{"id":111026,"date":"2023-07-28T18:56:57","date_gmt":"2023-07-28T18:56:57","guid":{"rendered":"https:\/\/learnexams.com\/blog\/?p=111026"},"modified":"2023-07-28T18:57:06","modified_gmt":"2023-07-28T18:57:06","slug":"nur-2063-exam-3-nur2063-essentials-of-pathophysiology-exam-3-latest-2023-real-exam-100-questions-and-correct-answers-rasmussen-agrade","status":"publish","type":"post","link":"https:\/\/www.learnexams.com\/blog\/2023\/07\/28\/nur-2063-exam-3-nur2063-essentials-of-pathophysiology-exam-3-latest-2023-real-exam-100-questions-and-correct-answers-rasmussen-agrade\/","title":{"rendered":"NUR 2063 EXAM 3\/NUR2063 ESSENTIALS OF PATHOPHYSIOLOGY EXAM 3 LATEST 2023 REAL EXAM 100+ QUESTIONS AND CORRECT ANSWERS RASMUSSEN |AGRADE"},"content":{"rendered":"\n

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pathophysiology exam 1 rasmussen test bank<\/p>\n\n\n\n

Physiology reactions during “Fight or Flight”<\/a><\/p>\n\n\n\n

– increased heart rate (tachycardia)
– anxiety
– sweating
– tremor
– increased blood glucose concentrations (due to glycogenolysis, or breakdown of liver glycogen).<\/a><\/p>\n\n\n\n

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Define Ventilation<\/a><\/p>\n\n\n\n

movement of air into and out of the lungs artificially<\/a><\/p>\n\n\n\n

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Causes of Edema<\/a><\/p>\n\n\n\n

– increased capillary hydrostatic pressure
– loss of plasma proteins (decreased capillary oncotic pressure)
– obstruction of lymphatic circulation
– increased capillary permeability<\/a><\/p>\n\n\n\n

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Define sign and how it’s used in diagnosis<\/a><\/p>\n\n\n\n

What can be seen or measured<\/a><\/p>\n\n\n\n

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Define symptom and how it’s used in diagnosis<\/a><\/p>\n\n\n\n

What the patient describes that is not visible to the healthcare practitioner<\/a><\/p>\n\n\n\n

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Define subjective data and how it’s used in diagnosis<\/a><\/p>\n\n\n\n

Information from the client’s point of view (“symptoms”), including feelings, perceptions, and concerns obtained through interviews.<\/a><\/p>\n\n\n\n

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Define contraindication and how it’s used in diagnosis<\/a><\/p>\n\n\n\n

A specific situation in which a drug, procedure, or surgery should not be used because it may be harmful to the person (Allergy to penicillin)<\/a><\/p>\n\n\n\n

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Know electrolytes that are higher in intracellular fluid<\/a><\/p>\n\n\n\n

Potassium (K+)
Phosphorus (PO4-)
Sulfate (SO4-)<\/a><\/p>\n\n\n\n

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Know clinical manifestation of appendicitis and how to identify it<\/a><\/p>\n\n\n\n

– Manifestations vary significantly in severity, from asymptomatic to sudden and severe.
– Pain near the umbilicus and McBurney point.
– The pain will temporarily subside if the appendix ruptures but then will return and escalate as peritonitis develops.
– Anorexia, nausea, vomiting, abdominal distention, and bowel pattern changes can also be associated with appendicitis. Fever, chills, and leukocytosis
– Monitored for signs and symptoms of peritonitis (e.g., abdominal rigidity, tachycardia, and hypotension).
Diagnostic procedures: history, physical examination, CBC, abdominal ultrasound, abdominal X-ray, abdominal CT, and laparoscopy.<\/p>\n\n\n\n

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Know clinical manifestation of peptic ulcer disease and how to identify it<\/a><\/p>\n\n\n\n

– Some are asymptomatic
– Dull, gnawing pain, burning sensation in back or low mid epigastric are, heartburn, constipation or diarrhea, sour taste in the mouth, burping, n\/v, bloating, urea present in breath, tarry stools<\/a><\/p>\n\n\n\n

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Know steps of laceration correction and what end goal is<\/a><\/p>\n\n\n\n

– Closing a wound or laceration by placing sutures or stitches or staples in the skin to hold the edges of the wound together for proper healing.
– To stop bleeding, prevent infection, speed healing, and preserve the appearance and function of the injured area.<\/a><\/p>\n\n\n\n

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Know clinical manifestations of ARF; high and low levels of what is in the lungs<\/a><\/p>\n\n\n\n

– A sudden inability of the respiratory system to provide O2 and\/or remove CO2 from the blood<\/a><\/p>\n\n\n\n

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Know cause of pulmonary embolism<\/a><\/p>\n\n\n\n

– occlusion in the pulmonary circulation, most often caused by a blood clot
– Pt. dehydrated, venous stasis from immobility, surgery or on birth control, clotting disorder, or heart arrhythmias like A-fib.<\/a><\/p>\n\n\n\n

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Know tool used to determine level of consciousness<\/a><\/p>\n\n\n\n

– A measurement of a person’s arousability and responsiveness to a stimulus.
– Glascow Coma Scale (GCS)
– Neurologic assessment of a patient’s best verbal response, eye opening, and motor function.<\/a><\/p>\n\n\n\n

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Define cystitis<\/a><\/p>\n\n\n\n

– Inflammation of the urinary bladder.
– It is often caused by infection and is usually accompanied by frequent, painful urination.<\/a><\/p>\n\n\n\n

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Define pyelonephritis<\/a><\/p>\n\n\n\n

– Inflammation of the kidney and renal pelvis due to bacteria.<\/a><\/p>\n\n\n\n

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Know outcome of imbalance in PTH when high? low?<\/a><\/p>\n\n\n\n

– This hormone helps regulate calcium levels in the blood. When calcium levels are low, the parathyroid glands increase PTH production. When calcium levels are high, the glands slow down the secretion of PTH.<\/a><\/p>\n\n\n\n

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Know outcome of imbalance in ADH when high? low?<\/a><\/p>\n\n\n\n

– Antidiuretic hormone. Low levels of anti-diuretic hormone will cause the kidneys to excrete too much water. A high ADH level causes the body to produce less urine. A low level results in greater urine production.<\/a><\/p>\n\n\n\n

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Know outcome of imbalance in Calcitonin when high? low?<\/a><\/p>\n\n\n\n

– A lack of calcitonin in the blood may increase a person’s risk of bone degradation and osteopenia,The overall effect of calcitonin is to lower the concentration of calcium in the blood when it rises above the normal value.<\/a><\/p>\n\n\n\n

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Know phases of acute kidney injury<\/a><\/p>\n\n\n\n

– Oliguric
– Diuretic
– Chronic<\/a><\/p>\n\n\n\n

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Know common findings of ARDS<\/a><\/p>\n\n\n\n

PCWP <18, CXR with bilateral pulmonary infiltrates, PaCO2:FiO2 ratio <200<\/a><\/p>\n\n\n\n

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Know clinical manifestations of left-sided heart failure<\/a><\/p>\n\n\n\n

1. Pnea, SOB
2. Crackles
3. Oliguria
4. Frothy Sputum
5. Displaced Apical Pulse (Hypertrophy)<\/a><\/p>\n\n\n\n

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Know pathophysiology of multiple sclerosis<\/a><\/p>\n\n\n\n

– Disease of the central nervous system characterized by the demyelination (deterioration of the myelin sheath) of nerve fibers, with episodes of neurologic dysfunction (exacerbation) followed by recovery (remission)<\/a><\/p>\n\n\n\n

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Define homeostasis<\/a><\/p>\n\n\n\n

– The maintenance of a constant internal environment within the body; it’s a dynamic equilibrium.<\/a><\/p>\n\n\n\n

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Define diffusion<\/a><\/p>\n\n\n\n

– Movement of molecules from an area of high concentration to an area of low concentration<\/a><\/p>\n\n\n\n

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Define osmosis<\/a><\/p>\n\n\n\n

– Diffusion of water through a selectively permeable membrane<\/a><\/p>\n\n\n\n

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Know Gigantism and causes<\/a><\/p>\n\n\n\n

– Growth Hormone hypersecretion in children<\/a><\/p>\n\n\n\n

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Know Acromegaly and causes<\/a><\/p>\n\n\n\n

– Excessive secretion of growth hormones in adults.<\/a><\/p>\n\n\n\n

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Know Dwarfism and causes<\/a><\/p>\n\n\n\n

– A condition caused by insufficient growth hormone in childhood<\/a><\/p>\n\n\n\n

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Know clinical manifestation of anaphylaxis<\/a><\/p>\n\n\n\n

– A severe response to an allergen in which the symptoms develop quickly, and without help, the patient can die within a few minutes.<\/a><\/p>\n\n\n\n

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Know presentation of liver disease<\/a><\/p>\n\n\n\n

1.) Changes in mentation are the first clinical signs. Cerebral edema, encephalopathy
2.) Jaundice
3.) Coagulation abnormalities
4.) Metabolic Acidosis
5.) Renal failure
6.) Multi-organ Failure<\/a><\/p>\n\n\n\n

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Know signs and symptoms of asthma<\/a><\/p>\n\n\n\n

coughing, wheezing, SOB, tachycardia, hypoxia, and Respiratory alkalosis or acidosis (hyperventilation or hypoventilation respectively)<\/a><\/p>\n\n\n\n

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Know what causes atherosclerosis plaques in the body<\/a><\/p>\n\n\n\n

