Patho Exam #2 Flashcards
Lymph nodes
Part of the immune and hematologic systems
o Facilitates maturation of lymphocytes
o Transports lymphatic fluid back to the circulation
o Cleanses the lymphatic fluid of MOs and foreign particles
Evaluation of the Hematologic System
• Tests of bone marrow function Bone marrow aspiration Bone marrow biopsy Measurement of bone marrow iron stores Differential cell count • Blood tests Large variety of tests – CBC
Aging and the Hematologic System
• Erythrocyte lifespan is normal, but are replaced more slowly
Possible causes
o Iron depletion
o Decreased total serum iron, iron-binding capacity, and intestinal iron absorption
Lymphocyte function decreases with age
Humoral immune system is less responsive
Quantitative disorders
Increases/decreases in cell numbers
o Leukopenia
Not normal and not beneficial
Low WBC predisposes a patient to infection
o Leukocytosis
Normal protective physiologic response to physiologic stressors
Bone marrow disorders or premature destruction of cells
Response to infectious MO invasion
Qualitative disorders
Disruption of cellular function
Neutropenia
• Reduction in circulating neutrophils
• Causes
Prolonged severe infection
Decreased production caused by chemotherapy
Reduced survival
Abnormal neutrophil distribution and sequestration
Leukemias
• Malignant disorder of the blood and blood-forming organs (Hematopoietic stem cells)
• Excessive accumulation of leukemic cells
In bone marrow mutation
Excessive accumulation of lymphocytic – B, T, or NK cells
Excessive accumulation of myelogenous – monocytes or granular leukocytes
Acute leukemia
Presence of undifferentiated or mature cells, usually blast (leukoblast) cells
Chronic leukemia
Predominant cell is mature but does not function normally
Leukemia Symptoms
• Related to suppressed bone marrow function
Infection – severe and/or recurrent
Night sweats, fever, lymphadenopathy
Anemia, pallor, fatigue, weight loss
Nose bleeds, bleeding gums, petechiae (small red or purple spot caused by bleeding into the skin), ecchymosis (bruise)
• Related to infiltration to other organs with immature cells
Enlarged spleen, liver, lymph nodes, bone and joint pain
CNS symptoms (ALL & AML): headache, nausea, vomiting
Leukemia Diagnosis
• Abnormalities in Complete blood cell count (CBC)
• X rays
• Bone marrow aspiration reveals leukemic blast cells and tumor markers
Syringe is used to suck marrow from the iliac crest or the sternum
Procedure used to examine bone marrow cells
• Lumbar puncture
Chemotherapy
Needs to be systemic
Goal is to rid body of leukemic cells without completely destroying bone marrow
Bone marrow transplant provides cure for some types of leukemia
Acute Lymphocytic Leukemia (ALL) & Acute Malloid Leukemia (AML)
Induction Therapy
o Intense combo of chemotherapy and radiation
o Given at time of diagnosis
o Goal to achieve remission
Consolidation Therapy
o Given once remission achieved
o Variation of chemotherapy given during induction
o Curative intent; may be one treatment or repeated cycles for 1 – 2 years
o CNS treatment in children
Maintenance Therapy
o Purpose to maintain remission
o Decreased dose of chemotherapy
o Usually given in cycles over several years (2-5)
Chronic Malloid Leukemia (CML)
Chemo agents – administered orally
In blast crisis
o Drugs similar to those used in AML
Leukapheresis (WBCs are separated from a sample of blood), plateletpheresis (platelets are separated from a sample of blood)
Bone marrow transplant before blast crisis
Chronic Lymphocytic Leukemia (CLL)
Goal – palliation (make a disease or its symptoms less severe or unpleasant without removing the cause)
Oral chemo agents to control WBC count
Malignant Lymphomas
• Uncontrolled proliferation of lymphocytes arising from lymphoid tissues
• Invade bone marrow and other organs
Hodgkin’s Lymphoma
Non-Hodgkin’s Lymphoma
Hodgkin’s Lymphoma (Disease)
Associated with Epstein-Barr Disease (EBV)
Form of lymphoma demonstrating the Reed-Sternberg cell, seen after doing a biopsy on a patient’s lymph node]
Bimodal incidence peak
o Teens to mid-twenties or after 50
Thought to be associated with inflammatory reaction to infectious agent, virus – EBV
Painless progression of single node or group of nodes; spreads in continuous pattern
Usually good prognosis
Non-Hodgkin’s Lymphoma:
Linked with chromosomal translocation
Worst type
Heterogeneic group of neoplastic disorders of lymphoid tissue; absence of Reed-Sternberg cell
