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hiv and gi

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Describe the effects that the retrovirus HIV and the disease AIDS have on the immune system.
The virus' RNA converts to DNA and integrates into the host cell's DNA. It then produces new HIV viruses which leave the cell and infect other T4 cells. These T4 cells are destroyed as the virus replicates. As T4 cells are lost, the body's immune system weakens and is unable to protect the body against common organisms and infections. These common organisms, usually kept under control by a healthy immune system, cause infections due to this opportunity of a weakened immune system, causing OIs or opportunistic infections.
Describe and differentiate CD4 count used to monitor HIV/AIDS.
CD4 count - shows damage to the immune system as CD4 cells are immune system cells. 1000 is the normal adult value, treat at 350, goal is stable count.
Describe and differentiate viral load used to monitor HIV/AIDS.
viral load - is the actual count of viral RNA or how much virus is there in the blood/serum. It shows the risk of disease progression (0 means no virus, >100,000 means there is a lot of virus). Usually a person is treated when >55,000, and the goal is <20 which is considered not detectable.
Describe and differentiate drug levels used to monitor HIV/AIDS.
detects levels of antiviral drugs in the blood. If it is too high, toxicity can occur. If it is too low, viral breakthrough can occur.
Describe and differentiate drug resistance used to monitor HIV/AIDS.
tests the efficacy of the medication. One type, genotypic assay, is a blood test checking for resistance while a phenotypic assay is a CF culture (?) (the virus mutates to survive; multiple drug regimes helpful to combat this; Cross-resistance can occur meaning resistance to drugs in one class results in resistance to all the drugs in that class; resistance is permanently archived) try to keep CD4 count stable and viral load as undetectable.
Understand how drug therapy for patients with HIV/AIDS is based upon the basic principles.
a. Delay progressions to AIDS and prolong life
b. Control viral replication and mutation (may cause resistance so be careful of which drugs to give and when): this will preserve immunologic fxn which then improves quality of life.
c. Decrease risk of drug toxicity.
d. Decrease emergence of resistant strains
Recognize examples of opportunistic infections (OI) that commonly occur with HIV/AIDS.
The following are examples of Ois:
Pneumocystis carinii pneumonia (PCP),
Tuberculosis,
Toxoplasma gondii,
Mycobacterium Avium Complex (MAC),
Varicella-Zoster virus (VZV).
Look at table 44.9 on pg. 812 for more info...
Describe the role of prophylaxis drug therapy to prevent OIs in HIV/AIDS patients.
OIs, or opportunistic infections, are caused by organisms normally found in our enviroment/body. The infections come when the CD4 count is low and the immune system is compromised. Certain OIs are commonly seen in patients with AIDS. By treating these with prophylactics, the infections can be avoided. (Infections can result in serious complications due to immunosuppression, like death, and that's mighty bad!) However, routine prophylaxis is not recommended. These common OIs have recommendations for ongoing prophylaxis. Their prophylactic treatments are as follows: PCP - Tx: Bactrim, Dapsone, or Pentamidine when CD4<200 or thrush occurs; Toxoplasmosis - Tx: Bactrim or Dapsone if IgG for toxo is absent & CD4<100; TB - Tx: INH or PZA and Rifampin if PPD is + or close contact w/ TB case; MAC - Tx: Clarithromycin or Azithromycin or Rifabutin when CD4<50; Candida - Tx: rarely done - Fluconazole or Nystatin when CD4<50; CMV - Tx; Ganciclovir if titer positive & CD4<50; Histoplasmosis - Tx: Intraconazole when CD4<100.
Identify vaccine recommendations for HIV/AIDS patients.
For Varicella, give VZIG after exposure or if AB negative (?blood type or antibodies), when CD4>200! Pneumocoocal pneumonia, HBV and HAV vaccinations are recommended early in disease. Influenza vaccine is recommended annually for most Pts.
Identify strategies the nurse can use to improve adherence with chronic drug therapy, such as for HIV treatment.
Adherence is crucial to prevent resistance! You cannot miss even one or two doses!! It is hard to predict who will adhere. Fit the drug regiment into the patient's lifestyle, work around their schedule. Provide written or pictorial instructions. Monitor for side effects and look for drug interactions, including those from OTC drugs.
Define Gastroesophageal reflux disease (GERD)
GERD- Digestive order of upper GI tract when gastric contents move back up into esophagus due to incompetent lower esophageal sphincter. Causes symptoms of heartburn, dyspepsia and ulceration of mucosal lining. Often result of hiatal hernia.
Define peptic ulcer disease
Peptic ulcer disease- inflammation and erosion of mucosal layers of stomach or duodenum.
Define flatulence
Flatulence- gas, normal byproduct of digestion. When excess flatus is produced by ingesting gas-producing foods or if person is unable to pass the gas through large intestines. Common occurrence after GI surgery d/t lack of peristalsis.
