Diseases and Treatments

Diabetes

Afrezza is a rapid-acting inhaled insulin that is also FDA-approved for use

before meals. It must be used in combination with long-acting insulin in
patients with type 1 diabetes and should not be used by those who smoke
or have chronic lung disease. It comes as a single dose cartridge. Premixed
insulin is also available for people who need to use more than one type of
insulin.

Lung/Breathing Diseases

Pulmonary hypertension (PH or PHTN) is a condition of increased blood

pressure within the arteries of the lungs. Symptoms include shortness of
breath, syncope, tiredness, chest pain, swelling of the legs, and a fast
heartbeat. The condition may make it difficult to exercise. Onset is
typically gradual.
The cause is often unknown. Risk factors include a family history, prior
blood clots in the lungs, HIV/AIDS, sickle cell disease, cocaine use,
COPD, sleep apnea, living at high altitudes, and problems with the mitral
valve. The underlying mechanism typically involves inflammation of the
arteries in the lungs. Diagnosis involves first ruling out other potential
causes.
There is no cure. Treatment depends on the type of disease. A number of
supportive measures such as oxygen therapy, diuretics, and medications to
inhibit clotting may be used. Medications specifically for the condition
include epoprostenol, treprostinil, iloprost, bosentan, ambrisentan,
macitentan, and sildenafil.A lung transplant may be an option in certain
cases.
Epiglottitis is inflammation of the epiglottis—the flap at the base of the
tongue that keeps food from going into the trachea(windpipe). Symptoms
are usually rapid in onset and include trouble swallowing which can result
in drooling, changes to the voice, fever, and an increased breathing rate. As
the epiglottis is in the upper airway, swelling can interfere with breathing.
People may lean forward in an effort to open the airway.As the condition
worsens stridor and bluish skin may occur.

Epiglottitis was historically mostly caused by infection by H. influenzae

type b. With vaccination it is now more often caused by other bacteria.
Other possible causes include burns and trauma to the area. The most
accurate way to make the diagnosis is to look directly at the epiglottis. X-
rays of the neck from the side may show a "thumbprint sign" but the lack
of this sign does not mean the condition is absent.

An effective vaccine, the Hib vaccine, has been available since the 1980s.
Then atibiotic rifampicin may also be used to prevent the disease among
those who have been exposed to the disease and are at high risk. The most
important part of treatment involves securing the airway, which is often
done by endotracheal intubation. Intravenous antibiotics such as
ceftriaxone and possibly vancomycin or clindamycin is then given.
Corticosteroids are also typically used. With appropriate treatment, the risk
of death among children with the condition is about one percent and
among adults is seven percent.

Esophageal achalasia, often called simple achalasia, is a failure of smooth

muscle fibers to relax, which can cause the lower esophageal sphincter to
remain closed. Without a modifier, "achalasia" usually refers to achalasia
of the esophagus. Achalasia can happen at various points along the
gastrointestinal tract; achalasia of the rectum, for instance, may occur in
Hirschsprung's disease.

Esophageal achalasia is an esophageal motility disorder involving the

smooth muscle layer of the esophagus and the lower esophageal sphincter
(LES). It is characterized by incomplete LES relaxation, increased LES
tone, and lack of peristalsis of the esophagus (inability of smooth muscle
to move food down the esophagus) in the absence of other explanations
like canceror fibrosis.

Achalasia is characterized by difficulty in swallowing, regurgitation, and

sometimes chest pain. Diagnosis is reached with esophageal manometry
and barium swallow radiographic studies. Various treatments are available,
although none cures the condition. Certain medications or Botox may be
used in some cases, but more permanent relief is brought by esophageal
dilatation and surgical cleaving of the muscle (Heller myotomy).

Lymphangioleiomyomatosis (LAM) is a rare, progressive and systemic

disease that typically results in cystic lung destruction. It predominantly
affects women, especially during childbearing years.

The average age of onset is the early to mid 30s. Exertional dyspnea
(shortness of breath) and spontaneous pneumothorax (lung collapse) have
been reported as the initial presentation of the disease in 49% and 46% of
patients, respectively.

Diagnosis is typically delayed 5 to 6 years. The condition is often

misdiagnosed as asthma or chronic obstructive pulmonary disease. The
first pneumothorax, or lung collapse, precedes the diagnosis of LAM in
82% of patients. The consensus clinical definition of LAM includes
multiple symptoms:

•Fatigue
•Cough
•Coughing up blood (rarely massive)
•Chest pain
•Chylous complications arising from lymphatic obstruction, including
•Chylothorax
•Chylous ascites
•Chylopericaridium
•Chyloptysis
•Chyluria
•Chyle in vaginal discharge
•Chyle in stool.
•Angiomyolipomas (fatty kidney tumors) are present in about 30% of
patients with sporadic LAM and up to 90% of patients with TSC-LAM.
Angiomyolipomas can sometimes spontaneously bleed, causing pain or
low blood pressure.
•Cystic lymphangiomas or lymph nodes with hypodense centers, which
mimic necrotizing lymphomas, ovarian or renal cancers, or other
malignancies can occur in the retroperitoneum, pelvis or mediastinum.
Lung destruction in LAM is a consequence of diffuse infiltration by
neoplastic smooth muscle-like cells that invade all lung structures
including the lymphatics, airway walls, blood vessels and interstitial
spaces. The consequences of vessel and airway obstruction include
chylous fluid accumulations, hemoptysis, airflow obstruction and
pneumothorax. The typical disease course displays progressive dyspnea on
exertion, spaced by recurrent pneumothoraces and in some patients,
chylous pleural effusions or ascites.

Most people have dyspnea on exertion with daily activities by 10 years

after symptom onset. Many patients require supplemental oxygen over that
interval.

LAM can come to medical attention in several ways, most of which trigger
a chest CT. Thin-walled cystic change in the lungs may be found
incidentally on CT scans of the heart, chest or abdomen (on the cuts that
include lung bases) obtained for other purposes. HRCTs of TSC patients
reveals that about 20% of women have cystic change by age 20 and about
80% of women have cystic changes after age 40. LAM is sometimes
revealed by chest CT in patients who present with an apparent primary
spontaneous pneumothorax, but more often CT scanning is not ordered (in
the United States) until recurrences occur. Progressive dyspnea on exertion
without the exacerbations and remissions that are characteristic of asthma
or COPD sometimes prompt a chest CT. A review of the CT by an expert
familiar with LAM may increase diagnostic accuracy. Chylothorax an also
bring LAM to attention.

In some cases, a LAM diagnosis can be made with confidence on clinical

grounds (without biopsy) in patients with typical cystic changes on high
resolution CT scanning of the lung and findings of tuberous sclerosis,
angiomyolipoma, lymphangioleiomyoma, chylothorax or serum VEGF-D
> 800 pg/ml.

An FDA-approved drug for treatment of LAM, the mTOR inhibitor

sirolimus, is available for stabilization of lung function decline. Lung
transplant remains the last resort for patients with advanced disease.
Pleurisy, also known as pleuritis, is inflammation of the membranes that
surround the lungs and line the chest cavity(pleurae). This can result in a
sharp chest pain with breathing. Occasionally the pain may be a constant
dull ache. Other symptoms may include shortness of breath, cough, fever
or weight loss, depending on the underlying cause.

The most common cause is a viral infection. Other causes include

pneumonia, pulmonary embolism, autoimmune disorders, lung cancer,
following heart surgery, pancreatitis, chest trauma, and asbestosis.
Occasionally the cause remains unknown. The underlying mechanism
involves the rubbing together of the pleurae instead of smooth gliding.
Other conditions that can produce similar symptoms include pericarditis,
heart attack, cholecystitis, and pneumothorax. Diagnosis may include a
chest X-ray, electrocardiogram (ECG), and blood tests.

Treatment depends on the underlying cause. Paracetamol (acetaminophen)

and ibuprofen may be used to decrease pain. Incentive spirometry may be
recommended to encourage larger breaths.

Infectious Diseases

Rat-bite fever (RBF) is an infectious disease that can be caused by two

different bacteria. Streptobacillary RBF is caused by Streptobacillus
moniliformis in North America while spirillary RBF or sodoku is caused
by Spirillum minus and occurs mostly in Asia. People usually get the
disease from infected rodents or consumption of contaminated food or
water. When the latter occurs, the disease is often known as Haverhill
fever. If not treated, RBF can be a serious or even fatal disease.
There are several ways people can get RBF. The most common include:

• Bites or scratches from infected rodents (such as rats, mice, and

gerbils).
 • Handling rodents with the disease (even without a bite or scratch).
• Consuming food or drink contaminated with the bacteria.
RBF is not spread from one person to another.
Symptoms include:
• Fever
• Vomiting
• Headache
• Muscle pain
• Joint pain
• Rash
Symptoms usually occur 3-10 days after exposure to an infected rodent,
but can be delayed as long as 3 weeks. By this time, any associated bite or
scratch wound has usually healed.

Within 2-4 days after fever onset, a maculopapular rash may appear on the
hands and feet. This rash is identified by flat, reddened areas with small
bumps. One or more joints may then become swollen, red, or painful.

If you have RBF, your doctor can give you antibiotics that are highly
effective at curing the disease. Penicillin is the antibiotic most often used.
If you are allergic to penicillin, your doctor can give you other antibiotics.

Without treatment, RBF can be serious or potentially fatal. Severe illnesses

can include:

•Infections involving the heart (endocarditis, myocarditis, or

pericarditis)

•Infections involving the brain (meningitis)

•Infections involving the lungs (pneumonia)

 •Abscesses in internal organs

While death from RBF is rare, it can occur if it goes untreated.

Meningitis is an inflammation (swelling) of the protective membranes

covering the brain and spinal cord. A bacterial or viral infection of the fluid
surrounding the brain and spinal cord usually causes the swelling.
However, injuries, cancer, certain drugs, and other types of infections also
can cause meningitis. It is important to know the specific cause of
meningitis because the treatment differs depending on the cause.

Vibrio vulnificus is a species of Gram-negative, motile, curved-rod shaped

(bacillus), pathogenic bacteria of the genus Vibrio. Present in marine
environments such as estuaries, brackish ponds, or coastal areas, V.
Vulnificus is related to V. cholerae, the causative agent of cholera.

Infection with V. vulnificus leads to rapidly expanding cellulitis or

septicemia. It was first isolated as a source of disease in 1976. The capsule,
made of polysaccharides, is thought to protect against phagocytosis. The
observed association of the infection with liver disease (associated with
increased serum iron) might be due to the capability of more virulent
strains to capture iron bound to transferrin.

V. vulnificus is an extremely virulent bacterium that can cause three types

of infections:

•Acute gastroenteritis from eating raw or undercooked shellfish: V.

Vulnificus causes an infection often incurred after eating seafood,
especially raw or undercooked oysters. It does not alter the appearance,
taste, or odor of oysters. Symptoms include vomiting, diarrhea, and
abdominal pain
•Necrotizing wound infections can occur in injured skin exposed to
contaminated marine water. V. Vulnificus bacteria can enter the body
through open wounds when swimming or wading in infected waters,or by
puncture wounds from the spines of fish such as stingrays. People may
develop a blistering dermatitis sometimes mistaken for pemphigus or
pemphigoid.
•Invasive septicemia can occur after eating raw or undercooked shellfish,
especially oysters. V. Vulnificus is 80 times more likely to spread into the
bloodstream in people with compromised immune systems, especially
those with chronic liver disease. When this happens, severe symptoms
including blistering skin lesions and septic shock can sometimes lead to
death. This severe infection may occur regardless of whether the infection
began from contaminated food or an open wound.
Among healthy people, ingestion of V. Vulnificus can cause vomiting,
diarrhea, and abdominal pain. In someone with a compromised immune
system, particularly those with chronic liver disease, it can infect the
bloodstream, causing a severe and life-threatening illness characterized by
fever and chills, decreased blood pressure (septic shock), and blistering
skin lesions.

V. vulnificus wound infections have a mortality rate around 25%. In people

in whom the infection worsens into septicemia, typically following
ingestion, the mortality rate rises to 50%. The majority of these people die
within the first 48 hours of infection. The optimal treatment is not known,
but in one retrospective study of 93 people in Taiwan, use of a third-
generation cephalosporin and a tetracycline (e.g., ceftriaxone and
doxycycline, respectively) were associated with an improved outcome.
Prospective clinical trials are needed to confirm this finding, but in vitro
data support the supposition this combination is synergistic against V.
vulnificus. Likewise, the American Medical Association and the Centers
for Disease Control and Prevention (CDC) recommend treating the person
with a quinolone or intravenous doxycycline with ceftazidime. The first
successful documented treatment of fulminant V. Vulnificus sepsis was in
1995. Treatment was Fortaz and intravenous (IV) Cipro and IV
doxycycline, which proved successful. Prevention of secondary infections
from respiratory failure and acute renal failure are crucial. Key to the
diagnosis and treatment was early recognition of bullae in an
immunocompromised person with liver cirrhosis and oyster ingestion
within the previous 48 hours, and request by the physician for STAT Gram
staining and blood cultures for V. vulnificus.

