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NSG 211 Exam 4 Review
Pathophysiology (NSG 211)
Marian University
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NSG 211 Exam 4 Review
1. Consider: Etiology, Process, Signs, and Symptoms, Complications 2. Respiratory control in the nervous system: Central (primary) receptors vs. Peripheral (secondary) receptors Control center: an elaborate network of neurons in the medulla, Carotid and Aortic Bodies: Dorsal & Ventral Respiratory Groups (DRG, VRG), pneumotaxic center, & apneustic center Brainstem: controls rhythm, rate, and depth Chemoreceptors: carbon dioxide (CO2), hydrogen Ion (H+), Oxygen HYPERCAPNIA – TOO MUCH CO2 – TRIGGERS THE BRAIN TO RESPOND TO RESPIRATORY ACIDOSIS Central (primary) receptor - chemoreceptors in the brainstem ● Elevated CO2, Elevated H+ in the Cerebrospinal Fluid (CSF) ● Hypercapnia is the major stimulus for the healthy CNS respiratory center (elev. H+) Peripheral (secondary) receptor - chemoreceptors in carotid arteries and aortic body ● Decreased oxygen concentration in blood is major stimulus ● Oxygen levels must become quite low (60 torr) for secondary receptor activation LUNG DISEASE: in the presence of chronic hypercapnia primary receptors “burn out” (“reset”). Hypoxia from peripheral receptors become primary stimulus and control Over Administration of O2 can shut off respiratory drive - don’t give full O 3. Pneumonia Etiology: ● Acute infection of lungs ● Infection of the lower respiratory tract caused by bacteria, viruses, fungi, protozoa or parasites (p) ● Classified by agent (viral, bacterial) and location (RLQ, LLQ, etc) ● Classified by CAP or HAP (community-acquired, hospital acquired) ● HAP usually more resistant to antibiotics Pneumococcal Pneumonia (“lobar” pneumonia) ● Caused by streptococcus pneumoniae (“pneumococcus”) ● Infection localized in 1 or more lobe (lobar) Process : Inflamm/congestion of alveolar wall→exudate interfere w/O2 diffusion→RBCs/WBCs accumulate in alveolar exudate (forming a solid mass “consolidation”) ● Mass shows on X Ray “lobar” ● RBCs in exudate create rusty sputum often associated w/pneumococcal pneumonia Signs/Symptoms : ● Sudden onset, systemic signs of high fever, chills, marked fatigue, leukocytosis
● Dyspnea, tachypnea, tachycardia, pleuritic chest pain, rales initially (clears w/consolidation) ● Productive cough, w/typical rusty colored sputum (RBC in exudate) ● Confusion and disorientation if infection is severe and several lobes involved (hypoxemia) Complications : aspiration, death 4. Aspiration risks (what type of patient is at risk?), complications Def: passage of food, fluid, drugs, or other foreign material into trachea & lungs Risks Factors: ● Decreased level of consciousness (LOC) - vomit ○ Sedation, drug abuse, anesthesia ● Nasogastric Tube Feedings (elevate HOB & check those residuals) Complications: inflammation, bronchospasm, lost ciliary function ● Aspiration pneumonia: material becomes medium for bacteria growth ● ARDS - massive inflammation response leads to : ○ Loss of lung compliance (“stiff lungs”, higher ventilation pressure) ○ Pulmonary edema & hypoxemia (oxygen can’t swim) ○ Tissue hypoxia and acidosis 5. Respiratory failure: Definition, signs, symptoms, complications Definition: inadequate gas exchange, which is characterized by PaO2 ≤60 mmHg (hypoxemic respiratory failure) and/or PaCO2 ≥50 mmHg, pH ≤7 (hypercapnic respiratory failure) (p) Signs/Symptoms and Complications: ● CNS depression Hypoxemia→tissue hypoxia→anaerobic metabolism→lactic acidosis Hypercapnia →respiratory acidosis Eventually respiratory arrest will occur 6. ARDS: PaO2, PCO2: Normal arterial levels, how levels are affected in disease processes ARDS : Adult Respiratory Distress Syndrome (mortality rate 40%) PaO2: Normal - 85- Severe hypoxemia - 50- ● If the respiratory failure is primarily hypoxemic it is the result of inadequate exchange of oxygen between the alveoli and the capillaries and the individual must receive supplemental oxygen therapy (p) PCO2: Normal - 35- Severe hypercapnia - ≥
