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Cardiology > Pathology > Flashcards

Pathology Flashcards

1
Q

what is atherosclerosis?

A

a disease where there is the formation of fatty deposits (lesions) within the large and medium sized arteries known as sclerotic plaques

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2
Q

an atherosclerotic plaque contains what components

A

connective tissues (collagen) produced by smooth muscle cells providing structural strength, inflammatory cells- macrophages, lipid deposits known as fatty streaks, and foam cells- taken up lipoproteins via specialised membrane bound scavenger receptors

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3
Q

what are the most common sites of atherosclerosis?

A

points of arterial branching and bifurcation, where the lumen of the vessel is narrower- increases pressure on the endothelium hence there is a more likely chance of damage.

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4
Q

name 5 risk factors of atherosclerosis

A

obestiy, asian prevalence, smoker, inactivity and hypertensive

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5
Q

What are the treatments/interventions for atherosclerosis?

A

plasminogen inhibitors and alpha-2 antiplasmin- inhibits plasminogen being converted into plasmin.

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6
Q

what is high blood pressure?

A

a blood pressure where the treatment to reduce it will reduce the risk of complications arising. It is beneficial to treat

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7
Q

describe primary hyperaldosteronism (conns syndrome)

A

it is a benign adenoma in the adrenal gland (one or both) which results in excessive production and release of aldosterone.
Characterised by: Hypertension (increases sodium retention in the kidneys) Hypokalaemia- increases potassium loss and Alkalosis.

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8
Q

what is produced excessively in Cushings syndrome, and what does this result in?

A

cortisol, it acts in a similar way to aldosterone- increases BP but also increases glucose levels

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9
Q

What is fibromuscular dysplasia of the artery wall?

A

this is increased muscle cells in the artery wall- increased thickness

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10
Q

what are the treatments for hypertension?

A

ACE inhibitors, beta blockers, calcium channel blockers, diuretics

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11
Q

why are caucasians over the age of 55 and afro carribbeans given calcium channel blockers and diuretics to treat hypertension instead of ACE inhibitors?

A

As you get older you responsiveness to renin decreases, afro caribbeans are also less sensitive to renin and thus the ACE inhibitors have a lesser antihypertensive effect

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12
Q

What is heart failure?

A

the inability to expel blood out of the heart

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13
Q

what is cor pulmonale

A

a term used to describe right sided heart failure secondary to lung disease

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14
Q

give 5 reasons why blood supply to the heart may be impaired

A
  1. atherosclerosis of the arteries
  2. thrombosis within a blood vessel
  3. thromboembolic blocking a blood vessel supplying the heart
  4. arteritis
  5. reduced blood pressure
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15
Q

what is hypovolaemia?

A

shock resulting from a significantly decreased blood volume

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16
Q

What is polysythemia?

A

high production and thus levels of RBC’s in the blood plasma. It is usually a compensatory mechanism as a result of hyperaemia

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17
Q

Name 5 differential diagnosis for symptoms which suggest ischaemic heart disease

A
  1. Pericarditis
  2. pulmonary embolism
  3. chest infection
  4. dissection of the aorta
  5. gastro-oesophageal reflux
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18
Q

What is angina?

A

a mismatch of oxygen demand and supply in the heart because of a narrowed coronary artery which causes discomfort in the chest and adjacent areas

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19
Q

What is Prinzmetal’s angina?

A

this is the mismatch of perfusion and demand of the heart due to arterial spasms- its a type of unstable angina

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20
Q

unstable angina

A

unexpected chest pain whilst resting, due to atherosclerosis of the coronary vessels supplying the heart.

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21
Q

What is a myocardial infarction?

A

this is a term applied to necrosis of the heart after an acute interruption of the coronary blood supply

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22
Q

Describe the 3 types of infarction and the locations within the heart muscle where a myocardial infarction may occur.

A

Subendocardial infarction- death of the innermost layer of the myocardial tissue
Patchy infarction- throughout the myocardial tissue layers
Transmural infarction- tissue death the full thickness of the myocardial tissue from the epicardium to the endocardium

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23
Q

Describe 3 main features of a myocardial infarction

A
  1. severe angina
  2. raised ST segment on and ECG
  3. breathlessness
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24
Q

what anti-thrombotic therapy is given to reduce the risk of immediate vascular occlusion following a MI?

