Pathophysiology made incredibly easy!.—5th ed. p. ; cm. Includes bibliographical references It will make you smile as it enhances your knowledge and skills. One of the top-selling titles from the Incredibly Easy series, the fully updated 5th edition of Pathophysiology Made Incredibly Easy presents. download Pathophysiology Made Incredibly Easy! Series®) 5th Edition, Kindle Edition We're sorry, the Kindle Edition of this title is not currently available for.
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And the winner is no surprise here: Pathophysiology Made Incredibly Visual! Well, as you can see, Pathophysiology Made Incredibly Visual has swept The Visual Awards! Selected references Assessment made incredibly easy (4th ed.). () Rubin's pathology: Clinicopathologic foundations of medicine (5th ed.). pathophysiology? Gain confidence, with the newly updated Pathophysiology Made Incredibly Easy!®, 6th Edition. Jumpstarts. ▽. Home > Books > Pathophysiology Made Incredibly Easy! Pathophysiology Made Incredibly Easy! View PDF. Jan 4, Pathophysiology made incredibly Easy 5th Edition PDF Free Download Pathophysiology made incredibly Easy 5th Edition PDF Free Download If.
It may then subside spontaneously, followed by exacerbations in late childhood, adolescence, or early adulthood. How it happens In atopic dermatitis, the allergic mechanism of hypersensitivity results in a release of inflammatory mediators through sensitized antibodies of the IgE class.
Histamine and other cytokines induce acute inflammation. Partial remissions and unpredictable exacerbations mark the course of this potentially crippling disease. RA is three times more common in women than men. It occurs worldwide, affecting more than 2. When exposed to an antigen, a person susceptible to RA may develop abnormal or altered IgG antibodies.
By aggregating into complexes, rheumatoid factor causes inflammation. Eventually, inflammation causes cartilage damage. Immune responses continue, including complement system activation.
Complement system activation attracts leukocytes and stimulates the release of inflammatory mediators, which then exacerbate joint destruction. Life expectancy for a person with RA may be shortened by an average of about 5 years. Four stages of inflammation Stage 1 Synovitis develops from congestion and edema of the synovial membrane and joint capsule.
Stage 2 Formation of pannus thickened layers of granulation tissue , which covers and invades cartilage and eventually destroys the joint capsule and bone. Stage 3 Fibrous ankylosis fibrous invasion of the pannus and scar formation that occludes the joint space occurs.
Bone atrophy and misalignment cause visible deformities and restrict movement, causing muscle atrophy, imbalance and, possibly, partial dislocations. Stage 4 Fibrous tissue calcifies, resulting in bony ankylosis fixation of a joint and total immobility. Pain associated with movement may restrict active joint use and cause fibrous or bony ankylosis, soft-tissue contractures, and joint deformities. These joints can't move like they used to! Pannus forms. Ankylosis fibrous occurs.
Hip calcifies. Rebus riddle Solve the riddle to learn a characteristic of a skin disorder. Photo finish 3, 5, 1, 4, 2, 6; Rebus riddle Atopic dermatitis is characterized by superficial skin inflammation and intense itching.
Both forms can progress into adrenal crisis. Massive destruction usually results from an autoimmune process whereby circulating antibodies attack adrenal tissue. This leads to a rapid decline in the steroid hormones cortisol and aldosterone, which directly affects the liver, stomach, and kidneys. Adrenal crisis Adrenal gland Liver Decrease in hepatic glucose output Destruction of the adrenal cortex causing rapid decline in hormone levels, adversely affecting all body systems Cortisol absent or very low Secondary The secondary form of adrenal hypofunction is caused by a disorder outside the gland, such as a pituitary tumor with corticotropin deficiency, or abrupt withdrawal of long-term corticosteroid therapy.
In secondary forms of the disorder, aldosterone secretion may be unaffected. Brain Hypoglycemia Profound hypoglycemia Adrenal crisis and hypotension… Know how it happens and you learn your lesson! But I just crave salty foods! Type 1 formerly called insulin-dependent diabetes mellitus Type 2 formerly called non-insulin-dependent diabetes mellitus , the more prevalent form Several secondary forms also exist, caused by such conditions as pancreatic disease, pregnancy gestational diabetes mellitus , hormonal or genetic problems, and certain drugs or chemicals.
