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N5 471 > Weeks 1&2 > Flashcards

Weeks 1&2 Flashcards

1
Q

Assessment includes

A

Risk factors
Risk behaviors
Clinical manifestations

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2
Q

Interventions include

A

Medications

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3
Q

Collaborative management

A

Implementing provider orders
Nursing care
Involving other disciplines

  • making links between physical assessment findings and plans of care
  • clues to diagnostics & treatment
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4
Q

10 leading causes of death in US (All ages)

A
  1. ❤️ disease
  2. Cancer
  3. COVID
  4. Accidents
  5. Stroke
  6. Chronic lower respiratory disease
    Life expectancy: 78.8
    Infant mortality: 587/100,000 live births
  7. Alzheimer’s disease
  8. Diabetes
  9. Chronic renal disease
  10. Intentional self harm (suicide)

***noticing, interpreting, responding, reflecting

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5
Q

Airborne precautions

A

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)

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6
Q

Droplet precautions

A

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)

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7
Q

Contact precautions

A

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

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8
Q

Protective environment

A

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

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9
Q

HEPA

A

High-efficiency particulate air

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10
Q

Factors for emerging infections

A

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)

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11
Q

Emerging infection examples

A

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

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12
Q

Hines worm

A

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

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13
Q

Microbial resistance

A

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

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14
Q

MRSA Hospital acquired risk factors

A

Current or recent hospitalization

Residing in a long term care facility

Invasive devices

Recent antibiotic use

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15
Q

MRSA community acquired risk factors

A

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

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16
Q

Strategy one in preventing antimicrobioal resistance in healthcare settings

A

HAND HYGIENE!!!

Wetting, soaping, lathering, allying friction under running water for 15 seconds, rinsing, adequate drying

Alcohol based hand rubs (ABHRs)

No artificial nails

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17
Q

Strategy 2 to prevent antimicrobial resistance

A

Prevent infection:

  1. Vaccinate: annual influenza/H1N1 vaccines; appropriate pneumococcal vaccines
  2. Get the catheters out: use foley, IV, PICC, and central lines only when necessary; discontinue drains as soon as possible
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18
Q

Strategy 3 to prevent antimicrobial resistance

A

Diagnose and treat infection effectively

  1. Target the pathogen: culture the pt
  2. Access the experts: consult infectious disease experts for pts with serious infections
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19
Q

Strategy 4 to prevent antimicrobial resistance

A

Use antimicrobial wisely

  1. Practice antimicrobial stewardship: engage in local antimicrobial control efforts
  2. Use local data: know your antibiogram (ask your infection prevention practitioner/pharmacist for the current copy); know the specific risks of your patient population
  3. 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
  4. 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.
  5. 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.
  6. Stop antimicrobial treatment: when infection is cured; when cultures are negative and infection is unlikely; WHEN INFECTION IS NOT DIAGNOSED!
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20
Q

Strategy 5 to prevent antimicrobial resistance

A
  1. Isolate the pathogen: use standard infection control precautions; contain infectious bodily fluids (follow precautions); consult infection control experts early.
  2. Break the chain of contagion: STAY HOME WHEN YOU ARE SICK! WASH YOUR FUCKING HANDS!!! Encourage others to follow good hand hygiene protocols.
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21
Q

Infectious disease process cycle

A

Susceptible host

Portal of entry

Mode of transmission

Portal of exit

Reservoir of sources

Causative agent

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22
Q

Susceptible host factors

A 
Age
Immune status
Chronic disease
Malnutrition
Surgery
Burns
Antibiotics, steroids, chemotherapy 
Radiation therapy
Invasive procedures
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23
Q

Portal of entry examples

A 
Respiratory tract
Gastrointestinal tract
Genitourinary tract
Skin/ mucous membranes 
Blood
Transplacental
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24
Q

Mode of transmission examples

A 
Contact: Direct; Indirect
Droplet
Airborne vehicle 
Common vehicle
Vectorborne
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25
Q

Portal of exit examples

A 
Respiratory tract 
Gastrointestinal tract
Genitourinary tract
Skin/ mucous membranes
Blood
Transplacental
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26
Q

Reservoir of sources

A

Animate

Inanimate

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27
Q

Causative agent examples

A

Bacteria

Viruses

Fungi

Rickettsiae

Protozoa

Helminths

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28
Q

Airborne precautions (in addition to standard precautions)

A

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)
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29
Q

Droplet precautions (in addition to standard precautions)

A

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
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30
Q

Contact precautions (in addition to standard precautions)

A

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

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31
Q

Infection is accompanied by inflammation. True or false?

A

True

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32
Q

Inflammation is accompanied by infection. True or false?

