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NSG533 Week 4 Exam – Test 1 – End Term A+ Submission

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Course: NSG 533 – Advanced Pharmacology Exam: Test 1 | Week 4 | End Term | A+ Graded Level: Graduate Nursing (MSN / Nurse Practitioner Track) Includes: Full exam content from Week 4 Test 1 A+ level answers aligned with evidence-based pharmacological principles Topics include drug classifications, mechanisms of action, adverse effects, interactions, and prescribing guidelines

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NSG 533
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NSG 533 – Week 2/3 Exam 1 – End Term
A+ Graded Submission
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



Metabolic acidosis and a normal anion gap ... - ✔✔A loss of bicarb

Typically either GI or renal (RTA - type 1, type 2, or type 4)

"Hyperchloremic metabolic acidosis"

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