Module 2 Flashcards
Physical and Chemical Barriers to Infection?
Skin and Mucous Membranes/Secretions
Is the inflammatory response specific or non specific?
non specific
When does the inflammatory response occur?
after tissue injury or infection
Inflammatory Response leads to …
Inflammation and Fever
The inflammatory response is a ____ and ____ protection against invasion by a _____ range of pathogens
immediate, general, wide
What parts of the immune system does the inflammatory response involve?
phagocytic WBC, antimicrobial substances, natural killer cells
Is the immune response specific or no specific?
specific
The immune response leads to …
antigen-antibody response
Self vs Non-self
-host versus foreign substance
-used in the immune response
-leads to recognition and elimination of altered host cells
The immune system develops more ___ and involves _____ cells to combat a ____ ____
slowly; specific; particular pathogen
1st Line of Nonspecific Resistance to Disease
Skin
Mucous Membranes
Mucus
Hairs
Cilia
Lacrimal Apparatus
Saliva
Urine
Defecation and Vomiting
Acid pH of Skin
Unsaturated Fatty Acids
Lysozyme
Gastric Juice
Vaginal Secretions
(these are Mechanical and Chemical Factors)
2nd Line of Nonspecific Resistance to Disease
Antimicrobial Proteins: Interferons and Complement System
Natural Killer Cells
Phagocytes
Inflammation
Fever
Interferons are glycoproteins with _____ activity
anti viral
Important Structures of the Immune System
-Lymph Nodes
-Thymus
-Spleen
-Tonsils
-Red Bone Marrow
How do lymph nodes work in the immune system?
Distributes lymph fluid among the body to remove bacteria and toxins from circulation. Also causes proliferation of immune cells
How does the thymus work in the immune system?
- located in the mediastinum
- produces T lymphocytes
How does the spleen work in the immune system?
-largest lymph organ
-reservoir for blood
-macrophages clear cellular debris and process hemoglobin
How does the tonsils work in the immune system?
-produces lymphocytes
-guard against airborne and ingested pathogens
How does the red bone marrow work in the immune system?
houses stem cells that develop into lymphocytes
Primary Lymphatic Organs
-organs providing the environment for stem cells to divide and mature
-crucial to the inflammatory responses maintenance
-Red Bone Marrow and Thymus Gland
Secondary Lymphatic Organs
-sites where most immune responses occur
-Lymph nodes and nodules, and the spleen
Lymphatic Flow
-lymph flow is similar to blood with a lower protein count and no RBC
-its made in tissue spaces and then gathered in small vessels to carry it to the thoracic or right lymphatic duct
What does lymph flow allow for?
the removal of things to large to cross the capillary membrane
Right Lymphatic Duct
drains the right side of the thorax, head, and neck (1/4 of the person)
Thoracic Duct
drains the lymph for all parts of the body except for the upper right fourth
Pathogen
Disease Agent
Microbial factors to be aware of?
Virulence
Dose
Portal of Entry
Organ Preference
Virulence
refers to how sick a pathogen can make you
What 3 Things does Response to Disease Rely on?
Pathogen (microbial factors, microbes)
Host (resistance, susceptibility, host factors)
Environment (conditions)
Epidemiologic Triangle
Triad of things leading to the disease response: Agent(infectious factor), Host(intrinsic), and Environment(extrinsic)
Agent
originally referred to as infectious microorganism until it became more broad
Biologic Agents
Allergens and infectious organisms
Chemical Agents
toxins and dust
Physical Agents
kinetic energy, radiation, thermal energy, noise
Are social and psychological stressors agents of disease?
yes
Infection
-Host organism’s response to a pathogen caused by tissue destroying microorganisms entering and multiplying in the body
-emia means?
“in the blood”
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
Do Bacteremia and Viremia always become Septicemia?
no, competent immune systems can keep the infection localized
Viruses
- cause infection
-microscopic genetic obligate intracellular parasites - protein coat + nucleic acid core + DNA or RNA
-no Metabolic capability, need host cell
-some can reproduce outside a living cell
-can be dormant for long periods of times and produce symptoms years or months after infections
When do viruses activate?
in times of increased stress
Bacteria
-single celled microorganisms with no true nucleus
-larger than viruses
reproduce by cellular division
-contain cell damaging proteins
Endotoxins
released when the bacterial cell wall decomposes; can cause fever and are not affected by antibiotics
Exotoxins
released during cell growth from bacteria
How are bacteria classified?