○ Long term med treatment (up to 12 months) * INH (isoniazid) * Rifampin and/or Ethambutol *Compliance critical for eradication of organism, failure to comply could = “superbug” *MDR-TB=multi drug resistant TB *XDR TB=extremely drug resistant TB 8. Cystic Fibrosis: Respiratory and gi manifestations Respiratory Manifestations : airway obstruction from thick mucus causes: ● Air obstructed from leaving during exhalation ● Air trapping ● Atelectasis ● Bronchiole damage ● Obstructive disease of hyperinflation ● Stagnant mucus is a medium for infection (frequent pneumonia) ● Eventually respiratory failure or Cor Pulmonale (elevated pulm. Artery pressures) Cor Pulmonale – RV disorder caused by primary disorder of RESPIRATORY SYSTEM GI manifestations: ● First sign often meconium ileus in NB (thick secretions causes no first stool) Pancreas ● Deficit of pancreatic enzymes due to blocked exocrine glands ● malnutrition/malabsorption of proteins Liver/Gallbladder ● Bile ducts are blocked w/thick secretions, interfering w/fat absorption ● Malnutrition, dehydration, and fat-soluble vitamin def. (K.A.D) ● Back up of pressure behind the obstruction leads to inflamed tissue/damage Salivary Glands ● High chloride and mucus plugs may cause obstruction/infection (sialadenitis) Sweat Glands ● Secretion of high NaCl levels which leads to dehydration w/exercise (rationale behind NaCl sweat analysis skin test) Reproductive ● Thick mucus block vas deferens and cervix, often leading to infertility
9. Asthma: causes of 2 types. Effects on the lungs (think inflammation). Complications: short-term and long-term Causes of 2 types: ●
Effects on the lungs: ● Inflammation of mucosa ● Bronchial hyper-responsivenss Short-term Complications: Hypoxia, Hypoxemia, status asthmaticus (no response to bronchodilator, poss. fatal), RV afterload - cor pulmonale Long-term Complications: COPD Signs/Symptoms : Cough, wheezing, tachypnea (fast breathing) Treatment : Corticosteroids, Beta2 Adrenergic Agonists (relax smooth muscle), Anticholinergics (relax and lower secretions)
10: Emphysema and Chronic Bronchitis; Characteristics, patient profile, complications of each Emphysema Characteristics S/Sx: Blebs, Dyspnea, Barrel Chest, Prolonged expirations, Pursed lips, Hypoxia, Increased erythropoietin, Clubbed fingers, Flushed face Usually using accessory muscles because diaphragm is flat Patient Profile: Smoker - Decrease in genetic ability to repair damage (alpha- antitrypsin). Complications: pneumothorax/collapsed lung, chronic hypercapnia, burn out central receptors Bronchitis Characteristics S/Sx: Constant productive cough, hypoxia and cyanosis, dyspnea, pulmonary HTN, peripheral edema Patient Profile: Smoker or living around air pollution Complications: pneumonia, pneumothorax, RF, cor pulmonale 11: Vital Capacity and total lung capacity -- What changes are seen in chronic lung disease? Vital Capacity: Max amount that can move in/out with breaths Total Lung Capacity = vital capacity + residual volume Changes seen: Decrease in lung expansion = decrease vital capacity & increase residual volume Dead Space: no gas exchange (bronchi, bronchioles, collapsed alveoli, obstructions) 12 interpretations: What is affected by Metabolic (GI) and Respiratory Disorders?
