Midterm Exam: NR507/ NR 507 (Latest 2024/ 2025 Update) Advanced Pathophysiology Review| Questions and Verified Answers| 100% Correct |Grade A – Chamberlain
Midterm Exam: NR507/ NR 507 (Latest
2024/ 2025 Update) Advanced
Pathophysiology Review| Questions and
Verified Answers| 100% Correct |Grade A –
Chamberlain
Q: Autoimmune disease…
Answer:
…. can be familial.
Q: Hypersensitivity: Type 4
Answer:
-Delayed
-T-cell mediated
- Does NOT involve antigen/antibody complexes
Q: Type 2 & 4 Hypersensitivity relationship
Answer:
(Type 2) Organ rejection involves cytotoxicity -> (Type 4) T-cells also involved in organ
rejection -> (Type 2) Antigens from target cells stimulate T-cells to differentiate into cytotoxic Tcells -> (Type 4) T- cells have cytotoxic activity along with helper T-cells involved in delayed
hypersen- sitivity
Q: Hypersensitivity Type 4 RASH
Answer:
-Delayed several days following contact (e.g. poison ivy)
-contact dermatitis consisting of lesions only at the site of contact with the allergen
Q: Treatment of Type 4 Rash
Answer:
Topical corticosteroids
No epi or antihistamines as doesn’t act on mast cells/H1 receptors
Q: primary immunodeficiency
Answer:
Most primary immune deficiencies are the result of a single gene defect
*something lacking in the immune system itself
Q: secondary immunodeficiency
Answer:
Immunodeficiency as a complication of some other physiologic condition or disease
Q: Example of primary immunodeficiency
Answer:
B-lymphocyte Deficiency
Q: Example of secondary immunodeficiency
Answer:
Malnutrition is a cause of this
HIV pt gets pneumocystis carinii
Q: Recycling of RBCs
Answer:
Provides the body with most of its iron stores
Q: Mean Corpuscular Hemoglobin Concentration (MCHC)
Answer:
Measure of the av- erage concentration of hemoglobin inside a single red blood cell (color)
Q: Normochromic anemias
Answer:
MCHC 32-36%
Hemolytic
Aplastic
Post-hemorrhagic
Q: Hypochromic Anemias
Answer:
Pale RBCs
Sideroblastic anemia Iron deficiency anemia Thalassemia
Q: Hyperchromic anemias
Answer:
Liver disease
Sickle cell Hyperthyroidism Hereditary spherocytosis
Q: iron deficiency anemia
Answer:
microcytic, hypochromic
Caused by disorder of hb synthesis
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Hypersensitivity: Type 1 -Allergic reaction-Mediated by IgE-inflammation d/t mast cell degranulation*Most dangerous form is anaphylactic-systemic response-hypotension, sever bronchoconstriction~Main treatment: epi reverses the effects
Hypersensitivity: Type 2 -cytotoxic reaction; tissue specific (e.g. thyroid tissue) -macrophages are primary effectof cells involved -can cause tissue damage or alter function-example: Grave’s disease (hyperthyroidism) is example of altering thyroid function but does not destroy thyroid tissue- incompatible blood type- example of cell/tissue damage that occurs; severe transfusion reaction occurs and the transfused erythrocytes are destroyed by agglutination or complement-mediated lysis.-organ specific
Hypersensitivity: Type 1 Local & Systemic Symptoms -Local: itching, rash-Systemic: wheezing
Hypersensitivity: Type 3
Scope of damage of SLE- type 3 auto immune repítanse Facial rash confine to the cheeks (malar rash)Discoid rash (raised patches, scaling)PhotosensitivityOral or nasopharyngeal ulcersHematological disorders (hemolytic anemia, lymphopenia, or thrombocytopenia). Immunologic disordersNon-erosive arthritis of at least two peripheral jointsSerositis (pleurisy, pericarditis)Renal disorder Neuro disorder (seizure, psychosis)+ANA
Alloimmunity Term used to describe what an individuals immune system reacts against antigens on the tissues of other members of the same species
Examples of alloimmunity -neonatal disease, where the maternal immune system become sensitize against antigens, expressed by the fetus-Transplant rejection-Transfusion reaction
Autoimmunity The alteration in the ability of the body to tolerate its own self antigensCan occur when the immune system overreacts against self antigens to the extent that tissue damage occurs.
Autoantibodies T- and B-cells These autoantibodies react in associated body symptoms to produce signs and symptoms in autoimmune disorders
- ANA Seen and 90% of patients with systemic lupus erythematosus
Autoimmune disease… …. can be familial.
Hypersensitivity: Type 4
Type 2 & 4 Hypersensitivity relationship (Type 2) Organ rejection involves cytotoxicity -> (Type 4) T-cells also involved in organ rejection -> (Type 2) Antigens from target cells stimulate T-cells to differentiate into cytotoxic T-cells -> (Type 4) T- cells have cytotoxic activity along with helper T-cells involved in delayed hypersensitivity
Hypersensitivity Type 4 RASH -Delayed several days following contact (e.g. poison ivy)-contact dermatitis consisting of lesions only at the site of contact with the allergen
Treatment of Type 4 Rash Topical corticosteroidsNo epi or antihistamines as doesn’t act on mast cells/H1 receptors
primary immunodeficiency Most primary immune deficiencies are the result of a single gene defectsomething lacking in the immune system itself secondary immunodeficiency Immunodeficiency as a complication of some other physiologic condition or disease Example of primary immunodeficiency B-lymphocyte Deficiency Example of secondary immunodeficiency Malnutrition is a cause of thisHIV pt gets pneumocystis carinii Recycling of RBCs Provides the body with most of its iron stores Mean Corpuscular Hemoglobin Concentration (MCHC) Measure of the average concentration of hemoglobin inside a single red blood cell (color) Normochromic anemias MCHC 32-36%Hemolytic AplasticPost-hemorrhagic Hypochromic Anemias Pale RBCsSideroblastic anemiaIron deficiency anemiaThalassemia Hyperchromic anemias Liver disease Sickle cell Hyperthyroidism Hereditary spherocytosis iron deficiency anemia microcytic, hypochromicCaused by disorder of hb synthesis Ferritin level needed to show body’s total iron stores low serum ferritin iron deficiency anemia Hb hemoglobinOxygen carrying component of red cells Normal hb for men 13.5-17.5 Normal Hb for women 12-15.5 Hct hematocritVolume of cells as % of total volume of cells and plasma in whole blood Normal hct for men 42-45% Normal Hct for women 37-48% Mean Cell Volume (MCV) Mean Corpusular Hemoglobin (MCH) The average weight of hb per RBCNormal is 27 Red Cell Distribution Width (RDW) Quantitative estimate of the uniformity of individual cell size Normal is 11.5-14.5% Labs for IDA (Ferritin, RDW, serum iron, total iron binding capacity, transferrin) Ferritin- lowRDW- highSerum iron- lowTotal iron binding capacity- highTransferrin- low Labs for Thalassemia Ferritin- highRDW- normal to highSerum iron- normal to highTotal iron binding capacity- normalTransferrin- normal to high RDW is increased in … microcytic and macrocytic anemias Folate deficiency -Can cause megaloblastic anemia-In pregnancy there is increased risk of neural tube defects-ETOH pt high risk d/t malnutrition Vitamin B12 Deficiency Symptoms FatigueDyspneaPeripheral neuropathy in BLE Those at risk for Vitamin B12 deficiency Older adultsH. Pylori infectionS/p gastrectomyGastritis pernicious anemia a vitamin B12-deficiency disease, caused by lack of intrinsic factor and characterized by large, immature red blood cells and damage to the nervous system Who is at risk for Hemolytic anemia -Mismatched blood types – destroys RBCs (cytotoxic type2) -Auto immune hemolytic anemia, due to order antibodies against erythrocytes attack, immune system, and perceives as an antigen, and then attacks it. -Allergic reaction to a drug that causes drug induced hemolytic, anemia -newborn hemolytic disease, Rh incompatibility Acute blood loss anemia # of RBCs lost is greater that # of RBCs produced d/t direct result of blood loss Causes of blood loss anemia GI BleedingSever traumaSurgeryL&d complications Chronic blood loss from GI aplastic anemia diagnostics Blood test and bone marrow biopsy Blood results in aplastic anemia Low reticulocyte (less or equal to 40×109/L)Low granulocytes (less than 500/uL)Platelet count less that 20k causes of aplastic anemia RadiationViral inducedTumorsAbx or other medsCongenital defects (Fanconi’s)The agent destroys the blood cell producing red bone marrow which is replaced with fatty yellow marrow that cannot produce RBCs… leads to pancytopenia… hypoxia… clotting problems….. increased infections Sickle Cell Disease (SCD) a group of inherited, autosomal recessive disordersA single amino acid change in the beta-chain Elongated cells (HbS) that do not readily bind with O2 How long until sickled RBCs rupture? 10-15 days SCD is a type of … … hemolytic anemia and presents with classic anemia signs plus more SCD pts are at risk for Circulatory iron overloadStrokeSplenic damageKidney damage Thalassemia inherited defect in ability to produce hemoglobin, leading to hypochromia There are many _ with thalassemia. genetic mutations
Bicuspid valve Mitral Valve: Between left atrium and ventricle
aortic valve The semilunar valve separating the aorta from the left ventricle that prevents blood from flowing back into the left ventricle.
tricuspid valve valve between the right atrium and the right ventricle
pulmonary semilunar valve heart valve opening from the right ventricle to the pulmonary artery
Normal blood flow through the heart superior/inferior vena cava > r atrium > tricuspid valve > r ventricle > pulmonic valve > pulmonic artery > lungs > l atrium > l ventricle > aorta > body
Pulmonary veins carry _ blood to the LA Oxygenated
Cardiac Output (CO) Amount of blood pumped in 1 minute (ml/min)
Stroke Volume (SV) The volume of blood pumped for each heartbeat (ml/beat)~ 70 ml
Heart Rate (HR) number of heart beats per minute
Cardiac output formula CO = HR x SV
Preload “””Volume””Loading heart with blood prior to ejectionDegree of myocardial fiberlength stretch before contraction”
Afterload “””Pressure””””Unload””The amount of tension the ventricle must develop during systole to open semilunar valves and eject blood”
Contractility ability to shorten when an adequate stimulus is received
increases contractility Sympathetic stimuli: FeverAnxiety Increased thyroxine
decreases contractility Decreased ATP Levels:IschemiaHypoxiaAcidosisCardiomyopathy
Sustained tachycardia will the afterload. decrease
causes of increased afterload HTNPulmonary disease (COPD, pulm. HTN)Aortic damage/stenosis
HTN has most immediate effect on the __. …. afterload
Decrease la afterload d/t decreased volume Hemorrhage
What does increase preload do to SV in healthy heart? Increases SV
Preload decreases with blood volume loss vasodilationcardiac tamponade
Major risk factor in developing heart failure Long standing HTN
Normal EF 55-70%
EDV end diastolic volume Amount of blood in ventricle before systole (~120 ml)
ESV Amount of blood in ventricle after systole (50 ml)
Afterload decreases with HypotensionVasodilation
Three types of heart failure LHFRHFHigh-output failure
left heart failure Inability of LV to provide adequate blood flow into systemic circulation
Causes of LHF Systemic HTNLV MILV HypertrophyAortic or bicuspid valve damageRHF
symptoms of LHF FatigueDecrease urine production Rapid/irreg heartbeat Congestion Difficulty breathingPink tinged sputum OrthopneaParoxysmal nocturnal orthopneaWeight gain
Right heart failure Inability of RV to provide adequate blood flow into pulmonary circulation Cor pulmonale
Stage A of HF (ACC/AHA) Patient has risk factors (CAD) but no symptoms; no structural heart damage
Stage B of HF (ACC/AHA) Patient has structural heart damage(MI), but still has no symptoms
Stage C of HF (ACC/AHA) Patient is symptomatic with alteration in their daily functions due to dyspnea, swelling, etc. This is where the NYHA functional classifications come into play.
Stage D of HF (ACC/AHA) End stage heart failure – have maximize medication’s to treat it, may need a heart transplant or pacemaker
NYHA Functional Classifications Related to the impact on the patients activity caused by the heart failure symptoms
NYHA stage I Mild; no limitation of physical activity; ordinary physical activity does not cause symptoms
NYHA stage II Mild; slight limitation of physical activity; comfortable at rest; oh no physical activity, results and fatigue, competition, dyspnea, or anginal pain
NYHA stage III Moderate; Mark decreasing physical activity; marks, limitation of physical activity; comfortable at rest. Less than ordinary activity, causes fatigue, palpitations, dyspnea, or anginal pain.
NYHA stage IV Severe; in ability to carry on any physical activity without discomfort. Symptoms of heart, failure, or the anginal syndrome may be present even at rest. If any physical activities, undertaken, discomfort is increased.
aortic stenosis A tight aortic valve impeding blood flow from the left ventricle to aorta.Blood backs up in the left ventricle and decreases blood flow to the body
Causes of aortic stenosis Congenital- bicuspid aortic valve Age related calcification (CAD d/t smoking, HTN, HLD, DM)Rheumatic fever
aortic stenosis signs & symptoms
aortic stenosis murmur mid-systolic ejection murmur best heard at the 2nd right intercostal space (RU Sternal border)S4 gallopMid-systolic crescendo – decrescendo murmur, heard loudest at the base and radiating to the neck
aortic regurgitation “””Floppy aortic valve””Blood flows back into LV when aortic valve should be closed”
Aortic regurgitation causes Aneurysmal changes of annulus d/t:- tertiary syphilis-connective tissues disorder (Marfans, Ehlers) EndocarditisRheumatic fever
Aortic regurgitation signs & symptoms FatigueSyncopeSOB that progressively worsensPalpitations Wide pulse pressure (=SBP-DBP)L ventricular dilationCXR pulm edema or cardiomegaly
Aortic regurgitation murmur Early diastolic murmur that is high pitched located loudest at the left lower sternal borderDiastolic rumble sound heard at heart’s apexSystolic crescendo-decrescendo murmur at left upper sternal border
Mitral regurgitation “””Floppy mitral valve””Blood backflows from left ventricle into left atria and into pulmonary circulation”
Causes of mitral regurgitation Anything causing LV dilation:-remodeling post MI-dilated cardiomyopathy Rheumatic fever/heart diseaseEndocarditis Papillary muscle disfunction/ruptureChordae tendinae dysfunction/ruptureCalcification
Mitral regurgitation signs & symptoms Acute: papillary muscle rupture-Pulmonary edema/CHFChronic: dilated ischemic cardiomyopathy-FatigueSOBPulmonary congestion JVDcrackle in basesL atrial enlargement
Mitral regurgitation murmur A blowing, holosystolic (pansystolic) murmur at apexRadiates to back and axilla
FEV1 forced expiratory volume in 1 second
Hypersensitivity Type 1 RASH -Immediate-Atopic dermatitis (widely distributed lesions)
mitral valve prolapse When the valve billows or bulges into the left atria.This in itself doesn’t typically cause a murmur, but if it causes regurgitation it will cause a murmur
Mitral valve prolapse causes IdiopathicD/t connective tissues disorders (Marfans, Ehlers)
Mitral Valve Prolapse signs & symptoms Asymptomatic -OR-MVP Syndrome:Atypical chest painPalpitationsSOBdizzinesssyncope
Mitral valve prolapse murmur midsystolic click
Mitral valve prolapse has increase risk factors for these: Infective endocarditis Certain arrhythmiasProgression to MR
mitral valve stenosis “””Tight mitral valve””Blood cannot pass easily through mitral valve from the left atria to the left ventricle so it backs up in the left atria & in the lungs”
Mitral valve stenosis symptoms S/s of decrease COFatigueExercise intolerance SOBCoughLA enlargement Pulmonary edema JVDBilat cracklesLVH possibleAfib possible
Mitral valve stenosis murmur Diastolic rumbleOpening snap
FEV1/FVC Ratio that is useful in distinguishing between restrictive & obstructive diseases Normal is 70% or less that someone’s normal
Normal FEV1 > 80% predicted
Obstructive pulmonary disorders Decreased airflowSOB with exhaleAir trapping after full expirationCOPD & asthma
Restrictive pulmonary disorders •Occurs due to decrease compliance of lung tissue•Normal amount of elastin Issue with decreased compliance •Pulmonary fibrosis, decrees compliance equals decrease ventilation, due to amount of air flow into lungs •Not enough in = not enough out
TLC for restrictive lung disease < 80% TLC TLC for obstructive lung disease >120 % (hyperinflation)
FEV1/FVC ratio in obstructive disease Less than 70%
FEV1/FVC ratio in restrictive disease Normal or >70%
Asthma Chronic disease characterized by airway, inflammation, bronchial, hyperreactivity, and smooth muscle spasm, intermittent, reversible, airflow, obstruction
asthma results in Excess mucus production and accumulationHypertrophy of bronchial, smooth muscle Airflow obstruction/ bronchoconstrictionDecreased alveolar ventilation
extrinsic asthma •Triggered by allergic reaction (dust, mold, pollen, pet dander)• increase IgE levels is diagnostic• more common in children, males more than females
intrinsic asthma •Triggered by a variety of nonallergic factors (chemicals, airborne irritant, infections[viral], exercise, stress, anxiety, GERD, obesity).•No initial elevation in IgE levels•Typically seen in adults over age 40
Asthma symptoms CoughingWheezing Shortness of breath TachypneaChest tightness
Mucous plugging and pus from inflammatory process in asthma can block alveolar passageways and lead to….. Air trapping and hyperinflation
when are asthma symptoms worse? night and early morning
how to diagnose asthma PFT:FEV1/FVC ration < 70% Methacholine challenge test administer for mildest form of intermittent asthma Short-acting beta2-agonist (SABA) inhalers (albuterol) mild persistent asthma has night symptoms how many days/month 3-4 Sever persistent asthma has night symptoms how many days/month Every night COPD diagnosis History of symptomsPhysical examination PFTs- decreased FEV1, unresponsive to bronchodilatorsABG analysis CXR -hyper inflation, flattened diaphragm GOLD staging of COPD GOLD 1: MILD: FEV1 >/= 80% predictedGOLD 2: MODERATE: FEV1 50-80%GOLD 3: SEVERE: FEV1 30-50%GOLD 4: VERY SEVERE: < 30%
Emphysema
chronic bronchitis •Damage occurs in the airway•Productive cough w/ copious amts of sputum •Dyspnea •Wheezing•Rhonchi•cyanosis of skin and mucous membranes•Polycythemia Vera •cor pulmonale
Mitral valve stenosis causes Rheumatic fever- group A streptococcus- — strep pyogenes (pharyngitis) untreated 2-3 weeksEndocarditis