Define laxative.
Laxative- drugs used to treat constipation, which is the infrequent or incomplete passage of hard stools as a result of decreased peristalsis and slow movement of fecal matter through colon, allowing more water to be reabsorbed by body. Acts directly on the intestine to produce peristalsis and evacuation of bowel. Classifications are: saline, hyperosmotic, stimulants, bulk-forming, stool softeners/surfactants and lubricants.
Describe why treating H. pylori infection is needed in treating peptic ulcer disease.
H. pylori is a causative agent of peptic ulcer disease. Elimination of H. pylori improves healing and decreases the recurrence of ulcers. Eradication therapy is the standard of care for active or inactive peptic ulcer pts. The cure of H. pylori infection reduces significantly the resk of recurring ulcer disease.
Describe the rationale for multi-drug therapy in treating H. pylori infection.
Use of a single antibiotic is not recommended due to the potential of developing resistance. Double antibiotic therapy w/ antisecretory drug is very effective and is the most preferred therapy. Not triple or quad because more risk for adverse effects and less compliance.
Differentiate ALUMINUM AND MAGNESIUM BASED ANTACIDS in terms of major adverse effects and core pt variables. 686
Both can be used to balance the constipation and diarrhea. Possible hypermagnesemia in people w/ renal failure and hypophosphatemia.
Assess whether symptoms warrant the antacid: GI bleeding.
Pt. w/ history of renal insufficiency shouldn't take this because don't excrete magnesium at normal rate so can cause hypermagnesemia. Check phosphate level because aluminum binds w/ phosphate. Check OTC drugs. Diet, alcohol, smoking habits, spicy food can contribute to severity of symptoms. Can be administered anywhere.
Aluminum
Adverse Effect: constipation
Magnesium
Adverse Effect: diarrhea Pt: do not use in pt with renal failure-magnesium toxicity can result, used to treat hypomagnesium
State the pharmacodynamics of H2 antagonists (prototype Ranitidine (Zantac))
Blocks histamine competitively at the H2 receptors in the gastric parietal cells. Inhibits all phases of gastric secretion. Used for GERD and ulcers. Ranitidine inhibits both the daytime and nocturnal basal gastric acid secretions as well as gastric acid secretion stimulated by food, betazole, and pentagastrin. Ranitidine does not affect pepsin secretion. It has little or no effect on fasting or postprandial gastrin secretion. It has no effect on prolactin levels, gonadotropins, TSH, growth hormone, cortisol, aldosterone, androgen, estrogen levels or sperm count.
State the pharmacodynamics of Sucralfate
Used in treating duodenal ulcers. Unlike aluminum hydroxide with magnesium hydroxide, sucralfate does not lower the acidity of gastric juices. Sucralfate is an aluminum salt of sulfated sucrose. In the acidic medium of gastric fluid, the aluminum ion splits off, leaving a highly polar anion. The basically non-absorbing paste that forms adheres to the ulcer lesions and protects the lesion from acid, pepsin, and bile salts. This allows the ulcer to heal.
State the pharmacodynamics of SIMETHICONE, the prototype ANTIFLATULENT
Has a defoaming action that alters the surface tension of gas bubbles. As the surface tension is changed, gas bubbles unite, forming larger gas bubbles that are more easily eliminated by belching or expelled as flatus. Can be used with antacids to decrease flatulence. Also used w/ antacids to decrease flatulence. Off label use to treat infant colic.
State the nursing actions to maximize therapeutic effects for SIMETHICONE, the prototype ANTIFLATULENT.
Administer after meals and at bedtime to increase effectiveness.
Describe the pharmacodynamics for MAGNESIUM HYDROXIDE, THE PROTOTYPE LAXATIVE.
PD: it is a salt that works in large and small bowel by attracting and retaining water in the intestinal lumen, thereby increasing pressure within the intestine.
Describe the core patient variables for MAGNESIUM HYDROXIDE, THE PROTOTYPE LAXATIVE
HS: renal insufficiency. Asses for bowel sounds, palpate for abdominal distention, ask about usual pattern of bowel function.
LSG: patient must be 2 years or older to receive drug, older adults may experience constipation d/t decreased peristalsis. Also may be less active and eat fewer foods w/ roughage.
LDH: adequate fluid (at least 1000-1500 ml daily) and nutritional intake of fruits, vegetables and roughage, exercise? does patient ignore urge to defecate? All may contribute to constipation. Does patient use laxatives regularly? May be dependent on this.
E: OTC, in acute care settings, inpatient facility usually means pt. less active to greater chance of constipation
C: what does patient perceive normal elimination and constipation to be according to their culture?
Describe the nursing management for MAGNESIUM HYDROXIDE, THE PROTOTYPE LAXATIVE.
Follow drug administration with a full glass of water to prevent dehydration, limit fluid and electrolyte imbalance and promote a speedier effect.

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