Essentials of Pathophysiology - Final Exam review sheet PDF

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**Essentials of Pathophysiology – Final Exam Review Sheet Covers Material from Modules 1-10 NEED A 58% TO PASS CAN USE SCRAP PAPER (MUST BE BLANK @START) Be sure to look over review sheets from Exam #1 and #2 – all previous information is fair game for the Final exam Review the difference between ho...

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Essentials of Pathophysiology – Final Exam Review Sheet Covers Material from Modules 1-10 NEED A 58% TO PASS CAN USE SCRAP PAPER (MUST BE BLANK @START) 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.  homeostasis – a state in which all systems are in balance, a state of equilibrium o stability, balance, equilibrium  allostasis- ability to successfully adapt to challenges; o process to bring back to homeostasis from disturbance Homeostatic Systems-

ex) central chemoreceptor (receptors that detect changes in our systems) responses to changes in body core temperature  Stress and Hans Selye’s General Adaptation Syndrome (GAS) 2. What is epidemiology? Review the different levels of disease prevention such as primary, secondary, and tertiary as well as examples for each. epidemiology: study of the patterns involving populations to understand the transmission of diseases a. Examining the occurrence, incidence, prevalence, transmission, and distribution of diseases in large groups of populations/people b. Florence Nightingale- first practicing epidemiologists to start making changes in her patients’ lives i. Handwashing c. Levels of Disease Prevention: i. Primary- altering susceptibility or reducing exposure for susceptible persons; 1. Primary = prevention 2. Ex) immunizations: designed to introduce portions of the disease to prepare body to attack that infection ii. Secondary: early detection, screening, and management of disease 1. Secondary= Screening 2. Ex) cancer screening, performing monthly breast examinations, weight monitoring, BP monitoring iii. Tertiary: rehabilitation, supportive care, reducing disability, and restoring effective functioning 1. Tertiary=Therapy 2. focuses on restoration of functional ability after illness Ex) Physical Therapy or Occupational Therapy following stroke 3. Review the differences between the sympathetic vs the parasympathetic nervous systems. What happens to the body during “fight-or-flight” response? Parasympathetic Nervous System vs. Sympathetic Nervous Systems Parasympathetic: Rest & Digest Sympathetic: Fight or Flight Constricted pupils Dilate pupils Stimulate saliva Inhibit salivation Slow heartbeat Increase heart beat Constrict airways Relaxed airways- increased respirations Stimulate activity of stomach Inhibit activity of stomach- Gastrointestinal 

system suppressed; lost appetite under stress

Inhibit release of glucose Stimulate gallbladder Stimulate activity of intestines Contracts bladder

Stimulates release of glucose Inhibits gallbladder Inhibits activities of intestines Relax bladder- GU function suppressed Secretes epinephrine and norepinephrine

Promotes erection of genitals

Promotes ejaculation and vaginal contraction

Fight or Flight Responses: a. Reduced resistance to stressors- every little stressor will further active this fight or flight response b. increased secretion of (adrenaline, CRH, ACTH,) increased BP 4. Review the functions of the various organelles of the cell such as the nucleus, mitochondria, ribosome, lysosome, endoplasmic reticulum, peroxisome, golgi apparatus Cell Shape= Function of cell  Nucleus – control center/ brain of the cell; o Functions:  DNA and gene storage  Messenger RNA production o most cells only contain one nucleus, except liver and skeletal cells. o Red blood cells don’t contain a nucleus, DNA from blood comes from white blood cells  Mitochondria- power house of the cell; have their own set of DNA o Functions: provides energy to the cell in the form of ATP (Adenosine Triphosphate)  Ribosomeo Functions: site of protein production; RNA produced in the nucleus undergo translation to create protein  Translation: RNA from nucleus-> Protein  Endoplasmic Reticulum – series of folded membranes that move protein around the cell o Rough ER – ribosomes attached  Function:  Site of protein synthesis  Production of integral proteins and phospholipids found in cellular membranes o Smooth ER- found more in liver and kidneys  Functions:  Detoxification  Lipid metabolism  Synthesis of hormones  Calcium storage  Golgi apparatus – organelle made up of stacked, flattened membranes o Functions UPS Center of the cell-sorts and packages proteins produced in Rough ER  moves materials within the cell and out of the cell  Lysosome- spherical membranous organelles containing digestive enzymes o Functions:  digests particles- such as bacteria, viruses, and toxins- taken in by endocytosis  Degrades worn-out or nonfunctional organelles and tissues  Lysis= breakdown=garbage disposals of the cell  Peroxisome -membranous sacs containing a variety of powerful enzymes such as oxidase and catalase o Functions:  Oxidases detoxify harmful substances using molecular oxygen (O2), like alcohol and formaldehyde  Neutralize dangerous free radicals (highly reactive chemicals that can damage biological molecules) into hydrogen peroxide (H2O2)

