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Review of Knowledge (ROK)
Course NR
Exam Exam 3
Purpose
The Review of Knowledge (ROK) focuses on course outcomes, unit outcomes and key concepts to enhance student success on exams.
Key Concepts Chapters Student Notes
Hyperkalemia
C BIG K DROP
C= calcium gluconate or calcium chloride (cardioprootective)
Chapter 19
Alterations
of
Hormonal
Regulation
Hyperkalemia is a common complication of kidney failure. What does the administration of glucose and regular insulin infusions with sodium bicarbonate do to the potassium level of a patient with hyperkalemia?
- Hyperkalemia is a condition in which the potassium within the body is considered to be very high within the blood. Potassium is considered to be very essential for the body to function especially the muscle and nerve cells. When Sodium bicarbonate, glucose and also insulin is added to the body with a patient who is suffering from hyperkalemia, this will drive potassium intracellularly if the patient is
B= Beta2 agonists or bicarbonate I= insulin G= glucose
K= Kayexhalate
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D= diuretics/dialysis considered to^ be^ acidotic.
- A client with this condition will present symptoms including nausea, arrhythmia, general weakness, muscle fatigue and sometimes paralysis. Potassium play a big role in generation of action potentials. Nervous illness or medication may cause hyperkalemia. Addison’s disease
- Pathophysiology and clinical manifestations)
Chapter (^19) Addison's disease is a caused by primary adrenal insufficiency. Unlike previously stated alterations in secretion, the adrenal medulla is not known to experience hypofunction. Hyperfunction of the adrenal medulla is typically caused by tumors
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surrounding tissue injury
- causes in children: Congenital defects (primary) Parathyroid Dysfunction-
- Hyperparathyroidism (pathophysiology and causative factor
Chapter (^19) hyperparathyroid function is classified as either being primary (problem within the parathyroid gland itself, such as a tumor) or secondary (resulting from chronic hypocalcemia, vitamin D production or absorption or calcium deficiency, or medication side effects).
- Pathologic fractures, kyphosis of the dorsal spine, veterbral compression fractures, abnormal blood and urine levels of calcium and phosphate, and metabolic acidosis are common manifestations of hyperparathyroidism. Diabetes Mellitus (DM)
- Pathophysiology of type I and II (Please note important difference in patho of both types of DM and age of affected individuals)
Chapter (^19) group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both
slow wound healing, decreased blood flow, reduced/loss sensation to lower extremities, blindness, and even amputation.
TYPE 1
Autoimmune T-cell mediated destruction of beta cells; insulin dependent; develops prior to age 30
TYPE 2
Some insulin typically produced; controlled w/ oral agents; abdominal obesity; develops after age 40; not prone to ketosis
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Diabetes Mellitus
- Clinical manifestations and assessment findings
Chapter (^19) These sugar accumulate in the blood and they end up disturbing the acid balance in the blood causing a person to be at risk in having a coma.
Diabetes Mellitus
- Assessment findings in hypoglycemia
Chapter (^19) Another important area to educate our patients is regarding exercise related hypoglycemia. As nurses, it is important to provide education to our patient about the importance of checking their blood sugar, staying hydrated, and eating an appropriate snack before exercising. If the patient is on insulin, an important teaching point in relation to exercise
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Labs for GFR measurement
GFR and normal mean arterial pressure (MAP)
the creatinine clearance test is the most accurate measurement of glomerular filtration rate. This is because creatinine is only filtered by the glomeruli and not reabsorbed by the tubules.
Chapter (^30) Renal blood flow is extremely important in the function of the glomerulus and can impact the glomerular filtration rate
- How does the arterial pressure affect the GFR? What arterial blood flow range can keep the glomerular filtration rate constant?
- The rate at which plasma is filtered is known as the glomerular filtration rate or GFR. Filtration is the process of plasma and water moving from the glomerular capillaries, across the filtration membrane, and into the Bowman’s space. About 20% of the total volume of plasma that flows through the glomerular capillaries is filtered. Filtration involves bulk flow so the concentration is the same in the Bowman’s space as it is in the concentration in
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Mean arterial pressure is a measurement used to determine what the average blood pressure a person has during a complete cardiac cycle. to calculate it you need to know the blood pressure for instance 120/84. you then can use the following formula MAP = 2(diastolic) + Systolic/3. This helps to calculate the overall blood flow. The normal range though is 70 - 105 mmHg with a MAP greater then 105 indicating an increased workload on the heart.
the plasma. Filtration occurs with the high pressure in the glomerular capillaries. The glomerular capillaries lie between two arterioles, the afferent arteriole and the efferent arteriole. Due to the resistance of the efferent arteriole, the pressure is higher than the pressure in a typical capillary. Changes in the systemic blood pressure do not cause changes in pressure in the glomerular capillaries and therefore, there are no changes in the pressure in the glomerular capillaries. In normal healthy people, this does not happen because of renal autoregulation. Renal autoregulation involves feedback mechanisms only found in the kidney that cause either dilation or constriction of the afferent arteriole to counteract blood pressure changes and keep a steady pressure in the glomerular capillaries. So if the arterial pressure increases renal autoregulation causes the afferent arteriole to constrict, and this prevents the pressure increase from being transmitted to the glomerular capillaries, and it also keeps the the GFR from increasing. Renal autoregulation normally keeps pressure in the glomerular capillaries steady over a wide range of blood pressures. However, renal autoregulation is disrupted in chronic kidney disease.
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cannot get out of the kidney due to an obstruction such as a kidney stone
Acute kidney injury is classified as being prerenal, intrarenal, or postrenal. The classification is determined by the location of the injury. Prerenal injury is a result of anything that causes decreased circulating blood volume, which may result in shock (this includes hypovolemia, hypotension, hemorrhage and heart failure). Intrarenal injury occurs within the kidney itself. Conditions that may cause intrarenal injury are infection, tumors, glormerulnephritis, pyelonephritis, acute tubular necrosis (ATN), radiopaque dye, nephrotoxic drugs, coagulation defects and impaired blood flow within the kidneys. Postrenal injury usually results from urinary tract obstruction. This includes renal calculi, prostatic hypertrophy, neurogenic bladder and tumors (inside or outside the urinary tract).
Renal calculi pathophysiology causative factors
Chapter 30
Glomerulonephritis pathophysiology Also review: Types of glomerular lesions and characteristics
Chapter 30 Also review Table 30 - 4
Acute pyelonephritis pathophysiology
Chapter (^30) - patients with cystitis have an inflammation of the bladder. Thank you for also identifying that cystitis affects the lower urinary tract, while pyelonephritis affects the upper tract
- UTI can be divided into two variants. Cystitis are infections in the lower urinary tract particularly the bladder and the urethra. Cystitis is more common in women because of the shorter urethra and the closeness of the urethra to the anus (increasing the possibility of bacterial contamination).
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is the most common site of UTI. Cystitis is commonly caused by Escherichia coli, Staphylococcus saprophyticus, Klebsiella, Proteus, Pseudomonas, fungi, viruses, and parasites like in the case of schistosomiasis. Treatment is usually by antibiotic adminiatration. Pyelonephritis are infections in the upper urinary tract are also called kidney infections. Pyelonephritis may affect both or either of the ureters. The bacteria responsible for this disease are E. coli, Proteus, or Pseudomonas. Treatment is by specific antibiotic therapy
- clinical manifestations of cystitis include slight fever, feeling pressure in the lower abdomen, burning sensation when urinating, persistent urge to urinate, hematuria, passing particulate urine and pelvic discomfort. The clinical manifestations of pyelonephritis include high fever which is usually accompanied by headaches, fatigue loss of appetite, nausea and vomiting. Usually one will experience low back pain and tenderness around the kidney area. Dysuria and Urgency to urinate are apparent. Nephrotic syndrome- pathophysiology Also review nursing interventions including pertinent nursing diagnoses
Chapter 30 - More severe
- Nephrotic syndrome is the expelling of 3.5g/day or more protein in the urine per day (podocytes are lost and can’t keep protein in). The glomerular basement membrane has an interruption and podocyte injury that allows proteins to pass through and a loss of electrical charge. Plasma proteins, albumin (major protein; liver has to compensate = increased lipids), and some immunoglobulins are lost across the glomerular membrane. Edema occurs due to the loss of plasma proteins. Nursing interventions- Peripheral edema is characteristic of nephrotic syndrome, and a key nursing responsibility in the care of patients with the disease is close monitoring of abdominal girth, weights, and extremity size. Diagnoses- 1. Excess fluid volume (The glomerulus is involved in formation of urine, so when glomerular basement membrane is damaged the client sustains extensive urinary protein loss that leads to edema. Patients with nephrotic syndrome are usually
- kidney
- frothy urine
- thrombosis (DVT, PE)
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Pus in urine; bacterial infection
Chapter 36 Alterations^ in^ Digestive^ Function
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Paralytic ileus (pathophysiology)
Chapter 36
Gastroesophageal reflux (pathophysiology, sphincters involved)
Reflux esophagitis
Chapter (^36) Peristaltic movements are important for colon health as it promotes emptying of the colon GERD typically is caused by a malfunctioning lower esophageal sphincter (LES), a ringed muscle that acts as a valve between the esophagus and stomach. Dumping syndrome (pathophysiology)
Chapter 36 Dumping syndrome (after surgery) is a rapid emptying of a large volume of chyme from the stomach component remaining after gastric resection. (Too quickly; not processed before going into small bowel)
- Pain, flushing, diarrhea, dizziness (hormonal release) Pancreatic cancer (pathophysiology and diagnosis)
Chapter 36
Gall Bladder function Chapter^36
Sphincter of Oddi function Chapter 36
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production until the pancreas heals are common treatment modalities.
IBD (Inflammatory Bowel Disease)
- Crohns (pathophysiology, assessment findings, inflammation pattern, skip lesions, treatment)
- Ulcerative Colitis (pathophysiology, assessment findings)
Chapter 36
CHART ON PHONE!
Peptic Ulcer disease
- (pathophysiology, causative organism, complications {including complications in the elderly})
- Gastric (stomach) versus Duodenal ulcers (upper small intestine)
Chapter (^36) - patho= There is a lining in your stomach to help protect it from this acid, but sometimes that lining is damaged by H. pylori and or NSAID's; can cause inflammation in the lining of the stomach which allows the stomach acid to cause ulcers; Endoscopy is used to help with PUD and to stop the bleeding before a person ends up in surgery. With all these complications chronic PUD could lead to stomach cancer.
- complications= bleeding, perforation, penetration, to obstruction; could damage large blood vessels that are deeper in the digestive tract by perforation causing major bleeding in the intestinal tract
- causative organism = h.pylori, NSAIDs, stomach acids
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Esophageal cancer (pathophysiology and causative factors)
Chapter 36
Liver Cirrhosis (Review Types of cirrhosis and causative factors)
Chapter 36
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pattern)
Osteoarthritis
- Pathophysiology and causative factor
- Heberden and Bouchard nodes
Chapter (^39) Osteoarthritis is commonly referred to as a noninflammatory process. The loss of articular cartilage and subsequent alterations in bone anatomy cause pain and difficult mobility. Analgesic and anti-inflammatory medications are used to manage symptoms.
Osteoarthritis commonly effects the area's of the body that are responsible for bearing weight although it can affect any synovial joint. Hips,, knees spine, and hands are the most commonly affected area. Trauma is one of the main causes of Osteoarthritis.
1 Nodes – balls formed near fingertips 2 nodes - cysts Rheumatoid arthritis pathophysiology
Chapter 39 Rheumatoid arthritis is an autoimmune disease associated with genetic predisposition for disease development. The synovial membrane becomes inflamed, leading to joint destruction and alterations. Systemic manifestation of inflammation may include fever, rash, lymph node enlargement, and other indicators of inflammation. Early treatment typically includes administration of disease-modifying antirheumatic drugs.
The immune system see's the tissue in the synovial joints as a foreign body. This causes an immune response. Inflammation occurs within the synovial joints, which causes structural changes to certain proteins. Because of these changes T-cells start the promotion of osteoclast formation. This causes the breakdown of bone.
- Anemia can occur as a result of rheumatoid arthritis. This occurs because of the destruction of the bone itself.
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