Mind Map by , created almost 6 years ago

Doctorate Pathology (Systems Pathology) Mind Map on Cardiopathology, created by melian.yates on 11/06/2013.

Created by melian.yates almost 6 years ago
General Pathoanatomy Final MCQs (201-300)- 3rd Year- PMU
Med Student
patho. practical slides
Pancreas Pathology
German GCSE Vocab
Mapas mentales con ExamTime
Pathology of Alimentary Tract 2 (Ruminant Forestomachs/ Glandular stomach)
Musculoskeletal Pathology
Liver Pathology
General Pathoanatomy Final MCQs (301-400)- 3rd Year- PMU
Med Student
General Pathoanatomy Final MCQs (401-519)- 3rd Year- PMU
Med Student
1 Congenital Diseases
1.1 1) Septal Defects (Chamber development/partitioning)
1.1.1 Atrial Septal Defect Persistent foramen ovale 1) LA -> RA -> RV RA dilation Increased RV Preload => Eccentric RV Hypertrophy 2) Pulmonary overperfusion Increased pulmonary return => LA dilation
1.1.2 Ventricular Septal Defect (VSD) 1) LV -> RV Increased RV Preload & Afterload => Eccentric RV Hypertrophy 2) Pulmonary overperfusion Increased pulmonary return => Dilation & Increased LV Preload => LV Eccentric Hypertrophy Development of ventricular septum: Ventral -> Dorsal (Opening Dorsal near Pulmonary valve or Mitral Valve)
1.2 2) Great Vessel Vascular Anomaly (Great vessels & Valve origins)
1.2.1 Pulmonic Stenosis 1) Increased RV Afterload => RV Concentric Hypertrophy 2) Pulmonary Artery Poststenotic Dilation Dilation of base of pulmonary artery
1.2.2 Aortic Stenosis 1) Increased LV Afterload => LV Concentric Hypertrophy 2) Aortic Poststenotic Dilation
1.2.3 Tetralogy of Fallot Uncommon Calves, Pigs, Dogs Multiple congenital abnormalities simultaneously 1) Pulmonic Stenosis Increased RV Afterload => 3) RV HYpertrophy 2) VSD: RV -> LV Systemic Hypoxia 4) Dextro-rotated aorta
1.2.4 Patent Ductus Arteriosus Calves (Major vessels - Don't close until 2 weeks after birth (Normal)) 3-5cm distal to Aortic & Pulmonary valves 1) Aorta -> Pulmonary artery (Blood flow) => Increased RV Afterload => RV Concentric Hypertrophy 2) Pulmonary Overperfusion => Increased Pulmonary return -> LA Dilation & LV Preload -> LV Eccentric Hypertrophy
1.2.5 Shunting Sequelae Blood shunts from Left -> Right => Pulmonary Hyperperfusion => Sustained Pulmonary Hypertension => Vascular changes in lung & arteriosclerosis => Increased resistance (Increased pressure in RT) => SHUNT REVERSAL (Right -> Left => Cyanosis)
1.2.6 Aortic Arch Syndrome Abnormal development of the Aorta from the foetal brachial arches Aortic Arch (LT side = Normal) Mechanical disruption Persistent Aortic Arch Most Common Aorta arises from anomalous right side (RT 4th brachial arch) + Persistent Ductus Arteriosus (ligamentum arteriosum) Consequence: Vascular ring formation => Stricture of the oesophagus => Megaoesophagus => Regurgitation (undigested) Double Aortic Arch Vascular ring formed by persistence of both 4th brachial arches around the oesophagus Very rare Anomalous Subclavian Arteries Aberrant origin of one or both subclavian arteries causes oesophageal stricture
1.3 3) Valvular Dysplasias
1.3.1 Usually atrioventricular valves affected
1.3.2 Leaflets of endocardium
1.3.3 1) Valve leaflets replaced by web-like structure
1.3.4 2) Short chordae with small papillary muscles
1.3.5 Combination of 2 forms possible
1.4 Result of impaired development during embryogenesis
1.4.1 Genetics, Mother (issues during pregnancy), Chemicals, Infectious agent
1.5 Others: Coarctation of the aorta, Ectopia cordia, Endocardial fibroelastosis (Endocardium increases thickness), Pericardial abnormalities (absent or malformed)
2 Pathophysiological Mechanisms
2.1 Pump failure
2.1.1 Heart not contracting as hard as it should
2.2 Obstruction to forward blood flow
2.2.1 Systemic - Valves, Lungs (Increased PVR), Hypertension
2.3 Regurgitant Blood Flow
2.3.1 Malformed valves not closing adequately - Esp. AV valves - Reflux back into Atria
