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Questions and Answers
What is the effect of angiotensin II on blood pressure?
What condition is characterized by the excessive secretion of anti-diuretic hormone (ADH)?
In metabolic acidosis, what typically characterizes the anion gap?
What causes respiratory alkalosis?
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What is the main physiological effect of aldosterone?
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What happens in Diabetes Insipidus in terms of urine concentration?
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What causes metabolic alkalosis?
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What is a typical symptom of hyponatremia due to excessive ADH secretion?
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What is the primary role of aldosterone in blood pressure regulation?
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Which structure is primarily responsible for the reabsorption of most ions in the nephron?
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How does the countercurrent mechanism in the Loop of Henle affect urine concentration?
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What triggers the release of renin from the Juxtaglomerular Apparatus (JGA)?
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What is the primary action of anti-diuretic hormone (ADH) in the nephron?
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Which effect does decreased GFR have on blood volume and blood pressure?
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Which of the following correctly describes the tubular secretion process?
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What is the main difference between tubular reabsorption and excretion?
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What is the primary difference between necrosis and apoptosis?
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Which of the following is NOT considered a hallmark of cancer?
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Which characteristic is common to benign neoplasms?
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Which of the following factors can lead to cell injury?
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What describes hyperkalemia?
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What effect does increased capillary permeability have on the body?
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Which of these conditions is characterized by low sodium levels?
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Which process leads to lipid peroxidation and damage to cell membranes?
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How does malignant neoplasm differ from benign neoplasm?
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Which extracellular ions are typically found at higher concentrations outside the cell?
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What is the primary consequence of decreased GFR in terms of blood pressure regulation?
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Which part of the nephron is primarily responsible for the dilution of urine?
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What physiological process primarily occurs in the thick ascending limb of the Loop of Henle?
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What effect does aldosterone have on the kidneys?
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How does the presence of anti-diuretic hormone (ADH) influence urine concentration?
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What is a normal ejection fraction percentage?
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What could lead to increased heart rate as a compensatory mechanism?
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Which layer of the heart is primarily responsible for its pumping action?
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Which of the following represents the normal range for cardiac output?
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Which mechanism does the Frank-Starling mechanism increase?
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What is the role of the SA node in the heart?
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What is a major consequence of atherosclerosis?
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Which structure is located in the pericardial cavity?
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What does increased stroke volume indicate?
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What is a potential effect of ventricular remodeling?
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What is the effect of inadequate ADH secretion on urine composition?
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Which process contributes to the development of metabolic acidosis?
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What happens to sodium levels in the syndrome of inappropriate ADH secretion (SIADH)?
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Which of the following correctly identifies a condition associated with respiratory acidosis?
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How does the anion gap help to diagnose the cause of metabolic acidosis?
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What common result occurs from an excessive concentration of aldosterone?
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What is a characteristic feature of metabolic alkalosis?
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What physiological change occurs during hypernatremia due to inadequate ADH?
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What is the primary function of IgG antibodies?
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Which stage of infectious disease is characterized by initial exposure to the onset of first symptoms?
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What type of immunity occurs when antibodies are received from an external source?
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What is a significant outcome of endotoxic shock caused by Gram-negative bacteria?
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Which immunoglobulin is primarily found in the gastrointestinal, respiratory, and genitourinary tracts?
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How does HIV infect a CD4+ T cell?
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What is the immediate response antibody that indicates acute exposure to an antigen?
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What major effect does opsonization have on phagocytosis?
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During which stage of an infectious disease does initial discomfort and fatigue occur?
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What is NOT a characteristic of passive immunity?
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What characterizes a true aneurysm?
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Which of the following is a common cause of varicose veins?
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What is a primary symptom of chronic venous insufficiency?
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Which statement accurately describes deep vein thrombosis (DVT)?
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Which of the following best describes coronary artery disease (CAD)?
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What is one of the non-traditional risk factors for coronary artery disease?
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In acute coronary syndrome, what triggers the sudden coronary obstruction?
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What is a primary characteristic of a false aneurysm?
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Which symptom indicates the risk of venous stasis ulcers?
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Which of the following is a risk factor for developing deep vein thrombosis?
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Which condition is indicated by the significant obstruction leading to urine build-up in the kidney?
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What does increased plasma creatinine levels indicate in terms of renal function?
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Which of the following symptoms are characteristic of nephrotic syndrome?
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In cases of acute glomerulonephritis, which clinical manifestation is expected?
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What effect do diuretics have on renal function?
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What characterizes innate immunity?
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What is the role of mast cells in inflammation?
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Which cells are primarily involved in communicating between the innate and adaptive immune systems?
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What is a primary function of cytokines in the immune response?
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What component of the immune response is activated to prevent the spread of infection?
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Which type of immune cell is responsible for rapid response to virus-infected cells?
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What effect does bradykinin have in the immune response?
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Which of the following statements is true about the complement system?
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Which symptom is primarily associated with right heart failure?
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What condition is characterized by impaired left ventricle pumping?
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Which clinical manifestation is typical for diastolic heart failure?
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How does the renal system primarily maintain homeostasis?
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What is a key feature of the kidneys regarding urine formation?
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What role does the renal capsule play in kidney function?
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Which blood condition is commonly associated with renal hormone secretion?
