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Clinical Pathology Year 2 > Cardiovascular Pathology > Flashcards

Cardiovascular Pathology Flashcards

1
Q

How can infectious agents enter the CNS?

A

a) Hematogenous spread (most common, usually arterial route)
b) Direct implantation (most often is traumatic. Rare. Can be congenital)
c) Local extension (secondary to established infections eg) mastoid, frontal sinus, infected tooth)
d) Along peripheral nerves (usually viruses eg Rabies, Herpes Zoster)

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2
Q

What are 3 classifications of Meningitis?

A

Acute Pyogenic (usually bacterial meningitis)
Aseptic (viral meningitis)
Chronic (Myobacterium TB, cryptococcus)

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3
Q

Common pathogens of meningitis and age…

a) 0-4 weeks
b) 4-12 weeks
c) 3m-18yrs
d) 18yrs+

A

a) Strep. agglactiae, E coli, Listeria monocytogenes, Enterococcus
b) Strep. agglactiaea, E coli, Listeria monocytogenes, Strep. pneumoniae, Neisseria meningitides
c) H. influenzae, N. meningitidis, S. pneumoniae
d) N. meningitidis, S. pneumoniae

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4
Q

CSF abnormalities in Meningitis…

a) Bacterial
b) Viral
c) TB

A

a) (cloudy). High protein, low glucose
b) (clear) Normal protein & glucose
c) (clear) High protein, low glucose

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5
Q

Some features of viral meningitis?

What does the CSF show?

A

Mainly affects children & young adults
Milder signs & symptoms (usually full recovery)
CSF shows raised lymphocyte count.
Main cause: enteroviruses (coxsackie, polio)

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6
Q

Some features of Tuberculous meningitis?

A

High freq of complications (cranial nerve palsy)

CSF shows raised lymphocytic response, but polymorphs also present.

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7
Q

What is Encephalitis and what is the most common cause?

A

An acute inflammatory process affecting the brain parenchyma.
Viral infection is most common cause

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8
Q

Some causes of Encephalitis?

A 
Herpes virus (most common- causes severe haemorrhagic encephalitis affecting temporal lobes)
Adenoviruses
Influenza A
Enteroviruses, Poliovirus
MMR viruses
Rabies
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9
Q

What is the link between Encephalitis & Rabies?

A

Rabies causes acute, progressive viral encephalitis.

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10
Q

What are the clinical phases of rabies?

A

Prodromal Phase
Furious Phase
Dumb Phase
Coma Phase

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11
Q

What is a brain abscess?

A

It is a focal suppurative process within the brain parenchyma (pus in the substance of the brain)

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12
Q

What are some of the bacteria responsible for a brain abscess?

A

(they are often mixed- polymicrobial)

  • Streptococci (60-70%)
  • Staph aureus (most common in abscesses after trauma/ surgery)
  • Anaerobes
  • Gram negative enteric bacteria
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13
Q

Main antibiotic treatments of CNS infections?

A

Ampicillin, Penicillin, Cefotaxime, Ceftazidime, Metronidazole (all achieve therapeutic concentrations in intracranial pus).

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14
Q

(Neurosyphillis)
Early symptomatic forms cause what?
Late symptomatic forms cause what?

A

Early: acute meningitis, meningovascular
Late: General paresis, Tabes dorsalis

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15
Q

Clinical syndrome resulting from pressure on the heart due to a build-up of fluid in the pericardial space?

A

Cardiac Tamponade

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16
Q

Gram positive cocci that grown in pairs and is a common cause of meningitis?

A

Streptococcus pneumoniae

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17
Q

A cause of secondary hypertension, where there is increased levels of catecholamines in the blood?

A

Pheochromocytoma

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18
Q

An effective treatment for giant cell arteritis?

A

Corticosteroids

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19
Q

Most common congenital heart disease?

A

Ventricular Septal Defect

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20
Q

Type of cardiomyopathy that is due to mutations in the sarcomere gene?

A

Hypertrophic

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21
Q

The most common valve disorder in rheumatic heart disease?

A

Mitral Stenosis

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22
Q

What is the aetiology of Infective Endocarditis (in order of commonness)?

A

Staphylococci, Streptococci, Enterococci

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23
Q

Some clinical presentations of Infective Endocarditis?

A

Fever, Splinter haemorrhages, Osler nodes, Janeway lesions, Roth Spots

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24
Q

Aetiology of a Mycotic Aneurysm?

A

Salmonella spp, Staphylococcus aureus, Streptococcis spp, Pseudomonas aeruginosa, E coli

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25
Q

Common aetiologies of Infected DVT?

A

S. aureus, streptococci, and anaerobes

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26
Q

Features of peripheral vascular disease?

A

Narrowing of blood vessels that restricts blood flow (wall thickening by atheroma/ thrombosis- VIRCHOW’S TRIAD)
Progressive disease leading to increasing levels of tissue hypoxia (as decreased perfusion).
Asymptomatic –> Intermittent Claudication –> Critical Limb ischaemia

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27
Q

What is Giant Cell Arteritis?

