MODULE 4: Pulmonary System, Study notes of Pathophysiology

Download MODULE 4: Pulmonary System and more Study notes Pathophysiology in PDF only on Docsity! lOMoARcPSD|24365327 Pathophysiology Exam 2: Modules 4-8 MODULE 4: Pulmonary System Compare and contrast the concepts of ventilation, oxygenation, and perfusion. Topic: Etiology Analyze Ventilation: The process of inspiration and expiration of air through the pulmonary airways to the alveoli Oxygenation: The process of supplying oxygen to the cells and tissues of the body. Perfusion: The movement of blood through the pulmonary circulation to the alveoli Etiology Analyzing: Ask yourself, is this a ventilation or Perfusion problem? Normal conditions: ● Alveoli have air moving in and out effortlessly (ventilation) ● blood suppplied to the alveoli (perfusion) ● Adequate oxygen and CO2 exchange between alveoli walls and capillary bed (oxygenation) Ventilation Problem: Air cannot get to alveoli ● Asthma, COPD, Obstruction- in bronchi or mucus in alveoli ● Something is impeding flow of air called a shunt Perfusion Problem: Blood is unable to get to alveoli ● Hemorrhage or Pulmonary Embolism ● Known as a deadspace Describe the various types of pneumonia, the risk factors, prevention and treatment options. Topic: Etiology Analyze Community-Acquired: ● MOST COMMON: Streptococcus pneumoniae (bacteria) ○ Others include: H.influenza, Mycoplasma, Klebsiella, Staphylococcus, Legionella ● Inoculated outsides of the hospital setting Hospital-Acquired: ● MOST COMMON: MRSA or VRE ● Innoculated within the hospital stay Ventilator Associated: ● MOST COMMON: Enterococcus ● Innoculated for being on a mechanical vent system Aspiration ● Anaerobic bacteria swallowed from the oropharynx ● MOST COMMON: Staphylococcus ● RISK FACTORS: Stroke, dysphagia, coma, chronic gingivitus or periodontal disease, alcohol intoxication Walking Pneumonia: lOMoARcPSD|24365327 ● Mild infection caused by Mycoplasma ● Innoculation through close living quarters Risk Factors: ● Current infection with influenza (or other respiratory viral infections) ○ Secondary bacterial pneumonia ● Immunosuppressed patients (like HIV) ● Smoking ● Lung cancers or tumors ● COPD ● Bronchiolectisis ● Asthma ● Atelectas is Prevention: ● Pneumococcal vaccine ● Smoking cessation ● Social distancing ● Preventing aspiration ● Hand hygiene Treatment: ● Antibiotic therapy and Oxygen therapy ● IV fluids ● Bronchodialators if needed ● Analgesia and Antipyretics Identify the basic pathophysiologic concepts of respiratory function. Topic: Atelectasis Analyze Definition: A small number of alveoli collapsed resulting in a decrease in gas exchange. (Ventilation or perfusion problem?) ● Can be parietal collaspe of a lung or full lung Etiology: Something is inhibitng the alveoli from FULLY expanding resulting in them collasping caused by: ○ Some compressive force (tumor) ■ Pleural effusion ○ Post-operative respiratory depression ■ Shallow breaths and low rate ○ Obstruction of bronchioles ○ Even high amounts of supplemental O2 S/S: ● Cough, chest pain, dyspnea, hypoxia, cyanotic, tachycardia Treatmet: ● Deep breath and cough- the force of the cough forces air into the alveoli to help them reinflate Understand the etiology of select inflammatory upper airway disorders Topic: See outline/Flashcards Acute Rhinitis: “inflammation of the Nose” ● Etiology: Rhinovirus (most common) “the cold” and Allergies ● S/S: Viral versus Allergies lOMoARcPSD|24365327 Explain the pathophysiology and consequences of chronic hypercapnia and chronic hypoxia. Topic: COPD Understand and Evaluate Normal Person: ● Hypercapnia is what drives the breathing reflexes ○ Hypercapnic drive ● Chemoreceptors located: Medulla, periphery, aortic arch and carotid bodies. ○ Medulla and CSF - CO2 sensitive ■ LOW pH or HIGH CO2 = Increase respiration rate ○ Others are O2 sensitive than 2x per week and 2x at night per month. Brief and go away. Tx: albuterol Mild Persistent: Symptoms 2+ a week with occasional night waking less than 2x a month. Attack interfers with activity briefly. > or = 80% Normal; 70%+ Moderate Persistent: Daily symptoms and use of rescue inhaler daily. Intefere with daily life. Tx: corticosterioid, albuterol, allergy medication 60%-80% of normal Reduced by 5% Severe Persistent Continous attack, little to no relief. Night disturbances, activity disturbances. Lower than 60% Reduced by %5 or more lOMoARcPSD|24365327 ■ LOW O2 = increase respiration rate ■ This occurs only when CO2 accumulation is not stimulating the hypercapnic drive ● Hypoxic Drive COPD ● COPD patients are at a constant state of hypercapnia and hypoxia. ○ Poor ventilation = decrease CO2 removal and decrease O2 exchange ● Chronic hypercapnia state decreases the chemoreceptors sensitivity and shuts