1. Pyogenic liver abscesses may be caused by E. coli, Klebsiella, Streptococcus, Staphylococcus, Bacteroides, Pseudomonas, and fungi. 

Parasitic infections

1. Schistosomiasis is caused by different organisms in different parts of the world.

a. Clinical features include splenomegaly, portal hypertension, and ascites. Lesions are caused by the immune response to ova. 
2. Amebiasis is caused by Entamoeba histolytica. 
a. Clinical features include bloody diarrhea, pain, fever, jaundice, and hepatomegaly.

Drug-induced liver damage may be caused by agents that are direct hepatotoxins, such as carbon tetrachloride, acetaminophen, methotrexate, anabolic steroids, and oral contraceptive pills. 

Herpes zoster, or shingles
 - represents reactivation of a latent varicella-zoster infection.
 - virus lies dormant in sensory dorsal root ganglia and when activated involves the distribution (dermatome) of the sensory nerve with a painful vesicular eruption.
 - trigeminal verve distribution → Ramsay Hunt syndrome
 - may indicate the presence of advanced neoplastic disease or be a complication of chemotherapy.

NECROSIS

Definition: Necrosis is defined as the morphologic changes caused by the progressive degradative
action of enzymes on the lethally injured cell.

These changes are due to
I. Autolysis and
2. Heterolysis.

The cellular changes of necrosis i.e. death of circumscribed group of cells in continuity with living tissues are similar to changes in tissues following somatic death, except that in the former, there is leucocytic infiltration in reaction to the dead cells and the lytic
enzymes partly come from the inflammatory cell also. (Heterolysis). Cell death occurs in the normal situation of cell turnover also and this is called apoptosis-single cellular dropout.

Nuclear changes in necrosis

As cytoplasmic changes are a feature of degeneration ,similarly nuclear changes are the hallmark of necrosis. These changes are:
(i) Pyknosis –condensation of chromatin
(ii) Karyorrhexis - fragmentation
(iii) Karyolysis - dissolution

Types of necrosis

(1) Coagulative necrosis: Seen in infarcts. The architectural outlines are maintained though structural details are lost. E.g, myocardial infarct.
(2) Caseous necrosis: A variant of coagulative necrosis seen in tuberculosis. The architecture is destroyed, resulting in an  eosinophilic amorphous debris.
(3) Colliquative (liquifactive). Necrosis seen in Cerebral infarcts and suppurative necrosis.

Gangrenous necrosis: It is the necrosis with superadded putrefaction

May be:
a. dry - coagulative product.
b. Wet - when there is bacterial liquifaction.

Fat necrosis

May be:
a. Traumatic (as in breast and subcutaneous tissue).
b Enzymatic (as in pancreatitis). It shows inflammation of fat with formation of lipophages and giant cells.

This is often followed by deposition of calcium as calcium soaps.

Hyaline necrosis: Seen in skeletal muscles in typhoid and in liver ceIs in some forms of hepatitis.

Fibrinoid necrosis: In hypertension and in immune based diseases.
 

Pulmonary Hypertension 

Sustained elevation of mean pulmonary arterial pressure.

Pathogenesis 
Elevated pressure, through endothelial cell dysfunction, produces structural changes in the pulmonary vasculature. These changes ultimately decrease pulmonary blood flow and stress the heart to the point of failure. Based on etiology, pulmonary hypertension is divided into two categories.

Primary (idiopathic): The cause is unknown.
Secondary: The hypertension is secondary to a variety of conditions which increase pulmonary blood flow or increase resistance to blood flow. Example: Interstitial fibrosis.
Pathology 
The changes involve large and small pulmonary blood vessels and range from mild to severe. The major changes include atherosclerosis, striking medial hypertrophy and intimal fibrosis of small arteries and arterioles, and plexogenic arteriopathy. Refer to Figure 15-7 in your textbook.

Pathophysiology 
Dyspnea and fatigue eventually give way to irreversible respiratory insufficiency, cyanosis and cor pulmonale.

Abnormalities in chromosome number
Trisomy 21 (Down syndrome)
(1) The most common chromosomal disorder.
(2) A disorder affecting autosomes. It is generally caused by meiotic nondisjunction in the mother, which results in an extra copy of chromosome 21 or trisomy 21.
(3) Risk increases with maternal age.
(4) Clinical findings include mental retardation and congenital heart defects. There is also an increased risk of developing acute leukemia
and an increased susceptibility to severe infections.
(5) Oral findings include macroglossia, delayed eruption of teeth, and hypodontia.

Trisomies 18 and 13
(1) Trisomy 18 (Edwards syndrome):
characterized by an extra copy of chromosome 18. Oral findings include micrognathia.
(2) Trisomy 13 (Patau’s syndrome): characterized by an extra copy of chromosome 13. Oral findings include cleft lip and palate.
(3) Meiotic nondisjunction is usually the cause of an extra chromosome in both of these trisomies.
(4) Clinical findings for both of these trisomies are usually more severe than trisomy 21. Most children with these diseases die within months after being born due to manifestations such as congenital heart disease.

Klinefelter’s syndrome
(1) One of the most common causes of male hypogonadism.
(2) Characterized by two or more X chromosomes and one or more Y chromosomes. Typically, there are 47  chromosomes with the karyotype of XXY.
(3) The cause is usually from meiotic nondisjunction.
(4) Clinical findings include atrophic and underdeveloped testes, gynecomastia, tall stature, and a lower IQ.

Turner’s syndrome
(1) One of the most important causes of amenorrhea.
(2) Characterized by having only one X chromosome, with a total of 45 chromosomes and a karyotype of XO.
(3) Clinical findings include underdeveloped female genitalia, short stature, webbed neck, and amenorrhea. Affected females are usually
sterile. Unlike other chromosomal disorders, this one is usually not complicated by mental retardation.

Treacher Collins syndrome (mandibulofacial dysostosis)
(1) Genetic transmission: autosomal dominant.
(2) A relatively rare disease that results from abnormal development of derivatives from the first and second branchial arches.
(3) Clinical findings include underdeveloped zygomas and mandible and deformed ears. Oral findings include cleft palate and small or absent parotid glands.

Myocardial infarction (MI)—heart attack

A. Ischemia versus MI: Ischemia is a reversible mismatch between the supply and demand of oxygen. Infarction
is an irreversible mismatch that results in cell death caused by the lack of blood flow (oxygenation). For instance, chest pain caused by ischemia can be relieved by administering nitroglycerin (a vasodilator) to the patient. If the patient has an MI, the pain will not be relieved with nitroglycerin.

1. MIs most commonly occur when a coronary artery is occluded by a thrombus generated in an atherosclerotic artery.

2. Symptoms include:
a. Chest pain, shortness of breath.
b. Diaphoresis (sweating), clammy hands.
c. Nausea, vomiting.

3. Consequences:
a. Death (one third of patients).
b. Arrhythmias (most common immediate cause of death).
c. Congestive heart failure.
d. Myocardial rupture, which may result in death from cardiac tamponade.
e. Thrombus formation on infarcted tissue; may result in systemic embolism.