Essentials of Pathophysiology – Final Exam Review Sheet Modules 1-10, Exams of Pathophysiology

Download Essentials of Pathophysiology – Final Exam Review Sheet Modules 1-10 and more Exams Pathophysiology in PDF only on Docsity! Essentials of Pathophysiology – Final Exam Review Sheet Modules 1-10 Covers Material from Modules 1-10 Be sure to look over review sheets from Exam #1 and #2 – all previous information is fair game for the Final exam 1. Review the difference between homeostasis and allostasis. Allostasis is the overall process of adaptive change necessary 2. What is epidemiology? . Epidemiology the branch of medicine that deals with the study of the causes, distribution, and control of disease in populations….Review the different levels of disease prevention such as primary- preventionintermsofimprovednutrition,eco nomy,housing,andsanitation Secondary- prevention that lead to the early diagnosis of disease and, in some cases, cure tertiary- prevention- once a disease becomes established, treatment as well as examples for each. Epidemiology the branch of medicine that deals with the study of the causes, distribution, and control of disease in populations. Primary- preventionintermsofimprovednutrition,econ omy,housing,andsanitation… Secondary- prevention that lead to the early diagnosis of disease and, in some cases, cure… Tertiary prevention- once a disease becomes established, treatment 3. Review the differences between the sympathetic vs the parasympathetic nervous systems. What happens to the body during “fight-or-flight” response? Sympathetic- stressful stimulus and release of norepinephrine. Parasympathetic-rest/relax P a g e 1 | 21 Essentials of Pathophysiology – Final Exam Review Sheet Modules 1-10 s - 4. Review the functions of the various organelles of the cell such as the nucleus, mitochondria, ribosome, lysosome, endoplasmic reticulum- cytoplasm of a eukaryotic cell, has ribosomes attached and is involved in protein and lipid synthesis. peroxisome- breakdown of very long chain fatty acids through beta oxidation golgi apparatus- a complex of vesicles and folded membranes within the cytoplasm of most eukaryotic cells, involved in secretion and intracellular transport.protein molecules in sacs called cisternae and the transport of synthesized proteins in vesicles to the 5. Review the difference between active and passive immunity, know examples for each type. A c t i v e imm un i t y -vacine ocurswhenindividualsareexposedtoantigen,whichconfe rslong-term protectionbut maytakeseveralwekstodevelop.)and (Passive immunity-Newborns receive IgA antibodies through breast milk. serotherapy, involves direct injection of antibodies into an unprotected person P a g e 2 | 21 Essentials of Pathophysiology – Final Exam Review Sheet Modules 1-10 , e , 13.What are the function of the kidneys? drainexcesinterstitialfluidandproteinsreg ulateblod sup lyandreninreleas filtrationofwater-solublesubstances; (2)reabsorptionoffilterednutrients, P a g e 5 | 21 Essentials of Pathophysiology – Final Exam Review Sheet Modules 1-10 . water,andelectrolytes(3)secretionofwaste sorexcessubstances…How do we assess for renal disorders? ? BUN levels are used to monitor the progression of renal disease or to screen for occult renal insufficiency. Creatinineclearanceisfrequentlyusedtoase sGFR BUNandcreatininearemeasured together,andtheratioisdetermined.Acutec hangesinGFRarereflectedinahigherBUN-to- creatinine ratio,usuallygreaterthan20:1 14.What is cystic kidney disease? polycystic kidney disease, where cysts form in the kidneys. Genes code for proteins associated with the primary cilium 2types- autosomal- recesive(infant)andautosomal- dominant(adult)commonlyfoundinmen….What causes this condition? end stage renal disease 15.Review the following terms: nephrons- performingallfiltration,reabsorption,andse cretoryfunctions hematuria-- proteinuria- for biopsy, renal disease check.. nephrolithiasis-- -(stone) crystal ag regatescomposedoforganicandinorganicmate rials20and30years,loweramongAfrican AmericansandMexican…..pyelonephritis- -Chronic: smallatrophiedkidneyswithdiffusescaring andblunting.obstruction or ureteral reflux that allows contaminated urine to enter the kidney… cystitis-- inflammation of the bladder lining, may result from bacterial, fungal, or parasitic infections P a g e 6 | 21 Essentials of Pathophysiology – Final Exam Review Sheet Modules 1-10 16.Review signs and symptoms of acute kidney injury (AKI). Review causes of AKI including prerenal- S/S- fluid volume overload, oliguria, low urinary sodium.. Intrinsic- S/S: declining urine output. postrenal. - Obstruction of the normal outflow of urine, more common in the elderly.Know examples of each type of injury. 