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Pathophysiology > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Euploid Cells

A

Cells with a multiple of the normal # of chromosomes.

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2
Q

Haploid cells

A

Euploid cells- Gametes- Sperm/Egg-23 chromosomes

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3
Q

Diploid Cells

A

Euploid cells- normal body cells- 46 chromosomes

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4
Q

Aneuploid Cells

A

A cell that doesn’t contain a multiple of 23 chromosomes. Includes trisomy/monosomy

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5
Q

Down’s Syndrome

A

Trisomy of Chromosome 21
1:800-3 copies of 21st chromosome.
Risks: maturity of mother

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6
Q

Trisomy

A

A cell containing three copies of one chromosome

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7
Q

Nondisjunction

A

When chromosomes don’t split correctly

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8
Q

Locus

A

the position of a gene or mutation on a chromosome

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9
Q

Turner’s Syndrome

A

Monosomy of X chromosome

Occurs in females.

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10
Q

Klienfelter Syndrome

A

Duplicates X chromosomes along with one Y
chromosome
Female characteristics on a male

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11
Q

3 Modes of inheritance

A
  1. Autosomal dominant
  2. Autosomal recessive
  3. X-linked recessive
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12
Q

Autosomal dominant inheritance

A
  • Both mother and father exhibit the trait and are equally likely to transmit
  • No generations are skipped
  • Affected heterozygus individuals transmit the trait to approx. 50% of offspring
    Example: Huntington’s Disease
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13
Q

Autosomal recessive

A
  • Both sexes affected in equal proportions
  • Diseases seen in siblings, but not parents
  • Aprox 25% offspring affected

Example: cystic fibrosis

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14
Q

X-linked recessive

A
  • Trait seen much more in males
  • Never transmitted from father to son
  • Can be transmitted through many carrier females
  • Affected father —– all daughters affected

Example: muscular dystrophy

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15
Q

Recurrance Risk

A

The probability an individual will develop a genetic disease (Autosomal dominant inheritance: 50%/Autosomal recessive 25%)

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16
Q

Penetrance

A

Percentage of individuals with a specific genotype who also exhibit the expected phenotype.

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17
Q

Incomplete penetrance

A

Individuals with the disease causing genotype may not exhibit the disease. —- carriers

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18
Q

Expressivity

A

Extent of variation in phenotype associated with a particular genotype

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19
Q

Phenotype

A

Outward appearance of an individual—result of both genotype and environment

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20
Q

Genotype

A

Composition of genes at a given locus

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21
Q

Alleles

A

Different forms of a gene: homozygus (AA or aa) or heterozygus (Aa)

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22
Q

Expressivity

A

The extent of variation in phenotype associated with a particular genotype

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23
Q

Multifactorial Inheritance

A

When environmental factors influence the expression of a trait

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24
Q

Single gene trait

A

Traits caused by a single gene

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25
Q

Polymorphic

A

A locus that has two or more alleles that each occur with a significant frequency in a population

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26
Q

Sex-limited traits

A

Can only occur in one sex.

Example: uterine/testicular cancer

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27
Q

Sex-influenced trait

A

Occurs more often in one sex over the other.

Example: male pattern baldness

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28
Q

Polygenic inheritance

A

Traits resulting from several genes acting together

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29
Q

Epigenetics

A

Same gene sequence cause different phenotypes due to chemical modification, which alters expression of genes

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30
Q

Genomic imprinting

A

One parent inactivattes the gene during transmission to offspring—during fertilization

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31
Q

Threshold of liability

A

Stacking risk factors to reach a point where you definitely have the disease.

Example: diabetes—Eventually this person gets diabetes

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32
Q

Atrophy

A

Decrease/shrinkage in cellular size.

Most common in skeletal muscle, the heart, secondary sex organs, and the brain.

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33
Q

Physiologic (adaptive) cell adaptations

A

Normal or natural adaptations

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34
Q

Pathogenic cell adaptations

A

Result of a problem

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35
Q

Physiologic atrophy

A

Shrinkage of the thymus

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36
Q

Pathogenic atrophy

A

Occurs from decreased:

  • workload
  • use
  • blood supply
  • nutrition
  • hormonal stimulation
  • nervous stimulation
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37
Q

Hypertrophy

A

Increase in size of cells—> size of affected organ

Particularly in heart and kidneys

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38
Q

Hypertrophy is triggered by

A 
-Mechanical signals (stretch)
Trophic signals (growth factors, hormones, vasoactive agents)
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39
Q

Hyperplasia

A

Increased # of cells resulting from an increased rate of cell division. (epidermis/liver)

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40
Q

Hyperpasia occurs when:

A
  • Cells can synthesize DNA

- Cells can divide

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41
Q

Dysplasia

A

Abnormal change in size, shape, and organization of mature cells. Found adjacent to cancer, but doesn’t necessarily mean the pt has cancer.

