Pathopharm Study Guide PDF

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COMPREHENSION STUDY GUIDE Antifungal drugs Amphotericin B – systematic antifungal, candida and cryptococcal infection  Pump must be used!!!  Adverse effects: neurotoxicity, tinnitus, visual disturbances, hands or feet numbness, convulsions, renal toxicity, fever, chills, nausea, GI upset Anti-inflammatory drugs NSAIDs – ibuprofen, aspirin (acetylsalicylic acid; ASA)  Anti-pyretic  Analgesic  Anti-inflammatory

 Work through inhibition of the leukotriene pathway, the prostaglandin pathway, or both limiting the undesirable inflammatory effects of PGs  Differs from opioids which relieve pain by interfering with its recognition in the brain Aspirin/ASA/acetylsalicylic acid  Inhibit clots  Can cause bleeding  Irreversible inhibitor of COX-1 receptors within the platelets 

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Cardiovascular risk: o contraindicated by coronary artery bypass graft surgery o NSAIDS incrase the risk of CLOTS (MIs, STROKE) Gastrointestinal risk o Increase risk of bleeding, ulcers o Elderly pts at greater risk Metabolic o Sweating, thirst, hyperventilation hypo or hyper glycemia Children: hyperventilation, (CNS effects like) dizziness, drowsiness, lethargy, excitability, fever, hyperventilation  Toxic level is 12 adult or 48 baby aspirin Treat with Dialysis

Nonsalicylate Toxicity/Ibuprofen  Hemodialysis is not effective in removing it from bloodstream  NOT as dangerous as salicylate drugs overdose  Treat by administration of charcoal  Behavioral changes, N/V/D, intense headache, dizziness, cerebral edema, cardiac arrest

Bayer (ASA)  Most widely used drug in the world  Contraindicated with flu like symptoms in children  causes reyes syndrome o Reye syndrome: neurological deficits leads to coma, may cause liver and neurological damage INNATE DEFENSE INFLAMMATION Defense mechanisms 1. Physical, mechanical and biochemical barriers a. Are innate (from birth) b. Physical i. Normal flora: mutualistic, surface barriers that harbor a group of microorganisms ii. Skin: tight epithelial cells, low pH (3-5) iii. Includes 1. lining of GI: a. sterile a birth, produce vitamin K for klotting, compete for resources and block attachment to epithlium, produce toxins b. can be altered by antibiotic treatment c. clostridium difficile  pseudomembranous colitis 2. GU a. Altered by antibiotic tmt b. Candida albicans  vaginosis 3. respiratory tract c. Mechanical barriers i. Dead skin flaking off ii. Fluids expelled through coughing sneezing and vomiting iii. Urinating d. Biochemical barriers i. Mucus, sweat, tears, ear wax, saliva ii. Epithelial cells secrete “antimicrobial peptides” that are toxic to bacteria, fungi, viruses, etc (over 1000 have been found!) 2. Inflammation response: goal is to limit infection and control tissue damage a. limit damage b. prevent infection c. initiates repair d. Activated by Mast Cells, histamine release occurs in two ways i. Degranulation: release of the contents of mast cell granules ii. Synthesis: new production and release of mediators in response to a stimuli iii. Histamine: 1. Increased blood flow  redness and warmth 2. Increased vascular permeability  edema

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synthesize prostaglandins (cause pain), leukotrienes (longer vascular effects, same as histamine) and platelet activating factor iv. ALL HALLMARKS OF INFLAMMATION ARE CAUSED BY MAST CELLS 1. Loss of function 2. Redness 3. Swelling 4. Heat 5. pain v. Antihistamines: drugs that block the binding of histamine 1. H1: used to treat asthma, dipenhydramine 2. H2: blocks HCl in stomach, zantac ranitidine e. NONSPECIFIC f. DIVIDED INTO FOUR CATEGORIES 1. vascular response: edema, redness, heat 2. cellular response: pain, loss of function 3. formation of exudate 4. healing: removal of bacterial products, dead cells, other products Systematic inflammation clinical manifestation a. Elevated WBC count b. Malaise c. Fatigue d. Elevated RR and HR e. Fever (cause by prostaglandin  hypothalamus) f. nausea g. anorexia Temperature below set point a. Vasoconstrictions b. Shivering c. Increased metabolism Temperature above set point a. Vasodilation b. Sweating c. Conduction/convection/evaporation Acute inflammation a. No residual damage b. 2-3 weeks c. neutrophils chronic inflammation a. lymphocytes and macrophages b. rheumatoid arthritis c. leads to injury Granumomatosus: creates granuloma, giant cell encapsulated by collagen; the body attempts to wall off and isolate affected area

