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.

In the first stage which is called non-proliferative diabetic retinopathy (NPDR) there are no symptoms, the signs are not 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 be done to see the back of the eye. Narrowing or blocked retinal blood vessels can be seen clearly and 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. The symptoms of macular edema 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 the areas of

retinal thickening (due to fluid accumulation) of 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, also known as diabetic eye disease, is a medical condition in which damage occurs to the retina due to diabetes and is a leading cause of blindness.

It affects up to 80 percent of people who have had diabetes for 20 years or more. At least 90% of new cases could be reduced if there were proper treatment and monitoring of the eyes. The longer a person has diabetes, the higher his or her chances of developing diabetic retinopathy. Each year in the United States, diabetic retinopathy accounts for 12% of all new cases of blindness. It is also the leading cause of blindness for people aged 20 to 64 years.

Open-angle glaucoma is painless and does not have acute attacks, thus the lack of clear symptoms make screening via regular eye check-ups important. The only signs are gradually progressive visual field loss, and optic nerve changes (increased cup-to-disc ratio on fundoscopic examination).

About 10% of people with closed angles present with acute angle closure characterized by sudden ocular pain, seeing halos around lights, red eye, very high intraocular pressure (>30 mmHg), nausea and vomiting, suddenly decreased vision, and a fixed, mid-dilated pupil. It is also associated with an oval pupil in some cases. Acute angle closure is an emergency.

Opaque specks may occur in the lens in glaucoma, known as glaukomflecken.

Secondary glaucoma (H40.3-H40.6)

- Inflammatory glaucoma

- Phacogenic glaucoma

- Glaucoma secondary to intraocular hemorrhage

- Traumatic glaucoma

- Neovascular glaucoma (see below for more details)

- Drug-induced glaucoma

- Glaucoma of miscellaneous origin

Neovascular glaucoma, an uncommon type of glaucoma, is difficult or nearly impossible to treat, and is often caused by proliferative diabetic retinopathy (PDR) or central retinal vein occlusion (CRVO). It may also be triggered by other conditions that result in ischemia of the retina or ciliary body. Individuals with poor blood flow to the eye are highly at risk for this condition.

Neovascular glaucoma results when new, abnormal vessels begin developing in the angle of the eye that begin blocking the drainage. Patients with such condition begin to rapidly lose their eyesight. Sometimes, the disease appears very rapidly, especially after cataract surgery procedures. A new treatment for this disease, as first reported by Kahook and colleagues, involves the use of a novel group of medications known as anti-VEGF agents. These injectable medications can lead to a dramatic decrease in new vessel formation and, if injected early enough in the disease process, may lead to normalization of intraocular pressure. Currently, there are no high-quality controlled trials demonstrating a beneficial effect of anti-VEGF treatments in lowering IOP in people with neovascular glaucoma.

Toxic glaucoma is open angle glaucoma with an unexplained significant rise of intraocular pressure following unknown pathogenesis. Intraocular pressure can sometimes reach . It characteristically manifests as ciliary body inflammation and massive trabecular oedema that sometimes extends to Schlemm's canal. This condition is differentiated from malignant glaucoma by the presence of a deep and clear anterior chamber and a lack of aqueous misdirection. Also, the corneal appearance is not as hazy. A reduction in visual acuity can occur followed neuroretinal breakdown.

Associated factors include inflammation, drugs, trauma and intraocular surgery, including cataract surgery and vitrectomy procedures. Gede Pardianto (2005) reported on four patients who had toxic glaucoma. One of them underwent phacoemulsification with small particle nucleus drops. Some cases can be resolved with some medication, vitrectomy procedures or trabeculectomy. Valving procedures can give some relief, but further research is required.

Affected males develop generalized reticular hyper pigmentation in early childhood.

Hair often looks bedraggled or brushed backwards, hanging low on the forehead.

Among the associated extracutaneous manifestations are described:

- Respiratory infections

- Dyskeratosis corneal photophobia

- Hypohidrosis with large deficit of thermoregulation

- Growth retardation

- Gastrointestinal disorders

- Kidney disease

- Kidney stones

- Urinary infections

- Webbed feet or hands

- Electrolyte imbalance

- Retinitis pigmentosa

- Lymphoedema

- Thyroid abnormalities

Each patient shows some of the symptoms listed above. Not every sick person will show all of the listed symptoms.

In females the disease is characterized by skin rashes linear hyper pigmentation following the Blaschko's lines, morphologically similar to stage 3 pigment incontinence. There are no systemic manifestations associated with XLPDR in females.

X-linked reticulate pigmentary disorder (also known as "familial cutaneous amyloidosis", "Partington amyloidosis", "Partington cutaneous amyloidosis", "Partington syndrome type II", "reticulate pigmentary disorder", and "X-linked reticulate pigmentary disorder with systemic manifestations") is a cutaneous condition that has been described in adult women that had linear streaks of hyperpigmentation and in which male patients manifested a reticulated mottled brown pigmentation of the skin, which, on biopsy, demonstrated dermal deposits of amyloid.

