NUR333-Exam 2 Questions And Correct Answers
PROTOTYPE: Isoniazid (INH)
Therapeutic class: Anti-tuberculosis drug, antimycobacterial
Pharmacologic class: Mycolic acid inhibitor
Therapeutic effects: M. tuberculosis prophylaxis, mainstay of TB treatment Action:
Inhibits synthesis of mycolic acid, bactericidal for rapidly dividing
organisms, bacteriostatic for dormant mycobacteria
ADR: fever, rash, neurotoxicity
Black Box Warning: hepatotoxicity (monitor LFTs for 1-3 month), older adult, neuropathy
(B6/pyridoxine may be given to prevent neuropathy)
Contraindications: allergy, hx chronic hepatic disease, seizure disorder
Interactions: antacids, azole antifungals, alcohol, CYP450 inhibitors, carbamazepine,
food, herbs
Pregnancy Category C
Treatment of overdose: Pyridoxine to prevent seizures and to correct metabolic
acidosis
,Similar Drugs - Ethambutol (Myambutol), Rifampin (Rifadin), Pyrazinamide (PZA)
Stages of Wound Healing
hemostasis:
coagulation of blood to stop bleeding
- Exposed collagen of injury attracts platelets
- Platelets aggregate and secrete inflammatory mediators
- Vasoactive amines cause short-term vasoconstriction
- Proliferation and Granulation
- Fibroblasts
- Connective tissue cells
- Synthesize collagen
framework of scar tissue
inflammation
proliferation
new tissue, collagen
granulation tissue formation,
,angiogenesis (formation of new blood vessels)
epithelialization (epidermal cells migrate to cover wound gap)
contraction & remodeling
3 weeks after
scar tissue
primary intention
Well-defined wound edges
Surgical incision
No tissue loss
Simple epithelization (new skin growing)
By day 5, granulation tissue
At the end of first month, connective tissue covered by intact epidermis
Secondary Intention
Tissue loss significant
Regeneration with same cell type not possible
Granulation and fibrotic tissue formation
Longer healing time with wound contraction to close gap
Myofibroblasts
Scarring
tertiary intention
Large amount of deep tissue missing
Cleaned and left open
Temporary packing with sterile gauze
Highly visible scarring, often requires skin graft
Pressure ulcers and severe burns
acute inflammation
Occurs quickly in response to cell injury, clears the body of the offending agent,
, promotes healing and resolves after short time, hours or days
Lasts 1 to 2 weeks
Immediate onset
A result of the influx of neutrophils (6-24 hours)
Results in pain and edema
Phase 1 of acute inflammation
1. increased vascular permeability
Inflammatory mediators' histamine and bradykinin enable blood vessels to dilate and
become more permeable
Permeability allows for fluids, WBCs and platelets to make their way to the site of injury
or infection. After the onset of the inflammatory process, blood vessels surrounding the
site become permeable allowing phagocytic cells to reach and neutralize the antigen
Increased permeability of the blood vessels leads to edema of surrounding tissues.
Always obtain culture before starting antibiotics
phase 2 of acute inflammation
2. Cellular chemotaxis:
Chemical signals from WBC's, endothelial cells, microbial agents, attract other WBC's
and platelets
PROTOTYPE: Isoniazid (INH)
Therapeutic class: Anti-tuberculosis drug, antimycobacterial
Pharmacologic class: Mycolic acid inhibitor
Therapeutic effects: M. tuberculosis prophylaxis, mainstay of TB treatment Action:
Inhibits synthesis of mycolic acid, bactericidal for rapidly dividing
organisms, bacteriostatic for dormant mycobacteria
ADR: fever, rash, neurotoxicity
Black Box Warning: hepatotoxicity (monitor LFTs for 1-3 month), older adult, neuropathy
(B6/pyridoxine may be given to prevent neuropathy)
Contraindications: allergy, hx chronic hepatic disease, seizure disorder
Interactions: antacids, azole antifungals, alcohol, CYP450 inhibitors, carbamazepine,
food, herbs
Pregnancy Category C
Treatment of overdose: Pyridoxine to prevent seizures and to correct metabolic
acidosis
,Similar Drugs - Ethambutol (Myambutol), Rifampin (Rifadin), Pyrazinamide (PZA)
Stages of Wound Healing
hemostasis:
coagulation of blood to stop bleeding
- Exposed collagen of injury attracts platelets
- Platelets aggregate and secrete inflammatory mediators
- Vasoactive amines cause short-term vasoconstriction
- Proliferation and Granulation
- Fibroblasts
- Connective tissue cells
- Synthesize collagen
framework of scar tissue
inflammation
proliferation
new tissue, collagen
granulation tissue formation,
,angiogenesis (formation of new blood vessels)
epithelialization (epidermal cells migrate to cover wound gap)
contraction & remodeling
3 weeks after
scar tissue
primary intention
Well-defined wound edges
Surgical incision
No tissue loss
Simple epithelization (new skin growing)
By day 5, granulation tissue
At the end of first month, connective tissue covered by intact epidermis
Secondary Intention
Tissue loss significant
Regeneration with same cell type not possible
Granulation and fibrotic tissue formation
Longer healing time with wound contraction to close gap
Myofibroblasts
Scarring
tertiary intention
Large amount of deep tissue missing
Cleaned and left open
Temporary packing with sterile gauze
Highly visible scarring, often requires skin graft
Pressure ulcers and severe burns
acute inflammation
Occurs quickly in response to cell injury, clears the body of the offending agent,
, promotes healing and resolves after short time, hours or days
Lasts 1 to 2 weeks
Immediate onset
A result of the influx of neutrophils (6-24 hours)
Results in pain and edema
Phase 1 of acute inflammation
1. increased vascular permeability
Inflammatory mediators' histamine and bradykinin enable blood vessels to dilate and
become more permeable
Permeability allows for fluids, WBCs and platelets to make their way to the site of injury
or infection. After the onset of the inflammatory process, blood vessels surrounding the
site become permeable allowing phagocytic cells to reach and neutralize the antigen
Increased permeability of the blood vessels leads to edema of surrounding tissues.
Always obtain culture before starting antibiotics
phase 2 of acute inflammation
2. Cellular chemotaxis:
Chemical signals from WBC's, endothelial cells, microbial agents, attract other WBC's
and platelets
