{"id":131937,"date":"2024-01-27T07:23:41","date_gmt":"2024-01-27T07:23:41","guid":{"rendered":"https:\/\/learnexams.com\/blog\/?p=131937"},"modified":"2024-01-27T07:23:43","modified_gmt":"2024-01-27T07:23:43","slug":"midterm-exam-nr507-nr-507-latest-2024-2025-update-advanced-pathophysiology-review-questions-and-verified-answers-100-correct-grade-a-chamberlain-2","status":"publish","type":"post","link":"https:\/\/www.learnexams.com\/blog\/2024\/01\/27\/midterm-exam-nr507-nr-507-latest-2024-2025-update-advanced-pathophysiology-review-questions-and-verified-answers-100-correct-grade-a-chamberlain-2\/","title":{"rendered":"Midterm Exam: NR507\/ NR 507 (Latest 2024\/ 2025 Update) Advanced Pathophysiology Review| Questions and Verified Answers| 100% Correct |Grade A \u2013 Chamberlain"},"content":{"rendered":"\n<p>Midterm Exam: NR507\/ NR 507 (Latest 2024\/ 2025 Update) Advanced Pathophysiology Review| Questions and Verified Answers| 100% Correct |Grade A \u2013 Chamberlain<\/p>\n\n\n\n<p>Midterm Exam: NR507\/ NR 507 (Latest<br>2024\/ 2025 Update) Advanced<br>Pathophysiology Review| Questions and<br>Verified Answers| 100% Correct |Grade A \u2013<br>Chamberlain<br>Q: Autoimmune disease\u2026<br>Answer:<br>\u2026. can be familial.<br>Q: Hypersensitivity: Type 4<br>Answer:<br>-Delayed<br>-T-cell mediated<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Does NOT involve antigen\/antibody complexes<br>Q: Type 2 &amp; 4 Hypersensitivity relationship<br>Answer:<br>(Type 2) Organ rejection involves cytotoxicity -&gt; (Type 4) T-cells also involved in organ<br>rejection -&gt; (Type 2) Antigens from target cells stimulate T-cells to differentiate into cytotoxic Tcells -&gt; (Type 4) T- cells have cytotoxic activity along with helper T-cells involved in delayed<br>hypersen- sitivity<br>Q: Hypersensitivity Type 4 RASH<br>Answer:<br>-Delayed several days following contact (e.g. poison ivy)<br>-contact dermatitis consisting of lesions only at the site of contact with the allergen<\/li>\n<\/ul>\n\n\n\n<p>Q: Treatment of Type 4 Rash<br>Answer:<br>Topical corticosteroids<br>No epi or antihistamines as doesn&#8217;t act on mast cells\/H1 receptors<br>Q: primary immunodeficiency<br>Answer:<br>Most primary immune deficiencies are the result of a single gene defect<br>*something lacking in the immune system itself<br>Q: secondary immunodeficiency<br>Answer:<br>Immunodeficiency as a complication of some other physiologic condition or disease<br>Q: Example of primary immunodeficiency<br>Answer:<br>B-lymphocyte Deficiency<br>Q: Example of secondary immunodeficiency<br>Answer:<br>Malnutrition is a cause of this<br>HIV pt gets pneumocystis carinii<br>Q: Recycling of RBCs<br>Answer:<\/p>\n\n\n\n<p>Provides the body with most of its iron stores<br>Q: Mean Corpuscular Hemoglobin Concentration (MCHC)<br>Answer:<br>Measure of the av- erage concentration of hemoglobin inside a single red blood cell (color)<br>Q: Normochromic anemias<br>Answer:<br>MCHC 32-36%<br>Hemolytic<br>Aplastic<br>Post-hemorrhagic<br>Q: Hypochromic Anemias<br>Answer:<br>Pale RBCs<br>Sideroblastic anemia Iron deficiency anemia Thalassemia<br>Q: Hyperchromic anemias<br>Answer:<br>Liver disease<br>Sickle cell Hyperthyroidism Hereditary spherocytosis<br>Q: iron deficiency anemia<br>Answer:<br>microcytic, hypochromic<br>Caused by disorder of hb synthesis<br>Powered by <a href=\"https:\/\/learnexams.com\/search\/study?query=\" target=\"_blank\" rel=\"noopener\">https:\/\/learnexams.com\/search\/study?query=<\/a><br>Hypersensitivity Type 1 Anaphylasix &#8211; Fast! &#8211; IgE<br>Type 1 allergic reaction Inflammation. Mast cell dengranulatio<br>Type 1 allergic reaction local symptoms Itching. Rash.<br>Type 1 allergic reaction systemic symptoms Wheezing.<br>Type 1 allergic anaphylactic symptoms Systemic response hypotension.Severe bronchoconstriction.