– uncertain, believed to be related to injury to the endothelial lining
– condition in which fatty deposits called plaque build up on the inner walls of the arteries<\/a><\/p>\n\n\n\n

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Know what backwards effect of right-sided heart failure is<\/a><\/p>\n\n\n\n

1. Jugular Vein Distention
2. Ascending Dependent Edema
3. Weight Gain
4. Hepatomegaly (Liver Enlargement)<\/a><\/p>\n\n\n\n

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Know what causes barrel chest in emphysema<\/a><\/p>\n\n\n\n

– It occurs because the lungs are chronically overinflated with air, so the rib cage stays partially expanded all the time.<\/a><\/p>\n\n\n\n

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Know signs and symptoms of myocardial infraction<\/a><\/p>\n\n\n\n

– Heart attack; death of myocardial tissue (infarction) caused by ischemia (loss of blood flow) as a result of an occlusion (plugging) of a coronary artery; usually caused by atherosclerosis; symptoms include pain in the chest or upper body (shoulders, neck, and jaw), shortness of breath, diaphoresis, and nausea<\/a><\/p>\n\n\n\n

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Know symptoms of COPD<\/a><\/p>\n\n\n\n

– Chronic cough, excessive sputum production, wheezing, dyspnea, poor exercise tolerance<\/a><\/p>\n\n\n\n

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Know clinical manifestations of hyperthyroidism<\/a><\/p>\n\n\n\n

– Heat intolerance, weight loss, sweating, anxiety, irritability, hyperactive reflexes, palpitations, EXOPTHALMOS (lid lag when gaze moves from downward to upward)<\/a><\/p>\n\n\n\n

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Know complications of compartment syndrome<\/a><\/p>\n\n\n\n

– Rhabdomyolysis with AKI (due to myoglobinuria)- volksmanns ischemic contracture (necrosis followed by secondary fibrosis with calcification)<\/a><\/p>\n\n\n\n

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Define rheumatoid arthritis<\/a><\/p>\n\n\n\n

– Chronic inflammatory disease, the most serious and crippling form of arthritis.
– Systemic, autoimmune disease
– Arises from immune system malfunction, immune system mistakenly attacks bone coverings as if they were foreign tissue<\/a><\/p>\n\n\n\n

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Know causes of contact dermatitis<\/a><\/p>\n\n\n\n

– Contact with a skin allergen<\/a><\/p>\n\n\n\n

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Know the characteristics of coronary artery disease<\/a><\/p>\n\n\n\n

– Atherosclerosis of the coronary arteries that reduces the blood supply to the heart muscle
– Chest pain or discomfort (angina)Weakness, light-headedness, nausea (feeling sick to your stomach), or a cold sweat. Pain or discomfort in the arms or shoulder. Shortness of breath<\/a><\/p>\n\n\n\n

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Define Cushing’s syndrome and know presentation<\/a><\/p>\n\n\n\n

– A condition caused by prolonged exposure to high levels of cortisol

– Fatty hump between shoulders a rounded face, and pink purple stretch marks on skin, thinning fragile skin, slow healing of cuts, insect bites and infections, acne, decreased libido, decreased fertility, irregular or absent menstrual periods, fatigue, muscle weakness, cognitive difficulties, and headaches.<\/p>\n\n\n\n

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Know goal of treating anemia<\/a><\/p>\n\n\n\n

– To restore the hemodynamics of the vascular systems and to replace lost red blood cells.<\/a><\/p>\n\n\n\n

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Know presentation of cystic fibrosis<\/a><\/p>\n\n\n\n

1. Chronic lung disease (cough, sputum, hemoptysis, bronchiectasis, wheezing, dyspnea)
2. Recurrent episodes of infection
3. Sinus pain and polyps common<\/a><\/p>\n\n\n\n

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Know what happens in cerebral palsy patients and why it occurs<\/a><\/p>\n\n\n\n

– Paralysis caused by damage to the area of the brain responsible for movement<\/a><\/p>\n\n\n\n

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Know pathophysiology for type 1 diabetes<\/a><\/p>\n\n\n\n

– Diabetes caused by a total lack of insulin production; usually develops in childhood, and patients require insulin replacement therapy to control the disorder<\/a><\/p>\n\n\n\n

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Know characteristics of DIC<\/a><\/p>\n\n\n\n

– Bleeding, from many sites in the body. Blood clots. Bruising. Drop in blood pressure. Shortness of breath. Confusion, memory loss or change of behavior. Fever.

– The condition affects the blood’s ability to clot and stop bleeding. Life-threatening disorder.<\/a><\/p>\n\n\n\n

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What is used to identify a Myocardial Infarction in a patient?<\/a><\/p>\n\n\n\n

– Cardiac Troponin<\/a><\/p>\n\n\n\n

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Know presentation for Parkinson’s disease<\/a><\/p>\n\n\n\n

-Begins insidiously with a resting “pill-rolling” tremor of one hand
-Cardinal signs include tremor, rigidity, resistance to passive motion that is not velocity dependent (cogwheel or lead pipe), akinesia, postural instability, festinating gait, falling backwards (retropulsion) or forwards (propulsion), mask face, micrographia<\/a><\/p>\n\n\n\n

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Know which organs are involved in developing esophageal varices<\/a><\/p>\n\n\n\n

– Swollen, twisted veins in the esophagus that are especially susceptible to ulceration and hemorrhage. throat and stomach (esophagus).<\/a><\/p>\n\n\n\n

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Know which hormones raises blood sugar<\/a><\/p>\n\n\n\n

– glucagon<\/a><\/p>\n\n\n\n

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Know pathophysiology of exercise-induced asthma<\/a><\/p>\n\n\n\n

– A medical condition characterized by shortness of breath induced by sustained aerobic exercise<\/a><\/p>\n\n\n\n

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Know outcomes of gout<\/a><\/p>\n\n\n\n

– Permanent joint damage. Some people with gout can also develop other health problems, such as severe arthritis, kidney stones and heart disease.<\/a><\/p>\n\n\n\n

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Know what causes peptic ulcers<\/a><\/p>\n\n\n\n

family history of PUD
blood group type O
cigarette smoking
intake of foods and beverages containing caffeine
chronic aspirin and NSAID use**
stress
H. pylori infection**<\/a><\/p>\n\n\n\n

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Know what causes hepatic encephalopathy<\/a><\/p>\n\n\n\n

1. GI bleeding
2. Hypokalemia (think loop diuretics)
3. Hypovolemia
4. Hypoxia
5. Sedatives or tranquilizers
6. Hypoglycemia
7. Metabolic alkalosis
8. Infection (including SBP)<\/a><\/p>\n\n\n\n

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HPV causes which type of cancer?<\/a><\/p>\n\n\n\n

– Cervical cancer<\/a><\/p>\n\n\n\n

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Know cause of diabetic ketoacidosis and disease it is associated with<\/a><\/p>\n\n\n\n

– Profound deficiency of insulin
– Type 1 diabetes<\/a><\/p>\n\n\n\n

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Define modifiable risk factors<\/a><\/p>\n\n\n\n

Can be reduced; smoking, diabetes, obesity, elevated serum lipids, hypertension, sedentary lifestyle<\/a><\/p>\n\n\n\n

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Define nonmodifiable risk factors<\/a><\/p>\n\n\n\n

– Age, gender, race, family history<\/a><\/p>\n\n\n\n

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Know outcomes of hyponatremia<\/a><\/p>\n\n\n\n

– Cells swell because electrolyte concentration is higher inside than outside. Can produce CNS dysfunction and cerebral edema which is life threatening.
sodium levels drop rapidly \u2014 resulting in potentially dangerous effects, such as rapid brain swelling, which can result in a coma and death<\/a><\/p>\n\n\n\n

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Define hypovolemia<\/a><\/p>\n\n\n\n

– Decreased blood volume<\/a><\/p>\n\n\n\n

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Know ranges of a normal ABG<\/a><\/p>\n\n\n\n

pH: 7.35 – 7.45
PaCO2: 35 -45
HCO3 (bicarb): 22 – 26<\/a><\/p>\n\n\n\n

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Define passive immunity<\/a><\/p>\n\n\n\n

– The short-term immunity that results from the introduction of antibodies from another person or animal. A newborn baby acquires passive immunity from its mother through breast milk<\/a><\/p>\n\n\n\n

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Know what causes increased intracranial pressure<\/a><\/p>\n\n\n\n

– bleeding in the brain
– a tumor
– stroke
– aneurysm
– high blood pressure
– brain infection<\/a><\/p>\n\n\n\n

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What hormone decreases blood glucose and helps cells take up glucose?<\/a><\/p>\n\n\n\n

– Insulin<\/a><\/p>\n\n\n\n

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Know clinical manifestations of leukemia<\/a><\/p>\n\n\n\n

– Pallor, fatigue, purpura, fever<\/a><\/p>\n\n\n\n

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Know how to identify kidney disease<\/a><\/p>\n\n\n\n

– Common symptoms include nausea and loss of appetite, itching and dry skin, and numbness in the hands, blood in urine(hematuria) Patients may experience excessive thirst and breath malodor.<\/a><\/p>\n\n\n\n

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Know risk factors for hypertension<\/a><\/p>\n\n\n\n

– Non-Modifiable: Family history, age, gender, ethnicity [african american; male]<\/strong>Modifiable: Obesity, substance abuse, stress, diet, and sedentary lifestyle-Tobacco damages the lining of the artery walls, prone to plaque accumulation.-Nicotine constricts the blood vessels, elevate HR and BP.<\/a><\/p>\n\n\n\n

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Define intussusception<\/a><\/p>\n\n\n\n

– Telescoping of a segment of the intestine<\/a><\/p>\n\n\n\n

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Know causes of spinal cord injury<\/a><\/p>\n\n\n\n

– Trauma
– Slipped disk
– Infection
– Tumour growth
– Ischaemia\/infarction
– Sport injuries<\/a><\/p>\n\n\n\n

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Define meningitis<\/a><\/p>\n\n\n\n

– An inflammation of the meninges (membrane covering the brain) due to bacteria, viruses, yeast, fungus, toxins, or meningeal irritation resulting from other causations; bacterial from used to be the most common; however, with the advent of HIB and pneumococcal vaccines, the viral form may now be the most prevalent form.<\/a><\/p>\n\n\n\n

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Know properties of metastatic cancer<\/a><\/p>\n\n\n\n

– Cancer that has spread from the place where it first started to another place in the body<\/a><\/p>\n\n\n\n

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Know causes of cardiogenic shock<\/a><\/p>\n\n\n\n

– inadequate heart function
– the disease of muscle tissue
– impaired electrical system
– disease or injury<\/a><\/p>\n\n\n\n

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Know etiology of a Cerebral vascular accident<\/a><\/p>\n\n\n\n

– Stroke refers to an interruption of the cerebral arterial blood supply. A CVA is an infarction of the brain, so it is often referred to as a brain attack.<\/a><\/p>\n\n\n\n

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Know organs affected by hypertension<\/a><\/p>\n\n\n\n

– Brain
– Kidneys
– Eyes
– does not affect liver<\/a><\/p>\n\n\n\n

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Know causes of osteoporosis<\/a><\/p>\n\n\n\n

– Corticosteroids, heparin pharmacology reactions
a condition characterized by a progressive loss of bone calcium that leaves the bones brittle<\/a><\/p>\n\n\n\n

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Know risk factors for pneumonia<\/a><\/p>\n\n\n\n

– Advanced age
– Lung disease
– Smoking
– Immunosuppressed
– Bed ridden
– Post- Op<\/a><\/p>\n\n\n\n

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Define polycythemia<\/a><\/p>\n\n\n\n

– Increased RBCs ; red blood cells (high hematocrit)<\/a><\/p>\n\n\n\n

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Know clinical findings of shock<\/a><\/p>\n\n\n\n

-Tachycardia, tachypnea
-Cool, clammy extremities; peripheral pulses
-Decreased arterial BP (decompensation)
-Cyanosis and\/or pallor
-Restlessness, apprehension, decreased mental function
-Poor urinary output<\/a><\/p>\n\n\n\n

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Define tension pneumothorax and know interventions<\/a><\/p>\n\n\n\n

– A type of pneumothorax in which air that enters the chest cavity is prevented from escaping

– Immediate needle aspiration (14-16-gauge needle) 2nd ICS, MCL; Do not wait for CXR<\/a><\/p>\n\n\n\n

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Know cause of secondary brain injury after trauma<\/a><\/p>\n\n\n\n

– The “after effects” of the primary injury; includes abnormal processes such as cerebral edema, increased intracranial pressure, cerebral ischemia and hypoxia, and infection; onset is often delayed following the primary brain injury.

– Impairment or local declines in cerebral blood flow (CBF)
– Causes of secondary brain injury include hematoma, contusion, diffuse brain swelling, systemic shock and intracranial infection.<\/p>\n\n\n\n

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Define generalized seizures, know hemisphere<\/a><\/p>\n\n\n\n

– Seizures that involve the entire brain
Hemispheres of the brain
– The human brain is divided into two halves called the left and right hemispheres<\/a><\/p>\n\n\n\n

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Define sepsis<\/a><\/p>\n\n\n\n

– A toxic (life-threatening) inflammatory condition arising from the spread of microbes, especially bacteria or their toxins, from a response of infection.<\/a><\/p>\n\n\n\n

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Bone stores electrolytes and acts as an electrolyte pool<\/a><\/p>\n\n\n\n

Know this.<\/a><\/p>\n\n\n\n

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Know what lateral scoliosis looks like on x-ray<\/a><\/p>\n\n\n\n

– Sideways curvature of vertebrae<\/a><\/p>\n\n\n\n

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Define stress incontinence<\/a><\/p>\n\n\n\n

The leak of urine with an increase in abd pressure (cough, sneeze)
Unique to women
No nocturnal urine leak
Loss of urine < 50 mL. Occurs with increased intra-abdominal pressure (coughing, sneezing, laughing, lifting).<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Best was to prevent transmission of infectious agents<\/a><\/p>\n\n\n\n

– Washing hands with plain soap and water<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Know what patient with hypoventilation looks like<\/a><\/p>\n\n\n\n

– Decreased rate or depth of air movement into the lungs<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Decreased cardiac output is the common finding of all forms of heart failure<\/a><\/p>\n\n\n\n

know this.<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Know key marker of Hodgkin disease<\/a><\/p>\n\n\n\n

– CD30 antigen, a marker for Hodgkin’s lymphoma, is a receptor whose ligand defines an emerging family of cytokines with homology to TNF.<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Know clinical manifestations of septic shock<\/a><\/p>\n\n\n\n

-Fever
-Warm, flushed skin
-Abrupt personality changes
-Hypotension
-Oliguria
-Lactic acidosis<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

CT is the goal standard to diagnose ischemic\/hemorrhagic shock<\/a><\/p>\n\n\n\n

know this.<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Kidneys secrete this to increase RBC production<\/a><\/p>\n\n\n\n

– Erythropoietin (EPO)<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

The main functional process of the endocrine system is_______<\/a><\/p>\n\n\n\n

– To secrete hormones that coordinate and direct target cells and organs<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Know presentation for thrombocytopenia<\/a><\/p>\n\n\n\n

– A condition in which there is an abnormally small number of platelets circulating in the blood

– Easy or excessive bruising (purpura) Superficial bleeding into the skin that appears as a rash of pinpoint-sized reddish-purple spots (petechiae), usually on the lower legs. Prolonged bleeding from cuts.<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Know how mycobacterium tuberculosis is transmitted<\/a><\/p>\n\n\n\n

– spread by droplet nucle
i- immune system usually prevents spread
– bacteria can remain alive in the lungs for many years (latent TB infection)<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Know function of ribosomes<\/a><\/p>\n\n\n\n

– Protein synthesis<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

What is the best way to prevent spinal cord injuries?<\/a><\/p>\n\n\n\n

Driving defensively and using seat belts.
Follow sports safety guidelines for children, adolescents and adults.
Jumping rather than diving, into water.
Limiting use of medicines that lower blood-clotting ability, such as aspirin.
Don’t drive after drinking alcohol.<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Know treatment for hemophilia A<\/a><\/p>\n\n\n\n

– Clotting factor transfusions, recombinant clotting factors, desmopressin (DDAVP), and bleed precautions

– Hemophilia A is a hereditary bleeding disorder caused by a lack of blood clotting factor VIII.<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Know clinical manifestations for sickle cell crisis<\/a><\/p>\n\n\n\n

– Unexplained episodes of severe pain, such as pain in the abdomen, chest, bones or joints. Swelling in the hands or feet. Abdominal swelling, especially if the area is tender to the touch.<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Define unstable angina pectoris<\/a><\/p>\n\n\n\n

– Prolonged, worsening chest pain occurs without exertion, not relieved by rest or nitroglycerin.<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Define stable angina pectoris<\/a><\/p>\n\n\n\n

– Type of cardiac chest pain that is a result of ischemia that is initiated by increased demand (activity) and relieved with the reduction of that demand (rest).<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Virchow’s triad includes<\/a><\/p>\n\n\n\n

– The three factors of Virchow’s triad include intravascular vessel wall damage, stasis of flow, and the presence of a hypercoagulable state<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Why is dialysis necessary for end-stage renal disease?<\/a><\/p>\n\n\n\n

– With end-stage renal disease, you need dialysis or a kidney transplant to stay alive<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Define reperfusion injury<\/a><\/p>\n\n\n\n

– Injury to tissue that occurs after blood flow is restored<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Altered LOCs is the most sensitive indicator of altered brain function<\/a><\/p>\n\n\n\n

know this.<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Define renin and what it used for, what it does<\/a><\/p>\n\n\n\n

– Hormone secreted by the kidney that raises blood pressure<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

DIC is a severe complication of what?<\/a><\/p>\n\n\n\n

– Sepsis<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

What results in prerenal kidney injury?<\/a><\/p>\n\n\n\n

– Characterized by low GFR, oliguria, high urine specific gravity and osmolality, and low urine sodium<\/a><\/p>\n\n\n\n

\"Image:<\/figure>\n\n\n\n

Flickr Creative Commons Images<\/h4>\n\n\n\n

Some images used in this set are licensed under the Creative Commons through\u00a0Flickr.com<\/a>.<\/p>\n\n\n\n

Explain primary prevention
Preventing”; altering susceptibility or reducing exposure of disease for people<\/p>\n\n\n\n

Explain secondary prevention
“Screening”; early detection, screening, and management of disease to catch disease early before it spreads<\/p>\n\n\n\n

Explain tertiary prevention
“Treating” and preventing further complications from a disorder or disease after the person has the condition<\/p>\n\n\n\n

What are examples of primary prevention?
Vaccinations and Handwashing<\/p>\n\n\n\n

What are examples of secondary prevention?
PAP smears for STDs, lab work for HBA1C check, mammogram<\/p>\n\n\n\n

What are examples of tertiary prevention?
Rehab for hip surgery, relearning ADL’s after amputation, Wound care after stroke to prevent pressure ulcer<\/p>\n\n\n\n

What happens to the body during the sympathetic phase of the flight or fight response?
Pupils dilate, salivation inhibited, increase in HR, bronchodilation of airway, increased respirations, glucose release, inhibit GI\/GU.<\/p>\n\n\n\n

What happens to the body during the parasympathetic phase of the flight or light response?
Rest and Digest. Pupils constrict, salivation occurs, decreased HR, bronchoconstriction,decreased respiration, GI\/GU systems resume action<\/p>\n\n\n\n

Explain the role of the nucleus
control center of the cell, where DNA and genes are stored, produces mRNA to help build body proteins<\/p>\n\n\n\n

Explain the role of the mitochondria
Powerhouse of the cell. Provides energy in ATP, and has its own set of DNA<\/p>\n\n\n\n

Explain the role of the ribosome
produces RNA to produce proteins through transcriptions of DNA and translation of RNA into a protein<\/p>\n\n\n\n

Explain the role of the lysosomes
helps breakdown and digest dead cells, organelles, or tissues<\/p>\n\n\n\n

Explain the role of the rough ER
folded membranes that move proteins around the cell. Has ribosomes attached to it and helps produce proteins for the cell membrane<\/p>\n\n\n\n

Explain the role of the smooth ER
helps the Liver and kidney cells to detoxify, lipid metabolism, synthesis of hormones, and calcium storage<\/p>\n\n\n\n

Explain the role of the peroxisome
membrane cells that contain oxidase and catalase to detoxify harmful chemicals, breakdown hydrogen peroxide and filter metabolic wastes<\/p>\n\n\n\n

Explain the role of the Golgi body
stacked membranes that act as the sorter and packager for proteins from the ER. Helps move things in and out of cell<\/p>\n\n\n\n

Explain passive immunity
the transfer of preformed antibodies against specific antigens from a protected or immunized individual to an unprotected or non immunized person. Provides immediate and short term protection. No memory cells are produced. IgA and IgE. Passes protection<\/p>\n\n\n\n

What are examples of passive immunity?
mom to fetus through placenta or mom to infant through breast milk. Serotherapy<\/p>\n\n\n\n

Explain active immunity
a protective state owing to the immune system response as a result of active infection or immunization. It has to be activated in the body and the body has to fight it to have long term immunity<\/p>\n\n\n\n

What are examples of active immunity?
Vaccinations<\/p>\n\n\n\n

Explain what edema is
accumulation of fluid in the interstitial space. Leads to tissue swelling<\/p>\n\n\n\n

What are some causes of edema?
increase in the forces that move fluid from capillaries to interstitial compartments or decrease in the opposite.<\/p>\n\n\n\n

What are factors that contribute to edema?
Increase in hydrostatic forces in the capillaries that increases the blood volume, increased capillary permeability, CHF, HYPTN, decrease in plasma proteins like albumin (causes liver to hold onto more water- ascites, cirrhosis), blockage of lymph drainage<\/p>\n\n\n\n

What is a hypersensitivity?
an overreaction to antigens or allergens that is beyond the normal range, leading to damage<\/p>\n\n\n\n

What is a type 1 hypersensitivity?
anaphylactic. Occurs within 2-30mins of exposure. Can be systemic or localized. Binds to IgE and mast cells that release histamine, leukotrienes, and prostaglandins to create inflammation<\/p>\n\n\n\n

Mediating Factor for type 1 hypersensitivity
IgE<\/p>\n\n\n\n

Examples of type 1 hypersensitivity
allergic reaction to dust. someone eats peanuts and breaks out in hives and runny nose<\/p>\n\n\n\n

How do we treat type 1 hypersensitivity reactions?
antihistamines to block histamine, beta adrenergics to bronchodilator , corticosteroids, to decrease inflammation. IgE therapy, epinephrine given during anaphylaxis through IV or through IM in epipens<\/p>\n\n\n\n

What are signs and symptoms of a type 1 hypersensitivity reaction?
hives, runny nose, eczema, throat constriction, ,localized edema, wheezing, tachycardia, anaphylaxis.<\/p>\n\n\n\n

Explain Type 2 Hypersensitivity
The cells attack healthy organs and blood, causing symptoms<\/p>\n\n\n\n

Mediating factor for type 2 hypersensitivity
cytotoxic- IgM\/ IgG<\/p>\n\n\n\n

Examples of type 2 hypersensitivity
Blood transfusions when wrong blood given, hemolytic disease of newborn, grans disease, myasthenia gravis<\/p>\n\n\n\n

What is type 3 hypersensitivity?
The igG antibodies are stuck beneath the membranes of cells. Can activate immune responses that can damage tissues. Immune complex<\/p>\n\n\n\n

Mediating factor type 3 hypersensitivity
immune complexes<\/p>\n\n\n\n

Examples type 3 hypersensitivity
RA, lupus<\/p>\n\n\n\n

What is type 4 hypersensitivity?
there is a delayed cell reaction caused by the T cells. Antigens are phagocytized and are sensitized to receptors on the t cell. Reexposure causes the memory cells to release destructive cytokines.<\/p>\n\n\n\n

Mediating factor type 4 hypersensitivity
delayed cell mediated<\/p>\n\n\n\n

Examples type 4 hypersensitivity
TB test, contact dermatitis<\/p>\n\n\n\n

Characteristics of benign tumors
Localized growth that is curable. They more closely resemble the original tissue type, they grow slowly, have little vascularity, rarely necrotic, and usually have similar function to the original cells. Can be fatal depending on the location (brain, heart,etc), usually grows at the original areas of the body. Encapsulated<\/p>\n\n\n\n

Characteristics of malignant tumors
usually cancerous. They ignore growth controlling signals and replicate despite signals from the environment. They can escape signals and can die. they can also display different functions poorly or not at all related to the tissue. Greater degree of differentiation means that it is more aggressive. Can move around with a poor prognosis. Anaplasia, metastasis<\/p>\n\n\n\n

S\/S of peptic ulcer disease
epigastric burning pain that is usually relieved by food or antacids (gastric ulcers present on empty stomach but can be after food, duodenal ulcers present 2-3 hours after food and is relieved by food). Can also be life threatening as GI bleeding can occur without warning and cause a drop in H\/H and dark tarry stools and hematemesis<\/p>\n\n\n\n

What is H.pylori?
has a key role in promoting both gastric and duodenal ulcer formation and thrives in acidic areas. It slows down ulcer healing and can reoccur frequently, and taking it away can help ulcers heal<\/p>\n\n\n\n

What is a functional bowel obstruction?
problem with the act of the bowel actually moving, such as things that inhibit movement from surgery, medications, opioids, low fiber diets that can slow motility or shut off the GI system from the SNS stimulation<\/p>\n\n\n\n

What is a mechanical bowel obstruction?
blockage of the bowel inhibiting movement. adhesions, hernia, tumors, impacted feces, volvus or twisting of the intestines, intussusception<\/p>\n\n\n\n

adhesions
bands of scar tissue joining two surfaces that are normally separated in the bowel<\/p>\n\n\n\n

hernia
Protrusion of bowel through the wall of the cavity that normally contains it<\/p>\n\n\n\n

volvus
twisting of the bowel<\/p>\n\n\n\n

Intusseption
telescoping of the intestines<\/p>\n\n\n\n

S\/S of appendicitis
Periumbilical pain, RLQ pain, presence of a positive McBurneys point and rebound tenderness when one presses on the belly button and hip region and when the pressure is removed, the client has pain, nausea, vomiting, fever, diarrhea, RLQ tenderness, systemic signs of infection.<\/p>\n\n\n\n

how to assess appendicitis
McBurney’s point technique when pressing on the belly button and RLQ hip region and removing the pressure causes intense pain, indicates positive appendicitis. Rebound tenderness= positive<\/p>\n\n\n\n

rebound tenderness
pain that increases when pressure (as from a hand) is removed-in appendicitis<\/p>\n\n\n\n

S\/S of liver disease
hepatocellular failure (jaundice, decreased clotting, hypoalbuminemia, decreased vitamin D and K) and portal hypertension (GI congestion due to blockage of blood, more esophageal or gastric varies, hemorrhoids, enlarged spleen,)<\/p>\n\n\n\n

what is jaundice?
green yellow staining of tissues from increased level of bilirubin as the liver cannot metabolize extra bilirubin. Found on eyes, skin, and mouth. present with liver disease<\/p>\n\n\n\n

What is ascites?
pathological accumulation of fluid in the peritoneal cavity due to the loss of albumin in the liver, causing fluid to be free amongst the cells. It can cause a lot of pain in the abdomen, and it must be drained with a parenthesis<\/p>\n\n\n\n

What is hepatic encephalopathy?
neuropsychiatric syndrome from too much ammonia in the blood as the liver cannot break it down. Dementia=ammonia and psychotic symptoms common along with jerking<\/p>\n\n\n\n

What is portal hypertension?
Increased pressure in the portal venous system from a build-up of portal vein pressure due to progressive hepatic fibrosis which increases hepatic resistance<\/p>\n\n\n\n

What is esophageal varices?
a complication of portal hypertension resulting from alcoholism or hepatitis. Causes the vessels in the esophagus to become dilated and bleed, and the rupturing can be forceful enough for one to bleed out<\/p>\n\n\n\n

How do we treat esophageal varices?
reduce the hypertension, banding the varices to prevent rupturing and bleeding by cutting of the flow with a band<\/p>\n\n\n\n

What role does albumin play in the blood?
Albumin helps keep fluid in the blood stream and in cells so it does not leak into other tissues. It can also carry other substances in the body<\/p>\n\n\n\n

What happens to albumin during liver failure?
leads to low albumin levels, causing edema in the extremities and buildup of fluid in abdomen called ascites from fluid leaking through the cells and vessels into the tissues<\/p>\n\n\n\n

Three functions of the kidneys
elimination, excretion, regulation<\/p>\n\n\n\n

Explain elimination
discharge of waste (urine) from the body<\/p>\n\n\n\n

Explain Excretion
removal of organic wastes from the blood<\/p>\n\n\n\n

Explain regulation
regulating blood volume, ion concentration, blood pH and nutrients<\/p>\n\n\n\n

Manifestations of renal disorders
Pain: usually in the back-flank area, felt at the CVA angle when one palpates with a closed fist and it causes the client tenderness. Pain upon micturition<\/p>\n\n\n\n

What are abnormal urinalysis findings?
dark, strong smelling urine could denote decreased renal function, infection or dehydration, cloudy urine could denote infection or high WBC count. Ketones or glucose suggest diabetes, and proteinuria<\/p>\n\n\n\n

Normal GFR
125 mL\/min<\/p>\n\n\n\n

Normal urine output per hour
30 mL\/hr<\/p>\n\n\n\n

What is polycystic kidney disease?
a congenital abnormality of the kidney that is genetically transmitted, and it results in fluid filled cysts on one or both kidneys that can lead to renal failure, needing dialysis, or kidney transplantation<\/p>\n\n\n\n

What causes polycystic kidney disease?
genetics<\/p>\n\n\n\n

Explain nephron
in the kidney and helps to filter blood and remove waste products. The kidney has 1-2 million of them<\/p>\n\n\n\n

Explain hematuria
blood found in the urine not due to menstruation<\/p>\n\n\n\n

Explain proteinuria
protein found in the urine<\/p>\n\n\n\n

What is nephrolithiasis?
kidney stones that obstruct the ureters and kidneys. Usually made of calcium and can cause urinary stasis and pain<\/p>\n\n\n\n

What is pyleonephritis?
infected and inflamed kidney, usually caused by e.coli from the lower urinary tract that ascends<\/p>\n\n\n\n

Explain how to assess for pyelonephritis
Percussion at the CVA noting tenderness, pain when urinating, low GFR, concentrated urine with things in urine<\/p>\n\n\n\n

s\/s of pyelonephritis
CVA tenderness most common, fever, chills, N\/V, anorexia or not willing to eat, flank pain<\/p>\n\n\n\n

What is cystitis?
inflammation of the bladder (UTI)<\/p>\n\n\n\n

How to prevent pyelonephritis
remove catheters as early as possible to prevent infection as it can spread<\/p>\n\n\n\n

s\/s of acute kidney injury (AKI)
low urine output, concentrated urine, low GFR, high BUN\/CRE, sudden reduction in kidney function<\/p>\n\n\n\n

3 Causes of AKI
Prerenal, intrarenal, postrenal<\/p>\n\n\n\n

explain pre renal causes of AKI
disruption in renal perfusion and blood flow. It can cause low blood pressure, low blood volume, heart failure, renal artery obstruction, fever, vomiting, diarrhea, burns that lead to dehydration, Drugs such as ACE inhibitors or angiotensin 2 blockers, NSAIDs that can drop the blood pressure or cause bleeding<\/p>\n\n\n\n

Explain intrarenal causes of AKI
damage or disruptions within the kidney blood vessels, tubules, or glomeruli. It can cause reduced blood supply within the kidneys, toxic injury with medications, chemo, and contrast medias, renal inflammation, or prolonged prostate\/ stones\/ in the post renal stage<\/p>\n\n\n\n

Explain postrenal causes of AKI
caused by an obstruction in the urinary collecting system, urethra, bladder, or ureters due to stone, tumor, or enlarged prostate that results in elevated pressure in the Bowman’s capsule that impedes glomerular filtration. Prolonged injury can lead to intrinsic injury and irreversible damage<\/p>\n\n\n\n

Examples of prerenal causes of AKI
low BP, hypovolemia, heart failure, renal artery occlusion, fever, vomiting, diarrhea, burns leading to dehydration, NSAIDs, and antihypertensives that drop the BP<\/p>\n\n\n\n

Examples of intrarenal causes of AKI
chemo, contrast dye, prolonged kidney stones in the post renal stage<\/p>\n\n\n\n

Examples of postrenal causes of AKI
renal stones, enlarged prostate, tumor in the urethra<\/p>\n\n\n\n

What is compartment syndrome?
Damage to nerves and vasculature of an extremity due to compression. if untreated it can cause edema, increased pressure, reduced capillary flow, ischemia and necrosis<\/p>\n\n\n\n

What must be done in compartment syndrome?
fasciotomy to reduce pressure in the area<\/p>\n\n\n\n

What are the 5 P’s for compartment syndrome?
Pain paralysis paresthesia pallor pulselessness<\/p>\n\n\n\n

What are pressure ulcers?
localized area of cellular necrosis resulting from pressure between any boney prominence and with an external object<\/p>\n\n\n\n

Which populations are most likely to have a pressure ulcer?
elderly, bedridden patients, incontinent patients, those who are malnourished, bad hygiene, those with paralysis<\/p>\n\n\n\n

Risk factors for pressure ulcers
poor nutrition, aging, immobility, sensory loss, bowel and bladder incontinence<\/p>\n\n\n\n

Most common places to find pressure ulcers
buttocks, coccyx, heels, elbows, back of head, shoulders<\/p>\n\n\n\n

stage 1 pressure ulcer
Intact skin with non blanching redness<\/p>\n\n\n\n

stage 2 pressure ulcer
partial thickness skin loss involving the epidermis or dermis or both<\/p>\n\n\n\n

stage 3 pressure ulcer
full thickness tissue loss with visible fat<\/p>\n\n\n\n

stage 4 pressure ulcer
full thickness tissue loss with exposed bone, muscle or tendon<\/p>\n\n\n\n

How can we prevent pressure ulcers
turning patients every 2 hours who are bedridden. Appropriate nutrition and hydration. float heels off bed, clean linens, doing incontinence care, movement of patients<\/p>\n\n\n\n

What are electrolyte reservoirs?
where electrolytes are found at an abundance, usually in the bones<\/p>\n\n\n\n

Which electrolytes are stored in the bones?
calcium, phosphate, magnesium<\/p>\n\n\n\n

What is osteomyelitis?
severe pyogenic infection of bone and local tissues. the organism reaches the blood adjacent to soft tissue or directly into it. if not managed, necrotic bone can separate the bone into dead segments<\/p>\n\n\n\n

Causes of osteomyelitis
burns, sinus disease, trauma, tumors, periodontal infection and pressure ulcers, open fractures, penetration of wounds, surgical contamination or use of metal screws<\/p>\n\n\n\n

What is osteoporosis?
occurs when the rate of bone resorption is greater than bone formation. The bones end up becoming fragile and light<\/p>\n\n\n\n

Who is most likely to get osteoporosis?
women age 60-80 that are caucasian<\/p>\n\n\n\n

What are the causes of osteoporosis?
estrogen deficiency, poor calcium intake and disuse of supplements<\/p>\n\n\n\n

S\/S of osteoporosis
short stature, muscle wasting, back spasms and difficulty bending. bones will be porous and have holes in them, more fragile<\/p>\n\n\n\n

How do we diagnoses osteoporosis?
bone mineral density scan with levels being -1.0 to -2.5<\/p>\n\n\n\n

How do we treat osteoporosis?
calcium and vitamin D supplements, exercise, human parathyroid hormone, supplemental estrogen<\/p>\n\n\n\n

What is rickets?
defective mineralization of both bone and growth plate cartilage in children<\/p>\n\n\n\n

What causes rickets?
Vitamin D deficiency<\/p>\n\n\n\n

Which population is affected by rickets?
children<\/p>\n\n\n\n

S\/S of Rickets
bowleg, knock kneed, beading of ribs, improper formation of teeth, long ends of the bones, pelvis deformities<\/p>\n\n\n\n

What is osteomalacia?
a rare condition of the adult bone associated with vitamin D deficiency, resulting in decalcification and softening of bone.<\/p>\n\n\n\n

Which population is affected with osteomalacia?
adults<\/p>\n\n\n\n

What causes osteomalacia?
Low vitamin D in adults<\/p>\n\n\n\n

What is osteoarthritis?
local degenerative disorder associated with aging and wear and tear from repetitive stress. Characterized by loss of articular cartilage, calcification, wear of bone and bone spurs. Non inflammatory, and the weight bearing joints are affected<\/p>\n\n\n\n

What causes osteoarthritis?
long-term or excessive wear and tear on joints, aging, genetics<\/p>\n\n\n\n

s\/s of osteoarthritis
pain, stiffness, enlargement, tenderness, limited range of motion and deformity, crepitus<\/p>\n\n\n\n

What are Heberden’s and Bouchard’s nodes?
boney bumps on fingers and joints caused by joint inflammation in osteoarthritis and RA<\/p>\n\n\n\n