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What is the primary consequence of increased hydrostatic pressure in the pulmonary vascular bed?
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Which structure within the kidney mainly participates in urine excretion?
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What results from decreased compliance in the left ventricle?
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What is the primary effect of renin release from the Juxtaglomerular Apparatus (JGA)?
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Which part of the nephron is primarily responsible for the secretion of hydrogen ions and contributes to acid-base balance?
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What effect does the countercurrent mechanism in the Loop of Henle have on urine formation?
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What is the role of aldosterone in blood pressure regulation?
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What effect does anti-diuretic hormone (ADH) have on the distal convoluted tubule and collecting duct?
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Which physiological process occurs primarily in the thick ascending limb of the Loop of Henle?
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How does a decreased glomerular filtration rate (GFR) affect blood pressure?
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Which part of the nephron is primarily responsible for the reabsorption of most ions?
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What is the main result of tubular secretion in the nephron?
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What is the primary function of principal cells in the collecting duct?
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What defines unstable angina?
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Which type of myocardial infarction requires immediate intervention?
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Which of the following is a common cause of heart failure?
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What is a characteristic symptom of silent ischemia?
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What mechanism helps compensate for heart failure by increasing heart rate and peripheral vascular resistance?
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What type of angina is described as increasing in frequency, duration, or severity during minimal activity?
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Which condition is commonly recognized as the most prevalent form of heart failure?
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Which neurohormonal mechanism involves vasoconstriction and renal fluid retention?
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What does myocardial ischemia develop from?
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Which of the following best illustrates a characteristic feature of dyspnea in heart failure?
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Study Notes
Blood Pressure Regulation
- Angiotensin II causes vasoconstriction, increasing blood pressure.
- Aldosterone promotes sodium and water retention by the kidneys, increasing extracellular fluid volume and blood pressure.
- Antidiuretic hormone (ADH) is secreted by the posterior pituitary gland and promotes water reabsorption in the kidneys, leading to concentrated urine and reduced water loss.
Syndrome of Inappropriate ADH Secretion (SIADH)
- Excessive ADH secretion results in overly concentrated urine and excessive water retention.
- Leads to hyponatremia (low sodium levels in the blood).
Inadequate ADH - Diabetes Insipidus
- Results in excessively dilute urine due to excessive water loss.
- Leads to hypernatremia (high sodium levels in the blood).
Acid-Base Balance
- Even slight changes in hydrogen ion concentration can disrupt metabolic reactions, ion distribution, and hormone function.
Metabolic Acidosis
- Characterized by low pH, normal CO2, and low bicarbonate levels.
-
Anion gap helps determine the cause:
- Normal anion gap (12 mmol/L): Chronic diarrhea, pancreatic issues, renal tubular acidosis.
- Elevated anion gap: Excessive acid buildup (lactic acidosis, ketoacidosis, renal failure, medications, inherited metabolic disorders).
Metabolic Alkalosis
- Characterized by high pH, normal CO2, and high bicarbonate levels.
- Caused by loss of acid from the blood or excess bicarbonate (excessive vomiting, hyperaldosteronism, diuretics).
Respiratory Acidosis
- Characterized by low pH, high CO2, and normal bicarbonate levels.
- Caused by excessive carbon dioxide buildup (hypoventilation, respiratory depression, obstructive disease).
Respiratory Alkalosis
- Characterized by high pH, low CO2, and normal bicarbonate levels.
- Caused by excessive CO2 loss (hyperventilation, altitude sickness, panic attacks).
Cell Adaptation
- Cells can adapt to stress, but if the stress is too severe, it can lead to injury or death.
Cell Injury
- Cell injury can be caused by:
- Hypoxia/Ischemia (lack of oxygen)
- Chemical agents (drugs, alcohol)
- Physical agents (trauma, heat, radiation)
- Infections
- Psychosocial stress
- Genetic defects
- Nutritional defects
- Aging
Free Radicals
- Chemically unstable molecules that damage other molecules.
- They are created by ionizing radiation, redox reactions, metabolism, or exogenous substances.
- They can cause:
- Lipid peroxidation (membrane damage)
- Protein modification (increased degeneration or loss of activity)
- DNA damage (mutations)
Cell Death
- Necrosis: Uncontrolled, disorderly cell death; requires no energy; cellular contents leak out; inflammation present.
- Apoptosis: Controlled, orderly cell death; requires energy; cellular contents are packaged into apoptotic bodies for digestion; no inflammation; usually physiological (cell turnover).
Neoplasms
- Benign: Cells resemble normal tissue; slow growth; pushes on but does not invade surrounding tissue; does not metastasize.
- Malignant: Cells lack differentiation of normal cells; can grow slowly or quickly; invades surrounding tissues; metastasizes.
Hallmarks of Cancer
- Self-sufficiency in growth signals
- Insensitivity to growth inhibition
- Altered cellular metabolism
- Evasion of apoptosis
- Immortality
- Sustained angiogenesis (formation of new blood vessels)
- Ability to invade and metastasize
- Ability to evade the human immune response
How Cancer Spreads
- Invasion: Cancer cells move through the walls of nearby blood vessels or lymph nodes.
- Metastasis: Cancer cells grow in new tissue until a tiny tumor forms; create blood supply, allowing further growth.
