Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophysiology I > week 2 - inflammation, tissue healing & edema > Flashcards

week 2 - inflammation, tissue healing & edema Flashcards

1
Q

List 3 main actions of lymphatic system

A
  • fluid balance
  • immunity
  • fat absorption (fat from food - lacteal - lymphatic system)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are 2 main functions of albumin in plasma?

A
  • carry / transport lipid soluble
  • osmotic pressure
    albumin is the most abundant protein. its pressure pulls fluid back in the cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

List 5 types of leukocytes and their main function

A

Neutrophil - first responder. Kill bacteria and fungi.
Lymphocyte - kill viruses, make antibodies.
Monocyte - remove dead cells. (–> macrophage).
Eosinophil - kill parasites, allergic response
Basophil - inflammatory response. abundant in mucus membranes. (–> mast cell)

Never-Let-Monkey-Eat-Banana

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

WBC counts

What’s the difference betwen newborn/infants and eldery/immuno-compromised person?

A

newborn / infants - high WBC counts

elderly / person with immunocompromise - low WBC counts, might not have enough leukocytes in response to infection or injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Monocyte

How long do they live?
What are they?

A

10 - 20 hrs circulating in blood.
Receptors allow to adhere to capillary wall when needed in tissue, to move out of vessel into interstitial space –> alter to macrophage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Macrophage

Where are they?
What are 4 main functions?

A

live moths to years in tissue.
derived from monocyte

Phagocytosis:
recognize bacteria, antigens, danger signals on cell fragments –> phagocytosize / engulf –> “phagosome”
–> phagosome fusion with lysosome inside macrophage –> becomes phagolysosome –> digest by macrophage

Chemotaxis (CENTRAL ROLE - IMMUNE)
Release of cytokines (TNF, IL-1) / Initiate inflammation in tissue (alarm!)

Release growth factor –> Stimulate fibroblasts –> promote healing with fibrinogen

Antigen presentation to initiate adaptive arm of immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Macrophages - different name in different tissue

Brain
Neck
Lung
Liver
Spleen
Kidney
Joint
Blood
Lymph node
Skin
(Bone)

A

Brain - microglial cells
Neck - Cervical lymph nodes
Lung - alveolar macrophages
Liver - Kupffer cell
Spleen - macrophage
kidney - mesangial phagocytes
joint - synovial A cell
Blood - monocytes (mature to macrophage)
Lymph node - resident and recirculating macrophages
Skin - langerhans cells
(Bone - Precursors in bone marrow)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is selectin?

A

A type of receptor on macrophage (macrophage has many various receptors that enables to respond to many things).

Selectin on monocyte binds to the endothelium cells on the inner wall of blood vessel –> monocyte stops in the stream and go out to the interstitial space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Neutrophil

How long do they live?
What are they?

A

6 - 12 hours in circulation

early responders to tissue injury.
phagocytosis & cytokines release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is neutrophilia?

A

increased number of neutrophil in blood. Indicates possible infection / disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is neutropenia?
What is the risk?

A

decreased number of neutrophil in blood.
Susceptible to infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What patients might have neutropenic precautions?

A

Patients that don’t have many WBC.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does “shift to left” indicate regarding neutrophil?

A

With high rate of stimulation (e.g. new infection in the body), neutrophils produced at high rate and immature cells (“bands”) enter circulation.

“Shift to left” indicate decreased ratio of mature neutrophils and increased ratio of immature neutrophils (“bands”).

“Shift to left” on blood test indicates ongoing acute injection or injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Mast cell

How long do they live?
Where are they?
What are they?

A

5 weeks to months
derived from basophil.
lives in connective tissue (near blood vessels and under mucosal surfaces)

Have IgE receptors <– activation by antigens
=> hypersensitivity / allergic reactions
=> release histamine, a powerful activator of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is an unique thing about mast cell that differentiate from macrophage

A

Having IgE receptor. Release histamine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Explain the steps of mast cell in hypersensitivity reaction

A
  1. New stimuli arrives. e.g. pollen
  2. B cell (B-lymphocytes) creates antibody (one antibody per one B-cell)
  3. The antibody binds to Mast cell at receptor (one mast cell can have multiple antibodies attached)
  4. The same stimuli comes again
  5. The antigen on mast cell recognize it
  6. Degranulation of Mast cell
    - change its shape and release chemicals
    - histamine (activate inflammation)
    - cytokines (attract neutrophils & macrophages –> promote healing)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Be able to explain mechanisms of inflammation, tissue damage through symptoms

A

(study diagram)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

In case of tissue damage, what triggers vasodilation?

