Exam 3 Flashcards
One good sign of an infection
Elevated WBC (11,000-25,000) 3,500/5,000-10,000 (normal)
Leukemia WBC range
WBC 100,000-400,000
Eosinophils and basophils
Allergies and inflammation
Neutrophils
Fight infection
Lymphocyte
A lymphocyte is a type of white blood cell in the vertebrate immune system. Lymphocytes include natural killer cells, T cells, and B cells
Serous fluid
Watery, like plasma
Fibrinous fluid
Clotted
Serosanguious fluid
Clear pink, blood tinged
Sanguinous
Bloody
Shift to the left** of cells
*
Purulent
Pus (suppurative)
Serious, fibrinous, serosanguinous, sanguinous, purulent drainage are sisngs of
Local manifestations
ESR (erythrocyte sedimentation rate)
The erythrocyte sedimentation rate is the rate at which red blood cells in anticoagulated whole blood descend in a standardized tube over a period of one hour. It is a common hematology test, and is a non-specific measure of inflammation.
Stimulates angiogenesis
Chronic inflammation can cause
Cancer
Purpose of an inflammatory response
To prepare the injured area for healing
3 inflammatory responses:
- Leukocytes (neutrophils & macrophages) to
remove debris and provide growth factors - Nutrients (proteins, glucose, vitamins) to
provide the building blocks for cells - Clotting factors and platelets to limit damage
T/F every disease has some type of inflammation
True
3 plasma protein systems:
- Clotting cascade: prevents further bleeding
- Kinin cascade: produces bradykinin, causing pain, vasodilation, vascular permeability
- Complement cascade: stimulates opsonins,chemotactic factors, and anaphylatoxins which degrade Mast cells to release histamine, a potent vasodilator.
Vascular response to inflammation (4 steps)
Histamine and bradykinin stimulate vasodilation
and increased permeability, resulting in:
1. Increased blood flow to the area, causing redness
(rubor) and heat (calor)
2. Leakage of protein rich plasma into the
interstitial spaces, causing swelling (tumor)
3. Bradykinin also causes pain (dolor)
4. Cells are unable to function
Cellular response of inflammation (4 steps)
Chemotactic factors attract neutrophils to:
1. Marginate: move to the capillary walls
2. Emigrate: squeeze through capillary pores
3. Migrate: through chemotaxis to the injury
4. Phagocytosis facilitated by opsonization
(acts to facilitate adherence of WBC’s to
bacteria)
5 cardinal signs of inflammation
- redness
- swelling
- loss of function
- pain
- heat
3 systemic signs of inflammation
- Fever: caused by specific cytokines
(endogenous pyrogens) - Leukocytosis: increase in WBC’s (>11,000)
and in infection, a “left shift” ratio - Increase in plasma proteins as measured by ESR (erythrocyte sedimentation rate)
3 reasons chronic inflammation occurs and 3 results of it:
May occur due to: 1. Chronic infection or contamination 2. Continuous exposure to irritants 3. Immune system abnormalities May result in: 1. Granuloma formation 2. Giant cell formation 3. Cancers in genetically susceptible individuals
3 stages of wound healing
- Inflammation: usually lasts 1-2 days
- Proliferation and New Tissue Formation:
2-8 weeks until maximum strength achieved.
May involve regeneration and resolution, or
repair with scar tissue but loss of function - Remodeling and Maturation: up to 2 years
3 stages of wound healing
Hemostasis is first- wound being closed by clotting
1. Inflammation: usually lasts 1-2 days
2. Proliferation and New Tissue Formation:
2-8 weeks until maximum strength achieved.
