Inflammation and Repair Flashcards
inseparable and coexistent processes orchestrated
by leukocytes, chemical mediators, and GFs
present in tissue and blood
Inflammation and Repair
Follow a predictable sequence of events that includes:
- tissue injury
- vascular response
- cellular response
- resolution
Inflammation and Repair
- Response of living vascularized tissue to injury
- ROLE: destroy/isolate injurious agents to achieve healing and repair
Inflammation
Factors determining pattern of inflammation
- Inciting agent
- Time of observation
- Immune status of host
4 cardinal signs of inflammation
(D RCT = D Randomized Controlled Trials)
- Dolor – pain
- Rubor – redness
- Calor – warmth/heat
- Tumor – swelling
Fifth clinical sign of inflammation (later added by Virchow)
Functio laesa – loss of function
(iNIF)
Infections – bacterial, viral, fungal, parasitic and microbial toxins
Immune reactions/ hypersensitivity – autoimmune diseases, allergies
tissue Necrosis – ischemia, trauma, physical and chemical injury
Foreign bodies – splinters, dirt, sutures
Inciting agents/stimuli of inflammation
Typical Inflammatory Reactions: 5 Rs
- RECOGNITION of the injurious agent by macrophages, other sentinel cells in tissues
- RECRUITMENT of leukocytes and proteins – vasodilation, increased vascular permeability (edema)
- REMOVAL/Elimination of the agent – WBCs and CHONs activation
- REGULATION (control) of the response
- RESOLUTION/REPAIR of damaged tissue – fibroblasts, ECM and cells
Acute Inflammation: Hallmarks
Redness and Warmth – result of vessel dilatation and increased blood flow to the inflamed part
Swelling – caused by accumulation of fluid, esp exudate
Pain – due to increased pressure on nerve endings from swelling, and a direct effect of certain chemical factors which are released to mediate the response
Loss of function – When swelling and pain are marked, there is partial or complete loss of function of the inflamed structure
Immediate and early response to an injurious agent
Acute Inflammation
3 major components of acute inflammation
- Dilation of small vessels –> increase in blood flow
- Increased permeability of the microvasculature –> plasma proteins and leukocytes to leave the circulation
- Emigration of leukocytes from the microcirculation and their accumulation in the focus ofinjury, and their activation to eliminate the offending agent
- high protein content, may be with RBCs/WBCs
- formed in inflammation (vascular permeability
increases due to increased inter-endothelial spaces)
Exudate
- low protein content, few cells
- formed when fluid leaks out because of increased hydrostatic pressure or decreased oncotic pressure
Transudate
Vasodilation is induced by the action of several mediators, notably histamine on vascular smooth muscle
- involves first arterioles and opening of capillary beds resulting in increased blood flow
- redness (erythema) and warmth
Quickly followed by increased permeability of the microvasculature
Slowing of blood flow (stasis) - vascular congestion and localized redness
Leukocyte accumulation (principally neutrophils) along vascular endothelium
Vascular Changes (changes in blood flow and caliber) - Acute Inflammation
In inflammation, lymph flow is increased.
- secondarily inflamed lymphatics
- secondarily inflamed draining lymph nodes
¨ reactive or inflammatory lymphadenitis
Lymphangitis- secondarily inflamed lymphatics
Lymphadenitis- secondarily inflamed draining lymph nodes
*reactive or inflammatory lymphadenitis