Congestive heart disease is a misapplied term used when referring to a disorder named congestive heart failure (CHF); another mistake people make when talking or reading about this condition is that they don't know that the initials CHD which refers to congenital heart defects (which may be accompanied by congestive heart failure fact that confuses even more the people).


The symptoms of congestive heart failure occur in patients who have an abnormality (inherited or acquired) in heart structure or functioning. There are many causes that lead to this condition, the most frequent being miocardic infarction, miocardic ischemia, hypertension, genetic disorders, valvular diseases and infiltrative diseases.

The most common symptoms of congestive heart failure are fatigue and dyspnea. Fatigue is determined not only by the low cardiac output but also by the associated non-cardiac co-morbidities. Dyspnea occurs in the early stages only after exertion but, as the disease progresses it occurs after any physical activity and,ultimately it occurs even at rest. Orthopnea (shortness of breath while lying flat) and paroxysmal nocturnal dyspnea (severe breathlessness and coughing attacks in the nighttime, awakening the patient) are common in the late stages of the disease. Orthopnea may be relieved by sitting upright, unlike paroxysmal nocturnal dyspnea. Another respiratory feature of the disease is represented by the Cheyne-Stokes respiration. This sign consists in severe episodes of dyspnea or short, transient cessations of breathing.

The patient also complain of gatrointestinal symptoms such as fullness, nausea, anorexia, abdominal pain and early satiety, determined by a congested liver or the edema of the bowel. The congestion of the liver and the stretching of Glisson's capsule ill also lead to right-upper quadrant pain.

In patient with severe congestive heart failure neurological symptoms may occur. Sleep disturbances, confusion, mood disturbances and disorientation are common, especially among the elderly patients.

A very important sign is represented by hepatomegaly. When this sign is present the enlarged liver is tender and pulsates during systole in case tricuspid regurgitation is present. As a consequence of the increased blood pressure in the hepatic veins, ascites occurs. The liver congestion leads to an impaired hepatic function, whose consequence is jaundice, another late sign of congestive heart failure.

A cardinal sign of congestive heart failure is peripheral edema which occurs mainly in the pretibial region and in the ankles. In bedridden patients presacral edema may be found.

In the severe cases of the disease massive weight loss and cachexia may be found. These feature have not been entirely explained but they are considered to be multifactorial and determined by the anorexia, impairment of the intestinal function, nausea, vomiting due to abdominal fullness and hepatic congestion.

Other less specific signs and symptoms are: decreased daytime micturition, nocturia, postural light headedness, falls and muscle wasting. Other symptoms, determined by hypoxemia are severe cyanosis and impaired mental performance.

Pick's disease is a neurological disease which determines a rare type of dementia (frontotemporal dementia). The disease usually affects people of 40-55 years old but there have been documented cases of patient younger than 30 or older than 60; it has also been noticed that the disease affects more womnt than men. The disease causes the brain cells to shrink due to the apparition inside the brain cells of large proteic aggregates, also known as Pick's bodies. Although that the disease has similar symptoms to other diseases that cause frontotemporal dementia (eg Alzheimer) in Pick's disease the brain damage is focal, not diffuse.


The symptoms of Pick's disease, especially in the early stages are determinned by frontal lobe damage. This is why the first symptoms are affecting emotional functioning and social skills (unlike in Alzheimer's disease where the memory is impaired first). The patient presents mood swings, desinhibition, euphoria, light headaches and his social abilities deteriorate. At the beginning of the disease the behavioral changes may go unnoticed but as the disease progresses, the patient may become extremely withdrawn or extroverted, his / her sexual behavior may change and there may be noticed an increased libido. This feature and  other symptoms such as aggressivity, impatience, rudeness and the loss of inhibition may be very disturbing and it may even make necessary law enforcement  interventions.

In the early stages of the disease language problems may occur. The patient has difficulties in naming objects or finding words; instead of finding the word to name an object the patient will describe it; but these problems are not marked.


As the disease progresses the patient's alimentary habits changes. The person with Pick's disease may have an increased appetite, even gluttony, he/she may manifest an obsessive-compulsive behavior towards food such as overeating or eating only a few or even one type of food. Excessive drinking (alcohol) occurs, although prior the onset of Pick's disease the patient did not have drinking problems.