down the hypercapnic drive ● The hypoxic drive takes over due to the loss of hypercapnic drive ○ BE CAREFUL WITH SUPPLEMENTAL O2 ■ You can shut off the hypoxic drive and the person can go into respiratory arrest ■ Careful with respiratory depressive drugs too ● Chronic hypoxic states stimulates other compensatory mechanisms such as: ○ Anaerobic metabolism = increase lactic acid ○ Vasoconstriction of the pulmonary arterioles = increase BP → Pulmonary hypertension ■ R-HF can occur = Cor pulmonale ○ Chronic stimulation of EPO → erythropoiesis ■ Trying to increase O2 carrying capacity ○ Finger or toe clubbing Provide rationales for common clinical manifestations for obstructive lung disorders. Topic: Emphysema Analyze Emphysema: characterized by: ● Pathophysiology: ○ Distended alveoli due to elastin damage ■ Proteolytic enzymes released from WBCs due to chronic inflammatory response due to some inhalation of some irritant, attack the alveoli elastin. ● OR AAT-1 = elastase uninhibited and destroys elastin ● OR EDS or Marfans = connective tissue recoil reduced ● IV drug use ■ Loss of recoil and elasticity ■ Increased air trapping = hypercapnia + more overdistention of alevoli Manifestations: ● Barrel-shaped chest ○ Lungs are hyperinflatted and push on the rib cage and this results in structural changes to compensate for “bigger” lungs by widening the rib cage. lOMoARcPSD|24365327 ● Pursed-lip breathing ○ This slows the rate of air entering the airway and increasing the pressure while breathing in to force more air into the deeper parts of the lungs. ● Often thin (cachexia) ○ Due to increased metabolic demand to just breath- results in other resources to use as fuel to facilitate the increase in demand. ■ Muscle and fat ● Severe dyspnea/ SOB ○ Chest changes and CO2 trapping to get that air out results in difficulty breathing ○ Can occur at rest ○ The amount of effort it takes to breath results in this manifestation as well ● Diminished breath sounds ○ The barrel chest makes it difficult to ausculate breath sounds ○ impaired airflow = low and quiet breath sounds ● Activity Intolerance ○ Hypercapnic and hypoxic state = no energy ● Tachypnea ○ Increased rate of breathing compensation for hypoxic state ● Accessory muscles used for breathing ○ The diaphragm and intercostal muscles are unable to by pass the hyperinflatted alveoli so recruitment of other muscles are needed to try to get that CO2 out. Understand pathophysiology, and disease specific clinical manifestations for select pulmonary vascular disorders Topic: Emphysema Analyze Pulmonary Vascular Disorder/Changes with Emphysema ● Chronic hypoxic state = physiological mechanism engage ○ Increase ventilation ○ Pulmonary arteriole vasoconstriction = Pulmonary HTN over time ■ Right-Sided Heart failure r/t increase workload ■ Cor Pulmonale ● Distended alveoli = damages pulmonary capillary beds = increase in hypoxic state Understand etiology, pathophysiology, and disease Asthma: chronic inflammatory disease involving constriction of the bronchioles. lOMoARcPSD|24365327 ● Pursed lip breathing ● Accessory muscle recruitment ● Fatigued ● Cachexia (thin) ● Dyspnea/SOB Pleural Effusion: abnormal collection of fluid in pleural cavity that compresses the lungs and inhibits lung inflation Etiology: Atelectasis, cirrhosis, CHF, hypoalbuminemia, myxedema, nephrotic syndrome, peritoneal dialysis, TB, pancreatitis Pathophysiology: increase in hydrostatic pressure that exceeds oncotic pressure → fluid is pushed from capillaries → into pleur space → pleural effusion → decreases volume for lung expansion S/S: ● Dyspnea ● Tachypnea ● Sharp pleuritc chest pain upon inhalation ● Dullness to percussion ● Diminished breath sounds ● Tactile fremitus Understand diagnosis for types of pneumothoraces. Topic: Traumatic Analyze Pneumothorax: c ollapsed lung due to air in the pleural cavity 1. Primary spontaneous a. No trauma or underlying pulmonary condition i. Often Marfan’s or smoker b. Young thin men most common 2. Secondary Spontaneous a. Caused by a lung disease or some sort b. Ruptured blebs (overally distended or damaged alveoli) 3. Traumatic a. Penetrating wound to the thoracic cage b. Rib fracture can cause it too c. Pleural space is open to the air and negative pressure is lost resulting in lung collasping 4. Tension a. Increasing interpleural pressure of escalating air build up b. Air has no where to go 5. Iatrogenic a. Medical or surgical complication i. Thorocentisis, lung biopsy, mechanical ventilation injury lOMoARcPSD|24365327 Diagnosis: ● Chest X-ray shows: linear shadow of visceral pleura ● Pulse ox and ABG analysis ○ Acidosis and hypercapnia ● Hypoxemia ● Tracheal shift Total Number of Pulmonary Questions: 12 MODULE 5: Gastrointestinal System Understand the etiology and