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BIOL 317 > Test 1 > Flashcards

Test 1 Flashcards

1
Q

What is cancer?

A

Genetic disease in which abnormal cells divide without control and can invade other tissues

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2
Q

Tumor

A

Mass of tissue that results from growth of the abnormal cells that serves no physiological function

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3
Q

Benign tumor properties

A
  • Small
  • encapsulated
  • no metastasis
  • well differentiated
  • typical organization
  • slow growth
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4
Q

Malignant tumor properties

A
  • Large
  • Infiltrative/invasive
  • Metastasizing
  • poorly differentiated
  • atypical tissue structure
  • rapid growth
  • hemmorage
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5
Q

Two fundamental properties of cancer cells

A
  • unregulated cell proliferation

- metastatic spread

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6
Q

Multi-step concept of Carcinogenesis

A

Cancer does not occur after a single genetic change

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7
Q

Clonal

A

Originated from a common ancestral cell that accumulated numerous specific mutations. All cancer cells in primary and secondary tumors are this

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8
Q

Types of genomic alterations associated with cancer

A
  • single-nucleotide subs
  • large-scale chromosomal rearrangements
  • amplifications
  • deletions
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9
Q

Causes of cancer

A
  • any substance or event that damages DNA has the potential to be carcinogenic if it cause to occur in proto-oncogenes or tumor suppressor genes
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10
Q

what are Carcinogens

A

chemicals, radiation, and some viruses

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11
Q

How can DNA mutations result in abnormal cell proliferation

A
  • growth and differention of cells are strictly regulated
  • Many of the genes that control these functions are mutated or aberrant expressed, leading to uncontrolled cell proliferation
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12
Q

What happens normally vs cancer cells

A

normally if DNA damage is so severe that repair is impossible, the cell may initiate apoptosis, or programmed cell death. Cancer cells dont obey these rules

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13
Q

Two ways mutations in genes can lead to uncontrolled cell proliferation

A
  • Make stimulatory genes hyperactive (oncogenes)

- make inhibitory genes inactive (tumor suppressor genes)

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14
Q

Oncogenes

A
  • Originate from genes incolced in regulating normal cell growth
  • Mutations in these genes result in gain of function of the proteins they encode for
  • Accelerator stuck “on”
  • act in dominant manner
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15
Q

Tumor Suppressor Genes

A
  • normal role is to block uncontrolled cell proliferation
  • mutations in these genes result in loss of function of proteins they encode for
  • eliminates “brake” mechanism
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16
Q

Gatekeeper

A

Tumor suppressor genes that controls cell growth

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17
Q

Caretaker

A

Tumor suppressor gene that protects integrity of genome

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18
Q

Sporadic cancer

A

Two acquired mutations in SAME cell

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19
Q

Hereditary cancer

A
  • One mutation inherited (present in every cell)

- 2nd mutation is acquired (in any cell)

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20
Q

DNA repair genes

A
  • normal role is to repair DNA damage caused from DNA damaging agents or spontaneous errors from replication
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21
Q

Base excision repair

A

Removal of abnormal bases

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22
Q

Nucleotide excision repair

A

Removal of pyrimidine dimers, large chemical adducts

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23
Q

Mismatch repair

A

Corrects mismatched bases caused by mistakes in DNA replication

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24
Q

How to metastasize from primary tumor

A

Cancer cell must digest components of EM and basal lamina that normally inhibit migration of cells

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25
Q

Multistep process of metastasis

A
  • detachment
  • invasion
  • survival in circulation
  • attachment
  • extravasation
  • proliferation
  • induction of neovasculature
  • evasion of host defenses

MUST POSSESS ALL OF THESE FUNCTIONS

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26
Q

Proteolytic enzymes

A

Present at higher than normal levels in highly malignant tumors and are not susceptible to normal controls conferred by regulatory molecules

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27
Q

Metalloproteinases (MMP)

A

a type of proteolytic enzyme

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28
Q

Tissue inhibitors of metalloproteinases (TIMP)

A

Regulatory molecules which are normal controls for MMP

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29
Q

Angiogenesis

A

formation of new blood vessels. Required condition for cancer metastasis

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30
Q

properties of TIMP

A
  • slow binding, reversible inhibitors
  • inhibitory activity resides in N-terminal domain
  • inhibit all active MMPs, with different affinities
  • TMPs inhibit tumor invasion
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31
Q

Is there a way to prevent, cure or slow alzheimer’s

A

no

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32
Q

Age factor in AD

A
  • greatest risk factor

- risk of Alzheimer’s doubles every five years after age 65

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33
Q

Risk genes (in alzheimers)

A

Increase the likelihood of developing a disease, but does not guarantee it will happen

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34
Q

Deterministic genes

A

Directly cause a disease, guaranteeing that anyone who inherits one will develop a disorder

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35
Q

Inheritance of AD

A
  • 90% of AD cases are sporadic and occur at 60-90 years

- 10% show autosomal dominant inheritance and have earlier age of onset

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36
Q

Autosomal dominant familial AD can be attributed to mutations in one of three genes

A
  • amyloid presursor protein (APP)
  • presenilin 1 (PSEN1)
  • presenilin 2 (PSEN2)
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37
Q

Best known genetic risk factor for AD

A

Inheritance of the e4 allele of the apoliopoprotein E (APOE)

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38
Q

Amyloid beta precursor protein

A
  • Mutations affect its processing or expression levels

- speculated to bind other proteins on the surface of cells or help cells attach to one another

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39
Q

PSEN1 and PSEN2

A
  • proteins identified as part of the enzymatic complex, y-secretase, that cleaves the AB peptide from APP
  • mutations increase the AB42/AB40 ratio
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40
Q

APP is processed by 3 secretases

A
  • a-secretase
  • B-secretase
  • y-secretase
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41
Q

a-secretase

A
  • Transmembrane protease that cleaves APP within the AB domain, preventing AB generation
  • cuts 90% of APP
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42
Q

B-secretase

A
  • Directly involved in cleavage of APP at the site which generates the N-term end of AB
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43
Q

y-secretase

A
  • multiprotein catalytic complex

- Cleabes APP after a- or B- cleavage to generate the C-term end of AB

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44
Q

If APP is processed by a and y secretases…

A

AB NOT produced

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45
Q

If APP processed by B and y secretases

A

AB produced

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46
Q

Processive Processing

A

Multiple sequential cuts take place within transmembrance domain of APP to generate the AB peptides implicated in AD

47
Q

In vitro assay for gamma secretase

A

monitor cleave of substrate by looking for the accumulation of either AB or AICD-Flag

48
Q

Plaques (AD)

A

microscopic clumps AB peptide. May block signaling at synapses and may activate immune system cells that trigger inflammation and devour disabled cells

49
Q

Tangles (AD)

A

Hyperphosphorylated microscopic strands of the protein tau. This causes neurofibrility tangles and disintegrates the neuron’s transport system

50
Q

Hallmark changes in AD

A
  • Plaques
  • Tangles
  • Loss of connections among brain cells responsible for memory, learning and communication
  • Inflammation resulting from brain’s effort to fend off the lethal effects of the other changes
  • eventual death of brain cells and severe tissue shrinkage
51
Q

Protein misfolding disease

A

-Cause by accumulation of abnormally folded AB and tau proteins in the brain

52
Q

Effects of Alzheimer’s on brain

A
  • Cortex shrivels
  • Hippocampus shrinks
  • Ventricles grow larger
53
Q

Cholinesterade inhibitors (AD)

A

Slows down the disease activity that breaks down a key neurotransmitter

54
Q

NMDA Receptor antagonist (AD)

A

regulates the activity of glutamate, a chemical messenger involved in learning and memory.

