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COMPLETE Pathophysiology Notes - Part 4 (4.0ed the final exam!)

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NURS 2080

REPRODUCTIVE DISORDERS Acute bacterial prostatitis Infection or reflux into prostatic ducts An ascending urethral connection; considered a subtype of a UTI in men Caused by E. coli or other G- rods Risk factors Anyone with impaired host defenses (HIV/AIDS, people with diabetes mellitus) Any instrumentation done (catheter, etc.) Any narrowing within canal (urethral strictures) will cause urine to stay in bladder longer and can reflux into prostate Manifestations Fever & chills Malaise & myalgia (muscle pain) Frequent & urgent urination Dysuria Urethral discharge Dull achy pain (rectum, sacral coccygeal region, peritoneum) Warm prostate (because inflammation occurring) Chronic bacterial prostatitis Recurrent urinary tract infections Caused by G- rods; persistent strain Organisms similar to acute Symptoms Frequent & urgent urination Dysuria Perineal discomfort & low back pain Mostly afebrile Chronic prostatitis/chronic pelvic pain syndrome Symptoms Pain along penis, testicles & scrotum Painful ejaculation, decreased libido, impotence Low back pain Rectal pain radiating into inner thighs Urinary symptoms without bacteria present Inflammatory – nonbacterial prostatitis Inflamed prostate Elevated leukocytes & inflammatory cells in prostatic secretions Cause unknown Noninflammatory - prostatodynia Negative urine cultures and prostatic fluid Extraprostatic sources i.e. obstruction in bladder neck (urine cold shunt back into prostate and irritate it) *This is a gentleman who complains of pain and they can’t find any bacterial cause for it* Benign prostatic hyperplasia (BPH) Age related & non malignant Exact cause unknown – imbalance of cell proliferation & death Suspected cause is DHT (dihyrotestosterone) induced growth factors Increased # of epithelial cells & stromal components of periurethral area Decreased cell death resulting in accumulation of senescent cells Estrogens may also play role Lesions compress urethra, producing symptoms that affect outflow of urine Complications Frequency (bladder can’t fully empty), nocturia (becomes worse at night) Obstruction progresses – chronic urinary retention Urinary tract infections Destructive changes to bladder cell wall Hydroureter (urine in ureter) Hydronephrosis (enlargement of kidney from backed-up urine) Risk of renal failure (post-renal failure) Long-term results: using detrusor muscle, it hypertrophies to force urine out of bladder Eventually, detrusor muscle decompensates (gives up) If can’t empty bladder and urine becomes stagnant, it’s a medium for infection Destructive changes to bladder wall: this also hypertrophies Outpouchings between muscle layers occurs (diverticula of bladder wall), which can also become infected and cause diverticulitis of bladder Human Papilloma Virus Nonenveloped double stranded DNA virus Most common sexually transmitted infection Transmission Minor trauma to squamous epithelium Sign & Symptoms Most do not develop symptoms or health problems Genital warts Cell changes Cancer can occur in volva, vagina, cervix, anus, or oral pharynx (men can get HPV-related cancer) Prevention Pap smear HPV test Pelvic inflammatory disease Polymicrobial infection of upper reproductive tract Ascend through endocervical canal Factors predisposing Young women (16-24) Nulliparity Multiple partners Manifestations Lower abdominal pain & tenderness Purulent cervical discharge Fever & elevated WBC Painful intercourse Complications Scarred fallopian tubes (can lead to infertility) Abscesses Adhesions from healing of inflammatory process Peritonitis (bacterial infection spreads into fallopian tubes and then infects peritoneum) Endometriosis Functional endometrial tissue found outside of uterus This tissue can implant anywhere within abdominal cavity (i.e. peritoneum, bowel) Active; so tissue can bleed within that area Would normally bleed thru uterus Cause unknown Risk factors Early menarche Regular periods with Shorter cycles (< 27 days) Longer duration (> 7 days), Heavier flow Increased menstrual pain 1 degree relatives Symptoms – Pain (pelvic, back) Lesions stimulated by ovarian hormones More severe premenstrual, subsides on cessation Develop lesions/adhesions: no outlet when endometrial tissue bleeds Pelvic anatomy distorted: can cause infertility DIEBETES MELLITUS “sweet urine” Metabolic disorder characterized by