Pathophysiology study guide final exam review for nursing BSN for a semester length course, Study Guides, Projects, Research of Nursing

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Hyperplasi a Hypertroph y Metaplasia Dysplasia Atrophy Increase in the number of cells in an organ or tissue. -Responds to a stimulus and stops when the stimulus is removed. Example:  Physiologic hyperplasia = Breast enlargement during pregnancy vs.  Compensator y hyperplasia regeneration of the liver after a partial hepatectomy An increase in cell size and with an increase in tissue mass. Physiological hypertrophy: Increased muscle mass relating to exercise. Pathological hypertrophy: Disease conditions and may be adaptive. Adaptive: Thickening of the urinary bladder from long-continued obstruction of urinary flow. Compensatory: When one kidney is removed, the remaining one will enlarge to compensate for the loss. Reversible change in which one adult cell type replaces another adult cell type. More mature cells become replaced by immature cells EX: adaptive substitution of stratified squamous epithelial cells for the ciliated columnar epithelial cells in the trachea and large airways of a habitual cigarette smoker. (Barrett’s esophagus) Deranged cell growth of a specified tissue results in a vary in size, shape, and organs Potentially reversible is underlying cause is removed. This is a strong precursor of cancer The decrease in cell size. Physiological atrophy : When you don’t use your muscles, they get smaller, and this is usually reversible. Pathological Atrophy : This has to do with a disease which causes the cell size to shrink. Causes:

1. Disuse
2. Denervation
3. Loss of endocrine stimulation
4. Inadequate nutrition
5. Ischemia Adaptive and reversible

• Disease may be determined through lymphatic mapping and sentinel node biopsy
• This is done by injecting a radioactive tracer or blue dye into the tumor to determine the first lymph in the route of lymph drainage from cancer. Hematologic Spread: Risk factors Patho T score: Diagnostics A delayed menarche. Low body weight Menopause Current smoker. History of fractures after menopause (other than skull, facial bone, ankle, finger, or toe) History of a hip fracture in a parent Increase in osteoclasts activity, decrease in osteoblast activity Bone resorption exceeds bone formation. how we determine how much bone mineral density there is in a person The lower a person’s T-score, the lower the bone density -1 or UP is normal -2.5 is osteopenia -2.5 or less is osteoporosis osteoporosis and assess your risk of fracture and determine your need for treatment, your doctor will most likely order a bone density scan. This exam is used to measure bone mineral density (BMD). It is most commonly performed using dual-energy x-ray absorptiometry (DXA or DEXA) or bone densitometry. T score to determine BMD Downloaded by Manifestations of osteoarthritis (degenerative joint disease) pg. 1513-1517 (135-136) Risk Factors Pathophysiology Manifestation Treatment

s gender, and race AGE IS NOT A FACTOR Constant use of hand, knee, hip, foot, spine By 55 years of age, women are commonly affected (Hand OA more common) Obesity, risk factor for OA of the knee in women Excess fat may have direct metabolic effect *You can have this on ONE side. May arise suddenly or insidiously Aching pain, stiffness less than 30 mins in the AM, limited movement, hurts more throughout the day or after activity Difficult to locate Worsens with activity relieved by rest Crepitus and grinding Joint enlargement Hip, Knees, and Lumbar are mostly affected Joint Deformities: Herberden’s nodes : formation of hard nodules in DIP joints Bouchard’s nodes : formation of nodules in PIP joints Reduce pain Tylenol Maintain mobility Minimize swelling Articular cartilage

decreases friction during joint movement and displaces force of workload onto subchondral bone **-loss of Proteoglycans from the articular cartilage. What causes this loss? Enzymes that break down cartilage. If you have a normal proteoglycan that you will produce collagen. If you have a break down in this than you decrease in collagen formation.