Catalase breaks down the H2O2 into H2O and O2  H2O2 can be more damaging than cleansing, the O2 kills bacteria, good and bad, which damages healthy cells & tissues too and prevents from reproduction. Lysosomes and peroxisomes are like cousins- both contain digestive enzymes; peroxisome enzymes are more important to breaking down toxic waste products. 5. Review the difference between active and passive immunity, know examples for each type. a. Active Immunity: a protected state owing to the body’s immune response as a result of active infection or immunization i. Requires memory B cells 1. Second exposure -> quicker response ii. Immunizations – 1. vaccines contain altered microorganisms of toxins 2. retain ability to stimulate immune system (antigenic properties) 3. do not have pathogenic properties, do not cause harm to the host iii. Vaccines contain live and attenuated (altered) agents or killed infectious agents b. Passive Immunity: transfer of performed antibodies against specific antigen from a protected or immunized individual to an unprotected or nonimmunized individual i. Provides immediate but temporary protection ii. Used for: 1. B-cell immunodeficiencies (absence of a sufficient immune response) 2. Following exposure of individual with high susceptibility to a disease without adequate time for active immunization iii. Examples: 1. Mother to fetus: IgG can cross placenta 2. Mother to Infant: IgA from breast milk 3. Serotherapy: direct injection of infusion of antibodies from humans or animals into the bloodstream a. Antibody injection may alleviate or suppress effects of antigenic toxin b. Ex) rabies vaccination 6. What is edema? Review the various factors that can contribute to edema. Edema: Accumulation of fluid in the interstitial space, outside the cells, leading to localized or generalized tissue swelling Causes:  increases in the forces that move fluid from the capillaries into the interstitial compartment  decreases in forces that move fluid from the interstitial compartment into the capillaries Factors that can contribute to Edema:  increases in capillary hydrostatic pressure- force that fluid is placing on the vessels o blood vessel blockage, incompetent venous valves  increased capillary permeability (inflammation)  congestive heart failure- blood goes back into the body  High Blood volume or HTN  Decrease in plasma protein- such as albumin (protein produced by the liver that binds water to blood vessels to keep water in the bloodstream, production is inhibited when the liver is damaged b/c water from blood is released to the body) o Loss of albumin: jaundice, round abdomen= ascites,  Blockage of lymphatic drainage (due to cancer or removal of lymph node; lymphedema) 7. What is a hypersensitivity? Review the four different types of hypersensitivities: Type I (Anaphylactic), Type II (Cytotoxic), Type III (Immune complex), Type IV (Delayed cell-mediated). Know examples and mediating factors for each type. Refer to table 19.1- pg 14 of slides Hypersensitivity: antigenic response to antigens (allergens) beyond what is considered normal, in a way that is not beneficial to self, leading to damage 

Types of Hypersensitivity Reactions: THINK ACID a. Type I (Anaphylactic)i. occurs very quickly- within 2-30 minutes of antigen exposure, ii. Can be systematic or local iii. Antigens bind to IgE attached to mast cells and basophils- undergo degranulation (exocytosis of stored molecules contained in cytoplasmic vesicles), releasing mediators: histamines, leukotrienes, and prostaglandins 1. Examples: allergic reactions to shellfish, peanuts, mold, pollen b. Type II (Cytotoxic)- involves IgG or IgM antibodies that react with cell-surface antigens i. Examples: 1. transfusion reactions- transfused red blood cells destroyed by circulating antibodies 2. hemolytic disease of the newborn (erythroblastosis fetalis) a. can occur in situations with Rh- mother and Rh+ fetus (Father must be Rh+) i. maternal antibodies attack Rh+ red blood cells of the fetus, this usually occurs in the 2nd or 3rd pregnancy, not 1st. This is an ___ type of immunity, so it takes time to develop, mother can take medication to block production of these antibodies during pregnancy 3. graves’ disease- thyroid gland is attacked by antibodies, causing thyroid to release excessive thyroid hormones (hyperthyroidism) a. results in: extreme weight loss, increased blood pressure, affects sleep, hair loss 4. myasthenia gravis- antibodies attach acetylcholine receptors at neuromuscular junction, block acetylcholine from binding to receptors on muscle cells a. no muscle contraction will occur if acetylcholine is attacked -> muscle weakness c. Type III (Immune complex)- IgG antibodies and antigens from immune complexes circulate in the blood and can become lodged in basement membranes beneath cells -> activates inflammatory response which can cause damage to tissues i. Examples: rheumatoid arthritis (RA), glomerulonephritis (inflammation of kidneys), Systemic Lupus Erythematosus d. Type IV (Delayed cell-mediated)- cell-mediated responses caused by T-cells i. Antigens are phagocytized and presented to receptors on T-cells, causing sensitization ii. Re-exposure to antigen cause memory cells to release destructive cytokines iii. Basically, a delayed reaction so it can take lots of testing to find out what the causing factor is, can occur days later after exposure iv. Examples: 1. Mantoux screening test for TB 2. Contact dermatitis- reactions to poison ivy, certain metals, latex gloves (allergy can develop overtime) 8. Review the differences between benign and malignant tumors. Pg. 15 Module 2 Slides, Ch 7 Neoplasia – new growth, Implies abnormality of cellular growth/tumor a. Benign Tumors i. Benign growths tend to be more localized and can be cured. ii. Grows more slowly iii. Rarely necrotic- cell death iv. Often retains original function v. Rarely fatal, but can be life-threatening depending on location vi. Doesn’t invade adjacent tissues or spread to distant sites b. Malignant Tumors –

