1
Q
What is pathophysiology?
A
The study of the FUNCTIONAL changes of the normal structural, mechanical, and physical, and biochemical functions of our cells, tissues, and organs as a result of disease, injury, or condition
2
Q
Why Study Pathophysiology?
A
- Helps the nurse recognize the underlying mechanisms of disease that the patient is manifesting as clinical signs and symptoms
- Nurses use pathophysiology every time they come in contact with a patient
3
Q
Patho 4 interrelated topics
A
Etiology
Pathogenesis
Clinical manifestations
Treatment
4
Q
Pathology meaning
A
-Study of the STRUCTUAL (anatomical/physiological) changes in cells, tissues and organs caused by disease or injury
-Biopsy or autopsy FINDINGS are used to make a DIAGNOSIS of disease and PROGNOSIS of healing
5
Q
Pathologist’s use …
A
Findings/diagnostics to determine diagnosis, prognosis, and treatment
6
Q
Biopsy
A
Tissue removal from living individual
7
Q
Autopsy
A
Postmortem
Tissue removal following death of individual
8
Q
Tissue samples
A
From either biopsy or autopsy will undergo microscopic, genetic, biological, and/or chemical diagnostic analysis
9
Q
Findings
A
The diagnostics
Results of the lab and imaging tests utilized by the pathologist to determine diagnosis, prognosis, and treatment protocol
10
Q
Diagnosis
A
The identification of the specific disease
11
Q
Prognosis
A
The expected outcome of the disease
12
Q
Therapy/therapeutics
A
The method of TREATMENT of the disease/illness with the goal of curing or at least reducing the patients signs and symptoms to a level of near normal function
13
Q
Pathogen
A
- The disease causing organism/causative agent
- Sometimes called antigen
14
Q
Antigen
A
- Self or foreign chemical that elicits adaptive immune response ( B or T lymphocyte response )
- Most are foreign antigens (microbes, foods, drugs, toxins, animals)
- Self antigens (eg. Cellular proteins) are causes of autoimmune disease
- If cause common manifestations of allergies, may be called allergens
15
Q
Pathogenicity
A
The ability of the pathogen to cause disease
16
Q
Pathogenic success depends on
A
Communicability
Virulence
Extent of tissue damage
Host susceptibility
17
Q
Which is better, high pathogenicity of low
A
Low
18
Q
Which is better, highly virulent or low virulent
A
Low
19
Q
Which is better, highly susceptible host or low
A
Low
20
Q
Disease vs Illness
A
Disease > homeostatic imbalance occurs > diagnostic proof, medical history, clinical manifestations (signs and symptoms) > able to adapt and continue with activities of daily living
Illness > individual feels “unhealthy” > diagnostic proof, medical history, clinical manifestations (sign and symptoms) > difficulty with activities of daily living
21
Q
Disease
A
- The abnormal condition; the homeostatic imbalance
- Causes variations of cellular structure and/or function that are considered outside of normal range = loss of homeostatic balance required for optimal cellular functioning
22
Q
Illness
A
- Suggests that individual is aware of homeostatic imbalance
23
Q
Homeostatic imbalance
A
Presence of imbalance causing pathophysiologic clinical manifestations can be detected using diagnostic tools
24
Q
Diagnostic tool examples
A
Blood chemistry
Imaging
DNA analysis
25
Blood chemistry
- Blood glucose (BG)
- Presence of intracellular enzymes (should remain inside the cell to help it function normally)
- presence of extra cellular fluids such as blood plasma
- eg. Blood levels of cardiac enzyme (biomarkers) such as troponin and creatinine phosphokinase (CPK) are elevated in myocardial ischemia or infarction
26
Imagining
X rays, ultrasounds, CT scans, MRI scans
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Disease classifications
Hereditary
Congenital
Inflammatory
Degenerative
Metabolic
Neoplastic
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Etiology
The cause of the disease and/ or injury
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3 broad etiologic categories
Genetic Etiology
Congenital Etiology
Acquired Etiology
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Genetic Etiology
- Cause is a genetic abnormality
- Chromosomal defect/mutation
- Genetic defect/mutation
- Leads to changes in gene expression and consequent underproduction or overproduction of a particular protein therefore affecting normal biochemistry/ cell functioning
- Inherited traits, familial genetic predisposition “runs in family”
- Family history
- Developmental effects
- Increased susceptibility to specific diseases
- Random or due to environmental exposure
- Clinical manifestations may be present at or shortly after birth or develop years later
31
Genes
Specific regions of DNA, each gene codes for and regulates synthesis of a specific protein
32
Gene expression
Term used to the process by which the info encoded in a particular gene is used to synthesize the specific protein product of a gene
Eg. Gene transcription DNA > mRNA and translation > amino acid sequence
33
Genetic Disorders
Diseases that alter DNA sequences (ATCG)
34