pathophysiology of common disorders of the esophagus. Topics: Barrett’s Esophagus ; GERD Analyze GERD: The inability for the lower esophageal sphincter to close permitting backflow of acidic contents back into the esophgus. Etiology: Mechanical or Funtional ● Smoking, pregnancy, chocolate, coffee, high fat meals, anticholinergic drugs, beta agonists, CCB, Obesity, gastroparesis Pathophysiology: Etiology weakens LES → stomach contents are able to reflux upward into the esophagus → irritation of esophagus squamous epithelium → cells in esophgus not equipped to handle acid levels → metaplasia of esophgeal cells occur into columnar epithelium (more stomach like) → barret’s esophagus occurs (precancerous) Barrett’s Esophagus: cellular changes of the esophagus from squamous to columnar (metaplasia) This occurs due to the constant acidic contents irritating the cells. Compensatory mechanisms had to occur or a hole would bore into the esophagus Understand clinical manifestations of acute abdomen Topics: Peptic Ulcer Disease ; Appendicitis Analyze PUD Evaluate Appendicitis Peptic Ulcer Disease: Multiple small erosions of mucosa or submucosa related to the overproduction of HCL and pepsin in the stomach. Locations can be stomach (gastric) or duodenal (duodenum). Clinical Manifestations: ● Epigastric pain (burning sensation) ○ Gastric location: ■ While eating ■ 30min - 1 hour after eating ● Increased gastric secretions during times of eating and after a meal. ○ Duodenal location: ■ Pain relieved with eating ■ 2-3hours after a meal pain occurs lOMoARcPSD|24365327 ● Pyloric sphincter closed during time of a meal so nothing is pushed into the duodenum ● 2-3 hours chyme has been created to be pushed into the duodenum where the ulcer is. ● Nausea ○ Vagus nerve stimulation to CTZ centers ○ More associated with gastric ● Weight loss ○ Likely due to nausea ○ more associated with gastric ● Nocturnal epigastric pain ○ Increase in gastrin secretion at night due to basal secretion levels increasing. ■ “Rest and digest” ● H.pylor detectable in blood ● Low H/H = bleeding ulcer ○ Dark stools (melena)- duodenal ○ Coffee ground emsis (hematoemsis)- gastric ● Pain radiating to back followed by abdominal rigidity, pale skin, hematoesis and cold sweats = perforation Appendicitis: narrowing of the appendix lumen due to obstruction resulting in inflammation of the wall where bacteria can now grow related to that obsturction. **If uterus owner please conduct pregnancy test to rule out ectopic pregnancy** Clinical Manifestations: Abdominal pain begins generalized over the abdomen and increases in severity over time. *Begins in umbilicus or epigastric region* ● Pain increased with sudden movements such as ○ Quick movements ○ Coughing ○ Taking deep breaths ● Acute abdominal pain ○ Originating from umblicus radiating to RLQ ■ McBurney’s point ○ Rebound tenderness ■ Palpation of abdomen then when released the pain gets worse ● Related to peritoneal inflammation ○ Rovsing’s sign ■ Palpation of LLQ results in pain in the RLQ ● Referred pain ○ Psoas sign ■ Supine patient actively flexes right thigh at hip and if pain results = positive sign lOMoARcPSD|24365327 areas forming segmental pattern) →enlarged lymph nodes → superficial tiny ulcerations with fissures forming fistulas and abscesses over consistent inflammatory response → granuloma development due to inflammatory cells → cobblestoning → infections occur → fibrotic scar tissue → narrowing and thickening of the bowel wall → shortening colon. Clinical Manifestations: ● Remissions and exacerbation periods ● Episodes of diarrhea and abdominal pain ● increase d bowel tones ● steady/progressive weight loss ● N/V/D ● Pallor ● Fever ● Obstruction followed by borborygmi (hyperactive tones) ○ With distension and tympany ● Stool characteristics ○ Number of stools per day ○ Alleviating or aggravating factors ○ Bloody stool? ● Malabsorption and nutritional deficiencies ○ Anemic and fatigued ● Other issues such as: canker sores, uveitis, arthritis, dermological problems (erythema nodosum) can develop. Ulcerative Colitis: IBD condition only affecting the mucosal layer of the large intestine. This condition can lead to colon cancer. Pathophysiology: Immunological changes → Cytotoxic T cells accumulate on the large intestinal mucosal wall → Immunoglobulin G and E accumulate as well → inflammatory process causes crypt abscesses → goblet cell production declines → ulcerations occur covered by granulation tissue → pseudopolyps grow → continuous inflammatory response → increase risk of nerve damage and perforation resulting in necrotic/gangrene conditions → chronic irritation = cancer risk Clinical Manifestations: Episodic as well with diarrhea and abominable pain ● Abdominal pain ● Bloody diarrhea multiple times a day (up