All this disturbances plus the inability to function in social contexts, the affected judgment, and the difficulties in keeping a line of thought will make the patient unable to find or keep a job.




In time the language difficulties increase; echolalia (repeating words other people say), aphasia (difficulties in understanding speech or difficulties in speaking) may occur and writing and reading abilities are affected as well. Other emotional changes become more obvious: lack of empathy or warmth, a decreased interest in daily activities, impulsivity and lack of interest concerning personal hygiene.

There may also appear physical and neurological symptoms: urinary incontinence, weakness, stiffness and muscle rigidity, lack of movement coordination and progressive memory loss.

Unfortunately there is no treatment or cure for Pick's disease and the disease always leads to deterioration but there are treatments that ameliorate the behavioral problems; speech and occupational therapy may also be useful and behavioral modification techniques may have an impact on social integration. The life expectancy in Pick's disease it's usually 2-15 years and so, the treatment must focus on improving the patient's life quality.

Mercer disease is an extremely contagious disease caused by Methicillin Resistant Staphylococcus Aureus and therefore the disease is mostly known as MRSA infection. This bacteria is frequently acquired in hospitals, dialysis centers, nursing home and other health care facilities (health care associated MRSA). The health care associated MRSA affects mostly immunocompromised patients and old patients. Another type of MRSA has been discovered in otherwise healthy people in wider communities ( community associated MRSA) which is responsible for serious forms of pneumonia and skin infections.



The first symptoms in MRSA skin infections (the most common type of infection) are small red bumps like boils (the infection of hair follicles), pimples, abscesses (the infection of subcutaneous soft tissue), carbuncles (severe abscesses from which pus is draining), celulitis (the infection of fatty tissue ) or impetigo( superficial skin infection which appears as pus-filled vesicles). In short time, these skin conditions increase their severity, their surface increases, they become more painful,  and the patient develops more symptoms such as malaise, fever, and rashes. Although these skin conditions may be effectively treated, some community acquired MRSA strains may be highly virulent and may spread rapidly causing serious complications like sepsis, necrotizing fasciitis, toxic shock syndrome, necrotising pneumonia, pyomiositosis and infective endocarditis.




Necrotising fasciitis is a serious, deep infection of the subcutaneous tissue. Its symptoms are pain, subcutaneous swelling, crepitus, normal or reddish aspect of the skin in the first stage and skin necrosis and dark bullae in later stages. Necrotising fasciitis may be determined not only by Methicillin Resistant Staphylococcus Aureus, but also by other strains of bacteria and so, the antibiotic must be chosen after a microbiological analysis of the tissue.

Pyomiositosis is a deep muscular infection (it affects skeletal muscles, especially the quadriceps and the gluteal muscular group) and its symptoms are muscle swelling, pain, and high fever. The skin is usually minimally involved.

The pneumonia produced by MRSA is usually the result of a nosocomial (acquired during hospitalization) infection. Its features are not very different to those produced by other types of bacteria. The patient presents fever, cough with large quantities of purulent sputum and respiratory distress. The diagnosis is made after sputum cultures and Gram coloration.

TSS or toxic shock syndrome may be caused not only by MRSA but virtually by all Staphylococcus aureus strains. It is determined by the different bacterial toxins and its symptoms are: malaise, high fever, low blood pressure, characteristic rash, gastrointestinal disturbances (such as vomiting and diarrhea). Toxic shock syndrome progresses fast, leading to renal failure, hepatic inflammation, central nervous system involvement (confusion, stupor, coma). THis is a severe disorder and it frequently requires hospitalization.

Infective endocarditis occurs mainly in patients with intra-vascular devices, immunosupressed, that are going through hemodialysis, or patients with intra-vascular prosthetic devices. Most commonly the patient complains of fever, chills, night sweats, fatigue, shortness of breath, pleuritic chest pai. The clinical exam reveals muscular, red or hemorrhagic, painless patches on palms or soles known as Janeway's lesions, petechiae, splinter hemorrhage, and oval, pale retinal lesions surrounded by hemorrhage known as Roth's spots. Neurological manifestations may occur due to central nervous system embolization.

