U1A Flashcards

1
Q

HOMEOSTASIS

A

Homeostasis - the body’s ability to maintain a dynamic steady-state of INTERNAL BALANCE or equilibrium

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2
Q

HYPERPLASIA

A

Hyperplasia – INCREASED NUMBER of cells.

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3
Q

HYPERTROPHY

A

Hypertrophy - INCREASED SIZE of cell (2ry to ↑’d workload or a pathological condition (enlarged heart).

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4
Q

ATROPHY

A

Atrophy – REDUCED SIZE of cell (2ry to disuse, ↓’d blood flow, malnutrition, etc.

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5
Q

METAPLASIA

A

Metaplasia – REPLACEMENT of one cell type with another that can better endure the stress (but usually doesn’t work as well as the original tissue). Caused by chronic inflammation or irritation, i.e., a callous.

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6
Q

DYSPLASIA

A

Dysplasia – Abnormal cell growth of specific tissue resulting in abnormal SIZE, SHAPE, or APPEARANCE. Often precedes cancerous changes.

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7
Q

CELLULAR INJURY

A

1 - Free Radical Injury - Highly reactive chemical molecules with an unpaired electron in their outer orbit that pulls electrons off of healthy cell molecules → cell damage; cancers; other disease states result.
Treat with antioxidents such as Vitamin C & E

2 - Hypoxic Cell Injury – cellular oxygen deprivation. Brain/Heart/Kidneys are high consumers of O2. Caused by lack of O2 or impaired blood flow to the tissue → inflammatory response (see pg. 3 of outline).

  • Brain dies 4-6 minutes wo O2
  • Kidneys die in 20-30 minutes wo O2

3 - Impaired Calcium function – Ca++ is an important signalling ion for many cell responses. If the cell is injured, calcium builds up inside the cell and many cell structures are damaged.

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8
Q

REVERSIBLE CELL INJURY

A

Water- Sodium builds up in cell due to the breakdown of the sodium [Na+] – potassium [K+] pump. Consequently, sodium collects inside the cell and attracts water → intracellular swelling. Usually due to hypoxic injury.

Lipids (causing fatty changes in the cell) – lipid collects in cells leading to impairment of cell functions. “Fatty liver” is often the result. Fatty changes are a more ominous sign of cell injury than swelling, but can be reversed with dietary changes.

Calcium builds up in cell due to breakdown of the Calcium [Ca++] – Magnesium [Mg++] pump. Consequently, calcium collects inside the

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9
Q

IRREVERSIBLE CELL INJURY

A

APOPTOSIS: Controlled cell death (implosion). Cell membrane maintains integrity → cell contents are NOT released into the extracellular space, so there is no inflammatory response.

(death from inside out–cell membrane remains intact and as a result, doesn’t trigger an inflammatory response.)

NECROSIS: Uncontrolled cell death (explosion). Cell membrane loses integrity → cell contents released into EXTRACELLULAR space which triggers the inflammatory response.

(death from outside in–usually cause by three types of cell injury above)

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10
Q

TELOMERES

A

Outermost tails of the chromosome arms that are shortened during each replication of a cell. When the telomere is too short to replicate, the cell dies because it cannot reproduce itself any more.

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11
Q

EXAMPLES OF DAMAGE CAUSED BY CELLULAR AGING AND OTHER FACTORS (LIST 4)

A

Decrease in elasticity of blood vessels → atherosclerosis (“hardening of the arteries”] and high blood pressure

Loss of bowel motility due to aging or medications → Chronic constipation

Loss of muscle mass due to aging, malnutrition, eating disorders, etc. → muscle weakness, problems with balance

Loss of subcutaneous fat due to aging or extreme dieting, cancer, malnutrition, etc. → problems regulating temperature, and skin breakdown over bony areas especially if bed-bound

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12
Q

ORGANS OF THE IMMUNE SYSTEM

A

ORGANS of the Immune System

Bone Marrow: Source of ALL Blood components (Red blood cells, white blood cells, and platelets)

Thymus Gland: Produces T- Cells from lymphocytes

Lymph Nodes/Tonsils/Spleen

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13
Q

CELLS OF INFLAMMATION

A

CELLS of Inflammation

  1. Endothelial Cells – line the blood vessels - Produces chemicals that:
    a. vasodilate or vasoconstrict
    b. cause blood thinning/prevent clotting (to keep vein open)
    c. allow entrance/exit into and out of the blood vessel (vessel wall permeability)
    d. control inflammatory mediators
  2. Platelets – thrombocytes
    a. Responsible for blood coagulation/clotting
    b. Platelets release of over 300 potent inflammatory mediators
  3. Leukocytes – White blood cells
    They are the major cellular component of the inflammatory response
    The term “LEUKOCYTOSIS” means a higher than normal production of White Blood Cells (usually neutrophils) in the blood, and is a common indicator of inflammation and infection.
    WBCs are classified as either GRANULOCYTES or AGRANULOCYTES
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14
Q

SYMPTOMS OF INFLAMMATION

A

“S.H.A.R.P.”

