Final Review PDF

Title Final Review
Author Nicole Puccio
Course Pathophysiology
Institution Sam Houston State University
Pages 35
File Size 1.3 MB
File Type PDF
Total Downloads 23
Total Views 127

Summary

Pathophysiology Final Exam Review Chapter 2 Fluid, Electrolyte, and Acid-Base ImbalancesReview of Concepts and Processes The major component of the body is water in these compartments: Intercellular fluid (ICF) compartment Extracellular fluid (ECF) compartment Balance of water in the compartments es...


Description

Pathophysiology Final Exam Review Chapter 2 Fluid, Electrolyte, and Acid-Base Imbalances Review of Concepts and Processes • The major component of the body is water in these compartments: • Intercellular fluid (ICF) compartment • Extracellular fluid (ECF) compartment • Balance of water in the compartments essential for homeostasis Fluid Compartments • Intracellular compartment (ICF) • Extracellular compartment (ECF) • Intravascular fluid (IVF) or blood • Interstitial fluid (ISF) or intercellular fluid • Cerebrospinal fluid (CSF) • Transcellular fluids • Present in various secretions • Pericardial cavity • Synovial cavities Sodium Imbalance • Review of sodium • Primary cation in ECF • Sodium diffuses between vascular and interstitial fluids. • Transport into and out of cells by sodium-potassium pump • Actively secreted into mucus and other secretions • Exists in form of sodium chloride and sodium bicarbonate • Ingested in food and beverages

Hyponatremia • Causes • Losses from excessive sweating, vomiting, diarrhea • Use of certain diuretic drugs combined with low-salt diet • Hormonal imbalances • Insufficient aldosterone • Adrenal insufficiency • Excess ADH secretion • Diuresis • Excessive water intake

Effects of Hyponatremia • Low sodium levels • Cause fluid imbalance in compartments • Fatigue, muscle cramps, abdominal discomfort or cramps, nausea, vomiting • Decreased osmotic pressure in ECF compartment • Fluid shift into cells • Hypovolemia and decreased blood pressure • Cerebral edema • Confusion, headache, weakness, seizures Hyponatremia and Fluid Shift into Cells Hypernatremia • Cause is imbalance in sodium and water • Insufficient ADH (diabetes insipidus) • Results in large volume of dilute urine • Loss of the thirst mechanism • Watery diarrhea • Prolonged periods of rapid respiration • Ingestion of large amounts of sodium without enough water

Effects of Hypernatremia • Weakness, agitation • Dry, rough mucous membranes • Edema • Increased thirst (if thirst mechanism is functional) • Increased blood pressure Potassium Imbalance • Review of potassium • Major intracellular cation • Serum levels are low, with a narrow range. • Ingested in foods and excreted primarily in urine • Insulin promotes movement of potassium into cells • Level influenced by acid-base balance • Excess potassium ions in interstitial fluid may lead to hyperkalemia. • Abnormal potassium levels cause

changes in cardiac conduction and are life-threatening! Signs of Potassium Imbalance Role of sodium and potassium ions in the conduction of an impulse Causes of Hypokalemia • Definition of hypokalemia • Serum K+ < 3.5 mEq/L • Causes • Excessive losses caused by diarrhea • Diuresis associated with some diuretic drugs • Excessive aldosterone or glucocorticoids • Example: Cushing syndrome • Decreased dietary intake • May occur with alcoholism, eating disorders, starvation • Treatment of diabetic ketoacidosis with insulin Effects of Hypokalemia • Cardiac dysrhythmias • Caused by impaired repolarization leading to cardiac arrest • Interference with neuromuscular function • Muscles less responsive to stimuli • Paresthesia―“pins and needles” • Decreased digestive tract motility • Severe hypokalemia: • Shallow respirations • Failure to concentrate urine―polyuria Causes of Hyperkalemia • Definition of hyperkalemia • Serum K+ > 5 mEq/L • Causes • Renal failure • Deficit of aldosterone • “Potassium-sparing” diuretics • Leakage of intracellular potassium into extracellular fluids • In patients with extensive tissue damage • Displacement of potassium from cells by prolonged or severe acidosis Relationship of Hydrogen and Potassium Ions Effects of Hyperkalemia • Cardiac dysrhythmias • May progress to cardiac arrest • Muscle weakness common • Progresses to paralysis • May cause respiratory arrest • Impairs neuromuscular activity



Fatigue, nausea, paresthesia

Calcium Imbalance • Review of calcium • Important extracellular cation • Ingested in food • Stored in bone • Excreted in urine and feces • Balance controlled by parathyroid hormone (PTH) and calcitonin • Vitamin D promotes calcium absorption from intestine • Ingested or synthesized in skin in the presence of ultraviolet rays • Activated in kidneys Functions of Calcium • Provides structural strength for bones and teeth • Maintenance of the stability of nerve membranes • Required for muscle contractions • Necessary for many metabolic processes and enzyme reactions • Essential for blood clotting Causes of Hypocalcemia • Hypoparathyroidism • Malabsorption syndrome • Deficient serum albumin • Increased serum pH level • Renal failure Effects of Hypocalcemia • Increase in the permeability and excitability of nerve membranes • Spontaneous stimulation of skeletal muscle • Muscle twitching • Carpopedal spasm • Tetany • Weak heart contractions • Delayed conduction • Leads to dysrhythmias and decreased blood pressure Causes of Hypercalcemia • Uncontrolled release of calcium ions from bones • Neoplasms―malignant bone tumors • Hyperparathyroidism • Demineralization caused by immobility • Decrease stress on bone • Increased calcium intake • Excessive vitamin D • Excess dietary calcium



Milk-alkali syndrome

Effects of Hypercalcemia • Depressed neuromuscular activity • Muscle weakness, loss of muscle tone • Lethargy, stupor, personality changes • Anorexia, nausea • Interference with ADH function • Less absorption of water • Decrease in renal function • Increased strength in cardiac contractions • Dysrhythmias may occur. Magnesium Imbalances • Magnesium • Intracellular ion • Hypomagnesemia • Results from malabsorption or malnutrition; often associated with alcoholism • Caused by use of diuretics, diabetic ketoacidosis, hyperthyroidism, hyperaldosteronism • Hypermagnesemia • Occurs with renal failure • Depresses neuromuscular function • Decreased reflexes Changes in Acids, Bicarbonate Ion, and Serum pH in Circulating Blood Buffer Systems • Sodium bicarbonate–carbonic acid system • Major ECF buffer • Controlled by the respiratory system and kidneys • Other buffering systems: • Phosphate • Hemoglobin • Protein Compensation Mechanisms for pH Imbalance • Compensation limited, usually short term • Does not remove the cause of imbalance • Compensation occurs to balance the relative proportion of hydrogen ions and bicarbonate ions in circulation: • Buffers • Change in respiration • Change in renal function Decompensation • Occurs when: • Causative problem becomes more severe

• •

• Additional problems occur • Compensation mechanisms are exceeded or fail Requires intervention to maintain homeostasis LIFE-THREATENING!

Acid-Base Imbalance • Acidosis • Excess hydrogen ions • Decrease in serum pH • Alkalosis • Deficit of hydrogen ions • Increase in serum pH Acid-Base Imbalances Respiratory Acidosis • Acute problems • Pneumonia, airway obstruction, chest injuries • Drugs that depress the respiratory control center • Chronic respiratory acidosis • Common with chronic obstructive pulmonary disease • Decompensated respiratory acidosis • May develop if impairment becomes severe or if compensation mechanisms fail Metabolic Acidosis • Excessive loss of bicarbonate ions to buffer hydrogen • Diarrhea―loss of bicarbonate from intestines • Increased use of serum bicarbonate • Renal disease or failure • Decreased excretion of acids • Decreased production of bicarbonate ions • Decompensated metabolic acidosis • Additional factor interferes with compensation. Effects of Acidosis • Impaired nervous system function • Headache • Lethargy



• Weakness • Confusion • Coma and death Compensation • Deep rapid breathing • Secretion of urine with a low pH Changes in Blood Gases with Acidosis

Pain Chapter 4 Gate open: pain stimulus transmitted Gate closed: Pain stimulus blocked Gates closed: pain blocking system • Three ways gates can close 1. sensory stimuli move along competing pathways 2. brain produces outgoing transmissions through reticular system 3. brain releases Opiate-like chemicals • Endorphins • Block substance P at the synapse • Natural opiate receptors are throughout brain Inflammation and Healing Chapter 5 Normal Defenses of the Body  First line of defense—skin and mucous membranes, saliva, tears o Second line of defense our innate immune system o Non-specific process of: o Phagocytosis o Inflammation  Third line of defense is a  Specific defense o Sensitized t-lymphocytes o Production of antibodies

Acute & Chronic Inflammation  Acute inflammation  Chronic inflammation  Local Manifestations of Acute Inflammation  Systemic Manifestation of Acute Inflammation Diagnostics; Changes in the Blood with Inflammation Types of Healing • Resolution- minimal damage • Regeneration- damaged tissue is replaced by cells that are functional • Replacement-extensive tissue damage or cell’s can’t be replaced. • Can result in loss of function Infection Chapter 6 Chlamydia, Rickettsia, Mycoplasmas • Obligate intercellular parasites. • Chlamydia-very primitive forms • Rickettsia • Mycoplasmas Fungi  Eukaryotic organisms –Nucleus?  Found throughout environment  Fungal or mycotic infection  Examples Protozoa

   

Eukaryotic forms Unicellular, lack cell wall Many live independently, others are obligate parasites Pathogens are usually parasites.

Other Agents of Disease  Helminths (Flat or Round Worms)  Are not microorganisms  Parasites *Diseases??? Fungal Infections • Thick, tough cell wall & plasma membrane • Fungi live where • If untreated, • Superficial infections Principles of Infection • Normal flora • Infection o Sporadic o Endemic o Epidemic o Pandemic Transmission of Infectious Agents  Transmission from person to person o Reservoir o Carrier o Agent  Portal of exit  Mode of transmission  Portal of entry  Susceptible host

Chapter 7 Immunity Antibodies and Immunoglobulins

• • •

IgG • IgM • IgA •

Most common in blood First to increase in immune response In secretions • Tears • Saliva and mucous membranes • Colostrum

Antibodies and Immunoglobulins (Cont.) • IgE • Allergic response • Causes release of histamine and other chemicals • Results in inflammation • IgD • Attached to B cells • Activates B cells Review of the Major Components of the Immune System



Major components of the immune system and their function

Types of Acquired Immunity

Anaphylaxis: Anaphylactic Shock • Severe, life-threatening • Systemic hypersensitivity reaction • Decreased blood pressure caused by release of histamine • Airway obstruction

• •



Severe hypoxia Can be caused by: • Latex materials • Insect stings • Nuts or shellfish; various drugs Signs and symptoms • Generalized itching or tingling, especially in oral cavity • Coughing • Difficulty breathing • Feeling of weakness • Dizziness or fainting • Sense of fear and panic • Edema around eyes, lips, tongue, hands, feet • Hives • Collapse with loss of consciousness Signs and Symptoms of Anaphylaxis

Treatment for Anaphylaxis • Requires first aid response: • Administer EpiPen if available • Call 911 (many paramedics can start drug treatment and oxygen) • Treatment in emergency department: • Epinephrine • Glucocorticoids • Antihistamines • Oxygen • Stabilize BP

Blood and Circulatory System Disorders Chapter 10 Composition of Blood Blood Typing and ABO Blood Groups

Diagnostic Tests  Complete blood count (CBC)  Includes total red blood cells (RBCs), white blood cells (WBCs), and platelets  Leukocytosis (increased WBCs)  Associated with inflammation or infection  Leukopenia (decreased WBCs)  Associated with some viral infections, radiation, chemotherapy  Increased eosinophils o Common in allergic responses  Differential count for WBCs  Morphology  Observed with blood smears  Shows size, shape, uniformity, maturity of cells  Different types of anemia can be distinguished.  Hematocrit  Percent by volume of cellular elements in blood  Hemoglobin  Amount of hemoglobin per unit volume of blood  Mean corpuscular volume (MCV)  Indicates the oxygen-carrying capacity of blood o Reticulocyte count  Assessment of bone marrow function

o Chemical analysis  Determines serum levels of components, such as iron, vitamin B12, folic acid, cholesterol, urea, glucose o Bleeding time  Measures platelet function o Prothrombin time (PT) and partial thromboplastin time (PTT)  Measure function of various factors in coagulation process  International normalized ratio (INR) is a standardized version. Anemias • Causes a reduction in oxygen transport • Basic anemia problem is hemoglobin deficit • Oxygen deficit leads to: • Less energy production in all cells • Cell metabolism and reproduction diminished • Compensation mechanisms • Tachycardia and peripheral vasoconstriction • General signs of anemia • Fatigue, pallor (pale face), dyspnea, tachycardia Iron Deficiency Anemia  Pathophysiology  Insufficient iron impairs hemoglobin synthesis  Microcytic, hypochromic RBCs  Result of low hemoglobin concentration in cells  Etiology  Dietary intake  Chronic blood loss  Duodenal absorption  Severe liver disease  infections and cancers Pernicious Anemia Pernicious Anemia: Vitamin B12 Deficiency  Signs and symptoms  Tongue enlarged, red, sore, and shiny  digestive discomfort  Paresthesia in the extremities or loss of coordination and ataxia  Diagnostic tests  Megaloblastic on microscopic examination  Marrow is hyperactive  Vitamin B12 level  Presence of hypochlorhydria or achlorhydria Aplastic Anemia  Pathophysiology





 Impairment or failure of bone marrow Etiology  Often idiopathic but possible causes include:  Myelotoxins  Radiation, industrial chemicals, drugs  Viruses  Particularly hepatitis C  Genetic abnormalities  Myelodysplastic syndrome  Fanconi’s anemia Diagnostic tests  Blood counts indicate pancytopenia  A bone marrow biopsy to confirm pancytopenia

Hemolytic Anemias  Results from excessive destruction of RBCs  Causes  Genetic defects  Immune reactions  Changes in blood chemistry  Infections such as malaria  Toxins in the blood  Antigen-antibody reactions  Incompatible blood transfusion  Erythroblastosis fetalis  Sickle Cell  Thalassemia Sickle Cell Anemia • Genetic condition • Autosomal • Incomplete dominance • Anemia occurs in homozygous recessive • Diagnostic testing is available • More common in individuals of African ancestry • Heterozygous condition is somewhat protective against malaria • One in ten African Americans is heterozygous for the trait Comparison of Selected Anemias

Chapter 12 Cardiovascular System Disorders Heart: Conduction System • Conduction pathway • Sinoatrial (SA) node • Pacemaker • Sinus rhythm • Atrioventricular (AV) node • Located in floor of the right atrium • AV bundle (bundle of His) • Right and left branches • Purkinje fibers • Terminal fibers Heart: Conduction System (Cont) • Electrocardiogram (ECG) • P wave • Depolarization of atria • QRS wave • Depolarization of ventricles • T wave • Repolarization of ventricles Cardiac Cycle (Cont) Control of the Heart • Cardiac control center in medulla oblongata • Controls rate and force of contraction • Located in the medulla • Baroreceptors • Detect changes in blood pressure • Located in the aorta and internal carotid arteries • Sympathetic stimulation (cardiac accelerator nerve)



• Increases heart rate (tachycardia) Parasympathetic stimulation (cranial nerve [CN] X; vagus nerve) • Decreases heart rate (bradycardia)

