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A comprehensive overview of cirrhosis, a chronic and irreversible liver disease that disrupts liver function and structure. It delves into the pathophysiology of cirrhosis, including the development of fibrosis, portal hypertension, and ascites. The document also covers other related liver disorders, such as hepatitis, jaundice, and various skin conditions associated with liver disease. It explores the symptoms, causes, and consequences of these conditions, offering insights into the role of nurses in managing patients with these conditions. The document serves as a valuable resource for understanding the complex nature of liver diseases and their impact on patient health.
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in females -rectocele --low residue diet- not enough fiber --sedentary lifestyle --excessive use of antacids--decrease motility --changes in general-can be due to aging, no access to toilets, pregnancy, IBS
-change to the mucosal lining -excessive secretion of fluid and electrolytes
-fluid and electrolyte imbalance --> hyponatriema, hypokalemia -weight loss
-conditions that delay gastric emptying
regurgitation of chyme mid-epigastric pain within one hour of eating
cotents -normal in newborns because neuromuscular control of the gastroesophageal sphincter is not fully developed
lumen or failure of normal intestinal motility in the absence of an obstructing lesion
failure of intestinal motility often after abdominal surgery
intestine
distention; bowel sounds may be altered to be decreased or absent below the obstruction
esophagus, stomach, or duodenum
secreting mucosa of the body
-its usually after eating!!!
concentration of bile salts disrupting the gastric mucosa --> disrupted mucosa becomes edematous and loses plasma proteins --> destruction of small vessels cause bleeding --gastric secretion tends to be normal or less than normal
functions, immune reactions to intestinal flora, abnormal T cell responses
mucosa --sigmoid colon and rectum --age of onset 20-40 years old
colon --> mucosa is hyperemic --> small erosions form and ulcers/ab- scesses ensue --> necrosis of tissue --> edema and thickening of mucosae can narrow lumen of colon
quadrant since it affects the rectum... -bloody stools -cramping -diarrhea (10-20/day) usually watery
-chronic inflammation of the intestinal tract usually affecting the ileum and colon --rectum is seldom involved --10-20% of those diagnosed have a family history
in intestinal submucosa and spreads --> neutrophils and macrophages promote inflammation
-hypothalamus: many hormones and neurotransmitters are involved (control ap- petite and weight, GI motility; leptin resistance happens then the person doesnt realize they are full) -proinflammatory state (proinflammatory cytokines are activated)
structure -decreased hepatic function caused by nodular and fibrotic tissue synthesis (fibro- sis) --fibrosis alters or obstructs billiary channels and blood flow --regeneration no longer occurs and instead hypoxia, necrosis, atrophy and liver failure occurs --fibrosis yields a smaller or larger liver and hard to palpation
resistance to blood flow --caused by disorders that obstruct or impede blood flow through any component of the portal venous system or vena cava
heart failure
-cirrhosis is the most common cause but can also be from heart failure and other organ malfunction
--> portal hypertension and decreased albumin --> capillary hydrostatic pressure to exceed capillary osmotic pressure --> imbalance pushes water into the peritoneal cavity and you also have decreased circulating blood volume --> sodium and water retention --> activates RAAs system --> possible bacteria and toxin release leads...-> to peritonitis and inflammatory response --> furthers capillary permeability and more fluid into the cavity
increased abdominal girth dyspnea increased respiratory rate
hyperbilirubinemia -obstructive jaundice -hemolytic jaundice
absorption of a hematoma
Recovery phase
--activate vit D --micro-organisms, UV, body fluid loss, mechanical stress --regulate body temp -immune surveillance --touch and pressure receptors --commensal micro-organisms
-usually dark skinned individuals -excessive fibroblast activity and collagen formation -grow within one year of skin damage -claw-like appearance on flat surfaces
chronic skin alteration
contact dermatitis stasis dermatitis
-interaction of skin barrier function, reaction to irritants -genetic susceptibility examples: poison ivy, latex allergy
substances -irritating substances temporarily damage the epidermis examples: detergents, industrial cleaners
most common type of "plaque"... psoriasis vulgaris -diagnosis around age 20; hereditary -T helper cells secrete cytokines cause symptoms -epidermal shedding turnover 3-4 days instead of the usual 14-20 days -thickened epidermis and forms white-silver plaques of keratin
disease of skin and mucous membranes -T cell mediated immune response in which epithelial cells are identified as foreign, cytokine involvement -can last for months or years, recurrence possible, and pruritis is most distressing symptom
-furuncles "boils" -carbuncles -impetigo -cellulitis
--usually staph aureus
(cellulitis) --usually staph aureus
tissue
posterior neck, upper back, lateral thighs
-(staph aureus or beta-hemolytic strep)
-can follow any skin lesion
-herpes zoster/varicella zoster=shingles/chicken pox -human papillomavirus (HPV)
root ganglion latently and can reactivate through sensory nerve endings HSV2- usually genital; transmitted by mucous membrane contact during shedding; vertical transmission
root ganglion -20% pts postherapetic pain and reactivation -vaccines are usually given to reduce incidence
-genital wart (condyloma acuminata): highly contagious; can develop into cancer
-candida albicans
penis, skin folds
child, tanning bed before 30 yo, males, geography, 3 or more atypical nevi
--sunburn
--superficial: moist surface involving SUPERFICIAL DERMIS, blisters in minutes, intact pain sensors
dermis, +/- blisters, diminished pain sensation
subcutaneous tissue -dry leathery lift off paper like layer with visible veins and white/cherry/red/black apperance, no pain sensation ***will not heal; scar
-involves skin/subcutaneous tissue/tendon/muscle/bone
-urinary leakage, incontinence, increased chance for UTIs
-some stool moves forward, rest moves outward =floor is coming up, push for stool and so floor comes up higher, making it harder to pass stool
uterus -responds to hormone fluctuations of the menstral cycle -creates painful and heavy menestruation -possible causes: retrograde menstruation, spread through vascular or lymphatic system, genetic predisposition -looks like coffee grounds
bleeding, chronic pelvic pain and fatigue, painful sex, difficulty getting pregnant, infertility, bleeding between periods, pelvic pain, painful or heavy irregular periods, constant fatigue, urination and bowel pain
sexually transmitted disease (gonirrhea and chlymedia) -nonsexual origins can be caused by urologic procedures, insertion of foreign objects, anatomic abnormalities, or trauma
-commonly a result of trauma or untreated or severe urethral infections -trauma --> creates scar tissue --> creates urethral stricture
trouble getting flow started
-requires surgery, radiation, or chemo
-all related to cellular health
-caused by inadequate or absent valves in the spematic veins -varicose veins in scrotal sac
vaginalis -imbalance between fluid secretion and reabsorption -fluid where it shouldnt be -swelling after surgery will die down...