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Patho final exam
Pathophysiology Final Exam
| Question | Answer |
|---|---|
| What are the signs and symptoms of Inflammation? | Ruber (red) Tumor (swollen) Calor (warm) Dolar (pain) |
| What is the acute local inflammatory response? Part 1 | 1) Chemicals released such as prosteglandins, leukotrienes, kinins, opson, and histamine . 2) Stimulate pain receptors by leukocytosis |
| What is the acute local inflammatory response? Part 2 | 3) Increase in blood flow and stretch capillaries and dilation of arterioles which results in local edema and WBC’s (neutrophils) flow through capillaries. 4) Neutrophils are trapped in capillaries by the binding of selectin and integrin |
| What is the acute local inflammatory response? Part 3 | 5) Neutrophils move towards the walls of the capillaries and flatten. Margination – moving to walls and Pavementing – flatten 6) Neutrophils move from the blood to the exudates (diapedisis) |
| What is the acute local inflammatory response? Final Part 4 | 7) Neutrophils are attracted to the site of injury through chemotaxis 8) Activation of phagocytosis (opsonization) |
| What are the functions of the inflammatory response? | Pain makes it easier to repair because of less usage. Leukocytosis helps with the infection. Local edema carries material away from site of injury. Phagocytosis helps with demolition |
| What are the complications of repair? | Adhesions, Keloid Scarring, Contracture, and Sclerosis |
| What are adhesions? | Scar tissue binds to structures together that are normally independent |
| What is Keloid Scarring? | Overgrowth of scar tissue which affects function and flexability. |
| What is a Contracture? | Shrinking of scar tissue ; Stenosis - narrowing |
| What is Sclerosis? | Hardening of Scar tissue |
| What is chronic inflammation? | Inflammation that lasts 3 months or longer with less obvious signs and symptoms |
| What are the complications of Chronic Inflammation? | Regeneration no longer possible ; Necrosis = tissue death |
| What are the two types of treatment for inflammation? | Non-pharmacological and pharmacological |
| What is the non-pharmacological treatment of inflammation? | R.I.C.E. Rest, Ice, Compress, Elevate ; compress and elevate helps with edema |
| What is the pharmacological treatment of inflammation? | Steriods, Non-steroids |
| What is NAID’s (examples, Method of action, problems associated with long term use) | Examples : Aspirin and Ibuprofin; MOA: Decreasing production of prosteglandins (less inflammation) ; Problems associated: Cause Ulcers |
| What are Corticosteroids? (examples, Method of action, problems associated with long term use) | Examples: cortisone –made by adrenal gland, and prednisone ; MOA: Decrease bodies production of prostaglandin and leukotrienes; problems with long term use: Weakens immune system and increases risk of infection. |
| What is the Etiology/Pathophysiology of HIV/Aids? Part 1 | 1) HIV binds to CD4 protein located on membrane of helper T cell. AKA T4 lymphocyte, helper T cell 2) HIV fuses with the T-4 lymphocyte 3) Viral RNA and reverse transcriptase insert into target cell |
| What is the Etiology/Pathophysiology of HIV/AIDs? Part 2 | 4) Reverse transcriptase produces viral DNA from viral RNA (gets in nucleus through pores) 5) Viral DNA enters nucleus and splices into target cell. |
| What is the Etiology/Pathophysiology of HIV/AIDS? Part 3 | 6) The target cell uses the information on the viral DNA and produces the pieces needed for building copies of HIV. 7) The pieces are assembled into new copies of HIV. This process uses and enzyme called protease. |
| What is the Etiology/Pathogenesis of HIV/AIDS? Part 4 | 8) Copies are then released from cell in process called budding. |
| What is the first stage of HIV/AIDS? (S/S and Pathogenesis) | Prodromal Stage: Occurs within a month Lasts about a week Nonspecific Signs and Symptoms - such as body ache, lack of energy, and slight fever. |
