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 Anaphylasix – Fast! – IgE
Type 1 allergic reaction Inflammation. Mast cell dengranulatio
Type 1 allergic reaction local symptoms Itching. Rash.
Type 1 allergic reaction systemic symptoms Wheezing.
Type 1 allergic anaphylactic symptoms Systemic response hypotension.Severe bronchoconstriction.
Hypersensitivity Type 2 Cytotoxic. Tissue specific like thyroid tissue
Hypersensitivity Type 2- what effector cells is involved Macrophages
example of type II hypersensitivity -Penicillin reaction -Rh incompatibility-Grave’s disease- hyperthyroidism. It alters the thyroid but doesn’t destroy it
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
Hypersensitivity Type 2 versus Type 3 Type 2 is organ specific and binds to the antigen ON the cell surface
Hypersensitivity Type 3 Type 3 is NOT organ specific.Antibody binds to SOLUBE antigen OUTSIDE the cell surface
Hyper Type 2 2 Organ On it
Hyper Type 3 3 No organ Outside it
Hypersensitive type 3 examples Rheumatoid arthritis.Systemic Lupus Erythematous (SLE)
rheymatoid arthritis Antigen/antibodies are deposited in the joints.Autoimmune disorder
Systemic Lypus Erythematosus chronic inflammatory autoimmune disease. Antigen & antibodies deposited in organs. Causes tissue damage.
systemic lupus erythematosus (SLE) symptoms Facial rash on cheeks: malar rash.Discoid rash: raised patches, scaling Oral or nasopharyngeal ulcersSerositis: pleurisy or pericarditis
SLE photosensitivity Development of skin rash due to sunlight
SLE hematologic disorders Hemolytic anemia.Leukopenia.Lymphopenia. Thrombocytopenia.
SLE immunologic manifestations Antibodies against double-stranded DNA- dsDNA or Smith (Sm) antigen.False-positive serologic test for syphilis. Or antiphospholipid antibodies
SLE renal manifestations Persistent protein of >0.5/day or >3g/day on dipstick
SLE neurologic manifestations Seizures or psychosis with no known cause ‘
SLE presence with Antinuclear antibody (ANA)
Autoimmunity can be Familial but not all members have same disease or characteristics. Autoimmune and allergic reactions.
Autoimmunity is associated with Major histocompatibility complex (MHC) alleles or non-MHC genes
alloiummunity Individual’s own immune system reacts against antigen on the tissue of another member of same species
Alloimmunity: think about Same type of tissue just different person
Alloimmunity examples 1. Transfusion reactions2. RH Blood group 3. Transplant rejection4. Mom to fetus
Hypersensitivity Type 4 Delayed Type – T-cell mediated.Does NOT involve antigen/antibody complexes like Types 1, 2 and 3
Hypersensitivity Type 2 and 4 Type 2- antigens target cells which stimulate T-cells to differentiate Cytotoxicity- organ rejectionType 4-T cells reject organ & delayed hypersensitivity
Type 1 vs. Type 4 rashes- key words Type 1: immediate, atopic dermatitis. WidelyType 4: delayed. Contact. Local.
type 1 rash Immediate hypersensitivity. Atopic dermatitis. Widely distributed lesions
Type IV hypersensitivity delayed hypersensitivity. Contact dermatitis. Local or site of contact lesions.
Key determinant of Ty 1 or 4 rash timing Type 1: immediate.Type 4: delayed- several days afterwards
Type 4 rash treatment Non-severe, contact dermatitis= topical corticosteroid
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.
primary immunodeficiency are the result of Single gene defects. B-lymphocyte deficiency more severe kind
Secondary immunodeficiency are the result of Some other physiologic condition or disease. example: HIV patient gets pneumocystis caribouMost common: malnutrition
Hematology involves RBCs.
Most of our body’s iron stores come from the Recycling of iron from old RBCs
iron deficiency anemia Decreased: ferritin, iron, transferrin Increased: RBC distribution width, total iron-binding capacity
Thalassemia is a inherited defect in ability to produce hemoglobin, leading to hypochromia
Thalssemia Increased: ferritinNormal to increased: RBC width, Iron, transferrinNormal: iron binding capacity
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
Sideroblastic anemia Increased: RBC widthNormal to increased: ferritin, iron, transferrin Normal: iron-binding
Mean Corpuscular Hemoglobin Concentration (MCHC) average concentration of hemoglobin in red blood cells
Mean Corpuscular Hemoglobin Concentration (MCHC) normal in Aplastic anemia.Post-hemorrhagic anemia.Hemolytic anemia.
LOW Mean Corpuscular Hemoglobin Concentration (MCHC) Iron deficiency anemia. Sideroblastic anemia.Thalassemia.