A

Cytokines from mast cells / macrophages
Kirins (hormonal plasma protein)
Prostaglandins (lipid components from surrounding cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Explain the steps of neutrophil / monocyte emigration from blood vessel to interstitial tissue

A

(vasodilation –> increased blood flow)

  1. endothelial activation
    adhesion molecule / chemokines
  2. WBCs (neutrophils / monocytes) to tissue
    a) margination (move to sides, roll, adhesion)
    b) diapedesis / emigration (squeeze between endothelial cells)
    c) chemotaxis (guide to the site of tissue damage)
    d) phagocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Define cytokines

A

signaling protein.
involves with immunity, inflammation, hematopiesis

21
Q

Define chemokines

A

subset of cytokines (signaling protein).
induce directed cell movement

22
Q

Difine chemotaxis

A

Guiding cell to specific location

23
Q

Systemic inflammation

Explain how systemic inflammation happens

What are 3 common signs/symptoms?

A

Pyrogens
- some cytokines are pyrogens
- bacteria can produce pyrogens

Pyrogens reach to brain, induce hypothalamus to produce/release prostaglandins
–> conserves heat (SNS, vasoconstriction)
–> produce heat
–> systemic FEVER / fever = body trying to fight against

3 common signs/symptoms
- fatigue & lethargy (impaired sleep)
- anorexia
- leukocytosis

24
Q

What is leukocytosis. What is the normal range?

A

Elevated WBC count

Normal range: 5,000 - 10,000 mcL (for adult)

25
Q

Can inflammation occur in absence of infection?
Explain

A

Yes.

Infection (bacteria / virus involved)
Inflammation can happen from injury / tissue damage that does not involve infection.

26
Q

What is the difference between acute and chronic inflammation?

A

Acute: <2 weeks, = first step of healing

Chronic: >2 weeks
Can interfere with healing

27
Q

What are common causes of chronic inflammation?

A

Causes:
foreign body, toxins, infection, autoimmune disease, immunosuppression

28
Q

How continued tissue damage occurs in chronic inflammation?
Why is it problematic?

A

When macrophages phagocyte, they release:

Degradative enzyme (as a part of clean up) –> too much / too long can break down surrounding tissue

Growth factors (stimulate fibrosis to promote healing) –> too much / too long can increase the risks of clotting

29
Q

What is SIRS?

A

Systemic Inflammatory Response Syndrome

2 early indicators:
tachycardia (HR >90 bpm)
tachypnea (RR > 20)

Other:
Temp: too high or too low
WBC count: too high or too low

29
Q

What is sepsis?

A

SIRS (systemic inflammatory response syndrome) + Infection

30
Q

What are 2 types of tissue healing and their examples?
(categorize per replacing cell types)

A

Regeneration
- replaces the injured tissue with parenchymal (functional) cells = same cell type
e.g. epithelial tissue (skin),
e.g. bone (osteoblasts)
e.g. liver

Connective Tissue Repair
- replaces cells that cannot regenerate or cells that regenerate minimally, with connective tissue = scar
- scar tissue lacks properties of the original cell
e.g. heart muscle
e.g. liver - liver can regenerate, but after too much/long damage, fibrosis forms (interfere function)

31
Q

Explain liver tissue healing. Regeneration? Connective Tissue Repair?

A

Liver can regenerate. But after continued damage, fibrosis forms and interfere the functions of liver.

32
Q

What are 2 types of healing of surface wounds, and their examples?

A

Primary intention
- edges approximated (closed together but not united)
e.g. incision

Secondary intention
- heals bottom upward
e.g. pressure sore
e.g. burn injury

33
Q

What is the 3 phases of tissue healing?

