Weeks 1&2 Flashcards
Assessment includes
Risk factors
Risk behaviors
Clinical manifestations
Interventions include
Medications
Collaborative management
Implementing provider orders
Nursing care
Involving other disciplines
- making links between physical assessment findings and plans of care
- clues to diagnostics & treatment
10 leading causes of death in US (All ages)
- ❤️ disease
- Cancer
- COVID
- Accidents
- Stroke
- Chronic lower respiratory disease
Life expectancy: 78.8
Infant mortality: 587/100,000 live births - Alzheimer’s disease
- Diabetes
- Chronic renal disease
- Intentional self harm (suicide)
***noticing, interpreting, responding, reflecting
Airborne precautions
Droplet nuclei smaller than 5 microns
Ex: measles, chickenpox (varicella), disseminated varicella zoster, pulmonary or laryngeal tuberculosis
Protection: private room, negative pressure airflow of at least 6-12 exchanges per hour via HEPA filtration, mask or respiratory protection device, N95 respirator (depending on condition)
Droplet precautions
Droplets larger than 5 microns; being within 3 feet of patient
Ex: diphtheria (pharyngeal), rubella, streptococcal pharyngitis, pneumonia or scarlet fever in infants and young children, pertussis, mumps, mycoplasma pneumonia, meningococcal pneumonia or sepsis, pneumonic plague
Protection: private room or cohort patients; mask or respirator (refer to agency policy)
Contact precautions
Direct patient or environmental contact
Ex: colonization or infection with mullti-drug resistant organisms (VRE, MRSA, clostridium difficile, shigella, and other enteric pathogens), major wound infections, herpes simplex, scabies, varicella zoster (disseminated), respiratory syncytial virus in infants, young children, or immunocompromised adults
Protection: private room or cohort patients, gloves, gowns; patients may leave their room for procedures or therapy if infectious material is contained or covered and placed in a clean gown and hands cleaned
Protective environment
Allogenic hematopoietic stem cell transplants
Protection: private room, positive airflow with 12 or more air exchanges per hour; HEPA filtration for incoming air; mask to be worn by patient when out of room during times of construction in area
HEPA
High-efficiency particulate air
Factors for emerging infections
Microbial change and adaptation
Drug resistant malaria, drug resistant KPC (klebsiella pnuemoniae carbapenemase)
Population growth, urbanization, crowding, migration into previously uninhabited areas, deforestation
Inadequate public health measures: poverty, increased/overuse of antimicrobial agents, risky human behaviors (war/refugee camps)
Emerging infection examples
Food borne, waterborne diseases, close personal contact: Ebola, salmonella, escheria Coli, H1N1, SARS (Toronto hospital), SARS-CoV-2 (Variants), avian influenza (H5N1), dengue fever (mosquito borne), clostridium difficile (new strain)
Vectorborne & zoonotic: West Nile virus, Lyme disease (vector borne; deer tick), guinea-work disease, Zika (vector borne, mosquito)
Blood borne: bovine spongiform encephalopathy is
Hines worm
Looks like a complicated ass knot
Extracted or coaxed from the body which is performed in public
Villagers often make a party to get people to attend and learn how to protect themselves
Microbial resistance
Reemergence of bacterial diseases (e.g., TB, HIV, malaria, salmonella- drug resistant forms)
Mechanisms: non adherence, overuse, agricultural use of antibiotics
Biofilm-complex group of microorganisms, slimy gel coating
MRSA, VRE, carbapenem-resistant enterococcus, TB, penicillin-resistant streptococcus pneumoniae
Klebsiella pneumoniae carbapenemase (KPC): highly drug resistant gram negative bacteria
MRSA is most prevalent in long-term care facilities
MRSA Hospital acquired risk factors
Current or recent hospitalization
Residing in a long term care facility
Invasive devices
Recent antibiotic use
MRSA community acquired risk factors
Young age
Participating in contact sports
Sharing towels and athletic equipment
Having a weakened immune system
Living in crowded or unsanitary conditions
Association with healthcare workers
*often looks like a spider bite in appearance; ask pt if they remember being bit by a spider
Strategy one in preventing antimicrobioal resistance in healthcare settings
HAND HYGIENE!!!
Wetting, soaping, lathering, allying friction under running water for 15 seconds, rinsing, adequate drying
Alcohol based hand rubs (ABHRs)
No artificial nails
Strategy 2 to prevent antimicrobial resistance
Prevent infection:
- Vaccinate: annual influenza/H1N1 vaccines; appropriate pneumococcal vaccines
- Get the catheters out: use foley, IV, PICC, and central lines only when necessary; discontinue drains as soon as possible
Strategy 3 to prevent antimicrobial resistance
Diagnose and treat infection effectively
- Target the pathogen: culture the pt
- Access the experts: consult infectious disease experts for pts with serious infections
Strategy 4 to prevent antimicrobial resistance
Use antimicrobial wisely
- Practice antimicrobial stewardship: engage in local antimicrobial control efforts
- Use local data: know your antibiogram (ask your infection prevention practitioner/pharmacist for the current copy); know the specific risks of your patient population
- Treat infection, not contamination or colonization: use proper antisepsis for blood and other cultures; culture blood, not skin or catheter hub; use proper methods to obtain and process all cultures
- Treat infection, not colonization: Topical or systemic antimicrobial therapies DO NOT eradicate nasal or extra nasal MRSA. Treat pneumonia, not the tracheal aspirate. Treat bacteremia, not the catheter tip or hub (see CDC guidelines for how to obtain BC from existing catheters). Treat UTI, not the indwelling catheter.
- Know when to say “no” to Vanco: treat infection, NOT contaminants or colonization. Fever in a pt with an IV catheter is not a routine indication for Vancomycin.
- Stop antimicrobial treatment: when infection is cured; when cultures are negative and infection is unlikely; WHEN INFECTION IS NOT DIAGNOSED!
Strategy 5 to prevent antimicrobial resistance
- Isolate the pathogen: use standard infection control precautions; contain infectious bodily fluids (follow precautions); consult infection control experts early.
- Break the chain of contagion: STAY HOME WHEN YOU ARE SICK! WASH YOUR FUCKING HANDS!!! Encourage others to follow good hand hygiene protocols.
Infectious disease process cycle
Susceptible host
Portal of entry
Mode of transmission
Portal of exit
Reservoir of sources
Causative agent
Susceptible host factors
Age Immune status Chronic disease Malnutrition Surgery Burns Antibiotics, steroids, chemotherapy Radiation therapy Invasive procedures
Portal of entry examples
Respiratory tract Gastrointestinal tract Genitourinary tract Skin/ mucous membranes Blood Transplacental
Mode of transmission examples
Contact: Direct; Indirect Droplet Airborne vehicle Common vehicle Vectorborne
Portal of exit examples
Respiratory tract Gastrointestinal tract Genitourinary tract Skin/ mucous membranes Blood Transplacental
Reservoir of sources
Animate
Inanimate
Causative agent examples
Bacteria
Viruses
Fungi
Rickettsiae
Protozoa
Helminths
Airborne precautions (in addition to standard precautions)
Private room with negative airflow- air exchange and discharge to outside or through HEPA filter; door closed, enter through anti-room
Wear Powered Air purifying Respirator (PAPR) for known or suspected TB. Susceptible people wear PAPR or N95 HEPA filter
Pt to wear surgical mask if leaves room
Diseases transmitted by air: Rubeola (Measles) Mycobacterium tuberculosis (TB) Varicella (chickenpox) Disseminated varicella zoster virus (shingles)
Droplet precautions (in addition to standard precautions)
Private room preferred; may cohort with pt with same active infection (same microorganism)
Mask if working within 3 feet of patient
Transport with surgical mask on
Diseases transmitted by droplet: Diphtheria (pharyngeal) Streptococcal pharyngitis Pneumonia Influenza Rubella Mumps Pertussis Invasive disease caused by H. Influenza type B/ Neisseria meningitis: meningitis, pneumonia, sepsis
Contact precautions (in addition to standard precautions)
Private room preferably; may cohort pts with same active infection
Wear gloves when entering room
Wash hands with antimicrobial soap before leaving
Wear gown to prevent contact with pt or contaminated items
Remove gown before leaving room
Use necessary precautions when transporting pt
Use dedicated equipment for pt only
Diseases that are transmitted by direct contact:
Clostridium difficile (C Diff)
Colonization of infection caused by MDRO (MRSA/VRE)
Pediculosis (lice)
Respiratory syncytial virus (RSV)
Scabies
Infection is accompanied by inflammation. True or false?