More prevalent than Hodgkin’s Lymphoma
o More common in older adults
o Common among persons who are immunosuppressed
Viruses also implicated as possible cause
Multi-centric in origin, non-continuous spread to lymph nodes and early to liver, spleen, and bone marrow
Poorer prognosis
Malignant Lymphomas Symptoms
Painless, enlarged lymph nodes
Low grade fever, night sweats, weight loss, fatigue
Enlarged liver, spleen
Malignant Lymphomas Diagnosis
Biopsy lymph node
CT scan
Bone marrow aspiration
Malignant Lymphoma: Treatment
• Hodgkin’s Lymphoma
If localized, radiation therapy alone (Stage I & II)
Stage IIIA: radiation therapy and combination chemotherapy
Stage IIIB & IV: combination chemotherapy
• Usually combination of radiation therapy and chemotherapy as multicentric (multiple centers of origin) in nature
Multiple Myeloma
• Malignant disease of plasma cells – abnormal B cells
• Malignant plasma cells produce
Immune deficiency
Increased amount of nonfunctional immunoglobulin
o Called the M protein – increases blood viscocity
Substance that stimulates and enhances angiogenesis
• Malignant plasma cells can infiltrate other tissues
Multiple Myeloma Symptoms
Bone pain
Osteoclastic activity increased
o Osteolytic lesions and evidence of osteoporosis on X-ray
o Pathologic fractures
Hypercalcemia, anemia, leukopenia, thrombocytopenia
Renal failure (damage due to Bence Jones protein)
Multiple Myeloma Diagnosis
Serum protein electrophoresis
o Elevated monoclonal protein spike
Bone marrow aspiration
o Sheets of plasma cells present
Multiple Myeloma Treatment
Chemotherapy: control illness
o Various cheme agents + corticosteroids (Decadron)
Thalidomide (Thalomid) to prevent angiogenesis (used to be used to treat, but caused deformed limbs if mother took in early pregnancy)
Biologic agents – alpha-interferon to maintain remission
Radiation for bone lesions
Bisphosphonates to diminish osteoclastic activity
Promote renal function
Symptom management
o Pain, hypercalcemia, increased blood viscosity
o Prevent, treat infections
Anemia
• Reduction in total number of erythrocytes in circulating blood or in the quality or quantity of hemoglobin Impaired erythrocyte production Acute or chronic blood loss Increased erythrocyte destruction Combination of the above
Anemia Morphology
Morphology o Based on MCV, MCH, and MCHC values o Size Identified by terms that end in “-cytic” Macrocytic, microcytic, normocytic o Hemoglobin content Identified by terms that end in “-chromic” Normochromic and hypochromic
Anemia Physiology Manifestation
o Reduced oxygen-carrying capacity
o Heme iron: organ meats good source
o Non-heme irons: Vitamin C helps observe
Classic Anemia Symptoms
Fatigue, dypsnea, weakness, and pallor
Microcytic-Hypochromic Anemia
• Iron deficiency anemia
Most common type of amemia worldwide
Nutritional iron deficiency
Metabolic or functional deficiency
Characterized by RBCs that are abnormally small and contain reduced amounts of hemoglobin
Related to:
o Disorders of iron metabolism
o Alcoholism
o Progression of iron deficiency causes:
Brittle, thin, coarsely ridged, and spoon-shaped nails
A red, sore, and painful tongue
Macrocytic-Normochromic Anemia
• Folate deficiency anemia
Absorption of folate occurs in the upper small intestine
Not dependent on any other factor
Neurologic manifestations generally not seen
Treatment requires daily oral administration of folate
Normocytic-Normochromic Anemia
• Hemolytic anemia Accelerated destruction of RBCs Autoimmune hemolytic anemias Immunohemolytic anemia: blood transfusion reaction Drug-induced hemolytic anemia
Pernicious Anemia
• Lack in intrinsic factor, no B12 absorption
• Signs and symptoms
Nerve demyelination
Atrophic glossitis (redness and swelling of tongue, beefy red)
• People at risk usually obese due to surgeries
Mononucleosis
Infection of B lymphocytes
• Epstein Barr virus
• Most infectious two weeks before symptoms start to show
• Ruptured spleen can be caused by this which can cause death
• Diagnosed by monospot test
Burkitt-lymphoma
- B-cell, Epstein Barr
- Most common types of non-Lodgkins lymphoma in children
- Found in jaw and facial muscles
Gas transport
Ventilation of the lungs
Diffusion of oxygen from the alveoli into the capillary blood
Perfusion of systemic capillaries with oxygenated blood
Diffusion of oxygen into systemic capillaries into the cells
Diffusion of CO2 occurs in reverse order
Factors Affecting Alveolar-Capillary Gas Exchange
- Surface area available for diffusion
- Thickness of the alveolar-capillary membrane
- Partial pressure of alveolar gases
- Solubility and molecular weight of the gas
Lung compliance
- C=△V/△P
* △V Lung volume can be accomplished with given △P respiratory pressure
Airway resistance
- Volume of air that moves into and out of the air exchange portion of the lungs
- Directly related to the pressure difference between the lungs and the atmosphere
- Inversely related to resistance the air encounters as it moves through the airways
Cheyne-Stokes Respirations
o Characterized by oscillation of ventilation between apnea and hyperpnea
o Compensate for changing serum partial pressures
Kussmaul Respirations
o Deep and labored breathing pattern often associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA), but also renal failure
o Form of hypertentilation (reduces CO2 in blood due to increased rate or depth of respiration)
Signs and Symptoms of Pulmonary Disease
• Dyspnea: not breathing properly
Subjective sensation of uncomfortable breathing
• Orthopnea: difficulty breathing when laying down
• Paroxysmal nocturnal dyspnea (PND): sleeping and then wake up sharply, can be associated with cardiac
Mechanisms Involved in Dyspnea
• Stimulation of lung receptors
• Increased sensitivity to changes in ventilation perceived through CNS mechanisms
• Reduced ventilatory capacity or breathing reserve
• Stimulation of neural receptors in the muscle fibers of the intercostals and diaphragm and of receptors in the skeletal joints
• Associated conditions
Primary lung disease
Heart disease
Neuromuscular disorders
Signs and Symptoms of Pulmonary Disease
• Hypoventilation Hypercapnia • Hyperventilation Hypocapnia • Cough Acute cough Chronic cough • Hemoptysis: coughing up blood • Cyanosis • Pain: chest pain • Clubbing: finger nails, pulmonary obstructive disorders • Abnormal sputum: look for color (green, yellow, pink, brown), consistency, thickness, copious amounts of sputum, smell • Pulmonary edema: fluid in or around lungs, congestive heart failure (CHF)
Hypoxemia
• Shortness of breath, increased respiration, changing mental status (esp in elderly), pale or cyanosis
• Results from:
Inadequate O2 in air
Disease of respiratory system
Dysfunction of the neurological system
Alterations in circulatory function
• Mechanisms
Hypoventilation
Impaired diffusion of gases
Inadequate circulation of blood through the pulmonary capillaries
Mismatching of ventilation and perfusion
Mild Hypoxemia
Metabolic acidosis Increase in heart rate Peripheral vasoconstriction Diaphoresis Increase in blood pressure Slight impairment of mental performance
Chronic Hypoxemia
May be insidious in onset and attributed to other causes o Compensation masks condition Increased ventilation Pulmonary vasoconstriction Increased production of RBCs Cyanosis
Hypercapnia
• Increased arterial PCO2
• Caused by hyperventilation or mismatching or ventilation and perfusion
• Effects
Acid-base balance (decreased pH, respiratory acidosis)
Kidney function
NS function
Cardiovascular function
Pleural effusion
Abnormal collection of fluid in pleural cavity
Transudate or exudate, purulent (containing pus), chyle (fluid that consists of fat droplets and lymph), or sanguineous (bloody)
Spontaneous Pneumothorax
Occurs when air-filled blister on the lung surface ruptures
Traumatic Pneumothorax
Caused by penetrating or non-penetrating injuries
Can be from car accident, incident is involved
Tension Pneumothorax
Occurs when the intrapleural pressure exceeds atmospheric pressure
Build-up of air within pleural space, usually due to a laceration which allows air to escape in pleural space but doesn’t return
Characteristics and Symptoms of Pleural Pain
- Abrupt in onset
- Unilateral, localized to lower and lateral part of the chest
- May be referred to the shoulder
- Usually made worse by chest movements
- Tidal volumes are kept small
- Breathing becomes more rapid
- Reflex splinting of the chest may occur
Diagnosis of Pleural Effusion
Chest radiographs, chest ultrasound
Computed tomography (CT)
Treatment of Pleural Effusion
- Thoracentesis: inserting needle in lungs to draw out fluid
- Injection of sclerosing agent (develops scar tissue) into the pleural cavity
- Open surgical drainage (chest tube, usually used to inflate lungs that collapse)
Actelectasis
Incomplete expansion of a lung or portion of a lung
Causes of Actelectasis
Airway obstruction
Lung compression such as occurs in pneumothorax or pleural effusion
Increased recoil of lung due to loss of pulmonary surfactant
Causes of Respiratory Failure
• Impaired ventilation Upper airway obstruction Weakness of paralysis of respiratory muscles Chest wall injury • Impaired matching of ventilation and perfusion • Impaired diffusion Pulmonary edema Respiratory distress syndrome
Treatment of Respiratory Function
- Respiratory supportive care directed toward maintenance of adequate gas exchange
- Establishment of an airway
- Use of bronchodilating drugs
- Antibiotics for respiratory infections
- Ensure adequate oxygenation
Acute Respiratory Distress Syndrome (ARDS)
Damaged alveoli, oxygenation severely impaired
• Injury to pulmonary capillary endothelium
• Inflammation and platelet activation
• Surfactant inactivation
• Atelectasis
Causes of ARDS
- Aspiration in gastric contents
- Major trauma (with or without fat emboli)
- Sepsis secondary to pulmonary or non-pulmonary infections
- Acute pancreatitis
- Hematologic disorders
- Metabolic events
- Reactions to drugs and toxins
ARDS Manifestations
Hyperventilation Respiratory alkalosis Dyspnea and hypoxemia Metabolic acidosis Hypoventilation Respiratory acidosis Further hypoxemia Hypotension, decreased cardiac output, death
ARDS Evaluation and Treatment
- 100% oxygen
- Keep O2 levels above 90%
- Physical examination, blood gases, and radiologic examination
- Supportive therapy with oxygenation and ventilation and prevention of infection
- Surfactant to improve compliance
Chronic obstructive airway disease (COPD)
• Expiration is affected
• Progression can be slowed with treatment
• Inflammation and fibrosis of bronchial wall
• Hypertrophy of submucosal glands
• Hypersecretion of mucus (asthmatic patients, chronic bronchitis patients)
• Loss of elastic lung fibers
Impairs the expiratory flow rate, increases air trapping, and predisposes to airway collapse
• Alveolar tissue
Decreases the surface area for gas exchange
Causes of COPD
- Chronic bronchitis
- Emphysema
- Bronchiectasis
- Cystic fibrosis
Types of COPD
• Emphysema
Enlargement of air spaces (beyond terminal bronchioles, loss of recoil, harder and not as quick) and destruction of lung tissue
• Chronic obstructive bronchitis
Obstruction of small airways
Pulmonary Emphysema
- Smoking history
- Age of onset: 40-50 years
- Often dramatic barrel chest (1:1 ratio)
- Weight loss
- Decreased breath sounds
- Normal blood gases until late in disease process
- Slowly debilitating disease
Chronic Bronchitis
- Smoking history
- Age of onset 30-40 years
- Barrel chest may be present
- Shortness of breath predominant early symptom
- Rhonchi often present
- Sputum frequent early manifestation
- Often dramatic cyanosis
- Hypercapnia and hypoxemia may be present
- Frequent cor pulmonale and polycythemia
- Numerous life threatening episodes due to acute exacerbations
Pulmonary Embolism
• Development
Blood-borne substance lodges in a branch of the pulmonary artery and obstructs the flow
Thrombus: arising from DVT
Fat: mobilized from the bone marrow after a fracture or from a tramatized fat depot
Amniotic fluid: enters the maternal circulation after rupture of the membranes at the time of delivery
Asthma
Environmental o Construction (concrete dust) o Smoking o Pet hair Preventable o Control whatever triggers asthma attack Exercise induced Allergen induced Stress Induced
Asthma Symptoms
Wheezing, coughing throughout the night, difficulty breathing, and excess sputum
Pneumonia
6th leading cause of death Nosocomial Infection Spread of respiratory droplets Hospital/environmental acquired Can be caused by bacteria (strep) Haemophilis influenza most common cause
Tuberculosis
Caused by mycobacteria (rod-shaped) Acid-fast bacillus Airborne Patients in negative air-pressure rooms Droplet precautions Causeous necrosis (cheesy-looking granules) TB skin tests o Pos. needs further testing o Chest x-ray o 3 sputum cultures
Hyperthyroidism
Thyrotoxicosis: caused by too much thyroid hormone in body, most common type of hyperthyroidism
o Exopathalmos: bulging of eyes
o Too much T3 and T4 in body
o Cured with iodine
Graves disease
o Pretibial myxedema
o Most common type of hyperthyroidism
Hyperthyroidism resulting from nodular thyroid disease
o Goiter: result of iodine deficiency
Thyrotoxic crisis: immediate care needed, most extreme form of hyperthyroidism
Hypothyroidism