How it happens Normally, insulin allows glucose to travel into cells. Insulin also stimulates protein synthesis and free fatty acid storage in adipose tissue. The pathophysiology behind each type of diabetes differs. It figures! This lack of energy causes glucose to build up in the blood vessels, resulting in damage to all body organs. Age-old story Age and diabetes Type 1 diabetes is the most common form of diabetes in children, but type 2 is on the rise owing to the obesity epidemic.
Symptoms that are more typical for children include: The trigger for this autoimmune response is unclear; it may have several causes. Genetic factors may play a part because the disease tends to occur in identical twins. Immunologic factors may also be the culprit.
The disease occasionally coexists with other autoimmune endocrine abnormalities, such as type 1 diabetes mellitus, thyroiditis, and hyperparathyroidism. I feel grave. What to look for Anterior pituitary T-cell lymphocytes become sensitized to thyroid antigens.
T-cell lymphocytes stimulate B-cell lymphocytes to secrete autoantibodies. Thyroid gland Thyroid-stimulating antibodies bind to and stimulate TSH receptors of the thyroid gland.
Increased production of thyroid hormones and cell growth result. This slowing is caused by a deficit in triiodothyronine T3 or thyroxine T4 , both of which regulate metabolism.
Hypothyroidism is classified as primary or secondary. The primary form stems from a disorder of the thyroid gland itself. The secondary form stems from a failure to stimulate normal thyroid function.
The secondary form of hypothyroidism may progress to myxedema coma, a medical emergency.
Metabolic syndrome—also called syndrome X, insulin resistance syndrome, dysmetabolic syndrome, or multiple metabolic syndrome—is a cluster of conditions characterized by: How it happens In the normal digestion process, the intestines break down food into its basic components, one of which is glucose. Glucose provides energy for cellular activity, and excess glucose is stored in cells for future use. Insulin, a hormone secreted in the pancreas, guides glucose into cells for metabolism or storage.
Excess insulin is then required to overcome this resistance. This excess in quantity and force of insulin causes damage to the lining of the arteries, promotes fat storage deposits, and prevents fat breakdown.
This series of events can lead to diabetes, blood clots, and coronary events.
Abdominal obesity evidenced by a waist of more than 40" [ It occurs in all age-groups, especially in people who have undergone radiation treatment of the neck area. There are three main types: Lesser horn of the hyoid bone Hyoid bone How it happens Thyrohyoid membrane Papillary carcinoma accounts for one-half of all thyroid cancers in adults.
Follicular carcinoma is less common but more likely to recur and metastasize to the regional lymph nodes and through blood vessels into the bones, liver, and lungs. Medullary carcinoma originates in the parafollicular cells and contains amyloid and calcium deposits. This rare form of thyroid cancer is familial, associated with pheochromocytoma, and completely curable when detected before it causes symptoms.
Untreated, it progresses rapidly. Seldom curable by resection, these tumors resist radiation and metastasize quickly. Follicular adenoma This photograph shows an encapsulated mass of follicular adenoma with hemorrhage, fibrosis, and cystic changes.
What is a major component of diabetes mellitus? Solve the word scrambles to discover four major signs and symptoms of diabetes mellitus. Has anyone seen the close-up shot of the kidney in the hospital? An interruption in my work flow! This can lead to serious failure! Renal Acute renal failure is the sudden interruption of renal function. It can be caused by obstruction, poor circulation, or kidney disease. Each type has separate causes. Acute renal failure is a critical illness. Its early signs and symptoms are oliguria decreased urine output , azotemia excess levels of urea in blood and, rarely, anuria failure to secrete urine.
Electrolyte imbalance, metabolic acidosis, and other severe effects follow as the patient becomes increasingly uremic and renal dysfunction disrupts other body systems.
Acute tubular necrosis ATN , also called acute tubulointerstitial nephritis, destroys the tubular segment of the nephron, causing uremia excess accumulation of protein metabolism by-products in blood and renal failure.