| What is the second stage of HIV/AIDS? (S/S and Pathogenesis) | Asymptomatic stage : 6-10 years ;No symptoms ;Signs include: Viremia (virus in blood), Presence of antibodies, decrease in CD4 cells (helper T) |
| What is the third stage of HIV/AIDS? (S/S and Pathogenesis) | Acute (AIDS stage) ; CD4 Count less then 200 normal is 800 ;Opportunistic diseases develop ;Change in physiology in body , Cancer – All forms ; Karposi’s Sarcoma, Pneumo Cystis Carinii, TB, Salmonella (20xs more likely in HIV) |
| What is the treatment of HIV/AIDS | Starts at 350 CD4 Count ;Control Reproduction. Use cocktail of up to 4 types of drugs (HAART) 1) fusion inhibitor 2) Non-nucleoside reverse transcriptase 3) Nucleoside reverse transcriptase inhibitor 4) Protease inhibitors |
| What is the functions of the “Cocktail” of drugs known as HAART? | Fusion inhibitors: Interfere with binding of CD4 Protein ;Reverse transcriptase inhibitors – interfere with the conversion of RNA to DNA ;Protease Inhibitors – effects assembly of the virus. |
| What are the signs/symptoms and diagnosis of SLE (lupus)? Part 1 | Butterfly rash ;Discord skin rash – other areas ;Photosensitivity – exposure to sunlight ;Polyarthritis – two of more swollen, tender joints of extremities ;Pleuritis –dypsnea ;Pericarditis- may result in arrhythmias |
| What are the signs/symptoms and diagnosis of SLE (lupus) ? Part 2 | Glomerulonephritis –presence of cells, proteins in urine ;Encephalitis – manifested by convulsions and/or psychosis Low counts of red or white blood cells ;Abnormal immune test or positive LE prep |
| What are the signs/symptoms and diagnosis of SLE (lupus) ? Part 3 | Positive ANA test – presence of anti-nuclear antibodies ;Obvious exacerbation and remission ;Steroids – anti-inflammatory (cortisone, prednisone) |
| What is the risk factors of Colorectal Cancer? | Controllable = Fiber decrease, fat increases (type of fat) Non controllable = Age, history of inflammation of the intestine. |
| What is the screening test for Colorectal Cancer? When does it start? | Fecal occult blood test starts at around age 30. Colonoscopy starts at age 50 |
| What is the risk factors for Prostate Cancer? | Age |
| What is the screening test for Prostate Cancer? | Age 40 – Digital Rectal Exam ;Age 50 Blood test for prostate specific antigen |
| What is the risk factors for Lung cancer (Bronchiogenic cancer)? | Most common is Smoking ; Second hand smoking ;Occupational hazards |
| What is the screening test for Lung cancer (Bronchiogenic cancer)? | Most common is chest x-ray |
| What is the risk factors for breast cancer? | Estrogen receptor –inherited,genetic ;Early puberty ;Late menopause ;Large babies ;Family history |
| What is the Screening test of Breast Cancer? | Self breast exam – at 20years of age till death ;Clinical breast exam- at 40 years of age every year/ 20years of age ever three years ;Mammogram – age 40 every year |
| What is the S/S of Breast Cancer? | Lump in the axial, unusual discharge from breast, dimpling of the breast |
| What is the risk factors for Cervical Cancer? | HPV, Smoking, Diet (low fruits and vegetables), Family History, Birth control pills, Poverty (inadequate health care) |
| What is the S/S of Cervical Cancer? | Pelvic pain or pain during intercourse, watery bloody vaginal discharge, vaginal bleeding after intercourse |
| What is the screening test for Cervical Cancer? | Pap test, HPV DNA test (test for types of HPV) |
| What is the normal values for Erythrocytes? | 4.2 – 5.9 million/mm3 |
| What is the normal values for leukocytes? | 4,500 – 10,500mm3 |
| What is the normal values for thrombocytes? | 150,000 – 450,000 mm3 |
| What is the normal values for hemoglobin? | 12-18 g/dl |
| What is the normal values for Hematocrit? | 36-54 |
| What is the normal values for Mean corpuscular volume (MCV)? | 86-98mcm3 |
| Describe the microscopic perspective of Leukemias. | High WBC’s |
| What is the confirmation test for leukemias and aplastic anemia? | Bone marrow biopsy |
| Describe the microscopic appearance of aplastic anemia. | Lack of cells |
| Describe the microscopic appearance of hypochromic anemia. | Oval, Pale, Small RBC’s |
| Describe the microscopic appearance of pernicious anemia. | Large, no pale area |
| What is the confirmation test for hypochromic anemia and pernicious anemia? | Iron deficiency test |
| What is the microscopic appearance of thallasemias? | Look like hypochromic |
| What is the microscopic appearance of sickle cell anemia? | Low RBC, Sickle shaped |
| What is the confirmation test for thallasemias? | Iron test, Genetic screen, Test Alpha/Beta |
| What is the confirmation test for Sickle cell anemia? | Genetic screen, Electrophoresis |
| What is pernicious anemia’s deciding factor? | b12 |
| What 3 diseases have a normal MCV, Low Hematocrit, Low Hemoglobin, Low RBC count, Low WBC count, and low Platelet count? | Aplastic anemia, Leukemia, and Hemophilia |
| What 2 diseases have Low MCV, Hematocrit, and Hemoglobin, and Normal RBC count, WBC count, Platelet count? | Hypochromic, and thallasemia |
| What disease has a high MCV, normal Hematocrit, low Hemoglobin, Low RBC count, Normal/Low WBC count, and Normal/Low Platelet count? | Pernicious Anemia |
| What disease has a normal MCV, low Hematocrit, low Hemoglobin, low RBC count, normal WBC count, and normal Platelet count? | Sickle cell anemia |
| What is the Etiology of Right CHF? | Chronic respiratory disease (most common cause) increased afterload on right ventricle ;Incompetance (not able to perform job) of pulmonary or tricuspid valves ;damage to right ventricle |
| What is the Etiology of Left CHF? | Hypertension (most common) ;Incompetence of aortic and mitral ;Ischemia of left ventricle |
| What is the Pathogenesis of Left CHF? | Stage 1 – Tired, Pale, Increased heart rate/respiration rate |
| What is the Pathogenesis of Right CHF? | Stage 1 – Patient is going to be tired, pale ; Increase heart rate/ respiration rate |
| What is Cor. Pulmonale? | Right side CHF associated in respiratory disease (emphysema) |
| What is the treatment of CHF? | 1) Cardiac Glycosides (digoxin) – heart failure - desired affect increases force of contraction; negative effect decreases heart rate ; Diaretics (lasix) –treat congestive ;Negative effect causes hypokalemia ; Desired – to remove fluid |
| What is the treatment of CHF? Cont… | 3) Treat adverse affects ;- Potassium Supplements |
| What is Atherosclerosis? | Build up of plaques in the arteries |
| What are the risk factors for Atherosclerosis? | Smoking, Obesity, Hyperlipidema, Alcohol, Diabetes, Stress, Hypertension, Inactivity, Sex(gender) , Genetics. (Spending One Hour A Day Studying Helps Improve Science Grades) |
| What is the pathogenesis of CAD? | Stage 1 – Asymptomatic ischemia ; Stage 2 – Angina occurs ; Stage 3 – Necrosis occurs |
| What is the screening test for CAD? | Stress test and Cardiolyte test (done together) at age 50 ; Cardiolyte test is performed by at radioactive substance is injected through an IV and circulation occurs goes in tissue of heart muscle you will notice difference in blood flow. |
| What is Angina Pectoris? | Chest pains as a result of ischemia *Warning Symptom ;two types: Stable (chest pains only when active then stops at rest) Unstable – on without warning relieved with meds. |
| What is MI? | Ischemic necrosis of heart muscle |
| How do you diagnose MI? | EKG ;Test for cardiac marker (most common triponin) ;Chest x-ray |
| What do heart attacks always lead to? | Scar tissue formation in the heart |
| What is the treatment of CAD? | Lifestyle – address risk factors ;Address risk factors with medication such as take aspirin a day and take statin for cholesterol. |
| What is the treatment of CAD? Cont.. | - Treat symptom (angina) ;Surgery – put in stent ;Coronary Artery Bypass Graft (CABG) |
| What is the etiology of CBV (cerebral vascular disease)? | Idiopathic ;Risk factors* |
| What is the pathogenesis of CBV? | Stage 1 – Asymptomatic ischemia ;Stage 2 - Transient Ischemic attacks (TIA’s) ;Stage 3 – Necrosis |