True
Inflammation is accompanied by infection. True or false?
False
Human leukocyte antigens (HLA)
Found on surface of most body cells
Determine tissue type of person
Hey for recognition and self-tolerance
Unique proteins: identical only with an identical sibling
Because cell surface proteins are “non-self” to another person’s immune system, they are antigens capable of stimulating the immune response
About HLAs
Humans have about 40 major HLAs
Inherited from parents
When encounter another HLA if not a PERFECT match, inflammation is initiated
Immune function declines starting in our 30s
Inflammation
Neutrophils- nonspecific phagocytosis
Macrophages- nonspecific recognition of foreign proteins, ingestion, and phagocytosis
Monocytes- destruction of bacteria and cellular debris. Matured into macrophage
Eosinophils- releases vasoactive amines during an allergic reaction
Basophils- released histamine and heparin in areas of tissue damage
Antibody mediated immunity
B-lymphocytes- becomes sensitized to foreign cells with helper/inducer T-cells
Plasma cells- secrete immunoglobulins in response to specific antigens
Memory cells- remain sensitized to specific antigens. Secretes immunoglobulins in re-exposure
Cell mediated immunity
Helper/inducer T-cells- enhances immune activity through secretion of cytokines
Cytotoxic/cytolytic T-cells- selectively destroy non-self cells (virally infected cells)
Natural killer Cells- selectively destroys non-self cells (malignant cells)
Leukocyte immune function
Recognition of self vs non-self
Destruction of invaders and abnormal self cells
Production of antibodies directed against foreign invaders
Complement activation (innate immunity): activate plasma proteins that act as enzymes and attract agents to complement cell actions
Production of cytokines that stimulate the production and activity of leukocytes
3 processes of protection
Full immunity requires all 3
Inflammation
Antibody-mediated immunity (AMI): defense response produces antibodies directed against certain pathogens; antibodies inactivate pathogens and protect against future infection
Cell-mediated immunity (CMI): microbial resistance mediated by specifically sensitized T-lymphocytes action
Killing actions of AMI and CMI
Committed lymphocyte stem cell (exposed to specific foreign antigen) - - -> unsensitized B-lymphocyte (AMI) OR unsensitized T-lymphocyte (CMI) - - -> goes to sensitized B-lymphocyte (plasma cell), sensitized B-memory cell, sensitized T-memory cell, or sensitized T-lymphocyte (effector cell)
If goes to plasma cell: immediately begins secreting antibodies directed against the specific antigen
If goes to effector cell: immediately takes direct and indirect killing actions against the specific antigen
What happens when you get a paper cut?