A

Chronic granulomatous inflammation of arteries (predominantly in branches of external carotid artery- generally temporal arteries, also vertebral & opthalmic)
Treatment usually with corticosteroids.

28
Q

What is Endocarditis?

A

Inflammation of endocardium (mainly involves valves- ‘vegetation’ on valves made of thrombus & organisms)
Can occur in normal heart with virulent organisms, but more commonly on background of structural abnormality of valves.

29
Q

Aetiology of Endocarditis other than from an infection of the bloodstream?

A
  • Mouth = viridans streptococci
  • Prolonged indwelling vascular catheters
  • Gut & Perineum = Enterococci
  • Staph aureus from skin
  • S. epidermis from commonly infected prosthetic heart valve
30
Q

4 clinical features of endocarditis?

A
  • Immunologically mediated conditions eg) glomerulonephritis
  • Janeway lesions
  • Osler’s nodes
  • Roth spots (retinal haemorrhages in the eyes)
31
Q

What is Rheumatic Fever caused by? (cause of right ventricular hypertrophy)

A

Group A streptococcal pharyngitis

32
Q

Pathology of Rheumatic Fever?

A

It is due to hypersensitivity reactions = combined antibody & T-cell mediated response to self antigens in the heart.
GROUP A STREP –> antibodies & T-cells (which make cytokines that activate macrophages) –>cross react with self proteins in the heart.

33
Q

What are some pathological features of Rheumatic Fever?

A

Vegetations called veruccae
Mitral Valve changes
Fibrous bridging of valvular commissures & calcification… ‘fish mouth’ stenoses

34
Q

What is Pericarditis caused by? (3 things)

A

(inflammation of the pericardial sac)

  • Infections: Viruses (Coxsackie B), bacteria, TB, fungal
  • Autoimmune: Rheumatic Fever, SLE, scleroderma
  • Miscellaneous: post-MI, ureamia, cardiac surgery
35
Q

5 types of acute pericarditis? (inflamed)

A
  1. Serous (usually autoimmune)
  2. Serofibrinous/fibrinous (most common cause. Due to MI, Dressler’s syndrome, uraemia, radiation. Dry, granular surface)
  3. Purulent/ suppurative (infections. Features include red, granular exudate)
  4. Haemorrhagic (blood mixed with serous or suppurative. Neoplasia, infections, following cardiac surgery)
  5. Caseous (TB or fungal)
36
Q

What are the 3 types of chronic pericarditis? (stuck down)

A
  1. Adhesive (fibrosis/ stringy adhesions. Heart can become encased in a fibrous scar)
  2. Adhesive mediastinopericarditis
  3. Constrictive pericarditis
37
Q

4 main types of Cardiomyopathy?

A

Dilated
Hypertrophic
Restrictive
Arrythmogenic right ventricular cardiomyopathy (dysplasia)

38
Q

What does Dilated cardiomyopathy lead to? And what are 3 main causes of it?

A

Progressive dilation –> contractile (systolic) dysfunction
Causes:
1. Genetic (20-50%) Autosomal dominant
2. Alcohol (10-20%) & other toxins (chemotherapy)
3. Others: SLE, scleroderma, thiamine deficiency, diabetes

39
Q

What are the complications of Hypertrophic Cardiomyopathy?

A

(ie stiff ventrical that doesnt fill properly- 100% genetic)
There is a thick walled, poorly compliant left ventricular myocardium, causing obstruction to left ventricular outflow.

  • Atrial fibrillation
  • Mural thrombus formation
  • Cardiac failure
  • Ventricular arrythmias
  • Sudden death (most common cause of sudden death in athletes)
40
Q

Restrictive Cardiomyopathy… (rare)
Morphology?
Cause?

A

Primary decrease in ventricular compliance (impaired ventricular filling during diastole)
The ventricles are normal sized- but the myocardium is firm & noncompliant
Cause: Idiopathic or secondary (infiltration)… fibrosis, amyloidosis, sarcoidosis.

41
Q

What is Arrythmogenic right ventricular Cardiomyopathy?

A

Genetic disease: RV dilation & myocardial thinning
Fibrofatty replacement of RV, & disorder if cell-cell desmosomes
Exercise= cells detach & die. (sudden cardiac death in young/ exercise)

42
Q

What is Myocarditis and what is the pathology behind it?

A

Inflammation of the myocardium.
Infection/inflammatory trigger –> cytokines, cytotoxic damage, damage myocytes –> myocyte & endothelium malfunction –> electrical/mechanical problems.

43
Q

What are some causes of Myocarditis?

Infections, Immune-mediated, other

A

Infections: Viruses (coxsackie, HIV, influenza), Bacteria (C diptheriae, N meningococcus), Fungi (Candida), Protozoa, Helminths, Chlamydiae
Immune mediated: post-viral, post-streptococcal, SLE, Transplant rejection
Other: Sarcoidosis, Giant cell myocarditis

44
Q

In terms of cholesterol, what is a better indicator of of CVD risk?

A

Not total cholesterol but high HDL & a low TC:HDL ratio is a better indicator of CVD risk.

