Test 1 Flashcards
Health
A state of complete physical, mental, and social wellbeing, and not merely the a sense of disease and infirmity
Determinants of health
- Biology and behavior
- physical and social environment
- gov policies and interventions
- access to quality health care
Disease
Any deviation from or interruption of the normal structure or function of a part, organ, or system of the body that is manifested by a characteristic set of symptoms or signs
Organic disease
Structural changes
Examples of organic diseases
Inflammation, infection, bone break
Functional disease
No morphologic abnormalities
Asymptomatic
Disease present (abnormal physical finding) but NOT associated with symptoms or discomfort
Symptomatic
Disease present WITH associated symptoms
Disease continuum
One end: severe, life-threatening, disabling illness
Other end: complete mental and physical well-being
Pathology and physiology
Deals with the study of the structure and function of cells, tissues and organs within the body
Pathophysiology
The pathology and physiology of disease, focuses on the mechanisms underlying disease
What does pathophysiology do
Basis for preventive and therapeutic health measures and nursing practice
Etiologic factors
Causes of disease
Examples of etiologic factors
Biologic agents
Physical forces
Chemical agents
Nutritional excesses or deficits
Important concepts about etiology
- a single disease agent can affect more than a single organ
- a number of different disease agents can affect the same organ
- most diseases are multifactorial
Etiology
Describes what sets the disease process in motion
Risk factors
Predisposing conditions for a particular disease
Congenital risk factors
Present at birth
Acquired risk factors
Caused by events that occur after birth
Categories of risk factors
- genetic
- disease associated
- treatment associated
- environmental
- lifestyle/behavioral
Pathogenesis
Sequence of cellular and tissue events that take place from the time of initial contact with an agent until the ultimate expression of disease
- how the disease process evolves “how things come to be wrong”
Morphology
The fundamental structure of cells or tissues
- cells -> tissues -> organs -> organ systems
Histology
Relation to morphology
- deals with the study of the cells and extracellular matrix of body tissues
Lesions
Relation to morphology
- Represents a pathologic or traumatic discontinuity of body organ or tissue
Signs
Objective (can be measured) manifestation of an illness or disorder
- can be seen, heard, measured or felt by clinician
Symptoms
Subjective (cannot be measured) evidence of an illness or disorder
- changes in the body or its function that is perceived by the patient as indicating the presence of disease
Syndrome
A compilation of signs and symptoms characteristic of a specific disease state
Complications
Possible adverse extensions of a disease or outcomes from treatment
Sequelae
Lesions or impairments that follow or are caused by a disease
Diagnosis
Designation as to the nature or cause of a health problem
- involves weighing competing possibilities and selecting most likely one accounting for the clinical presentation
What diagnosis is based on
Health history and physical examination
Deductive reasoning
From general to specific
- concerned with the rules for determining when an argument is valid
Inductive reasoning
From specific to general
- concerned with the soundness of inferences for which the evidence is not conclusive
Probability theory
Inductive reasoning
- what is the probability that the conclusion is true given the evidence in question
Major categories of diagnostic tests
- clinical laboratory tests
- tests of electrical activity
- radioisotope studies
- endoscopy
- ultrasound
- x ray
- magnetic resonance imaging (MRI)
- positron emission tomography (PET scan)
-cytologic and histologic exams
Validity
(Accuracy)
- refers to the extent to which a measurement tool measures what it is intended to measure
Reliability
(Consistency)
- refers to the extent to which an observation, if repeated, gives the same result
Reference range
Determined for each test by each laboratory
- usually defined by testing healthy volunteers and plotting the frequency distribution
How reference ranges are conformed
Gaussian bell shaped curse
- hopefully fall in 95 percentile
- ranges are reported as 2 standard deviations away from the mean
Acute disorder
Usually self limiting and relatively severe
Chronic disorder
Implies long term process
- continuous symptoms/severity of disease over time
Exacerbation
Seen in chronic disorders
- varying degrees of aggravation of symptoms/severity of disease
Subacute disease
Intermediate between acute and chronic
- not as severe as acute and not as prolonged as chronic
Preclinical stage
Disease is not clinically evident but is destined to progress to overt clinical disease
Subclinical disease
Not clinically apparent and not destined to become clinically apparent
Clinical disease
Characterized by signs and symptoms
Carrier status
Refers to an individual who harbors an organism but is without clinical manifestation
- does not have the disease but can still infect others
Classifications of disease
- congenital and hereditary
- inflammatory
- degenerative
- metabolic
- neoplastic
Congenital and hereditary disease
Genetic abnormality, intrauterine injury or integration of genetic and environmental factors
Inflammatory disease
Non-specific reaction to an injurious agent
Degenerative disease
Deterioration of various parts of the body
Metabolic disease
Disturbances of cellular energy processes
Neoplastic disease
Benign or malignant
Characterized by abnormal cell growth
Stress response
State of affairs arising when a person relates to situations in certain ways
- successfully adapt
- maladaptive resulting in disease
How are people disturbed by situations
Not by the situation itself but by the way they appraise and react to situations
How stress effects health
Stressful demands that exceed a persons coping abilities result in reactions such as disturbances of cognition, emotion and behavior that can adversely affect health and well being
Homeostasis
Purposeful maintenance of a stable internal environment maintained by coordinated physiologic processes that oppose change
How the physiologic control system works
Opposes change by operating on negative feedback mechanisms
Components of physiologic control system
- sensor that detects change
- integrator/comparator that sums and compares incoming data
- effector system that returns the sensed function to within the set point range
Cannon’s general features of homeostasis
- constancy requires mechanisms that act to maintain it
-steady state conditions require that any tendency towards change automatically be met with facts that resist - the regulating system that determines the homeostatic state consists of a number cooperating mechanisms acting simultaneously or successively
- does not occur by chance, result of organized self governance
Control systems
A collection of interconnected components that function to keep physical or chemical parameter of the body relatively constant
Jobs of control systems