Crohn's disease consist in the chronic inflammation of the gatrointestinal tract. It commonly affects the colon or the distal ileum but it may affect virtually any part of the digestive tract. The causes of this disease are not certainly known but many authors consider it an autoimmune disorder (determined by an improper immune response). There are clues that suggest a hereditary predisposition to the disease; also smoking seems to have a contribution in triggering the attacks and affecting the course of the disease. Depending on the segment affected the disease may present as jejunoileitis, ileocolitis, colitis and perianal disease, or gastroduodenal disease.

In all these clinic forms of the disease, the first symptom of the disease is in most cases chronic diarrhea (especially if the patient complaining of this symptom has had surgery), accompanied by low-grade fever, anorexia, abdominal pain and weight loss.

In ileocolitis (the most common form of the disease) the signs and symptoms are chronic diarrhea, colicky lower right quadrant pain, a palpable mass in the same quadrant and fever. As a consequence of diarrhea, fear of eating and anorexia the patient suffers a weight loss of up to 20% of his body weight. The mass consists in swollen bowel and mesentery amd it may compress the right ureter leading to dysuria. Bowel obstruction causes symptoms that vary in intensity from postprandial pain to fibrostenotic stricture (over the years). Severe inflammation may lead to wall thinning thus leading to fistula formation to the adiacent structures (bowl, skin, mesenteric abscess).

Jejunoileitis determines loss of digestive surface, thus leading to malabsorbtion (followed by nutritional deficiencies) and steatorrhea. Diarrhea is a characteristic symptom. The nutritional deficiencies may have serious consequences such as pellagra (a severe disorder caused by niacin deficit) and  megaloblastic anemia (due to lack of vitamin B12).

The signs and symptoms of colitis ans perianal disease are diarrhea, fever, malaise, crampy abdominal pain, rectal bleeding. Due to colon strictures the patient may present symptoms of bowel obstruction. The disease may produce fistulas into the stomach and duodenum ,thus leading to feculent
vomiting, and 12% of women suffering of Crohn's disease will develop a rectovaginal fistula. Perianal disease occurs in 35% of patients with Crohn colitis and its symptoms are large hemorrhoidal tags, anorectal fistulae, anal strictures, incontinence and perirectal abscesses.

In gatroduodenal disease the symptoms are: nausea, vomiting and pain in the epigastric region.

Crohn's disease may have extra-intestinal symptoms too. The dermatological manifestations of the disease are perianal skin tags (up to 80% of the patients with Crohn's colitis), erythema nodosum (up to 17% of the patients) which consists in red nodules, measuring up to 5 cm in diameter on the calves, thighs and arms and pyoderma gangrenosum (just 7% of cases). The rheumatologic manifestations occur in 15 to 20% of cases and they are represented by ankylosing spondilitis and peripheral artritis. These manifestations worsen as the disease progresses.

Inspite the fact that anthrax has been usually observed in well defined areas or as an occupational hazard , nowdays it is very important due to its potential use as a biological weapon. Anthrax it is mainly a zoonosis; it mainly affects herbivores (horses, cattle, sheep), who come in contact with Bacillus antracis spores that contamine their pastures. The people are infected usually by direct contact with animals or their contaminated biological
The disease has three forms, with different symptoms and progression: cutaneous, pulmonary and gastrointestinal. In all three forms of the disease meningitis and sepsis may occur due to the lymphematogenous dissemination of bacteria from a primary lesion.

Cutaneous anthrax is the most frequent form of the disease (95% of cases). The bacteria or the spores are being inocculated into the skin through a cut, scratch, or insect bite. After two to five days (in some cases the incubation period lasts up to 3 weeks), at the infection site it appears an initial lesion, an erythematous papule which may be mistaken as an insect bite. In 2-4 days the papule enlarges and it is surrounded by a ring of small vesicles. The area surrounding this lesion is eritematous and edematous. The lesions' diameter is 1-3 cm, it is not painful and pus is absent. When the vesicular ring ruptures (day 7-12) the clear fluid from the vesicles is being discharged and the lesion progresses into an eschar - a specific black necrotic lesion which heals slowly (up to 60 days).Other symptoms are: regional lymphadenopathy, fever, malaise and headaches

In cutaneous anthrax, if the patient receives adequate treatment, mortality is rare; nevertheless in severe cases, less commonly the disease may progress with toxemia, bacteremia, massive local edema and painful adenomegaly, shock and fatal outcome.

