Studyguide Exam 4 2020 - Study guide for exam 4 PDF

Preview

Summary

Study guide for exam 4...

Description

STUDY GUIDE EXAM 4 – 2020 Unit 13 Chapter 43 o What predisposes men to cancer of prostate (is there a higher risk factor with race?), be able to describe screening tools, what is a Gleason score? What predisposes to cancer of the testes?  Predisposes of prostate cancer: age (85% > 65), race (AA), heredity, and environment (high fat diet)  Screening tools: transrectal ultrasound, Gleason grading system  Gleason Score: well differentiated Grade 1 to poorly differentiated Grade 5  Predisposes of testes cancer: cryptorchidism (undescended testes (higher the location, higher the risk)), genetics o ED- review causes, arterial insufficiency, what diseases cause, what is role of nitric oxide and cGMP?  Causes: Psychogenic (organic or mixed), Neurogenic (Parkinson’s, stroke, cerebral trauma, spinal cord (depends on location, level and extent of lesion)), Drugs (antidepressant, antipsychotic, antihypertensive), excessive alcohol and aging  Arterial insufficiency: Hypertension, hyperlipidemia, cigarette smoking, DM, pelvic irradiation  Diseases that cause: Parkinson’s, high bp, high cholesterol  Role of nitric oxide: make penial muscles relax  cGMP: inhibited by phosphodiesterase type 5 o What predisposes a patient to cancer of the testes?  Cryptorchidism; undescended testes, the higher the location, the higher the risk; genetics o Testicular torsion-why does this have more urgency for detection and treatment?  Twisting of spermatic cord that suspends testes; pain radiating to inguinal area, N&V, affected testes large and tender; differentiate from inflammation/infection o Cause of urinary retention in older male-what is the disease?  Benign Prostatic Hyperplasia and Prostate tumors o Priapism, what is it, what causes it, what patient population is at high risk for this? Priapism is a failure of __________  Definition: Involuntary, prolonged, abnormal, painful erection  Causes: Sickle cell; deoxygenation and stasis of cavernosal blood during erection thought to increase sickling  Patient Population: 6-42% AA males  Failure of: venous outflow o Nurses role in vasectomy-patient education  Fertility continues 4-5 weeks after a vasectomy o BPH: cause, symptoms, what determines when treatment occurs?  Cause: Dihydrotestosterone biologically active metabolite of testosterone-mediator  Symptoms: Incomplete emptying, frequency, intermittency, urgency, weak stream, straining, nocturia, urinary retention  When treatment occurs: rating on BPH symptom index (0-7) o Cryptorchidism  Incidence related to birth weight and gestational age, undescended testes, spontaneous descent often occurs during 3-6 months, consequences infertility, malignancy, and psychological effects Chapter 45 o Purpose of Pap smear; precipitating causes and symptoms of Ca of cervix, role of HPV causing dysplasia  Purpose: diagnose cervical cancer  Precipitating causes and symptoms of Ca of cervix: abnormal bleeding, abnormal vaginal discharge, palpable mass, pain during intercourse  Role of HPV causing dysplasia: causes vaginal and cervical cancer 1

o Polycystic ovary syndrome-pathophysiology and clinical manifestations  Pathophysiology: excessive ovarian and androgen hormones  Clinical Manifestations: oligomenorrhea, hyperandrogenism (acne and infrequent periods), elevated testosterone levels on blood testing, polycystic-appearing ovaries with numerous small cysts o Breast cancer: who is at risk (e.g. impact of menopause timing, age of first child), diagnosis, role of lumpectomy, should everyone who has had a lumpectomy have their regional nodes tested for metastasis?  Risk: age, history, promotion of breast maturation and cell mutation (early menarche, late menopause, 1st child >30, not term pregnancies), hormonal influences, obesity, long-term use of postmenopausal hormone therapy, alcohol, physical inactivity  Diagnosis: physical examination, mammography, ultrasonography, percutaneous needle aspiration, stereotactic needle biopsy, excisional biopsy  Lumpectomy role:  Regional nodes tested for metastasis with lumpectomy: o Endometrial cancer, endometriosis, fibroids –brief overview from PP, role of genetics BRCA1 and 2  Endometrial cancer: most frequent invasive cancer in US females; 15-25% of postmenopausal women w/ bleeding have endometrial cancer, 10-fold increase if 50# overweight, diabetes, nulliparity, early menarche and late menopause  Endometriosis: functional endometrial tissue found in ectopic sites outside the uterus  Fibroids: benign tumors of smooth muscle origin, ¼ women over 35, growth rate and size greater in AA, asymptomatic or may cause menorrhagia o Disorders of pelvic support and uterine position, what causes and what are symptoms (briefly)  Pelvic support disorders and uterine position  Cystocele, rectocele, uterine prolapse o Why is ovarian cancer detected late? What are highest risk factors for ovarian cancer? What is nulliparity? What decreases risk? Role of genetics.  Detected late: may be asymptomatic or vague; NO good screens  Highest risk factors: history and ovulatory age  Nulliparity: no kids  Decreases risk: long-term oral contraceptive use, acetaminophen, and aspirin; surgical reducing strategies- prophylactic removal of both fallopian tubes and ovaries  Genetics role: 2+ first- or second- degree relatives have a 50% risk of development Chapter 46 o Role of HPV and what does it cause, be familiar with cellular changes  Role: increases risk of cervical cancer  Causes: cervical cancer o Normal bacterial flora, how are diabetic and immunosuppressed patients affected?  `Normal bacterial flora can be messed up easily o Candidiasis and trichomonas including vaginal discharge characteristics  Candidiasis: Yeast infection or thrush; present in 20-55% of healthy women, can be asymptomatic,  Results in- inflammation and thick odorless discharge  Causes: antibiotic therapy (suppresses the normal protective bacterial flora); high hormonal levels owning to pregnancy; the use of oral contraceptives (cause increase in vaginal glycogen stores); DM or HIV infection (compromise the immune system)  Trichomonas: anaerobic protozoan that feeds on vaginal mucosa and ingests bacteria and leukocytes  Symptoms: copious, frothy, malodorous, green or yellow discharge; erythema and edema of the affected mucosa; occasional itching and irritation; sometimes strawberry spots appear on cervix; associated w/ tubular infertility or pelvic inflammatory disease o Where does herpes simplex virus reside?  The original effected neuron 2