| What are TIA’s? | Transient Ischemic attacks (temporary) <S – Sensory changes – vision change, numbness, tingling ;A – Affect – personality changes , memory gaps, and confusion ;M – Motor/ muscle/movement – weakness, paralysis, speech (slurred) |
| What is the necrosis of CVB? | Cerebral infarction – ischemic necrosis of the brain/stroke (CVA) |
| What is the treatment of CVB? | Confirm with CT scan ;Types of strokes ;- Occlusive (use TPA) ;- hemorrhagic (stroke cause by bleeding) |
| What is the Etiology of PVD/PAD? | Idiopathic with risk factors |
| What is the pathogenesis of PVD/PAD? | Stage 1 – Asymptomatic ischemia ; Stage 2 – pain/numbness/tingling – warning ; stage 3 – necrosis (can lead to amputation) |
| What is the obstruction to air flow of Emphysema? | Loss of elasticity ; mucous |
| What is the etiology of Emphysema? | Chronic bronchitis generally from smoking |
| What is the Signs and Symptoms of Emphysema? Pink Puffers | Skin flushed because of working to breath ;weight loss ; Barrel chested ; ABG’s will be normal or close to normal ; able to keep with bodies needs. |
| What are the Signs and Symptoms of Emphysema? Blue Bloaters | Blue due to hypoxia ; Respiratory acidosis ; labored breathing but body can’t keep controlled ;edema because of Cor. Pulmonale ; Edema cause of weight gain |
| What is the treatment of Emphysema? | Blue bloaters on oxygen and/or steroid inhalers ; No effective treatment |
| What is the obstruction to air flow on Bronchial Asthma? | Mucous ; Inflammation ; Constriction |
| What is the etiology of Bronchial Asthma? | Idiopathic ; More common in those with allergies ; more common in crowded areas |
| What is the Signs and Symptoms of Bronchial Asthma? | Sudden severe difficulty in breathing ; wheezing |
| What is the treatment of Bronchial Asthma? | Bronchodilator ; Steroid ; Used by injection, oral, or inhaler (lower side affects/lower dose); Bronchodilator used during attacks |
| What is the etiology of Cystic Fibrosis? | Auto-somal recessive genetic ; 1 out of 25 are carriers |
| What is the Signs and Symptoms of Cystic Fibrosis? | Thick mucous leads to DIB and infections <; Digestive : Thick mucous can block secretions from the gall bladder causing malnutrition ; Sterile : Thick mucous block sperm (male/female) ; Sweat : Excess of sodium – loss of sodium (heart problems – Na+) |
| What is the treatment of Cystic Fibrosis? | Mucolytics (break down mucous) + Percussion (break mucous free using vest or physical) ; Enzymes to help digest |
| What is Type 1 DM? | Less common- occurs when beta cells are destroyed ; idiopathic and auto-immune |
| What are the Risk Factors for Type 1 DM? | Family history |
| What is the treatment of Type 1 DM? | Insulin Injections ; Lifestyle changes – routine of diet and exercise ;Monitor and adjust when needed |
| What is Type 2 DM? | Problem with receptors on target cells making them less responsive (insulin resistant) ; Incidence climbing |
| What are the risk factors for Type 2 DM? | Weight (10x’s greater risk overweight ; 30x’s greater risk obese) |
| What is the treatment of Type 2 DM? | Lifestyle changes – diet and exercise ; Give oral hypoglycemic – increase insulin production and sensitivity of receptors ; Give insulin – not as common with type 2 ; Monitor and adjust |
| What are the classic S&S of DM? | Increase in urine production (frequent urination) ; Glucosurea ; thirst ; hunger ; High Blood Sugar (hyperglycemia) {normal is 70 – 100g/dl} |
| What are the tests performed with DM? | Fasting Blood sugar and oral glucose tolerance test |
| What is fasting blood sugar? | Screening test / routine during annual physical ; Procedure : 12 hour fast then single blood draw < 125 normal >125 diabetes ; Results : Less then 125 = Normal ; Greater then 125 = Diabetes |
| What is the oral glucose tolerance test? | Procedure: 12 hour fast then one blood draw ; drink heavy glucose – 75 grams of sugar ; pregnant = 100g of sugar ; Draw blood every 30minutes or 1 every hour<; Result: over 200 = positive ; 140-200 = at risk > glucose intolerant |
