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Pathophysiology > Vocab > Flashcards

Vocab Flashcards

1
Q

Pathology

A

the study and diagnosis of disease though the examination of organs, tissues, cells, and bodily fluids

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2
Q

Physiology

A

study of mechanical, physical, and biochemical functions of living organisms

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3
Q

Pathophysiology

A

study of abnormalities in physiologic functioning of living beings

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4
Q

Idiopathic Etiology

A

Cause is unknown

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5
Q

Iatrogenic Etiology

A

Cause is a result of an unintended or unwanted medical treatment

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6
Q

Primary Levels of Prevention

A

Altering susceptibility, reducing exposure for susceptible persons

Ex: Education, immunizations, condoms

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7
Q

Secondary Levels of Prevention

A

Early detection and screening; prevent further complications

Ex: Breast cancer screening, PAP smears

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8
Q

Tertiary Levels of Prevention

A

Individual has the disease; looking to get them back to better quality of life

Ex: rehabilitation (PT), supportive care, outreach programs

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9
Q

Incidence

A

New cases over a time period

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10
Q

Prevalence

A

Existing cases over a time period

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11
Q

Reliability

A

Same results when repeated

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12
Q

Validity

A

Measuring what was intended

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13
Q

Sensitivity

A

Correctly identifies a condition

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14
Q

Specificity

A

Correctly excludes a condition

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15
Q

Predictive Value

A

Ability to predict disease or condition

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16
Q

Morbidity

A

Causes disease, illness, consequences

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17
Q

Diffusion

A

Passive transport

Movement of area of high concentration to low concentration

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18
Q

Osmosis

A

Passive transport

Movement of water via osmotic pressure from high to low concentration

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19
Q

Facilitated diffusion

A

Passive transport that requires a protein carrier, such as glucose

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20
Q

Ischemia

A

Lack of blood flow

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21
Q

Hypoxic

A

Lack of oxygen –> cannot produce ATP

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22
Q

What is the first manifestation of most forms of reversible cell injury?

A

Hydropic swelling

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23
Q

What is Hydropic Swelling?

A

Cell swelling due to excess water from sodium/potassium pump malfunction (not receiving enough energy/ATP)

Pump malfunction –> sodium ions build up inside the cell –> water always follows salt –> cells swell

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24
Q

What is Intracellular Accumulation?

A

Build up of substances due sometimes to faulty metabolisms

  • Normal body substance buildup (melanin, lipid)
  • Buildup due to metabolic dysfunction (Tay-Sachs disease)
  • Exogenous products (black lung filled with coal dust)
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25
Q

How does free radical formation (UV/radiation) cause damage?

A

Lipid preroxidation by attacking fat

Attacks proteins disrupting transport channels

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26
Q

What is Necrosis?

A

Tissue destruction that occurs as a consequence of ischemia or toxic injury

Characteristics: cell rupture, spilling of contents into ECF, and inflammation

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27
Q

Coagulative Necrosis etiology

A

Ischemia –> loss of energy –> inefficiency of sodium potassium pump –> salt build up inside cell –> swelling –> rupture (triggers inflammatory response)

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28
Q

Liquefactive Necrosis etiology

A

spilled contents –> stimulates inflammatory response –> eaten up by lysosomes –> but healthy tissue gets eaten too –> forms abscesses –> liquid-filled cysts

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29
Q

Fat Necrosis

A

death of adipose tissue as a result of trauma

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30
Q

Caseus Necrosis

A

lung damage secondary to tuberculosis

-clumpy cheese appearance in granulomas

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31
Q

What is a gangrene?

A

Cellular death in a large area of tissue that results in interruption of blood supply to a particular part of the body

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32
Q

Describe Dry Gangrene

A
  • Form of coagulative necrosis
  • Blackened, dry, wrinkled tissue separated by a line of demarcation from healthy tissue
  • Spreads slowly
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33
Q

Describe Wet Gangrene

A

Form of liquefactive necrosis (abscesses) typically found in internal organs but also can be seen outwardly

  • No strict demarcation
  • Spreads quickly
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34
Q

Describe Gas Gangrene

A

Results from infection of necrotic tissue by Clostridium (anaerobic bacteria)
-Formation of gas bubbles in damaged tissue

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35
Q

What does Apoptosis do?

