Pallor mortis results from the cessation of capillary circulation throughout the body. Gravity then causes the blood to sink down into the lower parts of the body, creating livor mortis.

Pallor mortis occurs almost immediately (within 15–25 minutes) post-mortem; paleness develops so rapidly after death that it has little to no use in determining the time of death, aside from saying that it either happened less than 30 minutes ago or more, which could help if the body were found very soon after death.

Pallor is a pale color of the skin that can be caused by illness, emotional shock or stress, stimulant use, or anemia, and is the result of a reduced amount of oxyhaemoglobin and is visible in skin conjuctivae or mucous membrane.

Pallor is more evident on the face and palms. It can develop suddenly or gradually, depending on the cause. It is not usually clinically significant unless it is accompanied by a general pallor (pale lips, tongue, palms, mouth and other regions with mucous membranes). It is distinguished from similar presentations such as hypopigmentation (lack or loss of skin pigment) or simply a fair complexion.

Symptoms of OI are triggered by the following:

- An upright posture for long periods of time (e.g. standing in line, standing in a shower, or even sitting at a desk).

- A warm environment (such as in hot summer weather, a hot crowded room, a hot shower or bath, after exercise).

- Emotionally stressful events (seeing blood or gory scenes, being scared or anxious).

- Astronauts returning from space not yet re-adapted to gravity.

- Extended bedrest

- Inadequate fluid and salt intake.

Hemolytic anemia affects nonhuman species as well as humans. It has been found, in a number of animal species, to result from specific triggers.

Some notable cases include hemolytic anemia found in black rhinos kept in captivity, with the disease, in one instance, affecting 20% of captive rhinos at a specific facility. The disease is also found in wild rhinos.

Dogs and cats differ slightly from humans in some details of their RBC composition and have altered susceptibility to damage, notably, increased susceptibility to oxidative damage from consumption of onion. Garlic is less toxic to dogs than onion.

Hypochromic anemia occurs in patients with hypochromic microcytic anemia with iron overload. The condition is autosomal recessive and is caused by mutations in the SLC11A2 gene. The condition prevents red blood cells from accessing iron in the blood, which causes anemia that is apparent at birth. It can lead to pallor, fatigue, and slow growth. The iron overload aspect of the disorder means that the iron accumulates in the liver and can cause liver impairment in adolescence or early adulthood.

It also occurs in patients with hereditary iron refractory iron-deficiency anemia (IRIDA). Patients with IRIDA have very low serum iron and transferrin saturation, but their serum ferritin is normal or high. The anemia is usually moderate in severity and presents later in childhood.

Hypochromic anemia is also caused by thalassemia and congenital disorders like Benjamin anemia.

PRCA is considered an autoimmune disease as it will respond to immunosuppressant treatment such as ciclosporin in many patients, though this approach is not without risk.

It has also been shown to respond to treatments with Rituximab and Tacrolimus.

Hypochromic anemia may be caused by vitamin B6 deficiency from a low iron intake, diminished iron absorption, or excessive iron loss. It can also be caused by infections (e.g. hookworms) or other diseases (i.e. anemia of chronic disease), therapeutic drugs, copper toxicity, and lead poisoning. One acquired form of anemia is also known as Faber's syndrome. It may also occur from severe stomach or intestinal bleeding caused by ulcers or medications such as aspirin or bleeding from hemorrhoids.

Pure red cell aplasia (PRCA) or erythroblastopenia refers to a type of anemia affecting the precursors to red blood cells but not to white blood cells. In PRCA, the bone marrow ceases to produce red blood cells. The condition has been first described by Paul Kaznelson in 1922.

Patients with chronic orthostatic intolerance have symptoms on most or all days. Their symptoms may include most of the symptoms of acute OI, plus:

- Nausea

- Neurocognitive deficits, such as attention problems

- Pallor

- Sensitivity to heat

- Sleep problems

- Other vasomotor symptoms.

Iron is needed for bacterial growth making its bioavailability an important factor in controlling infection. Blood plasma as a result carries iron tightly bound to transferrin, which is taken up by cells by endocytosing transferrin, thus preventing its access to bacteria. Between 15 and 20 percent of the protein content in human milk consists of lactoferrin that binds iron. As a comparison, in cow's milk, this is only 2 percent. As a result, breast fed babies have fewer infections. Lactoferrin is also concentrated in tears, saliva and at wounds to bind iron to limit bacterial growth. Egg white contains 12% conalbumin to withhold it from bacteria that get through the egg shell (for this reason, prior to antibiotics, egg white was used to treat infections).

To reduce bacterial growth, plasma concentrations of iron are lowered in a variety of systemic inflammatory states due to increased production of hepcidin which is mainly released by the liver in response to increased production of pro-inflammatory cytokines such as Interleukin-6. This functional iron deficiency will resolve once the source of inflammation is rectified; however, if not resolved, it can progress to Anaemia of Chronic Inflammation. The underlying inflammation can be caused by fever, inflammatory bowel disease, infections, Chronic Heart Failure (CHF), carcinomas, or following surgery.