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42
Q

Metaplasia

A

Reversible replacement of one mature cell type by another, less differentiated cell. Loss of specialized function due to the cell’s environment.

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43
Q

Cellular injury

A

Most diseases begin with cell injury. (reversible/irreversible injury)

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44
Q

Hypoxia

A

partial depletion of O2

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45
Q

Hypoxia causes (5)

A
  • Reduced amount of O2 in air
  • Loss of hemoglobin/decreased efficiency of hemoglobin (anemia)
  • Under production of RBC
  • Disease of cardio/respiratory system
  • Poisoning of oxidating enzymes in cells
  • Ischemia
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46
Q

Cellular responses to hypoxia

A

ATP decreases»>failure of sodium-potassium pump and sodium-calcium exchange draws water into cell with high Na concentration»>swelling

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47
Q

Reperfusion injury

A

Reintroduction of O2 to oxygen startved cells causes oxygen starved cells causes oxygen intermediates (radicals) to enter the cell and cause cell damage or cell death

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48
Q

Ischemia

A

Most common cause of hypoxia. Reduced blood supply. Caused by narrowing of arteries/decreased circulation due to blood clots

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49
Q

Anoxia

A

total lack of O2

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50
Q

Oxidative stress

A

Injury induced by free radicals, especially by reactive oxygen species (ROS)

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51
Q

Free radical

A

electrically uncharged atom or group of atoms with an unpaired electron: unstable atoms-bond strongly>leads to chain reactions

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52
Q

Free radicals damage cells by (4)

A
  • antioxidants neutrilize lipid peroxidation-destruction of polyunsaturated lipids
  • alteration of protiens
  • alteration of DNA (fragmentation)
  • Mitochondrial damage
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53
Q

Chemical injury

A

toxic, mutagenic, and carcenogenic materials

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54
Q

Cellular injury mechanisms

A
  • Hypoxic
  • Free radicals/reactive oxygen species
  • Chemical injury
  • unintentional and intentional injury
  • Infectious
  • Immunologic/Inflammatory injury
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55
Q

Cellular damage from lead

A

Harms unborn fetuses/children

Affects:

  • nervous system
  • Production of blood cells (hematologic)
  • kidneys

Effects:

  • High calcium concentrations
  • Anemia
  • Convulsions/delerium
  • Wrist/finger/foot paralysis
  • Glucose in urine
  • GI problems
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56
Q

Cellular damage from Carbon monoxide

A

Interferes with cellular respiration. Causes O2 deprivation (hypoxic injury)

Effects:

  • Headache
  • Giddiness
  • tennitus
  • nausea
  • weakness
  • vomiting
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57
Q

Cellular damage from Alcohol

A

Affects nutritional status & deficiencies. Acetaldehyde is toxic

Effects:

  • liver disease
  • heart disease/hypertension
  • CNS
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58
Q

Asphyzial injuries

A

Caused by a failure of cells to receive or use oxygen. (ie. strangulation/suffocation/drowning/chemical suffocation like CO)

cells react like hypoxia

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59
Q

Blunt force injuries

A

Trauma to the body resulting in tearing, shearing, or crushing of tissues

  • contusions
  • hematoma
  • abrasion
  • laceration
  • fractures
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60
Q

Hematoma

A

collection of blood in soft tissue

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61
Q

Contusion

A

Typical bruise

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62
Q

Abrasion

A

Skinning skin

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63
Q

Laceration

A

ripping/tearing of skin

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64
Q

Fractures

A

broken bones

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65
Q

Sharp injuries

A
  • incised
  • stab
  • puncture
  • chopping
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66
Q

Incised

A

Longer than deep wound

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67
Q

Infectuous injury

A

Disease producing potential depends on:

  • ability to invade and destroy
  • produce toxins
  • hypersensitivity reactions
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68
Q

Immunologic and inflammatory injury

A

Membranes injured by direct contact to chemicals of immune response

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69
Q

Manifestations of cellular injury:Accumulations (7)

A

Accumulation of

  • water
  • lipids and carbs
  • glycogen
  • protiens
  • Pigment changes
  • electrolytes
  • Urate
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70
Q

Water accumulation

A

Due to ATP loss (hypoxia)

Cellular swelling due to solute irregularity. Reversible.

