Midterm Review Chapter 1 1)What is the definition of Etiology? -the cause of the disease 2)What are the differences between Idiopathic and Iatrogenic etiology? -Idiopathic means the causes is unknown and lactogenic means the cause is unwanted medical treatment and unintended. 3)Examples for modifiable and nonmodifiable risk? -modifiable → diet, exercise, stress level, smoking/drinking, preexisting condition -nonmodifiable→ genes, family history, gender, race, ethnicity 4)what are the differences between signs and symptoms? -signs are objective observed ( what nurses observed) -symptoms are subjective feeling from patients 5)what stage of illness that shows your first signs/symptoms appear? - prodromal period 6)is it possible for chronic situation happen after an acute situation? -YES 7) what is exacerbation? -a sudden increase in severity of disease, signs or symptoms. 8) what is remission? Can cancer be cured or remission? -decrease in severity, signs or symptoms. Cancer can not be cured but remission. 9) what is convalescence? -stage of recovery after a disease, injury or surgical procedure. 10) what is sequela? - subsequent pathologic condition resulting from an illness. 11) what are the three types epidemiology and what are the differences? - endemic → native to local region, Epidemic→ spread to many people at the same time, pandemic→ spread or large geographic areas, 12) what is primary, secondary and tertiary prevention? - primary→ eating healthy, vaccine, education/ secondary→screening, physical exam/ tertiary→ support care, therapy. “ Primary = Prevention, Secondary= Screening, Tertiary=Treatment” 13) what are the gender differences? - male has higher hemoglobin and muscle mass than female. 14) what is the stage that not yet show signs of the disease? -latent stage → maybe only mild symptoms will appear Chapter 2 1) what is homeostasis? - an “set point” despite alteration in the body and a state of equilibrium/ maintain stable. 2) what is allostasis ? - ability to successfully adapt to challenges/ refers to process of achieving homeostasis through behavioral change. 3)which terms refers to a state of tension that can lead to threaten physical and mental stability? -stress 4)what does GAS stand for? - General Adaptation Syndrome 5) what are the three stages for GAS? And what do they provide or do? - Alarm → fight or flight response. Resistance/Adaptation → activate nervous and endocrine system/ Exhaustion→ point where body can no longer return to homeostasis. 6) what is a stressor? - an agent or condition that can causes stress. 7) what are the hallmarks for catecholamines? -play roles in allostasis/ include both epinephrine and norepinephrine/ fight or flight response 8) what are the hallmarks for norepinephrine? -constricts blood vessel and raises blood pressure/reduces gastric secretions/ increase night & far vision 9) what are the hallmarks for epinephrine? - increase HR, increase cardiac output, causes bronchodilation (“EpiPen” for allergic reaction), increase glycogenolysis to increase glucose level in liver. 10) what are the hallmarks for cortisol? -glucocorticoid, affects protein metabolism, anti-inflammatory effects, anabolic effect on protein. 11) what ate the hallmarks for aldosterone? - mineralocorticoid, reabsorption of Na &H2o, increase blood pressure 12) what is our body’s natural pain reliver? - endogenous opioids from endorphins and enkephalins 13) what does immune cytokines do? - secreted by macrophages during stress response, enhance immune system response, prolonged stress can suppress immune functioning 14) what hormone is responsibility to lactation and interferes with ovulation ? -prolactin Chapter 4 1) what are the hallmarks for hydropic swelling? - cell swelling due to accumulation of h2o, results from malfunction of Na-K pump w/ accumulation of Na ions w/in the cell, loss of ATP 2) what is the term for selling of cells in organ that increase in size and weight? -megaly 3) What kind of cell injury is hydropic swelling? -reversible cell injury 4) what kind of cell injury is intracellular accumulations? -reversible cell injury 5) what can lead to intracellular accumulation? - toxicity, immune response, taking up cellular space 6) what are the common site of intracellular accumulation? - liver 7) The cellular response indicative of injury due to faulty metabolism of lipids, carbohydrates, glycogen and proteins is? - intracellular accumulation. 