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CR3 > Cardio-vascular Pathology > Flashcards

Cardio-vascular Pathology Flashcards

1
Q

Define HF

A

Inability of the heart to pump blood at a rate required of metabolising tissues

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2
Q

Examples of systolic dysfunction

A

IHD
Cardiomyopathy
Pressure or volume overload = systemic hypertension or AS

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3
Q

Examples of diastolic dysfunction

A

(inability to relax/fill)

  • amyloid
  • myocardial fibrosis
  • constrictive pericarditis
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4
Q

Frank-Starling Law

A

Stretching = increased contraction

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5
Q

Which mechanisms compensate dysfunction?

A
  • Starling law
  • hypertrophy = chamber dilatation
  • neurohormonal systems (noradrenaline, RAS, ANP)
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6
Q

Consequence of pressure overload

A

concentric hypertrophy

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7
Q

Consequence of volume overload

A

Cavity dilatation

Without thickening?

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8
Q

Consequence of hypertrophy

A

Capillary decrease
Fibrous tissue increase
Increased metabolic needs
Vicious cycle = failure

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9
Q

Left Sided Failure Define

A
  • due to peripheral pressure fall and pulmonary circulation damming
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10
Q

Symptoms of left sided failure

A

Lungs congested
Oedema
Dyspnoea, orthopnea, PND
Brain and kidneys affected if severe/hypoxia

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11
Q

Right Sided Failure Features

A

Secondary to LVF usually

Severe pulmonary HTN

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12
Q

Symptoms of right sided failure

A

Nutmeg liver = congested
Portal Vein pressure increase = splenomegaly, ascites
Kidneys and brain hypoxia
Peripheral oedema

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13
Q

Calculation for BP

A

CO x Peripheral Resistance

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14
Q

Renal causes of HTN

A 
CKD
Glomerulonephritis
APKD
RAS
Vasculitis
Renin tumour
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15
Q

Neurological causes of HTN

A

Stress
Psychogenic
Raised ICP

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16
Q

CV causes of HTN

A

Aortic coarctation
Systemic vasculitis
Increased intravascular volume or CO

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17
Q

Endocrine causes of HTN

A 
Cushings
Conns
Exogenous hormones
Phaeo
Acromegaly
Hyper/hypo thyroid
Pregnancy
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18
Q

What affects cardiac output?

A

HR
Contractility
Sodium, mineralocorticoids, atriopeptin

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19
Q

Hormone Constrictors

A 
Angiotensin II
Catecholamines
Thromboxane
Leukotrienes
Endothelin
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20
Q

Hormone Dilators

A

Prostaglandins
Kinins
NO

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21
Q

Neural constrictors

A

alpha-adrenergic

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22
Q

Neural dilators

A

beta-adrenergic

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23
Q

Local factors affecting peripheral resistance

A

Ions = pH, hypoxia

Autoregulation

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24
Q

How does HTN affect the heart?

A

LVH

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25
Q

How does HTN affect vessels?

A

Atheroma
Aortic dissection
Cerebrovascular haemorrhages
Degenerative changes = fibrointimal thickening

26
Q

How does HTN affect small vessels?

A

Hyaline arteriosclerosis
Hyperplasic arteriolosclerosis
Fibrinoid necrosis

27
Q

What is Cor pulmonale

A

Pulmonary HTN

28
Q

Causes of cor pulmonale?

A

Disease of lung parenchyma (COPD, CF, DIF)
Disease of pulmonary vessels (PEs, vasculitis, PH)
Disorders of chest movement (neuromuscular disease, kyphoscoliosis)
Disorders causing arterial constriction (chronic altitude sickness, hypoxaemia)

29
Q

Features of cor pulmonale

A 
Acute with massive PE
Or chronic
RV hypertrophy
RA hypertrophy and dilatation
Thickened R ventricle >0.5cm
Tricuspid regurg
30
Q

Vasculitis

A

inflammation of vessel walls
Infectious or non
Non are immune complex mediated = by ANCA, direct antibodies, cells, paraneoplastic or idiopathic

31
Q

Anti GBM disease

A

Immune complex small vessel vasculitis

e.g = cryoglobinemia, IgA Henoch Schonlein, hypocomplementemic urticarial

32
Q

ANCA Associated Small Vessel Vasculitis

A

Microscopic polyangiitis
Wegners = granulomatosis with polyangiitis
Churg Strauss = eosinophilic granulomatosis with polyangitis