What causes genetic disorders
- Caused by a mutation in one gene, multiple genes, or by a combination of gene mutations and environmental factors that change the gene sequence within a chromosome
- Random genetic mutations also occur
- Important to note that a genetic defect is a specific cell will be present in the offspring of that cell
35
Chromosomal defect/ mutation
Includes additions, deletions, or translocations of entire sections of chromosomes
36
Eg chromosomal defect/mutation
- 5p minus syndrome
- Deletion of the short arm of chromosome 5 (aka Cri du Chat)
- Trisomy 21
- Turners syndrome
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Increased risk of chromosomal defect/mutation
Advanced maternal age increases risk of chromosomal abnormalities; fetal assessments including karyotype analysis usually suggested
38
Genetic defect/mutation
- Implies that the DNA sequence of a single gene or group of genes on a single chromosome is/are defective
39
Genetic mutation
Eg. A single gene selection or addition or even the addition or deletion or switching of a single nitrogenous base (ATCG) may cause the gene coding for a particular protein to be defective
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Defective gene
Does not allow for proper protein synthesis; lack of a particular protein or production of the wrong protein can result in a biochemical change that may be detrimental to the individual
41
Examples genetic defect/mutation
Cystic fibrosis
Hemophilia
Sickle cell
Phenylketonuria (PKU)
All are genetic disorders that affect production of normal body proteins
42
Genetic and chromosomal disorders often have
Developmental effects
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Example developmental effects
Eg. Down syndrome (Trisomy 21) often manifests with mental and physical issues such as increased risk of learning disorders, cardiac abnormalities and earlier onset dementia
44
Inheritable traits
- May cause increased disease susceptibility
- Eg. UV skin damage in those with very fair or very dark skin
- Eg. Increased risk of early onset heart disease in families with hypercholesterolemia or sickle cell
45
Environmental exposure
Gene mutation
Eg lung cancer resulting from cigarette smoke exposure
46
Examples chromosomal and genetic disorders
Down syndrome = Chromosomal defect = xtra chromosome in autosomal pair 21
Sickle cell = Genetic defect (point mutation) = faulty gene expression incorrectly replaces one amino acid in the protein hemoglobin =hemoglobin sickles (changes morphology) =when blood o2 levels are lower than normal (ie during hypoxic episodes) = lots of microthrombi develop and block blood flow causing tissue hypoxia/anoxia
47
Congenital Etiology
Results in a genetic defect, injury/exposure, or micronutrient deficiency that occurred during embryonic or fetal development in utero or during labour and delivery of child, sometimes called a birth defect since disorder may be present before or at birth
48
Examples Congenital Etiology
Includes mental deficits, physical anomalies, structural malformations, and some diseases or syndromes
49
What are Congenital due to
Intrauterine exposure to a teratogen
Timing of exposure is significant to degree of malformation
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1st Trimester exposure
Embryonic period has most severe outcomes
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1st trimester exposure organs
Major organs affected: brain, spinal cord, heart, eyes, ears, limbs, and palate
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Common Congenital Manifestations 1st Trimester
Mental deficiency
Motor control deficiency
Structural heart defect
Blindness
Deafness
Club foot and/or cleft palate
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Approx _ amount of babies worldwide are born with a congenital anomaly. The majority _ occur in low or middle income families
6%, 94%
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Embryonic development
Beginning of week 3 to end of week 8, is the most dangerous period for intrauterine exposure to teratogens
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Fetal development
Week 9- 38
Developmental issues may still occur but usually not as severe as embryonic exposure
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Micronutrient deficiencies
- Lack of maternal folic acid = neural tube defects eg. Spinal bifida
- Lack of maternal iodine = maternal and fetal hypothyroidism and impaired fetal neurological development
57
What is a Teratogen
A substance or condition that impairs normal embryonic or fetal development, causing fetal deformity
Timing of exposure greatly influences susceptibility and resulting degree of malformation
Known: chemical toxins, radiation, specific infective agents
58
Prevention of teratogen’s include
Avoid exposure, get maternal vaccination, fortification of foods (folic acid, iodine), adequate perinatal care, keep maternal blood glucose levels in normal range