Fluid Regulation
- Intracellular fluid is inside the cells.
- Extracellular fluid is divided into interstitial fluid (between cells) and intravascular fluid (within blood vessels).
Intracellular & Extracellular Ions
- Intracellular fluid: High concentration of potassium (K+), phosphate, and organic ions.
- Extracellular fluid: High concentration of sodium (Na+), chloride (Cl-), and bicarbonate (HCO3-)
Ion Imbalances
- Hypernatremia: High sodium levels in the blood; symptoms include thirst, confusion, neuromuscular excitability, seizures, and coma.
- Hyponatremia: Low sodium levels in the blood; symptoms include headache, confusion, stupor, seizures, and coma.
- Hyperkalemia: High potassium levels in the blood; symptoms include progressive muscle weakness, placid paralysis, and arrhythmia.
- Hypokalemia: Low potassium levels in the blood; symptoms include spastic paralysis, fatigue, cramps, and arrhythmia.
- Hypercalcemia: High calcium levels in the blood; symptoms include cognitive changes, confusion, coma, muscle weakness, and arrhythmias.
- Hypokalemia: Low calcium levels in the blood; symptoms include irritability, anxiety, paresthesia (numbness or tingling), bronchospasms, heart failure, and muscle cramps.
Capillaries & Leaky Syndrome
- Capillaries can become leaky, increasing capillary permeability.
- Causes include infection, medications, inflammation, and burns.
- Leakage allows water, ions, proteins, and cells to move into the interstitial space.
Fluid Pressure
- Hydrostatic pressure: Pressure exerted by a fluid against a barrier (e.g., blood vessel wall).
- Oncotic pressure: Osmotic pressure generated by large molecules, like proteins, attracting water.
Decreased Glomerular Filtration Rate (GFR)
- Decreases excretion of sodium and water.
- Leads to an increase in blood volume, which increases blood pressure.
Renin-Angiotensin-Aldosterone System (RAAS)
- Renin, released from the juxtaglomerular apparatus (JGA) when blood pressure or GFR is low, triggers the formation of angiotensin.
- Angiotensin stimulates the release of aldosterone from the adrenal cortex.
- Aldosterone causes vasoconstriction, increased thirst, and antidiuretic hormone secretion, all of which increase blood pressure and/or blood volume.
Tubular Reabsorption & Secretion
- Tubular reabsorption: Movement of fluids and solutes from the tubular lumen to the peritubular capillary plasma.
- Tubular secretion: Movement of fluids and solutes from the capillary to the tubular lumen.
Nephron Segments & Function
- Proximal Convoluted Tubule (PCT): Reabsorption of most ions.
-
Loop of Henle:
- Thin Descending Limb: Highly permeable to water.
- Thick Ascending Limb: Actively transports ions into the interstitium, leading to diluted urine passing into the distal convoluted tubule (DCT).
- Distal Convoluted Tubule (DCT): Reabsorption and secretion of ions; creates dilute fluid; secretes H+, contributing to acid-base balance.
- Collecting Duct: Principal cells reabsorb Na+ and water, secrete K+; intercalated cells secrete H+ and reabsorb K+.
Urine Concentration & Dilution
- Concentration: Countercurrent mechanism in the loop of Henle; fluid flows in opposite directions along parallel loops, creating concentration gradients.
- Dilution: Antidiuretic hormone (ADH) decreases the permeability of the DCT and collecting ducts to water, allowing more water to move in and dilute the urine.
Blood Pressure Regulation
- Angiotensin II constricts arterioles, increasing blood pressure.
- Aldosterone causes the kidneys to retain sodium and water, expanding extracellular fluid volume and raising blood pressure.
Antidiuretic Hormone (ADH)
- Secreted by the posterior pituitary gland.
- Promotes the production of concentrated urine to reduce water loss.
- Syndrome of inappropriate ADH secretion (SIADH) results in excess ADH secretion, leading to hyperconcentrated urine, water retention, and hyponatremia (low sodium levels).
- Diabetes insipidus occurs due to insufficient ADH, resulting in excessively dilute urine, excessive water loss, and hypernatremia (high sodium levels).
Acid-Base Balance
- Even slight deviations in hydrogen ion concentration can significantly alter metabolic reactions, ion distribution, and hormone function.
Metabolic Acidosis
- Characterized by an excessive buildup of acid or loss of bicarbonate.
-
Anion gap helps identify the cause:
- Normal anion gap (12 mmol/L): Occurs in conditions like chronic diarrhea, pancreatic issues, and renal tubular acidosis.
- Elevated anion gap (above 12 mmol/L): Suggests an excessive buildup of acid due to causes such as lactic acidosis, ketoacidosis, renal failure, medications, or inherited metabolic disorders.
- Metabolic acidosis is characterized by low pH, normal CO2 levels, and low HCO3 levels.
Metabolic Alkalosis
- Occurs due to a loss of acid from the blood or an excess of bicarbonate.
- Common causes include excessive vomiting, hyperaldosteronism, and diuretic use.
- Metabolic alkalosis is characterized by high pH, normal CO2 levels, and high HCO3 levels.
Respiratory Acidosis
- Caused by an excessive buildup of carbon dioxide due to hypoventilation (inadequate breathing).
