Podcast
Questions and Answers
Which of the following accurately describes the pathogenesis of HIV/AIDS?
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?
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?
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?
Which of the following is a common clinical manifestation observed with HIV/AIDS due to its pathogenesis?
Which of the following is NOT a typical etiological factor for HIV/AIDS?
Which of the following is NOT a typical etiological factor for HIV/AIDS?
What is the primary effect of increased vascular permeability during inflammation?
What is the primary effect of increased vascular permeability during inflammation?
Which of the following compensatory mechanisms is directly triggered by acute systemic hypoperfusion?
Which of the following compensatory mechanisms is directly triggered by acute systemic hypoperfusion?
How does the renal system typically respond to maintain function during the initial stages of hypoperfusion?
How does the renal system typically respond to maintain function during the initial stages of hypoperfusion?
What is the purpose of peripheral vasoconstriction in response to hypovolemia?
What is the purpose of peripheral vasoconstriction in response to hypovolemia?
What is the effect of antibodies on bacteria that makes them more susceptible to phagocytosis?
What is the effect of antibodies on bacteria that makes them more susceptible to phagocytosis?
Which of the following is a key differentiating factor between pernicious anemia and folate-deficiency anemia?
Which of the following is a key differentiating factor between pernicious anemia and folate-deficiency anemia?
Increased capillary hydrostatic pressure contributes to edema by which mechanism?
Increased capillary hydrostatic pressure contributes to edema by which mechanism?
How does alkalosis contribute to hypocalcemia?
How does alkalosis contribute to hypocalcemia?
Which of the following factors primarily influences magnesium metabolism?
Which of the following factors primarily influences magnesium metabolism?
How does hypermagnesemia affect neurological function?
How does hypermagnesemia affect neurological function?
Which hormone directly prevents osteoclast function, impacting calcium levels?
Which hormone directly prevents osteoclast function, impacting calcium levels?
Certain medications, pregnancy and alcohol use are factors for which type of anemia?
Certain medications, pregnancy and alcohol use are factors for which type of anemia?
What type of cellular adaptation involves the replacement of one type of adult cell with another?
What type of cellular adaptation involves the replacement of one type of adult cell with another?
How does allostasis contribute to maintaining homeostasis in the body when facing stressors?
How does allostasis contribute to maintaining homeostasis in the body when facing stressors?
What is the primary role of altered autocrine and paracrine signaling in carcinoma cells?
What is the primary role of altered autocrine and paracrine signaling in carcinoma cells?
In carcinoma cells, what is the effect of overexpressed or mutated growth factor receptors found on the cell surface?
In carcinoma cells, what is the effect of overexpressed or mutated growth factor receptors found on the cell surface?
How does protein deprivation affect the body's ability to maintain essential physiological functions?
How does protein deprivation affect the body's ability to maintain essential physiological functions?
Why does protein deprivation lead to edema, particularly in the abdomen and lower extremities?
Why does protein deprivation lead to edema, particularly in the abdomen and lower extremities?
Which of the following is a consequence of enzyme deficiencies resulting from protein deprivation?
Which of the following is a consequence of enzyme deficiencies resulting from protein deprivation?
Which of the following scenarios would most likely lead to cellular necrosis?
Which of the following scenarios would most likely lead to cellular necrosis?
What is the long-term effect of a negative nitrogen balance caused by protein deprivation?
What is the long-term effect of a negative nitrogen balance caused by protein deprivation?
Gangrene, a form of cell death, directly impacts which aspect of cellular function?
Gangrene, a form of cell death, directly impacts which aspect of cellular function?
How might severe protein deprivation impact liver function in children?
How might severe protein deprivation impact liver function in children?
Which of the following cellular adaptations is most likely a reversible response to a temporary increase in physical exertion?
Which of the following cellular adaptations is most likely a reversible response to a temporary increase in physical exertion?
A patient experiences a prolonged period of malnutrition. Which of the following compensatory mechanisms is least likely to occur?
A patient experiences a prolonged period of malnutrition. Which of the following compensatory mechanisms is least likely to occur?
In the process of hemostasis, what is the primary role of vasoconstriction?
In the process of hemostasis, what is the primary role of vasoconstriction?
Which of the following best describes the role of nitric oxide (NO) in hemostasis?
Which of the following best describes the role of nitric oxide (NO) in hemostasis?
If a patient has a condition that impairs their ability to produce thromboxane A2, which of the following is most likely to occur?
If a patient has a condition that impairs their ability to produce thromboxane A2, which of the following is most likely to occur?
What is the primary function of complement proteins as part of the body's first line of immune defense?
What is the primary function of complement proteins as part of the body's first line of immune defense?
Which of the following is an example of the body’s regulatory mechanism in response to bleeding?
Which of the following is an example of the body’s regulatory mechanism in response to bleeding?
Which statement describes the role of the body's immune compensatory mechanisms in the presence of cell mutations?
Which statement describes the role of the body's immune compensatory mechanisms in the presence of cell mutations?
During shock, the complement system contributes to hypovolemia and hypotension by:
During shock, the complement system contributes to hypovolemia and hypotension by:
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?
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?
What is the primary nutritional issue in marasmus, differentiating it from kwashiorkor?
What is the primary nutritional issue in marasmus, differentiating it from kwashiorkor?
Edema is a distinguishing feature of kwashiorkor but not typically of marasmus. What explains the presence of edema in kwashiorkor?
Edema is a distinguishing feature of kwashiorkor but not typically of marasmus. What explains the presence of edema in kwashiorkor?
In Type II hypersensitivity reactions, how do antibodies typically cause cell damage?
In Type II hypersensitivity reactions, how do antibodies typically cause cell damage?
Which of the following mechanisms primarily mediates tissue damage in Type III hypersensitivity reactions?
Which of the following mechanisms primarily mediates tissue damage in Type III hypersensitivity reactions?
What is the fundamental difference in the causes of Type II and Type III hypersensitivity reactions?
What is the fundamental difference in the causes of Type II and Type III hypersensitivity reactions?
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?
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?
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?
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?
How does the renal system initially respond to hypoperfusion during shock, and how can this response become maladaptive?
How does the renal system initially respond to hypoperfusion during shock, and how can this response become maladaptive?
Flashcards
Etiology
Etiology
The study of the causes or origins of diseases or disorders.
Pathogenesis
Pathogenesis
The manner in which a disease develops.
Immunosuppression
Immunosuppression
Suppression of the immune system's ability to fight infection.
HIV
HIV
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AIDS
AIDS
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Bacterial Aggregation
Bacterial Aggregation
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Vascular Permeability Impact
Vascular Permeability Impact
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Nervous System Response
Nervous System Response
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Acute Systemic Hypoperfusion
Acute Systemic Hypoperfusion
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Renal System Response
Renal System Response
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Pernicious Anemia
Pernicious Anemia
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Folate-Deficiency Anemia
Folate-Deficiency Anemia
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Edema
Edema
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Hypocalcemia Pathogenesis
Hypocalcemia Pathogenesis
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Hypomagnesemia
Hypomagnesemia
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Hypermagnesemia
Hypermagnesemia
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Cellular Adaptation
Cellular Adaptation
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Metaplasia
Metaplasia
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Differentiation gene
Differentiation gene
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Allostasis
Allostasis
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Carcinoma
Carcinoma
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Autocrine signaling (cancer)
Autocrine signaling (cancer)
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Paracrine signaling (cancer)
Paracrine signaling (cancer)
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Muscle wasting (cachexia)
Muscle wasting (cachexia)
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Edema in protein deprivation
Edema in protein deprivation
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Effects of protein deprivation in children
Effects of protein deprivation in children
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Necrosis
Necrosis
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Gangrene
Gangrene
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Atrophy
Atrophy
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Hypertrophy
Hypertrophy
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Hyperplasia
Hyperplasia
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Dysplasia
Dysplasia
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Ghrelin
Ghrelin
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Leptin
Leptin
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Skin Boundary Surfaces
Skin Boundary Surfaces
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Complement System
Complement System
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Marasmus
Marasmus
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Kwashiorkor
Kwashiorkor
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Type II Hypersensitivity
Type II Hypersensitivity
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Type III Hypersensitivity
Type III Hypersensitivity
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Vascular Permeability
Vascular Permeability
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Cardiac compensation in shock
Cardiac compensation in shock
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Oliguria/Anuria in Shock
Oliguria/Anuria in Shock
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Autoimmune Response
Autoimmune Response
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Hypoxia leading to Hypercapnia in shock
Hypoxia leading to Hypercapnia in shock
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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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