Unit 10 Chapter 32(partial)  Urine Formation including rate, role of anti-diuretic hormone, renal threshold definition e.g. blood glucose o Rate: 125 ml of filtrate/min but only 1ml of 125ml filtrate excreted in urine; 60 ml/hr o Role of anti-diuretic hormone: opens water channels on luminal aide of tubular cells producing a marked increase in water permeability; without ADH, water channels are closed, tubular cells lose water permeability and dilute urine is formed o Renal threshold definition: the plasma level at which the substance appears in the urine- exceeds the transport mechanism (e.g. uncontrolled diabetes 320 mg/min spills into urine (over 300, you spill glucose into urine)  Regulation of renal blood flow o SNS innervates; Angiotensin II, ADH, and endothelins produce vasoconstriction of renal vessels; Dopamine, nitric oxide, and prostaglandins dilate; constancy of blood flow maintained by autoregulation; Juxtaglomerular complex represents feedback control system linking GFR with renal blood flow, controls release of renin  Elimination function of kidney including role of creatinine/urea, aldosterone, and pH regulation o Creatinine/urea: product of creatine metabolism in muscles; formation/release are relatively constant; freely filtered in glomeruli and not reabsorbed and minimally secreted into tubules; serum value depends closely on GFR- used as measure of renal function o Aldosterone: regulation of NA and K; atrial natriuretic peptide-synthesized in muscle cells of atria and released with atria are stretched; vasodilation of arterioles, inhibits Na reabsorption/ ADH release o pH regulation: conserves HCO3/ eliminates H+  Endocrine function of kidney including RAA, erythropoietin, and Vitamin D (activation occurs where?) o RAA: renin is synthesized and stored in juxtaglomerular cells of kidney, release in response to decrease in renal blood flow or change in composition of distal tubular fluid or SNS stimulation o Erythropoietin: polypeptide hormone that regulates the differentiation of RBC in bone marrow, 8995% formed in kidneys, tissue hypoxia is stimulus for production o Vitamin D: activation occurs in kidney; needed to increase Ca absorption from GI tract and regulate deposition in bone  Urine and blood tests for kidney function (you will not be responsible for actual values). o Urine: 24-hour specimen; first voided and fresh; casts are molds of distal nephron lumen; less than 150 mg of protein /24 hour; specific gravity valuable index of hydration status and functional statues of kidney- 1.010-1.025 o Blood: serum creatinine- 0.6-1.2 screening measure, reflects GFR; blood urea nitrogen (8-20mg); influenced by protein intake, GI bleeding and hydrogen status; normal BUN to creatinine ration 10:1- ratios greater than 15:1 represent a prerenal condition such as CHF or GI bleeding  What substances are normally found in urine? o Water, waste products, excess electrolytes, unwanted substances  What impact does aldosterone have on NA? What effect does ADH have on water? What conditions have decreased ADH? o Aldosterone impact on NA: inhibits reabsorption o ADH effect on water: opens the water channels on luminal aide of tubular cells which increase water permeability; mediates reabsorption of water o Conditions decreasing ADH: Chapter 33  Glomerular, tubulointerstial, and cystic kidney disease. What is relationship between strep oropharynx infection and kidney disease? What is the pathophysiology? When does glomerulonephritis occur? 3





o Glomerular: Nephritic syndromes produce a proinflammatory response; nephrotic syndromeconstellation of clinical findings that results from increases glomerular permeability to plasma proteins  Acute Nephritic Syndrome: clinical correlate acute proliferative inflammation; onset of oliguria as GFR decreased followed by hematuria w/ red cell casts, proteinuria; decreased GFR leads to hypertension and edema; caused by renal limited disorder such as post strep infection (7-12 days post pharyngitis or impetigo) or secondary complication disorder such as SLE  Rapidly Progressive Glomerulonephritis: clinical syndrome characterized by signs of severe glomerular injury not associated with specific cause; focal and segmental proliferation glomerular cells with recruitment of monocytes and macrophages that form structures obliterating Bowmans space; SLE, small vessel vasculitiedes, and Goodpasture syndrome  Nephrotic Syndrome: not a specific disease- constellation of clinical findings that results from increases glomerular permeability to plasma proteins; primary disorders or secondary to changes of systemic diseases such as DM or SLE; massive proteinuria, lipiduria, hypoalbuminemia, generalized edema, and hyperlipidemia; disruption of coagulation system-risk for thrombotic complications o Tubulointerstial: ATN to follow; drug related nephropathies involve functional or structural changes in the kidneys after exposure to a drug; kidney are active in metabolic transformation of drugs and are exposed to toxic metabolites because of high flow and filtration pressure; tolerance varies w/age, renal function, state of hydration, bp, and pH of urine; elderly particularly susceptible; danger of nephrotoxicity w/ 2+ drugs; decrease in renal blood flow, obstructing urine flow; direct damage, or hypersensitivity reactions  Pyelonephritis: inflammation of parenchyma and pelvis  Acute Pyelonephritis: bacterial infection of upper urinary tract: source lower urinary tract and bloodstream, produce abrupt systemic signs (shaking chills, fever, headache, ill, pain over costovertebral angle- CVA tenderness)  Chronic: progressive process with scarring and deformation of the renal calices and pelvis; infection superimposed on obstructive abnormalities and/or reflux o Cystic:  Renal: fluid filled sacs or segments of dilated nephron interspersed with normally functioning nephrons; may arise as a developmental abnormality but most are hereditary  Autosomal Dominant Polycystic Kidney Disease: most common form; may also be formed in liver, pancreas; pain, hematuria, infection, hypertension; progress is slow, ESRF uncommon o Strep oropharynx infection and kidney disease:  Pathophysiology: elevated antistreptococcal antibody titer  Glomerulonephritis occurs: 7-12 days post pharyngitis Renal calculi-know general prevention measures-how does diet and disease impact development? o Prevention measures: fluid intake plus correcting cause with diet/meds o Diet and disease impacts development: bad diet and underlying disease increase/speed up development Urinary tract infections including etiology, host defenses, pathogen virulence, obstruction/reflux, catheters, manifestations, and diagnosis. o Etiology: Escherichia coli o Host defenses: distal urethra has pathogens, urine sterile o Pathogen virulence: o Obstruction/ reflux: increase risk o Catheters: CAUTI remains a significant risk in critical illness; prevention strategies include avoiding unnecessary use of urinary catheters; insertion of urinary catheters using aseptic technique; 4





adoption of evidence-based standards for maintenance of urinary catheters; daily clinical review of the need for the urinary catheter and if not needed prompt removal o Manifestations: frequency, dysuria, abdominal/back discomfort o Diagnosis: presence of 10 to the 5 or more bacterial per ml of urine Pyelonephritis onset and symptoms o Onset: abrupt o Symptoms: shaking chills, fever, headache, ill, pain over costovertebral angle- CVA tenderness Renal neoplasms-symptoms, population at risk, survival. o Wilms Tumor: solid mass in any part of kidney  Symptoms: asymptomatic abdominal mass and hypertension  Pop. at Risk: those with chromosomal abnormalities  Survival: >60% o Renal Cell Carcinoma: 3% of all cancers  Symptoms: denote advanced disease: hematuria and renal mass  Pop. at Risk: smokers, obese, asbestos, 55-84 years old  Survival: 30% if metastasis