 Chest discomfort with cough and dyspnea.  Fever, night sweats  Weight loss  Pruritus (itching)  Advance stages of HL: liver, spleen, lungs,  digestive tract, and CNS are involved. Diagnostic Test à Presence of Reed Sternberg cells in biopsy à CT scans of chest and abdomen. à Thrombocytosis, leukocytosis, eosinophilia, elevated erythrocyte sedimentation rate (ESR), elevated alkaline phosphatase

Hodgkin lymphoma is a specialized form of

lymphoma that features the presence of an

abnormal

cell called a Reed-Sternberg cell.

Signs and Symptom  Painless lymphadenopathy  ENLARGED NODES  Fever  Night sweats  Weight loss  Increased infections  Dyspnea  Renal failure  Weight loss Diagnostic Test and Treatments  Lymph node biopsy  immune-phenotyping to determine the lineage  Bone marrow biopsy, blood studies, chest and  abnormal CT scans, MRI  Staging the disease is important to determine the treatment Determine whether patients has DI, SIADH, Addison’s SIADH DI SIADH is due to excess water because of the excessive secretion of ADH or water. It is NOT due to a deficit is sodium. The volume is causing this. o HYPONATREMIA o Serum osmolality is decreased o Urine osmolality is increased o Urinary output is decreased o Fluid overload INTRAVASCULARLY o HYPERNATREMIA o Elevated serum osmolality o Decreased Urine osmolality o Urinary output is increased o Specific gravity = 1.015 if vasopressin is effective.

Megaloblastic, and different anemias Iron Deficiency Anemia Megaloblastic Anemia Aplastic Anemia Chronic Disease Anemia Iron deficiency anemia is a Microcytic anemia, smaller size. You also have hypochromic meaning the color is less. You have a decrease in H&H (Decrease in hemoglobin and hematocrit) you will have: increase RR, you will also be dizzy. Iron deficiency anemia is usually related through chronic blood loss from the stool. Usually related to the GI tract. Iron cannot be recycled. The other things that patients will exhibit is cracked lips. Large hemorrhoids can cause iron deficiency anemia Vitamin b12 deficiency o Folic Acid deficiency With Vitamin b12 deficiency and folic: you still tend to have a normal hemoglobin, but the RBC have a shorter half-life. They live less than the average individual ”MEGA” meaning bigger, and enlarged RBC. MCV is greater. LARGE RBC

- Vitamin b12: help with the transmission of nerve symptoms. o Will have a tingling sensation in hands and feet. o NEUROLOGIC SYNDROME o Schilling Test: done for vitamin B 12 deficiency. It can be able to tell you if your body is absorbing the correct amount of b12. This test makes sure there is intrinsic factor which is needed for production of b12. Folic acid: MCV is big, normal color. o GI disturbances o Malnutrition Aplastic Anemia: Your bone marrow is not working. Result in reduction of everything RBC. WBC, platelets. You need bone marrow transplant. Radiation can cause this, Chemicals, etc.. CBC values are low, but size and hemoglobin content of RBC’s are normal, Aplastic Anemia IS CAUSED BY A STEM CELL DEFICIENCY Anemia that occurs from chronic conditions. Chronic kidney disease, erythropoietin is produced here. RBC will be impaired. Crohn’s, ulcerative colitis, and inflammatory bowel diseases will cause chronic anemia. Downloaded by

Common for a patient with COPD void the bicarb by urinating. respiratory rate Main patho of ARDs  A form of pulmonary edema. There is a direct lung injury causing alveolar collapse. Alveolar are severely impaired, this results in in increased permeability of alveolar blood vessels which allows fluid to accumulate in alveolar spaces and alveoli become airless.  As alveoli are damaged, hypoxia and eventually cell injury and death occur.  O2 does NOT improve this condition!  Decreased O2 in acute respiratory distress syndrome is caused by alveolocapillary membrane injury; ie pt in a motor vehicle accident is at risk for ARDS Stable, unstable, MI MI ATI Question: -A 55-year-old male died of myocardial infarction. The nurse understands that an autopsy would most likely reveal platelet aggregation within the atherosclerotic coronary artery. o 20 minutes before an irreversible cell injury occurs MI o Myocardial Infarct is due to a FULL OCLUSION. o Damaged cells cause a decrease in myocardial contractibility o Coronary artery occlusion leads to cell death or necrosis w/o exertion that limits PT ac tivity Chest pain occurrin g

