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CARDIO/RESP > Pathology > Flashcards

Pathology Flashcards

1
Q

What is the leading cause of mitral stenosis and what are some clinical features?

A

Cause: Rheumatic fever
Features: AF due to thrombi, haemoptysis, pulmonary congestion and HTN, RV hypertrophy

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2
Q

What are the causes of and clinical features present with aortic stenosis?

A

Causes: degenerative calcification, old age, rheumatic aortic valve disease
Features: small pulse, LV hypertrophy, angina, syncope, LV failure, death

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3
Q

What type of murmur does mitral stenosis and aortic stenosis produce?

A

Mitral - rumbling diastolic

Aortic - ejection systolic murmur

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4
Q

What is infective endocarditis?

A

Infection of heart valves or mural endocardium by a microbe with formation of vegetations

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5
Q

What are the clinical forms of infective endocarditis?

A

(1) Acute endocarditis - caused by virulent organisms, large vegetations, valvular destruction (staph aureus)
(2) Subacute endocarditis - less virulent organisms, grow slowly on damaged valves (more common) - strep viridian’s

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6
Q

What are some of the pathological features of dilated cardiomyopathy?

A

Hypertrophy and dilatation of all 4 chambers, with bowing of the iV septum to the right side

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7
Q

What are the pathological features of hypertrophic cardiomyopathy?

A

Myocardial hypertrophy and abnormal diastolic filling due to increased wall thickness

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8
Q

What are the pathological features of restrictive cardiomyopathy?

A

Ventricles are normal sized, cavities not dilated, but the myocardium is firm and non-compliant

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9
Q

What is myocarditis?

A

Inflammation of the myocardium with lymphocytic infiltration

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10
Q

What are the infectious causes and immune mediated causes of myocarditis?

A

Infectious - virus, bacteria, protozoa, rickettsial, fungal

Immune mediated - post viral, post strep, SLE, RF, Polymyositis, drug

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11
Q

What is the most common tumour of the heart and where is it found?

A

Myxoma - commonly found in the atria in the fossa ovalis

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12
Q

What anatomical location is affected by chronic bronchitis? and is the pathology, etiology, symptoms?

A

Bronchus - mucous gland hyperplasia and hyper secretion
cause - smoke, pollutants
signs - cough, sputum

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13
Q

What is the anatomical location of emphysema and what are the pathological changes, ethology and signs?

A

Acinus - airspace enlargement, wall destruction due to tobacco smoke
- dyspnea, barely chest, wheeze, cough

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14
Q

What types of emphysema are there?

A

Centriacinar - upper lobes, proximal portion of acinus

Panacinar - all lung fields, particularly bases

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15
Q

What is the pathogenesis of emphysema?

A

Imbalance between enzymes being produced - smoking inhibits the anti-proteases found in normal bronchial mucous

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16
Q

What is bronchiectasis and what are the clinical and pathological features?

A

Permanent dilation of the bronchi/bronchioles as a result of obstruction or infection.
Features: constant cough, smelly sputum, finger clubbing
Pathology: dilatation, purulent material, inflamed and ulcerated, fibrosis and lymphoid folicle formation

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17
Q

What is the pathogenesis of asthma?

A

Various stimuli/allergens resulting in reversible bronchoconstriction.
Also mucous plugging, focal necrosis, deem of bronchiole walls, hypertrophy of mucous glands and smooth muscle

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18
Q

What are some obstructive lung diseases?

A
  • Chronic bronchitis
  • Bronchiectasis
  • Asthma
  • Emphysema
  • Small airway/bronchiolitis
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19
Q

What are the 4 stages of the acute inflammatory response in bacterial pneumonia?

A

(1) Congestion
(2) Red hepatisation
(3) Grey hepatisation
(4) Resolution

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20
Q

What are the common causative organisms of bacterial community acquired acute pneumonia?

A 
o	Streptococcus pneumoniae
o	Haem. Influenza
o	Moraxella catarrhalis
o	Staph aureus 
o	Klebsiella pneumoniae 
o	Pseudomonas aeruginosa
o	Legionella pneumophilia
21
Q

What are the community acquired atypical pneumonias mostly caused by?

A

Viral (influenza, adenovirus) and mycoplasma

22
Q

What are the common organisms causing pneumonia in the immunocompromised host?

A

o Bacterial – pseudomonas aeruginosa, mycobacterium, legionella listeria monocytogenes
o Viruses – CMV, Herpes
o Fungi

23
Q

What are some clinical manifestations of heart failure?

A

Abdominal and cerebral symptoms, peripheral deem, dyspnoea, fatigue and weakness, cachexia

24
Q

What does ‘forward failure’ and ‘backward failure’ in heart failure mean?

A

FF - diminished cardiac output, reduced tissue perfusion

BF - Pooling of blood in venous system + edema

25
Q

In hypertensive heart disease, which side of the heart is affected by systemic HTN and pulmonary HTN?

