Walden University NUR 2063 Essentials of Pathophysiology – Final Exam Review Sheet Covers, Exams of Nursing

Download Walden University NUR 2063 Essentials of Pathophysiology – Final Exam Review Sheet Covers and more Exams Nursing in PDF only on Docsity!

Essentials of Pathophysiology – Final Exam Review

Sheet Covers Material from Modules 1-

1. Review the different levels of disease prevention such as primary, secondary, and tertiary as well as examples for each. LEVELS OF DISEASE PREVENTION- Primary- prevention of diseases- vaccination, handwashing, educating, social distancing Secondary- early detection before big problems. Eg- pap Smear or screening tests Tertiary- rehabilitation- eg- therapies.
2. Review the differences between the sympathetic vs the parasympathetic nervous systems. What happens to the body during “fight-or-flight” response?
3. Review the functions of the various organelles of the cell such as the nucleus, mitochondria, ribosome, lysosome, endoplasmic reticulum, peroxisome, golgi apparatus
4. Review the difference between active and passive immunity, know examples for each type. in order to achieve active immunity - the body must be exposed to m/o- vaccinations- weakened form of m/o. passive immunity- how the immune protection can be passed- mother to fetus in the placenta or the mother to baby. passive immunity doesn’t last very long.
5. What is edema? Review the various factors that can contribute to edema. Edema - accumulation of fluid in the interstitial space - leading to tissue swelling. Can be localized or generalized. Can be due to an increase in the forces that move fluid from the

capillaries into the interstitial compartment. Or a decrease in forces that move fluid from the interstitial compartment into the capillaries. Factors that contribute to edema include: Increases in capillary hydrostatic pressure (blood vessel blockage, incompetent venous

valves), Increased capillary permeability (inflammation),Congestive heart failure, High blood volume or HTN, Decrease in plasma proteins (such as albumin), Blockage of lymphatic drainage (due to cancer or removal of lymph tissue)

6. What is a hypersensitivity? Review the four different types of hypersensitivities: Type I (Anaphylactic), Type II (Cytotoxic), Type III (Immune complex), Type IV (Delayed cell- mediated). Know examples and mediating factors for each type. Too much activation of immune system is hypersensitivity. Type I- IgE, Type II- IgG and IgM, Type III- IgG, Type IV- T- cells.
7. Review the differences between benign and malignant tumors. Benign - encapsulated, localized, grows slowly and usually and doesn’t invade, doesn’t usually reoccur after treatment. Malignant - not capsulated, spread, all over body, grows fast, can reoccur.
8. Review signs and symptoms of peptic ulcer disease. Signs and symptoms are- pain on empty stomach or 2-3 hours after eating when food moves from stomach to large intestine where the ulcers are. H. Pylori thrives in acidic conditions and breaks down the lining and causes the ulcers to bleed.
9. Review differences between functional and mechanical bowel obstructions, know examples for each Inability to move stool. Functional obs - somethings that stops the peristalsis movement of the intestine- paralytic ileus. Causes of functional obs- certain medications like anticholinergics - it activates the flight or fight and person can’t poop, pee, spit or see. Poop and pee due to digestive and genitourinary system is slowed down, and salivary glands stop producing saliva and hence dry mouth and can’t see due to pupil dilation. Opioids and low fiber diet also cause functional obs. Mechanical obs- adhesions,

hernia, tumor, impacted feces, volvulus and intussusception (something that blocks the intestinal track.

10.Review signs and symptoms of appendicitis. How do we assess for this condition? Appendicitis- inflammation in the vermiform appendix. S/S - RLQ pain and tenderness, nausea, vomiting, fever, diarrhea and systemic signs of inflammation 11.Review signs and symptoms of liver disease. Review complications of liver disease such as ascites, hepatic encephalopathy and esophageal varices. How are esophageal varices managed/treated? Jaundice- green/yellow skin due to bilirubin due to impaired bilirubin metabolism. Ascites- accumulation of fluid in peritoneal cavity due to portal hypertension and hypoalbuminemia. Check total protein and albumin and fluid examination. Hepatic Encephalopathy- neuropsychiatric syndrome from too much ammonia. S/s- dementia, asterixis, mild confusion and lethargy to stupor and coma. Cirrhosis- end stage liver disease- irreversible- acute, chronic and toxic hepatitis, metal storage disease and alcoholism. Esophageal Varices- dilated blood vessels in the esophagus. Can rupture due to high blood pressure. We must reduce blood pressure to manage it and put rubber bands to control bleeding when it ruptures. 12.What role does albumin play in the blood? What happens to albumin production with liver failure? -Removes excess fluid and waste products, maintains pH, CVA tenderness, GFR. 13.What are the functions of the kidneys? How do we assess for renal disorders? Functions- excretion - removal of waste products, elimination -discharge of waste productions, regulation of blood volume levels, ions conc, blood pH and nutrients. Assessment of renal disorders- dialysis, glomerular filtration rate. Some findings are- CVA tenderness and blood in urine. 14.What is polycystic kidney disease? What causes this condition? genetically transmitted, many fluid filled cyst. Can lead to renal failure. Two types- autosomal recessive forms or autosomal dominant types. 15.Review the following terms: nephrons, hematuria, proteinuria, nephrolithiasis, pyelonephritis, cystitis Nephrons - filters in the kidney Hematuria - blood in urine- abnormal finding Proteinuria - protein in urine- abnormal finding Nephrolithiasis - kidney stones Pyelonephritis - kidney inflammation due to infection Cystitis - inflammation of the bladder.

16.Review signs and symptoms of acute kidney injury (AKI). Review causes of AKI including prerenal, intrinsic, and postrenal. Know examples of each type of injury. Prerenal injury is anything that impacts blood flow to the kidney. Examples of causes of damage due to prerenal injury is hypotension, hypovolemia, heart failure, renal artery obstruction, fever, vomiting, burns and drugs. Intrinsic or Inter renal damage is within the kidney, example tumors, inflammation in the kidneys, chemotherapy or contrast media. Post renal kidney injury is any that impacts the urine flow outside the kidney, example stones, ureter and tumor. 17.What is compartment syndrome? Why does it occur and what are the signs? Remember the 5 P’s Dangerous complication of soft-tissue injury-results from swelling of injured tissue within a restrictive fascia- swelling in tissue and tingling effect are the signs. Five P’s : Pain out of proportion to the injury, paralysis, paresthesia, pallor, and pulselessness. 18.What are pressure ulcers? How are the staged and how can we prevent them? Ulcers caused due to unequal load of pressure on a particular bony part. Stage I-Intact skin with nonblanchable redness Stage II-Partial-thickness skin loss involving epidermis, dermis, or both Stage III-Full-thickness tissue loss with visible fat Stage IV-Full-thickness tissue loss with exposed bone, muscle, or tendon First-degree burn: affects only the epidermis and cause pain, erythema, and edema Second-degree burn: affects the epidermis and dermis and cause pain, erythema, edema, and blistering Third-degree burn: extends into deeper tissues and cause white or blackened, charred skin that may be numb 19.What are electrolyte reservoirs? What electrolytes are found stored in bones? These reservoirs are back ups or storage of electrolytes. They are used when the body is in short of the electrolyte. Ca, Mg, Phosphorus are found in the bones 20.Review diseases of the bone including: osteomyelitis, osteosarcoma, osteomalacia, rickets, and osteoporosis Osteomyelitis- infection in bone after bone break through skin or surgeries or bacteria. Osteosarcoma- cancer in bones osteomalacia, rickets, - adults and children- deficient of calcium and vitamin D causing weakening of bones.

Osteoporosis- increased bone breakdown with little bone building- lack of estrogen in women after menopause causes it.

21.Review disorders of the joints including: rheumatoid arthritis, osteoarthritis, psoriatic arthritis, and gout. Know causes and signs/symptoms for each. rheumatoid arthritis- autoimmune- affects small joints due to inflammation in them. Bone cysts and fissures. osteoarthritis- aging process, use and overuse of joints. psoriatic arthritis- linked with psoriasis- genetic cause NSAIDS gout- uric acid excess in blood causes crystals and these crystals gets stuck in joints and causes pain. Medications to reduce uric acid treats gout. 22.Review endocrine disorders of the pituitary gland including: gigantism, dwarfism, acromegaly, diabetes insipidus, SIADH gigantism - childhood- excessive amount of growth hormone- lengthwise increase. Acromegaly - adulthood, excessive amount of growth hormone, widthwise increase. Dwarfism - lack of GH, short height. Diabetes insipidus - lack of ADH- very dilute urine in large amounts, no fluids= hypovolemia, electrolytes increase. Dehydration and extreme thirst. Dizziness, disorientation, rapid heart rate and headaches. SIADH - excessive ADH- water retention, oliguria, conc urine. Hyponatremia can lead to cerebral edema. 23.Review which organisms/viruses contribute to the following conditions: pelvic inflammatory disease, cervical cancer, UTIs, herpes, syphilis Pelvic Inflammatory disease- caused by Neisseria gonorrhoeae, Chlamydia trachomatis ,- cervical cancer - HPV ( diagnosed by papsmear), UTIS- E. coli , herpes (type II)- herpes simplex virus, syphilis- Treponema pallidum 24.What is parathyroid hormone (PTH)? Which electrolyte is primarily affected by PTH disorders?

PTH - increase Ca in blood and decrease Ca in bones. Calcitonin - decrease Ca in blood and increase bring it back to the bones. Calcitonin is produced by thyroid gland.

25.Review differences between Cushing’s syndrome (hypercortisolism) versus Addison’s disease (adrenocortical insufficiency) Cushing’s Syndrome - excessive glucocorticoids. Caused due to pituitary tumor. Swelling due to fluid retention, hyperglycemia. Hypertension, edema, hypernatremia, moon face- fat on posterior neck- buffalo hump. Addison’s disease - adrenocortical insufficiency. Can be caused due to removal of adrenal glands. Fatigue, Bronzing of skin, hypoglycemia and hyperkalemia. Reduced cardiac output. Should not stop steroids suddenly. 26.Review the differences between clinical manifestations of hypothyroidism and hyperthyroidism. What labs can be drawn to determine if an individual is suffering from a thyroid disorder? Hypothyroidism - common cause- hashimoto or autoimmune thyroiditis. Bradycardia, slow metabolism-weight gain and feels cold, tired and sluggish, dry skin, poor hair and nail growth. Iodine deficiency (required for T 3 /T 4 formation) Leads to lack of T 3 /T 4 , stimulates TSH secretion, Increased TSH causes thyroid cells to secrete large amounts of thyroglobulin, which leads to goiter. Hyperthyroidism - tachycardia, diarrhea, tremors, lose weight rapidly, bulging of eyes. 27.Review the difference between Type 1 diabetes versus Type 2 diabetes Type 1 diabetes mellitus. Typically diagnosed in young children/adolescents. Autoimmune disorder – beta cells in pancreas destroyed. Unable to produce insulin. Insulin dependent. Type 2 diabetes mellitus- Cells become resistant to insulin, decrease insulin receptors on target cells. Overtime insulin production by pancreas decreases. Gestational diabetes- Hormones produced during pregnancy inhibit effects of insulin

28.What are signs and symptoms of hyperglycemia versus hypoglycemia. What are the three Ps? Hyperglycemia - increased glucose. Polyuria - excessive urination. Polydipsia - excessive thirst. Polyphagia - excessive hunger. Hypoglycemia - cold, pallor, fatigue, hungry, low blood sugar, sweaty, more fatal than hyperglycemia. 29.Review the difference between primary and secondary brain injury Primary brain injury - occurs as a direct result of the initial insult. Example – Stroke, concussion. Secondary injury - refers to progressive damage resulting from the body’s physiologic response to the initial insult. Example – brain swelling secondary to stroke 30.Review causes of intracranial pressure; how does it lead to impaired neurological function? Increased Intracranial Pressure (ICP) l eads to impaired neurological functions due to: ► Compression of brain tissue due to swelling of the brain ► Inability of the cranium to expand in adults – bones of skull fused in adulthood ► Reduced blood flow to the brain from increased pressure 31.What are signs of increased ICP? Headache, vomiting, and altered level of consciousness (drowsiness), Blurry vision, Pupil responsiveness to light becomes impaired, Altered respiratory patterns and unresponsive to stimulation, Patient may become unable to move, verbalize, or open the eyes 32.Review the Glasgow coma scale , what is it used to assess? How we measure patients’ level of consciousness related to brain trauma. Can they open their eyes spontaneously, name, DOB, where they are, are they confused, are they mumbling words? Motor response- Can they move their arms and legs? Push and use fingers. Score and add them. 33.Review the different types of stroke: ischemic versus hemorrhagic. How is a stroke diagnosed? Ischemic - blockage in blood vessels within the brain. Prevents blood flow to the tissues down stream of the blockage. Clot busters for management. Hemorrhagic - bleeding, management is different. CT scan to check which kind of stroke it is. 34.Review the difference between meningitis versus encephalitis Meningitis - inflammation of the meninges (tissue surrounding the brain and spinal cord). Can be due to bacterial, virus or fungal

Encephalitis - inflammation of the actual brain.

35.Review the different types of seizures. How are seizures diagnosed? Generalized seizure - whole brain surface is affected during the seizure a. Absence (petite mal): occurs in children, staring spells that last only seconds b. Myoclonic: single/several jerks of limbs, upper body c. Atonic (drop attack): loss of muscle tone, can cause falls d. Tonic-clonic (grand mal): jerking of many muscles Focal (Partial) seizures - abnormal electrical activity restricted to one brain hemisphere Status epilepticus - continuing series of seizures without a period of recovery between episodes. Can be life-threatening Diagnose - EEG- electrical patterns of brain regions., CT, MRI to identify structural causes. 36.Review the etiology of cerebral palsy. Is cerebral palsy reversible? Etiology- diverse group of disorder- cause could be Infection, trauma before, during or shortly after birth. Decreases oxygen during birthing. It is not reversible. 37.What causes Parkinson’s disease? What does this condition affect? Progressive loss of dopamine producing neurons within the brain Dopamine deficiency associated with motor impairment s/s- motor impairment, tremors, shaking, mask like facial expression, move their feet across the floor, absent arm swing, shuffling or propulsive gait, pill rolling movement of the fingers. 38.What are the major mechanisms of spinal cord injury? How do we treat if we suspect someone has a spinal cord injury? Spinal cord injury during vehicle accident, fall. Mechanisms of injury- Hyperflexion, hyperextension, compression. We must stabilize the injury to prevent shock. Immobilize. Head and neck midline. 39.What happens with oxygen and carbon dioxide levels in the blood and lung with hypoventilation? Hyperventilation? ► Hypoventilation causes hypercapnia (high carbon dioxide) and hypoxemia (low O 2 in blood). Causes of hypoventilation - morphine, barbiturates, obesity, myasthenia gravis, obstructive sleep apnea, chest wall damage, paralysis of respiratory muscles, surgery of the thorax or abdomen ► Hyperventilation - Increase of air entering the alveoli leads to hypocapnia (carbon dioxide exhaled at a quicker rate than the body cells produce). Causes - pain, fever, anxiety, sepsis, high altitude, and brainstem injury

40.Be able to identify normal versus abnormal ABG values and example of causes for metabolic acidosis/alkalosis, respiratory acidosis/alkalosis. 41.What is the normal pH range of blood? CO2? HCO3?

42. Review conditions that affect the lungs such as: asthma (extrinsic, intrinsic, exercise- induced), mycobacterium tuberculosis, COPD, cystic fibrosis, ARDS, pneumonia. Asthma- wheezing, Airway inflammation, airway obstruction, Increased airway responsiveness to a variety of stimuli. Extrinsic – allergic asthma Intrinsic – non-allergic- body’s response to bacterial infection. Develops in middle age with less favorable prognosis. No history of allergies. Triggers include upper respiratory infections, air pollution, emotional stress, smoke, exercise, and cold exposure Allergen- specific immunotherapy and environmental control not helpful

Exercise-induced asthma- bronchospasm. Bronchoconstriction following

aerobic exercise.

mycobacterium tuberculosis- TB- airborne, N95 repirators, negative pressure rooms. Cough with bloody sputum, weight loss. And night sweats. COPD- lose ability to move air from the lungs. Air is trapped due to loss of lung elasticity. Barrel chest, finger clubbing.

ARDS- damage to the alveolar- capillary membrane. Lungs fill with fluid, pulmonary edema. Shortness of breath, hypoxemia, frothy sputum. High level of CO2. pH is going low- acidosis. Pneumonia- fluid in lungs and fluid is thick and hard to move out of longs. Elderly are at increased risk or pneumonia, sedentary and immunocompromised and no gag reflux are prone to pneumonia. 43.What are signs of ARDS? 44.What is a tension pneumothorax , how is it treated? Accumulation of air in the pleural spaces. Cause- air compressed the lungs or heart due to puncture wound, stab wound, gun wound, surgery in the chest wall. Cover the hole and use chest tube to pull the air out. 45.What is Virchow’s Triade? How do these factors increase a patient’s risk for developing a pulmonary embolus? Virchow’s triad - factors causing thromboemboli formation include: a. Venous stasis/sluggish blood flow b. Hypercoagulability c. Damage to the venous wall (intimal injury) Common risk factors - immobility, trauma, pregnancy, cancer, heart failure, and estrogen use 46.What are different causes/types of emboli? Types of emboli include : blood clot, fat emboli, amniotic fluid with debris, air, tumor, foreign bodies, parasites 47.What are causes of anemia? Complications of anemia? Goal in treatment? Reduced number of red blood cells- Can be the result of blood loss (hemorrhagic anemia), hemolysis, bone marrow failure ( aplastic anemia ), renal failure (decreased erythropoietin from kidneys) Low hemoglobin levels- Can be caused by nutritional deficiency as in iron-deficient anemia or pernicious anemia (result of vitamin B12 deficiency) Abnormal hemoglobin- Example – sickle cell anemia Complication- kidney failure, fatigue, hypoxemia, pale, feels cold and reduced metabolic actives, delayed wound healing. Goal in treatment- give oxygen, increase RBC and oxygen carrying capacity.

48.Review the following conditions of the blood including causes: polycythemia, thrombocytopenia, disseminating intravascular coagulation (DIC). How do we treat DIC? Polycythemia - abnormal excess of erythrocytes leading to increased blood viscosity

Thrombocytopenia - low platelet count. Patient has high risk of bleeding. DIC - disseminating intravascular coagulation- using up all the clotting factors and platelets and hence high risk of bleeding. Bleeding and clotting at the same time. Needs transfusion and clotting factors, heparin to break clots. 49.What hormone plays a role in RBC production? What organ produces this hormone? Erythropoietin helps in RBC production and produced by kidneys. That is why patients during kidney failure are anemic as they kidney cannot produce RBC. 50.Review the difference between Hodgkin’s vs Non-Hodgkin’s lymphoma. How are these cancers diagnosed? Diagnose- blood smear or tissue biopsy. Looking for the presence of Reed-Sternberg cells in the blood smear. Hodgins has the cells and Non-Hodgkin’s does not have. 51.Review modifiable versus nonmodifiable risk factors for hypertension. How is hypertension managed/treated? What medications are often prescribed to manage HTN? What are complications of hypertension if left unmanaged? Risk factors- Modifiable- Dietary factors, Sedentary lifestyle, Obesity/weight gain, Metabolic syndrome, Elevated blood glucose levels/diabetes, Elevated total cholesterol, Alcohol and smoking. Nonmodifiable- Family history, Age, Ethnicity/Genetics Manage - reduce salt and fat intake. Educate about need to exercise. Medications to lower blood pressure. -Diuretics – reduce blood volume and Antihypertensives like Beta blockers, ACE inhibitors, Angiotensin II receptor blockers, Calcium channel blockers Complication- higher risk for stroke, risk for kidney and heart failure, hemorrhage, aneurism and can affect vision. 52.Review the steps of the renin-angiotensin-aldosterone system in managing blood pressure. Renin-Angiotensin-Aldosterone System (RAAS) – occurs when arterial blood pressure declines Cells of the kidneys release renin into the blood – triggers production of hormone called

angiotensin I

Angiotensin I converted to Angiotensin II by enzyme called ACE (angiotensin converting enzyme) Angiotensin II is a potent vasoconstrictor – increases blood pressure by increasing peripheral resistance Aldosterone is a mineral corticoid and retains salt, reabsorption of sodium and hence retains water. Blood volume increases and hence blood pressure increases.

53. What is coronary artery disease?

Blockage and obstruction in coronary artery that can cut off the blood supply to the heart muscles. This can occur due to atherosclerosis 54.What is atherosclerosis? How does plaque formation begin? atherosclerosis- buildup of fat or plaque within the blood vessel. Plaque formation begins due to damage to the endothelium. Due to hypertension, bacteria, virus or due to lipids. And hence causes reduction in blood flow through the pipe. 55.Review the difference between stable versus unstable angina Due to plaque when the blood vessels cut blood flow to the heart muscles, the heart muscles cause pain because not enough oxygen and blood flow and the tissue becomes ischemic. Chest pain can be stable or unstable distinguished by periods of relief with rest and nitroglycerin (vasodilator). Stable pain predicted with physical or emotional stress. Unstable is unpredictable and happened with increased intensity and duration. 56.What diagnostic tool is used to identify acute coronary syndrome? 12 lead EKG- to see partial or complete blockage. And continue to monitor. 57.Review the following terms: afterload, preload, cardiac output Afterload - pressure needed to eject the blood from the heart Preload - amount of blood returning to the ventricle Cardiac output - the amount of blood pumped out by each ventricle in 1 minute. 58.Review the differences between left-sided versus right-sided heart failure, know signs/symptoms for each.

Left sided heart failure- blood in left side of the heart is coming from the lungs and hence s/s will be related to the lungs. Crackles sound on auscultation and look blue. Orthopnea or Tripod position. Pulmonary edema. Right side of the heart- peripheral edema (hands and legs) JBD, enlargement of spleen and liver, Asities (fluid in the abdomen). 59.Review the signs and symptoms of shock. Review the causes of different types of shock including anaphylactic shock, cardiogenic shock, hypovolemic shock, obstructive shock, septic shock (distributive shock) hypotension causes shock. Imbalance between oxygen supply and oxygen demand. Great demand but not enough supply. Anaphylactic shock- distributive, bronchoconstriction, angioedema, widespread inflammation due to allergens or antigens. Cardiogenic - problem with the heart. Severe ventricular disfunction, patient with heart failure, MI, or heart attack, portions of the heart is necrotic and ischemic. Heart cannot beat effectively. Hypovolemic - low blood volume- loss of fluid, patient that’s hemorrhaging, faced burns.

obstructive

septic - inflammation due to infection- bacterial, fungal, viral. 60.What are complications of shock? Complication of shock- DIC, bleeding, clotting, renal failure, multiple organ dysfunction, particular with septic shock. 61.What are the stages of hemostasis? What medications can affect hemostasis? Hemostasis- stopping of the bleeding and it involves platelets and the clotting factors. Vascular spasms- constriction of blood vessels to try to stop the blood flow. Platelet plug formation, coagulation. Clot retraction and dissolution (break down of clots). Medications like heparin, luvinox. These medications need to be balanced coz excess can put patients at the risk of bleeding. 62.What is hemophilia? What is the treatment for hemophilia? Hemophilia- genetic bleeding disorder, absence of clotting factor. Give them transfusion of the missing factors depending on the factors that they are missing.