How it happens ATN results from ischemic or nephrotoxic injury, most commonly in debilitated patients, such as the critically ill and those who have undergone extensive surgery. In ischemic injury, disruption of blood flow to the kidneys may result from circulatory collapse, severe hypotension, trauma, hemorrhage, dehydration, cardiogenic or septic shock, surgery, anesthetics, or reactions to transfusions.
Ischemic ATN can damage the epithelial and basement membranes and cause lesions in the renal interstitium and is, therefore, irreversible. Nephrotoxic injury may result from ingestion of certain chemical agents such as contrast media administered during radiologic procedures , administration of antibiotics aminoglycosides , or a hypersensitive reaction of the kidneys.
Vasoconstriction of the afferent arteriole, caused by tubuloglomerular feedback, results in decreased glomerular capillary filtration pressure. Injury to the tubule results and the increased intraluminal pressure causes fluid to leak back from the lumen into the interstitium.
How it happens In nearly all types of glomerulonephritis, the epithelial layer of the glomerular membrane is disturbed. Acute poststreptococcal glomerulonephritis results from an immune response that occurs in the glomerulus.
Glomerular injury occurs as a result of the inflammatory process. When someone tries to change us, we stimulate antibody formation. Acute poststreptococcal glomerulonephritis Yeah, lodge it into the glomerular capillaries! This inflammatory process has the antigen-antibody complexes initiating the release of immunologic substances! Glomerulonephritis Age-old story Age and glomerulonephritis In children, the characteristic features of glomerulonephritis are usually encephalopathy with seizures and local neurologic deficits.
An elderly patient with glomerulonephritis may report vague, nonspecific symptoms, such as nausea, malaise, and arthralgia. Immune complex deposits on the glomerulus The severity of glomerular damage and renal insufficiency is related to the size, number, location, duration of exposure, and type of antigenantibody complexes.
An abnormal dilation of the renal pelvis and the calyces of one or both kidneys, hydronephrosis is caused by an obstruction of urine flow in the genitourinary tract. How it happens If the obstruction is in the urethra or bladder, hydronephrosis usually affects both kidneys. If the obstruction is in a ureter, it usually affects one kidney. Obstructions distal to the bladder cause the bladder to dilate and act as a buffer zone, delaying hydronephrosis. Total obstruction of urine flow with dilation of the collecting system ultimately causes complete atrophy of the cortex the outer portion of the kidney and cessation of glomerular filtration.
Dilated calyces Cross section of hydronephrotic kidney Signs and symptoms of hydronephrosis depend on the cause of the obstruction. The disease affects males and females equally and appears in three distinct forms. Another inherited form is called autosomal recessive PKD. In most cases, progressive compression of kidney structures by the enlarging mass causes renal failure about 10 years after symptoms appear. Acquired cystic kidney disease is the third form. How it happens Multiple spherical cysts, a few millimeters to centimeters in diameter and containing straw-colored or hemorrhagic fluid, cause grossly enlarged kidneys.
The cysts are distributed evenly throughout the cortex and medulla. Hyperplastic polyps and renal adenomas are common. Renal parenchyma may have varying degrees of tubular atrophy, interstitial fibrosis, and nephrosclerosis. The cysts cause elongation of the renal pelvis, flattening of the calyces, and indentations in the kidney. Intracranial aneurysms, colonic diverticula, and mitral valve prolapse also occur. Cysts can develop on the liver, spleen, pancreas, and ovaries.
Age-old story Age and polycystic kidney disease Renal deterioration is more gradual in adults than infants. However, in both age-groups, the disease progresses relentlessly to fatal uremia. Note that cysts have taken the place of almost all of the parenchyma. Pyelonephritis Acute pyelonephritis, also known as acute infective tubulointerstitial nephritis, is a sudden inflammation caused by bacteria that primarily affects the interstitial area and the renal pelvis or, less commonly, the renal tubules.
With treatment and continued follow-up care, the prognosis is good, and extensive permanent damage is rare. Pyelonephritis is more common in females, probably because of the shorter female urethra and the proximity of the urinary meatus to the vagina and the rectum.