9. I don't got no type (exudates) a. Serous = white  early inflammation b. Sanguinous = red  rupture of blood vessel, after surgery c. Serosanguinous = pink  midpoint of healing after surgery d. Purulent = Yellow or green  bacterial infection e. Fibrinous = thick, clotted, lung of pneumonia pt, advanced inflammation 10. Adaptive (acquired) Immune response: a. increases the bodys long term protection against specific and dangerous infectious agents b. SPECIFIC: it involves memory c. Slower, specific process Infection 1. Classic symptoms of infection: fever, chills, sweats, redness, pain and swelling, fatigue, weight loss, increased white blood cell (WBC) count, and the formation of pus a. 11,000 WBC count  infection b. 12,000 WBC count  systematic inflammatory response 2. What factors influence the capacity of a pathogen to cause disease? a. Communicability: Ability to spread from one individual to others and cause disease—for example, measles and pertussis spread very easily; human immunodeficiency virus (HIV) is of lower communicability b. •Immunogenicity: Ability of pathogens to induce an immune response c. •Infectivity: Ability of the pathogen to invade and multiply in the host d. •Mechanism of action: Manner in which the microorganism damages tissue e. •Pathogenicity: Ability of an agent to produce disease—success depends on communicability, infectivity, extent of tissue damage, and virulence f. •Portal of entry: Route by which a pathogenic microorganism infects the host: direct contact, inhalation, ingestion, or bites of an animal or insect g. •Toxigenicity: Ability to produce soluble toxins or endotoxins, factors that greatly influence the pathogen's degree of virulence h. •Virulence: Capacity of a pathogen to cause severe disease—for example, measles virus is of low virulence; rabies virus is highly virulent 3. BACTERIA CAUSES INFECTION IN TWO WAYS a. Enter body and grow inside human cells  TB b. Secrete toxins that damage cells  S. aureus 4. Vocab a. Bacteremia?  presence of bacteria in the blood b. Septicemia  growth of bacteria in the blood (sepsis) c. Endotoxins: (lipopolysaccharides) are contained in the cell walls of gramnegative bacteria, antibiotics can NOT prevent toxic effects of these 5. C Difficile infections are growing

6. Superinfection  Normal intestinal flora compromised allowing the overgrowth of C difficile and the development of pseudomembranous colitis (bacterial infection of the intestines) OTC OTC drugs are for short term tmt of common minor illness Can delay tmt of serious disorders Do not address cause of the disorder Hepatic toxicity associated with acetaminophen OD (leading cause of liver failure) 5. NSAIDS associated with GI ulcers 6. OTC shouldn't be used on children 95% +/-2

1. Respiratory Acidosis a. As a result of hypoventilation  COPD causes this b. Compensatory response: Kidney retains HCO3 2. Respiratory Alkalosis a. Hyperventilation b. Compensatory response: Kidneys release HCO3 3. Metabolic Acidosis a. Depression of HCO3 OR increase in noncarbonic acids b. Decrease of pH c. Compensatory action: CO2 excretion hyperventilation 4. Metabolic Alkalosis a. Elevation of HCO3, loss of metabolic acids b. Increase of pH c. Compensatory action: respiratory depression, hold on the paCO2

Urinary Tract Infections   

Most common bacterial infection in women  UTI (esp pregnant women) 2nd most common bacterial disease most common pathogen  E Coli 1. Termz a. Pyelonephritis: inflammation usually d/t infection of the renal parenchyma, renal pelvis and collecting system b. Cystitis: inflammation of the bladder wall c. Urethritis: inflammation of the urethra d. Urosepsis: UTI that has spread to the circulatory system

2. Lower UTI (bladder and urethra) a. Dysuria b. Urgency c. Dribbling d. Cloudy urine e. Frequency f. Urethritis = inflammation of the urethra g. Bacterial infection  chlamydia, gonococcal, trichomonas h. Are cultures negative?  interstitial cycstitis d/t viral, fungal or radiation 3. Upper UTI a. Flank pain b. Fever c. Chills d. Renal edema e. Purulent urine f. Pyelonephritis: acute infection of the renal parenchyma and collecting system including the renal pelvis i. Acute pyelonephritis leads to chronic pyelonephritis ii. Inflammation  interstitial spaces between tubules Immunologic disorders of kidney 4. Glomerulonephritis: inflammation of the glomeruli a. 3rd leading cause of renal failure in US b. STREPTOCOCCUS c. DAMAGE TO THE GLOMERULUS  CHANGE IN GFR  PROTEINURIA AND HEMATURIA 5. Good pasture syndrome a. Young male smokers, RARE b. Pulmonary symptoms in addition to hematuria, weakness, anemia and renal failure 6. Nephrotic Syndrome Etiology: Results when the glomerulus is excessively permeable to plasma protein, causing proteinuria that leads to low plasma albumin and tissue edema a. Increased glomerular injury due to hyper excretion of protein i. >3.5 g/day b. Leads to hypoalbuminemia and ascites c. Hyper excretion of lipoproteins in liver d. Vitamin D deficiency, hypertension e. Hypercoagulability Urinary Tract Obstructions 1. Kidney Stones a. Most common  calcium b. Severe pain, N/V

c. “kidney dance” 2. Hematuria types a. RBC escaping through the glomerular membrane i. Smoky brown tinged urine ii. No clots iii. proteinuria b. Lower Urinary Tract bleeding i. Pink or red urine ii. Clots Incontinence and Retention 1. Incontinence: uncontrolled leakage of urine a. Urge: i. Involuntary loss of urine preceded by urgency ii. Abrupt strong desire to void iii. Involuntary contractions of the detrusor b. Overflow i. Pressure of urine in overfull bladder overcomes sphincter control ii. Leakage of small amounts of urine throughout day iii. Urinate frequent small amounts iv. Bladder palpable c. Stress i. Involuntary loss of urine ii. Abdominal pressure iii. Coughing iv. Sneezing v. Laughing vi. Leakage is small amounts may not be daily 2. Retention a. Acute urinary retention is the total inability to pass urine via micturition; It is a medical emergency!!!! Acute Kidney Injury Blood urea nitrogen levels measure: serum level of the end products of protein metabolism  Male client with a kidney stone: severe flank pain radiating towards testicles  s/s of cystitis (UTI) o frequency o dysuria o nocturia o urgency 1. Follows prolonged hypotension or hypovolemia OR exposure to nephrotoxic agent

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2. Azotemia: an accumulation of nitrogenous waste products (urea, nitrogen, creatinine) in the blood 3. Prerenal Acute Kidney Injury a. Can lead to intrarenal disease if ischemia is prolonged b. Oliguria:...