17.What is compartment syndrome? trauma to soft tissue caused Why does it occur and what are the signs? decreased compartment size, increased compartment content, or externally applied pressure….Remember the 5 P’s-- Pain. Pressure. Paresthesia (numbness). Paralysis. Pulselessness 18.What are pressure ulcers? bedsores, are localized damage to the skin and/or underlying tissue.. How are the staged and how can we prevent them? Stage I:The skin is intact, Stage II: An open wound, Stage III: A deep wound- Deep damage may expose a fat layer, Stage IV: Large scale tissue loss- exposes bone, muscle or tendons. 19.What are electrolyte reservoirs? Electrolytes come from the food and liquids you consume. What electrolytes are found stored in bones? Ca P a g e 7 | 21 Essentials of Pathophysiology – Final Exam Review Sheet Modules 1-10 26.Review the differences between hypothyroidism--- intrinsic dysfunction of the thyroid gland, Congenital hypothyroidism, developmentmaybereferedtoascretinism and hyperthyroidism— increasedsynthesis andsecretionofT4 andT3, , Gravesdisease.What labs can be drawn to determine if an individual is suffering from a thyroid disorder? TSH 27.Review the difference between Type 1 diabetes characterizedbydestructionoftheβcellsof the pancreas-,verproductionofglucagonbypanc reaticαcellsstimulatesglycogenolysis ( type II- need insulin, 2diabetesmelitusareresistantotheactionofinsulin onperipheraltisues 28.What are signs and symptoms of hyperglycemia- Blurred vision. Fatigue. Weight loss. Poor or delayed wound healing. ( hypoglycemia-- hunger,visualdisturbance,weaknes,parest hesias, confusion,agitation,coma,anddeath (What are the three Ps? polyuria, polydipsia and polyphagia 29.Review the difference between primary and secondary brain injury. TBI, primary injuries result immediately from the initial trauma…Secondary injury is an indirect result of the injury. It results from processes initiated by the trauma.. What is a P a g e 10 | 21 Essentials of Pathophysiology – Final Exam Review Sheet Modules 1-10 reperfusion injury? Celdeathresultingfrom ischemia occurs and blood supply to the tissues has been restored called reperfusion injury 30. Review causes of intracranial pressure; how does it lead to impaired neurological function? LOC, decrease motor function, speech issues, sbp ^ & pulse down, headache…(cause Aneurysm rupture , Encephalitis, Hydrocephalus (increased fluid around the brain) 31.What are signs or increased ICP? The signs of increased ICP include: headache, increased blood pressure , confusion , double vision, pupils that don’t respond to changes in light, loss of consciousness, coma 32.Review the Glasgow coma scale, what is it used to assess?checks for impairment of conscious level in response to defined stimulus. Eye opening, Verbal response, Motor response, P a g e 11 | 21 Essentials of Pathophysiology – Final Exam Review Sheet Modules 1-10 33.Review the different types of stroke: ischemic-- blood vessel carrying blood to the brain is blocked or restricted versus hemorrhagic-blood vessel in the brain ruptures or breaks . How is stroke diagnosed?CT or MRI 1st step, blood test, ECG-EKG 34.Review the difference between meningitis-- infection to the outer layer of the brain, cause Bacteria, Viruses,Fungi, rash, DX blood . versus encephalitis- acute inflammation to the brain itself cause Virus, no rash, DX mri ct. 35.Review the different types of seizures- tonic-clonic or convulsive seizures or grand mal) absence seizures or petit mal, atonic seizures or drop attacks) (How are seizures diagnosed? Electroencephalogram (EEG), blood testing to check for electrolyte imbalances , a spinal tap rule out infection, a toxicology screening 36.Review the etiology of cerebral palsy-- disorder of movement, muscle tone or posture that is caused by damage that occurs to the immature, developing brain, most often before birth ) (Is cerebral palsy reversable? No,Lifelong condition, caused by a static, non- progressive lesion in the brain. P a g e 12 | 21 Essentials of Pathophysiology – Final Exam Review Sheet Modules 1-10 43.What is a tension pneumothorax, how is it treated? air escapes into the pleural cavity, increasing air pressure in the pleural cavity causes progressive collapse of the lung. TX-by Needle in chest remove excess air 44.What is Virchow’s Triade? named for (Rudolf Virchow) contribute to thrombosis, Hypercoagulability Hemodynamic changes (stasis, turbulence) Endothelial injury/dysfunction How do these factors increase a patient’s risk for developing a pulmonary embolus? Beccuase thrombi occurring within the veins and migrate to the pulmonary vasculature P a g e 15 | 21 Essentials of Pathophysiology – Final Exam Review Sheet