Both conditions allow bacteria to reach the bladder more easily. In males, pyelonephritis may occur due to a lack of the antibacterial prostatic secretions normally produced in males. How it happens Typically, the infection spreads from the bladder to the ureters, then to the kidneys, as in vesicoureteral reflux. Vesicoureteral reflux may result from congenital weakness at the junction of the ureter and the bladder.
Bacteria refluxed to intrarenal tissues may create colonies of infection within 24 to 48 hours. Infection may also result from instrumentation such as catheterization, cystoscopy, or urologic surgery , from a hematogenic infection as in septicemia or endocarditis or, possibly, from lymphatic infection.
Pyelonephritis may also result from an inability to empty the bladder for example, in patients with neurogenic bladder , urinary stasis, or urinary obstruction due to tumors, strictures, or benign prostatic hyperplasia.
In children younger than age 2, fever, vomiting, nonspecific abdominal complaints, and failure to thrive may be the only signs of acute pyelonephritis. In the first photo, you can see many reddish areas that indicate scarring.
In the second photo, you can see severe dilation of the calyces as well as atrophy and scarring of the cortex. Also called nephrolithiasis, renal calculi stones can form anywhere in the urinary tract, although they most commonly develop in the renal pelves or calyces.
They may vary in size and may be solitary or multiple. Fin Calculi form when substances that are normally dissolved in the urine, such as calcium oxalate and calcium phosphate, precipitate. Dehydration may lead to renal calculi as calculus-forming substances concentrate in urine. Many calculi are less than 5 mm in diameter and are usually passed in the urine.
Staghorn calculi can continue to grow in the pelves and extend to the calyces, forming a branching calculus and, ultimately, resulting in renal failure if not surgically removed. Calculi may be composed of different substances, and the pH of the urine affects the solubility of many calculus-forming substances.
Hop along with me and see how it all happens! A crystal evolves in the presence of calculus-forming substances calcium oxalate, calcium carbonate, magnesium, ammonium, phosphate, or uric acid and becomes trapped in the urinary tract, where it attracts other crystals to form a calculus. A high urine saturation of these substances encourages crystal formation and results in calculus growth.
Calculi form around a nucleus in the appropriate environment. Renal calculi A look at staghorn calculi This photo shows a kidney with hydronephrosis and staghorn calculi, which are casts of the dilated calyces. Renovascular hypertension Renovascular hypertension occurs when systemic blood pressure increases due to intrarenal atherosclerosis or stenosis of the major renal arteries or their branches.
This narrowing sclerosis may be partial or complete, and the resulting blood pressure elevation may be benign or malignant. Renovascular hypertension is the most common type of secondary hypertension. How it happens The kidneys normally play a key role in maintaining blood pressure and volume by vasoconstriction and regulation of sodium and fluid levels.
In renovascular hypertension, these regulatory mechanisms fail. This potent vasoconstrictor heightens peripheral resistance and blood pressure.
Check for headache, nausea, anorexia, an elevated renin level, and hypertension. Angiotensin I 1 Certain conditions, such as renal artery stenosis and tumors, reduce blood flow to the kidneys. This reduced flow causes juxtaglomerular cells to continuously secrete renin—an enzyme that converts angiotensinogen a plasma protein to angiotensin I.
In this stage, be alert for flank pain, systolic bruit in the epigastric vein over the upper abdomen, reduced urine output, and an elevated renin level. Assess for hypertension, diminished urine output, albuminuria, hypokalemia, and hypernatremia. Expect worsening symptoms. Angiotensin II Aldosterone Angiotensin II 5 Intermittent pressure diuresis causes excretion of sodium and water, reduced blood volume, and decreasing cardiac output.
Check for blood pressure that increases slowly, drops but not as low as before , and then increases again. Headache, high urine specific gravity, hyponatremia, fatigue, and heart failure also occur. Excessive aldosterone and angiotensin II can damage renal tissue, leading to renal failure. Expect to find hypertension, pitting edema, anemia, decreased level of consciousness, and elevated blood urea nitrogen and serum creatinine levels. Identify the assessment technique being used in each illustration.
