Vocab Flashcards
Pathology
the study and diagnosis of disease though the examination of organs, tissues, cells, and bodily fluids
Physiology
study of mechanical, physical, and biochemical functions of living organisms
Pathophysiology
study of abnormalities in physiologic functioning of living beings
Idiopathic Etiology
Cause is unknown
Iatrogenic Etiology
Cause is a result of an unintended or unwanted medical treatment
Primary Levels of Prevention
Altering susceptibility, reducing exposure for susceptible persons
Ex: Education, immunizations, condoms
Secondary Levels of Prevention
Early detection and screening; prevent further complications
Ex: Breast cancer screening, PAP smears
Tertiary Levels of Prevention
Individual has the disease; looking to get them back to better quality of life
Ex: rehabilitation (PT), supportive care, outreach programs
Incidence
New cases over a time period
Prevalence
Existing cases over a time period
Reliability
Same results when repeated
Validity
Measuring what was intended
Sensitivity
Correctly identifies a condition
Specificity
Correctly excludes a condition
Predictive Value
Ability to predict disease or condition
Morbidity
Causes disease, illness, consequences
Diffusion
Passive transport
Movement of area of high concentration to low concentration
Osmosis
Passive transport
Movement of water via osmotic pressure from high to low concentration
Facilitated diffusion
Passive transport that requires a protein carrier, such as glucose
Ischemia
Lack of blood flow
Hypoxic
Lack of oxygen –> cannot produce ATP
What is the first manifestation of most forms of reversible cell injury?
Hydropic swelling
What is Hydropic Swelling?
Cell swelling due to excess water from sodium/potassium pump malfunction (not receiving enough energy/ATP)
Pump malfunction –> sodium ions build up inside the cell –> water always follows salt –> cells swell
What is Intracellular Accumulation?
Build up of substances due sometimes to faulty metabolisms
- Normal body substance buildup (melanin, lipid)
- Buildup due to metabolic dysfunction (Tay-Sachs disease)
- Exogenous products (black lung filled with coal dust)
How does free radical formation (UV/radiation) cause damage?
Lipid preroxidation by attacking fat
Attacks proteins disrupting transport channels
What is Necrosis?
Tissue destruction that occurs as a consequence of ischemia or toxic injury
Characteristics: cell rupture, spilling of contents into ECF, and inflammation
Coagulative Necrosis etiology
Ischemia –> loss of energy –> inefficiency of sodium potassium pump –> salt build up inside cell –> swelling –> rupture (triggers inflammatory response)
Liquefactive Necrosis etiology
spilled contents –> stimulates inflammatory response –> eaten up by lysosomes –> but healthy tissue gets eaten too –> forms abscesses –> liquid-filled cysts
Fat Necrosis
death of adipose tissue as a result of trauma
Caseus Necrosis
lung damage secondary to tuberculosis
-clumpy cheese appearance in granulomas
What is a gangrene?
Cellular death in a large area of tissue that results in interruption of blood supply to a particular part of the body
Describe Dry Gangrene
- Form of coagulative necrosis
- Blackened, dry, wrinkled tissue separated by a line of demarcation from healthy tissue
- Spreads slowly
Describe Wet Gangrene
Form of liquefactive necrosis (abscesses) typically found in internal organs but also can be seen outwardly
- No strict demarcation
- Spreads quickly
Describe Gas Gangrene
Results from infection of necrotic tissue by Clostridium (anaerobic bacteria)
-Formation of gas bubbles in damaged tissue
What does Apoptosis do?
Intracellular cascade that activates cellular suicide response
- Does NOT cause inflammation
- Neat clean matter through cascade signaling
- No further damage
- Removes dead cells, leaving room for new, better functioning cells
Component Acquired Capability - leading up to cancer
- Self sufficiency in growth signals (autonomous)
- Insensitivity to antigrowth signals
- Evading apoptosis
- Limitless replicative potential
- Sustained Angiogenesis
- Tissue invasion and metastasis
How do Mutator Genes lead to cancer?
Increases the rate of mutation of one or more other genes
What are proto-oncogenes and how can they lead to cancer?
Proto-Oncogenes are normal genes for proliferation (cell differentiation)
Thus when they mutate, they turn into oncogenes, enabling cells for autonomy
What is an oncogene?
An oncogene is a mutated proto-oncogene, aka CANCER CAUSING GENE
What are Tumor-Supressor Genes and how can they lead to cancer?
They are the genes that suppress tumors –> however if they are mutated, they no longer can inhibit the growth of tumors
What are other genes that when mutated, can lead to cancer?
