exam 2 patho merged

Essential Thrombocytosis

• occurs in bone marrow

• unknown cause

• increased number of platelets enhances risk of clot formation

• occlusions in arteries of heart, spleen, and liver may occur; whereas bleeding in GI may occur

• diagnosis: CBC, bone marrow biopsy

• treatment: drugs to inhibit platelet formation

Acute Immune Thrombocytopenic Purpura

• etiology: autoantibodies to GPIIb/IIIa complex,

• in children → acute, often follows viral infection, normally self-limiting

• s/sx: presents with petechiae and purpura, thrombocytopenia, hemolytic anemia, vascular occlusions, fever, neurological abnormalities, renal disease

• diagnosis: exclusion

• treatment: plasmapheresis (80%-90% recovery)

Hemolytic Uremic Syndrome

• etiology: hemolytic anemia, breakdown RBCs

• two forms are Stx-HUS (Shiga-toxin that produced HUS, bacteria related from contaminated foods/water) and non Stx-HUS (fungi, drugs)

• s/sx: bloody diarrhea, fever, can cause renal failure

• diagnosis: stool culture

• treatment: supportive therapy, antibiotics, hemodialysis, renal transplantation

Heparin

• anticoagulent (anti-clot)

• activates anti-thrombin (AT)

• limits the extension of a clot

• faster, more unpredictable response

• binds to plasma proteins

• varies among people

• risk for bleeding

• monitor bleeding with aPTT (if pt is bleeding more than normal)

• antidote: protamine sulfate

Warfarin

• anticoagulant (anti-clot), Vitamin K antagonist

• interferes with Vitamin K dependent clotting factors

• peak ~90 min after

• PT and INR monitoring

• variable responses

• antidote: Vitamin K

Anemia is a condition in which there is insufficient delivery of ___________ to tissues caused by an inadequate number of mature, healthy ______ in the blood.

oxygen, RBCs

Insufficient oxygen delivery to the tissues produces

signs and symptoms related to cellular hypoxia and lack of cell energy

Normal Hgb values for males

13-18 g/dL

Normal Hgb values for females

12-16 g/dL

Normal Hct values for males

42-52%

Normal Hct values for females

37-48%

Hematocrit

packed RBC volume, fraction of the whole blood that consists of RBCs

S/sx of anemia

jaundice, pallor of skin, conjunctiva, nailbeds, and buccal mucosa, excessive fatigue, weakness, SOB, exercise intolerance
palpitations (tachycardia), chest pain, dizziness or feeling faint, headache, nutritional anemias can cause glossitis, cheilitis, koilonychia, or pica

Sickle cell anemia

• etiology: genetic mutation, abnormal Hgb (Hbg S) which distorts the RBC shape, unable to deliver O2 to tissues, fragile

• recessive, homozygous (worse) and heterozygous

• s/sx: hypoxia, dehydration, severe stress and infection increase risk of distorted cell shapes, hyperbilirubinemia, large spleen

• diagnosis: blood sample for newborns, Hgb electrophoresis can differentiate, CBC, reticulocytosis

• treatment: avoid triggers of vaso-occlusive crises, folic acid to assist in RBC synthesis, blood transfusions, bone marrow transplant

• increased resistance to malaria

Secondary Polycythemia

• etiology: high EPO, prolonged hypoxia, as a compensatory effort by the body to improve oxygen delivery

• s/sx: can be asymptomatic, headache, dizziness, weakness, shortness of breath, splenic enlargement, vision changes, red/itchy skin, and unexplained bleeding, angina, abdominal pain

• diagnosis: CBC, Hgb levels usually do not become greater than 17 or 18 g/dL. Abnormally high Hgb or Hct level and a high EPO level

• treatment: may be reversed depending on whether the underlying cause of hypoxia can be eliminated

• people with COPD or living in high altitude areas

Normal RBCs

4-6 million

Normal platelet count

150,000-400,000

Name the types of WBCs

neutrophils, lymphocytes, monocytes, eosinophils, basophils

Monocytes

• 2-10%
• macrophages: mature monocytes in tissues
• phagocytosis, cytokine synthesis
• dendritic cells