V. vulnificus often causes large, disfiguring ulcers that require extensive

debridement or even amputation.

Clostridium difficile infection (CDI or C-dif) is a symptomatic infection

due to the spore-forming bacterium, Clostridium difficile. Symptoms
include watery diarrhea, fever, nausea, and abdominal pain. It makes up
about 20% of cases of antibiotic-associated diarrhea. Complications may
include pseudomembranous colitis, toxic megacolon, perforation of the
colon, and sepsis.

Clostridium difficile infection is spread by bacterial spores found within

feces. Surfaces may become contaminated with the spores with further
spread occurring via the hands of healthcare workers. Risk factors for
infection include antibiotic or proton pump inhibitors use, hospitalization,
other health problems, and older age. Diagnosis is by stool culture or
testing for the bacteria's DNA or toxins. If a person tests positive but has
no symptoms, the condition is known as C. Difficile colonizationrather
than an infection.

Prevention is by hand washing, terminal room cleaning in hospital, and

limiting antibiotic use. Discontinuation of antibiotics may result in
resolution of symptoms within three days in about 20% of those infected.
Often the antibiotics metronidazole, vancomycin or fidaxomicin will cure
the infection. Retesting after treatment, as long as the symptoms have
resolved, is not recommended, as the person may remain colonized.
Recurrences have been reported in up to 25% of people. Some tentative
evidence indicates fecal microbiota transplantation and probiotics may
decrease the risk of recurrence.

Giardiasis, popularly known as beaver fever, is a parasitic disease caused

by Giardia lamblia. About 10% of those infected have no symptoms. When
symptoms occur they may include diarrhea, abdominal pain, and weight
loss. Vomiting, blood in the stool, and fever are less common. Symptoms
usually begin 1 to 3 weeks after exposure and without treatment may last
up to six weeks.

Giardia usually spreads when Giardia lamblia cysts within feces

contaminate food or water which is then eaten or drunk. It may also spread
between people and from other animals. Risk factors include travel in the
developing world, changing diapers, eating food without cooking it, and
owning a dog. Cysts may survive for nearly three months in cold water.
Diagnosis is via stool tests.

Prevention is typically by improved hygiene. Those without symptoms do

not usually need treatment. When symptoms are present treatment is
typically with either tinidazole or metronidazole. People may become
temporarily lactose intolerant after an infection and therefore it is often
recommended milk be avoided for a few weeks. Resistance to treatment
may occur.

Treatment is not always necessary as the infection usually resolves on its

own. However, if the illness is acute or symptoms persist and medications
are needed to treat it, a nitroimidazole medication is used such as
metronidazole, tinidazole, secnidazole or ornidazole.

Enterovirus 68 (EV68, EV-D68, HEV68) is a member of the

Picornaviridae family, an enterovirus. First isolated in California in 1962
and once considered rare, it has been on a worldwide upswing in the 21st
century. With some uncertainty, it has been implicated in cases of a polio-
like disorder called acute flaccid myelitis.

EV68 almost exclusively causes respiratory illness, which varies from

mild to severe, but can cause a range of symptoms, from none at all, to
subtle flu-like symptoms, to debilitating respiratory illness and a suspected
rare involvement in a syndrome with polio-like symptoms. Like all
enteroviruses, it can cause variable skin rashes, abdominal pain and soft
stools. Initial symptoms are similar to those for the common cold,
including a runny nose, sore throat, cough, and fever. As the disease
progresses, more serious symptoms may occur, including difficulty
breathing as in pneumonia, reduced alertness, a reduction in urine
production, and dehydration, and may lead to respiratory failure.

The degree of severity of symptoms experienced seems to depend on the

demographic population in question. Experts estimate that the majority of
the population has, in fact, been exposed to the enterovirus, but that no
symptoms are exhibited in healthy adults. In contrast, EV-D68 is
disproportionately debilitating in very young children, as well as the very
weak. While several hundred people (472), mostly youth, have been
exposed to the disease, less than a hundred of those patients have been
diagnosed with severe symptoms (such as paralysis), and during the recent
outbreak in the US just a single death was recorded over the last weekend
of September 2014. The death was of a 10-year-old girl in New
Hampshire.

The virus has been suspected as one cause of acute flaccid myelitis, a rare
muscle weakness, usually due to polio- since two California children who
tested positive for the virus had paralysis of one or more limbs reaching
peak severity within 48 hours of onset. "Recovery of motor function was
poor at 6-month follow-up."

There is no specific treatment and no vaccine, so the illness has to run its
course; treatment is directed against symptoms (symptomatic treatment).
Most people recover completely; however, some need to be hospitalized,
and some have died as a result of the virus. Five EV68 paralysis cases
were unsuccessfully treated with steroids, intravenous immunoglobulin
and/or plasma exchange. The treatment had no apparent benefit as no
recovery of motor function was seen. A 2015 study suggested the antiviral
drug pleconarilmay be useful for the treatment of EV-D68.
Malaria is a mosquito-borne infectious disease affecting humans and other
animals caused by parasitic single-celled microorganisms belonging to the
Plasmodium group. Malaria causes symptoms that typically include fever,
tiredness, vomiting, and headaches. In severe cases it can cause yellow
skin, seizures, coma, or death. Symptoms usually begin ten to fifteen days
after being bitten by an infected mosquito. If not properly treated, people
may have recurrences of the disease months later. In those who have
recently survived an infection, reinfection usually causes milder
symptoms. This partial resistancedisappears over months to years if the
person has no continuing exposure to malaria.

The disease is most commonly transmitted by an infected female

Anopheles mosquito. The mosquito bite introduces the parasites from the
mosquito's saliva into a person's blood. The parasites travel to the liver
where they mature and reproduce. Five species of Plasmodium can infect
and be spread by humans. Most deaths are caused by P. Falciparum
because P. Vivax, P. ovale, and P. Malariae generally cause a milder form
of malaria. The species P. Knowlesi rarely causes disease in humans.
Malaria is typically diagnosed by the microscopic examination of blood
using blood films, or with antigen-based rapid diagnostic tests. Methods
that use the polymerase chain reaction to detect the parasite's DNA have
been developed, but are not widely used in areas where malaria is common
due to their cost and complexity.

The risk of disease can be reduced by preventing mosquito bites through

the use of mosquito nets and insect repellents, or with mosquito control
measures such as spraying insecticides and draining standing water.
Several medications are available to prevent malaria in travellers to areas
where the disease is common. Occasional doses of the combination
medication sulfadoxine/pyrimethamine are recommended in infants and
after the first trimester of pregnancy in areas with high rates of malaria.
Despite a need, no effective vaccine exists, although efforts to develop one
are ongoing. The recommended treatment for malaria is a combination of
antimalarial medications that includes an artemisinin. The second
medication may be either mefloquine, lumefantrine, or
sulfadoxine/pyrimethamine. Quinine along with doxycycline may be used
if an artemisinin is not available.

Infectious mononucleosis (IM, mono), also known asvglandular fever, is

an infection usually caused by the Epstein–Barr virus (EBV). Most people
are infected by the virus as children, when the disease produces few or no
symptoms. In young adults, the disease often results in fever, sore throat,
enlarged lymph nodes in the neck, and tiredness. Most people get better in
two to four weeks; however, feeling tired may last for months. The liver or
spleen may also become swollen, and in less than one percent of cases
splenic rupture may occur.

While usually caused by Epstein–Barr virus (EBV), also known as human

herpesvirus 4, which is a member of the herpes virus family, a few other
viruses may also cause the disease. It is primarily spread through saliva but
can rarely be spread through semen or blood. Spread may occur by objects
such as drinking glasses or toothbrushes. Those who are infected can
spread the disease weeks before symptoms develop. Mono is primarily
diagnosed based on the symptoms and can be confirmed with blood tests
for specific antibodies. Another typical finding is increased blood
lymphocytes of which more than 10% are atypical. The monospot test is
not recommended for general use due to poor accuracy.

There is no vaccine for EBV. Prevention is by not sharing personal items

with or kissing those infected. Mono generally gets better on its own.
Recommendations include drinking enough fluids, getting sufficient rest,
and taking pain medications such as paracetamol (acetaminophen) and
ibuprofen.

Leptospirosis is an infection caused by corkscrew-shaped bacteria called

Leptospira. Signs and symptoms can range from none to mild such as
headaches, muscle pains, and fevers; to severe with bleeding from the
lungs or meningitis. If the infection causes the person to turn yellow, have
kidney failure and bleeding, it is then known as Weil's disease. If it also
causes bleeding into the lungs then it is known as severe pulmonary
hemorrhage syndrome.

Up to 13 different genetic types of Leptospira may cause disease in

humans. It is transmitted by both wild and domestic animals. The most
common animals that spread the disease are rodents. It is often transmitted
by animal urine or by water or soil containing animal urine coming into
contact with breaks in the skin, eyes, mouth, or nose. In the developing
world the disease most commonly occurs in farmers and low-income
people who live in cities. In the developed world it most commonly occurs
in those involved in outdoor activities in warm and wet areas of the world.
Diagnosis is typically by looking for antibodies against the bacterium or
finding its DNA in the blood.

Efforts to prevent the disease include protective equipment to prevent

contact when working with potentially infected animals, washing after this
contact, and reducing rodents in areas people live and work. The antibiotic
doxycycline, when used in an effort to prevent infection among travellers,
is of unclear benefit. Vaccines for animals exist for certain type of
Leptospira which may decrease the risk of spread to humans. Treatment if
infected is with antibiotics such as: doxycycline, penicillin, or ceftriaxone.
Weil's disease and severe pulmonary haemorrhage syndrome result in
death rates greater than 10% and 50%, respectively, even with treatment.

Entamoeba histolytica is an anaerobic parasitic amoebozoan, part of the

genus Entamoeba. Predominantly infecting humans and other primates
causing amoebiasis, E. Histolytica is estimated to infect about 50 million
people worldwide. E. Histolytica infection is estimated to kill more than
55,000 people each year. Previously, it was thought that 10% of the world
population was infected, but these figures predate the recognition that at
least 90% of these infections were due to a second species, E. Dispar.
Mammals such as dogs and cats can become infected transiently, but are
not thought to contribute significantly to transmission.
The active (trophozoite) stage exists only in the host and in fresh loose
feces; cysts survive outside the host in water, in soils, and on foods,
especially under moist conditions on the latter. The infection can occur
when a person puts anything into their mouth that has touched the feces of
a person who is infected with E. histolytica, swallows something, such as
water or food, that is contaminated with E. histolytica, or swallows E.
histolytica cysts (eggs) picked up from contaminated surfaces or fingers.
The cysts are readily killed by heat and by freezing temperatures, and
survive for only a few months outside of the host. When cysts are
swallowed they cause infections by excysting (releasing the trophozoite
stage) in the digestive tract. The pathogenic nature of E. Histolytica was
first reported by Lösch in 1875, but it was not given its Latin name until
Fritz Schaudinn described it in 1903. E. histolytica, as its name suggests
(histo–lytic = tissue destroying), is pathogenic; infection can be
asymptomatic or can lead to amoebic dysentery or amoebic liver abscess.
Symptoms can include fulminating dysentery, bloody diarrhea, weight
loss, fatigue, abdominal pain, and amoeboma. The amoeba can actually
'bore' into the intestinal wall, causing lesions and intestinal symptoms, and
it may reach the blood stream. From there, it can reach different vital
organs of the human body, usually the liver, but sometimes the lungs,
brain, spleen, etc. A common outcome of this invasion of tissues is a liver
abscess, which can be fatal if untreated. Ingested red blood cells are
sometimes seen in the amoeba cell cytoplasm.
There are a number of effective medications. Generally several antibiotics
are available to treat entamoeba histolytica. The infected individual will be
treated with only one antibiotic if the E. Histolytica infection has not made
the person sick and most likely be prescribed with two antibiotics if the
person has been feeling sick. Otherwise, below are other options for
treatments.

Intestinal infection: Usually nitroimidazole derivatives (such as

metronidazole) are used because they are highly effective against the
trophozoite form of the amoeba. Since they have little effect on amoeba
cysts, usually this treatment is followed by an agent (such as paromomycin
or diloxanide furoate) that acts on the organism in the lumen.

Liver abscess: In addition to targeting organisms in solid tissue, primarily

with drugs like metronidazole and chloroquine, treatment of liver abscess
must include agents that act in the lumen of the intestine (as in the
preceding paragraph) to avoid re-invasion. Surgical drainage is usually not
necessary except when rupture is imminent.

People without symptoms: For people without symptoms (otherwise

known as carriers, with no symptoms), non endemic areas should be
treated by paromomycin, and other treatments include diloxanide furoate
and iodoquinol. There have been problems with the use of iodoquinol and
iodochlorhydroxyquin, so their use is not recommended. Diloxanide
furoate can also be used by mildly symptomatic persons who are just
passing cysts.

Aspergillosis is the name given to a wide variety of diseases caused by

infection by fungi of the genus Aspergillus. The majority of cases occur in
people with underlying illnesses such as tuberculosis or chronic
obstructive pulmonary disease (COPD), but with otherwise healthy
immune systems. Most commonly, aspergillosis occurs in the form of
chronic pulmonary aspergillosis (CPA), aspergilloma or allergic
bronchopulmonary aspergillosis (ABPA). Some forms are intertwined; for
example ABPA and simple aspergilloma can progress to CPA.

