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Pathophysiology > Module 1 Foundations > Flashcards

Module 1 Foundations Flashcards

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

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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
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3
Q

Patho 4 interrelated topics

A

Etiology
Pathogenesis
Clinical manifestations
Treatment

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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

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5
Q

Pathologist’s use …

A

Findings/diagnostics to determine diagnosis, prognosis, and treatment

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6
Q

Biopsy

A

Tissue removal from living individual

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7
Q

Autopsy

A

Postmortem
Tissue removal following death of individual

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8
Q

Tissue samples

A

From either biopsy or autopsy will undergo microscopic, genetic, biological, and/or chemical diagnostic analysis

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9
Q

Findings

A

The diagnostics
Results of the lab and imaging tests utilized by the pathologist to determine diagnosis, prognosis, and treatment protocol

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10
Q

Diagnosis

A

The identification of the specific disease

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11
Q

Prognosis

A

The expected outcome of the disease

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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

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13
Q

Pathogen

A
  • The disease causing organism/causative agent
  • Sometimes called antigen
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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
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15
Q

Pathogenicity

A

The ability of the pathogen to cause disease

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16
Q

Pathogenic success depends on

A

Communicability
Virulence
Extent of tissue damage
Host susceptibility

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17
Q

Which is better, high pathogenicity of low

A

Low

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18
Q

Which is better, highly virulent or low virulent

A

Low

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19
Q

Which is better, highly susceptible host or low

A

Low

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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

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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
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22
Q

Illness

A
  • Suggests that individual is aware of homeostatic imbalance
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23
Q

Homeostatic imbalance

A

Presence of imbalance causing pathophysiologic clinical manifestations can be detected using diagnostic tools

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24
Q

Diagnostic tool examples

A

Blood chemistry
Imaging
DNA analysis

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25
Q

Blood chemistry

A
  • 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
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26
Q

Imagining

A

X rays, ultrasounds, CT scans, MRI scans

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27
Q

Disease classifications

A

Hereditary
Congenital
Inflammatory
Degenerative
Metabolic
Neoplastic

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28
Q

Etiology

A

The cause of the disease and/ or injury

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29
Q

3 broad etiologic categories

A

Genetic Etiology
Congenital Etiology
Acquired Etiology

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30
Q

Genetic Etiology

A
  • 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
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31
Q

Genes

A

Specific regions of DNA, each gene codes for and regulates synthesis of a specific protein

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32
Q

Gene expression

A

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

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33
Q

Genetic Disorders

A

Diseases that alter DNA sequences (ATCG)

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34
Q

What causes genetic disorders

A
  • 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
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35
Q

Chromosomal defect/ mutation

A

Includes additions, deletions, or translocations of entire sections of chromosomes

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36
Q

Eg chromosomal defect/mutation

A
  • 5p minus syndrome
  • Deletion of the short arm of chromosome 5 (aka Cri du Chat)
  • Trisomy 21
  • Turners syndrome
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37
Q

Increased risk of chromosomal defect/mutation

A

Advanced maternal age increases risk of chromosomal abnormalities; fetal assessments including karyotype analysis usually suggested

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38
Q

Genetic defect/mutation

A
  • Implies that the DNA sequence of a single gene or group of genes on a single chromosome is/are defective
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39
Q

Genetic mutation

A

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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40
Q

Defective gene

A

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

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41
Q

Examples genetic defect/mutation

A

Cystic fibrosis
Hemophilia
Sickle cell
Phenylketonuria (PKU)
All are genetic disorders that affect production of normal body proteins

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42
Q

Genetic and chromosomal disorders often have

A

Developmental effects

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43
Q

Example developmental effects

A

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

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44
Q

Inheritable traits

A
  • 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
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45
Q

Environmental exposure

A

Gene mutation
Eg lung cancer resulting from cigarette smoke exposure

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46
Q

Examples chromosomal and genetic disorders

A

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

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47
Q

Congenital Etiology

A

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

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48
Q

Examples Congenital Etiology

A

Includes mental deficits, physical anomalies, structural malformations, and some diseases or syndromes

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49
Q

What are Congenital due to

A

Intrauterine exposure to a teratogen
Timing of exposure is significant to degree of malformation

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50
Q

1st Trimester exposure

A

Embryonic period has most severe outcomes

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51
Q

1st trimester exposure organs

A

Major organs affected: brain, spinal cord, heart, eyes, ears, limbs, and palate

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52
Q

Common Congenital Manifestations 1st Trimester

A

Mental deficiency
Motor control deficiency
Structural heart defect
Blindness
Deafness
Club foot and/or cleft palate

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53
Q

Approx _ amount of babies worldwide are born with a congenital anomaly. The majority _ occur in low or middle income families

A

6%, 94%

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54
Q

Embryonic development

A

Beginning of week 3 to end of week 8, is the most dangerous period for intrauterine exposure to teratogens

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55
Q

Fetal development

A

Week 9- 38
Developmental issues may still occur but usually not as severe as embryonic exposure

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56
Q

Micronutrient deficiencies

A
  • Lack of maternal folic acid = neural tube defects eg. Spinal bifida
  • Lack of maternal iodine = maternal and fetal hypothyroidism and impaired fetal neurological development
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57
Q

What is a Teratogen

A

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

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58
Q

Prevention of teratogen’s include

A

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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59
Q

teratogen exposure yellow zone

A

Yellow zone: Week 0-2
Exposure unlikely to cause birth defects since pre-embryonic period does not rely on maternal blood supply for support

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60
Q

Teratogen exposure red zone

A

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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61
Q

Red zone teratogen organ sensitivity

A

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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62
Q

Pink zone teratogen

A

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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63
Q

Brain development and teratogens

A

Fetal brain development sensitive throughout entire pregnancy, no safe time period for exposure to teratogens such as alcohol or nicotine or drugs or radiation

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64
Q

Teratogens TORCH

A

T- toxoplasmosis
O- other, includes certain viruses, bacteria, chemicals (toxins/drugs), and radiation
R- rubella (German measles)
C- cytomegalovirus (CMV)
H- herpes simplex 2

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65
Q

Other infections that are teratogens

A

Coxsackie virus, hepatitis, HIV, parvovirus, syphilis, v-z virus, zika virus, Lyme disease

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66
Q

Other chemicals that are teratogens Smoking

A

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

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67
Q

Other chemicals that are teratogens alcohol

A

Associated with a variety of potential physical, neurological, and behavioural changes that are categorized as FASD =umbrella of FAS

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68
Q

Maternal diabetes

A

Increased risk of brain, sacrum, lower GI tract, heart, and limb defects

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69
Q

Radiation

A

Both teratogenic and mutagenic
Causes gene mutations that are harmful

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70
Q

Thalidomide exposure

A

Caused upper limb defects in 1950’s and early 1960’s

71
Q

Cleft palate

A

Has been linked to a variety of factors including maternal cigarette smoking

72
Q

Acquired Etiology

A
  • Most common
  • Genetics and intrauterine embryonic/fetal development are normal; damage occurs after birth or later in life
  • Includes environmental factors
73
Q

General causes of acquired tissue damage

A

-Infectious agents (microbial, biological)
-Physical agents
-Chemical agents
-Malnutrition (nutritional, fluid, electrolyte, pH imbalances)
-abnormal immune response
-psychological agents

74
Q

Environmental factors

A

Air pollutants, air or water borne organisms, ergonomic factors

75
Q

pH imbalances

A

Classified as acidosis (ph <7.35) or alkalosis ( ph >7.45)

76
Q

2 major causes of pH imbalances

A

Respiratory disorder of metabolic (biochemical) change

77
Q

Respiratory acidosis

A

Eg. Hypoventilation ^C02

78
Q

Respiratory Alkalosis

A

Eg. Hyperventilation v Co2

79
Q

Metabolic acidosis

A

Eg. Overuse of acidic drugs, diarrhea, DKA

80
Q

Metabolic alkalosis

A

Eg. Overuse of basic drugs, vomiting

81
Q

Nosocomial

A

Nurse did not properly wash hands prior to changing a surgical dressing

82
Q

Idiopathic

A

I’m sorry but we don’t know the cause of the seizure

83
Q

Iatrogenic

A

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
Q

Predisposing risk factors

A

-increase the possibility of developing a disease or injury
-NOT the actual cause of the disease

85
Q

Predisposing factors examples

A

Family history of heart disease

86
Q

Precipitating risk factor

A

Causes the disease or injury to develop

87
Q

Precipitating examples

A

Cigarette use led to development of atherosclerosis which progressed to heart disease

88
Q

Both predisposing and precipitating may be further categorized to

A

Modifiable and non-modifiable

89
Q

Modifiable risk factors

A

Risk factors that can be changed by the individual Eg lifestyle or environment

90
Q

Non-modifiable risk factors

A

Cannot be changed, Eg. Age, genetics, biological sex

91
Q

Multifactorial diseases

A

Result from a combination of genetic and environmental risk factors that effect onset and progression
Eg. Type 2 diabetes

92
Q

Sequelae

A

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
Q

Comorbidity

A

2 or more disease or medical conditions that are present in a patient at the same time, Are pre existing or concurrent diseases

94
Q

Sequelae and comorbidity

A

Both affect the disease prognosis of each patient

95
Q

Pathogenesis

A

-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
Q

Pathogenic changes

A

Changes in structural, functional and/or biochemical mechanisms may lead to homeostatic imbalance and probably present with clinical manifestations

97
Q

Pathologic vs pathophysiologic vs biochemical

A

Pathologic = structural changes
Pathophysiologic = functional changes/effects
Biochemical = body’s chemical and metabolic changes/effects (fluids electrolytes, nutrients, wastes

98
Q

Principal elements involved in disease pathogenesis

A

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
Q

Parenchyma

A

Functional cells of the organ
Eg. Skeletal muscle cell, hormone secreting endocrine cells, neurons, myocardium (cardiac muscle cells)

100
Q

Stromal

A

-Connective tissue (CT cells, fibroblasts, extra cellular matrix, ECM)
-Tissue immune cells (mast cells, macrophages)
-Microvasculature (arterioles, capillaries, venules)
-Nerve endings

101
Q

Exceptions parenchyma vs stromal

A

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
Q

Morphology

A

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
Q

Morphological change

A

Adaptive property of damaged cells as they try to survive the injury
If cells cannot adapt, they die

104
Q

Pathologists

A

Study changes in cellular morphology to diagnose disease

105
Q

Morphology researchers

A

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
Q

Lesion

A

The actual site(s) of tissue damage, the “wound”

107
Q

Classifications of lesions

A

Local/focal, diffuse/multifocal, systemic

108
Q

Local/focal

A

Limited to specific, defined body location, an organ or body part

109
Q

Diffuse (multifocal) lesion

A

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
Q

Systemic lesion

A

Tissue damage is widespread across one or several body systems
Eg. Metastatic cancer

111
Q

Signs

A

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
Q

Symptoms

A

Patients experiences
Subjective
Part of patient medical HX
Eg. Pain level, malaise, anxiety, headache, fatigue

113
Q

Assessment

A

Mechanism used to determine the specific plan of care for an individual patient

114
Q

Prognosis

A

Based upon the patients response to therapy and medical professionals knowledge of the disease pathogenesis and clinical experience of the disease

115
Q

Disease onset

A

The time over which the disease or condition develops
Eg. Acute, chronic, insidious, latent/dormant, subclinical/subacute

116
Q

Hypertension

A

Chronic

117
Q

Broken leg

A

Acute

118
Q

Myocardial infarction

A

Acute

119
Q

Cystic fibrosis

A

Chronic

120
Q

HIV

A

Latent/dormant

121
Q

Acute condition

A

-Rapid or sudden onset of signs and symptoms, often severe
-Short duration possibly hours/days
-Self-limiting
-Eg. food poisoning

122
Q

Acute examples

A

Flu, broken bones, infections like UTI or pink eye, strep throat, burns, cold, heart attack, pneumonia

123
Q

Chronic condition

A

-Rapid or slow (insidious) onset of signs and symptoms
-Continuous, longer duration, weeks, months, lifetime

124
Q

Chronic examples

A

Rheumatoid arthritis, diabetes mellitus, Alzheimer’s, asthma, cancer, dementia, Crohn’s disease, IBS, IBD, obesity, Diabetes

125
Q

Latent/dormant condition

A

Asymptomatic period of quiescence before signs and symptoms manifest

126
Q

Latent/dormant

A

HIV, shingles, TB, herpes

127
Q

Subclinical/subacute

A

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
Q

Subclinical examples

A

Subacute endocarditis, pertussis

129
Q

Disease course

A

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
Q

Acute disease course

A

Time trim from illness to wellness measured in days to about 2 weeks
Allows time for adaptive immune response to antigen if necessary

