Pallor mortis (Latin: "pallor" "paleness", "mortis" "of death"), the first stage of death, is an after death paleness that occurs in those with light/white skin.

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 can include:

- pallor

- tachycardia

- decreased activity

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.

Patients who suffer from acute OI usually manifest the disorder by a temporary loss of consciousness and posture, with rapid recovery (simple faints, or syncope), as well as remaining conscious during their loss of posture. This is different from a syncope caused by cardiac problems because there are known triggers for the fainting spell (standing, heat, emotion) and identifiable prodromal symptoms (nausea, blurred vision, headache). As Dr. Julian M. Stewart, an expert in OI from New York Medical College states, "Many syncopal patients have no intercurrent illness; between faints, they are well."

Symptoms:

- Altered vision (blurred vision, "white outs"/gray outs, black outs, double vision)

- Anxiety

- Exercise intolerance

- Fatigue

- Headache

- Heart palpitations, as the heart races to compensate for the falling blood pressure

- Hyperpnea or sensation of difficulty breathing or swallowing (see also hyperventilation syndrome)

- Lightheadedness

- Sweating

- Tremulousness

- Weakness

A classic manifestation of acute OI is a soldier who faints after standing rigidly at attention for an extended period of time.

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.

Symptoms of iron deficiency can occur even before the condition has progressed to iron deficiency anemia.

Symptoms of iron deficiency are not unique to iron deficiency (i.e. not pathognomonic). Iron is needed for many enzymes to function normally, so a wide range of symptoms may eventually emerge, either as the secondary result of the anemia, or as other primary results of iron deficiency. Symptoms of iron deficiency include:

- fatigue

- dizziness/lightheadedness

- pallor

- hair loss

- twitches

- irritability

- weakness

- pica

- brittle or grooved nails

- hair thinning

- Plummer–Vinson syndrome: painful atrophy of the mucous membrane covering the tongue, the pharynx and the esophagus

- impaired immune function

- pagophagia

- restless legs syndrome

Continued iron deficiency may progress to anaemia and worsening fatigue. Thrombocytosis, or an elevated platelet count, can also result. A lack of sufficient iron levels in the blood is a reason that some people cannot donate blood.

In general, signs of anemia (pallor, fatigue, shortness of breath, and potential for heart failure) are present. In small children, failure to thrive may occur in any form of anemia. Certain aspects of the medical history can suggest a cause for hemolysis, such as drugs, consumption of fava beans due to Favism, the presence of prosthetic heart valve, or other medical illness.

Chronic hemolysis leads to an increased excretion of bilirubin into the biliary tract, which in turn may lead to gallstones. The continuous release of free hemoglobin has been linked with the development of pulmonary hypertension (increased pressure over the pulmonary artery); this, in turn, leads to episodes of syncope (fainting), chest pain, and progressive breathlessness. Pulmonary hypertension eventually causes right ventricular heart failure, the symptoms of which are peripheral edema (fluid accumulation in the skin of the legs) and ascites (fluid accumulation in the abdominal cavity).

Iron-deficiency anemia is characterized by the sign of pallor (reduced oxyhemoglobin in skin or mucous membranes), and the symptoms of fatigue, lightheadedness, and weakness. None of these symptoms (or any of the others below) are sensitive or specific. Pallor of mucous membranes (primarily the conjunctiva) in children suggests anemia with the best correlation to the disease, but in a large study was found to be only 28% sensitive and 87% specific (with high predictive value) in distinguishing children with anemia [hemoglobin (Hb) <11.0 g/dl] and 49% sensitive and 79% specific in distinguishing severe anemia (Hb < 7.0 g/dl). Thus, this sign is reasonably predictive when present, but not helpful when absent, as only one-third to one-half of children who are anemic (depending on severity) will show pallor.

Because iron-deficiency anemia tends to develop slowly, adaptation occurs to the systemic effects that anemia causes, and the disease often goes unrecognized for some time. In severe cases, dyspnea can occur. Pica may also develop; pagophagia has been suggested to be "the most specific for iron deficiency."

Other possible symptoms and signs of iron-deficiency anemia include:

Depending upon what exact meaning of the word glossitis is implied, signs and symptoms might include:

- Smooth, shiny appearance of the tongue, caused by loss of lingual papillae.

- Tongue color changes, usually to a darker red color than the normal white-pink color of a healthy tongue.

- Tongue swelling.

- Difficulty with chewing, swallowing, or speaking (either because of tongue soreness of tongue swelling).

- Burning sensation. Some use the term secondary burning mouth syndrome in cases where a detectable cause, such as glossitis, for an oral burning sensation.

Depending upon the underlying cause, there may be additional signs and symptoms such as pallor, oral ulceration and angular cheilitis.

Iron-deficiency anemia is anemia caused by a lack of iron. Anemia is defined as a decrease in the number of red blood cells or the amount of hemoglobin in the blood. When onset is slow, symptoms are often vague, including feeling tired, weakness, shortness of breath, or poor ability to exercise. Anemia that comes on quickly often has greater symptoms, including: confusion, feeling like one is going to pass out, and increased thirst. There needs to be significant anemia before a person becomes noticeably pale. Problems with growth and development may occur in children. There may be additional symptoms depending on the underlying cause.