hyperglycemia Decrease in insulin secretion, insulin action, or both Glucose Brain/Nervous system rely on glucose as a fuel source Extra glucose  stored as glycogen in skeletal muscles and liver When we exhaust intake within these places, extra glucose is converted to fatty acids and stored as triglycerides in fat/adipose tissue Terminology Glucogenolysis Glycogen is broken down Release of glucose from the liver between meals Maintains the blood glucose with in a normal range Glyconeogenesis Liver can also synthesize glucose From excess amino acids, fats, or other non-carbohydrate sources. Insulin secretion Secreted in response to a rise in glucose Promotes glucose uptake by target cells and provides for glucose storage as glycogen Prevents fat and glycogen breakdown Inhibits gluconeogenesis and increases protein synthesis Counterregulatory hormones can affect glucose Increase in epinephrine (catecholamine) Growth hormone has a lot to do with protein synthesis Cortisol can stimulate gluconeogenesis by the liver Pancreas produces hormones for metabolism/ cellular utilization of carbs, proteins, and fats Alpha cells secrete glucagon (glucagon used when blood sugar falls below normal, which is 70) Helps boost blood sugar in between meals Beta cells secrete insulin Delta cells secrete somatostatin and have inhibitory functions Acini cells secrete digestive enzymes Insulin unlocks channels so glucose from bloodstream can enter cells (gives us energy) Unlocks tyrosine (a signaling protein), which allows us to mediate affects of glucose, fat, and protein (allows synthesis or those products) No insulin in cells = glucose in bloodstream = cannot do synthesis Blood tests for diagnosis of DM Fasting Plasma Glucose ≥126mg/dl OR Oral glucose tolerance test ≥200mg/dl OR HA1C ≥6.5% OR Casual Blood Glucose test (if sugar > 200, indicates DM esp. if other symptoms present) Type 1 DM Destruction of pancreatic beta cells  loss of beta cell function with ABSOLUTE insulin deficiency Genetic and environmental Factors Type 1B: (5-10%) beta cell destruction, NO autoimmunity present. Mostly African or Asian descent; varying degrees of insulin deficiency Type 1A = autoimmune disorder Genetic component and environmental triggering factor They think T lymphocytes make changes to their beta antigen on pancreas T cells attack beta cells of pancreas Juvenile diabetes Because insulin deficiency, these patients prone to diabetic ketoacidosis Type 2 DM (90-95%) NIDDM = not insulin dependent diabetes mellitus Insulin resistance with: Relative insulin deficiency (decreased uptake) Liver can overproduce glucose Impaired release of insulin r/t blood glucose levels (beta cell dysfunction) 90-95% of DM Obesity, family predisposition In type 2, insulin is produced In type 1, virtually no insulin is produced Clinical manifestations 3 P’s (3 p’s = polyuria, polydipsia, polyphagia) Polyuria = lots of urine Has to do with body’s ability to pull fluid Fluid pulled into vascular space (serum) With increased fluid; kidneys filter it out Polydipsia = thirst from fluid loss Polyphagia = hungry Seen more often in type 1; decrease in energy production because insulin not getting into cells Type 1 symptoms arise suddenly; wt. loss Weight loss due to body breaking down a lot of tissue Type 2 symptoms develop more insidiously; polyuria/polydipsia more common Other S&S of hyperglycemia Blurry vision, fatigue, numbness (paresthesia), increase in skin infections (i.e. yeast) Hypoglycemia Below normal blood glucose levels Results from excess of insulin Could give themselves too much insulin, or took insulin/diabetic pills and forgot to eat Altered cerebral function – brain needs glucose See symptoms of decreased function (altered mental behavior, cannot problem solve, confusion, headache, seizures, diabetic coma if blood sugar is low enough) Activation of ANS (autonomic nervous system) Anxiety/jitters Cold/clamminess to skin (constriction of blood vessels) *Exercising increases demands; problems in type 1 DM* Acute complication Type 1 Acute complication: DKA (diabetic ketoacidosis) *This is how many Type I diabetics are diagnosed Ketosis results from incomplete metabolism of fatty acids Type I Acute, life threatening Osmotic diuresis causes massive fluid loss Causes Stress, stress of illness Not taking enough insulin Diagnosis Hyperglycemia Ketosis Incomplete metabolism of fatty acids  end up with ketones Metabolic acidosis Breaking down fatty acids Additional Symptoms Rapid breathing, fruity breath (sign of ketosis) N/V  abdominal pain, dehydration Acute complication Type 2: HHS (hyperosmolar hyperosmotic syndrome) Causes Profound dehydration brought on by infection and stressors Stressors include MI, acute pancreatitis Diagnosis: Hyperglycemia Hyperosmolarity/dehydration Absence of ketoacidosis Just enough insulin to prevent this Depression of sensorium Confusion, depression, even coma and seizures Because water pulled out of brain cells and body tissues Seen more in elderly Hydrogen/K+ exchange – in order to buffer acids, H ions shift into cell in exchange for K K disturbances seen here Labs DKA (acidotic state) Serum Glucose >250mg/dL Serum and urine ketones + Serum pH: <7.3 (because lose base; have low bicarbonate) Serum HCO3 <15mEq/L HHS Serum Glucose >600mg/dL Serum & urine ketones - Serum pH >7.4 (normal pH because normal bicarbonate) Serum HCO3: >20mEq/L Serum Osmo >320mOsm/L (profound dehydration; lots of solutes within vasculature) Normal HCO3 22-26 mEq/L Chronic complications over time Microvascular and macrovascular problems Micro – thickening of vessel membranes – can happen in capillaries and arterioles Microvascular complications – nephropathy, retinopathy, and neuropathy Macrovascular problems – effect heart, brain, vasculature (arteries) Microvascular complications: diabetic nephropathy *Leading cause of renal failure in US Proteinuria >500mg/24 hrs & dx of DM Lesions of glomeruli Early: Kidney enlargement Nephron hypertrophy Hyperfiltration Thickening of capillary membrane and sclerosis (scarring) of tissues Creates problems with filtration Increased urinary albumin secretion (losing proteins) Microalbuminuria first, then numbers get greater *both type 1 and type 2 have this problem Microvascular complications: diabetic retinopathy *Leading cause of acquired blindness in US Affecting capillaries and small arterioles within eye (because it’s a microvascular problem) Characterized by: Abnormal retinal vascular permeability Microaneurysm formation Neovascularization & associated hemorrhage Scarring Retinal detachment Increased risk for cataracts/glaucoma *Both type 1 and type 2 have this problem Microvascular complication: diabetic neuropathy Peripheral nerve dysfunction Somatic:  perception of vibration, pain, temp, esp. in lower extremities Autonomic: Disorders of vasomotor function,  cardiac response, inability to empty bladder, GI motility problems, sexual dysfunction Can lead to dizziness, syncope from postural hypotension Stomach loses good motility and contraction from nerve damage – GI issues Demyelination of schwann cells affects nerve conduction Increased risk falling (problem with vasomotor function – numbness), serious burns/injuries to feet; altered biomechanics of foot Macrovascular complications Combined with hypertension, hyperlipidemia, etc. accelerates complications DM major risk factor for CAD (coronary artery disease) MIs = most common cause of death for both type I and type II Cerebrovascular disease – strokes Type II diabetics at risk Peripheral arterial disease Accelerated atherosclerosis (more foot problems; less blood flow to feet combined with decreased sensation and altered immune function – patients more susceptible to infections that don’t heal and gangrene of foot; ischemic lesions) Foot ulcers If severe enough  ulceration, infection, amputation Lesions represent the effects of neuropathy & vascular insufficiency Infections follow trauma Common sites – back of heel, plantar part of metatarsals, great toe Prevention & patient teaching *Diabetics should inspect feet daily; many are unaware of foot infections (numbness) Infections Certain types occur, seen with frequency Hyperglycemia & glucosuria may influence the growth of microorganisms & increase severity of infections Increased risk of UTI because retaining urine – ascends to kidneys (polynephritis) DM & elevated blood sugar may impair host defenses Neutrophils Chemotaxis Phagocytosis Because of foot issues, vascularity of foot can cause osteomillitus of foot/bone ENDOCRINE ALTERATIONS Disorders Primary (target gland affected) Secondary (target hormone is normal; most hormones stimulated from pituitary) Tertiary (problem is hypothalamus) Results in pituitary and target hormone being not properly stimulated Many hormones are regulated by negative feedback mechanism Function is similar to that of a heating system (hypothalamus like a thermostat) Endocrine sensors detect a change in the hormone level Adjust secretion to maintain levels within