to 20) ● Colicky ● Dehydration ● Anemia ● Abdominal distention lOMoARcPSD|24365327 ● Abdominal guarding ● Fever ● Leukocytosis ● Inflammation of liver and bile ducts Compare the various types of hepatitis including modes of transmission Topic: Hepatitis A, B, C Remember Hepatitis A: Fecal oral route ● Sanitation condition related ○ Food ○ Person to person ○ Water ● Vaccine available (often given in childhood in United States) ● S/S: Flu-like, abdominal pain, jaundice/hepatomegaly. Dark urine, pale stools. ● Self-limiting disease- recovery Hepatitis B: “Baby, Booty, Body fluid”: blood products, bodily fluids like semen, and mom to baby transmission. ● No cure, treatable ● Gets host immune system to attacks hepatocytes ● Treatment involves interferon ● Vaccine is available Hepatitis C: transmission via blood, needle sharing ● Low grade fever, n/v, fatigue, malaise, anorexia, weight loss ● Can be curable Differentiate between non- alcoholic liver disease and alcoholic liver disease. Topic: Pathophysiology of both Analyze Non Alcoholic fatty liver disease (NAFLD) PATHO ● Patient typically has comorbidities ○ Obesity ○ Hypertriglyceridemia ○ Diabetes Liver becomes infiltrated with fat & fibrotic tissue → fulminant hepatic failure = acute liver failure complicated by hepatic encephalopathy Alcoholic liver disease PATHO Heavy alcohol use → chronic inflammation in liver → stellate cells in liver are stimulated to synthesize collagen and fibrotic tissue Understand the pathophysiology and complications for the patient with cirrhosis. Topic: Encephalopathy Understand Hepatic encephalopathy d ue to cirrhosis ● Altered mental status and cognitive function in the presence of liver failure S/Sx: ● Confusion ● Personality change ● Stupor lOMoARcPSD|24365327 ● Asterixis may be present ○ Flapping hand tremors PATHO: GI toxins and nitrogenous waste (ie. NH3 [ammonia]) not removed by liver due to impairment = toxic to brain Understand the pathophysiology and clinical manifestations for gallbladder. Cholelithiasis (gallstones) *most frequent* Motility disturbances → bile stasis → biliary sludge (bile salts, bile acids, bile pigments, lecithin, cholesterol) → biliary stasis → forms calculi (gallstones) Topic: Gallbladder Apply 3 Types of gallstones 1. Cholesterol stones a. Most common - 80% 2. Black pigment stones a. Due to alcohol liver disease, chronic hemolysis, aging 3. Brown pigment stones a. Often located in bile ducts b. Cause obstruction and inflammation Cholangitis → gallstone that causes inflammation of the cystic duct Choledocholithiasis→ gallstones travel and obstruct the common bile duct ● Complete obstruction leads to hyperbilirubinemia → jaundice Gallstones can move into the pancreas → pancreatitis = potentially fatal inflammatory disorder Cholecystitis (inflammation of the gallbladder) → caused by cholelithiasis CLINICAL MANIFESTATIONS ● Pain after eating fatty foods ● Jaundice ● Temp/ elevated WBC = possible sign of infection Biliary Colic - syndrome of spasmodic pain associated with irritation of gallbladder ● Commonly secondary to gallstones CLINICAL MANIFESTATIONS ● Steady, intense pain ● Nausea, vomiting, RUQ pain, right flank pain/mid chest pain ● Murphy’s sign ○ Sharp RUQ pain upon palpation of abdomen lOMoARcPSD|24365327 g. Hyperkalemia h. Metabolic acidosis 3. Diuresis phase: a. High UOP (1-2L output/day) i. Not concentrated continuation of nitrogenous waste build up b. Hypovolemia . Renal Caliculi: the formation of calculi in the kidney (if it goes to the ureters and obstructs urine flow it is called a urolithiasis) ● Commonly made out of calcium others are: ○ Struvite, Uric acid, Cytesine stones Risk Factors: ● Metabolic condition: ○ Hypercalcemia (high calcium) ○ Hyperoxaluria (high oxalate) ○ Hyperuricemia (high uric acid r/t diet or alcohol) ○ Hyperparathyroidism (increases calcium in blood) ○ Goat (increase uric acid in blood) ● Low fluid intake (dehydration) ● Age greater than 40 ● Male ● Certain medications ● Dietary factors (high red meat) ● Gastric bypass ● Geographic locations (hot climates) ● High sodium diet ● IBD ● Inherited kidney conditions ● Obesity ● UTIs Pathophysiology: Condition based, the perfect conditions have to occur for example: Hyperabsorption of calcium and oxalate in GI or hyperparathyroidism → calcium stones Chronic UTI + alkaline pH of urine → struvite High protein (purine) intake + goat = high uric acid → uric acid stones Renal failure to reabsorb cytasine → super saturates urine →crystal deposition → crystaline stones Either way: the stones form in the kidney → deposit into the tissue → block the flow of urine to the bladder ● Deposit in the kindey, renal papilla, minor calyx, or ureter lOMoARcPSD|24365327 ● Hydronephrosis can occur due to blockage lOMoARcPSD|24365327 