-Shape
-growth requirements
-motility
-oxygen requirements
-gram stain
Gram Positive Stains?
purple
Gram negative stains?
it does not stain
Do gram positive or negative have more virulence?
Gram negative
Mycoplasmas
-1/3 the size of bacteria
-can reproduce independently
-NO rigid cell wall
-can cause atypical pneumonia (especially in crowded living conditions)
Rickettsiae
-needs a host for nutrients
-uses cell division
-has a rigid cell call
-infection caused by bite of infected arthropod
Examples of Infections/Diseases caused by Rickettsiae?
Typhus
Rocky Mountain Spotted Fever
Fungi
-non photosynthetic microorganisms
-asexual cell division or sexual division
-all fungi are spore based regardless of division type
-contains a true nucleus
-relatively large
-causes mycoses
Classifications of Fungi
Yeasts
Molds
Yeast
round, single cells, facultative anaerobes (live with or without oxygen)
Molds
filament like, multi nucleated, aerobic organisms
Mycoses
infections caused by fungi that release mycotoxins
When do mycoses become severe?
when the patients immune system is compromised (opportunistic infection) or if the fungi becomes systemic
Most mycotic infections are…
mild (athlete’s foot, candidiasis)
Parasites that cause infection?
Protozoa
Helminths
Arthropods
Ectoparasites
Parasite
depend on host for food and protective environment
Protozoa
-unicellular animals
-transmitted via arthropod vector or contaminated food/water
What causes malaria or amebic dysentary?
protozoa
Helminths
-worm like parasites
-transmitted by ingestion of fertilized eggs or larva penetration of the skin
-common in developing countries
Arthropods
-jointed exoskeleton and paired jointed legs
-can serve as vectors for other diseases
Examples of Arthropods
ticks, mosquitoes, biting flies
Ectoparasites
organism that lives on the outside of the body
How are ectoparasites transmit?
contact with infected clothing, bedding, or grooming articles
examples of Ectoparasites?
mites, lice, chiggers
Normal Body Flora
harmless microorganisms that reside in or on the body
Where is normal body flora found
skin, mouth, nose, pharynx, distal intestine, colon, distal urethra, vagina
Intestinal flora help synthesize …
Vitamin K
When can normal body flora become opportunistic?q
incompetent/compromised immune systems
What are host factors?
factors responsible for the degree to which the individual is able to adapt to the stressors produced by the agent (resistance). These can be controllable or not controllable depending.
Examples of Host Factors
-Genotype/Phenotype
-Nutritional Status
-Immune System
-Social Behaviors
How does environment influence infection?
influences the probability and circumstances of contact between the host and agent
What things does environment include?
sanitation, living conditions, pollution, social/political/economic factors
Chain of Infection
a model to conceptualize the transmission of a communicable disease from its source to a susceptible host
What do we want to do with the chain of infection?
break it!
What are the six links of the chain of infection?
Pathogen - Reservoir - Portal of Exit - Transmission - Portal of Entry - New Host
Reservoir
the habitat in which an infectious agent normally lives or grows (person, animal, environment)
Zoonoses
infectious animal reservoir
Important Cellular Elements in Infection/Inflammation
Granulocytes
Agranulocytes
Red Blood Cells
Platelets
Granulocytes
-Have granules in cytoplasm
-releases histamine and heparin in the inflammatory response
1. Neutrophils and Bands
2. Basophils
3. Eosinophils
Agranulocytes
-lymphocytes
-monocytes
Hematopoiesis
formation of new cells in the bone marrow
Hematopoietic Stem Cell Differentiation
Stem cell –> Common Lymphoid Progenitor –> B-cell or T-Cell –> Plasma Cell and Activated T Cell
Stem Cell –> Myeloid Progenitor –> Megakaryocyte and Erthrythroblast –> Platelets and Erythrocytes
Stem Cell –> Myeloid progenitor –> Leukocytes - - -> Basophils become Mast cells to release histamine and Monocytes become Macrophages
How much of the blood is WBC
less than 1 percent
What do WBC do?
protect the body against harmful bacteria and infection
Pyogenic
pus eating (this is WBCs)
the 3 Granulocytes are…
neutrophils, basophils, and eosinaophils
the 2 agranulocytes are…
monocytes and lymphocytes
Neutrophils
-WBC
-they phagocytosis “pyogenic infections”
Bands
-immature neutrophils (1-3 % of neutrophils)
How much of the Neutrophils are Bands?
1 to 3 %
What is a “shift to the left”?
When mature neutrophils have died battling infection and the average/mean size of the neutrophil gets smaller due to the release of Bands to compensate and the lessening of fighting ability, the whole bell curve shape shift left. This means a more bacterial infection is occurring
What does a shift to the left indicate
a bacterial infection
Basophils
- become mast cells
-involved in allergies and inflammatory responses
-release histamine and heparin once they are mast cells
Eosinophils
- release heparin and histamine
-involved in delayed allergic reactions and parasitic infections - Hay fever leads to decreased amount
Monocytes
become macrophages which phagocytose in severe infections - more delayed in response (2nd responders)
Life span of neutrophils?
48 hours
Lymphocytes indicate what?
viral infection
2 Types of Lymphocytes
B and T Cells
B-Cells
-become plasma cells and release antibodies
T-Cells (T4 and T8)
-regulate cell mediated immunity
-T4 secrete cytokines to amplify inflammatory response, and T8 cells do cell to cell recognition and killing
Macrophages
-scavenger cell created when monocytes enter tissue
-have receptors for Fc region and for complement
-they ingest and process antigen to tag
-secrete cytokines
- in both humoral and cell mediated responses
How do macrophages tag after phagocytosis?
MHC (Major histo compatability complex) - MHCI are normal cell surface markers on all nucleated cells and platelets that are unique to you, while MHCII are specific tags telling T-lymphocytes to kill the macrophage that has phagocytosed an invader
What cytokines do Macrophages release?
TNF(Tumor necrosis factor) and Interleukin-1
What do cytokines cause?
fever
Reticuloendothelial System
-System of macrophages throughout the body that filter and destory invaders, bad stuff, and worn out/abnormal cells
ex of name changing:
Lung - alveolar macrophages
Liver - kupffers cells
spleen - macrophages
lymph nodes - macrophages
intestine- peyers patches
CNS - microglial cells
skin - langerhans cells
connective tissue - histiocytes
Function of Neutrophils
Bacterial Infection
Inflammatory Disorders
Stress
Certain Drugs
Function of Eosinophils
Allergic Disorders
Parasitic Infestations
Function of Basophils
Inflammation
Allergic Reaction
Function of Lymphocytes
Viral Infection
Function of Monocytes
Severe Infection
Relative Count
percentage count of WBC adding up to 100%
Absolute count
actual number of WBC in WBCC/CBC
What do myelocytes indicate if on a blood count smear?
leukemia or severe bacterial infection since theyre only in bone marrow
Absolute Value Equation
Relative Value (% put into decimal) * Total WBC
Relative count values always add to 100%, so…
if one cell type increases, the others must decrease
Relative increase and decreases are _____ but Absolute increase and decreases are _____.
relative = not important
absolute - absolutely important
Total WBC Count
12.8x10^3 cells/mm^3 (12800)
High Neutrophils indicate…
usually pyogenic bacterial infection
Low neutrophil levels might indicate?
cancer
low lymphocyte levels indicate what?
that it probably is not a viral infection
Increased Values are indicated by what suffixes?
-cytosis and -philia
Decreased values are indicated by what suffixes?
-penia
What things can increased WBC count indicate?
infection
inflammation
tissue necrosis
leukemic neoplasia
What things can decreased WBC count indicate?
chemotherapy
radiation therapy
marrow infiltrative diseases
overwhelming infections
dietary deficiencies
autoimmune diseases
What may a persistent increase in WBC count indicate?
worsening of an infection
What may a drastic decrease in WBC count indicate?
bone marrow failure and risk of infection
Critical WBC count values?
anything less than 2500 or greater than 30,000
WBC values are __ related?
age
Normal Newborns and infants tend to have ___ WBC values
higher
Elderly WBC count does what during infection?
potentially does not increase in the presence of severe bacterial infection
ANC
Absolute Neutrophil count
ANC calculation
WBC x(%neutrophils + %bands in decimal) = ANC
ANC critical value
less than 1000
How much of ANC should be bands/stabs?
