Human Chorionic Gonadotropin

The syncytiotrophoblast is responsible for producing a hormone called human chorionic gonadotropin (hCG). This hormone signals other parts of the female reproductive system that fertilization and implantation have occurred, so the uterine lining should continue to grow and develop (rather than being shed as menstruation). By the end of the second week of development, sufficient quantities of hCG are produced to be detected in a woman’s urine. The presence of hCG in urine indicates a woman is pregnant, and thus hCG is the basis for modern-day pregnancy tests. For the first 3 months of pregnancy, hCG levels remain high, but after that they decline. By this time, hCG is no longer needed because the placenta is producing its own hormones to maintain the pregnancy.

source :human anatomy

Chromosomal Abnormalities and Their Effect on the Blastocyst

Abnormalities in chromosome number, shape, or form occur regularly. These abnormalities can occur during gametogenesis, fertilization, or cleavage. If the chromosomal abnormalities are severe enough, they result in the spontaneous abortion (miscarriage) of the blastocyst or embryo. Many of these spontaneous abortions occur early in pregnancy (within 2 to 3 weeks after fertilization), so a woman often spontaneously aborts without realizing she was ever pregnant.



Some estimates propose that approximately 50% of all pregnancies terminate as a result of spontaneous abortion; perhaps half of these are caused by chromosomal abnormalities in the developing organism. As a consequence, fewer organisms are stillborn or born with severe congenital malformations (birth defects).
Thus, while 2–3% of all infants are born with some type of birth defect, this percentage would be much higher if not for the high frequency of spontaneous abortions very early in pregnancy.

source : human anatomy

Cystic Fibrosis and Chloride Channels

The inherited disease cystic fibrosis (CF) involves defective plasma membrane proteins that affect chloride ion (Cl − ) channels in the membrane. These channels are transport proteins that use facilitated diffusion to move chloride ions across the plasma membrane. The genetic defect that causes CF results in the formation of abnormal chloride channel proteins in the membranes of cells lining the respiratory passageways and ducts in glands, such as the pancreas. The primary defect in these chloride channels results in an abnormal flow of chloride ions across the membrane, causing salt to be trapped within the cytoplasm of affected cells.
Ultimately, the normal osmotic flow of water across the plasma membrane breaks down. The concentration of salt within the cytoplasm of these cells causes an increase in the osmotic flow of water into the cell, thereby resulting in thickening of the mucus in the respiratory passageways and the pancreatic ducts. The aggregation of thickened mucus plugs the airways of the lungs, leading to breathing problems and increasing the risk of infection.
Therefore, a single genetic and biochemical defect in a transport protein produces significant health problems.

source : human anatomy

Hypertension: The “Silent Killer”

Hypertension is chronically elevated blood pressure, defined as a systolic pressure greater than 140 mm Hg and/or a diastolic pressure greater than 90 mm Hg. About 90–95% of all hypertension cases are essential hypertension, in which the cause is idiopathic (unknown).
Secondary hypertension accounts for the other 5–10% of cases, meaning that the high blood pressure is caused by another condition, usually renal disease or an adrenal gland tumor.


Hypertension has many serious effects on the body. It causes changes in the blood vessel walls, making them prone to further injury.
Increased damage makes the blood vessels more likely to develop atherosclerosis (see Clinical View: In Depth on page 708). In addition, hypertension causes undue stress on arterioles, resulting in thickening of the arteriole walls and reduction in luminal diameter, a condition called arteriolosclerosis. Furthermore, hypertension causes thickening of the renal arteries, leading to renal failure, and it can greatly damage the cerebral arteries, making them prone to rupture, which results in a fatal brain hemorrhage or stroke. Finally, hypertension is a major cause of heart failure owing to the extra workload placed on the heart.