5 stages: injury, vascular response, fluid exudation, cellular exudation, and repair/healing (may never be repair/healing)
Significance: physical assessment findings
Regional manifestations: lymphadenitis
Systemic manifestations: increased temp, high WBCs, high ESR (erythrocytes sedimentation rate)
Shift to the left or bandemia: sign of significant ongoing infection; immature cells: bands/stabs
Understanding WBCs
Bands (stabs)- immature neutrophils
Neutrophils (Segs/Poly)- circulating phagocytes, 55-70% of the total WBCs; 109 billion released from the bone marrow daily
Eosinophils- ~1.5% of total WBCs; kill microbes that are too large for phagocytosis (parasites) by the process of degranulation
Basophils- ~0.5% of the total WBCs; release vasoactive mediators (cause the manifestations of infection= fever, lymphadema)
Lymphocytes- ~28% of WBCs; respond to viral infections
Monocytes- 2-8% of WBCs; circulating phagocytes
Neutrophils
Mature neutrophils are called segmented (segs) or polymorphonuclear (poly) cells
Less mature neutrophils are called bands/stabs
12-14 days for a stem cell to grow into mature neutrophils
Life span is very short: 12-18 hours
Function: phagocytosis
Each neutrophil= 1 episode of phagocytosis and then it is exhausted
Phagocytosis process
- Exposure/invasion
- Attraction
- Adherence
- Recognition
- Cellular ingestion
- Phagosome formation
- Degradation
Stem cell into mature segmented neutrophil
Committed stem cell -> myeloblast -> promyelocyte -> metamyelocyte -> band neutrophil -> mature segmented neutrophil
Total WBC lab meaning
<5000 is r/t disease or treatment affecting bone marrow
> 11000 from increased inflammation, infection, sepsis, trauma
> 100,000 is r/t leukemia
Neutrophils lab meaning
<500 with radiation/chemo; >70% bacterial
Immature neutrophils = bands, segs (shift to the left)
Bands lab meaning
> 5% of total BIG infection or inflammation
Monocytes lab meaning
> 500 fungal infections, mono (Epstein-barr virus/EBV), chronic inflammatory disease
Takes 24 hours to come out
Lymphocytes lab meaning
<1000 steroid or immunocompromised, drug treatment, HIV, renal disease
> 5000 viral infections, immune disease
Sequence of inflammatory response
Five cardinal manifestations of inflammation:
Warmth
Redness
Swelling
Pain
Decreased function
Stage 1 of the inflammatory response (Acute)
Vascular changes due to histamine/serotonin/kinins to increase arteriole flow
Macrophage deployment
Stage 2 of the inflammatory response (tissue formation- proliferation)
Neutrophilia phase (count can increase 5 times normal in 12 hours)
Exudate/pus
Anti-inflammatory drugs work in this phase
If this phase lasts more than a few days, we see a shift to bands (shift to the left)
Stage 3 of the inflammatory response (remodeling/chronic)
Tissue repair and replacement phase (scar tissue)
Acute inflammation: vascular phase
Vasodilation of arterioles and venules
Increased vascular permeability
Acute inflammation: cellular phase
Delivery of leukocytes, mainly neutrophils
After extravasation, leukocytes migrate in the tissues toward the site of injury
Acute inflammation: leukocyte activation phase
Phagocytosis
Cell killing: 4 step process -> degradation of the microbe
Specific immunity
Adaptive internal protection resulting in long-term resistance to effects of invading microorganisms
Body must learn to generate specific immune responses (squired immunity) when infected by or exposed to specific organisms
Lymphocytes develop actions and products that provide true immunity
2 divisions are AMI and CMI
Acquiring Antibody-Mediated Immunity (AMI) or Humoral Immunity
Uses antigen-antibody interaction to neutralize, eliminate, or destroy foreign proteins (antigens) produced by bone marrow-derived B-lymphocytes (B-cells)
Adaptive response to invasion by organisms or foreign proteins
Active immunity
Specific antibodies against antigen
Natural active immunity
Antigen enters naturally
Artificial active immunity
Protection developed by vaccination/immunization (may require booster)
Passive immunity
Antibodies are transferred after first being made in another human/animal to provide immediate short term protection (rabies, tetanus, poisonous snake bite)
Natural passive immunity
Passed from mother to fetus
Cell-mediated immunity (CMI) or cellular immunity
Involves many WBC actions and interactions
Another type of adaptive/acquired true immunity
For total immunocompetence, CMI must function optimally
Important cell types for CMI: T-lymphocytes (T cells) and Natural Killer cells (NK cells)
Cytokines- small protein hormones produced by WBCs that regulate CMI
