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HSC-Class 1 Flashcards

0
Q

Define etiology

A
  • causes of disease

- could be physical forces, biological agents, nutritional excesses/deficits or chemical agents

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1
Q

Define Disease

A

study of a cellular and organ changes occurring with diseases, and their affects on body functions

-interruption, cessation, or disorder of a body system or organ structure that is characterized usually by a recognized etiologic agent or agents an identifiable group of signs and symptoms, or consistent anatomic alteration

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2
Q

Define Risk Factors

A

pre-disposers of the disease

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3
Q

Define Pathogenesis

A

-sequence of cellular and tissue events from time of contact with etiological event until expression of disease

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4
Q

Define Manifestation

A

signs and symptoms

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5
Q

Define Syndome

A
  • signs and symptoms characteristics of a specific disease state
  • usually Etiology unknown
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6
Q

Define Complication

A

possible/actual adverse extensions of disease or as a result of treatment

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7
Q

Define sequelae

A

-impairments that are caused by disease

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8
Q

Hematologic System comprise of

A 
RBC
WBC
Platelets
Coagulation Factors
Bone Marrow
Lymph nodes
Spleen
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9
Q

What is atrophy and the conditions which these changes occur

A

-the decrease in cell size

Conditions - disuse, denervation, loss of endocrine stimulation, inadequate nutrition and ischemia

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10
Q

What is Hypertrophy and the condition which this occur

A

-is the increase in cell size and with it an increase in the amount of functioning tissue mass

Two types - physiologic and non-physiologic
Exercising is physiologic
myocardial hypertrophy is pathologic

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11
Q

What is Hyperplasia and what condition does this change occur

A

-increase in the number of cells in an organ or tissue

Physiologic

  • Hormonal (breast and uterine enlargement)
  • compensatory (regeneration of the liver)

Non-physiologic
-excessive hormonal or growth factors

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12
Q

What is Metaplasia and the conditions this occurs

A

-reversible change in which on cell type is replaced with another cell type

  • occurs in response to chronic irritation and inflammation
    eg. smoker
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13
Q

What is dysplasia and what are the conditions which this occurs

A

-characterized by deranged cell growth of a specific tissue that results in different size, shaped and organization.

  • minor degree of dysplasia are associated with chronic irritation or inflammation
  • strongly precursor of cancer
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14
Q

What is Intracellular Accumulation and cite 4 sources

A

-the buildup of substances that cells cannot immediately use or eliminate.

3 Categories

  1. normal body substances (lipids, proteins, carbs, melanin, and bilirubin that are present in abnormally large amounts
  2. abnormal endogenous products, such as those resulting from inborn error of metabolism.
  3. exogenous products, such as tattoo, lead, coal dust
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15
Q

Causes of cell injury

A 
physical agents
radiation
chemical injury
biologic agents
nutritional imbalance
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16
Q

Describe the mechanism whereby physical agent such as mechanical forces produces cell injury

A
  • injury or trauma due to mechanical forces as a result of body impact with another object
  • split and tear tissues, fracture bones, injure blood vessels, and disrupt blood flow
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17
Q

Describe mechanism of extreme temp on cell injury

A
  • burns and severe heat stroke causes injury by inducing vascular injury, accelerating cell metabolism, inactivating temperature sensitive enzymes and disrupting the cell membrane
  • exposure to cold increases blood viscosity and induces vasoconstriction by direct action on blood vessels and through reflex activity of the sympathetic nervous system. The resultant decrease in blood flow may lead to hypoxic tissue injury.
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18
Q

Mechanism of electrical forces on cell injury

A

AC (alternating current) - causes violent muscle contractions, preventing the person from releasing the electrical source.
DC - in and out quick, early cataracts

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19
Q

What is radiation? Differentiate between the effects of ionizing and nonionizing radiation in terms of their ability to cause cell injury

A

-interferes with DNA synthesis and mitosis

Ionizing Radiation affects cells by causing ionization of molecules and atoms in the cell, by directly hitting the target molecules in the cell or by producing free radicals that interacts with critical cell components. It can immediately kill cells, interrupt cell replication or cause a variety of genetic mutations. EG: cancer treatment, occupational/accidental exposure

-UV (just above the visible range) interrupts cellular bonds

Nonionizing Radiation

  • infrared lights, ultrasound, microwaves, and laser energy. Causes vibration and rotation of atoms and molecules =>thermal energy
  • injury from these is mainly thermal involving dermal and subcu injury
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20
Q

What is chemical Injury

A

Drugs - alcohol, prescription, OTC, street drugs
Lead toxicity -paint, glazes, cosmetic (Absorbed via GI tract or lungs)(children more susceptible because their blood-brain barrier is more permeable), can inactivate enzymes, interferes with enzymes for hemoglobin formation. Damages nerves (demyelination). S&S - anemia, fatigue, abd pain, mentation changes

Mercury

  • fish, amalgams in dentistry, and vaccines.
  • depending on the form involving can affect the CNS and kidneys
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21
Q

Explain how the injurious effects of biologic agents differ from those produced by physical and chemical agents

A

Biologic agents differ in that they are able to replicate and can continue to produce their effects. They injure cell by diverse mechanism.

  • Virus enter cell and become incorporated into its DNC.
  • Bacteria secrete exotoxin that interfere with cellular production of ATP
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22
Q

How is nutritional imbalances contribute to cell injury

A

nutritional excesses and deficiencies predispose cell to injury

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23
Q

Describe the three major mechanisms whereby most injurious agents exert their effects

A

Free Radicals

  • highly reactive chemical species with an unpaired electron in the outer orbit. The unpaired electron causes free radicals to be unstable and highly reactive, reacting to nonspecifically with molecules in the vicinity.
  • reacts with proteins, lipids, and carbohydrate (damaging cell membrane, inactivating enzymes, and damaging nuclei acids in DNA)
  • Antioxidants inhibits free radicals

Hypoxic Cell Injury

  • deprives the cell of oxygen and interrupts metabolism and generation of ATP
  • Damage 4-6 min
  • hypoxia can result from air, respiratory disease, vasoconstriction, anemia, edema, or inability of cells to use oxygen
  • hypoxia causes a power failure in the cell, with widespread effects on the cell’s structural and functional components = aerobic metabolism ceases, cell reverts to anaerobic metabolism, using glycogen stores to maintain cell functions, reduced ATP = cell swelling.

Impaired Calcium Homeostasis
-cell usually maintains low intracellular calcium
-when calcium is released into the cell it:
=acts as a “second messenger” inside the cell
=turns on intracellular enzymes, some of which can damage the cell
=can open more calcium gates in the cell membrane which lets in more calcium (calcium cascade)

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24
Q

What is Reversible Cell Injury

A

-impaired cell function, does not result in cell death

Cellular Edema
-reversible when ATP pump reactivates

Fat Accumulation

  • usually do to a disease process
  • Can be partially reversible
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25
Q

What is Programmed Cell Death

A

Cell death occurs by necrosis or by programmed cell death called apoptosis

  • Inhibitors of apoptosis are thought to contribute to cancer and autoimmune disease
  • Apoptosis (cell suicide), controlled cell destruction to remove/replace cells in excess, improperly developed, genetically damaged, worn out

NECROSIS
-cell death and degradation (unregulated)

Cell may undergo

  • liquefaction
  • coagulation
  • infarction

Cell contents are often released
triggers inflammation

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26
Q

Compare dry, wet, and gas gangrene in regards to pathophysiology and physical outcomes

A

-gangrene is applied when a considerable mass of tissue undergoes necrosis. May be classified as dry or moist
DRY
-dry and shrinks, wrinkles, and color dark brown or black
-interference with arterial blood supply to the part without interference with venous return and is a form of coagulation necrosis.

WET

  • area is cold, swollen and pulseless. Skin is moise, black and under tension. Liquefaction occurs and a foul odour is caused by bacterial action.
  • interference with venous return.

GAS

  • special type that results from infection (clostridium)
  • trauma, fractures in which dirt are embedded
  • bacteria produce toxins that dissolve membrane, muscle cell death, edema, hemolysis, renal failure
  • characteristics are bubbles of hydrogen sulfide gas that form in muscle
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27
Q

What are the five cardinal signs of acute inflammation, describe the physiologic mechanisms involved in the production of these signs

A
  • redness, swelling, heat, pain, loss of function

- characterized by exudation of fluid and plasma proteins and emigration of leukocytes, predominantly neutrophils.