Genes that control apoptosis, genes that regulate repair of DNA damage
Are mutations that occur in somatic cells passed down to progeny?
No
Are mutations that occur in gremlin (stem) cells passed to future generations?
Maybe!
GERD can lead to what type of cancer?
Esophageal cancer
Chronic Pancreatitis can lead to…
Pancreatic cancer
How can viruses cause cancer?
Viruses can insert their own DNA structure/genes –> change the existing genes –> leads to cancer
What are the local effects of tumors?
- Pain (which can be absent until late stages –> late diagnosis)
- Tissue Integrity (compressed and eroded blood vessels, ulceration, necrosis, hemorrhage, frank bleeding)
What are the systemic effects of (malignant) tumors?
- Weight loss and cachexia (anorexia, fatigue, pain, stress due to the increased demands from tumor cells on the body)
- Anemia (lack of RBC)
- Severe fatigue (due to inflammatory changes, cachexia, anemia, stress of treatment schedule, psychological factors)
- Effusions from the inflammation
- Infections (as a result of immunodeficiency)
- Paraneoplastic syndrome (tumor cells release substances that affect neurologic function and may have hormonal effects)
Cachexia
Weakness and wasting of body
Effusions
Fluid buildup in body cavities
How does the TNM Classification System work?
TX = primary tumor, number is based on size N = regional lymph nodes and the number of lymph nodes involved M = distant metastasis; 0 = no metastasis, 1 = metastasis present
For what type of cells is radiation therapy most effective?
Rapidly dividing cells
What are adverse effects of radiation therapy?
Bone marrow depression, epithelial damage, infertility, GI upset
What type of drugs does chemotherapy use?
Antineoplastic drugs
How can a diagnosis of malignancy be confirmed?
Biopsy
Remission of cancer is generally defined as a period in which….
An individual no longer has any detectable signs or symptoms of cancer
What is margination?
Margination is the process of neutrophils and macrophages sticking and accumulating to the blood vessel wall in the area of injury
How do the marginated WBC stick?
They stick via selections which are released by endothelial cells when trigger by cytokines
What is emigration and diapedesis?
The movement of leukocytes out of the circulatory system towards the site of tissue damage or infection
What is chemotaxis and how is it created?
Chemical gradient that promotes leukocytes out of the circulatory system towards the site of injury.
The gradient is created by proteins of the complement system + chemokines
What are the elements of cellular stage of the inflammatory response?
margination, emigration/diapedesis, chemotaxis, phagocytosis
What are the elements of the vascular stage of the inflammatory response?
Bradykinin –> vasodilation –> parin receptors –> mast cells/basophils –> histamine –> (eventually prostaglandins and leukotrienes)
How does increased vascular permeability effect osmotic pressure?
Increased vascular permeability –> outpouring of protein-rich exudate into extravascular spaces –> loss of proteins –> reduces capillary osmotic pressure and increases the interstitial osmotic pressure
What are inflammatory exudates and what are their functions?
Inflammatory exudates: the fluid that leaks out of blood vessels and into nearby tissues in the inflammatory response
- Transport leukocytes and antibodies
- Dilutes toxins and irritating substances
- Transport nutrients for tissue repair
Serous inflammatory exudate =
watery
Sanguinous inflammatory exudate =
bloody
Serosanguinous inflammatory exudate
mostly serous (mostly watery)
Fibrinous
sticky, thick, very high cell content
Purulent
pus, thick, yellow-green, high in WBC and microorganisms
What plasma proteins would show increased levels in diagnostic findings for inflammation?
Fibrinogen and Prothrombin
What is C-Reactive Protein and what does it indicate?
It is a protein not normally in the blood but appears with acute inflammation and necrosis within 24-48 hours
-Inflammatory marker
What is different about RBC when there is inflammation?
They have an increased ESR (erythrocyte sedimentation rate) due to the elevated plasma protein count
-Inflammatory marker
Local effects of inflammation
Redness, swelling, heat, pain, loss of function
Systemic effects of inflammation
Mild fever = pyrexia Malaise Fatigue Headache Anorexia or weight loss
Which leukocytes infiltrate more in chronic inflammation than acute inflammation?
Infiltration by macrophages and lymphocytes instead of neutrophils.
Neutrophils are the first responders in acute inflammation.
What are there increased presences of in chronic inflammation than acute?
Lymphocytes, macrophages, and fibroblasts
What is there less of in chronic inflammation than acute?
There is less swelling and exudate in chronic inflammation than acute.