Other, non-invasive manifestations include fungal sinusitis (both allergic

in nature and with established fungal balls), otomycosis (ear infection),
keratitis (eye infection) and onychomycosis (nail infection). In most
instances these are less severe, and curable with effective antifungal
treatment.

People with deficient immune systems—such as patients undergoing

hematopoietic stem cell transplantation, chemotherapy for leukaemia, or
AIDS—are at risk of more disseminated disease. Acute invasive
aspergillosis occurs when the immune system fails to prevent Aspergillus
spores from entering the bloodstream via the lungs. Without the body
mounting an effective immune response, fungal cells are free to
disseminate throughout the body and can infect major organs such as the
heart and kidneys.

The most frequently identified pathogen is Aspergillus fumigatus—a

ubiquitous organism that is capable of living under extensive
environmental stress. It is estimated that most humans inhale thousands of
Aspergillus spores daily, but they do not affect most people’s health due to
effective immune responses. Taken together, the major chronic, invasive
and allergic forms of aspergillosis account for around 600,000 deaths
annually worldwide.

A fungus ball in the lungs may cause no symptoms and may be discovered
only with a chest X-ray, or it may cause repeated coughing up of blood,
chest pain, and occasionally severe, even fatal, bleeding. A rapidly
invasive Aspergillus infection in the lungs often causes cough, fever, chest
pain, and difficulty breathing.

Poorly controlled aspergillosis can disseminate through the blood stream to

cause widespread organ damage. Symptoms include fever, chills, shock,
delirium, seizures and blood clots. The person may develop kidney failure,
liver failure (causing jaundice), and breathing difficulties. Death can occur
quickly.

Aspergillosis of the ear canal causes itching and occasionally pain. Fluid
draining overnight from the ear may leave a stain on the pillow.
Aspergillosis of the sinuses causes a feeling of congestion and sometimes
pain or discharge. It can extend beyond the sinuses.

In addition to the symptoms, an X-ray or computerised tomography (CT)

scan of the infected area provides clues for making the diagnosis.
Whenever possible, a doctor sends a sample of infected material to a
laboratory to confirm identification of the fungus.

On chest X-ray and CT, pulmonary aspergillosis classically manifests as a

halo sign, and, later, an air crescent sign. In hematologic patients with
invasive aspergillosis, the galactomannan test can make the diagnosis in a
noninvasive way. False positive Aspergillus galactomannan tests have been
found in patients on intravenous treatment with some antibiotics or fluids
containing gluconate or citric acid such as some transfusion platelets,
parenteral nutrition or PlasmaLyte.

On microscopy, Aspergillus species are reliably demonstrated by silver

stains, e.g., Gridley stain or Gomori methenamine-silver.

The current medical treatments for aggressive invasive aspergillosis

include voriconazole and liposomal amphotericin B in combination with
surgical debridement. For the less aggressive allergic bronchopulmonary
aspergillosis findings suggest the use of oral steroids for a prolonged
period of time, preferably for 6–9 months in allergic aspergillosis of the
lungs. Itraconazole is given with the steroids, as it is considered to have a
"steroid sparing" effect, causing the steroids to be more effective, allowing
a lower dose.

Other drugs used, such as amphotericin B, caspofungin (in combination

therapy only), flucytosine (in combination therapy only), or itraconazole,
are used to treat this fungal infection. However, a growing proportion of
infections are resistant to the triazoles. A. fumigatus, the most commonly
infecting species, is intrinsically resistant to fluconazole.

Fungal meningitis refers to meningitis caused by a fungal infection.

Symptoms of fungal meningitis are generally similar to those of other

types of meningitis, and include: a fever, stiff neck, severe headache,
photophobia (sensitivity to light), nausea and vomiting, and altered mental
status (drowsiness or confusion).

Fungal meningitis may be caused by the following (and also other) types
of fungi:

•Candida - C. Albicans is the most common Candida species causing CNS

infection.

•Coccidioides - it is endemic to southwestern United States and Mexico. A

third of patients presenting with disseminated coccidioidomycosis have
developed meningitis.

•Histoplasma - occurs in bird and bat droppings and is endemic to parts of

the United States, South, and Central America. CNS involvement occurs in
10-20% of disseminated histoplasmosis cases.

•Blastomyces - occurs in soil rich in decaying organic matter in the

Midwest United States. Meningitis is an unusual manifestation of
blastomycosis and can be very difficult to diagnose.

•Cryptococcus (Cryptococcal meningitis) - it is thought to be acquired

through inhalation of soil contaminated with bird droppings. C.
Neoformans is the most common pathogen to cause fungal meningitis.

•Aspergillus – Aspergillus infections account for 5% of CNS fungal

infections.

•If suspected, fungal meningitis is diagnosed by testing blood and Cerebral

Spinal Fluid (CSF) samples for pathogens. Identifying the specific
pathogen is necessary to determine the proper course of treatment and the
prognosis. Measurement of opening pressure, cell count with differential,
glucose and protein concentrations, Gram's stain, India ink, and culture
tests should be performed on Cerebral Spinal Fluid (CSF) samples when
fungal meningitis is suspected.

Prognosis depends on the pathogen responsible for the infection and risk
group. Overall mortality for Candida meningitis is 10-20%, 31% for
patients with HIV, and 11% in neurosurgical cases (when treated).
Prognosis for Aspergillus and coccidioidal infections is poor.

Botulism poisoning can occur due to preserved or home-canned, low-acid

food that was not processed using correct preservation times and/or
pressure.

Foodborne botulism "Signs and symptoms of foodborne botulism

typically begin between 18 and 36 hours after the toxin gets into your
body, but can range from a few hours to several days, depending on the
amount of toxin ingested."
•Double vision
•Blurred vision
•Drooping eyelid
•Nausea, vomiting, and abdominal cramps
•Slurred speech
•Trouble breathing
•Difficulty in swallowing
•Dry mouth
•Muscle weakness
•Constipation
•Reduced or absent deep tendon reactions, such as in the knee.

Wound botulism Most people who develop wound botulism inject drugs
several times a day, so it's difficult to determine how long it takes for signs
and symptoms to develop after the toxin enters the body. Most common in
people who inject black tar heroin, wound botulism signs and symptoms
include:
•Difficulty swallowing or speaking
•Facial weakness on both sides of the face
•Blurred or double vision
•Drooping eyelids
•Trouble breathing
•Paralysis

Infant botulism If infant botulism is related to food, such as honey,

problems generally begin within 18 to 36 hours after the toxin enters the
baby's body. Signs and symptoms include:
•Constipation (often the first sign)
•Floppy movements due to muscle weakness and trouble controlling the
head
•Weak cry
•Irritability
•Drooling
•Drooping eyelids
•Tiredness
•Difficulty sucking or feeding
•Paralysis

Beneficial effects of botulinum toxin: Purified botulinum toxin is diluted

by a physician for treatment:
•Congenital pelvic tilt
•Spasmodic dysphasia (the inability of the muscles of the larynx)
•Achalasia (esophageal stricture)
•Strabismus (crossed eyes)
•Paralysis of the facial muscles
•Failure of the cervix
•Blinking frequently
•Anti-cancer drug delivery

Adult intestinal toxemia: A very rare form of botulism that occurs by the
same route as infant botulism but is among adults. Occurs rarely and
sporadically. Signs and symptoms include:
•Abdominal pain
•Blurred vision
•Diarrhea
•Dysarthria
•Imbalance
•Weakness in arms and hand area

Physicians may consider the diagnosis of botulism based on a patient’s

clinical presentation, which classically includes an acute onset of bilateral
cranial neuropathies and symmetric descending weakness. Other key
features of botulism include an absence of fever, symmetric neurologic
deficits, normal or slow heart rate and normal blood pressure, and no
sensory deficits except for blurred vision. A careful history and physical
examination is paramount in order to diagnose the type of botulism, as
well as to rule out other conditions with similar findings, such as Guillain-
Barre syndrome, stroke, and myasthenia gravis. Depending on the type of
botulism considered, different tests for diagnosis may be indicated.
Foodborne Botulism: serum analysis for toxins by bioassay in mice should
be done, as the demonstration of the toxins is diagnostic.
Wound Botulism: isolation of C. botulinum from the wound site should be
attempted, as growth of the bacteria is diagnostic.
Adult Enteric and Infant Botulism: isolation and growth of C. botulinum
from stool samples is diagnostic. Infant botulism is a diagnosis which is
often missed in the emergency room.
Other tests that may be helpful in ruling out other conditions are:
•Electromyography (EMG) or antibody studies may help with the
exclusion of myasthenia gravis and Lambert-Eaton myasthenic syndrome
(LEMS).
•Collection of cerebrospinal fluid (CSF) protein and blood assist with the
exclusion of Guillan-Barre syndrome and stroke.
•Detailed physical examination of the patient for any rash or tick presence
helps with the exclusion of any tick transmitted tick paralysis.
Cytomegalovirus

Most people infected with CMV who are otherwise healthy experience few
if any signs and symptoms. People at greater risk of signs and symptoms
of CMV include:

•Newborns infected with CMV before birth (congenital CMV).

•Infants who become infected during birth or shortly afterward
(perinatal CMV). This group includes babies infected through breast
milk.
•People with weakened immune systems, for example due to organ
transplant or HIV infection.
Babies

Most babies with congenital CMV appear healthy at birth.

A few babies with congenital CMV who appear healthy at birth can
develop signs over time — sometimes not for months or years after birth.
The most common of these late-occurring signs are hearing loss and
developmental delay. A small number of babies may also develop vision
problems.

Babies with congenital CMV who are sick at birth tend to have significant
signs and symptoms, including:

•Premature birth
•Low birth weight
•Yellow skin and eyes (jaundice)
•Enlarged and poorly functioning liver
•Purple skin splotches or a rash or both
•Abnormally small head (microencephaly)
•Enlarged spleen
•Pneumonia
 •Seizures
People with weakened immunity

If your immune system is weakened, you might experience more-serious

signs and symptoms affecting your:

•Eyes
•Lungs
•Liver
•Esophagus
•Stomach
•Intestines
•Brain
Otherwise healthy adults

Most people infected with CMV who are otherwise healthy experience few
if any signs or symptoms. When first infected, some adults may have
symptoms similar to infectious mononucleosis, including:

•Fatigue
•Fever
•Sore throat
•Muscle aches
CMV mononucleosis is less likely than infectious mononucleosis to cause
enlarged lymph nodes and spleen.

Human alveolar echinococcosis is characterized by a lengthy incubation

period of 5 to 15 years in immunocompetent individuals. The progression
of disease is potentiated in immunocompromised patients. Following the
ingestion of the eggs of E. multilocularis, the metacestode (larval) stage of
the parasite typically embeds in the liver. As the disease progresses, the
larval stage proliferates exogenously within the tissue, behaving similar to
hepatic neoplasia. Patients with human alveolar echinococcosis typically
present with headache, nausea, vomiting, abdominal pain. Jaundice is rare,
but hepatomegaly is a common physical finding.
Serological and imaging tests are commonly used to diagnose this disease.
Since the serological tests for alveolar echinococcosis only indicate
exposure to the parasite and not ongoing infection, visualization of the
parasitic mass is required to confirm the diagnosis. Frequently used
serological tests include antibody tests, ELISA and indirect
hemaglutination (IHA). Also, an intradermal allergic reaction test (Casoni
test) has also been used to diagnose patients. Imaging tests include: X-
rays, CT scans, MRI, and ultrasound.
If no specific therapy is initiated, in 94% of patients the disease is fatal
within 10–20 years following diagnosis.
•Currently, benzimidazoles (such as albendazole) are used to treat AE:
only halt their proliferation and do not actually kill the parasites, side
effects such as liver damage
•2-ME2, a natural metabolite of estradiol, is tested with some results in
vitro: decreased transcription of 14-3-3-pro-tumorogenic zeta-isoform,
causes damage to germinal layer but does not kill parasite in vivo
•Treatment with a combination of albendazole/2-ME2 showed best results
in reducing parasite burden
•Despite the improvements in the chemotherapy of echinococcosis with
benzimidazole derivatives, complete elimination of the parasitic mass
cannot be achieved in most infected patients, although studies indicate that
long-term treatment with mebendazole may cause the death of the parasite.

Neurocysticercosis is a specific form of the infectious parasitic disease

cysticercosis which is caused by infection with Taenia solium, a tapeworm
found in pigs. Neurocysticercosis occurs when cysts formed by the
infection takes hold within the brain causing neurologic syndromes such as
epileptic seizures. It has been called a "hidden epidemic" and "arguably the
most common parasitic disease of the human nervous system".
The epidemiology of Taenia solium cysticercosis is solely associated with
local cultural practices especially poor sanitation and is highly endemic in
Sub-Saharan Africa, Latin America and Asia. Infection by Taenia solium
cysticercosis, the pork tapeworm larvae in human, spares no ethnic group.
Cysticercosis in the United States, which commonly presents in the form
of neurocysticercosis, has been classified as a "neglected tropical disease",
which commonly affects the poor and homeless, particularly those without
access or in the habit of inadequate hand-washing and in the habit of
eating with their hands. Neurocysticercosis most commonly involves the
cerebral cortexfollowed by the cerebellum. The pituitary gland is very
rarely involved in neurocysticercosis. The cysts may rarely coalesce and
form a tree-like pattern which is known as racemose neurocysticercosis,
which when involving the pituitary gland may result in multiple pituitary
hormone deficiency.