A

Intracellular cascade that activates cellular suicide response

  • Does NOT cause inflammation
  • Neat clean matter through cascade signaling
  • No further damage
  • Removes dead cells, leaving room for new, better functioning cells
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36
Q

Component Acquired Capability - leading up to cancer

A
  • Self sufficiency in growth signals (autonomous)
  • Insensitivity to antigrowth signals
  • Evading apoptosis
  • Limitless replicative potential
  • Sustained Angiogenesis
  • Tissue invasion and metastasis
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37
Q

How do Mutator Genes lead to cancer?

A

Increases the rate of mutation of one or more other genes

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38
Q

What are proto-oncogenes and how can they lead to cancer?

A

Proto-Oncogenes are normal genes for proliferation (cell differentiation)

Thus when they mutate, they turn into oncogenes, enabling cells for autonomy

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39
Q

What is an oncogene?

A

An oncogene is a mutated proto-oncogene, aka CANCER CAUSING GENE

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40
Q

What are Tumor-Supressor Genes and how can they lead to cancer?

A

They are the genes that suppress tumors –> however if they are mutated, they no longer can inhibit the growth of tumors

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41
Q

What are other genes that when mutated, can lead to cancer?

A

Genes that control apoptosis, genes that regulate repair of DNA damage

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42
Q

Are mutations that occur in somatic cells passed down to progeny?

A

No

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43
Q

Are mutations that occur in gremlin (stem) cells passed to future generations?

A

Maybe!

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44
Q

GERD can lead to what type of cancer?

A

Esophageal cancer

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45
Q

Chronic Pancreatitis can lead to…

A

Pancreatic cancer

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46
Q

How can viruses cause cancer?

A

Viruses can insert their own DNA structure/genes –> change the existing genes –> leads to cancer

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47
Q

What are the local effects of tumors?

A
  • Pain (which can be absent until late stages –> late diagnosis)
  • Tissue Integrity (compressed and eroded blood vessels, ulceration, necrosis, hemorrhage, frank bleeding)
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48
Q

What are the systemic effects of (malignant) tumors?

A
  • Weight loss and cachexia (anorexia, fatigue, pain, stress due to the increased demands from tumor cells on the body)
  • Anemia (lack of RBC)
  • Severe fatigue (due to inflammatory changes, cachexia, anemia, stress of treatment schedule, psychological factors)
  • Effusions from the inflammation
  • Infections (as a result of immunodeficiency)
  • Paraneoplastic syndrome (tumor cells release substances that affect neurologic function and may have hormonal effects)
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49
Q

Cachexia

A

Weakness and wasting of body

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50
Q

Effusions

A

Fluid buildup in body cavities

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51
Q

How does the TNM Classification System work?

A 
TX = primary tumor, number is based on size 
N = regional lymph nodes and the number of lymph nodes involved
M = distant metastasis; 0 = no metastasis, 1 = metastasis present
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52
Q

For what type of cells is radiation therapy most effective?

A

Rapidly dividing cells

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53
Q

What are adverse effects of radiation therapy?

A

Bone marrow depression, epithelial damage, infertility, GI upset

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54
Q

What type of drugs does chemotherapy use?

A

Antineoplastic drugs

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55
Q

How can a diagnosis of malignancy be confirmed?

A

Biopsy

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56
Q

Remission of cancer is generally defined as a period in which….

A

An individual no longer has any detectable signs or symptoms of cancer

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57
Q

What is margination?

A

Margination is the process of neutrophils and macrophages sticking and accumulating to the blood vessel wall in the area of injury

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58
Q

How do the marginated WBC stick?

A

They stick via selections which are released by endothelial cells when trigger by cytokines

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59
Q

What is emigration and diapedesis?

A

The movement of leukocytes out of the circulatory system towards the site of tissue damage or infection

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60
Q

What is chemotaxis and how is it created?

A

Chemical gradient that promotes leukocytes out of the circulatory system towards the site of injury.

The gradient is created by proteins of the complement system + chemokines

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61
Q

What are the elements of cellular stage of the inflammatory response?

A

margination, emigration/diapedesis, chemotaxis, phagocytosis

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62
Q

What are the elements of the vascular stage of the inflammatory response?

A

Bradykinin –> vasodilation –> parin receptors –> mast cells/basophils –> histamine –> (eventually prostaglandins and leukotrienes)

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63
Q

How does increased vascular permeability effect osmotic pressure?

A

Increased vascular permeability –> outpouring of protein-rich exudate into extravascular spaces –> loss of proteins –> reduces capillary osmotic pressure and increases the interstitial osmotic pressure

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64
Q

What are inflammatory exudates and what are their functions?