Lymphocytes

• 20-40%
white blood cells; provide long-term immunity

T cells

CD4 and CD8 cells

B cells

produce antibodies (Igs)

Granulocytes

cytoplasm, contain chemicals

Basophils

• <2%
• levels elevate during infection and inflammation
• contain histamine → signal neutrophil migration

Eosinosphils

• 1-7%
• elevate during parasitic infections and allergies

Neutrophils

• 40-80%
• carry out phagocytosis
• first responders
• release enzymes to destroy microbes
• release free radicals

PMNs

polymorphonuclear leukocytes; mature neutrophils, SEGS

BANDS

immature neutrophils

Normal WBC value

4,000-11,000 WBCs

Leukocytosis

> 11,000 WBCs

Leukemoid reaction

> 50,000 WBCs

Leukopenia

< 4,000 WBCs

Neutrophilia

> 7,000 neutrophils

Neutropenia

< 1,500 neutrophils

Leukocytosis v. leukopenia v. lymphocytosis

Leukocytosis: WBC above 11,000 cells/microliter

Leukopenia: WBC less than 4,000/microliter

Lymphocytosis: Lymphocyte count greater than 4,000/microliter

Common cause for elevated level of Neutrophils

Bacterial infection

Common cause for elevated level of Lymphocytes

Viral infection

Common cause for elevated level of Eosinophils

Allergic reaction

Common cause for elevated level of Basophils

parasitic infection or allergic reaction

Common cause for elevated level of Monocytes

inflammation, chronic infection, malignancy, autoimmune disease

Risk factors for hematologic neoplasms

• repeated exposure to benzene
• repeated exposure to herbicides and pesticides
• certain genetic disorders
• past chemotherapy or radiation treatment (cancer)
• history of blood cancers or disorders
• viral causes (HIV, EBV, HTLV)
• bacteria (H. pylori)

Acute lymphoblastic leukemia

• etiology: many chromosomal and genetic alterations, pH chromosome, immature T or B cells (lymphoblasts)

• s/sx: nonspecific, anemia, increased bleeding, lymph node enlargement, splenomegaly, increased infection risk, bone pain

• diagnosis: history and physical assessment, unusually high WBC count, bone marrow biopsy

• treatment: chemotherapy, Bone marrow transplant, CAR-T

Nursing interventions for a neutropenic patient

• isolate patient

• immunocompromised --> be aware of exposure to microbes/germs

• hand hygiene

• do not share equipment/machines with other pt's

• no live plants or flowers

• make sure food is cooked

List all of the complications of healing

keloid, contractures, dehiscence, evisceration, stricture, fistula, adhesions

Keloid

hyperplasia (enlargement of tissue/organ due to increase in reproduction rate of cells) of scar tissue

Contractures

inflexible shrinkages of wound tissue that pulls the edges toward the center of the wound

Dehiscence

opening of a wound's suture line

Evisceration

opening of wound with extrusion of tissue and organs

Stricture

an abnormal narrowing of a tubular body passage from the formation of scar tissue (esophagus)

Fistula

an abnormal connection between two epithelium-lined organs or vessels that normally do not connect (e.g., tracheoesophageal fistula)

Adhesions

internal scar tissue between tissues or organs

Fever is a common manifestation of

inflammation and infection

Ferbile is

fever

Pyrogens

substances that cause fever, activate prostaglandins to reset hypothalamic temperature-regulation center to a higher level

A higher body temperature increases the

efficiency of WBCs in their defense of the body against foreign invaders

Skin wounds heal by three processes which include

primary, secondary, and tertiary intention

The ______ of the wound determines the process the body uses

nature

Primary intention

• least complicated type

• edges of wound are clearly demarcated, cleanly lacerated, and easily brought together

• no missing tissue

• ex: surgical wound healing

Steps of primary intention healing

• within 24 hours, WBCs congregate and a fibrin clot develops at the site
• after 24 to 48 hours, simple epithelialization predominates as the major process that closes the wound
• by day 5, granulation tissue progressively fills in the incision space and new blood vessel growth is maximal