Gastrointestinal anthrax is determined by the ingestion of spores in contaminated water or food. After the incubation period wich lasts up to one week, the disease may have two clinical forms: intestinal or oropharyngeal.

Initially the symptoms of intestinal anthrax are non-specific: fever, malaise, vomiting, nausea and anorexia. Later on, the disease progresses and severe abdominal pain, massive ascites, hematemesis (vomiting blood) and bloody diarrhea appear. Toxemia develops, then shock, leading to death (25% to 60% of cases).

In oropharyngeal anthrax the lesion is more frequently localized on the tongue, the buccal mucous membrane, the posterior pharyngeal wall or the tonsils. The main symptoms in this form of the disease are: sore throat, high fever, dysphagia, local lymphadenopathy. The infection may lead to bacteremia and toxemia thus leading to shock and death, in spite of the treatment (50% mortality).

The inhalation of spores leads to pulmonary anthrax. Its initial symptoms are insidious and are similar to a cold. After a short incubation (up to 1 week) the disease begins with unproductive cough, fever, malaise, dyspnea. In a few days the illness worsens and progresses to its next stage characterized by high fever, cianosis, dyspnea, respiratory distress. The bacteria spreads massively to CNS ad bloodstream and toxemia occurs.Once bacteremia has developed the progression to shock and death is very rapid. In spite treatment, pulmonary anthrax is, in most cases, fatal.

Lyme disease or Lyme borreliosis is a spirochettal disease, whose etiological agent, the bacteria Borrelia burgdoferi, is transmitted by ticks. The bacteria spreads hematogenously, thus determining the three stages of the disease.

The signs and symptoms in the first stage of Lyme disease consist in cutaneous manifestations. After the incubation period, which lasts up to 30 days, erythema migrans, the characteristic, expanding skin lesion appears at the site of the bite. The erythema migrans is at first a red macule but in time it slowly expands to an anular lesion with a bright red outer border and central clearing. In some cases the center of the lesion may become necrotic, vesiculous or erythematous. This type of lesion is not usually painful. The most common sites of erythema migrans are thigh, axilla and groin, but the lesion may virtually be located anywhere.

In the second stage of Lyme borreliosis the bacteria spreads hematogenously to many sites. The early signs and symptoms of the disease are usually changing and sometimes intermittent, except for fatigue which is constant. The most common symptoms in this stages are skin lesions, fever, severe headaches,chills, musculoskeletal pain, malaise, arthralgias.

Less common features of the disease are: hepatitis, lymphadenopathy, splenomegaly, iritis, nonproductive cough, dyspnea and sore throat.

In this stage it may appear symptoms suggesting meningeal irritation and after several weeks up to 15% untreated patients present neurological abnormalities such as meningitis, encephalitic signs, radiculoneuropathy, myelitis an cranial neuritis. A serious complication of neurological involvement happens in children, where due to the inflammation and the increased intracranial pressure the optic nerve may be affected, leading to blindness.

Another 8% of the untreated patiens develop cardiac symptoms, the most common cardiac abnormality being atrioventricular block, myopericarditis and chronic cardiomyopathy, pancarditis and cardiomegaly.
A very common feature of Lyme disease in this stage is articular and musculoskeletal pain. This typical feature consist in migratory pain in muscles, joints, bones, and tendons.In the third stage of the disease , several months after the infection more than 60% of the untreated patients develop arthritis. This feature usually presents as intermittent attacks of oligoarticular arthritis, especially in large joints (most commonly the knee).

A less common feature, chronic neurologic involvement may also manifest. The most common forms of neurological involvement are:encelopathy affecting mood, memory and sleep and axonal polyneuropathy (manifested as distal paresthesia or spinal radicular pain).In this stage of the disease the late skin manifestation is acrodermatitis chronica atrophicans. This lesion usually begins with reddish-violaceous discoloration; over the years it becomes sclerotic or atrophic.

