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Y5 Histopathology > Cardiac Histopath Qs > Flashcards

Cardiac Histopath Qs Flashcards

1
Q

What are the 3 prinicple components of atherosclerotic plaques?

A

Cells - including SMC, macrophages, and other leukocytes; ECM including collage, Intracellular and extracellular lipid

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2
Q

What areas are most at risk of atherosclerosis?

A

Abdominal aora affected more than thoracic aorta. More prominent around origins (ostia) of major branches (turbulent blood flow has low/oscillatory sheer stress which is athrogenic). High laminar flow is protective.

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3
Q

What are the modifiable risk factors for atherosclerosis?

A

TIIDM, HTN, High cholesterol, smoking

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4
Q

What are the non modifiable risk factors for atherosclerosis?

A

Gender (Male), increasing age, FHx

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5
Q

Steps of Atherogenesis (7)

A
  1. Endothelial injury
  2. LDL enters intima and is trapped in sub-intimal space
  3. LDL is converted into modifies and oxidised LDL causing inflammation
  4. Macrophages take up ox/modLDL via scavenger receptors and become foam cells
  5. Apoptosis of foam cells causes inflammation and cholesterol core of plaque
  6. Increase in adhesion molecules on endothelium results in more macrophages and T cells entering the plaque
  7. Vascular smooth muscle cells form the fibrous cap
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6
Q

Pathogenesis of MI

A

dynamic interaction between coronary atherosclerosis, plaque rupture, superimposed platelet activation, thrombosis and vasospasm leading to occlusive intracoronary thrombus overlying a disrupted plaque. This results in necrosis secondary to ischaemia

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7
Q

How long must ischaemia last to cause irreversible injury and myocyte death?

A

Over 20 mins

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8
Q

What liver enzymes is raised after an MI?

A

ALP

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9
Q

Complications of an MI (mneumonic)

A

DARTHVADER: Death, Arrhythmia (VF), Rupture (Ventricular wall, septum, papillary muscle), Tamponade (from pericardial effusion), HF, Valve disease (MR), Aneurysm of ventricles (over 4 weeks post MI), Dresslers Syndrome (and other Pericarditis), Embolism (due to mural thrombus), Recurrence of MI

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10
Q

Mechanical Complications of MI (Path guide division)

A

Contractile dysfunctioon leading to cardiogenic shock, Congestive CF due to ventricular dysfunction, LV infarct leading to papillary muscle dysfunction/necrosis/rupture leading to MR; Cardiac rupture of ventricular wall, septum, papillary muscle; ventricular aneurysm

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11
Q

What is the result of a cardiac rupture of: Ventricular wall, Septum, Papillary muscle?

A

Ventricular wall - haemopericardium; septum - left to right shunt (VSD); Papillary muscle - MR

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12
Q

How long after an MI does a ventricular aneurysm appear?

A

Over 4 weeks post MI

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13
Q

What Arrhythmia commonly presents after an MI? How long after an MI does it occur? What can it cause?

A

VF, usually occurs in the first 24hrs, common cause of sudden death

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14
Q

How many petients develop an arrhythmis following an MI?

A

90%

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15
Q

What are the pericardial complications of an MI?

A

Early (Peri-infarct associated) pericarditis, Pericardial effusion (+/- tamponade), Dressler’s Syndrome, Fibrinous Pericarditis#

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16
Q

What is Dressler’s syndrome? When and how does it present?

A

Secondary form of pericarditis due to cardiac injury; presents weeks-months after an MI with fever, pleuritic pain, pericarditis and/or a pericardial effusion.

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17
Q

When would fibrinous pericarditis be a complication of an MI? (what must occur during the MI?)

A

When the infarct extended to the epicardium

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18
Q

Histological findings post MI: under 6 hrs

A

Normal (CK-MB also normal)

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19
Q

Histological findings post MI: 6-24 hrs

A

Loss of nuclei, homogenous cytoplasm, necrotic cell death

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20
Q

Histological findings post MI: 1-4 days

A

Infiltration of polymorphs then macrophages (celaring up debris)

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21
Q

Histological findings post MI: 5-10 days

A

Removal of debris

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22
Q

Histological findings post MI: 1-2 weeks

A

Granulatioon tissue, new blood vessels, myofibroblasts, collagen synthesis

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23
Q

Histological findings post MI: weeks - months

A

Strengthening, decellularising scar tissue

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24
Q

What can be seen on histology of Early pericarditis?

A

Dusky haemorrhagic tissue

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25
6 common causes of Heart Failure
Ischaemic heart disease, valve disease, myocarditis, hypertension, dilated cardiomyopathy, arrhythmias
26
Complications of Heart Failure
Sudden death, Systemic emboli, arrhythmias, deep vein thrombosis and PE, pulmonary oedema with superimposed infection, hepatic cirrhosis (nutmeg liver)
27
What system is activated when there is reduced cardiac output? What does this system then do? What complication does this cause in HF?
Renin-angiotensin system is activated Renin -> AGT1 -> AGT2 -> Aldosterone -> salt and water retention; maintains perfusion, however overtime leads to fluid overload
28
What causes ventricular hypertrophy in HF? (Full mechanism, starts with decrese in SV)
Decresed Stroke Volume activatea the sympathetic NS via baroreceptors; prolonged activation --> increase in total peripheral resistance --> increased afterload --> ventricular hypertrophy
29
What causes ventricular dilatation in HF?
Increased afterload (due to high total peripheral resistance) --> increased EDV --> dilatation of the ventricle and worsening contractile function
30
What is seen macroscopically in HF?
LV is hypertrophied and dilated with myocardial fibrosis
31
What can result from the systemic effects of HF?
Pulmonary oedema, Hepatic cirrhosis (Nutmeg liver)
32
What is the crucial (exam key word) symptom of pulmonary oedema?
Cough producing a frothy pink transudate
33
What are the key symptoms of LV failure?
Damning of blood within the pulmonary circulation --> dyspnoea, orthopnoea, PND, wheeze, fatigue
34
What are the causes of RV Failure?
Chronic severe pulmonary HTN, or Secondary to LVF
35
Clincal Symptoms of RV Failure
Symptoms: peripheral oedema, ascites, facial engorgement
36
Investigations for ? RV Failure
BNP, CXR, ECG, Echo
37
Is nutmeg liver is assoicated with RV or LV Failure?
RVF
38
Pathology of RVF, pulmonary and systemically.
Engorgement of systemic and portal venous systems, minimal pulmonary congestion (unless caused by LVF)
39
What are the 3 patterns of cardiomyopathy?
Dilated, Hypertrophic, Restrictive
40
Which cardiomyopathy is associated with diastolic dysfunction and which with systolic dysfunction?
Dilated = Systolic dysfunction; Hypertrophic = Diastolic Dysfunctioon; Restrictive = Diastlic Dysfunction
41
Causes of Dilated Cardiomyopathy
Idiopathic, ALCOHOL, peripartum, genetic, sarcoidosis, haemochromatosis, myocarditis
42
Causes of Hypertrophic Cardiomyopathy
Genetic, storage diseases
43
Causes of Restrictive Cardiomyopathy
Sarcoidosis, Amyloidosis, radiation-induced fibrosis
44
What is the inheritance pattern for genetic HCM?
Autosomal dominant
45
What genetic mutations are commonly associated with HCM? What protein do they endcode for?
Beta-MHC = most common; MYBP-C, Trop-T. Genes encode for sarcomeric proteins. N.B Different mutations result in diffeent amout of hypertrophy and effects the incidence of arrhythmias.
46
For genetic HCM, which mutation gives you a high risk of sudden cardiac death?
Troponin-T mutations
47
How does the heart typically look in Hypertrophic Cardiomyopathy?
Thick-walled, heavy and hyper-contracting
48
Common phenotype of Hypertrophic Cardiomyopathy
Myocardial hypertrophy without ventricular dilation
49
In Hypertrophic Cardiomyopathy, what areas of the heart is hypertrophy most prominent?
Septum and left ventricle
50
What from of Cardiomyopathy can people with HOCM go on to develop?
15-20% go on to develop a DCM phenotype
51
What is HOCM?
Hypertrophic Obstructive Cardiomyopathy: septal hypertrophy resulting in an outflow tract obstruction
52
What is ARVC/D?
Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia: type of nonischaemic cardiomyopathy
53
What causes ARVC?
Genetic: many different mutations of genes which encode for cardiac desmosomes
54
Histological characteristics of ARVC
Hypokinetic areas in the free wall of the RV, with fibrofatty replacement of the RV myocardium (loss of myocytes). Associated with arrhythmias of the RV.
55
Acute Rheumatic Fever occurs at what age? (peak age)
5-15 years
56
What systems are affected by Acute Rheumatic Fever?
Cardiac, Bone, Skin, Neurological
57
What are the cardiac presentations of Acute Rheumatic Fever?
Pancarditis i.e Endocarditis, myocarditis, pericarditis
58
What are the joint presentations of Acute Rheumatic Fever?
Arthritis (migrating polyarthritis) and synovitis
59
What are the skin presentations of Acute Rheumatic Fever?
Erythema marginatum, subcutaneous nodules
60
What are the neurological presentations of Acute Rheumatic Fever?
Encephalopathy, Sydenham's chorea
61
What is the main pathogen associated with Acute Rheumatic Fever?
Lancefield Group A Strep (Grup A beta haemolytic Strep)
62
What precedes Acute Rheumatic Fever?
Strep throat infection 2-4 weeks prior
63
Histological findings in Acute Rheumatic Fever.
Beady fibrous vegetations (verrucae), Aschoff bodies (small giant cell granulomas), Anitschkov myocytes (regenerating myocytes)
64
