Week 10: Pancreatitis, Pancreatic Cancer, & HIV

pancreatitis

inflammation of the pancreas that can be serious/life threatening

pancreas

both an endocrine and exocrine gland; exocrine function is to break down starches, proteins, and fats; enzymes usually secreted in inactive forms

acute pancreatitis

inflammation from excessive pancreatic enzymes resulting in autodigestion and fibrosis of the pancreas

an obstruction of the pancreatic duct can cause ductal rupture ans pillage of pancreatic enzymes into the pancreatic tissues; early activation of the enzymes occur in the pancreas, causing inflammation; pancreatic cells are damaged by enzymes (trypsin, lipase, elatase) and autodigestion occurs)

complications of pancreatitis

pseudocyst (fluid becomes walled off by fibrous tissue), abscess, pulmonary complications (pleural effusions, atelectasis, pneumonia in older patients, ARDS (form of pulmonary edema)), cardiovascular complications (hypovolemia), hypocalcemia, abdominal compartment syndrome

DIC

disseminated intravascular coagulation

hypercoagulation of blood, development of microthrombi, excess bleeding

causes of pancreatitis

alcoholism (most common, men), gallstones (biliary tract disease, women), blunt abdominal trauma, operative manipulation and trauma, drug use, infection, unknown causes

consequences of pancreatitis

edema, necrosis (fat necrosis), hemorrhage, vascular permeability, vasodialtion (decrease BP), shock (hypovolemic)

autodigestion in acute pancreatitis

obstruction in the pancreatic duct can cause ductal rupture and spillage of pancreatic enzymes into the pancreatic tissues; early activation of these enzymes occurs in the pancreas, causing inflammation; pancreatic cells are damaged by the enzymes (trypsin, lipase, elastase) and autodigestion occurs

increased risk for pancreatitis

gallbladder disease— gallstone causing obstruction; most common (women)

after cholecystectomy, Whipple procedure, partial gastrectomy

complication of ERCP (endoscopic retrograde cholangiopancreatography)

chronic alcohol intake— 2nd most common (men)

smoking

hypertriglyceridemia

trauma

assessment for acute pancreatitis

abdominal pain: mid epigastric or LUQ; sudden onset and radiates to the back, left flank or left shoulder; worse lying in the supine position, relief in the fetal position

nausea & vomiting: weight loss

low-grade fever

leukocytosis

hypotension: shock from vasodilation and increased vascular permeability

tachycardia

jaundice: swelling of the head of the pancreas, slows bile flow through common bile duct

Grey Turner’s Spots/Sign: discoloration of left flank

Cullen’s Sign: gray/blue hemorrhagic discoloration on abdomen

hyperglycemia from release of glucagon and decreased insulin due to damage of the islet cells, can lead to T1DM

coagulation defects: physiologic changes in the pancreas cause the release of necrotic tissue and enzymes into the blood resulting in altered coagulation; DIC involves hypercoagulation of the blood with development of microthrombi

lab tests for acute pancreatitis

increased amylase (within 12-24 hours, elevated for 2-3 days), lipase (up to 2 weeks), liver enzymes (ALT), triglycerides, glucose, bilirubin, alkaline phosphatase (elevated if biliary obstruction), WBC elevated, ESR elevated

decreased calcium & magnesium with fat necrosis, albumin a serum total protein

diagnostic assessment for acute pancreatitis

abdominal ultrasound, contrast-enhanced CT, abdominal x-ray, ERCP

interventions for acute pancreatitis

pain: possibly PCA; acute pancreatitis pain subsides in 2-3 days, chronic pancreatitis 2 wks

prevention or alleviation of shock: IV fluids

reduction of pancreatic secretions: NPO

correction of F/E imbalances: calcium and magnesium replacements, I&O’s

prevention/treatment of infections: antibiotics

removal of precipitating cause (if possible)

nutrition intervention for acute pancreatitis

NPO (reduce secretions), enteral feedings, small/frequent feedings high in carbohydrates, abstain from alcohol

drugs for pancreatitis

morphine, antispasmodics (dicyclomine), carbonic anhydrase inhibitor (acetazolamide), antacids, PPI, pancreatic enzyme products, insulin

morphine for pancreatitis

relief of pain

antispasmodics for pancreatitis- dicyclomine (Bentyl)

decrease vagal stimulation, motility, pancreatic overflow

carbonic anhydrase inhibitor (aceteazolamide) for pancreatitis

decrease volume and bicarbonate concentration of pancreatic secretion

antacids for pancreatitis

neutralize gastric HCl acid secretion

PPI for pancreatitis

decrease HCl acid secretion

pancreatic enzyme products for pancreatitis

replacement therapy for pancreatic enzymes

insulin for pancreatitis

treatment for hyperglycemia (if needed)

chronic pancreatitis

progressive destructive disease of pancreas characterized by remissions and exacerbations; inflammation and fibrosis of tissue contribute to pancreatic insufficiency

types: chronic calcifying pancreatitis (CCP), chronic obstructive pancreatitis (gallstones), autoimmune pancreatitis, idiopathy and hereditary pancreatitis

