Week 7 Quiz (Wound healing and alt. of Hematologic fx) Flashcards
1
Q
Resolution definition
A
- injured tissue is replaced by cells of the same type
- restoration of the original structure and function
2
Q
Repair definition
A
- destroyed tissue is replaced by connective tissue (scar)
- fills in lesion and restores tensile strength but can not carry out physiologic functions of the destroyed tissue
3
Q
when do resolution/repair occur?
A
they begin early during the inflammatory process
4
Q
Regenerative capacity of different cell types
A
- Labile cells
- Quiescent cells
- Permanent cells
5
Q
Labile cells and examples
A
- continuously dividing (proliferate thought life)
- skin, oral cavity, GI tract lining, urinary tract, bone marrow
6
Q
Quiescent cells and examples
A
- stable cells
- usually demonstrate low level of replication, but stimulation can lead to rapid increases in division
- bone, kidney, pancreas, fibroblasts, liver
7
Q
Permanent cells and examples
A
- nondividing cells
- stopped dividing during prenatal life
- nerve cells, cardiac m., skeletal m.
8
Q
Skeletal muscle fiber repair
A
- multinucleated, provide multiple copies of genes to speed up production of enzymes and structural proteins
- myoblasts: embryonic cells which fuse to create the muscle fibers
- satellite cells: assist with repair of damaged fibers = left-over myoblasts
9
Q
Other factors which influence wound healing
A
- site of the wound
- mechanical factors
- size of wound
- infection (won’t heal until get rid of infection)
- circulatory status (cartilage example)
- nutritional and metabolic factors
- age
10
Q
Tension lines
A
- most collagen and elastin fibers are in parallel bundles
- their orientation depends on the stress placed on the skin during normal movement
- clinical significance in surgery
11
Q
Debridement
A
- the first, absolutely essential step in wound healing is debridement
- “clean-up” of particulate matter in the inflammatory exudate by phagocytosis
- dissolution of fibrin clots by fibrinolytic enzymes
- natural debridement occurs, but is slow (inflammation and phagocytosis)
- surgical debridement speeds up healing
12
Q
First intention healing
A
- primary union
- wounds with minimal tissue loss
- example: sutured surgical wound
- always preferred if possible
- more likely to lead to resolution
13
Q
Second intention healing
A
- large, open defects and infected wounds
- examples: degloving injuries, burns
- formation of granulation tissue
- more likely to lead to repair
14
Q
Healing by second intention involves
A
- formation of a healthy granulation bed (happy pink)
- filling in the wound defect
- covering or sealing the wound (epithelialization)
- shrinking the wound (contraction)
- wound maturation
- remodeled (scars)
15
Q
granulation tissue
A
- has a soft, pink, granular appearance
- represents a temporary scaffolding that changes over time
- contains angioblasts and fibroblasts
- angioblasts are cells that form new blood vessels
- fibroblasts form collagen fibers for strong scar tissue
16
Q
Repair involves and occurs in what two phases?
A
- filling in the wound defect
- epithelialization (covering or sealing the wound)
- contraction (shrinking the wound)
- reconstruction phase
- maturation phase (think about us remodeling)
17
Q
Epithelialization
A
- epithelial cells from the surrounding healthy tissue migrate onto the granulation bed
- use proteolytic enzymes to sever the connection between the clot and the wound surface and slide in between
- make contact with similar cells from all sides of the wound and seal it (contact inhibition allows the cells to meet up and say they are done sealing)
- epithelialization can be aided by keeping the wound moist
18
Q
Phases of wound healing
A
- inflammation
- granulation tissue
- wound contraction
- collagen accumulation remodeling starts near the end of granulation tissue phase
19
Q
Reconstructive phase
A
- wound is initially sealed off by a blood clot containing fibrin and trapped cells
- debridement by macrophages and neutrophils (or by a surgeon)
- chemical mediators of inflammation are secreted by macrophages and promote growth and activity of angioblasts, and fibroblasts
- granulation tissue forms in 2-5 days
20
Q
Angiogenesis
A
- capillary buds sprout out of vascular endothelial cells on wound margins
- new endothelial cells migrate into the scaffolding and organize into vessels
- allows influx of blood with oxygen, nutrients, and more phagocytic cells and chemical mediators
- also called neovascularization
21
Q
Fibrosis (Fibroplasia)
A
- fibroblasts enter the area and proliferate
- they deposit fibrous structural proteins
- fibroblasts produce collagen which gradually develops more strength (scar tissue made of collagen and there are several types of collagen)
- collagen not inside of cells
- original collagen that is laid down is later replaced by better collagen that is more parallel to tension lines
22
Q
wound contraction
A
- myofibroblasts have features of both fibroblasts and smooth muscle cells
- the myofibroblasts establish connections with neighboring cells
- they anchor themselves to the wound bed and exert pull on neighboring cells
- contraction alone may move the wound edge by 0.5mm per day (just like a muscle)
23
Q
Maturation phase of healing (scar remodeling)
A
- continuation of collagen deposition, tissue repair, and wound contraction
- scar tissue is remodeled and gains its maximum strength
- collagen fibers are initially almost random, but now become highly organized
- “immature” type III collagen is replaced by stronger type I collagen
- this process often continues for months
24
Q
Wound healing order
A
- Induction of acute inflammatory response by the initial injury
- Debridement
- Formation of a healthy granulation bed