The signs and symptoms of Addison's disease (also known as primary adrenal insufficiency) are produced by the reduced serum concentration of steroid hormones. The oset of the disease is insidious and in many cases the patients consider that the first symptoms are the result of stress.

The most common signs and symptoms of the disease are: fatigue, hyperpigmentation of skin and mucous membranes, anorexia, nausea, diarrhea, vomiting and muscle weakness.

The most specific symptom of this disorder is fatigue, which at the onset of the disease is sporadic but whose intensity and frequency increases as adrenal function is impaired. This symptom is determined mainly by deficient neuromuscular function which is determined by the following process: the lack of glucocorticoid hormones disturbs the glucidic, lipidic and proteic metabolism; due to the lack of cortisol, the amount of glucose produced from proteins decreases, thus diminishing the muscle and liver glycogen deposit and so, weakness occurs. It also may occur muscular or articular pain.




Hypoglicemia also determines the diminished resistance to infection and trauma in addison's disease patients and the myocardial weakness reduces cardiac output (leading to hypotension).

Although hyperpigmentation may be absent, it is a specific feature of the disease. It appears as a tanny aspect of the skin, even in areas not expose to the sun. The most affected areas are: skin creases, old scars, the areolae, and the mucous membranes. Other disorders that produce skin abnormalities and which may co-exist with Addison's disease are goitre (6%) and vintiligo (3%).

Many patients also complain of gastrointestinal abnormalities. The gastrointestinal symptoms vary from anorexia, nausea and weight loss to severe nausea, fulminating vomiting and diarrhea with marked dehydratation.

Some patients also have neurological disturbances such as postural dizziness, syncope, the enhancement of hearing and olfaction and reduced sensory modality of taste. They may also have personality changes, mood swings increased irritability and restlessness which may lead to an incorrect diagnosis of neurosis. In 12% of cases it has been observed a decreased tolerance to cold.

Due to the loss of adrenal androgens, axilary and pubic hair may be decreased in women. Amenorrhea may also occur as a result of metabolical disturbances.


Addisonian crisis (adrenal crisis) is a very severe complication of Addison's disease. It represents a rapid intensification of the disease and it is usually triggered by sepsis or by surgical stress. The adrenal crisis signs and symptoms are: severe abdominal pain, profound astenia, severe lower back and leg pain, low temperature or fever (in case the crisis has been triggered by infection), fulminating vomiting and diarrhea (leading to severe dehydratation), confusion or psychosis, convulsions, hypotension, rapid heart rate and loss of consciousness. This is a life-threatening state and immediate treatment is imperative. In all cases the precipitating or the triggering cause must be sought. Delay in diagnosis and treatment can result in poor outcomes.

The signs and symptoms of liver disease can be determined either by the liver disease itself or by the complications of the disease; for example, the portal hypertension syndrome- a complication of cirrhosis may determine acute GI bleeding.  The most common signs and symptoms of liver disease are: jaundice, right upper quadrant pain, abdominal distension, fatigue, intestinal bleeding, and itching. Fever may occur in viral (most common) or alcoholic hepatitis. Jaundice (the yellow pigmentation of sclerae, mucous membranes and skin) is the most common feature of liver disease, and many hepatologists consider it to be a very reliable marker of severity. Many patient observe the darkening of the urine before the noticing the pigmentation of sclerae. Jaundice is accompanied in many cases by steatorrhea (fatty stools) and the lightening of the colour of the stool, due to cholestasis.

Another common symptom of liver disease is fatigue. The patients describe it variously as lack of stamina, increased need for sleep, malaise, lethargy, weakness and poor energy. This symptom usually occurs after exercise or physical activity. Its severity is reduced in the morning or after adequate rest. The fatigue is intermittent in liver disease and it varies in severity from hour to hour.

Right upper quadrant pain is caused by the extension of liver's capsule (which is very rich in nerve endings) and it is another common feature of liver disease. Right upper quadrant pain is usually accompanied by hepatomegaly. Due to the variability in size and shape of the liver hepatomegaly is not a very reliable feature of liver disease. Hepatomegaly is a typical finding in alcoholic hepatitis, cirrhosis, amiloidosis, venoocclusive disease and liver cancer.

