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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
Q

The sodium concentration is regulated by

A

The sodium concentration is regulated by the renal effects of aldosterone

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26
Q

Water balance is regulated primarily by

A

Water balance is regulated primarily by antidiuretic hormone (ADH) , also known as vasopressin

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27
Q

Primary ECF cation

A

Sodium (Na+) accounts for 90% of the ECF cations (positively charged ions)

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28
Q

Primary ECF cation

A

chloride and bicarbonate, the two major anions (negatively charged ions),

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29
Q

Aldosterone

A

Hormonal regulation of sodium (and potassium) balance is mediated by aldosterone, a mineralocorticoid synthesized and secreted from the adrenal cortex.

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30
Q

Water balance is regulated by

A

Water balance is regulated by the secretion of ADH, also known as vasopressin .

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31
Q

When is ADH produced?

A

ADH is secreted when plasma osmolality increases or circulating blood volume decreases, causing a drop in blood pressure

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32
Q

When does increased plasma osmolality occur?

A

Increased Plasma osmolality occurs when there is a decrease in water or an excess concentration of sodium in relation to total body water.

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33
Q

Stimulation of osmoreceptors results in

A

The increased osmolality stimulates hypothalamic osmoreceptors , resulting in thirst.

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34
Q

Three things that stimulate thirst and the release of pituitary ADH, which prompt fluid consumption

A
  1. Osmoreceptors
  2. Volume Sensitive Receptors
  3. Baroreceptors
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35
Q

When do sodium imbalances occur?

A

Sodium imbalances occur with gains or losses of body water.

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36
Q

When do water imbalances occur?

A

Water imbalances develop with gains or losses of salt.

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37
Q

Tonicity

A

the change in the concentration of solutes in relation to the amount of water present

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38
Q

What causes hypovolemia?

A

Isotonic fluid loss causes hypovolemia

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39
Q

What causes hypervolemia?

A

Isotonic fluid excess causes hypervolemia.

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40
Q

What are the three defenses involved in immunity?

A

First line: Innate Immunity

Second line: Inflammation/rapid nonspecific response

Third: Adaptive (acquired) (specific) immunity/ Antibodies-immunoglobins

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41
Q

First line of defense in immunity:

A

Innate immunity

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42
Q

Innate immunity

A

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.

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43
Q

Second line of immune defense

A

inflammatory response

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44
Q

Inflammation response characteristics

A

rapid
nonspecific response
same generic response no matter what issue is

45
Q

Inflammatory response

A

the inflammatory response, is activated to protect the body from further injury, fight infection, and promote healing.

46
Q

Third line of defense

A

adaptive immunity (also known as acquired or specific immunity)

47
Q

Another word for an immunoglobin

A

Ig

An immunoglobin is an antibody

48
Q

Adaptive immunity (also known as acquired or specific immunity)

A

is induced through a slower and more specific process and targets particular invaders and diseased tissues for the purpose of eradicating them.

49
Q

Five pillars of local inflammation

A
  1. Rubor (redness, erythema)
  2. Calor (heat)
  3. Tumor (swelling)
  4. Dolor (pain)
  5. Functio laesa (loss of function)
50
Q

Why does heat/redness occur as a response to inflammation?

A

Heat occurs because increased blood flow to the site. Vasodilation occurs

Arterial blood is warm

51
Q

Why does swelling/loss of function occur in inflammation?

A

leaky capillaries- capillaries are more permeable to substances

swelling causes lack of function

52
Q

Ultimate result of inflammation:

A

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
Q

Three key plasma protein systems that are essential to an effective inflammatory response

A
  1. Complement system
  2. Clotting system
  3. Kinin system
54
Q

The complement system

A

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
Q

Coagulation system

A

is a group of plasma proteins, which, when activated sequentially, form a blood clot

56
Q

Kinin System

A

series of proteins

end result is primarily reana kinin, which is associated with pain

57
Q

Systemic Manifestations of Acute Inflammation

A
  1. fever
  2. leukocytosis
  3. increased levels of circulating plasma proteins
58
Q

What are mediators in inflammation do?

A

Mediators are substances released from cells that stimulate a response

59
Q

Other ways to measure inflammation in the blood

A
  1. C-reactive protein
  2. ESR: how long for rbc to settle at bottom of test tube
60
Q

How is adaptive immunity characterized?

A

specific and involves antibodies

61
Q

Passive immunity

A

You have immunity but you didn’t make the antibodies

62
Q

Example of passive imunity

A

breastmilk

63
Q

Active immunity

A

Develops after exposure to the antigen

Antigen is then able to stimulate an immune response

64
Q

Antigen

A

Substance is able to stimulate an immune system

65
Q

Example of artificial active immunity

A

Vaccine

66
Q

Example of natural active immunity

A

disease

67
Q

Five antibodies circulating in blood classes

A

IgG

IgA

IgM

IgE

IgD

68
Q

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?

A
  1. it’s either going to be that my immune system is working too much.
  2. not working enough

3.