Clinical Manifestations: ● Pain in flank and upper outer quadrant of abdomen of affected kidney ○ Radiates to the lower abdomen and groin ● Patient is bent over, writhe in pain, pace, and consistently change positions to get comfortable ● Pain can be dull, deep, or ache in flank or back ○ This is related to distention of renal pelvis or calyces ○ Commonly associated with increase fluid intake ● cool/clammy skin ● n/v ● Hematuria noted Identify the types of renal failure including pathophysiology, clinical manifestations and diagnostic tests. Topics: Chronic renal failure (CRF), Nephrotic Syndrome, Lab Values Analyze Labs Understand: Nephrotic Syndrome Apply CRF Chronic Renal Failure: w hen 90-95% of nephrones deteriorate and the kidneys are unable to filter nitrogenous wastes or exrete fluid. This is a gradual onset with months to years of development. Progresses to End Stage Renal Disease. ● Risk factors: HTN and DM, glomerulonephritis, PKD, SLE Pathophysiology: ● Based on Stages 1-5: ○ 1: Kidney damage with normal or increased GFR (90mL/min or greater) ○ 2: mild reduction in GFR (60-90mL/min) ○ 3: moderate reduction in GFR (30-59 mL/min) ○ 4: severe reduction in GFR (15-29 mL/min) ○ 5: kidney failure (GFR lower than 15mL/min) Clinical manifestations: ● Altered LOC (confusion, stupor, coma) ○ Nitrogenous wastes affects brain ● Bruising ○ Thrombocytopenia from lack of EPO ● Fatigue/Dyspnea on exertion ○ Result of anemia ● Edema ○ Fluid overload from inability to exrete fluid ● Oliguira ○ Unable to excrete fluid ● Muscle spasms or seizure ○ Due to hypocalcemia ● Amenorrhea ○ Decrease in excretion of sex hormones ● Sex hormones negatively feed back to organs ● HTN ● Pallor Diagnostic Tests: ● U/A shows proteinuria, RBCs and WBCs ● Elevated creatine and BUN lOMoARcPSD|24365327 osteoclast activity to release calcium from bones Compare and contrast treatment options for renal replacement Topic: All types Remember Big Concept: ● Treatment of renal diseases where renal function is severely impaired to maintain homeostasis . ○ Balances: ■ Fluid ● Removes or replaces fluid ■ Electrolytes ■ acid/base ● Adds sodium bicarb ■ Blood glucose ■ monitor s RBC production ● Epogen to stimulate RBC Peritoneal Dialysis: filling the patient’s peritoneal cavity with dialysis solution that pulls waste and extra fluid from the blood into the abdominal cavity through diffusion processes ● Dwell time refers to amount of time fluid remains in cavity after complete infusion ○ 4 hours-6hours ○ Infusion and removal takes 30-40min ● After dwell time fluid is drained from cavity and discarded ● Average 4 exchanges per day with dwell time of 4- 6hours Hemodialysis: blood drawn out of patient at a rate of 200- 400mL/minute through a dialyzer device. ● Patient commonly has a ateriovenous fistula to facilitate process ○ Made from brachiocephalic artery and cephalic vein with a tubular connection ● Blood drawn from brachiocephalic artery → dialyzer → removes exces solutes and fluid → returns blood to cephalic vein ● Sterile solution of electrolytes used ● Entire patien’ts blood volume circulates (5000mL) every 15 minutes ● Average done 3x a week for 4-6hour sessions Continuous Renal Replacement Therapy (CRRT): ● Like hemodalysis but for SEVERELY hemodynamically unstable and fluid overloaded patients ● Dialyzer hooked up for 24 hours Understand common etiologies and pathophysiology of common urinary disorders. Topic: UTI Urinary tract infections (UTI): Etiology: ● Bacteria in nature can be fungal ○ Most common E.Coli- improper hygiene ● CAUTI- improper hygiene lOMoARcPSD|24365327 Apply ○ Polymicrobial ● Diabetes ● Baths ● Anal-intercourse ● Urinary stasis ○ Reflux ○ Blockage- kidney stone ○ Neurological issue- unable to empty ○ BPH Pathophysiology: Bacteria inoculation → climbs up urethra → colonates in urine → immune/inflammtory response ● IgA usually in urinary system but women often are non- secretors or IgA Can present with symptoms or non symptomatic (asymptomatic bacteruria) Interpret basic urinalysis results. Topic: Table 23.2 Analyze Bacteriuria ● Bacteria in urine ● Indicative of UTI or aymptomatic UTI Bilirubinria ● Bilirubin in urine ● Indicative of liver disorder or excessive hemolysis Crystalluria ● Crystals of pieces of kidney stones in urine (calcium or uric acid) ● Inidicative of nephrolithiasis or urolithiasis Glucosuria ● Glucose in urine ● Indicative of uncontrolled diabetes Hematuria ● Blood in urine ● Indicative of UTI, Nephrolithiasis or urolithiasis, urological malignancy Ketonuria ● Ketones in urine ● Indicative of fasting, starvation, uncontrolled DM Lekucyte esterase ● WBCs in urine ● Inidcative of UTI or ASB Nitrites ● Bacteria presents in urine ● Indicative of ASB Proteinuria ● Abnormal protein content- greater than 200mg/L ● Indicative of: ○ glomerular injury ○ Kidney dysfunction r/t diabetes or HTN ○ kidney inflammation Pyuria lOMoARcPSD|24365327 ● WBCs (neutrophils) in the urine ● Indicative of: UTI or ASB Urinary Casts ● Mucoproteins found in sediment can be hyaline, waxy, granular, fatty, crystal like ● Indicative of ○ Nephrotic syndrome ○ Dehyrdation ○ Vigerous exercise ○ Diuretics ○ Tubular necrosis ○ Autoimmune disorder ○ Pyelonephritis ○ Other kidney diseases Differentiate between the four types of urinary incontinence. Understand Stress Incontinence: involuntary leakage of urine due to increased abdominal pressure. ● Poor pelvic support ● Sneezing ● Coughing ● Weak urethral sphincter ● Laughing Urge Incontinence (overactive bladder-OAB): detrusor muscle is overactive and flexes resulting in leakage of urine. ● Sense of urgency and frequency ● Etiology unclear Overflow incontinence: chronically overdistended and urinary retension in the bladder results in leakage. ● BPH ● Failure of detrusor muscle due to spinal damage Neurogenic bladder: interruption of sensory nerver fibers between bladder and spinal cord or afferent nerve tracts to the brain. ● The bladder becomes overdistended chronically Functional Incontinence: in ability to hold urine ● CNS problems or stroke ● Psychiatric disorders ● Prolonged immobility ● Dementia ● delirium Mixed Incontinence: combination of stress incontinence and OAB Total Number of Renal Questions: 12 lOMoARcPSD|24365327 increased ICP Treatment: ● Clot forming agents ● Surgerical procedures to stop bleeding ● BP management ● IV mannitol ● Intubation Transient Ischemia Attack (TIA): di sruption of cerebral circulation with neurological deficits that are reversible within 24 hours. ● Body will naturally dissolve the clot ● TIA is a warning sign for future strokes Treatment: ● Wait it out ● Aspirin ● Anticoagulant therapy ● Carotid stenosis therapy (endarterectoomy) Clincal manifestations with Strokes: ● FAST acronym: ○ Face droop ○ Arm weakness ○ Speech difficulty ○ Time to call 911 ● Right Hemisphere = Left body weakness/paralysis ● Left Hemisphere = Right body weakness/paralysis ○ Hemiparesis (weakness) ○ Hemiplegia (paralysis) ● Aphasia occurs with left affected ● Change in LOC ○ Subarachnoid hemorrhage ● Headache ○ Subarachnoid hemorrhage Differentiate the various types of seizures: Etiology and Pathophysiology Topic: Focal ; Unwitnessed Analyze Unwitnessed Understand Focal ETIOLOGY: ● Epilepsy ● Brain neoplasms ● Cerebrovascular Disease ○ Stroke, heart attack ● Congenital malformation ● Degenerative Brain Disorders ○ Ex. Alzheimer's Disease ○ Dementia leading cause among older adults ● Developmental Disorders ○ Down Syndrome, autism ● Environmental stimuli ○ Blinking lights, loud noises, certain music, odors ● Genetic predisposition lOMoARcPSD|24365327 ○ Est. 500 genes associated with condition ● Head Trauma ○ Severe, penetrating head trauma ■ Car accident/other traumatic injury ● Infections/Viruses ○ Meningitis, AIDS, viral encephalopathy ● Metabolism disturbances ○ Hypoglycemia, hyponatremia, respiratory alkalosis ● Prenatal Injury ○ Infection in mother, poor nutrition, O2 deficiencies ■ Can lead to cerebral palsy ● Perinatal injury ○ Hypoxia ● Substance abuse ● Withdrawal ○ Alcohol, sedative-hypnotic drugs GENERALIZED ONSET SEIZURE: ● Motor Symptoms ○ Clonic, tonic, myoclonic muscle activity, atonic, or epilectic spasms ● Nonmotor Symptoms (absent seizures) ○ Patient unaware of seizure activity ○ Staring spells without movement ○ Brief twitches (myoclonus) ■ Can affect specific body part or just eyelids FOCAL ONSET SEIZURE: → arise from a neuronal area localized in one cerebral hemisphere and are RESTRICTED to that hemisphere Motor, sensory, autonomic or psychic symptoms ● With or without impaired cognition May cause: (MOTOR) ● Abnormal hand movements ● Abnormal facial expression ● Automatisms (repeated automatic movements) ○ Clapping hands, lip smacking/chewing, running May cause: (NONMOTOR) changes in: ● Sensation ● Emotions ● Thinking or cognition ● Autonomic function ○ GI sensation, waves of heat or cold, goosebumps, heart racing ○ Lack or movement ■ Called behavioral arrest ● EEG - abnormal spike discharges in a very limited region over the related area of the cerebral cortex lOMoARcPSD|24365327 SEIZURE PATHO: abrupt, abnormal, excessive, and uncontrolled electrical discharge of neurons within the brain → cause alterations in LOC, changes in motor/sensory ability and/or behavior Discuss the assessment and impact of Parkinson’s Disease and Alzheimer’s Disease including pathophysiology. Topci: Alzheimer’s ; Parkinson’s Understand Alzheimer’s Evaluate: Parkinson’s Parkinson’s Disease PATHO: progressive loss of dopamine-producing cells in the substantia nigra ( inside the basal