- Common causes include respiratory depression, airway obstruction, and chronic lung diseases.
- Respiratory acidosis is characterized by low pH, high CO2 levels, and normal HCO3 levels.
Respiratory Alkalosis
- Results from an excessive loss of carbon dioxide due to hyperventilation (rapid breathing).
- Causes include anxiety, altitude sickness, and panic attacks.
- Respiratory alkalosis is characterized by high pH, low CO2 levels, and normal HCO3 levels.
Body Fluid Compartments
- The human body consists of a large amount of water distributed between the intracellular and extracellular compartments (interstitial fluid and plasma).
- Ions and other solutes are maintained within these compartments through energy-dependent mechanisms.
Antibody Functions
- Antibodies play a critical role in immune defense. Their functions include:
- Neutralization: Binding and inactivating pathogens or toxins.
- Agglutination: Clumping pathogens together, facilitating their removal by phagocytes.
- Precipitation: Forming insoluble complexes with soluble antigens, aiding in their removal.
-
Indirect functions include:
- Complement activation: Triggering the complement cascade, leading to pathogen lysis.
- Opsonization: Coating pathogens to make them more recognizable to phagocytes.
Antibody Types
- IgG: The most abundant antibody, responsible for long-term immunity and transplacental transfer.
- IgA: Found in mucosal surfaces like the gastrointestinal, respiratory, and genitourinary tracts.
- IgM: The primary antibody produced during acute exposure, responsible for the initial immune response.
- IgE: Specializes in mediating allergic reactions and parasitic infections.
Passive Immunity
- A type of immunity acquired by receiving antibodies from another source rather than producing them through the individual's immune system.
- Immunoglobulin transfer occurs through the placenta or colostrum.
- Offers temporary protection, lasting only weeks or months.
Stages of Infectious Disease
- Incubation period: The interval between initial exposure to the onset of symptoms; duration varies from hours to years.
- Prodromal stage: Marked by early, nonspecific symptoms, such as fatigue and discomfort.
- Invasion stage: Pathogens spread from the initial site of infection into other tissues.
- Covalescence stage: Convalescence phase, characterized by recovery, potential complications like death or latency.
Infectious Agents
- Infectious diseases are caused by various agents, including:
- Bacteria
- Viruses
- Protozoa
- Fungi
- Prions
- Parasites
Endotoxic Shock
- A severe form of septic shock triggered by bacterial endotoxins, primarily lipopolysaccharide (LPS) from the cell wall of Gram-negative bacteria.
-
Endotoxin release leads to:
- Cytokine storm: Massive production of pro-inflammatory cytokines.
- Tissue damage: Inflammation and tissue injury.
- Multi-organ failure: Widespread organ dysfunction and failure.
HIV Infection
- HIV targets CD4+ T cells (helper T cells).
- Viral entry: HIV binds to the CD4 receptor on the surface of the target cell and fuses with the cell membrane, releasing viral RNA and proteins into the host cell.
- Reverse transcription: The enzyme reverse transcriptase converts viral RNA into DNA.
- Viral integration: The newly formed viral DNA is transported to the host cell nucleus and integrated into the host's genome.
- Viral replication: The host cell's machinery is used to produce new viral RNA and proteins based on the integrated viral DNA.
- Viral assembly and release: Immature HIV particles bud off the host cell and mature into infectious virions.
- Immune system weakening: Repeated infection of CD4+ T cells weakens the immune system, increasing vulnerability to opportunistic infections.
- AIDS diagnosis: Confirmed when the CD4+ count falls below a specific threshold.
Cardiac Output
- The volume of blood pumped by the heart per minute.
- Cardiac output = Stroke volume x Heart rate (liters per minute).
- Normal cardiac output at rest: 5-6 liters per minute.
-
Factors influencing stroke volume:
- Increased stretch of cardiac muscle fibers: Leads to increased contraction and stroke volume up to a certain point.
- Ejection fraction: Percentage of blood ejected from the heart with each beat; normal ejection fraction is 50% or higher.
Compensatory Mechanisms for Low Cardiac Output
- Several mechanisms try to restore or increase cardiac output when it decreases:
- Increased heart rate: The heart beats faster to pump more blood.
- Increased stroke volume: The heart pumps more blood with each contraction.
- Increased cardiac muscle mass: Long-term adaptation to increased workload, leading to a larger and stronger heart.
- Increased blood volume: The body increases blood volume to enhance cardiac output.
- Increased cardiac filling pressure: The heart muscle stretches more before contraction, increasing stroke volume.
- Sympathetic nervous system activation: Release of catecholamines (adrenaline, noradrenaline) to constrict blood vessels and increase heart rate.
- Ventricular remodeling: Changes in ventricular size and thickness in response to increased workload.
- Neurohormonal system activation: The body activates various neurohormonal systems to maintain blood flow to essential organs.
- Frank-Starling mechanism: Increased stretch of cardiac muscle fibers enhances the force of contraction, improving cardiac output.
Heart Structure
- Epicardium: The outermost smooth layer, part of the pericardium.
- Myocardium: The muscular wall of the heart.
- Endocardium: The innermost layer lining the heart chambers.
-
Pericardium: A double-walled sac surrounding the heart:
- Parietal layer: The outer layer.
- Visceral layer: The inner layer, also known as the epicardium, adhering to the heart surface.
- Pericardial cavity: The space between the parietal and visceral layers, containing pericardial fluid (about 20 ml).
-
Functions of the pericardium:
- Prevents displacement of the heart during movement.
- Protects the heart from infection and inflammation.
- Contains receptors that regulate heart rate and blood pressure.
Cardiac Conduction System
- SA node: The pacemaker of the heart, generating electrical impulses at a rate of 60-100 beats per minute.
- Impulse conduction: The action potential travels from the SA node to the AV node, then to the Bundle of His, the right and left bundle branches, Purkinje fibers, and the ventricular apex.
- Ventricular contraction: The electrical impulses trigger ventricular contraction, pumping blood out of the heart.
Cardiac Conditions
Atherosclerosis
- A chronic inflammatory disease leading to thickening and hardening of the arteries.
- Endothelial dysfunction: Damage to the lining of blood vessels, initiating the process.
- Plaque formation: Accumulation of cholesterol, fat, and other substances within the artery walls.
- Plaque instability: The plaque can rupture, triggering thrombosis and vascular events like heart attack or stroke.
Aneurysms
- True aneurysm: Involves all three layers of the artery wall, weakening the wall and leading to localized dilation.
- False aneurysm: A blood clot formed outside the artery wall, creating a pulsating hematoma (collection of blood).
Varicose Veins
- Distorted, inflamed veins due to blood pooling.
- Typically affect the saphenous veins.
- Enlarged, twisted, and palpable veins.
- Caused by trauma or gradual venous distention, leading to valve incompetence.
- Increase the risk of blood clots.
Chronic Venous Insufficiency
- Inadequate venous return over an extended period, often caused by varicose veins or valve incompetence.
- Symptoms include pain, swelling, skin changes, venous stasis ulcers, and an increased risk of infection.
Deep Vein Thrombosis (DVT)
- A blood clot forming in a deep vein, usually the saphenous vein.
-
Virchow's triad: Contributing factors:
- Venous stasis: Slow blood flow in the veins.
- Venous endothelial damage: Injury to the lining of blood vessels.
- Hypercoagulable state: Increased tendency for blood clotting.
- DVT can dislodge (embolize) and travel to the lungs, causing pulmonary embolism (PE).
Coronary Artery Disease (CAD)
- Any vascular disease that narrows or blocks the coronary arteries, supplying blood to the heart.
- Imbalance: Occurs between the coronary blood supply and the heart's oxygen and nutrient demands.
- Atherosclerosis: The most common cause of CAD.
- Myocardial ischemia or infarction: Impaired blood flow to the heart muscle can cause ischemia (reduced oxygen supply) or infarction (heart attack).
Non-Traditional Risk Factors for CAD
- C-reactive protein: A marker of inflammation.
- Troponin I: A protein released from damaged heart muscle.
- Hyperhomocysteinemia: Elevated levels of homocysteine, an amino acid linked to cardiovascular disease.
- Adiponectin and leptin: Hormones released from adipose tissue (fat), associated with metabolic health.
- Microorganisms and periodontal disease: Chronic inflammation related to gum disease can increase cardiovascular disease risk.
- Air pollution: Exposure to pollutants can damage blood vessels and contribute to CAD.
- Coronary artery calcification and carotid wall thickness: These physical changes in blood vessels can indicate increased risk of CAD.
Acute Coronary Syndrome (ACS)
- A sudden event caused by coronary artery blockage, typically due to thrombus formation over a ruptured atherosclerotic plaque.
- Complications: Can lead to myocardial infarction, unstable angina, or sudden cardiac death.
Renal Function
- Glomerular filtration rate (GFR): The volume of fluid filtered by the kidneys per minute.
-
Decreased GFR:
- Reduces excretion of sodium and water.
- Increases blood volume, raising blood pressure.
Renin-Angiotensin-Aldosterone System (RAAS)
- A hormonal system regulating blood pressure and fluid balance.
- Renin: Released from the juxtaglomerular apparatus (JGA) in the kidneys in response to low blood pressure or GFR.
- Angiotensin I: Formed by renin's action on angiotensinogen.
- Angiotensin II: Converted from angiotensin I by angiotensin-converting enzyme (ACE).
- Aldosterone: Released from the adrenal cortex, triggered by angiotensin II.
-
Actions of aldosterone:
- Vasoconstriction: Narrowing blood vessels, increasing blood pressure.
- Increased thirst: Encouraging fluid intake.
- Antidiuretic hormone secretion: Promoting water retention.
Renal Tubule Transport
-
Tubular reabsorption: Movement of fluids and solutes from the tubular lumen to the peritubular capillary plasma.
-
Tubular secretion: Movement of substances from the capillaries to the tubular lumen.
-
Excretion: Elimination of waste products in the urine.
-
Proximal convoluted tubule (PCT): Responsible for the reabsorption of most ions, water, and nutrients.
-
Loop of Henle:
- Thin descending limb: Highly permeable to water.
- Thick ascending limb: Actively transports ions into the interstitium, creating a concentrated environment.
-
Distal convoluted tubule (DCT):
- Continues reabsorption and secretion of ions.
- Creates a dilute fluid.