| What are the 3 types of monitoring therapy? | Home glucose monitoring, Hemoglobin A1c, and Microalbumin |
| What is home glucose monitoring? | Patients perform on their own; allow for control and adjustment |
| What is hemoglobin A1c? | Tests for amount of sugar in hemoglobin; Tests for amount of control of diabetes |
| What is Microalbumin? | Small protein in the blood; Urine test for protein – identify kidney damage (complications of kidney damage) |
| What are the acute complications of DM? | Hypoglycemia and Hyperglycemia |
| What is the etiology of Hypoglycemia? | skipped meal (too few calories) ; too much insulin; more active then normal |
| What is the S&S of Hypoglycemia? | Skin – moist and cool, clammy ;Respiration – shallow (breathing less) ; Behavior – drunk (slurred speech, uncoordinated, combative) |
| What is the treatment of Hypoglycemia? | Calories (food intake) |
| What is the prognosis of Hypoglycemia? | No response can lead to insulin shock which can be fatal |
| What is the etiology of Hyperglycemia? | Forget to take insulin or meds ; too many calories ; less active then normal ;infection or inflammation |
| What are the S&S of Hyperglycemia? | Skin – red and dry ; Respiration – deep, fruity odor (burning fat in place of sugar) ; Behavior – Lethargy, Drowsiness (stoner like) |
| What is the treatment of Hyperglycemia? | Take to hospital to receive insulin ; professional care |
| What is the prognosis of Hyperglycemia? | Develop into keytoacidosis (build up of keyto’s; PH and CO2 low) ; form into possible diabetic coma |
| What are the Chronic Complications of DM? | Vascular damage, Neuropathy, Hyperlipidema |
| What is the vascular damage of DM? | Damage to small capillaries (kidneys, hands and feet, retina) |
| What is the neuropathy damage of DM? | Nerve damage affects feeling and hands and feet ; more susceptible to infection ; gastropharosis –doesn’t sense food (digestive system not functioning properly) |
| What is the Hyperlipidema damage of DM? | Lead to atherosclerosis (CAD, CVD,PVD) |
| What helps prevent complications of DM? | Tight control |
| What is the Prognosis of DM? | Depends on control ; Diabetes is leading cause of amputation and blindness ; Heart attack and stroke are leading causes of death in kidney failure |
| What is a new treatment for DM? | Transplant procedure for type 1 diabetes ; dissolve pancreas then run through screens ; trap islets ; Give them by IV through the portal vein. |
| What therapeutic class(s)/drugs is involved with hypertension? | Alpha blockers, Ace inhibitors, Angiotensin receptor blockers,Diuretics, Calcium channel blockers, Beta blockers |
| What therapeutic class/drugs is involved with high cholesterol? | Statins |
| What therapeutic class/drug is involved with prevention/treatment of a thromboembolism? | Vitamin K analogs |
| What therapeutic class/drug is involved with CAV, especially after a stent? | Platelet aggregation inhibitors |
| What therapeutic class/drug is involved with hypokalemia? | Potassium Supplements |
| What therapeutic class/drug is involved with hypertension and edema? | Diuretics |
| What therapeutic class/drug is involved with CHF and atrial fibrillation? | Cardiac Glycosides |
| What therapeutic class/drugs only deal with hypertension? | Alpha blockers, ACE inhibitors, and Angiotensin Receptor blockers. |
| What therapeutic class/drug is involved with prevention of angina and hypertension? | Calcium Channel Blockers |
| What therapeutic class/drug is involved with the prevention of Angina; reduce risk of a MI in those with a history; and hypertension? | Beta-blockers |
| What therapeutic class/drug is involved with prevention of angina and treatment of angina? | Nitrates |
| Now work on the Review questions in the handouts and answer each one!!!! | |
| NOW REST!!! Get at least 7 hours of sleep before final exam!!! | |
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fender87_2