Blood Pressure • Changes in blood pressure • Sympathetic branch of ANS • Increased output → vasoconstriction and increased BP • Decreased output → vasodilation and decreased BP • BP is directly proportional to blood volume. • Hormones • Antidiuretic hormone (↑ BP); aldosterone (↑ blood volume, ↑ BP); reninangiotensin-aldosterone (vasoconstriction; ↑ BP) Angina Pectoris • Occurs when there is a deficit of oxygen to meet myocardial needs • Chest pain may occur in different patterns. • Classic or exertional angina • Variant angina • Vasospasm occurs at rest. • Unstable angina • Prolonged pain at rest—may precede myocardial infarction Angina: Imbalance of Oxygen Supply and Demand Emergency Treatment for Angina • Rest, stop activity • Patient seated in upright position • Administration of nitroglycerin—sublingual • Check pulse and respiration. • Administer oxygen, if necessary. • Patient known to have angina • Second dose of nitroglycerin • Patient without history of angina • Emergency medical aid Myocardial Infarction • Occurs when coronary artery is totally obstructed • Atherosclerosis is most common cause • Thrombus from atheroma may obstruct artery • Vasospasm is cause in a small percentage. • Size and location of the infarct determine the damage.

Warning Signs of Heart Attack • Feeling of pressure, heaviness, or burning in chest—especially with increased activity • Sudden shortness of breath, weakness, fatigue • Nausea, indigestion • Anxiety and fear • Pain may occur and, if present, is usually • Substernal • Crushing • Radiating Myocardial Infarction (MI) Myocardial Infarction • Diagnostic tests • Changes in ECG • Serum enzyme and isoenzyme levels • Serum levels of myosin and cardiac troponin are elevated. • Leukocytosis, elevated CRP and ESR common • Arterial blood gas measurements may be altered in severe cases. • Pulmonary artery pressure measurements helpful Myocardial Infarction: Treatment • Reduce cardiac demand. • Oxygen therapy • Analgesics • Anticoagulants • Thrombolytic agents may be used. • Tissue plasminogen activator • Medication to treat: • Dysrhythmias, hypertension, congestive heart failure • Cardiac rehabilitation begins immediately. Congestive Heart Failure • Heart is unable to pump out sufficient blood to meet metabolic demands of the body. • Usually a complication of another cardiopulmonary condition • May involve a combination of factors • Various compensation mechanisms maintain cardiac output. • Some of these often aggravate the condition.

Signs and Symptoms of Congestive Heart Failure • Forward effects (similar with failure on either side) • Decreased blood supply to tissues, general hypoxia • Compensation mechanisms • Left sided • cough • Right sided • JVD Congestive Heart Failure (CHF) Shock • Hypovolemic shock • Loss of circulating blood volume • Cardiogenic shock • Inability of heart to maintain cardiac output to circulation • Distributive, vasogenic, neurogenic, septic, anaphylactic shock • Changes in peripheral resistance leading to pooling of blood in the periphery Types of Shock

Respiratory System Disorders

Chapter 13 Pulmonary Volumes

Respiratory Control Diffusion of Gases Factors Affecting Diffusion of Gases • Partial pressure gradient • Thickness of the respiratory membrane • Fluid accumulation in alveoli or interstitial tissue impairs gas exchange. • Total surface area available for diffusion • If part of alveolar wall is destroyed, surface area is reduced, so less exchange • Ventilation-perfusion ratio Transport of Oxygen and Carbon Dioxide • Oxygen • Most is bound (reversibly) to hemoglobin. • Binding and release of oxygen to hemoglobin depend on: • PO2, PCO2, temperature, plasma pH • Carbon dioxide • Waste product from cellular metabolism • About 7% dissolved in plasma • About 20% reversibly bound to hemoglobin

Factors Affecting Diffusion of Gases • Partial pressure gradient • Thickness of the respiratory membrane

• •

• Fluid accumulation in alveoli or interstitial tissue impairs gas exchange. Total surface area available for diffusion • If part of alveolar wall is destroyed, surface area is reduced, so less exchange Ventilation-perfusion ratio

Transport of Oxygen and Carbon Dioxide • Oxygen • Most is bound (reversibly) to hemoglobin. • Binding and release of oxygen to hemoglobin depend on: • PO2, PCO2, temperature, plasma pH • Carbon dioxide ...


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