Medications
Drug-induced psoriasis may occur with beta blockers, lithium, antimalarial medications, nonsteroidal anti-inflammatory drugs, terbinafine, calcium channel blockers, captopril, glyburide, granulocyte colony-stimulating factor, interleukins, interferons, lipid-lowering medications,: 197  and paradoxically TNF inhibitors such as infliximab or adalimumab. Withdrawal of corticosteroids (topical steroid cream) can aggravate psoriasis due to the rebound effect. Pathophysiology
Psoriasis is characterized by an abnormally excessive and rapid growth of the epidermal layer of the skin. Abnormal production of skin cells (especially during wound repair) and an overabundance of skin cells result from the sequence of pathological events in psoriasis. The sequence of pathological events in psoriasis is thought to start with an initiation phase in which an event (skin trauma, infection, or drugs) leads to activation of the immune system and then the maintenance phase consisting of chronic progression of the disease. Skin cells are replaced every 3–5 days in psoriasis rather than the usual 28–30 days. These changes are believed to stem from the premature maturation of keratinocytes induced by an inflammatory cascade in the dermis involving dendritic cells, macrophages, and T cells (three subtypes of white blood cells). These immune cells move from the dermis to the epidermis and secrete inflammatory chemical signals (cytokines) such as interleukin-36γ, tumor necrosis factor-α, interleukin-1β, interleukin-6, and interleukin-22. These secreted inflammatory signals are believed to stimulate keratinocytes to proliferate. One hypothesis is that psoriasis involves a defect in regulatory T cells, and in the regulatory cytokine interleukin-10.
Surgical intervention in the form of sigmoid colectomy or proctocolectomy and ileostomy may be required only when all conservative measures of evacuation fail. Attempts at removal can have severe and even lethal effects, such as the rupture of the colon wall by catheter or an acute angle of the fecaloma (stercoral perforation), followed by sepsis. It may also lead to stercoral perforation, a condition characterized by bowel perforation due to pressure necrosis from a fecal mass or fecaloma. See also
Aerosol impaction
Colon
Dental impaction
Impaction (animals)

References
Further reading
Wrenn K (September 1989). "Fecal impaction". The New England Journal of Medicine. 321 (10): 658–62. doi:10.1056/NEJM198909073211007. PMID 2671728. Dugdale, David C. (January 31, 2011). "Fecal impaction". A.D.A.M., Inc.
Gattuso JM, Kamm MA, Halligan SM, Bartram CI (April 1996). "The anal sphincter in idiopathic megarectum: effects of manual disimpaction under general anesthetic". Diseases of the Colon and Rectum. 39 (4): 435–9. doi:10.1007/bf02054060. PMID 8878505. S2CID 40482887. == External links ==