33
Q

Large vessel Vasculitis

A

Takayasu Arteritis

Giant Cell Arteritis

34
Q

Medium Vessel Vascultiis

A

Polyarteritis Nodosa

Kawasaki Disease

35
Q

Effects of vasculitis

A

Mural necrosis and haemorrhage
Secondary ischaemia of down stream tissue
May cause infarction
Localised/organ specific/ systemic

36
Q

Polyarteritis Nodosa Features

A 
Systemic vasculitis
Arteries 
Often spares lungs
At branching sites
Segmental necrotising inflammation of arteries = renal, cardiac, GI tract
37
Q

Effects of polyarteritis nodosa

A

Aneurysms, infarcts, haemorrhage
Transmural inflammation and fibrinoid necrosis (all 3 layers)
Thrombosis of vessel
Fibrosis becomes nodular

38
Q

Polyarteritis Nodosa Presentation

A 
Young Adults
Episodic
Fever, malaise, weight loss, HTN, abdo pain, melaena, muscular pain, renal involvement, peripheral neuritis
Gangrene
Migraine
Liver infarcts
No haematuria
39
Q

Therapy for polyarteritis nodosa

A

Steroids

Cyclophosphamide

40
Q

Causes of polyarteritis nodosa

A

Hep B
Hep C
Cryoglobulins

41
Q

ANCA related vasculitis features

A

Systemic or renal limitied
Flu like illness
Fever, arthralgia, myalgia, purpura, peripheral neuropathy, GI
Provoked by drugs = PPU, penciliiamine, hydralazine

42
Q

Wegners granulomatosis geatures

A 
URT/LRT
Occular/ear
Necrotising granulomas
Vasculitis
c-ANCA usually
PR3
43
Q

Presentation of Wegners granulomatosis

A 
Sore eye
Sore ear
Stuffy nose
Sore joints
Gangrene
Permanent kidney failure
Destruction of face
Lung cavities and bleeds
44
Q

How to treat ANCA associated vasculitis

A

Cyclophosphamide
Steroids
Aggressive otherwise 1 year mortality if untreated

45
Q

Define cardiomyopathy

A

Cardiac disease from primary intrinsic myocardial abnormality
Exclude ischaemia as a cause

46
Q

3 main types of cardiomyopathy

A

Dilated - ventricles enlarge
Hypertophic - walls thickened
Restrictive - walls stiff but not necessarily thickened

47
Q

Features of dilated cardiomyopathy

A

Contractile dysfunction
valves/arteries normal mostly
Thrombi
Myocardial hypertrophy/fibrosis

48
Q

Causes of dilated cardiomyopathy

A 
Idio
Genetic
Post myocarditis
Alcohol/toxicity
Pregnancy associated
Haemochromatosis
Sarcoidosis
49
Q

Presentation of dilated cardiomyopathy

A

20-50yrs
LVF and RVF
Death from failure or sudden arrhythmia

50
Q

How to treat dilated cardiomyopathy?

A

Transplantation

51
Q

Hypertrophic Cardiomyopathy Effects

A

Poor diastolic filling
Outflow obstruction
Disproportionate thickening of septal myocardium
micro hypertrophy and fibrosis

52
Q

Causes of hypertrophic cardiomyopathy

A

Beta myosin mutation (muscle protein)
Familial
Many different mutations

53
Q

Treatment of hypertrophic cardiomyopathy

A

May need surgery

54
Q

Restrictive cardiomyopathy causes

A

Idio

secondary to amyloidosis, sarcoidosis, tumour metastases

55
Q

Features of restrictive cardiomyopathy

A

Dilated atria

Firm ventricles

56
Q

Myocarditis define

A

inflammation causing myocardial injury and no response to it

57
Q

Infections causing myocarditis

A

Enterovirus, HIV, chalmydia, rickettsiae, bacteria, fungi, protozoa

58
Q

Immunological causes of myocarditis

A

SLE, drug reactions, transplant rejections

59
Q

Other causes of myocarditis

A

Sarcoidosis, giant cell myocarditis

60
Q

Features of myocarditis

A

Direct damage or T cell mediated to antigens of myocyte surface
Inflammation
Myocyte necrosis
Fatigue, fever, chest discomfort, HF, arrhythmias, sudden death

61
Q

What can myocarditis lead to

A

Dilated cardiomyopathy

CR3 (30 decks)

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