypovolaemic- haemorrhage or fluid shock
    3. Septic- gram neg bacterial infection
    4. Anaphylactic
    5. Neurogenic
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6
Q

Define heart failure

A

Typical symptoms (breathlessness) and signs caused by structural and functional cardiac abnormality causing a reduced cardiac output and or elevated intracardiac pressures at rest or during stress

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7
Q

How do you calculated ejection fraction

A

ejection fraction = stroke volume
end diastolic volume

Normal Left ventricle EF= >50% reduced= <40%

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8
Q

What is the classification heart failure symptoms

A
  1. No limits to physical exercise
  2. Mild limitation- comfy at rest but normal activity gives fatigue, sob and palp
  3. Comfortable at rest but gentle activity gives symptoms
  4. Symptoms at rest
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9
Q

Discuss the Frank Starling Mechanism

A

There is increased blood left behind after systole but not all of it is ejected which increases diastolic volume stretches myocardial fibres and enhances contractility and stroke volume

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10
Q

How is the RAAS system activated in heart failure

A

Reduced cardiac output leads to decreased renal perfusion
This activates the RAA system
This leads to enhanced salt and water retention
Which further increases venous pressure leads to direct toxic effects on myocardial cells

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11
Q

How is the sympathetic nervous system activated in HF

A

Cardiac output= stroke volume x heart rate

  • Stroke volume is reduced caused by myocardial impairment and is compensated for by increased heart rate
  • Chronic sympathetic nervous system activation has effects causing myocyte apoptosis - this explains the effectiveness of b- blockers
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12
Q

How are natriuretic peptides activated in heart failure

A

ANP and BNP- help to mark HF in bloods

  • Counter regulatory system for the RAAS system
  • Decreases blood volume, arterial pressure , central venous pressure and cardiac output
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13
Q

Explain left sided HF

A
  • Pooling of blood in pulmonary circulation causing dyspnoea, orthopnoea, PND
  • Leads to inadequate perfusion of downstream tissues causing renal and cerebral hypoxia
  • Also causes stasis of blood in left sided chambers causes dilation of the left atrium leading to atrial fibrillation and increased risk of stroke
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14
Q

Explain the causes of right sided heart failure

A 
Most commonly caused by left sided heart failure 
-May occur with 
pulmonary HTN 
Right ventricular infarction 
Right ventricular cardiomyopathy 
Adult congenital heart disease

Cor pulmonale= only when the right side of the heart is affected

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15
Q

How does right sided heart failure affect other parts of the body

A
  1. Systemic venous congestion causes spleen and bowel enlargement
  2. Liver and Portal system affected by congestive hepatomegaly
  3. Kidney and brain affected
  4. Hepatic necrosis when left side of heart is also involved
  5. Fluid accumulation in pleural, pericardial and peritoneal spaces
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16
Q

What is arterial blood pressure

A

Measure of the force exerted onto the arterial walls by circulating blood
Systolic diagnostic threshold= 140mmHg
Diatolic 90mmHg

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17
Q

What are the primary and secondary causes of hypertension

A

Primary -No single cause but a number of risk factors
- age, gamily history, African or Carribean, high salt diet, no exercise , overweight , smoking , alcohol, stress , urban dwelling

Secondary - specific cause can be identified

  • Renal- parenchymal and renovascular disease
  • Endocrine- Phaechromocytoma, Cushing’s , Juperaldosteronism
  • Coarctation of aorta
  • Medications- NSAIDs, OCP, Steroids
  • Pregnancy
18
Q

What are the renal parenchymal diseases

A
  • Diabetic nephropathy
  • Chronic glomerulonephritis (autoimmune)
  • PCKD
  • Chronic tunulointerstital nephritis
  • Hypertensive renal disease
19
Q

Explain renovascular disease

A
  • Renal artery stenosis due to atherosclerosis or fibromuscular dysplasia (younger females- pathological thickening of artery wall) causes decreased blood flow through main renal arteries or branches
  • This causes refractory hypertension and may lead to chronic kidney disease
20
Q

What are the endocrine causes of hypertension

A
  • Elevated aldosterone due to a benign tumour of the adrenal gland
  • Elevated noradrenaline and adrenaline due to phaeochromocytoma
  • Cushings syndrome- high cortisol
  • Ectopic ACTH from lung cancer
  • Steroid medication
21
Q

Explain coarctation of the aorta

A

Congenital narrowing of the aorta causing reduced blood flow to the lower half of the body so blood pressure is lower than normal in the legs and higher than normal in the arms

22
Q

What is the difference between atherosclerosis and arteriosclerosis

A

Atherosclerosis - Asymmetrical narrowing of the lumen of larger vessels by lipid accumulation in the intimate

Arteriosclerosis- Symmetrical narrowing of lumen of smaller vessels by deposition of protein in the wall of the blood vessel

23
Q

What is a haemorrhagic stroke

A

Stroke resulting from ruputure of small cerebral micro-aneurysms that have been weakened usually by chronic arterial hypertension

24
Q

What is hypertensive nephrosclerosis

A
  • Progressive renal impairment caused by chronic poorly controlled HTN due to damage of small blood vessels, glomeruli, renal tubules and interstitial fluids
  • Progressive chronic kidney disease can develop
25
Q

What is hypertensive retinopathy

A

Seen in long term HTN
-Thickened blood vessel walls cause reduced blood flow to retina leading to ischaemia and infarction leading to loss of vision