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teratogen exposure yellow zone
Yellow zone: Week 0-2
Exposure unlikely to cause birth defects since pre-embryonic period does not rely on maternal blood supply for support
60
Teratogen exposure red zone
Red zone: week 3-8
First trimester, embryonic period = major morphological abnormalities
Because period of very rapid organogenesis (development of internal organs) and limb development
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Red zone teratogen organ sensitivity
CNS, eyes, ears, heart, limbs and palate most sensitive because they are rapidly developing during this time
Time many woman do not know they are pregnant
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Pink zone teratogen
Week 9-36/38
Functional defects and minor morphological abnormalities
All organs have developed but are still growing and maturing
Fetal cells are still sensitive to teratogens but deficits to exposure should be less than in embryonic period
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Brain development and teratogens
Fetal brain development sensitive throughout entire pregnancy, no safe time period for exposure to teratogens such as alcohol or nicotine or drugs or radiation
64
Teratogens TORCH
T- toxoplasmosis
O- other, includes certain viruses, bacteria, chemicals (toxins/drugs), and radiation
R- rubella (German measles)
C- cytomegalovirus (CMV)
H- herpes simplex 2
65
Other infections that are teratogens
Coxsackie virus, hepatitis, HIV, parvovirus, syphilis, v-z virus, zika virus, Lyme disease
66
Other chemicals that are teratogens Smoking
Maternal smoking = cause low birth weight due to decreased placental perfusion (nicotine causes arteriole vasoconstriction, including placental arterioles resulting in less oxygen rich blood reaching developing embryo or fetus
67
Other chemicals that are teratogens alcohol
Associated with a variety of potential physical, neurological, and behavioural changes that are categorized as FASD =umbrella of FAS
68
Maternal diabetes
Increased risk of brain, sacrum, lower GI tract, heart, and limb defects
69
Radiation
Both teratogenic and mutagenic
Causes gene mutations that are harmful
70
Thalidomide exposure
Caused upper limb defects in 1950’s and early 1960’s
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Cleft palate
Has been linked to a variety of factors including maternal cigarette smoking
72
Acquired Etiology
- Most common
- Genetics and intrauterine embryonic/fetal development are normal; damage occurs after birth or later in life
- Includes environmental factors
73
General causes of acquired tissue damage
-Infectious agents (microbial, biological)
-Physical agents
-Chemical agents
-Malnutrition (nutritional, fluid, electrolyte, pH imbalances)
-abnormal immune response
-psychological agents
74
Environmental factors
Air pollutants, air or water borne organisms, ergonomic factors
75
pH imbalances
Classified as acidosis (ph <7.35) or alkalosis ( ph >7.45)
76
2 major causes of pH imbalances
Respiratory disorder of metabolic (biochemical) change
77
Respiratory acidosis
Eg. Hypoventilation ^C02
78
Respiratory Alkalosis
Eg. Hyperventilation v Co2
79
Metabolic acidosis
Eg. Overuse of acidic drugs, diarrhea, DKA
80
Metabolic alkalosis
Eg. Overuse of basic drugs, vomiting
81
Nosocomial
Nurse did not properly wash hands prior to changing a surgical dressing
82
Idiopathic
I’m sorry but we don’t know the cause of the seizure
83
Iatrogenic
I went to the hospital to have my baby and now I have a really bad guy infection
Cause of disease and/or injury is related to a medical intervention Eg surgery or drug side effect
84
Predisposing risk factors
-increase the possibility of developing a disease or injury
-NOT the actual cause of the disease
85
Predisposing factors examples
Family history of heart disease
86
Precipitating risk factor
Causes the disease or injury to develop
87
Precipitating examples
Cigarette use led to development of atherosclerosis which progressed to heart disease
88
Both predisposing and precipitating may be further categorized to
Modifiable and non-modifiable
89
Modifiable risk factors
Risk factors that can be changed by the individual Eg lifestyle or environment
90
Non-modifiable risk factors
Cannot be changed, Eg. Age, genetics, biological sex
91
Multifactorial diseases
Result from a combination of genetic and environmental risk factors that effect onset and progression
Eg. Type 2 diabetes
92
Sequelae
Unwanted outcomes of a disease or trauma that can lead to further, often chronic health issues, often multisystemic and may be described as the complications of a specific disease
Eg. Long covid
93
Comorbidity
2 or more disease or medical conditions that are present in a patient at the same time, Are pre existing or concurrent diseases
94
Sequelae and comorbidity
Both affect the disease prognosis of each patient
95
Pathogenesis
-The pathologic, physiologic, or biochemical patter of TISSUE changes leading to development of disease
-How does this disease progress/evolve over time?