- Secretes hydrogen ions (H+), contributing to acid-base balance.
-
Collecting duct:
- Principal cells: Reabsorb sodium and water, secrete potassium.
- Intercalated cells: Secrete hydrogen ions and reabsorb potassium.
Urine Concentration & Dilution
-
Concentration:
- Occurs primarily in the loop of Henle, DCT, and collecting duct.
- Countercurrent mechanism: Fluids flow in opposite directions along the parallel loops of Henle, creating concentration gradients. The longer the loops, the more concentrated the urine becomes.
-
Dilution:
- Regulated by antidiuretic hormone (ADH).
- ADH: Increases water permeability of the DCT and collecting ducts, allowing more water to move in and dilute the urine.
- Final adjustments: The distal tubule and collecting duct fine-tune the urine concentration and composition.
Immune Response
-
Adaptive immunity is highly specific.
- It can be immediate the second time an immune system is exposed to the same pathogen.
- Key cells - lymphocytes, macrophages and dendritic cells
- Memory cells help with a faster response during re-exposure.
- Peptides, antibodies and complement are involved in this process.
-
Innate immunity is broad, non-specific, and responds the same way every time.
- It comprises the first and second lines of defense – barriers and inflammation.
-
Inflammation involves various cells like mast cells, monocytes, neutrophils, dendritic cells, NK cells, and various substances like histamine, cytokines, clotting factors, complement, and kinins.
- Mast cells release histamine, causing vascular dilation and increased capillary permeability.
- Monocytes/macrophages surround and kill microorganisms, ingest foreign material, boost immune response, and remove dead cells.
- Granulocytes are the first responders to cellular injury/infection. They participate in phagocytosis and inflammation.
- Dendritic cells connect the innate and adaptive immune systems through cytokine communication by migrating to lymph nodes to present antigens to lymphocytes.
-
Cytokines can be pro- or anti-inflammatory.
- Interleukins are produced by white blood cells in response to antigens or inflammation.
- Interferons protect against viral infections and modulate inflammatory responses.
-
Plasma protein system
- Clotting prevents infection spread, traps microorganisms, and forms clots to stop bleeding.
- Kinins (like bradykinin) dilate blood vessels, cause smooth muscle contraction, increase vascular permeability, and white cell recruitment.
- Complement is made up of plasma proteins that can directly destroy pathogens or activate or collaborate with other inflammatory response components.
- NK cells are cytotoxic lymphocytes providing a rapid response to virus-infected cells and tumor formation by recognizing injured or infected cells. They release cytokines to trigger apoptosis in infected cells.
### Myocardial Ischemia
- Myocardial ischemia happens when coronary blood supply cannot meet the myocardium's oxygen and nutrient demands.
- Stable angina is predictable chest pain.
- Prinzmetal angina is unpredictable.
- Silent ischemia has no symptoms.
- Angina pectoris is short-lasting chest discomfort under the breastbone.
- Unstable angina can happen even at rest, lasts over 20 minutes, is new onset, or involves an increase in frequency, duration, or the amount of activity needed to trigger it. It indicates plaque rupture, potentially leading to infarction soon.
-
MI (myocardial infarction) There are two main types: subendocardial and transmural.
- STEMI requires immediate intervention.
- non-STEMI suggests that additional myocardium is at risk of recurrent ischemia or infarction.
Heart Failure
- Heart failure occurs when the heart's pumping or filling capacity is reduced, leading to reduced cardiac output and fluid buildup in the lungs.
- The heart becomes unable to adequately perfuse vital tissues.
Causes of Heart Failure:
- Coronary artery disease
- Myocardial infarction
- Hypertension
- Smoking
- Obesity
- Diabetes
- Cardiomyopathy
- Heart valve disease
- Congenital heart disease (common in pediatric cases)
- Arrhythmia
- Endocarditis
- Anemia
- Lung disease
- Certain medications
Neurohormonal Mechanisms Contributing to Heart Failure:
- Catecholamines increase heart rate and contractility.
- Vasopressin causes vasoconstriction and renal fluid retention.
- RAAS increases preload and afterload.
- Natriuretic peptides aim to decrease preload but are often ineffective in compensation.
- Cytokines are inflammatory and cause vasoconstriction.
Signs and Symptoms of Heart Failure:
-
Right-sided heart failure:
- Jugular venous distention (JVD)
- Peripheral edema
- Liver and spleen enlargement
- Ascites (fluid buildup in the abdomen)
- Gastrointestinal venous congestion: bloating, nausea, constipation, anorexia
- Fatigue and weakness
-
Left-sided heart failure:
- Dyspnea (shortness of breath) during exertion or at night
- Blood-tinged sputum
- Orthopnea (difficulty breathing when lying down)
- Cough
- Cyanosis (bluish skin discoloration)
- Rales/crackles (rales/crackles in lungs)
- Fatigue
- S3 gallop
- Oliguria (reduced urine output)
Systolic vs. Diastolic Heart Failure
-
Systolic heart failure is characterized by impaired left ventricle pumping, causing blood to back up into the atrium.
- The left atrium's capacity to accept blood from the pulmonary veins is reduced.
- Blood backs up in the pulmonary veins.
- Increased hydrostatic pressure in the pulmonary vascular bed leads to fluid accumulation in the interstitial and alveolar spaces, causing pulmonary congestion.
-
Diastolic heart failure is characterized by a decreased ejection fraction, reduced LV compliance and diastolic relaxation.
- Clinical manifestations include dyspnea on exertion and fatigue.
Diagnosis of Heart Failure:
- History and physical exam
- Labs
- EKG
- Chest X-ray
- WHO classification
- BNP
Renal System
-
The primary function of the kidneys is to maintain a stable internal environment for optimal cell and tissue metabolism.
-
Functions:
- Balancing solute and water transport.
- Excreting metabolic waste products.
- Conserving nutrients.
- Regulating acids and bases.
- Endocrine functions - by secreting hormones like:
- Renin (for blood pressure regulation).
- EPO (for red blood cell production).
- Vitamin D3 (for calcium metabolism).
- Gluconeogenesis (synthesizing glucose from amino acids).
-
Features of the genitourinary (GU) system:
- Urine formation is achieved through glomerular filtration, tubular reabsorption, and secretion within the kidneys.
- The bladder stores urine.
- Ureters transport urine from the kidneys to the bladder.
- Urine is removed through the urethra.
-
Kidney location and structure:
- Kidneys are paired organs located in the posterior region of the abdominal cavity behind the peritoneum.
- The renal capsule surrounds each kidney, which is embedded in a mass of fat.
- The outer layer of the kidney is the cortex containing glomeruli, most proximal tubules, and segments of distal tubules.
- The medulla forms the inner part of the kidney and consists of regions called pyramids.
- The apexes of the pyramids project into minor calyces that form major calyces.
- The major calyces join to form the renal pelvis.
-
Decreased GFR reduces excretion of Na and water, leading to increased blood volume and consequently higher blood pressure.
-
RAAS (Renin-Angiotensin-Aldosterone System):
- Renin is produced in the juxtaglomerular apparatus (JGA) and released when blood pressure or GFR are low.
- It triggers the formation of angiotensin, which stimulates aldosterone secretion from the adrenal cortex.
- Aldosterone causes vasoconstriction, increases thirst, and promotes anti-diuretic hormone secretion—all working to increase blood pressure and/or blood volume.
-
Tubular reabsorption refers to the movement of fluid and water from the tubular lumen back into the peritubular capillary plasma.
-
Tubular secretion is the movement of substances from the capillary lumen into the tubular lumen.
-
Excretion refers to the elimination of waste products in the final urine.
-
Specific functions of different parts of the nephron:
- Proximal convoluted tubule (PCT): Reabsorption of most ions.
-
Loop of Henle:
- Thin descending limb: Highly permeable to water.
- Thick ascending limb: Actively transports ions into the interstitium and passes urine into the DCT.
- Distal convoluted tubule (DCT): Reabsorption and secretion of ions, creating dilute fluid, secreting H+ to contribute to acid-base balance.
-
Collecting duct:
- Principal cells: Reabsorb Na and water, secrete K.
- Intercalated cells: Secrete H+ and reabsorb K.
-
Concentration and dilution of urine:
- Mostly happens in the loop of Henle, DCT, and collecting duct.
- Final adjustments are made by the distal tubule and collecting duct.
- Concentration: Countercurrent mechanism in the loop of Henle involves fluid flowing in opposite directions along parallel loops, creating concentration gradients—the longer the loop, the more concentrated the urine.
- Dilution: Anti-diuretic hormone (ADH) reduces the DCT and collecting duct's permeability to water, allowing more water to move in and dilute the urine.
-
Reabsorption predominantly occurs in the PCT and collecting duct.
-
Secretion occurs primarily in the PCT, loop, and DCT.
Renal Failure
-
Renal failure can lead to:
- Hypertension
- Edema
- Anemia
- Hypocalcemia
- Vitamin D deficiency
- Sometimes, hypoglycemia
- Accumulation of toxic metabolites
### Diuretics
- Enhance urine flow.
- Interfere with renal Na+ reabsorption, decreasing extracellular fluid volume.
- Common types:
- Osmotic diuretics
- Loop diuretics
- Thiazide diuretics
- Potassium-sparing diuretics
GU System Tests
-
Urine dipstick
- Glucose: Negative
- Leukocyte esterase: Negative
- Nitrates: Negative (positive with some bacteria)
- Ketones: Byproducts of fat, positive during starvation or diabetic ketoacidosis.
- Albumin: Negative (positive with glomerular failure).
- Hemoglobin: Negative (positive with RBC breakdown)
- Myoglobin: Negative (positive with muscle breakdown).
-
Urine sediment/cytology:
- Microscopic analysis reveals crystals, casts, red blood cells, white blood cells, and cancer cells.
-
Blood urea nitrogen (BUN)
- Reflects urine-concentrating ability and glomerular filtration.
- BUN is a waste product from the liver.
- BUN increases when GFR drops.
- Normal range: 10-20 mg/dL.
- Levels rise in dehydration, acute and chronic renal failure (reduced passage of fluid in renal tubules).
-
Plasma creatinine:
- Increases proportionally when GFR declines (doubling creatinine = 50% reduction in GFR).
- Useful for monitoring over time, as it takes 7-10 days to stabilize following a GFR decline.
- Normal range: 0.7-1.2 mg/dL.