13 Embolus: etiology, manifestations, complications Def: a blood clot or other occlusion that obstructs the pulmonary artery or branch of it
● LV heart failure (backup pressure/increased hydrostatic pressure causes edema) Pathophysiological changes - ● Fluid shifts from capillaries into alveoli (inflammation, high hydrostatic pressure, low protein) ● Hypoxia results from interference in O2 diffusion (Oxygen can’t swim) ● Eventual atelectasis from decreased surfactant and alveolar collapse (LaPlace Law) ● Capillary engorgement and rupture can produce pink frothy sputum Signs/Sx- ● Cough ● Orthopnea (SOB/DYSPNEA lying down) ● Rales ● Hemoptysis (if really bad): often pink frothy sputum (bubbly) ● Labored breathing ● Feeling of drowning (paroxysmal Nocturnal Dyspnea) - “air hunger at night” ● Cyanosis (V/Q mismatch - deoxygenated blood passing through pulmonary artery and surviving into the pulmonary vein circuit - “blue blood” passes through to periphery) Why does hypoxia develop? hypoxia results from interference in oxygen diffusion 16 Chest: causes, definition, signs, and symptoms. Major Risks associated with Flail Chest. Causes : chest trauma Definition : 3-6 ribs fractured in 2 places “free floating ribs” Signs/Symptoms : dyspnea, tachycardia, Paradoxical movement of “free” ribs Major risks : HIGH risk for pneumothorax (air in the pleural cavity) 17: Effects on acid-base balance. (Consider early vomiting Vs. prolonged vomiting) Early vomiting - initially, vomiting causes Metabolic ALKALOSIS due to loss of H+ in HCl gastric contents. Prolonged vomiting - causes dehydration→ Anaerobic metabolism (dehydration)--> ACIDOSIS. 18: effects on acid-base balance. (Consider the loss of HCO3, plus anaerobic metabolism from fluid dehydration). Acid-Base balance effects: Loss of Bicarb (HCO3) and anaerobic metabolism (dehydration)→ LEADS to METABOLIC ACIDOSIS. The GI stores much of Bicarb, leading to further metabolic acidosis. Hypovolemia : tissue ischemia leads to anaerobic metabolism/lactic acidosis 19 disease: etiology, causes, and manifestations of liver disease a. Hepatitis: Inflammation of the liver Etiology:
Idiopathic (fatty liver)
Viral/Infections: both local and systemic (group of virus that specifically target hepatocyte)
Toxicity: drug (acetaminophen) or chemicals (inhalants, ETOH) Patho : May be asymptomatic carrier (HBV, HCV, HDV. Manifestations: liver cell damage by a) direct action of virus (hep C), 2) cell-mediated immune response to the virus (Hep B). Cell injury leads to inflammation/ necrosis in the liver. Signs/Sx: (Stages) Stage 1: (Pre-Iteric) - fatigue, malaise, anorexia, sometimes RUQ pain Stage 2: (Icteric)- jaundice, clay stools, dark urine, pruritic skin, hepatomegaly In severe cases, blood clotting is prolonged (prothrombin/fibrinogen) Stage 3: (Post-Icteric/”Recovery”) - marked reduction in symptoms versus liver failure (Icteric) **b. Cirrhosis: Progressive destruction of liver
- 50 % of deaths are alcohol related. Patho/Etiology:** Extensive diffuse fibrosis and loss of lobular organization→ Regenerated tissue can be non-functional due to vascular disorganization. Effects of cirrhosis/Liver failure evolve from two factors:
- Loss of liver function
- Interference with blood and bile flow in liver. Signs/Sx:
- decreased removal and circulation of bilirubin -decreased bile production
- decreased blood clotting factors
- impaired glucose/glycogen
- inadequate storage of iron and vitamin B
- increased Aldosterone, ADH, and Estrogen
- decreased removal of toxic substances such as ammonia and drugs. Patho/ Etiology: of Alcohol Liver Disease (several steps)
- Fatty Liver which is an accumulation of fat cells in liver→ Hepatomegaly. Asymptomatic
- Alcohol Hepatitis which is an inflammation and cell necrosis; Fibrous tissue forms in liver.
