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Patho > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Components of the Cell

A
  • plasma membrane
  • cytoplasm & organelles
    • endoplasmic reticulum
    • golgi apparatus
    • lysosomes
    • mitochondria
  • nucleus
  • cytoskeleton
  • cilia
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2
Q

Endoplasmic Reticulum

A

extension of nucleus

  • rough: contains ribosomes
  • smooth: participates in metabolism of carbs, lipids,
  • sarcoplasmic reticulum: Ca storage which is needed for muscle contraction
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3
Q

Golgi Apparatus

A

packages molecules in vesicles and transports

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4
Q

Lysosomes

A

packed w/ enzymes that break down damaged products

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5
Q

Mitochondria

A

produces energy

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6
Q

Nucleic Acids

A

DNA & RNA

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7
Q

DNA

A

made up of nucleotides (3 phosphates, a sugar, and 1 of 4 bases)

  • T-A, C-G - held together by H bonds
  • essential for life
  • replication happens during mitosis
  • sequencing: determing base pair
  • codon: 3 nucleotides code for amino acid
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8
Q

RNA

A

mRNA: copies DNA & transported to cytoplasm - ribosome
*template for protein
*1 strand of mRNA = 1 gene = 1 protein
tRNA: transfers amino acids to ribosome
*contains anticodon- matches w/ codon on mRNA

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9
Q

rRNA

A

together w/ protein makes ribosomes

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10
Q

Central Dogma

A

DNA -transcription-> RNA -translation-> protein

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11
Q

Cellular Functions

A
  • transport
  • Ingestion (endocytosis) & Secretion (exocytosis)
  • respiration
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12
Q

Diffusion

A

movement of solutes from high concentration to low concentration
passive

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13
Q

Osmosis

A

movement of h2o from decreased pressure to high pressure

* cell will expand due to increase in water and rupture
* passive
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14
Q

Facilitated Diffusion

A

uses transport proteins to get solutes from high concentration to low concentration
passive

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15
Q

Active Transport

A

uses transport proteins to move molecules from low to high concentration

* ex. sodium/potassium pump
   - needed for creating membrane potential
  - maintaining osmotic balance & stabilizing cell volume
  - failure results in cell death
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16
Q

Respiration

A 
energy production through oxidation of fuel molecules (carbs and lipids)
    *glucose oxidation- 1st source of energy used by
      bodies
      -anaerobic glycolysis
      -aerobic glycolysis
    *lipid fatty acid oxidation
      -beta oxidation
    *protein metabolism
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17
Q

Anaerobic glycolysis

A
  • happens in cytoplasm
  • 1 molecule of glucose = 2 molecules ATP
  • end product- pyruvic acid –> lactic acid (decreases pH)
  • LDH
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18
Q

LDH

A
  • enzyme that catalyzes pyruvic acid to lactic acid
  • only found inside the cell, if present in blood- cells have ruptured
  • can tell what tissue is damaged based of markers in LDH
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19
Q

Aerobic glycolysis

A
  • happens in mitochondria
  • krebs cycle
  • oxidative phosphorylation in ETC
  • 1 molecule of glucose = 34 molecules ATP
  • more efficient than anaerobic and faster than beta oxidation
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20
Q

Cyanide poisioning

A

cyanide binds to an enzyme in ETC which disrupts cell respiration
no energy- cells die

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21
Q

Lipid (fatty acid) respiration

A
  • stored in adipocytes as triglycerides
  • lipolysis: breakdown of triglycerides into fatty acids and glycerol
  • Circulation: adipocytes - blood bound to albumin - mitochondria
  • beta oxidation
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22
Q

Beta oxidation

A
  • 2 carbon fragments are released in repeated cycles to form acetyl CoA
  • acetyl CoA enters citric acid cycle - oxidative phosphorylation
  • 1 molecule of palmitate - 106 ATP
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23
Q

Protein Metabolism

A
  • composed of amino acids
  • digested in GI tract and broken down into amino acids
  • turnover of endogenous proteins
  • nitrogen waste from proteins breakdown (ammonia) is removed as ureas
    • produced to bind N from amino acid break down
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24
Q

Glycogenesis

A

glucose –> glycogen (stored in m and liver)

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25
Q

Glycogenolysis

A

glycogen –> glucose

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26
Q

Gluconeogenesis

A

proteins, fat –> glucose

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27
Q

Cell Communication

A
  • receptors
  • channels
  • adhesion molecules
  • signal transduction
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28
Q