2.4 Shunted Blood Flow
2.4.1 Congenital defects (Septal defects, Persistant ductus arteriosus)
2.5 Rupture of Heart or Major
2.5.1 Hypovolemia => Shock, fluid build-up in pericardium, Increase in P
2.6 Cardiac Conduction Disorders
2.6.1 Arrhythmias - Unsynchronized contractions, blood not being pumped in proper direction
3 Myocardial Compensation
3.1 Responses of the myocardium to heart failure
3.2 Cardiomyocytes do NOT divide, can only undergo HYPERTROPHY, NOT Hyperplasia
3.3 Types
3.3.1 Concentric Hypertrophy Response to increased Afterload (Ventricular volume </= Normal) HYPERTROPHY ONLY Increase in Mass (Thicker/larger wall)
3.3.2 Eccentric Hypertrophy Response to increased Preload (Ventricular volume > Normal) HYPERTROPHY & DILATION Increase in Mass & Volume of chambers
3.4 Progression
3.4.1 Chronic Hypertrophy => Myofibre degeneration + Interstitial fibrosis
3.4.2 1:1 Ratio of Cardiomyocytes to Blood not held => Cardiomyocytes not properly perfused => Degeneration
3.4.3 Dilation can compensate up to a limit Frank Starling Mechanism Increase in Preload => Increase in SV (Functional) Congestion earlier for failing heart
4 Aquired Diseases
4.1 Pericardial Diseases
4.1.1 Non-inflammatory Hydropericardium Excessive fluid accumulates in the pericardial cavity Cardiac tamponade Haemopericardium Blood accumulates in the pericardial sac Cardiac tamponade Idiopathic Effusions
4.1.2 Inflammatory Pericarditis Causes: 1) Haemotogenous Result of septicemia (Most Common) 2) Extension from surrounding tissues Lungs, pleura, mediastinum > myocardium 3) Traumatic Ex. Traumatic Reticulopericarditis Serofibrinous/haemorrhagic Purulent Staph, strep Leakage of fibrin Sequelae Resolution Adhesion Constriction Myocarditis
4.2 Myocardial Diseases
4.2.1 Functional Ex. Concentric/ Eccentric Hypertrophy
4.2.2 Metabolic Disturbances (Degeneration) Hydrophobic degeneration Fatty change/degeneration Fatty infiltration Hylaine degeneration Mineralization (Calcification - Metastatic vs. Dystrophic) Urate deposition (visceral gout) Dehydration/Infectious agent (Impairing renal function) Uric acid accumulates in tissues (not as soluble as urea) Diet (too much Vit. D) Parathyroid problems
4.2.3 Infarction (rare in animals) Impairs contractability of heart Embolism Hyperthyroidism, Diabetes mellitus (Dogs) Acute Red (haemorrhage, hyperaemia) Grey
4.2.4 Inflammation (Myocarditis) Acute & Suppurative Acute & Non-suppurative Chronic Lymphocytes, macrophages (No Neutrophils) Infectious lesion (elsewhere) => infectious embolis
4.2.5 Parasitic Fibrous sacs
4.2.6 Nutritional (deficiencies)
4.2.7 Cardiomyopathies (Nutritional & Idiopathic) Nutritional (Vit. E/Se deficiency) Antioxidant function Mulberry heart disease White muscle disease Oxidative damage of myocytes => Necrosis Genetic Malignant hyperthermia (Pigs) - Point mutation in Ca2+ channel => Necrosis Endocrine Feline hyperthyroidism Sxs: Thin, tachycardia, hypertension, hyperactive, (possibly aggressive), Increased BMR, Increased appetite Pathology: LV Concentric Hypertrophy Uni/bi-lateral thyroid involvement Neoplasia (older)/ Hyperplasia (younger) Idiopathic Dilated cardiomyopathy (DCM) Cats (Taurine deficiency) Horses, Dogs (Toxicity) Hypertrophic cardiomyopathy (HCM) Cats LV Concentric hypertrophy Saddle thrombus (10-20% of cases) Myofibre disarray/ loss + fibrosis Point mutation in contractile proteins Turbulence in Atrium Thrombus of LA => Aortic arch Restrictive cardiomyopathy Fibrosis of endocardium Arrythmogenic RT ventricular cardiomyopathy Primarily Boxers (familial) Affects RV & S Myocardial replacement adipose tissue + fibrosis => Disruption of conduction tissue
4.3 Epicardial Disease
4.3.1 Ex. Serous atrophy of Fat
4.4 Endocardial Disease