• Primary hypothyroidism Subacute thyroiditis Autoimmune thyroiditis (Hashimoto disease) Painless thyroiditis Postpartum thyroiditis Myxedema coma: life threatening • Congenital hypothyroidism • Thyroid carcinoma • Overweight, fatigue, thyroid gland can atrophy, constipation, sensitivity to cold, dry skin and nails, constant pain • Creatinism 44 in or less Scamp or no hair Umbilical hernia Underdeveloped breasts
Type 1 Diabetes Mellitus
- Demonstrates pancreatic atrophy and specific loss of beta cells
- Macrophages, T- and B-lymphocytes, and natural killer cells are present
Type 1 Diabetesx Mellitus
- T cells attack and destroy islet cells in pancreas
- Body can make insulin but body can’t use it
- Obesity
- Hypertension
- Poor wound healings
- Peripheral neuropathy
- Amputations
- Frequent infections
- Liver and kidney disease
- End-stage renal disease
- retinopathy
Type 1 DM
• Genetic susceptibility
Glycogen
• Environmental factors
• Immunologically mediated destruction of beta cells by T cells
• Manifestations
Hyperglycemia, polydipsia, polyuria, polyphagia, weight loss, and fatigue
Have to have insulin
Type 2 DM
Insulin resistance
• Body makes insulin, but doesn’t produce enough for glucose in body
• Usually seen in 35 years +
• Normal should be 70-100
• Orange juice given to help instantly (monosaccharide)
• Milk if no OJ present (dissacharide)
• Glucose given under gum or by IV
Acute Complications of DM
- Hypoglycemia
- Diabetic ketoacidosis
- Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)
- Somogyi effect
- Dawn phenomenon
Diabetic ketoacidosis
Sweet smelling pee
Fat begins to be broken down
Carbs aren’t broken down, glucose not used for energy
Ketones enter bloodstream
Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)
Life threatening
Enough insulin produced to not get NKA
Not enough insulin produced to not prevent hyperglycemia
High blood sugarm but body still making enough insulin
Ketones aren’t spilled into blood
Somogyi effect
Blood glucose drops in sleep, Hormones increase blood sugar too much
Dawn phenomenon
Higher blood sugar than anticipated when waking up
Chronic Complications of DM
• Hyperglycemia and nonenzymatic glycosylation • Hyperglycemia and the polyol pathway Protein kinase C • Microvascular disease Retinopathy Diabetic nephropathy • Macrovascular disease Coronary artery disease Stroke Peripheral arterial disease • Diabetic neuropathies • Infection
Disseminated Intravascular Coagulation (DIC)
• Complex, acquired disorder in which clotting and hemorrhage simultaneously occur
• Result of increased protease activity in the blood caused by unregulated release of thrombin with subsequent fibrin formation and accelerated fibrinolysis
• Endothelial damage is the primary initiator of DIC
• By activating fibrinolytic system (plasmin), patient’s fibrin degradation product (FDP) and D-dimer levels will increase
• Because of the patient’s clinical state, the disorder has a high mortality rate
• Treatment is to remove the stimulus and maintain hemodynamic status
• Clinical signs and symptoms demonstrate wide variability
Bleeding from venipuncture sites
Bleeding from arterial lines
Purpura, petechiae, and hemotomas
Symmetric cyanosis of the fingers and toes
Vitamin K deficiency
Alteration of Coagulation
Necessary for synthesis and regulation of prothrombin, the prothrombin factors (II, VII, XI, X) and proteins C and S (anticoagulants)
Liver disease
Causes a broad range of hemostasis disorders
o Defects in coagulation, fibrinolysis, and platelet number and function
Thrombocytopenia
Platelet count <150,000/mm3
Hemorrhage from minor trauma
<50,000/mm3
Spontaneous bleeding
<15,000/mm3
Severe bleeding
<10,000/mm3
Sickle Cell Anemia
Mutation in beta chains of HbG
When HbG deoxygenated, beta chains link together forming long protein rods that make the cell sickle
Problems caused by Sickle Cell
Blocked capillaries, causing acute pain, infarctions cause chronic damage to liver, spleen, heart, kidneys, eyes and bones
Pulmonary infarction > acute chest syndrome
Cerebral infarction > stroke
Sickled cells more likely to be destroyed
Ventilation
the movement of air between the atmosphere and the respiratory portion of the lungs
Inspiration
air is drawn into the lungs as the respiratory muscles expand the chest cavity
Expiration
air moves out of the lungs as the chest muscles expand the chest cavity becomes smaller
Perfusion
the flow of blood through the lungs
Diffusion
transfer of gases between air-filled spaces in the lungs and the blood
