Summary
Summary NSG 211 Final Study Guide
- Course
- NSG 211
- Institution
- Marian University
This is a comprehensive and detailed study guide on;finals exam for NSG 211. *An Essential Study Resource!!
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Pathophysiology: NSG 211 Exam 5 ReviewConsider: Etiology, Process, Signs and Symptoms, Complications of topics below…
Pyelonephritis
Glomerulonephritis: signs symptoms
Urolithiasis: causes, signs / symptoms, complications
Renal failure: causes, signs / symptoms, complications
Comas, Vegetative state: definitions
Posturing: prognosis
Aphasia: types, areas affected
Types of speech and writing dysfunctions from neurological injury
ICP: early signs and symptoms of increased ICP
Cushing Reflex
Meningitis
Meningitis: Inflammation of the brain meninges or spinal cord
Pathophysiology:
o Micro-organisms reach the brain via the blood by...
*Nearby tissue (mucosa)
*Direct Trauma / Surgery
Microbes bind to nasopharyngeal wall and cross mucosal
barrier attaching to choroid plexus
o After entering CSF, infection spreads rapidly in CNS
Inflammatory response leads to Increased ICP, as pia
mater become edematous
Exudate covers the brain and fills the sulci
(grooves)
Exudate is present in CSF (spinal tap), blood
vessels of brain dilate and rupture
Etiology:
o Can be Viral or Bacterial Bacterial: MOST Deadly
Children: predominantly less than 1 year old Spinal Tap: CSF
Neisseria meningitis (meningococcus)
Turbid/cloudy (WBC)
Streptococcus pneumonia
Low Glucose
Signs & Symptoms:
o HA or Irritability
o Back Pain
o Photophobia
o Nuchal Rigidity (move chin to chest it hurts/ or when laying on back and lift chin up,
the knees will pop up)
Kernig’s / Brudzinski’s signs
, (Lie them down on back, bring chin to chest, knees will come up to relieve pressure
on spine – Nuchal rigidity)
Bending knees decreases ICP
o Fever / Chills
o Leukocytosis
o Signs of Increased ICP
(Vomiting, Irritability, Lethargy, Seizures)
Bacterial: Most Deadly
Spinal Tap: CSF
Turbid / Cloudy (WBC)
Low Glucose (bt. Eat glucose
***Most antibiotics will not pass through the blood brain barrier, so hard to treat bacterial infection.
Autonomic dysreflexia: Causes, process
Autonomic Dysreflexia
Sudden massive reflex sympathetic discharge
o Associated with spinal injuries at T-6 and above
Pathophysiology:
o Stimulus initiates positive feedback stimulation of
ANS
Hypertension, Bradycardia, and risk for
death
How?
o Most often stimulus: distended bladder or colon
Stimulus below injury ascends to send
message to brain; however, it is blocked
by spinal lesion at site of injury
Injury “Fireworks” stimulate
SNS below lesion
SNS => Vasoconstriction => Hypertension=>
Diaphoresis
HTN stimulates baroreceptors to activate
PNS:
1. PNS signals to SNS to shut off, But
Cannot reach site due to lesion below
2. PNS (Vagus) signals SA node to slow HR
Causes bradycardia
o Since ascending SNS stimulus not blocked, and original stimulus not relieved, SNS
stimulation increases
More Vasoconstriction induces more severe HTN
, Complications:
o SNS stimulation HTN PNS Vagus nerve stimulation
SA Node bradycardia Malignant Hypertension
CVA, MI, Aneurysm, Resp. Failure
Treatment:
o Stimulus must be relieved
Periodic Caths (q8h), bladder Scans, Bowel Hygiene
Degenerative disorders such as Multiple Sclerosis, Parkinson’s Disease, ALS, Myesthenia
Gravis, Huntingtons Disease
Multiple Sclerosis - MS
Definition:
o a progressive demyelination and sclerosis of the neurons in the CNS
o Neurons of brain, spinal cord and cranial nerves are affected
o Characterized by remissions and exacerbations with progressive debilitation
2 steps forward, 1 step back moving toward debilitation.
o Several Types: Different types have different progression and severity characteristics
Pathophysiology:
o Loss of myelin interferes with impulse conduction in CNS (Brain and Spinal Cord)
All types of fibers may be effected (Motor, Sensory, Autonomic)
What do we see?
Initially:
o lesions occur as inflammatory response with loss of myelin in white matter of CNS
Later:
o larger areas of inflammation and demyelination cause plaques (sclerosis)
Plaques are frequently visible in the ventricles, brainstem, and optic nerve
o As inflammation subsides, some neurologic function may return (“remission”)
Neural degeneration becomes irreversible with permanent loss of
neurologic function
Etiology:
o Age = 20-40 years
o More common in Women
o More frequent in European descent
o Idiopathic: Believed to be autoimmune (Type II and Type III hypersensitivity Reactions)
Genetics, immunologic, environmental, or viral infections as possible triggers
Signs & Symptoms:
o Tingling / numbness / burning sensation Neuropathies / Muscle Spasticity
Diplopia / loss of visual acuity / blindness Weakness / Paralysis
Diagnostic Tests:
o Patient history and physical exam key
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