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113 Cards in this Set
- Front
- Back
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Homeostasis
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stable state
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Single Gene disorders:
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autosomal dominant-huntingtons and marfans, autosomal recessive-cystic fibrosis and sickle cell anemia
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Chromosomal disorder:
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Down syndrome-on 21st chromosome---has three---presents mental retardation, no dimple in upper lip as child, cardiac deficiency, shorter lifespan
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Intracellular electrolytes:
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potassium
Essential for transmission and conduction of nerve impulses, normal cardiac rhythms, and skeletal and smooth muscle contraction |
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Extracellular electrolytes:
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sodium
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pH:
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7.35-7.45
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sodium:
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135-145
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potassium:
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3.5-4.5
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Hypernatremia:
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sodium >145
Related to sodium gain or water loss Causes – Diabetes and fluid loss Water movement from the ICF to the ECF Intracellular dehydration Manifestations Intracellular dehydration, convulsions, pulmonary edema, hypotension, tachycardia, etc. |
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Hyponatremia:
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<135(too much water can cause this)
Sodium deficits cause plasma hypo-osmolality and cellular swelling Causes – SIADH (Syndrome of inappropriate antidiuretic hormone) Manifestations Lethargy, confusion, decreased reflexes, seizures, and coma |
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Hyperkalemia:
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>4.5, could present due to renal failure, burns(CAN EFFECT CARDIAC)
Hyperkalemia is rare because of efficient renal excretion Caused by increased intake, shift of K+ from ICF, decreased renal excretion, insulin deficiency, or cell trauma Burns Renal Failure (patient) |
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Hypokalemia:
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<3.5-weakness, could be caused by diarrhea, vomiting, or NG tube that is taking out potassium
-Give them dialysis or make em poop Potassium balance is described by changes in plasma potassium levels Causes can be reduced intake of potassium, increased entry of potassium, and increased loss of potassium Diarrhea Vomiting Diuretics Excessive sweating |
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First line of defense
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Innate resistance (natural or native immunity)
Skin Linings of the gastrointestinal, genitourinary, and respiratory tracts Sloughing off of cells Coughing and sneezing Flushing Vomiting Mucus and cilia |
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Second line of defense
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Inflammatory response
Caused by a variety of materials Infection, mechanical damage, ischemia, nutrient deprivation, temperature extremes, radiation, etc. Local manifestations Vascular response Blood vessel dilation, increased vascular permeability and leakage, white blood cell adherence to the inner walls of the vessels and migration through the vessels |
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Mast Cells
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Most important activator of the inflammatory response activated with injury
Located in the loose connective tissues close to blood vessels Stimuli will activate mast cells to produce inflammation Degranulation (release of contents of the mast cell) |
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Mast Cell Degranulation---Histamine
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Causes temporary, rapid constriction of the large blood vessels and the dilation of the postcapillary venules
Increased vascular permeability |
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Mast Cell---Chemotactic Factors
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Neutrophil – kill bacteria early in the stages of inflammation
Ingest bacteria, dead cells, and cellular debris Cells are short lived and become a component of the purulent exudate Eosinophil – help to regulate the inflammatory process Defense against parasites and regulation of vascular mediators |
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Local inflammation:
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redness, pain, swelling
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Exudative fluids:
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serous-clear, purulent-pus, hemorrhagic-bloody
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HIV infection
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Treatment and prevention
Highly active antiretroviral therapy (HAART) Reverse transcriptase inhibitors Protease inhibitors New drugs Entrance inhibitors Integrase inhibitors Vaccine development |
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Lupus:
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Systemic lupus erythematosus (SLE)
Deposition of circulating immune complexes containing antibody against host DNA More common in females Clinical manifestations Arthralgias or arthritis (90% of individuals) Vasculitis and rash (70%-80%) Renal disease (40%-50%) Hematologic changes (50%) Cardiovascular disease (30%-50%) |
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Third line of defense
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Adaptive (acquired) immunity
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Monocytes:
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produced in the bone marrow, enter the circulation, and migrate to the inflammatory site, where they develop into macrophages
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Macrophages:
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typically arrive at the inflammatory site 24 hours or later after neutrophils
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General Adaptation Syndrome (GAS)