o Pain is NOT relieved with NTG and rest o Number one cause of cardiogenic shock is an MI Diagnostics of MI o ECG or EKG which can determine a STEMI or ST segment elevation o Troponin Biomarkers will be elevated (TnI and TnT) ▪ CPKII or MB to see if MI has occurred ▪ Echocardiography- To check the valves ▪ Q wave- this can be seen on someone who has had a prior MI o Remodeling of the heart = Hypertrophy of the heart, which will make heart lose contractility Know your lab values (Hemoglobin, WBC, hematocrit)

 ketone present in urine – dt lack of lipids Ketones will be stored  DKA! Metabolic acidosis! Graves and Addison’s disease Graves’ Disease- Pathophysiology: Adrenal glands do not produce Aldosterone or Cortisol. Potassium levels are increased which will cause the patient to have a decrease cardiac output. You will not have volume due to the deficiency in NA which is why you will have cardiovascular collapse. (BP issues) Inability to conserve water and sodium due to aldosterone deficiency Hypoglycemia Manifestations o Hypoglycemia o Weight loss o Lethargy o Weakness o Fever o Dehydration o Hypovolemia, hypotension o Patient will present with o Hyperpigmentation due to increased ACTH o Craving salty food Mineralocorticoid deficiency  ↓NA, ↓CO, ↑K+  Dehydration  Weakness, fatigue  CV collapse  Orthostasis Exophthalmos (budging eyes) Goiter Hyperthyroidism, t3/t4 is elevated

Glucocorticoid deficiency  Hypoglycemia  Lethargy, weakness  Fever  GI symptoms Hypothyroidism: T3, T4 are low so TSH will be high Hyperthyroidism: T3, T4 are high so TSH will be low GAS general adaptation syndrome Stress – Seyle’s definition- a state manifested by a specific syndrome of the body developed in response to any stimuli that made an intense systemic demand on it. The body adapts to stress by GAS (general adaptation syndrome). General – the effect was a general systemic reaction Adaptive – the response was in reaction to a stressor Syndrome - the physical manifestations were coordinated and dependent on each other.

1. The alarm stage – stimulation of SNS and HPA (hypothalamic- pituitary-

adrenal) this in turn releases catecholamine and cortisol.

2. Resistance stage - the body selects the best defense. Cortisol levels drop

because they are no longer needed.

3. The exhaustion phase - prolonged stressor overwhelms the body, wear and

tear or systemic damage appears. Patho of Asthma Mass cell degranulation you will release histamine and immunoglbin IGE. o Elevated IGE in a patient you will think obstructive asthma. IGE results in vasodilatation. Characteristics of Asthma. Bronchi spasms -> mucous secretion (released from goblets)-

Thicken airway walls -> lumen of the airway shrinks -> causes

childhood viral infection Considered a type 4 hypersensitivity reaction Relapse/ remitting Disturbance of Mood swings, depression, OR any emotional upsets o Euphoria, apathy, forgetfulness, loss of memory o VISION is AFFECTED scar tissue forms, replacing axons and leading to permanent disability. The term gliosis leads to the term sclerosis which means scarring Characterized by exacerbations and remissions over many years in several different sites in the CNS Initially, there is normal or nearnormal neurologic function between exacerbations. As the disease progresses, there is less improvement between exacerbations Corticosteroids are used, plasmapheresis Intraocular pressure Reflects that of the aqueous humor (fluid behind the eye) that fills anterior and posterior chambers of the eye Intraocular pressure results from a balance of several factors:

1. Rate of aqueous humor production (Fluid behind the eye) To much fluid
2. Resistance to flow, there is a blockage
3. Rate of removal by drainage system Impaired fasting plasma glucose o Fasting plasma glucose < 100 mg/dL is normal o FPG 100- mg/dL= “Pre-diabetes” o Calorie restriction/weight reduction o FPG > 126 mg/dL = criteria for diagnosis of DM

o EX: A1c of 6 and 126 glucose this is considered a diabetic because of their blood sugar Modifiable risk factors for coronary artery disease Cigarette smoking Hyperlipidemia Diabetes mellitus Dietary habits Abdominal obesity Physical inactivity Metabolic syndrome Obesity, BP Pathophysiology of cataracts = As lens ages, new layers of fibers are added and the lens nucleus is compressed Insulin, and glucagon, know the differences o The purpose of insulin is to draw glucose into the cell; by doing this, this will help to lower the blood sugar. In type 1 diabetes there is NO insulin due to destruction of the beta cells in the pancreas. In type 2 diabetes (insulin resistance) there is insulin production, however it is not sufficient enough. o Glucagon Stroke patients and their manifestations, how would they present or look Manifestations: Sudden in onset Focal One-sided Weakness of face/arm/leg Unilateral numbness Vision loss in one eye or to one side Language disturbance Slurred speech Unexplained imbalance Pre-renal, intra-renal and Post renal failure Pre-renal Intra-renal Post-renal

Know stroke volume, cardiac output Skull fractures Complications related to spinal cord injuries What type of change occur when we are stressed out? In terms of vitals and how body reacts to stress. Signs for right/ left heart failure Left sided heart failure Right sided heart failure If you have left sided heart failure volume will start to back up into your pulmonary and you will have respiratory symptoms Why? All your arteries and veins, you will have pulmonary congestion. o Pulmonary Congestion & Edema o Manifestoed first by restlessness due to SOB o Cyanosis (periorbital) o Frothy Sputum o Hypoxia in the gums o Orthopnea o Decreased Cardiac output o Pulmonary Crackles Pathophysiology Right sided heart failure follows Left sided heart failure. Why? Pressure on left side of heart is higher than pressure on the right. Now you already have pulmonary, now you will have systemic backup. The right sided heart failure patient will have peripheral edema, hepatomegaly (jugular vein distension, only is seen on the right sided because it is systemic). What’s going on essentially? The pulmonary vascular is backing up into the right ventricle, right ventricle is backing up into the right atrium, backwards, right atrium now into my o Diminished cardiac output o Decreased injection fraction Etiology o Acute Myocardial Infarct o Hypertension Worsening heart failure complication: potential for pulmonary edema periphery. Will have edema. o Interstitial edema , fluid between the vascular space and tissue. (capillaries leaking form the intervascular into the outside space)o Your hydrostatic pressure has increased. Fluid will be pulled out.

Right Sided heart failure: They will have 3 rd. spacing, fluid accumulation outside. o Number one cause is left sided heart failure. o Asciteso Liver Congestiono Impaired Liver Function Edema to both lower legs is related to right sided heart failure. Auditory issues Conductive Hearing Loss Sensorineural Hearing Loss o Auditory stimuli are not transmitted through or not effectively transmitted through the auditory canal, TM, or middle or inner ear o Temporary or permanent o Occurs with disorders that affect inner ear, auditory nerve or auditory pathways of brain o Sound waves are conducted to inner ear; but abnormal cochlear apparatus distort/decrease transfer of information to the brain Pathophysiology for Parkinson’s pg. 472-475 o Widely believed that most cases are caused by an interaction of environmental and genetic factors o Oxidative stress, apoptosis, and mitochondrial disorders might lead to degeneration o Dopamine depletion results from degeneration of the dopamine nigrostriatal system o Develops from a postencephalatic syndrome o Side effect of therapy with antipsychotic drugs which block dopamine receptors o Toxic reaction to a chemical agent o Outcome of severe carbon monoxide poisoning TIA and a stroke differences TIA Stroke Similar symptoms to a stroke but go away