an appropriate range Decrease stimulate hormone production Increased levels – production and release decrease Sensors are in either the hypothalamus or pituitary gland Which of the following structures controls greatest number target glands and cells? Pituitary gland Pituitary gland Hypofunction Not releasing enough hormones Congenital disorders Absence of the gland or absence of the enzyme needed for hormone synthesis Glands can be destroyed Graves disease when thyroid destroyed Adenomas Tumor pushes on pituitary; affecting function Decreased blood flow to that gland Age (as we age we can have atrophy of glands and decreased hormone release) Hyperfunction (excessive production related to hyperplastic gland) Hyperplasia – glands enlarged, an enlarged gland puts out more hormones Paraneoplastic disorders Can mimic hormones (particularly ADH; exogenous hormones) Pituitary gland (cont.) Anterior lobe produces Thyroid-stimulating hormone (TSH) Adrenocorticotropic hormone (ACTH) Growth hormone (GH) Gonadotropic hormones – sex hormones Posterior lobe Antidiuretic hormone (ADH) Oxytocin (important in pregnancy for uterine contractions and breast milk production) Growth hormone Helps bones grow & have to do with protein synthesis (regulates metabolic functions) GH can be stimulated by Hypoglycemia Starvation Stress GH can be inhibited by Pre-fatty acid release Increased glucose levels Deficiency = short stature; interferes with linear bone growth Excess = gigantism (longer face, extremities, organs including heart) Acromegaly GH excess in adulthood (insidious; might take >7 years to notice) Excess GH after linear plates have fused and we can’t grow any larger Common cause Adenomas; can increase GH release Soft tissue growth occurs Cartilage enlargement Gradual overgrowth of hands, feet, skull/face (change in facial features*) Other manifestations Excessive sweating Sexual disorders Hypertension Sleep apnea (affects breathing) Overgrowth of organs Enlarged heart, thyroid Hyperglycemia (develop insulin resistance; decreased glucose uptake) Thyroid gland Needs dietary iodine (iodine in ionized table salt) To help with T3 and T4 protein synthesis Bound to plasma proteins in blood Carries these hormones Hormone regulation by feedback Released in times of need When body has enough T3 and T4, feeds back to hypothalamus Important for protein synthesis Body functions affected by TH Metabolic rate Cardiovascular Both hypofunction and hyperfunction Gastrointestinal Neuromuscular TRH (Thyropin releasing hormone) produced by hypothalamus Releases TSH from anterior pituitary gland TSH increases overall activity of thyroid gland by increasing thyroglobulin breakdown & release of thyroid hormone from follicles into blood stream activating the iodide pump Increased levels of thyroid hormone T3 & T4 act in feedback inhibition of TRH or TSH Thyroid hormone deficit decreases metabolism, which alters the function of all major organs in body Hypothyroidism Tied to metabolic activity Primary Low T4 and elevated TSH levels Secondary Low TSH and TH, high levels TRH Tertiary Low levels TRH, TSH, and TH Causes Primary (destruction of gland) Hashimoto thyroiditis (antibodies attack gland) Iodine deficiency Postpartum women Cancers (head, neck, throat – radiation therapy affects thyroid gland) Secondary (problem with pituitary) Tertiary (problem with hypothalamus) Manifestations (caused by slowing of metabolic rate) Weakness/fatigue from decreased energy metabolism Weight gain despite loss of appetite (because metabolism is so slow) Cold intolerance; always cold Constipation (slowing things down) Course, dry hair Slow pulse Myxedema (puffy eyes, fat tongue, swelling of feet; all from accumulation of fluid) Myxedema coma Extreme form of hypothyroidism from metabolic rate slowing so dramatically – cardiac and respiratory failure Abnormal stimulation of thyroid gland by TSH–receptor antibodies is implicated in cases of graves disease Hyperthyroidism Eating a lot and stil losing weight; metabolism extremely fast Causes Graves Disease (form of hyperthyroidism) Overstimulation comes from thyroid stimulating antibodies Goiter (thin patients with big neck) Thyroiditis Infection of thyroid gland can stimulate hyperthyroid state Adenomas Autoimmune Thyroid stimulating antibodies created Increased metabolic rate (elevated T3 and T4) Increased sympathetic activity (tremor can occur, palpations, increases HR and RR) Thin, silky hair Diarrhea Person always warm Exophthalmosis Startled/sunken