Modules 1-10 45.What are different causes/types of emboli? (pulmonary embolism- deep vein thrombosis or DVT), lodges in one of the arteries of the lungs. Types-- brain embolism, fat embolism, air embolism. Causes-- smoking and heart disease-- cancer, previous surgery, a broken leg or hip 46.What are causes of anemia? blood loss, decreased production of RBC, and destruction of RBC. What are complications of anemia? tissue hypoxia. Shock, hypotension, or coronary and pulmonary insufficiency What is the goal in treating anemia? treated based on the cause 47.Review the following conditions of the blood including causes: (polycythemia- red cells are present in excess, increasing blood viscosity thrombocytopenia Caused by: lung and heart diseases, sleep apnea, tumors, dehydration,) (Disseminating intravascular coagulation (DIC)--- hemorrhagic syndrome in which both clotting and bleeding occur simultaneously . How do we treat DIC- Replacementofdepleted clotingfactorswithfreshfrozenplasma,pack edredblodcells,platelets,orcryoprecipit ate 48.What hormone plays a role in RBC production? erythropoietin (EPO). What organ produces this hormone? Kidney(Formation in the bone marrow) P a g e 16 | 21 Essentials of Pathophysiology – Final Exam Review Sheet Modules 1-10 49.Review the difference between Hodgkin’s-dx’s Is early stages treatable, also begins in the upper body neck , armpits chest vs Non-Hodgkin’s lymphoma-begins in lymph nodes dx’s Is later stages harder to treat.. How are these cancers diagnosed? 50.Review modifiable- Dietary factors, Sedentary lifestyle, Obesity/weight gain// nomodifiable —Family history,Age,Ethnicity/Genetics risk factors for hypertension. How is hypertension managed/treated? What medications are often prescribed to manage HTN? What are complications of hypertension if left unmanaged? Stroke, atherosclerosis, MI, organ damage 51.What is the role of renin-angiotensin-aldosterone system in managing blood pressure? restore blood volume, Angiotensin 1 not strong enough Instead, converted to angiotensin II, much more powerful hormone to change blood act directly on blood vessels. 52.What is coronary artery disease? major blood vessels that supply your heart with blood, oxygen and nutrients (coronary arteries) become damaged or diseased P a g e 17 | 21 Essentials of Pathophysiology – Final Exam Review Sheet Modules 1-10 y 60.Review the signs and symptoms of shock. Review the causes of different types of shock including: anaphylactic shock- Antibiotic therapy, Peanuts and tree nuts, Insect stings, Snake bites cardiogenic shock-- Loss of consciousness, Pallor of the skin hypovolemic shock-- elevated HR, vasoconstriction, increased contractility obstructive shock- Confusion or lack of alertness, Loss of ability to concentrate, Unconsciousness, Chest pain. septic shock--- Activation of clotting cascade, DIC, Hypotension, Cellular hypoxia, Increased capillary permeability with edema formation (Distributive shock)--- abnormal distribution of blood flow, not enough oxygen-carrying blood Neurogenic shock massive vasodilation, spinal cord sympathetic nerves damage 61.What are complications of shock? They are Disseminated Intravascular Coagulation occurs in septic shock Immune activation of the clotting.. Acute Renal Failure - Kidneys undergo long periods of hypoperfusion. Vasoconstriction causes decreased glomerular blood flow.. Multiple Organ Dysfunction Syndrome (MODS) Occurs when 2 or more organ systems are affected 62.What are the stages of hemostasis?- initial, interaction between platelets and the endothelium of the injured blood vessel. The secondcomponentofprimar hemostasis isformationofaplateletplug-formationof afibrinclot,orcoagulation.Clot retraction, the final stage of clot formation, This stage takes approximately 1 hour P a g e 20 | 21 Essentials of Pathophysiology – Final Exam Review Sheet Modules 1-10 e , s 63. What medications can affect hemostasis? vascularpurpuraincludesremovalofcausativeagentifo neis identified(e.g.,penicilin).extensivebledingtocontro lth bleedingarenecessary. 64.What is hemophilia? most common severe inherited coagulation disorder. Excessive bleeding adevelop bleeding) Review the differences between Hemophilia A is a bleeding disorder associated with a deficiency of factor VIII, a protein necessary for blood clotting TX - administration of cryoprecipitate or other preparations of factor VIII concentrate desmopresinandantifibrinolytic .. Hemophilia B- results from factor deficiency or the abnormal function of factor IX, TX-- administration of fresh or fresh frozen plasma or cryoprecipitate What is the treatment for each? P a g e 21 | 21 Essentials of Pathophysiology – Final Exam Review Sheet Modules 1-10