Since hypertension is initially asymptomatic (meaning no noticeable symptoms are present), it has been dubbed the “silent killer.”
Everyone is encouraged to have their blood pressure checked early in life, and regularly, to make sure they are not suffering from hypertension. Mild hypertension may be controlled by losing weight, eating a healthy diet, exercising regularly, and not smoking. Stress is also associated with hypertension; thus, reducing stress, or learning to manage it, is important in treatment. In many instances, however, medication may be needed to control hypertension. Diuretics increase urine output, thereby reducing salt and water retention and consequently lowering blood volume. Beta-blockers slow the heart rate and lower heart output, while ACE (angiotensin-converting enzyme) inhibitors block angiotensin II (a protein that constricts arterioles), thereby increasing vasodilation.

source : human anatomy

Deep Vein Thrombosis

Deep vein thrombosis (throm-bō ′sis; a clotting) (DVT) refers to a thrombus,
which is a blood clot in a vein. The most common site for the thrombus is a vein in the calf (sural) region; the femoral region is another common site. The blood clot partially or completely blocks the flow of blood in the vein. DVT typically occurs in individuals with heart disease or those who are inactive or immobile for a long period of time, such as bedridden patients or those who have been immobilized in a cast. Even healthy individuals who have been on a long airline trip may develop DVT. In fact, DVT is sometimes called “economy class syndrome” in reference to the reduced amount of leg room in economy class seating on airlines.

DVT may also be a complication in pregnancy, where fluid accumulation in the legs and impingement of the fetus on the inferior vena cava may prevent efficient blood flow back to the heart. For inactive individuals, the leg muscles (e.g., gastrocnemius and soleus) do not contract as often and can’t help propel blood through the deep veins, thus allowing the blood to pool and potentially to clot. Initial signs of DVT include fever, tenderness and redness in the affected area, severe pain and swelling in the areas drained by the affected vein, and rapid heartbeat. A person experiencing these symptoms should seek immediate medical attention. The most serious complication of DVT is a pulmonary embolus (em′bō -lū s; a plug), in which a blood clot breaks free within the vein and travels through vessels to the lung, eventually blocking a branch of the pulmonary artery and potentially causing respiratory failure and death. If a DVT is diagnosed, the patient is given anticoagulation medication (such as low-molecular-weight heparin) to help prevent further clotting and break up the existing clot.


To reduce the risk for DVT, a person should maintain a healthy weight, stay active, and treat medical conditions that may increase the risk for DVT. On a long airline flight or car trip, stretching the legs and moving the feet frequently assist venous circulation in the legs.
Bedridden individuals may wear full-length compression stockings to assist circulation in the lower limbs.



Source : human anatomy

varicose veins

Varicose (var′i-kōs; varix = dilated vein) veins are dilated, tortuous (having many curves or twists) veins. The valves in these veins have become nonfunctional, causing blood to pool in one area and the vein to swell and bulge. Varicose veins are most common in the superficial veins of the lower limbs. They may be a result of genetic predisposition, aging, or some form of stress on the venous system that inhibits venous return (such as standing for long periods of time, obesity, or pregnancy). Varicose veins may become inflamed and painful, especially if fluid leaks from them into the tissues.

Symptoms of varicose veins may be alleviated by elevating the affected body part or wearing compression stockings (to promote blood movement in the lower limbs). In a procedure called sclerotherapy, an irritant is injected into small varicose veins to make them scar and seal off. Typically, a patient needs multiple sclerotherapy sessions before optimal results are seen. For larger varicose veins, an outpatient surgical procedure called stripping or vein removal (phlebectomy) is necessary.