i. growths can travel throughout the body, tend to be a lot more lethal in nature ii. Continue to grow in the absence of oxygen, nutrients, or other growth-initiating signals, and ignore growth-controlling signals iii. Escape signals to die and achieve a kind of immortality iv. Anaplasia- Display lack of differentiated features and contribute poorly or not at all to the function of their tissue- they don’t look like or function like their surrounding cells/tissue v. Metastasis- process by which cancer cells escape their tissue of origin and initiate new colonies of cancer in distant sites 9. Review signs and symptoms of peptic ulcer disease. Peptic Ulcer Disease- disorders of the upper GI tract caused by the action of hydrochloric acid and pepsin; irritation to the lining of the stomach that’s actually eating away at the stomach tissue; these ulcerations can cause a lot of bleeding Signs and Symptoms – a. epigastric burning pain that is usually relieved by the intake of food (especially dairy products) or antacids b. pain of gastric ulcers typically occurs on an empty stomach, but may present soon after a meal. c. nausea, abdominal upset (dyspepsia), and chest discomfort 10. Review signs and symptoms of appendicitis. How do we assess for this condition? Appendicitis- inflammation of the vermiform appendix; obstruction of the appendiceal lumen by a fecalith causes most cases Signs and Symptoms: periumbilical pain, RLQ pain “McBurney’s Point,” nausea, vomiting, fever, diarrhea, RLQ tenderness, systemic signs of inflammation Assessment: McBurney’s Point- rebound pressure a. Place thumb on belly button (site of pain) and pinky finger on hip bone, rebound tenderness/pressure on the center where palm is i. Less pain with pressure application ii. Tenderness/ pain @ release of pressure 11. Review signs and symptoms of liver disease. Review complications of liver disease such as ascites, hepatic encephalopathy and esophageal varices. How are esophageal varices managed/treated? General Manifestations of Liver Disease  Hepatocellular failure – Jaundice, decreased clotting factors, hypoalbuminemia, decreased vitamins D and K o Jaundice - Characteristic sign of liver disease  Green-yellow staining of tissues by bilirubin  Results from impaired bilirubin metabolism  Portal Hypertension- GI congestion, development of esophageal or gastric varices, hemorrhoids, splenomegaly (enlargement of spleen), and ascites o Gastroesophageal Varices - Complication of portal hypertension resulting from alcoholic or viral hepatitis  In developing countries, Schistosoma species of liver flukes major cause  Affects more than half of cirrhotic patients  High mortality rate

 How are esophageal varices managed/treated? 

Portal Systemic Encephalopathy – o Hepatic Encephalopathy – Complex neuropsychiatric syndrome from too much ammonia  Clinical manifestations  Dementia  Psychotic symptoms  Asterixis “liver flap” (classic sign)

