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TNCC FINAL EXAMS, PRACTICE EXAM AND STUDY GUIDE 2024 WITH ACTUAL CORRECT QUESTIONS AND VERIFIED DETAILED ANSWERS BY EXPERTS |FREQUENTLY TESTED QUESTIONS AND SOLUTIONS |ALREADY GRADED A+ |NEWEST |LATEST UPDATE | GUARANTEED PASS CA$29.37   Add to cart
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TNCC FINAL EXAMS, PRACTICE EXAM AND STUDY GUIDE 2024 WITH ACTUAL CORRECT QUESTIONS AND VERIFIED DETAILED ANSWERS BY EXPERTS |FREQUENTLY TESTED QUESTIONS AND SOLUTIONS |ALREADY GRADED A+ |NEWEST |LATEST UPDATE | GUARANTEED PASS

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TNCC FINAL EXAMS, PRACTICE EXAM AND STUDY GUIDE 2024 WITH ACTUAL CORRECT QUESTIONS AND VERIFIED DETAILED ANSWERS BY EXPERTS |FREQUENTLY TESTED QUESTIONS AND SOLUTIONS |ALREADY GRADED A+ |NEWEST |LATEST UPDATE | GUARANTEED PASS

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  • April 8, 2024
  • 169
  • 2023/2024
  • Exam (elaborations)
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  • tncc final exams
  • tncc
  • already graded a newest
  • tncc final exams practice exam and study guide 2
  • tncc final exams practice exam and study guide
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By: drjohna • 6 months ago

very accurate

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By: Dredward • 6 months ago

very accurate and well detailed ...highly recommended

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1 | P a g e TNCC FINAL EXAMS , PRACTICE EXAM AND STUDY GUIDE 2024 WITH ACTUAL CORRECT QUESTIONS AND VERIFIED DETAILED ANSWERS BY EXPERTS |FREQUENTLY TESTED QUESTIONS AND SOLUTIONS |ALREADY GRADED A+ |NEWEST |LATEST UPDATE | GUARANTEED PASS What is renal response? Renal ischemia activates release of renin. Kidneys do not receive adequate blood supply, renin is release into circulation. Renin causes angiotensinogen, normal plasma protein, to release angiotensin I. Angiotensin -converting enzyme from the lungs converts into angiotensin II. Angiotensin II cau ses: - Vasoconstriction of arterioles and some veins - Stimulation of sympathetic nervous system - Retention of water by kidneys - Stimulation of release of aldosterone from the adrenal cortex (sodium retention hormone) *Decreased urinary output = early s ign renal hypoperfusion and an indicator that there's systemic hypoperfusion . Explain adrenal gland response. When adrenal glands are stimulated by SNS, release of catecholamines (epinephrine and norepinephrine) from adrenal medulla will increase. Epi sti mulates receptors in heart to increase force of cardiac contraction (positive inotropy) and increase HR (positive chronotropy) to improve cardiac output, BP and tissue perfusion. Shock stimulates hypothalamus to release corticotropin -releasing hormone tha t stimulates pituitary to release ACTH that stimulates adrenal gland to release cortisol. Effect of cortisol release is elevation in blood sugar and increased insulin resistance and gluconeogenesis, hepatic process to produce more sugar. 2 | P a g e Cortisol also ca uses renal retention of water and sodium, a compensatory mechanism to conserve body water. Explain Hepatic Response. Liver can store excess glucose as glycogen. As shock progresses, glycogenolysis is activated by epi to break down glycogen into glucose. In a compensatory response to shock, hepatic vessels constrict to redirect blood flow to other vital areas. Explain Pulmonary Response. Tachypnea happens for 2 reasons: 1. Maintain acid -base balance 2. Maintain increased supply of oxygen * Metabolic acido sis from anaerobic metabolism will be a stimulus for the lungs to increase rate of ventilation. Increased RR is an attempt to correct acidosis + augments oxygen supply to maximize oxygen delivery to alveoli. Explain Irreversible Shock. Shock uncompensated or irreversible stages will cause compromises to most body systems. - Inadequate venous return - inadequate cardiac filling - decreased coronary artery perfusion - Membranes of lysosomes breakdown within cells and release digestive enzymes that cause intra cellular damage. How would you assess a pt in hypovolemic shock? (Use Initial Assessment) and then: Inspect: - LOC - Rate and quality of respirations - External bleeding? - Skin color and moisture - Assess jugular veins and peripheral veins Auscultate: - BP - Pulse pressure - Breath sounds - Heart sounds - Bowel sounds Percuss: 3 | P a g e - Chest and abdomen Palpate: - Central pulse (carotid or femoral) - Positive inotropic effect (force of contraction) may be evidence by a bounding central pulse - Palpate peripheral pulses - Palpate skin temp and moisture Diagnostic Procedures: - Xrays and other studies - Labs Planning and Implementation - Oxygen - IV's with warmed replacement fluids - Control external bleeding with direct pressure - Elevate LE's - NGT - Foley - Monitor and pulse oximeter - Monitor for development of coagulopathies - Surgery? ICP is a reflection of what three volumes? What happens when one increases? 1. Brain 2. CSF 3. Blood within the nonexpansible cranial vault As volume of one increases, the volume of another decreases to maintain ICP within normal range. As ICP rises, CPP decreases, leading to cerebral ischemia and potential for hypoxia and lethal secondary insult. Hypotensive pt w/marginally elevated ICP can be harmful. Slightly elevated BP could protect against brain ischemia in a pt with high ICP. Cerebral ischemia can lead to increased concentration of CO2 and decreased concentration of O2 in cerebral vessels. CO2 dilates cerebral blood vessels = increase blood volume and ICP. What are the early signs and symptoms of increased ICP? - Headache - N/V - Amnesia regarding events around the injury - Altered LOC - Restlessness, drowsiness, changes in speech, or loss of judgement What are the late observable signs of symptoms of i ncreased ICP? - Dilated, nonreactive pupil - Unresponsiveness to verbal or painful stimuli 4 | P a g e - Abnormal motor posturing patterns - Widening pulse pressure - Increased systolic blood pressure - Changes in RR and pattern - Bradycardia What is Cushing's phenome non or Cushing's Reflex? Triad of progressive HTN, bradycardia and diminished respiratory effort. What are the two types of herniation that occurs with ICP? 1. Uncal herniation 2. Central or transtentorial herniation Why does herniation occur? What are the symptoms? Because of uncontrolled increases in ICP. S/E's - Unilateral or bilateral pupillary dilation - AsyDimmetric pupillary reactivity - Abnormal motor posturing - Other evidence of neurologic deterioration Define uncal herniation. The uncus (medial aspect of the temporal lobe) is displaced over the tentorium into the posterior fossa. This herniation is the more common of the two types of herniation syndromes. Define central or transtentorial herniation. A downward movement of the cerebral hemispheres with herniation of the diencephalon and midbrain through the elongated gap of the tentorium. Disruptions of the bony structures of the skull can result in what? Displaced or nondisplaced fx's causing CSF leak age b/c of lac to the dura mater, creating a passage for CSF. CSF leaks through the nose (rhinorrhea) or the ears (otorrhea). A potential entrance for invading bacteria. Also: meningitis or encephalitis or brain abscess Define Minor Head Trauma. GCS 13 -15 Define Moderate Head Trauma Postresuscitative state with GCS 9 -13.

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