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Pathophysiology Final Exam Study Guide
Modules 1-
Module 1 Chapter 2 I. General Adaptation Syndrome and Allostasis a. Alarm Stage: Fight-or-Flight response due to stressful stimuli. b. Resistance Stage: Nervous & Endocrine systems returning the body to homeostasis c. Exhaustion Stage: Point where bofy can no longer return to homeostasis Chapter 24 II. Body Fluid Homeostasis: Pertains to water within the body and the particles dissolved in it. i. Fluid Distribution: Occurs through osmosis, water moves to higher osmolality, cell membranes permeable to water, not elec- trolytes. ii. Extracellular Fluid: OUTSIDE THE CELL
1. 1/3 BODY FLUID IN ADULTS 2. Infants have more extracellular fluid as compared to intracel- lular iii. Intracellular Fluid: INSIDE THE CELL 1. 2/3 BODY FLUID IN ADULTS III. Fluid Imbalances a. Volume Deficit i. Etiology: Caused by removal of a sodium-containing fluid from the body ii. Clinical Manifestations: Sudden weight loss, postural blood pres- sure decrease with concurrent increased heart rate, flat neck veins, lightheadedness, dizziness, syncope, oliguria, decreased skin tur- got, dryness of oral mucus membranes, hard stools, soft sunken eyeballs, lonitudinal furrows in the tongue 1. INFANTS: fontanel may be sunken, neck veins are not reli- ably assessed in infants b. Volume Excess i. Etiology: Amount of extracellular fluid is abnormally increased, vascular and intersitial areas have too much fluid **ii. Clinical Manifestations:
- Circulatory Overload:** Bounding pulse, neck vein distention in upright position, crackles in dependent portions of lungs, dyspnea, orthopnea 2. Sudden Weight Gain : A sensitive measure of extracellular fluid 3. INFANT: Bulging fontanel, assessment of neck
veins is not effective in infants
2. HYPER-
ii. a. Clinical Manifestations: decreased neuromuscular excitability, muscle weakness, diminished reflexes, cardiac dysrhythmias, anorexia, nausea, emesis, fa- tigue, polyuria, constipation, headache, confusion, lethargy, personality change, renal calculi, pathologic fractures Module 2 Chapter 8 I. Transmission of Infection a. Chain of Transmission: RESERVOIR PORTAL OF EXIT MODE OF TRANSMISSION PORTAL OF EN- TRY SUSCEPTIBLE VICTIM HUMAN NASAL MU- INSECT BITE NASAL MU- MALNOUR- ANIMAL COSE NASAL COSA ISHED INSECT ORAL MU- DROPLETS ORAL MU- UNIMMUNIZED SOIL (^) COSA SEMEN (^) COSA SKIN ABRA- IMMUNE COM- PROMISED SION SKIN PUNCTURE Chapter 9 I. Innate Defenses and Inflammation a. Inflammation i. Neutrolize and destroy invading and harmful agents ii. limit spread of harmful agents to other tissue iii. prepare damaged tissue for repair iv. Redness, swelling, heat, pain, loss of function b. Histamine : Most important mediatior i. Causes: Increased vascular permeability, vasodilation, urticaria, smooth muscle constriction, increased mucus secretion, pruritis Clinical Manifestations:
1. Mild: Hives, seasonal alergic rhinitis, eczema 2. More problematic symptoms: throat constriction, localized edema, wheezing, tachycardia 3. Anaphylaxis: Most life-threatening reaction; occurs in very small number of highly allergic individuals iii. Treatment: 1. Antihistamines: block effects of histamine 2. Beta-Adrenergics: decrease bronchoconstriction 3. Corticosteroids: decrease inflammatory response 4. Anticholinergics: Block parasympathetic system 5. IgE therapy: Inhibits binding of IgE to mast cells 6. Epinephrine: Adrenergic agent given subQ or IV
c. Systemic Manifestations of Inflammation II. Passive Immunity: Provided when a person is given antibodies to a disease rather than producing them on their own. (from mother/ artificial) III. Active Immunity: Production of antibodies by the immune system in re- sponse to the presence of an antigen (Vaccines/Illness) Chapter 10 I. Excessive Immune Responses a. Autoimmunity : Immune system attacks own tissues b. Hypersensitivity: Normal immune response that it inapropritately trig- gered, excessive, produces undesireable effects on the body i. Type I Sensitivity (Immediate Hypersensitivity)