A

Dual anti-platelet therapy- GP2b/3a given IV, anticoagulant fondaparinux (inhibits fibrin and thrombin formation)

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25
Q

When are fibrinolytic drugs offered to a patient with a recent MI? and name one

A

Offered to patients who cannot have a percutaneous coronary laparoscopy within 90 minutes of hospital admission. Streptokinase.

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26
Q

What is valvular incompetence?

A

the loss of a normal functioning valve- it fails to prevent regurgitation of blood after contraction of an individual chamber

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27
Q

What is a vegetation on the heart?

A

an infective thrombotic nodule developing on the valves of the heart that impairs normal functions- motility and closure

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28
Q

what is calcific aortic stenosis?

A

the narrowing of the aortic valve due to calcific deposits in the cusps, progressively distorting the valve shape and ability to close properly

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29
Q

what are the 3 main symptoms of aortic stenosis?

A
  1. chest pain
  2. dizziness
  3. occasional fainting
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30
Q

what is an Austin flint murmur?

A

this is a sound heard in aortic regurgitation because the regurgitating jet impinges on the anterior mitral valve lobe causing it to vibrate

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31
Q

what is myxomatous degeneration of the mitral valve and what can it lead to?

A

this is the dysfunction of the mitral valve because there is too much length of papillary muscle making the tension weak and allowing the valve to invert

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32
Q

Name 3 signs of mitral regurgitation

A
  1. Auscultation- a soft 1st heart murmur at the apex radiating to the axilla
  2. 3rd heart sound- due to left arterial overload
  3. displaced apex beat
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33
Q

Name 3 signs of mitral stenosis

A
  1. diastolic mumur- low pitched rumble at the apex
  2. loud S1 snap at the apex beat due to the initial rapid opening of the valve (the tips are often fused and so a force is required to open them)
  3. shorter time interval between S1 and S2
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34
Q

What is rheumatic fever?

A

this is a condition which develops after a streptococcal infection in the upper respiratory tract. Immune reactions to the pathogen produces antibodies which cross react with myocytes and valvular glycoproteins in the heart.

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35
Q

Giant cell myocarditis

A

a rare and often fatal cardiac disease with areas of muscle cell death due to macrophage giant cells.

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36
Q

name 5 predisposing factors to endocarditis

A
  1. rheumatic fever
  2. abnormal/prosthetic heart valve
  3. dental sepsis
  4. IVDU
  5. age- young and elderly
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37
Q

What is infective endocarditis and what bacterial pathogen commonly causes it?

A

infection of the endocardial layer of the heart (this lines the valves and innermost layer of the heart.) Staphylococcus Aureus

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38
Q

what is a roth spot? and what condition is it commonly found in?

A

it is a vegetation in the retina. commonly seen in infective endocaridits.

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39
Q

What criteria is used for the diagnosis of infective endocarditis?

A

Modified Dukes criteria

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40
Q

What is the most effective method of treating infective endocarditis?

A

4-6 weeks IV penicillin or gentamicin.

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41
Q

what is the function of Lidocaine?

A

it blocks the inactivation gate of Na channels, therefore is effective in treating ventricular tachycardia

42
Q

why is digoxin a useful drug to treat supra ventricular tachycardia?

A

it blocks the ATPase Na+/K+ pump in the cell membrane making the membrane potential positive and thus preventing depolarisation

43
Q

How do amlodipine and verapamil work as anti-arrhythmic agents?

A

they block the calcium channels preventing depolarisation

44
Q

why is verapamil more effective as an anti-arrhythmic agent than amlodipine?

A

it has no effect on the calcium channels at rest

45
Q

why is propranolol the most useful beta blocker to help control arrhythmia following an MI?

A

it is a Na channel blocker

46
Q

what is the function of the loop diuretic Furosemide?

A

it is a inhibitor of the Na/K/2Cl transporter channel in the loop of henle (ascending limb) in the kidney.

47
Q

Name one potential side effect from beta blockers?

A

Bronchospasm

48
Q

name one common side effect from ACE inhibitors

A

dry cough

49
Q

what CVS drug is most likely to induce postural hypotension as a potential side effect?

A

Calcium antagonists

50
Q

what effect does digoxin have on the force of contraction of the heart muscle?