How is antigenic mimicry associated with Acute Rheumatic Fever?
Cell mediated immunity and antibodies to streptococcal antigen cross-react with myocardial antigens, causing rheumatic heart disease
65
What criteria is used for diagnosis of Acute Rheumatic Fever? What else is used?
Jones Criteria: Along with lab test showing raised ESR and ASOT titres.
66
What valve is most commonly affected in Acute Rheumatic Fever?
Mitral valve
67
Symptoms of Rheumatic Fever (Mneumonic)
JONES: Joints (arthritis + synovitis), Heart (pancarditis), Nodules (Subcut), Erythema Marginatum, Sydenhams Chorea
68
Treatment for Acute Rheumatic Fever
Benzylpenicillin. Erythromycin if penicillin-allergic
69
4 types of Vegetative Endocarditis
Rheumatic Heart Disease, Infective Endocarditis, Non-bacterial thrombotic endocarditis, Libman-Sacks endocarditis
70
What are the characteristics of the vegetations seen in Rheumatic Heart Disease?
Small, warty vegetation found along the lines of closure of valve leaflet - 'verrucae'
71
What are the characteristics of the vegetations seen in Infective Endocarditis?
Large, irregular masses on valve cusps, extending into the chordae; friable vegetations.
72
What are the characteristics of the vegetations seen in Non-Bacterial thrombotic endocarditis (Marantic)?
Small, bland vegetations attached to lines of closure. Formed of thrombi.
73
What are the characteristics of the vegetations seen in Libman-Sacks endocarditis?
Small (up to 2mm), warty vegetations that are sterile and platelet-rich
74
What disorders are associated with Libman-Sacks Endocarditis?
SLE and anti-Phospholipid syndrome (Hugh's Syndrome)
75
What casues Non-Bacterial thrombotic endocarditis?
DIC, Hypercoagulable states
76
What are the predisposing factors for Infective Endocarditis?
Rheumatic Heart Disease, Mitral valve prolapse, Calcified valves, Bicuspid aortic valve, prosthetic valves, congenital defects
77
Infective endocarditis is colonization of the endocaridum due to a bacteraemia. What can cause this bactaraemia?
Poor dental hygeine, IVDU, soft tissue infection, dental treatments, cannulae/lines, cardiac surgery/pacemakers
78
What are the causative organisms of Acute Infective Endocarditis?
Staph Aureus, Strep pyogenes
79
Which causative organism of Infective Endocarditis is more associated with healthy valves? And unhealthy valves?
Healthy - Staph aureus; Unhealthy valve = Strep. Pyogenes
80
What are the causative organisms of Subacute Infective Endocarditis?
Strep viridans, Staph epidemis, Coxiella, Mycoplasma, Candida, HACEK (culture -ve)
81
HACEK?
HACEK?
82
Clinical Features of Infective Endocarditis (menumonic)
FROMJANE: Fever, Roth spots, Osler nodes, Murmur (new), Janeway lesions, Anaemia, Nail haemorrhage (splinter haemorrhages), Emboli
83
What valves are most commonly affected in Infective Endocarditis? What is the exception?
Mitral and Aortic valves. Exception = IVDU when Tricuspid and Pulmonary more involved
84
What criteria is used to diagnose Infective Endocarditis?
Dukes Criteria
85
What is the treatment for Infective Endocarditis?
Benzylpenicillin + Gentamicin
86
Rank the valves in order of most affected to least affected in chronic rheumatic valve disease.
Mitral > Aortic > Tricuspid > Pulmonic
87
What happens in chronic rheumatic valve disease?
thickening of valve leaflet, especially along lines of closure and fusion of commissures. There is alos thickening, shortening and fusion of chordae tendineae.
88
Clincial presentation of Mitral Valve prolapse. Who is most often affected?
Short of breath with chest pain - intermittent. Mainly affects middle aged women
89
What would you hear on auscultation of a mitral valve prolapse?
Late systolic murmur with a mid-systolic click
90
What causes aortic stenosis? What non-modifiable factor can speed up this process?
Calcification, process sped up if have bicuspid valve
91
What causes aortic regurgitation? (3 subtitles)
Rigidity: rheumatic, degenerative; Destruction: endocarditis; Dilatation: cystic medial degeneration; Marfan's syndrome, Dissecting aneuryms, Syphilitic aortitis, ankylosing spondylitis.
92
What are the 5 types of pericarditis?
Fibrinous, Purulent, Granulomatous, Haemorrhagic, Fibrous
93
What are the causes of Fibrinous pericarditis?
MI, uraemia
94
What are the causes of Purulent pericarditis?
Staphylococcus
95
What are the causes of Granulomatous pericarditis?
TB
96
What are the causes of Haemorrhagic pericarditis?
Tumour, TB, uraemia
97
What are the causes of Fibrous/Constrictive Pericarditis?
MI, uraemia, staph, TB, tumour
98
What s a pericardial effusion?
Serous fluid in the pericardial sac
99
What is the most common cause of pericardial effusion?
Chronic Heart Failure
100
What would cause an exudative pericardial effusion?
Exudative fluids occur secondary to inflammatory, infectious, malignant,, or autoimmune processes within the pericardium.
101
What is haemopericardium?
myocardial rupture from myocardial infarction or trauma

Y5 Histopathology (3 decks)

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