55
Q

Diagnosis of AD

A
  • ask Qs about overall health, past medical problems, ability to carry out daily activities, changes in behavior and personality
  • conduct tests of memory, problem solving
  • standard medical tests such as blood or urine
  • Perform brain scans such as CT or MRI
56
Q

Tests used in animal models of AD

A
  • morris water maze
  • novel object recognition
  • passive avoidance
57
Q

Problems with animal model in AD

A
  • mouse models are incomplete models of the human phenotype-most represent familial form of AD, which is small % of total AD cases
  • Behavioral results not as robust
58
Q

Stroke definition

A

Brain damage caused by a sudden and sustained loss of blood flow to the brain

59
Q

Who has high risk of stroke

A
  • Elderly
  • Men have higher risk, but more women die
  • African Americans have almost twice the risk
60
Q

Other risk factors of stroke

A
  • Previous stroke
  • High cholesterol
  • high clood pressure
  • heart disease
  • carotid artery disease
  • smoking/drinking
61
Q

Infarction

A

Tissue death

62
Q

Reperfusion

A

Reestablishment of blood flow

63
Q

Embolus

A

An abnormal particle circulating in the blood

64
Q

Thrombus

A

Clot of blood formed within a blood vessel and remaining attached to its place of origin

65
Q

Thromboembolism

A

Blocking of a blood vessel by a particle that has broken away from a blood clot at its site of formation

66
Q

Cardioembolism

A

Blood clot formed in the Heart

67
Q

Artherosclerosis

A

Hardening of the arteries, caused by cholesterol or plaque build up

68
Q

Ischemic stroke

A
  • loss of blood flow

- Occurs when arteries are blocked by blood clots or by gradual build-up of plaque and other fatty deposits

69
Q

Hemorrhagic stroke

A
  • bleeding

- occurs when a blood vessel in the brain breaks leaking blood into brain

70
Q

Embolic stroke

A

Blood clot or plaque fragment forms somewhere in the body and moves through the bloodstream to the brain. Once in the brain, clot blocks a blood vessel and leads to a stroke

71
Q

Thrombotic stroke

A

Formation inside an artery that supplied blood to the brain

72
Q

Aneurysm

A

Weak spot on wall of an artery that may balloon out, forming a thin-walled bubble. As it gets bigger, the aneurysm gets weaker and can burst, leaking blood into or outside the brain

73
Q

Intercerebral hemorrhage

A

Hemorrhagic stroke. caused when a burst blood vessel bleeds into brain

74
Q

Subarachnoid hemorrhage

A

Blood vessel bursts near surface of brain and blood pours into area around outside of brain

75
Q

when strok strikes act FAST

A

Face, does one side droop?
Arms does one arm drift downward
Speech repeat a sentance
Time time is critical

76
Q

Antithrombotics

A

Prevent formation of blood clots that can cause stroke

77
Q

Antipletlet drugs

A

Prevent clotting by decreasing activity of platelets. Ex. aspirin

78
Q

Anticoagulants

A

Reduce stroke risk by reducing clotting property of blood. ex. warfarin, heparin, enoxaparin

79
Q

Thrombolytic drugs

A

Dissolve thrombi by activating plasminogen to form plasmin, which breaks crosslinks between fibrin molecules to destabilize structural integrity of blood clots

80
Q

Tissue plasminogen activator (tPA)

A

Thrombolytic drug that is only effective within 3 hours of stroke

81
Q

Endovascular procedure (ischemic stroke)

A

Try removing blood clot by sender catheter to site of the blocked blood vessel in the brain.

82
Q

Hemorrhagic stroke Treatment

A
  • Endovascular procedures. Use of catheter to deposit a mechanical agent to prevent rupture
  • Surgical treatment. Metal clip may be placed at base of aneurysm to secure it
83
Q

Penumbra

A

Hyroperfused tissue that will die unless reperfused properly

84
Q

Infarct core cell death

A

Necrosis occurs within a few minutes of vessel occlusion

85
Q

Penumbra cell death

A

Apoptotic cell death may occur and progress more slowly than necrosis

86
Q

Neuroprotection

A

Designed to block cascades that lead to ischemic brain injury

87
Q

In Vitro models of stroke

A

Osygen-Glucose deprivation. Cell or tissue culture incubated in glucose free medium. Then incubated in glucose containing medium, which simulated reperfusion stage/
Pro: Eliminates technical challenges
Con: too simple

88
Q

TTC-Staining

A

Ischemic areas do not metabolize TCC and appear white

89
Q

Limitation with animal models of stroke

A
  • Timing, in some human trials, treatments given outside effective window
  • Age. Animal studies conducted on healthy, young animals under control
  • Morphological and anatomical differences in animal and human brain
  • Plasma conc. of drugs and side effects
90
Q

Obesity Definition

A

abnormal or excessive fat accumulation that presents a risk to health

91
Q

BMI calculation

A

a person’s weight (in kg) divided by the square of his or her height (in m).

92
Q

As a person’s BMI increases

A

so does their mortality rate

93
Q

Feeding is a…

A

complex motivational behavior

94
Q

Fundamental cause of obesity

A

cause of obesity and overweight is an energy imbalance between calories consumed and calories expended.

95
Q

(Obesity) Globally there has been an

A
  • an increased intake of energy-dense foods that are high in fat
  • an increase in physical inactivity due to the increasingly sedentary nature of many forms of work, changing modes of transportation, and increasing urbanization
96
Q

Calories burned depend on

A
  • activity level
  • age
  • height and build
97
Q

How does the body deal with excess dietary calories?

A

1 convert excess fuel to fat and store it in adipose tissue
2 burn excess fuel by extra exercise
3 “waste” fuel by diverting it to heat production

98
Q

Long-term maintenance of body weight

A
  • Periods of food deprivation are followed by periods of increased food intake
  • Periods of forced feeding are followed by periods of lower food intake.
99
Q

Adiposity indirectly influences food intake

A
  • Loss of body fat reduces the efficacy of meal-generated “satiety” signals and increases the efficacy of “hunger” signals.
  • Gain of body fat increases the efficacy of meal-generated satiety signals and reduces the efficacy of “hunger” signals
100
Q

Heritability

A

describes the proportion of total phenotypic variation in a population due to genetic factors

101
Q

heritability estimate

A

tells the proportion of phenotypic variation that can be attributed to genetic variation within a certain population in a particular environment

102
Q

For identical twins obesity observations

A

phenotypic variance equals environmental variance, as there is no genotypic variance

103
Q

For fraternal twins obesity observations

A

phenotypic differences represent both environmental variance and approximately half the genotypic variance

104
Q

adipokines

A

produce changes in fuel metabolism and feeding behavior that reestablish adequate fuel reserves and maintain body mass.

105
Q

Adipose tissue

A

synthesizes, stores, and mobilizes triacylglycerides

106
Q

Leptin

A

upon reaching the brain, acts on receptors in the hypothalamus to curtail appetite.

107
Q

Central weight-control center

A

Hypothalamus

108
Q

When leptin is injected into ob/ob mice

A

lose weight and increase their activity and thermogenesis

109
Q

Mice with two defective copies of Leptin gene (ob/ob) show the behavior and physiology of animals in a constant state of starvation

A
  • they are unable to stay warm
  • exhibit unrestrained appetite (become severely obese)
  • they have metabolic disturbances very similar to those seen in diabetes (are insulin-resistant)
110
Q

Leptin’s Central Actions

A
  • Increase energy expenditure (via physical activity, sympathetic nervous system activity)
  • Decrease food intake
  • Decrease body weight
  • Increase insulin sensitivity
  • Help signal the onset of puberty
  • Regulate other pituitary hormone axes
111
Q

neuropeptide Y (NPY)

A

appetite-stimulating neurons stimulate eating by producing and releasing NPY

112
Q

melanocyte– stimulating hormone (melanocortin)

A

appetite-suppressing neurons in the brain produce this

113
Q

The DB gene encodes for

A

leptin receptor

114
Q

Ghrelin

A

a powerful appetite stimulant that works on a shorter time scale (between meals) than leptin and insulin.

BIOL 317 (1 decks)

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