Swelling – Heat - Altered function – Redness - Pain

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15
Q

TYPES OF LEUKOCYTES

A

Granulocytes “Granpa B.E.N.”

~ Neutrophils (60% of WBC), ↑’d in ACUTE bacterial infection [“First Responder (within minutes”]
They live 1-5 days; 5 days to make a new one too
We want them to be 60% of the force bc they are the green berets
If Neutrophils are elevated, infection is current and acute

~ Eosinophils (↑’d in allergic rxn & parasites)
~ Basophils (release histamine)

Agranulocytes [then add, “And Granma Loves Money”
~ Lymphocytes (25-30% of WBC) B & T cells - ↑’d in VIRAL and CHRONIC infection (see types of Lymphocytes below) Lymphocytes Days to respond but fight for months ie National Guard

If Lymphocytes are elevated on a CBCD, then you know the infection is chronic. Also, lymphocytes can detect if it is a viral infection.
~ Monocytes circulate in the bloodstream. When called into action they migrate into tissue
to become macrophages (cells that can “eat” foreign particles in a process called
phagocytosis).

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16
Q

LYMPHOCYTES

A

T cells: [“Timely” - respond before “B” cells do] - Cell-mediated immune response
Produced from lymphocytes in the THYMUS gland

T memory cells —Remain in lymph nodes for many years after an infection. Should the same pathogen enter the body again, these cells produce new clones of T cells so that a rapid response is possible

Helper T-cells: activate/regulate T & B cells

Killer T-cells: Attack virus-infected cells and tumor cells. Ingests antigens* via phagocytosis

Natural killer Cells (NK cells) —Attack abnormal cells such as cancer cells. These are lymphoid cells that can destroy cancer cells (have different cell surface markers than killer T Cells).

Suppressor T-cells: Returns the functioning of the immune system to normal operation after infection; prevents autoimmunity

B cells: [“Back up Response” and “Makes
AntiBodies”] - Humoral immune response
slower response time than T Cells
antibodies
Produced from lymphocytes in the BONE marrow
Releases antiBodies and assists activation of T cells
It takes time to make antibodies in response to a specific antigen, unless they were already made at the time of a previous exposure to the same antigen.

17
Q

WHAT ARE ANTIGENS

A

Antigens reside on the surfaces of cells. They are identifiers that tell the body a cell belongs in the body or is foreign and must be eliminated. Each cell in our body has an antigen that tells the immune system that it is part of us and should not be eliminated

18
Q

WHAT ARE ANTIBODIES

A

They are proteins made by the body to attach to corresponding antigens to destroy invaders

19
Q

REMINDER HOW ANTIBODIES (IMMUNOGLOBULINS) ARE MADE

A

WBC (leukocytes) are made in the bone marrow
Lymphocytes a type of WBC, in the bone marrow make B Cells
B cells make antibodies (IgA, IgD, IgE, IgG, Ig) (GAMED)
When an antigen enters the body (on a pollen, dust, food, etc.) antibodies attack and destroy the antigen.

20
Q

TWO TYPES OF RESPONSES OF INFLAMMATION

A

Local: Contained to a localized site in the body
Systemic: Involves the entire body

Note: both local and systemic have ACUTE and CHRONIC phases

21
Q

CHRONIC PHASE OF LOCAL INFLAMMATION

A

Chronic inflammation can last for weeks, months or years.
Does not trigger the same response as Acute Inflammation does
In CHRONIC inflammation, a WBC blood test shows elevated LYMPHOCYTE levels (NOT elevated neutrophils)
Can be caused by recurrent and persistent infections; low grade infections.
Can be caused by persistent exposure to damaging sources (i.e., smoking, chemical exposure, etc.)
Can be caused by obesity. Adipose tissue (“white fat”) excretes hormones and chemical mediators.

