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NSG 533 Exam 1 | Questions & Answers (100 %Score) Latest Updated 2024/2025 Comprehensive Questions A+ Graded Answers | With Expert Solutions $13.48   Add to cart

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NSG 533 Exam 1 | Questions & Answers (100 %Score) Latest Updated 2024/2025 Comprehensive Questions A+ Graded Answers | With Expert Solutions

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NSG 533 Exam 1 | Questions & Answers (100 %Score) Latest Updated 2024/2025 Comprehensive Questions A+ Graded Answers | With Expert Solutions

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  • August 7, 2024
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  • 2024/2025
  • Exam (elaborations)
  • Questions & answers
  • NSG 533
  • NSG 533
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VasilyKichigin
NSG 533 Exam 1 | Questions & Answers (100 %Score) Latest Updated 2024/2025
Comprehensive Questions A+ Graded Answers | With Expert Solutions


5 essential components of pathophysiology - 1. Etiology (causative mechanisms)
2. Epidemiology (risk factors and distribution in populations)
3. Pathogenesis (disease mechanisms)
4. Clinical manifestations (signs, symptoms, and diagnostic criteria)
5. Outcomes (cure, remission, chronicity, or death)

7 general mechanisms of cell injury - 1. ATP depletion
2. Mitochondrial damage
3. Accumulation of oxygen and oxygen-derived free radicals
4. Membrane damage (depletion of ATP)
5. Protein folding defects
6. DNA damage defects
7. Calcium level alterations

3 cellular events that occur with ischemia-induced hypoxic injury - 1. Since not enough
oxygen is reaching the cell, the amount of ATP production within the mitochondria
declines
2. When ATP production through oxidative phosphorylation declines, glycolysis
(anaerobic metabolism) increases
3. The decline in pH leads to rupture of already swollen lysosomes and release of their
proteolytic enzymes = autodigestion of cell contents and cell membrane

4 A&P occurrences that characterize all cell injury and death - 1. Impaired energy (ATP)
production
2. Direct cell membrane damage/injury
3. Genetic alteration
4. Metabolic derangements

4 critical points at which ATP production may be impaired - 1. Hypoxia (the most
common)
2. Hypoglycemia (far less common than hypoxia)
3. Inhibition of enzymes within the cell (extremely rare)
4. Uncoupling of oxidation and phosphorylation (extremely rare)

5 forms of direct cell membrane damage/injury - 1. The effect of free radicals (reactive
oxygen species)
2. Activation of the complement system
3. Lysis by enzymes
4. Lysis by viruses
5. Physical and chemical stressors

2 forms of endogenous accumulations (metabolic derangements) - 1. Fat

, 2. Bilirubin

4 effects of free cytosolic calcium - 1. Activation of protein kinases
2. Activation of phospholipases with phospholipid degradation and loss
3. Activation of proteases
4. Activation of endonuclease

Pyknosis - Clumping of nuclear material

Karyorrhexis - Fragmentation of the nuclear material

Karyolysis - Dissolution of the nuclear material

3 mechanisms involved in apoptosis - 1. Apoptosis triggered by internal signals: the
intrinsic or mitochondrial pathway
2. Apoptosis triggered by external signals: the extrinsic or death receptor pathway
3. Apoptosis-inducing factor (AIF)

Current TBW for water deficit - weight in kg x (0.4 for women, 0.5 for men, 0.6 for
infants)

Ideal TBW - (current Na X TBW) / 140

Water deficit - (Current Na X TBW) / 140 - TBW

Current TBW for water excess - weight in kg (0.5 for women, 0.6 for men, 0.7 for
infants)

Water excess - weight (kg) X (0.5 for women, 0.6 for men, 0.7 for infants) x (1 -
[Na/125])

Serum osmolality - OSM (calc) = 2 X [sodium concentration] + [glucose
concentration/18] + [BUN/2.8]

Corrected serum sodium - Corrected sodium = 1.6 mEq/L X (every increase of 100
mg/dl in glucose concentration over 100)

5 mechanisms of edema formation - 1. Increased capillary venous hydrostatic pressure
2. Decreased capillary oncotic pressure
3. Lymphatic obstruction/dysfunction
4. Increased capillary permeability
5. Sodium and water retention

Metabolic acidosis and an elevated anion gap ... - "Abnormal" numbers and types of
anions present

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