<br>Hypersensitivity Type 2 Cytotoxic. Tissue specific like thyroid tissue<br>Hypersensitivity Type 2- what effector cells is involved Macrophages<br>example of type II hypersensitivity -Penicillin reaction -Rh incompatibility-Grave&#8217;s disease- hyperthyroidism. It alters the thyroid but doesn&#8217;t destroy it<br>type II hypersensitivity incompatible blood type Cell tissue damage that occurs; severe transfusion reaction where the transfused erythrocytes are destroyed by agglutination or complement-mediated lysis<br>Hypersensitivity Type 2 versus Type 3 Type 2 is organ specific and binds to the antigen ON the cell surface<br>Hypersensitivity Type 3 Type 3 is NOT organ specific.Antibody binds to SOLUBE antigen OUTSIDE the cell surface<br>Hyper Type 2 2 Organ On it<br>Hyper Type 3 3 No organ Outside it<br>Hypersensitive type 3 examples Rheumatoid arthritis.Systemic Lupus Erythematous (SLE)<br>rheymatoid arthritis Antigen\/antibodies are deposited in the joints.Autoimmune disorder<br>Systemic Lypus Erythematosus chronic inflammatory autoimmune disease. Antigen &amp; antibodies deposited in organs. Causes tissue damage.<br>systemic lupus erythematosus (SLE) symptoms Facial rash on cheeks: malar rash.Discoid rash: raised patches, scaling Oral or nasopharyngeal ulcersSerositis: pleurisy or pericarditis<br>SLE photosensitivity Development of skin rash due to sunlight<br>SLE hematologic disorders Hemolytic anemia.Leukopenia.Lymphopenia. Thrombocytopenia.<br>SLE immunologic manifestations Antibodies against double-stranded DNA- dsDNA or Smith (Sm) antigen.False-positive serologic test for syphilis. Or antiphospholipid antibodies<br>SLE renal manifestations Persistent protein of >0.5\/day or >3g\/day on dipstick<br>SLE neurologic manifestations Seizures or psychosis with no known cause &#8216;<br>SLE presence with Antinuclear antibody (ANA)<br>Autoimmunity can be Familial but not all members have same disease or characteristics. Autoimmune and allergic reactions.<br>Autoimmunity is associated with Major histocompatibility complex (MHC) alleles or non-MHC genes<br>alloiummunity Individual&#8217;s own immune system reacts against antigen on the tissue of another member of same species<br>Alloimmunity: think about Same type of tissue just different person<br>Alloimmunity examples 1. Transfusion reactions2. RH Blood group 3. Transplant rejection4. Mom to fetus<br>Hypersensitivity Type 4 Delayed Type &#8211; T-cell mediated.Does NOT involve antigen\/antibody complexes like Types 1, 2 and 3<br>Hypersensitivity Type 2 and 4 Type 2- antigens target cells which stimulate T-cells to differentiate Cytotoxicity- organ rejectionType 4-T cells reject organ &amp; delayed hypersensitivity<br>Type 1 vs. Type 4 rashes- key words Type 1: immediate, atopic dermatitis. WidelyType 4: delayed. Contact. Local.<br>type 1 rash Immediate hypersensitivity. Atopic dermatitis. Widely distributed lesions<br>Type IV hypersensitivity delayed hypersensitivity. Contact dermatitis. Local or site of contact lesions.<br>Key determinant of Ty 1 or 4 rash timing Type 1: immediate.Type 4: delayed- several days afterwards<br>Type 4 rash treatment Non-severe, contact dermatitis= topical corticosteroid<br>Why would you NOT use epinephrine, antibiotics or antihistamine ? Epinephrine is or Type 1: anaphylactic reactions.Antihistamine acts of H1 receptors. Type 4 does NOT involve mast cells or H1 receptors.Antibiotics no right bc this is not an infections.<br>primary immunodeficiency are the result of Single gene defects. B-lymphocyte deficiency more severe kind<br>Secondary immunodeficiency are the result of Some other physiologic condition or disease. example: HIV patient gets pneumocystis caribouMost common: malnutrition<br>Hematology involves RBCs.