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PATHO/PHARM I > Week 3 Lecture: Fluid Balance and Inflammation > Flashcards

Week 3 Lecture: Fluid Balance and Inflammation Flashcards

1
Q

Total Body Water (TBW):

A

sum of all fluids within body compartments

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2
Q

How much is TBW in adults?

A

Is about 60% of body weight in adults

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3
Q

How is TBW usually expressed?

A

Volume of TBW is usually expressed as a percentage of body weight in kilograms
One liter of water weighs 2.2lb (1kg)

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4
Q

Intracellular fluid (ICF)

A

is all the fluid within cells and comprises about two-thirds of TBW.

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5
Q

How much TBW does intracellular fluid fluid comprise of?

A

comprises about two-thirds of TBW.

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6
Q

Extracellular fluid (ECF)

A

Extracellular fluid (ECF) is all the fluid outside the cells and comprises about one-third of TBW. ECF includes the interstitial fluid, the intravascular fluid, and the various transcellular fluids

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7
Q

How much tbw does ecf comprise of?

A

comprises about one-third of TBW.

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8
Q

What does ECF include?

A

ECF includes the interstitial fluid, the intravascular fluid, and the various transcellular fluids

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9
Q

interstitial fluid

A

The interstitial fluid is the fluid found in the spaces between cells but not within the blood vessels.

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10
Q

Intravascular Fluid

A

is the fluid found within blood vessels

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11
Q

What is Intravascular Fluid commonly known as:

A

it is more commonly known as the blood plasma

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12
Q

Transcellular fluids

A

the smallest component of extracellular fluids, are the fluids contained within epithelial-lined cavities of the body.

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13
Q

Examples of transcellular fluid

A

Examples of transcellular fluid include synovial fluid, cerebral spinal fluid, gastrointestinal fluids, pleural fluids, pericardial fluids, peritoneal fluids, and urine.

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14
Q

Filtration

A

Refers to fluid movement out of the capillary and into the interstitial space

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15
Q

Reabsorption

A

Reabsorption refers to fluid movement into the capillary from the interstitial space.

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16
Q

Capillary hydrostatic pressure (blood pressure)

A

facilitates the movement of water from the capillary into the interstitial space.

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17
Q

Capillary (plasma) oncotic pressure

A

osmotically attracts water from the interstitial space into the capillary.

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18
Q

Interstitial hydrostatic pressure

A

facilitates the inward movement of water from the interstitial space into the capillary.

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19
Q

Interstitial oncotic pressure

A

osmotically attracts water from the capillary into the interstitial space.

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20
Q

What occurs at arterial end of the capillary?

A

hydrostatic pressure exceeds capillary oncotic pressure; thus fluid moves into the interstitial space (filtration).

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21
Q

What happens at the venous end of the capillary?

A

At the venous end of the capillary, oncotic pressure within the capillary exceeds capillary hydrostatic pressure; thus fluids move into the capillary to enter into the circulation (reabsorption).

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22
Q

Edema

A

Edema is the excessive accumulation of fluid within the interstitial spaces.

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23
Q

How does edema result?

A

It results from a shift of fluid from the capillaries (intravascular fluid) or lymphatic vessels into the tissues

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24
Q

Physiologic conditions that promote fluid flow into the tissues that lead to edema include

A

(1) increased capillary hydrostatic pressure,
(2) decreased plasma oncotic pressure,
(3) increased capillary membrane permeability, and
(4) lymphatic channel obstruction.

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25
The sodium concentration is regulated by
The sodium concentration is regulated by the renal effects of aldosterone
26
Water balance is regulated primarily by
Water balance is regulated primarily by antidiuretic hormone (ADH) , also known as vasopressin
27
Primary ECF cation
Sodium (Na+) accounts for 90% of the ECF cations (positively charged ions)
28
Primary ECF cation
chloride and bicarbonate, the two major anions (negatively charged ions),
29
Aldosterone
Hormonal regulation of sodium (and potassium) balance is mediated by aldosterone, a mineralocorticoid synthesized and secreted from the adrenal cortex.
30
Water balance is regulated by
Water balance is regulated by the secretion of ADH, also known as vasopressin .
31
When is ADH produced?
ADH is secreted when plasma osmolality increases or circulating blood volume decreases, causing a drop in blood pressure
32
When does increased plasma osmolality occur?
Increased Plasma osmolality occurs when there is a decrease in water or an excess concentration of sodium in relation to total body water.
33
Stimulation of osmoreceptors results in
The increased osmolality stimulates hypothalamic osmoreceptors , resulting in thirst.
34
Three things that stimulate thirst and the release of pituitary ADH, which prompt fluid consumption
1. Osmoreceptors 2. Volume Sensitive Receptors 3. Baroreceptors
35
When do sodium imbalances occur?
Sodium imbalances occur with gains or losses of body water.
36
When do water imbalances occur?
Water imbalances develop with gains or losses of salt.
37
Tonicity
the change in the concentration of solutes in relation to the amount of water present
38
What causes hypovolemia?
Isotonic fluid loss causes hypovolemia
39
What causes hypervolemia?
Isotonic fluid excess causes hypervolemia.
40
What are the three defenses involved in immunity?
First line: Innate Immunity Second line: Inflammation/rapid nonspecific response Third: Adaptive (acquired) (specific) immunity/ Antibodies-immunoglobins
41
First line of defense in immunity:
Innate immunity
42
Innate immunity
includes natural barriers and inflammation Innate barriers form the first line of defense at the body's surfaces. They serve to prevent damage by the environment and thwart infection by pathogenic microorganisms.
43
Second line of immune defense
inflammatory response
44
Inflammation response characteristics
rapid nonspecific response same generic response no matter what issue is
45
Inflammatory response
the inflammatory response, is activated to protect the body from further injury, fight infection, and promote healing.
46
Third line of defense
adaptive immunity (also known as acquired or specific immunity)
47
Another word for an immunoglobin
Ig An immunoglobin is an antibody
48
Adaptive immunity (also known as acquired or specific immunity)
is induced through a slower and more specific process and targets particular invaders and diseased tissues for the purpose of eradicating them.
49
Five pillars of local inflammation
1. Rubor (redness, erythema) 2. Calor (heat) 3. Tumor (swelling) 4. Dolor (pain) 5. Functio laesa (loss of function)
50
Why does heat/redness occur as a response to inflammation?
Heat occurs because increased blood flow to the site. Vasodilation occurs Arterial blood is warm
51
Why does swelling/loss of function occur in inflammation?
leaky capillaries- capillaries are more permeable to substances swelling causes lack of function
52
Ultimate result of inflammation:
The ultimate result of these changes is the migration of leukocytes, plasma proteins, and other biochemical mediators from the circulation into the nearby damaged tissue, where they can work together to destroy invaders, limit tissue injury, and promote healing. `
53
Three key plasma protein systems that are essential to an effective inflammatory response
1. Complement system 2. Clotting system 3. Kinin system
54
The complement system
intensifies or complements the capacity of antibodies and phagocytes to clear pathogens and damaged cells and activate inflammation. proteins normally in blood further triggers inflammation
55
Coagulation system
is a group of plasma proteins, which, when activated sequentially, form a blood clot
56
Kinin System
series of proteins end result is primarily reana kinin, which is associated with pain
57
Systemic Manifestations of Acute Inflammation
1. fever 2. leukocytosis 3. increased levels of circulating plasma proteins
58
What are mediators in inflammation do?
Mediators are substances released from cells that stimulate a response
59
Other ways to measure inflammation in the blood
1. C-reactive protein 2. ESR: how long for rbc to settle at bottom of test tube
60
How is adaptive immunity characterized?
specific and involves antibodies
61
Passive immunity
You have immunity but you didn't make the antibodies
62
Example of passive imunity
breastmilk
63
Active immunity
Develops after exposure to the antigen Antigen is then able to stimulate an immune response
64
Antigen
Substance is able to stimulate an immune system
65
Example of artificial active immunity
Vaccine
66
Example of natural active immunity
disease
67
Five antibodies circulating in blood classes
IgG IgA IgM IgE IgD
68
So when we have an immune problem, if I have a problem with my immune response. Or if I have a disease of my immune system , Why might that be?
1. it's either going to be that my immune system is working too much. 2. not working enough 3.
69
Hypersensitivity
Your response is dramatic
70
Different types of immune sensitivity
Type I- IgE mediated Type 2- Tissue-related reactions Type 3-Immune-complex mediated Type 4- Cell mediated-delayed
71
Type I-IgE mediated
allergic response (hives to analphylaxis)
72
Type 2: Tissue Specific reactions
body overreacting to specific tissue ex; thyroid disease
73
Allo-immunity
Blood transfusion reaction
74
What type of hypersensitivity are blood transfusions?
Type 2 sensitivities
75
Type 3: Immune complex-mediated
are not organ specific ex; rhemetoid arthritis (abnormal antibody attacks another antibody)
76
Type 4: Cell-mediated delayed
symptoms occur 48 hours after exposure no antibody involved T cells are involved
77
Which hypersensitivity type does not have antibody involved at all and is not humoral mediated
Type 4: T cells are involved not humoral or antibody mediated
78
Two types of immune deficiencies:
1. Primary (congenital) immunodeficiencies 2. Secondary (acquired) immunodeficiency
79
1. Primary (congenital) immunodeficiencies
Genetic anomaly
80
2. Secondary (acquired) immunodeficiency
Caused by another illness more common malignancy, immunosuppressive, AIDS
81
As a general rule, what do we think of immunosuppressants?
As a general rule, immunosuppressants are good, and are frequently used to do things like prevent organ rejection and are very important for treatment of autoimmune diseases
82
Immunosuppressants
Inhibit immune response
83
Uses of Immunosuppressants
1. Prevention of organ rejection 2. Treatment of autoimmune diseases
84
Toxicity caused by immunosuppressants:
1. increased risk of infection 2. increased risk of neoplasms (cancers)- our cells scavenge around for abnormal cells
85
Calcineurin Inhibitors- principle use
Prevention of organ rejection in transplant recipients
86
What does inhibition of calcineurin cause?
Inhibition of calcineurin suppresse production of interleukin (IL-2)
87
What is interleukin (IL-2) needed for?
IL-2 is needed for T-cell proliferation
88
Example of calcineurin inhibitors that are the most effective immunosuppressants available
Cyclosporine tacrolimus pimecrolimus
89
What is the drug of choice for organ rejection?
Cyclosporine
90
Adverse effects of Calcineurin Inhibitors
Nephrotoxicity Infection Hepatotoxicity Lymphoma Hypertension
91
Of all adverse effects of calcineurin inhibitors, what is common but manageable?
Hypertension
92
Food and Drug Interactions having to do with calcineurin inhibitors
Grapefruit juice- p450 inhibitor that leads to cyclosporin toxicity that can lead to nephrotoxicity/hepatotocity Nephrotoxic meds- other nephrotoxic drugs +nephrotoxic drugs = bad; be concerned if pt is on another nephrotoxic drug
93
What are glucocorticoids used for
1. Used to widely suppress immune response 2. Large doses used to prevent rejection
94
Glucocorticoids are used to suppress immune response, what are some examples:
Suppression of allograft rejection treatment of asthma rhemetoid arthritis systemic lupus erythematosus (SLE) MS
95
What are the adverse effects of glucocorticoids associated with in regards to usage?
More adverse effects are associated with long term use or high dosage cortical steriods
96
Ways that glucocorticoids can be administered?
1. systemic administration- more likely to have adverse effects 2. local administration
97
Which type of glucocortisoids have an effect on sodium, water and aldosterone?
The shorter acting glucocortisoids have greatest effect on the aldosterone and sodium and water retention
98
Short term adverse effects of glucocorticoids?
Mental agitation lack of sleep (insomnia)
99
Large doses of glucocortisoids used to prevent rejection cause what:
Increased risk of infection thinning of skin bone dissolution with fracture impaired growth in children suppression of hypothalmic-pituitary adrenal axis
100
Adverse effects of long term use:
osteoporosis fat redistribution/muscle loss hyperglycemia
101
How do you stop cortisol and why do it this way?
You taper off the med This is because your own adrenal glands shut down their cortisol factories. The brain senses plenty of cortisol, so adrenal gland has no signal to make more
102
What happens if you abruptly stop cortisol?
Your adrenal glands cannot produce enough fast enough to replace what you were taking. You need to slowly wean to allow adrenal glands to make more
103
Why do we care that body can make enough cortisol?
Because our body won't respond well to stress hypoglycemia low bp from low cortisol
104
Cytotoxic Drugs
Suppress immune response by killing B and T lymphocytes undergoing proliferation
105
Negative effect of cytotoxic drugs
they are nonspecific; toxic to all proliferating cells (rbcs and platelets too)
106
Adverse effects of cytotoxic drugs
Bone marrow suppression GI disturbances Reduced fertility alopecia
107
Bone marrow suppression caused by cytotoxic drugs lead to:
1. Neutropenia 2. Thrombocytopenia
108
How should you handle cytotoxic drugs? why?
Use PPE You are at risk when you are exposed to it, even by touching

PATHO/PHARM I (28 decks)

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