May involve regeneration and resolution, or
repair with scar tissue but loss of function
3. Remodeling and Maturation: up to 2 years
3 types of wound healing
- First Intention: must be clean; able to
approximate wound edges; fastest; preferred - Second Intention: used in contaminated wounds;
large amount of tissue lost; very slow; large scar - Third Intention: rarely used to close large
wounds that are clean enough. Example: skin
grafting
3 types of wound healing
- First Intention: must be clean; able to
approximate wound edges; fastest; preferred - Second Intention: used in contaminated wounds;
large amount of tissue lost; very slow; large scar - Third Intention: rarely used to close large
wounds that are clean enough. Example: skin grafting
Adherence
Wound staying together
Wound vacuum
for 2nd intentiton
Wound healing process
- Macrophages: dissolve clots; clear debris; add
a. TGF-B, transforming growth factor-beta to
stimulate collagen precursor procollagen
b. VEGF, vascular endothelial growth factor
stimulates angiogenesis
c. MMPs, Matrix metalloproteinases, remodel collagen and fibrin2. Collagen lattice forms - Granulation tissue fills in wound
- Hypertrophic scar tissue overfills wound
- Cicatrization (maturation) of wound
may take 1-2 years. Collagen contracts
& scar becomes lighter and smoother
Non-union
failure of adherence
Dehiscence
wound edges separate, exposing underlying tissues
Evisceration
underlying viscera are exposed
Abscess
A walled pocket of infection
Sinus tract
A narrow tunnel forming
Cellulitis
A bacterial infection that enters the skin, affected skin appears swollen and red and may be hot and tender. edema is a big risk factor with cellulitis
Necrosis
Death of tissues/ cells
Gangrene
Type of tissue death caused by a lack of blood supply
Fistula
An abnormal connection between two body parts, such as an organ or blood vessel and another structure.
Excess fibrin or dysfunctional collagen
synthesis may result in abnormalities such
as: (5)
- fistula formation
- adhesions
- contractures
- strictures
- keloids
Patients that have the hardest time healing from wounds
Diabetics
Systemic markers of vascular inflammation
Homocysteine level: elevated in reduced
levels of folate, B vitamins, and riboflavin.
Inhibits anticoagulation cascade and
increases endothelial damage in arteries.
• C-Reactive Protein: increases to neutralize
inflammatory chemicals
• Infectious agents: often found in plaques
• Endothelial dysfunction: lack of NO
Granulation tissue
New connective tissue and microscopic blood vessels that form on the surfaces of a wound during the healing process. Granulation tissue typically grows from the base of a wound and is able to fill wounds of almost any size. Bleeds easily
Define CHF and the mortality rate in 5 years
A complex syndrome resulting from any cardiac dysfunction that results in low cardiac output (CO) and symptoms of pulmonary or systemic fluid congestion. In adults, the mortality rate is 50% within 5 years. It is considered an end-stage disease.
Risk factors of CHF
Age: generally seniors
• High cholesterol, HTN, DM, obesity
• Pre-existing heart conditions, CAD, MI
• Valve problem or other mechanical issue
• Fluid overload conditions: renal disease
• Alcoholism, liver disease
Cicatrization
scar formation at the site of a healing wound
Causes of CHF
- Coronary Artery Disease/atherosclerosis
- Hypertension/myocardial hypertrophy
- Myocardial Infarction
- Heart Valve Disease
- Pericardial restriction/pericarditis
- Fluid overload conditions
Hypertrophic cardiomyopathy
Hypertrophic: walls are thickened,
reducing ventricular volume.