Protection provided by CMI
Helps protect the body through the ability to differentiate self from non-self
Watches and ride body of self cells that may potentially harm body
Prevents development of cancer and metastasis after exposure to carcinogens
The liver
Mostly RUQ of abdomen
R/L Lobes
Largest vascular organ
Palpate the lower margin edge (2 finger width)
Performs >400 functions
Effects entire body system
Liver diseases range
Vascular functions of the liver
Blood storage- protective function
Stores 2 units
Blood filtration- Kupffer cells (phagocytic)
Secretory functions of the liver
Bile salt production
Conjugation and secretion of bilirubin
Cholesterol removal
Metabolic functions of the liver
Carbohydrate metabolism
Maintenance of glucose levels by:
Glycogenesis (glucose storage)
Glycogenolysis (breakdown of stored glycogen)
Gluconeogenesis (formation of glucose from protein and fat- starvation)
Fat and metabolism storage
Protein metabolism:
Albumin synthesis-serum osmotic pressure and keeping fluid in vascular system
Conversion of ammonia (NH3) to urea (NH2) which is water soluble
Synthesis of blood clotting factors II, V, VII, VIII, IX, and X (Vitamin K dependent)
Detoxification of hormones (sex, thyroid, cortisone, adrenal) and harmful compounds (drugs, alcohol, chemicals)
Storage functions of the liver
Blood
Glucose
Fat
Minerals: iron and magnesium
Vitamins A, B12, D, E, and K (switch fat soluble vitamins to water soluble)
Hepatocytes: single cell responsible for all the functions of the liver
Common hepatotoxic drugs
Tylenol Aspirin Anesthetics (e,g., halothane) Librium Valium Dilantin Phenobarbital Elavil Methotrexate Rifampin INH Haldol Tagamet Amiodarone
Risk of drug toxicity increases with aging and decreased liver function
Hepatic portal circulation
Blood from GI organs/spleen delivered to liver
Stomach, pancreas, portions of large intestine via splenic vein to hepatic portal vein
Small intestine and portion of large intestine, stomach, pancreas via superior mesenteric vein
Liver processes substances from blood and pass into general circulation
Liver receives oxygenated blood from hepatic artery
Kupffer cells kill most of the bacteria that escapes from the GI tract
Cirrhosis
Extensive irreversible scarring caused by inflammation and necrosis
Tissues become nodular, block normal flow and bile ducts
Inflammation causes swelling= increased pressure in portal system; hepatocytes are asymmetrical
What happens with advanced cirrhosis
Swelling
Scarring
Hepatitis
Necrosis
Inflammation
Liver function tests (LFTs) that are insensitive and nonspecific
Abnormalities occur only after significant damage
Liver enzymes (hepatocytes hold enzymes):
AST: aspartate aminotransferase (0-35 U/L)
ALT: alanine aminotransferase (4-36 U/L)
Alkaline phosphatase (30-120 U/L)
Gamma Glutamyl Transferase (GGT)
Bilirubin
Total protein
Albumin (liver is the only organ that makes this)
Ammonia (NH3)
Clotting factors (PT/PTT)
Magnesium
Platelets
Hormone levels
What is expected to happen with a patient with hepatitis with the lab values AST and ALT?
A.) increase
B.) decrease
C.) stay about the same
A.) increase
Liver injury will typically cause elevated transaminases that are released into the serum as a result of cell injury or death. These enzymes essentially will leak out into the bloodstream, causing the levels to be high.
What would be expected to happen to the albumin level in a patient with hepatitis?
A.) increase
B.) decrease
C.) stay about the same
B.) decrease
Albumin is made in the liver. Patients with Hepatitis B will have a low albumin level due to the damage to the liver resulting in a liver no longer able to produce albumin.
A low albumin level in patients with Hepatitis C can be a sign of cirrhosis. Very low albumin levels can cause symptoms including edema in the lower extremities as well as as items (fluid retention in the abdomen)
What is expected to happen with a patient with hepatitis with the lab values PT/PTT
A.) increase
B.) decrease
C.) stay about the same
C.) stay about the same with acute liver disease and chronic hepatitis
However, these levels tend to increase significantly with cirrhosis.
What would be expected to happen to the ammonia level of a patient with hepatitis?
A.) increase
B.) decrease
C.) stay about the same
A.) increase
Ammonia levels are elevated in patients with acute and chronic liver diseases. It is also known to affect the brain in disorders including Reye syndrome and certain metabolic disorders.
Ammonia is normally converted to urea in the liver and cleared out of the body through the urine. Ammonia is highly toxic to the brain.