The syndrome is also referred with the acronym X-Linked-PDR or even XLPRD.It's a very rare disease, genetically determined, with a chronic course.

It was characterized in 1981. Mutation of the "POLA1" gene leads to loss of expression of the catalytic subunit of DNA polymerase-α and is responsible for XLPDR. Loss of POLA1 expression results in reduced levels of RNA:DNA hybrids in the cytosol and unexpectedly triggers aberrant immune responses (e.g. type I interferon production) which at least in part can account for the symptoms associated with XLPDR.

In the subgroup of patients where an inoculating event was noted, the mean incubation period of acute melioidosis was 9 days (range 1–21 days). Patients with latent melioidosis may be symptom-free for decades; the longest period between presumed exposure and clinical presentation is 62 years. The potential for prolonged incubation was recognized in US servicemen involved in the Vietnam War, and was referred to as the "Vietnam time-bomb". A wide spectrum of severity exists; in chronic presentations, symptoms may last months, but fulminant infection, particularly associated with near-drowning, may present with severe symptoms over hours.

Symptoms usually appear 2 to 4 weeks after exposure. There are four general types of infection including localized, pulmonary, blood-borne, or disseminated throughout the body. The type and location of the infection usually determines which symptoms appear first as well as which symptoms are more prominent.

Patients with melioidosis usually present with fever. Pain or other symptoms may be suggestive of a clinical focus, which is found in around 75% of patients. Such symptoms include cough or pleuritic chest pain suggestive of pneumonia, bone or joint pain suggestive of osteomyelitis or septic arthritis, or cellulitis. Intra-abdominal infection (including liver and/or splenic abscesses, or prostatic abscesses) do not usually present with focal pain, and imaging of these organs using ultrasound or computed tomography should be performed routinely. In one series of 214 patients, 27.6% had abscesses in the liver or spleen (95% confidence interval, 22.0% to 33.9%). "B. pseudomallei" abscesses may have a characteristic "honeycomb" or "swiss cheese" architecture (hypoechoic, multiseptate, multiloculate) on CT.

Regional variations in disease presentation are seen: parotid abscesses characteristically occur in Thai children, but this presentation has been described only once in Australia. Conversely, prostatic abscesses are found in up to 20% of Australian males, but are rarely described elsewhere. An encephalomyelitis syndrome is recognised in northern Australia.

Patients with melioidosis usually have risk factors for disease, such as diabetes, thalassemia, hazardous alcohol use, or renal disease, and frequently give a history of occupational or recreational exposure to mud or pooled surface water. However, otherwise healthy patients, including children, may also get melioidosis.

In up to 25% of patients, no focus of infection is found and the diagnosis is usually made on blood cultures or throat swab. Melioidosis is said to be able to affect any organ in the body except the heart valves (endocarditis). Although meningitis has been described secondary to ruptured brain abscesses, primary meningitis has not been described. Less common manifestations include intravascular infection, lymph node abscesses (1.2–2.2%), pyopericardium and myocarditis, mediastinal infection, and thyroid and scrotal abscesses and ocular infection.

Chronic melioidosis is usually defined by a duration of symptoms greater than two months and occurs in about 10% of patients. The clinical presentation of chronic melioidosis is protean and includes such presentations as chronic skin infections, chronic lung nodule, and pneumonia. In particular, chronic melioidosis closely mimics tuberculosis, and has sometimes been called "Vietnamese tuberculosis".

Stunted growth, also known as stunting and nutritional stunting, is a reduced growth rate in human development. It is a primary manifestation of malnutrition (or more precisely undernutrition) and recurrent infections, such as diarrhea and helminthiasis, in early childhood and even before birth, due to malnutrition during fetal development brought on by a malnourished mother. The definition of stunting according to the World Health Organisation (WHO) is for the "height for age" value to be less than two standard deviations of the WHO Child Growth Standards median.

As of 2012 an estimated 162 million children under 5 years of age, or 25%, were stunted in 2012. More than 90% of the world's stunted children live in Africa and Asia, where respectively 36% and 56% of children are affected. Once established, stunting and its effects typically become permanent. Stunted children may never regain the height lost as a result of stunting, and most children will never gain the corresponding body weight. Living in an environment where many people defecate in the open due to lack of sanitation, is an important cause of stunted growth in children, for example in India.

Multiple drug resistance (MDR), multidrug resistance or multiresistance is antimicrobial resistance shown by a species of microorganism to multiple antimicrobial drugs. The types most threatening to public health are MDR bacteria that resist multiple antibiotics; other types include MDR viruses, fungi, and parasites (resistant to multiple antifungal, antiviral, and antiparasitic drugs of a wide chemical variety). Recognizing different degrees of MDR, the terms extensively drug resistant (XDR) and pandrug-resistant (PDR) have been introduced. The definitions were published in 2011 in the journal "Clinical Microbiology and Infection" and are openly accessible.

Stunted growth in children has the following public health impacts apart from the obvious impact of shorter stature of the person affected:

- greater risk for illness and premature death

- may result in delayed mental development and therefore poorer school performance and later on reduced productivity in the work force

- reduced cognitive capacity

- Women of shorter stature have a greater risk for complications during child birth due to their smaller pelvis, and are at risk of delivering a baby with low birth weight

- Stunted growth can even be passed on to the next generation (this is called the "intergenerational cycle of malnutrition")

The impact of stunting on child development has been established in multiple studies. If a child is stunted at age 2 they will have higher risk of poor cognitive and educational achievement in life, with subsequent socio-economic and inter-generational consequences. Multi-country studies have also suggested that stunting is associated with reductions in schooling, decreased economic productivity and poverty. Stunted children also display higher risk of developing chronic non-communicable conditions such as diabetes and obesity as adults. If a stunted child undergoes substantial weight gain after age 2, there is a higher chance of becoming obese. This is believed to be caused by metabolic changes produced by chronic malnutrition, that can produce metabolic imbalances if the individual is exposed to excessive or poor quality diets as an adult. This can lead to higher risk of developing other related non-communicable diseases such as hypertension, coronary heart disease, metabolic syndrome and stroke.

At societal level, stunted individuals do not fulfill their physical and cognitive developmental potential and will not be able to contribute maximally to society. Stunting can therefore limit economic development and productivity, and it has been estimated that it can affect a country's GDP up to 3%.

Cholangiocarcinoma, also known as bile duct cancer, is a form of cancer that is composed of mutated epithelial cells (or cells showing characteristics of epithelial differentiation) that originate in the bile ducts which drain bile from the liver into the small intestine. Other biliary tract cancers include gallbladder cancer and cancer of the ampulla of Vater.

Cholangiocarcinoma is a relatively rare neoplasm that is classified as an adenocarcinoma (a cancer that forms glands or secretes significant amounts of mucins). It has an annual incidence rate of 1–2 cases per 100,000 in the Western world, but rates of cholangiocarcinoma have been rising worldwide over the past few decades.

Prominent signs and symptoms of cholangiocarcinoma include abnormal liver function tests, abdominal pain, jaundice, and weight loss. Other symptoms such as generalized itching, fever, and changes in color of stool or urine may also occur. The disease is diagnosed through a combination of blood tests, imaging, endoscopy, and sometimes surgical exploration, with confirmation obtained after a pathologist examines cells from the tumor under a microscope. Known risk factors for cholangiocarcinoma include primary sclerosing cholangitis (an inflammatory disease of the bile ducts), infection with the parasitic liver flukes "Opisthorchis viverrini" or "Clonorchis sinensis", some congenital liver malformations, and exposure to Thorotrast (thorium dioxide), a chemical formerly used in medical imaging. However, most people with cholangiocarcinoma have no identifiable risk factors.

Cholangiocarcinoma is considered to be an incurable and rapidly lethal cancer unless both the primary tumor and any metastases can be fully removed by surgery. No potentially curative treatment exists except surgery, but most people have advanced stage disease at presentation and are inoperable at the time of diagnosis. People with cholangiocarcinoma are generally managed - though not cured - with chemotherapy, radiation therapy, and other palliative care measures. These are also used as additional therapies after surgery in cases where resection has apparently been successful (or nearly so).

Common multidrug-resistant organisms are usually bacteria:

- Vancomycin-Resistant Enterococci (VRE)

- Methicillin-Resistant "Staphylococcus" "aureus" (MRSA)

- Extended-spectrum β-lactamase (ESBLs) producing Gram-negative bacteria

- "Klebsiella" "pneumoniae" carbapenemase (KPC) producing Gram-negatives

- Multidrug-Resistant gram negative rods (MDR GNR) MDRGN bacteria such as "Enterobacter species", "E.coli", "Klebsiella pneumoniae", "Acinetobacter baumannii", "Pseudomonas aeruginosa"

A group of gram-positive and gram-negative bacteria of particular recent importance have been dubbed as the ESKAPE group ("Enterococcus faecium", "Staphylococcus aureus", "Klebsiella pneumoniae", "Acinetobacter baumannii", "Pseudomonas aeruginosa" and Enterobacter species).

- Multi-drug-resistant tuberculosis

The most common physical indications of cholangiocarcinoma are abnormal liver function tests, jaundice (yellowing of the eyes and skin occurring when bile ducts are blocked by tumor), abdominal pain (30%–50%), generalized itching (66%), weight loss (30%–50%), fever (up to 20%), and changes in the color of stool or urine. To some extent, the symptoms depend upon the location of the tumor: patients with cholangiocarcinoma in the extrahepatic bile ducts (outside the liver) are more likely to have jaundice, while those with tumors of the bile ducts within the liver more often have pain without jaundice.

Blood tests of liver function in patients with cholangiocarcinoma often reveal a so-called "obstructive picture," with elevated bilirubin, alkaline phosphatase, and gamma glutamyl transferase levels, and relatively normal transaminase levels. Such laboratory findings suggest obstruction of the bile ducts, rather than inflammation or infection of the liver parenchyma, as the primary cause of the jaundice.