A

it increases the force of contraction and subsequently increases the ejection fraction from the heart.

51
Q

what is colchine used to treat?

A

gout

52
Q

name a virus and bacteria commonly causing pericarditis

A 
Virus= coxsackie virus, EBV
Bacteria= rheumatic fever
53
Q

define shock

A

circulatory failure resulting in inadequate organ perfusion

54
Q

name the 5 types of shock

A 
haemorrhagic
circulatory/cardiogenic
septic
anaphylactic
neurogenic
55
Q

how do you treat shock (generic emergency treatment)

A 
ABC
raise foot above the bed
IV access
diamorphine for pain
identify and treat underlying cause
infuse crystalloid to raise BP
investigations; allergy, general appearance(cold, palor), respiratory function, postural hypotension, ECG- HR, ischaemia, rhythm, pulse
56
Q

describe the 3 phases of shock

A
  1. Exudative: reversible phase, cells begin to change due to reduced perfusion and oxygenation.
  2. proliferation (compensatory phase) reorganisation of exudates, fibroblast proliferation and increased ventillation
  3. fibrotic phase: irreversible necrosis of tissues
57
Q

name 5 signs of shock

A 
temperature>38 
pallor
systolic blood pressure 
increased respiratory rate >20pmin
tachycardia >100bpm
58
Q

what is an aortic dissection?

A

high blood pressure causing a tear in the intimal layer of the aorta. This results in blood flowing into the intima and media layers of the vessel forming a clot. as the dissection gets bigger it can occlude branches of the aorta

59
Q

how would an aortic dissection resulting in occlusion of the carotid artery present?

A

hemiplagia

60
Q

how does an aortic dissection usually present?

A

acute chest pain radiating to the back

61
Q

name the 2 types of aortic dissection and what each involved

A

Type A: more serious involving the ascending aorta- needs surgical repair
Type B: less serious, not involving the ascending aorta, treated with Beta blockers.

62
Q

what is an aortic aneurysm?

A

an abnormal and permanent dilation of all layers of the abdominal wall associated with fibrosis and atrophy of myocytes

63
Q

what is the difference between a true aneurysm and a pseudo aneurysm?

A

a pseudo aneurysm only involves collection of blood in the adventitia whereas a true aneurysm involves all layers of the arterial wall

64
Q

what age are men invited for screening of abdominal aortic aneurysms?

A

the year they turn 65, from 2013,

65
Q

what are the key features of an abdominal aneurysm?

A

expansile, pulsatile mass involving all layers of the arterial wall

66
Q

when is surgical repair recommended in an aortic aneurysm?

A

when the aneurysm is >5.5cm and growing at a rate of >1cm p.a

67
Q

how does an aortic aneurysm present?

A

it is usually asymptomatic until ruptured

may present with intermittent/continuous abdominal pain radiating to the back and groin

68
Q

what is a berry aneurysm?

A

a rounded berry like dilation in the cerebellar circulation, most commonly in the sites of anastomosis in the circle of willis- eg at where the posterior communicating and internal carotids meet

69
Q

name 3 differences between skeletal and cardiac muscle

A
  1. skeletal is not branched cardiac is
  2. skeletal has no intercalated discs- cardiac does
  3. cardiac myocytes secrete atrial natiuretic peptide, skeletal muscles dont.
70
Q

how long is a QRS complex normally?

A

0.06- 0.12 s

71
Q

how long is the PR interval normally?

A

0.12-0.2s

72
Q

how long is the ST segment

A

0.2-0.4s

73
Q

how long is the P wave?

A

0.08-0.1s

74
Q

how long is the T wave usually?

A

0.4s

75
Q

name the 6 peripheral pulses

A
  1. carotid artery
  2. brachial atery
  3. radial artery
  4. femoral artery
  5. popliteal artery (behind the knee)
  6. posterior tibial artery (ankle)
  7. dorsalis pedis (foot)
76
Q

what percentage of the lumen needs to be occluded for ischaemia to present?