assessment for chronic pancreatitis

abdominal pain, ascites (buildup of excess fluid in the abdominal cavity), respiratory compromise, steatorrhea (malabsorption of fats, fat in stool), weight loss (muscle wasting), jaundice, dark urine, polyuria/polydipsia/polyphagia

interventions for chronic pancreatitis

managing pain (first opioids, then others), maintain adequate nutrition (avoid high fat foods, alcohol,caffeine, nicotine, spicy foods; parenteral nutrition; PERT- pancreatic enzyme replacement therapy), prevent disease recurrence

pancreatic cancer

leading cause of cancer deaths; tumor is discovered late and 5 year survival rates are low

tumor may be a primary cancer or secondary from lung, breast, thyroid, kidney or skin; usually it’s an adenocarcinoma- grows rapidly and spreads to surrounding organ, VTE is a common complication

risk factors for pancreatic cancer

diabetes, chronic pancreatitis, chirrhosis, obesity, males, smoking, family history

clinical manifestations of pancreatic cancer

jaundice may be a first sign but indicates advanced disease

diagnostic studies for pancreatic cancer

serum amylase, lipase, alkaline phosphatase, and bilirubin increased; carcinoembryonic antigen levels- indicates pancreatic cancer; abdominal US and CT to confirm diagnosis, ERCP

treatment for pancreatic cancer

more palliative; chemotherapy and radiotherapy used to relieve pain by shrinking the tumor; may insert biliary stents to relieve the pain from biliary obstruction

chemotherapy, radiation, surgery

assessment for pancreatic cancer

slow, vague presentation, jaundice (late, advanced disease, often 1st sign), icterus (yellowing eyes), weight loss, anorexia, nausea, vomiting

surgical management of pancreatic cancer

Partial pancreatectomy: for tumors smaller than 3 cm; minimal invasive surgery, remove pancreatic tumor laparoscopically

for large tumors: radical pancreatectomy or perform a Whipple; traditionally an open surgical approach but may be carried out under laparoscopic conditions; there are three anastomoses; head of the pancreas is removed (duodenum, some of the jejunum, a bit of the stomach and the gall bladder are removed)

post op care for pancreatic cancer

Diabetes Hemorrhage, Wound infection, Bowel obstruction, Intra-abdominal abbcess, NPO, NGT, Monitor electrolytes, Monitor serum protein and albumin to prevent osmotic pressure (may cause third spacing of fluid into the interstitial space leading to shock, less likely to occur with laproscopic procedure, monitor Hgb&Hct, Monitor glucose (hyper or hypo glycemia from stress of manipulation of the pancreas), Drains– drainage should be serosanguineous (usually jackson-pratt), Position in semi fowlers to reduce tension on suture line and anastomoses site

most common pancreatic cancer post op complication

development of fistula, from partial or complete breakdown of the anastomosis; leakage of bile, pancreatic enzymes, or gastric secretions are corrosive, peritonitis can occur – board like abdominal rigidity call surgeon or RRT

HIV demographic considerations

Disproportionally affects individuals who are Black/ African American; Hispanic/Latinx; multiple races; and gay, bisexual, and men who have sex with men.

HIV transmission

Sexual: genital, anal, or oral sexual contact with exposure of mucous membranes to infected semen or vaginal secretions. Most common mode

Parenteral: ie sharing needles or equipment contaminated with infected blood or receiving contaminated blood products, needlestick injuries for health care workers

Perinatal Transmission – from the placenta, during birth – exposure to infected mother’s blood and vaginal secretions, breast milk from infected mother to child

ways HIV is NOT transmitted

Casual contact in the home, school or workplace

Sharing household utensils, towels, linens and toilet facilities

Mosquitoes or other insects

safer sexual practices

Use a new latex or polyurethane condom for each intercourse encounter

Use a water-based lubricant in addition to the condom

Use a condom or latex barrier (dental dam) over the genitals or anus during oral-genital or oral-anal sexual contact

Use latex gloves for finger or hand contact with the vagina or rectum. Change gloves when moving sites.

stage HIV-I

acute; onset of acute infection after invasion by the virus; relatively short stage that progresses to the chronic stage of HIV (HIV II)

stage HIV-II

chronic; this stage can last for years (with treatment) before progressing to HIV III AIDS acquired immune deficiency syndrome

stage HIV-III

AIDS; the last stage is characterized by a profound reduction of immunity with poor protection against infection and increased risk of cancer; not everyone progresses to this stage

HIV infectious process

HIV virus is an RNA virus (retrovirus)

The virus binds to specific CD4+T cells

Fusion inhibitor drugs work to prevent the entry of the HIV particle into the cell

Inside the cell, the HIV’s genetic material (the strand of RNA) is converted to DNA by reverse transcriptase. This is now compatible with the hosts DNA, and turns the cell into a virus factory. Infected CD4+T cell no longer functions as an immune system cell

Nucleoside reverse transcriptase inhibitors NRTI’s and non-nucleoside reverse transcriptase inhibitors NNRTI’s work to prevent this viral replication

HIV then uses the enzyme integrase to get its DNA into the hosts DNA

Effects of HIV

When the virus enters the CD4+T cell, the cell stops being an active immune cell and becomes a virus factory.

Eventually the number of HIV particles overwhelms the immune system, the CD4+T cell level decreases and the viral load increases. As the CD4+T cell drops,the patient is at risk for bacterial fungal and viral infections and some cancers

reverse transcriptase inhibitors (NARTI/NNRTIs)

prevent virus from converting to DNA

integrase inhibitors

prevent integration of viral DNA to CD4+T cell DNA

AIDS diagnosis (HIV III)

CD4+T-cell count of less than 200 cells/mm³ (0.2 X 109/L) or a percentage of less than 14%. Any patient, regardless of CD4+T-cell counts or percentages who has an AIDS-defining illness (opportunistic infection)

HIV progression

can take months to years

timing depends on: how HIV is acquired, health problems, personal factors, interventions, frequency of re-exposure, presence of other STIs, nutrition status, stress

Pre-exposure prophylaxis – PrEP

use of antiretroviral drugs by an uninfected adult to prevent HIV infection

Examples: Injection drug users, men who have sex with men (MSM), non monogamous heterosexually active men and women, adults who are HIV negative and in a relationship with a partner who is HIV+ve

Truvada (tenofovir/emtricitabine) and Discovy (emtricitabine/tenofovir)

once a day drug to prevent HIV infection. Black box warning: not to be taken by anyone infected with Hepatitis B as it can cause a severe exacerbation of hep B. Both drugs are toxic to the liver and kidney so individuals taking the drug need to test kidney function and for HIV infection every 3 months. The individual is not protected until they have completed at least 7 days of consistent dosing

Post exposure prophylaxis cART

for adults who have had an occupational exposure (needlestick injury, contact with bodily fluids to broken skin or mucous membranes (eyes, mouth nose)), non occupational exposure (sexual contact with person of unknown HIV status inc. sexual assault victims)

Start cART within 36 hours, 3 drug regimen for 28 days or until the HIV status of the source has been determined to be negative. Sharps injury – wash site for a full minute and contact employee health, starting cART within 2 hours has the best outcome

assessment for HIV

history: age, gender, occupation, current illness (when did it start, when HIV diagnosed), problems since diagnosis, sexual practices, STI’s, TB, hepatitis, injection drug use, understanding of disease

physical assessment: few symptoms but as the disease progresses – more severe health problems occur; assess for clusters of symptoms

oportunistic infections, malignancies, endocrine or cardivascualr complications

monitor for HIV (+lab tests)

monitor: lymphocytes (often AIDS patients are leukopenic with a WBC less than 3500 cells/mm³), CD4+ T cell count

Antibody-Antigen tests: tests the amount of HIV RNA particles in 1 ml of blood– indirect test of HIV

Viral load tests: the higher the viral load the higher the risk of transmission – used to measure therapy effectiveness

Other labs to measure patient’s overall health: CMP, LFT’s TB testing, Hepatitis screen, lipid profile

opportunistic infections in HIV

Candida albicans: yellowish white plaques in the mouth and throat; also esophagitis, pt has pain and difficulty swallowing; women may also get vaginal candida

Kaposi sarcoma: most common AIDS related malignancy; small purplish brown raised lesions on the skin and mucous membranes

analysis for HIV

Potential for infection – due to reduced immunity

Inadequate gas exchange – due to anemia, respiratory infection or pulmonary Kaposi sarcoma

Pain – due to neuropathy, myelopathy, cancer or infection

Inadequate nutrition – due to increased metabolic need, nausea, vomiting, diarrhea, difficulty chewing or swallowing or anorexia

Diarrhea – due to infection, food intolerance or drugs

Potential for reduced tissue integrity – due to Kaposi sarcoma, infection, reduced nutrition, incontinence, immobility, hyperthermia or cancer

Cognitive decline

Psychosocial distress

interventions for HIV

Prevent the development of opportunistic diseases – handwashing, bathing, avoiding crowds. Detect and treat opportunistic diseases – report temperatures greater than 100oF, persistent cough, cloudy urine, boils/abscess

Enhancing gas exchange: treatment of PCP – trimethoprim with sulfmethoxazole, monitor for cyanosis, O2 therapy,pulmonary hygiene, ABG’s

Managing pain, comfort measures, drug therapy - NSAIDS

Enhancing nutrition: dependent on patients ability to swallow, presence of candida etc. include dietician in care. Monitor weight, I&O’s and calorie count

Managing diarrhea: Antidiarrheals eg loperamide, assess perineal skin, IV fluids may be necessary

Restoring skin integrity: treatment of KS, HSV, VZV

Addressing psychosocial distress

Prevent further transmission of HIV

transition management for HIV

Management of the disease most often in the home

Hospitalization occurs for severe infections or acute exacerbations of symptoms especially at stage III

May need long term care or hospice care.

Teach patient family friends about transmission and preventative behaviors

Self care strategies including good hygiene