Reflecting this link between iron bioavailability and bacterial growth, the taking of oral iron supplements in excess of 200 mg/day causes a relative overabundance of iron that can alter the types of bacteria that are present within the gut. There have been concerns regarding parenteral iron being administered whilst bacteremia is present, although this has not been borne out in clinical practice. A moderate iron deficiency, in contrast, can provide protection against acute infection, especially against organisms that reside within hepatocytes and macrophages, such as malaria and tuberculosis. This is mainly beneficial in regions with a high prevalence of these diseases and where standard treatment is unavailable.

A moderate degree of iron-deficiency anemia affects approximately 610 million people worldwide or 8.8% of the population. It is slightly more common in females (9.9%) than males (7.8%). Mild iron deficiency anemia affects another 375 million.

The prevalence of iron deficiency as a cause of anemia varies among countries; in the groups in which anemia is most common, including young children and a subset of non-pregnant women, iron deficiency accounts for a fraction of anemia cases in these groups ("25% and 37%, respectively"). Iron deficiency is a more common cause of anemia in other groups, including pregnant women.

Within the United States, iron-deficiency anemia affects about 2% of adult males, 10.5% of Caucasian women, and 20% of African-American and Mexican-American women.

Possible reasons that athletics may contribute to lower iron levels includes mechanical hemolysis (destruction of red blood cells from physical impact), loss of iron through sweat and urine, gastrointestinal blood loss, and haematuria (presence of blood in urine). Although small amounts of iron are excreted in sweat and urine, these losses can generally be seen as insignificant even with increased sweat and urine production, especially considering that athletes' bodies appear to become conditioned to retain iron better. Mechanical hemolysis is most likely to occur in high-impact sports, especially among long distance runners who experience "foot-strike hemolysis" from the repeated impact of their feet with the ground. Exercise-induced gastrointestinal bleeding is most likely to occur in endurance athletes. Haematuria in athletes is most likely to occur in those that undergo repetitive impacts on the body, particularly affecting the feet (such as running on a hard road, or Kendo) and hands (e.g. Conga or Candombe drumming). Additionally, athletes in sports that emphasize weight loss (e.g. ballet, gymnastics, marathon running, and wrestling) as well as sports that emphasize high-carbohydrate, low-fat diets, may be at an increased risk for iron deficiency.

Acquired hemolytic anemia may be caused by immune-mediated causes, drugs and other miscellaneous causes.

- Immune-mediated causes could include transient factors as in "Mycoplasma pneumoniae" infection (cold agglutinin disease) or permanent factors as in autoimmune diseases like autoimmune hemolytic anemia (itself more common in diseases such as systemic lupus erythematosus, rheumatoid arthritis, Hodgkin's lymphoma, and chronic lymphocytic leukemia).

- Spur cell hemolytic anemia

- Any of the causes of hypersplenism (increased activity of the spleen), such as portal hypertension.

- Acquired hemolytic anemia is also encountered in burns and as a result of certain infections (e.g. malaria).

- Lead poisoning resulting from the environment causes non-immune hemolytic anemia.

- Runners can suffer hemolytic anemia due to "footstrike hemolysis", owing to the destruction of red blood cells in feet at foot impact.

- Low-grade hemolytic anemia occurs in 70% of prosthetic heart valve recipients, and severe hemolytic anemia occurs in 3%.

The body normally gets the iron it requires from foods. If a person consumes too little iron, or iron that is poorly absorbed (non-heme iron), they can become iron deficient over time. Examples of iron-rich foods include meat, eggs, leafy green vegetables and iron-fortified foods. For proper growth and development, infants and children need iron from their diet. A high intake of cow’s milk is associated with an increased risk of iron-deficiency anemia. Other risk factors for iron-deficiency anemia include low meat intake and low intake of iron-fortified products.

Many conditions can cause glossitis via malnutrition or malabsorption, which creates the nutritional deficiencies described above, although other mechanisms may be involved in some of those conditions listed.

- Alcoholism

- Sprue (celiac disease, or tropical sprue), secondary to nutritional deficiencies

- Crohn’s disease

- Whipple disease

- Glucagonoma syndrome

- Cowden disease

- Acquired immunodeficiency syndrome (AIDS)

- Carcinoid syndrome

- Kwashiorkor amyloidosis

- Veganism and other specialized diets,

- Poor hydration and low saliva in the mouth, which allows bacteria to grow more readily

- Mechanical irritation or injury from burns, rough edges of teeth or dental appliances, or other trauma

- Tongue piercing Glossitis can be caused by the constant irritation by the ornament and by colonization of Candida albicans in site and on the ornament

- Exposure to irritants such as tobacco, alcohol, hot foods, or spices

- Allergic reaction to toothpaste, mouthwash, breath fresheners, dyes in confectionery, plastic in dentures or retainers, or certain blood-pressure medications (ACE inhibitors)

- Administration of ganglion blockers (e.g., Tubocurarine, Mecamylamine).