A

Inflammatory exudates: the fluid that leaks out of blood vessels and into nearby tissues in the inflammatory response

  • Transport leukocytes and antibodies
  • Dilutes toxins and irritating substances
  • Transport nutrients for tissue repair
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65
Q

Serous inflammatory exudate =

A

watery

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66
Q

Sanguinous inflammatory exudate =

A

bloody

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67
Q

Serosanguinous inflammatory exudate

A

mostly serous (mostly watery)

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68
Q

Fibrinous

A

sticky, thick, very high cell content

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69
Q

Purulent

A

pus, thick, yellow-green, high in WBC and microorganisms

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70
Q

What plasma proteins would show increased levels in diagnostic findings for inflammation?

A

Fibrinogen and Prothrombin

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71
Q

What is C-Reactive Protein and what does it indicate?

A

It is a protein not normally in the blood but appears with acute inflammation and necrosis within 24-48 hours

-Inflammatory marker

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72
Q

What is different about RBC when there is inflammation?

A

They have an increased ESR (erythrocyte sedimentation rate) due to the elevated plasma protein count

-Inflammatory marker

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73
Q

Local effects of inflammation

A

Redness, swelling, heat, pain, loss of function

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74
Q

Systemic effects of inflammation

A 
Mild fever = pyrexia 
Malaise
Fatigue
Headache
Anorexia or weight loss
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75
Q

Which leukocytes infiltrate more in chronic inflammation than acute inflammation?

A

Infiltration by macrophages and lymphocytes instead of neutrophils.

Neutrophils are the first responders in acute inflammation.

76
Q

What are there increased presences of in chronic inflammation than acute?

A

Lymphocytes, macrophages, and fibroblasts

77
Q

What is there less of in chronic inflammation than acute?

A

There is less swelling and exudate in chronic inflammation than acute.

78
Q

ASA =

A

Acetylsalicylic Acid
Example: Aspirin
-lowers prostaglandins synthesis at the site –> decreases inflammatory response –> anti-inflammatory

  • Analgesic
  • Antipyretic
  • Anti-Inflammatory

Can increase bleeding, therefore is NOT given to someone with cuts/wounds

79
Q

Acetaminophen

A

Example: Tylenol
It is an analgesic but has no effects on the inflammatory response

Can also increase bleeding

80
Q

NSAIDs

A

Non-steroidal anti-inflammatory drugs
Example: Ibuprofen (advil, motrin) or Naproxen Sodium (aleve)

-Anti-Inflammatory, analgesic (relieves pain), and antipyretic

Can increase bleeding

81
Q

What are the side effects of ASAs and NSAIDs?

A

Increased bleeding
GI stress
Stomach Ulcerations
Delayed blood clotting

82
Q

What are glucocorticoids?

A

Corticosteroids that decrease capillary permeability, decrease leukocytes and mast cells at site
–> decreased release of histamines and prostaglandins

Anti-finlammatory

83
Q

What are the side effects of Glucocorticoids?

A

Risk of infection
GI distress
Stomach ulceration
Edema
Increased BP
Atrophy of lymphoid tissue –> decrease in WBC count and hematopoiesis (formation of blood cellular components in bone marrow
Catabolic Effects (tissue breakdown, less protein synthesis ) –> osteoporosis, muscle wasting, thinning of skin
Altered feedback response system –> decrease in release of production of normal hormones –> atrophy of adrenal glands
Delayed healing (and growth in children)
Retention of sodium and water due to aldosterone-like effect in the kidney

84
Q

Resolution Healing

A

Minimal tissue damage

85
Q

Regenration

A

Damaged tissues replaced with cells that are capable of mitosis and are still functional

86
Q

Replacement

A

Functional tissue replaced by scar tissue

87
Q

Primary intention

A

Approximated wound edges and ALL areas heal simultaneously

88
Q

Secondary intention

A

Heals from the inside out / bottom up

  • Greater risk for infection and scarring
  • Examples: Pressure ulcers, fractures
89
Q

What phase of healing occurs 3-4 days after injury?

A

Proliferative Phase

Foreign material and cell debris removed by phagocytosis and granulation tissue grows into the gap

90
Q

What phase of healing occurs about 2 weeks after injury?

A

Remodeling phase

-scar tissue build up

91
Q

What is hypertorphic scar tissue and how does it complicate healing?

A

Overgrowth of fibrous tissue, leading to hard ridges of scar tissue or keloid formation

92
Q

What is ulceration and how does it complicate healing?