69
Q

Hypersensitivity

A

Your response is dramatic

70
Q

Different types of immune sensitivity

A

Type I- IgE mediated

Type 2- Tissue-related reactions

Type 3-Immune-complex mediated

Type 4- Cell mediated-delayed

71
Q

Type I-IgE mediated

A

allergic response (hives to analphylaxis)

72
Q

Type 2: Tissue Specific reactions

A

body overreacting to specific tissue

ex; thyroid disease

73
Q

Allo-immunity

A

Blood transfusion reaction

74
Q

What type of hypersensitivity are blood transfusions?

A

Type 2 sensitivities

75
Q

Type 3: Immune complex-mediated

A

are not organ specific

ex; rhemetoid arthritis (abnormal antibody attacks another antibody)

76
Q

Type 4: Cell-mediated delayed

A

symptoms occur 48 hours after exposure

no antibody involved

T cells are involved

77
Q

Which hypersensitivity type does not have antibody involved at all and is not humoral mediated

A

Type 4: T cells are involved

not humoral or antibody mediated

78
Q

Two types of immune deficiencies:

A
  1. Primary (congenital) immunodeficiencies
  2. Secondary (acquired) immunodeficiency
79
Q
  1. Primary (congenital) immunodeficiencies
A

Genetic anomaly

80
Q
  1. Secondary (acquired) immunodeficiency
A

Caused by another illness

more common

malignancy, immunosuppressive, AIDS

81
Q

As a general rule, what do we think of immunosuppressants?

A

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
Q

Immunosuppressants

A

Inhibit immune response

83
Q

Uses of Immunosuppressants

A
  1. Prevention of organ rejection
  2. Treatment of autoimmune diseases
84
Q

Toxicity caused by immunosuppressants:

A
  1. increased risk of infection
  2. increased risk of neoplasms (cancers)- our cells scavenge around for abnormal cells
85
Q

Calcineurin Inhibitors- principle use

A

Prevention of organ rejection in transplant recipients

86
Q

What does inhibition of calcineurin cause?

A

Inhibition of calcineurin suppresse production of interleukin (IL-2)

87
Q

What is interleukin (IL-2) needed for?

A

IL-2 is needed for T-cell proliferation

88
Q

Example of calcineurin inhibitors that are the most effective immunosuppressants available

A

Cyclosporine

tacrolimus

pimecrolimus

89
Q

What is the drug of choice for organ rejection?

A

Cyclosporine

90
Q

Adverse effects of Calcineurin Inhibitors

A

Nephrotoxicity

Infection

Hepatotoxicity

Lymphoma

Hypertension

91
Q

Of all adverse effects of calcineurin inhibitors, what is common but manageable?

A

Hypertension

92
Q

Food and Drug Interactions having to do with calcineurin inhibitors

A

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
Q

What are glucocorticoids used for

A
  1. Used to widely suppress immune response
  2. Large doses used to prevent rejection
94
Q

Glucocorticoids are used to suppress immune response, what are some examples:

A

Suppression of allograft rejection

treatment of asthma

rhemetoid arthritis

systemic lupus erythematosus (SLE)

MS

95
Q

What are the adverse effects of glucocorticoids associated with in regards to usage?

A

More adverse effects are associated with long term use or high dosage cortical steriods

96
Q

Ways that glucocorticoids can be administered?

A
  1. systemic administration- more likely to have adverse effects
  2. local administration
97
Q

Which type of glucocortisoids have an effect on sodium, water and aldosterone?

A

The shorter acting glucocortisoids have greatest effect on the aldosterone and sodium and water retention

98
Q

Short term adverse effects of glucocorticoids?

A

Mental agitation

lack of sleep (insomnia)

99
Q

Large doses of glucocortisoids used to prevent rejection cause what:

A

Increased risk of infection

thinning of skin

bone dissolution with fracture

impaired growth in children

suppression of hypothalmic-pituitary adrenal axis

100
Q

Adverse effects of long term use:

A

osteoporosis

fat redistribution/muscle loss

hyperglycemia

101
Q

How do you stop cortisol and why do it this way?

A

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
Q

What happens if you abruptly stop cortisol?

A

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
Q

Why do we care that body can make enough cortisol?

A

Because our body won’t respond well to stress

hypoglycemia

low bp from low cortisol

104
Q

Cytotoxic Drugs

A

Suppress immune response by killing B and T lymphocytes undergoing proliferation

105
Q

Negative effect of cytotoxic drugs

A

they are nonspecific; toxic to all proliferating cells (rbcs and platelets too)

106
Q

Adverse effects of cytotoxic drugs

A

Bone marrow suppression
GI disturbances
Reduced fertility
alopecia

107
Q

Bone marrow suppression caused by cytotoxic drugs lead to:

A
  1. Neutropenia
  2. Thrombocytopenia
108
Q

How should you handle cytotoxic drugs? why?

A

Use PPE
You are at risk when you are exposed to it, even by touching

PATHO/PHARM I (28 decks)

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