Neurology Diseases
Pseudobulbar affect (PBA), or emotional incontinence, is a type of
emotional disturbance characterized by uncontrollable episodes of crying
and/or laughing, or other emotional displays. PBA occurs secondary to a
neurologic disorder or brain injury. Patients may find themselves crying
uncontrollably at something that is only moderately sad, being unable to
stop themselves for several minutes. Episodes may also be mood-
incongruent: a patient may laugh uncontrollably when angry or frustrated,
for example. Sometimes, the episodes may switch between emotional
states, resulting in the patient crying uncontrollably before dissolving into
fits of laughter.

The Pseudobulbar affect, also referred to as emotional lability, should not

be confused with labile mood or labile emotions that stem from emotional
instability – affective dysregulation – commonly seen in personality
disorders, such as borderline personality disorder.

Education of patients, families, and caregivers is an important component

of the appropriate treatment of PBA. Crying associated with PBA may be
incorrectly interpreted as depression; laughter may be embarrassing. It is
therefore critical for families and caregivers to recognize the pathological
nature of PBA and the reassurance that this is an involuntary syndrome
that is manageable. Traditionally, antidepressants such as sertraline,
citalopram, nortriptyline and amitriptyline have been prescribed with some
efficacy.
Polyneuropathy (poly-+neuro-+-pathy) is damage or disease affecting
peripheral nerves (peripheral neuropathy) in roughly the same areas on
both sides of the body, featuring weakness, numbness, and burning pain. It
usually begins in the hands and feet and may progress to the arms and legs
and sometimes to other parts of the body where it may affect the
autonomic nervous system. It may be acute or chronic. A number of
different disorders may cause polyneuropathy, including diabetes and some
types of Guillain–Barré syndrome.
Among the signs/symptoms of polyneuropathy, which can be divided (into
sensory and hereditary) and are consistent with the following:

•Sensory polyneuropathy – ataxia, numbness, muscle wasting and

paraesthesiae.

•Hereditary polyneuropathy – scoliosis and hammer toes

In the treatment of polyneuropathies one must ascertain and manage the

cause, among management activities are: weight decrease, use of a
walking aid, and occupational therapist assistance. Additionally BP control
in those with diabetes is helpful, while intravenous immunoglobulin is
used for multifocal motor neuropathy.
Dravet syndrome, previously known as severe myoclonic epilepsy of
infancy (SMEI), is a type of epilepsy with seizures that are often triggered
by hot temperatures or fever. It is treated with anticonvulsant medications.
It often begins around six months of age.
Dravet syndrome has been characterized by prolonged febrile and non-
febrile seizures within the first year of a child’s life. This disease
progresses to other seizure types like myoclonic and partial seizures,
psychomotor delay, and ataxia. It is characterized by cognitive impairment,
behavioral disorders, and motor deficits. Behavioral deficits often include
hyperactivity and impulsiveness, and in more rare cases, autistic-like
behaviors. Dravet syndrome is also associated with sleep disorders
including somnolence and insomnia. The seizures experienced by people
with Dravet syndrome become worse as the patient ages, as the disease is
not very observable when symptoms first appear. This coupled with the
range of severity differing between each individual diagnosed and the
resistance of these seizures to drugs has made it challenging to develop
treatments.

Dravet syndrome appears during the first year of life, often beginning
around six months of age with frequent febrile seizures (fever-related
seizures). Children with Dravet syndrome typically experience a lagged
development of language and motor skills, hyperactivity and sleep
difficulties, chronic infection, growth and balance issues, and difficulty
relating to others. The effects of this disorder do not diminish over time,
and children diagnosed with Dravet syndrome require fully committed
caretakers with tremendous patience and the ability to closely monitor
them.

Seizures in Dravet syndrome can be difficult to manage but may be

reduced by anticonvulsant medications such as clobazam, stiripentol,
topiramate and valproate. Because the course of the disorder varies from
individual to individual, treatment protocols may vary. A diet high in fats
and low in carbohydrates may also be beneficial, known as a ketogenic
diet. Although diet adjustment can help, it does not eliminate the
symptoms. Until a better form of treatment or cure is discovered, those
with this disease will have myoclonic epilepsy for the rest of their lives.

Certain anticonvulsant drugs that are classed as sodium channel blockers

are now known to make seizures worse in most Dravet patients. These
drugs include carbamazepine, gabapentin, lamotrigine, and phenytoin.

Treatments include cognitive rehabilitation through psychomotor and

speech therapy. In addition, valproate is often administered to prevent
recurrence of febrile seizures and benzodiazapine is used for long lasting
seizures, but these treatments are usually insufficient.

A generalized tonic–clonic seizure (also known as a grand mal seizure) is a

type of generalized seizure that affects the entire brain. Tonic–clonic
seizures are the seizure type most commonly associated with epilepsy and
seizures in general, though it is a misconception that they are the only
type.

Autoimmune Diseases

Hyperimmunoglobulinemia E syndrome (HIES), of which the

autosomal dominant form is called Job's syndrome or Buckley
syndrome, is a heterogeneous group of immune disorders. Job's is also
very rare at about 300 cases currently in the literature.
It is characterized by recurrent "cold" staphylococcal infections, unusual
eczema-like skin rashes, severe lung infections that result in
pneumatoceles (balloon-like lesions that may be filled with air or pus or
scar tissue) and very high concentrations of the serum antibody IgE.
Inheritance can be autosomal dominant or autosomal recessive. Many
patients with autosomal dominant STAT3 hyper-IgE syndrome have
characteristic facial and dental abnormalities, fail to lose their primary
teeth, and have two sets of teeth simultaneously.
Most patients with hyper IgE syndrome are treated with long-term
antibiotic therapy to prevent staphylococcal infections. Good skin care is
also important in patients with hyper IgE syndrome. High-dose
intravenous gamma-globulin has also been suggested for the treatment of
severe eczema in patients with HIES and atopic dermatitis.
Pediatric autoimmune neuropsychiatric disorders associated with
streptococcal infections (PANDAS) is a hypothesis that there exists a
subset of children with rapid onset of obsessive-compulsive disorder
(OCD) or tic disorders and these symptoms are caused by group A beta-
hemolytic streptococcal (GABHS) infections. The proposed link between
infection and these disorders is that an initial autoimmune reaction to a
GABHS infection produces antibodies that interfere with basal
gangliafunction, causing symptom exacerbations. It has been proposed that
this autoimmune response can result in a broad range of neuropsychiatric
symptoms.
In addition to an OCD or tic disorder diagnosis, children may have other
symptoms associated with exacerbations such as emotional lability,
enuresis, anxiety, and deterioration in handwriting. In the PANDAS model,
this abrupt onset is thought to be preceded by a strep throat infection. As
the clinical spectrum of PANDAS appears to resemble that of Tourette's
syndrome, some researchers hypothesized that PANDAS and Tourette's
may be associated; this idea is controversial and a focus for current
research.
Treatment for children suspected of PANDAS is generally the same as the
standard treatments for TS and OCD. These include cognitive behavioral
therapy and medications to treat OCD such as selective serotonin reuptake
inhibitors (SSRIs); and "conventional therapy for tics"

Fibromyalgia (FM) is a medical condition characterised by chronic

widespread pain and a heightened pain response to pressure. Other
symptoms include tiredness to a degree that normal activities are affected,
sleep problems and troubles with memory. Some people also report restless
legs syndrome, bowel or bladder problems, numbness and tingling and
sensitivity to noise, lights or temperature. Fibromyalgia is frequently
associated with depression, anxiety and posttraumatic stress disorder.
Other types of chronic pain are also frequently present.
The cause of fibromyalgia is unknown; however, it is believed to involve a
combination of genetic and environmental factors, with each playing a
substantial role. The condition runs in families, and many genes are
believed to be involved. Environmental factors may include psychological
stress, trauma and certain infections. The pain appears to result from
processes in the central nervous system, and the condition is referred to as
a "central sensitization syndrome". Fibromyalgia is recognized as a
disorder by the US National Institutes of Health and the American College
of Rheumatology. There is no specific diagnostic test. Diagnosis involves
first ruling out other potential causes and verifying that a set number of
symptoms are present.
The treatment of fibromyalgia can be difficult. Recommendations often
include getting enough sleep, exercising regularly and eating a healthy
diet. Cognitive behavioral therapy (CBT) may also be helpful. The
medications duloxetine, milnacipran or pregabalin may be used. Use of
opioid pain medication is controversial, with some stating their use is
poorly supported by evidence and others saying that weak opioids may be
reasonable if other medications are not effective. Dietary supplements also
lack evidence to support their use. While fibromyalgia can last a long time,
it does not result in death or tissue damage.

Genetic Diseases
Hypertrichosis is an abnormal amount of hair growth over the body. The
two distinct types of hypertrichosis are generalized hypertrichosis, which
occurs over the entire body, and localized hypertrichosis, which is
restricted to a certain area. Hypertrichosis can be either congenital (present
at birth) or acquired later in life. The excess growth of hair occurs in areas
of the skin with the exception of androgen-dependent hair of the pubic
area, face, and axillary regions.

Heart Diseases
Ventricular tachycardia (V-tach or VT) is a type of regular and fast heart
rate that arises from improper electrical activity in the ventricles of the
heart. Although a few seconds may not result in problems, longer periods
are dangerous. Short periods may occur without symptoms or present with
lightheadedness, palpitations, or chest pain. Ventricular tachycardia may
result in cardiac arrest and turn into ventricular fibrillation. Ventricular
tachycardia is found initially in about 7% of people in cardiac arrest.

Ventricular tachycardia can occur due to coronary heart disease, aortic

stenosis, cardiomyopathy, electrolyte problems, or a heart attack.
Diagnosis is by an electrocardiogram (ECG) showing a rate of greater than
120 bpm and at least three wide QRS complexes in a row. It is classified as
non-sustained versus sustained based on whether or not it lasts less than or
more than 30 seconds. The term "ventricular tachycardias" refers to the
group of irregular heartbeats that includes ventricular tachycardia,
ventricular fibrillation, and torsades de pointes.

In those who have a normal blood pressure and strong pulse, the
antiarrhythmic medication procainamide may be used. Otherwise
immediate cardioversion is recommended. In those in cardiac arrest due to
ventricular tachycardia, cardiopulmonary resuscitation (CPR) and
defibrillation is recommended. Biphasic defibrillation may be better than
monophasic. While waiting for a defibrillator, a precordial thump may be
attempted in those on a heart monitor who are seen going into an unstable
ventricular tachycardia. In those with cardiac arrest due to ventricular
tachycardia, survival is about 45%. An implantable cardiac defibrillator or
medications such as calcium channel blockers or amiodarone may be used
to prevent recurrence.

Costochondritis, also known as chest wall pain, costosternal syndrome, or

costosternal chondrodynia is an acute and often temporary inflammation of
the costal cartilage, the structure that connects each rib to the sternum at
the costosternal joint. The condition is a common cause of chest pain.
Though costochondritis often resolves on its own, it can be a recurring
condition that has little or no signs of onset.

Costochondritis symptoms can be similar to the chest pain associated with

a heart attack. Chest pain is considered a medical emergency until life-
threatening cardiac issues (such as an acute coronary syndrome) can be
ruled out. Severe cases of costal cartilage inflammation that also involve
painful swelling are sometimes referred to as Tietze's syndrome, a term
sometimes used interchangeably with costochondritis. However, some
physicians view costochondritis and Tietze's syndrome as separate disease
states due to the absence of costal cartilage swelling in costochondritis.

Treatment options are quite limited and usually involve a combination of

rest, analgesics, or anti-inflammatory medications. Cases with persistent
discomfort may be managed with cortisone injections or surgery may be
indicated if the condition is severe. Individuals with costochondritis are
typically instructed to avoid strenuous physical activity to prevent the
onset of an attack.

Myocarditis, also known as inflammatory cardiomyopathy, is

inflammation of the heart muscle. Symptoms can include shortness of
breath, chest pain, decreased ability to exercise, and an irregular heartbeat.
The duration of problems can vary from hours to months. Complications
may include heart failure due to dilated cardiomyopathy or cardiac arrest.

Myocarditis is most often due to a viral infection. Other causes include

bacterial infections, certain medications, toxins, and autoimmune
disorders. A diagnosis may be supported by an electrocardiogram (ECG),
increased troponin, heart MRI, and occasionally a heart biopsy. An
ultrasound of the heart is important to rule out other potential causes such
as heart valve problems.