A

The blood supply may be impaired around the scar, resulting in further tissue breakdown and ulceration at a future time.

93
Q

What is dehiscence?

A

Previously closed wound reopening

94
Q

What are the 4 basic stages of inflammation and healing?

A

Hemostasis (blood clotting) –> Inflammation –> Proliferation –> Remodeling

95
Q

Why does Hypovolemia impede healing?

A

Hypovolemia causes decreased blood flow to the affected area, not allowing adequate oxygen and nutrients to the area that promote healing

96
Q

Briefly describe Autoimmunity

A

An individual recognizes its own cells as foreign due to a breakdown of self-tolerance, and develops antibodies to their own cells

  • it can be polygenic and multifactorial
  • can have more than one autoimmune disorder at once
97
Q

Briefly describe Alloimmunity

A

An immune response to foreign antigens from members of the same species

Examples: Hyperacute graft rejection, Blood transfusion reaction, Graft vs host disease

98
Q

What is a hypersensitivity reaction?

A

A normal immune response that is either inappropriately triggered, excessive, or produces undesirable effects on the body

99
Q

How does Host Defense Failure happen?

A

Host Defense Failure is a result from functional decrease in one or more components of the immune system

Ex: AIDS, malnutrition can lead to immune deficiency due to the lack of proteins

100
Q

What are examples of autoimmunity?

A

Lupus, a chronic inflammatory disease that effects multiple organs

Addison’s disease

Celiac disease

Grave’s Disease

Hashimoto’s Thyroiditis

Multiple Sclerosis

101
Q

What are the first clinical indicators of host defense failure?

A

Signs and symptoms of infection

102
Q

What is the principle mediating antibody of Type I hypersensitivity reactions and what do they bind to?

A

IgE binds to sensitized mast cells

103
Q

What is a severe clinical manifestation of Type I Hypersensitivity?

A

Anaphylaxis (swelling, hives, itchiness)

104
Q

How do you manage Type I Hypersensitivity reactions?

A 
Antihistamines 
Corticosteroids 
IgE therapy 
Epinhephrine 
Immunotherapy 
Pharmacologic desensitization 
Stay away from allergen (environmental control)
105
Q

What is the principle mediating antibody for Type II Hypersensitivity and what is its pathogenesis?

A

AKA tissue-specific or cytotoxic hypersensitivity, IgG attack antigens on specific cells or tissues

106
Q

Examples of Type II Hypersensitivity

A 
Transfusion reaction
Hyperacute graft rejection (rejection of transplanted donor tissue)
Graves Disease (hyperthyroidism - autoimmune)
Myasthenia Gravis (neuromuscular - autoimmune)
107
Q

Describe the etiology and pathogenesis of Type III Hypersensitivity

A

Immune Complex Reaction

  • Antigen combines with the antibody to form a complex that is deposited into tissue, activating the complement system
  • Immune and phagocytic systems fail to effectively remove antigen-antibody immune complexes
108
Q

Examples of Type III Hypersensitivity

A
  • Rheumatoid arthritis
  • Immune complex glomerulonephritis
  • Systemic lupus erythematosus
109
Q

Type IV Hypersensitivity etiology and pathogenesis

A

Delayed response by sensitized T lymphocytes, resulting in the release of lymphokines and other chemical mediators that cause inflammatory response and destruction of the antigen

110
Q

What is the principle mediating antibody for Type IV?

A

None!

There are no antibodies involved, but rather it is regulated by T CELLS

111
Q

Examples of Type IV Hypersensitivity

A

Contact dermatitis, PPD test (for TB)

112
Q

A patient reports hives associated with eating peanuts has which type of hypersensitivity reaction?

A

Type I

113
Q

What do HLA do?

A

The Human Leukocyte Antigen are proteins that label cells of the individual

114
Q

CD8

A

Cytotoxic T Lymphocytes

115
Q

CD4

A

Helper T Lymphocytes (Th1 and Th2)

116
Q

Th1

A

Recruit other T cells to the injured area, activate macrophages, and secrete cytokines and chemokines

117
Q

Th2

A

Trigger B cells

118
Q

How are MHC molecules involved in immunity?

A

Major Histocompatibility Complex display HLAs as MHC-presented peptides on the surface of cells to help immune cells discriminate between normal antigens and those that are foreign/dangerous

Prevents immune system from attacking our own cells as well

119
Q

MHC 1

A

Present on virtually all nucleated cells - triggers cytotoxic T cells

120
Q

MHC 2

A

Restricted to immune cells, antigen-presenting cells, B cells, and macrophages

The engulfed antigen is then degraded into free-peptide fragments within cytoplasmic vesicles –> complexed with MHC 2 molecules –> present on surface of cell –> T Helper cells recognize them and become activated

121
Q

Cell mediated immunity involves which type of lymphocyte?

A

T cells

122
Q

B lymphocytes are involved in what type of immunity?

A

Humoral

123
Q

What is the smallest in size but most common antibody?

A

IgG

-can cross placenta

124
Q

Which antibody is best for secondary exposure?

A

IgG

125
Q

Which antibody is the first responder to antigens at initial response?

A

IgM

-supplements IgG on subsequent exposure

126
Q

Which antibody is found in mucous secretions and is critical in mucosal immunity (part of first line of defense)

A

IgA

127
Q

IgD is co expressed with which antibody?

A

IgM

128
Q

What does IgD activate?

A

B cells

129
Q

Which antibody stimulates histamine/allergic response?

A

IgE

130
Q

Which antibody is transferred from mother to fetus through breast milk?

A

IgG

131
Q

What is a Titre?

A

It is a diagnostic test that measures levels of serum immunoglobulins

132
Q

What does an Indirect Coombs test measure?

A

Detects Rh blood incompatibility

-affects blood transfusions, mother-child

133
Q

What does an Elisa test detect?

A

Detects for HIV antibodies

134
Q

Receiving the influenza vaccination provides which type of immunity?

A

Active artificial

135
Q

What is influenza and how is it transmitted?

A

Influenza is a viral infection of epithelial cells, leading to infected epithelial cell necrosis of the upper respiratory tract, impairing cilia and mucous production.

Transmitted by respiratory droplet transmission

136
Q

What are the clinical manifestations of influenza?

A

Cough, sore throat, nasal congestion/drainage, chills, fever, body aches, malaise, anorexia

137
Q

What should you avoid giving children with influenza?

A

Aspirin –> Reye Syndrome

138
Q

What are the nursing implications when treating influenza?

A

Droplet precautions!

139
Q

Symptoms of fatigue, low grade fever, and generalized muscle aches would most likely be present in which stage of acute infection?

A

Prodromal

140
Q

What does leukocytosis, specifically neutrophilic, frequently indicate?

A

Bacterial infections

141
Q

What would an increase in eosinophils indicate?

A

Allergic reaction

142
Q

What does a decrease in leukocytes and or neutrophils indicate?

A

Immunosupression or bone marrow damage

143
Q

Hand washing is an example of an action to break the chain of infection at which link?

A

Means of transmission

144
Q

Contents of ECF

A

Sodium, chloride, bicarbonate

145
Q

Contents of Intravascular Fluid:

A

protein rich fluid (plasma), large amounts of albumin

146
Q

Interstitial Fluid

A

Fluid between cells and location of most extracellular fluid

  • hardly any protein
  • rich in electrolytes (sodium, chloride, bicarbonate)
147
Q

Transcellular fluid

A

contained in specialized body cavities

148
Q

What is Hydrostatic Pressure/Filtration?

A

Movement of fluid and solutes from an area of higher hydrostatic pressure to lower

The pressure is created by the weight of fluids that forces fluids through the capillary walls into the interstitial spaces.

149
Q

Osmolality

A

osmotic pull exerted by particles per kg of water

150
Q

What type of pressure influences water movement between vascular and interstitial membranes?

A

Hydrostatic and osmotic

151
Q

Why is blood pushed out of the capillary into interstitial compartment?

A

At the arterial end of the capillary, the blood hydrostatic pressure exceeds opposing interstitial hydrostatic pressure and plasma pressure of blood –> blood is pushed out of capillary into interstitial compartment

152
Q

How is blood pulled back into capillary

A

At venous end of capillary, blood hydrostatic pressure is decreased and osmotic pressure is higher –> therefore blood is pulled back into capillary

153
Q

Describe Hypothalamic Regulation

A

Osmoreceptors in the hypothalamus regulate the fluid

154
Q

Pituitary Regulation

A

Posterior Pituitary releases ADH –> water retention in kidneys

155
Q

Adrenal Cortical Regulation

A

Glucocorticoids and mineralcorticoids secreted by adrenal cortex help regulate both water and electrolytes

156
Q

In Hypotension when there is decreased renal perfusion…

A

Kidneys release renin –> causes kidneys to release angiotensiongen –> converted to angiotensin I –> then to angiotensin II –> vasoconstrictor to raise BP

Angiotensin II also simulates secretion of aldosterone by adrenal context –> causes tubules of kidneys to increase reabsorption of water and sodium in blood and excrete potassium –> increase in fluid volume

157
Q

What is the primary extracellular electrolyte?