ganglia of the midbrain) ● Basal ganglia → modulate movements ○ Ie. posture, standing, walking, writing ○ Neurotransmitters = Ach and dopamine ■ Ach - stimulates muscle movement ■ Dopamine - inhibits movements Parkinson’s creates an imbalance between Ach and dopamine → unopposed Ach = tremors, spasmodic muscle movements ALSO: accumulation of an abnormal protein ● Alpha-synuclein found in Lewy bodies in brainstem, spinal cord, regions of cortex ○ Associated with neurodegeneration and cell death ASSESSMENT: TRAP Tremor at rest Rigidity Akinesia (bradykinesia) - slowness of movement Postural/gait instability Symptoms are disabling and affect ● Socialization ● Motivation ● Quality of life Alzheimer’s Disease PATHO: progressive neurological degenerative disease → significant changes in the brain tissue ● Accumulation of neurofibrillary tangles ● Senile plaques ● Cerebrocortical atrophy of the brain Microtubules (support structures of neurons that guide nutrients down cell body to axon and back up) are stabilized by tau (specialized protein) ALZHEIMERS BRAIN: tau pair with other threads of tau → neurofibrillary tangle → microtubule disintegration → neuron’s transport system collapses → tangles and plaques build up and take over normal neural tissue in brain → communication malfunction and brain lOMoARcPSD|24365327 Presentation ; Figure 6.11, Read Chronic Pain and Chronic Stress article Understand stimuli ● Found in ○ Skin ○ Muscle ○ Connective tissue ○ Bone ○ Circulatory system ○ Abdominal, pelvic and thoracic viscera Inflammation pathways of PGs and sites of anti inflammatory drug action… PAIN RELIEF! SITE: inside the WBC ● Inflammation activates → phospholipase ○ Corticosteroids block this pathway (IE. prednisone) ● Arachidonic Acid → 2 pathways (NSAIDs block this pathway) ○ 1. Cox - 1 → PG1 ■ Produce gastric mucus ■ Enhance renal perfusion ■ Assist in thrombus formation ○ 2. Cox -2 → PG2 (uncomfortable side effects of inflammation) ○ Cox -2 inhibitors block here → celecoxib ■ Pain ■ Edema ■ Fever ■ Stim cycle of inflammation Recognize concepts of stress and adaptation as identified by three theorists. Topics: 3 phases of stress response Selye Stress Response Theory 1. Alarm a. Stage of arousal i. CNS & adrenal gland stimulation ii. SNS stim (aka adrenergic nervous system) lOMoARcPSD|24365327 theory Apply 1. Releases catecholamine norepinephrine a. Increases alertness and stims cardiorespiratory and vascular responses b. NE: vasoconstriction of arterial blood vessels 2. Fight or flight Hypothalamus releases corticotropin releasing factor which stimulates the anterior pituitary gland to release ACTH. This stimulates the adrenal cortex to secrete cortisol & aldosterone. Stimulates adrenal medulla to secrete epi & norepi. Posterior pituitary gland secrete ADH which enhances water reabsorption into the bloodstream. 2. Resistance a. Body attempts to stave off effects of stress i. Continual hormone secretion ii. Catecholamine secretion b. Time limited stage i. If stress stops → SNS and adrenal stimulation stop → PSNS resumes relaxation 3. Exhaustion a. IF stressor does NOT subside → high level of hormone and catecholamine secretion cannot be sustained → EXHAUSTION! b. Stress overwhelms body's ability to defend itself i. Resources are depleted ii. Signs of systemic dysfunction occur 1. Feel rundown, unable to cope, depressed, anxious, physically ill Identify physiologic, Responses to short term stress: lOMoARcPSD|24365327 pathophysiologic, and psychological responses to short and long term stress Topic: Allostatic Overload, Read Chronic Pain and Chronic Stress article, Fight/fight alarm, figure 4.1 Remember Fight/Flight and Figure 4.1 Understand Allosteric Overload; Read ChronicPain/Chronic Stress Article ● Fight or flight *see above* Responses to long term/chronic stress: ● Long term cortisol secretion → suppresses immunity (MAJOR ADVERSE EFFECT) ● Atrophy of the thymus gland → decline in T lymphocytes ○ Another cause of immunosuppression ■ Predisposes to other infection and disease ● Hormones and catecholamines have a cumulative, noxious effect contributing to allostatic load on body ○ Load can accumulate → stress exceeds body’s ability to adapt ● Pathophysiological conditions ○ Ex. diabetes and insulin resistance secondary to obesity that causes stress on the body ○ Autoimmune disease, cancer, heart disease, depression McEwen’s Stress Response Theory Allostasis - dynamic state of balance that changes according to exposure of stressors ● Theory: frequent stressors change the body’s physiological balance and create new set points for homeostasis ● Ex. daily job stress → high BP → chronic stress → high BP persists in and out of work Allostatic load - wear and tear in the body systems caused by stress reactions Load