Treatment depends on both the severity and the cause. Medications such as
ACE inhibitors, beta blockers, and diuretics are often used. A period of no
exercise is typically recommended during recovery. Corticosteroids or
intravenous immunoglobulin (IVIG) may be useful in certain cases. In
severe cases an implantable cardiac defibrillator or heart transplantmay be
recommended.
Asystole (1860, from Modern Latin, from Greek privative a "not, without"
+systolē"contraction")is the absence of ventricular contractions. Asystole
is the most serious form of cardiac arrest and is usually irreversible. A
cardiac flatline is the state of total cessation of electrical activity from the
heart, which means no tissue contraction from the heart muscle and
therefore no blood flow to the rest of the body.

Asystole should not be confused with very brief pauses in the heart's
electrical activity, even those that produce a temporary flat line, in
electrical activity that can occur in certain less severe abnormal rhythms.
Asystole is different from very fine occurrences of ventricular fibrillation,
though both have a poor prognosis, and untreated fine VF will lead to
asystole. Faulty wiring, disconnection of electrodes and leads, and power
disruptions should be ruled out.

Asystolic patients (as opposed to those with a "shockable rhythm" such as

ventricular fibrillation or ventricular tachycardia, which can be potentially
treated with defibrillation) usually present with a very poor prognosis:
asystole is found initially in only about 28% of cardiac arrest cases, but
only 15% of these patients ever leave the hospital alive, even with the
benefit of an intensive care unit, with the rate being lower (only 6%) for
those already prescribed drugs for high blood pressure.

Asystole is treated by cardiopulmonary resuscitation (CPR) combined with

an intravenou vasopressor such as epinephrine(a.k.a. adrenaline).
Sometimes an underlying reversible cause can be detected and treated (the
so-called 'Hs and Ts', an example of which is hypokalaemia). Several
interventions previously recommended—such as defibrillation (known to
be ineffective on asystole, but previously performed in case the rhythm
was actually very fine ventricular fibrillation) and intravenous atropine—
are no longer part of the routine protocols recommended by most major
international bodies. Asystole may be treated with 1 mg epinephrine by IV
every 3–5 minutes as needed. Vasopressin is no longer part of ACLS
protocol for PEA as of AHA 2015 guidelines due to lack of evidence of
benefit vs. Epinephrine only every 3-5 minutes.

Survival rates in a cardiac arrest patient with asystole are much lower than
a patient with a rhythm amenable to defibrillation; asystole is itself not a
"shockable" rhythm. Out-of-hospital survival rates (even with emergency
intervention) are less than 2 percent.

Third-degree atrioventricular block (AV block), also known as complete

heart block, is a medical condition in which the nerve impulse generated
in the sinoatrial node (SA node) in the atrium of the heart does not
propagate to the ventricles.

Because the impulse is blocked, an accessory pacemaker in the lower

chambers will typically activate the ventricles. This is known as an escape
rhythm. Since this accessory pacemaker also activates independently of the
impulse generated at the SA node, two independent rhythms can be noted
on the electrocardiogram (ECG).

•The P waves with a regular P-to-P interval (in other words, a sinus
rhythm) represent the first rhythm.

•The QRS complexes with a regular R-to-R interval represent the second
rhythm. The PR interval will be variable, as the hallmark of complete heart
block is lack of any apparent relationship between P waves and QRS
complexes.
People with third-degree AV block typically experience severe bradycardia
(an abnormally-low measured heart rate), hypotension, and at times,
hemodynamic instability.

Many conditions can cause third-degree heart block, but the most common
cause is coronary ischemia. Progressive degeneration of the electrical
conduction system of the heart can lead to third-degree heart block. This
may be preceded by first-degree AV block, second-degree AV block,
bundle branch block, or bifascicular block. In addition, acute myocardial
infarction may present with third-degree AV block.

An inferior wall myocardial infarction may cause damage to the AV node,

causing third-degree heart block. In this case, the damage is usually
transitory. Studies have shown that third-degree heart block in the setting
of an inferior wall myocardial infarction typically resolves within 2 weeks.
The escape rhythm typically originates in the AV junction, producing a
narrow complex escape rhythm.

An anterior wall myocardial infarction may damage the distal conduction

system of the heart, causing third-degree heart block. This is typically
extensive, permanent damage to the conduction system, necessitating a
permanent pacemaker to be placed. The escape rhythm typically originates
in the ventricles, producing a wide complex escape rhythm.

Third-degree heart block may also be congenital and has been linked to the
presence of lupus in the mother. It is thought that maternal antibodies may
cross the placenta and attack the heart tissue during gestation. The cause of
congenital third-degree heart block in many patients is unknown. Studies
suggest that the prevalence of congenital third-degree heart block is
between 1 in 15,000 and 1 in 22,000 live births.

Hyperkalemia in those with previous cardiac disease and Lyme disease can
also result in third-degree heart block.

Atropine is often used as a first line treatment of a third-degree heart block

in the presence of a narrow QRS which indicates a nodal block, but, may
have little to no effect in an infra-nodal block. Atropine works by reducing
vagal stimulation through the AV node but will not be effective in those
who have had a previous heart transplant. Other drugs may be utilized
such as epinephrine or dopamine which have a positive chronotropic
effects and may increase the heart rate. Treatment in emergency situations
can involve electrical tracscutaneous pacing in those who are acutely
hemodynamically unstable and can be used regardless of the persons level
of consciousness. Sedative agents such as a benzodiazapine or opiate may
be used in conjunction with transcutaneous pacing to reduce the pain
caused by the intervention.

In cases of suspected beta-blocker overdose, the heart-block maybe treated

with pharmacological agents to reverse the underlying cause with the use
of glucagon. In the case of a calcium channel blocker overdose treated
with calcium chloride and digitalis toxicity may be treated with the
digoxin immune Fab.

Third-degree AV block can be treated more permanently with the use of a

dual-chamber artificial pacemaker. This type of device typically listens for
a pulse from the SA node via lead in the right atrium and sends a pulse via
a lead to the right ventricle at an appropriate delay, driving both the right
and left ventricles. Pacemakers in this role are usually programmed to
enforce a minimum heart rate and to record instances of atrial flutter and
atrial fibrillation, two common secondary conditions that can accompany
third-degree AV block. Since pacemaker correction of third-degree block
requires full-time pacing of the ventricles, a potential side effect is
pacemaker syndrome, and may necessitate use of a biventricular
pacemaker, which has an additional 3rd lead placed in a vein in the left
ventricle, providing a more coordinated pacing of both ventricles.

The 2005 Joint European Resuscitation and Resuscitation Council (UK)

guidelines state that atropine is the first line treatment especially if there
were any adverse signs, namely: 1) heart rate < 40 bpm, 2) systolic blood
pressure < 100 mm Hg, 3) signs of heart failure, and 4) ventricular
arrhythmias requiring suppression. If these fail to respond to atropine or
there is a potential risk of asystole, transvenous pacing is indicated. The
risk factors for asystole include 1) previous asystole, 2) complete heart
block with wide complexes, and 3) ventricular pause for > 3 seconds.
Mobitz Type 2 AV block is another indication for pacing.

As with other forms of heart block, secondary prevention may also include
medicines to control blood pressure and atrial fibrillation, as well as
lifestyle and dietary changes to reduce risk factors associated with heart
attack and stroke.

Congestive heart failure facts

•Congestive heart failure (CHF) is a condition in which the heart's function as a

pump is inadequate to meet the body's needs.
•Many disease processes can impair the pumping efficiency of the heart to
cause congestive heart failure.
 •The symptoms of congestive heart failure vary, but can include:
•fatigue,
•diminished exercise capacity,
•shortness of breath, and
•swelling (edema).

Heart failure describes the inability or failure of the heart to adequately meet the
needs of organs and tissues for oxygen and nutrients. This decrease in cardiac
output, the amount of blood that the heart pumps, is not adequate to circulate the
blood returning to the heart from the body and lungs, causing fluid (mainly water) to
leak from capillary blood vessels. This leads to the symptoms that may include
shortness of breath, weakness, and swelling
the most common causes of congestive heart failure are:

•Coronary artery disease

•High blood pressure (hypertension)
•Longstanding alcohol abuse
•Disorders of the disorders of the heart valves
•Unknown (idiopathic) causes, such as after recovery from myocarditis

Less common causes include viral infections of the stiffening of the heart
muscle, thyroid disorders, disorders of the heart rhythm, and many others.

Right heart failure, left heart failure, or both

•Patients with right heart failure leak fluid into the tissue and organs that
deliver blood to the right heart through the vena cava.
•Back pressure in capillary blood vessels cause them to leak water into the
space between cells and commonly the fluid can be found in the lowest parts
of the body.
•Gravity causes fluid to accumulate in the feet and ankles but as more fluid
accumulates, it may creep up to involve all of the lower legs.
 •Fluid can also accumulate within the liver causing it to swell (hepatomegaly)
and also within the abdominal cavity (ascites).
•Ascites and hepatomegaly may make the patient feel bloated, nauseated, and
have abdominal pain with the feeling of distension.

Congestive heart failure is often a consequence of atherosclerotic heart disease and

therefore the risk factors are the same: poorly controlled high blood pressure, high
cholesterol, diabetes, smoking, and family history. Heart valve disease becomes a
risk factor as the patient ages.

Other causes of heart failure have their own set of risk factors and predispositions
and it becomes a complication of those diseases. Such causes may include
obstructive sleep apnea, alcohol and drug abuse, infections, and connective tissue
disorders like systemic lupus erythematosus, sarcoidosis, and amyloidosis.

Many patients have stable congestive heart failure but can decompensate when a
change occurs to their body. For example, a patient with congestive heart failure may
be doing well but then develops pneumonia, an infection of the lungs, or suffers
a heart attack. The patient's heart may not be able to react to the body's changing
environment and does not have the capability or reserve to meet the body's energy
needs.

Congestive heart failure can be a medical emergency, especially if it acutely

decompensates and the patient can present extremely ill with the inability to breathe
adequately. In this situation, the ABCs of resuscitation (Airway, Breathing,
Circulation) need to be addressed while at the same time, the diagnosis of
congestive heart failure is made.

Electrocardiogram (EKG, ECG) to help assess heart rate, rhythm, and indirectly, the

size of the ventricles and blood flow to the heart muscle.

•Chest X-ray to look at heart size and the presence or absence of fluid in the
lungs.
•Blood tests may include a complete blood count (CBC), electrolytes, glucose,
BUN, and creatinine (to assess kidney function).
 •B-type natriuretic peptide (BNP) may be helpful in deciding if a patient has
shortness of breath from congestive heart failure or from a different cause. It
is a chemical that is located in the heart ventricles and may be released when
these muscles are overloaded.
•Echocardiography or ultrasound testing of the heart is often recommended to
assess the anatomy and the function of the heart. In addition to being able to
evaluate the heart valves and muscle, the test can look at blood flow within the
heart, watch the chambers of the heart contract, and measure the ejection
fraction (percentage of blood ejected with each beat - normal = 50% to 75%).

Treatment may try to decrease fluid within the body so that the heart does not have to
work as hard to circulate blood through the blood vessels in the body.

Fluid restriction and a decrease in salt intake may be very helpful. Diuretic
medications (water pills) may be prescribed if appropriate. Common diuretics
include furosemide (Lasix), bumetanide (Bumex), and hydrochlorothiazide.

Medications are available that can make the heart pump more efficiently, increase
cardiac output, and increase ejection fraction, as well as improve long-term survival

ACE inhibitors (angiotensin converting enzyme inhibitors) and ARBs (angiotension

receptor blockers) are medicines that are also shown to increase survival by
decreasing systemic resistance and favorable altering the hormonal milieu, which
affects the cardiac performance; they are often used with other drugs. Beta
blockers may control heart rate and increase cardiac output and ejection fraction,
and provide a beneficial response to circulating epinephrine
("adrenalin"). Digoxin (Lanoxin) is an older medicine that may help increase cardiac
output and control symptoms.

A very mild newer diuretic, spironolactone, has been shown to be of long-term benefit

as well.
Cardiac risk factor modification is the cornerstone of  prevention  but may also benefit
patients with established congestive heart failure.
Weight loss, establishing an exercise program, stopping smoking, and
controlling high blood pressure, high cholesterol, and diabetes may help in the
management of congestive heart failure.

End stage congestive heart failure (NYHA stage IV) patients may require aggressive
treatments including left ventricular assist devices (LVAD), an implanted pump that
helps increase the heart's ability to squeeze, or even heart transplantation. In older
patients, not considered transplant candidates, LVAD may be a permanent treatment.

When you have heart failure, your heart makes two proteins. Your doctor will call them B-
type natriuretic peptide (BNP) and N-terminal-pro-BNP. Levels of both in your blood go up
when your heart failure gets worse and go down when it gets better. A test called a BNP
blood test measures those two important levels. It’s able to spot heart failure more than
80% of the time.

Endocrine Diseases
Graves' disease, also known as toxic diffuse goiter, is an autoimmune
disease that affects the thyroid. It frequently results in and is the most
common cause of hyperthyroidism. It also often results in an enlarged
thyroid. Signs and symptoms of hyperthyroidism may include irritability,
muscle weakness, sleeping problems, a fast heartbeat, poor tolerance of
heat, diarrhea, and unintentional weight loss. Other symptoms may include
thickening of the skin on the shins, known as pretibial myxedema, and eye
bulging, a condition caused by Graves' ophthalmopathy. About 25 to 80%
of people with the condition develop eye problems.

The exact cause is unclear; however, it is believed to involve a

combination of genetic and environmental factors. A person is more likely
to be affected if they have a family member with the disease. If one twin is
affected, a 30% chance exists that the other twin will also have the disease.
The onset of disease may be triggered by stress, infection, or giving birth.
Those with other autoimmune diseases such as type 1 diabetes and
rheumatoid arthritis are more likely to be affected. Smoking increases the
risk of disease and may worsen eye problems. The disorder results from an
antibody, called thyroid-stimulating immunoglobulin (TSI), that has a
similar effect to thyroid stimulating hormone (TSH). These TSI antibodies
cause the thyroid gland to produce excess thyroid hormone. The diagnosis
may be suspected based on symptoms and confirmed with blood tests and
radioiodine uptake. Typically, blood tests show a raised T3 and T4, low
TSH, increased radioiodine uptake in all areas of the thyroid, and TSI
antibodies.

The three treatment options are radioiodine therapy, medications, and

thyroid surgery. Radioiodine therapy involves taking iodine-131 by mouth,
which is then concentrated in the thyroid and destroys it over weeks to
months. The resulting hypothyroidism is treated with synthetic thyroid
hormone. Medications such as beta blockers may control some of the
symptoms, and antithyroid medications such as methimazole may
temporarily help people while other treatments are having effect. Surgery
to remove the thyroid is another option. Eye problems may require
additional treatments.

Hypogonadism means diminished functional activity of the gonads—the

testes or the ovaries—that may result in diminished sex hormone
biosynthesis.

Low androgen (e.g., testosterone) levels are referred to as

hypoandrogenism and low estrogen (e.g., estradiol) as hypoestrogenism,
and may occur as symptoms of hypogonadism. Other hormones produced
by the gonads that hypogonadism can decrease include progesterone,
DHEA, anti-Müllerian hormone, activin, and inhibin. Spermatogenesis and
ovulation may be impaired by hypogonadism, which, depending on the
degree of severity, may result in partial or complete infertility.

Women with hypogonadism do not begin menstruating and it may affect

their height and breast development. Onset in women after puberty causes
cessation of menstruation, lowered libido, loss of body hair and hot
flashes. In boys it causes impaired muscle and beard development and
reduced height. In men it can cause reduced body hair and beard, enlarged
breasts, loss of muscle, and sexual difficulties. A brain tumor (central
hypogonadism) may involve headaches, impaired vision, milky discharge
from the breast and symptoms caused by other hormone problems.

Male primary or Hypergonadotropic hypogonadism is often treated with

testosterone replacement therapy if they are not trying to conceive.

For women with hypogonadism, estradiol and progesterone are often

replaced. Some types of fertility defects can be treated, others cannot.
Some physicians also give testosterone to women, mainly to increase
libido.

Hypothyroidism, There is an inadequate production of thyroid hormones:

1.It is characterized by decreased  T4.

2.Ther is an increased level of  TSH.
3.Signs and Symptoms of Hypothyroidism
1.The signs and symptoms of hypothyroidism vary widely,
depending on the severity of the hormone deficiency.
2.At first, you may barely notice symptoms such as fatigue and
sluggishness.
3.Increased sensitivity to cold
4.Constipation.
 5.Skin is pale and dry skin.
6.There is puffiness of face due to edema.
7.The patient develops Hoarseness of voice.
8.There is an increased level of cholesterol.
9.The patient also gain weight.
10.There are Muscle aches, tenderness, and stiffness.
11.There is Muscle weakness
12.There may be Pain, stiffness or swelling of joints.
13.Female patients develops heavier menstrual periods.
14.The patient may develop signs of Depression.
15.Usually, these patients become obese.
16.There may be joint pain.
17.This patient may suffer from infertility.
18.These patients may develop heart problems.
19.In untreated cases, signs and symptoms become worse.
20.Constant stimulation of thyroid give rise to enlargement of
the gland, that is called Goiter.
21.Advanced hypothyroidism is known as Myxedema.
4.Myxedema includes more signs and symptoms like :

1.Low blood pressure.

2.Decreased breathing.
3.Decreased body temperature.
4.Unresponsiveness and the even patient may go into a coma.
5.Myxedema may be fatal in some patient.
5.Causes of hypothyroidism
1.Autoimmune thyroid disease.
2.Iodine deficiency.
3.iodine-induced.
4.Goitrogen exposure.
5.A defect in hormone synthesis.
6.Thyroid ablation by surgery or radiation.
7.Thyroid agenesis or dysgenesis.
8.Hypothalamic-pituitary disease.
Hyperthyroidism (Thyrotoxicosis), There is excessive production of
thyroid hormones:

1.It is characterized by elevated  T4.

2.There is decreased or even absent level of    TSH.
3.Signs and Symptoms of Hyperthyroidism
1.Hyperthyroidism can significantly accelerate your body’s
metabolism, causing :
2.Sudden weight loss, even appetite, and food intake remain
normal or increase.
3.Rapid or irregular heartbeat ( Tachycardia, Palpitation may be
more than 100 beats/minutes.).
4.The patient may even develop Arrhythmias.
5.The patient develops sweating.
6.Nervousness or irritability.
Graves disease This is an autoimmune disorder.
7.Grave’s Disease is due to Hyperthyroidism.
8.symptoms of hyperthyroidism:
1.Tremor, these are usually fine trembling with hands and
fingers.
2.Patients have increased sensitivity to heat.
3.Changes in bowel patterns, especially more frequent
bowel movements.
4.An enlarged thyroid gland (goiter).
5.The patient will have Fatigue, muscle weakness.
6.The patient will have sleep difficulty.
9.Beta blockers can mask many of the symptoms of
hyperthyroidism
4.Causes of hyperthyroidism

1.Multinodular goiter.
2.Single toxic goiter.
3.Subacute thyroiditis.
4.Autoimmune thyroid disease.
5.Pituitary adenoma (thyrotropin producing tumor).
6.Gestational trophoblastic tumor.
7.Postpartum Thyroid disease.
8.Hyperemesis gravidarum.
 9.Exogenous thyroid hormones.
10.Metastatic thyroid cancer.
11.iodine-induced.

Goiter

1.Definition This is enlarged thyroid gland because of any cause.

2.Causes are :
1.Inflammatory.
2.A function which may be normal increased or decreased.
3.Neoplastic.
3.Most of the goiter have normal function seen in 90 % of the
multinodular goiter and these are almost all are a colloid goiter.
4.Euthyroid sick syndrome This is also known low T3 syndrome
1.There is biochemical hypothyroidism as T4 is shifted away to
form T3.
2.Total T4 and TSH usually remain within normal limits.

Bone and Muscle Injuries

Shoulder impingement syndrome, also called subacromial impingement,
painful arc syndrome, supraspinatus syndrome, swimmer's shoulder,
and thrower's shoulder, is a clinical syndrome which occurs when the
tendons of the rotator cuff muscles become irritated and inflamed as they
pass through the subacromial space, the passage beneath the acromion.
This can result in pain, weakness and loss of movement at the shoulder.
The most common symptoms in impingement syndrome are pain,
weakness and a loss of movement at the affected shoulder. The pain is
often worsened by shoulder overhead movement and may occur at night,
especially when lying on the affected shoulder. The onset of the pain may
be acute if it is due to an injury or may be insidious if it is due to a gradual
process such as an osteoarthritic spur. The pain has been described as dull
rather than sharp, and lingers for long periods of a time, making it hard to
fall sleep. Other symptoms can include a grinding or popping sensation
during movement of the shoulder.

The range of motion at the shoulder may be limited by pain. A painful arc
of movement may be present during forward elevation of the arm from 60°
to 120°. Passive movement at the shoulder will appear painful when a
downwards force is applied at the acromion but the pain will ease once the
downwards force is removed.

Impingement syndrome is usually treated conservatively, but sometimes it

is treated with arthroscopic surgery or open surgery. Conservative
treatment includes rest, cessation of painful activity, and physical therapy.
Physical therapy treatments would typically focus at maintaining range of
movement, improving posture, strengthening shoulder muscles, and
reduction of pain. Physical therapists may employ the following treatment
techniques to improve pain and function: joint mobilization, interferential
therapy, acupuncture, soft tissue therapy, therapeutic taping, rotator cuff
strengthening, and education regarding the cause and mechanism of the
condition. NSAIDs and ice packs may be used for pain relief.

Therapeutic injections of corticosteroid and local anaesthetic may be used

for persistent impingement syndrome. The total number of injections is
generally limited to three due to possible side effects from the
corticosteroid. A recent systematic review of level one evidence showed
corticoestroid injections only give small and transient pain relief.
Hip dysplasia is an abnormality of the hip joint where the socket portion
does not fully cover the ball portion, resulting in an increased risk for joint
dislocation. Hip dysplasia may occur at birth or develop in early life.
Regardless, it does not typically produce symptoms in babies less than a
year old. Occasionally one leg may be shorter than the other. The left hip is
more often affected than the right. Complications without treatment can
include arthritis, limping, and low back pain.
Hip dysplasia can range from barely detectable to severely malformed or
dislocated. The congenital form, teratologic or non-reducible dislocation
occurs as part of more complex conditions.

The condition can be bilateral or unilateral:

•If both hip joints are affected one speaks of "bilateral" dysplasia. In this
case some diagnostic indicators like asymmetric folds and leg-length
inequality do not apply.
•In unilateral dysplasia only one joint shows deformity, the contralateral
side may show resulting effects. In the majority of unilateral cases the left
hip has the dysplasia.
If the joint is fully dislocated a false acetabulum often forms (often higher
up on the pelvis) opposite the dislocated femoral head position.

In acetabular dysplasia the acetabulum (socket) is too shallow or

deformed. The center-edge angle is measured as described by Wiberg. Two
forms of femoral dysplasia are coxa vara, in which the femur head grows
at too narrow an angle to the shaft, and coxa valga, in which the angle is
too wide.

A rare type, the "Beukes familial hip dysplasia" is found among Afrikaners
that are members of the Beukes family. The femur head is flat and
irregular. People develop osteoarthritis at an early age.

Sacroiliitis is a medical condition caused by any inflammation within one,

or both, of the sacroiliac joints. Sacroiliitis is a feature of
spondyloarthropathies, such as axial spondyloarthritis (including
ankylosing spondylitis), psoriatic arthritis, reactive arthritis or arthritis
related to inflammatory bowel diseases, including ulcerative colitis or
Crohn's disease. It is also the most common presentation of arthritis from
brucellosis.

Sacroiliitis is a condition caused by inflammation within the sacroiliac

joint. This joint is located where the base of the spine, known as the
sacrum, and the pelvis, known as the ilium, intersect. "Itis" is a latin term
denoting inflammation.

Since sacroiliitis can describe any type of inflammation found within the
sacroiliac joint, there can be a number of issues that cause it. These
include:

•Degenerative arthritis, or osteoarthritis of the spine, can cause

degeneration within the sacroiliac joints and lead to inflammation and joint
pain.

•Any form of spondyloarthropathies, which includes ankylosing

spondylitis, psoriatic arthritis, reactive arthritis or arthritis related to
inflammatory bowel diseases, including ulcerative colitis or Crohn's
disease.

•Pregnancy can cause inflammation as a result of the widening and

stretching of the sacroiliac joints to prepare for childbirth. Additionally, the
added weight carried during childbearing can put an extra amount of stress
on the SI joints, leading to abnormal wear.

•Traumatic injury such as a fall or car crash that affects the lower back,
hips, buttocks or legs.

•Though rare, infection within the sacroiliac joints or another part of the
body, such as a urinary tract infection, can cause inflammation.

In most cases sacroiliitis can be treated without surgery. Often patients will
find relief through a combination of rest, heat / ice therapy and anti-
inflammatory medication, like ibuprofen. Together these simple treatments
help reduce inflammation and allow the body to deliver healing nutrients
to the affected SI joints.

For more severe forms of sacroiliitis, sacroiliac joint injections might be

recommended to help combat symptoms. If chosen, a physician will inject
a numbing agent, usually lidocaine, and a steroid containing powerful anti-
inflammatory medication into the joint using fluoroscopic guidance. These
steroid injections can be delivered up to three or four times a year and
should be accompanied with physical therapy to help rehabilitate the
affected joint.

Intestinal Diseases
A volvulus is when a loop of intestine twists around itself and the
mesentery that supports it, resulting in a bowel obstruction. Symptoms
include abdominal pain, abdominal bloating, vomiting, constipation, and
bloody stool. Onset of symptoms may be rapid or more gradual. The
mesentery may become so tightly twisted that blood flow to part of the
intestine is cut off, resulting in ischemic bowel. In this situation there may
be fever or significant pain when the abdomen is touched.