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1. Alarm stage (Fight and Flight)
Arousal of body defenses Release of epinephrine and norepinephrine 2. Stage of resistance (adaptation) Responds to stress and attempts to return to homeostasis Coping mechanisms used 3. Stage of exhaustion Progressive breakdown of compensatory mechanisms Onset of disease |
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Benign
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grows slowly, well-defined capusle, not invasive, well differentiated, low mitotic index, does not metastasize
(-oma) |
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Malignant
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grows rapidly, not encapsulated, invasive, poorly differentiated, high mitotic index, metastasizes
(carcinomas and sarcomas) |
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Stages of Cancer
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Stage 1 – Cancer confined to the site of origin
Stage 2 – Cancer that is locally invasive Stage 3 – Cancer spread to regional structures such as lymph nodes Stage 4 – Cancer spread to distant sites |
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Environmental Risk Factors For Cancer
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Tobacco
Multipotent carcinogenic mixture Linked to cancers of the lung, lower urinary tract, aerodigestive tract, liver, kidney, pancreas, cervix uteri Linked to myeloid leukemia |
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mental Risk Factors For Cancer
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Ionizing radiation
Emission from x-rays, radioisotopes, and other radioactive sources Exposure causes cell death, gene mutations, and chromosome aberrations Bystander effects Poor gene repair Changes in gap junction intercellular communication |
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mental Risk Factors For Cancer
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Ultraviolet radiation
Causes basal cell carcinoma, squamous cell carcinoma, and melanoma Principal source is sunlight Ultraviolet A (UVA) and ultraviolet B (UVB) Promotes skin inflammation and release of free radicals |
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mental Risk Factors For Cancer
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Alcohol consumption
Risk factor for oral cavity, pharynx, hypopharynx, larynx, esophagus, and liver cancers Cigarette/alcohol combination increases a person’s risk |
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mental Risk Factors For Cancer
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Sexual reproductive behavior
Carcinogenic types of human papillomavirus High-risk HPV |
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mental Risk Factors For Cancer
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Occupational hazards
Substantial number of occupational carcinogenic agents Asbestos Dyes, rubber, paint, explosives, rubber cement, heavy metals, air pollution, etc. Radon |
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mental Risk Factors For Cancer
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Diet
Xenobiotics Toxic, mutagenic, and carcinogenic chemicals in food Activated by phase I activation enzymes Defense mechanisms Phase II detoxification enzymes Examples Compounds produced in the cooking of fat, meat, or proteins Alkaloids or mold by-products |
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Environmental Risk Factors For Cancer
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Obesity-In response to endocrine and metabolic signaling, adipose tissue releases free fatty acids
Increased free fatty acids gives rise to insulin resistance and causes chronic hyperinsulinemia Correlates with colon, breast, pancreatic, and endometrial cancers |
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Cachexia
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Most severe form of malnutrition
Present in 80% of cancer patients at death Includes: Anorexia, early satiety, weight loss, anemia, asthenia, taste alterations, and altered protein, lipid, and carbohydrate metabolism |
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Side Effects of Cancer Treatment
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Gastrointestinal tract
Bone marrow Hair and skin Reproductive tract |
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Hematologic System
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Chief function
Delivery of substances needed for cellular metabolism Removal of wastes Defense against microorganisms and injury Maintenance of acid-base balance |
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Erythrocytes
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most abundant
responsible for tissue oxygenation |
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Leukocytes(WBC)
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defends body against infection and remove debris
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Granulocytes: destroys microorganisms
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Neutrophils: phagocytes in early inflammation
Eosinophils: ingest antigen-antibody complexes, induced by IgE hypersensitivity Mast Cells: central cell in inflammation, found in vascularized connective tissue Basophils: structurally and functionally similar to mast cells |
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Agranulocytes
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Monocytes and macrophages make up the mononuclear phagocyte system (MPS)
Monocytes Lymphocytes Natural killer (NK) cells |
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spleen:
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disposes of components of blood cell retaining the iron, filters and recycles
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hemostasis:
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stopping bleeding
Requires: Platelets Clotting factors Blood flow and shear forces Endothelial cells Fibrinolysis |
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lymphadenopathy:
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enlarged lymph nodes
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thrombocytopenia:
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decrease in platelets causes bleeding
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Macrocytic-Normochromic Anemias
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Pernicious anemia-Caused by a lack of intrinsic factor from the gastric parietal cells
Required for vitamin B12 absorption Results in vitamin B12 deficiency Loss of appetite, abdominal pain, beefy red tongue (atrophic glossitis), icterus, and splenic enlargement Treatment: parenteral or high oral doses of vitamin B12 |