eye look from breakdown of fat tissue from excess metabolism Thyroid Storm Extreme form of hyperthyroidism: high temperature elevated HR, delirium Life-threatening, high mortality rate Primary adrenal cortical insufficiency (Addison Disease) Autoimmune disorder Adrenal cortical hormones Mineralocorticoid deficiency Aldosterone Patient thin from fluid loss; dehydrated;hypotensive Glucocorticoid deficiency Cortisol (important for glucose, protein, fat metabolism) Patient may suffer from lethargy, weakness, hypoglycemia Elevated ACTH levels Pigmentation (tan, dark creases, gums, mucous membranes) Other causes Infections, adrenal hemorrhage, cancer, AIDS Acute Adrenal Crisis (adrenal gland sits on top of kidneys) Extreme form of Addison’s disease Can occur if patients experience illness or stress Can also occur from massive bilateral adrenal hemorrhage, adrenal trauma Life threatening Hypoglycemia Glucocorticoid hormone excess (Cushing’s Syndrome) Opposite of Addison’s Cause: Pituitary (excess production of ACTH by pituitary gland) Adrenal (tumor of this gland) Ectopic (any other tumors within body that may secrete ACTH) Hypercorticolism – exaggeration of cortisol Moon face from altered fat metabolism Deposition of fat in body/face Buffalo hump on back Muscle weakness Extremity wasting (thin arms and legs from protein breakdown; weakened skin and tissues; purple striae along abdomen; osteoporosis from destruction of bone proteins) Elevated cortisol levels  immune dysfunction (poor wound healing) Elevated blood sugars from poor glucose metabolism – many of these patients become diabetic Patients can develop facial hair from elevated androgen levels Disorders of ADH Diabetes Insipidus Deficiency of ADH or decreased response to ADH Unable to concentrate urine; body cannot hold onto water Polyuria 2 types Neurogenic (neural problem) Decreased synthesis of ADH itself or release of ADH from posterior pituitary Nephrogenic (kidney problem) Related to genetics, drugs, electrolyte imbalances *We worry about elderly, because they cannot sense thirst well Syndrome of inappropriate ADH (SIADH) Failure of negative feedback ADH secretion continues despite serum osmolality Super-saturated with water, can’t get rid of water Holding onto excess fluid: hypertension and weight gain Dilutional hyponatremia (diluting serum from holding onto water) Causes Paraneoplastic syndromes Tumors (lung, GI, pancreas) because they release their own ADH CNS disorders Anything that compresses hypothalamus Encephalitis, meningitis, intracranial hemorrhage, trauma, tumors Drugs Diabetes Insipidus (Neurogenic) SIADH ADH Deficiency Excess Kidneys Inability to concentrate urine Renal collecting ducts -kidney unable to increase -increases permeability to H2O permeability to H2O -Causes water reabsorption Water excretion Water retention -excretion of large volumes of -expansion of ECF urine -dilutional hyponatremia -dehydration (hypertonic) Symptoms Polyuria Urine output decreased Polydipsia, continuous thirst HCT, BUN & Serum Na levels Hypernatremia & hyperosmolar Urine osmolality high, serum low Urine dilute (low specific gravity) May see weight gain, crackles, edema NERVOUS SYSTEM ALTERATIONS Alzheimer’s disease (atrophy of brain; not receiving nutrients) 60 – 80% of all cases of dementia Subtle onset of memory loss Slowly progressive dementia follows Exact cause unknown Forms Familial (onset before age 65) Non-familial (onset after age 65) Pathologic changes Brain tissue shrinks Atrophy of cerebral cortex Enlargement of ventricles Shrinking hippocampus Crucial in acquisition of new memories and retrieval of old ones Cause: Neuritic plaques & tangles Has to do with breakdown of protein within neurons Beta-amyloid builds up in places between nerves Tao protein used within neurons to keep tract straight Breakdown of tao: tracks no longer lay straight Tangling: transmission can’t go down tracts Brain tissue can’t get nutrients  atrophies In unhealthy brains, beta amyloid does not get cleared It sticks together Greater amount of plaque,  greatest amount of tangles within brain  greater the dementia Manifestations of Alzheimer’s Hallmark symptoms Loss of short-term memory with denial of memory loss Initial Short-term memory loss Forget random details Mild personality changes (social withdrawal, lack of spontaneity and humor) Moderate stage (progression occurring) More global cognitive impairment Lack of insight; disorientation  extrem
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