Keratic precipitate (KP) is an inflammatory cellular deposit seen on corneal endothelium. Acute KPs are white and round in shape whereas old KPs are faded and irregular in shape. Mutton-fat KPs are large in shape and are greasy-white in color and are formed from macrophages and epithelioid cell. They are indicative of inflammatory disease. Mutton fat Kps are due to granulomatous iridocyclitis. Another variant called red KPs may be seen in hemorrhagic uveitis.

Those with conjunctivitis may report mild irritation or scratchiness, but never extreme pain, which is an indicator of more serious disease such as keratitis, corneal ulceration, iridocyclitis, or acute glaucoma.

This condition is usually unilateral, and its symptoms vary from none to mild blurring and discomfort. Signs include diffuse iris atrophy and small white keratic precipitates (deposits on the inner surface of the cornea), cells presenting in the anterior chamber as well as the anterior vitreous. Glaucoma and cataract occur frequently.

Fuchs heterochromic iridocyclitis (FHI) is a chronic unilateral uveitis appearing with the triad of heterochromia, predisposition to cataract and glaucoma, and keratitic precipitates on the posterior corneal surface. Patients are often asymptomatic and the disease is often discovered through investigation of the cause of the heterochromia or cataract. Neovascularisation (growth of new abnormal vessels) is possible and any eye surgery, such as cataract surgery, can cause bleeding from the fragile vessels in the atrophic iris causing accumulation of blood in anterior chamber of the eye, also known as hyphema.

A reduction in visual acuity in a 'red eye' is indicative of serious ocular disease, such as keratitis, iridocyclitis, and glaucoma, and never occurs in simple conjunctivitis without accompanying corneal involvement.

As of 2012, the rate of hyphemas in the United States are about 20 cases per 100,000 people annually.

Hyphema (or hyphaema, see spelling differences) is blood in the front (anterior) chamber of the eye. It may appear as a reddish tinge, or it may appear as a small pool of blood at the bottom of the iris or in the cornea.

A corneal dystrophy can be caused by an accumulation of extraneous material in the cornea, including lipids and cholesterol crystals.

Corneal dystrophy may not significantly affect vision in the early stages. However, it does require proper evaluation and treatment for restoration of optimal vision. Corneal dystrophies usually manifest themselves during the first or second decade but sometimes later. It appears as grayish white lines, circles, or clouding of the cornea. Corneal dystrophy can also have a crystalline appearance.

There are over 20 corneal dystrophies that affect all parts of the cornea. These diseases share many traits:

- They are usually inherited.

- They affect the right and left eyes equally.

- They are not caused by outside factors, such as injury or diet.

- Most progress gradually.

- Most usually begin in one of the five corneal layers and may later spread to nearby layers.

- Most do not affect other parts of the body, nor are they related to diseases affecting other parts of the eye or body.

- Most can occur in otherwise totally healthy people, male or female.

Corneal dystrophies affect vision in widely differing ways. Some cause severe visual impairment, while a few cause no vision problems and are diagnosed during a specialized eye examination by an ophthalmologist. Other dystrophies may cause repeated episodes of pain without leading to permanent loss of vision.

Acne fulminans begins as pain and inflammation in the joints. It eventually progresses into a swelling of the lymph nodes located at the base of the neck, causing inflexibility in the neck within weeks after the nodes swell. This swelling will eventually decrease, but this decrease will be accompanied by an increased inflammation and swelling of the joints, as well as a complete loss of appetite, though these symptoms are often ignored. After some time, the disease will cause an extreme loss of weight and atrophy of the muscles, leading to the decline of physical abilities.

Any potential ocular involvement should be assessed by an ophthalmologist as complications such as episcleritis and uveitis may occur.

Herpes zoster ophthalmicus (HZO) and also known as ophthalmic zoster is a disease characterised by reactivation of dormant varicella zoster virus residing within the ophthalmic nerve (the first division of the trigeminal nerve). This condition is an important subtype of shingles, representing 15% of all cases.

Herpes zoster ophthalmicus is transmitted via direct contact or droplets. Varicella zoster virus is a DNA virus which produces acidophilic intranuclear inclusion bodies. The virus is neurotrophic in nature.

The frontal nerve is more commonly affected than the nasociliary nerve or lacrimal nerve.

Acne fulminans (also known as "acute febrile ulcerative acne") is a severe form of the skin disease, acne, which can occur after unsuccessful treatment for another form of acne, acne conglobata. The condition is thought to be an immunologically induced disease in which elevated level of testosterone causes a rise in sebum and population of "Propionibacterium acnes" bacteria. The increase in the amount of "P acnes" or related antigens may trigger the immunologic reaction in some individuals and lead to an occurrence of acne fulminans. In addition to testosterone, isotretinoin may also precipitate acne fulminans, possibly related to highly increased levels of "P acnes antigens" in the patient's immune system. Acne fulminans is a rare disease. Over the past several years, fewer cases of this disease have occurred, possibly because of earlier and better treatment of acne. Approximately 100 patients with acne fulminans have been described.

Giant-cell arteritis and Takayasu's arteritis have much in common, but usually affect patients of different ages, with Takayasu's arteritis affecting younger people, and giant-cell arteritis having a later age of onset.

Aortitis can also be considered a large-vessel disease.

Takayasu arteritis. Primarily affects the aorta and its main branches. At least 3 out of 6 criteria yields sensitivity and specificity of 90.5 and 97.8%:

- onset < 40 years affects young and middle -aged women (ages 15–45)

- claudication of extremities

- decreased pulsation of one or both brachial arteries

- at least 10 mmHg systolic difference in both arms

- bruit over one or both carotid arteries or abdominal aorta

- arteriographic narrowing of aorta, its primary branches, or large arteries in upper or lower extremities

- Ocular manifestation

- visual loss or field defects

- Retinal hemorrhages

- Neurological abnormalitis

- Treatment: steroids

Giant cell (temporal) arteritis. Chronic vasculitis of both large and medium vessels, primarily affecting cranial branches of the arteries arising from the aortic arch. At least 3 out of 5 criteria yields sensitivity and specificity of 95 and 91%:

- Age at onset ≥ 50 years

- New onset headache with localized tenderness

- Temporal artery tenderness or decreased pulsation

- Elevated ESR ≥ 50 mm/hour Westergren

- Temporal artery biopsy showing vasculitis with mononuclear cell infiltrate or granulomatous inflammation, usually with multinucleated giant cells

Incomitant esotropias are conditions in which the esotropia varies in size with direction of gaze. They can occur in both childhood and adulthood, and arise as a result of neurological, mechanical or myogenic problems. These problems may directly affect the extra-ocular muscles themselves, and may also result from conditions affecting the nerve or blood supply to these muscles or the bony orbital structures surrounding them. Examples of conditions giving rise to an esotropia might include a VIth cranial nerve (or Abducens) palsy, Duane's syndrome or orbital injury.

These conditions are sometimes considered together with the small vessel vasculitides.

Polyarteritis nodosa (PAN). Systemic necrotizing vasculitis and aneurysm formation affecting both medium and small arteries. If only small vessels are affected, it is called microscopic polyangiitis, although it is more associated with granulomatosis with polyangiitis than to classic PAN. At least 3 out of 10 criteria yields sensitivity and specificity of 82 and 87%:

- unexplained weight loss > 4 kg

- livedo reticularis

- testicular pain

- myalgias, weakness

- Abdominal pain, diarrhea, and GI bleeding

- mononeuropathy or polyneuropathy

- new onset diastolic blood pressure > 90 mmHg

- elevated serum BUN (> 40 mg/dL) or serum creatinine (> 1.5 mg/dL)

- hepatitis B infection

- arteriographic abnormalities

- arterial biopsy showing polymorphonuclear cells

Kawasaki disease. Usually in children(age<4), it affects large, medium, and small vessels, prominently the coronary arteries. Associated with a mucocutaneous lymph node syndrome. Diagnosis requires fever lasting five days or more with at least 4 out of 5 criteria:

- bilateral conjunctival injection

- injected or fissured lips, injected pharynx, or strawberry tongue

- erythema of palms/soles, edema of hands/feet, periungual desquamation

- polymorphous rash

- cervical lymphadenopathy (at least one node > 1.5 cm)

Isolated cerebral vasculitis. Affects medium and small arteries over a diffuse CNS area, without symptomatic extracranial vessel involvement. Patients have CNS symptoms as well as cerebral vasculitis by angiography and leptomeningeal biopsy.

