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NURS 5315 Module 1 Exam Questions and Answers 2024( A+ GRADED 100% VERIFIED).
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NURS 5315 Module 1 Exam Questions and Answers 2024( A+ GRADED 100% VERIFIED).
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NURS 5315 Module 1Cell membrane composed of - ANS phospholipids, cholesterol, glycolipid
Role of phospholipids - ANS repairing the cell by folding
Cell membrane is highly permeable to - ANS CO2, O2, fatty acids, steroid hormones
Resting membrane potential - ANS slight difference in charge between ICF and ECF. Charge is
-70 to -85mV
Action potential - ANS sudden impulse and rapid change in resting membrane potential.
Depolarization - ANS charge is moving closer to zero and becoming more positive
Threshold potential - ANS occurs when the inside of the cell does not change at least 15 to
20mV and the action potential is not successfully reached
Repolarization - ANS occurs when the charge reaches zero and then returns back to the
baseline of -70 to -85mV
Refractory period - ANS cell membrane resists repolarization and cannot depolarize
Absolute refractory period - ANS membrane does not respond to any stimulus
Relative refractory period - ANS repolarization only occurs to very strong stimulus
Hyperpolarized - ANS charge is greater than -85mV. Cell is less excitable
Hyperpolarized - ANS charge is less than -65mV. Cell is very excitable
Hypokalemia effects of resting membrane potential - ANS hyperpolarized, less excitable
Decrease in neuromuscular excitability, weakness, smooth muscle atony, paresthesias and
cardiac dysrhythmias
Hyperkalemia effects of resting membrane potential - ANS hyperpolarized, more excitable
Peak T waves, K+ increases, widening QRS, cardiac standstill
Hypercalcemia effects of resting membrane potential - ANS hyperpolarized, less excitable
Weakness, hyporeflexia, lethargy, confusion, encephalopathy, short QT, depressed T waves
, Hypocalcemia effects of resting membrane potential - ANS hyperpolarized, more excitable
Tetany, hyperreflexia, circumoral paresthesias, seizures, dysrhythmias
Atrophy - ANS E: shrinkage of cell size
P: imbalance between protein synthesis and degradation, less mitochondrial, myofilaments, and
endoplasmic reticulum. Autophagy is also present.
CM: shrinkage of thymus gland in childhood, skeletal muscle atrophy d/t being bedridden
Physiologic atrophy:
Pathologic atrophy: - ANS -shrinkage of thymus gland in childhood
-skeletal muscle shrinkage d/t being bedridden or paralyzed. Also brain shrinkage d/t age
Hypertrophy - ANS E: increase in size of cells
P: hormonal stimulation or increased functional demand which increases cellular protein in
mitochondria and endoplasmic reticulum
CM: skeletal muscle growth d/t lifting weights and working out, kidney enlargement d/t other
kidney being removed, cardiomegaly d/t increased workload
Physiologic hypertrophy:
Pathologic hypertrophy: - ANS -skeletal muscle enlargement d/t lifting weights, surgical removal
of one kidney causes the other kidney to enlarge to compensate
-cardiomegaly d/t increased workload, hypertension
Hyperplasia - ANS E: increase in number of cells
P: happens only in cells capable of mitosis d/t growth factors that stimulate the cells to multiply
CM: increase in tissue mass as damage or resection, removal of part of liver, uterine and
mammary enlargement in pregnancy, endometrial lining of the uterus d/t estrogen secretion
Physiologic hyperplasia:
Pathologic hyperplasia: - ANS compensatory hyperplasia d/t increase in tissue mass after
damage or resection, removal of part of the liver will result in it to regenerate, uterine and
mammary gland enlargement d/t pregnancy
abnormal increase in hormonal stimulation, endometrial lining undergoes hyperplasia as a result
of estrogen however progesterone will halt this. It becomes a problem when progesterone does
not halt it and it will lead to cancer
Metaplasia - ANS E: reversible, adult cell is replaced by another adult cell
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