Receptors

A

proteins outside the membrane that respond to signals coming from different molecules (hormones, growth factors, chemical transmitters, drugs)

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29
Q

Channels

A

proteins embedded in membrane that help ions go through

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30
Q

Signal Transduction

A

process by which a cell converts one kind of signal or stimulus (extracellular) into another (cellular response)

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31
Q

Classes of surface cell receptors

A
  • g-protein coupled receptors
  • enzyme linked receptors
  • ion channel receptors
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32
Q

Ligand

A

primary messenger

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33
Q

Receptor

A

all have a chain of amino acids that span the membrane 7 times - domain

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34
Q

Intracellular signaling molecules

A
  • g-proteins
  • effector proteins - produce 2nd messengers
  • 2nd messenger proteins: stay in the membrane
    • catalyze and change molecules so signal can be read
  • target proteins
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35
Q

2nd messenger proteins

A

cyclic AMP, cAMP and cyclic GMP
calcium ion
IP3
DAG

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36
Q

Cholera

A

protein that modifies G-protein so its activation is disrupted- constantly being stimulated to produce 2nd messenger.
activates NA channels to open- water flows into cell
causes diarrhea

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37
Q

G-protein coupled receptor (GPCR) - components of signal transduction

A
  • ligand
  • receptor
  • intracellular signaling molecules
    • g-proteins
    • effector proteins
    • 2nd messengers
    • target proteins
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38
Q

Growth factor receptor (enzyme linked receptor)

A
  • 1 transmembrane domain
  • ligand binds outside & changes the shape of the receptor (2 come together and modify each other)
  • protein inside cell gets phosphorylated then phosphorylates another protien etc
  • phosphorylated proteins look for target protein inside nucleus (through nucleopore)
  • target protein gets together with another protein, together the form a transcription factor and bind to the promoter
  • old proteins must be deactivated by enzymes in cell
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39
Q

Insulin Resistance

A
  • receptor or downstream components are unresponsive- insulin cant act on cells
  • insulins role is to promote glucose mvmt
  • only way glucose gets into cell is through facilitated diffusion
  • glucose transporters found in cytoplasm migrate to membrane and form channel where glucose comes in after activation of insulin receptor
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40
Q

Receptor Channels

A

ligand binds to receptor causing the channel to be opened and ions can move through

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41
Q

Reproduction

A
  • cell growth controlled by growth factors
  • excessive growth prevented by cell cycle inhibitors inside the cell
  • cell cycle
  • terminally differentiated cells
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42
Q

Cell cycle

A
  • cell grows, dna replication starts
  • goes through mitosis
  • stops dividing when telomere gets too short
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43
Q

Telomere

A

determines how many times a cell will divide

  • piece of DNA at end of chromosome
  • each time cell divides a piece is lost
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44
Q

Terminally differentiated cells

A

cells that dont go through cell cycle

  • for specific function
  • cant divide, once they die, can’t be regenerated
  • neurons, cardiomyocytes
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45
Q

Proliferation

A

increasing number of cells

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46
Q

Differentiation

A

each cell type differentiates (becomes specialized) to carry out a particular function

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47
Q

Mitosis

A

cell division

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48
Q

Mutation

A

if Dna in parent cell is altered and passed on, offspring cells will carry the mutation

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49
Q

Stressors

A
  • oxygen
    • temp
    • electrolytes
    • molecular toxins
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50
Q

Reversible changes

A
  • ceases once the stressor is removed
  • no damage done to cell
  • physiological hypertrophy of heart - athletes
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51
Q

Irreversible changes

A

eventually results in cell death

  • damage done and cant be reversed
  • pathological hypertrophy of hear - high BP
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52
Q

Atrophy

A
  • decrease in cell size
  • results in reduced tissue mass
  • reduced use
  • malnutrition
  • decreased hormonal stimulation
  • aging
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53
Q

Hypertrophy

A
  • increase in cell size
  • results in enlarged tissue mass
  • training: cardiac and skeletal muscles
  • hypertension
  • increased hormonal stimulation - acromegaly
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54
Q

Hyperplasia

A
  • increased number of cells
  • may be accompanied by hypertrophy
  • resulting in an enlarged tissue mass
  • hormonal changes in puberty
  • liver regeneration after partial hepatoectomy
  • exposure to high altitudes
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55
Q

Metaplasia

A
  • mature cell type is replaced by a different cell type
  • occurs in response to chronic irritation
  • chronic smokers: ciliated columnar epithelium is substitutes with stratified squamous epithelium
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56
Q