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Macrocytic-Normochromic Anemias
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Folate deficiency anemia-Absorption of folate occurs in the upper small intestine
Not dependent on any other factor Similar symptoms to pernicious anemia except neurologic manifestations generally not seen Treatment requires daily oral administration of folate |
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Microcytic-Hypochromic Anemias
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Iron deficiency anemia-Most common type of anemia worldwide
Nutritional iron deficiency Metabolic or functional deficiency Progression of iron deficiency causes: Brittle, thin, coarsely ridged, and spoon-shaped nails A red, sore, and painful tongue |
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Posthemorrhagic Anemia
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Acute blood loss from the vascular space
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Infectious Mononucleosis
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Acute, self-limiting infection of B-lymphocytes transmitted by saliva through personal contact
Commonly caused by EBV Symptoms: fever, sore throat, swollen cervical lymph nodes, increased lymphocyte count, and atypical (activated) lymphocytes |
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Leukemias
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Malignant disorder of the blood and blood-forming organs
Excessive accumulation of leukemic cells Acute leukemia Presence of undifferentiated or immature cells, usually blast cells Chronic leukemia Predominant cell is mature but does not function normally Signs and symptoms of leukemia Anemia, bleeding purpura, petechiae, ecchymosis, thrombosis, hemorrhage, DIC, infection, weight loss, bone pain, elevated uric acid, and liver, spleen, and lymph node enlargement |
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Lymphadenopathy
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Enlarged lymph nodes that become palpable and tender
Local lymphadenopathy Drainage of an inflammatory lesion located near the enlarged node General lymphadenopathy Occurs in the presence of malignant or nonmalignant disease |
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Infectious Mononucleosis
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Acute, self-limiting infection of B-lymphocytes transmitted by saliva through personal contact
Commonly caused by EBV Symptoms: fever, sore throat, swollen cervical lymph nodes, increased lymphocyte count, and atypical (activated) lymphocytes |
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Hodgkin Lymphoma
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Characterized by the presence of Reed-Sternberg cells in the lymph nodes
Physical findings Adenopathy, mediastinal mass, splenomegaly, and abdominal mass Symptoms Fever, weight loss, night sweats, pruritus Laboratory findings Thrombocytosis, leukocytosis, eosinophilia, elevated ESR, and elevated alkaline phosphatase Paraneoplastic syndromes |
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Leukemias
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Malignant disorder of the blood and blood-forming organs
Excessive accumulation of leukemic cells Acute leukemia Presence of undifferentiated or immature cells, usually blast cells Chronic leukemia Predominant cell is mature but does not function normally Signs and symptoms of leukemia Anemia, bleeding purpura, petechiae, ecchymosis, thrombosis, hemorrhage, DIC, infection, weight loss, bone pain, elevated uric acid, and liver, spleen, and lymph node enlargement |
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Lymphadenopathy
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Enlarged lymph nodes that become palpable and tender
Local lymphadenopathy Drainage of an inflammatory lesion located near the enlarged node General lymphadenopathy Occurs in the presence of malignant or nonmalignant disease |
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Non-Hodgkin Lymphoma
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Generic term for a diverse group of lymphomas
The lymphomas can be differentiated based on etiology, unique features, and response to therapies Non-Hodgkin lymphomas are linked to chromosome translocations, viral and bacterial infections, environmental agents, immunodeficiencies, and autoimmune disorders |
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Hodgkin Lymphoma
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Characterized by the presence of Reed-Sternberg cells in the lymph nodes
Physical findings Adenopathy, mediastinal mass, splenomegaly, and abdominal mass Symptoms Fever, weight loss, night sweats, pruritus Laboratory findings Thrombocytosis, leukocytosis, eosinophilia, elevated ESR, and elevated alkaline phosphatase Paraneoplastic syndromes |
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Non-Hodgkin Lymphoma
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Generic term for a diverse group of lymphomas
The lymphomas can be differentiated based on etiology, unique features, and response to therapies Non-Hodgkin lymphomas are linked to chromosome translocations, viral and bacterial infections, environmental agents, immunodeficiencies, and autoimmune disorders |
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Stages of Bone Repair
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Inflammation/hematoma formation
Procallus formation Callus formation Callus replacement Remodeling |
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Muscle Contraction
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Excitation
Coupling Contraction Relaxation Isometric contraction Isotonic contraction |
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Muscle Metabolism
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Requires constant supply of ATP and phosphocreatine
Strenuous activity requires oxygen |
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Older Adults
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muscles decrease=sarcopenia, bone decreases, joints=osteoarthritis
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Bone Fracture:
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a break in the continuity of a bone
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Sprain
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Tear or injury to a ligament
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Strain
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Tear or injury to a tendon
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Bursitis