<br>Most of our body&#8217;s iron stores come from the Recycling of iron from old RBCs<br>iron deficiency anemia Decreased: ferritin, iron, transferrin Increased: RBC distribution width, total iron-binding capacity<br>Thalassemia is a inherited defect in ability to produce hemoglobin, leading to hypochromia<br>Thalssemia Increased: ferritinNormal to increased: RBC width, Iron, transferrinNormal: iron binding capacity<br>Anemia of chronic disease Normal to increased: ferritin Normal: RBC width Normal to slightly decreased: transferrin Normal to decreased: iron Slightly decreased: Iron-binding capacity<br>Sideroblastic anemia Increased: RBC widthNormal to increased: ferritin, iron, transferrin Normal: iron-binding<br>Mean Corpuscular Hemoglobin Concentration (MCHC) average concentration of hemoglobin in red blood cells<br>Mean Corpuscular Hemoglobin Concentration (MCHC) normal in Aplastic anemia.Post-hemorrhagic anemia.Hemolytic anemia.<br>LOW Mean Corpuscular Hemoglobin Concentration (MCHC) Iron deficiency anemia. Sideroblastic anemia.Thalassemia.<br>High Mean Hemoglobin Concentration (MCHC) Hereditary spherocytosis. Liver diseased.Hyperthyroidism.Sickle cell disease<br>iron deficiency anemia is a hypochromic, microcyticHIM<br>iron deficiency anemia is caused Poor hemoglobin synthesis<br>iron deficiency anemia is measured by what lab value? Ferritin- measures the body&#8217;s total iron stores<br>Low ferritin levels indicate\u2026 Reflects anemia, but doesn&#8217;t tell you the type<br>Earliest Lab Marker for Anemia Increased RBC distribution width (RDW). Earliest sign for developing microcytic or macrocytic anemia<br>Folate deficiency can lead to megaloblastic anemia<br>Who is at high risk for folate deficiency? Alcoholics<br>Signs and symptoms B-12 deficiency Fatigue. Dyspnea. Peripheral neuropathy in BLE- numbness and tingling<br>Risk factors for Vitamin B-12 deficiency Older adults.H-pylori infection. affects Vit. B-12 absorption<br>hemolytic anemia- the RBCs are Destroyed<br>hemolytic anemia causes Mismatched blood types- Type 2 Cytotoxic. Allergic reaction to a drug. Autoimmune reactions against own erythrocytes<br>Autoimmune hemolytic anemia immune system misidentifies red blood cells (RBCs) as foreign. creates autoantibodies that attack them<br>What is drug-induced hemolytic anemia? Allergic reaction to a drug<br>What is blood loss anemia? hemorrhagic anemia due to rapid blood loss<br>Aplstic Anemia is diagnosis by A blood test and bone marrow biopsy<br>Aplsatic anemia lab values Low circulating erythrocytes, leukocytes and platelets<br>aplastic anemia granulocyte count will be Less than 500\/uL<br>aplastic anemia platelet count will be Less than 20,000\/uL<br>aplastic anemia absolute reticulocyte count will be Less than or equal to 40 x 109\/L<br>sickle cell anemia is a autosomal recessive disorder. One normal gene and one abnormal gene.<br>thalassemia anemia causes Decreased circulating hemoglobin<br>thalassemia anemia is caused by Several possible genetics<br>Blood flow through the heart:start on right side to lungs Superior &amp; Inferior Vena Cava, Right Atrium, Tricuspid Valve, Right Ventricle, Pulmonary Valve, Pulmonary Artery, Lungs-pick up oxygen<br>Blood flow from lungs to body Pulmonary Veins,Left Atrium. Mitral Valve or Bicuspid. Left Ventricle,Aortic ValveAorta,Body<br>Cardiac output is the the amount of blood pumped out of each ventricle in one minute<br>stroke volume is The amount of blood ejected from the heart in one contraction.<br>Heart rate is the number of beats per minute<br>Stroke volume times heart rate= Cardiac output<br>Preload is defined as: Ventricular end-diastolic volume. How much blood volume is in the bottom of the heart.<br>Afterload is the amount of resistance to ejection of blood from the ventricle<br>Sustained tachycardia leads to Decrease stroke volume. Pumps are too fast to get more blood out<br>ischemia, acidosis, cardiomyopathy all lead to Decreased contractility<br>What has the most immediate effect on afterload, the resistance to eject blood Hypertension<br>hemorrhage creates a decrease afterload due to A decreased volume<br>Increased preload causes increased stroke volume bc the heart can compensate to the extra volume<br>Hemorrhage or anything that reduces blood volume will Decrease preload<br>What is the underlying patho of heart failure There is less cardiac output to meet the body&#8217;s oxygen demands<br>Over time there in heart failure is decreased in Contractility and stroke volume<br>With heart failure there is an increase in Left ventricular end-diastolic volume (lVEDV)<br>With decrease contractility and stroke, and increase left ventricular end-diastolic in cases the heart Will dilate and have an increase in preload.