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28
Q

Compare vascular and cellular stages of the inflammatory response

A

Vascular
-increased blood flow (vasodilation)
=-increase in capillary blood flow, causing heat and redness.(cardinal sign)
-increased vascular permeability allowing plasma proteins to leave the circulation. This reduces capillary osmotic pressure and increases the interstitial osmotic pressure. In addition, increase in capillary pressure, causes a marked outflow of fluid and its accumulation in the tissue spaces produces
-swelling, pain, impaired function (cardinal signs)

Cellular Stage
-emigration of leukocytes (mainly neutrophils) and their accumulation at the site of injury

Margination + Adhesion (leukocytes accumulate and adhere to endothelium, cytokines released)

Transmigration (Leukocytes move through vessel wall to tissue)

Chemotaxis (Leukocytes are guided by a gradient called chemokines to the site of injury)

Activation and phagocytosis (neutrophils, monocytes, and tissue macrophages engulf and degrade the bacteria and cellular debris

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29
Q

Name and Describe the five types of inflammatory exudates

A

Serous - watery fluids low in protein content that result from plasma entering the inflammatory site

Hemorrhagic exudates- occur when there is severe tissue injury that causes damage to blood vessels or when there is significant leakage of red cells from the capillaries

Fibrinous exudate - contains large amounts of fibrinogen and form a thick and sticky meshwork.

Membranous - develop on mucous membrane surfaces and are composed of necrotic cells enmeshed in a fibropurulent exudate

Purulent - contains pus, which is composed of degraded white blood cells, proteins, and tissue debris.

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30
Q

Contrast acute and chronic inflammation

A
  • in contrast to acute inflammation, which is usually self-limited and short duration, chronic inflammation is self-perpetuating and may last for weeks, months or even years
  • characterized by infiltration with mononuclear cells (macrophages, lymphocytes, and plasma cells) and attempted connective tissue repair involving new vessel formation.

*begins insidiously, often asymptomatic (atherosclerosis, lung disease, rheumatoid arthritis, and Inflammatory bowel disease.

  • macrophages accumulate and release inflammatory mediators
  • fibroblasts proliferate
  • scar tissue forms
  • macrophages mass around foreign bodies
  • connective tissue surrounds and isolates the mass
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31
Q

Causes of Chronic Inflammation

A

Foreign bodies - talc, silica, asbestos, and surgical suture materials

  • Virus, bacteria, fungi, and parasites.
  • diseases that cause excessive and inappropriate activation of the immune system
  • presence of a injured tissue such as that surrounding a healing fracture
  • Obesity, white adipose tissue is to be an active endocrine organ and a source of an inflammatory mediator
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32
Q

Define core temperature

A
  • Core body temperature (36 to 37.5) temperature of the deep body tissue.
  • reflection of the balance between heat gain and heat loss by the body
  • intracranial, intrathoracic, intra-abdominal
  • caused by cytokine induced upward displacement of the set point in the hypothalamus center
  • temp body is almost entirely regulated by the nervous system
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33
Q

Mechanism of heat production

A
  • shivering (hypothalamus impulse, general increase in muscle tone, oscillating rhythmic tremor, which results in heat
  • Physical exertion
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34
Q

Mechanism of heat retention

A

-Vasoconstriction- closing of the arteriovenous shunt

Pilomotor muscle contraction - raises skin hair (goosebumps), traps air and decreases surface area available for heat loss

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35
Q

Mechanism of heat loss

A

RADIATION - transfer of heat through the air (opening of AV shunt)
CONDUCTION - direct transfer of heat from one molecule to another (cooling blanket)
CONVECTION - air currents
EVAPORATION - use of body heat to convert water on the skin to water vapor
EXHALATION
URINE/FECES
HEAT EDEMA
INCREASED HR

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36
Q

Pathogenesis of Pyrexia

A
  • exogenous pyrogen enters body -> engulfed and digested by macrophages
  • interleukin released and travel to hypothalamus
  • prostaglandin binds to hypothalamus which increases the setpoint
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37
Q

Explain intermittent, remittent, sustained and relapsing fevers

A

Intermittent - temp returns to normal at least once every 24h
Remittent - never returns to normal and varies
Sustained - never returns to normal but varies (only minimal)
Recurrent/relapsing - episode of fever with episodes with normal temp, both lasting days at time

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38
Q

Describe the four stage of fever

A

Prodromal - headache, fatigue, general malaise, aches
Chills - chilled, shaking, although temperature rising, AV shunt closed, pilorection, pale skin, rigor
Flush - vasodilation, warm, and redded, AV shunts open
Defervescence - sweating provides heat loss

39
Q

What are treatments for fever

A
  • modifications of the external environment intended to increase heat transfer from the internal to the external environment
  • support hypermetabolic state that accompanies fever
  • protection of vulnerable body organs and systems
  • treatment of the infection or condition
40
Q

Discuss fever in children

A
  • often fever without source
  • immune system not as developed
  • rectal temp of 38 degree or greater requires monitoring and or treatment
  • vaccination have decreased occurrence of some bacterial infections
41
Q

Fever in elderly

A

afebrile or blunted fever response is due to disturbance in hypothalamus ability to recognize change in body state

altered release of endogenous pyrogens

inability to respond to set point change

42
Q

Define Neoplasm and explain how the growth differs with normal adaptive changes in tissues

A

-growth is uncoordinated and autonomous, lack normal cpontrols over cell growth and division
-Normal renewal and repairs involves proliferation, the process of cell division. However it is the genetic change that allow excessive and uncontrolled proliferation that is unregulated by normal growth-regulating stimuli.
Differentiation is the process of specialization where by new cells acquire the structural, microscopic and functional characteristic of cells they replace.

