1.What is cardiac cirrhosis and centrilobular necrosis?
RHF/CHF→ “chronic passive congestion of the liver, the central regions of the hepatic lobules are grossly red-brown and slightly depressed (owing to a loss of cells) and are accentuated against the surrounding zones of uncongested tan liver (nutmeg liver). Microscopically, there is evidence of centrilobular necrosis with loss of hepatocytes dropout and hemorrhage, including hemosiderin-laden macrophages. In severe, long-standing hepatic congestion (most commonly associated with heart failure), there may even be grossly evident hepatic fibrosis (cardiac cirrhosis). Because the central portion of the hepatic lobule is the last to receive blood, centrilobular necrosis can also occur whenever there is reduced hepatic blood flow (including shock from any cause); there need not be previous hepatic congestion.” (Robbins et al 7E, pg 122)
2.What is the mechanism of chronic ischemic heart disease?
“In more than 90% of cases, the cause of myocardial ischemia is reduction in coronary blood flow due to atherosclerotic coronary arterial obstruction. Thus, IHD is often termed coronary artery disease (CAD) or coronary heart disease. In most cases, there is a long period (decades) of silent, slowly progressive, coronary atherosclerosis before these disorders become manifest. Thus, the syndromes of IHD are only the late manifestations of coronary atherosclerosis that probably began during childhood or adolescence.” (Robbins et al 7E, pg 571)
1. Cardiac Cirrhosis
Lon standing severe right hart failure leads to elevated central venous pressure which spreads directly to the liver via the inferior vena cava and hepatic veins. The venous congestion in the liver blocks drainage of the sinusoidal blood flow into terminal hepatic venules which will cause atrophy and fibrosis around the central areas.
Right heart failure in the presence of left heart failure there is severe central hypoxia producing necrosis around the central areas with seinusoidal congestion.
2. Mechanism of chronic ischemic heart disease
Prior myocardial infarction sometimes with previous coronary artery bypass graft --> damage to myocardium will cause decrease in contractility and cardiac output--> blood backs up into left ventricle --> left ventricular dilates to hold volume and then hypertrophy to increase contractility --> postinfarction decompensation due to exhaustion of the compensatory hypertrophy of the noninfarcted myocardium
1a. Cardiac cirrhosis- after RHF (preceded by LHF), there is backup of the IVC. Venous congestion impeds efficient drainage of the sinusoidal blood flow into the terminal hepatic venules. Therefore there is sinusoidal stasis which leads to an accumulation of deoxygenated blood. Therefore with the accumulation of the deoxygenated blood there is necrosis which is followed by deposition of collagen and then finally, fibrosis.
1b. The Nutmeg liver is also seen due to chronic passive congestion of the liver which is secondary to RHF. THe central lobules of the liver are red and or brown as they are engorged by the hepatic vein from the backed up IVC and hence stand out against the non-congested part of the liver which appears tan.
2. Chronic Ischemic Heart Disease- Is a condition where there is a reduced blood supply to the heart, which eventually will turn into a complete obstruction of the heart. The major pathogenesis lies in the formation of an atheroma (CAD), with the risk factors including hypertension, diabetes, smoking and hypercholesteremia/hyperlipidemia. Once the atheroma is present and occlusions are formed a patient may present with various forms of angina. If the occlusion is less than 75%, it is stable angina where pain is only felt upon stress. The coronary plaque is fixed and is not changing. Nitroglycerine can be used to relieve such cases. Once the occlusion or atheromatous plaque exceeds 75%, therefore the plaque changes, but does not reach 100% occlusion, it is considered Unstable Angina. In unstable angina pain is felt even without a stressor. There is a small thrombus in addition to the plaque formation. C-Reactive protein can be used as a biochemical marker in cases of angina to see the risk of MI. An MI will occur once a 100% occlusion has been reached. This 100% occlusion in an MI can be reached by one of three categories: 1) rupture of a plaque where the clot ruptures, ulcerates, hemorrhages and then erodes. 2)Prolonged coronary artery spasms which may be effected by smoking or using street drugs such as cocaine or 3) Emboli from some other pathophysiological problem such as vegetative endocarditis or a paradoxical embolism usually occuring due to a VSD or ASD. Overall ischemic heart disease manifests its way from the beginning of the atheroma into either angina, MI, cardiac death or will prolong to produce chronic ischemic heart disease.
Cardiac cirrhosis is the appearance the liver takes in response to chronic passive congestion secondary to right heart failure. Cardiac cirrhosis also called nutmeg liver is where hepatic lobules are red-brown and slightly depressed and are against the surrounding zones of uncongested tan liver.
Centrilobular necrosis- the central portion of the hepatic lobule is the last to receive blood and necrosis can occur due to reduced or insufficient blood flow.
What is the mechanism of chronic ischemic heart disease? Ischemic heart disease (Coronary Heart Disease/ Coronary Artery Disease) is the reduction of coronary blood flow due to atherosclerotic arterial obstruction. Coronary heart disease risk increases with age, smoking, hypercholesterolaemia (high cholesterol levels), diabetes, hypertension (high blood pressure) and is more common in men and those who have close relatives with ischaemic heart disease.
Cardiac Cirrhosis (nutmeg liver) is due to long standing severe right-sided congestive heart failure. The congestion leads to a build up of venous pressure within the circulation, which the heart cannot handle, causing blood to back up in the body’s major veins. Eventually, the liver becomes engorged and swollen with blood for a prolonged period of time. This leads to chronic liver injury and inflammation and the formation of scar tissue in the liver (fibrosis). The liver appears "speckled" like a grated nutmeg kernel, from the dilated, congested central veins (dark spots) and paler, unaffected surrounding liver tissue.
2. What is Centrilobular Necrosis?
It is a necrosis restricted to the hepatocytes immediately surrounding the central venule. Occurs when left-sided heart failure and right-sided heart failure are both present and severe central hypoxia produces such a necrosis along with sinusoidal congestion.
3. Mechanism of Chronic ischemic Heart Disease?
It is a disease characterized by inadequate coronary perfusion relative to the myocardial demand. The disease process underlying most ischemic heart disease is atherosclerosis of the coronary arteries. The arteries become "furred up" by fat-rich deposits in the vessel wall (plaques), reducing blood supply to the heart muscle.