Secondary intention

• extensive loss of tissue within a wound, complex

• regeneration of the same cells to replace lost tissue is not possible

• more intense and longer inflammation process

• wound contraction: myofibroblasts cause contraction of the wound's edges to close the tissue gap

• susceptible to infection, complications, and deformity

Tertiary intention

• wound is missing a large amount of deep tissue, contaminated

• cleaned, left open for 4-5 days

• temporary packing w/ sterile gauze, drainage tube

• scarring with healing

• usually require skin graft

• ex: severe burns, pressure ulcers

Phases of wound healing (HIP WOUND)

1. Hemostasis
2. Inflammatory
3. Proliferation
4. Wound contraction and remodeling

Hemostasis phase of wound healing

• occurs shortly after injury as exposed collagen surfaces attract platelets

• stops blood flow

• platelets aggregated and secrete inflammatory mediators

• vasoactive amines cause short-term vasoconstriction to limit blood loss

Inflammation phase of wound healing

• occurs next in the acute phase, after injury

• vasodilation, increased vascular permeability, and chemotaxis

• acute or chronic

Phases of inflammation

• decreasing vascular permeability
• cellular chemotaxis
• systemic response of inflammation: patient becomes febrile

Signs of infection

redness, loss of function, heat, swelling, pain

Proliferation phase of wound healing

• granulation tissue formation, angiogenesis, and epithelialization

• granulation tissue forms

• after injury, fibroblasts form the granulation tissue that serves as the foundation of scar tissue

• granulation tissue then secretes growth factors and cytokines

• epithelial cells migrate and proliferate to form a new surface and fill in the gap between the wound edges.

• fibroblasts produce collagen

Wound contraction and remodeling phase of wound healing

• ~3 weeks after injury

• scar tissue is structurally refined and reshaped by fibroblasts and myofibroblasts

Factors involved in wound healing include (NO-CCIMA)

nutrition, oxygenation, circulation, immune strength, contamination, mechanical factors, age

Histamine originates from

mast cells, basophils, platelets

Effects of histamine

vasodilation, increase vascular permeability, activates endothelium

Prostaglandins originate from

leukocytes

Effects of prostaglandins

pain, fever, vasodilation, muscle spasms

IgA

• location: breast milk, tears

• function: protect mucous membranes of genitourinary, pulmonary systems

• most active: activity not related to infection, protective/preventive

IgD

• location: attached to surface of B cells

• function: binds antigens to B cells

• most active: early stage, when antigen has first entered the body

IgE

• location: found on mast cells in pulmonary and GI

• function: active in allergic rxns, bind to mast cells and basophils to release histamine and leukotrienes

• most active: not related to infection, found in people with allergies

IgG

• location: throughout bloodstream

• function: activates complement to release inflammatory and bactericidal mediators, confers long-term immunity, active against viruses, bacteria, antitoxins, moves across maternal-fetal barrier

• most active: late disease, recovery, and long after

IgM

• location: throughout bloodstream

• function: initiates complement activity and further immune responses; controls ABO blood reactions

• most active: early infection

Bacterial meningitis

• etiology: fatal infectious disease, caused by inflammation of the meningeal layers that surround and protect brain and spinal cord, caused by viruses or strains of bacteria

• Kernig and Brundzinski’s sign

• s/sx: fever, nuchal rigidity, headache, and photophobia

• diagnosis: lumbar puncture (sample and culture the CSF)

• treatment: high-dose antibiotics, self-limiting, prevented by vaccines

-more acute and severe than viral

-@ risk: people living in close quarters (dorms, jail, apartments, military)

Erythema Infectiosum (Fifth Disease)

• etiology: human parvovirus B19, common childhood viral exanthem

slapped-cheek appearance! headache, low-grade fever, pharyngitis, and malaise

• diagnosis: physical exam and history

• treatment: supportive measures like antipyretics, antihistamines, and hydration

Rubella

• etiology: RNA virus, droplet infection (cough/sneeze) infects respiratory epithelium

• s/sx: rash, fever, sore throat, rhinitis, petechiae (mouth), Forchheimer’s spots, red macules!