Abdominal distension and shifting dullness suggests ascites (fluid in the peritoneal cavity). Ascites in hepatic disease is determined usually by portal hypertension (90% cases), but also by chronic hepatitis, severe alcoholic hepatitis and  Budd-Chiari syndrome.

In acute liver disease itching may occur. Itching appears early in obstructive jaundice and later in acute hepatitis. It may also occur in chronic cholestatic liver diseases such as primary biliary cirrhosis and sclerosing cholangitis.

The physical examination also shows palmar erythema and spider angiomata in both acute and chronic disease, but they are not very reliable signs since they can occur in normal individuals, especially during pregnancy. Spider angiomata are visible, superficila, tortuous arteries which occur only on the face, arms, and upper torso.

In advanced liver disease the signs are more proeminent including edema, muscle wasting, bruising and weight loss. Other signs of advanced liver disease are:umbilical hernia caused by ascites, hydrothorax and caput medusa- proeminent collateral veins radiating from the umbilicus. Severe cirrhosis and portal hypertension may lead to hepatopulmonary syndrome which consists in liver disease,  pulmonary arteriovenous shunting and hypoxemia.

Skin changes may also occur in liver disease. Hyperpigmentation is typical in chronic conditions such as primary cirrhosis and sclerosing cholangitis. Mucocutaneous vasculitis is a common feature of cryoglobulinemia in  chronic hepatitis C but it can also appear  in chronic hepatitis B.

Cushing' s syndrome is determined by the excess cortisol in blood and therefore, its signs and symptoms are the direct result of the action of  glucocorticoid hormones.

Cushing's syndome most common causes are: adrenal hyperplasia, adrenal macronodular hyperplasia, Carney's syndrome, adrenal neoplasia, prolonged use of glucocorticoids and prolonged use of ACTH. The ectopic ACTH syndrome is determined by tumors (nonpituitary) that secrete ACTH and determine adrenal hyperplasia. The symptoms of cushing's syndrome determined by the ectopic ACTH syndrome are subtle or even absent but the laboratory tests show many important changes in the biochemical values.

Cushing's syndrome most common symptoms are: truncal obesity, fatigue, hirsutism, hypertension, amenorrhea, edema, osteoporosis and purplish abdominal striae. The laboratory analysis of urine shows glucosuria.

The action of glucocorticoid hormones on the tissue metabolism determines muscle weakness and fatigability. decreased bone mineralization is very frequent among children and in adults osteoporosis, which is an important clinical issue since it can lead to fractures of the bones and to the colaps of vertebral bodies.

The increased gluconeogenesis (the body's production of glucose) and the increased resistance to insulin may reduce the glucose tolerance and therefore diabetus mellitus may occur (approximately in 20% cases).

Another common sign of Cushing's syndrome is the rapid weight gain, in which adipous tissue deposits in specific sites (lipodystrophy): the face ("moon face" aspect), the back of the head and the interscapular area ("the buffalo hump") and the mesenteric area, thus producing the "truncal obesity". The cause of this lipodystrophy is unknown , but it may be determined by by the elevated insulin levels and the insulin resistance.  The patient presents polydipsia (excessive thirst) excessive sweating and polyuria (large quantity of urine). The face is frequently plethoric (red face) even though the red cell count is normal. The massive weight gain causes the skin to stretch and therefore it can easily bruise or hemorrage, causing the purple striae( a frequent feature of Cushing's)

A common cardio-vascular manifestation of Cushing's syndrome is hypertension determined by the fact that epinephrine's vasoconstrictive effect is enhanced by cortisol. The hypertension and the hyperglicemia may also lead to different heart disease, increasing the mortality among the Cushing's syndrome patients. Cushing's syndrome may also have psychological manifestations such as profound emotional changes, irritability, depression, confusion, anxiety, emotional lability or even psychosis.

In women, cushing's syndrome may determine oligomenorhhea (reduced frequency and length of menstruation) hirsutism (male hair growth pattern in a woman) or dry, brittle hair and nails. Male patients may complain of reduced libido, impotence and infertility.Due to the fact that cortisol reduces the immune and the inflammatory response the wound healing is impaired and many patients may contact opportunistic infections.Other (less frequent symptoms of Cushing's syndrome are:acne, episternal fatty tumors and aching, sore joints (especially shoulders or lower back).