22
Q

ACUTE PHASE OF LOCAL INFLAMMATION

A
  1. Vascular Phase: 5 signs of inflammation are: “S.H.A.R.P.” =
    SWELLING, HEAT, ALTERED FUNCTION, REDNESS, AND PAIN”
    Vasodilation cause HEAT and REDNESS
    Plasma brings WBCs and proteins to the site causing SWELLING and PAIN.
    Proteins are pushed from the blood vessel into the tissue. These proteins draw more fluid from blood into the tissue, which increases the swelling and pain.
    Fluid trapped in the tissue keeps the infection from moving into the rest of the body, but also causes ALTERED FUNCTION due to swelling.
    Chemical Mediators are released into tissue: Histamine, Serotonin, Cytokines and the “kinins” control the inflammation response by:
    Causing vasodilation
    Causing capillary permeability (“leaky capillary syndrome”) (contributes to swelling).
    Causing blood flow to slow down so clotting can begin
    Chemical mediators signal WBCs to congregate in the area of damage (contributes to swelling).

**vasodilation decreases bp in addition to, capillary permeability which also lowers bp

  1. Cellular Phase
    Leukocytes (primarily neutrophils – “first responders”) are delivered to the site of infection/injury and EMIGRATE through the blood vessel wall into the tissue
    WBCs move through the tissue by CHEMOTAXIS (“chemical taxi’s”) or moving along a chemical gradient
  2. Leukocyte Activation and Phagocytosis
    Leukocytes encase the microbe
    Lysosomal enzymes and oxygen free radicals in the leukocyte digest the microbe
    The accumulation of plasma, WBCs and chemical mediators create a fluid called EXUDATE
23
Q

ACUTE PHASE OF SYSTEMIC INFLAMMATION

A

Acute-phase Proteins
Proteins provide protective functions during systemic inflammation/infection
Liver makes these acute-phase proteins
Fibrinogen - causes a high ESR (erythrocyte sedimentation rate) which is a blood test for systemic inflammation (not very specific to any particular body system)
C-Reactive Protein (CRP) – can be a marker for Myocardial Infarction risk
Serum Amyloid A protein (SAA) – provides cellular energy

Fever – the most common objective sign of systemic inflammation, especially during the acute response phase. See Fever on pg. 8 below.

White Blood Cell (WBC) Response
Elevated WBC lab test shows TOTAL of all WBCs - normal range is 5,000 10,000
WBCs have a life span of about 10 hours
A WBC “WITH DIFFERENTIAL” – blood test that shows blood levels for all the various leukocytes (granulocytes and agranulocytes).
“Bands” are immature WBCs. When elevated, this indicates that the body has “run out of” adult neutrophils

24
Q

*WHAT DOES IT MEAN WHEN THESE LEUKOCYTES ARE ABNORMAL?

A

Elevated Neutrophils = acute bacterial infection
Elevated Lymphocytes = viral or chronic bacterial infection
Elevated eosinophils = parasite infection or allergic reaction
Low WBC = Overwhelming infection has exhausted the WBC supply or the bone marrow is not able to keep up production.

25
Q

SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS)

A

This condition is the potential “WORST CASE SCENARIO” of systemic inflammation. SIRS can result WITH or WITHOUT infection. Cytokines are released into circulation causing:
Massive generalized vasodilation
Increased vascular (capillary) permeability (→ fluid leaks from the blood vessels into the tissue)
Heart failure
Circulatory shock (not enough blood pressure to circulate blood through the body → death)

26
Q

HYPERTHERMIA

A

primarily caused by bacterial or viral infections, such as pneumonia or influenza and are the *Most common objective sign of systemic inflammation, especially during the acute phase

Fevers can also be caused by a damaged hypothalamus (temperature-controlling function) which could result from a head injury, stroke, brain tumor, etc.

Hypermetabolic states (i.e., thyroid storm, head injury, burns, some medications/drugs, multiple traumas

27
Q

PYROGEN

A

Anything that triggers a fever

ie microbes, chemical mediators (interleukin 1)

28
Q

Interleukin 1

A

*Interleukin 1 (one of the CYTOKINES) is an endogenous chemical mediator
that directly affects the set point in the hypothalamus

*Fever is caused by cytokines changing the body’s temperature “set point”.

29
Q

NORMAL TEMPERATURE

A

97 - 99.5 F

105-108 cause cell damage

109 fatal

*2 degrees above the normal baseline is normal

  • *children can tolerate higher fevers
  • neonates cannot
  • elderly have lower body temperatures so they could have an infection w apparent fever (So, chills can be an indicator of infection)
  • slightly elevated after surgery and childbirth
30
Q

TESTS TO DETERMINE CAUSE OF ELEVATED TEMPERATURE

A
CBC
BX see if pathogen is in blood
UA see if infection is in urine
XRCH check for pneumonia 
LP check spinal fluid for bacteria