A

75% or more

77
Q

name 5 risk factors for IDH

A
  1. smoking
  2. obesity
  3. FH
  4. diabetes
  5. hypertension
78
Q

name 5 causes of IDH

A
  1. High blood pressure
  2. atherosclerosis
  3. thrombosis
  4. thromboemboli
  5. arteritis
79
Q

name 4 complications of IDH

A
  1. polycythemia- compensatory mechanism where the bone marrow produced more RBC to counteract low levels of oxygen in the blood
  2. hypoxaemia- low oxygen in the blood due to restricted blood vessel lumen
  3. anaemia- reduced bone marrow perfusion thus reduced RBC production
  4. hypovolaemia- reduced cardiac output results in reduced blood volume
80
Q

what class of drug is bisoprosol?

A

class 2 anti-arrhythmic drug

81
Q

briefly describe the mechanism of action of bisoprosol

A

it is a beta-adrenergic antagonist. it acts on the B1 receptors in the SAN and AVN (and the b2 adrenergic receptors in the lungs) inhibiting sympathetic innervation. Therefore causing reduced SAN depolarisation, reducing atrial contraction and HR.

82
Q

what is the target INR when on warfarin

A

between 2-3

83
Q

name 2 bacteria commonly causing infective endocarditis

A

streptococcus viridans

staphylococcus aureus

84
Q

patient with longstanding rheumatic mitral valve disease (malfunctioning valve as a result of previous Rheumatic fever infection) presents with pansystolic murmur loudest at the apex. what is the first line investigation?

A

BLOOD CULTURES!!!!

85
Q

what effect do ACE inhibitors have on the arterioles of the kidneys?

A

They inhibit the conversion of angiotensin 1 into angiotensin 2. This prevents efferent arteriolar constriction

86
Q

what is the most appropriate prophylaxis of a DVT in a patient recently undergone surgery?

A

LMWH- eg Dalteparin

87
Q

what is the treatment for rheumatic fever>

A

benzylpenicillin IV, then penicillin PO for 10 days. Bed rest until CRP is normal

88
Q

describe the initial stages of management of a STEMI

A
  1. attach ECG
  2. IV access- take bloods
  3. Aspirin (unless already given)
  4. Morphine IV (+ antiemetic)
  5. if percutaneous coronary implementation is not available within 120 minutes fibrinolysis is necessary
89
Q

what is the acronym used to assess the risk of stroke following a atrial fibrillation?

A

CHA2DS2 VASc score (congestive heart failure, hypertension, age >75, Diabetes, stroke previously, Vascular disease, Age 65-74, Sex category - female)

90
Q

what treatment would you give for thrombolysis in acute non haemorrhagic stroke?

A

iv recombinant tissue plasminogen activator

91
Q

name 2 places where alpha receptors are found and what it does

A

alpha 1 receptors= smooth muscle and sphincters- vasoconstriction and contraction
alpha 2 receptors= nerve endings, inhibit release of neurotransmitters

92
Q

name 2 places where beta receptors are found and what they do

A

beta 1 receptors= heart and kidneys; increase HR and force, stimulate the release of renin
Beta 2 receptors= in the smooth muscle bronchi, liver and skeletal muscles. Cause vasodilation in the bronchi (bronchodilation), gluconeogenesis in the liver and skeletal msucles

93
Q

which clotting factors require vitamin K for their synthesis?

A

2,7,9,10

94
Q

what 3 key features do you see on a barium swallow?

A

left bronchus
left aorta
aortic arch

95
Q

name 4 other features you may see on a barium swallow

A

tumour, hiatus hernia, oesophageal strictures, oesophageal reflux

96
Q

what is Barlow syndrome?

A

mitral valve prolapse- a mid systolic click followed by a late systolic murmur heard at the apex of a thickened mitral valve slightly displaced into the left atrium during systole

97
Q

how might a patient present with an aortic dissection?

A

3 day history of severe TEARING pain that radiates towards the back and sometimes to the jaw.

98
Q

what happens to the JVP wave in atrial fibrillation?

A

the “a” waves are absent due to dysfunctional atrial systole

99
Q

name 4 signs seen in mitral stenosis

A

malar flush, atrial fibrillation, tapping apex beat and right ventricular heave.

100
Q

what heart sound is usually heard in mitral valve regurgitation

A

pan-systolic murmur

101
Q

describe 3 features seen in coarctation of the aora

A

bruitis over the intercostal spaces, notching of the lower margins of the ribs on Xray, midsystolic murmur maximal at the aortic area radiating to the back. (LVH can also be seen)

Cardiology (3 decks)

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