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Pathophysiology > Intro (Exam 1) > Flashcards

Intro (Exam 1) Flashcards

1
Q

Physiology

A

The study of life processes work at the molecular, organ/system and whole level; focused how systems in the body operate

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2
Q

Pathophysiology

A

The study of functional changes due to disease or injury

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3
Q

Inflammation

A

Response to tissue injury/infection; release of chemical mediators

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4
Q

Examples of chronic inflammation

A

Rheumatoid arthritis, IBS

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5
Q

Pathogens

A

Disrupts normal cell processes, release toxins, induce inflammatory responses

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6
Q

Examples of pathogens

A

Bacteria, viruses, fungi and parasites

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7
Q

Cancer

A

Uncontrolled cell growth and the ability to invade surrounding tissues.

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8
Q

Cardiovascular diseases

A

Affects the heart and blood vessels; accumulation of fatty plaques in arteries

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9
Q

Metabolic disorders

A

Defects in the biochemical processes that regulate energy production and utilization

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10
Q

Examples of metabolic disorders

A

Imbalances in hormone levels, impaired glucose metabolism

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11
Q

Neurological disorders

A

Affects brain, spinal cord and peripheral nerves; induce progressive loss of neurons and impaired neuronal communication leads to cognitive decline, sensory deficits, etc.

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12
Q

Neurological Disorders examples

A

Alzheimer’s disease, Parkinson’s disease, multiple sclerosis

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13
Q

Disease

A

Any disturbance of structure/function of the body; can be symptomatic or asymptomatic

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14
Q

Pathology

A

Study of structural/functional changes in the body caused by disease

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15
Q

Etiology

A

Cause of the disease

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16
Q

Pathogenesis

A

Sequence of the events that lead to the disease

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17
Q

Congenital and heredity diseases (with example)

A

Changes in DNA; Down’s syndrome, fragile x syndrome

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18
Q

Inflammatory diseases

A

Body’s reaction to an injurious agent; autoimmune disorder

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19
Q

Degenerative diseases

A

Degeneration of various parts due to aging; arthritis

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20
Q

Metabolic diseases

A

disturbance in some metabolic process; diabetes, hyper/hypothyroidism

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21
Q

Neoplastic

A

Conditions that cause tumor growth- both benign and malignant (cancer, fibroids)

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22
Q

Goal of cell adaptation/how it’s done

A

Goal: maintain homeostasis in internal/external environment
Done by: changing cell size, number or type of

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23
Q

Physiologic adaptation example

A

Enlargement of the uterus during pregnancy (normal physiological change)

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24
Q

Pathologic adaptation example

A

Enlargement of heart due to hypertension, formation of plaques due to high cholesterol (response to adverse conditions)

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25
Atrophy
Wasting away due to reduction in size of the cells
26
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
27
Hyperplasia
Increase in cell number and tissue mass ONLY in cells that can actively divide
28
Metaplasia
one cell type is replaced by another, stays within the same tissue type usually occurs in response to chronic irritation or inflammation
29
Dysplasia
Abnormal development of cells; associated with chronic inflammation/irritation; can lead to cancer but can be reversible if irritation is removed
30
5 ways for cells to get injured
Nutritional imbalances physical agents radiation chemical biological agents
31
Hypoxia
Lack of oxygen- most common cellular injury
32
Ischemia
Reduce blood flow, can lead to hypoxia
33
Anoxia
Total lack of oxygen
34
Free radical
Contains a single unpaired electron in an outer orbit can lead to heart attack, cancer, etc, DNA damage, mutations
35
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
36
Reactive oxygen species (ROS)
Chemically reactive oxygen molecules; usually balanced by antioxidants
37
Oxidative stress
Imbalance between the production of ROS and antioxidant defenses
38
Reasons for chemical injury (3)
1. Xenobiotics (carbon tetrachloride, lead, carbon monoxide, ethanol, mercury, social or street drugs) 2. chemical agents including agents (OTC and prescribed drugs) 3. direct damage, hypersensitivity reactions
39
What is the leading cause of child poisoning?
Chemical injury - Xenobiotics, OTC
40
What is the most susceptible organ/ initial site of contact for most ingested chemicals?
Liver
41
Infectious injury
pathogenicity of microorganisms, disease producing potential (invasion and destruction, toxin production, production of hypersensitivity reactions)
42
Immunologic and inflammatory injury (3)
Phagocytes cells membrane alterations immune/inflammatory substances (histamine, antibodies)
43
Fever
Release of endogenous pyrogens (intetleukin-1) from macrophages/bacteria
44
functional plasma enzymes
Present more in plasma than tissues, known functions, substrates present in blood, synthesis in liver, decreased liver diseases
45
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
46
4 sources of non functional plasma enzymes
1. Increase in the rate of enzyme synthesis 2. Obstruction of normal pathway 3. Increase permeability of cell membrane 4. Cell damage with the release of its content of enzymes into the blood
47
Medical importance of non functional plasma enzymes (2)
1. Diagnosis of diseases - diseases of different organs cause elevation of different plasma enzymes 2. Prognosis of the disease - the effect of treatment can be followed up by measuring plasma enzymes before and after treatment
48
apoptosis
Programmed cell death involved in normal cell deletion or renewal
49
necrosis
cell death due to extensive damage, cellular swelling, rupture of the cell membrane and inflammation due to injury
50
autophagy
Conserved degradation of the cell that removes unnecessary/dysfunctional components through a lysosome dependent regulated mechanism
51
autophagy paradox
destruction and recycling of cells prevents but also promotes tumors
52
mutagen
Agent known to increase the frequency of mutations
53
Tumor cells typically exhibit genome wide hypomethylation; tumor suppressor genes often hypermethylated
DNA methylation leading to cancer
54
pathophysiology of infectious diseases
involves invasion and proliferation of microorganisms within the body
55
pathophysiology of cancer
involves genetic mutations that lead to abnormal cell division, reduced apoptosis and angiogenesis.
56
pathophysiology of cardiovascular diseases
involves accumulation of fatty plaques in the arteries leading to atherosclerosis and in severe cases, myocardial infarction or stoke
57
pathophysiology of metabolic disorders
involves imbalances in hormone levels, impaired glucose metabolism, and dysregulations of lipid and protein metabolism
58
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
59
how do organisms adapt to stress
in the external environment
60
how do cells adapt to stress
in the internal environment
61
causes of atrophy
disuse denervation loss of endocrine stimulation inadequate nutrition ischemia or decrease in blood flow
62
brain atrophy
also known as cerebral atrophy; loss of neurons and connections between neurons
63
physiologic hypertrophy
increased muscle mass associated with exercise
64
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
65
physiologic hyperplasia
result of hormonal stimulation, increased workload - breast enlargement, pregnancy, tissue healing
66
non-physiologic hyperplasia
result of excessive hormonal stimulation and growth factors- skin warts, excess estrogen
67
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
68
How are ROS formed?
during normal cellular processes and balanced by endogenous antioxidants
69
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
70
cell injury
occurs if the adaptive responses are exceeded or compromised by injurious agents, stress, mutations
71
reversible injury
if it is mild or transient
72
irreversible injury
if the stimulus persists the cell suffers and eventually dies
73
what is the most common cause of cellular injury?
hypoxia
74
direct damage
chemicals and drugs injure cells by combining directly with critical molecular substances, chemo drugs, drugs of abuse
75
hypersensitivity reactions
range from mild skin rashes to immune-mediated organ failure
76
tachycardia
due to increase in metabolic processes resulting from fever
77
pain
due to various mechanisms including release of bradykinin, obstruction, presure
78
presence of cellular enzymes in blood
Creatinine kinase - SKELETAL MUSCLE, heart Aspartate aminotransferase - liver Alanine aminotransferase - liver Amylase - pancreas Troponins - HEART, skeletal muscle
79
lethal cell injury results in
cell death
80
a pt's blood work shows elevation in both AST and ALT which organ is inidicating there is damage?
liver
81
mutations
any inherited alteration of genetic material base pair substitution frameshift spontaneous hot spots

Pathophysiology (18 decks)

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