Risk factors include a birth defect known as intestinal malrotation, an

enlarged colon, Hirschsprung disease, pregnancy, and abdominal
adhesions. Long term constipation and a high fiber diet may also increase
the risk. The most commonly affected part of the intestines in adults is the
sigmoid colon with the cecum being second most affected. In children the
small intestine is more often involved. The stomach can also be affected.
Diagnosis is typically with medical imaging such as plain X-rays, a GI
series, or CT scan.

Initial treatment for sigmoid volvulus may occasionally occur via

sigmoidoscopy or with a barium enema. Due to the high risk of recurrence,
a bowel resection within the next two days is generally recommended. If
the bowel is severely twisted or the blood supply is cut off, immediate
surgery is required. In a cecal volvulus, often part of the bowel needs to be
surgically removed. If the cecum is still healthy, it may occasionally be
returned to a normal position and sutured in place.

Hirschsprung's disease (HD or HSCR) is a birth defect in which nerves

are missing from parts of the intestine. The most prominent symptom is
constipation. Other symptoms may include vomiting, abdominal pain,
diarrhea, and slow growth. Symptoms usually become apparent in the first
two months of life. Complications may include enterocolitis, megacolon,
bowel obstruction, and intestinal perforation.

The disorder may occur by itself or in association with other genetic

disorders such as Down syndrome or Waardenburg syndrome.About half
of isolated cases are linked to a specific genetic mutation and about 20%
occur within families. Some of these occur in an autosomal dominant
manner. The cause of the remaining cases is unclear. If otherwise normal
parents have one child with the condition, the next child has a 4% risk of
being affected. The condition is divided into two main types, short-
segment and long-segment, depending on how much of the bowel is
affected. Rarely, the small bowel may be affected, as well. Diagnosis is
based on symptoms and confirmed by biopsy.

Treatment is generally by surgery to remove the affected section of bowel.

The surgical procedure most often carried out is known as a "pull
through". Occasionally, an intestinal transplantation may be recommended.

Crohn's disease is a type of inflammatory bowel disease (IBD) that may

affect any part of the gastrointestinal tract from mouth to anus. Signs and
symptoms often include abdominal pain, diarrhea (which may be bloody if
inflammation is severe), fever, and weight loss. Other complications may
occur outside the gastrointestinal tract and include anemia, skin rashes,
arthritis, inflammation of the eye, and tiredness. The skin rashes may be
due to infections as well as pyoderma gangrenosum or erythema nodosum.
Bowel obstruction may occur as a complication of chronic inflammation,
and those with the disease are at greater risk of bowel cancer.

While the cause of Crohn's disease is unknown, it is believed to be due to a

combination of environmental, immune, and bacterial factors in
genetically susceptible individuals.It results in a chronic inflammatory
disorder, in which the body's immune system attacks the gastrointestinal
tract possibly directed at microbial antigens. While Crohn's is an immune-
related disease, it does not appear to be an autoimmune disease (in that the
immune system is not being triggered by the body itself). The exact
underlying immune problem is not clear; however, it may be an
immunodeficiency state. About half of the overall risk is related to genetics
with more than 70 genes found to be involved. Tobacco smokers are twice
as likely to develop Crohn's disease as nonsmokers. It also often begins
after gastroenteritis. Diagnosis is based on a number of findings including
biopsy and appearance of the bowel wall, medical imaging and description
of the disease. Other conditions that can present similarly include irritable
bowel syndrome and Behçet's disease.

There are no medications or surgical procedures that can cure Crohn's

disease. Treatment options are intended to help with symptoms, maintain
remission, and prevent relapse. In those newly diagnosed, a corticosteroid
may be used for a brief period of time to rapidly improve symptoms
alongside another medication such as either methotrexate or a thiopurine
used to prevent recurrence. Stopping smoking is recommended in people
with Crohn's disease. One in five people with the disease is admitted to
hospital each year, and half of those with the disease will require surgery
for the disease at some point over a ten-year period. While surgery should
be used as little as possible, it is necessary to address some abscesses,
certain bowel obstructions, and cancers. Checking for bowel cancer via
colonoscopy is recommended every few years, starting eight years after
the disease has begun.

Coeliac disease, also spelled celiac disease, is a long-term autoimmune

disorder that primarily affects the small intestine. Classic symptoms
include gastrointestinal problems such as chronic diarrhoea, abdominal
distention, malabsorption, loss of appetite and among children failure to
grow normally. This often begins between six months and two years of
age. Non-classic symptoms are more common, especially in people older
than two years. There may be mild or absent gastrointestinal symptoms, a
wide number of symptoms involving any part of the body or no obvious
symptoms. Coeliac disease was first described in childhood; however, it
may develop at any age. It is associated with other autoimmune diseases,
such as diabetes mellitus type 1 and thyroiditis, among others.

Coeliac disease is caused by a reaction to gluten, which are various

proteins found in wheat and in other grains such as barley and rye.
Moderate quantities of oats, free of contamination with other gluten-
containing grains, are usually tolerated. The occurrence of problems may
depend on the variety of oat. It occurs in people who are genetically
predisposed. Upon exposure to gluten, an abnormal immune response may
lead to the production of several different autoantibodies that can affect a
number of different organs. In the small bowel, this causes an
inflammatory reaction and may produce shortening of the villi lining the
small intestine (villous atrophy). This affects the absorption of nutrients,
frequently leading to anaemia.

Diagnosis is typically made by a combination of blood antibody tests and

intestinal biopsies, helped by specific genetic testing. Making the
diagnosis is not always straightforward. Frequently, the autoantibodies in
the blood are negative, and many people have only minor intestinal
changes with normal villi. People may have severe symptoms and be
investigated for years before a diagnosis is achieved. Increasingly, the
diagnosis is being made in people without symptoms, as a result of
screening. Evidence regarding the effects of screening, however, is not
sufficient to determine its usefulness. While the disease is caused by a
permanent intolerance to wheat proteins, it is not a form of wheat allergy.

The only known effective treatment is a strict lifelong gluten-free diet,

which leads to recovery of the intestinal mucosa, improves symptoms and
reduces risk of developing complications in most people. If untreated, it
may result in cancers such as intestinal lymphoma and a slightly increased
risk of early death.

Peritonitis is inflammation of the peritoneum, the lining of the inner wall

of the abdomen and cover of the abdominal organs. Symptoms may
include severe pain, swelling of the abdomen, fever, or weight loss. One
part or the entire abdomen may be tender. Complications may include
shock and acute respiratory distress syndrome.

Causes include perforation of the intestinal tract, pancreatitis, pelvic

inflammatory disease, stomach ulcer, cirrhosis, or a ruptured appendix.
Risk factors include ascites and peritoneal dialysis. Diagnosis is generally
based on examination, blood tests, and medical imaging.

Treatment often includes antibiotics, intravenous fluids, pain medication,

and surgery. Other measures may include a nasogastric tube or blood
transfusion. Without treatment death may occur within a few days.
Approximately 7.5% of people have appendicitis at some point in time.
About 20% of people with cirrhosis who are hospitalized have peritonitis.

The main manifestations of peritonitis are acute abdominal pain,

abdominal tenderness and abdominal guarding, which are exacerbated by
moving the peritoneum, e.g., coughing (forced cough may be used as a
test), flexing one's hips, or eliciting the Blumberg sign (a.k.a. rebound
tenderness, meaning that pressing a hand on the abdomen elicits less pain
than releasing the hand abruptly, which will aggravate the pain, as the
peritoneum snaps back into place). Rigidity (involuntary contraction of the
abdominal muscles) is the most specific exam finding for diagnosing
peritonitis (+ likelihood ratio: 3.9). The presence of these signs in a patient
is sometimes referred to as peritonism. The localization of these
manifestations depends on whether peritonitis is localized (e.g.,
appendicitis or diverticulitis before perforation), or generalized to the
whole abdomen. In either case, pain typically starts as a generalized
abdominal pain (with involvement of poorly localizing innervation of the
visceral peritoneal layer), and may become localized later (with the
involvement of the somatically innervated parietal peritoneal layer).
Peritonitis is an example of an acute abdomen.
Other symptoms include:
Diffuse abdominal rigidity ("abdominal guarding") is often present,
especially in generalized peritonitis
•Fever
•Sinus tachycardia
•Development of ileus paralyticus (i.e., intestinal paralysis), which also
causes nausea, vomiting and bloating.
Perforation of part of the gastrointestinal tract is the most common cause
of peritonitis. Examples include perforation of the distal esophagus
(Boerhaave syndrome), of the stomach (peptic ulcer, gastric carcinoma), of
the duodenum (peptic ulcer), of the remaining intestine (e.g., appendicitis,
diverticulitis, Meckel diverticulum, inflammatory bowel disease (IBD),
intestinal infarction, intestinal strangulation, colorectal carcinoma,
meconium peritonitis), or of the gallbladder (cholecystitis). Other possible
reasons for perforation include abdominal trauma, ingestion of a sharp
foreign body (such as a fish bone, toothpick or glass shard), perforation by
an endoscope or catheter, and anastomotic leakage. The latter occurrence is
particularly difficult to diagnose early, as abdominal pain and ileus
paralyticus are considered normal in patients who have just undergone
abdominal surgery. In most cases of perforation of a hollow viscus, mixed
bacteria are isolated; the most common agents include Gram-negative
bacilli (e.g., Escherichia coli) and anaerobic bacteria (e.g., Bacteroides
fragilis). Fecal peritonitis results from the presence of faeces in the
peritoneal cavity. It can result from abdominal trauma and occurs if the
large bowel is perforated during surgery.

•Disruption of the peritoneum, even in the absence of perforation of a

hollow viscus, may also cause infection simply by letting micro-organisms
into the peritoneal cavity. Examples include trauma, surgical wound,
continuous ambulatory peritoneal dialysis, and intra-peritoneal
chemotherapy. Again, in most cases, mixed bacteria are isolated; the most
common agents include cutaneous species such as Staphylococcus aureus,
and coagulase-negative staphylococci, but many others are possible,
including fungi such as Candida.
•Spontaneous bacterial peritonitis (SBP) is a peculiar form of peritonitis
occurring in the absence of an obvious source of contamination. It occurs
in patients with ascites, in particular, in children.
•Intra-peritoneal dialysis predisposes to peritoneal infection (sometimes
named "primary peritonitis" in this context).
•Systemic infections (such as tuberculosis) may rarely have a peritoneal
localisation.
Depending on the severity of the patient's state, the management of
peritonitis may include:

•General supportive measures such as vigorous intravenous rehydration

and correction of electrolyte disturbances.
•Antibiotics are usually administered intravenously, but they may also be
infused directly into the peritoneum. The empiric choice of broad-
spectrum antibiotics often consist of multiple drugs, and should be targeted
against the most likely agents, depending on the cause of peritonitis (see
above); once one or more agents grow in cultures isolated, therapy will be
target against them.
•Gram positive and gram negative organisms must be covered. Out of the
cephalosporins, cefoxitin and cefotetan can be used to cover gram positive
bacteria, gram negative bacteria, and anaerobic bacteria. Beta-lactams with
beta lactamase inhibitors can also be used, examples include
ampicillin/sulbactam, piperacillin/tazobactam, and ticarcillin/clavulanate.
Carbapenems are also an option when treating primary peritonitis as all of
the carbapenems cover gram positives, gram negatives, and anaerobes
except for ertapenem. The only fluoroquinolone that can be used is
moxifloxacin because this is the only fluoroquinolone that covers
anaerobes. Finally, tigecycline is a tetracycline that can be used due to its
coverage of gram positives and gram negatives. Empiric therapy will often
require multiple drugs from different classes.
•Surgery (laparotomy) is needed to perform a full exploration and lavage
of the peritoneum, as well as to correct any gross anatomical damage that
may have caused peritonitis. The exception is spontaneous bacterial
peritonitis, which does not always benefit from surgery and may be treated
with antibiotics in the first instance.
Bowel obstruction, also known as intestinal obstruction, is a mechanical
or functional obstruction of the intestines which prevents the normal
movement of the products of digestion. Either the small bowel or large
bowel may be affected. Signs and symptoms include abdominal pain,
vomiting, bloating and not passing gas. Mechanical obstruction is the
cause of about 5 to 15% of cases of severe abdominal pain of sudden onset
requiring admission to hospital.
Causes of bowel obstruction include adhesions, hernias, volvulus,
endometriosis, inflammatory bowel disease, appendicitis, tumors,
diverticulitis, ischemic bowel, tuberculosis and intussusception. Small
bowel obstructions are most often due to adhesions and hernias while large
bowel obstructions are most often due to tumors and volvulus. The
diagnosis may be made on plain X-rays; however, CT scan is more
accurate. Ultrasound or MRI may help in the diagnosis of children or
pregnant women.
The condition may be treated conservatively or with surgery. Typically
intravenous fluids are given, a tube is placed through the nose into the
stomach to decompress the intestines, and pain medications are given.
Antibiotics are often given. In small bowel obstruction about 25% require
surgery. Complications may include sepsis, bowel ischemia and bowel
perforation

Diverticulitis, specifically colonic diverticulitis, is a gastrointestinal

disease characterized by inflammation of abnormal pouches – diverticuli -
which can develop in the wall of the large intestine. Symptoms typically
include lower abdominal pain of a sudden onset. The onset of symptoms,
however, may also occur over a few days. In North America and Europe
the abdominal pain is usually on the left lower side, while in Asia it is
usually on the right. There may also be nausea; and diarrhea or
constipation. Fever or blood in the stool suggests a complication. Repeated
attacks may occur.
The causes of diverticulitis are uncertain. Risk factors may include obesity,
lack of exercise, smoking, a family history of the disease, and nonsteroidal
anti-inflammatory drugs (NSAIDs). The role of a low fiber diet as a risk
factor is unclear. Having pouches in the large intestine that are not
inflamed is known as diverticulosis. Inflammation occurs in between 10%
and 25% at some point in time and is due to a bacterial infection.
Diagnosis is typically by CT scan, though blood tests, colonoscopy, or a
lower gastrointestinal series may also be supportive. The differential
diagnosis includes irritable bowel syndrome.
Preventive measures include altering risk factors such as obesity,
inactivity, and smoking. Mesalazine and rifaximin appear useful for
preventing attacks in those with diverticulosis. Avoiding nuts and seeds as
a preventive measure is no longer recommended since there is no evidence
these play a role in initiating inflammation in diverticula. For mild
diverticulitis, antibiotics by mouth and a liquid diet is recommended. For
severe cases, intravenous antibiotics, hospital admission, and complete
bowel rest may be recommended. Probiotics are of unclear use.
Complications such as abscess formation, fistulaformation, and perforation
of the colon may require surgery.