o Spastic jerking of hands held in forced extension  Mild confusion and lethargy to stupor and coma  Complications of Advanced Liver Disease – o Ascites- Pathologic accumulation of fluid in peritoneal cavity  Occurs with portal hypertension and hypoalbuminemia  Diagnosis:  Fluid examination from abdominal paracentesis o Total protein o Albumin 12. What role does albumin play in the blood? What happens to albumin production with liver failure? a. Albumin – protein produced by the liver that binds water to blood vessels to keep water in the bloodstream, production is inhibited when the liver is damaged b/c water from blood is released to the body b. albumin production with liver failure 13. What are the function of the kidneys? How do we assess for renal disorders? a. Functions: i. Excretion ii. Elimination iii. Regulation b. Assessment: i. Palpating Costovertebral Angle- pounding of the back at this area, jumping from tenderness or flank pain is an indicator ii. Abnormal Urinalysis Findings 14. What is cystic kidney disease? What causes this condition? a. A congenital abnormality; Genetically transmitted renal disorder resulting in fluid-filled dilations (cysts on kidneys); may be localized to one area or affect both kidneys b. Can lead to renal failure, requiring dialysis or transplantation c. Two types: 1. Autosomal recessive forms 2. Autosomal dominant types – most common, symptoms appear later in life 15. Review the following terms: nephrons, hematuria, proteinuria, nephrolithiasis, pyelonephritis, cystitis a. Nephrons – the functional unit of the kidney, performing all filtration, reabsorption, and secretory functions b. Hematuria - blood in the urine c. Proteinuria – protein in the urine d. Nephrolithiasis - the formation and passage of calculi anywhere within the urinary tract. e. Pyelonephritis - Infection of the kidney; Most common cause is ascending infection from an untreated UTI, from which e. coli travels up to the kidneys f. Cystitis - inflammation of the bladder lining, may result from bacterial, fungal, or parasitic infections; chemical irritants; foreign bodies (e.g., stones); or trauma. 16. Review signs and symptoms of acute kidney injury (AKI). Review causes of AKI including prerenal, intrinsic, and postrenal. Know examples of each type of injury. a. Signs and Symptoms: i. Disruptions in fluid, electrolyte, and acid-base balances ii. Retention of nitrogenous waste products iii. Increased serum creatinine iv. Decreased glomerular filtration rate (GFR) b. Causes: i. Prerenal- disruption to renal perfusion (Blood flow to kidneys) 1. Hypovolemia, hypotension, heart failure

2. Renal artery obstruction 3. Fever, vomiting, diarrhea 4. Burns 5. Overuse of diuretics 6. Edema, ascites 7. Drugs: ACE inhibitors, angiotensin II blockers, NSAIDs ii. Intrinsic/ intrarenal- damage/disruptions within the kidney blood vessels, tubules, or glomeruli 1. Berger disease 2. Contrast dye/media 3. Nephrotoxic medication, chemotherapy, amphetamines iii. Postrenal – disruption of urine flow distal (down) to the kidney 1. Kidney stones stuck in the ureter or in the urethra are blocking the flow of urine 2. Enlarged 17. What is compartment syndrome? Why does it occur and what are the signs? Remember the 5 P’s 18. What are pressure ulcers? How are the staged and how can we prevent them? 19. What are electrolyte reservoirs? What electrolytes are found stored in bones? a. Bones act as an electrolyte reservoir to calcium, phosphate, and magnesium; can be withdrawn or deposited to maintain balance 20. Review diseases of the bone including: osteomyelitis, osteosarcoma, osteomalacia, and osteoporosis a. Osteomyelitis- severe pyogenic infection of bone and local tissue i. Causes: IV drug abusers, open fracture, surgical contamination ii. Organisms reach bone through bloodstream, adjacent soft tissue or direct introduction of organism into bone 1. Adjacent soft tissue injury caused by to burns, sinus disease, trauma, malignant tumor necrosis, periodontal infection, infected pressure ulcer 2. Direct infection causes open fracture, penetrating wounds, surgical contamination, or insertion of prostheses, metal plates, or screws iii. Treatment: very difficult to treat, a lot of times, patients are on long term IV and antibiotics b. Osteosarcoma - Extremely malignant bone-forming tumor and most common i. Grows rapidly, very destructive c. Osteomalacia- softening of the bones due to lack of calcium and vitamin D i. Precursor to osteoporosis ii. Equivalent to Rickets- which occurs in children, and Osteomalacia occurs in adults iii. Treatment - drinking milk (fortified in vitamin D) and exposing skin to sunlight d. Osteoporosisi. Most common metabolic disease- occurs when rate of bone resorption is greater than bone formation ii. Bones become fragile, porous and light iii. Shortened stature, muscle wasting, back muscle spasms, difficulty bending over iv. Causes: estrogen deficiencies, poor calcium intake, and disuse v. Treatment - calcium and vitamin D supplements, exercise, bisphosphonates, recombinant human parathyroid hormone 21. Review disorders of the joints including: rheumatoid arthritis, osteoarthritis, psoriatic arthritis, and gout. Know causes and signs/symptoms for each. Joint Disorders: a. rheumatoid arthritis- systematic autoimmune inflammatory disease vi. genetically predisposed individuals vii. Signs and Symptoms: bilateral symmetric polyarthritis involving smaller joints, malaise, fatigue, and diffuse musculoskeletal b. osteoarthritis-

viii. Usually associated with the elderly ix. Initial Cause: The wear and tear or overuse of joints that develops over time; loss of protective cartilage layer causing bone on bone contact, can lead to inflammation and swelling of joints, but main cause is non-inflammatory x. Treatment: Viscosupplementation: replenishment of synovial fluid; Synovial fluid is impacted from bone- to bone grinding c. psoriatic arthritis- condition is associated with individuals who have psoriasis d. gouty arthritis - due to production of uric acid xi. Uric acid is produced in response to xii. Uric acid has a tendency to crystalize and get trapped in joint cavities Kahoot Questions: 1. The ability of the or...