Clinical manifestations of liver disease (“hepatitis”)
N/V
Anorexia
Weight loss (may be masked by water retention; be attentive to extremities)
Pain
Constipation
Flatulence
Fatigue
Fever
Later signs of liver disease: jaundice
Disturbed bilirubin metabolism, liver can’t secrete so increased.
20-25% of patients have puritis (itching) from bilirubin deposited in the skin.
Other etiology: hemolysis (increased RBC destruction)
Later signs of liver disease: portal hypertension
Persistent increase within portal vein >5mmHg
Fluid retention, hydrothorax, splenomegaly, collateral circulation (varices)
Later signs of liver disease: ascites and esophageal varices
Caused by increased hydrostatic pressure
Later signs of liver disease: portal systemic encephalopathy
Also know as hepatic coma
Buildup of ammonia, mercaptans (sulfur containing compounds)
Later signs of liver disease: hepatorenal syndrome
Decreased urine (oliguria)
Increased BUN/CR (azotemia)
Decreased urine sodium excertion
Other Later signs of liver disease:
Coagulation defects
Spontaneous bacterial peritonitis (SBP): bacteria🦠 usually from bowels
Splenomegaly: from blood flow back into the spleen, veins become dilated
Ascites
Collection of plasma in peritoneal fluid
Reduces circulating plasma protein
Liver is NOT producing albumin (due to impaired hepatocytes)
Serum colloid osmotic pressure decreases in circulating system (third spacing)
Paracentesis
A procedure that removes peritoneal fluid from the abdomen through a slender needle.
It is collected and sent to the lab for analysis to determine what’s causing the excess fluid.
Purpose: to diagnose an infection is the most common reason for performance
Contains: water, albumin, sodium, potassium
LeVeen Peritoneovenous Shunt
Direct ascitic fluid into vena cava through a one way valve
Bypass liver and Kupffer cells
Complications: Clotting issues/bleeding Fever Infection Cardiopulmonary compromise
Paraumbilical vein
Paraumbilical vein patency
May affect hepatic hemodynamics and function
Paraumbilical vein can be varicosed and visible
Spider angioma
Vascular lesions with a red center and radiating branches
Nose, cheeks, upper thorax, and shoulders
Caused from increased estrogen levels
Found more commonly in alcoholic cirrhosis
Palmar erythema
Warm and bright red palms
Abnormal serum estradiol levels (~20% of patients with hepatic disease)
Estrogen CANNOT be converted from fat soluble to water soluble and excreted
Preicteric stage of hepatitis
Before evidence of jaundice
Fatigue
Headache
Urticaria (itching)
Icteric stage of hepatitis
Jaundice or acute phase
Inflammation
Low-grade fever
Chills
Lymphadenopathy
Enlarged liver/spleen
RUQ pain (vague)
N/V
Anorexia
Weight loss
Decreased bilirubin metabolism & decreased liver function
Jaundice- high bilirubin, ALT, AST, Alk Phos, ammonia, dark yellow urine, light clay-colored stools (from lack of bile), and large globules of fat in the stool (from undigested fat)
Posticteric stage of hepatitis
Same as the icteric phase with improvement
Blood levels remain abnormal for extended time
What causes inflammation in hepatitis?
Immunologic damage
Infections (e.g., viruses, bacteria, fungi, Protozoa)
Toxic damage (e.g., alcohol, drugs, poisons/chemicals)
Hepatitis includes
Fatigue
Infection
Nutritional deficit/fluid volume overload or deficit
Comfort
Skin integrity
Bleeding
Injury/falls
Social isolation (involve family, social workers, counselors, mental/behavioral health professionals)
Lack of knowledge
Hepatitis NANDA NRSG Dx
Nutrition,
Management of cirrhosis
Fatigue: short activity/rest
Nutrition: small meals, vitamins
Excess fluid volume: monitor fluid, meds
Ineffective breathing pattern: respiratory support
Impaired skin integrity: positioning, barrier
Risk for infection: hand hygiene
Cirrhosis
Encephalopathy (confusion)
Sparse body hair
Muscle wasting
Spider angioma
Hobnail fibrotic liver
Dilated vessels
Red palms
Ascites
Jaundice (yellow itchy skin)
Collaborative treatment for cirrhosis
Medications: Diuretics to decrease portal HTN Potassium Vitamins (folic acid, thiamine, K, and C) Lactulose Antibiotics/probiotics
Surgical treatment:
Shunts to reduce blood flow through obstructed area
Paracentesis
Transplant
Esophageal varices
Most dangerous complication of portal HTN
50% mortality with hemorrhage
Endoscopy to diagnose and treat
Beta-blockers (propranolol) to decrease HR and pressure gradient
If hemorrhage occurs: NG with lavage Hemodynamic stability (PRBCs, FFP, Vit K) Vasopressin (IV or into SVC) for vasoconstriction Sandostatin for vasoconstriction Endoscopy sclerotherapy- inject Balloon tamponade Shunt
Sengstaken-Blakemore Tube
Holds pressure
Clots off varices
3 ports:
- Suction for gastric aspiration
- Esophageal balloon inflation
- Gastric balloon inflation
Balloon tamponade of GE varices indications
Unstable pts with massive variceal bleeding in the following scenarios-
Endoscopy is not available
Endoscopy is unsuccessful at controlling bleeding
Consultant physicians are unavailable and vasoactive agents have failed to stop bleeding
Balloon tamponade of GE varices contraindications
History of esophageal stricture
Recent esophageal or gastric surgery
Balloon tamponade of GE varices complications
Airway obstruction
Esophageal rupture
Aspiration pneumonitis
Pain
Ulceration of lips, mouth, tongue, or nares
Esophageal and gastric mucosal erosions
Balloon tamponade of GE varices equipment
Nasal spray
Viscous lidocaine
60mL syringe (catheter-tip)
Bulb inflator
Manometer
Tube clamps
“Y” tube
Scissors
Sengstaken-Blakemore tube
How esophageal varices form and what they are like
Varices are enlarged veins in the esophagus
Varices develop in order to decompress the hypertensive portal vein and return blood to the systemic circulation
Form when pressure gradient between portal and hepatic veins rises >12 mmHg
Hepatitis A cases and how it spreads
About 24,900 new infections each year
Effective vaccine available
Outbreaks still occur in the US; currently there are widespread person-to-person outbreaks that are recent
Spread when a person ingests fecal matter (even in microscopic amounts) from contact with objects, food, or drinks contaminated by fevers or stool from an infected person
Hepatitis B cases and how it spreads
About 22,600 new infections in 2018; ~862,000 people living with Hep B
Effective vaccine available
About 2 in 3 infected do not know they are infected
About 50% of those with Hep B in the US are Asian
Hep B is a leading cause of liver cancer
It is spread when blood, semen, or other body fluids infect another person by:
- Birth to an infected mother
- sex with an infected person
- sharing needles, syringes, medical equipment (e.g., glucose monitor)
- sharing toothbrushes or razors
- poor infection control leading to outbreaks in healthcare facilities
Hepatitis C cases and how it spreads
About 50,300 new cases in 2018; ~2.4 million living with Hep C
~50% of people with Hep C don’t know they have it
Hep C is a leading cause of liver transplants and liver cancer
It is spread when blood from an infected individual enters the body of someone who is not infected
It can also be transmitted from:
- sharing equipment contaminated with blood such as needles or syringes
- receiving a blood transfusion or organ transplant before 1992 (when widespread screening virtually eliminated Hep C from the blood supply)
- poor infection control resulting in outbreaks in health care facilities
- birth to an infected mother
Blood tests Hepatitis A
Hepatitis A Virus (HAV) antibodies (anti-HAV)
+ anti-HAV IgG= immune (previous infection)
+ anti-HAV IgM= acute infection (4-6 weeks)
+ anti-HAV IgM & -IgG= no immunity, needs immunization
Hepatitis B (HBV) prevalence, transmission, incubation, prophylaxis, and antibodies
Prevalence: 5% of the world population: 3,322 new cases in 2018; 59% are heterosexuals with multiple partners , homosexual men, IV drug users; 3% are health care workers
Transmission: blood or bodily fluids, sexually, during birth, body piercing/tattoos
Incubation of 60-150 days
A hardy organism- can survive outside the human body for at least 7 days on environmental surfaces
Prophylaxis: Hep B vaccine since 1982
Antibodies: antiHBc (core) AntiHBs (surface)
Who is at risk for Hep B?
IV drug users
Sharing needles, razors, toothbrush
People having unprotected sex
Healthcare workers
People with compromised immunity
Blood transfusions prior to 1992
Patient receiving chronic dialysis
Born to infected mother
HBV Treatment
Antiviral and immunomodulating meds
Interferon: 3 injections/week for 4-6 months; side effects: depression, fatigue, muscle pains, body aches, fever, nausea; keep hydrated
Oral antiviral meds to prevent replication for 1 year (e.g., entecavir (Baraclude), tenofovir (Viread), lamivudine (Epivir), adefovir (Hepsera), and telbivudine (Tyzeka); monitor kidney functions
Rest
Eat small, high card, moderate fat, and protein diet
Avoid alcohol, acetaminophen/other hepatotoxic meds
Prevent transmission
HBV Health Promotion
Vaccination (95% of HBV can be prevented with vaccine)
Wear gloves
Needle-less system in healthcare
Protected sex
Avoid sharing needles
Immune globulin after exposure
Do not share personal items
Do not donate blood if HBV positive/risky behaviors
Hepatitis C (HCV) prevalence, transmission, incubation, prophylaxis, antibodies
Prevalence: 20-50% of cases will develop chronic hepatitis (1990- HCV 1st identified)
Transmission: parenteral
Incubation: 2 weeks to 6 months (6-9 weeks common)
Prophylaxis: immune globulin, donor screening since 1985
Antibodies: AntiHCV (can exist without an active infection); HCV ribonucleic acid (RNA) confirms presence of active infection
Vaccine: in development for 25 years; 7 genotypes and 67 subtypes
Alcohol consumption speeds the process
Who is at risk for Hepatitis C?
Baby boomers (born between 1945-1965)
IV drug users that share needles
Unprotected sex
HIV
Chronic dialysis
Unsanitary tattoos done in prison or a non-licensed establishment
Blood recipients or organ transplants prior to 1992
Healthcare workers via needlestick, sharps, mucosa
Clotting factors before 1987
Born to an HCV-infected mother
Hepatitis C symptoms
~70-80% of those with acute Hep C do not have any symptoms
If symptoms occur, the average time is 6-7 weeks after exposure, but can range from 2weeks to 6 months
Symptoms include: Fever Fatigue Loss of appetite N/V Abdominal pain Dark urine Clay-colored bowel movements Joint pain Jaundice (yellowing of the skin/eyes)
Current Hep C Treatmebt according to the CDC and FDA (issues revolve around cost and access)
Common Tx: SQ Pegylated interferon alpha every week and oral ribavirin
CoPegus- ribavirin
Incivek- telaprevir-monitor CBC (SE: anemia)
Infergen- interferon aphacon-1
Intron A- interferon alpha-2b
Olysio- simeprevir (~80% cure rate)
Harvoni- sofoburvir + ledipasvir ($98,500 for 12 weeks; $197,000 for 24 weeks
Pegasys- pegylated interferon
Pegintron- pegylated interferon alpha-2b
Rebetol- ribavirin
Roferon- interferon alpha-2a
Sovaldi- sofoburvir ($84,000 for 12 weeks; $168,000 for 24 weeks)
Victrelis- boceprevir - monitor CMP
Viekira Pak- ombitasvir, panitaprevir, and ritonavir tablets
Autoimmune Hepatitis (AIH)
Non-contagious, chronic, inflammatory, autoimmune disease
Exact cause is unknown; believed to be a combo of environmental, genetic, immunologic, and other factors; med-induced linked to nitrofurantoin, minocycline, and hydralazine; infections such as viral hepatitis (A, B, C, and D), herpes simplex virus, and cytomegalovirus
Persistent inflammation can result in scarring, ultimately cirrhosis
Treatment: corticosteroids, azathioprine, or mycophenolate mofetil
