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NR507 Final EXAM Study Guide 2024, Exams of Nursing

NR507 Final EXAM Study Guide Lecture notes New Advanced Pathophysiology (NR-507) Family Nurse Practitioner (MSc)Nursing (MSN) AGACNP Track (MSc)Nursing (MSN) Chamberlain University 15 pages 2023/2024

Typology: Exams

2023/2024

Available from 04/09/2024

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FINAL EXAM STUDY GUIDE

Concepts:  Genitourinary disorders  Gastrointestinal disorders  Neurobiological disorders  Endocrine disorders  Neurodegenerative disorders  Demyelinating diseases  Convulsions  Headache syndromes  Cranial nerve disorders  Central nervous system inflammation  Central nervous system ischemia  Dermatologic conditions GENITOURINARY DISORDERS  Acute Renal Failure o Reversible o Prognosis- kidneys respond to diuretic with good output= kidneys are functioning well  Acute Pyelonephritis o Pathophysiology  Bacterial colonization  Adherence and invasion  Inflammation and immune response  Renal injury and complications (upper urinary system) o Assessment  Diagnosing by clinical symptoms alone can be difficult; can be similar to cystitis; pyelonephritis involves the upper tract and cystitis involves the lower tract.  Flank pain, abdominal tenderness, and fever. Systemic signs, such as high fever, chills, and tachycardia, may suggest severe infection. o Diagnosis  Urinalysis: Positive urine culture with significant bacteriuria (>10^5 CFU/mL) and the presence of pyuria (≥10 white blood cells per high-power field) on urinalysis. WBC casts indicates pyelonephritis, but may not always be present  CBC: Complete blood count (CBC) elevated white blood cell count =infection.  Imaging studies: renal ultrasound or computed tomography (CT) scan, can help identify structural abnormalities and complications like abscess formation or obstruction.  Renal Calculi o Pathophysiology  Supersaturation: urine becomes oversaturate with certain substances like calcium  Nucleation: crystals act as nucleation sites, where further crystal deposition can occur.

 Crystal retention: urinary stasis or inadequate urine flow allows crystals to remain in the urinary tract  Stone growth and composition: overtime, crystals accumulate and grow into stones. o Assessment  Medical history: identify risk  Physical exam: flank or abdominal pain; costovertebral angle (CVA) tenderness; hematuria  Imaging studies: crucial for assessing the presence, size, location and composition of the stones- CT scan, renal ultrasound or x-ray  Lab tests: urinalysis (blood, crystals or infection); blood tests evaluate renal function and identify metabolic abnormalities o Treatment  Conservative treatment: for stones <5 mm that are asymptomatic or causing mild symptoms  Medical management: thiazide diuretics or allopurinol can be used for calcium stones or uric acid stones, respectively  Stone removal: larger stones >5 mm or stones causing severe symptoms-lithotripsy.  The goals of treatment:  Manage acute pain  Promote passage of stone  Reduce the size of stone already formed  Prevent new stone formation  Chronic Renal Failure o Review who is a candidate for dialysis o Chronic kidney disease (CKD) is the progressive loss of renal function associated with systemic diseases such as hypertension, diabetes mellitus (most significant risk factor) systemic lupus erythematosus, or intrinsic kidney disease o CKD stage is determined by estimates of GFR and albuminuria. o Review 5 stages of CKD Stage Description eGFR (mL/min) Complications of Decreased GFR 1 There is kidney damage with normal or elevated GFR 90-120  Anemia  Hypertension  Decreased calcium absorption  Hyperlipidemia  Heart failure  Left ventricular hypertrophy  Fluid volume overload  Hyperkalemia 2 There is kidney damage with mild decrease in GFR

60-

3 There is a moderate decrease in GFR 30-

Stage Description eGFR (mL/min) Complications of Decreased GFR  Hyperparathyroidism  Hyperphosphatemia  Metabolic acidosis  Malnutrition (late complication) 4 There is a severe decrease in GFR 15- 5 Kidney failure- End-stage renal disease < (dialysis) o Once Stage IV is reached, progression to Stage V is inevitable as well as dialysis or kidney transplant. o Candidates for Dialysis  Based on symptoms, kidney function, overall health status and individual circumstances  Symptomatic uremia  Fluid overload and hypertension  Hyperkalemia  Acid/base imbalances  Progressive loss of kidney function GASTROINTESTINAL DISORDERS  GERD o Warning signs of GERD include: Symptoms over the age of 50: o Dysphagia (difficulty with swallowing food) o Odynophagia (pain on swallowing) o Nausea and vomiting o Weight loss o Melena o Early satiety (feeling full after eating very little food). o Pathophysiology  Lower esophageal sphincter (LES) dysfunction: reduced pressure or improper relaxation allows gastric acide to flow back into the esophagus  Hiatal hernia: contributes to GERD by disrupting the normal barrier between the esophagus and stomach  Esophageal motility disorders: impaired esophageal peristalsis and reduces esophageal clearance can lead to pooling of gastric acid in the esophagus  Acidic acid contents: Gastric acid, bile acids, and pepsin are the major components of the gastric contents that reflux into the esophagus. These substances can cause direct

mucosal damage and trigger inflammation, leading to the characteristic symptoms of GERD. o Assessment  Subjective: Patients often report symptoms such as heartburn (burning sensation in the chest), regurgitation (acidic taste in the mouth), dysphagia (difficulty swallowing), and chest pain, which may mimic cardiac chest pain.  Objective: The physical examination is usually normal in uncomplicated cases of GERD, although there may be signs of esophagitis or other complications in severe cases.  Diagnostic tests: If symptoms are severe or persistent, additional diagnostic tests may be performed, including upper gastrointestinal endoscopy, esophageal pH monitoring, and esophageal manometry. o Diagnosis  Clinical symptoms  Response to empiric therapy-if pt responds to omeparozole  Diagnostic tests  Upper GI series  Endoscopy  Esophageal manometry o Treatment  Lifestyle modification  Medications  Antacids  H2 receptor antagonists and proton pump inhibitors  Prokinetic agents to improve esophageal motility  Surgery  Hiatal Hernia o Diagnosis  Diaphragmatic weakness  Sliding hiatal hernia  Contributing factors:  Aging  Obesity  Pregnancy  Increased intra-abdominal pressure (chronic coughing or Valsalva maneuver)  Structural abnormalities of the diaphragm o Assessment and Diagnosis  Treat symptoms

 Upper GI Barium swallow or EGD o Treatment  Lifestyle modification  Medications:  Antacids  Prokinetic agents  Surgery  Duodenal Ulcer o Pathophysiology  H. pylori  Gastric acid hypersecretion  Impaired mucosal defense mechanisms  Disruption of the balance between aggressive and defensive factors o Assessment  Medical history  Symptoms:  The characteristic manifestation of a duodenal ulcer is chronic intermittent pain in the epigastric area.  The pain begins 30 minutes to 2 hours after eating, when the stomach is empty.  It is not unusual for pain to occur in the middle of the night and disappear by morning.  Physical exam o Diagnosis  Upper GI endoscopy  H. pylori testing  Imaging studies o Treatment  Medications:  Proton pump inhibitors and H2-receptor blockers  Antibiotics  Antacids and cytoprotective agents  Lifestyle modifications  Follow-up and monitoring  Peptic Ulcer o A peptic ulcer is a break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum. o Least likely to occur in the large intestine

o Pathophysiology  Aggressive factors  H. pylori  Gastric acid hypersecretion  NSAIDS  Lifestyle factors  Protective mechanisms:  Mucus and bicarbonate secretion  Prostaglandins  Mucosal blood flow  Epithelial cell renewal o Assessment and Diagnosis  Medical History  Symptoms  Physical exam o Diagnostic Testing  Endoscopy  H. pylori testing  Imaging studies o Treatment  Medications:  Proton pump inhibitors  Antibiotics  H2-receptor antagonists  Cytoprotective agents  Lifestyle modifications:  Avoidance of NSAIDS  Smoking cessation  Dietary changes  Follow-up and maintenance therapy NEUROBIOLOGICAL DISORDERS  Major Depressive Disorder (MDD) o Neurotransmitter imbalance:  Serotonin  Norepinephrine  Dopamine

o Neuroendocrine dysregulation-abnormalities in the hypothalamic-pituitary-adrenal axis- elevated cortisol levels o Inflammatory processes: chronic inflammation o Neuroplasticity and structural changes o SSRIs are the standard first-line treatment for major depression. o Initial selection of an antidepressant includes:  includes an assessment of the person's symptoms  age  side effects  safety  cost  Social Anxiety Disorder o Key features of social anxiety disorder:  fear and avoidance of social situations.  For example, the anxious person may feel very uncomfortable having a conversation or interacting with others and very conscious of being scrutinized and humiliated or rejected by others.  Review patient exemplars in E-dapt to distinguish among the various anxiety disorders  Schizophrenia o Schizophrenic symptoms are classified into positive, negative, and cognitive categories. o Positive symptoms:  hallucinations, delusions, formal thought disorder, and bizarre behavior. o Negative symptoms:  flattened affect, alogia, anhedonia, attention deficits, and apathy. Cognitive symptoms are the inability to perform daily tasks requiring attention and planning. o Diagnosis  Advanced neuroimaging techniques have revealed structural brain abnormalities in schizophrenia.  A consistent finding is the enlargement of the lateral and third ventricles and the widening of frontocortical fissures and sulci ENDOCRINE  Hypothyroidism o most common disorder of thyroid function o affects between 0.1% and 2% of the U.S. population o is more common in women and the elderly. o Treatment

 Hormone replacement therapy with the hormone levothyroxine is the treatment of choice for hypothyroidism.  Thyroid-Stimulating Hormones o TSH is released by the anterior pituitary o Review the hypothalamic-pituitary axis o Thyroid-releasing hormone (hypothalamus)  Hyperthyroidism-Grave’s Disease o Two categories of ophthalmopathy associated with Grave’s disease are: o (1) functional abnormalitiesresulting from hyperactivity of the sympathetic division of the autonomic nervous system (lag of the globe on upward gaze or a lag of the upper lid on downward gaze) o (2) infiltrative changesinvolving the orbital contents with enlargement of the ocular muscles. These changes affect more than half of individuals with Graves’ disease. Increased secretion of hyaluronic acid, adipogenesis, inflammation, and edema of the orbital contents result in exophthalmos (protrusion of the eyeball), periorbital edema, and extraocular muscle weakness leading to strabismus and diplopia (double vision). o The two most distinguishing factors of Grave's disease is pretibial myxedema and exophthalmos. o Treatment:  Treatment is directed at controlling excessive TH production, secretion, or action and includes antithyroid drug therapy (methimazole or propylthiouracil), radioactive iodine therapy (absorbed only by thyroid tissue, causing death of cells), and surgery.  The goal of radioactive iodine ablation for the treatment of Grave's disease is to destroy overactive thyroid tissue  Type 1 Diabetes o Environmental factors associated with Type 1 diabetes:  Viral infections, particularly enteroviruses, coxsackievirus, other infectious microorganisms  H. pylori  exposure to cow's milk proteins;  lack of vitamin D o Diagnostic Criteria:  Hemoglobin A1C greater than or equal to 6.5% o Actions of Insulin  insulin promotes glucose uptake mostly in the liver, muscle and adipose tissue  Autonomic Neuropathy-complication of diabetes o Autonomic neuropathy includes:

o gastrointestinal symptoms:  decreased esophageal motility,  gastroparesis  delayed gastric emptying  Hypoglycemia o Neurogenic reactions occur when the decrease in blood glucose level is rapid and presents with:  Tachycardia  Palpitations  Diaphoresis  Tremors  Pallor  Arousal anxiety  Hyperparathyroidism o Primary hyperparathyroidism-usually caused by parathyroid gland tumor.  hypercalcemia o Secondary hyperparathyroidism is increased PTH secretion in response to hypocalcemia  Is usually caused by CKD  As PTH increases, it can lead to hypercalcemia  Hypercalcemia o Hypercalcemia and hypophosphatemia (also due to increased PTH) may be asymptomatic or affected individuals may present with symptoms related to the neuromuscular changes that include paresthesia and muscle cramps o Patients with hypercalcemia can have low bone density (osteoporosis) that is most noted in the distal one-third of the radius o Other issues: kidney stones, pathological fractures, ventricular hypertrophy, depression, gastric issues  Hypoparathyroidism o Hypomagnesemia inhibits PTH secretion. o Hypomagnesemia may be related to chronic alcoholism, malnutrition, malabsorption, increased renal clearance of magnesium caused by the use of aminoglycoside antibiotics or certain chemotherapeutic agents, or prolonged magnesium-deficient parenteral nutritional therapy.  Hypocalcemia o Symptoms of hypocalcemia include:  Dry skin  Loss of body and scalp hair  Hypoplasia of developing teeth

 Horizontal ridges on the nails  Cataracts  Basal ganglia calcifications  Bone deformities  Bowing of the long bones  Hypocortisolism o Pathophysiology  Adrenal tumors  Produces cortisol independent of the normal regulatory mechanisms of the HPA axis  Suppression of ACTH: due to high cortisol levels that exert negative feedback on the pituitary gland and hypothalamus which inhibits secretion of ACTH  Pituitary tumors (Cushing’s disease): hypercortisolism caused by a pituitary tumor that secretes excess ACTH o Glucose intolerance is associated with hypercortisolism; o Glucose intolerance occurs because of cortisol-induced insulin resistance and increased gluconeogenesis and glycogen storage by the liver. o Cushing's syndrome is characterized by patterns of fat deposition have been described as “truncal [central] obesity,” “moon face,” and “buffalo hump o Adrenal Crisis  Insufficient cortisol production  Lack of aldosterone  Stress response failure  Fluid and electrolyte imbalances  Adrenal crisis triggers:  Infection  Surgery  Trauma  Sudden discontinuation of corticosteroid therapy o Adrenal Crisis-Hhyporcortisolism  Onset of adrenal crisis is signified by hypotension  Hypotension can progress to complete vascular collapse and shock. This is known as adrenal crisis or addisonian crisis, and develops with undiagnosed disease, acute withdrawal of glucocorticoid therapy, or the occurrence of infection or other comorbid stressful events o Primary Hypocortisolism-Adrenal Insufficiency  Lab work that indicates primary hypocortisolism: