NURS 2063 (Pathophysiology) FINAL EXAM
STUDY GUIDE LATEST UPDATED AND 100%
VERIFIED RATED A.
Parkinson's disease etiology
✔✔idiopathic, acquired or drugs
Parkinson's disease pathophysiology
✔✔Dopamine deficiency in the basal ganglia (substantia nigra) associated with
motor impairment;
LEWY BODIES in nerves
Parkinson's disease manifestations
✔✔difficulty initiating and controlling movements results in akinesia, tremor, and
rigidity
stooped posture
forward tilt of trunk
reduced arm swinging
flexed elbows and writs
constipation
drooling
anosmia
masklike face
Parkinson's treatment
✔✔no cure, control symptoms
,levodopa, dopamine agonists, monoamine oxidase B inhivitors MAO-B, catechol
O-methyltransferase COMT inhibitors, and anticholinergic agents
can increase levels of dopanine, but effects diminish overtime.
deep brain stimulation
Stroke/CVA diagnosis
✔✔history, physical examination including neurologic assessment
head CT, head MRI, carotid ultrasound, cerebral arteriogram, serum clotting
studdies, blood chemistry, and CBC
determine whether it is ischemic or hemorrhagic in orgin prior to treatment is
crucial becasue the interventions vary on type.
assessment of brain function
✔✔SLUMS test
mental status test
Tuberculosis Etiology
✔✔Mycobacterium tuberculosis, a slow-growing aerobic bacillus.
person-to-person trasmission occurs through inhalation of tiny infected aerosol
droplets.
Only people with active TB can spread the disease to others.
opportunistic infection
TB pathogenesis
✔✔primary TB infection-when bacillus first enters body, macrophages engulf
microbe causing local inflammatory response. some bacilli travel to lymph nodes
and activate type IV sensitivity.
,lypmhatic and hematogenous spread, t cells and macrophages surround
organisms in granulomas (infection is contained here)
T cells become sensitive about 2-12 weeks, evidenced by positive TB test
can lay dormant
Secondary (active) may occur years later, impaired immunes system causes
reactivation. HIV, corticosteroid use, silicosis, and diabetes mellitus found to be
associated with reactivation
TB treatment
✔✔6-9 months of antimicrobial therapy: 2 months inital intensive-phase
treatment and 4-7 monts of continuation-phase treatment.
asthma etiology
✔✔allergies/allergens, smoke, cold exposure, pollution, epinephrine, cortisol
and histamine, exercise induced, occupational asthma, drug induced (frequently
aspirin)
chronic disorder that results in intermittent, reversible airway obstruction.
stages of asthma attack
✔✔stage one:
bronchospasms, signaled by coughing
peaks within 15-30 minutes
inflammatory mediators responsible include leukotrienes, histamine, and some
interleukins
Stage 2:
peaks within 6 hours of onset
airway edema and mucus production
, alveolar hyperinflation causes air trapping
bronchospasm, smooth muscle contraction, inflammation, mucus production
combine to narrow airways
manifestations of asthma
✔✔wheezing, SOB, dyspnea, chest tightness, cough, tachypnea, anxiety
status asthmaticus-life threatening prolonged asthma attack not responding to
usual treatment
can lead to repiratory alkalosis and respiratory failure quickly
asthma treatments
✔✔inhaled and systemic corticosteroids, bronchodilaters, beta agonists, nebs,
leukotriene mediators, mast cell stabilizers, anticholinergics
Asthma treatment plan
RAAS system
✔✔renin-angiotensin-aldosterone system
BP falls, causes pathway
kidneys release Renin --> activating angiotensin I, which is then converted to
angiotensis II (a vasoconstrictor) and stimulating aldosterone secretion.
aldosterone (salt retention, increased blood volume, blood pressure rises)
afterload
✔✔pressure the LV must overcome to move blood into circulation
STUDY GUIDE LATEST UPDATED AND 100%
VERIFIED RATED A.
Parkinson's disease etiology
✔✔idiopathic, acquired or drugs
Parkinson's disease pathophysiology
✔✔Dopamine deficiency in the basal ganglia (substantia nigra) associated with
motor impairment;
LEWY BODIES in nerves
Parkinson's disease manifestations
✔✔difficulty initiating and controlling movements results in akinesia, tremor, and
rigidity
stooped posture
forward tilt of trunk
reduced arm swinging
flexed elbows and writs
constipation
drooling
anosmia
masklike face
Parkinson's treatment
✔✔no cure, control symptoms
,levodopa, dopamine agonists, monoamine oxidase B inhivitors MAO-B, catechol
O-methyltransferase COMT inhibitors, and anticholinergic agents
can increase levels of dopanine, but effects diminish overtime.
deep brain stimulation
Stroke/CVA diagnosis
✔✔history, physical examination including neurologic assessment
head CT, head MRI, carotid ultrasound, cerebral arteriogram, serum clotting
studdies, blood chemistry, and CBC
determine whether it is ischemic or hemorrhagic in orgin prior to treatment is
crucial becasue the interventions vary on type.
assessment of brain function
✔✔SLUMS test
mental status test
Tuberculosis Etiology
✔✔Mycobacterium tuberculosis, a slow-growing aerobic bacillus.
person-to-person trasmission occurs through inhalation of tiny infected aerosol
droplets.
Only people with active TB can spread the disease to others.
opportunistic infection
TB pathogenesis
✔✔primary TB infection-when bacillus first enters body, macrophages engulf
microbe causing local inflammatory response. some bacilli travel to lymph nodes
and activate type IV sensitivity.
,lypmhatic and hematogenous spread, t cells and macrophages surround
organisms in granulomas (infection is contained here)
T cells become sensitive about 2-12 weeks, evidenced by positive TB test
can lay dormant
Secondary (active) may occur years later, impaired immunes system causes
reactivation. HIV, corticosteroid use, silicosis, and diabetes mellitus found to be
associated with reactivation
TB treatment
✔✔6-9 months of antimicrobial therapy: 2 months inital intensive-phase
treatment and 4-7 monts of continuation-phase treatment.
asthma etiology
✔✔allergies/allergens, smoke, cold exposure, pollution, epinephrine, cortisol
and histamine, exercise induced, occupational asthma, drug induced (frequently
aspirin)
chronic disorder that results in intermittent, reversible airway obstruction.
stages of asthma attack
✔✔stage one:
bronchospasms, signaled by coughing
peaks within 15-30 minutes
inflammatory mediators responsible include leukotrienes, histamine, and some
interleukins
Stage 2:
peaks within 6 hours of onset
airway edema and mucus production
, alveolar hyperinflation causes air trapping
bronchospasm, smooth muscle contraction, inflammation, mucus production
combine to narrow airways
manifestations of asthma
✔✔wheezing, SOB, dyspnea, chest tightness, cough, tachypnea, anxiety
status asthmaticus-life threatening prolonged asthma attack not responding to
usual treatment
can lead to repiratory alkalosis and respiratory failure quickly
asthma treatments
✔✔inhaled and systemic corticosteroids, bronchodilaters, beta agonists, nebs,
leukotriene mediators, mast cell stabilizers, anticholinergics
Asthma treatment plan
RAAS system
✔✔renin-angiotensin-aldosterone system
BP falls, causes pathway
kidneys release Renin --> activating angiotensin I, which is then converted to
angiotensis II (a vasoconstrictor) and stimulating aldosterone secretion.
aldosterone (salt retention, increased blood volume, blood pressure rises)
afterload
✔✔pressure the LV must overcome to move blood into circulation