26
Q

What is ischaemic heart disease

A

Clinical problems including angina, MI or sudden death that are due to an imbalance between demand for oxygen and its supply by the coronary arteries mainly caused by atheroma

27
Q

What are the risk factors for IHD

A
  • Fam history
  • Smoking***
  • Diet- high salt
  • Lifestyle- no exercise
  • More common in white people
  • Age
  • Male
  • DM
  • Obesity
  • HTN
  • Hyperlipidaemia
28
Q

What is the pathophysiology of IHD

A
  • Blood supply becomes insufficient due to
    1. Reduction in blood supplying vessel due to atheroma
    2. Increased demand of muscle (ventricular hypertrophy- due to HTN)
    3. Reduced oxygen carriage (anaemia)
29
Q

What are the 3 most common coronary arteries affected in an MI

A
  1. LAD
  2. Right coronary artery
  3. Left circumflex
30
Q

Describe the areas of the heart affected by an MI in the different coronary arteries

A
  1. LAD- Anterior infarction- ECG changes in leads 1-4 - artery of sudden death
  2. Right coronary artery- Inferior infarction- ECG changes in leads 2, 3 and AVF, can involve posterior septum
  3. Circumflex artery- Lateral infarction- ECG changes in leads 1, AVL and lateral chest leads 4-6
31
Q

What are the complications of an MI

A

Sudden death- due to VF (early)
Arrhythmias due to damaged conduction system (early days)
Angina- ischaemia (varies)
Cardiac failure- muscle necrosis (varies)
Mitral Incompetence- papillary muscle damage
Pericarditis- transmural infarct and pericardial inflame (2-4 days)
Cardiac rupture- weaker tissue following muscle necrosis and acute inflammation (3-5 days )
Mural thrombosis- Ischaemia and endothelial damage (week or more)
Ventricular aneurysm- muscle necrosis/ arrhythmia (late)
Dressler’s sundrome (chest pain, fever, effusions) autoimmune (late)

32
Q

What is the difference between a myocardial rupture and a ventricular aneurysm

A

Myocardial rupture

  • Early 3-5 days
  • Mechanism= muscle necrosis with acute inflammation
  • Happens in ventricle wall to give acute blood in pericardial sac, septum to give left to right shunt and papillary muscle to give mitral incompetence

Ventricular Aneurysm

  • Late- weeks to months
  • Mechanism= dilation of fibrous scar
  • Effects- dyskinetic segment, heart failure and mural thrombosis
33
Q

Describe rheumatic fever and it’s symptoms

A
  • Occurs in children due to throat infection with Group A haemolytic streptococci
  • 2-6 week latency period
  • Causes valve disease

Need 2 major or 1 major and 2 minor symptoms

Major Minor
Carditis Fever
Polyarthritis Arthralgia
Sydenham’s chorea (neuro disorder) Abnormal lab results (high CRP) Erythema Marginatum ECG abnormalities- prolonged PR interval
Subcutaneous nodules Strep infection

34
Q

Describe the characteristic symptoms of rheumatic fever

A
  • Hallmark= a pancarditis (inflame of entire heart- pericardium, myocardium and endocardium(
    -Pleural effusion and fibrous pericarditis producing a fibrous rub on auscultation
    Myocarditis will show a lesion - ischial body
    -Endocarditis development
35
Q

Describe the two types of value disease

A
  1. Stenosis- Thickened or calcified valve causing obstruction to flow
  2. Incompetence (regurgitation)- loss of normal function and leakage

Mixed mitral valve disease can have both

36
Q

What are the causes of valve disease

A
  • Age related changes- calcification
  • Functional changes
  • Rhuematic fever
  • Congenital defects
  • Infective endocarditis
37
Q

Discuss the different types of aortic valve disease

A

Aortic stenosis - caused by calcific degeneration and rheumatic fever, can lead to left ventricular hypertrophy, angina, syncope, dyspnoea, left ventricular heart failure and sudden death

Aortic incompetence can be caused by aortic root dilatation (patients will present with HF) or rheumatic valve disease

Congenital bicuspid valve stenosis - Aortic valve normally has 3 cusps but if at birth it only has two calficific degeneration will occur at an earlier age

38
Q

Discuss the types of mitral valve diseases

A

Mitral Stenosis - Caused by rheumatic fever, can lead to pulmonary hypertension, with left atrial and right ventricular hypertrophy due to pressure changes in atria and pulmonary circulation

Mitral Incompetence- Caused by floppy valve, rheumatic fever, dilated mitral valve annulus, papillary muscle dysfunction
-Floppy valves are prone to AF

39
Q

What is infective endocarditis

A

Acute or chronic disease resulting from infection of a focal area of the endocardium- usually over a heart valve

  • When an infective organism enters the bloodstream and settles on a thumbs on a valve leaflet and it forms a vegetation
  • Classified by the causative organism
  • Life threatening
Organisms 
-Virdans Strep- oropharynx - dentist 
-Staph-Skin - surgery or cannulation 
-Enterococci- Gi tract/ UG tract -endoscopy, cystoscopy/ prostatectomy 
IV drug abuse
40
Q

What are the risk factors and complications of infective endocarditis

A

Risk factors - structura cardiac abnormalities, Prostheses and catheters, factors causing bacteraemia, immunosuppression

Complications
1. Local - Cusp/ chord rupture , valve incompetence, myocarditis
2. Systemic- non specific, fever, weight loss, malaise, multisysytem involvement
Part of the vegetation can embolism and break off going elsewhere in the body

Pathology (12 decks)

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