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71
Q

Lipid an carbohydrate accumulation

A

Mostly in spleen, liver, and CNS.

Narrows arteries

72
Q

Glycogen accumulation

A

Results in excessive vacuolation of cytoplasm

73
Q

Protein accumulation

A

Primarily in renal tubules and B-lymphocytes

74
Q

Proteinuria

A

protein accumulation in relan tubules

75
Q

Multiple myeloma

A

Protein accumulation in B-lymphocytes

76
Q

Pigment accumulation

A
  • melanin
  • hematoproteins cause bruising
  • Biliruben in liver causes yellowing from jaundice
77
Q

Calcium accumulation

A

Accumulates in injured and dead cells. Clusters and hardens.

78
Q

Dystrophic calcification

A

Injured/dead/dying tissue

79
Q

Metastatic calcification

A

Clusters in normal/undamaged tissue from high calcium levels

80
Q

Urate accumulation

A

Causes gout

81
Q

Systemic manifestations of cellular injury

A
  • Fatigue
  • Loss of well being
  • Altered appetite
  • fever
  • increased heart rate
  • increased leukocytes (WBC)
  • pain
  • presence of cellular enzymes
82
Q

Necrosis

A

Death of a group of cells.

Main outcome to several cellular injuries. Can be programmed.

83
Q

Apoptosis

A

Death of a single cell

Programmed cell death. Active process.

84
Q

Coagulative necrosis

A

Occurs in kidney, heart, and adrenal gland.

Caused by hypoxia.

Gellies

85
Q

Liquefactive necrosis

A

Occurs in the brain. Injury to neurons/glial cells in the brain.

Tissue becomes soft and liquefies, forming cysts

86
Q

Caseous necrosis

A

Combination of coagulative and liquefactive necrosis. Tissue soft and granular.

Teburculosis

87
Q

Fat necrosis

A

Occurs in breasts, pancreas, abdominal structures

Free fatty acids combine with calcium, magnesium, and sodium forming soaps. Lipases dissolve fats.

White/opaque

88
Q

Gangrenous necrosis

A

hypoxic injury»>death of tissue

89
Q

Algor mortis

A

Drop in body temp

90
Q

Livor mortis

A

Skin discoloration

91
Q

Rigor mortis

A

Stiff muscles

92
Q

Putrefaction: postmortem autolysis

A

Enzymes-lytic dissolution

93
Q

Hydrostatic pressure

A

Pushes water

94
Q

Osmotic pressure

A

Pulls water in

95
Q

Capillary hydrostatic pressure

A

Outward movement of water from the capillary to the interstitial space. ie soaker hoses

96
Q

Capillary oncotic pressure

A

Osmotically attracts water from the interstitial fluid

97
Q

Interstitial hydrostatic

A

inward movement from the interstitial space to the capillary

98
Q

Interstitial oncotic

A

osmotically attracts water from the capillary into interstitial fluid

99
Q

Edema

A

Swelling. Accumulation of fluid in the interstitial space

100
Q

Mechanisms of edema

A
  • increased capillary hydrostatic pressure
  • increased capillary membrane permeability
  • decreased capillary oncotic pressure
  • lymphatic channel obstrucion (lymphedema)
101
Q

Causes of increased capillary hydrostatic pressure

A
  • Venous obstruction

- Salt/water retention (heart failure, renal failure, cirrhosis of the liver, pregnancy)

102
Q

Causes in decreased capillary oncotic pressure

A

Plasma protiens lost in blood-burns, underproduction of albumin, liver disease

103
Q

Causes of increased membrane permeability

A
  • Inflammation/immune response
  • allergic reations

proteins escape

104
Q

Causes of lymphatic channel obstruction

A
  • removal of lymph nodes

- tumors

105
Q

lymphedema

A

when lymphatic channels are blocked/removed proteins and fluid accumulate in interstitial space

106
Q

Localized edema

A

Surrounding a cut/burn/sprain

107
Q

Generalized edempa

A

-dependet edema:a fluid accumulation in the tissues that is influenced by gravity. It is usually greater in the lower part of the body than in the part above the level of the heart.

108
Q

Mechanism for retaining sodium

A
  1. Blood pressure drops
  2. Renin released by juxtaglomerular
  3. Renin stimulates angiotensin I
  4. ACE converts angiotension I to angiotensin II in pulmonary vessels
  5. Angiotensin II stimilates secretion of aldosterone/causes vasoconstriction
  6. Aldosterone promotes sodium and water resorption and excretion of potassium, increasing blood volume/blood pressure
109
Q

Mechanism to excreting excess sodium

A

Naturitic peptides released at high blood pressure-Cause vasodialation and decreases blood pressure.

110
Q

Water balance regulation

A

regulated by secretion of ADH in response to high plasma osmolality or low circulating blood volume

111
Q

Low water/high sodium

A

Causes:

  • thirst
  • release of Antidiuretic hormone (ADH)
112
Q

Hypertonic solution

A

High sodium in interstitial space

Cells shrink

113
Q

Hypotonic solution

A

Low sodium in interstitial space

cells swell

114
Q

Causes of isotonic fluid loss

A

hypovolemia

  • hemorrhage
  • severe wound drainage
  • excessive sweating
  • inadequate fluid intake
  • skin dryness
  • increased urine output
115
Q

Causes of isotonic fluid excess

A

hypervolemia

  • Increased aldosterone
  • excessive iV administration
  • effects of drugs that cause reabsorption of sodium/water
116
Q

Manifestations of isotonic fluid loss

A
  • Rapid heart rate
  • Flattened neck veins
  • Normal/decreased blood pressure
  • weight loss
  • dryness
  • decreased urine output
117
Q

Manifestations of isotonic fluid excess

A
  • Neck veins distend
  • Blood pressure increases
  • edema formation
118
Q

Hypertonic water deficit

A

Dehydration

  • headache
  • thirst
  • dry skin/mucus membranes
  • elevated temp
  • weight loss
  • decreased urine output
  • more concentrated urine
119
Q

Hypotonic water excess

A

Overhydration (nearly impossible)

  • cerebral edema
  • confusion
  • convulsions
  • weakness
  • nausea
  • headache
  • weight gain
120
Q

Normal range of Calcium

A

8.5mg/dl-10.5mg/dl

121
Q

Normal range of Phosphate

A

2.0 mg/dl-4.7mg/dl

122
Q

Normal range of Magnesium

A

1.5mEq/L-3.0mEq/L

123
Q

Normal range of Sodium

A

135mEq/L-145mEq/L

124
Q

Normal range of Potassium

A

3.5mEq/L-5.5mEq/L

125
Q

Role of Potassium in the body

A

“Cardiac”

  • Normal cardiac rhythems
  • Nerve impulses
  • Electrical neutrality
  • skeletal smooth muscle contraction
126
Q

Role of Sodium in the body

A

“neurologic”

  • Regulates osmotic forces, thus water
  • Axon action potentials
  • Acid-base balences
  • Membrane transport
  • cellular chemical reactions
127
Q

Role of Calcium in the body

A

“musculoskeletal”

  • Fundemental metabolic practices
  • structure of bone and teeth
  • blood clotting
  • contraction of muscles
128
Q

Role of Phosphate in the body

A
  • Activates B-complex vitamins
  • Forms/activates ATP
  • Acid-base balance
  • Calcium homeostasis
129
Q

Role of Magnesium in the body

A
  • Smooth muscle function
  • Neuromuscular excitability
  • blood coagulation
  • ATP formation
  • Carbohydrate metabolism
130
Q

Innate immunity

A
  • Natural barriers (physical, mechanical, biochemical)
  • Inflammation
  • In place at birth
131
Q

Adaptive immunity

A
  • Aquired
  • Specific
  • Slower
  • Uses “memory”
132
Q

Defense mechanisms-3 lines of defense

A

1-Physical and biochemical barriers/normal flora
2-Innate immunity in response to tissue injury or infection (inflammation)
3-Adaptive immunity

133
Q

Inflammation benefits (4)

A
  • prevents infection and further damage
  • limits and controls inflammatory process-prevents spread to healthy tissue
  • Elicits specific response from adaptive immune system
  • Prepares area for healing
134
Q

Compliment system

A

destroys pathogens via:

  • obsinias
  • chemotactic factors
  • anaphylaxtoxins
135
Q

Clotting system

A

Forms blood clots that:

  • plug damaged vessels
  • stop bleeding
  • stop WBC to help affected area
  • Form framework for healing
136
Q

Kinin system

A

Bradykinin is final product. Functions:

  • dialation of blood vessels (like histamine)
  • Induces pain
  • Smooth muscle cell contraction
  • Increased membrane permeability (like histamine)
137
Q

Characteristics of inflammation

A
  • Occurs in tissues with blood supply
  • Activated rapidly
  • Depends on activity of both cellular and chemical components
  • Nonspecific: occurs same way no matter what type of stimulus
  • Acute vs. Chronic
138
Q