Other skin disorders need medical attention! There are two types of acne: How it happens 1 Excessive sebum production Androgens stimulate sebaceous gland growth and the production of sebum, which is secreted into dilated hair follicles that contain bacteria. Epithelial cells Sebaceous follicle 2 Increased shedding of epithelial cells The bacteria, usually Propionibacterium acne and Staphylococcus epidermidis, are normal skin flora that secrete the enzyme lipase. This enzyme interacts with sebum to produce free fatty acids, which provoke inflammation.
Sorry, guys! Adolescent facial acne Age-old story Age and acne Acne occurs in both males and females. What to look for 3 Inflammatory response in follicle Hair follicles also produce more keratin, which joins with the sebum to form a plug in the dilated follicle.
Ruptured follicle The acne plug may appear as: How it happens The injuring agent denatures cellular proteins. Some cells die because of traumatic or ischemic necrosis. Loss of collagen cross-linking also occurs with denaturation, creating abnormal osmotic and hydrostatic pressure gradients, which cause the movement of intravascular fluid into interstitial spaces.
Cellular injury triggers the release of mediators of inflammation, contributing to local and, in the case of major burns, systemic increases in capillary permeability. Superficial partial-thickness burns A superficial partial-thickness burn causes localized injury or destruction to the epidermis only by direct such as chemical spill or indirect such as sunlight contact.
The barrier function of the skin remains intact. Superficial partial-thickness burns Deep partial-thickness burns Deep partial-thickness burns involve destruction to the epidermis and some dermis. Color can be a major assessment factor when it comes to burns. A white waxy burn is a superficial partial-thickness burn.
A leathery black or silver-colored burn is full-thickness. Burns Age-old story Age and burns Burn victims younger than age 4 and older than age 60 experience a higher incidence of complications and thus a higher mortality rate. Full-thickness burns moderate edema and pain. As these blisters break, the nerve endings become exposed to the air. Pain and tactile responses remain intact, so subsequent treatments are painful. The barrier function of the skin is lost.
A major full-thickness burn affects every body system and organ. A fullthickness burn extends through the epidermis and dermis and into the subcutaneous tissue layer. If the burn is fourth-degree, muscle, bone, and interstitial tissues would also be involved. Within hours, fluids and protein shift from capillary to interstitial spaces, causing edema.
The immediate immunologic response to the burn injury makes burn wound sepsis a potential threat. Lastly, an increase in calorie demand after the burn injury increases metabolic rate.
It may follow damage to the skin, such as a bite or wound. As the cellulitis spreads, fever, erythema, and lymphangitis may occur. If cellulitis is treated in a timely manner, the prognosis is usually good. How it happens As the offending organism invades the compromised area, it overwhelms the defensive cells neutrophils, eosinophils, basophils, and mast cells that break down the cellular components, which normally contain and localize the inflammation.
As cellulitis progresses, the organism invades tissue around the initial wound site. Phases of acute inflammatory response 1 Wound Age-old story Age and cellulitis Cellulitis of the lower extremity is more likely to develop into thrombophlebitis in an elderly patient. The classic signs of cellulitis are erythema and edema surrounding the initial wound. The tissue is warm to the touch. It can also appear as an irritation of the skin resulting from contact with concentrated substances to which the skin is sensitive, such as perfumes, soaps, chemicals, or metals and alloys for instance, the nickel used in jewelry.
Requires 1 hour. Processing, presentation, and sensitization takes 24 hours. They just have to be careful of their sensitive skin! T cells Sensitized T cells 4 Sensitized T cells enter a lymphatic vessel. Lymphatic vessel 5 Sensitized T cells transported to regional lymph nodes, where T-cell hyperplasia is induced. It usually occurs in adults and produces localized vesicular skin lesions and severe neuralgic pain in peripheral areas.
Complete recovery is common, but scarring may occur as well as vision impairment with corneal damage or persistent neuralgia. This infection progresses to viremia, seeding of fixed macrophages, and dissemination of VZV to the skin the rash seen in chickenpox. After the initial infection, the virus lays dormant in the dorsal spinal ganglion, where it remains for many years. The virus is reactivated, probably because of decreased cellular immunity, and spreads from ganglia along the sensory nerves to the peripheral nerves of sensory dermatomes, causing shingles.
However, the incidence in younger age-groups is increasing because of increased sun exposure or, possibly, a decrease in the ozone layer.
Incomplete or incorrect repair of UV radiation—induced DNA damage is largely responsible for the growth of precancerous cells and malignant cells. Bring me the sunscreen! A closer look Malignant melanoma can arise on normal skin or from an existing mole. If not treated promptly, it can spread to other areas of skin, lymph nodes, or internal organs.
So wear that sunblock or put on a hat and pants! What to look for Just as I suspected. Lots of clues here that lead me straight to malignant melanoma. These ulcers may be superficial caused by local skin irritation with subsequent surface maceration or deep originating in underlying tissue.
Deep lesions commonly remain undetected until they penetrate the skin, but by then, they have usually caused subcutaneous damage. Most pressure ulcers develop over five body locations: Patients who have contractures are at an increased risk for developing pressure ulcers because of the added pressure on the tissue and the alignment of the bones.
How it happens A pressure ulcer is caused by an injury to the skin and its underlying tissues. The pressure exerted on the area causes ischemia and hypoxemia to the affected tissues because of decreased blood flow to the site. As the capillaries collapse, thrombosis occurs, which subsequently leads to tissue edema and then tissue necrosis.
Ischemia also adds to an accumulation of waste products at the site, which in turn leads to the production of toxins. The toxins further break down the tissue and eventually lead to the death of the cells.
Age-old story Age and pressure ulcers Age plays a role in the incidence of pressure ulcers. Muscle is lost with aging, and skin elasticity decreases. Both of these factors increase the risk of developing pressure ulcers. One singular sensation of a stage II pressure ulcer is a shallow open wound—like the blisters these heels are giving me! Match the definitions with their corresponding disorders.
Most lethal skin cancer 2. Localized areas of cellular necrosis that are most common over bony prominences 3. Chronic inflammatory disease of the sebaceous glands 4.
Inflammation or irritation of the skin due to contact with irritating chemical or atopic allergen 5. Infection of the dermis or subcutaneous layer of the skin 6. Acute inflammation caused by infection with herpesvirus 3. Cellulitis Herpes zoster Acne Contact dermatitis E. Malignant melanoma F. Pressure ulcers Answers: Matchmaker 2.
How it happens Regardless of the cause, BPH begins with nonmalignant changes in periurethral glandular tissue. The growth of the fibroadenomatous nodules masses of fibrous glandular tissue progresses to compress the remaining normal gland nodular hyperplasia. The hyperplastic tissue is mostly glandular, with some fibrous stroma and smooth muscle.
As the prostate enlarges, it may extend into the bladder and obstruct urinary outflow by compressing or distorting the prostatic urethra. Periodic increases in sympathetic stimulation of the smooth muscle of the prostatic urethra and bladder neck also occur. Progressive bladder distention may cause a pouch to form in the bladder that retains urine when the rest of the bladder empties. This retained urine may lead to calculus formation or cystitis.
The urethra has been compressed to a slit about as wide as a paperclip. Characteristically, the condition starts with a group of symptoms known as prostatism, which are caused by enlargement, and include: As the obstruction increases, it causes: Carcinoma of the breast Higher risk Genetic mutations are just one of the major risk factors for breast cancer.
Preinvasive disease, also known as precancerous dysplasia, cervical intraepithelial carcinoma, or cervical cancer in situ, is more frequent than invasive cancer and occurs more commonly in younger women. How it happens Preinvasive disease can range from mild cervical dysplasia in which the lower third of the epithelium contains abnormal cells , to carcinoma in situ in which the full thickness of epithelium contains abnormally proliferating cells.
In invasive carcinoma, cancer cells penetrate the basement membrane and can spread directly to adjacent pelvic structures or disseminate to distant sites by lymphatic routes.
A closer look Carcinoma in situ Normal cells Premalignant cells In almost all cases of cervical cancer, the histologic type is squamous cell carcinoma, which varies from well-differentiated cells to highly anaplastic spindle cells. Endometrial cancer originates in the endometrium or lining of the uterus. How it happens In most cases, endometrial cancer is an adenocarcinoma that metastasizes late, usually from the endometrium to the cervix, ovaries, fallopian tubes, and other peritoneal structures.