ASA =
Acetylsalicylic Acid
Example: Aspirin
-lowers prostaglandins synthesis at the site –> decreases inflammatory response –> anti-inflammatory
- Analgesic
- Antipyretic
- Anti-Inflammatory
Can increase bleeding, therefore is NOT given to someone with cuts/wounds
Acetaminophen
Example: Tylenol
It is an analgesic but has no effects on the inflammatory response
Can also increase bleeding
NSAIDs
Non-steroidal anti-inflammatory drugs
Example: Ibuprofen (advil, motrin) or Naproxen Sodium (aleve)
-Anti-Inflammatory, analgesic (relieves pain), and antipyretic
Can increase bleeding
What are the side effects of ASAs and NSAIDs?
Increased bleeding
GI stress
Stomach Ulcerations
Delayed blood clotting
What are glucocorticoids?
Corticosteroids that decrease capillary permeability, decrease leukocytes and mast cells at site
–> decreased release of histamines and prostaglandins
Anti-finlammatory
What are the side effects of Glucocorticoids?
Risk of infection
GI distress
Stomach ulceration
Edema
Increased BP
Atrophy of lymphoid tissue –> decrease in WBC count and hematopoiesis (formation of blood cellular components in bone marrow
Catabolic Effects (tissue breakdown, less protein synthesis ) –> osteoporosis, muscle wasting, thinning of skin
Altered feedback response system –> decrease in release of production of normal hormones –> atrophy of adrenal glands
Delayed healing (and growth in children)
Retention of sodium and water due to aldosterone-like effect in the kidney
Resolution Healing
Minimal tissue damage
Regenration
Damaged tissues replaced with cells that are capable of mitosis and are still functional
Replacement
Functional tissue replaced by scar tissue
Primary intention
Approximated wound edges and ALL areas heal simultaneously
Secondary intention
Heals from the inside out / bottom up
- Greater risk for infection and scarring
- Examples: Pressure ulcers, fractures
What phase of healing occurs 3-4 days after injury?
Proliferative Phase
Foreign material and cell debris removed by phagocytosis and granulation tissue grows into the gap
What phase of healing occurs about 2 weeks after injury?
Remodeling phase
-scar tissue build up
What is hypertorphic scar tissue and how does it complicate healing?
Overgrowth of fibrous tissue, leading to hard ridges of scar tissue or keloid formation
What is ulceration and how does it complicate healing?
The blood supply may be impaired around the scar, resulting in further tissue breakdown and ulceration at a future time.
What is dehiscence?
Previously closed wound reopening
What are the 4 basic stages of inflammation and healing?
Hemostasis (blood clotting) –> Inflammation –> Proliferation –> Remodeling
Why does Hypovolemia impede healing?
Hypovolemia causes decreased blood flow to the affected area, not allowing adequate oxygen and nutrients to the area that promote healing
Briefly describe Autoimmunity
An individual recognizes its own cells as foreign due to a breakdown of self-tolerance, and develops antibodies to their own cells
- it can be polygenic and multifactorial
- can have more than one autoimmune disorder at once
Briefly describe Alloimmunity
An immune response to foreign antigens from members of the same species
Examples: Hyperacute graft rejection, Blood transfusion reaction, Graft vs host disease
What is a hypersensitivity reaction?
A normal immune response that is either inappropriately triggered, excessive, or produces undesirable effects on the body
How does Host Defense Failure happen?
Host Defense Failure is a result from functional decrease in one or more components of the immune system
Ex: AIDS, malnutrition can lead to immune deficiency due to the lack of proteins
What are examples of autoimmunity?
Lupus, a chronic inflammatory disease that effects multiple organs
Addison’s disease
Celiac disease
Grave’s Disease
Hashimoto’s Thyroiditis
Multiple Sclerosis
What are the first clinical indicators of host defense failure?
Signs and symptoms of infection
What is the principle mediating antibody of Type I hypersensitivity reactions and what do they bind to?
IgE binds to sensitized mast cells
What is a severe clinical manifestation of Type I Hypersensitivity?
Anaphylaxis (swelling, hives, itchiness)
How do you manage Type I Hypersensitivity reactions?
Antihistamines Corticosteroids IgE therapy Epinhephrine Immunotherapy Pharmacologic desensitization Stay away from allergen (environmental control)
What is the principle mediating antibody for Type II Hypersensitivity and what is its pathogenesis?
AKA tissue-specific or cytotoxic hypersensitivity, IgG attack antigens on specific cells or tissues
Examples of Type II Hypersensitivity
Transfusion reaction Hyperacute graft rejection (rejection of transplanted donor tissue) Graves Disease (hyperthyroidism - autoimmune) Myasthenia Gravis (neuromuscular - autoimmune)
Describe the etiology and pathogenesis of Type III Hypersensitivity
Immune Complex Reaction
- Antigen combines with the antibody to form a complex that is deposited into tissue, activating the complement system
- Immune and phagocytic systems fail to effectively remove antigen-antibody immune complexes
Examples of Type III Hypersensitivity
- Rheumatoid arthritis
- Immune complex glomerulonephritis
- Systemic lupus erythematosus
Type IV Hypersensitivity etiology and pathogenesis
Delayed response by sensitized T lymphocytes, resulting in the release of lymphokines and other chemical mediators that cause inflammatory response and destruction of the antigen
What is the principle mediating antibody for Type IV?
None!
There are no antibodies involved, but rather it is regulated by T CELLS
Examples of Type IV Hypersensitivity
Contact dermatitis, PPD test (for TB)
A patient reports hives associated with eating peanuts has which type of hypersensitivity reaction?
Type I
What do HLA do?
The Human Leukocyte Antigen are proteins that label cells of the individual
CD8
Cytotoxic T Lymphocytes
CD4
Helper T Lymphocytes (Th1 and Th2)
Th1
Recruit other T cells to the injured area, activate macrophages, and secrete cytokines and chemokines
Th2
Trigger B cells
How are MHC molecules involved in immunity?
Major Histocompatibility Complex display HLAs as MHC-presented peptides on the surface of cells to help immune cells discriminate between normal antigens and those that are foreign/dangerous
Prevents immune system from attacking our own cells as well
MHC 1
Present on virtually all nucleated cells - triggers cytotoxic T cells
MHC 2
Restricted to immune cells, antigen-presenting cells, B cells, and macrophages
The engulfed antigen is then degraded into free-peptide fragments within cytoplasmic vesicles –> complexed with MHC 2 molecules –> present on surface of cell –> T Helper cells recognize them and become activated
Cell mediated immunity involves which type of lymphocyte?
T cells
B lymphocytes are involved in what type of immunity?
Humoral
What is the smallest in size but most common antibody?
IgG
-can cross placenta
Which antibody is best for secondary exposure?
IgG
Which antibody is the first responder to antigens at initial response?
IgM
-supplements IgG on subsequent exposure
Which antibody is found in mucous secretions and is critical in mucosal immunity (part of first line of defense)
IgA
IgD is co expressed with which antibody?
IgM
What does IgD activate?
B cells
Which antibody stimulates histamine/allergic response?
IgE
Which antibody is transferred from mother to fetus through breast milk?
IgG
What is a Titre?
It is a diagnostic test that measures levels of serum immunoglobulins
What does an Indirect Coombs test measure?
Detects Rh blood incompatibility
-affects blood transfusions, mother-child
What does an Elisa test detect?
Detects for HIV antibodies
Receiving the influenza vaccination provides which type of immunity?
Active artificial
What is influenza and how is it transmitted?
Influenza is a viral infection of epithelial cells, leading to infected epithelial cell necrosis of the upper respiratory tract, impairing cilia and mucous production.
Transmitted by respiratory droplet transmission
What are the clinical manifestations of influenza?
Cough, sore throat, nasal congestion/drainage, chills, fever, body aches, malaise, anorexia
What should you avoid giving children with influenza?
Aspirin –> Reye Syndrome
What are the nursing implications when treating influenza?
Droplet precautions!
Symptoms of fatigue, low grade fever, and generalized muscle aches would most likely be present in which stage of acute infection?
Prodromal
What does leukocytosis, specifically neutrophilic, frequently indicate?
Bacterial infections
What would an increase in eosinophils indicate?
Allergic reaction
What does a decrease in leukocytes and or neutrophils indicate?
Immunosupression or bone marrow damage
Hand washing is an example of an action to break the chain of infection at which link?
Means of transmission
Contents of ECF
Sodium, chloride, bicarbonate
Contents of Intravascular Fluid:
protein rich fluid (plasma), large amounts of albumin
Interstitial Fluid
Fluid between cells and location of most extracellular fluid
- hardly any protein
- rich in electrolytes (sodium, chloride, bicarbonate)
Transcellular fluid
contained in specialized body cavities
What is Hydrostatic Pressure/Filtration?
Movement of fluid and solutes from an area of higher hydrostatic pressure to lower
The pressure is created by the weight of fluids that forces fluids through the capillary walls into the interstitial spaces.
Osmolality
osmotic pull exerted by particles per kg of water
What type of pressure influences water movement between vascular and interstitial membranes?