What is rheumatoid arthritis?
a chronic progressive inflammatory disease causing inflammation in the joints and resulting in painful deformity and immobility, especially in the fingers, wrists, feet, and ankles.<\/p>\n\n\n\n

What causes rheumatoid arthritis?
autoimmune disorder<\/p>\n\n\n\n

s\/s of rheumatoid arthritis
s\/s similar to osteoarthritis, malaise and fatigue.<\/p>\n\n\n\n

What is psoriatic arthritis?
inflammation of the joint cavities associated with psoriasis<\/p>\n\n\n\n

What is psoriatic arthritis associated with?
psoriasis<\/p>\n\n\n\n

What causes psoriatic arthritis?
automimmune disorder where cells attack the joints if not corrected earlier<\/p>\n\n\n\n

s\/s of psoriatic arthritis
similar to RA, but secondary to psoriasis. oligoarthritis, combined soft tissue and peripheral joint disease<\/p>\n\n\n\n

What is gout?
disorder in which the disturbance of uric acid metabolism leads to deposition of uric acid crystals in the joints<\/p>\n\n\n\n

What is associated with gout?
uric acid and uric acid crystals<\/p>\n\n\n\n

What causes gout?
hyperuricemia<\/p>\n\n\n\n

s\/s of gout
Severe pain in a peripheral joint, often great toe
Swelling of joint, redness
Trophi in lower extremities (small, white nodules visible through the skin)
Renal stones<\/p>\n\n\n\n

What is gigantism?
occurs in childhood as a result of too much growth hormone. Occurs before skeletal plates fuse at the ends of bones. Leaves client with increased risk for cardiac problems<\/p>\n\n\n\n

Which population is affected by gigantism?
children<\/p>\n\n\n\n

What is dwarfism?
occurs when there is too little growth hormone. It causes short stature, hypoglycemia, delayed dental eruption, thin hair, poor nail growth, greater fat mass, decreased muscle mass, and delayed bone formation and puberty. Often is congenital or idiopathic.<\/p>\n\n\n\n

What is acromegaly?
occurs in adults as a result of too much growth hormone. Occurs when the cells grow width wise amongst the bones.<\/p>\n\n\n\n

Which population is affected by acromegaly?
adults<\/p>\n\n\n\n

How do the bones grow in gigantism?
vertically or horizontally from the ends of bone.<\/p>\n\n\n\n

How do the bones grow in acromegaly?
width wise<\/p>\n\n\n\n

What is diabetes insipidus caused by?
lack of ADH<\/p>\n\n\n\n

What does diabetes insipidous result in?
Results in the kidneys being unable to retain water in the body and a lot of urine output that is dilute. Extreme thirst. Lack of water leads to dehydration.<\/p>\n\n\n\n

s\/s of diabetes insipidus
dizziness, disorientation, nausea, tachycardia, headaches, low blood pressure, hypovolemia, high electrolytes in the blood- sodium, large volumes of dilute urine\/ fluid are excreted, weight loss<\/p>\n\n\n\n

What are patient with diabetes insipidus at high risk for developing?
hypovolemic shock<\/p>\n\n\n\n

What is SIADH?
too much ADH in the body. Causes the body to retain too much water<\/p>\n\n\n\n

S\/S of SIADH
low urine output, high osmolarity, electrolytes are at a lower concentration, edema, weight gain, hyponatremia, cereal edema, seizures, confusion, coma<\/p>\n\n\n\n

What are patients with SIADH at risk of developing?
cerebral edema<\/p>\n\n\n\n

What organism causes pelvic inflammatory disease
Neisseria gonorrhoeae, chlamydia trachomatis<\/p>\n\n\n\n

What organism causes cervical cancer
human papillomavirus or HPV<\/p>\n\n\n\n

What organism causes UTI
e.coli<\/p>\n\n\n\n

What organism causes herpes
herpes simplex 1\/ 2 virus (depending on area of body)<\/p>\n\n\n\n

What organism causes syphillis
Treponema pallidum<\/p>\n\n\n\n

What is parathyroid hormone?
increases the calcium levels in the blood to be released from bone reservoirs by activating osteoclasts. It increases Ca absorption in the intestine and decreases Ca excretion in the urine<\/p>\n\n\n\n

What is calcitonin?
decreases calcium levels in the blood and increases calcium levels in the bone. puts calcium back into the bones.<\/p>\n\n\n\n

What electrolyte is affected by parathyroid hormone and calcitonin?
calcium<\/p>\n\n\n\n

What is Cushing’s disease?
caused by excessive glucocorticoids from either a pituitary tumor or tumor or adrenal cortex or secondary to prescribed glucocorticoids<\/p>\n\n\n\n

S\/S of Cushing’s Disease
hyperglycemia, loss of muscle and bone, excess water and salt retention, weight gain, edema, hypernatremia, characteristic signs: moon face and the buffalo hump due to swelling and redistribution of fat, high BP and blood volume<\/p>\n\n\n\n

What is Addison’s disease?
caused by adrenocortical insuffiency from not having enough steroids or glucocorticoids. Primarily from autoimmune conditions or removal of the adrenals, secondary to removal of corticosteroid therapy<\/p>\n\n\n\n

S\/S of Addison’s disease
weight loss, salt wasting of fluids, weakness, malaise, hyperpigmentation or bronzing of skin, hypoglycemia, and hyperkalemia. Reduced cardiac output, inadequate blood volume, low blood pressure<\/p>\n\n\n\n

Hypothyroidism causes
caused by cells attacking the thyroid gland or surgical removal of tissues, iodine deficiency. Leads to a lack of T3\/T4 and too much of TSH. The TSH recognizes the lack of the T3\/T4 so more is pushed into it yet the thyroid cannot produce it.<\/p>\n\n\n\n

Lab values for hypothyroidism
elevated TSH, low T3\/T4<\/p>\n\n\n\n

S\/S hypothyroidism
low metabolism, weakness, lethargy, cold intolerance, low appetite, bradycardia, weight gain, dry skin, constipation, depression, difficulty concentrating, menstrual problems<\/p>\n\n\n\n

Hyperthyroidism causes
excessive iodine, Graves’ disease, nonmalignant thyroid tumors, thyroid inflammation, and taking large amounts of thyroid hormone replacement<\/p>\n\n\n\n

Lab values for hyperthyroidism
High T3\/T4 levels, low TSH<\/p>\n\n\n\n

S\/S of hyperthyroidism
exophthalmos or eye budging, lid lag, vision changes, light sensitivity, high metabolism, rapid weight loss, insomnia, restlessness, cannot concentrate, tremors and irritability, palpitations, heat intolerance, diaphoresis, diarrhea, amenorrhea<\/p>\n\n\n\n

type 1 diabetes mellitus patho
the inability for one to produce insulin needed to transport glucose into cells. They are insulin dependent. The beta cells in the pancreas are destroyed or not present. No insulin to stimulate production of glucagon, causing glucose levels to rise.<\/p>\n\n\n\n

What must type 1 diabetes do with their condition?
take lifelong insulin<\/p>\n\n\n\n

type 2 diabetes mellitus
caused by the cells of the pancreas becoming resistant ot insulin, and decrease of receptors on the target cells. They lose the ability to respond to cells. Results in decreased insulin production.<\/p>\n\n\n\n

What must type 2 diabetics do with their condition?
take insulin or oral diabetic agents. can have a low sodium diet and exercise regularly to keep stress levels low, keep their blood pressure low and weight gain at a minimum<\/p>\n\n\n\n

Normal blood sugar range
60-120<\/p>\n\n\n\n

Hypoglycemia blood sugar levels
lower than 60<\/p>\n\n\n\n

Hyperglycemia blood sugar levels
above 120<\/p>\n\n\n\n

How do we diagnose diabetes?
random sampling of blood glucose over 200 mg, fasting blood glucose level of 126, or and Hgba1C over 6.5<\/p>\n\n\n\n

Normal A1C level
4-6<\/p>\n\n\n\n

Diabetic A1c level
above 6.5<\/p>\n\n\n\n

Where should any diabetic aim their A1C level to be at?
less than 7<\/p>\n\n\n\n

S\/S of hyperglycemia
Dry mouth, increased thirst, blurry vision, weakness, headache, frequent urination “sugar high”<\/p>\n\n\n\n

S\/S of hypoglycemia
cold, pale, sweating, sleepy, lack of coordination, irritability, hunger<\/p>\n\n\n\n

Which takes priority: hyperglycemia or hypoglycemia?
hypoglycemia<\/p>\n\n\n\n

What do we need to do to treat hypoglycemia?
by giving 15g of carbs or D50 over time and rechecking the sugar every 15 minutes<\/p>\n\n\n\n

What are the 3 P’s of diabetes?
polyuria, polydipsia, polyphagia<\/p>\n\n\n\n

Explain polyuria
increased urination<\/p>\n\n\n\n

Explain polydipsia
increased thirst<\/p>\n\n\n\n

Explain polyphagia
increased hunger<\/p>\n\n\n\n

Primary Brain Injury
occurs as a direct result of the initial insult to the brain<\/p>\n\n\n\n

Examples primary brain injury
stroke, concussion, trauma<\/p>\n\n\n\n

Secondary Brain injury
occurs as the response to the initial impact or trauma. Can be progressive damage resulting from the body’s response to the initial insult<\/p>\n\n\n\n

Examples of secondary brain injury
brain swelling secondary to stroke or trauma<\/p>\n\n\n\n

What is intracranial pressure?
the volume of the craniums brain tissue, CSF, and blood, overall pressure in the skull and spinal cord<\/p>\n\n\n\n