Dysplasia

A
  • cells vary in size and shape within a tissue
  • occurs in response to chronic irritation (infection)
  • DNA mutations
  • may be precancerous
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57
Q

Anaplasia

A
  • undifferentiated cells with variable nuclear and cell structures
  • characteristic of cancer
58
Q

Neoplasm

A

new growth - tumor

59
Q

Hypoxia

A
  • due to reduced oxygen of breathed air (altitude)

* low oxygen saturation in blood

60
Q

Ischemia

A
  • most common injury to cell
  • due to lack/reduction of blood supply
  • oxygenation deprivation to a tissue
    • respiratory problems & circulatory problems
  • lack of oxygen interferes w/ energy production - oxygen not present, metabolism shifts to anaerobic, decreases pH
  • energy production decreases, Na/K pump stops working, Na goes into cell bringing water - dies
  • when cell swells, decreases integrity of membrane - lets in ions (Ca) which stimulate proteolytic enzymes that digest internal components and apoptotic enzymes - cause cell death
61
Q

Infarction

A

cell/tissue death due to oxygen deprivation due to absence of blood supply

62
Q

Cell damage

A
  • drugs: anticancer; immunosuppressants’acetaminophen
  • microorganisms: bacteria, viruses
  • abnormal metabolites: genetic disorders (inborn errors) & altered metabolism
  • nutritional deficits
  • imbalance of fluids of electrolytes
  • extreme temps
  • chemical agents (exogenous & endogenous)
63
Q

High temps

A
  • inactivation of temp sensitive enzymes
  • protein misfolding
  • protein coagulation
  • damage to organelles
  • disrupting cell membrane
64
Q

Low temps

A
  • increase vasoconstriction
  • reduced oxygen supply
  • ice crystal formation
65
Q

Exogenous

A
  • from environment

* carbon monoxide, tobacco smoke, carbon tetrachloride

66
Q

Endogenous

A
  • from inside body
  • reactive oxygen species or free radicals (can damage proteins, lipids, irreversible)
  • from oxidative phosphorylation
  • role of vitamine E- fat soluble compound incorporates itself into the membrane and when free radicals present, sequesters and neutralizes them
67
Q

Apoptosis

A
  • programmed cell death
  • controlled by genetic elements
  • may increase in development and aging
  • occurs when cell number is excessive or cells are injured
  • cells self destruct
  • tumor cells lack apoptotic mechanisms
68
Q

Necrosis

A
  • disrupted cell metabolism
  • lack energy
  • inflammation
  • Ca flux activates lysosomal enzymes - cell swells & ruptures- inflammation to neighboring cells- cell components leak in blood
  • specific enzymes can be measure by diagnostic tests to identify the dype of damaged cells
69
Q

Growth and differentiation changes

A
  • atrophy
  • hypertrophy
  • hyperplasia
  • metaplasia
  • dysplasia
  • anaplasia
  • neoplasia
70
Q

First line of defense- mechanical barriers

A
  • Physical barriers: unbroken skin, mucous membranes, nasal hair, blood clot
  • fluids: saliva, tears, gastric juices, seat glands
71
Q

Second line of Defense

A

*Phagocytosis
neutrophils & macrophages engulf and destroy
*inflammation: limits effects of invading agents - destroy foreign bodies, clean space from debris, prepare site for healing

72
Q

Third Line of Defense

A
  • antibodies

* Cell-mediated immunity

73
Q

Inflammation

A

response to vascular tissue to injury

localize, neutralize and remove harmful agents and remove dead tissues

74
Q

Granulocytes

A

WBC

  • neutrophils: phagocytosis
  • basophils: release histamine
  • eosiniophils: combat histamine
75
Q

Agranulocytes

A

wbc

  • monocytes: enter tissue become macrophages
  • lymphocytes: produce cytokines
76
Q

Mast cells

A

located in tissues
release chemicals from granules in response to injury
histamine
bradykinin

77
Q

Macrophages

A

monocytes that entered tissues

act as phagocytes

78
Q

Cytokines

A

made by lymphocytes & macrophages
small proteins that affect cell behavior
include: interleukins, lymphkines & chemokines

79
Q

Interferons

A

made by leukocytes
produced to prevent virus replication in cells
stimulate immune system

80
Q

Histamine

A

vasodilation

increase capillary permeability

81
Q

Bradykinin

A

vasodilation
increase capillary permeability
pain
chemotaxis

82
Q

Leukotrines

A

released by damaged cells
vasodilation
increase capillary permeability
chemotaxis