45
Q

What 4 things can myocardial infarction lead to?

A
  • Impaired contractility
  • Tissue necrosis
  • Electrical instability
  • Pericardial inflammation
46
Q

What can impaired contractility lead to?

A

Ventricular thrombus (= stroke/ embolism)
Hypotension & reduced coronary perfusion (= cardiogenic shock)
Congestive heart failure

47
Q

What are the changes in the myocardium that occur in Ischaemic heart muscle?

A

<24hrs: normal
1-2days: pale, oedema, myocyte necrosis, neutrophils
3-4days: yellow with haemorrhagic edge, myocyte necrosis, macrophages
1-3weeks: pale, thin, granulation tissue then fibrosis

48
Q

What are 5 blood markers of IHD?

A
  1. Troponins T & I (proteins released by damaged myocytes) Raised post MI (but also in PE, myocarditis)
  2. Creatine kinase MB (primary source of CKMB is the myocardium)
  3. Myoglobin (also released from damaged skeletal muscle)
  4. Lactase dehydrogenase isoenzyme 1
  5. Aspartate transaminase (also present in liver)
49
Q

What system regulates blood pressure (and therefore vascular resistance)?

A

Renin-Angiotensin-Aldosterone System (RAAS)

50
Q

How does the RAAS work?

A

Renin (released from kidneys into blood), acts upon angiotensinogen (from liver)- which undergoes proteolytic cleavage to angiotensin I.
ACE (enzyme from lungs vascular endothelium) cleaves off 2 amino acids to form angiotensin II (acts directly on blood vessels- vasoconstriction).
This acts on the adrenal gland to stimulate the release of aldosterone–> stimulates kidneys to reabsorb salt & water.

51
Q

What are some causes of secondary hypertension?

A

Endocrine: Cushings (cortisol has aldosterone-like action on the kidneys), Thyroid disease
Renal: Diabetic nephropathy, Chronic glomerulonephritis, Polycystic disease
CVS: Aortic coarctation, renal artery stenosis
Drugs: NSAIDS, oral contraceptives

52
Q

What is Cor Pulmonale?

A

Pulmonary (right sided) hypertensive heart disease.
Right ventricular hypertrophy, dilation & potential heart failure secondary to pulmonary artery hypertension (caused by disorders of the lung)

53
Q

What are some causes of Cor Pulmonale?

A
  • Diseases of the pulmonary parenchyma (COPD, CF, bronchiectasis)
  • Diseases of the pulmonary vessels
  • Disorders affecting chest movement
  • Disorders inducing pulmonary arterial compression
54
Q

What is the difference between a true aneurysm and a pseudoaneurysm?

A

True aneurysm= when bounded by arterial wall components

Pseudoaneurysm= a breach in the vascular wall leading to an extravascular haematoma.

55
Q

Aetiology of aneurysms?

A

Atherosclerosis, cystic medial degeneration, trauma, congenital defects, infections

56
Q

What can left-sided heart failure lead to?

A

CONGESTION: Lungs (pulmonary oedema & congestion), Dyspnoea, Orthopnoea, blood tinged sputum, cyanosis
LOW CARDIAC OUTPUT: reduced kidney perfusion (RAAS= salt & fluid retention), cerebral hypoxia

57
Q

What can right-sided heart failure lead to?

A

(engorgement of systemic & portal venous systems)

  • Liver & spleen portal congestion (nutmeg liver, ascites)
  • Pleura/ pericardium (systemic congestion) effusions.
  • Oedema of peripheral body parts
58
Q

Valvular heart disease… opening problems and closing problems?

A

Opening problems= stenosis

Closing problems= regurgitation

59
Q

What is the most common cause of VHD?

A 
Aortic Stenosis (70%): calcification of a deformed valve
Mitral Stenosis: Rheumatic heart disease, which follows a group A strep infection.
60
Q

What are 4 congenital defects causing L>R SHUNT

A

Ventricular Septal Defect
Atrial Septal Defect
Patent Ductus Arteriosus
Atrioventricular Septal Defect

61
Q

What are 4 congenital defects causing R>L SHUNT

A

Tetrology of Fallot
Transposition of great arteries
Truncus Arteriosus
Tricuspid Atresia

62
Q

Difference in features concerning L>R shunt and R>L shunt?

A 
L>R = no cyanosis, pulmonary hypertension
R>L = cyanosis, venous emboli become systemic
63
Q

What is the most common CHD defect?

A

Ventricular Septal Defects (often with Tetrology of Fallot)

64
Q

What chromosome is important in heart development?

A

22q11.2 - a region of chromosome 22. Deletion= conotruncus, branchial arch

65
Q

Where does the Left Main Carotid Artery (LMCA) supply blood?

A

Supplies blood to the left ventricle & left atrium.
Left Anterior Descending= 40-50%
Left circumflex= 15-20%

66
Q

Where does the Right Coronary Artery (RCA) supple blood?

A

Supplies blood to the right ventricle, right atrium & the SA and AV nodes.
30-40%

Clinical Pathology Year 2 (11 decks)

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