1-3 percent (if more it indicates a shift to the left)
Serologic Indicators of Inflammation and infection
- ESR - Erythrocyte Sedimentation Rate
- C Reactive Protein (CRP)
3.WBC count and differential
ESR
-Erythrocyte Sedimentation Rate
-Rate that RBC settle out of anticoagulated blood in 1 hour
-RBC form a Rouleaux when inflammation or necrosis is occuring thus leading to an increased ESR
Is ESR diagnostic?
no, just provides info on disease processes to investigate
When does ESR elevate?
in acute infections, it wont elevate for 6 to 24 hours and then peaks after several days
C-Reactive Protein (CRP)
-abnormal liver protein present in blood during any process of necrosis, trauma, inflammation, or infection
-appears rapidly in injury situations
-a classic and most dramatic acute phase reactant increasing 1000x normal rapidly and then rapidly declining
CRP is ____ _____
non specific; can say if theres inflammation, but not where
Culture and Sensitivity - Lab Specimen In Vitro Growth Purpose?
to ID the organism and test antimicrobial effectiveness
Remember that in vitro tests…
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 drug activity
What is serial dilution used for?
to obtain a culture plate yielding a countable number of separate colonies and then calculate number of viable cells in original solution
Gram Negative Bacteria are more …
virulent
Urinalysis
-urine screening test that can give markers of infection due to appearance and color, odor, pH, leukocyte esterase test, nitrates
Vaginal Secretions can cause what in urinalysis?
a false positive on nitrite screening/test
Leukocyte Esterase
urinalysis test used to detect leukocytes in the urine with 90% accuracy
When is a stool culture performed?
when patients have unrelenting diarrhea, fever, and abdominal bloating
Examples of bacteria that can act as pathogens in a stool culture?
Salmonella
Shigella
Campylobacter
Yersinia
Acute Inflammatory Response
a rapid and nonspecific protective response to cell injury of any cause only occuring in vascularized tissue
Acute inflammatory response can only occur where?
in vascularized tissue
“itis”
means inflammation
Acute Inflammatory Response results in …
accumulation of fluid and cells at the inflammatory site
Hallmarks of Inflammation
1.Redness (rubor)
2. Swelling (Tumor)
3. Heat (calor)
4. Pain (dolor)
5. Loss of Function (functio laesa)
What causes swelling, redness, and heat in inflammation responses?
increased capillary permeability leading to more blood in the area
Colonization of microorganisms alone _____ inflammation
DOES NOT PRODUCE (infection may just lead to cell injury and inflammation)
The inflammation reaction of vascularized tissue is …
Active
Aggressive
Nonspecific
The inflammation tissue response is _____ regardless of cause
the same
Causes of inflammation
Infection by microorganisms
Heat burns and cold frostbite
radiation
trauma
chemicals
ischemic damage
Hypoxia
lack of sufficient oxygen (can lead to cell injury and inflammation)
Ischemia
reduced blood supply (can lead to cell injury and inflammation)
Anoxia
Total lack of oxygen
Infarction
cell death
What are hypoxia, ischemia, anoxia, and infarction as they relate to inflammation?
they are etiologic factors of inflammation
You can have ____ without Ischemia, but if theres Ischemia there is always ___
hypoxia, hypoxia
Hyperemia
excess blood in vessels
What is the vascular response of the acute phase response for inflammation?
- Instant vasoconstriction followed by vasodilation leading to swelling (edema) and erythema (redness) due to hyperemia
-The increased capillary permeability allows fluid to escape tissue and cause edema to dilute toxins
-pain and impaired function determine tissue swelling and release of chemical mediators
What is the cellular response of the acute phase response for inflammation?
-WBC move to damaged cells and do phagocytosis of dead cells and microorganisms
-Platelets move to damaged cells and controll excess bleeding
-Mast cells release heparin to maintain blood flow in the area
Granulocyte job in acute phase response?
-neutrophils arrive early to phagocytosis
-eosinophils arrive to release chemical mediators of inflammation for allergies and parasites
-basophils release histamine to mediate inflammation and release heparin for blood flow
-Leukocytosis occurs causing increased WBC count
Mononuclear Phagocyte job in acute phase response?
within 48 hours arrive and become the predominant cell, largest WBC, much longer lifespan, wall off material that cannot be digested to cause chronic inflammation, eat bad stuff, migrate to lymph nodes and play role in specific immunity
Margination and Emigration of Leukocytes in acute phase response?