 These veins can be removed without affecting the circulation, since the blood may be shunted to other veins that are not varicose. Even after treatment, it is possible for varicose veins to recur.
Varicose veins in the anorectal region are called hemorrhoids (hem′ō -royd). Hemorrhoids occur due to increased intra-abdominal pressure, as when a person strains to have a bowel movement or is in labor during childbirth. Hemorrhoids may need to be surgically excised if they become too painful or bleed excessively.


source : human anatomy

Cardiac Arrhythmia

Cardiac arrhythmia (ā-rith ́mē -ā ; a = not, rhythmos = rhythm), also called dysrhythmia, is any abnormality in the rate, regularity, or sequence of the cardiac cycle. Several common arrhythmias have been described:

• Atrial flutter occurs when the atria attempt to beat at a rate of 200 to 400 times per minute, and as a consequence literally bombard the AV node with muscle impulses. Abnormal muscle impulses flow continuously through the atrial conduction system, thus stimulating the atrial musculature and AV node over and over. This condition may persist for years, and frequently degenerates into atrial fibrillation.
• Atrial fibrillation (fı¯-bri-lā ́shūn) differs from atrial flutter in that the muscle impulses are significantly more chaotic, leading to an irregular heart rate. The ventricles respond by increasing and decreasing contraction activities, which may lead to serious disturbances in the cardiac rhythm.
• Premature ventricular contractions (PVCs) often result from stress, stimulants such as caffeine, or sleep deprivation. They occur either singly or in rapid bursts due to abnormal impulses initiated within the AV node or the ventricular conduction system. All of us experience an occasional PVC, and they are not detrimental unless they occur in great numbers. Most PVCs go unnoticed, although occasionally one is perceived as the heart “skipping a beat” and then “jumping” in the chest.

A more serious arrhythmia is ventricular fibrillation, a rapid, repetitious movement of the ventricular muscle that replaces normal contraction. This is a life-threatening condition caused by scattered impulses originating at different times and places throughout the entire myocardium. Because the contractions of a heart in fibrillation are uncoordinated, the heart does not pump blood, and blood circulation stops. This cessation of cardiac activity is called cardiac arrest.
Fibrillation almost certainly results in death unless the normal rhythmic contractions of the heart are promptly restored. To restore normal heart contractions, medical personnel apply a strong electrical shock to the skin of the chest using paddle electrodes. The electrical current passes through the chest wall to completely and immediately depolarize the entire myocardium. This procedure is analogous to pushing the reset button on a computer—and as in rebooting the computer, the hope is that when the heart begins to function again, it will work as intended.


Source : human anatomy

Valve Defects and Their Effects on Circulation

Structural damage to the heart valves can impair blood circulation and lead to serious health problems. Damage may result from developmental abnormalities, infection, hypertension, or other cardiovascular problems.


Valvular insufficiency, also termed valvular incompetence, occurs when one or more of the cardiac valves leaks (called “regurgitant flow”) because the valve cusps do not close tightly enough. Inflammation or disease may cause the free edges of the valve cusps to become scarred and constricted, allowing blood to regurgitate back through the valve. As the heart works to overcome the effect of the backflow, blood must be forced through the valve openings and this effort may cause heart enlargement. As a result, the heart must work harder to circulate the normal amount of blood.




Valvular stenosis (ste-nō ́sis; narrowing) is scarring of the valve cusps so that they become rigid or partially fused and cannot open completely. A stenotic valve is narrowed and presents resistance to the flow of blood, so that output from the affected chamber decreases.
Often the affected chamber hypertrophies and dilates—both conditions that may have deleterious consequences. Heart function may become so reduced that the rest of the body cannot receive adequate blood flow. A primary cause of valvular stenosis is rheumatic heart disease.




Rheumatic (roo-mat ́ik) heart disease may follow a streptococcal infection of the throat. It results when antibodies produced to kill the bacteria cross-react with the body’s own connective tissue, thereby initiating an autoimmune disease. All parts of the heart are subject to injury, but the endocardium, the valve cusps, and the left AV valve are typically most affected. Significantly scarred and narrow valves must be surgically repaired or replaced. Patients with a history of rheumatic heart disease must take antibiotics before undergoing dental or medical procedures that are likely to introduce bacteria into the bloodstream.

source : human anatomy