Diagnosis
Graves disease may present clinically with one or more of these characteristic signs:
Rapid heartbeat (80%)
Diffuse palpable goiter with audible bruit (70%)
Tremor (40%)
Exophthalmos (protuberance of one or both eyes), periorbital edema (25%)
Fatigue (70%), weight loss (60%) with increased appetite in young people and poor appetite in the elderly, and other symptoms of hyperthyroidism/thyrotoxicosis
Heat intolerance (55%)
Tremulousness (55%)
Palpitations (50%)Two signs are truly diagnostic of Graves disease (i.e., not seen in other hyperthyroid conditions): exophthalmos and nonpitting edema (pretibial myxedema). Goiter is an enlarged thyroid gland and is of the diffuse type (i.e., spread throughout the gland). Diffuse goiter may be seen with other causes of hyperthyroidism, although Graves disease is the most common cause of diffuse goiter. A large goiter will be visible to the naked eye, but a small one (mild enlargement of the gland) may be detectable only by physical examination. Occasionally, goiter is not clinically detectable, but may be seen only with computed tomography or ultrasound examination of the thyroid. Another sign of Graves disease is hyperthyroidism; that is, overproduction of the thyroid hormones T3 and T4. Normal thyroid levels are also seen, and occasionally also hypothyroidism, which may assist in causing goiter (though it is not the cause of the Graves disease). Hyperthyroidism in Graves disease is confirmed, as with any other cause of hyperthyroidism, by measuring elevated blood levels of free (unbound) T3 and T4.Other useful laboratory measurements in Graves disease include thyroid-stimulating hormone (TSH, usually undetectable in Graves disease due to negative feedback from the elevated T3 and T4), and protein-bound iodine (elevated).
Neck pain associated with tender, swollen lymph nodes, referred ear pain and foul breath are also common. While these signs may be present in tonsillitis itself, a PTA should be specifically considered if there is limited ability to open the mouth (trismus). Complications
While most people recover uneventfully, there is a wide range of possible complications. These may include:
Retropharyngeal abscess
Extension of abscess in other deep neck spaces leading to airway compromise (see Ludwigs angina)
Airway obstruction
Aspiration pneumonitis
Lung abscess (following rupture)
Sepsis
Life-threatening hemorrhage (following erosion or septic necrosis into the carotid sheath of the neck)
Glomerulonephritis and rheumatic fever (chronic complications of strep throat)Difficulty swallowing can lead to decreased oral intake and dehydration. Causes
PTA usually arises as a complication of an untreated or partially treated episode of acute tonsillitis. The infection, in these cases, spreads to the peritonsillar area (peritonsillitis). This region comprises loose connective tissue and is hence susceptible to formation of an abscess. PTA can also occur de novo. Both aerobic and anaerobic bacteria can be causative. Commonly involved aerobic pathogens include Streptococcus, Staphylococcus and Haemophilus. The most common anaerobic species include Fusobacterium necrophorum,  Peptostreptococcus, Prevotella species, and Bacteroides. Diagnosis
Diagnosis is usually based on the symptoms. Medical imaging may be done to rule out complications. Medical imaging may include CT scan, MRI, or ultrasound is also useful in diagnosis. Treatment
Medical treatment with antibiotics, volume repletion with fluids, and pain medication is usually adequate, although in cases where airway obstruction or systemic sepsis occurs, surgical drainage may be necessary. Steroids may also be useful.