Blood viscosity increases since fluid is leaving the capillaries which leads to chemical mediator release (kinins, leukotrienes, and histamine) and cytokines to make endothelial cells of the capillaries more adhesive/sticky, marginate the area with leukocytes , and allow emigration/diapedesis through the capillary walls
Diapedesis
movement of leukocytes through the capillary wall once it is more adhesive and marginates with leukocytes
Commonality between histamine, leukotrienes, kinins, and cytokines
all help make the capillary wall more adhesive for leukocyte margination and emigration
Chemotaxis
cytokines (chemokines and IL8), bacterial and cellular debris, and complement fragments (c3a and C5a) allow migration of leukocytes to the localized cellular response for inflammation
4 Steps of the complete Phagocytosis process
- Chemotaxis
- Adherence plus opsonization (cover with Fc or C3a antigen)
- Engulfment (pseudopod inclosure and merge with lysosome and digest)
- Intracellular killing via enzymes, defensins,and toxic product
5 Steps of phagocytosis?
attachment
ingestion
fusion of the lysosome and phagosome
digestion
release of digested products
What cells do phagocytosis
neutrophils and macrophages
Leukocyte
white blood cells
Results of the Acute Phase Response
- changes in concentration of plasma proteins
- increase in ESR
- fever
- increase in leukocyte number
- skeletal muscle catabolism
- negative nitrogen balance
Endotoxins stimulate fever, so what does the body need to do?
break skeletal muscle down for nitrogen when needed
Main chemical mediator of inflammation?
Histamine
Things Histamine does?
-Both parts of vascular response (increased blood flow and increased capillary permeability)
-bronchoconstriction
-gastric acid secretion
Stress ulcers or asthma can be caused by…
histamine
Bradykinin
plasma protease causing increased capillary permeability and pain
Kinin
plasma proteases activated by complement proteins and clotting factors
Prostaglandins (PGE)
-tissue injury leads to their production which makes fever very common (but does not mean infection)
-increase blood flow and capillary permeability
-potentiate histamine effects, cause fever, stimulate pain receptors
What blocks prostaglandins?
NSAIDS like aspirin or ibuprofen (so blocking good prostaglandins in GI tract lead to GI bleeding)
Does fever = infection?
no
Leukotrienes
-increase vascular permeability
-affects WBC adhesion to capillary
-work in chemotaxis
SRSA
-Slow reacting substance of anaphylaxis leading to bronchoconstriction in asthma
-this is due to leukotrienes
Platelet Activating Factor
-from lipid in cell membranes
-affects many cell types
-induces platelet aggregation
-draws in eosinophils
-activates neutrophils
Cytokines
-peptides made by many inflammatory cells and non inflammatory cells (fibroblasts and endothelial cells)
-named according to their function or a numbered interleukin
-act as local hormone to affect host response to injury or infection
-many effects: act as immune and inflammatory communication links (chemotaxis)
Important Chemical Inflammatory mediators/
Histamine
Plasma Proteases (kinin, bradykinin)
Prostaglandins (PGE 1 and 2)
Leukotrienes
Platelet Activating Factor
Cytokines (IL-#)
What chemical mediators cause swelling, redness, and tissue warmth?
histamine
prostaglandins
leukotrienes
bradykinin
platelet activating factor
What chemical mediators cause tissue damage?
lysosomeal enzymes and products released by leukocytes and other inflammatory cells
What chemical mediators cause chemotaxis?
complement fragments
What chemical mediators cause pain?
prostaglandins
bradykinin
What chemical mediators cause fever?
cytokines (IL)
What chemical mediators cause leukocytosis?
cytokines (IL)
Inflammatory Exudate
fluid, plasma protein, and cell contents in inflammation
Serous Exudate
watery, low protein (plasma)
Fibrinous Exudate
fibrinogen –> thick sticky meshwork like a clot
Membranous Exudate
develop on mucous membrane surface–> necrotic cells enmeshed in fibrino purulent exudate
Purulent or Suppurative Exudate
contains pus
Hemorrhagic Exudate
RBC leakage
Difference between Acute and chronic Inflammation?