It may spread to distant organs, such as the lungs and the brain, through the blood or lymphatic system. Lymph node involvement can also occur. Most postmenopausal women who develop uterine cancer have a history of anovulatory menstrual cycles or other hormonal imbalance.
Ectopic endometrial tissue is generally confined to the pelvic area, usually around the ovaries, uterovesical peritoneum, uterosacral ligaments, and the cul-de-sac, but it can appear anywhere in the body. How it happens The ectopic endometrial tissue responds to normal stimulation in the same way as the endometrium, but more unpredictably.
The endometrial cells respond to estrogen and progesterone with proliferation and secretion. During menstruation, the ectopic tissue bleeds, which causes inflammation of the surrounding tissue. This inflammation causes fibrosis, leading to adhesions that produce pain and infertility. After cancers of the lung, breast, and colon, primary ovarian cancer ranks as the most common cause of cancer death among women in the United States.
In women with previously treated breast cancer, metastatic ovarian cancer is more common than cancer of any other organ. The prognosis varies with the histologic type and staging of the disease. Ovarian tumors spread rapidly intraperitoneally by local extension or surface seeding and, occasionally, through the lymphatic system and the bloodstream.
In most cases, extraperitoneal spread is through the diaphragm into the chest cavity, which may cause pleural effusions. Other metastasis is rare. Ovarian cysts Ovarian cysts are usually nonneoplastic sacs on an ovary that contain fluid or semisolid material. Although these cysts are usually small and produce no symptoms, they may require thorough investigation as possible sites of malignant change. Cysts may be single or multiple. Common physiologic ovarian cysts include follicular cysts, corpus luteum cysts, and dermoid cysts.
The prognosis for nonneoplastic ovarian cysts is excellent. How it happens Ovarian cysts can develop any time between puberty and menopause, including during pregnancy. During the proliferative phase of the menstrual cycle, many follicles are released but only one reaches maturity and produces estrogen. The follicular cyst eventually matures to a corpus luteum after ovulation and produces progesterone until the beginning of the next menstrual cycle.
Follicular cysts occur in the first 2 weeks of the cycle. Two functional ovarian cysts may develop: This type of cyst can become very large and can contain hair, teeth, bone, and cartilage.
Adenocarcinoma is the most common form. Malignant prostatic tumors seldom result from the benign hyperplastic enlargement that commonly develops around the prostatic urethra in older men. Typically, when primary prostatic lesions spread beyond the prostate gland, they invade the prostatic capsule and then spread along the ejaculatory ducts in the space between the seminal vesicles or perivesicular fascia. When prostatic cancer is fatal, death usually results from widespread bone metastasis.
Signs of advanced disease are due to obstruction caused by tumor progression. The more individuals in a family who have the disease, the greater the risk for others in the family to develop it.
Metastatic carcinoma Lymph node metastasis We may not be the cause of urinary problems when prostate cancer is involved. The prognosis depends on the cancer cell type and stage. When treated with surgery, chemotherapy, and radiation, almost all patients with localized disease survive beyond 5 years. These tumors, which are characterized by uniform, undifferentiated cells, resemble primitive gonadal cells.
Other tumors—nonseminomas—show various degrees of differentiation. Typically, when testicular cancer extends beyond the testes, it spreads through the lymphatic system to the iliac, para-aortic, and mediastinal nodes. Metastases affect the lungs, liver, viscera, and bone. Are you saying that seminoma tumors look like us primitive cells? A closer look Vas deferens Epididymis Age-old story Age and testicular cancer Testicular cancer seldom occurs in children.
Malignant testicular tumors are the most prevalent solid tumors in men ages 20 to Reproductive disorders Uterine fibroids Uterine fibroids, the most common benign tumors in women, are also known as myomas, fibromyomas, or leiomyomas. Uterine fibroids are tumors composed of smooth muscle and usually occur in the uterine corpus, although they may appear on the cervix or on the round or broad ligament.