High Mean Hemoglobin Concentration (MCHC) Hereditary spherocytosis. Liver diseased.Hyperthyroidism.Sickle cell disease
iron deficiency anemia is a hypochromic, microcyticHIM
iron deficiency anemia is caused Poor hemoglobin synthesis
iron deficiency anemia is measured by what lab value? Ferritin- measures the body’s total iron stores
Low ferritin levels indicate… Reflects anemia, but doesn’t tell you the type
Earliest Lab Marker for Anemia Increased RBC distribution width (RDW). Earliest sign for developing microcytic or macrocytic anemia
Folate deficiency can lead to megaloblastic anemia
Who is at high risk for folate deficiency? Alcoholics
Signs and symptoms B-12 deficiency Fatigue. Dyspnea. Peripheral neuropathy in BLE- numbness and tingling
Risk factors for Vitamin B-12 deficiency Older adults.H-pylori infection. affects Vit. B-12 absorption
hemolytic anemia- the RBCs are Destroyed
hemolytic anemia causes Mismatched blood types- Type 2 Cytotoxic. Allergic reaction to a drug. Autoimmune reactions against own erythrocytes
Autoimmune hemolytic anemia immune system misidentifies red blood cells (RBCs) as foreign. creates autoantibodies that attack them
What is drug-induced hemolytic anemia? Allergic reaction to a drug
What is blood loss anemia? hemorrhagic anemia due to rapid blood loss
Aplstic Anemia is diagnosis by A blood test and bone marrow biopsy
Aplsatic anemia lab values Low circulating erythrocytes, leukocytes and platelets
aplastic anemia granulocyte count will be Less than 500/uL
aplastic anemia platelet count will be Less than 20,000/uL
aplastic anemia absolute reticulocyte count will be Less than or equal to 40 x 109/L
sickle cell anemia is a autosomal recessive disorder. One normal gene and one abnormal gene.
thalassemia anemia causes Decreased circulating hemoglobin
thalassemia anemia is caused by Several possible genetics
Blood flow through the heart:start on right side to lungs Superior & Inferior Vena Cava, Right Atrium, Tricuspid Valve, Right Ventricle, Pulmonary Valve, Pulmonary Artery, Lungs-pick up oxygen
Blood flow from lungs to body Pulmonary Veins,Left Atrium. Mitral Valve or Bicuspid. Left Ventricle,Aortic ValveAorta,Body
Cardiac output is the the amount of blood pumped out of each ventricle in one minute
stroke volume is The amount of blood ejected from the heart in one contraction.
Heart rate is the number of beats per minute
Stroke volume times heart rate= Cardiac output
Preload is defined as: Ventricular end-diastolic volume. How much blood volume is in the bottom of the heart.
Afterload is the amount of resistance to ejection of blood from the ventricle
Sustained tachycardia leads to Decrease stroke volume. Pumps are too fast to get more blood out
ischemia, acidosis, cardiomyopathy all lead to Decreased contractility
What has the most immediate effect on afterload, the resistance to eject blood Hypertension
hemorrhage creates a decrease afterload due to A decreased volume
Increased preload causes increased stroke volume bc the heart can compensate to the extra volume
Hemorrhage or anything that reduces blood volume will Decrease preload
What is the underlying patho of heart failure There is less cardiac output to meet the body’s oxygen demands
Over time there in heart failure is decreased in Contractility and stroke volume
With heart failure there is an increase in Left ventricular end-diastolic volume (lVEDV)
With decrease contractility and stroke, and increase left ventricular end-diastolic in cases the heart Will dilate and have an increase in preload.
What is major risk factor in the development of heart failure Long-standing hypertension
right sided heart failure can occur due to Left-sided heart failure because of fluid back up from the left to right side
Other cause of right-sided heart failure Long-standing pulmonary issues like COPD
Right sided heart failure symptoms Right JVD distinction. Peripheral edema. Hepatosplenomegaly.
Stages of Heart Failure: Stage A patients has high risk for developing heart failure. No symptoms.no structural abnormalities
Stage B heart failure patients who have structural heart disease but demonstrate no symptoms of heart failure
Stage C heart failure Symptoms with alterations to daily life: dyspnea, swelling.
Heart failure stage D End stage heart failure. Maximized medications.May need transplant or pacemaker
Class 1 heart failure is no limitation of ordinary physical activity
Class 2 heart failure is Slight limitation of physical activity. Okay at rest. Physical activity causes symptoms of HF
class 3 heart failure (moderate) Marked by limitation of physical activity. Ok at rest. Not much activity cause HF symptoms.
HF class 4 is severe and the patient is Unable to do physical activity without HF symptoms. Give has symptoms at rest.
Right sided heart failure Jugular vein distentionHepatosplenomegaly. Peripheral edema. Cor Pulmonale.Tricuspid valve damage
Left sided heart failure pulmonary edema.Increased left ventricular after load. Decreased ejection fraction .Increased LV preload Dyspnea.
Cor pulmonale is defined as: Right sided heart failure secondary to chronic lung disease
What causes Cor Pulmonale right side heart failure? Pulmonary disease than causes pulmonary hypertension. Right ventricular MI or hypertrophy. Tricuspid valve damage.
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’t eject normal amount of blood
Mitral stenosis murmur sounds like Rumbling. Decrescendo.Diastolic. Heard at apex of the heart.
aortic stenosis murmur Mid-systolic crescendo-decrescendo. heard loudest at the base and radiating to the neck
Mitral regurgitation murmur Blowing. Holosystolic.Apex to axilla.
What valve is between the right atrium and right ventricle? tricuspid valve
What valve is between the left atrium and left ventricle? mitral valve or bicuspid valve
What valve is between the right ventricle and lungs ? pulmonary semilunar valve
What valve is between the left ventricle and aorta? aortic semilunar valve
Symptoms of aortic stenosis Fainting, chest pressure upon exercising. Angina, S4.gallop present. Heart murmur, apical pulse displacement
What does an aortic stenosis sound like Mid-systolic crescendo-decrescendo murmur heard loudest at the base and radiating to the neck
with aortic regurgitation, shortness of breath gets Progressively worse
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’s apex And A Systolic crescendo-decrescendo murmur heard at the left upper sternal border
An aortic regurgitation causes a backflow of blood into the left ventricle during?
What causes aortic regurgitation? Widening or aneurysmal changes. Ballooning or out-pouching of a vessel.Annulus
What is an annulus? Ring of fibrous tissue surrounding aortic valve
aortic regurgitation conditions Tertiary syphillis. Connective tissue disorders like Marfan syndrome or Ehlers-Danilo’s.Endocarditis.Valve Infection. Rheumatic fever.
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
murmur of aortic regurgitation can be heard Along the left sternal border.
In aortic regurgitation a chest x-ray will show Pulmonary edema and cardiomegaly
An aortic regurgitation chest x-ray will show signs of pulmonary edema and cardiomegaly
What is mitral stenosis? narrowing of the mitral valve. Blocks blood flow
As the mitral valve stenosis progresses; what is compromised? The ability of the valve to open decreases more. Decreased cardiac output- especially with exertion.
Symptoms of mitral valve stenosis SOB on exertion, dry cough, jugular vein distention, crackles,Pounding/racing heart.
mitral valve stenosis heart sounds Low-pitched murmur auscultated at the heart’s apex and radiates to the back and axilla
Another major mitral stenosis symptoms Jugular vein distention and bilateral crackles at the lung based
Mitral valve EKG will show Atrial fibrillation and ventricular hypertrophy
obstructive pulmonary disease indicates increased airway resistance/ obstruction FEV1/FVC ration low, 56%
Restrictive pulmonary disease
Asthma- the airways are Constricted
entrinsic asthma is triggered by An external factor. Environmental: dust, pet dander
Intrinsic asthma triggered by Something internal: anxiety
Mildest form of asthma- intermittent treatment is Beta 2 agonist inhalers.
Mild persistent asthma occurs 3-4 days a month
COPD is diagnosed by History of symptoms. Physical examination.Chest X-ray. Pulmonary function tests. Blood gas analyses.
COPD is what two diseases chronic bronchitis and emphysema
COPD pulmonary function tests shows Airway obstruction- decreased FEV1.That have progressed are unresponsive to bronchodilators.
COPD Staging- Gold: based on degree of limitation Gold 1: mild >= 80%;Gold 2: moderate >=50<80%Gold 3: severe : 30<50% Gold 4: very severe: FEV <30% predicted GOLD 1: Mild COPD FEV1 > 80% predicted
GOLD 2: Moderate COPD 50% < FEV1 < 80% predicted
Gold 3 severe COPD FEV1/FVC 30-50% predicted
GOLD 4: Very Severe COPD FEV1 < 30% predicted
Emphysema damage Occurs in the alveoli
Emphysema Emphysema Alveoli
Emphysema (COPD) expiration issue because they Can get air in but can’t get it out.Air-trapping
signs of emphysema barrel chestpursed lip breathingdyspnea on exertion
X-ray of emphysema Lateral view. Flattened diaphragm. Increased AP diameter
chronic bronchitis damage occurs in the AIRWAY- not the alveoli
What are some causes of mitral valve stenosis? Rheumatic heart disease→group A streptococcus→GAS. Endocarditis→staph aureus.Molecular mimicry- antibody attacks pathogen and heart it looks the same.
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
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
What are the symptoms of mitral valve regurgitation? Echo- blue flash of blood going backwards.. Heart has no time to compensate. Dyspnea. JVD. Crackles.
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
dilated cardiomyopathy dysfunctional heart muscle because of an enlarged heart. Genetic or caused by alcohol or toxins
Endocarditis is caused by Infection on valves