43
Q

What is Benign Neoplasm

A
  • enclosed in a fibrous capsule
  • grow by expansion
  • lost ability to control cell proliferation
  • well-differentiated cell that resemble normal cell
44
Q

Malignant Neoplasm

A
  • no well define capsule or margins
  • lost ability to control both proliferation and differentiation
  • invading/extension surrounding tissues (crablike, cause a release in toxins and enzymes)
  • ability to break loose
  • cancer in situ= is a localized pre-invasive lesion that can be removed or treated
45
Q

Distinguish between cell proliferation and differentiation

A

Cell proliferation is the process of cell division, mechanism for cell replacement when old cells die or additional cells are needed.

Differentiation is the process of specialization whereby new cells acquire the structural, microscopic, and functional characteristics of the cells they replace

46
Q

State the differences in characteristics between benign and malignant neoplasm

A
  • characteristics of turmor cells
  • rate of growth
  • local invasion
  • ability to metastasize

BENIGN

  • well differentiated cells that resemble the cell of the tissue of origin
  • slow, progressive rate of growth
  • grow by expansion and remain localized to their site of origin
  • does not infiltrate, invade or metastasize

MALIGNANT

  • grow rapidly
  • invade and infiltrate nearby tissue
  • lack a well define capsule
  • secrete hormones and cytokines, liberate enzymes and toxins, induce inflammatory response that injures normal tissue
47
Q

Trace the pathway for hematologic spread of a metastatic cancer cell

A
  1. Direct invasion and extension - aided by enzyme secretion
  2. Seeding in body cavities
  3. Metastatic spread thru lymphatic or vascular pathways
    - “Sentinel Node” is the initial lymph node draining cancer cell
48
Q

What is Angiogenesis

A
  • development of new blood vessels
  • growth, wound healing
  • transition of benign state to malignant in tumor
  • process is triggered and regulated by tumor-secreted growth factor
49
Q

How does factors such as heredity, levels of edogenous hormones, obesity and immune system function increase the risk for selected cancers

A

Heredity - cancers exhibit an autosomal dominant inheritance pattern that greatly increases the risk of tumor. The inherited mutation is usually a point mutation occurring in a single allele of a tumor-suppressor gene. A person who inherit the mutant gene are born with one normal and one mutant copy. (In order for cancer to develop, the normal gene must be inactivated, usually through a somatic mutation.

Hormones - the ability to drive the cell division of a malignant phenotype

Obesity - Insulin and growth factor are anabolic molecules that can promote tumor development by stimulating cell proliferation and inhibiting apoptosis, therefore increase the chance of a malignant cell, particularly the breast, and colon. Obesity has been related to chronic inflammation characterized by abnormal production of inflammatory cytokines that can contribute to the development of malignant

Immunologic Mechanism - immune system plays a central role in resistance against the development of tumors. The mechanism provides detection, classification and prognostic evaluation. Development of cancer might be associated with impairment or decline in the surveillance capacity of the immune system.

50
Q

What are the effects of factors such as chemical carcinogens, radiation and oncogenic viruses on cancer development

A

Chemical Carcinogens - binds with DNA, RNA or proteins and cause cell mutation or alteration that alters cell replication and interferes with cell regulatory controls. EG. Smoking, alcohol, smoked meats

Radiation - type of cancer that developed depends on dose, sex, age.

Viral and Microbial Agents - Human papilloma virus (HPV), Epstein-Barr virus (EBV), and human herpevirus 8 (HHV-8), Hepatitis B virus (HBV)

51
Q

Define and Describe typical clinical manifestation of cancer

A
  • the initial manifestations of cancer reflect the function of the primary site of involvement
  • bleeding, hemorrhage, bowel obstruction, SOB, chest pain, abd discomfort, anemia
  • anorexia and cachexia, fatigue and sleep disorders
  • Paraneoplastic syndomes are symptoms unrelated to the tumor site.
  • often as a result of inappropriate hormone
  • Cushing symdrome due to ectopic ACTH production and hypercalcemia.
  • associated with production of circulating mediator that produce hematologic complication
52
Q

Diagnosing of Cancer

A

Tumor Marker (not reliable) - antigen released from tumor, or substances released in response to tumor

Cytologic studies - papanicolaou test, tissue biopsy, DNA microarray

-U/A, X-RAY, MRI, CT, PET

53
Q

Discuss the grading and staging of cancer

A

Grading - microscopic examination of cancer cells to determine their level of differentiation and the number of mitoses.
Grade 1 - neoplasm are well differentiated and Grade 4 poorly differentiated and display marked anaplasia

Staging - determine the extent and spread of the disease. Criteria used is vary with organs, size of tumor, extent of local growth, lymph node involvement, metastasis.

54
Q

What are some treatment for Cancer

A

Surgery
Radiation - ionizing radiation, damages cancer cells moreso than normal. Also damages to all proliferating cells (GI, bone marrow)

Chemotherapy - toxic to all cells

Hormone Therapy - alter abnormal hormonal activity (breast, prostate)

Biotherapy - interferon to inhibit viral replication or tumor protein synthesis

Targeted Therapy - specific to tissue and cell, only developed for certain types of cancer

55
Q

What are factors in determining BMI and explain its use in evaluating body weight ion terms of undernutrition and overnutrition

A
  • Weight(kg)/height(m)
  • if BMI is less that 18.5 then it is considered underweight
  • if BM is more than 30 than it is considered obesity

-upper body obesity if when ratio of waist ratio to hip >1 in men + >.8 in women

56
Q

What are the causes of obesity and health risks associated with it

A 
Causes - diet and physical activity, hereditary, environmental such as eat pattern, inactivity because of labor-saving devices and time spent on the computer and watch TV.
Using food as reward, comfort.
Eat may be ways to cope with tension, anxiety, and mental fatigue
Risk associated
-systemic insulin resistance
-hypertension
-cardiovascular disease (upper body fat more at risk)
-diabetes
-cancer (breast, endometrial)
-gallbladder disease
-osteoarthritis
-menstrual irregularities
-infertility
-skeletal degradation
57
Q

Define Marasmus and Kwashiokor and compare.

A 
Marasmus is a progressive loss of muscle mass and fat stores due to inadequate food intake that is equally deficient in calories and proteins.
Childhood Presentation
-wasted appearance
-loss of SC fat
-protuberant abdomen (muscle hypotonia)
-stunted growth (sign)
-wrinkled skin
-spare/dry/dull hair (sign)
-diarrhea
-slow HR, low BP, low temp
-concurrent infections
Kwashiokor results from a deficiency in protein in diet but high in carbohydrate
Childhood Presentation
-growth stunted but has SC fat
-generalized edema (hypoalbuminemia)
-distended abd
-flaky lesions on skin, face, perineum
-decreased cardiac output, Tachy
-red hair (sign)
-cold extremities
-anorexia, apathy
58
Q

What are the effect of malnutrition on muscle mass, respiratory function, immune function, and wound healing

A
  • decrease in immune cells, wound healing is poor and the body is unable to fight off infection because of multiple immunologic malfunction
  • gastrointestinal tract undergoes mucosal atrophy
  • cardiac muscle leads to decrease in myocardial contractility and cardiac output
  • respiratory function becomes compromised as muscles for breathing becomes weakened
59
Q

State the causes of malnutrition in trauma and illness

A

protein-energy malnutrition often occurs secondary to trauma or illness

  • kwashiorkor like secondary protein-energy malnutrition occurs with hypermetabolic acute illness, such as trauma, burns, and sepsis
  • Marasmus secondary protein-energy malnutrition results from COPD, CHF, cancer and HIV
60
Q

Explain Anorexia Nervosa and its complication

A

-refusal to maintain minimally normal body weight for age and height
-intense fear of gaining weight
-altered perception about own body size, weight and hshape
-amenorrhea happens before 12% BF percentile
-less than 85% normal weight
COMPLICATION
-amenorrhea, loss of secondary sex characteristic
-osteoporosis, kyphosis, compression fractures
-constipation
-cold intolerance, failure to shiver
-decreased HR & BP, dysrhythmias
-hematologic and electrolyte abnormalities
-lanugo
-decreased cognitive function
-inability to recognize the issue
-depression
-alcohol and substance abuse

61
Q

Explain Bulimia Nervosa and its complication

A

-recurrent binge eating and activities including vomiting, fasting, excessive exercise, and use of diuretics, laxatives or enemas to compensate for that behavior.
-recurrent binging 2 or more per week for 3 months
-inappropriate behaviors -> vomitting, laxatives, fasting and exercising
-self evaluation influenced by body shape/weight
-usually maintains normal weight
COMPLICATION
-overeating, vomiting
-dental caries, parotitis(swollen glands), pariodontal disease, fluid and electrolyte disorders
-tooth enamel to dissolve, esophagitis, esophageal strictures
-gastric reflux;aspiration pneumonia
-feeling of shame
-predisposes to metabolic acidosis with hypokalemia

62
Q

Explain Binge Eating

A
  • reuccrent episodes of binge eating at least 2 days per week for 6 months plus at least 2 of the following
  • eating rapidly
  • eating until becoming uncomfortably full
  • eating large amounts when not hungry
  • eating alone because of embarrassment
  • disgust, depression or guilt
63
Q

Define Leukopenia

A

-decrease number of white blood cells in the blood

64
Q

Define neutropenia

A

decrease in number of neutrophils less than 1500/UL

can be further graded as mild, moderate, or severe

65
Q

Define granulocytopenia

A

abnormally low concentration of granulocytes

66
Q

Define aplastic anemia

A

deficiency in bone barrow maturation of all cell types from stem cells
all the myeloid stem cells are affected, resulting in anemia, thrombocytopenia, and agranulocytosis

67
Q

What are two general causes of neutropenia

A

Congenital (kostmann syndrome)
Acquired (drug reaction
neoplasm
autoimmune

68
Q

Describe the mechanism of symptom production in neutropenia

A
  • depends on the severity of neutropenia
  • risk of infection
  • usually the first line of defence against skin and gastro
  • respiratory tract is most serious infection
  • signs of inflammatory response may be absent
  • fever in person with neutropenia should be assumed to be of infectious origin
69
Q

Define infectious mononucleosis and describe the pathogenesis, clinical manifestations, and treatment

A

-self limiting lymphproliferative disorder cause by Epstein-Barr virus, acute phase lasting 2 to 3 weeks
-adolescent and young adult
-oral secretion
PATHO
-penetrates the nasopharyngeal, oropharyngeal, and salivary epithelial cell.
-Spread to the underlying oropharyngeal lymphoid tissue and B lymphocytes.
-infected B cell either dies or incorporate into the genome and becomes heterophil antibodies
CLINICAL MANIFESTATION
-insidious
-initial malaise, anorexia, and chills
-fever, pharyngitis, and lymphadenopathy
-lymph node are enlarged
-hepatitis(nausea and jaundice) and splenomegaly
Complications to 1%
-cranial nerve palsies, encephalitis, meningitis, Guillain0Barre syndrome

70
Q

What is Leukemia

A
  • malignant neoplasms arising from stem cells such as myeloid or lymphoid
  • immature and poorly differentiated
  • long life span
  • proliferate rapidly via blood stream
  • interfere with normal maturation of cells
  • commonly thought as a childhood disease but is 10x more frequent in adult
  • it is classified according to either lymphocytic or myelocytic and whether acute or chronic
  • There are 4 types of leukemias- acute and chronic lymphocytic, and myelocytic leukemia
  • Lymphocytic involve immature lymphocytes and their progenitors that originate in the bone marrow but infiltrate the spleen, lymph node, CNS.
  • Myelogenous leukemia involves the pluripotent myeloid stem cells in bone marrow, interfering with the maturation of all blood cells, granulocytes, erythrocytes, and thrombocytes
71
Q

What is Chronic Myelogenous Leukemia

A

-disorder of the pluriopotent hematopoetic progenitor cell. It is characterized by excessive proliferation of granulocytes, erythroid, and megakaryocytes. CML cells harbor a distinctive chromosome called the philadelphia

Three Phases

  1. chronic phase
    - slow, nonspecific symptoms such as weakness, weight loss. Anemia, and thrombocytopenia develops. Splenomegaly
  2. short accelerated phase
    - enlargement of spleen, fever, bone bane, weight loss, night sweat, bruising.
  3. terminal blast crisis
    - increase of blast cells in blood, infiltration of skin, lymph, bone and CNS
    - symptoms of leukocytosis
72
Q

What is Chronic Lymphocytic Leukemia

A
  • malignancy of the B lymphocyte, most common in adults in western world
  • signs are related to progressive infiltration of bone marrow.
  • often asymptomatic at time of diagnosis
  • lymphadenopathy, hematosplenomegaly, fever, abd pain, weight loss, anemia

Hypogammaglobulinemia -increase susceptibility to infection reflects an inability to produce speciofic antibodies.

73
Q

What is Acute Leukemia

A
  • cancer of the hematopeitic progenitor cells
  • sudden onset
  • symptoms of depressed bone marrow
  • ALL is most common in children and adults
  • AML is mostly older adults
  • anemia, fever, night sweat, weight loss, bruising, bone pain, CNS disorders
74
Q

What are the signs and symptoms of Non-Hodgkin Lymphoma

A

NHL is unknown but related to impaired immune system
unpredictable spread
originates in the lymphatic tissue or nodes
-painless lymphadenopathy
-many will transform into more aggressive form of lymphoma
-fever, night sweats, weight loss
-increase infections

treatment - radiation or chemo, or combined

75
Q

What are signs and symptoms of hodgkin Lymphoma

A

-presence of an abnormal cell called a Reed-Sternberg cell
-HL arises in a single node or grouping and spreads to related lymphoid tissues; whereas, NHL originates at extranodal sites and spreads in a unpredictable fashion
-characterized by large, atypical, mononuclear tumor cells
SIGNS
-lymph node enlargement above level of diaphragm
-night sweats, fever, chills, weight loss, pruritus, anemia

TREATMENT - staged, radiation and chemotherapy

76
Q

Define Multiple Myeloma and its complication

A
  • proliferation of malignant plasma cells in the bone marrow and osteolytic bone lesion throughout the skeletal system
  • abnormal proliferation of marrow plasma cells
  • activation of osteoclasts leading to bone resorption and destruction (prone to fractures) and prone to infection

SIGNS

  • pathologic fracture
  • hyper-viscosity of body fluids
  • heart failure/nephropathy
  • myeloma nephrosis
  • bacterial infections
  • plasma cell tumor
  • bone pain
  • symptoms of bone marrow suppression

Treatment

  • medications
  • highdose chemo and stem cell transplantation
77
Q

Define hemostasis

A

-stoppage of blood flow, to prevent hemmorhage and blood loss
-so either inappropriate clotting or
-insufficient clotting (bleeding)
-compose of platelets,
coagulation systems - plasma protein and clotting factors
endothelium - promote smooth blood flow, inhibits clot formation, synthesis von willebrand factor to promote clotting

78
Q

Stages of hemostasis

A
  1. VESSEL SPASM - smooth muscle contraction + reduce blood flow (less than 1 min)
  2. PLATELET PLUG FORMATION - adhesion of platelets and the addition of platelets because of the VWB factor
  3. COAGULATION CASCADE - activation of two pathways: intrinsic or extrinsic to create a clot to stabilize
  4. CLOT RETRACTION - actin and myosin in platelets contracts and the strands of clot are pulled in, squeezing plasma from clot and causes it to shrink
  5. CLOT DISSOLUTION - conversion of plasminogen to plasma. Plasma will digest fibrin strands and clot dissolve. (FIBRINOLYSIS)
79
Q

State the causes and effects of increased platelet function (hypercoaguluability)

A
  • increase number of platelets, disturbances in blood flow, damage to vessel wall and increase sensitivity of platelets to factors that cause adhesiveness.
  • reactive disorder such as iron-deficiency anemia, splenectomy, cancer.

Increased Clotting Activity
-inherited or acquired disorders altering coagulation such as bed rest, immobility, stasis of blood.

Effects - thrombosis, occulsions, polycythemia vera (excess platelets predispose to thrombosis)

80
Q

What is thrombocytopenia and its manisfestation

A
  • decrease in platelet count
  • either decreased production or increase destruction
  • bruising, purpura, petechiae
81
Q

Describe role of Vitamin K in coagulation

A
  • synthesis in the gut

- necessary for synthesis of factors, prothrombin and protein C

82
Q

Describe hemophilia A and its mechanism

A
  • inherited bleeding disorder affect factor VIII
  • if severe, it occurs in childhood and is spontaneous, if mild, bleeding does not usually happen until local lesion or trauma
  • joint bleeding occurs when a child walks leading to inflammation, pain and swelling
83
Q

Describe Von willebrand disease and its mechanism of bleeding

A

-deficiency of the VWB factor
-defect of platelet function and coagulation pathway
-usually diagnosed in adult
-generally no treatment
SIGNS
-spontaneous bleeding (nose, mouth, GI tract, menstrual)
-normal platelet count with prolonged bleeding time