The tumors become malignant leiomyosarcoma in less than 0. How it happens Leiomyomas occur from an overgrowth of smooth muscle and connective tissue in the uterus. A genetic predisposition exists. Both estrogen and progestin receptors are present in fibroids and elevated estrogen levels may cause fibroid enlargement. Some fibroids may decrease in size during pregnancy.
Fibroids shrink after menopause, but some regrowth may occur if the woman begins hormonal therapy. Genetically speaking, some women are predisposed to uterine fibroids. In the illustration, label the anatomic structures involved in prostatic enlargement. Which reproductive disorder usually has a poor prognosis? Philadelphia, PA: Atlas of pathophysiology 3rd ed.
Bickley, L. Brender, E. Cardiogenic shock. Journal of the American Medical Association, 21 , Gandhi, S. Echocardiography, 25 3 , — Grimard, B. Aortic stenosis: Diagnosis and treatment. American Family Physician, 78 6 , — McCance, K. The biologic basis for disease in adults and children 6th ed.
Murdoch, D. Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: Archives of Internal Medicine, 5 , — Pathophysiology made incredibly easy 4th ed. Porth, C. Concepts of altered health states 8th ed. Rubin, E. Clinicopathologic foundations of medicine 5th ed. Hall, J. Thank you for your feedback. Share your thoughts with other customers. Write a customer review. Read reviews that mention incredibly easy nursing school easy to understand nursing student recommend for anyone easy to read made incredibly pathophysiology made care plans highly recommend great book textbook easy to follow made easy must have for nursing advanced pathophysiology helped me understand patho book good book pathophysiology class.
Top Reviews Most recent Top Reviews. There was a problem filtering reviews right now. Please try again later. Paperback Verified download. Bought as a refresher for Advanced Pathophysiology for FNP school, and while it helped review the basics it was not sufficient for in-depth study.
But it's a fabulous product for a basic refresher. This book was downloadd on recommendation by my text book's website, and I have NOT been disappointed! For beginning Pathophysiology, this book is incredibly easy to understand and the visual depictions of processes helps you "see development in progress" in your mind's eye. This concept is incredibly important when it comes time for exam, because you have NO IDEA what questions will be asked about the processes.
With this guide, you understand the process all the way through, so you're prepared to answer ANY questions! The textbook will be useful as a reference I even have the Pathophysiology Made Incredibly Visual, which is another great reference, but overall, this book is my favorite!
I hope this review helps you in your download decision I found this helpful when taking Patho last semester. If I would have spent more time reading through it early on it would have been more beneficial. It is definitely worth having to reference for simplified clarification. Be aware though, it is not comprehensive. There were many topics that were missing from the book. As one might guess given it's small size compared to a patho text book.
I got an A in patho and all I can say is know causes, manifestations, and the reasons why those are what they are. Know this inside and out and you will be okay. downloadd this book as a resource for my graduate level Pathophysiology book. I truly don;t even think it would be any help to a beginning student. The book contains nothing more than headings you would find in a patho text.
There is no explanation and no explaining of information. The content is truly what you would find in the summary bullet points at the end of a chapter. This is not a book I would recommend on any level, save your money for sure.
This is an awesome book. I am a nurse practitioner student who's taking advanced pathophysiology, but haven't had pathophysiology.
This book is an excellent bridge between the two. Colorful and easy reading. An excellent resource. Helped me understand the class versus just memorizing material. Would recommend for anyone having issues with patho or anyone who needs more in depth explinations. I love this book, it really made a difference in nursing school. Urinary system Makes it easy to learn the basics of nursing science, concepts and skills. Series Incredibly Easy! This is not a physical book but a ebook.
What is an eBook?. All platforms are able to g This practical reference uses a unique, conversational writing style that breaks down complex concepts and information to make ECG interpretation easier to understand. In addition, the book explains h All pages are intact, and the cover is intact. The spine may sho RN2ED, a nurse education consultancy. Assessment Made Incredibly Easy! Condition is Good. Fluids and Electrolytes Made Incredibly Easy!
The sp The spine may Made Incredibly Easy: Item in good condition. Wound Care Made Incredibly Easy! Fairly worn, but readable and intact.
If applicable: Dust jacket, disc or access code may not be included.