A

Systemic - Left

Pulmonary - Right

26
Q

What are the heart changes occurring in systemic hypertension?

A

Concentric LV hypertrophy with increased wall thickness

It impairs diastolic filling, leading to atrial enlargement

27
Q

What is Cor Pulmonale?

A

Right ventricular enlargement due to pulmonary hypertension caused by disorders of the lungs or pulmonary vessels

28
Q

What are the types of Angina pectoris?

A
  1. stable angina - induced by exercise, relieved by GTN or rest
  2. variant form - recurrent prolonged attacks of severe ischaemia caused by spasm of coronary artery
  3. unstable angina - pain at rest that persists
29
Q

What is a transmural (STEMI) and a subendocardial (NSTEMI) MI?

A

STEMI - full thickness necrosis in area supplied by single coronary artery
NSTEMI - circumferential necrosis around inner 1/2-1/3 of V wall

30
Q

What are complications of MI?

A

Sudden death

other: arrhythmia, cardiogenic shock, pericarditis, mural thrombus, PE, tamponade

31
Q

Whats the difference between arteriosclerosis and atherosclerosis?

A

arterio - thickening/hardening of arteries for any reason

Athero - due to fatty material (atheroma/plaque)

32
Q

What are the stages in the inflammatory response resulting in atherosclerosis?

A

(1) endothelial injury - LDL/cholesterol etc
(2) inflammation - monocytes, T cells, foam cells
(3) fibroproliferative response - smooth muscle cells migrate and produce CT elements
(4) plaque formation in tunica intima

33
Q

What is a fibrous plaque?

A

A raised lesion with a soft lipid core, covered by a firm fibrous cap and usually involves a partial circumference of the wall

34
Q

What are the 5 complications of atherosclerosis?

A
  1. calcification
  2. ulceration
  3. rupture
  4. haemorrhage
  5. aneurysmal dilatation
35
Q

What are major consequence of atherosclerosis in the heart, brain, peripheral arteries and aorta?

A

heart - MI, Angina
brain - CVA, TIA
Peripheral - gangrene
Aorta - abdominal aortic aneurysm

36
Q

What are the two types of small blood vessel disease?

A
  1. hyaline arteriosclerosis - due to endothelial damage = smooth muscle hypertrophy and fibrosis
  2. hyperplastic - occurs in HTN emergency patients - concentric prolif. of smooth muscle (onion skin)
37
Q

How would a patient with pulmonary HTN present?

A

RH failure (peripheral edema, failure to oxygenate (anginal chest pain, SOB), arrhythmias

38
Q

What are aneurysms and how can they be classified?

A

Abnormal localised dilatation of a vessel or part of the heart (media)

  1. Cause
  2. Morphology - saccular or fusiform
  3. Anatomical site
39
Q

What are 3 main complications of aneurysms?

A
  1. rupture - rapidly fatal
  2. occlusion - disturbance in blood flow leads to thrombus
  3. mass effect - compress other structures
40
Q

What is an intracranial berry aneurysm? clinical features and complications

A

Saccular cerebral aneurysm, form from defective smooth muscle in the artery.
Features - before rupture usually nothing, after = thunderclap headache, vomiting, collapse, seizure, death

41
Q

What is an abdominal aortic aneurysm, features and complications?

A

Fusiform aneurysm
complications - rupture, peripheral thromboembolism
features - asymptomatic maybe back pain, then rupture = abdominal pain + pulsatile mass

42
Q

What is an aortic dissection? complications and clinical features?

A

Blood enters wall of the aorta through a tear in the intimate, separating the media. (*marfans)
complications - rupture, extension to branches of aorta/occlusion (MI, stroke)
features - sudden onset chest pain/between shoulder blades, collapse, shock, death

43
Q

What is Marfan’s syndrome?

A

Autosomal dominant genetic disorder with mutation of fibrillin gene (results in abnormal elastic tissue)

44
Q

What is vasculitis?

A

Inflammation of the blood vessels leading to thickening (ischaemia via occlusion) or thinning (aneurysm)

45
Q

What is temporal arteritis?

A

Inflammation of large and medium sized arteries - often branch of carotid

46
Q

What is polyarteritis nodosa?

A

Multisystem necrotising vasculitis involving medium sized arteries
Fibrinoid necrosis, neutrophils, lymphocytes infiltrate, narrowing of lumen, thrombosis, ischaemia

47
Q

Granulomatosis with polyangitis - Wegener’s?

A

Small vessel vasculitis affecting upper and lower resp tract + kidney

48
Q

What are some factors that may increase the load on a persons heart?

A
  • Anaemia
  • Sepsis
  • Thyroid disease
  • Pregnancy
  • Medications
  • Renal/resp failure

CARDIO/RESP (5 decks)

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