Acute inflammation

A 
Self limiting
8-10 days
-pain
-redness
-exudate
-swelling
-heat
-leukocytes value over 11k/mL
-Left shift
139
Q

Chronic inflammation

A

over 2 weeks-months

  • pus formation
  • incomplete healing
  • lyphocytes and macrophages at site trying to clean site for healing
  • granulomas-walled off infection
140
Q

Granulomer formation

A

Contains infection’s remains so it is walled off from the functioning body.
Tuberculosis

141
Q

Leukocytes

A

WBC

  • Lymphocytes
  • Monocytes»>Macrophages
  • Granulocytes:
    - Neutrophil
    - Eosinophil
    - Basophil
142
Q

Mast cells

A

Release histamine

143
Q

Histamine

A
  • Causes vasodialation (swelling/heat/redness)
  • Increases capillary membrane permeability
  • Begins synthesis of other mediators of inflammation
144
Q

Neutrophils

A

Predominant phagocytes in early inflammation. 6-12 hours after injury
-short lived/incapable of division

145
Q

Functions of neutrophils

A
  • removal of debris/dead cells in sterile locations (pus)

- destruction of bacteria in non sterile locations

146
Q

Left shift

A

More immature leukocytes synthesized to combat infection

147
Q

erythema

148
Q

Types of exudate

A
  • serous
  • Fibrinogen
  • Purulent
  • Hemorrhagic
149
Q

Serous exudate

A
  • Watery
  • Few leukocytes/plasma proteins
  • Fluid in blister
150
Q

Fibrinogen exudate

A
  • Thick and clotted

- Mucus in lungs with pneumonia

151
Q

Purulent exudate

A
  • Walled off lesions (abcess/pus)
  • Many leukocytes
  • Chronic inflammation
152
Q

Platelets

A

Activated to:

  • Stop bleeding
  • Degranulation, releasing mediators with histamine-like effects
  • Would healing
153
Q

Basophils

A

Responsible for allergic reactions/antigen response

Releases histamine/heparin

154
Q

Heparin

A

Anticoagulent=more WBC to the area

155
Q

Monocytes

A

Phagocytes. Longer lived than neutrophils. Antibody response via Tcells. Become macrophages

156
Q

Macrophages

A

Engulfs/digests cellular debris

  • Enter site after 24 hours to gradually replace neutrophils
  • Orchestrate wound healing by cleaning up area
157
Q

Eosinophils

A

Mildly phagocytic.

  • Defense against parasites
  • Regulate mast cell mediators (contains inflammation-histamin-ase)
158
Q

Cytokines

A

Variety of molecules that affect other cells: pro-inflammatory/noninflammatory

159
Q

Opsonins

A

Coats bacteria so WBC can ingest

160
Q

Chemotactic factors

A

Attract phagocytic cells to site

161
Q

Anaphylactoxins

A

Induce rapid degranulation of mast cells, release histamine

162
Q

Primary intention in wound healing

A

Resolution: wounds that heal and are functional again

163
Q

Secondary intention of wound healing

A

Repair: Doing the best you can to get the body back to normal. Loss of function.

164
Q

Phases of wound healing (3)

A

1-Inflammation: 1-2 days(neutrophils, macrophages, platelets)
2-Proliferation & New tissue formation: 3-4 days (red/pink tissue: granulation tissue)
3- Remodeling and maturation: weeks-years. scar formation and cellular differentiation.

165
Q

Ishemia and wound healing

A

lack of O2 leads to infection

166
Q

Excessive bleeding and wound healing

A

Large clots means more space to fill

167
Q

Excessive fibrin deposits

A

Leads to adhesions: thick bands of fibrin that binds structures together (organs)

168
Q

Diabetes

A

Prolongs wound healing: hyperglycemia suppresses macrophages

169
Q

Wound infection

A

pathogens delay wound healing

170
Q

Inadequate nutrition

A

cells need adequate nutrition to heal

171
Q

Medications

A

Anticancer agents, NSAIDs, Steroids delay wound healing

172
Q

Obesity

A

Adipose tissue hard to suture

173
Q

Red flags for bad wound healing

A
  • pain
  • redness after healthy looking granulation tissue
  • excessive swelling
  • purulent exudate
174
Q

Dehiscence

A

Wound pulls apart at suture line

175
Q

Impared contraction

A

When contraction is excessive, joints are immobilized

Pathophysiology (6 decks)

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