4.4.1 Valvular Disease Consequences: Stenosis More common in AV or PV (Semi-lunar valves) Help flow to be unidirectional => Increased afterload > Concentric hypertrophy Insufficiency/ Incompetence AV Valves Large surface area => Regurgitation > upstream congestion > Increased preload > Eccentric Hypertrophy Valvular Endocardiosis Mostly Canine > 6 yrs old Small breeds (Ex. Cavalier King Charles Spaniel) Mostly arterioventricular: Mitral valve => Valvular Insufficiency (NOT Stenosis) Equine Valvulopathy Valvular lesions subtle in Horses Fibrosis AV valves => Insufficiency Aortic valve => Stenosis/Insuffiiciency
4.4.2 Endocarditis Common: Cow, Sheep, Pig Rare: Horse, Dog, Cat Septicaemia/pyaemia from septic/purulent foci Colonize/infect endothelium Septic embolism -> deposit -> Thrombus Septic Thrombi (from leaflets of valves) Usually valvular (can extend to mural) RT side: Cow LT side: Other species Both sides: Pig Sequelae: Post endocarditis valvular obliteration Septic embolism Thromboembolic infarction (post LAV endocarditis -> Kidney) Pulmonary thromboembolism (post RAV endocarditis)
4.4.3 Necrotising Mural Endocarditis
4.4.4 Endocardial Calcification
4.4.5 Valve " Cysts" Congenital Haematomas/lymphatic (AV)
4.4.6 Jet lesions Valvular insufficiency
4.4.7 Melanosis Non-significant
4.5 Cardiac Neoplasia
4.5.1 Primary Arises in Heart itself Haemangiosarcoma Endothelum (Mesenchymal) RT Atrium Chemodectoma (Heart base tumor) Epithelial
4.5.2 Secondary Lymphoma Metastasis
5 Secondary Cardiac Disease
5.1 Cor pulmonale
5.1.1 => Pulmonary disease -> Cardiac disease
5.1.2 Primary pulmonary disease Pulmonary Thromboembolism Mechanical vascular obstruction Resp. Impairment Altitude Disease (> 2000m) Pulmonary hypertension Increased Pulmonary resistance => Increased RT ventricle afterload
5.2 Systemic Disease
5.2.1 LT side of Heart affected Ex. Cats: Renal failure => Hypertension
6 Vascular Disease
6.1 Arterial Disease
6.1.1 Hypertension Intimal hypertrophy/ arteriosclerosis Obliterates lumen in artery Thickened tunica media Proliferation of tunica intima Decrease in size of lumen
6.1.2 Intramural Substance Deposit Arteriosclerosis Plaque lesions, poorly demarcated Atherosclerosis Amyloidosis Spleen or Kidney Result of chronic inflammation Alpha sheet (soluble), Beta sheet (animals -> INSOLUBLE => Deposits in tissues) Acute phase proteins (SAA) -> Normally alpha helix + inflammation => Beta pleated sheet Systemic Reactive Amyloidosis (Most common), Heritary amyloidosis (sharpei, asian cats), AL amyloidosis (Increase in plasma cells (Tumor)) Calcification Ca2+ deposits on walls of tissue Metastatic or Dystrophic Poor intestinal function Base of Aorta -> Not hypercalceamic (mimicing metastatic)
6.1.3 Fibrinoid necrosis Looks like Fibrin, but is NOT fibrin (degeneration of cells) Wall has become necrotic & died
6.1.4 Inflammation (Arteritis) Infectious (Generalized/local) Bacterial Thrombosis of vessels in skin (Infarcts) Viral Virus targeting endothelium -> infarction -> ulcers Mycotic Lush pasture/ High concentrates -> Dec. pH -> Inc. Lactic acid bacteria -> Mucosal erosion (Rumen/abomasum) -> FUNGAL INVASION (mucosa & vasculature) -> Thrombosis (obliteration of lumen) -> Necrosis Parasitic Upstream: Venacava -> obliteration Downstream: Arteriosclerosis Non-infectious Type III Hypersensitivity Ag-Ab complex (deposit in vasculature & glomeruli) Immune complex mediated inflammation & tissue injury Ex. Purpura haemorrhagica (Horses) Sequella of infection Idiopathic Ex. Polyarteritis nodosa, Beagle pain syndrome
6.1.5 Mural/luminal changes Aneurysms Aortic rupture Thrombosis
6.2 Venous Disease
6.2.1 Thrombosis/phlebitis Jugulars, Venacava, Portal vein
6.2.2 Rupture Exercise induced (Horses)
6.3 Mural/Luminal Structural Chamges
6.3.1 Aneurysm
6.3.2 Rupture
6.3.3 Thrombosis 1) Damage to Endothelium 2) Changes in BF 3) Changes in coagubility
6.3.4 Idiopathic (Ex. Hypertrophic cardiomyopathy)

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