83
Q

Prostaglandins

A

released by damaged cells
vasodilation
increased capillary permeability
pain

84
Q

Increased Vascular Permeability

A

epithelial cells stick together tightly
inflammatory mediators increase size- contents less tightly packed
creates gap junctions- allow larger molecules in
immunoglobulins (antibodies) migrate to extracellular space
fibrinogen repair vessel or block infectious agent

85
Q

4 Cardinal Signs of Inflammation (local effects)

A 
redness
warmth
swelling
pain
loss of function
86
Q

Systemic Effects

A 
mild fever
malaise
fatigue
headache
loss of appetite
87
Q

Inflammation Protection

A

removes harmful agents
removes dead tissues
enables tissue to heal

88
Q

Inflammation Harmful

A

too much- becomes chronic
misdirected- infectious agent contiained by healing process to keep occurring
may be accompanied by loss of function

89
Q

Acute Inflammation

A 
Early reaction
short duration
neutrophils
followed by repair
vasodilation
increased capillary permeability
migration of inflammatory cells (neutrophils) to the site of injury
90
Q

Chronic Inflammation

A

slow onset; may follow acute
longer duration
lymphocytes, macrophages & fibroblasts
simultaneous inflammation and repair
less swelling and exudate
collagen produced- fibrous scar tissue
granuloma- small mass of cells w/ necrotic center and covered by connective tissue

91
Q

Complications of Inflammation

A

Infection
Deep ulcers
skeletal muscle spasm
local complications (obstruction, loss of sensation, decreased cell function)

92
Q

Treatments

A 
Acetylsalicylic acid - aspirin
acetaminophen - tylenol
glucocorticoids
ibprofen
COX inhibitors
93
Q

Anti inflammatory Effects of Glucocorticoids

A

made in adrenal cortex gland
decrease capillary permeability
enhance effectiveness of epinephrine and norepinephrine (vasoconstrictors)
reduce number of leukocytes and mast cells
reduce immune response - immunosuppressants (side effect)

94
Q

Adverse effects of glucocorticoids

A

atrophy of lymphoid tissue; reduce production of WBC
catabolic effects: increase tissue breakdown; decrease protein synthesis (affects healing)
delay healing
delay growth in children
retention of Na and H2O- lead to high BP and edema

95
Q

Resolution

A

minimal tissue damage

sun burn

96
Q

Regeneration

A

damaged tissue replaced with cells that are functional
cell must be able to divide
new cells laid down on extracellular matrix
growth factors stimulate local cells to divide
*endothelial cells proliferate
-fill the wound cavity
-promote angiogenesis
*granulation tissue appears- extensive network of capillaries
-highly vascular
- fragile
-need as precursor for blood supply

97
Q

Replacement

A

functional tissue replaced by scar or fibrous tissue
loss of function
no new cell proliferation OR injury to where cells don’t divide

98
Q

Humoral Immunity

A

antibodies produced to neutralize foreign antigen

99
Q

Cell-Mediated Immunity

A

lymphoctyes programmed to attack non-self cells

100
Q

Antigen

A

something that elicits an immune response

101
Q

Major histocompatibility complex (MHC)

A

cell surface proteins that allow immune system to recognize self
every cell in body has same MHCs
changed when cell membrane is altered- not self anymore

102
Q

MHC Class I

A

in all nucleated cells
process and present antigens INSIDE the cell
*proteins produced w/in cell broken down into fragments (antigens) –> rough ER and combine w/ MHC –> transported to golgi–> plasma membrane - t-cells activated and destroy cell

103
Q

MHC Class II

A

present on macrophages & other immune cells
process & present on exogenous antigen
*phagocyte ingests foreign particles & breaks into particles w/ in vesicle - combines w/ MHC vesicle and combines - complex transported to cell membrane - immune cells respond

104
Q

Lymphoid Structures

A 
lymph nodes
spleen
thymus
intestinal lymphoid tissue
lymphatic circulation
105
Q

Tissues where immune cells develop

A

bone marrow - origination & maturation of immune cells

thymus- maturation of t-lymphocytes

106
Q

Macrophages

A 
produced when monocytes move into tissue
MHC class II
secrete interleukins- activate lymphocytes
107
Q

Lymphocytes

A 
primary cells in immune response
WBC
mature lymphocytes- immunocompetent cells
t- lymphocytes
b- lymphocytes
natural killer cells
108
Q

T-lymphocytes

A

derive from bone marrow
differentiate in thymus
participate in cell-mediated immunity
cytotoxic, helper, suppressor, memory

