NR507 Advanced Pathophysiology MidTerm With 100% correct answers + rationales 2026

Hypersensitivity: Type 1

Type 1: Allergic reaction, Mediated by IgE, Inflammation due to mast cell degranulation

Local symptoms:

-itching

-rash

Systemic symptoms:

-wheezing

Most dangerous = anaphylactic reaction

systemic response of hypotension, severe bronchoconstriction

Main treatment: epinephrine reverses the effects

Hypersensitivity: Type 2

Type 2: Cytotoxic reaction; tissue specific (ex: thyroid tissue)

Macrophages are the primary effectors cells involved

Can cause tissue damage or alter function

Grave's disease (hyperthyroidism) - 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.

Type 1 Hypersensitivity VS. Type 2 Hypersensitivity

Type 1 Hypersensitivity

Organ Specific

Antibody binds to the antigen on the cell surface

Type 2 Hypersensitivity

Not Organ Specific

Antibody binds to the soluble antigen outside the cell surface that was released into the blood or body fluids, and the complex is then deposited in the tissues

Hypersensitivity: Type 3 - Examples

Rheumatoid arthritis: Antigen/antibodies are deposited in the joints

Systemic Lupus Erythematosus (SLE)- very closely related to autoimmunity- antigen/antibodies deposit in organs that cause tissue damage

Hypersensitivity: Type 4

Delayed response

Does not involve antigen/antibody complexes like Types 1, 2 and 3

Is T-cell mediated

Differentiating Between the Rash of a Type 1 vs. Type 4 Reaction:

Type 1: Immediate hypersensitivity reactions, termed atopic dermatitis, are usually characterized by widely distributed lesions

Type 4: Contact dermatitis (delayed hypersensitivity) consists of lesions only at the site of contact with the allergen

The key determinant is the timing of the rash:

-Type 1 = Immediate

-Type 4 = Delayed: Several days following contact, ex would be poison ivy

Treatment of Type 4 Rash

A non-severe case of contact dermatitis would be treated with topical corticosteroid.

Why not epinephrine or antihistamines?

-Epinephrine is for emergent Type 1 anaphylactic reactions. Antihistamines act on the H1 receptors. Type 4 does not involve mast cells and H1 receptors.

Antibiotics not appropriate since not an infection

Autoimmunity

Autoimmune disease can be familial, Affected family members may not all develop the same disease, but several members may have different disorders characterized by a variety of hypersensitivity reactions, These include autoimmune and allergic reactions

Associations with particular autoimmune diseases have been identified for a variety of major histocompatibility complex (MHC) alleles or non-MHC genes

Alloimmunity

General term used to describe when an individual's immune system reacts against antigens on the tissues of other members of the same species.

Examples: Neonatal disease where the maternal immune system becomes sensitized against antigens expressed by the fetus, Transplant rejection, Transfusion reaction

Primary Immunodeficiency

Most primary immune deficiencies are result of single gene defects

Something is lacking with the immune system itself.

Example: B-lymphocyte deficiency - one of the most severe forms of a primary immunodeficiency

Secondary Immunodeficiency

Complication of some other physiological condition/disease, Malnutrition one of most common causes worldwide. Example: Pt. with HIV gets pneumocystis carinii

Hematology

Anemias, Involve RBCs, Most of body's iron stores come from the recycling of iron from old RBCs

Iron Deficiency Anemia

Microcytic/Hypochromic Anemia, Caused by disorders of hemoglobin synthesis, particularly iron deficiency, Ferritin is an important measurement that reflects the body's total iron stores, The NP will order a ferritin level to get an idea of the body's total iron stores, Low ferritin reflects anemia

Major Lab Marker for Anemia

Increased RBC distribution width (RDW) is one of the earliest lab markers in developing microcytic or macrocytic anemia

Folate Deficiency

Can cause megaloblastic anemia, Alcoholics can easily get folate deficiency

Ferritin level normal

Hgb low

Hct low

Vitamin B-12 Deficiency

Fatigue, Dyspnea, Peripheral Neuropathy in BLE (numbness and tingling)

Risk Factors: Older adults, H-pylori infection

Affects Vitamin B-12 absorption

Hemolytic Anemia

Who is at risk?

RBCs destroyed, Mismatched blood types destroy RBCs.

Autoimmune hemolytic anemia due to autoantibodies against erythrocytes that the immune system perceives as an antigen and then attacks it. Allergic reaction to a drug causes drug-induced hemolytic anemia

Acute Blood Loss Anemia

Trauma victims who are losing blood, GI bleed (Acute)

Aplastic Anemia

Diagnosis made by blood tests and bone marrow biopsy.

AA is suspected if levels of circulating erythrocytes, leukocytes and platelets diminished:

-Granulocyte count less than 500/ uL

-Platelet count less than 20,000/ uL

-Absolute reticulocyte count less than or equal to 40 x 109/ L

Sickle Cell Anemia

Patients encountered who have sickle cell trait, Inherited a normal Hb gene from one parent and an abnormal Hb gene from the other parent

Thalassemia

Inherited blood disorder causing decreased circulating hemoglobin, Many possible genetic mutations

Heart Failure

Pathophysiology (Wk 2 Discussion)

Underlying patho is that there is less cardiac output to meet the body's oxygen demands.

Over time there is decreased contractility, decreased stroke volume, increased left ventricular end-diastolic volume (LVEDV)

When contractility is decreased, stroke volume falls, and LVEDV increases. This causes dilation of the heart and an increase in preload.

Major risk factor is long standing hypertension. Preload = stretch Afterload = resistance

Differentiate between Right and Left Heart Failure

Sometimes right-sided heart failure can occur due to left-sided heart failure due to the back up of fluid from the left side to the right.

Sometimes right-sided heart failure can occur without there being left-sided heart failure; this usually occurs because the person has long standing pulmonary issues (COPD).

Patients will have classic R. sided heart failure symptoms without L. sided heart failure symptoms: Right JVD distention, Peripheral edema, Hepatosplenomegaly

Stages of Heart Failure (ACC/AHA)

-Stage A: patient has risk factors (CAD) but no symptoms; no structural heart damage

-Stage B: patient has structural heart damage (MI), but still has no symptoms

-Stage C: 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: end-stage heart-failure - have maximized medications to treat it. May need heart transplant or pacemaker

NYHA Functional Classifications- It's all about the impact on the patient's activity caused by the HF symptoms:

-Stage I: Mild- no limitation of physical activity; Ordinary physical activity does not cause symptoms -Stage II: Mild- slight limitation of physical activity; comfortable at rest; Ordinary physical activity results in fatigue, palpitation, dyspnea or anginal pain.

-Stage III: Moderate- marked decrease in physical activity; marked limitation of physical activity; comfortable at rest. Less than ordinary activity causes fatigue, palpitation, dyspnea or anginal pain. -Stage IV: Severe- inability to carry on any physical activity without discomfort. Symptoms of HF or the anginal syndrome may be present even at rest. If any physical activity undertaken, discomfort is increased.

Heart Valve Disorders

Signs and Symptoms (Edapt Scenarios), Murmur Characteristics, Important to know Anatomy

Aortic Stenosis

Blood backed up into left ventricle causing perfusion problems for the rest of the body

Causes:

Bicuspid aortic valve- congenital condition (only two cusps to the aortic valve which usually has three cusps)- the two cusps get damaged quicker because they are doing the work of three

Age related calcification- obstruction/ stenosis

Smoking, High BP, Hypertension, Hyperlipid, Diabetes

Rheumatic Fever

Signs & Symptoms = SAD

S: Syncope

A: Angina

D: Dyspnea

**Fainting

Chest pressure upon exercising

Sustained, laterally displaced apical pulse

Mid-systolic crescendo-decrescendo murmur heard loudest at base and radiating to the neck

S4 gallop present**

Aortic Regurgitation

Blood is coming back from the Aorta into the L. Ventricle through the Aortic Valve

Causes

Widening or aneurysmal change of the aortic annulus (ring of fibrous tissue surrounding the aorta)

Endocarditis

Rheumatic Fever

Signs & Symptoms

Fatigue

Syncope

SOB

Palpitations

Widened Pulse Pressure

L. Ventricular Dilation

Early diastolic murmur along left sternal border

**Shortness of breath that progressively worsens

High pitched early diastolic murmur heard loudest at left lower sternal border

Diastolic rumbling sound at the heart's apex

Systolic crescendo-decrescendo murmur heard at the left upper sternal border

A chest x-ray may show signs of pulmonary edema and cardiomegaly**

Mitral Stenosis

Blood is going to back up into the L. Atrium and Lungs

Causes

Rheumatic Fever / Rheumatic Heart Disease

Endocarditis

Signs & Symptoms

Fatigue

SOB

Exercise intolerance

Cough

L. Atrial enlargement

Pulmonary congestion/edema

Diastolic rumble

Opening snap before Diastolic rumble

**As mitral stenosis progresses, symptoms of decreased CO occur, especially during exertion Shortness of breath on activity

Pounding/racing heart

Associated w/ history of Rheumatic HD

A low-pitched murmur auscultated at the heart's apex

JVD and bilateral crackles in lung bases noted

ECG demonstrates A-FIB and Left Ventricular Hypertrophy**

Mitral Regurgitation

Blood goes from L. Ventricle to L. Atrium and then to the Lungs

Causes - Anything that causes LV dilation

Remodeling process (post MI)

Dilated cardiomyopthathy

Rheumatic Fever/ Rheumatic Heart Disease

Endocarditis

Papillary muscle dysfunction/rupture/ chordae tendinae

Calcification of the valve/around the valve

Signs & Symptoms

Acute

Chronic

**Shortness of breath

JVD, Crackles in bilateral lung bases

Blowing pansystolic murmur heard best at heart's apex and radiates to back and axilla**

Obstructive vs. Restrictive Pulmonary Disease

Obstructive: decreased FEV1 indicates airway obstruction along with low FEV1/FEV ratio 56%

Restrictive: FEV1/FVC ratio above 70%, Review EDapt examples

Asthma

Airways constricted

Intrinsic: triggered by something internal such as anxiety

Extrinsic: triggered by something in outside environment- something in the air (dust mites/pet dander)

In mildest form of asthma (intermittent), short acting beta2-agonist inhalers are prescribed

Mild-persistent asthma will have night symptoms 3-4 days a month

COPD

Diagnosis based on Hx of symptoms, physical exam, chest imaging, pulmonary function tests and blood gas analysis

Pulmonary function testing reveals airway obstruction (decreased FEV1) that is progressive and unresponsive to bronchodilators, Emphysema, Chronic bronchitis

COPD Staging According to GOLD Guidelines- Based on degree of airway limitation

Gold 1: Mild: FEV1≥80% predicted

Gold 2: Moderate: 50% ≤FEV1 <80% predicted

Gold 3: Severe: 30% ≤FEV1 <50% predicted

Gold 4: Very Severe: FEV < 30% predicted

Emphysema

Damage occurs in the alveoli, Impairs gas exchange, Issue is in expiration- they can get air in but cannot get air out

Air trapping, Pursed lip-breathing

Increased A&P diameter, Barrel chest

Chronic Bronchitis

Productive cough with copious amounts of sputum

dyspnea

wheezing

rhonchi and cyanosis of the skin and mucous membranes

Damage occurs in the airway- not the alveoli, Mucous Plugs

Forced Vital Capacity (FVC)

Normal 80-120%

The FVC measures the volume of air in the lungs that can be exhaled.

Patient inhales as deep as possible and then exhales as long and as forcefully as possible.

Obstructive: Will be decreased or normal

Restrictive: Will be decreased

Forced Expiratory Volume in 1 second (FEV1)

Normal 80-120%

Amount of air forcefully exhaled from the lungs in the first second.

The patient inhales and forcefully exhales as fast as possible.

Obstructive: Will be decreased

Restrictive: Will be decreased

FEV1/FVC ratio

Determines if the pattern is obstructive, restrictive or normal

Normal is 70% or less than the lower limit of normal for the patient

This is a calculated ratio that represents the proportion of a person's vital capacity that they are able to expire in the first second of forced expiration to the full, forced vital capacity.

Obstructive: Less than 70%

Restrictive: Normal or > 70%

Diffusing capacity

The diffusing capacity is simply how well the lungs are able to exchange gas

Residual volume (RV)

RV is the amount of air that remains in the lungs after a forceful exhalation

Total Lung Capacity (TLC)

RV + FVC = TLC

Normal range is 80-120% of predicted

Obstructive: >120% (represents hyperinflation)

Restrictive: <80%

Microcytic anemia

(MCV<80 fL) describes RBCs that are small.

Iron deficiency

Sideroblastic

Thalassemia

Anemia of chronic disease

Macrocytic anemia

(MCV>100 fL) describes RBCs that are large.

B12 deficiency (pernicious anemia)

Folate deficiency

Normocytic anemia

(MCV 80-99 fL) describes RBCs that are normal in size.

Anemia of inflammation and chronic disease

Hereditary spherocytosis

G6PD deficiency

Paroxysmal nocturnal hemoglobinuria

Hypochromic anemia

RBCs with less hemoglobin than normal. As a result, the RBCs appear pale in color (MCHC is low).

Hyperchromic anemia

RBCs with more hemoglobin than normal. As a result, the RBCs appear a dark hue or red than normal cells (MCHC is high).

Normochromic anemia

RBCs that have a normal amount of hemoglobin. As a result, the RBCs appear neither pale nor dark (MCHC is normal).

Decreased tissue oxygenation from anemia can manifest as signs and symptoms of the following:

Severe fatigue

Pallor

Weakness

Dyspnea

Dizziness

Cardiac Output (CO)

The amount of blood that the heart pumps in 1 minute. CO is also known as cardiac contractility.

CO=heart rate (HR) x stroke volume (SV).

Stroke Volume (SV)

The volume of blood pumped out of the left ventricle during each systolic cardiac contraction.

Afterload

The force, or load, which the heart must contract against in order to pump blood.

Afterload is also known as systemic vascular resistance (SVR).

Preload

The amount of stretch that the cardiac muscle exhibits at the end of ventricular filling.

Right-sided Heart Failure

S/Sx:

Jugular vein distention

Hepatosplenomegaly

Peripheral edema

CorPulmonale

Tricuspid valve damage

Right ventricle

superior vena cava (preload)

pulmonary artery (afterload)

Causes of right heart failure include: 1) pulmonary disease that causes pulmonary hypertension. This is the most common cause; 2) right ventricular myocardial infarction (MI), which weakens the cardiac muscle; 3) right ventricular hypertrophy (secondary to cardiac damage); 4) tricuspid valve damage (causing backflow of the blood into the right atrium or right ventricle after ejection); 5) secondary failure as a result of left heart failure due to the build-up of pressure in the damage left ventricle

Left-Sided Heart Failure

S/Sx:

Increased left ventricular afterload

Decreased ejection fraction

Increased left ventricular preload

Pulmonary edema

Dyspnea

Left ventricle

Pulmonary vein (preload)

Aorta (afterload)

This increased pressure will force fluid from the pulmonary capillaries into the pulmonary tissues, which essentially floods those areas. The result is pulmonary edema and dyspnea. If left ventricular heart failure is unresolved, volume and pressure will continue to build until it reaches the right side of the heart, contributing to right heart failure as well