- Oral lichen planus, erythema multiforme, aphthous ulcer, pemphigus vulgaris

- Heredity

- Albuterol (bronchodilator medicine)

- Schizophrenia

A painful tongue may be an indication of an underlying serious medical condition and nearly always merits assessment by a physician or dental surgeon.

Any dermatitis may heal leaving pale skin, as may excessive use of corticosteroid creams used to treat episodes of eczema. The hypopigmentation is due to both reduced activity of melanocytes with fewer and smaller melanosomes.

The condition is most often seen in children between the ages of 3 and 16 years and is more common in males than females. However adults can also suffer from this disease.

It may occur more frequently in lighter-skinned patients, but is more apparent in those with darker complexions.

Up to a third of US school children may at some stage have this condition. Single-point prevalence studies from India have shown variable rates from 8.4%,

to 31%.

Other studies have shown prevalence rates in Brazil of 9.9%,

Egypt 13.49%,

Romania 5.1%,

Turkey 12% where higher rates were seen in those with poor socioeconomic conditions,

and just 1% in school children in Hong Kong.

Bacterial, viral or fungal infections can cause glossitis. "Candida" species are involved in median rhomboid glossitis.

Syphilis is now relatively rare, but the tertiary stage can cause diffuse glossitis and atrophy of lingual papillae, termed "syphilitic glossitis", "luetic glossitis" or "atrophic glossitis of tertiary syphilis". It is caused by Treponema pallidum and is a sexually transmitted infection.

The average age at onset is 3–7 years, but CVS has been seen in infants who are as young as 6 days and in adults who are as old as 73 years. Typical delay in diagnosis from onset of symptoms is 2.7 – 3 years. Females show a slight predominance over males; the female-to-male ratio is 57:43.

How common the condition is, is not clear. A prospective study found that 3 in 100,000 five-year-olds are diagnosed with the condition. Two published studies on childhood CVS suggest nearly 2% of school-age children may have CVS. However, diagnosis is problematic and, as knowledge of CVS has increased in recent years, more and more cases are emerging.

There is little hard evidence of death as a result of the condition. However, in severe cases the fluid loss can lead to potentially life-threatening electrolyte imbalances. The patient can also become malnourished if the attacks last too long without adequate replenishment of nutrients. With adequate medical interventions, most patients can be properly supported during an episode.

Untreated, severe aplastic anemia has a high risk of death. Modern treatment, by drugs or stem cell transplant, has a five-year survival rate that exceeds 85%, with younger age associated with higher survival.

Survival rates for stem cell transplant vary depending on age and availability of a well-matched donor. Five-year survival rates for patients who receive transplants have been shown to be 82% for patients under age 20, 72% for those 20–40 years old, and closer to 50% for patients over age 40. Success rates are better for patients who have donors that are matched siblings and worse for patients who receive their marrow from unrelated donors.

Older people (who are generally too frail to undergo bone marrow transplants), and people who are unable to find a good bone marrow match, undergoing immune suppression have five-year survival rates of up to 75%.

Relapses are common. Relapse following ATG/ciclosporin use can sometimes be treated with a repeated course of therapy. In addition, 10-15% of severe aplastic anemia cases evolve into MDS and leukemia. According to a study, for children who underwent immunosuppressive therapy, about 15.9% of children who responded to immunosuppressive therapy encountered relapse.

Milder disease can resolve on its own.

The patches of pityriasis alba may last from 1 month to about one year, but commonly on the face last a year. However it is possible that the white patches may last for more than 1 year on the face.

The cause of TEC is unknown, but it thought to be triggered by a viral infection. While rare cases have been attributed to infection with Parvovirus B19, the majority of cases are not related to Parvovirus infection. This is in contrast to transient aplastic crisis, seen in patients with hemoglobinopathies such as sickle cell disease, which is usually caused by Parvovirus infection.

The cause of PVS is unknown; however, genetic factors and nutritional deficiencies may play a role. It is more common in women, particularly in middle age (peak age is over 50). In these patients, esophageal squamous cell carcinoma risk is increased; therefore, it is considered a premalignant process.

The condition is associated with koilonychia, glossitis, inflammation of the lips (cheilitis), and splenomegaly.

Esophageal web in Plummer-Vinson syndrome is found at upper end of esophagus(post cricoid region) and Schatzki ring may be found at the lower end of esophagus.

Raynaud's disease, or "Primary Raynaud's", is diagnosed if the symptoms are "idiopathic", that is, if they occur by themselves and not in association with other diseases. Some refer to Primary Raynaud's disease as "being allergic to coldness". It often develops in young women in their teens and early adulthood. Primary Raynaud's is thought to be at least partly hereditary, although specific genes have not yet been identified.

Smoking increases frequency and intensity of attacks, and there is a hormonal component. Caffeine, estrogen, and non-selective beta-blockers are often listed as aggravating factors, but evidence that they should be avoided is not solid. People with the condition are more likely to have migraines and angina.