- End Stage Cirrhosis. Hepatitis Symptoms become exacerbated. Hepatocytes are replaced with fibrotic tissue **Signs/Sx:
- Portal Hypertension and Low albumin: ascites, generalized edema, and esophageal varices, hemorrhoids.
- Decreased clotting factors and immunity:** anemia, increased bleeding, splenomegaly - leukopenia/Thrombocytopenia - Hepatic encephalopathy: High ammonia (CNS toxins); tremors, confusion, coma, & death.
● Beefy red tongue of Vit B12 deficiency Management/Dietary Restrictions: absolutely cannot have any gluten (will cause severe reaction) 22 obstruction: Dangers of obstruction. Physiological changes during obstruction. Complications. Dangers: ● Fluid/gas build up in GI tract ● Distention/colic ● Vomiting/dehydration/electrolyte imbalances ○ Initially metabolic ALKALOSIS, becomes metabolic ACIDOSIS ● Wall pressure as more fluid shifts in ● Third spacing (too much fluid moves from the intravascular space into the interstitial space) becomes hypovolemic shock ● Mucosal wall edema and ischemia leads to more fluid/edema and less peristalsis ● Increased permeability of intestinal wall allows bacteria to cross intestinal wall into blood, which leads to peritonitis and/or bacterial septicemia ● More hypovolemic shock, more metabolic acidosis Physiological changes during obstruction: Non-obstructive “ILEUS” ● Neurologic impairment ● Lack of propulsion in intestine ○ Abdominal surgery ○ Spinal cord injury ○ Severe ischemia ○ Acute gastritis ○ Pancreatitis ○ Hypokalemia/Hypocalcemia ○ Mesenteric thrombosis ○ Toxemia/sepsis ○ Decreased/absent bowel sounds ○ Steady pain ○ Vomiting ○ Abdominal distention ○ No stool or gas passed Complications: ● Restlessness ● Tachycardia ● Hypovolemia ● Electrolyte imbalances ● Weakness ● Confusion ● Shock
23 diseases/types. definitions associated with gallbladder diseases Definition: Types of gallbladder diseases: ● Choledocholithiasis/GALLSTONES ○ Formation of gallstones, which are masses of solid material/calculi formed in bile ○ Form in bile ducts, gallbladder cyst duct ○ Consist of cholesterol, bile pigment (Bilirubin), calcium salts ● Cholecystitis ○ Often precipitated by a fatty meal ○ Sudden waves of pain (“biliary colic”) in RUQ/epigastrium that often radiates to the back and right shoulder ○ Nausea, vomiting, dehydration ○ Jaundice indicates common bile duct blockage (posthepatic jaundice) ○ Leukocytosis, fever
24 associated with gastrointestinal disorders Definition: Anorexia: Loss of appetite. Often precedes nausea/vomiting. Non-specific (common in many disorders) Nausea: Unpleasant, subjective feeling stimulated by distention, irritation, inflammation of the GI tract Retching: Usually precedes vomiting (muscular action of vomiting, but nothing expelled) Vomiting (emesis): Forceful expulsion of chyme from the stomach ● Activated by the vomiting center of the medulla oblongata ● Increased intracranial pressure (ICP) “projectile vomiting” ● Stimulation of chemoreceptor trigger zone in the medulla by drugs or toxins Character of vomitus can be diagnostic ● Blood (hematemesis): “Coffee grounds” - upper GI. “Coffee grounds” suggest it is somewhat digested ● Yellow/Green: Bile Diarrhea: Presence of loose, watery stools. Can be acute (less than 14 days) or chronic (more than 14 days) ● Large volume diarrhea: water/infection or rapid transit from excessive water or mucous secretions ● Small volume diarrhea: excessive GI motility without increased stool ● Steathorhea: foul-smelling, greasy, fat stools that float indicate malabsorption disorders Hematochezia (Blood in stool): Occult (hidden by naked eye), Frank (visible), Melena (red, tarry stool) Risks of diarrhea dehydration: ● Hypovolemia: tissue ischemia leads to anaerobic metabolism and lactic acidosis
Signs/Sx: ● Duodenal: ○ Epigastric pain, burning (especially 2-3 hours after eating or at night) ○ Pain often relieved by ingestion of foods or antacids ● Gastric ○ Epigastric pain, burning occurs IMMEDIATELY after eating ○ Heartburn, nausea, vomiting, weight loss ● Iron deficient anemia or occult blood in stool ○ If severe, black tarry stool likely (melena) Complications: Stress ulcers - CAN DEVELOP SUDDENLY Etiology: ● Severe trauma (massive burns ● Serious systemic problems (hemorrhage or sepsis) Pathophysiology : ● Multiple ulcers, usually gastric, form within HOURS of the precipitating event ● As blood flow is reduced to gastric mucosa from stress, there is reduced secretion of mucosa and epithelial regeneration, which act as a protective barrier to the effects of the acidic chyme ● The acid barrier is lost, so acid erodes the sensitive mucosa Complications: ● Hemorrhage with blood vessel ulceration ● Bacterial peritonitis with gastric muscle perforation into peritoneum ● Obstruction if ulceration/fibrous tissue narrows passageway, such as duodenum
27: etiology/ risk factors for both acute and chronic gastritis Etiology: Risk factors (acute): Risk factors (chronic): 28 syndrome: etiology, complications Etiology: Gastric resection ● Surgical loss of pyloric sphincter ○ Usually controls slow chyme release into duodenum Complications: ● Severe diarrhea (body doesn’t have ability to absorb nutrients - fluid/electrolyte loss too) ● Hypovolemia (tachycardia, dizzy) ● Hypoglycemic (2-3 hours after) ● Vitamin deficiency (loss of intrinsic factors)
● Anemia (folic and iron deficiency) 29: liver changes associated with Hepatitis B, C, Liver Failure Liver changes (hep B): (cell-mediated immune response to the virus which leads to inflammation and destruction of hepatocyte). Chronic inflammation with hep B/C leads to inflammation and necrosis that lasts greater than 6 months. Permanent liver damage could then lead to cirrhosis, and then could lead to liver cancer. Liver Changes (hep C): (the virus itself attacks the hepatocyte) Chronic inflammation with hep B/C leads to inflammation and necrosis that lasts greater than 6 months. Permanent liver damage could then lead to cirrhosis, and then could lead to liver cancer. Liver changes (liver failure) : Cirrhosis =progressive destruction of liver tissue *not sure if i should put the signs/symptoms for alcohol liver disease too?? ● Loss of liver function ● Interference w/blood and bile flow in the liver ○ Decreased removal & circulation of bilirubin (intrahepatic jaundice) ○ Decreased bile production; impaired absorption of nutrients (K.A.D.) ○ Decreased blood clotting factors (fibrinogen/prothrombin) and plasma protein (albumin) ○ Impaired glucose/glycogen metabolism (hypoglycemic risk) ○ Inadequate storage of iron and vitamin B6 (folate) - anemia ○ Increased aldosterone, antidiuretic hormone & estrogen activity ○ Decreased removal of toxic substances such as ammonia & drugs
30 Bowel Diseases: Etiologies, Manifestations in Stool. Locations of disorders. Complications a. Crohn’s disease vs. Ulcerative Colitis Crohn's disease Etiology: ● “Skip lesions” - inflammation begins in intestinal submucosa and spreads in discontinuous pattern Manifestations in Stool: ● Soft, semi-formed stools Location: ascending & transverse colon, ileum Complications: ● Hypoproteinemia ● Avitaminosis ● Malnutrition ● Steatorrhea - fatty stools ● Adhesions (thick walls) ● Fistulas - inappropriate connection between two areas ● Adhesions can lead to bowel obstructions and peritonitis Ulcerative Colitis
NSG 211 Exam 4 Review
Course: Pathophysiology (NSG 211)
University: Marian University
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