-From first contact with etiological agent until disease or injury becomes evident (clinical manifest)
96
Pathogenic changes
Changes in structural, functional and/or biochemical mechanisms may lead to homeostatic imbalance and probably present with clinical manifestations
97
Pathologic vs pathophysiologic vs biochemical
Pathologic = structural changes
Pathophysiologic = functional changes/effects
Biochemical = body’s chemical and metabolic changes/effects (fluids electrolytes, nutrients, wastes
98
Principal elements involved in disease pathogenesis
Etiological agent causes —> initial injury —-> defective cellular/tissue function —> defective organ/organ system function —> related systemic effects
-at any time signs and symptoms of disease
99
Parenchyma
Functional cells of the organ
Eg. Skeletal muscle cell, hormone secreting endocrine cells, neurons, myocardium (cardiac muscle cells)
100
Stromal
-Connective tissue (CT cells, fibroblasts, extra cellular matrix, ECM)
-Tissue immune cells (mast cells, macrophages)
-Microvasculature (arterioles, capillaries, venules)
-Nerve endings
101
Exceptions parenchyma vs stromal
In CNS stromal tissue is composed of neuroglial cells that surround and protect the functional neurons
In basic CT fibroblasts are the functional parenchyma cells
102
Morphology
The science of structure and form (shape)
The size/ shape of cells
Specific to each cell type; required for the cell to function normally
103
Morphological change
Adaptive property of damaged cells as they try to survive the injury
If cells cannot adapt, they die
104
Pathologists
Study changes in cellular morphology to diagnose disease
105
Morphology researchers
Study effects of new treatment and new etiological agents at the cellular level
Eg. If pharm company wants to market a new drug, changes to parenchyma or stromal morphology are part of potential side effects that must be proven to not be overly severe
106
Lesion
The actual site(s) of tissue damage, the “wound”
107
Classifications of lesions
Local/focal, diffuse/multifocal, systemic
108
Local/focal
Limited to specific, defined body location, an organ or body part
109
Diffuse (multifocal) lesion
Tissue damage is within one organ or body part but the damage is uniformly distributed throughout the organ or body party
Eg. Fatty liver
110
Systemic lesion
Tissue damage is widespread across one or several body systems
Eg. Metastatic cancer
111
Signs
Detectable, testable patient info
Objective Eg vital signs
Physical exam, lab test, or medical procedure
Eg. Blood glucose, X-ray, biopsy, redness, swelling, fever
112
Symptoms
Patients experiences
Subjective
Part of patient medical HX
Eg. Pain level, malaise, anxiety, headache, fatigue
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Assessment
Mechanism used to determine the specific plan of care for an individual patient
114
Prognosis
Based upon the patients response to therapy and medical professionals knowledge of the disease pathogenesis and clinical experience of the disease
115
Disease onset
The time over which the disease or condition develops
Eg. Acute, chronic, insidious, latent/dormant, subclinical/subacute
116
Hypertension
Chronic
117
Broken leg
Acute
118
Myocardial infarction
Acute
119
Cystic fibrosis
Chronic
120
HIV
Latent/dormant
121
Acute condition
-Rapid or sudden onset of signs and symptoms, often severe
-Short duration possibly hours/days
-Self-limiting
-Eg. food poisoning
122
Acute examples
Flu, broken bones, infections like UTI or pink eye, strep throat, burns, cold, heart attack, pneumonia
123
Chronic condition
-Rapid or slow (insidious) onset of signs and symptoms
-Continuous, longer duration, weeks, months, lifetime
124
Chronic examples
Rheumatoid arthritis, diabetes mellitus, Alzheimer’s, asthma, cancer, dementia, Crohn’s disease, IBS, IBD, obesity, Diabetes
125
Latent/dormant condition
Asymptomatic period of quiescence before signs and symptoms manifest
126
Latent/dormant
HIV, shingles, TB, herpes
127
Subclinical/subacute
Rather recent onset or change
Time frame intermediate between acute and chronic