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Inflammation of a bursa
Skin over bone, skin over muscle, and muscle and tendon over bone Caused by repeated trauma Septic bursitis is caused by a wound infection |
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Rhabdomyolosis
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a life-threatening complication of severe muscle trauma with muscle cell loss
Crush syndrome Compartment syndromes Flush kidneys to save them |
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Osteoporosis
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Porous bone
Poorly mineralized bone Decreased Bone density Potential causes Decreased levels of estrogen and testosterone Decreased activity level Inadequate levels of vitamins D and C, or Mg++ |
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Tendinopathy
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Tendinitis
Inflammation of a tendon Tendinosis Painful degradation of collagen fibers |
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Osteomyelitis
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Manifestations
Acute and chronic inflammation, fever, pain, necrotic bone Treatment Antibiotics, débridement, surgery, hyperbaric oxygen therapy Can be caused by Staph |
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Osteoarthritis
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Degeneration and loss of articular cartilage, sclerosis of bone underneath cartilage, and formation of bone spurs (osteophytes)
Also known as DJD chances increase w age Manifestations Pain, stiffness, enlargement of the joint, tenderness, limited motion, and deformity |
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Rheumatoid arthritis
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Systemic autoimmune damage to connective tissue, primarily in the joints (synovial membrane)
Similar symptoms to osteoarthritis Presence of rheumatoid factors (RA or RF test) Antibodies (IgG and IgM) against antibodies Joint fluid presents with inflammatory exudate |
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Gout
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Metabolic disorder that disrupts the body’s control of uric acid production or excretion
Gout manifests high levels of uric acid in the blood and other body fluids Occurs when the uric acid concentration increases to high enough levels to crystallize Crystals deposit in connective tissues throughout the body When these crystals occur in the synovial fluid, the inflammation is known as “gouty arthritis” Mechanisms for crystal deposition Lower body temperatures, decreased albumin or glycosaminoglycan levels, changes in ion concentration and pH, and trauma |
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Disorders of Skeletal Muscle
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Contracture
Muscle fiber shortening without an action potential Caused by failure of the sarcoplasmic reticulum (calcium pump) even with available ATP Stress-induced muscle tension Neck stiffness, back pain, clenching teeth, hand grip, and headache Associated with chronic anxiety Disuse Atrophy-Reduction in the normal size of muscle cells as a result of prolonged inactivity Bed rest, trauma, casting, or nerve damage Treatment Isometric movements and passive lengthening exercises |
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Stages of Pressure Ulcers
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Stages
Nonblanchable erythema of intact skin Partial-thickness skin loss involving epidermis or dermis Full-thickness skin loss involving damage or loss of subcutaneous tissue Full-thickness skin loss with damage to muscle, bone, or supporting structures |
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Disorders of Skin
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Allergic contact dermatitis-Caused by a hypersensitivity reaction
The allergen comes in contact with the skin Atopic dermatitis-Type I hypersensitivity—activation of mast cells, eosinophils, T-lymphocytes, and other inflammatory cells Causes red, weeping crusts and chronic inflammation, lichenification Irritant contact dermatitis-Nonimmunologic inflammation of the skin Chemical irritation from acids or prolonged exposure to irritating substances Symptoms similar to allergic contact dermatitis Treatment—remove stimulus |
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Skin Cancer
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Basal-most common, does not metastasize, risk=sunlight, slow growth rate
Squamous-in situ and invasive, more malignant, sunlight exposure and xray are risks, can spread to regional lymph nodes Malignant-originates from melanocytes, metastasizes |
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Disorders of Skin
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Stasis dermatitis-Occurs in the legs as a result of venous stasis, edema, and vascular trauma
Sequence of events: erythema, pruritus, scaling, petechiae, ulcerations Seborrheic dermatitis-Inflammation of the skin involving the scalp, eyebrows, eyelids, nasolabial folds, and ear canals Scaly, white, or yellowish plaques |
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Psoriasis
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Psoriasis
Chronic, relapsing, proliferative skin disorder T cell immune–mediated skin disease Scaly, thick, silvery, elevated lesions, usually on the scalp, elbows, or knees caused by a high rate of mitosis in the basale layer |
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Burns
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Partial-thickness burns
First degree Superficial and deep partial Second degree Full-thickness burns Third degree “Rule of nines” |
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Kaposi's Sarcoma
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vascular malignancy related to immunodeficiency states, such as transplant recipients
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Normal in Cardiac Cycle
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Blood goes in superior and inferior venae cavae--->R atrium--->R ventricle--->pulmonary artery to lungs--->pulmonary veins--->L atrium--->L aortic valve--->L ventricle--->aorta
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Diastole:
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filling
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Systole:
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contraction
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S1:
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mitral and tricuspid (AV) valves closing
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S2:
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pulmonic and aortic valves closing
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Conduction of the heart:
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pacemaker is at the top(SA node), next halfway down to AV node, bottom of heart and spreads each ventricle to bund of His and bundle branches (R and L), Purkinje fibers at end
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ECG tracing:
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T wave at end...QRS is big ^...P wave is at beginning; atrial depolarization, ventricular depolarization, ventricular repolarization
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PVC:
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preventricular contraction because of stress or caffeine
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Sympathetic Nerves
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speeds up HR
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Parasympathetic Nerves
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slows HR(like a parachute settling)
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Vagus nerve:
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para-vagal maneuver(going to the bathroom)...done when pt is tachy
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Preload
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Left ventricular end-diastolic volume
Laplace law Frank-Starling law of the heart during diastole |
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Afterload
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resistance coming out(meds that can increase or decrease each)
Load muscle must move after it starts to contract |
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Varicose Veins
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pooling of blood
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Venous Insufficiency
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not getting enough blood...it is pooling---->can cause venous stasis ulcer
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DVTs
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Obstruction of venous flow leading to increased venous pressure
Factors Venous stasis Venous endothelial damage Hypercoagulable states a clot, aka thrombus, that can be caused by inactivity; if it travels it can go to lungs and become pulmonary embolus -PE presents w chest pain and SOB |
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Superior Vena Cava syndrome
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person was blue w swelling in head and upper extremity...couldn't lay down...has orthopenia.
Progressive occlusion of the superior vena cava that leads to venous distention of upper extremities and head Oncologic emergency |
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HTN
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primary is most common; different stages=different treatments; if not treated then vascular and tissue level problems
Secondary hypertension Caused by a systemic disease process that raises peripheral vascular resistance or cardiac output Isolated systolic hypertension Elevations of systolic pressure are caused by increases in cardiac output, total peripheral vascular resistance, or both Complicated hypertension Chronic hypertensive damage to the walls of systemic blood vessels Smooth muscle cells undergo hypertrophy and hyperplasia with fibrosis of the tunica intima and media Malignant hypertension Rapidly progressive hypertension Diastolic pressure is usually >140 mm Hg |
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Aneurysm:
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bulge/pocketing in aorta, can be in diff spots such as thoracic or abdominal; want to catch and treat early otherwise if it blows pt will die
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Thrombus vs. embolus
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Thrombus-clot
Embolus-moving thromboembolus=moving clot |
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Peripheral Artery Disease:
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arterial disease of arteries; artery vs. venous, may be a decrease in pulses and cold extremities/Raynauds have vasospasm, pain, and are white
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Arteriosclerosis
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Chronic disease of the arterial system
Ischemia(lack of O2) vs. infarction(death of tissue) Myocardial ischemia ex. angina Myocardial infarction ex. heart attack |
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CAD:
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Any vascular disorder that narrows or occludes the coronary arteries
risk factors=smoking, HTN, obesity, diabetes, sodium intake(all modifiable), genetics, race, gender[woman postmenopausal], age(all not modifiable) |
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Valve Disorders:
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stenosis=stiff, regurgitation or insufficiency=pushes it back
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Left heart failure
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Systolic heart failure
Inability of the heart to generate adequate cardiac output to perfuse tissues Ventricular remodeling Diastolic heart failure Pulmonary congestion despite normal stroke volume and cardiac output backs up in to lungs, which can lead to Right sided |
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Right heart failure
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Most commonly caused by a diffuse hypoxic pulmonary disease
Can result from an increase in left ventricular filling pressure that is reflected back into the pulmonary circulation backs up in the system(edema) |
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Shock:
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perfusion of heart is not happening so tissues die
Cardiovascular system fails to perfuse the tissues adequately Impaired oxygen use Impaired glucose use |
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Phagocytosis
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Process by which a cell ingests and disposes of foreign material
Monocytes are produced in the bone marrow, enter the circulation, and migrate to the inflammatory site, where they develop into macrophages Macrophages typically arrive at the inflammatory site 24 hours or later after neutrophils |
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Platelets
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activation results in degranulation and interaction with components of the coagulation system
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