1. Reation occurs 15 to 30 minutes after exposire to antigen/al- lergen 2. Clinical Manifestations: a. Mild: Hived, seasonal allergic rhinitis, eczema b. More Problematic symptoms: throat constriction, local- ized edema, wheezing, tachycardia c. Anaphylaxis: most life-threatening reaction Chapter 7 I. Benign: No potential to kill host II. Malignant Growth: Can kill host if untreated, invasive/matastasizing nature, grows rapidly III. Metastasis: Process by which cancer cells escape their tissue of origin and initiate new colonies of cancer in distant sites IV. Effects of Cancer on the Body a. Cachexia: Overall weight loss and generalized weakness i. Loss of appetitie, increased metabolic rate, nausea/vomiting b. Warning signs: Change in bowel/bladder habits, a sore that does not heal, unusual bleeding or discharge, thickening or lump in breast or else- where, indigestion or difficulty swallowing, obvious change in wart or mole, nagging cough or hoarseness i. Warning signs in children: continued unexplained weight loss, headaches with vommiting in the morning, increased swelling/per- sistant pain in bones/joints, lump or mass in abdomen, neck or elsewhere, development of whitish appearance in pupil, recurrent fevers not caused by infection, excessive bleeding or bruising, no- ticeable paleness or prolonged tiredness Module 3 Chapter 51 I. Contractile Soft Tissue Injuries a. Compartment Syndrome: Complication of soft tissue injury,
results from swelling of injured tissue within a restrictive fascia i. Symptoms: Pain, pallor, parethesia, pulselessness, paralysis
i. Etiology: NSAIDS, stress, smoking, genetics, H. Pylori
1. Gastric: Caused by breakdown of protective mucous layer that normally prevents diffusion of acids into gastric epithelia because of chronic inflammation. (Asprin, NSAIDS, alcohol,& bile acids) 2. Duodenal: Inappropriate excess secretion of acid, increased basal activity of vagus nerve. ii. Pathogenesis: epithelial cells of the stomach and duodenum se- crete mucus in response to irritation of the epithelial lining and as a result of cholunergic stimulation II. Inflammatory Bowel Disease a. Ulcerative Colitis: Inflammatory disease of the mucosa of the rectum and colon. i. Clinical Manifestations: Bloody and/or chronic diarrhea, passage of mucus, fecal urgency and lower abdominal pain. b. Crohn’s Disease: Inflammation of the GI tract that extends through all the layers of the intestinal wall. i. Clinical Manifestations: Intermittent bouts of fever, diarrhea, if bloody, not as severe as crohn’s disease. Constant LRQ pain, may have RLQ mass, tenderness. III. Enterocolitis a. Antibiotic-Associated Colitis (Pseudomembranous Colitis): Acute ind- lammation and necrosis of large intestine. Caused by Clostridium difficile (Exposure to antibiotics) *Medicated by bacterial toxins i. Clinical Manifestations: Diarrhea (often bloody), abdominal pain, fever, leukocytosis, sepsis, colonic perforation(rare) Chapter 27 I. Infection a. Risk factors for UTI’s: female anatomy, sexual activity, menopause, cer- atin types of birth control, Urinary tract abnormalities, blockages in the uri- nary tract, suppressed immune system, catheter use, recent urinary pro- cedure b. Acute Pyelonephritis: Infection of renal pelvis/parenchyma usually from ascending UTI i. Clinical Manifestations: CVA tenderness, accompanied by fever, chills, N/V, anorexia, which increased fever-induced dehydration II. Glomerular Disorders (Glomerulopathies)
a. Postinfectious acute glomerulonephritis: Immune response to variety of potential triggers. Inflammation results in degradation of the basement membrane. b. Clinical Manifestations: Proteinuria, oliguria, azotemia, edema & hyper- tention c. Treatment: Supportive measures (dietary & fluid), management of sys- temic and renal hypertension Chapter 28 I. Acute Kidney Injury a. Prerenal: Due to conditions that diminish perfusion of the kidney i. Characterized by: low GFR, oliguria, high urine specific gravity, and osmalality ii. *can lead to acute tubular necrosis b. Intrarenal: due to primary dysfunction of the nephrons and the kidney it- self c. Postrenal: caused by obstruction within the urinary collecting system dis- tal to the kidney; elevated pressure in Bowman capsule; impedes glomerular filtration II. Chronic Kidney Disease: III. Pathophysiology: Outcome of progressive and irrevocable loss of functional nephrons a. Complications of CKD: Hypertension & Cardiovascular disease, Uremic syndroma, metabolic acidosis, electrolyte imbalances, bone & mineral dis- orders, malnutrition, anrmia, pain, depression Chapter 29 I. Incontinence: Any involuntary Urine loss, never normal, not a part of aging. a. Stress Urinary Incontinence (SUI): Occurs when urine is involuntarily lost with increases in intraabdominal pressure i. Causes: Weakening of pelvic muscles or intrinsic urethral sphincter deficiency; obesity, childbirth-related trauma, pelvic surgery, dia- betes, degenerative neurologic diseases that impair nerves that in- nervate the bladder b. Urgency Urinary Incontinence (UUI): Involuntary sudden leakage of urine alone with or immediately following the sensation of a need to uri- nate (urgency)
b. Clinical Manifestations: pharync, conjunctivae, & anus inflammation i. Women: Usually asymptomatic, purulent vaginal discharge, dy- suria, abnormal vaginal bleeding ii. Men: Dysuria, urethritis, purulent urethral discharge, redness and swelling at infection site III. Human Papilloma Virus Infections a. Treatment: Prevention and by treating symptoms. Treatment depends on stage. Module 6 Chapter 40 I. Thyroid Hormone Disorders a. Hypothyroidism i. Pathogenesis:
1. Primary: intrinsic thyroid gland dysfunction 2. Congenital Hypothyroididm typically cause by thyroid dys- genesis (lack of development) 3. Secondary: result of defects in TSH production usually asso- ciated with head/brain conditions 4. Lymphocytic thyroiditis, irradiation of the thyroid glans, surgi- cal removal of thyroid tissue, iodine deficiency (required for T3 & T4 formation) ii. Clinical Manifestations: Decreased basal metabolic rate, weak- ness, lethargy, cold intolerance, decreased appetite, bradycardia, narrowed pulse pressure, mild/moderate weight gain, elevated serum cholesterol & triglycerides, enlarged thyroid, dry skin, consti- pation, depression, difficulties with concentration/memory, loss of eyebrow, menstrual irregularity b. Hyperthyroidism i. Clinical Manifestations: Insomnia, restlessness, tremor, irritability, palpations, heat intolerance, diaphoresis, diarrhea, inability to con- centrate, enlarged thyroid gland, Increased basal metabolic weight which leads to weight loss even with increase in appetite and di- etary intale, amenorrhea/scant menses II. Parathyroid Hormone Disorders
a. Hypoparathyroidism i. Clinical Manifestations: kidney stones, bone demineralization (os- teoporosis), polyuria & dehydration, anorexia, vomiting, constipa- tion, bradycardia, heart block, cardiac arrest, decrease in neuro- muscular excitability. III. Antidiuretic Hormone Chapter 41 I. Diabetes Mellitus a. Type I Diabetes i. Pathogenesis: caused by destruction of beta cells of the pancreas ii. Clinical Manifestations: hyperglycemia, polyuria, polydipsia, polyphagia b. Type II Diabetes i. Pathogenesis : Insulin resistance and beta cell dysfunction lead to a relative lack of insulin ii. Clinical Manifestations: Acute hyperglycemia, dawn phenome- non, pulyuria, polydipsia, polyphagia, nausea, fatigue, blurred vi- sion II. Clinical Manifestations and Complications a. Vascular complications i. Macrovascular: damage to large blood vessels; leads to cardio- vascular disease, peripheral vascular disease, and stroke ii. Microvascular: retinopathy and nephropathy from abnormal thick- ening of the basement membrane in capillaries; may lead to blind- ness and renal failure III. What is a Hemoglobin AIC? Evaluated the average amount of glucose in the blood over the last 2-3 months by measuring the percentage of glycared hemoglobin in the blood Module 7
