N-Trivia

Posted: 13 Jan 2011 06:37 PM PST

Definition

Implantation is the penetration of the growing structure to the uterine endothelium. It occurs approximately 8 to 10 days after fertilization.

Sequential Events in Implantation

Immediately after fertilization, the fertilized ovum or zygote stays in the fallopian tube for 3 days. During this time a rapid cell division (mitosis) or cleavage is taking place.
The first cleavage occurs at about 24 hours and it continues to rapidly divide at a rate of one in every 22 hours.
The developing cells are now termed as BLASTOMERES.
When 16 to 50 blastomeres (developing cells) are present, the cells tend to create a bumpy appearance and it is now called MORULA. Morula comes from a Latin word "morus" meaning mulberry.
In this morula form, it will start to travel by ciliary action and peristaltic contractions of the Fallopian tube to the uterus. It continues to multiply as it floats free in the uterine cavity for 3 or 4 days.
Large cells tend to accumulate at the side of the structure. Because of this peripheral accumulation, a fluid space surrounding the inner cell mass is created. When a cavity is formed in the morula the structure is now called a BLASTOCYST.
Blastocyst is the structure that penetrates to the uterine endothelium. Cells form on the outer ring of the blastocyst, which are called trophoblast cells. Trophoblast cells enable the blastocyst to invade the endometrium. These cells will later form the placenta and membranes.
The brushing of the blastocyst to the uterine endometrium is a process called APPOSITION.
The attachment of the blastocyst to the uterine endometrium is termed as ADHESION.
The settling down of the blastocyst down into its soft folds is a process called INVASION. Invasion is made possible because as the growing structure touches the endometrial wall a proteolytic enzyme is produced that dissolve the tissues that they come in contact with.
The blastocyst burrows deep into the endometrial wall to receive nourishment from the endometrial glands.
Continued invasion establishes an effective communication network with the maternal circulation.
Once implanted the zygote is now termed embryo and the uterine endometrium is now termed decidua.
Implantation bleeding is characterized by a small amount of vaginal spotting that appears with implantation as capillaries are ruptured by the penetrating trophoblast cells. (This should not be mistaken for the woman's last menstrual period or LMP.)

image from science.tjc.edu

Megaloblastic Anemias

Posted: 13 Jan 2011 03:12 PM PST

Definition

Megalosblastic anemias are characterized by the presence of enlarged red cells (megaloblasts) due to the impaired cell division. Because the erythrocytes that reach the circulation are enlarged, a macrocytic and normochromic anemia results.

Pathophysiology

Causes

Vitamin B12 deficiency
Folic acid deficiency

Vitamin B12 and Folic acid are essential for normal DNA synthesis of erythrocyte formation. When these vitamins are deficient erythrocyte's DNA synthesis is affected. Mitosis in the progenitor lines is suppressed and abnormal increase in the number of normal cells or hyperplasia occurs. Since there is no impairment of the RNA or protein synthesis cell growth still proceeds. However, because mitosis or cell division can't occur (because of the absence of Vitamin B12 and Folic Acid) the marrow precursors (erythroid and myeloid cells) remain enlarged which are termed as MEGALOBLASTS. Many of these cells die within the marrow so the mature cells that leave the marrow is decreased in number. As a result, pancytopenia (deficiency of all cellular elements of the blood) develops.

Types of megaloblastic anemia

Vitamin B12 deficiency

Vitamin B12, also known as cobalamin, is not synthesized in the tissues. Thus, the body relies on the dietary intake of meat, liver, seafood and dairy products to supply our needs. The body stores more than a 3-year supply of vitamin B12 in the liver.

Causes:

Inadequate dietary intake
Impaired gastrointestinal absorption (absence of intrinsic factor, pernicious anemia, gastrectomy, chronic gastritis)

Clinical Manifestations:

Weakness
Listless
Pale
Smooth sore red tongue and diarrhea (those with pernicious anemia)
Neurologic manifestations (confusion, paresthesia, paralysis, severe neuropathy)

Diagnostic evaluation:

Schilling test (to determine the cause of Vitamin B12 deficiency)

Management:

Vitamin B12 replacement

Oral supplementation if the cause is inadequate cobalamin intake.
In cases of defective absorption or absence of intrinsic factor, replacement is by intramuscular (IM) injection of Vitamin B12.

Folic Acid Deficiency

Folic Acid is another vitamin that is necessary for normal red blood cell production. It is stored in the body as folates. The dietary sources of folate are meats, eggs and leafy vegetables. Body stores of folic acid provide a five-month period of tolerance from proven deficient folic acid in the diet.

Causes:

Inadequate folate in the diet
Alcoholism (alcohol increases folic acid requirements in the body)

Clinical Manifestations:

Symptoms of folic acid and Vitamin B12 deficiency are the same however, neurologic manifestations of Vitamin B12 deficiency do not occur when folic acid is deficient.

Management: