Pathophysiology

Patho

100

• Etiology

• The cause(s) that result in a disease

200

• Local vs systemic illness

• A local illness is one that affects only one body part/organ whereas a systemic illness is one that has entered the bloodstream and affects multiple body parts/organs

300

• Syndrome

• A set of signs and symptoms that occur together that suggests the presence of a disease/illness

400

Exacerbation

• An acute increase in the severity of an illness/disease and its signs and symptoms

500

• Homeostasis

• A state of normalcy within a system that has self-regulated mechanics of give and take through positive and negative feedback loops

600

• Prognosis

• The likely outcome or course of a disease/illness

700

• Give examples of traumatic cell injury.

Low intensity heat/extreme heat, cold/extreme cold, UV radiation, electric current, viruses, drugs/toxins

800

• Describe in detail the what can happen when normal cell homeostasis is disrupted by increased stress, demand or injury.

The stimulus that results in disruption of homeostasis are noticed by the body through sensors/receptors which cause a response by the cell. The responses could be adaptive or injury can occur if the cell is unable to adapt. If the injury is still reversible, the cell can return to normal functioning. If the injury is not reversible and the cell is unable to adapt, apoptosis or necrosis will result.

900

• Give examples of cell injury caused by substrate deficiency

• An infection which results in the cell substrates being used up by the infected cells
• Genetic diseases/disorders that lead to impaired metabolite regulation and synthesis
• Primary nutrient deficiency such as a decrease in glucose consumption
• Secondary nutrient deficiency such as pernicious anemia (intrinsic factor not synthesized -> B12 not absorbed -> RBC not effectively produced -> O2 delivery compromised leading to cell damage)
• These can all lead to a state of substrate deficiency and ultimately cell injury

1000

Give an example of reversible cell injury

An example is an individual getting a sunburn. Overtime, the cell will repair the injury and return to their normal state.

GAS EXCHANGE

100

A patient with pneumonia develops impaired gas exchange. Which assessment finding is the earliest indicator of hypoxemia?

A. Cyanosis
B. Restlessness and anxiety
C. Bradycardia
D. Clubbing of fingers

B

Restlessness and anxiety are early signs of hypoxemia. Cyanosis is a late finding.

200

A patient with chronic obstructive pulmonary disease (COPD) has an oxygen saturation of 88%. Which pathophysiologic process primarily contributes to impaired gas exchange?

A. Increased cardiac output
B. Ventilation-perfusion mismatch
C. Increased hemoglobin production
D. Increased lung compliance

B

COPD causes ventilation-perfusion (V/Q) mismatch, resulting in inadequate oxygenation.

300

Which arterial blood gas (ABG) value indicates hypoxemia?

A. PaO₂ 95 mmHg
B. PaCO₂ 40 mmHg
C. PaO₂ 58 mmHg
D. HCO₃ 24 mEq/L

C

A PaO₂ less than 60 mmHg indicates significant hypoxemia. Normal PaO₂ is 80–100 mmHg.

400

A patient with pulmonary edema experiences impaired gas exchange because fluid in the alveoli:

A. Increases oxygen diffusion
B. Improves ventilation
C. Increases the distance for oxygen diffusion
D. Enhances carbon dioxide removal

C

Fluid in the alveoli increases the diffusion distance for oxygen, impairing gas exchange.

500

Which patient is at highest risk for impaired gas exchange?

A. Patient with a fractured wrist
B. Patient with severe asthma exacerbation
C. Patient with gastroenteritis
D. Patient with hypertension

B

Severe asthma causes airway narrowing and impaired oxygen movement into the alveoli.

600

Which assessment finding is the best indicator that gas exchange is improving in a patient with pneumonia?

A. Respiratory rate of 28 breaths/min
B. Oxygen saturation increasing from 88% to 95%
C. Presence of a productive cough
D. Temperature of 101.2°F (38.4°C)

B

Improved oxygen saturation indicates better oxygenation and gas exchange.

700

A patient with chronic lung disease develops clubbing of the fingers. This finding is most associated with:

 A. Acute hyperglycemia

B. Chronic hypoxia

C. Hyperventilation

D. Dehydration

B

Clubbing develops over time in response to chronic hypoxia and low oxygen levels.

800

Which structure is the primary site of gas exchange in the lungs?

A. Bronchi
B. Trachea
C. Alveoli
D. Larynx

C

Alveoli are the primary site where oxygen and carbon dioxide are exchanged.

900

A patient with pulmonary embolism suddenly develops shortness of breath. The impaired gas exchange occurs because:

A. Alveoli collapse completely
B. Blood flow to part of the lung is blocked
C. Excess mucus fills the bronchioles
D. The diaphragm becomes paralyzed

C

Tachypnea, nasal flaring, and accessory muscle use are classic signs of respiratory distress.

1000

Which patient is showing signs of respiratory distress?

A. Respiratory rate 16/min, SpO₂ 98%
B. Respiratory rate 14/min, relaxed posture
C. Respiratory rate 32/min, nasal flaring, use of accessory muscles
D. Respiratory rate 18/min, clear lung sounds

C

Tachypnea, nasal flaring, and accessory muscle use are classic signs of respiratory distress.

Adaptive Immune System

100

•  What are the three major cell types in the adaptive immune system?

• B cells
• T cells
• Antigen presenting cells (APCs)

200

•  What are the differences between the innate and adaptive immune system?

• Innate immunity is fast (very fast onset) and messy (non-specific targeting). It provides protection in a destructive/napalm matter.
• Adaptive immunity, while slower, is precise and targeted to specific antigens. This type of immunity results in long memory for quicker response on repeated exposure.

300

• What does an antigen presenting cell do and which cells can be antigen presenting cells?

APCs are the bridge between the innate an adaptive immune system. Once phagocytosis has occurred and the pathogen has been destroyed, the APC will take a portion of the foreign material (antigen) and present on its surface through MHC-II for a naïve T-cells to recognize.

400

• Describe how humoral immunity works and what cells are involved.

An activated T-Helper cell will activate a B-cell similarly to how the T-Helper cell was activated. Recognition occurs where the antigen is presented to the B-cell. Once this occurs, co-stimulation occurs to ensure the information being communicated is correct. Lastly, chemical mediators are released which fully activates the B-cell. Once activated, clonal expansion occurs to proliferate and become B-memory cells or Plasma cells. B-memory cells “remember” the antigen that is being targeted for a faster response on subsequent exposures. Plasma cells release antibodies against the antigen and send them into circulation. These antibodies can be IgM, IgD, IgA, IgG, or IgE depending on the requirements. The antibodies will then neutralize the pathogen or opsonize the pathogen for phagocytosis

500

• Describe the three steps of T helper cell activation.

• The three steps are recognition, co-stimulation, release of chemical mediators.
• 
  
• In the recognition step, APCs present an antigen through their MCH-II molecule to the naïve T-cell. Once this initial connection has been made, it needs to be co-stimulated. In this step, separate receptors on both the APC and the naïve T-cell connect to ensure the information being communicated is correct. After both connections have been made, chemical mediators (cytokines) are released by both the APC and the T-cell. Once all three steps have occurred, the naïve T-cell is now activated.

600

• Describe how cell mediated immunity works and what cells are involved.

• This is a type of immunity that does not involve any antibodies. This is done through interactions between different cells. When a T-cell is first released, it is naïve and needs to be activated. This is done through a series of connections. First is known as recognition. In this step, APCs present an antigen through their MCH-II molecule to the naïve T-cell. Once this initial connection has been made, it needs to be co-stimulated. In this step, separate receptors on both the APC and the naïve T-cell connect to ensure the information being communicated is correct. After both connections have been made, chemical mediators (cytokines) are released by both the APC and the T-cell. Once all three steps have occurred, the naïve T-cell is now activated.
• 
  
• The activated T-Helper cell undergoes clonal expansion to proliferate and activate other T-cells (such as the cytotoxic T-cells) and B-cells.
• 
  
• °NK cells are not cell mediated. They are surveillance cells.

700

Self-Discrimination

• MHC-I molecules are used to identify self-cells from foreign objects. This allows for the immune response (under normal circumstances) to not attack the self.

800

IgM

It is a pentamer that is seen earlier in infection. It results in opsonization, activation of complement cascade (C1), or agglutination

900

The primary function of neutrophils is to:

a. Produce Antibodies

b. Destroy bacteria through phagocytosis

c. Release histamine 

d. Produce clotting factors

B. 

Neutrophils are the first responders of bacterial infections and perform phagocytosis.

1000

IgA

The most abundant type of antibody. It is a monomer that is produced by plasma cells to either 1) precipitate, 2) activate MAC, or 3) neutralize the pathogen

Hypersensitivity

100

• What is the immune mediator of each of the hypersensitivity reactions?  (i.e. type of Ig, etc)

Type I: IgE

Type II: IgM or IgG

Type III: IgG and antigen-antibody complexes

Type IV: T-Helper cells

200

• Where do self antigens come from?

Self-antigens come from healthy tissue that shed component proteins and from cells that have undergone apoptosis. In the bone marrow, stromal cells and hematopoietic cells result in the production of self-antigens that are used to screen B-cells for auto-reactivity.

300

• Which hypersensitivity reaction relies on the complement cascade the most?

Type III hypersensitivity. In this reaction, a HUGE complement response occurs which attracts cells that hope to phagocytosize the complex. Most of the time, they are unable to do and “puke” out their contents and indiscriminately destroy the surrounding tissue. The tissue damage results in inflammation and further damage which results in further inflammation and further damage which…. a vicious cycle.

400

• Describe the 3 components of B cell central tolerance.

Just like T-cells, B-cells need to be checked to ensure they are not auto-reactive. If they escape, they can create antibodies to self and cause autoimmune diseases. Just like T-cells, B-cells are produced in the bone marrow. Unlike T-cells, B-cells stay in the bone marrow to mature.

Similar to how the strength of binding determines auto-reactive from normal T-cells, the same goes for B-cells. If the immature B-cell has no interaction with a self-antigen, it is allowed to exit the bone marrow and travel to the lymphoid tissue. If there is a strong interaction with self-antigens, the development of the B-cell is arrested in the bone marrow.

Once arrested in the bone marrow, three mechanisms are used to induce tolerance: receptor editing (the antigen receptor is modified through gene editing), clonal deletion (if receptor editing is unsuccessful then apoptosis occurs), and anergy (the auto-reactive B-cell stays arrested and becomes unresponsive).

500

Describe central tolerance of T cells – 3 possible outcomes

Central tolerance is “training camp” for T-cells. Once produced in the bone marrow, they travel to the thymus to mature. Whether the T-cell matures and can leave the thymus depends on its interactions with self-antigens that are presented by thymus cells. Thymus cells present the self-antigen for the thymus cell receptors (TCRs) on immature T-cells to recognize.

If the T-cell does not recognize the self-antigen on MHC-I molecules, they undergo apoptosis because they are not able to do their job.

If the T-cell recognizes the self-antigen and MODERATELY binds to it, this is referred to as positive selection. This guy survives and goes to the lymph node!

If the T-cell recognizes the self-antigen and STRONGLY binds to it, this is referred to as negative selection. This guy also undergoes apoptosis because there’s a chance they’ll target the self.

600

• Describe peripheral tolerance of T cells – prevention and control

While central tolerance does a good job of catching the T-cells that shouldn’t be allowed to live, it’s not always perfect. Some auto-reactive T-cells escape to the lymph nodes. To stop these T-cells from reacting and attacking the self, peripheral tolerance is a method to stop their attack. The overall goal of peripheral tolerance is to either prevent their activation or control the immune response.

Normally recognition, co-stimulation, and release of chemical mediators is required to activate T-cells. To prevent activation, T-cells that do not co-stimulate due to their strong affinity for self-antigens, peripheral clonal deletion occurs where the T-cell undergoes apoptosis or anergy occurs where the T-cell is “put to sleep”.

In addition, the immune response can be controlled to further protect against the auto-reactive T-cells. These methods include an immune deviation (a less harmful response results), immune privilege regions exist where no immune cells are found (eyes, CNS, testes), cytokines are immunosuppressed, and regulatory T-cells further control the response.

700

• Name and describe the three different types of Type 2 hypersensitivity reactions and give examples.

• Antigen-antibody complexes activate the complement system to kill the cell via opsonization or MAC attack. An example is hemolytic anemia or Rh reaction of the mother to their baby during pregnancy.
• Antibody dependent cell mediated cytotoxicity. Antigen-antibody complexes attract WBCs that will phagocytosize the cell and destroy it. An example is Good Pasture Syndrome or graft rejection
• Target cell dysfunction can also happen where the antibodies produced can block or overstimulate receptors without killing the cell needed for normal functioning. Examples include Myasthenia Gravis or Grave’s Disease.

800

Describe the type of hypersensitivity with examples. Type III

This type of hypersensitivity is mediated by immune complexes (antigen-antibody complexes). This occurs due a double failure of tolerance. Not only did a self-recognizing T-cell escape, but a self-recognizing B-cell escaped as well. Due to co-stimulation, B-cells produce IgG antibodies and bind to antigens that are soluble (free-floating and not attached to cell). If the antibody is binding to an antigen on a cell that is Type 2 hypersensitivity. Since the antibodies formed are binding to small antigens, macrophages aren’t attracted as they would be if it were a cell. This results in the complexes floating in circulation for a while before getting trapped in spaces (ie: blood vessel walls, glomeruli, synovium). Once trapped, a HUGE complement response occurs which attracts cells that hope to phagocytosize the complex. Most of the time, they are unable to do and “puke” out their contents and indiscriminately destroy the surrounding tissue. The tissue damage results in inflammation and further damage which results in further inflammation and further damage which…. a vicious cycle.

900

Describe the type of hypersensitivity with examples. Type II

This type of hypersensitivity occurs due to a failure of central tolerance that is antibody mediated and generally leads to cytotoxicity. Normally, central tolerance takes care of T-cells and B-cells that are auto-reactive, but some escape and circulate the system. These cells produce IgM antibodies that can bind to molecules they shouldn’t have and create an antigen-antibody complex. These complexes can result in different mechanisms to kill the cell. First, they can activate the complement system (C1 binds to the antibody) which will result in the destruction of the cell through the MAC (membrane attack complex). Second, they can opsonize the cell which will attract immune cells a macrophage to phagocytosize the cell and destroy it. If phagocytosis cannot be done, macrophages or neutrophils “puke” out perforins, enzymes, or free radical species (found in lysosomes and peroxisomes) and indiscriminately destroy the area the antigen is in.

1000

Describe the type of hypersensitivity with examples. Type IV

This type of hypersensitivity is referred to as T-cell mediated hypersensitivity. Certain foreign molecules are very small and can cross through barriers and be picked up by APCs. If a naïve T-Helper cell recognizes the antigen, activation of the T-Helper cell can occur (recognition, co-stimulation, and release of chemical mediators). The now activated T-Helper will proliferate and activate other immune cells like macrophages to release cytokines. The cytokine release widens the endothelial gaps and allows for immune cells to enter (the 4 pillars of inflammation - swelling, redness, heat, and pain occur!).

CD4+ cells are not the only players in this type of hypersensitivity though! Killer T-cells (CD8+) are present and can directly destroy cells like a silent assassin. They scan cells and monitor their MHC-I receptor. When changes occur to the MHC-I molecule, CD8+ cells bind to it and release perforins and granzymes to induce apoptosis in the infected cells.

Examples include poison ivy, TB, type 1 diabetes mellitus, multiple sclerosis, and rheumatoid arthritis. This hypersensitivity takes the longest to occur.

IMMOBILITY

100

A patient has been on bed rest for several weeks. Which complication is most directly related to impaired mobility?

A. Hyperthyroidism
B. Deep vein thrombosis (DVT)
C. Hyperglycemia
D. Hyperkalemia

B

Venous stasis from immobility increases the risk of DVT formation.

200

Prolonged immobility increases the risk for pressure injuries because it:

A. Increases tissue perfusion
B. Decreases capillary blood flow to tissues
C. Increases oxygen delivery to skin
D. Improves nutrient transport

B

Constant pressure reduces capillary blood flow, leading to tissue ischemia and skin breakdown.

300

Which assessment finding is most consistent with a developing deep vein thrombosis (DVT)?

 A. Bilateral leg numbness

B. Cool pale extremities

C. Unilateral calf swelling and pain

D. Bilateral pedal edema

C

Classic DVT findings include unilateral swelling, warmth, redness, and calf pain.

400

A nurse is caring for a patient with limited mobility following surgery. Which intervention best helps prevent complications of immobility?

 A. Restrict fluids

B. Encourage early ambulation

C. Limit activity to bed rest

D. Elevate the head of bed at all times

B

Early ambulation reduces risks of DVT, atelectasis, muscle atrophy, and constipation.

500

Immobility can contribute to atelectasis because:

A. Patients take deeper breaths while resting
B. Secretions are more effectively cleared
C. Alveoli collapse due to reduced lung expansion
D. Oxygen demand decreases

C

Reduced movement and shallow breathing promote alveolar collapse (atelectasis).

600

Why does iron deficiency cause problems for red blood cells?

Key components of RBCs are hemoglobin and iron. There are tons of molecules of heme that are bound to iron. This interaction allows for iron to bind to oxygen molecules which then allows RBCs to carry and deliver oxygen to various tissues of the body. With a deficiency of iron, RBC production becomes compromised, and they often are smaller in size which decreases their ability to deliver oxygen.

700

1. Describe how platelets are made in the marrow and what they do in the circulation.

In the bone marrow, hematopoiesis leads to the production of megakaryoblasts. When undergoing mitosis, they do not cleave (cytokinesis) and instead remain fused. This results in the multinucleated megakaryocyte. This cell breaks off pieces of itself that are anucleated. These broken off pieces are platelets. Once broken off, platelets circulate in the blood for ~10 days in an inactive form. When bleeding occurs in the body, they become active to make fibrin clots to stop it.

800

1. Why do RBCs sickle?  How does this effect the body?

In normal RBC development, Hgb A is present that allows RBCs to be flexible and slip through tiny gaps (such as the ones in capillaries) without any issues. In sickle cell, however, there is a mutation which turns Hgb A into Hgb S. This mutation results in RBCs to more rigid and form in a crescent shape. Due to these changes, RBCs undergo premature hemolysis and only circulate the body for ~20 days compared to the normal ~120 days. Since turnover occurs more often, the body can’t produce enough RBCs needed to deliver the appropriate amount of oxygen to the tissues that is required. This results in the individual experiencing hypoxia and feeling cold. In addition, due to the crescent shape, the sickled RBCs can no longer slip through gaps. This results in them getting stuck in places like capillaries, the spleen, kidneys, and etc further resulting in the symptoms described earlier along with the possibility of blocking blood flow and resulting in necrosis of tissues which causes pain, inflammation, and increased risk of infection for the individual.

900

1. What happens if platelets are destroyed by the immune system?

Destruction of platelets by the immune system is known as ITP (immune thrombocytopenia purpura). In this autoimmune disease, antibodies are created against platelets. Their destruction can result in purpura (small bleeding spots beneath the skin) or, in severe cases, epistaxis (nose bleeding). Normally, hemostasis occurs where bleeding is stopped by plugging the vessel that is leaking through platelet clumping at the site. In ITP, due to destruction of platelets, bleeding becomes harder to stop.

1000

Describe TTP and its clinical findings

TTP (Thrombotic thrombocytopenia purpura) is a blood disease where small blood clots occur throughout the body. During blood clot formation, von Willebrand factor sticks to exposed tissue and acts like a glue for platelets to stick to. Once the clot needs to be broken down, an enzyme breaks down von Willebrand factor but in TTP, there is a deficiency of that enzyme. Without the regulatory effects of this enzyme, small blood clots form frequently throughout the body. These blood clots can block blood flow and lead to the clinical findings of decreased platelet count, purpura (small bleeding spots beneath the skin), brain dysfunction, GI problems, and heart-related symptoms.

Cancer

100

Define -oma, -carcinoma, -sarcoma

-oma is tumor

-carcinoma is cancer of epithelial tissue (endo- or ectodermal tissue0

-sarcoma is cancer of connective tissue (mesodermal tissue)

200

What is benign tumor?

Benign Tumor: Well-differentiated so they can continue their function, grow faster than normal cells but not as much as malignant tumors, remains localized (does not infiltrate/invade/metastasize), surrounded by fibrous capsule (which is easier to remove during resection than malignant tumors)

300

• What is pleomorphism?

Pleomorphism is cells having variation in size and shape. They have lost their differentiation and organization that they previously had. As a result, pleomorphic cells have their own autonomy and create cells whenever, wherever, and whatever shape/size they feel like with no consistency. These unstructured cells can become invasive and enter the bloodstream.

400

• What is the mechanism of tumor invasion?

Tumors attempting to invade do so by binding to the extracellular matrix and basement membrane. When bound, the tumor will release enzyme to degrade the ECM and basement membrane. In addition, due to mutations and secretions, they have reduced adhesion and release chemotactic factors. These changes allow for them to have enhanced motility which leads to invasion to neighboring tissue and through the blood.

500

• Describe the stages of the cell cycle and what happens in each.

G0: The resting state of the cell (out of the cycle of division) where it performs it function

G1: When ready for division, the cell will enter this phase where it will grow and prepare. To do this, organelles and cytoplasm of the cell begin to duplicate along with performing transcription and translation of DNA.

S: DNA synthesis and duplication occurs here

G2: The cell continues to prepare for cell division by duplicating organelles and cytoplasm.

M: Mitosis

Cytokinesis: After completing mitosis, the two daughter cells split and become individual cells

Once completing mitosis and cytokinesis, the cell can either remain in the cycle to divide again, or it may leave and return to G0.

600

• Where are the check points and what do they do?

There are multiple checkpoints within the cell cycle that monitor the progress of the cell through the different phases and attempt to prevent mutant replication and detect DNA damage. If damage is detected, the cell will attempt to repair it, enter G0, or undergo apoptosis.

The first checkpoint is found between the G1 and S phases to ensure the DNA is ready for duplication and so that the cell size, nutrients, and growth factors can be checked. The second checkpoint is found between the G2 and M phases to ensure everything is ready for mitosis and ensuring DNA replication didn’t lead to damage or errors. There is also one last checkpoint during mitosis that ensures the spindles (attach the chromosomes to the metaphase plate) are functioning properly.

700

• Paraneoplastic syndrome may involve a lot of secondary symptoms related to cancer.  Name 5 of the paraneoplastic syndrome findings.

There are many findings, these include: cachexia (weakness), anemia (due to chronic loss and suppression of bone marrow), infection (due to suppression of immune system), pain (due to pressure, destruction, and nerve involvement), anorexia (loss of appetite/weight loss), pallor, depression, anxiety

800

• What are the mechanisms which alters the normal cell cycle and result in tumor formation?

In normal conditions, there checks that keep the cell from dividing uncontrollably. The cyclin-CDK complex activate the proteins required to continue through checkpoints and proceed through the cell cycle. If there is damage to DNA, cyclin is not present and the cell cycle will be halted to repair DNA, return to G0, or undergo apoptosis.

In oncogenesis (development of a tumor), this mechanism is broken and results in excessive cell division, reduced cell loss, and an increase in retention of cells. Proto-oncogenes are required in normal cell growth and division, but in oncogenesis these genes become defective and become oncogenes. These oncogenes are like pressing on the gas pedal and continuously speeding through checkpoints. There are suppressor genes (ie: p53), however, that act as brakes and promote DNA repair and apoptosis.

In oncogenesis, suppressor genes can become inhibited and damaged DNA is allowed to replicate, or oncogenes can be activated by excess of promoter growth factors can override suppressor genes and lead to tumor production (without the promoter, this would not be possible).

900

• How can benign tumors cause devastating outcomes?

By definition benign tumors are not cancerous and will not lead to metastasis. However, these cells can continue to grow and crush/damage neighboring cells (this phenomenon is known as mass effect).

There are places in the body where space is limited (ie: the skull) where a benign tumor can grow large enough to damage brain cells, disrupt flow of CSF, and other devastating effects. Another example is obstruction of passageways (ie: respiratory tract where the benign tumor can result in blockage of air).

1000

• Describe the interaction between promoters and initiators and how they result of predisposition to tumor formation.

In oncogenesis (development of a tumor), the mechanism that checks before continuing through the cell cycle is broken and results in excessive cell division, reduced cell loss, and an increase in retention of cells. Proto-oncogenes are required in normal cell growth and division, but in oncogenesis, initiators cause these genes to become defective and become oncogenes.

Compared to normal functioning cells, promoters have a stronger effect in cancerous cells and oncogenes can be activated by excess of promoter growth factors which overrides suppressor genes and lead to tumor production.

HORMONAL AND GLUCOSE REGULATION

100

Which hormone is primarily responsible for lowering blood glucose levels?

A. Glucagon
B. Cortisol
C. Insulin
D. Epinephrine

C

Insulin lowers blood glucose by promoting glucose uptake into cells and storage as glycogen.

200

A patient with type 1 diabetes mellitus develops hyperglycemia because:

A. The body's cells become resistant to insulin
B. The pancreas produces excessive glucagon
C. Autoimmune destruction of pancreatic beta cells reduces insulin production
D. The liver stores excessive glycogen

C

Type 1 diabetes results from autoimmune destruction of pancreatic beta cells, leading to insulin deficiency.

300

Which assessment finding is most characteristic of hyperglycemia?

A. Diaphoresis
B. Tremors
C. Polyuria and polydipsia
D. Bradycardia

C

Hyperglycemia causes osmotic diuresis, resulting in polyuria, polydipsia, and dehydration.

400

A patient becomes shaky, diaphoretic, and confused. Which glucose value would the nurse expect?

A. 45 mg/dL
B. 120 mg/dL
C. 150 mg/dL
D. 180 mg/dL

A

Symptoms of hypoglycemia include shakiness, diaphoresis, confusion, and blood glucose typically less than 70 mg/dL.

500

Which hormone increases blood glucose levels by stimulating glycogen breakdown in the liver?

A. Insulin
B. Glucagon
C. Aldosterone
D. Oxytocin

B

Glucagon raises blood glucose by stimulating glycogenolysis and gluconeogenesis.

600

Excess secretion of cortisol, as seen in Cushing syndrome, commonly results in:

A. Hypoglycemia
B. Hyperglycemia
C. Decreased blood pressure
D. Weight loss

B

Cortisol promotes gluconeogenesis and insulin resistance, causing elevated blood glucose levels.

700

Which laboratory finding is most consistent with uncontrolled diabetes mellitus?

A. Hemoglobin A1C of 5.2%
B. Fasting blood glucose of 85 mg/dL
C. Hemoglobin A1C of 9.5%
D. Random glucose of 100 mg/dL

C

An A1C of 9.5% indicates poor long-term glucose control. Goal for many patients is <7%.

800

A patient with hypothyroidism would most likely exhibit which manifestation?

A. Tachycardia and weight loss
B. Heat intolerance and anxiety
C. Fatigue and weight gain
D. Hyperactivity and insomnia

C

Hypothyroidism slows metabolism, causing fatigue, weight gain, cold intolerance, and constipation.

900

Which hormone is responsible for increasing water reabsorption by the kidneys?

A. Antidiuretic hormone (ADH)
B. Insulin
C. Glucagon
D. Growth hormone

A

ADH acts on the kidneys to increase water reabsorption and reduce urine output.

1000

A patient with diabetes insipidus would most likely experience:

A. Excessive urine output and thirst
B. Weight gain and edema
C. Severe hypoglycemia
D. Decreased urine production

A

Diabetes insipidus involves ADH deficiency or resistance, leading to polyuria and polydipsia.

Pulmonary II

100

• What is the mechanism of intrinsic restrictive lung disease?  How do the lung get stiff?

The lung is elastic and it is very important that it remains that way, but pathologies can result which compromise that elasticity. Intrinsic restrictive lung disease occurs due to changes (ie: scarring, chronic inflammation, microinjuries, etc) in the lung tissue between the alveoli and blood vessels which results in the lungs becoming fibrotic and stiff which makes it hard for them to expand and allow air to enter.

200

• How does their lung function compare with that of normal lungs?

Individuals will intrinsic restrictive lung disease have reduced vital capacity, residual volume, functional residual volume, tidal volume, and total lung capacity.

300

• What are the steps that lead to cor pulmonale?

Cor Pulmonale typically occurs when an individual has chronic lung disease. This causes pulmonary vasoconstriction which manifests as pulmonary hypertension. Due to the increase in blood pressure in the pulmonary blood vessels, the right ventricle of the heart pumps harder to compensate. This compensation leads to enlargement of the right side of the heart and eventually right sided heart failure as the heart is unable to keep up with the demand.

400

• What are the clinical symptoms associated with intrinsic restrictive lung disease?

The symptoms that can be experienced by individuals with intrinsic restrictive lung disease are cough, dyspnea (especially on exertion), sputum production, cyanosis (due to large concentration of deoxygenated blood), and fatigue

500

• List 5 of the causes of intrinsic restrictive lung disease.

The causes are occupational/exposure (particles that get trapped in the lung that lead to an immune response), drugs, autoimmune diseases (Lupus, Rheumatoid arthritis, scleroderma, etc), idiopathic (pulmonary fibrosis, interstitial pneumonia, etc), or smoking.

600

How does the fibrosis develop? Explain the pathophysiology

Foreign materials or a chronic irritant can lead to an immune response to be mounted. Macrophages that are present in the area attempt to engulf the foreign material and clear the alveoli. Unable to do, macrophages may undergo oxidative burst or disintegrate to clear it instead. This leads to a buildup of fibrous tissue (collagen) within the alveoli. This tissue affects diffusion and stiffens the lung as collagen is not as elastic.

700

• What are granulomas?  How do they develop?

Granulomas are clumps of immune cells. Chronic infection/inflammation leads to multiple immune cells to be present at the site. These immune cells clump in such a way that a necrotic core and fibrotic capsule forms that walls off the pathogen from the rest of the body.

800

• Name the three most common causes of obstructive lung disease.  Compare and contrast the disorders and their symptoms.

In the lumen: This type of obstruction is where an object is blocking the passageway of the lumen itself.

• Oropharynx: the tongue is swollen and blocking air from traveling from the upper airway to the lower airway.
• Laryngitis: the vocal cords become inflamed and obstructs the airway
• Epiglottitis: The epiglottis is inflamed and obstructs the airways
• Chronic Bronchitis: Destruction and inflammation block exhalation and inhalation and results in a loss of elasticity and outflow obstruction.
• Asthma: mucus is hyper secreted which obstructs the airways and results in air trapping

Outside the lumen, pushing in: This type of obstruction is where an object is blocking the passageway of the lumen from outside.

• Goiter or neck mass: smashes the airway from outside of the lumen and obstructs the airway
• Asthma: The bronchial constriction results in less space within the lumen and can ultimately lead to obstruction of the airway

In the wall: This type of obstruction is where an object is blocking the passageway from the wall of the lumen.

• Asthma: Inflammation of the vessel causes narrowing and results in obstruction of the airway
• Tumors: a mass that forms within the wall of the lumen can reduce the size of the lumen and ultimately lead to obstruction

900

• Describe the 5 different causes of impaired gas exchange at the alveolar level.

• Collapse (atelectasis): Lung volume decreases due to the collapse of alveoli. Can result due to obstruction within the airway, compression (excess air, water, blood), fibrosis of the lung, or decrease attachment of the alveoli to each other
• Architectural destruction (emphysema): The alveoli can have trapped particles within them (typically seen in individuals who chronically smoke) which results in an inflammatory response. The chemicals released during the response can dissolve the walls of individual alveoli, resulting in a large air cavity lined with the carbon deposits. Due to the loss of many small alveoli, the surface area of the lung decreases, resulting in less efficient gas exchange
• Fluid within the alveoli (Water, Blood, Pus): Water can leak into the alveoli can impair gas exchange (as seen in heart failure), Pus can build up within the alveoli (as seen in pneumonia), or Blood can enter the alveoli (as seen in lung contusion and other traumatic injuries)

1000

• What are the toxic causes of shortness of breath?  How do they cause hypoxia?

The toxic causes of shortness of breath are CO2, CO, cyanide, and particles that result in the fibrosis of the lung (as listed above).

• CO2: High levels of CO2 within the body trigger the chemoreceptors within the brain (specifically the medulla) to increase the rate of respiration
• CO: CO competes with O2 in terms of hemoglobin binding, as such, high flow O2 is given to outcompete CO.
• Cyanide: Cyanide interferes with oxidative phosphorylation by binding to a protein within the electron transport chain and inhibiting it.