"Congenital esotropia," or "infantile esotropia," is a specific sub-type of primary concomitant esotropia. It is a constant esotropia of large and consistent size with onset between birth and six months of age. It is not associated with hyperopia, so the exertion of accommodative effort will not significantly affect the angle of deviation. It is, however, associated with other ocular dysfunctions including oblique muscle over-actions, Dissociated Vertical Deviation (DVD,) Manifest Latent Nystagmus, and defective abduction, which develops as a consequence of the tendency of those with infantile esotropia to 'cross fixate.' Cross fixation involves the use of the right eye to look to the left and the left eye to look to the right; a visual pattern that will be 'natural' for the person with the large angle esotropia whose eye is already deviated towards the opposing side.

The origin of the condition is unknown, and its early onset means that the affected individual's potential for developing binocular vision is limited. The appropriate treatment approach remains a matter of some debate. Some ophthalmologists favour an early surgical approach as offering the best prospect of binocularity whilst others remain unconvinced that the prospects of achieving this result are good enough to justify the increased complexity and risk associated with operating on those under the age of one year.

Kawasaki disease often begins with a high and persistent fever that is not very responsive to normal treatment with paracetamol (acetaminophen) or ibuprofen. It is the most prominent symptom in Kawasaki disease, is a characteristic sign of the acute phase of the disease, is normally high (above 39–40 °C), is remittent, and is followed by extreme irritability. Recently, it is reported to be present in patients with atypical or incomplete Kawasaki disease; nevertheless, it is not present in 100% of cases. The first day of fever is considered the first day of illness, and the duration of fever is on average one to two weeks; in the absence of treatment, it may extend for three to four weeks. Prolonged fever is associated with higher incidence of cardiac involvement. It responds partially to antipyretic drugs and does not cease with the introduction of antibiotics. However, when appropriate therapy is started – intravenous immunoglobulin and aspirin – the fever is gone after two days.

Bilateral conjunctival inflammation was reported to be the most common symptom after fever. It typically involves the bulbar conjunctivae, is not accompanied by suppuration, and is not painful. It usually begins shortly after the onset of fever during the acute stage of the disease. Anterior uveitis may be present on slit-lamp examination. Iritis can occur, too. Keratic precipitates are another eye manifestation (detectable by a slit lamp but are usually too small to be seen by the unaided eye).

Kawasaki disease presents with set of mouth symptoms, the most characteristic changes are the red tongue, swollen lips with vertical cracking and bleeding. The mucosa of the mouth and throat may be bright red, and the tongue may have a typical "strawberry tongue" appearance (marked redness with prominent gustative papillae). These mouth symptoms are caused by the typical necrotizing microvasculitis with fibrinoid necrosis.

Cervical lymphadenopathy is seen in 50% to 75% of people, whereas the other features are estimated to occur in 90% of patients, but sometimes it can be the dominant presenting symptom. According to the definition of the diagnostic criteria, at least one impaired lymph node ≥ 15 mm in diameter should be involved. Affected lymph nodes are painless or minimally painful, nonfluctuant, and nonsuppurative; erythema of the neighboring skin may occur. Children with fever and neck adenitis who do not respond to antibiotics should have Kawasaki disease considered as part of the differential diagnoses.

In the acute phase of the disease, changes in the peripheral extremities can include erythema of the palms and soles, which is often striking with sharp demarcation and often accompanied by painful, brawny edema of the dorsa of the hands or feet. This is why affected children frequently refuse to hold objects in their hands or to bear weight on their feet. Later, during the convalescent or the subacute phase, desquamation of the fingers and toes usually begins in the periungual region within two to three weeks after the onset of fever and may extend to include the palms and soles. Around 11% of children affected by the disease may continue skin-peeling for many years. One to two months after the onset of fever, deep transverse grooves across the nails may develop (Beau’s lines), and occasionally nails are shed.

The most common skin manifestation is a diffuse macular-papular erythematous rash, which is quite nonspecific. The rash varies over time and is characteristically located on the trunk; it may further spread to involve the face, extremities, and perineum. Many other forms of cutaneous lesions have been reported; they may include scarlatiniform, papular, urticariform, multiform-like erythema, and purpuric lesions; even micropustules were reported. It can be polymorphic, not itchy, and normally observed up to the fifth day of fever. However, it is never bullous or vesicular.

In the acute stage of Kawasaki disease, systemic inflammatory changes are evident in many organs. Joint pain (arthralgia) and swelling, frequently symmetrical, and arthritis can also occur. Myocarditis, diarrhea, pericarditis, valvulitis, aseptic meningitis, pneumonitis, lymphadenitis, and hepatitis may be present and are manifested by the presence of inflammatory cells in the affected tissues. If left untreated, some symptoms will eventually relent, but coronary artery aneurysms will not improve, resulting in a significant risk of death or disability due to myocardial infarction. If treated quickly, this risk can be mostly avoided and the course of illness cut short.

Other reported nonspecific symptoms include cough, rhinorrhea, sputum, vomiting, headache, and seizure.

The course of the disease can be divided into three clinical phases.

- The acute febrile phase, which usually lasts for one to two weeks, is characterized by fever, conjunctival injection, erythema of the oral mucosa, erythema and swelling of the hands and feet, rash, cervical adenopathy, aseptic meningitis, diarrhea, and hepatic dysfunction. Myocarditis is common during this time, and a pericardial effusion may be present. Coronary arteritis may be present, but aneurysms are generally not yet visible by echocardiography.

- The subacute phase begins when fever, rash, and lymphadenopathy resolve at about one to two weeks after the onset of fever, but irritability, anorexia, and conjunctival injection persist. Desquamation of the fingers and toes and thrombocytosis are seen during this stage, which generally lasts until about four weeks after the onset of fever. Coronary artery aneurysms usually develop during this time, and the risk for sudden death is highest.

- The convalescent stage begins when all clinical signs of illness have disappeared, and continues until the sedimentation rate returns to normal, usually at six to eight weeks after the onset of illness.

The presentation between adults and children differs, as adults' neck lymph nodes are more affected (93% of adults versus 15% of children), hepatitis (65% versus 10%), and arthralgia (61% versus 24–38%). Some people have atypical presentations and may not have the classical symptoms. This occurs in particular in young infants; those people are especially at higher risk for cardiac artery aneurysms.

Some clinical examples:

Other examples are:

- Subacute bacterial endocarditis

- Symptoms of malaria

Type III hypersensitivity occurs when there is accumulation of immune complexes (antigen-antibody complexes) that have not been adequately cleared by innate immune cells, giving rise to an inflammatory response and attraction of leukocytes. Such reactions progressing to the point of disease produce immune complex diseases.

Symptoms can take as long as 14 days after exposure to appear, and may include signs and symptoms commonly associated with hypersensitivity or infections.

- rashes

- itching

- joint pain (arthralgia), especially finger and toe joints

- fever, as high as 40 °C and usually appears before rash

- lymphadenopathy (swelling of lymph nodes), particularly near the site of injection, head and neck

- malaise

- hypotension (decreased blood pressure)

- splenomegaly (enlarged spleen)

- glomerulonephritis

- proteinuria

- hematuria

- shock

Other Kawasaki disease complications have been described, such as aneurysm of other arteries: aortic aneurysm, with a higher number of reported cases involving the abdominal aorta, axillary artery aneurysm, brachiocephalic artery aneurysm, aneurysm of iliac and femoral arteries, and renal artery aneurysm. Other vascular complications can occur such as increased wall thickness and decreased distensibility of carotid arteries, aorta, and brachioradial artery. This change in the vascular tone secondary to endothelial dysfunction. In addition, children with Kawasaki disease, with or without coronary artery complications, may have a more adverse cardiovascular risk profile, such as high blood pressure, obesity, and abnormal serum lipid profile.

Gastrointestinal complications in Kawasaki disease are similar to those observed in Henoch–Schönlein purpura, such as: intestinal obstruction, colon swelling, intestinal ischemia, intestinal pseudo-obstruction, and acute abdomen.

Eye changes associated with the disease have been described since the 1980s, being found as uveitis, iridocyclitis, conjunctival hemorrhage, optic neuritis, amaurosis, and ocular artery obstruction. It can also be found as necrotizing vasculitis, progressing into peripheral gangrene.

The neurological complications per central nervous system lesions are increasingly reported. The neurological complications found are meningoencephalitis, subdural effusion, cerebral hypoperfusion, cerebral ischemia and infarct, cerebellar infarction, manifesting with seizures, chorea, hemiplegia, mental confusion, lethargy and coma, or even a cerebral infarction with no neurological manifestations. Other neurological complications from cranial nerve involvement are reported as ataxia, facial palsy, and sensorineural hearing loss. Behavioral changes are thought to be caused by localised cerebral hypoperfusion, can include attention deficits, learning deficits, emotional disorders (emotional lability, fear of night, and night terrors), and internalization problems (anxious, depressive or aggressive behavior).

Cryofibrinogenmic disease commonly begins in adults aged 40–50 years old with symptoms of the diseases occurring in the almost always affected organ, skin. Cutaneous symptoms include on or more of the following: cold contact-induced urticarial (which may be the first sign of the disease); painful episodes of finger and/or toe arterial spasms termed Ranaud phenomena; cyanosis, s palpable purpura termed Cryofibrinogenemic purpura), and a lace-like purplish discoloration termed livedo reticularis all of which occur primarily in the lower extremities but some of which may occur in the nose, ears, and buttocks; non-healing painful ulcerations and gangrene of the areas impacted by the cited symptoms. Patients also have a history of cold sensitivity (~25% of cases), arthralgia (14-58%), neuritis (7-19%), myalgia (0-14%); and overt thrombosis of arteries and veins (25-40%) which may on rare occasions involve major arteries such of those of the brain and kidney. Signs of renal involvement (proteinuria, hematuria, decreased glomerular filtration rate, and/or, rarely, renal failure) occur in 4-25% of cases. Compared to secondary cryofibrinogemia, primary crygofibrinogenemia has a higher incidence of cutaneous lesions, arthralgia, and cold sensitivity while having a far lower incidence of renal involvement. Patients with secondary cryofibrinogenemia also exhibit signs and symptoms specific to the infectious, malignant, premalignant vasculitis, and autoimmune disorders associated with their disease. While rare, individuals with cryofibrinogemic disease may experience pathological bleeding due to the consumption of blood clotting factors consequential to the formation of cryofibrinogen precipitates.

Diagnosis is based on history given by patient, including recent medications.

Symptoms generally begin around puberty but can occur earlier. These individuals have recurrent swelling in the extremities, genitals, face, lips, larynx or GI tract. Some patients describe a sensation of fullness but not pain or itching in the affected area except for those with abdominal swellings who often experience acute abdominal pain. Others experience an intense amount of pain, described as radiating from the bone outward along with intense itching just beneath the skin and intense heat, regardless of the area targeted.

Instances of swelling around the throat or larynx can cause difficulties in breathing should the swelling obstruct airways. This has been known to cause a large number of fatalities in those afflicted with the disorder. Episodes that attack the gastrointestinal tract can cause a number of complications including dehydration from being unable to keep anything down (which, depending on length of the episode, can prove fatal). Symptoms from gI tract swelling including violent vomiting, intense pain from the midsection, dehydration, and intense exhaustion.

Some suffered of HAE suffer from 'wandering' attacks. These attacks will center around an extremity. For example: Should the sufferer's hand swell up, it will go through the normal swelling cycle before 'transferring' to either the connection limb (In this case wrist to forearm) or move to the opposite hand. Sufferers with this symptom may find their episodes last longer, and may find their triggers more difficult to track.