2024-02-16T19:36:54+03:00[Europe/Moscow] en true <p>Mechanism of chloride transport in respiratory tract</p>, <p>PFT- Residual Volume</p>, <p>PFT-Functional residual capacity</p>, <p>PFT- Tidal volume</p>, <p>PFT- Total lung capacity</p>, <p>PFT- Vital Capacity</p>, <p>Surfactant producing cells</p>, <p>Lung protections</p>, <p>Genetic disorder that predisposes people to emphysema</p>, <p>Forced expiratory (FE) maneuvers</p>, <p>Mediator of acute asthma attacks</p>, <p>Site of renal filtration </p>, <p>Site of renal processing and reabsorbtion</p>, <p>Hormones produced by kidneys</p>, <p>Glomerular Filtration Rate (GFR)</p>, <p>Diabetic nephropathy results from persistent elevations in glucose levels that promote glucose/protein bonding. This is called:</p>, <p>inflammation within glomeruli</p>, <p>Presentation of glomerular disease</p>, <p>Autoregulation</p>, <p>Water has been reabsorbed under normal conditions of antidiuresis due to the actions of:</p>, <p>Implications of Acute Tubule Dysfunction</p>, <p>RAAS</p>, <p>Compensation for hypotension and/or hypovolemia</p>, <p>Renal compensations for HTN and/or hypervolemia</p>, <p>Most common cause of kidney damage in children</p>, <p>Markers of Renal Function</p>, <p>Scarring of the nephrons</p>, <p>Process of breaking down large amounts of unused glucose (hyperglycemia)</p>, <p>the pressure surrounding the lung, within the pleural space</p>, <p>the pressure difference between the pleural space and the alveolar space</p>, <p>Pleural effusion</p> flashcards

Lungs and Kidneys

Advanced Pathophysiology Module 6- Chapters 11 and 12

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  • Mechanism of chloride transport in respiratory tract

    the cystic fibrosis transmembrane conductance regulator (CFTR). Mutation in allele for this gene is the cause of cystic fibrosis

  • PFT- Residual Volume

    amount of air in the lungs after a maximal expiration, measured with plethysmography or helium dilution

  • PFT-Functional residual capacity

    amount of air in the lungs after a normal, quiet expiration

  • PFT- Tidal volume

    volume of air moved in a normal breath

  • PFT- Total lung capacity

    volume of air in the lungs after a maximal inspiration

  • PFT- Vital Capacity

    volume of air moved during complete expiration from total lung capacity (also equals TLC – RV)

  • Surfactant producing cells

    type 2 alveolar epithelial cells (AEC)

  • Lung protections

    1. Mucociliary clearance 2. Immunoglobulin A (IgA) 3. Alveolar macrophages phagocytose invaders and kill them with proteases and ROS 4. Alpha-1 antiprotease (also called alpha-1 antitrypsin)—made by the liver, blocks leukocyte proteases from damaging self-cells and tissues

  • Genetic disorder that predisposes people to emphysema

    alpha-1 antitrypsin (AAT) deficiency- homozygotes for abnormal AAT gene have greater emphysema risk, particularly if they smoke

  • Forced expiratory (FE) maneuvers

    subjects take maximal inspiration, then attempt to blow the air out as fast and hard as possible, the amount expelled in the first second (FEV1) is typically around 80%. FEV1 is limited by compression of small airways

  • Mediator of acute asthma attacks

    Type 1 hypersensitivity (allergic) reaction. Mediated by histamine

  • Site of renal filtration

    glomerulus

  • Site of renal processing and reabsorbtion

    Tubule

  • Hormones produced by kidneys

    Renin, erythropoietin and activated Vitamin D (bone strength, mood and immune function)

  • Glomerular Filtration Rate (GFR)

    Primary indicator of global kidney function. Measured in mL/min. Directly proportional to the number of functioning nephrons (declines in kidney disease)

  • Diabetic nephropathy results from persistent elevations in glucose levels that promote glucose/protein bonding. This is called:

    Glycated protein formation

  • inflammation within glomeruli

    Glomerulonephritis

  • Presentation of glomerular disease

    Urinary: oliguria, proteinuria, hematuria, red blood cell casts and dark, tea-colored urine

    Systemic: Azotemia (Increased serum CR and BUN), HTN, Edema of face, upper extremities and ascites (in children), fatigue

  • Autoregulation

    Property of maintaining relatively constant flow over a wide range of perfusion rates

  • Water has been reabsorbed under normal conditions of antidiuresis due to the actions of:

    arginine vasopressin (AVP)

  • Implications of Acute Tubule Dysfunction

    1.Retention of sodium, chloride, and water cause hypertension and edema 2. Failure of bicarbonate reabsorption and hydrogen ion secretion cause metabolic acidosis 3. Blood levels of wastes increase, including urea and creatinine 4. Renally excreted drugs build up to toxic levels 5. Renal replacement therapy (RRT—dialysis) can be used as needed until normalkidney function recovers (If it recovers)

  • RAAS

    Angiotensin promotes thirst and drinking, as well as vasoconstriction. Aldosterone secretion promotes late distal tubule sodium transport, restoring

    total body sodium (H2O follows sodium)

  • Compensation for hypotension and/or hypovolemia

    SNS (vasoconstriction), RAAS. AVP

  • Renal compensations for HTN and/or hypervolemia

    Inhibition of hypotensive responses and stimulation natriuretic hormones from the heart (inhibiting sodium reabsorption and promoting vasodilation)

  • Most common cause of kidney damage in children

    Poststreptococcal glomerulonephritis

  • Markers of Renal Function

    Serum CR (to estimate GFR), Lab meausre of GFR (requires IV infusion of marker), Cystatin C, BUN (blood urea nitrogen), Urine albumin/creatinine ratio (ACR), UA, MicroUA

  • Scarring of the nephrons

    Glomerulosclerosis

  • Process of breaking down large amounts of unused glucose (hyperglycemia)

    Glycation

  • the pressure surrounding the lung, within the pleural space

    Pleural pressure

  • the pressure difference between the pleural space and the alveolar space

    transpulmonary pressure

  • Pleural effusion

    buildup of too much fluid between the pleura and lungs. Associate with painful inspiration