8) what is hydropic swelling results from malfunction of ? -Na and K pump 9) what kind of situation can lead to cell atrophy? - Disuse ( didn’t use muscle for a long time), denervation ( lack of nerves supply), ischemia ( lack of blood ), nutrient starvation (lack of nutrient cells), interruption of endocrine signals, persistent cell injury ( damaging), aging. 10) what is the differences between atrophy, hypertrophy, hyperplasia, metaplasia and dysplasia? - atrophy → decrease in size, Hypertrophy → increase in size, Hyperplasia→ increase in numbers, Metaplasia→ replace one cell to another ( different shape), dysplasia → disorderly growth. 11) why does dysplasia different than other cellular adaptation? - dysplasia is an irreversible cell, which means a cancer cell that will need to be removed. So this will be the greatest concern if found on a biopsy report. 12) when intense contraction for heat will cause cell? - hypertrophy 13) what happened to the cell when response to increased physiologic demands or hormonal stimulation? - hyperplasia 14) when does necrosis usually occur? - ischemia or toxic injury. 15) are necrosis and gangrene reversible or irreversible? -irreversible 16)What are four types of necrosis? - coagulative, liquefactive, Fat necrosis, caseous Necrosis 17) what is the most common necrosis? -coagulative 18) Necrotic death of brain tissue usually produces____ necrosis? - liquefactive 19) what does death of adipose tissue bursting causing an accumulation of fat in that area? - fat necrosis 20) Lung damage secondary to TB resembles clumpy cheese produces _____ necrosis? - caseous necrosis 21) what kind of necrosis do dry, wet and gas gangrene form of? - Dry → coagulative, Wet and Gas → liquefactive 22) The cellular change that is considered preneoplastic is? -dysplasia → (preneoplastic lesions means pre-cancer cell and has to be removed) Chapter 7 Malignant tumor Benign tumor Can kill host if untreated Doesnt have potential to kill host, but may be life-threatening because of its location Confirmed by invasive or metastasizing nature Does not invade adjacent tissue or spread to distant sites Tissue-specific differentiation( does not closely resemble tissue type of origin) Many are encapsulated Greater degree of anaplasia indicates aggressive malignancy More closely resembles original tissue type Grows rapidly Grows more slowly May initiate tumor vessel growth Little vascularity Frequently necrotic Rarely necrotic Dysfunctional Often retains original function “ carcinoma” → epithelial origin “adenoma” “ Sarcoma” → mesenchymal origin “Oma” “Leukemia” → WBC **Lymphomas, Hepatomas, Melanomas ( exceptions ) Not mobile (hard, stuck in the tissue) mobile 1) Does tobacco use only linked to lung cancer? - No, it could linked to pancreatic, kidney, bladder, mouth, esophageal and cervical cancers. 2) what does Neoplasia means? - new growth 3) what does one third of cancer-related deaths may be attribute to ? -lifestyle factors→ tobacco use, nutrition, obesity, sun exposure, sexual exposure 4) what are two types of carcinogens? And what do they cause or promotes? - initiator → causes genetic damage, promoter→ promotes tumor growth 5) what does metastasis means? - process by which cancer cells escape their tissue of origin and initiate new colonies of cancer in distant sites. Specialized enzymes and receptors enable them to escape their tissue of origin and metastasize. 6)where does cancer cell generally spread? - circulatory or lymphatic systems ( blood and lymph nodes) 7) what are the differences between grading and staging of tumors? - grading → histologic characterizations, staging → location, patter of spread, size 8) what does TNM stand for ? - primary Tumor, regional lymph Nodes, distant Metastasis 9) adult’s warning signs of cancer.(CAUTION) -Change in bowel or bladder habits -A sore that does not heal -Unusual bleeding or discharge -Thickening or lump in breast or elsewhere -Indigestion or difficulty swallowing -Obvious change in wart or mole -Nagging cough or hoarseness 10)Children’ warning signs of cancer. ( CHILDREN) -Continued, unexpected weight loss -headaches with vomiting in the morning -Increased swelling or persistent pain in bones or joints -Lump or mass in abdomen, neck or elsewhere -Development of whitish appearance in pupil of the eye -Recurrent fevers not caused by infections -Excessive bleeding or bruising -Noticeable paleness or prolonged tiredness 11) what does cachexia means? - overall weight loss and generalized weakness. 12) what does bone marrow suppression contributes to anemia, leukopenia and thrombocytopenia? -Anemia→ deficiency in circulating in RBC, leukopenia→ WBC, thrombocytopenia→ platelets Chapter 10 A Type I (Atopic Anaphylactic) Mediated by IgE (immunoglobulin E) Immune response Antigen (Ag) plus IgE leading to Mast cell degranulation Peak Reaction Cause of reaction 15-30 mins T cell deficiency abnormal mediator feedback environmental factors and Ag Manifestation Asthma, rhinitis, atopic eczema, bee sting reaction, anaphylactic shock, may lead to hypertension and bronchoconstriction. C Type II (Cytotoxic Cytolytic “cell death” IgM or IgG Surface antigen( Ag) and Antibody (Ab), leading to killer cell cytotoxic action or complementmediated lysis 15-30 mins Exposure to Ag or foreign tissue, cells or graft I Type III (arthus reaction, immune complex) IgG Ag-Ab complex in tissue; complement activated and PMNS attracted 6 hrs Persistent infection microbe Ag extrinsic environmental Ag. Autoimmunity-self Ag. ABO transfusions, Glomerulonephritis, hemolytic disease SLE(infection in of newborn ( RH- kidney and pretty and RH+) persistent) , myasthenia gravis farmer’s lung arthritis vasculitis D Type IV (delayed hypersensitivity) T cell Ag-sensitized T cells release lymphokines, leading to inflammatory reactions, and attack macrophages, which release mediator. 24-48 hrs Intradermal Ag, Epidermal Ag, Dermal Ag Guillain-Barre’ disease, TB test, contact dermatitis, multiple sclerosis. Transplant rejection, graft vs host. Chapter 11 1) what are granulocyte and agranulocyte? -Granulocyte (phil family) → Eosinophil, Neutrophil, Basophil / Agranulocyte (cyte family)→ Monocyte, Lymphocyte 2)what is leukemias, lymphoma, plasma cell myeloma? -leukemias→ malignant disorder of RBC/ Lymphoma→ malignant disorder of WBC/ plasma cell myeloma→ malignant disorder of B cell. 3) where does myeloid lineage travel through? -only travel through blood.. RBC, platelets, monocytes and granulocyte ( eosinophil, neutrophil, basophil) 4) where does lymphoid lineage travel though? -travels through blood and lymphatic tissue, B cells, T cells, NK cells. Leukopenia → lymphadenopathy, joint swelling and pain, weight loss, anorexia, hepatomegaly, splenomegaly Anemia→ pallor, fatigue, malaise, shortness of breath, decreased activity tolerance Thrombocytopenia→ petechiae, easy bruising, bleeding gums, occult( dark ) hematuria (blood urine), retinal hemorrhages 5) what is the differences between allogenic and autologous bone marrow transplant? - Allogenic is when patient gets bone marrow from others and autologous is when patient uses their own bone marrow. 6) which component of the blood is protecting the body by phagocytosis of micro-organism and other debris? -erythrocytes Chronic Myeloid Leukemia (CML) -presence of Philadelphia chromosome (Ph+) -bcr/abl gene -elevated granulocyte count -Sweats -weight loss -abdominal discomfort -15% of all cases of leukemia -average age: 40-5-0 yrs old Acute Myeloid Leukemia (AML) Chronic Lymphoid Leukemia (CLL) -Malignant immature WBC >20% -Increased infection susceptibly -increased infection susceptibility -defective apoptosis=longer lifespan of CLL cells -80% of all cases are adults -average age: 64 yrs old -30% of all cases of leukemia -95% of malignant B cell = asymptomatic -5% malignant T-cell= aggressive Acute Lymphoblastic Leukemia/ Lymphoma (ALL) -Primarily children’s disease: 2nd leading cause -increased infection susceptibility -bone pain -anemia -fatigue -weight loss -anorexia -lymphadenopathy -splenomegaly -bone pain -infection -fever -enlarged liver -bruising Hairy Cell Leukemia (HCL) -90% of all cases have associated splenomegaly -hair-like projection on cell -splenomegaly -anemia -bleeding disorder -2% adult leukemia -average age: 55 yrs old Plasma Cell Myeloma (Multiple Myeloma) -malignant plasma cells invade tissue and form multiple tumor -presence of Bence Jones Protein in the urine -bone pain -anemia -bleeding disorder -occur in adults > 40 yrs old -average age: 65 years old -male > female -80% malignant B cell -20% malignant T cell -Peak incident → 3 – 7 yrs old -2nd peak → middle age -honeycomb x rays -Renal insufficiency -presence of hypercalcemia which can contribute compression fracture -Reed-Sternberg cell → found in Epstein-Barr Virus Hodgkin Disease Non- Hodgkin Disease -Epstein-Barr Virus w/o Reed Sternberg cell -night sweats -pruritus (itchy skin) -fever -night sweats -pruritus ( itchy skin) -fever -30% malignant lymphoma -half cases between 20 – 40 yrs old -95% in older adults -males > female -incidence increasing AIDS population Chapter 13 1) what is the differences between anemia and polycythemia ? - anemia is deficit of RBC / polycythemia is an excess of RBC 2) what is aplastic Anemia? -stem cell disorder characterized by reduction of hematopoietic tissue in the bone marrow, fatty marrow replacement and pancytopenia ( a deficiency of all type RBC decrease ) 3)The primary source of erythropoietin is provided by? -kidney 4) when renal failure occur which means ____production will be impaired? -erythropoietin 5)what is the most common anemia? -iron deficiency anemia o o o o o o Aplastic anemia: History of toxic or radiation injury to bone marrow. Accompanying leukopenia and thrombocytopenia. Red cells are normocytic and normochromic. Chronic renal failure: History of renal disease. Decreased erythropoietin level and erythropoietin responsiveness. Red cells are normocytic and normochromic. Vitamin B12 and folate deficiency: History of poor nutrient intake or gastrointestinal disease. Accompanying neurologic dysfunction. Red cells are megaloblastic (macrocytic). Iron deficiency: History of poor nutrient intake or chronic blood loss. Decreased serum ferritin and iron levels. Red cells are microcytic and hypochromic. Hemolytic: History of ABO or Rh incompatibility or drug exposure. Increased bilirubin level, jaundice, positive direct antiglobulin test. Red cells are normocytic and normochromic. Acute blood loss: History of trauma, surgery, or known bleeding. Accompanying manifestations of volume depletion. Red cells are normal. Anemia may not be apparent until fluid loss is replaced. Chapter 14 1) what should you do before performing a surgery? - screening for coagulation 2) A commonly ingested substance associated with prolongation of the bleeding time ? -aspirin 3)What assesses the extrinsic pathway of coagulation? -PT/INR (prothrombin time / international normalized ration) 4)What assesses the intrinsic pathway of coagulation? - aPPT ( activate partial thromboplastin time ) 5) what does vascular purpura? - looks like a rash, can see membrane and blood on skin 6)what is the treatment for Hemophilia A? - factor VIII replacement 7) what is the treatment for Hemophilia B? -frozen plasma or cryoprecipitate Chapter 15 Beurger’s Disease Definition → inflammatory occlusions of distal arteries veins Risk factor→ young men, around 20-45 yrs old, smoker, genetic or autoimmune S/S-> claudication, tingling and numbness Treatment→ stop smoking, vasodilator drugs, keep warm Raynaud’s Syndrome Definition→ Episodic Vasospasms of the small cutaneous arteries, usually involving the fingers and toes, primarily seen in young women, S/S→ cold, numb, cyanosis, ulcer, may progress to gangrene Treatment→ stop smoking, vasodilator drugs, keep warm Aneurysms (bulging effect of the vessel wall) Definition → the wall of the vessel will start to weaken and keep stretching, will be caused by a pulling of blood Risk factor→ smoking, hypertension, age over 40, women, tumor. S/S→ localized arterial dilations, true or false aneurysms, poor vision, tingling treatment → medically and surgically Varicose veins Definitions → impaired venous return result in increased capillary pressure causing edema, superficial darkened, raised and tortuous veins Treatment → reduce venous pressure Deep Vein Thrombosis (Venus Issue) Definition → thrombosis formation→ a blood clot that is stationary Risk factor→ obesity, prolonged standing, sitting, immobility, smoking and birth control pills 1) A serious complication of Deep Vein Thrombosis is ? - pulmonary embolus Chapter 16 1) cardiac output is the product of both____? - stroke volume and heart rate 2) what is one of the example of direct measurement of blood pressure? -catheter 3) what is one of the example of indirect measurement of blood pressure? -auscultation of korotkoff sounds 4)what does activates a1 receptors in smooth muscle of arterioles does to the blood pressure? -constrict 5) what does activated b1 receptors of the heart does to the blood pressure? -contract 6)what are microcirculation? -arteries to arterioles, capillaries, venules, veins 7)what are fast acting hypertension medications? -alpha and beta blockers 8) what are slow acting hypertension medications? ACE inhibitors, vasodilator, diuretic, aldosterone receptor blocker 9) blood pressure is regulated on a short-term basis through_____? - activation of SNS, interaction of carotid and artic baroreceptors, vasomotor center in brainstem. 10) blood pressure is regulated on a long-term basis through___? -activation of RAAS (Renin, Angiotensin-converting enzyme, Aldosterone blocker System) BLOOD PRESSURE CHART SYS DIA Normal <120 <80 Prehypertension 120-139 80-89 Stage 1 140-159 90-99 Stage 2 > 160 > 100 11) if a patient has 118 sys / 98 dia which stage of hypertension does this patient consider ? -Stage1 12)what organs can be damage from hypertension? -heart, arterioles, brain, eye, kidneys 13) what are the differences between hypertension emergency and hypertension urgency ? -hypertension emergency leads to organ damage and hypertension urgency does not cause organ damage. Chapter 18 1)Atherosclerosis predisposes to a number of processes that are factors in MI, these processes include____? - thrombus formation, coronary vasospasm, endothelial cell dysfunction 2) what does LDL do? - take cholesterol through the body and put it at the surface of the tissue of an organ. So we want LOW LDL 3) what does HDL do? -take cholesterol to liver to break it down. We want HIGH HDL Cholesterol HDL LDL Trig <200 Men >40 Women >50 <130 <165 4) when does ischemia occurs? -when oxygen supply is insufficient to meet metabolic demands 5)what does acute coronary syndrome (ACS) associate with? - plaque morphology and thrombosis 6)how long does cardiac marker stay in blood stream? -48-72 hrs Presentation→ working diagnose → ECG → cardiac biomarkers → final diagnosis 7) what is the differences between stenosis and regurgitation? stenosis→ failure of valve to open, and regurgitation → inability of a valve to close 8)mitral stenosis can lead to - right-sided heart failure which side heart failure? 9)mitral regurgitation can lead -left-sided heart failure to which side heart failure? 10)what can mitral valve prolapse cause? -infective endocarditis, sudden cardiac death, cerebral embolic event and progression to mitral regurgitation. 11) what can aortic stenosis may result in ? - ischemia and left-sided heart failure 12)what are the differences between endocarditis and myocarditis? -endocarditis is caused by a bacterial infection and myocarditis is caused by a virus infection. Chapter 19 1)what kind of disorder for heart failure, cardiac arrest and MI? -heart failure is chronic disorder/ cardiac arrest and MI are acute disorder 2) what are the most common cause for myocardial ischemia? -hypertension and dilated cardiomyopathy( heart muscles) Left sided HF - Backward Effects Dyspnea on exertion Orthopnea Cough Paroxysmal Nocturnal Dyspnea Cyanosis Basilar Crackles - Forward Effects Fatigue Oliguria Increase heart rate Faint pulses Restlessness Confusion Anxiety Right sided HF - Backward Effects Hepatomegaly Ascites Splenomegaly Anorexia Subcutaneous edema Jugular vein distension - Forward Effects Fatigue Oliguria Increase heart rate Faint pulses Restlessness Confusion Anxiety Chapter 20 1)Hypotension associated with neurogenic and anaphylactic shock is due to ? - peripheral pooling of blood 2) Which type of chock is characterized by generalized vasodilation and peripheral pooling of blood? - septic, anaphylactic and neurogenic 3)what does anaerobic metabolism lead to? - lactic acid production 4) what does free radical production lead to? -cell destruction 5)what does macrophage induction will cause? -destruction 6)what is the compensation disorder for cardiac? -SNS Cardiogenic Shock -Myocardial Infection -Cardiomyopathy -Valvular Heart Disease -Ventricular Rupture -Congenital Heart Defects -Papillary Muscle Rupture Obstructive Shock -Pulmonary Embolism -Cardiac Tamponade -Tension Pneumothorax -Dissecting Aortic Aneurism Hypovolemic Shock -Acute hemorrhage -Dehydration from vomiting, diarrhea -overuse of diuretics -Burns -Pancreatitis Distributive Shock -Anaphylaxis -Neurotrauma -Spinal Cord Trauma -Sepsis -Spinal anesthesia 7) what does septic shock caused by ? -common causes by Gram -/+ bacterial and fungal infection. Chapter 22 Hallmark Etiology Asthma (Reversible) -Eosinophils elevated -Hyperplasia of goblet cells -skin testing -airway inflammation -most common chronic disease for children Acute Bronchitis ( Reversible) -loss of ciliated function -inflamed airways -swelling from exudation of fluid -inflammation of trachea caused by viruses→ influenza virus, A or B -Atopy is an immediate hypersensitivity reaction Pathogenesis Clinical Manifestations -infiltration by neutrophils, eosinophils, and lymphocytes -remodeling can hypertrophied smooth muscle, edema, mucous gland hypertrophy and mucus in lumen -hyperplasia of goblet cells -wheezing, feeling of tightness of the chest -dyspnea, dry cough, increased sputum production -skin testing -elevated WBC ( eosinophils) Intrinsic ( non-allergic asthma) - Attacks are often sever - Short of breath - Occurs with patient has no history of allergy parainfluenza, respiratory syncytial virus, coronavirus, rhinovirus, coxsackie virus and adenovirus -Non-virus → streptococcus pneumonia, Haemophilus influenza, mycoplasma, Moraxella, and chlamydia pneumonia -loss of ciliary function and loss of portion of ciliated epithelium -Chest X-ray → shows normal x-ray ( acute bronchitis, shows fluid in lungs ( pneumonia) Extrinsic (allergic Asthma) - Stimulate stem cell - Family history of allergy Chronic Bronchitis (Irreversible) -Type B COPD -pulmonary hypertension ( lead to right side HF or right ventricular hypertrophy -mucus plugs in airway Emphysema ( Irreversible) -Type A COPD -destruction of alveoli -tapping of air in the distal air sacs Etiology -caused from 90% smoking Pathogenesis -resulting scarring -inflammation bronchia walls Clinical Manifestations -shortness of breath -right arterial dysthymias -right ventricular hypertrophy -secondary polycythemia -increase RBC -cigarette smoking 70 packs a yr - emphysema also associated with A1 antitrypsin deficiency in lungs→ no smoking history, age <50, enzyme levels below normal -Alveoli wall destruction -decrease in size of smaller bronchioles -loss radial traction -patient become thin due to increase respiratory effort and decrease ability to consume adequate calories - Blebs (outside lung air pocket) -Bullae ( inside lung air pocket) Hallmark 1)what are two conditions need skin test? -Asthma and hypersensitivity pneumonitis 2)What are the two conditions that loss function of the ciliary? -Acute bronchitis and Occupational lung disease Chapter 23 1) pulmonary function testing for restrictive diseases reveals which of following to be decreased? -vital capacity, total lung capacity, diffusing capacity Hallmark Fibrotic Diffuse Interstitial Lung Disease -fibrosis of the alveoli ( irreversible) -honeycomb lung Sarcoidosis -activation of large amount of macrophages, that leads to alveoli destruction -noncaseating epithelial granulomas Etiology -Thickening of alveolar interstitium -unknown cause Pathogenesis - inflammation → reversible - fibrosis → irreversible Clinical Manifestation -Nonproductive cough -honeycomb lung Hallmark Etiology Hypersensitivity Pneumonitis -Predominantly in nonsmokers -Hypersensitivity (TYPE III) -Pneumonitis (TYPE IV) -restrictive and occupational disease Pathogenesis -Hypersensitivity (TYPE III) -Pneumonitis (TYPE IV) Clinical Manifestation -skin test -respiratory → dyspnea at rest, dry cough, tachypnea and chest discomfort -develop multiple, uniform, noncaseating epithelioid granulomas -Erythema nodosum, macules, papules, hyperpigmentation and subcutaneous nodes. Occupation lung disease - ciliary function paralyzed -toxic gasses or foreign particles -preexisting lung disease -paralyzed ciliary function -macrophages attempt to engulf remove inorganic dust -symptom free for 20-30 yrs -late stage→ no turning back Chapter 25 1)how do the kidneys work to neutralize metabolic acidosis or alkalosis? -if metabolic alkalosis exists, the kidneys slow their acid excretion.