• diagnosis: IgM by enzyme immunoassay (EIA)

• treatment: supportive therapy with antipyretics, hydration, and oatmeal baths

-cariogenic effect: passed from mom to baby, causes spontaneous abortion of the fetus via placenta

Tapeworm

• etiology: contained in undercooked beef or contaminated vegetation

• s/sx: abdominal pain, nausea, anorexia, weight loss, and passage of eggs in the stool

• diagnosis: stool test

• treatment: Freezing meats to –4°F for 24 hours also kills tapeworm eggs. Antihelminthic medications include praziquantel and niclosamide

Coccidiomycosis (Valley Fever)

• etiology: spores disperse into the air with any disruption of the soil, such as during construction → infection is caused by inhalation of the particles; not spread from person to person

• s/sx: similar to flu; cough, fever, muscle aches, headache, macular skin rash

• diagnosis: chest x-ray, CT scan, serology, and blood culture

• treatment: consists of antifungal medications such as fluconazole; self-limiting

Vaginal Candidiasis

• yeast infection

• not sexually transmitted

• caused by long-term antibiotic use --> kills the good bacteria in vagina which is called lactobacillus

• can cause fatal disseminated infection = septicemia

-immunocompromised

Innate immunity

• body's first line of defense
• body's natural barriers, normal flora, WBCs, enzymes, and chemicals
• non-specific
• cytokines and NK cells

Cytokines

• produced by WBCs
• coordinate immune response
• regulate inflammation

Natural killer cells

• granular lymphocytes
• destroy tumor cells and virus-infected cells
• acts as a first line of defense

Adaptative immunity

• acquired, specific, memory
• developed after exposure to antigens
• active and passive acquired

Active acquired immunity

• immunization
• re-exposure to antigen

Passive acquired immunity

• passive transfer of antibodies
• ex: breastfeeding

Four hypersensitivity reactions

Type I immediate hypersensitivity, type II cytotoxic hypersensitivity, type III immune complex disorders, Type IV delayed hypersensitivity

Type I immediate hypersensitivity

• allergic or atopic disorder
• previously exposed to an antigen
• mast cells are distributed to tissues --> vasodilation
• reactions: hives, urtiaria, nasal and conjunctival discharge

Type II cytotoxic hypersensitivity

• mediated by Igs
• directed toward antigens on cells
• usually a transfusion reaction with incompatible donor
• antibody-mediated cell destruction and phagocytosis

Type III immune complex disorders

• antigen combines with Ig in circulation and these complexes are deposited into tissues
• autoimmune
• organ dysfunction
• system-wide
• ex: systemic lupus erythematosus (SLE) in kidney, blood vessels, lungs, and skin; and rheumatoid arthritis

Type IV delayed hypersensitvity

• initiated by T lymphocytes
• do not attack antigen until days after exposure
• inflammatory reaction = contact dermatitis
• ex: poison ivy and transplant reaction

Rheumatoid arthritis (RA)

chronic autoimmune, inflammatory disorder, affects joints and system

• etiology: unknown; genetic, hormonal, immune, and infectious factors

• s/sx: symmetrical, tender, swollen joints, common in fingers, wrists, hips, knees, and feet

• diagnosis: criteria include morning joint stiffness, polyarthritis, symmetrical arthritis, subcutaneous rheumatoid nodules for ~6 wks

• treatment: early diagnosis/treatment, patient education, diet, exercise

Systemic lupus erythematosus (SLE)

multisystem autoimmune disease, autoantibodies

• etiology: unknown, multiple genetic alterations are possible

• s/sx: fever, skin rash, joint inflammation, and damage to the kidney, lungs, and serosal membranes, fever, fatigue, myalgias, arthralgia

• classic sign: butterfly rash across nose and cheeks

• diagnosis: based on history physical, labs, 11 criteria (no single lab test), anti-nuclear antibody test

• treatment: NSAIDs, corticosteroids, methotrexate

Preventative treatment for HIV

pre-exposure prophylaxis (PrEP) and postexposure prophylaxis (PEP)

After exposure to HIV, ____ must be started within ____ ______ to be effective.

PEP; 72 hours

Mantoux test

• intradermal test that determines presence of tuberculosis

• tb protein is injected into the forearm

• wait for 48 hrs