Summary NSG 211 Final Study Guide

Pathophysiology: NSG 211 Exam 5 Review

Consider: 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