131
Q

Chronic disease course

A

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
Q

Remission

A

Periods where clinical manifestations disappear completely or are significantly decreased

133
Q

Exacerbation

A

Periods where clinical manifestations become more obvious and severe
Often called flare ups

134
Q

4 distinct stages of infectious disease course

A

Initial exposure to microbe followed by:
1. Incubation period
2. Prodromal stage
3. Invasion period
4. Convalescence

135
Q

Incubation period

A

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
Q

Prodromal stage

A

Initial non-specific symptoms of infection occur
Usually mild such as tiredness, discomfort
** most contagious stage **
Microbes multiplying but individual often ignores symptoms

137
Q

Invasion period

A

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
Q

Convalescence

A

Time required to return to health and strength after illness

139
Q

Communicable diseases

A

Infectious and easily transmissible from on individual to others and causes disease in most exposed individuals

140
Q

Common communicable diseases

A

Measles, mumps, rubella, pertussis, chicken pox, cold and flu, diphtheria, amoebic dysentery
Usually airborne or water borne

141
Q

Portal of entry (4)

A

Transdermal
Inhalation
Ingestion
Injection

142
Q

Body systems most commonly compromised

A

Skin
Resp
GI
Urogenital
Transplacental

143
Q

Injection

A

Includes needles, and bites/stings

144
Q

Transplacental

A

Could cause congenital defect

145
Q

Skin and mucous membrane

A

Major components of innate (born with) defence
Act as physical barriers to pathogens
When compromised, cell injury will occur

146
Q

Syndrome

A

Disease or condition had a defined group of lesions and signs/symptoms with a common Etiology

147
Q

Down syndrome

A

Genetic Etiology

148
Q

AIDS

A

Acquired

149
Q

FAS

A

Congenital

150
Q

Reye’s syndrome

A

Acquired

151
Q

Metabolic syndrome

A

Acquired

152
Q

Complication

A

Disease or condition that occurs in addition to the original tissue damage
May add to a difficulty of treatment; life threatening

153
Q

Epidemiology

A

Study of distribution and determinants of health in a specific population and application of this info to control the specific health proble.

154
Q

Epidemiology asks the questions

A

Who is at risk
Where is the risk
When did the health issue begin
How is it spread
How is it controlled

155
Q

Agencies involved in epidemiology

A

World health organization
National microbiology lab
Center for disease control
Public health agency of Canada

156
Q

Prevalence

A

Number of existing cases in a population/specific time
More subject to change
Common? Rare ?

157
Q

Incidence

A

Number of NEW cases in a population/ specific time
If endemic, should be constant year by year
Contained ? Spreading ?

158
Q

Endemic

A

Disease has high, but constant rates of infection within a particular population
Eg. TB, malaria,

159
Q

Epidemic

A

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
Q

Pandemic

A

Epidemic that is spread over large area of population, continent, global
Eg. Black Plague, Spanish flu, corona virus

161
Q

Notifiable (reportable) disease

A

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
Q

Mortality rate

A

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
Q

Morbidity rate

A

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
Q

Comorbidity

A

The presence of two or more diseases or medical conditions in a patient simultaneously

165
Q

Epigenetics

A

Study of chemical modifications (DNA), histones, or RNA that alter the expression of genes (the phenotype) resulting in cellular differentiation or disease

166
Q

Gene expression

A

Mechanisms that turn genes on or off
Eg. Oncogenes, hypersensitivity, stress related diseases, in utero influences (malnutrition, alcohol exposure, BPA exposure)

167
Q

Types of acquired etiologies

A

Infectious agents
Physical agents
Chemical agents
Nutritional imbalances
Fluid/electrolyte/pH imbalances
Abnormal immune response
Psychological agents

168
Q

Infectious agents

A

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
Q

Physical agents

A

External cause of homeostatic imbalance
Eg. Mechanical trauma, temp, trauma, radiation, noise pollution, light pollution, electrocution

170
Q

Chemical agents

A

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
Q

Nutritional Imbalances

A

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
Q

Fluid, electrolyte and ph imbalance

A

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
Q

Abnormal immune response

A

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

Pathophysiology (8 decks)

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