1. Manifestations of Brain Injury a. Level of Consciousness: State of alertness and attentiveness to one’s enviornment and situation a. Change in level of conciousness is most sensitive indicatior of al- tered brain function
paroxysmal abnormal or excessive cortical electrical discharges
b. Dementia: Syndrome associated with many pathologies; characterized by progressive deterioration and coninuing decline of memory and other cog- nitive changes c. Parkinson disease: difficulty initiating and controlling movements, results in akinesia, tremor, and rigidity
6. Spinal cord and peripheral nerve disorders a. Multiple sclerosis: Chronic demyelinating disease of the CNS that pri- marily affects young adults b. Spinal cord injury: Usually traumatic, cord may be compressed, tran- sected, or contused. Secondary injury may result from hemorrhage, swelling, ischemia, inflammation c. Guillian-Barre syndrome: Inflammatory demyelinating disease of the pe- ripheral nervous system or a lower motor neuron disorder Module 8 1. Alterations in Pulmonary Function a. Hypoxemia: deficient blood oxygen as measured by low artetial O2 and Low hemoglobin saturation b. Hypoxia: decrease in tissue oxygenation 2. Diagnostic tests a. Pulmonary function testing 3. Alterations in Pulmonary Vasculature a. Pulmonary venous thromboembolism: An undissolved, detaches material (blood clot, fat embolu, amniotic fluid, air, tumor, foreign bodies, septic, parasites) that occludes blood vessels a. 90% in deep veins of lower extremeties 4. Obstructive Pulmonary Disorders a. Obstruction From Conditions in the Wall of the Lumen i. Asthma: Airway obstruction/ inflammation that is reversible i. Intrinsic: Non-allergic, Adult onset
Module 9 Chapter 13 I. What is erythropoietin? a. Hormone Produced by the kidney b. Promotes the formation of red blood cells by bone marrow c. Can be synthesized and used as a treatment of some forms of anemia II. Anemia: Deficit of red blood cells a. General Effects of Anemia: Reductions in oxygen-carrying capacity (Tis- sue Hypoxia) i. Mild Anemia: usually no clinical symptoms, Elderly with cardiovas- cular, pulmonary disease ,ay have symtoms ii. Mild to Moderate Anemia: Fatigue, Generalized Weakness, Loss of stamina, followed by tachycardia and xertional dyspnea. iii. Moderate to Severe Anemia: Orthostatic and generalized hy- potension, vasoconstriction, pallor, tachypnea, dyspnea, tachycar- dia, transient murmurs, angina pectoris, heart failure, intermittent claudication, night cramps in muscles, headache, lightheadedness, faintness, tinnitus, roaring in the ears b. Aplastic Anemia i. Etiology: Caused by toxic, radiant, or immunologic injury to red blood cells (Immune systems attacking stem cells in blood marrow) ii. Pathogenesis:
1. Late Symptoms: weakness, fatigue, lethargy, pallor, dysp- nea, palpitations, transient murmurs, and tachycardia related to low RBC’s c. Iron Deficiency Anemia i. Clinical Manifestations: Pica, Blue Sclerae, Koilonychias (spoon- shaped nails) d. Sickle Cell Anemia i. Pathogenesis: caused by mutation in the beta-globin chain of the hemoglobin molecule
ii. Laboratory features e. Acute Blood Loss i. Clinical Manifestations:
**1. 10%: rarely causes signs, other thn vasovagal syncope
- 20%: no clinical symptoms at rest, tachycardia is** **seen with exercise
- 30%: flat neck veins when supine, postural** **hypotension, exercise tachycardia
- 40%: central venous pressure, cardiac output, & arterial** blood pressure to fall below normal while patient is supine and at rest; with associated hunger, **tachycardia, and cold, clammy skin
- 50%: causes shock and often death ii. Treatment: blood replacement therapy, w/ crystaloid solutions colloid solutions (Plasma protein, albumin, or dextran) f. Polycythemia Vera i. Pathogenesis ii. Clinical Manifestations g. Secondary Polycythemia i. Etiology:** Caused ny chronic hypoxemia with resultant increase in erythropoietin production