Iron-deficiency anemia is usually caused by blood loss, insufficient dietary intake, or poor absorption of iron from food. Sources of blood loss can include heavy periods, childbirth, uterine fibroids, stomach ulcers, colon cancer, and urinary tract bleeding. A poor ability to absorb iron may occur as a result of Crohn's disease or a gastric bypass. In the developing world, parasitic worms, malaria, and HIV/AIDS increase the risk. Diagnosis is generally confirmed by blood tests.

Prevention is by eating a diet high in iron or iron supplementation in those at risk. Treatment depends on the underlying cause and may include dietary changes, medications, or surgery. Iron supplements and vitamin C may be recommended. Severe cases may be treated with blood transfusions or iron injections.

Iron-deficiency anemia affected about 1.48 billion people in 2015. A lack of dietary iron is estimated to cause approximately half of all anemia cases globally. Women and young children are most commonly affected. In 2015 anemia due to iron deficiency resulted in about 54,000 deaths – down from 213,000 deaths in 1990.

Hemolytic anemia or haemolytic anaemia is a form of anemia due to hemolysis, the abnormal breakdown of red blood cells (RBCs), either in the blood vessels (intravascular hemolysis) or elsewhere in the human body (extravascular, but usually in the spleen). It has numerous possible consequences, ranging from relatively harmless to life-threatening. The general classification of hemolytic anemia is either inherited or acquired. Treatment depends on the cause and nature of the breakdown.

Symptoms of hemolytic anemia are similar to other forms of anemia (fatigue and shortness of breath), but in addition, the breakdown of red cells leads to jaundice and increases the risk of particular long-term complications, such as gallstones and pulmonary hypertension.

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.

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.

The dry scaling appearance is most noticeable during the winter as a result of dry air inside people's homes. During the summer, tanning of the surrounding normal skin makes the pale patches of pityriasis alba more prominent.

Individual lesions develop through 3 stages and sometimes are itchy:

1. Raised and red – although the redness is often mild and not noticed by parents

2. Raised and pale

3. Smooth flat pale patches

Lesions are round or oval raised or flat, of 0.5–2 cm in size although may be larger if they occur on the body (up to 4 cm), and usually number from 4 or 5 to over 20. The patches are dry with very fine scales. They most commonly occur on the face (cheeks), but in 20% appear also on the upper arms, neck, or shoulders.

The diagnostic differential should consider tinea and vitiligo amongst other causative factors.

PVS sufferers often complain of a burning sensation with the tongue and oral mucosa, and atrophy of lingual papillae produces a smooth, shiny, red, dorsum of the tongue. Symptoms include:

Serial contrasted gastrointestinal radiography or upper gastrointestinal endoscopy may reveal the web in the esophagus. Blood tests show a hypochromic microcytic anemia that is consistent with an iron-deficiency anemia. Biopsy of involved mucosa typically reveals epithelial atrophy (shrinking) and varying amounts of submucosal chronic inflammation. Epithelial atypia or dysplasia may be present.It may also present as a post-cricoid malignancy which can be detected by loss of laryngeal crepitus. Laryngeal crepitus is found normally and is produced because the cricoid cartilage rubs against the vertebrae.

Iron-deficiency anemia is mainly caused by blood loss, such as may occur during menses or gastrointestinal hemorrhage. This often results in a depapilled, atrophic glossitis, giving the tongue a bald and shiny appearance, along with pallor (paleness) of the lips and other mucous membranes a tendency towards recurrent oral ulceration, and cheilosis (swelling of the lips). The appearance of the tongue in iron deficiency anemia has been described as diffuse or patchy atrophy with tenderness or burning. One cause of iron deficiency anemia is sideropenic dysphagia (Plummer–Vinson or Paterson–Brown–Kelly syndrome) which is also characterized by esophageal webbing and dysphagia.

Pernicious anemia is usually caused by autoimmune destruction of gastric parietal cells. Parietal cells secrete intrinsic factor which is required for the absorption of vitamin B12. Vitamin B12 deficiency results in megaloblastic anemia and may present as glossitis. The appearance of the tongue in vitamin B12 deficiency is described as "beefy"

or "fiery red and sore". There may be linear or patchy red lesions.

People may vomit or retch six to twelve times an hour, and an episode may last from a few hours to well over three weeks, and in some cases months, with a median episode duration of 41 hours. Acid, bile and (if the vomiting is severe) blood may be vomited. Some sufferers will ingest water to reduce the irritation of bile and acid on the esophagus during emesis. Between episodes the sufferer is usually normal and healthy otherwise but can be in a weak state of fatigue or suffer from muscle pain. In approximately half of cases the attacks, or episodes, occur in a time-related manner. Each attack is stereotypical; that is, in any given individual, the timing, frequency and severity of attacks is similar.