<br>What is major risk factor in the development of heart failure Long-standing hypertension<br>right sided heart failure can occur due to Left-sided heart failure because of fluid back up from the left to right side<br>Other cause of right-sided heart failure Long-standing pulmonary issues like COPD<br>Right sided heart failure symptoms Right JVD distinction. Peripheral edema. Hepatosplenomegaly.<br>Stages of Heart Failure: Stage A patients has high risk for developing heart failure. No symptoms.no structural abnormalities<br>Stage B heart failure patients who have structural heart disease but demonstrate no symptoms of heart failure<br>Stage C heart failure Symptoms with alterations to daily life: dyspnea, swelling.<br>Heart failure stage D End stage heart failure. Maximized medications.May need transplant or pacemaker<br>Class 1 heart failure is no limitation of ordinary physical activity<br>Class 2 heart failure is Slight limitation of physical activity. Okay at rest. Physical activity causes symptoms of HF<br>class 3 heart failure (moderate) Marked by limitation of physical activity. Ok at rest. Not much activity cause HF symptoms.<br>HF class 4 is severe and the patient is Unable to do physical activity without HF symptoms. Give has symptoms at rest.<br>Right sided heart failure Jugular vein distentionHepatosplenomegaly. Peripheral edema. Cor Pulmonale.Tricuspid valve damage<br>Left sided heart failure pulmonary edema.Increased left ventricular after load. Decreased ejection fraction .Increased LV preload Dyspnea.<br>Cor pulmonale is defined as: Right sided heart failure secondary to chronic lung disease<br>What causes Cor Pulmonale right side heart failure? Pulmonary disease than causes pulmonary hypertension. Right ventricular MI or hypertrophy. Tricuspid valve damage.<br>HIgh pulmonary vascular pressure or increased after load will cause Right ventricular contraction force in order to eject the blood=reduces the ejection fraction=right ventricle can&#8217;t eject normal amount of blood<br>Mitral stenosis murmur sounds like Rumbling. Decrescendo.Diastolic. Heard at apex of the heart.<br>aortic stenosis murmur Mid-systolic crescendo-decrescendo. heard loudest at the base and radiating to the neck<br>Mitral regurgitation murmur Blowing. Holosystolic.Apex to axilla.<br>What valve is between the right atrium and right ventricle? tricuspid valve<br>What valve is between the left atrium and left ventricle? mitral valve or bicuspid valve<br>What valve is between the right ventricle and lungs ? pulmonary semilunar valve<br>What valve is between the left ventricle and aorta? aortic semilunar valve<br>Symptoms of aortic stenosis Fainting, chest pressure upon exercising. Angina, S4.gallop present. Heart murmur, apical pulse displacement<br>What does an aortic stenosis sound like Mid-systolic crescendo-decrescendo murmur heard loudest at the base and radiating to the neck<br>with aortic regurgitation, shortness of breath gets Progressively worse<br>An aortic regurgitation murmur is best heard as High pitched early diastolic murmur heard loudest at the left lower eternal border . Diastolic rumbling sound at the heart&#8217;s apex And A Systolic crescendo-decrescendo murmur heard at the left upper sternal border<br>An aortic regurgitation causes a backflow of blood into the left ventricle during?<br>What causes aortic regurgitation? Widening or aneurysmal changes. Ballooning or out-pouching of a vessel.Annulus<br>What is an annulus? Ring of fibrous tissue surrounding aortic valve<br>aortic regurgitation conditions Tertiary syphillis. Connective tissue disorders like Marfan syndrome or Ehlers-Danilo&#8217;s.Endocarditis.Valve Infection. Rheumatic fever.<br>aortic regurgitation signs and symptoms Dyspnea.orthopnea.Fatigue. Palpitations. Angina (reduced diastolic coronary flow due to elevated LV end-diastolic pressure)Left ventricular dilatation and failureWide pulse pressureBounding pulses<br>murmur of aortic regurgitation can be heard Along the left sternal border.<br>In aortic regurgitation a chest x-ray will show Pulmonary edema and cardiomegaly<br>An aortic regurgitation chest x-ray will show signs of pulmonary edema and cardiomegaly<br>What is mitral stenosis? narrowing of the mitral valve. Blocks blood flow<br>As the mitral valve stenosis progresses; what is compromised? The ability of the valve to open decreases more. Decreased cardiac output- especially with exertion.<br>Symptoms of mitral valve stenosis SOB on exertion, dry cough, jugular vein distention, crackles,Pounding\/racing heart.<br>mitral valve stenosis heart sounds Low-pitched murmur auscultated at the heart&#8217;s apex and radiates to the back and axilla<br>Another major mitral stenosis symptoms Jugular vein distention and bilateral crackles at the lung based<br>Mitral valve EKG will show Atrial fibrillation and ventricular hypertrophy<br>obstructive pulmonary disease indicates increased airway resistance\/ obstruction FEV1\/FVC ration low, 56%<br>Restrictive pulmonary disease<br>Asthma- the airways are Constricted<br>entrinsic asthma is triggered by An external factor. Environmental: dust, pet dander<br>Intrinsic asthma triggered by Something internal: anxiety<br>Mildest form of asthma- intermittent treatment is Beta 2 agonist inhalers.<br>Mild persistent asthma occurs 3-4 days a month<br>COPD is diagnosed by History of symptoms. Physical examination.Chest X-ray. Pulmonary function tests. Blood gas analyses.<br>COPD is what two diseases chronic bronchitis and emphysema<br>COPD pulmonary function tests shows Airway obstruction- decreased FEV1.That have progressed are unresponsive to bronchodilators.<br>COPD Staging- Gold: based on degree of limitation Gold 1: mild >= 80%;Gold 2: moderate >=50&lt;80%Gold 3: severe : 30&lt;50% Gold 4: very severe: FEV &lt;30% predicted GOLD 1: Mild COPD FEV1 > 80% predicted<br>GOLD 2: Moderate COPD 50% &lt; FEV1 &lt; 80% predicted<br>Gold 3 severe COPD FEV1\/FVC 30-50% predicted<br>GOLD 4: Very Severe COPD FEV1 &lt; 30% predicted<br>Emphysema damage Occurs in the alveoli<br>Emphysema Emphysema Alveoli<br>Emphysema (COPD) expiration issue because they Can get air in but can&#8217;t get it out.Air-trapping<br>signs of emphysema barrel chestpursed lip breathingdyspnea on exertion<br>X-ray of emphysema Lateral view. Flattened diaphragm. Increased AP diameter<br>chronic bronchitis damage occurs in the AIRWAY- not the alveoli<br>What are some causes of mitral valve stenosis? Rheumatic heart disease\u2192group A streptococcus\u2192GAS. Endocarditis\u2192staph aureus.Molecular mimicry- antibody attacks pathogen and heart it looks the same.<br>What are some signs and symptoms of mitral valve stenosis? Fever.chills.elevated WBC.Exercise intolerance.Coughing due to increased fluid in lung. Left atrial enlargement.Pulmonary congestion or edema.Diastolic rumble<br>What is mitral valve regurgitation? mitral valve does not close completely.blood backs up into L atrium. Blood does not go into the aortasame result as mitral stenosis-atrium stretches<br>What are the symptoms of mitral valve regurgitation? Echo- blue flash of blood going backwards.. Heart has no time to compensate. Dyspnea. JVD. Crackles.<br>What causes mitral regurgitation? rheumatic heart disease is main cause.Mitral valve damage. Remodeling process after heart attachment. Dilated cardiomyopathy. Endocarditis. Papillary muscle dysfunction.Chordate tendineae rupture<br>dilated cardiomyopathy dysfunctional heart muscle because of an enlarged heart. Genetic or caused by alcohol or toxins<br>Endocarditis is caused by Infection on valves<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Midterm Exam: NR507\/ NR 507 (Latest 2024\/ 2025 Update) Advanced Pathophysiology Review| Questions and Verified Answers| 100% Correct |Grade A \u2013 Chamberlain Midterm Exam: NR507\/ NR 507 (Latest2024\/ 2025 Update) AdvancedPathophysiology Review| Questions andVerified Answers| 100% Correct |Grade A \u2013ChamberlainQ: Autoimmune disease\u2026Answer:\u2026. can be familial.Q: Hypersensitivity: Type 4Answer:-Delayed-T-cell mediated Q: Treatment of Type 4 RashAnswer:Topical [&hellip;]<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"site-sidebar-layout":"default","site-content-layout":"","ast-site-content-layout":"default","site-content-style":"default","site-sidebar-style":"default","ast-global-header-display":"","ast-banner-title-visibility":"","ast-main-header-display":"","ast-hfb-above-header-display":"","ast-hfb-below-header-display":"","ast-hfb-mobile-header-display":"","site-post-title":"","ast-breadcrumbs-content":"","ast-featured-img":"","footer-sml-layout":"","ast-disable-related-posts":"","theme-transparent-header-meta":"","adv-header-id-meta":"","stick-header-meta":"","header-above-stick-meta":"","header-main-stick-meta":"","header-below-stick-meta":"","astra-migrate-meta-layouts":"default","ast-page-background-enabled":"default","ast-page-background-meta":{"desktop":{"background-color":"","background-image":"","background-repeat":"repeat","background-position":"center center","background-size":"auto","background-attachment":"scroll","background-type":"","background-media":"","overlay-type":"","overlay-color":"","overlay-opacity":"","overlay-gradient":""},"tablet":{"background-color":"","background-image":"","background-repeat":"repeat","background-position":"center center","background-size":"auto","background-attachment":"scroll","background-type":"","background-media":"","overlay-type":"","overlay-color":"","overlay-opacity":"","overlay-gradient":""},"mobile":{"background-color":"","background-image":"","background-repeat":"repeat","background-position":"center center","background-size":"auto","background-attachment":"scroll","background-type":"","background-media":"","overlay-type":"","overlay-color":"","overlay-opacity":"","overlay-gradient":""}},"ast-content-background-meta":{"desktop":{"background-color":"var(--ast-global-color-5)","background-image":"","background-repeat":"repeat","background-position":"center center","background-size":"auto","background-attachment":"scroll","background-type":"","background-media":"","overlay-type":"","overlay-color":"","overlay-opacity":"","overlay-gradient":""},"tablet":{"background-color":"var(--ast-global-color-5)","background-image":"","background-repeat":"repeat","background-position":"center center","background-size":"auto","background-attachment":"scroll","background-type":"","background-media":"","overlay-type":"","overlay-color":"","overlay-opacity":"","overlay-gradient":""},"mobile":{"background-color":"var(--ast-global-color-5)","background-image":"","background-repeat":"repeat","background-position":"center center","background-size":"auto","background-attachment":"scroll","background-type":"","background-media":"","overlay-type":"","overlay-color":"","overlay-opacity":"","overlay-gradient":""}},"footnotes":""},"categories":[25],"tags":[],"class_list":["post-131937","post","type-post","status-publish","format-standard","hentry","category-exams-certification"],"_links":{"self":[{"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/posts\/131937","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/comments?post=131937"}],"version-history":[{"count":0,"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/posts\/131937\/revisions"}],"wp:attachment":[{"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/media?parent=131937"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/categories?post=131937"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.learnexams.com\/blog\/wp-json\/wp\/v2\/tags?post=131937"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}