- Acute - intact immune system leading to self limited and rapidly controlled by host defenses
- Chronic- lasts for a long time, involves fibroblast proliferation rather than exudate leading to increased scarring risk, involves low grade and persistent irritants or moderate/low virulence things that cant spread rapidly or penetrate deeply
Abcess
-localized area of inflammation containing purulent exudate
-fibroblasts can enter and wall it off making antibiotics inaccessible and requiring surgical removal
Ulceration
-inflammation where epithelial surface is necrotic and eroded or as a result of injury to epithelial surface from vascular compromise
-in chronic ulceration, fibroblastic proliferation leads to scarring and chronic inflammatory cell accumulation
Granuloma Formation
-when acute response fails to rid of foreign particles, chronic inflammation occurs leading to a granuloma
-for example, cassius granuloma is due to Tb
-its a 1-2 mm lesion of macrophages surrounded by lymphocytes, where the outside is a collagen network that may calcify and become isolate, but the inside is a decris decay and liquid that has a “cheesy” necrotic center
What things cause Granuloma formation?
foreign bodies like splinters, sutures, silica, asbestos, and microorganism that cause TB and syphilis since they cannot be easily digested and controlled
Tumor Necrosis factor (TNF) and Interleukins cause…
lethargy
Systemic Manifestation of Inflammation/Infectioin
- Lethargy from IL and TNF
- Skeletal muscle catabolism and negative nitrogen balance
- overwhelming infections when other debilitating diseases like cancer are present
- fever due to pyrogenic cytokines
Lymphadenopathy
localized or generalized enlargement of the lymph nodes or vessels
Lymphadenitis
-inflammation of lymph nodes
-nodes may be enlarged, hard, smooth, red, feelt hot, tender
Location of lymphadenitis is indicative of …
where the origin of the disease/infection is
Painful Lymph Nodes are associated with
inflammation
Non-painful lymph nodes are associated with
neoplasms
Opportunistic Infection
infections that occur as a result of altered or weakened host immune systems
Autoimmune disorders
inflammatory response related to injury of ones own body tissue due to a hyperactive immune system
Pyrexia
fever (cardinal manifestation of disease)
A major surgery can be followed by
a normal 48-72 hour low grade fever
The bodys thermostat is the …
hypothalamus
Fever occurs when …
the hypothalamus is reset by the toxins released during the inflammatory process
Pyrogens
fever producers
exogenous: microorganisms
endogenous: macrophages, T4 cells, prostaglandin, bradykinin
What causes hyperthermia
the hypothalamus does not reset so the body keeps heating out of control
How do endogenous pyrogens cause fever?
they stimulate prostaglandin E release from the hypothalamus which causes EP from the adrenal medulla to release and cause shaking chills from a lower calcium concentration and faster firing rate
Stages of Fever
Prodromal
Stage 1: Cold or shaking chill stage
Stage 2: flush
Stage 3: Defervescence
Prodromal Phase
general malaise, aches, pains, energiless - first part of a fever
Stage 1 of a Fever
10-40 minutes with rapid and steady temperature rising and increased cell metabolism leading to no sweating and vasoconstriction = cold/shaking chills
Stage 2 of a Fever
thermostat resets and vasodilation occurs leading to the skin being warm and flushed with potential dehydration
Stage 3 of a Fever
Defervescence - sweating
Defervescence
sweating
Patterns of Fever
- Intermittent
- Remittent
3.Sustained or continuous - Recurrent or Relapsing
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 remains with minimal variation
Recurrent or Relapsing Fever
one or more episodes of fever each lasting several days with one or more days of normal temperature between
Manifestations of Fever
Anorexia
Myalgia
Arthralgia
Fatiguq
Diaphoresis
Dehydration
Metabolic Acidosis
headache
Delirium and confusion
Incoordination and agitation
febrile convulsions
herpetic leasions or fever blisters
Myalgia
muscle aches and pains
Arthralgia
joint aches and pains
FUO
fever of unknown origin: increased temperature of 101 present for more than 3 weeks
100.5 fevers usually..
run their course
fevers of 101 usually..
can sustain, and if so for over 3 weeks must be looked at for a root cause
Persistent fever is a common indicator of…
cancer or liver cirrhosis
Ways to treat fevers?
Modify external environment
treatment of underlying cause
fluid replacement and simple carbs
antipyretics like tylenol, NSAIDS, and ASA (aspirin)
Fever in children…
are very common
When is a child’s fever concerning?
when there is lethargy, poor feeding,k hypoventilation, poor oxygenation, cyanosis
Elders and Fever
- May not have a febrile response or it is blunted
- they have lower basal temperatures, so a low grade fever may actually be more severe for them
- if an elder suddenly is falling, they may have pneumonia or a UTI