Symptoms not as sudden as onset or severe as acute and usually shorter duration than chronic
Signs may not be detectable by clinical tests
128
Subclinical examples
Subacute endocarditis, pertussis
129
Disease course
How does the disease behave over time, describes the continuous progression
Patient history including a time frame is an important component in describing the course of a specific disease
If acute disease course measured in days to 2 weeks
If chronic disease measured in weeks, months
130
Acute disease course
Time trim from illness to wellness measured in days to about 2 weeks
Allows time for adaptive immune response to antigen if necessary
131
Chronic disease course
Time frame from illness to wellness measured in weeks or months or longer
If disease described as chronic in nature, then the terms remission or exacerbation may be used in disease progression
132
Remission
Periods where clinical manifestations disappear completely or are significantly decreased
133
Exacerbation
Periods where clinical manifestations become more obvious and severe
Often called flare ups
134
4 distinct stages of infectious disease course
Initial exposure to microbe followed by:
1. Incubation period
2. Prodromal stage
3. Invasion period
4. Convalescence
135
Incubation period
Time from initial exposure to the onset of first symptoms
Microorganisms have colonized, invaded, and are multiplying but infected individual is still asymptotic, although may be contagious
Incubation period of childhood diseases like chicken pox, measles, mumps are well documented
136
Prodromal stage
Initial non-specific symptoms of infection occur
Usually mild such as tiredness, discomfort
** most contagious stage **
Microbes multiplying but individual often ignores symptoms
137
Invasion period
Microbial infection is multiplying quickly and spreading to other tissues/organs either locally or systemically depending on severity
Clinical manifestations specific to disease causing organism present as inflammatory and immune responses are triggered to fight the infection =pain, malaise, headache, generalized aching, loss of appetite or other GI effects, skin rashes etc
NOTE: if fever develops = sign of systemic infection
138
Convalescence
Time required to return to health and strength after illness
139
Communicable diseases
Infectious and easily transmissible from on individual to others and causes disease in most exposed individuals
140
Common communicable diseases
Measles, mumps, rubella, pertussis, chicken pox, cold and flu, diphtheria, amoebic dysentery
Usually airborne or water borne
141
Portal of entry (4)
Transdermal
Inhalation
Ingestion
Injection
142
Body systems most commonly compromised
Skin
Resp
GI
Urogenital
Transplacental
143
Injection
Includes needles, and bites/stings
144
Transplacental
Could cause congenital defect
145
Skin and mucous membrane
Major components of innate (born with) defence
Act as physical barriers to pathogens
When compromised, cell injury will occur
146
Syndrome
Disease or condition had a defined group of lesions and signs/symptoms with a common Etiology
147
Down syndrome
Genetic Etiology
148
AIDS
Acquired
149
FAS
Congenital
150
Reye’s syndrome
Acquired
151
Metabolic syndrome
Acquired
152
Complication
Disease or condition that occurs in addition to the original tissue damage
May add to a difficulty of treatment; life threatening
153
Epidemiology
Study of distribution and determinants of health in a specific population and application of this info to control the specific health proble.
154
Epidemiology asks the questions
Who is at risk
Where is the risk
When did the health issue begin
How is it spread
How is it controlled
155
Agencies involved in epidemiology
World health organization
National microbiology lab
Center for disease control
Public health agency of Canada
156
Prevalence
Number of existing cases in a population/specific time
More subject to change
Common? Rare ?
157
Incidence
Number of NEW cases in a population/ specific time
If endemic, should be constant year by year
Contained ? Spreading ?
158
Endemic
Disease has high, but constant rates of infection within a particular population
Eg. TB, malaria,
159
Epidemic
Number of new infections within a particular population far exceeds expected occurrence
Eg. TB and HIV in northern communities, influenza outbreaks, Ebola in South Africa, zika in South America
160
Pandemic
Epidemic that is spread over large area of population, continent, global
Eg. Black Plague, Spanish flu, corona virus
161
Notifiable (reportable) disease
Required by law to be reported to public health authorities in an attempt to prevent further spread
Listed by public health associated of Canada
Eg TB
162
Mortality rate
Death rate due to specific disease/cause in a specific population or time frame
Often stated as a % within a population
Impacts public health policy
Impacts public health policy
Eg. Seat belt, texting and driving, cigarette packaging
163
Morbidity rate
Incidence/rate if a specific disease/cause in a specific population
Possible long term health consequences for the individual
Impacts health care costs
Eg. Workplace repetitive strain, obesity
164
Comorbidity
The presence of two or more diseases or medical conditions in a patient simultaneously
165
Epigenetics
Study of chemical modifications (DNA), histones, or RNA that alter the expression of genes (the phenotype) resulting in cellular differentiation or disease
166
Gene expression
Mechanisms that turn genes on or off
Eg. Oncogenes, hypersensitivity, stress related diseases, in utero influences (malnutrition, alcohol exposure, BPA exposure)
167
Types of acquired etiologies
Infectious agents
Physical agents
Chemical agents
Nutritional imbalances
Fluid/electrolyte/pH imbalances
Abnormal immune response
Psychological agents
168
Infectious agents
Aka microbial/biological
May of direct or indirect (via toxin production) affects on host
Eg. Bacteria, viruses, fungi, chlamydia, rickettsia, mycoplasma, parasites, insect vectors, prions, food poisoning
169
Physical agents
External cause of homeostatic imbalance
Eg. Mechanical trauma, temp, trauma, radiation, noise pollution, light pollution, electrocution
170
Chemical agents
Exposure to abnormally high or low level of specific chemical (inhaled or ingested, or transdermal) exposure; common target organs, neurological, heart, liver, kidney damage
Eg. Poisons, toxins, heavy metals, carcinogens, hypoxia, hypercapnia m, chemotherapeutics
171
Nutritional Imbalances
Carbs, proteins, fats, vitamins, minerals, and water
Malnutrition = poor nutritional status
Over nutrition = excessive consumption of 1 or more class of nutrients; may cause toxicity, obesity
Undernutrition= insufficient ingestion or production of 1 or more classes, may cause specific deficiencies of systemic Effects (starvation, anorexia, kwashiorkor)
172
Fluid, electrolyte and ph imbalance
Fluid = water + dissolved solutes (nutrients and wastes
Electrolytes = ions that carry an electric charge (na, k, cl) required for neurologic and muscle signals
Edema = excess tissue (interstital) fluid
Third spacing = occurs when fluid shifts out of the bloodstream and into a body cavity or interstitial space and is no longer part of circulating blood plasma or lymph Eg ascites
Over hydration = excess fluid intake or insufficient fluid loss (hypervolemia)
Under hydration = insufficient fluid intake or excessive fluid loss (hypovolemia, dehydration)
Electrolyte imbalance = hyper or hyponatremia, hyper or hypokalemia, hyper or hypocalcemia
Acidosis= decreased in physiological pH (<7.35) respiratory acidosis = asthma, COPD, ARDS metabolic acidosis = diabetic ketoacidosis
Alkalosis = resp alkalosis = hyperventilation, metabolic alkalosis Eg alkaline drug OD
173
Abnormal immune response
Increased or decrease innate immune functions Eg histamine secretion, phagocytosis, mucous secretion, complement proteins
Increase or decrease in adaptive immune function Eg B cell IG secretion, cytotoxic and/or helper T cell response
Hypersensitivities =allergies, immune system overreacts to relatively innocuous (not harmful) environmental agents/antigens
Autoimmunity= adaptive immune system reacts ti normal self antigens Eg type 1 diabetes, multiple sclerosis, rheumatoid arthritis
Immunodeficiencies= immune system does not elicit a normal response to foreign antigen Eg hiv/aids, ig deficenies