What is increased ICP?
occurs when there is a rise in pressure from trauma, stroke, swelling, tumor, obstruction, etc. There is often compression occurring from the skull that does not allow the brain to expand, adding to the pressure becoming high<\/p>\n\n\n\n

Result of increased ICP
cutting off of the blood supply, tissue damage, ischemia, hypoxia and eventually necrosis. brain cannot expand<\/p>\n\n\n\n

Normal ICP range
0-15 mmHg<\/p>\n\n\n\n

Increased ICP range
above 15 mmHg<\/p>\n\n\n\n

S\/S of increased ICP
LOC changes, headache, vomiting, drowsiness, impaired speech, low arousal, blurry vision, impaired pupil responsiveness to light reflex, unequal pupil size, fixed and dilated pupils, altered respiratory pattern, lack of movement<\/p>\n\n\n\n

Explain the Glasgow Coma Scale
A scale that measures the degree or level of consciousness (LOC is always number #1 with neurological assessment)<\/p>\n\n\n\n

What 3 categories is the Glasgow coma scale based on?
eye opening, verbal utterances, and motor reactions<\/p>\n\n\n\n

Mild Range Glascow coma scores
Above 12<\/p>\n\n\n\n

Moderate Range Glascow coma scores
9-12<\/p>\n\n\n\n

Severe Range Glascow coma scores
less than 8<\/p>\n\n\n\n

What score does it mean a patient is dead on the Glasgow coma scale?
3 or less<\/p>\n\n\n\n

What is the most powerful predictor of outcome according to the Glasgow coma scale?
motor response<\/p>\n\n\n\n

Explain decorticate posturing
abnormal flexion towards the core of the body<\/p>\n\n\n\n

Explain decerebrate posturing
abnormal extension away from the body<\/p>\n\n\n\n

What is an ischemic stroke?
From a sudden blockage of the cerebral artery secondary to a clot or emboli formation. Associated with atherosclerosis and clotting disorders and cardiac conditions that can push the clot to the brain.<\/p>\n\n\n\n

Most common type of stroke is?
ischemic stroke<\/p>\n\n\n\n

S\/S of ischemic stroke
contralateral paralysis (Right brain controls left side, left brain controls right side) on one side of the body, facial drooping, ptosis, hemi-sensory loss, contralateral visual blindness, aphasia or speech difficulty<\/p>\n\n\n\n

What is a hemorrhagic stroke?
results from a bleed within the brain. From secondary to severe and chronic hypertension, severe head trauma, aneurysm, weakness or rupture of a vessel, anticoagulant use, or arteriovenous malformation.<\/p>\n\n\n\n

S\/S of hemorrhagic stroke
one sided weakness, someone with right sided weakness – has a problem on the left side of the brain, drop on face, headache caused by bleeding, difficult to communicate, high blood pressure, impaired vision, nausea, seizures, unequal pupils, difficult respiration<\/p>\n\n\n\n

How do we diagnose a stroke (type and location)?
Brain CT scan<\/p>\n\n\n\n

Explain meningitis
inflammation of the meninges of the brain<\/p>\n\n\n\n

Causes of meningitis
strep pneumonia, meningococcus, hemophilic influenza or can be viral. it reaches the person through the ears<\/p>\n\n\n\n

S\/S of meningitis
headache, fever, stiff neck (patient cannot touch chin to chest without pain), photophobia, purple rash, confusion delirium<\/p>\n\n\n\n

Explain encephalitis
inflammation of the brain with swelling<\/p>\n\n\n\n

Causes of encephalitis
west nile virus, HSV, equine cephalitis<\/p>\n\n\n\n

S\/S of encephalitis
fever, headache, malaise, muscle pain, rash, seizure, confusion, stupor, coma<\/p>\n\n\n\n

How do we diagnose meningitis\/ encephalitis?
CT, MRI lumbar puncture with pathogens in it- either clear or cloudy straw color<\/p>\n\n\n\n

Generalized Seizure
whole brain surface is affected by the seizure<\/p>\n\n\n\n

Absence Seizure
staring spells that last seconds<\/p>\n\n\n\n

Myoclonic Seizure
single\/ several jerks of the body<\/p>\n\n\n\n

Atonic Seizure
loss of muscle tone, can cause falls as people drop during it<\/p>\n\n\n\n

Tonic Clonic Seizure
jerking of many muscles<\/p>\n\n\n\n

Focal Seizure
abnormal brain activity related to one hemisphere<\/p>\n\n\n\n

Status Epilepticus
continuing series of seizures without recovery. Life threatening due to low perfusion and o2 to brain.<\/p>\n\n\n\n

1st degree burn
Only the epidermis (red, painful, and edema)<\/p>\n\n\n\n

2nd degree burn
epidermis and part of dermis (blistered)<\/p>\n\n\n\n

3rd degree burn
Full thickness damage through skin into nerves and muscles. Absence of pain and neuropathy<\/p>\n\n\n\n

How do we diagnose Seizures?
EEG is gold standard. lab work to rule out toxins or malnutrition, MRI, lumbar puncture<\/p>\n\n\n\n

What should you do during a seizure?
maintain an airway, remove clothes that could constrict, lay person on left side, have suction and o2 at bedside, prevent aspiration, protect injury, document start and stop time of seizures, do not put anything in the mouth, dim room and quiet, give time to rest after the seizure as it deprives the brain of oxygen and energy<\/p>\n\n\n\n

What is cerebral palsy?
A permanent impairment affecting automatic postural control and movement as a result of a non-progressive brain disorder<\/p>\n\n\n\n

What is cerebral palsy caused by?
by prenatal infections or mechanical trauma to the head before, during or after birth or exposure to nerve damaging poisons or reduced oxygen supply to the brain<\/p>\n\n\n\n

Is cerebral palsy reversible?
No but ti can be managed with surgery, casts, braces, rehab<\/p>\n\n\n\n

What causes Parkinson’s disease?
the loss of dopamine producing neurons over time that are in the brain, dopamine deficiencies associated with motor impairment<\/p>\n\n\n\n

S\/S of Parkinson’s disease
difficulty initiating and controlling movements, slow movements, tremors that occur at rest, loss of facial expression, shuffling gait, absent arm swing<\/p>\n\n\n\n

What are spinal injuries caused by?
trauma, MVA, fall, GSW, injury resulting in the spinal cord being compressed, transected or bruised. Secondary to bleeding, swelling, ischemia or inflammation<\/p>\n\n\n\n

Types of spinal cord injuries
hyperflexion, hyperextension or compression<\/p>\n\n\n\n

What is spinal shock?
occurs right away and is a loss of reflexes below the injury. The muscles are flaccid and at the end the flaccidity is replaced with spasms<\/p>\n\n\n\n

What is neurogenic shock?
there is peripheral vasodilation resulting in hypotension, bradycardia, and circulatory collapse due to no pressure to move the blood in the body. Can potentially affect the respiratory system.<\/p>\n\n\n\n

What is autonomic dysreflexia?
reflexive response due to sympathetic activation below the injury level such as visceral stimulation, hypertension, headache. Leads to flushing above the level of injury and clammy skin below it.<\/p>\n\n\n\n

How do we treat spinal cord injuries?
do not move head or spine. stabilize with a brace to maximize recovery<\/p>\n\n\n\n

What happens to co2 and o2 levels during hypoventilation?
causes o2 to not be able to get into the lungs and for co2 to be retained and not expelled from the lungs<\/p>\n\n\n\n

What happens to co2 and o2 levels during hyperventilation?
causes too much co2 to be eliminated and too much o2 to be let into the lungs too fast<\/p>\n\n\n\n

Normal pH
7.35-7.45<\/p>\n\n\n\n

Normal CO2 range
35-45<\/p>\n\n\n\n

Normal HCO3
22-26<\/p>\n\n\n\n

Acidosis pH
less than 7.35<\/p>\n\n\n\n

Alkalosis pH
greater than 7.45<\/p>\n\n\n\n

Acidosis CO2
greater than 45<\/p>\n\n\n\n

Alkalosis CO2
less than 35<\/p>\n\n\n\n

Acidosis HCO3
less than 22<\/p>\n\n\n\n

Alkalosis HCO3
greater than 26<\/p>\n\n\n\n

What happens during respiratory acidosis?
pH is low and CO2 is high; leads to more CO2 retained and not enough O2<\/p>\n\n\n\n

Examples of respiratory acidosis?
hypoventilation, opioid overdose, impaired airway, respiratory depression, COPD<\/p>\n\n\n\n

What happens during respiratory alkalosis?
pH is high and CO2 is low; leads to not enough CO2 retained and too much oxygen held on<\/p>\n\n\n\n

Examples of respiratory alkalosis?
hyperventilation, fever, anxiety, sepsis, brain trauma, ventilation<\/p>\n\n\n\n

What happens during metabolic acidosis?
pH is low and HCO3 is low<\/p>\n\n\n\n

Examples of metabolic acidosis?
aspirin toxicity, excessive alcohol use, lactic acid buildup. DKA, starvation, persistent diarrhea, kidney failure<\/p>\n\n\n\n

What happens during metabolic alkalosis?
pH is high and HCO3 is high<\/p>\n\n\n\n

Examples of metabolic alkalosis?
excessive vomiting or NG suctioning<\/p>\n\n\n\n

What is asthma?
chronic inflammatory disorder of the airways from stimuli<\/p>\n\n\n\n

