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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
Q

Atrophy

A

Wasting away due to reduction in size of the cells

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26
Q

Hypertrophy

A

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

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27
Q

Hyperplasia

A

Increase in cell number and tissue mass ONLY in cells that can actively divide

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28
Q

Metaplasia

A

one cell type is replaced by another, stays within the same tissue type
usually occurs in response to chronic irritation or inflammation

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29
Q

Dysplasia

A

Abnormal development of cells; associated with chronic inflammation/irritation; can lead to cancer but can be reversible if irritation is removed

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30
Q

5 ways for cells to get injured

A

Nutritional imbalances
physical agents
radiation
chemical
biological agents

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31
Q

Hypoxia

A

Lack of oxygen- most common cellular injury

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32
Q

Ischemia

A

Reduce blood flow, can lead to hypoxia

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33
Q

Anoxia

A

Total lack of oxygen

34
Q

Free radical

A

Contains a single unpaired electron in an outer orbit
can lead to heart attack, cancer, etc, DNA damage, mutations

35
Q

Mechanism for ischemic/hypoxic injury (5 steps)

A

Reduction in ATP > dysfunction of Na+/K+ ATPase > altered intracellular levels > altered enzyme activation > cell death if oxygen not restored

36
Q

Reactive oxygen species (ROS)

A

Chemically reactive oxygen molecules; usually balanced by antioxidants

37
Q

Oxidative stress

A

Imbalance between the production of ROS and antioxidant defenses

38
Q

Reasons for chemical injury (3)

A
  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
Q

What is the leading cause of child poisoning?

A

Chemical injury - Xenobiotics, OTC

40
Q

What is the most susceptible organ/ initial site of contact for most ingested chemicals?

A

Liver

41
Q

Infectious injury

A

pathogenicity of microorganisms, disease producing potential (invasion and destruction, toxin production, production of hypersensitivity reactions)

42
Q

Immunologic and inflammatory injury (3)

A

Phagocytes cells
membrane alterations
immune/inflammatory substances (histamine, antibodies)

43
Q

Fever

A

Release of endogenous pyrogens (intetleukin-1) from macrophages/bacteria

44
Q

functional plasma enzymes

A

Present more in plasma than tissues, known functions, substrates present in blood, synthesis in liver, decreased liver diseases

45
Q

non-functional plasma enzymes

A

Present in plasma lower than tissues, no known functions, substrates absent from blood, synthesis in different organs, different enzymes inc in different diseases

46
Q

4 sources of non functional plasma enzymes

A
  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
Q

Medical importance of non functional plasma enzymes (2)

A
  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
Q

apoptosis

A

Programmed cell death involved in normal cell deletion or renewal

49
Q

necrosis

A

cell death due to extensive damage, cellular swelling, rupture of the cell membrane and inflammation due to injury

50
Q

autophagy

A

Conserved degradation of the cell that removes unnecessary/dysfunctional components through a lysosome dependent regulated mechanism

51
Q

autophagy paradox

A

destruction and recycling of cells prevents but also promotes tumors

52
Q

mutagen

A

Agent known to increase the frequency of mutations

53
Q

Tumor cells typically exhibit genome wide hypomethylation; tumor suppressor genes often hypermethylated

A

DNA methylation leading to cancer

54
Q

pathophysiology of infectious diseases

A

involves invasion and proliferation of microorganisms within the body

55
Q

pathophysiology of cancer

A

involves genetic mutations that lead to abnormal cell division, reduced apoptosis and angiogenesis.

56
Q

pathophysiology of cardiovascular diseases

A

involves accumulation of fatty plaques in the arteries leading to atherosclerosis and in severe cases, myocardial infarction or stoke

57
Q

pathophysiology of metabolic disorders

A

involves imbalances in hormone levels, impaired glucose metabolism, and dysregulations of lipid and protein metabolism

58
Q

pathophysiology of diabetes

A

involves the increase of blood glucose from:
carb intake
increase in hepatic glucose production
decrease in peripheral glucose uptake
decrease in insulin secretion

59
Q

how do organisms adapt to stress

A

in the external environment

60
Q

how do cells adapt to stress

A

in the internal environment

61
Q

causes of atrophy

A

disuse
denervation
loss of endocrine stimulation
inadequate nutrition
ischemia or decrease in blood flow

62
Q

brain atrophy

A

also known as cerebral atrophy; loss of neurons and connections between neurons

63
Q

physiologic hypertrophy

A

increased muscle mass associated with exercise

64
Q

pathologic hypertrophy

A

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
Q

physiologic hyperplasia

A

result of hormonal stimulation, increased workload - breast enlargement, pregnancy, tissue healing

66
Q

non-physiologic hyperplasia

A

result of excessive hormonal stimulation and growth factors- skin warts, excess estrogen

67
Q

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:

A

hyperplasia

68
Q

How are ROS formed?

A

during normal cellular processes and balanced by endogenous antioxidants

69
Q

mechanism for ischemia-reperfusion injury

A

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
Q

cell injury

A

occurs if the adaptive responses are exceeded or compromised by injurious agents, stress, mutations

71
Q

reversible injury

A

if it is mild or transient

72
Q

irreversible injury

A

if the stimulus persists the cell suffers and eventually dies

73
Q

what is the most common cause of cellular injury?

A

hypoxia

74
Q

direct damage

A

chemicals and drugs injure cells by combining directly with critical molecular substances, chemo drugs, drugs of abuse

75
Q

hypersensitivity reactions

A

range from mild skin rashes to immune-mediated organ failure

76
Q

tachycardia

A

due to increase in metabolic processes resulting from fever

77
Q

pain

A

due to various mechanisms including release of bradykinin, obstruction, presure

78
Q

presence of cellular enzymes in blood

A

Creatinine kinase - SKELETAL MUSCLE, heart
Aspartate aminotransferase - liver
Alanine aminotransferase - liver
Amylase - pancreas
Troponins - HEART, skeletal muscle

79
Q

lethal cell injury results in

A

cell death

80
Q

a pt’s blood work shows elevation in both AST and ALT which organ is inidicating there is damage?

A

liver

81
Q

mutations

A

any inherited alteration of genetic material
base pair substitution
frameshift
spontaneous
hot spots

Pathophysiology (16 decks)

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