- Angiogenesis and fibroplasia
- Epithelialization
- Wound contraction
- remodeling of tissue elements to restore function and to increase wound strength
25
glucocorticoids
- aka steroids
- strong anti-inflammatory drugs
- slows the migration of phagocytic cells to the site of injury
- cause phagocytic cells already in the area to become less active
- mast cells exposed to steroids are less likely to release histamine and other chemicals that promote inflammation
- good: decrease excess inflammation
- bad: suppress immune system & affect normal adrenal gland function
- NSAID's (these drugs don't affect the immune system)
26
hematocrit
% of whole blood that is made up of RBC's
27
anemia
-conditions in which there is a decrease in the quality or quantity of hemoglobin and/or RBCs (decreased hematocrit)
28
causes of anemia
- defective RBC's or defective hemoglobin (sickle cell, CO)
- blood loss (trauma, neoplasms, ulcers)
- increased RBC destruction (= hemolysis) which is autoimmune or blood parasites
29
Polycythemia vera
conditions in which there are excessive RBC numbers or volume (dehydration ism most common cause of increased hematocrit)
30
Clinical manifestations of anemia
- acute vs chronic
- decrease of RBC's or hemoglobin function -> hypoxia
- signs are:
* energy level: fatigue
* skin/mucus membrane color: pale or jaundice
* respiratory rate: increased rate and depth
* CNS: dizziness, lethargy
31
compensation for anemia occurs by
- cardiovascular system (increased heart rate, capillary dilation)
- respiratory system (increased rate & depth)
- renal system (decreased blood flow to kidney triggers renin-angiotensin system)
- hematologic system (bone marrow stimulation: erythropoietin)
32
classification of anemias by bone marrow activity
- regenerative vs non-regenerative
- reticulocyte count = # immature RBC's in blood
- regenerative: bone marrow working hard to fix problem
* hemolytic blood disorders, or blood loss
- non-regenerative: bone marrow is the problem
* decreased erythropoiesis
33
Normal reticulocyte count in %
<1%
34
Classification of anemias by cell size and color
- macrocytic-normochromic anemias (result from abnormal DNA synthesis and die prematurely, larger than normal)
- Microcytic-hypochromic anemias (disorders of iron metabolism, disorders of porphyrin, heme, or globin synthesis, smaller than normal)
- Normocytic-normochromic anemias (relatively normal size and color, but insufficient number)
35
macrocytic-normochromic anemias
- pernicious anemia
| - folate deficiency
36
pernicious anemia
- can't take oral supplement
- cause by malabsorption of vitamin B12
- lack of gastric intrinsic factor which is needed for vitamin B12 absorption
37
folate deficiency anemia
- lack of folic acid which is essential for RNA and DNA synthesis in the RBC
- humans are totally dependent on dietary intake of folate
38
Microcytic-hypochromic anemias
- iron deficiency anemia
- lack of iron can also result in gastritis, irritability, headache, numbness, etc.
- 26mg iron needed daily for new RBCs (dietary requirement is 1-2 mg/day)
39
iron deficiency anemia
- women- pregnancy and menorrhagia
- ulcers, ulcerative colitis, cancer, etc
- medications that cause GI bleeding (NSAIDs)
- insufficient dietary intake of iron
- children < 2 yrs of age
40
Normocytic-normochromic anemias
- aplastic anemia
- posthemorrhagic anemia
- hemolytic anemia
- anemia of chronic inflammation
41
aplastic anemia
infiltrative bone marrow disorders
42
posthemorrhagic anemia
sudden blood loss with N iron stores
43
hemolytic anemia
auto immune, drugs, toxins, blood parasites
44
anemia of chronic inflammation
AIDS, SLE, malignancies, renal failure
45
Sickle cell disease
- homozygous
- production of abnormal hemoglobin S due to an inherited autosomal recessive disorder
- RBC become stretched into an elongated "sickle" shape
- the abnormally shaped RBC's are very prone to hemolysis
- high incidence of sickle cell trait in Afro-americans and east africans which may provide protection against malaria
46
Quantitative disorders of leukocyte function
- WBCs
- absolute # or relative number (%)
- decreased bone marrow activity
- premature destruction or WBC's in circulation
47
Qualitative disorders of leukocyte function
altered function of WBC's in inflammation or immune processes
48
Actual Quantitative WBC disorders
- leukocytosis
| - leukopenia
49
leukocytosis
- increased number WBC
- can be a normal protective response
- can also be caused by pathologic conditions
50
leukopenia
- decreased # of WBC
| - never a normal response, never beneficial
51
Neutrophil disorders
- neutrophilia
- neutropenia
- agranulocytosis
52
neutrophilia
=increased number
- seen in early phases of infection (esp. bacterial), inflammation or tissue necrosis
- "left shift"= premature release of somewhat immature neutrophils into the circulation (bands - protective mech.)
- physiologic: stress
- with hemorrhage or hemolysis
- some drugs, metabolic disorders, and neoplasms
53
neutropenia
- decreased number
- severe prolonged infections
- abnormal distribution and sequestration (collect in one spot)
- decreased bone marrow production
* chemo (doesn't allow bone marrow to produce), aplastic anemia, radiation
- neupogen: recombinant DNA engineered: stim. bone marrow production (G-CSF) (granulocytes = G)
- increased destruction
* splenomegaly, immune reactions
54
agranulocytosis
-drastically low neutrophils, eosinophils, and basophils (all 3 granulocytes)
55
Eosinophil disorders
- eosinophilia
| - eosinopenia
56
eosinophilia
- increased number
- allergic disorders
- dermatologic disorders
- parasite infestation
- some malignancies
- some drugs
57
eosinopenia
- decreased number
- stress responses
- Cushing's syndrome (glucocorticoids)
