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CR Year 3 > Cardio-Vascular pathology > Flashcards

Cardio-Vascular pathology Flashcards

1
Q

Heart Failure Definition

A

Inability of heart to pump blood at rate commensurate with the requirements of the metabolising tissues

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2
Q

HF usually develops…

A

Slowly on background of cardiac hypertrophy

BUT may be acute e.g. MI, acute valve dysfunction

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3
Q

HF Systolic dysfunction causes

A

Ischaemic heart disease
Pressure or volume overload such as systemic hypertension or AS
Cardiomyopathy

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4
Q

HF Diastolic dysfunction causes

A

Inability to relax/fill
Amyloid
Myocardial fibrosis
Constrictive pericarditis

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5
Q

HF problems forwards + backwards

A

Decreased output

Damming of blood in venous system

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6
Q

HF Compensation mechanisms

A

Frank-Starling law: stretching leads to increased contraction •hypertrophy +/-chamber dilatation
•activation of neurohormonal systems including noradrenaline, RAS and atrial natriuretic peptide

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7
Q

HF Consequences

A

Heart size/weight increase
•hypertrophy not hyperplasia (sudden death)
•pressure overload -concentric hypertrophy
•volume overload -cavitary dilatation maybe without thickening
•hypertrophy -capillary decrease -increase in fibrous tissue -increased metabolic needs -vicious circle ——> failure

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8
Q

Left sided HF- main features

A

Decreased peripheral pressure + damming of blood in pulmonary circulation
brain + kidneys affected if severe (hypoxia)

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9
Q

Left sided HF symptoms

A

Lungs congested
Oedema
Accumulation of haemosiderin laden macrophages in alveoli- leads to dyspnoea, orthopnoea, PND

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10
Q

Right sided HF

A

Usually secondary to LVF

Primary association with severe pulmonary HT

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11
Q

Right sided HF autopsy

A

Liver congested- “nutmeg” appearance, centrilobular necrosis + fibrosis

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12
Q

Right sided HF signs

A

Portal vein pressure increase- splenomegaly, ascites

Kidneys + brain hypoxia, peripheral oedema

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13
Q

Hypertension

A 
Elevated BP
Systolic >140, Diastolic >90
Important RF for IHD, CVD (cerebro vascular disease), aortic dissection, cardiac failure, renal failure
Primary/essential (95%)
Secondary
"benign" or "malignant/accelerated" (5%)
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14
Q

Biventricular failure

A

Both Right and Left side features

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15
Q

Secondary Hypertension causes

A

Renal
Neurological
Cardiovascular
Endocrine

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16
Q

2dary hypertension- renal

A 
Chronic renal disease
Glomerulonephritis
Polycystic kidney disease
Renal artery stenosis
Vasculitis
Renin tumour
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17
Q

2dary hypertension- neurological

A

Stress inducing surgery
Psychogenic
Raised intracranial pressure

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18
Q

2dary hypertension- cardiovascular

A

Coarctation of aorta
Systemic vasculitis
Increased intravascular vol. or CO

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19
Q

2dary hypertension- endocrine

A 
Adrenocortical hyperfunction (Cushings/Conns)
Exogenous hormones
Phaeochromocytoma
Acromegaly
Thyroid disease (hyper or hypo)
Pregnancy
20
Q

BP equation

A

BP = Cardiac Output x Peripheral Resistance

21
Q

Hypertension pathological features

A

LVH
Vessels- atheroma, dissection, cerebrovascular haemorrhage, degenerative changes such as fibrointimal thickening
Small vessels- hyaline arteriolosclerosis esp. kidneys, hyperplastic arteriosclerosis (onion skinning), fibrinoid necrosis in vessel wall

22
Q

Cor pulmonale

A

Heart disease consequent to lung disease

23
Q

Pulmonary HT

A

High BP in pulmonary circulation

24
Q

Pulmonary HT/Cor pulmonale causes

A

Disease of lung parenchyma e.g. COPD, cystic fibrosis, diffuse interstitial fibrosis
Diseases of pulmonary vessels e.g. recurrent PEs, primary PH, severe vasculitis
Disorders affecting chest movement e.g. kyphoscoliosis, neuromuscular disease
Disorders causing arterial constriction e.g. hypoxaemia, chronic altitude sickness

25
Q

Cor pulmonale

A

Acute or chronic (acute with passive PE, normally chronic)
See RV hypertrophy, RA hypertrophy + dilatation of both chambers
Tricuspid regurg
Clinical features as of RVF plus primary disease

26
Q

Thickened R ventricle criteria

A

Normal <0.5cm

27
Q

Vasculitis

A

Inflammation of vessel walls
Infectious or non-infectious
Non-infective are immune complex, ANCA mediated, direct antibody mediated, cell mediated, paraneoplastic or idiopathic

28
Q

Vasculitis in general

A

All show vascular injury with mural necrosis and haemorrhage
Localised, organ restricted or systemic
Some are granulomatous
Secondary ischaemia of down-stream tissue
May cause infarction

29
Q

Polyarteritis nodosa

A

Systemic vasculitis
Small/medium sized arteries (not veins or smaller vessels)
Often spares lungs
Segmental necrotising inflammation of arteries especially renal, cardiac and GI tract
Branching sites particularly

30
Q

Polyarteritis nodose diagnosing

A

Angiogram

See hallmark changes- usually aneurysms

31
Q

Polyarteritis nodose can lead to

A

Aneurysms, infarcts, haemorrhage
Microscopically transmural inflammation and fibrinoid necrosis
Possible thrombosis of vessel
After healing, there is fibrosis which later becomes nodular
Lesions of different ages

32
Q

Polyarteritis nodosa features

A 
Young adults
More men than women
Acute, subacute or chronic
Fever, malaise, weight loss, HT abdo pain + melaena, muscular pains, renal involvement (not gloms), peripheral neuritis
30%  have Hep B antigen +
Therapy- steroids + cyclophosphamide
33
Q

ANCA related vasculitis

A

Systemic/renal limited/other
85% ANCA positive
Flu-like illness
Fever, arthralgia, myalgia, purpura, peripheral neuropathy, GI involvement
May be provoked by drugs (propylthiouracil, penicillamine, hydralazine)

34
Q

ANCA related vasculitis staining patterns

A

cytoplasmic and perinuclear (c and p) by IMF
c-ANCA- targeting proteinase r (PR3)
p-ANCA- targeting myeloperoxidase (MPO)

35
Q

ANCAs in patients without vasculitis

A

Non-MPO p-ANCA in UC, PSC, autoimmune hep, RA/Felty’s

36
Q

Wegener’s granulomatosis (aka granulomatosis with polyangitis)

A 
Upper/lower RT
Eyes/ears
Necrotising granulomas
Vasculitis
c-ANCA usually
Proteinase 3 (PR3)
Often have kidney involvement
37
Q

ANCA treatment

A

NEED TO BE TREATED- Untreated 80% 1 year mortality
Treated 75% 5 year survival
Aggressive immunosuppression with cyclophosphamide + steroids

38
Q

Cardiomyopathy

A

Cardiac disease resulting from primary intrinsic myocardial abnormality
Exclude other causes e.g. ischaemia
Causes are idiopathic or secondary to known cause
3 types (mainly involving left ventricle)- dilated, hypertrophic + restrictive
4th type- arrhythmogenic right ventricular CM

39
Q

Dilated cardiomyopathy

A

Progressive cardiac dilatation + contractile dysfunction
Big heart
4 chamber dilatation
Valves/arteries not significantly abnormal
May be thrombi
Microscope -myocardial hypertrophy/fibrosis

40
Q

Dilated cardiomyopathy features

A 
Idiopathic
Genetic 930%)
Post myocarditis
Alcohol or other toxicity e.g. doxorubicin
Pregnancy associated
Haemochromatosis
Sarcoidosis
41
Q

Dilated cardiomyopathy patients

A 
any age but usually 20-50
Progressive CCF
Signs of LVF + RVF
Death from failure or sudden death (arrhythmia)
Need transplant
42
Q

Hypertrophic cardiomyopathy

A

Hypertrophic heart
Poor diastolic filling
Often outflow obstruction
Little or no dilatation
Classically disproportionate thickening of septal myocardium esp. subaortic
Microscope- hypertrophy, disarray + fibrosis

43
Q

Hypertrophic cardiomyopathy features

A

Mutation of muscle protein esp. beta-myosin heavy chain
Most familial
Many diff. mutations
Leads to poor compliance + reduced LV chamber size +/- outflow obstruction
Clinically heterogenous, may need surgery to remove muscle in LV and let blood flow through

44
Q

Restricted cardiomyopathy

A

Primary decrease in ventricular compliance
Idiopathic
Secondary to irradiation fibrosis, amyloid, sarcoid, tumour metastases, other
Firm ventricles (otherwise normal) with dilated atria
Microscopy may reveal cause

45
Q

Myocarditis

A

Inflammation causing myocardial injury and not a response to it
Infections- viruses (most common) e.g. Coxacjieviruses, enteroviruses, HIV; chlamydia, rickettsiae, bacteria, fungi, protozoa, Helminths
Immunological- post-viral, SLE, drug reactions, transplant rej
Others- sarcoidosis, giant cell mypcarditis

46
Q

Myocarditis injury

A

May be direct damage or T cell mediated injury to antigens on myocyte surface
Inflammation and myocyte necrosis
Clinically fatigue, fever, chest discomfort, HF, arrhythmias, sudden death
May mimic acute infarct
May lead to dilated cardiomyopathy

CR Year 3 (7 decks)

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