Pathology Flashcards
Risk factors of artherosclerosis?
- : Hyperlipidemia (high LDL is bad, high HDL is good)
- Hypertension
- Smocking
- Homocysteine
- Hemodynamic factors
- Toxins
- Viruses
- Immune reactions
- Estrogen therapy or low estrogen before menopause
Describe the Pathogenesis of endothelial chronic injury
- Risk factors to chronic endothelial injury
- Endothelial dysfunction: monocyte adhesion and emigration
- Macrophage activation and smooth muscle recruitment
- Macrophages and smooth muscle engulfs lipid
- Smooth muscle proliferation, collagen and other ECM deposition, extracellular lipid
- Arherromatous Plaque: necrotic center and fibrous cap in the Intima
What’s the difference between stable and vulnerable atherosclerotic plaque ?
Stable Plaque
- Thickened fibrous cap
- Smaller lipid core
- Less inflammatory agents
Vulnerable Plaque
- Large lipid pool
- Thin fibrous cap
- Many inflammatory cells
* ***Can cause a thrombi, rupture, aneurysm**
What are the infarct terrotories of the different coronary arteries?
In which order to we autopsy the heart?
Open in direction of blood flow: IVC → RA → RV → PA → LA → LV → aorta
What are the types of heart failure?
- Circulatory failure: inability to meet metabolic demands of body
- Cardiac or heart failure: inability to pump at sufficient rate and/or pressure too high
- Circulatory overload/congestion: excess in blood volume
- Congestive heart failure (CHF): cardiac failure + abnormal circulatory congestion
What are the possible Etiologies of heart failure?
- ↓ contractility
- ↓ preload
- ↑ preload or overload
- ↑ afterload
- Electrophysioligical abnormalities (arrhythmias, conduction)
- Aggravating factors (anemia, fever, hyperthyroidism)
What are the 2 main categories of heart failure?
- Systolic dysfunction (½ patients) FORWARD FAILURE
- end-diastolic volume and pressure → pulmonary congestion and edema and ischemia
- Diastolic dysfunction (½ patients) BACKWARD FAILURE
Reduced ventricular compliance causes ↑ end-diastolic pressure for given volume → pulmonary edema
By wich mechanism the heart tries to compensate before being in heart failure?
- Frank-Starling mechanism
- Activation sympathetic nervous system
- Renin-angiotensin system, aldosterone, ADH
- Hypertrophy (Laplace equation)
- Volume overload → ↑ stress by ↑ radius → sacomeres replicate in serie → ↑ length sarcomeres → ECCENTRIC HYPERTROPHY
- Pressure overload → stress by pressure → sacomeres replicate in parallel ↑ diam. sarcomeres → CONCENTRIC HYPERTROPHY
- Dilatation
↑ EDV → ↑ radius → ↑ stress of myocardium → stretches → pulmonary edema
How doest heart failure manifests itself in the heart itself?
- Left heart failure
→ Dyspnea, orthopnea, fatigue, paroxysmal nocturnal dyspnea
- Right heart failure
→ Jugular venous distention, hepatomegaly, peripheral edema
What are the systemic manifestations of heart failure?
- Lungs: acute (pulmonary oedema in capillaries → interstitial → alveolar) OR chronic (brown induration), we can measure with the wedge pressure (pulmonary capillary pressure – left atrial pressure) with with a balloon
- Liver: ↑ hepatic venous pressure congestive hepatomegaly, centrilobular congestion ± hepatocyte necrosis → pain, altered liver function tests and portal hypertension → congestive splenomegaly
- Pleural, pericardial, peritoneal effusions
- Edema subcutaneous tissue → pedal edema
What are the types of cardiomyopathies?
- Dilated [dilatation + systolic dysfunction]
Most common, transplantation cause, high mortality, caused by alcohol, pregnancy, nutrition, myocarditis, fat and fibrotic heart
- Hypertrophic [hypertrophy + diastolic dysfunction]
Cause of sudden cardiac death, genetic, without outflow obstruction of with outflow obstruction
- Restrictive [restriction + diastolic dysfunction]
Genetic, familial amyloidosis
- Unclassified
What are the types of shock ?
- Hypovolemic
- Cardiogenic
A. Myocardial, valvular
B. Electrophysiological
C. Pericardial - Septic
- Other
A. Neurogenic
B. Hypo-adrenal
C. Anaphylactic - Post-traumatic
Mixed of hypovolemic, tissue damage and septic
What is the pathogenesis of hypovolemic shock?
- stroke volume → ↓ cardiac output → ↓ blood pressure
- Severe: > 40% blood loss
- Compensation/decompensation: Se, Renin-angiotensine, hematocrit fall → ischemia, hypoxia, cell damage and death
What is the pathogenesis of septic shock?
Deregulated host response to infection, Organ dysfunction assessed by the Sequential [sepsis-related] organ failure assessment (A SOFA score of 2 = mortality risk of ~10%)
Primary cause of death from infection, may be occult but may be the cause of new-onset organ dysfunction
Effects include:
- Systemic necrosis (circumferential subendocardial infarct in the heart, tubular and cortical in kidney and adrenal necrosis and hemorrhage)
- Acute respiratory distress syndrome: diffuse alveolar damage + acute exudative phase of ARDS → edema and hyaline membranes: that resolves in (1) resolution, (2) proliferative phase or (3) fibrotic phase
- GI tract: gastric erosions, acute ulcers and severe ischemic necrosis in intestine
- Liver: abnormal liver function
- Brain: micro-infarcts
Systolic 120-139
Diastolic 85-89
Pre-hypertension
Stage 1 hypertension?
S: 140-159
D: 90-99
Stage 2 hypertension?
S: ≥ 160
D: ≥ 100
What organs are affected by Systemic hypertension?
- Vascular
- Renal
- Cerebral
- Retinal
What are the vascular effects of systemic hypertension?
- Arteriolar lesions (hyaline and hyperplastic arteriolosclerosis)
- Large arterial lesions (atherosclerosis)
What are the renal effects of systemic hypertension?
- Benign nephrosclerosis (scleroses glomerulus)
- Malignant” nephrosclerosis = benign nephrosclerosis plus
What are the cerebral effects of systemic hypertension?
- Large hypertensive hemorrhages related to rupture of “Charcot-Bouchard” microaneurysms
- Lacunar infarcts 2o to occlusion of small arteries
- Hypertensive encephalopathy: edema, petechial hemorrhages, necrotizing arteritis (with severe or very severe hypertension)
- Multi-infarct dementia
What are the retinal effects of systemic hypertension?
retinopathy
What are the normal pressures in the lungs?
- Normal pulmonary artery pressure (Ppa): 15-30/4-12, mean ≈ 15 mmHg
- Normal (pulmonary capillary) wedge pressure (Pw) 2-10 (5) mm Hg
What is pulmonary hypertenison?
Mean Ppa ≥ 25, systolic > 30 mmHg.
What is the mechanism of pulmonary hypertension?
Increased pressure, blood flow: “hyperkinetic” –> Active vasoconstriction –> Passive, due to elevated pulmonary venous pressure –> Vascular lesions or remodeling or destruction of the vasculature –> Obstruction of lumen –> Elevated blood viscosity (contributing factor)
What are the 5 types or pulmonary hypertenion and on what are they based?
The classification is based on the etiology of the PH.
- Pulmonary arterial hypertension: high Ppa, normal Pw (< 15 mmHg) a.k.a. “pre-capillary”
- Pulmonary hypertension owing to left heart disease: moderate ↑ Ppa and ↑ Pw (abnormality is on venous end of pulmonary circulation)
- Pulmonary hypertension owing to lung diseases/hypoxia: moderate ↓ PO2, ↑ Ppa
- Chronic thromboembolic pulmonary hypertension (CTEPH): obstruction > 3 mo
- Pulmonary hypertension with unclear or multifactorial mechanisms (idiopathic)
What are the characteristics of Pulmonary arterial hypertension?
- Associated with connective tissue diseases, HIV infection, portal hypertension or congenital (ex. Eisenmenger syndrome)
- Therapy includes vasodilators, Endothelin receptor antagonists (bosentan…) or transplantation
What are the characteristics of Pulmonary hypertension owing to left heart disease: ?
- Second to left-sided cardiac failure, mitral valvular lesions
- Leads to Arterialization of veins
What are the characteristics of Pulmonary hypertension owing to lung diseases/hypoxia?
- Due to hypoxia or vascular destruction by the disease
- Atherosclerosis large elastic arteries and peripheral muscularization arteries and pulmonary fibrosis
What are the characteristics of Chronic thromboembolic pulmonary hypertension (CTEPH)?
- Important diagnostic clue:abnormal ventilation/perfusion (V/Q) scan
- Two main forms:
1. In proximal arteries (require surgical treatment)
2. In small distal arteries (require medical therapy)