A

Sodium!

158
Q

What is the primary intracellular electrolyte?

A

Potassium!

159
Q

Isotonic

A

Same osmolality as intracellular fluid

160
Q

Hypotonic

A

Lower osmolality of ICF (more solutes inside the cell than outside)

161
Q

Hypertonic

A

Higher osmolality of ICF (more solutes outside the cell)

162
Q

What is the most abundant cation in the ECF?

A

Sodium

163
Q

What is the ECF low in/ the ICF high in?

A

Potassium, magnesium, and phosphate ions

164
Q

In fluid balance at the capillary level, which force is caused by proteins or other molecules that can pull fluid from the interstitial space into the intravascular space?

A

Osmotic pressure

165
Q

If cells are in a hypotonic solution…

A

fluid is pulled IN to the cell, causing the cell to burst

166
Q

If cells are in a hypertonic solution…

A

fluid is pulled OUT of the cell, causing the cell to shrink

167
Q

Aldosterone release causes _____ retention with _____ excretion

A

Aldosterone release causes sodium retention with potassium excretion

168
Q

How do Loop Diuretics remove fluid?

A

They inhibit sodium and chloride reabsorption from the LOOP OF HENLEYS

Example: Lasixs

169
Q

How does Thiazide remove fluid?

A

Inhibits reabsorption of sodium and chloride from the DISTAL CONVOLUTED TUBULES

Example: HCTZ

170
Q

What are Potassium-Sparing diuretics?

A

Competitive antagonists for aldosterone - lose lots of fluid but retain or reabsorb potassium –> prevents reabsorption of sodium

171
Q

Clinical manifestations of Hypovolemia

A 
Tachycardia (rapid HR)
dry mouth/thirst 
skin turgor 
Syncope 
Low BP 
Oliguria (low urine output)
Low RBC and hemoglobin 
Nausea 
Substantial weight loss
172
Q

Treating Hypovolemia

A

Correct underlying cause and replace both water and electrolytes

173
Q

2% weight loss is a

A

Mild deficit

174
Q

Moderate deficit is

A

5% weight loss

175
Q

8% weight loss is considered

A

Severe dehydration

176
Q

Lab analyses check blood of dehydrated patients for…

A

Electrolytes, bicarbonate, BUN (blood urea nitrogen) (waste product of digestion of protein), creatinine, and specific gravity

177
Q

Serum electrolytes in Isotonic Dehydration

A

Stay in normal range

178
Q

Causes of Isotonic Dehydration

A

fasting, diarrhea, vomiting, burns, hemorrhage

179
Q

In Hypertonic Dehydration…

A

More fluid loss than electrolytes –> increase in serum electrolytes

180
Q

Causes of Hypertonic Dehydration

A

Extended fever, diabetes insipidus, DM, reduced fluid intake

181
Q

What type of dehydration does Diabetes Insipidus cause and how?

A

Diabetes insipidus causes hypertonic dehydration to the reduction in the release of ADH

182
Q

Hypotonic Dehydration

A

Loss of more electrolytes than fluid –> decrease in serum electrolytes

*HYPONATREMIA

183
Q

What causes Hypotonic Dehydration?

A

Addison’s disease
overuse of diuretics
Not enough electrolyte intake (only H2O)

184
Q

What does an overproduction of ADH lead to?

A

SIADH = syndrome of inappropriate ADH

  • water retention –> decreased urine output
  • decrease in plasma osmolality; increase in urine osmolality
185
Q

What is third-spacing?

A

Fluid shifts out of the blood into a body cavity or tissue and can no longer reenter vascular compartment

186
Q

Which of the following would cause edema?

Increased hydrostatic pressure
Increased interstitial fluid osmotic pressure
Blockage of lymphatic drainage
Decreased capillary osmotic pressure

A

All!

187
Q

Which of the following terms refers to a combination of decreased circulating blood volume combined with excess fluid in a body cavity?

Dehydration
Hypovolemia
Water Retention
Third Spacing

A

Third Spacing

Pathophysiology (8 decks)

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