accumulates due to: 1. Repeated stressful experiences 2. Inability of the individual to adapt to stress 3. Prolonged reaction to stressor 4. Inadequate response to stressor Adaptive ability influenced by ● Genetic make-up ● Cognitive ability ● Developmental level ● Socioeconomic status ● Lifestyle choices ● Diet ● Exercise ● Pre-existing conditions ● Past life experiences ● Support of others Identify adaptive and maladaptive coping mechanisms to stress. Topics: Chronic stress and Chronic pain Understand: Stress Adaptive Ability Apply Coping Mechanisms Selye’s Stress Response Theory ADAPTIVE ● The way an individual manages stress and reduces stressor’s effect on their life ● Effective adaptive ability = maintaining homeostasis ● Face problems and deal with them lOMoARcPSD|24365327 Remember a. Influenced by descending nerve tracts from brain or ascending nerve tracts from spinal cord 3. Third neuron a. Impulse projects upward into brain TO PRODUCE PAIN: 3-neuron chain goes thru 4 processes ● Transduction ○ Initial process occurring after ■ Direct tissue injury or inflammation ○ Converts painful stimuli → neuronal impulses ● Transmission ○ Impulse travel along the axon ● Modulation ○ Influence on the afferent nephron by ascending or descending nerve tracts front he brain ■ Spinothalamic tract most prominent nociceptive pathway in spinal cord ● Travels from spinal cord to brain ○ Effect of the interneuron on the afferent neuron = ■ Amplification of dampening of pain ● Perception ○ Conscious awareness of the experience of pain ■ Results from impulse transmission up to the thalamus, limbic system, midbrain, cerebral cortex and reticular system ■ Influenced by ● Developmental level, memory, past experience, attention, distraction, fatigue, fear, stress, anxiety, depression Differentiate between acute, chronic and neuropathic pain. Topic: Definitions Remember ● Acute ○ New onset of tissue injury or inflammation ○ Sudden ○ Lasts hours to days ○ Resolves when disorder heals ○ Biologically protective ■ Facilitates tissue repair and healing → individual avoids exposing injury to outside stimuli = undisturbed healing process ○ Ex. post-surgery, fracture, MI, appendicitis ● Chronic ○ Duration longer than 6 months ○ Ex. persistent inflammation, cancer, osteoarthritis, rheumatological disease ○ Debilitating ○ Does NOT serve any biological or protective function ○ Does NOT subside when condition no longer exists ○ Does NOT respond to common analgesic lOMoARcPSD|24365327 treatments ● Neuropathic ○ Caused by injury or malfunction of spinal cord and/or peripheral nerves ○ Described as “burning, tingling, shooting, pins-and- needles” ■ Paresthesia ○ Can occur within days, weeks, or months of an injury ○ Occurs in waves of frequency and intensity ○ Occurs at wither the level of or below the level of injury ■ Most often legs, back, feet, thighs, toes ■ Can occur in the upper body ○ Treatment ■ TENS, antidepressants, anticonvulsants, acupuncture Identify five sources of pain. Understand Localized = pain from areas rich in nociceptors Referred = pain far from the origin of injury 1. Cutaneous Pain a. Injury to skin or superficial tissue b. Cutaneous nociceptors terminate just below skin → high concentration of nerve endings c. Well defined, localized pain with a SHORT duration d. Ex. minor cuts, bruises, 1st degree burns, lacerations 2. Deep Somatic Pain a. From ligaments, tendons, bones, blood vessels, and nerves b. Pain receptors are scarce → dull, poorly localized pain with LONGER duration c. Ex. sprains, broken bones d. Myofascial pain i. Caused by tender points in muscles, tendons, fascia ii. May be localized or referred 3. Visceral Pain a. Emanates from deep organs → usually a result from disease process b. Vague, not well localized c. Described as “pressure-like” “deep squeezing” “dull” “collicky” “diffuse” d. Most pain occurs in GI tract, GU tract, gallbladder i. Nerves are stretched with distention and pain signal is sent to the brain e. Inflammation i. Due to PGs → edema, pain, fever, constant inflammation lOMoARcPSD|24365327 ii. Ex. pancreatitis, cystitis f. Systemic symptoms i. Malaise, weakness, nausea g. Referred Pain = hallmark of visceral pain 4. Phantom Pain a. Sensation of pain originating in an amputated part of the body b. Described as “burning” “stinging” “cramping” c. Constant and most intense right after amputation d. Usually worse at night e. Due to well developed neuro pathways that still perceive extremities despite their amputation 5. Referred Pain a. Occurs when nerve fibers from regions of high sensory input (skin) and low sensory input (organs) converge on same levels of the spinal cord b. Ex. myocardial infarction i. Pain in heart is felt as chest and left arm pain Total Number of Pain/Stress Questions: 12