A

False

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33
Q

Human leukocyte antigens (HLA)

A

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

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34
Q

About HLAs

A

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

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35
Q

Inflammation

A

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

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36
Q

Antibody mediated immunity

A

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

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37
Q

Cell mediated immunity

A

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)

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38
Q

Leukocyte immune function

A

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

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39
Q

3 processes of protection

Full immunity requires all 3

A

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

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40
Q

Killing actions of AMI and CMI

A

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

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41
Q

What happens when you get a paper cut?

A

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

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42
Q

Understanding WBCs

A

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

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43
Q

Neutrophils

A

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

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44
Q

Phagocytosis process

A
  1. Exposure/invasion
  2. Attraction
  3. Adherence
  4. Recognition
  5. Cellular ingestion
  6. Phagosome formation
  7. Degradation
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45
Q

Stem cell into mature segmented neutrophil

A

Committed stem cell -> myeloblast -> promyelocyte -> metamyelocyte -> band neutrophil -> mature segmented neutrophil

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46
Q

Total WBC lab meaning

A

<5000 is r/t disease or treatment affecting bone marrow

> 11000 from increased inflammation, infection, sepsis, trauma

> 100,000 is r/t leukemia

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47
Q

Neutrophils lab meaning

A

<500 with radiation/chemo; >70% bacterial

Immature neutrophils = bands, segs (shift to the left)

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48
Q

Bands lab meaning

A

> 5% of total BIG infection or inflammation

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49
Q

Monocytes lab meaning

A

> 500 fungal infections, mono (Epstein-barr virus/EBV), chronic inflammatory disease

Takes 24 hours to come out

50
Q

Lymphocytes lab meaning

A

<1000 steroid or immunocompromised, drug treatment, HIV, renal disease

> 5000 viral infections, immune disease

51
Q

Sequence of inflammatory response

A

Five cardinal manifestations of inflammation:

Warmth

Redness

Swelling

Pain

Decreased function

52
Q

Stage 1 of the inflammatory response (Acute)

A

Vascular changes due to histamine/serotonin/kinins to increase arteriole flow

Macrophage deployment

53
Q

Stage 2 of the inflammatory response (tissue formation- proliferation)

A

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)

54
Q

Stage 3 of the inflammatory response (remodeling/chronic)

A

Tissue repair and replacement phase (scar tissue)

55
Q

Acute inflammation: vascular phase

A

Vasodilation of arterioles and venules

Increased vascular permeability

56
Q

Acute inflammation: cellular phase

A

Delivery of leukocytes, mainly neutrophils

After extravasation, leukocytes migrate in the tissues toward the site of injury

57
Q

Acute inflammation: leukocyte activation phase

A

Phagocytosis

Cell killing: 4 step process -> degradation of the microbe

58
Q

Specific immunity

A

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

59
Q

Acquiring Antibody-Mediated Immunity (AMI) or Humoral Immunity

A

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

60
Q

Active immunity

A

Specific antibodies against antigen

61
Q

Natural active immunity

A

Antigen enters naturally

62
Q

Artificial active immunity

A

Protection developed by vaccination/immunization (may require booster)

63
Q

Passive immunity

A

Antibodies are transferred after first being made in another human/animal to provide immediate short term protection (rabies, tetanus, poisonous snake bite)

64
Q

Natural passive immunity

A

Passed from mother to fetus

65
Q

Cell-mediated immunity (CMI) or cellular immunity

A

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

66
Q

Protection provided by CMI

A

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

67
Q

The liver

A

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

68
Q

Vascular functions of the liver

A

Blood storage- protective function

Stores 2 units

Blood filtration- Kupffer cells (phagocytic)

69
Q

Secretory functions of the liver

A

Bile salt production

Conjugation and secretion of bilirubin

Cholesterol removal

70
Q

Metabolic functions of the liver

A

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)

71
Q

Storage functions of the liver

A

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

72
Q

Common hepatotoxic drugs

A 
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

73
Q

Hepatic portal circulation

A

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

74
Q

Cirrhosis

A

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

75
Q

What happens with advanced cirrhosis

A

Swelling

Scarring

Hepatitis

Necrosis

Inflammation

76
Q

Liver function tests (LFTs) that are insensitive and nonspecific

Abnormalities occur only after significant damage

Liver enzymes (hepatocytes hold enzymes):

A

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

77
Q

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

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.

78
Q

What would be expected to happen to the albumin level in a patient with hepatitis?

A.) increase

B.) decrease

C.) stay about the same

A

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)

79
Q

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

A

C.) stay about the same with acute liver disease and chronic hepatitis

However, these levels tend to increase significantly with cirrhosis.

80
Q

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

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.

81
Q

Clinical manifestations of liver disease (“hepatitis”)

A

N/V

Anorexia

Weight loss (may be masked by water retention; be attentive to extremities)

Pain

Constipation

Flatulence

Fatigue

Fever

82
Q

Later signs of liver disease: jaundice

A

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)

83
Q

Later signs of liver disease: portal hypertension

A

Persistent increase within portal vein >5mmHg

Fluid retention, hydrothorax, splenomegaly, collateral circulation (varices)

84
Q

Later signs of liver disease: ascites and esophageal varices

A

Caused by increased hydrostatic pressure

85
Q

Later signs of liver disease: portal systemic encephalopathy

A

Also know as hepatic coma

Buildup of ammonia, mercaptans (sulfur containing compounds)

86
Q

Later signs of liver disease: hepatorenal syndrome

A

Decreased urine (oliguria)

Increased BUN/CR (azotemia)

Decreased urine sodium excertion

87
Q

Other Later signs of liver disease:

A

Coagulation defects

Spontaneous bacterial peritonitis (SBP): bacteria🦠 usually from bowels

Splenomegaly: from blood flow back into the spleen, veins become dilated

88
Q

Ascites

A

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)

89
Q

Paracentesis

A

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

90
Q

LeVeen Peritoneovenous Shunt

A

Direct ascitic fluid into vena cava through a one way valve

Bypass liver and Kupffer cells

Complications:
Clotting issues/bleeding
Fever
Infection
Cardiopulmonary compromise
91
Q

Paraumbilical vein

A

Paraumbilical vein patency

May affect hepatic hemodynamics and function

Paraumbilical vein can be varicosed and visible

92
Q

Spider angioma

A

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

93
Q

Palmar erythema

A

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

94
Q

Preicteric stage of hepatitis

A

Before evidence of jaundice

Fatigue

Headache

Urticaria (itching)

95
Q

Icteric stage of hepatitis

A

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)

96
Q

Posticteric stage of hepatitis

A

Same as the icteric phase with improvement

Blood levels remain abnormal for extended time

97
Q

What causes inflammation in hepatitis?

A

Immunologic damage

Infections (e.g., viruses, bacteria, fungi, Protozoa)

Toxic damage (e.g., alcohol, drugs, poisons/chemicals)

98
Q

Hepatitis includes

A

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

99
Q

Hepatitis NANDA NRSG Dx

A

Nutrition,

100
Q

Management of cirrhosis

A

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

101
Q

Cirrhosis

A

Encephalopathy (confusion)

Sparse body hair

Muscle wasting

Spider angioma

Hobnail fibrotic liver

Dilated vessels

Red palms

Ascites

Jaundice (yellow itchy skin)

102
Q

Collaborative treatment for cirrhosis

A 
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

103
Q

Esophageal varices

A

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
104
Q

Sengstaken-Blakemore Tube

A

Holds pressure
Clots off varices

3 ports:

  1. Suction for gastric aspiration
  2. Esophageal balloon inflation
  3. Gastric balloon inflation
105
Q

Balloon tamponade of GE varices indications

A

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

106
Q

Balloon tamponade of GE varices contraindications

A

History of esophageal stricture

Recent esophageal or gastric surgery

107
Q

Balloon tamponade of GE varices complications

A

Airway obstruction

Esophageal rupture

Aspiration pneumonitis

Pain

Ulceration of lips, mouth, tongue, or nares

Esophageal and gastric mucosal erosions

108
Q

Balloon tamponade of GE varices equipment

A

Nasal spray

Viscous lidocaine

60mL syringe (catheter-tip)

Bulb inflator

Manometer

Tube clamps

“Y” tube

Scissors

Sengstaken-Blakemore tube

109
Q

How esophageal varices form and what they are like

A

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

110
Q

Hepatitis A cases and how it spreads

A

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

111
Q

Hepatitis B cases and how it spreads

A

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
112
Q

Hepatitis C cases and how it spreads

A

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
113
Q

Blood tests Hepatitis A

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

114
Q

Hepatitis B (HBV) prevalence, transmission, incubation, prophylaxis, and antibodies

A

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)

115
Q

Who is at risk for Hep B?

A

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

116
Q

HBV Treatment

A

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

117
Q

HBV Health Promotion

A

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

118
Q

Hepatitis C (HCV) prevalence, transmission, incubation, prophylaxis, antibodies

A

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

119
Q

Who is at risk for Hepatitis C?

A

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

120
Q

Hepatitis C symptoms

A

~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)
121
Q

Current Hep C Treatmebt according to the CDC and FDA (issues revolve around cost and access)

A

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

122
Q

Autoimmune Hepatitis (AIH)

A

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

N5 471 (5 decks)

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