-
Creatinine clearance:
- Estimates GFR.
- Requires a 24-hour urine collection and one blood draw.
- GFR = (urine creatinine x urine volume) / plasma creatinine.
Renal Dysfunctions
- Renal and urinary function can be affected by:
- Infection
- Obstruction from stones, tumors, or inflammatory edema
- Dysfunction due to kidney disease or systemic disease
New Renal Dysfunction:
- Vascular: Due to blood vessel issues.
- Prerenal: Caused by factors outside the kidneys (e.g., dehydration, congestive heart failure).
- Renal: Originating from the kidneys themselves (e.g., nephrotic or nephritic syndromes, acute tubular necrosis, interstitial nephritis).
- Postrenal: Obstructive issues.
Urinary Tract Obstruction
-
Interference with urine flow anywhere in the urinary tract.
-
Increases the risk of infection.
-
Anatomical changes due to obstruction are called obstructive uropathy.
-
It is not a primary disease.
-
Compression, stones, masses: Increase pressure, dilate the ureter, renal pelvises, calyces, and parenchyma before obstruction.
-
Increased pressure transmits back to the glomerulus, reducing glomerular blood flow and GFR.
-
Hydronephrosis: Urine buildup in the kidney due to significant obstruction—the renal pelvis expands, increasing intra-renal pressure. Renal pyramids infarct, nephrons are destroyed, and the kidney becomes dysfunctional.
-
Calculi (stones): Form in the ureters, urethra, or bladder, composed of crystals, proteins, etc.
- Cause: Renal colic: Severe, intermittent flank pain; urinary urgency, frequency, hematuria (blood in urine).
Lower Urinary Tract Obstruction
- Disorders of the bladder impacting urine storage or emptying.
- Incontinence
- Neurogenic bladder
- Urethral obstruction
- Pregnancy-related
### Urinary Tract Infection (UTI)
-
Inflammation of the urinary epithelium, usually caused by gut bacteria.
-
Can occur anywhere in the urinary tract.
-
Symptoms: Frequency, dysuria (painful urination), urgency, low back pain, and/or supraubic pain.
-
Can be asymptomatic.
-
Urine culture: 10,000 colony forming units (CFU)/mL or more in urine.
-
Treatment: Antibiotics.
-
Uncomplicated UTIs: Mild.
-
Complicated UTIs: Fever, occur when there are abnormalities in the urinary tract.
-
Recurrent UTIs: 3+ in 12 months, or 2+ in 6 months.
-
Cystitis: Bladder inflammation.
-
Pyelonephritis: Inflammation of the upper urinary tract.
-
UTI risk factors:
- Premature infants, pre-pubertal children, pregnant and sexually active women, indwelling catheters, diabetes mellitus, neurogenic bladder, obstruction.
Glomerular Disorders
-
Glomerulopathies: Directly affect the glomerulus.
- Nephrotic vs. nephritic
- Primary glomerular injury: Immunologic response, ischemia, free radical damage, drugs, toxins, vascular disorders, infection.
- Secondary glomerular injury: Systemic disease (e.g., diabetes, lupus).
-
Significant cause of chronic kidney disease (CKD).
-
Acute glomerulonephritis (AGN):
- Inflammation of the glomerulus.
- Primary glomerular injury: Immunologic response, ischemia, free radicals, drugs, toxins, vascular disorders, infection.
- Secondary glomerular injury: Systemic diseases like diabetes or lupus.
- Formation of immune complexes in the circulation: Deposition in glomerulus, activation of complement, recruitment and activation of immune cells.
- Results in:
- Decreased GFR
- Decreased glomerular perfusion due to inflammation.
- Scarring and thickening of the basement membrane, but increased protein and RBC permeability.
Acute Glomerulonephritis Symptoms:
-
Nephrotic:
- Increased permeability, loss of plasma proteins, decreased oncotic pressure, leading to edema.
- Loss of immunoglobulins, increasing susceptibility to infections.
- Hypoalbuminemia.
- Frothy/foamy urine.
- Anasarca (generalized edema).
- Urine contains protein >3 g/day, and microscopic amounts of blood or no blood.
-
Nephritic:
- Increased permeability of the glomerular filtration membrane.
- Pore size enlargement, allowing RBCs and proteins to pass through.
- Advanced stages of HTN, uremia, oliguria.
- Often associated with extra-renal syndromes (e.g., lupus, Goodpasture's syndrome, strep).
- Urine contains massive amounts of blood and protein (not as severe, between 300 mg to 500 mOsm).
Clinical Symptoms of Glomerulonephritis:
- Azotemia: Increased levels of serum urea, creatinine, etc.
- Uremia: Pro-inflammatory state associated with the buildup of waste and toxins.
- Hypertension, anorexia, nausea, vomiting, diarrhea or constipation, malnutrition, weight loss, pruritus (itching), edema, anemia, neurological complications, cardiovascular disease, skeletal changes.
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Description
This quiz covers key concepts in blood pressure regulation, including the roles of Angiotensin II, Aldosterone, and Antidiuretic hormone (ADH). Additionally, it discusses conditions like SIADH and Diabetes Insipidus, as well as the importance of acid-base balance and metabolic acidosis. Test your understanding of these critical physiological processes.