Chapter 34  Types and causes of acute renal failure with emphasis on acute tubular necrosis o Prerenal: decreased blood supply; hypovolemia, sepsis, anaphylaxis, cardiogenic shock, heart failure, decreased renal perfusion due to drugs, contrast agents and vasoactive mediators o Postrenal: urine flow is blocked; stones, tumors, enlarged prostate (bladder outlet obstruction) o Intrinsic: kidney tubule function is decreased- acute tubular necrosis; prolonged renal ischemia, nephrotoxic drugs/metals/organic solvents, intratubular obstruction (myoglobinuria), acute renal disease (glomerulonephritis)  Acute Tubular Necrosis: GFR does not improve with restoration of blood flow; characterized by destruction of tubular epithelial cells with acute suppression of renal function  Ischemic: major surgery, severe hypovolemia, trauma, burns, sepsis (toxins sensitize renal tubular cells to damaging effects of ischemia); frequently multifactorial  Nephrotoxic: induce varying combination of renal vasoconstriction, direct tubular damage or intratubular obstruction; antimicrobials including aminoglycosides, chemotherapy, radiocontrast, heavy metals, and organic solvents; vulnerable because of rich blood supply and ability to concentrate toxins  Intratubular Obstruction: myoglobin (muscle trauma), hemoglobin (transfusion reaction), uric acid and myeloma (widespread malignancy or massive tumor destruction by therapeutic agents)  Effect of sex and age on post renal failure? Name the organ that is impacted. o  Early signs of renal failure o  Phases of ATN including recovery; What is the mortality? o Onset/ initiating phase: lasts hours or days from onset of precipitating event until tubular injury occurs o Maintenance phase: marked decrease in GFR, sudden retention of urea, K, and creatinine; low urine output, edema, pulmonary congestion; may be non-oliguric o Recovery or convalescent phase: renal tissue repair occurs; diuresis may begin before renal function has fully returned to normal; BUN and creatinine begin to return to normal  Chronic renal failure- know definitions of stages by effect on GFR (mL/min/1.73 m2) o Stage 1: kidney damage w/ normal or increased GFR- ≥90 5



o Stage 2: kidney damage w/ mild decrease in GFR- 60-89 o Stage 3: moderate decrease in GFR- 30-59 o Stage 4: severe decrease in GFR- 15-29 o Stage 5: Kidney failure 30% of epidermis detaches), papulosquamous dermatoses (scaling papules and plaques), Psoriasis (complex, chronic, multifactorial, inflammatory disease involving hyperproliferation of the keratinocytes in the epidermis), Arthropod infestations (scabies, pediculosis, ticks)  German measles: diffuse, punctate, macular rash begins on trunk and spreads to arms/legs, mild fever, postauricular suboccipital and cervical lymph node adenopathy common w/ cold like symptoms Be able to recognize based on description or picture the following: simple mole vs malignant melanoma, deep candida infections,  Simple Mole vs Malignant Melanoma  Melanoma: Asymmetry, Border irregularity, Color variation, Diameter >0.6 cm, Evolving change over time  Deep candida infections: normal inhabitant of GI tract, mouth, and vagina; release of irritating toxins on skin level; predisposed: DM, antibiotics, poor nutrition, and/or immune status; thrive in intertriginous folds; well defined border with satellite lesions Stages of Pressure Injury (ulcers) Stage 1 only  Characterized by a defined area of persistent redness in lightly pigmented skin or an area of persistent redness with blue or purple hues in darker pigmented skin  Nonblanchable erythema of intact skin, the heralding lesion of skin ulceration; in individuals with darker skin, discoloration of the skin, warmth, edema, induration, or hardness may be indicators Braden score is used to assess patients’ risk for developing pressure injury-what are the risk factors you should include in your assessment?  Sensory perception, moisture, activity, mobility, nutrition, friction & shear Where do candida infections thrive? What factors predispose patients to this infection  Thrive in intertriginous folds  Predispositions: DM, antibiotics, poor nutrition, and/or immune status First priority to take care of a major burn. 

o

o

o

o

o

o

10



o o

o o o

o

Airway Assessment and Management  Stop the burning process; ensure patent airway; carbon monoxide- provide high FIO2; upper airway damage; circumferential burns of thorax; then move to fluid resuscitation, pain, and wound management Mechanism for burn shock-mechanism for burn patients becoming edematous  How does a major burn impact other organ systems?  Respiratory system dysfunction, hemodynamic instability, hypermetabolic responses, renal insufficiency, gastric ulceration, sepsis, systemic infection, constriction of areas under circumferential burns (can’t expand chest wall) Full thickness burn affects what skin layers  Epidermis, dermis, subcutaneous tissue (can damage muscle, bone, blood vessels) Premalignant skin lesion in elderly  Keratoses Characteristics of psoriasis including pathophysiology  complex, chronic, multifactorial, inflammatory disease that involves hyperproliferation of the keratinocytes in the epidermis; increase in the epidermal cell turnover rate; environmental, genetic, and immunologic factors appear to play a role; commonly manifests on the skin of the elbows, knees, scalp, lumbosacral areas, intergluteal clefts, and glans penis, joints can be affected  Triggers include: cold, trauma, stress, infections, alcohol, and drugs Can drugs cause dangerous skin eruptions? Describe? Name condition  Yes; sulfonamides, nonsteroidal, anti-infl...