Regulate cellular function
Control life processes
Integrate functions of different organ systems
Negative feedback mechanisms
- maintains stability in system
When function or value decreases below the set point of the system interjects and causes it to increase and vis Vera with an irregular increase
Positive feedback mechanism
- interjects instability in the system
Produces a cycle in which the initiating stimulus produces more of the same
Stress
State manifested bu a specific syndrome of the body developed in response to stimuli
Stimuli
Stressors
- endogenous: internal
- exogenous: external
General Adaption Syndrome (GAS)
- G: the effect is a general systemic reaction
- A: the response is in reaction to a stressor
- S: the physical manifestations are coordinated and dependent on each other
Alarm (stage of GAS)
- CNS aroused and defenses mobilized
- epinephrine and norepinephrine released, increases heart rate, force on contraction, O2 intake and mental activity
Resistance or adaption (stage of GAS)
- Sympathetic NS response
-“adrenaline rush” - body responds to stressor & attempts to return to homeostasis
Exhaustion (stage of GAS)
- continuous stress causes progressive breakdown of compensatory mechanisms
- body can no longer produce hormones and organ damage begins (onset of disease)
Properties of the stressor
Type:
Eustress (good stress)
Distress (disease infection)
Intensity/severity:
Mild
Moderate
Severe
Duration:
Acute
Chronic
Conditions of the person being stressed
Physical, psychological, emotional and social state
Conditions of person being stresses effects
Susceptibility
Adaptive capacity and response
Eustress
Mild, brief, controllable
- perceived as positive stimuli to emotional and intellectual growth and development
Distress
Severe, protracted, uncontrollable situations of psychological and physical health
- disruptive of health
Conditioning factors
Refers to influence of the adaptive capacity of the person
Internal: genetic predisposition, age, sex
External: exposure to envi agents, life experiences dietary, social support
How stress response is mediated
Neuroendocrine-immune interactions
Combined efforts of the nervous and endocrine systems
- they integrate signals received along neurosensory pathways and from circulating mediators in the bloodstream
Stress effect on immune system
- response is meant to protect person from acute threats to homeostasis
- neural response and hormones are usually not around long enough to damage tissues
If a stress response is hyperactive…
Also occurs if stress response becomes habituated
psychological and behavioral changes can become a threat to homeostasis
If a stress response is hypoactive…
Person may be more susceptible to diseases associated with overactivity of the immune system
Hypothalamic-Pituitary-Adrenal cortex (HPA)
Neuroendicrine response
- mediated by glucocorticoids secreted by the adrenal cortex
- cortisol
Sympathetic nervous system (SNS)
Neuroendicrine response
- mediated by catecholamines secreted by the adrenal medulla
- epinephrine and norepinephrine
Major glucocorticoid in body
Cortisol
Functions of cortisol in stress response
- stimulates the breakdown of muscular protein in AA
- help lipids break down fatty acids and glycerol
- promotes hepatic gluconeogenesis (synthesis of glucose) from AA, glycerol and fatty acids
- inhibits tissues from utilizing glucose, making more available to the brain
Permissive action of cortisol
- allows small amounts of glucose to be used for lipolysis and bronchodilation needed for the stress response
- decreases hormone production, reproductive function, bone formation and RBC and WBC formation (inhibits immune response)
Adrenal catecholamines
Epinephrine and norepinephrine
- almost all norepinephrine is converted to epinephrine
- exert their effects in target organs as they travel through alpha and beta receptors
Alpha receptors
- found in arteries in smooth muscle
- when stimulated by epinephrine and norepinephrine, cause arteries to constrict to help return blood to heart
Beta 1 receptors
- located in heart
- when stimulated, cause the heart to beat faster and contract more forcefully to increase cardiac output
Beta 2 receptors
- located in the lungs
- when stimulated cause the bronchioles to dilate
Epinephrine and norepinephrine during stress response
Keep blood glucose levels high, thereby inhibiting metabolic activities like digestion
Epinephrine increases
- Preparation for fight or flight response
- mobilizes energy stores and increases blood glucose and fatty acids
Cortisol increases
- mobilizes energy stores by increasing blood glucose, amino acids and fatty acids
Glucagon increases
Hormone that releases glucose from the liver
- increases blood glucose and fatty acids
Insulin decreases
Allows glucose to stay in the blood
Systems that keep circulating volume and blood pressure high (stress)
Renin-angiotensin-aldosterone system (RAA)
Anti-diuretic hormone system (ADH or Vasopressin)
Renin-angiotensin-aldosterone system (RAA) stress response
- conservation of salt and water
- increase in plasma volume
- increase in arteriolar vasoconstriction to maintain/elevate blood pressure
Anti-diuretic hormone system (ADH) stress response
- increase in plasma volume (control water)
- increase in arteriolar vasoconstriction to maintain/elevate blood pressure
HPA Axis stress response
Secretion of cortisol to mobilize energy stores
- raise blood glucose, AA and fatty acids (use as energy)
Sympathetic nervous system stress response
Epinephrine (facilitated by cortisol)
- raise blood glucose and fatty acids
- vasoconstrict as it flows through alpha receptors that cause the initiation of the RAA system due to less flow to the kidneys
stress effects which hormones
Growth, thyroid, reproductive
Body system adaption to stress Growth
Acute stress: increased levels of thyroid hormones to generate energy and respond to threat
Chronic stress: decreased levels of growth and thyroid hormones (conserve energy)
Body system adaption Immunity
Exact mechanisms unclear BUT share common pathways
Hormones and neuroopeptides can alter immune function
Immune system can modulate Neuroendicrine function
Body system adaption Reproduction
Inhibition of reproductive hormones cause amenorrhea (a sense of menstruation) and infertility
Cerebral cortex and stress
Involved with vigilance, cognition and focused attention
Limbic system and stress
Involved with emotional response (fear, excitement, rage, anger)
Thalamus and stress
Relay center - important in receiving, sorting and distribution sensory input
Hypothalamus and stress
Coordinates response of the endocrine system and autonomic nervous system
Pituitary gland and stress
Releases hormones that govern vital processes
Reticular activating system (RAS) and stress
Modulates mental alertness
Definition of stress
A state manifested by symptoms that arise from the coordinated activation of the neuroendocrine and immune systems
Purpose of hormones and neurotransmitters released during stress
Catecholamines (epinephrine) and cortisol
- alert the individual to a threat or challenge to homeostasis
- enhance cardiovascular and metabolic activity of other systems in order to manage the stressor
- focus the energy of the body by suppressing the activity of other systems that are not immediately needed
What systems are suppressed during stress response
Immune ,digestive and reproductive
What is the stress response designed to be
Acute and self limited
SUPPOSED TO BE
When pathophysiologic changes occur (stress response)
- a component of the system fails
- the neural & hormonal connections among the components of the system are dysfunctional
- the original stimulus for the activation of the system is prolonged or of such magnitude that it overwhelms the ability of the system to respond appropriately
Physiologic stress
Chemical or physical disturbance in the cells or tissue fluid produced by a change, either in the external environment or within the body itself, that requires a response to counteract the disturbance
Components of physiologic stress
- exogenous or endogenous stressors initiating the disturbance
- chemical or physical disturbance produced by the stressor
- the body counteracting response to the disturbance
Adaption
The ability to respond to challenges of physical or psychological homeostasis and to return to a balanced state
- affected by individual differences
Appraisal of the event
Cognitive perception of the meaning or significance of the threat
Coping mechanisms
Emotional and behavioral responses used to manage threats to physiologic or psychological homeostasis
Factors affecting ability to adapt
- previous learning
- physiologic and anatomic reserves
- time
- genetic endowment
- age
- health status
- nutrition
- sleep wake cycle
- hardiness
- psychosocial factors
Effects of acute stress ANS
(fight or flight) pounding headache, moist skin, stiff neck, arousal, alertness, vigilance, cognition, attention
Effects of acute stress (life saving ability)
diversion of blood to essential body function increases alertness and cognitive functional
Effects of acute stress (detrimental)
Overwhelm response mechanisms can be life threatening
Effects of chronic stress
- neural and hormonal connections among the components becomes dysfunctional
- system may become over or under active
- NIOSH: stress in a health hazard of the work place
Effects of chronic stress are linked to
Cardiovascular, gastrointestinal, immune and neurological diseases
Depression, alcoholism, drug abuse, eating disorders, accidents and suicide
Causes of PTSD
Combat, major catastrophic events, airplane crashes, terrorist bombings and rape or child abuse
PTSD is characterized by
Intrusion: occurrence of flashbacks in which past traumatic event is relived
Avoidance: emotional numbing and disruption of important personal relationships - often associated w/ depression
Hyperarousal: increases irritability and exaggerated startle reflex
Treatment of PTSD
Debriefing, crisis intervention, medications for anxiety and depression
Methods for studying physiologic manifestations of the stress responses
- electrocardiographic recording of heart rate
- blood pressure measurement
-electrodermal measurement of skin resistance associated with sweating
Biochemical analyses of hormone levels
Treatment of stress disorders
Relaxation
Imagery
Music therapy
Massage therapy
Biofeedback
Physical and chemical barriers to infections
- skin
- mucous membranes and secretions
Inflammatory response
Non specific
- fever and inflammation
- occur after tissue injury or infection
- immediate and general protection against invasion by a wide range of pathogens
- involves phagocytic WBCs, anti microbial substances, natural killer cells
Immune response
Specific
- identifies self from non-self
- recognizes & eliminates altered host cells
- develops more slowly & involves specific cells to combat a particular pathogen
1st line of defense mechanical factors
- skin
- mucous membrane
- mucus
- hairs
- cilia
- lacrimal apparatus
- saliva
- urine
- defecation & vomiting
1st line of defense chemical factors
- acid pH of skin
- unsaturated fatty acids
- lysozyme
- gastric juice
- vaginal secretions
2nd line of defense internal defenses
- antimicrobial proteins: interferons and complement system
- natural killer cells
- Phagocytes
- inflammation
- fever
Natural killer cells
Help induce apoptosis of viral/tumor cells
Complement system
Proteins kill organisms that don’t belong
Phagocytes
Engulf and destroy bacteria, foreign particles and dead cells
Lymph nodes
- distribute along lymphatic vessels
- filter lymph fluid & remove bacteria and toxins from circulation through phagocytic activity
- proliferation of immune cells
Thymus
- located in mediastinum
- produces T- lymphocytes
Spleen
- largest lymph organ
- reservoir for blood
- macrophages clear cellular debris and process hemoglobin
Tonsils
- Produce lymphocytes
- guard against airborne and ingested pathogens
- last organ to catch pathos before digestion
Red bone marrow
Houses stem cells that develop into lymphocytes
Primary lymphatic organ
Provide environment for stem cells to divide and mature
Red bone marrow: RBC WBC platelets mature
Thymus gland: T cells mature
Secondary lymphatic organs and tissues
Sites where most immune responses occur
Lymph nodes: macrophages
Spleen: macrophages
Lymphatic nodules: collect and filter debris
Lymphatic flow
Drains toxins, waste and infectious things to large blood vessels
- lymph fluids does NOT have RBC but is similar to blood (low protein count)
Microbial factors
Virulence: how serious it is
Dose: how much exposure
Portal of entry: eyes, ears, nose, cut, urethra, anus, surgery
Organ preference
Host resistance
Ability of the body to ward off disease
Host susceptibility
Vulnerability or lack of resistance to disease
Host factors
Age, immunity, genetics, nutrition, underlying or pre-existing diseases, health habits, stress, psychological factors
Environment and disease
Humidity, poor sanitation, crowded living, pollution, dust
Biologic agents
Allergens
Infectious organisms
- viruses, bacteria, mycoplasma, rickettsiae, fungi, parasites
Vaccines can combat
Chemical agents
Toxins
Dust
Physical gents
Kinetic energy
- ex: bullet wounds, blunt trauma, vehicular injuries
Radiation
Thermal
Social and psychologic stressors
Infection
Tissue destroying microorganisms enter and multiply in the body
Categorization by severity
- Minor: colds, ear infections
- life-threatening: sepsis
Sepsis
Infection, contamination
Bacteremia
Presence of bacteria in the blood
Viremia
Presence of virus particles in the blood
Septicemia
Systemic infection in which pathogens are present in the blood having spread from an infection in any part of the body
Viruses
Microscopic genetic parasites
- consist of a protein coat that surrounds a nucleic acid core which may contain RNA or DNA
- have no metabolic capability, most require a host cell to replicate (obligate intracellular parasites)
- some can reproduce outside of a living cell
- capable of remaining dormant for long periods of time
Bacteria
- single celled microorganisms
- no true nucleus
- reproduce by cell division
Cell damaging proteins of bacteria
Endotoxins: released when the bacterial cell wall decomposes
Exotoxins: released during cell growth
Classifications of bacteria
Shape: coccus (spherical), spirillum (helical), bacillus (elongated)
Growth requirements
Motility
O2 requirements: aerobic vs anaerobic
Gram stain: positive purple, negative does not retain stain
Mycoplasmas
- 1/3 the size of bacteria
- capable of reproducing independently
- do NOT have a rigid cell wall
- some cause pneumonia
Rickettsiae
- depends upon host cell division
- have a rigid cell division
- human infection caused by bite of an infected arthropod
Fungi
- non-photosynthetic microorganisms that reproduce asexually (cell division)
- relatively large
- contain a true nucleus
Classifications of Fungi
Yeasts: round, single-celled facultative anaerobes (can live w/ or w/out O2)
Molds: filament-like , multinucleated, aerobic microorganisms
Mycotic infections or mycoses
Infections caused by fungi that release mycotoxins
- most are mild, unless they become systemic or the patient’s immune system is compromised, opportunistic infection
Parasites
- depend on a host for food and protective environment
Protozoa
Parasite
- minute unicellular animals
-transmission by arthropod vector or contaminated food/water
Examples of Protozoa infections
Malaria, amebic dysentery
Helmiths
Worm like parasites
- transmitted by ingestion of fertilized eggs or larva penetration of the skin
- most common in developing countries
Arthropods
Parasite
- have jointed exoskeletons and paired jointed legs
- can serve as vectors for other diseases
Examples of arthropods
Ticks, mosquitoes, biting flies
Ectoparasites
Organisms that live on the outside of the body
- transmitted through contact with infected clotting, bedding or grooming articles
Examples of ectoparasites
Mites, lice and chiggers
Normal body flora
Harmless microorganisms that reside in or on the body
- found on skin and in the nose, mouth, pharynx, distal intestine, colon, distal urethra and vagina
- many useful functions
Normal body flora on skin
About 100,000 per square centimeter
Useful function of intestinall flora
Synthesize vitamin K
Host factors are influenced by
Genotype/phenotype
Nutritional status
Immune system
Social behavior
Environment and infection
Influences the probability and circumstances of contact between the host and the agent
Includes:
Sanitation and living conditions
Pollution
Social, political and economic factors
Pathogen
Disease causing agent
Reservoir
Habitat in which an infectious agent normally lives and grows
Examples of reservoirs
Human: symptomatic or asymptomatic
Animal: zoonoses
Environmental: plants, soil and water
Portal of exit
Path by which an agent leaves the source host
Transmission
How pathogens are passed
Modes of transmission
Direct: direct contact, droplet spread
Indirect: airborne, vehicleborne, vectorborne
Portal of entry
A gent enters susceptible host
Respiratory
Oral
Skin
Intravenous
Gastrointestinal
New host
Final link is a susceptible host
Granulocytes
Type of immune cell (WBC) w/ granules (small particles) w/ enzymes realized during infection, allergic reactions and asthma
Types of granulocytes
Neutrophils
Bands (immature neutrophils)
Basophils
Eosinophils
Agranulocytes
Types of WBC that lacks granules
Types of agranulocytes
Lymphocytes
Monocytes
Cellular elements of peripheral smear
Granulocytes
Agranulocytes
RBC
Platelets
White blood cells
Protect body against harmful bacteria and infection
Neutrophils
WBC type of Granulocyte
Phagocytosis “pyogenic” infections
Basophils
WBC type of Granulocyte
Involved in allergies and inflammatory response
Eosinophils
WBC type of Granulocyte
Release heparin and histamine
- involved in delayed allergic reaction
- has role in parasitic infections
Monocytes
WBC type of agranulocyte
Phagocytosis
Severe infections
Lymphocytes
WBC type of agranulocyte
Viral infections
B-cells
W/ lymphocytes
Mature into plasma cells and release antibodies
T-cells
W/ lymphocytes
Regulate cell mediated immunity
Macrophages
- Lack surface receptors for specific antigens
- Have receptors for Fc region (tail region of antibody) and for the compliment
- ingest and process antigen and deposit it on its own surface
MHC
Group of membrane bound proteins that code for antigens
MHC class 1
Communicate w/ macrophages to alert T cells to destroy foreign antigen (help identify foreign vs host)
Each person has unique
MHC class 2
Send chemicals to T cells to organize the killing of macrophages that have engulfed foreign invades
Secreting cytokines
Job of macrophages
Tumor necrosis factor (TNF) and interleukin-1 which produce fever
Dendritic cells
Mononuclear phagocytes that are another type of antigen presenting cell
- different function than dendritic cells in the nervous system
- communicate w/ innate and adaptive immune systems with central role in fighting infection and maintaining organ integrity
Main function of dendritic cells not NS
Activation of naive T cells not previously subjected to an antigen
Reticuloendothelial system
Destroy abnormal cells or at end of life cells
Lung macrophages
Alveolar macrophages
Liver macrophages
Kupffer’s cells
Tissue macrophages
Lymph nodes and spleen
Intestine macrophages
Peyer’s patches
CNS macrophages
Microglial cells
Skin macrophages
Langerhans’ cells
Connective tissue macrophages
Histiocytes
Absolute WBC count
Actual number
More important
Relative WBC count
Percentage
Finding absolute value WBC
Relative value (%) x total WBC
Increased values of WBC terms
Leukocytosis
Neutrophilia
Lymphocytosis
Monocytosis
Eosinophilia
Basophilia
Decreased values WBC terms
Leukopenia
Neutropenia
Lymphopenia
Monocytopenia
Eosinophilia
Basopenia
Increased WBC count means
Infections, inflammation, tissue necrosis, leukemia neoplasia (cancer)
Also trauma and stress
Decreased WBC count means
Chemotherapy, radiation therapy, marrow infiltrative diseases, overwhelming infections, dietary deficiencies, autoimmune diseases
Age and WBC count
Newborns and infants have higher WBC values
Elderly may not develop increased WBC even with severe infection
Critical WBC values
< 2500 cells/mm3
> 30,000 cells/mmm3
Erythrocyte sedimentation rate (ESR)
Serologic indicator of inflammation and infection
- rate that RBCs settle out of anti-coagulated blood in 1 hour
How ESR works
Inflammatory and necrotic processes cause an alteration in blood proteins, RBCs rend to clump together in a column like manner and thus are heavier and settle out faster when in vertical tube
-NOT diagnostic just provides info
ESR and acute infections
Usually does not elevate for 6 to 24 hours and peaks after several days
C-Reactive Protein (CRP)
Serologic indicator of inflammation and infection
- an abnormal protein synthesized by the liver and present in blood during ant process that involves tissue necrosis, trauma, inflammation or infection
- classic and most dramatic acute phase reactant
NONSPECIFIC
Readings of CRP
Levels increase up to 1000 x normal and decrease rapidly when inflammatory process regresses
Good indication of healing and response to Tx
Culture
Saliva, blood, urine and CSF (cerebral spinal fluid) and other specimen
- sample placed in culture media to allow organism to grow and be identified
Sensitivity with cultures
Antimicrobial effectiveness determined by placing various antibiotic disks on the culture medium
Important to remember about in vitro tests
They do NOT reflect plasma concentrations or attainable concentrations at the site of infection and do NOT take into account local factors (like pH) that may affect the activity of the drug
Serial dilution
Way of performing Calc to determine how many separate colonies are present
- from this a Calc of viable cells in the original suspension can be made
Urinalysis markers of infection
Appearance and color
Odor
PH
Leukocyte esterase
Nitrates
Appearance and color urinalysis
Could may be caused by pus (necrotic WBC, RBC or bacteria)
Pseudomonas may make it green
Odor urinalysis
Foul because of UTI
PH urinalysis
Bacteria may cause increase
Urea-splitting bacteria case urine to be alkaline (increase)
Leukocyte esterase urinalysis
Screening test to detect leukocytes
90% accurate
Nitrites urinalysis
Screening test for identification of UTIs
Bacteria produce an enzyme called reductase which can reduce nitrates to nitrites
50% accuracy
False + if contaminated with vaginal sec reactions
Stool culture
Normal stool contains indigenous bacteria and fungo
Presence of urine may inhibit bacterial growth causing false neg
- unrelenting fever and abdominal pain
- if immunocompromised normal flora in stool can become pathogenic
Pathogenic bacteria found in stool
Salmonella, shingella, campylobacter, yersinia
Acute inflammatory response
Rapid and nonspecific
Protective response to cellular injury from any cause
Can only occur in vascularized tissue
Acute inflammatory response results in
Accumulation of fluids and cells at the site
“-itis” : inflammation
Inflammation
Reaction of vascularized tissue to local injury
It is active, aggressive and nonspecific
NOT synonymous with infection; colonization alone does NOT produce inflammation
Tissue response is the same regardless of the cause
Causes of inflammation
Infection by microorganisms
Heat and cold
Radiation
Trauma
Chemicals
Ischemic damage
Hypoxia
Lack of sufficient O2 in cells
Hypoxemia
Lack of O2 in blood
Ischemia
Reduced blood supply
Gradual porgessive or sudden acute
Arteriosclerosis
Gradual narrowing of the arteries
Causes ischemia
Thrombosis
Complete blockage of an artery by a blood clot
Causes ischemia
Embolus
A blood clot that has traveled from a distant site
Causes ischemia
Anoxia
Total lack of O2
Infarction
Cell death
Acute vascular response
- immediate arteriolar vasoconstriction -> vasodilation -> swelling (edema) and erythema (redness) -> hyperemia
- increased capillary permeability -> allows fluid to escape into tissue -> swelling -> fluid dilutes toxins
- pain and impaired function d/t tissue swelling and release of chemical mediators
Acute cellular response WBC
Move towards damaged cells
Phagocytosis of dead cells and organisms
Acute cellular response platelets
Move towards damaged cells and control any excess bleeding in area
Acute cellular response mast cells
Release heparin to maintain blood flow to area
Acute phase response cellular response
Granulocytes
Mononuclear phagocytes
Margination and emigration of leukocytes
Chemotaxis
Phagocytosis
Acute cellular response neutrophil
Primary phagocyte
- arrive early
- polymorphonuclear (PMNs or polys) or segmented (segs)
Acute cellular response eosinophils
Allergic reactions and parasitic infection s
Release chemical mediators causing inflammation
Acute cellular response basophils
Mast cells in tissues
Inflammation and allergic reaction
Contain histamine -> mediator of inflammation
Acute cellular response Leukocytosis
Increase WBCs
Mononuclear phagocytes
Largest WBC (3-8%)
3-4x longer lifespan
Mature into macrophages
Acute cellular response mononuclear phagocytes
W/in 48 hours monocytes and macrophages are predominant cell type
Can phagocytize larger material than neutrophils
Migrate to local lymph nodes and play role in specific immunity
Role in chronic inflammation -> wall off material that cannot be digested
Margination of leukocytes
- release of chemical mediators and cytokines affect endothelial cells of capillaries
- causes expression of adhesion molecules
- leukocytes marginate (pavementing)
Adhesion molecules
Cause WBC to stick to area of vessels
Pavementing
Moving to the side closer to the invader
Chemical mediators
Histamine, leukotrienes and kinins
Emigration of leukocytes
Follows Margination
Diapedesis (moving) through capillary walls in order to attack
Acute response chemotaxis
- Leukocytes wander through tissue guides by:
Secreted cytokines (chemokines, IL-8)
Bacterial and cellular debris
Complement fragments (C3a C5a) - migration in response to chemical signal -> increases probability of sufficiently localized cellular response
Acute response phagocytosis
Neutrophils and macrophages engulf and degrade bacteria and cellular debris
4 steps of phagocytosis
Chemotaxis: chemical attraction of WBC to area
Adherence plus opsonization: coats the antigen with antibody (Fc) or complement (C3a)
Engulfment
Intracellular killing: via enzymes, defensins, toxic products
Phagocytosis engulfment
Pseudopods surround and enclose particle in phagocytic vesicle (phagosome)
Merge with lysosome
Antibacterial molecules and enzymes digest
Acute phase response
- changes in concentrations of plasma proteins
- increase in erythrocyte sedimentation rate
- fever
- increase in number of leukocytes
- skeletal muscle catabolism (break down)
- negative nitrogen balance
Histamine
Main chemical mediator of inflammation
- released by basophils, platelets, and mast cells
- responsible for both parts of vascular response to inflammation
Vasodilation causes (inflammation)
Increased blood flow + increased capillary permeability
Histamine also stimulates
Bronchoconstriction (H1 receptors)
Gastric acid secretion (H2 receptors)
Plasma proteases
Inflammatory mediator
Contributes to vascular phase of inflammation through fibrinopeptides formed during final step of clotting process
Bradykinins (inflammatory mediator plasma protease)
increases capillary permeability and causes pain
Kinins (inflammatory mediator plasma proteases)
activated complement proteins and clotting factors
Prostaglandins
Inflammatory mediator
- produces from arachodonic acid found in the cell membranes via cyclooxygenase metabolic pathway
- PGE and PGE2 important in inflammation
- increase blood flow and capillary permeability
Cause fever
Stimulate pain receptors
What blocks proglandins
NSAIDs
Ibuprofen, alive, etc
Leukotrienes
Inflammatory mediator
- increase vascular permeability
- affects adhesion of WBC to capillary
- acts as chemo-attractants
SRSA
Slow reacting substance of anaphylaxis
Key role in bronchoconstriction in asthma
Platelet activation factor
Inflammatory mediator
- generated from a complex lipid in cell membranes
- affect a variety of cell types
- induces PLT aggregation
- activates neutrophils
- potent eosinophil chemo-attractant
Cytokines
Inflammatory mediator
- peptide produced by variety of immune and inflammatory cells
- function as local hormones that affect host response to injury or infect
- multiple effects -> serve as a communication link between immune and inflammatory system
Producers of cytokines
Macrophages, monocytes, neutrophils, lymphocytes
Noninflammatory cells: fibroblasts and endothelial cells
Inflammatory cytokines
IL-1, IL-6, TNF, interferon-y
- promote fever and malaise + stimulate T-cell activity
- released from macrophages and monocytes ( IL-1 and TNF) or activated T-cells (IL-6, TNF and interferon)
- activate B-cells: plasma cells and secrete antibodies
IL-2
Cytokine
Decreased by activated T-helper
This with TNF: stimulate cytotoxic T-cells which attack and kill cancer cells or cells infected with a virus
Alerts macrophages to increase phagocytosis
Hematopoietic colony stimulating factors
Increase WBC during infection
IL-10
Noninflammatory cytokine
Decrease activation of B-cells
Inflammatory exudates
Fluid, plasma protein, cell contents
Serous
Watery, low protein (plasma)
Ex: blister that pops
Fibrinous
Fibrinogen -> thick sticky mesh work, like a clot
Ex: strep throat, bacterial pneumonia
Membranous
Develop on mucous membrane surface -> necrotic cells enmeshed in fibrino-purulent (pus) exudate
Ex: colon inflammation
Purulent or suppurative
Contains pus
Pus
WBCs - neutrophils and macrophages, proteins, tissue debris)
Hemorrhagic
Leakage of RBCs (blood)
Acute inflammation
With intact immune system - usually self limited and rapidly controlled by host defenses
Chronic inflammation
Self-perpetuating and last for weeks or months
- involves proliferation of fibroblasts instead of exudates which increases the risk of scarring
Irritants found in chronic inflammation
Typically low grade, persistent (talc, silica, asbestos) or moderate to low virulence (tubercle bacillus, treponema pallium, actinomyces) that are unable to penetrate deeply or spread rapidly
Types of chronic inflammation
Non-specific
Granulomatous
Abscess
A localizes area of inflammation containing a purulent exudate
Typical set up of an abscess
typically have a central necrotic core containing purulent exudates surrounded by a layer of neutrophils
Fibroblasts and abscesses
May eventually enter area and wall off to make it inaccessible to antibiotics
- often requires surgical incision and drainage
Ulceration
A site of inflammation on an epithelial surface (skin and GI tract), have become necrotic and eroded
What is ulceration usually associated with
Subendothelial inflammation
What can cause ulceration
Injury to epithelial surface to because of vascular compromise
Chronic lesions and ulceration
The area surrounding the ulceration develops fibroblast in proliferation with scarring and accumulation of chronic inflammatory cells
Chronic inflammatory cells
Macrophages and lymphocytes
Granuloma formation
Happens when the acute inflammatory response is unsuccessful at ridding the body of foreign particles which causes chronic inflammation
When does granuloma formation occur
When giant cells (fused macrophages) engulf large foreign particles
How granuloma formation works
A 1-2 mmm lesion - mass of macrophages surrounded by lymphocytes
Outside: encases by a collagen network and may eventually calcify -> lesion becomes encapsulated and isolated
Inside: debris decays and forms a liquid that may diffuse out leaving behind only a tick walled casing
What is granuloma formation associated with
Foreign bodies such as splinters, sutures, silica, asbestos and microorganisms that cause Tb and syphilis
Acute phase response: systemic manifestations
- changes in concentrations of plasma proteins: liver increases synthesis of acute phase proteins such as fibrinogen and C-reactive proteins
- increased ESR
- fever
- lethargy (effects of interleukins and TNF)
Systemic manifestations in bacterial infections
^ number of leukocytes
^ number and immaturity of circulating neutrophils by stimulating production in the bone marrow
“Shift to the left”
Increase in the number of bands (immature neutrophils)
Systemic manifestations in parasitic infections and allergic reactions
Eosinophilia
Systemic manifestations in viral infections
Neutropenia and lymphocytosis
Systemic manifestations in overwhelming infections in the presence of other debilitating diseases
Leukopenia
Systemic manifestations in skeletal muscle catabolism & neg nitrogen balance
Amino acids are used for immune response and tissue repair
Lymphadenopathy
Characterized by a localized or generalized enlargement of the lymph nodes or lymph vessels
Lymphadenitis
Inflammatory condition of the lymph nodes
- may be enlarged hard, smooth or irregular
- may be red, feel hot or tender to the touch
Location of node in lymphadenitis
Indicative of the site of origin of disease
- affected nodes are proximally located along the lymphatic drainage pathway
Pain of nodes
Painful: associated with inflammatory process
Non-painful: more characteristic of neoplasms
Opportunistic infection
Infections that occur as a result of altered or weakened host immune system
Autoimmune disorders
Hyperactive immune system
- inflammatory response related to injury to one’s own body tissues
Pyrexia
Fever - elevation in body temp
- cardinal manifestation of disease
- raised by toxins released during inflammatory process
- do NOT minimize or ignore
Fever following major surgery or MI
Low grade temp is normal for 1st 48-72 hours
Where is body’s thermostat
Hypothalamus
Pyrogens
Fever producers
Exogenous pyrogens
Gram +/- bacteria
Endotoxins
Viruses
Fungi
Yeast
Protozoa
Endogenous pyrogens
PMNs
Macrophages
T4 cells release fever producers in response to injury (IL1,IL6, TNF)
Malignancies, Ag-Ab reactions and graft rejections
Fever production
Endogenous pyrogens stimulate release of PgE from hypothalamus
Stimulates release of NE from adrenal medulla
Lowers Ca around hypothalamic cells
Increases firing rate
Prodromal stage of fever
General malaise, fleeting aches and pains
Stage 1 of fever
Cold and shaking chill state
- 10-40 min with rapid, steady rise in Temp ->
- cellular metabolism ->
- vasoconstriction and cessation of sweating
Stage 2 of fever
Flush stage
- Thermostats rest cutaneous vasodilation ->
- Skin warm and flush ->
- Dehydration
Stage 3 of fever
Defervescence
- initiation of sweating
Intermittent fever
Returns to normal at least every 24 hours
Remittent fever
Varies a few degrees in either direction
Sustained or continuous fever
Increased temperature with minimal variation
Recurrent or relapsing fever
One or more episode of fever each lasting several days with one or more days of normal temp b/w episodes
Fever of Unknown Origin
T> 101 present for > 3 weeks
Causes: malignancies, infections, cirrhosis
Treatment for fever
- Modifications of external environment: tepid baths & cooling blanket
- treatment of underlying causes
- fluid replacement and simple carbohydrates
- antipyretics: acetaminophen, NSAIDs, ASA (aprinin)
fever in children
- Common: 2/3 of all children < 3 yrs
- low vs high risk: based on prob of progression to bacteremia and meningitis
- S/S toxicity: lethargy, poor feeding, hypoventilation and poor O2, cyanosis
Fever in elderly
- normal body temp and circadian pattern often altered in elderly
- lower basal temp
- 20-30% with serious infection present with absent or blunted febrile response
only liquid tissue
Blood
Has some solid components
RBC WBC platelets
Composition of blood
-Plasma (55%)
About 50% water
About 5% plasma substances
-Formed Elements (45%)
Less than 1% WBC and platelets
Almost 45% RBC
Plasma proteins in blood
Albumin, globulins, fibrinogen, electrolytes, dissolved gases, waste products of metabolism, nutrients, vitamins, cholesterol
All cells start as
Pluripotent stem cells
Control of progenitor cell differentiation
- hematopoietic growth factors (stimulate cells to proliferate and differentiate)
- each progenitor cell responds to only a certain growth factor
- some growth factors act non-specifically on several
Where are many growth factors released from
Immune and inflammatory cells
Colony stimulating factors
Growth factors for specific lines of cells
- GCSF: granulocyte colony stimulating factor erythropoietin
RBCs
- no nucleus, mitochondria or ribosomes
- cannot reproduce
- contain hemoglobin that carry O2 to cells
Shape of RBCs
Biconcave disks
High surface area allows for rapid diffusion
Small and flexible -> squeeze through capillary beds
Growth of RBCs
- unipotential stems cells are in bone marrow
- response to growth factors and become erythoblasts (6 days in bone marrow)
- turn into reticulocytes (1 day in bone marrow one day in blood)
- become erythrocytes (RBC)
Lifespan of erythrocyte
120 days
Required for synthesis of erythrocyte
Iron, folic acid, vitamin B12
Erythoblast
Progenitor for Erythrocyte
Reticulocyte
Immature RBC
Erythrocyte
RBC
Myeloblast
Progenitor for granulocyte
Monoblast
Progenitor for monocyte which becomes macrophages
Prolymphoblast
Progenitor for lymphoid stem cells which become B-lymphocytes and T-lymphocytes
Breakdown of RBCs
RBC disintegrate and release Hgb into circulation
Liver and spleen and breakdown of RBCs
Phagocytize old RBCs
- globulin: converted into AA (build into proteins) to be reused in body
- iron: stored in liver and spleen until reused
- rest of molecules: converted to bilirubin and excreted in stool a bile or in urine
Transferrin
Carries iron to bone marrow where Hgb synthesized
Hemoglobin
Consists of heme and protein globulin
- about 300 molecules per RBC
Hemoglobin binding sites
4 sites for O2 per Hgb
Abnormal Hgb molecules
> 100 types that carry O2 poorly and can make patients anemic
Hematocrit
% of blood taken up by RBCs
Range depends on sex and age
Rules of 3
RBC x 3 = HGB
Hgb x 3 + Hct
Mean Corpuscular Volume
MCV = Hct / RBC
Relates to cell size
Normal: 87 - 103 micrometer^3
Microcytic
Cells too small in size
Normocytic
Cells of normal size
Macrocytic
Cells too large in size
Mean Corpuscular Hemoglobin Concentration
MCHC = Hgb / Hct
Norm: 32- 36 g/dL
Hypochromic
Cells with too little Hgb
Normochromic
Cells with normal amount of Hgb
Hyperchromic
Cells with too dense Hgb
Mean Corpuscular Hemoglobin
MCH = Hgb / RBC
Normal: 27 - 32 pg
Reflects both size of RBC and concentration of Hgb in RBC
Low value of MCH
Cause hypochromia or microcytosis or both
Not particularly helpful because it doesn’t differentiate
Red cell distribution width
Standard deviation of the MCV
Measure of the degree of uniformity of RBC size
Thalassemia
Uniform sized cells (normal level RDW)
Iron deficiency anemia and clinical descriptors
Decreased cell size
Increased RDW
Problem with MDW
Sensitivity is high but specificity is low
So if it is normal you can rule out iron deficiency anemia but if its high it can be many types of anemia
Reticulocyte count
The number of RBCs containing RNA (convert to DNA within 24 hrs)
Good indicator of bone marrow function
Most reliable measure of RBC production
Reticulocyte count (# of reticulocytes vs %)
Automated methods more accurate than manual
Absolute Reticulocyte count
% reticulocytes x RBC count
Spherocytes
RBC shape
Small and round
Decrease O2 carrying ability
Ellipyocytes
RBC shape
Elliptical or oval
Decrease O2 carrying ability
Sickle
RBC shape
Crescent shaped
Decrease O2 carrying ability
Target cells
RBC shape
Thin cells with less Hgb
Anisocytosis
Abnormal size of RBC
Caused by severe anemia
Poikilocytosis
Abnormal shape of RBC
Caused by severe anemia
Spherocytosis
Spherical RBCs without pale center
Caused by heredity
Stomatocytosis
RBC with slit-like areas of enteral pallor
Caused by congenital hemolytic anemia
Target cells on peripheral smear
RBCs with dark center + periphery and clear ring in between
Caused by thalassemia and hemoglobinopathies
Basophilic stippling
Punctuate stippling when Wright-stained
Caused by lead posioning
Anemia
Decreased RBCs or Hgb or Hct
Causes of Anemia
Disorder in RBC production
Evelvated loss of RBCs
- chronic bleeding (loosing a little everyday for months)
- sudden hemorrhage (trauma)
- excess lysis/cell destruction (destroying more than making)
Anemia symptom expression depends on
Duration and severity
Age and health status of host
Symptoms of anemia manifestation
Relates to reduction in delivery of O2 to cells (hypoxemia)
Symptoms of anemia
- Listlessness, FATIGUE, irritability, WEAKNESS, PALLOR
- ^ RR DYSPNEA AND SOB, - ^ HR, palpitations, angina (chest pain)
- heart failure & ischemia id pre-existing CV disease: pictorial, intermittent claudication, dizziness or giddiness
Classifications of anemia
Rate of development: acute or chronic
Morphology (shape)
Hemoglobin content
Type of defect or etiology
Production defect
Lack of necessary building blocks to make RBCs
Destruction defect
Bone marrow destruction or hemolysis
Genetic defects in Hemoglobin
Sickle cell anemia
Microcytic hypochromic anemia causes
Iron deficiency
Thalassemia
Chronic systemic diseases
Microcytic normochromic anemia causes
Chronic systemic disease
Normocytic normochromic anemia causes
Anemia of chronic disease
Acute blood loss
Hemolytic anemia
Renal failure
Liver disease
Hypothyroidism
Sickle cell anemia
Hypersplenism
Normocytic hypochromic anemia causes
Lead poisoning (plumbism)
Chronic systemic diseases
Normocytic hyperchromic anemia causes
Hereditary spherocytosis
Marcocytic normochromic anemia causes
Folic acid deficiency
Vitamin B 12 deficiency
Alcoholism
Chromic liver disease
Hypothyroidism
Aplastic anemia
Myelodysplastic syndromes
Drug induced (chemo)
Macrocytic hypochromic anemia causes
Some Macrocytic anemias with superimposed iron deficiency
Disorders of Red Cell production anemias causes
Inadequate/inaccessible iron
Lack of folic acid
Lack of vitamin B12
Lack of globulin
Bone marrow disease (leukemia)
Deficiency of erythropoietin (as in renal failure)
Causes of aplastic anemia
Idiopathic
Radiation
Chemo
Aplastic anemia
Disease where the body stops producing enough new blood cells
Lab results of aplastic anemia
Normocytic
Normochromic
Decreased Reticulocyte count
S/S of aplastic anemia
Hypoxemia
Decrease in bone marrow function (myelosuppression)
Infection
Bleeding
Tx for aplastic anemia
Stop drugs
Transfusions
Bone marrow transplant
Causes of iron deficiency
Decreased intake or absorption
Chronic blood loss
S/S of iron deficiency
Hypoxemia
Lab results of iron deficiency
Microcytic
Hypochromic
Increase total iron binding capacity
Decreased ferritin
Tx of iron deficiency
Iron- dietary, supplements, parenteral iron (IV)
Iron deficiency anemia
Microcytic (decreased MCV)
Hypochromic (decreased MCHC)
Decreased production of Hgb due to decreased availability of iron
Most common cause of anemia (all ages)
Iron deficiency
Menorrhagia
Heavy menstrual bleeding, often with clots for 7-10 days
One of the most common causes of iron deficiency anemia
Occult GI loss
Up to 50-75 mL of blood per day
Even a well-balanced diet and increased Fe uptake by transferrin cannot offset losses
One of the most common causes of iron deficiency anemia
Normal serum iron results
Male: 75-275
Females: 65-165
Newborn: 100-250
Child: 50-129
Where iron in the body is stored
70% in Hgb of RBCs
30% in form of ferritin and hemosiderin
Serum iron tests
Test usually measures iron bound to transferrin
Provides indirect measure of rate of dilevery to tissues
Of little diagnostic value by itself
Serum iron tests affected by
Hemolysis, time of day, transfusion, menstruation, supplementation
Iron-phosphorous-protein complex
Contains about 23% iron
Formed in intestinal mucosa by union of ferric iron with the protein apoferritin
Serum ferritin test
Amount of ferritin is directly related to total body iron stores
Good marker for iron deficiency anemia
Contradictions of serum ferritin test
Increased tissue damage causes false elevation
Administration of iron supplements ^ levels 2-3 for oral and within 24 hrs for parenteral
Not affected by blood transfusion
Transferrin concentration test
Transferrin is globulin in the blood that binds and transports iron 1/3 bound with iron 2/3 reserve
Can be measured directly or estimated from the total iron binding capacity (TIBC)
Total iron binding capacity (TIBC)
Maximum iron-binding capacity of transferrin and other iron binding globulins
- some labs do not perform - more of an indication of liver function and nutrition
Transferrin and iron stores
Inversely relates b/c stores are there and don’t need to move as much
Things that affect transferrin
Inflammation, loss of protein, nutritional status, liver disease
Transferrin saturation test
The % of transferrin and other mobile iron-binding proteins that are saturated with iron
The ration of serum iron to iron binding capacity
Transferrin sat (%) = [(serum iron level)/(TIBC)]
Normal transferrin saturation
20-50%
Iron deficiency associated with low sat (<15%)
Dietary iron
10-20 mg Fe in average diet
Only 1-2 mg of Fe absorbed from intestines
Menstruating females and dietary iron
Lose 30 mg with each period
Pregnancy and children birth and dietary iron
Loss of 650 mg to fetus and intrapartal bleeding
Storage of dietary iron
500-1500 mg stored as ferritin and hemosiderin in reticuloendothelial cells of macrophage system (liver, spleen and bone marrow) and muscle as myoglobin
Manifestations of iron deficiency anemia
Same as those for all anemias
- brittle, spoon shaped nails
Glossitis
Web in upper esophagus
Pica
Glossitis
Smooth, red sore tongue
Pica
Habitual eating of non-nutritive substances (clay, laundry starch, ice, paint)
Tx of iron deficiency anemia
Correct underlying causes
Ferrous sulfate given with meals
- give liquid form w/ straw bc stains teeth
- IM must use Z-track tech in deep tissue
Reticulocytosis in 4-5 days
Therapy
Transfusion
Megaloblastic anemia
Impaired synthesis of DNA in RBC precursors in bone marrow
Macrocytic, ^ MCV and fewer in number
Causes of megaloblastic anemias
Most often due to Vitamin B12 or folic acid deficiency
Vitamin B12
Must be supplied in food: meat, eggs, milk, cheese
Absorbed in terminal ileum
Absorbed only when in complex with intrinsic factor
Largely stored in liver
Intrinsic factor
A mucoprotein secreted by parietal cells of gastric mucosa
Help absorb Vitamin B12 by binding with ingested cobalamine (VB12) and then adhering to receptor site in the distal ileum where it is absorbed into the blood and transported to the lover for storage or bone marrow for erythropoiesis
How vitamin B12 cause anemia
Dietary inadequacy
Intrinsic factor problem (does not produce for years)
Decreased Absorption from defect in ileum
Consumption by parasites or unusual bacteria
Serum vitamin B12 and folate test
Vitamin B12: 100-700 pg/ml
Folic acid: 2-20 neg/ml
Interfering factors of serum vitamin B12 and folate test
VB12: ^ in pregnancy, oral contraception, high does Vitamin A or C, smoking
Folic acid: folic acid antagonists, hemolysis, transfusion
Pernicious anemia causes
Inadequate production of IF (intrinsic factor)
Interference with bonding of IF-cobalamine (type 1 blocking antibody)
Interference with bonding of IF and cobalamine complex at the ideal receptor sites (type 2 binding antibody)
Test with intrinsic factor antibody test
Causes of vitamin B12 deficiency
Decreased intake, intrinsic factor or ETOH use
Vitamin B12 lab results
Macrocytic
Normochromic
Decreased B12
S/S of VB12 deficiency
Hypoxemia
Neurological symptoms
Premature grey hairs
Vitiligo
Low BP
Lemon-yellow skin
Fever
Splenomegaly
Yellow-blue color blind
Neurologic VB12 deficiency S/S
Early:
Inability to preform fine motor skills
Loss of vibratory sense and 2 point discrimination
Progressive:
Paresthesias (hallmark of VB12 def) numbness and tingling
Weakness
Uncoordination
Ataxia
Personality changes
Late:
Urinary/fecal incontinence
Spastic paralysis
Confusion
Psychosis
Tx of VB12 deficiency
^ VB12 in diet
Parenteral VB12
Other causes of VB12 deficiency
Pernicious Anemia
Total gastrectomy (removes source of intrinsic factor)
Vegetarian diet
Chronic alcoholism
Spruce and celiac disease
Resection of ileum
Causes of folic acid deficiency
Decreased intake
Increase ETOH use
Increased demand
Drugs
Lab results folic acid deficiency
Macrocytic
Normochromic
Decreased serum folate
S/S folic acid deficiency
Hypoxemia
Tx of folic acid deficiency
^ intake
Supplements
Causes of acute anemia d/t blood loss
Trauma
Surgery
Lab results of acute anemia d/t blood loss
Normocytic
Normochromic
^ Reticulocyte count
S/S of acute anemia d/t blood loss
Volume depletion
Decreased BP
^ HR
Shock
Tx of acute anemia d/t blood loss
Hemostasis
Oxygen
Transfusion
Causes of chronic anemia d/t blood loss
GI bleed (ulcer)
Menstruation
Lab results of chronic anemia d/t blood loss
Microcytic
Hypochromic
^ Reticulocyte count
S/S of chronic anemia d/t blood loss
Hypoxemia
Tx of chronic anemia d/t blood loss
Treat cause
Iron therapy
Anemia of chronic disease (anemia of inflammation)
Very common
Seen with malignancy, chronic infection or inflammation
Anemia of chronic disease lab results
Typically Normocytic and normochromic
Or slightly hypochromic
Results of anemia of chronic disease
RBC survival softened but no compensatory ^ in production
R/T hyperactive immune system resulting in ^ destruction w/out ^ production
Polycythemia
Defined as an abnormally high total red cell mass
Hct> 50% taken up by RBC
Often accompanies rise in WBC and PLT
Relative polycythemia
Hct rises with loss of plasma volume
Absolute polycythemia
Primary = polycythemia Vera - common in men between 40-60, proliferative disorder
Secondary = arises from an ^ in erythropoietin, usually as compensation rom chromic hypoxia
Complication of polycythemia
^ blood volume and viscosity
Viscosity can interfere with cardiac blood flow
Hypertension
Venousstasis
Thromboembolism
Treatments for polycythemia
Primary: focus is to reduce blood viscosity, often with periodic phlebotomy, drug therapy or bone marrow transplant
Secondary to hypoxia: correct that proble with O2