Hydrostatic and osmotic
Why is blood pushed out of the capillary into interstitial compartment?
At the arterial end of the capillary, the blood hydrostatic pressure exceeds opposing interstitial hydrostatic pressure and plasma pressure of blood –> blood is pushed out of capillary into interstitial compartment
How is blood pulled back into capillary
At venous end of capillary, blood hydrostatic pressure is decreased and osmotic pressure is higher –> therefore blood is pulled back into capillary
Describe Hypothalamic Regulation
Osmoreceptors in the hypothalamus regulate the fluid
Pituitary Regulation
Posterior Pituitary releases ADH –> water retention in kidneys
Adrenal Cortical Regulation
Glucocorticoids and mineralcorticoids secreted by adrenal cortex help regulate both water and electrolytes
In Hypotension when there is decreased renal perfusion…
Kidneys release renin –> causes kidneys to release angiotensiongen –> converted to angiotensin I –> then to angiotensin II –> vasoconstrictor to raise BP
Angiotensin II also simulates secretion of aldosterone by adrenal context –> causes tubules of kidneys to increase reabsorption of water and sodium in blood and excrete potassium –> increase in fluid volume
What is the primary extracellular electrolyte?
Sodium!
What is the primary intracellular electrolyte?
Potassium!
Isotonic
Same osmolality as intracellular fluid
Hypotonic
Lower osmolality of ICF (more solutes inside the cell than outside)
Hypertonic
Higher osmolality of ICF (more solutes outside the cell)
What is the most abundant cation in the ECF?
Sodium
What is the ECF low in/ the ICF high in?
Potassium, magnesium, and phosphate ions
In fluid balance at the capillary level, which force is caused by proteins or other molecules that can pull fluid from the interstitial space into the intravascular space?
Osmotic pressure
If cells are in a hypotonic solution…
fluid is pulled IN to the cell, causing the cell to burst
If cells are in a hypertonic solution…
fluid is pulled OUT of the cell, causing the cell to shrink
Aldosterone release causes _____ retention with _____ excretion
Aldosterone release causes sodium retention with potassium excretion
How do Loop Diuretics remove fluid?
They inhibit sodium and chloride reabsorption from the LOOP OF HENLEYS
Example: Lasixs
How does Thiazide remove fluid?
Inhibits reabsorption of sodium and chloride from the DISTAL CONVOLUTED TUBULES
Example: HCTZ
What are Potassium-Sparing diuretics?
Competitive antagonists for aldosterone - lose lots of fluid but retain or reabsorb potassium –> prevents reabsorption of sodium
Clinical manifestations of Hypovolemia
Tachycardia (rapid HR) dry mouth/thirst skin turgor Syncope Low BP Oliguria (low urine output) Low RBC and hemoglobin Nausea Substantial weight loss
Treating Hypovolemia
Correct underlying cause and replace both water and electrolytes
2% weight loss is a
Mild deficit
Moderate deficit is
5% weight loss
8% weight loss is considered
Severe dehydration
Lab analyses check blood of dehydrated patients for…
Electrolytes, bicarbonate, BUN (blood urea nitrogen) (waste product of digestion of protein), creatinine, and specific gravity
Serum electrolytes in Isotonic Dehydration
Stay in normal range
Causes of Isotonic Dehydration
fasting, diarrhea, vomiting, burns, hemorrhage
In Hypertonic Dehydration…
More fluid loss than electrolytes –> increase in serum electrolytes
Causes of Hypertonic Dehydration
Extended fever, diabetes insipidus, DM, reduced fluid intake
What type of dehydration does Diabetes Insipidus cause and how?
Diabetes insipidus causes hypertonic dehydration to the reduction in the release of ADH
Hypotonic Dehydration
Loss of more electrolytes than fluid –> decrease in serum electrolytes
*HYPONATREMIA
What causes Hypotonic Dehydration?
Addison’s disease
overuse of diuretics
Not enough electrolyte intake (only H2O)
What does an overproduction of ADH lead to?
SIADH = syndrome of inappropriate ADH
- water retention –> decreased urine output
- decrease in plasma osmolality; increase in urine osmolality
What is third-spacing?
Fluid shifts out of the blood into a body cavity or tissue and can no longer reenter vascular compartment
Which of the following would cause edema?
Increased hydrostatic pressure
Increased interstitial fluid osmotic pressure
Blockage of lymphatic drainage
Decreased capillary osmotic pressure
All!
Which of the following terms refers to a combination of decreased circulating blood volume combined with excess fluid in a body cavity?
Dehydration
Hypovolemia
Water Retention
Third Spacing
Third Spacing
