REACTIVE AIRWAY DISTRESS SYNDROME
Acute lung injury – onset w/in 1 week of injury or increasing severity of respiratory issues, & bilateral opacities
o Pt. exposed to cleaning chemical in elevator at her residence. CT showed subsegmental atelectasis w/
opacities
Individuals do not necessarily have pre-existing respiratory issue.
o Pt. has no previous diagnosis for respiratory issues
Causes respiratory issues & hyperactive airways w/ inflammation i.e. – wheezing, dyspnea, asthma like cough which
impairs gas exchange
o Pt. has expiratory wheezes, asthma like cough – non-productive wheeze like cough
Length of S/S are unknown some can be as long as 1 year
o Pt. admitted Feb. 24/17 & tx w/ Hydrocortisone, Prednisone, Combivent, and oxygen.
OSTEOARTHRITIS
Cartilage destruction begins b/w 20-30 y/o.
Women affected more than men – r/t estrogen levels
o Pt. is female
Cause is unknown
Secondary cause r/t cartilage damage & joint instability
Genetic predisposition
Modifiable risk factors – obesity, moderate exercise
o Pt. obese and limited activity levels, uses walker
Cartilage becomes softer, less elastic & becomes thinner causing joint surfaces to touch resulting in pain
o Pt. prescribed Morphine & Acetaminophen for pain
GERD
Reflux of stomach acid into esophagus – no single cause.
o Pt. is being treated for GERD w/ Omeprazole (Losec)
Predisposing factors – hiatus hernia, incompetent lower esophageal sphincter, decreased esophageal clearance,
decreased gastric emptying.
Causes irritation & inflammation can be exacerbated by caffeine, drugs, fatty foods, anticholinergics which manifests
as a burning sensation below sternum spreading up into throat
o Pt prescribed Combivent – Ipratropium, Pt. has elevated cholesterol may have had fatty diet.
No labs or S/S in research to support diagnosis
Risk associated w/ GERD include respiratory issues – wheezing, coughing, dyspnea, bloating, pneumonia d/t
aspiration of gastric contents into respiratory system, & dental erosion.
o Pt. has wheezes on expiration, non-productive cough, opacities in lower lobes of lungs
HYPERLIPIDEMIA
Caused by diets high in fat, genetics, malnutrition, medication, or illnesses.
High levels of low-density lipoprotein (LDL) “bad” fats lead to hypertension and atherosclerosis which causes CAD.
LDLs cause fatty deposits in the intima (inner lining) of the arterial wall leading to chronic injury and inflammation.
3 developmental stages:
1. Fatty streak
• Early atherosclerotic lesions – smooth muscle filled w/ lipids causes yellow-tinge
• Begins by 15 y/o
• Cholesterol tx may reverse
2. Fibrous plaque
• Endothelium in arterial wall begins changes and can be seen by 30 y/o and continues w/ aging
• Endothelium unable to repair itself d/t LDLs, and production of muscle and thickening of arterial wall as a
result of growth factors from platelets.
• Lipoproteins carry cholesterol into the intima & collagen covers the fatty streak forming a fibrous plaque
which narrows the artery and decreases blood flow to tissue.
3. Complicated lesion
• Most dangerous and final stage of development of atherosclerotic lesions
• Chronic inflammation may cause instability, ulceration or rupturing of a plaque which causes platelets to form
a clot further occluding or narrowing the artery.
Page 1 of 3
Acute lung injury – onset w/in 1 week of injury or increasing severity of respiratory issues, & bilateral opacities
o Pt. exposed to cleaning chemical in elevator at her residence. CT showed subsegmental atelectasis w/
opacities
Individuals do not necessarily have pre-existing respiratory issue.
o Pt. has no previous diagnosis for respiratory issues
Causes respiratory issues & hyperactive airways w/ inflammation i.e. – wheezing, dyspnea, asthma like cough which
impairs gas exchange
o Pt. has expiratory wheezes, asthma like cough – non-productive wheeze like cough
Length of S/S are unknown some can be as long as 1 year
o Pt. admitted Feb. 24/17 & tx w/ Hydrocortisone, Prednisone, Combivent, and oxygen.
OSTEOARTHRITIS
Cartilage destruction begins b/w 20-30 y/o.
Women affected more than men – r/t estrogen levels
o Pt. is female
Cause is unknown
Secondary cause r/t cartilage damage & joint instability
Genetic predisposition
Modifiable risk factors – obesity, moderate exercise
o Pt. obese and limited activity levels, uses walker
Cartilage becomes softer, less elastic & becomes thinner causing joint surfaces to touch resulting in pain
o Pt. prescribed Morphine & Acetaminophen for pain
GERD
Reflux of stomach acid into esophagus – no single cause.
o Pt. is being treated for GERD w/ Omeprazole (Losec)
Predisposing factors – hiatus hernia, incompetent lower esophageal sphincter, decreased esophageal clearance,
decreased gastric emptying.
Causes irritation & inflammation can be exacerbated by caffeine, drugs, fatty foods, anticholinergics which manifests
as a burning sensation below sternum spreading up into throat
o Pt prescribed Combivent – Ipratropium, Pt. has elevated cholesterol may have had fatty diet.
No labs or S/S in research to support diagnosis
Risk associated w/ GERD include respiratory issues – wheezing, coughing, dyspnea, bloating, pneumonia d/t
aspiration of gastric contents into respiratory system, & dental erosion.
o Pt. has wheezes on expiration, non-productive cough, opacities in lower lobes of lungs
HYPERLIPIDEMIA
Caused by diets high in fat, genetics, malnutrition, medication, or illnesses.
High levels of low-density lipoprotein (LDL) “bad” fats lead to hypertension and atherosclerosis which causes CAD.
LDLs cause fatty deposits in the intima (inner lining) of the arterial wall leading to chronic injury and inflammation.
3 developmental stages:
1. Fatty streak
• Early atherosclerotic lesions – smooth muscle filled w/ lipids causes yellow-tinge
• Begins by 15 y/o
• Cholesterol tx may reverse
2. Fibrous plaque
• Endothelium in arterial wall begins changes and can be seen by 30 y/o and continues w/ aging
• Endothelium unable to repair itself d/t LDLs, and production of muscle and thickening of arterial wall as a
result of growth factors from platelets.
• Lipoproteins carry cholesterol into the intima & collagen covers the fatty streak forming a fibrous plaque
which narrows the artery and decreases blood flow to tissue.
3. Complicated lesion
• Most dangerous and final stage of development of atherosclerotic lesions
• Chronic inflammation may cause instability, ulceration or rupturing of a plaque which causes platelets to form
a clot further occluding or narrowing the artery.
Page 1 of 3