109
Q

Cytotoxic T-cells

A

bind to the antigen, release enzymes and chemicals and destroy the cell
CD8+

110
Q

Helper T-cells

A

facilitate immune response by secreting cytokines

activate and regulate all cells in the immune system

111
Q

Regulatory T-cells

A

suppress immune response

protect against auto immune response

112
Q

Memory T-cells

A

after being exposed, remembers antigen for quicker response next time

113
Q

Cluster of Differentiation

A

cell surface molecules
Each CD is 1 molecule
Identify cell type
Identify stage of differentiation - each stage has different
change as cell matures and differentiates
recognized by antibodies- used to label & identify CD

114
Q

B lymphocytes

A

made and mature in bone marrow
proceed to spleen and lymphoid tissue
humoral immunity
*become antibody producing plasma cells after exposure to antigen w/ help from t-helper
*b-memory: clone plasma cell so already have genetic material for antibody

115
Q

Natural Killer Cells

A

destroy tumor cells and virus infected cells

cell mediated immunity

116
Q

IgG

A 
most common in blood (75%)
primary and secondary immune response
antibacterial, antiviral, antitoxin, antibody
activate complement
cross placenta
117
Q

IgM

A

early immune response

natural antibodies- involved in ABO incompatibility reaction

118
Q

IgA

A

in secretions

protection for newborns

119
Q

IgE

A

allergic reaction

bind to mast cells- release histamine

120
Q

IgD

A

attached to B cells

needed for cell maturation

121
Q

Complement System

A

activated by antigen-antibody complex
complex binds to C1 - cascade activation
complement gets incorporated into membrane of bact. making pore-cell dies
triggers release of mast or basophils - inflammatory response
makes neutrophils/macrophages release lysosomal enzymes - cell damage tissue destruction

122
Q

Titer

A

diagnostic test

measures levels of serum immunoglobins

123
Q

Determining specific antibody

A

enzyme linked immunosorbent assay (ELISA)- detects HIV virus

124
Q

MHC typing

A

tissue matching before transplant

125
Q

Primary Response

A

first exposure to antigen
antigen processed and presented (develop antibody, sensitized t cells)
1-2 weeks antibody titer to reach efficacy

126
Q

Secondary Response

A

repeat exposure to same antigen

more rapid response with efficacy in 1-3 days due to memory b cells

127
Q

Innate Immunity

A

nonspecific
always present
attacks non self antigens

128
Q

Active natural immunity

A

natural exposure to antigen- making antibody, producing sensitized t- cells
flu, cold

129
Q

Active artificial immunity

A

antigen purposefully introduced to body to have memory cells built up
immunizations

130
Q

passive natural immunity

A

protection of infant for first few months
IgG transfer through placenta
IgM transferred through breast milk

131
Q

Passive artificial immunity

A

injection of antibodies for short term protection - when body can’t produce enough antibodies
someone w/ no immune system

132
Q

Immunosuppression

A

reduction of immune response to prevent transplanted tissue rejection

133
Q

Type I Hypersensitivity (Immediate)

A

allergic reactions
exposed to allergen, produce IgE
Mast cells sensitzed by binding to IgEs
second exposure- already have complex, allergen binds to antibodies- mast cells release histamine - inflammation

134
Q

Anaphylaxis

A 
decreased blood pressure (vasodilation)
edema (increased vessel permeability)
airway obstruction
severe hypoxia
treates w/ eminephrine, glucocorticoids, antihistamines, oxygen
135
Q

Type II (antibody mediated cytotoxic)

A

antigen present on membrane
circulating IgGs react w/ antigen
complement activated
antigen carrying cells are destroyed by phagocytosis
response to incompatible blood transfusion

136
Q

Type III (immune complex mediated)

A

antigen combines w antibody forming immune complexes - deposited in tissue - complement activated
stays in tissues and activates neutrophils - destroy tissue

137
Q

Type IV (cell-mediated or delayed)

A

no antibodies present
delayed response by sensitized t cells
release of lymphokines (attract immune cells)
inflammatory response
lyse and destroy antigen bearing cell, destroy normal tissue

138
Q

Primary immune deficiencies

A

basic development failure somewhere

139
Q

Secondary or acquired immune deficiencies

A

loss of immune response due to specific causes

140
Q

AIDS

A

caused by HIV
destroys CD4+ helper t cells
loss of immune response
increased susceptibility to secondary infections
prolonged latent period
development may be suppressed by antiviral agents

141
Q

HIV positive

A

virus is known to be in the body

no evidence of immune suppression - no symptoms

Patho (3 decks)

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