Episodes may happen every few days, every few weeks or every few months. For some there is not a pattern in time that can be recognized. Some sufferers have a warning of an attack. They may experience a prodrome, usually intense nausea and pallor, heightened sensitivity, especially to light, though sensitivity to smell, sound, pressure, and temperature, as well as oncoming muscle pain and fatigue, are also reported by some patients. The majority of sufferers can identify triggers that may precipitate an attack. The most common are various foods, infections (such as colds), menstruation, extreme physical exertion, lack of sleep, and psychological stresses both positive and negative.

A sufferer may also be light-sensitive (photophobic) during an attack, as well as sound-sensitive (phonophobic) and, less frequently, temperature- or pressure-sensitive. Some sufferers also have a strong urge to bathe in warm or cold water. Some sufferers report that they experience a restless sensation or stinging pain along the spine, hands, and feet followed by weakness in both legs. Some of these symptoms may be due to dehydration rather than the underlying cause of CVS.

Iron deficiency happens when a body has not enough (or not qualitatively enough) iron to supply its eventual needs. Iron is present in all cells in the human body and has several vital functions, such as: carrying oxygen to the tissues from the lungs as a key component of the hemoglobin protein; acting as a transport medium for electrons within the cells in the form of cytochromes; facilitating oxygen enzyme reactions in various tissues. Too little iron can interfere with these vital functions and lead to morbidity and death.

Total body iron averages approximately 3.8 g in men and 2.3 g in women. In blood plasma, iron is carried tightly bound to the protein transferrin. There are several mechanisms that control human iron metabolism and safeguard against iron deficiency. The main regulatory mechanism is situated in the gastrointestinal tract. When loss of iron is not sufficiently compensated by adequate intake of iron from the diet, a state of iron deficiency develops over time. When this state is uncorrected, it leads to iron deficiency anemia. Before anemia occurs, the medical condition of iron deficiency without anemia is called latent iron deficiency (LID) or Iron-deficient erythropoiesis (IDE).

Untreated iron deficiency can lead to iron deficiency anemia, a common type of anemia. Anemia is a condition characterized by inadequate red blood cells (erythrocytes) or hemoglobin. Iron deficiency anemia occurs when the body lacks sufficient amounts of iron, resulting in reduced production of the protein hemoglobin. Hemoglobin binds to oxygen, thus enabling red blood cells to supply oxygenated blood throughout the body. Children, pre-menopausal women (women of child-bearing age) and people with poor diet are most susceptible to the disease. Most cases of iron deficiency anemia are mild, but if not treated can cause problems like fast or irregular heartbeat, complications during pregnancy, and delayed growth in infants and children.

Signs and symptoms of CSWS include large amounts of urination (at least 3 liters of urine output over a 24-hour period for adults) due to inadequate sodium retention in the body, high amounts of sodium in the urine, low blood sodium concentration, excessive thirst, extreme salt cravings, dysfunction of the autonomic nervous system, and dehydration. Patients often self-medicate by naturally gravitating toward a high-sodium diet and by dramatically increasing their water intake. Advanced symptoms include muscle cramps, lightheadedness, dizziness or vertigo, feelings of anxiety or panic (not mentally induced), increased heart rate or slowed heart rate, low blood pressure and orthostatic hypotension sometimes resulting in fainting. Other symptoms frequently associated with dysautonomia include: headaches, pallor, malaise, facial flushing, constipation or diarrhea, nausea, acid reflux, visual disturbances, numbness, nerve pain, trouble breathing, chest pains, loss of consciousness and seizures.

Following clinical presentations may be used in the diagnosis of this condition.

1. Dizziness

2. Pallor of the conjuctiva and face

3. Erythematous oral mucosa with burning sensation

4. Breathelessness

5. Atropic and smooth tongue

6. Peripheral rhaggades around the oral cavity

The following tests are helpful in the diagnosis of Plummer–Vinson syndrome.

Transient erythroblastopenia of childhood (TEC) is a slowly developing anemia of early childhood characterized by gradual onset of pallor.

Individuals with TEC have a median age of presentation of 18–26 months; however, the disorder may occur in infants younger than 6 months and in children as old as age 10 years.

Because of the gradual onset of the anemia, children are often healthier than expected from their low hemoglobin levels.

This benign patch appears on the skin at birth or in early childhood. In most people these are under 10cm in size. If there is doubt about the diagnosis, rubbing the area causes the skin around the lesion to become red while the lesion itself does not change in color. Often the patches are difficult to see against the background color of the patient’s skin, but if sunburn develops, then the white area stands out prominently. The involved area is lighter than the normal skin, not because of a loss of pigment occurs, but because blood vessels are constricted, producing a permanent blanching of the area. This blanching is a functional rather than a structural abnormality, presumed to be caused by local increased sensitivity to catecholamines. Although the cutaneous vasculature appears normal histologically, the blood vessels within the nevus do not respond to injection of vasodilators. It has been postulated that the persistent pallor may represent a sustained localized adrenergic vasoconstriction. Results of a skin biopsy would be interpreted as normal and only physiological testing can reveal the nevus in contrast to normal skin. Stroking the patch elicits no red flare. Only the normal skin would react with a characteristic erythematous response. Examination under a Wood lamp can also reveal the nevus anemicus patch will not emphasize as a patch of vitiligo would.