84
Q

Describe the physiologic basis of acute disseminated intravascular coagulation

A
  • it is not a disease, but a complication
  • widespread coagulation and bleeding

RISK FACTORS

  • obstetric disorders
  • massive trauma
  • burns
  • shock
  • sepsis
85
Q

Describe the effects of vascular disorders on hemostasis

A
  • vascular disorder d/t weakened vessel walls or damage to vessel by inflammation or immune response
  • may not be able to constrict as well or develope von willbrand factor which leads to coagulation disorder.
  • bruising, petechiae, purpura
  • blood work normal
86
Q

Describe the usual cause of anemia

A
  • excessive blood loss
  • hemolysis of RBC
  • deficient RBC production d/t lack of nutritional element or bone marrow failure
87
Q

Describe the manifestations and mechanism of blood loss

A

RAPID - circulatory shock or collapse, d/t loss of intravascular volume
S&S - hypoxemia, shock, heart collapse, symptoms due to loss of blood volume

CHRONIC - due to iron-deficiency anemia and does not affect blood volume. Causes are GI bleeding + menstruation
S&S - pale, weak, fatigue , tachycardia, asymptomatic until low of Hgh less than 8

88
Q

Describe the mechanism and manifestation of hemolytic anemias

A

-premature destruction, retention of iron and compensatory increase in erythropoiesis
S&S - hyperbilirubinemia, jaundice, dyspnea, pigment gallstone, fatigue
-either be intrinsic (hereditary)
-extrinsic (toxin or infection)

89
Q

Explain the causes and risk factors associated with sickle cell anemia

A

-causes is HBs gene and is inherited
-cold, stress, physical exertion, infection, illnesses, hypoxia, dehydration and acidosis
S&S - pain, infarcts to liver, spleen, heart, kidneys, eyes, bone.

Results in chronic hemolytic anemia and blood vessel occlusion

TREATMENT should be as early as 2 months old

  • penicillin
  • antibiotics
  • folic acid
  • dialysis kidney transplant
  • analgesia
  • bone marrow transplant
90
Q

Describe Thalassemia

A
  • inherited gene mutation impairing hemoglobin synthesis resuktin gin rbc weaking/hemolysis
  • a deficiency in hemoglobin due to the decreased synthesis of the affect chain, coupled with excess production of the unaffected chain. The accumulation of the unaffected chain interferes with normal red blood cell production

Manifestation
-bone marrow hyperplasia, bone deformities, splenomegaly, hepatomegaly, iron deposits

91
Q

Describe Iron-deficiency anemia

A

-caused by dietary deficiency, blood loss, increased demands
-because iron is a component of heme, a deficiency leads to decreased in hemoglobin synthesis and consistent impairment of oxygen delivery
S&S
-hypoxia
-pica (neurologic or chemical imbalance)

92
Q

Describe Megaloblastic anemia (VITAMIN b12 and FOLIC ACID)

A
  • caused by impaired DNA synthesis that results in enlarged red cell due to impaired maturation and division
  • two principal causes: vitamin b12 and folic acid deficiencies

VITAMIN B12-Deficiency can be caused by gastritis which damages gut wall so VIT B12 cannot be absorbed (PERNICIOUS ANEMIA)
-inflammation, neoplasms, gastric issues, dietary deficiency

93
Q

What are three causes of aplastic anemia

A
  • exposure to radiation, chemicals, toxin that suppress hematopoiesis
  • bone marrow depression
  • slow and abrupt on set
94
Q

What are chronic diseases/conditions that are commonly associated with anemia

A

-aid, chronic liver failure, cancer, autoimmune disorders, systemic lupus, inflammatory bowel disease, kidney diease

95
Q

Differentiate from primary and secondary Polycythemia Vera.

A

Primary (myeloproliferative disorder)

  • neoplastic disease of bone marrow
  • over production of rbc’s wbc’s and platelets
  • more common in elderly male
  • viscosity rises with the increase in hematocrit
  • hypertension, headaches, dizziness, weight loss, night sweats
  • thromboembolism and hemorrhage due to platelet abnormalities

Secondary

  • increase in erythropoietin as a result of hypoxia
  • causes by living in high altitudes, chronic heart and lung disease, and smoking, COPD.
  • neoplasm that secrete erythropoietin may also be cause of secondary polycythemia

S&S

  • increase viscosity, hypertension, thromboembolism
  • pruritus, pain, discoloration in hands, feet, night sweats, weight loss, gout

Treatment
Primary - phlebotomy, ASA, hydroxyurea
Secondary - underlying disease

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