A
  1. Inflammation
    Macrophage secrete growth factors
  2. Proliferation / Reconstruction
    Epithelial proliferation and migration
  3. Remodeling / Maturation
    Reorganization of collagen / scar tissue
34
Q

What are systemic factors that impair healing? (leads to chronic inflammation). list 4.

A
  • Factors that suppress inflammation (e.g. taking corticosteroids)
  • poor oxygen supply
  • poor nutrition supply
  • impaired function of fibrosis
35
Q

What is lymphedema? What are common causes globally and in U.S.?

A

Blocked lymph flow.
By lymph not collecting interstitium:
- inflammatory response
- hypertrophy of subcutaneous adipose tissue
- fibrotic changes (leads to permanent edema)

Globally
often caused by parasitic nematode (worms) in lymph node

in U.S.
often caused by lymph node removal (e.g. breast cancer), or
damage to lymph with radiation treatment

36
Q

Explain 5 stages of bone healing

A

Bone healing = Regeneration

  1. Hematoma (bleeding at the fracture)
  2. Fibrocartilage (“collar” formation) - weight bearing
  3. Callus (calcification of fibrocartilage) - harden
  4. Ossification
  5. Remodeling
37
Q

Improper bone healing: delayed union

A

Union of bone ends occur later than expected

38
Q

Improper bone healing: malunion

A

healing in incorrect anatomical position

39
Q

Improper bone healing: nonunion

A

failure of bone ends to grow together - gap of bone filled with dense fibrous tissue, not bone

40
Q

What does macrophage release when tissue damage happens?

A

Macrophage release cytokines (TNF, IL-1) to alert neutrophils and monocytes.

Cytokines is pyrogenic. cause fever.

41
Q

What is dependent edema?

A

Edema due to gravity. Common on lower extremities

42
Q

Explain how edema happens in tissue?

A

At capillary bed

Arterial side: Hydrostatic pressure > Oncoic (colloid osmotic) pressure –> fluid out to interstitial space

Venous side: Hydrostatic pressure < Oncoic (colloid osmotic) pressure.
Most abundant plasma protein: albumin, pulls fluids back into vessel

10% of fluid won’t get back to vessel
Taken by Lymphatic system

43
Q

Explain 4 causes of edema at capillary mechanism

A
  1. Increased hydrostatic pressure
    - increased capillary flow
    - venous congestion
  2. Decreased oncoic (colloid osmotic) pressure
    - loss of albumin (excess excretion with urine)
    - decreased albumin synthesis (by liver)
  3. Increased microvascular permeability
    - leads to leakage of plasma proteins to interstitial space
    - leads to increase of interstitial oncoic pressure
  4. Impaired lymphatic drainage (lymphedema)
44
Q

What causes loss of albumin in plasma?

A

Liver disease / decreased liver function
(albumin is synthesized only at liver, hepatocytes)

Kidney/Renal disease / decrease kidney function
(albumin is filtered & reabsorbed at renal tubule. Excess loss of albumin in urine leads to hypoalbuminemia)

45
Q

What are 3 common causes of osteomyelitis (bone infection)?

A
  1. hematogenous osteomyelitis
    via bloodstream. bone is well perfused
    more common in children, elderly, with IV drug use, with central lines
  2. contiguous spread
    via adjacent soft tissue
    e.g. patient with necrotic tissue (high risk of infection) on toes
  3. direct introduction of microbes to bone
    e.g. wound penetrates the bone
    e.g. broken bone that breaks through the skin
46
Q

How to treat osteomyelitis (bone infection)?

What happens if treatment is insufficient?

A

Urgent treatment is necessary.
Eliminate the infection ASAP.

If treatment is not sufficient, necrotic bone can separate and the infection can continue to proliferate.

Osteoblasts may lay a layer of new bone around the infection –> decreases successful phagocytosis of the infected bone. Result in chronic infection.

47
Q

Explain how edema occur when an individual is at starvation?

A

No food / nutrition –> decreased body fluid (water) -
-> decreased hydrostatic pressure & decreased colloid pressure
–> overall lowered blood osmotic pressure
–> edema

48
Q

How edema increase the risk of injury and infection?

A

Excess fluid in interstitial space
Cells are pushed abnormally far apart
–> tissues are easy to get damaged

Pathophysiology I (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions