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Questions and Answers

Which of the following accurately describes the pathogenesis of HIV/AIDS?

  • HIV disrupts electrolyte balance, causing severe dehydration and acid/base imbalances that ultimately compromise the immune system.
  • HIV directly attacks malignant tumors, leading to their rapid growth and spread throughout the body.
  • HIV alters cellular metabolism by accelerating the production of red blood cells, leading to hyperviscosity and reduced oxygen delivery to tissues.
  • HIV primarily infects and destroys CD4 WBCs, impairing immune function and leading to opportunistic infections and other complications. (correct)

A patient with HIV is currently asymptomatic. What is the MOST likely reason for this?

  • The patient's immune system is effectively suppressing the virus without any intervention.
  • The opportunistic infections are being effectively managed with prophylactic antibiotics.
  • There are still enough circulating immune cells to maintain a functional level of immunity. (correct)
  • The virus is in a dormant state and not actively replicating.

How does HIV infection lead to immunosuppression?

  • By inducing a chronic state of allergic reactions weakening the body's responses.
  • By accelerating the aging process. This causes premature decline in immune function.
  • By promoting an overproduction of antibodies that results in hyperinflammation.
  • By directly attacking and destroying T lymphocytes which provide cell-mediated immunity. (correct)

Which of the following is a common clinical manifestation observed with HIV/AIDS due to its pathogenesis?

<p>Opportunistic infections due to a compromised immune system. (A)</p> Signup and view all the answers

Which of the following is NOT a typical etiological factor for HIV/AIDS?

<p>Casual contact, such as shaking hands or sharing a meal with an infected individual. (A)</p> Signup and view all the answers

What is the primary effect of increased vascular permeability during inflammation?

<p>Shift of fluid from the intracellular space (ICF) to the extracellular space (ECF), leading to hypovolemia and hypotension. (C)</p> Signup and view all the answers

Which of the following compensatory mechanisms is directly triggered by acute systemic hypoperfusion?

<p>Increased heart rate and cardiac contractility (C)</p> Signup and view all the answers

How does the renal system typically respond to maintain function during the initial stages of hypoperfusion?

<p>By exhibiting a vasodilatory response in the glomeruli to maintain filtration. (B)</p> Signup and view all the answers

What is the purpose of peripheral vasoconstriction in response to hypovolemia?

<p>To increase cardiac ventricular preload. (A)</p> Signup and view all the answers

What is the effect of antibodies on bacteria that makes them more susceptible to phagocytosis?

<p>Increasing bacterial aggregation (B)</p> Signup and view all the answers

Which of the following is a key differentiating factor between pernicious anemia and folate-deficiency anemia?

<p>Pernicious anemia is characterized by neurological symptoms due to B12 deficiency, while folate-deficiency anemia lacks these neurological effects. (A)</p> Signup and view all the answers

Increased capillary hydrostatic pressure contributes to edema by which mechanism?

<p>Pushing fluid out of the capillaries and into the interstitial space. (B)</p> Signup and view all the answers

How does alkalosis contribute to hypocalcemia?

<p>By enhancing the binding of calcium to albumin, reducing free calcium levels. (C)</p> Signup and view all the answers

Which of the following factors primarily influences magnesium metabolism?

<p>Renal function. (C)</p> Signup and view all the answers

How does hypermagnesemia affect neurological function?

<p>It inhibits the release of acetylcholine, impairing nerve transmission. (D)</p> Signup and view all the answers

Which hormone directly prevents osteoclast function, impacting calcium levels?

<p>Calcitonin (D)</p> Signup and view all the answers

Certain medications, pregnancy and alcohol use are factors for which type of anemia?

<p>Folate-deficiency anemia (D)</p> Signup and view all the answers

What type of cellular adaptation involves the replacement of one type of adult cell with another?

<p>Metaplasia (A)</p> Signup and view all the answers

How does allostasis contribute to maintaining homeostasis in the body when facing stressors?

<p>By activating the Sympathetic Nervous System and other systems to counteract the stressor and restore balance. (A)</p> Signup and view all the answers

What is the primary role of altered autocrine and paracrine signaling in carcinoma cells?

<p>To support tumor growth and invasion through self-stimulation and communication with surrounding cells. (C)</p> Signup and view all the answers

In carcinoma cells, what is the effect of overexpressed or mutated growth factor receptors found on the cell surface?

<p>Continuous growth signaling. (D)</p> Signup and view all the answers

How does protein deprivation affect the body's ability to maintain essential physiological functions?

<p>It impairs growth, immune function, and tissue repair due to insufficient production of essential components. (D)</p> Signup and view all the answers

Why does protein deprivation lead to edema, particularly in the abdomen and lower extremities?

<p>Due to reduced albumin levels, leading to fluid imbalances. (C)</p> Signup and view all the answers

Which of the following is a consequence of enzyme deficiencies resulting from protein deprivation?

<p>Disrupted metabolic functions. (A)</p> Signup and view all the answers

Which of the following scenarios would most likely lead to cellular necrosis?

<p>A cell dying in an organ due to a lack of blood supply while the organism is still alive. (A)</p> Signup and view all the answers

What is the long-term effect of a negative nitrogen balance caused by protein deprivation?

<p>Exacerbates muscle wasting. (C)</p> Signup and view all the answers

Gangrene, a form of cell death, directly impacts which aspect of cellular function?

<p>The cell's ability to receive adequate oxygen and nutrients. (C)</p> Signup and view all the answers

How might severe protein deprivation impact liver function in children?

<p>Leads to fatty liver. (C)</p> Signup and view all the answers

Which of the following cellular adaptations is most likely a reversible response to a temporary increase in physical exertion?

<p>Hypertrophy (A)</p> Signup and view all the answers

A patient experiences a prolonged period of malnutrition. Which of the following compensatory mechanisms is least likely to occur?

<p>The body increasing leptin production to stimulate appetite. (A)</p> Signup and view all the answers

In the process of hemostasis, what is the primary role of vasoconstriction?

<p>To reduce blood flow to the injured area. (D)</p> Signup and view all the answers

Which of the following best describes the role of nitric oxide (NO) in hemostasis?

<p>Inhibits platelet aggregation and causes vasodilation. (A)</p> Signup and view all the answers

If a patient has a condition that impairs their ability to produce thromboxane A2, which of the following is most likely to occur?

<p>Increased vasodilation. (A)</p> Signup and view all the answers

What is the primary function of complement proteins as part of the body's first line of immune defense?

<p>To aid in the destruction of pathogens. (B)</p> Signup and view all the answers

Which of the following is an example of the body’s regulatory mechanism in response to bleeding?

<p>Formation of a fibrin plug. (D)</p> Signup and view all the answers

Which statement describes the role of the body's immune compensatory mechanisms in the presence of cell mutations?

<p>Recognizing and removing cells with abnormal growth. (A)</p> Signup and view all the answers

During shock, the complement system contributes to hypovolemia and hypotension by:

<p>Increasing vascular permeability, causing fluid shift from intravascular to extravascular spaces. (B)</p> Signup and view all the answers

The body attempts to compensate for hypotension during shock by shunting blood to essential organs. Which set of organs are given priority during this compensation?

<p>Brain, heart, and lungs. (D)</p> Signup and view all the answers

What is the primary nutritional issue in marasmus, differentiating it from kwashiorkor?

<p>Severe calorie and protein deficiency. (C)</p> Signup and view all the answers

Edema is a distinguishing feature of kwashiorkor but not typically of marasmus. What explains the presence of edema in kwashiorkor?

<p>Protein deficiency causing fluid retention. (C)</p> Signup and view all the answers

In Type II hypersensitivity reactions, how do antibodies typically cause cell damage?

<p>Via complement activation, phagocytosis, or cytotoxicity. (D)</p> Signup and view all the answers

Which of the following mechanisms primarily mediates tissue damage in Type III hypersensitivity reactions?

<p>Deposition of antigen-antibody complexes causing inflammation and tissue damage. (C)</p> Signup and view all the answers

What is the fundamental difference in the causes of Type II and Type III hypersensitivity reactions?

<p>Type II involves reactions against self-antigens, while Type III involves deposition of immune complexes. (C)</p> Signup and view all the answers

A patient in shock exhibits increased heart rate and cardiac contractility. Which of the following best explains why these compensatory mechanisms might ultimately fail to maintain adequate tissue perfusion?

<p>Prolonged vasoconstriction and shunting of blood lead to inadequate tissue perfusion and organ damage. (A)</p> Signup and view all the answers

A patient with suspected kwashiorkor presents with edema, but their weight is within the normal range. What is the most likely explanation for this seeming contradiction?

<p>Edema is masking the underlying muscle wasting. (A)</p> Signup and view all the answers

How does the renal system initially respond to hypoperfusion during shock, and how can this response become maladaptive?

<p>Vasodilation of the glomeruli to maintain filtration, but continued hypoperfusion leads to decreased urine output and oliguria. (A)</p> Signup and view all the answers

Flashcards

Etiology

The study of the causes or origins of diseases or disorders.

Pathogenesis

The manner in which a disease develops.

Immunosuppression

Suppression of the immune system's ability to fight infection.

HIV

Human Immunodeficiency Virus; causes AIDS.

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AIDS

Acquired Immunodeficiency Syndrome; caused by HIV, weakens the immune system, leading to opportunistic infections.

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Bacterial Aggregation

Enhances antibody activity and bacterial clumping, promoting phagocytosis.

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Vascular Permeability Impact

Increased permeability causes fluid shift from ICF to ECF, leading to reduced blood volume and low blood pressure.

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Nervous System Response

The nervous system prioritizes blood flow to vital organs (brain, heart, lungs) by constricting blood vessels elsewhere.

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Acute Systemic Hypoperfusion

A state where tissues are not receiving enough oxygen due to decreased blood flow.

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Renal System Response

Kidneys attempt to maintain filtration via vasodilation, but ongoing low blood flow leads to decreased urine output or complete cessation.

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Pernicious Anemia

Vitamin B12 deficiency affecting DNA synthesis, leading to abnormal RBC formation and neurological symptoms.

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Folate-Deficiency Anemia

Folate (B9) deficiency that disrupts DNA synthesis (RBC production) without neurological effects.

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Edema

Excess interstitial fluid accumulation in tissues.

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Hypocalcemia Pathogenesis

Inhibition of PTH leading to decreased calcium release & reduced kidney reabsorption.

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Hypomagnesemia

An electrolyte that helps with cellular and nerve function within the body.

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Hypermagnesemia

Influences the cardiovascular and neurological systems.

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Cellular Adaptation

How cells adapt to stress, altering size (atrophy/hypertrophy), number (hyperplasia), and form (metaplasia).

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Metaplasia

Replacement of one adult cell type with another.

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Differentiation gene

A gene that causes cells to become specialized.

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Allostasis

Processes by which the body responds to stressors to regain homeostasis.

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Carcinoma

Cancer that begins in the skin or tissues that line or cover internal organs.

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Autocrine signaling (cancer)

Self-stimulation of cancer cells.

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Paracrine signaling (cancer)

Communication between cancer cells and their neighbors.

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Muscle wasting (cachexia)

Breakdown of muscle tissue due to lack of protein.

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Edema in protein deprivation

Fluid imbalances and swelling, especially in the abdomen and lower extremities, due to reduced albumin.

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Effects of protein deprivation in children

Growth retardation, developmental delays, and reduced immune function in children.

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Necrosis

Cell death in a living person's organ or tissue.

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Gangrene

Tissue death due to lack of blood supply.

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Atrophy

Decrease in cell size, often due to disuse or decreased blood flow.

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Hypertrophy

Increase in cell size, often due to increased workload.

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Hyperplasia

Increase in the number of cells in a tissue or organ.

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Dysplasia

Abnormal changes in cell size, shape, and organization in a tissue.

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Ghrelin

Hormone that stimulates appetite.

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Leptin

Hormone produced by fat tissue; helps regulate energy balance by inhibiting hunger.

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Skin Boundary Surfaces

First line of defense = physical and chemical barriers against pathogens

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Complement System

System in blood, essential for antibody activity; causes fluid shift from blood to tissues during shock.

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Marasmus

Severe calorie and protein deficiency. Symptoms include wasting of muscles and very thin appearance.

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Kwashiorkor

Adequate calorie intake but severe protein deficiency. Causes edema, especially in the abdomen.

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Type II Hypersensitivity

Antibodies bind to cell surfaces, causing inflammation and cell damage via complement activation or phagocytosis.

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Type III Hypersensitivity

Immune complexes deposit in tissues, causing inflammation and tissue damage via complement activation.

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Vascular Permeability

Shift of fluid from blood to tissues leading to hypovolemia and hypotension.

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Cardiac compensation in shock

Increased heart rate to maintain cardiac output in response to hypotension.

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Oliguria/Anuria in Shock

Systemic hypoperfusion leads to reduced urine output to retain cardiovascular volume.

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Autoimmune Response

Reaction against self; inflammation, opsonization, lysis of cells causing autoimmune disorders.

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Hypoxia leading to Hypercapnia in shock

Decreased systemic perfusion leading to hypoxia and hypercapnia then multisystem failure.

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Study Notes

  • A1 - UNIT 1

Immunosuppressant Disorders: HIV/AIDS

  • Etiology: HIV transmission occurs via bodily fluids.
  • Pathogenesis: HIV targets and destroys CD4 WBCs, leading to altered immune function and opportunistic infections, malignant tumors, nervous system manifestations, wasting syndrome, and metabolic disorders.
  • Clinical Manifestations: HIV-infected individuals can remain asymptomatic while still circulating immune cells; immunosuppression develops when circulating cells drop below a critical level (CD4 WBC<200), leading to AIDS diagnosis.

Autoimmune Disorders

  • Etiology: The immune system fails to distinguish self from non-self.
  • Pathogenesis: Autoantibodies and immune complexes are formed, causing direct damage or forming tissue-damaging complexes with corresponding antigens.
  • Clinical Manifestations: Various conditions arise from auto immune failures
  • Systemic lupus erythematosus: Causes Inflammation and damage to tissues and organs.
  • Rheumatoid arthritis: Results in Inflammation of the joints
  • Grave's disease: Causes Thyroid gland damage, which leads to hyperthyroidism
  • Diabetes mellitus 1: Results in Destruction of insulin-producing beta cells
  • Autoimmune hemolytic anemia: Results in RBCs destruction
  • Pemphigus vulgaris: Causes painful blisters on skin and mucous membranes
  • Hashimoto's: Inflammation and damage to the thyroid gland

Hematopoietic Disorders: Clotting Disorders

  • Etiology: Hypercoagulability states and DIC.
  • Pathogenesis: Increased risk of clot or thrombus formation in arterial or venous circulations due to turbulent blood flow, platelet adherence, and increased coagulation factor concentration.
  • Clinical Manifestations: Inappropriate formation of blood clots within the vascular system.

Vascular Disorders

  • Etiology: Decreased circulating platelets and impaired platelet function.
  • Pathogenesis: Not explained

Vascular Disorders: Hereditary and Acquired Diseases

  • Hereditary diseases: Hemorrhagic telangiectasia (HHT) leads to thin-walled dilated capillaries and arterioles.
  • Scurvy: Poor collagen synthesis causes fragile endothelial cells.
  • Cushing disease: Protein wasting and loss of vessel tissue lead to excess cortisol.
  • Senile purpura: Aging.
  • Clinical Manifestation: Bleeding

Coagulation Defects

  • Etiology: Defective synthesis, inherited disease, or increased consumption of clotting factors.
  • Pathogenesis: Disruption in the normal cascade of blood clotting mechanisms.
  • Clinical Manifestations: Abnormal bleeding, bruising, or pain.

Infections

  • Etiology: Bacterial, viral, fungal, parasites (protozoa, helminths, arthropods).
  • Pathogenesis: Microorganisms invade and multiply in body tissues, causing local cellular injury through competitive metabolism, toxins, intracellular replication, or antigen-antibody response.
  • Clinical Manifestations: Fever, chills, fatigue, and pain alongside skin and changes in breathing/urination with accompanying inflammation

Altered Cellular Metabolism: Cancer

  • Etiology: Cell changes/damage, inherited traits, errors in cell division, environmental factors, and aging effects.
  • Pathogenesis:
  • Initiation: Cells become susceptible to malignant transformation upon exposure to carcinogenic agents
  • Promotion: Unregulated accelerated growth in already cells caused by various chemicals and growth factors
  • Progression: Tumor cells exhibit malignant phenotypic changes that promote invasiveness, metastatic competence, autonomous growth, and increased karyotypic instability
  • Clinical Manifestations: Tumor

Regulation: Neoplasms, Fluid and Electrolyte Imbalances and Acid/Base Imbalances

  • Etiology: Unspecified
  • Pathogenesis: Unspecified
  • Clinical Manifestations: Unspecified

Fluid Imbalances: Deficit

  • Etiology: Negative fluid balance due to diuretics, vomiting, diarrhea, and burns.
  • Pathogenesis:
  • Pure H20 Loss: Dehydration leads to hypernatremia
  • H20 and Na+ Loss: Hypovolemia reduces circulating volume which leads to ECF deficit
  • Clinical Manifestations:
  • Hypernatremia: Body compensates by increasing ADH production and stimulation of the thirst center.
  • ECF Deficit: Body activates ADH, atrial receptor suppression, and RAAS to retain H20 and Na+.

Fluid Imbalances: Excess

  • Etiology: Fluid volume excess from disease states (HF, liver cirrhosis, kidney disease/injury) and excessive IV therapy.
  • Pathogenesis:
  • Imbalance of fluid intake and output causes body to retain more H20
  • HF: Decreased tissue perfusion causes retention of H20 and NA
  • Liver Cirrhosis: Decreased renal perfusion causes retention of H20 and NaCl
  • Kidney Disease: Acute kidney injury leads to fluid, electrolyte, and acid-base or chronic kidney injury prevents fluid removal
  • Excessive IV Fluids: Hypervolemia may cause an acute kidney injury
  • Clinical Manifestations: Development of Peripheral edema, pulmonary edema, pleural effusion, ascites, and hypervolemia.

Electrolyte Imbalances: Hyponatremia

  • Normal Range: (135-145)
  • Etiology: Renal and external fluid loss (vomiting, diarrhea, third spacing) and increased ADH secretion, excess IV fluids or H20, and increase total body weight and Na+.
  • Types and Pathogenesis:
  • Hypovolemic Hyponatremia: ADH increases to maintain vascular volume causing kidneys to retain water, which exacerbates Na+ deficit
  • Euvolemic Hyponatremia: Total body weight increases without changes to Na+ or ECF
  • Hypervolemic Hyponatremia: Total body weight > Na+ leading to cellular edema
  • Clinical Manifestations: High Urine Sodium Concentration, etc...
  • Stupor/coma, anorexia, lethargy, tachycardia, muscle weakness, orthostatic hypotension, seizure, HA and stomach cramping

Electrolyte Imbalances: Hypernatremia

  • Etiology: Intake of high-Na+ foods or drinks, excessive fluid loss through the body system, insufficient fluid intake.
  • Pathogenesis:
  • Hypervolemia: Increased Na+ and H20 in ECF causes to moves out of cells which leads to cell shrink
  • Euvolemic Hypernatremia: Osmolality (concentration) of ECF increases, and H20 moves out of cells to equalize ECF and ICF
  • Hypovolemic Hypernatremia: Na+ and H20 are decreased from the ECF which leads to loss in the ECF
  • Clinical Manifestations: Flushed skin, restlessness, anxiety, edema etc

Potassium Imbalances

Hypokalemia

  • Normal Range: (3.5-5.0)
  • Etiology: Poor dietary intake, excessive losses (renal and GI), or fluid compartment shifts.
  • Pathogenesis: ECF K+ increases, and the kidneys excrete K+ by releasing aldosterone.
  • Clinical Manifestations: N/v, EKG changes (flat/inverted T wave), decreased reflexes, hypotension etc...

Hyperkalemia

  • Etiology: Metabolic acidosis, cellular injury, DKA, or impaired potassium excretion.
  • Pathogenesis:
  • K+ shifts from ICF to ECF or as a result of Inadequate insulin which causes K+ to shift from ICF to ECF, or impaired excretion.
  • Clinical Manifestations: Muscle cramps/weakness, urine abnormalities, respiratory distress etc...

Magnesium Imbalances

Hypomagnesemia

  • Normal Range: (1.1-3)
  • Etiology: Poor intake and/or impaired absorption from GI tract, phytic acids, PPIs, Calcium phosphate, fats, etc. Also, kidney with creatinine clearance <20 mL/min.
  • Pathogenesis: Lowers Mg affects cardiovascular function, electrical activity, vascular tone.
  • Clinical Manifestations: Cardiac dysrhythmias

Hypermagnesemia

  • Etiology: Ingestion of Na+ and vitamin D, Hormones like growth hormone, parathormone and thyroid hormone, acute or chronic kidney disease
  • Pathogenesis: inhibits electrophysiological function and affects hemodynamic stability of cardiovascular, release of acetlycholine affects neurological
  • Clinical Manifestations: Cardiac & Neuroligical

Calcium Normal Range (9-11) and Calcium Imbalances

Hypocalcemia

  • Etiology: Decreased Parathyroid hormone, or from Hyopmagnesemia.
  • Also form alkalosis, low Vit D, Calcitonin, and/or Pancreatitis
  • Pathogenesis: Injury/removal of Parathyroid, or from HypoMg+
  • Also from Low Vit D preventing reabsorption.
  • Clinical Manifestations: Possible life-threatening seizures and Cardiac Dysrhythmias

Respiratory & Metabolic Acidosis and Alkalosis

Respiratory Acidosis

  • Etiology: Hypoventilation and increased physiological dead space
  • Pathogenesis: pH < 7.35 and ↑CO2 → ↑ H+ concentration in the blood
  • Clinical Manifestations: Compensation = simulation of ventilation to normalize C02 / HCO3 levels. If prolonged or increase in ICP

Respiratory Alkalosis

  • Etiology: Hyperventilation: decreased carbonic acid, cerebral vasoconstriction, less O2
  • Pathogenesis: pH > 7.35 and ↓CO2 → ↓ H+ concentration in the blood
  • Clinical Manifestations: Compensation = excreting HCO3 through kidneys

2. Differentiate between Pathophysiological Changes and Identify Regulatory and Compensatory Mechanisms

  • Pathophysiological changes & regulatory/compensatory functions for maintaining homeostasis, the cellular environment, nutrition
  • Also, for hemostasis, immunity, stress, and coping. (CO 2, 4)
  • Insufficient gas exchange
  • Hypoxemia
  • Hypercapnia
  • Renal and respiratory compensation

The cellular environment: Pathophysiological changes - cell injury

  • Physical/Biological agents:
  • extreme temperatures
  • electrical injuries
  • Nutrition imbalances: excesses or deficiencies
  • Radiation: ionized RT, UV light, non-ionizing RT
  • Regulatory Mechanisms
    • Reversible injury = impairs cell function, doesn't kill
    • Cellular Swelling
      • not enough O2 increases anaerobic metabolism & decreases ATP to cause disruption in cellular functions such as cellular swelling resulting in edema.
    • Fatty Change = Accumulation

Apoptosis & Necrosis

  • Apoptosis = programmed cell death, aka suicide.
    • cells age, cell injury and damage
  • Necrosis = unprogrammed cell death while organ/tissue is attached to living person -intereference in cell repair/replacement

Tissue integrity

  • altered for:
  • atrophy: decreases in cell size
  • hypertrophy: increases in cell size
  • hyperplasia: increase in cell numbers
  • metaplasia: Transformation
  • dysplasia: abnormal growth

4. Explore Alterations in Nutrition

  • Pathophysiological: weight loss, muscle wasting, weakness, dry skin, and dehydration due to inadequate food intake.
  • Compensatory: Eating behaviors or altered metabolic processes

Maintaining Hemostasis

  • process of clotting
  • Compensatory: Regulated food intake

Immunity Alterations

  • Pathophysiological - body attacks its own cells, or recognizes and removes mutated/cancerous cells Regulatory - skin is the first line of defense to prevent pathogen invasions Compensatory - inflammatory response to vasodilation and fluids flowing into areas of injury

Stress Alterations

Pathophysiological - cardiovascular, neurologic Regulatory - the stages of adaptation to stress (alarm, resistance, and exhaustion)

3. Differentiate between the manifestations and outcomes of inflammation

  • Causes: immunological
  • Manifestations: (4 potential outcomes), injury, infection, or allergy

Distributive Types of Shock

  • Anaphylactic - hypersensitivity/allergy
  • Neurogenic- loss of sympathetic
  • Septic- inflammatory mediators

Anemia

  • Pernicious Anemia - genetic
  • low levels of B12
  • affects DNA synthesis
  • can cause megaloblastic alteration and neurological
  • Folate-deficiency Anemia
  • affects DNA, but lacks neurological

Edema

  • fluid in tissues

Abnormal PTH

  • low lvls of Ca

Magnesemia

  • absorbed in GI tract
  • affects function

Carcinoma

  • Genetic Alterations
  • altered cellular communication

protein alterations

  • causes tissue damage

SLE & autoimmune response

  • body attacks itself

Gas Exchange-

-results from the lack of oxygen

Elimination-

-elimination from the kidneys

Cognition-

-altered due to the lack of neurons

Mobility-

-Mobilityperipheral arterial disease reduces the mobility

Nutrition-

Patient Education-

-the importance of walking and a healthy lifestyle

Type III hypersensitivity and Systemic Lupus Erythematosus (SLE):

What is SLE: is an autoimmune disease where the body's immune system mistakenly attacks its own cells and tissues ==END OF SUMMARY==

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