A volvulus is when a loop of intestine twists around itself and the

mesentery that supports it, resulting in a bowel obstruction. Symptoms
include abdominal pain, abdominal bloating, vomiting, constipation, and
bloody stool. Onset of symptoms may be rapid or more gradual. The
mesentery may become so tightly twisted tha blood flow to part of the
intestine is cut off, resulting in ischemic bowel. In this situation there may
be fever or significant pain when the abdomen is touched.
Risk factors include a birth defect known as intestinal malrotation, an
enlarged colon, Hirschsprung disease, pregnancy, and abdominal
adhesions. Long term constipation and a high fiber diet may also increase
the risk. The most commonly affected part of the intestines in adults is the
sigmoid colon with the cecum being second most affected. In children the
small intestine is more often involved. The stomach can also be affected.
Diagnosis is typically with medical imaging such as plain X-rays, a GI
series, or CT scan.
Initial treatment for sigmoid volvulus may occasionally occur via
sigmoidoscopy or with a barium enema. Due to the high risk of recurrence,
a bowel resection within the next two days is generally recommended. If
the bowel is severely twisted or the blood supply is cut off, immediate
surgery is required. In a cecal volvulus, often part of the bowel needs to be
surgically removed. If the cecum is still healthy, it may occasionally be
returned to a normal position and sutured in place.
Eye Diseases

Diabetic retinopathy, also known as diabetic eye disease, is a medical

condition in which damage occurs to the retina due to diabetes mellitus. It
is a leading cause of blindness.

Diabetic retinopathy often has no early warning signs. Even macular

edema, which can cause rapid vision loss, may not have any warning signs
for some time. In general, however, a person with macular edema is likely
to have blurred vision, making it hard to do things like read or drive. In
some cases, the vision will get better or worse during the day.

The first stage, called non-proliferative diabetic retinopathy (NPDR), has

no symptoms. Its signs aren't visible to the eye and patients will have
20/20 vision. The only way to detect NPDR is by fundus photography, in
which microaneurysms (microscopic blood-filled bulges in the artery
walls) can be seen. If there is reduced vision, fluorescein angiography can
show the back of the eye and narrowing or blocked retinal blood vessels
clearly. This is called retinal ischemia (lack of blood flow).

Macular edema, in which blood vessels leak their contents into the macular
region, can occur at any stage of NPDR. Its symptoms are blurred vision
and darkened or distorted images that are not the same in both eyes. Ten
percent (10%) of diabetic patients will have vision loss related to macular
edema. Optical Coherence Tomography can show areas of retinal
thickening due to fluid accumulation from macular edema.

In the second stage, abnormal new blood vessels (neovascularisation) form

at the back of the eye as part of proliferative diabetic retinopathy(PDR);
these can burst and bleed (vitreous hemorrhage) and blur the vision,
because these new blood vessels are fragile. The first time this bleeding
occurs, it may not be very severe. In most cases, it will leave just a few
specks of blood, or spots floating in a person's visual field, though the
spots often go away after a few hours.

These spots are often followed within a few days or weeks by a much
greater leakage of blood, which blurs the vision. In extreme cases, a person
may only be able to tell light from dark in that eye. It may take the blood
anywhere from a few days to months or even years to clear from the inside
of the eye, and in some cases the blood will not clear. These types of large
hemorrhages tend to happen more than once, often during sleep.

On funduscopic exam, a doctor will see cotton wool spots, flame

hemorrhages (similar lesions are also caused by the alpha-toxin of
Clostridium novyi), and dot-blot hemorrhages.

Diabetic retinopathy is detected during an eye examination that includes:

•Visual acuity test: Uses an eye chart to measure how well a person sees at
various distances (i.e., visual acuity).
•Pupil dilation: The eye care professional places drops into the eye to
dilate the pupil. This allows him or her to see more of the retina and look
for signs of diabetic retinopathy. After the examination, close-up vision
may remain blurred for several hours.
•Ophthalmoscopy or fundus photography: Ophthalmoscopy is an
examination of the retina in which the eye care professional: (1) looks
through a slit lamp biomicroscope with a special magnifying lens that
provides a narrow view of the retina, or (2) wearing a headset (indirect
ophthalmoscope) with a bright light, looks through a special magnifying
glass and gains a wide view of the retina. Hand-held ophthalmoscopy is
insufficient to rule out significant and treatable diabetic retinopathy.
Fundus photography generally captures considerably larger areas of the
fundus, and has the advantage of photo documentation for future reference,
as well as availing the image to be examined by a specialist at another
location and/or time.
•Fundus Fluorescein angiography (FFA): This is an imaging technique
which relies on the circulation of fluorescein dye to show staining,
leakage, or non-perfusion of the retinal and choroidal vasculature.
•Optical coherence tomography (OCT): This is an optical imaging
modality based upon interference, and analogous to ultrasound. It produces
cross-sectional images of the retina (B-scans) which can be used to
measure the thickness of the retina and to resolve its major layers,
allowing the observation of swelling.
The eye care professional will look at the retina for early signs of the
disease, such as:

1.leaking blood vessels,

2.retinal swelling, such as macular edema,
3.pale, fatty deposits on the retina (exudates) – signs of leaking blood
vessels,
4.damaged nerve tissue (neuropathy), and
5.any changes in the blood vessels.
There are three major treatments for diabetic retinopathy, which are very
effective in reducing vision loss from this disease. In fact, even people
with advanced retinopathy have a 95 percent chance of keeping their
vision when they get treatment before the retina is severely damaged.
These three treatments are laser surgery, injection of corticosteroids or
anti-VEGF agents into the eye, and vitrectomy.

Although these treatments are very successful (in slowing or stopping

further vision loss), they do not cure diabetic retinopathy. Caution should
be exercised in treatment with laser surgery since it causes a loss of retinal
tissue. It is often more prudent to inject triamcinolone or anti-VEGF drugs.
In some patients it results in a marked increase of vision, especially if there
is an edema of the macula.

Avoiding tobacco use and correction of associated hypertension are

important therapeutic measures in the management of diabetic retinopathy.

Acanthamoeba keratitis (AK) is an infection of the cornea, the clear

‘window’ at the front of the eye, that can be very painful. The infection is
caused by a microscopic organism called Acanthamoeba, which is
common in nature and is usually found in bodies of water (lakes, oceans
and rivers) as well as domestic tap water, swimming pools, hot tubs, soil
and air.

Many different species of Acanthamoeba exist. Acanthamoeba organisms

do not generally cause harm to humans (we come into contact with them
when we wash, swim, drink water etc), but they can cause a serious eye
disease if they infect the cornea. Not all species of Acanthamoeba have
been found to cause corneal infections. AK is most common in people who
wear contact lenses, but anyone with a corneal injury is susceptible to
developing the infection.
Your ophthalmologist will use a standard slit lamp microscope to look for
signs of inflammation in your cornea, including specific clinical signs
characteristic of AK. This is sometimes followed by a corneal scrape and
culture (a process by which some cells from the surface of your cornea are
removed and sent to a laboratory for further analysis), or a swab of the
cornea to check for Acanthamoeba DNA using a test called “PCR”. Results
for both these tests take a few days to come through. In some cases, AK
can be detected using a confocal microscope, a powerful scanner that can
see Acanthamoeba cysts within the various layers of the cornea. Your
ophthalmologist will use these tests together with other clinical signs and
symptoms in order to decide on the appropriate treatment plan.
Typically treatment is with antiseptic drops, including PHMB,
Chlorhexidine, Brolene or Hexamidine, which have an anti-amoebic effect.
Usually you’ll need to take these eye drops every hour for the first few
days (including overnight), reducing to 2-hourly by day only, and then less
frequently as the treatment progresses. It can be quite difficult to take eye
drops through the night during the first few days, but it’s very important to
try and stick to the regime outlined by the doctor as best you can.

In addition to the anti-amoebic eye drops, you may be given anti-

inflammatories or painkillers to help with the pain. You may also be
given a dilating drop early in the infection to stop painful spasms of the
coloured part of the eye, the iris. Around 10% of Acanthamoeba
infections have dual pathology, which means that another infection,
usually bacterial, is also present. If this is the case for you, we may also
prescribe you with antibiotics as well as your other drops. Sometimes
these are also given to guard against bacterial infection while the eye
surface is disrupted in the early stages of the disease. Patients with
severe inflammation or scleritis (inflammation of the white part of the
eye)are sometimes prescribed steroid eye drops, although not every
patient requires these and their use needs to be carefully managed.

OBGYN Diseases
Ectopic pregnancy is a complication of pregnancy in which the embryo
attaches outside the uterus. Signs and symptoms classically include
abdominal pain and vaginal bleeding. Fewer than 50 percent of affected
women have both of these symptoms. The pain may be described as sharp,
dull, or crampy. Pain may also spread to the shoulder if bleeding into the
abdomen has occurred. Severe bleeding may result in a fast heart rate,
fainting, or shock. With very rare exceptions the fetus is unable to survive.
Risk factors for ectopic pregnancy include: pelvic inflammatory disease,
often due to chlamydia infection, tobacco smoking, prior tubal surgery, a
history of infertility, and the use of assisted reproductive technology. Those
who have previously had an ectopic pregnancy are at much higher risk of
having another one. Most ectopic pregnancies (90%) occur in the
Fallopian tubewhich are known as tubal pregnancies. Implantation can also
occur on the cervix, ovaries, or within the abdomen. Detection of ectopic
pregnancy is typically by blood tests for human chorionic gonadotropin
(hCG) and ultrasound. This may require testing on more than one
occasion. Ultrasound works best when performed from within the vagina.
Other causes of similar symptoms include: miscarriage, ovarian torsion,
and acute appendicitis.

Prevention is by decreasing risk factors such as chlamydia infections

through screening and treatment. While some ectopic pregnancies will
resolve without treatment, this approach has not been well studied as of
2014. The use of the medication methotrexate works as well as surgery in
some cases. Specifically it works well when the beta-HCG is low and the
size of the ectopic is small. Surgery is still typically recommended if the
tube has ruptured, there is a fetal heartbeat, or the person's vital signs are
unstable. The surgery may be laparoscopic or through a larger incision,
known as a laparotomy. Outcomes are generally good with treatment.

Dificiency Diseases
Hypokalemia, also spelled hypokalaemia, is a low level of potassium (K+)
in the blood serum. Normal potassium levels are between 3.5 and 5.0
mmol/L (3.5 and 5.0 mEq/L) with levels below 3.5 mmol/L defined as
hypokalemia. Mildly low levels do not typically cause symptoms.
Symptoms may include feeling tired, leg cramps, weakness, and
constipation. It increases the risk of an abnormal heart rhythm, which is
often too slow, and can cause cardiac arrest.
Causes of hypokalemia include vomiting, diarrhea, medications like
furosemide and steroids, dialysis, diabetes insipidus, hyperaldosteronism,
hypomagnesemia, and not enough intake in the diet. It is classified as
severe when levels are less than 2.5 mmol/L. Low levels can also be
detected on an electrocardiogram (ECG). Hyperkalemia refers to a high
level of potassium in the blood serum.
The speed at which potassium should be replaced depends on whether or
not there are symptoms or ECG changes. Mildly low levels can be
managed with changes in the diet. Potassium supplements can be either
taken by mouth or intravenously. If given by intravenous, generally less
than 20 mmol are given over an hour. High concentration solutions (>40
mmol/L) should be given in a central line if possible. Magnesium
replacement may also be required.
Hypokalemia is one of the most common water–electrolyte imbalances. It
affects about 20% of people admitted to hospital. The word "hypokalemia"
is from hypo- means "under"; kalium meaning potassium, and -emia
means "condition of the blood"