Intro (Exam 1) Flashcards
Physiology
The study of life processes work at the molecular, organ/system and whole level; focused how systems in the body operate
Pathophysiology
The study of functional changes due to disease or injury
Inflammation
Response to tissue injury/infection; release of chemical mediators
Examples of chronic inflammation
Rheumatoid arthritis, IBS
Pathogens
Disrupts normal cell processes, release toxins, induce inflammatory responses
Examples of pathogens
Bacteria, viruses, fungi and parasites
Cancer
Uncontrolled cell growth and the ability to invade surrounding tissues.
Cardiovascular diseases
Affects the heart and blood vessels; accumulation of fatty plaques in arteries
Metabolic disorders
Defects in the biochemical processes that regulate energy production and utilization
Examples of metabolic disorders
Imbalances in hormone levels, impaired glucose metabolism
Neurological disorders
Affects brain, spinal cord and peripheral nerves; induce progressive loss of neurons and impaired neuronal communication leads to cognitive decline, sensory deficits, etc.
Neurological Disorders examples
Alzheimer’s disease, Parkinson’s disease, multiple sclerosis
Disease
Any disturbance of structure/function of the body; can be symptomatic or asymptomatic
Pathology
Study of structural/functional changes in the body caused by disease
Etiology
Cause of the disease
Pathogenesis
Sequence of the events that lead to the disease
Congenital and heredity diseases (with example)
Changes in DNA; Down’s syndrome, fragile x syndrome
Inflammatory diseases
Body’s reaction to an injurious agent; autoimmune disorder
Degenerative diseases
Degeneration of various parts due to aging; arthritis
Metabolic diseases
disturbance in some metabolic process; diabetes, hyper/hypothyroidism
Neoplastic
Conditions that cause tumor growth- both benign and malignant (cancer, fibroids)
Goal of cell adaptation/how it’s done
Goal: maintain homeostasis in internal/external environment
Done by: changing cell size, number or type of
Physiologic adaptation example
Enlargement of the uterus during pregnancy (normal physiological change)
Pathologic adaptation example
Enlargement of heart due to hypertension, formation of plaques due to high cholesterol (response to adverse conditions)
Atrophy
Wasting away due to reduction in size of the cells
Hypertrophy
Increase in cell size and tissue mass due to increase workload on the body part or organ. cells increase in size to meet demand. common in cardiac and skeletal muscle
Hyperplasia
Increase in cell number and tissue mass ONLY in cells that can actively divide
Metaplasia
one cell type is replaced by another, stays within the same tissue type
usually occurs in response to chronic irritation or inflammation
Dysplasia
Abnormal development of cells; associated with chronic inflammation/irritation; can lead to cancer but can be reversible if irritation is removed
5 ways for cells to get injured
Nutritional imbalances
physical agents
radiation
chemical
biological agents
Hypoxia
Lack of oxygen- most common cellular injury
Ischemia
Reduce blood flow, can lead to hypoxia
Anoxia
Total lack of oxygen
Free radical
Contains a single unpaired electron in an outer orbit
can lead to heart attack, cancer, etc, DNA damage, mutations
Mechanism for ischemic/hypoxic injury (5 steps)
Reduction in ATP > dysfunction of Na+/K+ ATPase > altered intracellular levels > altered enzyme activation > cell death if oxygen not restored
Reactive oxygen species (ROS)
Chemically reactive oxygen molecules; usually balanced by antioxidants
Oxidative stress
Imbalance between the production of ROS and antioxidant defenses
Reasons for chemical injury (3)
- Xenobiotics (carbon tetrachloride, lead, carbon monoxide, ethanol, mercury, social or street drugs)
- chemical agents including agents (OTC and prescribed drugs)
- direct damage, hypersensitivity reactions
What is the leading cause of child poisoning?
Chemical injury - Xenobiotics, OTC
What is the most susceptible organ/ initial site of contact for most ingested chemicals?
Liver
Infectious injury
pathogenicity of microorganisms, disease producing potential (invasion and destruction, toxin production, production of hypersensitivity reactions)
Immunologic and inflammatory injury (3)
Phagocytes cells
membrane alterations
immune/inflammatory substances (histamine, antibodies)
Fever
Release of endogenous pyrogens (intetleukin-1) from macrophages/bacteria
functional plasma enzymes
Present more in plasma than tissues, known functions, substrates present in blood, synthesis in liver, decreased liver diseases
non-functional plasma enzymes
Present in plasma lower than tissues, no known functions, substrates absent from blood, synthesis in different organs, different enzymes inc in different diseases
4 sources of non functional plasma enzymes
- Increase in the rate of enzyme synthesis
- Obstruction of normal pathway
- Increase permeability of cell membrane
- Cell damage with the release of its content of enzymes into the blood
Medical importance of non functional plasma enzymes (2)
- Diagnosis of diseases - diseases of different organs cause elevation of different plasma enzymes
- Prognosis of the disease - the effect of treatment can be followed up by measuring plasma enzymes before and after treatment
apoptosis
Programmed cell death involved in normal cell deletion or renewal
necrosis
cell death due to extensive damage, cellular swelling, rupture of the cell membrane and inflammation due to injury
autophagy
Conserved degradation of the cell that removes unnecessary/dysfunctional components through a lysosome dependent regulated mechanism
autophagy paradox
destruction and recycling of cells prevents but also promotes tumors
mutagen
Agent known to increase the frequency of mutations
Tumor cells typically exhibit genome wide hypomethylation; tumor suppressor genes often hypermethylated
DNA methylation leading to cancer
pathophysiology of infectious diseases
involves invasion and proliferation of microorganisms within the body
pathophysiology of cancer
involves genetic mutations that lead to abnormal cell division, reduced apoptosis and angiogenesis.
pathophysiology of cardiovascular diseases
involves accumulation of fatty plaques in the arteries leading to atherosclerosis and in severe cases, myocardial infarction or stoke
pathophysiology of metabolic disorders
involves imbalances in hormone levels, impaired glucose metabolism, and dysregulations of lipid and protein metabolism
pathophysiology of diabetes
involves the increase of blood glucose from:
carb intake
increase in hepatic glucose production
decrease in peripheral glucose uptake
decrease in insulin secretion
how do organisms adapt to stress
in the external environment
how do cells adapt to stress
in the internal environment
causes of atrophy
disuse
denervation
loss of endocrine stimulation
inadequate nutrition
ischemia or decrease in blood flow
brain atrophy
also known as cerebral atrophy; loss of neurons and connections between neurons
physiologic hypertrophy
increased muscle mass associated with exercise
pathologic hypertrophy
result of a disease
adaptive: thickening of bladder after continuous obstruction of urine flow, cardiac hypertrophy after hbp
compensatory: increase in size of single kidney if second kidney is removed
physiologic hyperplasia
result of hormonal stimulation, increased workload - breast enlargement, pregnancy, tissue healing
non-physiologic hyperplasia
result of excessive hormonal stimulation and growth factors- skin warts, excess estrogen
in this condition, the size of the prostate gland increases in part due to a hormone mediated increase in cell proliferation. this cellular change is most accurately described as:
hyperplasia
How are ROS formed?
during normal cellular processes and balanced by endogenous antioxidants
mechanism for ischemia-reperfusion injury
during ischemia, degradation of aTP produces hypoxanthine -> during reperfusion, oxygen catalyzes xanthine oxidase to dgrade hypoxanthine to uric acid and releasing highly reactive superoxide anion -> superoxide converted to hydrogen proxide and hydroxyl radical -> radical causes peroxidation of lipid structures of cell membranes resulting in the relase of proinflammatory eicosanoids
cell injury
occurs if the adaptive responses are exceeded or compromised by injurious agents, stress, mutations
reversible injury
if it is mild or transient
irreversible injury
if the stimulus persists the cell suffers and eventually dies
what is the most common cause of cellular injury?
hypoxia
direct damage
chemicals and drugs injure cells by combining directly with critical molecular substances, chemo drugs, drugs of abuse
hypersensitivity reactions
range from mild skin rashes to immune-mediated organ failure
tachycardia
due to increase in metabolic processes resulting from fever
pain
due to various mechanisms including release of bradykinin, obstruction, presure
presence of cellular enzymes in blood
Creatinine kinase - SKELETAL MUSCLE, heart
Aspartate aminotransferase - liver
Alanine aminotransferase - liver
Amylase - pancreas
Troponins - HEART, skeletal muscle
lethal cell injury results in
cell death
a pt’s blood work shows elevation in both AST and ALT which organ is inidicating there is damage?
liver
mutations
any inherited alteration of genetic material
base pair substitution
frameshift
spontaneous
hot spots