What is extrinsic asthma?
caused by external factor such as pet dander, pollen dust from an IgE response<\/p>\n\n\n\n

What is intrinsic asthma?
from internal factors such as inflammation, upper respiratory infections, air pollution, emotional stress, smoke<\/p>\n\n\n\n

What is exercised induced asthma?
occurs 10-15 minutes after the end of exercise as a compensatory mechanism to warm airways<\/p>\n\n\n\n

What are s\/s of ALL asthma types?
wheezing, tight chest, dyspnea, cough, increased sputum production, hyper inflated chest, decreased breath sounds<\/p>\n\n\n\n

Which organism causes TB?
mycobacterium tuberculosis<\/p>\n\n\n\n

How does TB enter the body?
inhalation of small droplets containing the bacteria that are expelled with cough, sneeze or talking. It enters into the lungs and the macrophages ingest the microorganism. Seen on the chest x ray as chon complexes for the small clusters<\/p>\n\n\n\n

How is TB classified?
primary is asymptomatic but when reactivated can impair the immune system<\/p>\n\n\n\n

S\/S TB
low grade fever, chronic cough with bloody sputum, night sweats, fatigue, weight loss<\/p>\n\n\n\n

How do we diagnose TB?
sputum culture, PPD test but does not work when one is exposed, CXR<\/p>\n\n\n\n

How do we prevent the spread of TB?
wear N95 mask, place patient in negative pressure room<\/p>\n\n\n\n

What is COPD?
result of both chronic bronchitis and emphysema that causes irreversible decrease for the lungs to force air out, lower lung elasticity and move air out<\/p>\n\n\n\n

What can COPD result in?
hypoventilation, co2 retention, decrease in pH, hypoxemia.<\/p>\n\n\n\n

Causes of COPD
smoking or air pollution<\/p>\n\n\n\n

S\/S of COPD
SOB, will be thin due to increased respiratory effect, increased calorie use, working hard to breathe, use of accessory muscles in a tripod position, pursed lip breathing, cough, clubbing of fingers, barrel chest. Will need o2<\/p>\n\n\n\n

What is cystic fibrosis?
Excess mucus in the lungs, digestive track and liver<\/p>\n\n\n\n

What causes cystic fibrosis?
genetics<\/p>\n\n\n\n

s\/s of cystic fibrosis
cough, thick sputum that is overproduced, recurrent infections and bronchitis, dyspnea, tachycardia, sternal retractions, unequal breath sounds, crackles and rhonchi, barrel chest, clubbing, fatty stools<\/p>\n\n\n\n

What is pneumonia?
inflammation of the lungs from an infection<\/p>\n\n\n\n

Etiology of Pneumonia
The organism enters the lung, multiplies and triggers pulmonary inflammation that invade alveolar sacs that fill with fluid that is hard to cough up.<\/p>\n\n\n\n

Causes of pneumonia
aspiration, inhaled contaminants from the mouth, virus, hospital or community acquired infections.<\/p>\n\n\n\n

Who is most at risk for getting pneumonia?
elderly, intubated patients, ill patients, hypoxic patients, immunocompromised patients.<\/p>\n\n\n\n

s\/s of pneumonia
crackles and bronchi breath sounds over affected tissue, chills, fever, cough with white or cloudy sputum.<\/p>\n\n\n\n

What is ARDS?
damage to the alveolar capillary membrane that causes wide spread pulmonary edema and severe shortness of breath. Associated with decline in o2 that does not respond to supplementary o2. the client becomes hypercapnia and acidotic.<\/p>\n\n\n\n

Etiology of ARDS
atelectasis and decrease in lung compliance and surfactant, fibrosis, pulmonary edema, disruptions in o2 transport, hypoxemia. Lungs fill with fluid- dyspnea, o2 will drop, frothy sputum, hypoximea, co2 is trapped low Ph<\/p>\n\n\n\n

Causes of ARDS
severe trauma, sepsis, aspiration, fat emboli, shock.<\/p>\n\n\n\n

S\/S of ARDs
Dyspnea, labored and shallow respirations productive cough with frothy sputum, crackles or rales, hypoxia, cyanosis, fever, hypotension, tachycardia, restlessness, confusion, lethargy and anxiety.<\/p>\n\n\n\n

What is a tension pneumothorax?
Accumulation of air in the pleural space usually from trauma that creates an open sucking chest wall where air enters during inspiration but does not escape during expiration. Creates low venous return and cardiac output.<\/p>\n\n\n\n

S\/S of pneumothorax
tachycardia, hypotension, tracheal shift with deviated trachea, neck vein distension, subcutaneous emphysema<\/p>\n\n\n\n

How do we treat tension pneumothorax?
depends on severity of the problem and cause of leak. Must remove air to restore pressure. Chest tube with h2o seal that draws air out of the lung without leaks.<\/p>\n\n\n\n

What is Virchow’s triad?
conditions that promote thrombus formation.<\/p>\n\n\n\n

3 parts of Virchow’s triad
Endothelial injury, sluggish blood flow, and increased coagulopathy<\/p>\n\n\n\n

How does virchows triad increase a patients risk for a PE?
additional platelets and inflammatory mediators come to the site, stagnant blood low allow platelets and clotting factors to form and adhere to the vessel and increased coagulopathy states promotion of the clot that can be dislodged and sent to the lungs from a peripheral site.<\/p>\n\n\n\n

What is a thrombus?
blood clot that is stasis and has platelets, fibrin and dead cells<\/p>\n\n\n\n

What is a pulmonary embolism?
blood clot in the lungs<\/p>\n\n\n\n

What is an emboli?
Intravascular mass that travels and occludes downstream vessels<\/p>\n\n\n\n

What is a DVT?
Blood clot in an extremity (usually in calf) in the vein<\/p>\n\n\n\n

What is an arterial thrombus?
blockage of an artery<\/p>\n\n\n\n

What is a venous thrombus?
blockage of vein<\/p>\n\n\n\n

causes of anemia
reduced number of red blood cells from the result of blood loss, bone marrow failure, renal failure, nutritional deficiencies, and abnormal hemoglobin<\/p>\n\n\n\n

hemorrhagic anemia
caused by blood loss<\/p>\n\n\n\n

aplastic anemia
failure of blood cell production in the bone marrow<\/p>\n\n\n\n

iron deficiency anemia
from lack of iron in the diet, resulting in insufficient hemoglobin<\/p>\n\n\n\n

What is PICA?
craving for nonfood substances such a dirt, clay, ice, Landry starch, cardboard or hair<\/p>\n\n\n\n

Problem with PICA
often indigestible, toxic and can cause infection<\/p>\n\n\n\n

perncious anemia
from lack of vitamin b12<\/p>\n\n\n\n

sickle cell anemia
from a mutated hemoglobin molecule that causes RBCs to be in a spiky or crescent shape. Cells are stiff, rupture easily, do not carry enough o2 and can clog small vessels. crises are painful<\/p>\n\n\n\n

Thalessemia
blood disorder causing reduced hemoglobin on the rbcs. Target shaped cells. S\/S: fatigue, weakness, paleness, slow growth.<\/p>\n\n\n\n

What types of disorders are sickle cell and thalassemia?
genetic<\/p>\n\n\n\n

What are the complications of anemia?
renal failure, fatigue, dyspnea, hypoxima, pale, cold, low metabolic activity<\/p>\n\n\n\n

How do we treat anemia?
from the causes! can give o2, blood transfusion if needed<\/p>\n\n\n\n

What is polycythemia?
abnormal excess of RBCs leading to thicken blood that clots easily<\/p>\n\n\n\n

What is polycythemia vera?
bone marrow cancer that causes high RBC count<\/p>\n\n\n\n

What is a secondary cause of polycythemia?
due to low o2 available, affects those at high altitudes<\/p>\n\n\n\n

How do we treat polycythemia?
blood dilution where blood is removed and replaced with saline<\/p>\n\n\n\n

What is thrombocytopenia?
low platelet count due to bone marrow suppression from chemo, decreased production, decreased platelet survival, intravascular dilation of circulating platelets<\/p>\n\n\n\n

What results from thrombocytopenia?
longer bleeding time, petechial, purpura, bleeding gums, hematuria<\/p>\n\n\n\n

What do we educate clients with thrombocytopenia?
no contact sports, physical trauma, use electric razors, soft tooth brush, put pressure on wounds.<\/p>\n\n\n\n

What is DIC?
life threatening condition in which there is widespread coagulation followed by massive bleeding due to depletion of clotting factors, causing one to bleed out<\/p>\n\n\n\n

DIC causes
trauma, malignancy, burns, sepsis, shock and abuptio placente. There is widespread clot formation in small vessels.<\/p>\n\n\n\n

S\/S DIC
bleeding from multiple sites of the body, clots, bruising and petechiae, hypotension due to low blood volume, shortness of breath, confusion, LOC changes, fevers. Bleed at some time as clotting<\/p>\n\n\n\n

How do we treat DIC?
removal or correction of the cause, support major organs, give fresh plasma or packed rbcs, platelets, etc, use heparin to minimize further consumption of clotting factors. Monitor aPTT with heparin use!<\/p>\n\n\n\n

What hormone plays a role in RBC production?
erythropoietin<\/p>\n\n\n\n

Where is erythropoietin produced?
kidneys<\/p>\n\n\n\n

What is a key feature of Hodgkins lymphoma?
Has Reed-Sternberg cells that look like owl eyes<\/p>\n\n\n\n

S\/S of Hodgkin’s Lymphoma<\/p>\n\n\n\n