• Causes: HTN, CAD, valve stenosis,
remodeling
Dilated cardiomyopathy
Dilated: walls are weakened and bulge
out, reducing contractility
• Causes: MI with extensive scar, valve
regurgitation
Fluid overload condition
CHF
Decrease cardiac output causes: (3 things)
Reduced blood flow to kidneys,
stimulating the RAAS and fluid retention
• Less stimulation to baroreceptors in aortic
arch, stimulating hypothalmus to increase
thirst and ADH production
• Stress response stimulates catecholamines,increasing HR and O2 demand of heart
Increase fluid retention in CHF causes
Increase in preload and afterload
Increased stress hormones/catecholamines vasoconstrict and…
Increase afterload, HR and O2 demand increase, causing ischemia
Ischemia reduces
Compliance, elasticity, and contractility
In CHF, wall stress is increased causing CO to
decrease
S/S of CHF (8)
SOB climbing stairs • SOB lying flat/orthopnea • SOB with activities • Increased abdominal girth • Lower leg edema • Cough, white sputum • Increased weight • Decreased appetite
Assessment findings of CHF
• SOB on exertion or at rest • Lungs may have crackles, esp at bases • Point of maximal impulse (heart) moved lower and left, indicating enlargement • X-rays: cardiac enlargement, pulmonary congestion. • Ascites & liver congestion, leg edema, distended jugular veins • Decreased urinary output
Left-sided HF s/s
- SOB
- Orthopnea
- Low O2 sat
- Pulmonary crackles
- S1 or S2 gallop
- Weak thready pulse
- Probably low BP
- left backs up into the lungs
Right-sided HF s/s
- weight gain
- leg edema
- ascites/liver enlargement
- jugular vein distension
- right backs up to the rest of the bpdy
Diagnostic testing of CHF
Echocardiogram/Stress Test/Stress Echo • Chest X-ray: heart and lungs • Blood tests: BNP and ANP • Kidney function: BUN, creatinine • Liver function: LFT’s • Cardiac Angiography/catheterization • Right-sided heart catheterization: Swan- Ganz catheter (ICU only)
Diagnostic criteria of CHF
- Ejection fraction less than 40%
- Atrial Natriuretic Peptide greater than 77 pg/mL
- Brain Natriuretic Peptide greater than 100 pg/mL
- S&S of fatigue, SOB, edema, activity intolerance
- S&S at rest indicate increased disease burden
- Structural heart disease: decreased wall motion,
coronary artery blockage on angiogram
AHA classification system
• Stage A: High risk/ no abnormalities (example: DM/CAD/HTN) • Stage B: Abnormalities/no S & S • Stage C: Abnormalities with S & S • Stage D: advance abnormalities and S & S at rest on maximum med therapy
Staging of CHF
• Stage 1: SOB with brisk walk/stairs • Stage 2: OK at rest. HR or SOB when walking or stairs. • Stage 3: HR up, tired, daily activity is an effort. • Stage 4: HR up, SOB at rest, fatigue, anxiety, palpitations
S/S Pulmonary Edema
Falling O2 sat, confusion, jugular vein distension, infarct, S3 gallop, tachycardia, enlarged spleen and liver, decreased urine output, weak pulse, cool or most skin, skin pale, grey, or cyanotic, dyspnea, orthopnea, crackles, wheeze, cough
CHF treatments
CHF medications are used to:
1. Improve cardiac efficiency by strengthening
contractions and slowing rate: glycosides
2. Reduce peripheral vascular resistance:
vasodilators
3. Reduce fluid retention: diuretics
Other treatments include:
1. Exercise: strengthens myocardium & vasodilates
2. Surgery: Bypass or valve repair as needed
Mechanical treatments for CHF
• Cardiac Resynchronization and Implantable Cardioverter-Defibrilators • Balloon Pumps: temporary • L-VAD: left ventricular assist devices • Heart transplantation • LV remodeling surgery
T/F: CHF is an end-stage disease
True
Atrophic scar
A smaller than normal scar that’s atrophied
Hypertrophic scar
A bigger, thicker hypertrophied scar, not as thick as a keloid
Ways to prevent CHF
Prevent CHF by controlling risk factors: • Blood pressure (HTN: meds/diet/exercise) • Blood sugar (DM: meds/diet/exercise) • Blood cholesterol (meds/diet/exercise) • Weight: keep normal • Exercise: keep it up! Resistance training, walking, isometrics • Diet: DASH diet (Dietary Approaches to Stop Hypertension), Mediterranean diet
Define renal failure
Renal failure is a condition in which
the kidneys fail to remove metabolic
end products from the blood and
regulate the fluid, electrolyte, and pH
balance of the extracellular fluids. It is
on the list of top 10 causes of mortality
in the United States.
Pre-renal failure
Reduced blood flow to the kidneys (CHF, HT, shock, clots, stenosis)