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216 Cards in this Set
- Front
- Back
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Physiologic changes with somatic death
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Means: Death of an organism- absence of heart rate and respiration that usually follows “brain death.”
Signs: • Algor Mortis • Livor Mortis • Rigor Mortis • Pale Skin |
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Algor Mortis
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Decrease in body temperature
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Livor Mortis
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Accumulation of blood and fluids; blood settles in dependent areas
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Rigor Mortis
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cellular changes create stiff muscles throughout the body (muscle rigidity), downward progression (head to toe), eventually gives way to flaccidity as tissues deteriorate (24 to 48 hrs.)
Putrefaction- smell of dead body (not permanent) |
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Pale Skin
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Blood is not flowing
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Pathogenesis
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Development or evolution of disease in the body (what’s happening in the body)
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Classification of Disease
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• Intrinsic
• Extrinsic (Inanimate) • Extrinsic (Animate) • Idiopathic (unknown) |
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Intrinsic
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inherited, psychogenic, congenital, metabolic, degenerative, neoplastic, immunologic, nutritional deficiency
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Extrinsic (Inanimate)
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Iatrogenic, physical agent induced, force, temp, humidity, radiation, electricity, chemicals
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Extrinsic (Animate)
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infections, pathogenic organisms, viruses, bacteria, fungi, protozoa, pathogenic animals, insects, worms
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Types of cellular changes
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Reversible
Irreversible |
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Reversible
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Cells can get back to normal stage
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Irreversible
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Cellular death, cells cannot do what it is suppose to do due to cellular swelling and alteration
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Necrosis
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(Irreversible)- the cells are injured and eventually die due to decrease supply or lack of oxygen to cell
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Necrosis: Clinical Manifestations
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-specific to organ/tissue
-body will attempt to compensate -changes are progressive |
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Types of Necrosis
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• Coagulation
• Liquefactive • Fat • Caseous |
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Coagulation
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(most common)- typically seen in the heart, surgical wounds, cells die and form together to form a solid mass and then are dissolved; basic tissue is maintained and repair itself; Ischemia can lead to this type
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Liquefactive
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typically seen in the brain, cells breakdown quickly and leave degree (cysts)
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Fat
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typically seen in pancreas, death of adipose( fat tissue) by enzymes, look like white chalky area
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Caseous
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typically seen in lungs, Tuberculosis, bacteria comes in and infectious cells die off, look like clumpy cheese
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Types of wound drainage
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• Serous (serum)
• sanguineous (blood) • serosanguineous (blood & serum) • purulent (pus) |
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Processes associated with phagocytosis
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1. Binding (clustering of receptors)
2. Activation (clusters activate & initiate membrane motility) 3. Entry (increased membrane motility leads to either complete engulfment or shrinking of cytoplasm) |
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Dehydration
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• Type of volume deficit that includes a decreased volume of fluid that is too concentrated. (Hypernatremia)
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Symptoms of dehydration
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•Sudden weight loss
•2%- mild •5%- moderate •8%- severe •10%- life threatening •Hypotension, postural hypotension, oliguria, absence of sweat and tears, confusion, coma, shock |
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Fluid Volume Deficit
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Water and sodium are lost in proportional amounts (isotonic fashion- fluid and sodium lost together)
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Fluid Volume Deficit: Etiologies
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Vomiting, Diarrhea, Gastric loss by suction, Renal Disease, Diuretics, Excessive blood loss, Massive Diaphoresis, Third-spacing Edema
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Fluid Volume Deficit: Clinical Manifestations
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Sudden weight loss, Decrease in BP (postural hypotension), Dizziness, Oliguria (decrease urine production), Skin Tenting
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Fluid Volume Excess
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Water and sodium are gained or retained in proportional amounts
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Fluid excess: etiologies
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• Intravenous infusions
• Disease process- CHF, Adrenal Dysfunction, Renal Disease, Steroid Therapy |
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Fluid Excess: Clinical Manifestations
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Sudden weight loss, Edema, Bounding Pulse, Neck Vein Distention (JVD), Dyspnea (difficulty breathing), Orthopnea (difficulty breathing while supine), Frothy Sputum (due to a lot of fluid buildup around capillaries)
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Electrolytes Normal Values
Na, K, Ca, Mg, Plasma Phosphate |
• Sodium (136-145)
Hypernatremia (> 145) Hyponatremia (<136) • Potassium (3.5-5.0) Hyperkalemia (>5.0) Hypokalemia (<3.5) • Calcium (9.0-10.5) Hypercalcemia(>10.5) Hypocalcemia (<9.0) •Magnesium (1.3-2.1) Hypermagnesemia (>2.1) Hypomagnesemia (<1.3) •Plasma Phosphate (3.0-4.5) Hyperphosphatemia (>4.5) Hypophosphatemia (<3.0) |
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Main function of Na, K, Ca, Mg, P
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Sodium- transmission of nerve impulses; fluid balance
Potassium- cardiac, skeletal and smooth muscle function Magnesium- Na/K pump, energy production of the body muscle function Calcium- Transmission of nerve impulses, clotting mechanisms, formation of bones and teeth Phosphorus- carbohydrates, protein, bone formation, fat metabolism |
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Hypernatremia: Etiologes
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Excessive water loss or sodium gain, Salt tablets, Processed foods, IV fluids, Diabetes Insipidus, Deficiency of ADH(antidiuretic hormone)
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Hyponatremia: Etiologes
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Water gain or sodium loss, Excess GI loss, Renal disease, Water intoxication, Diuretics
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Hyperkalemia: Etiologes
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Rapid IV infusion or intake of potassium, Large transfusion of stored blood (sickle cell), Insufficient insulin (uncontrolled diabetes), Medications, Renal disease
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Hypokalemia: Etiologies
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Decrease intake, Excess excretion (diarrhea, gastric suction, laxative abuse, diuretics), Excess insulin intake, Renal disease
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Hypercalemia: Etiologies
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Vitamin D overdose, Prolonged immobilization, Bone tumors, Chemotherapy, Hyperparathyroidism, Hypophosphatemia, Prolonged bed rest
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Hypocalcemia: Etiologies
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Insufficient Dietary Intake, Pancreatitis, Malabsorption, Presence of Hypomagnesemia (calcium and magnesium have a direct relationship), Excess phosphorus intake (calcium and phosphorus have an indirect relationship), Renal disease, Vitamin D deficiency (low calcium)
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Hypermagnesemia: Etiologies
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Increased intake, Bone demineralization, Milk of Magnesium, Renal disease (excretion of MN is impaired), Excessive antacids can result in Hypermagnesemia
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Hypomagnesemia: Etiologies
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Chronic alcohol abuse, Malnutrition (both most common), Laxative abuse/diarrhea, Pancreatic disease
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Hyperphosphatemia: Etiologies
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Excessive use of phosphate replacement, Phosphate enemas, Renal failure (most common)
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Hypophosphatemia: Etiologies
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Chronic Alcoholism, Intractable Diarrhea/vomiting, Antacid abuse (Low phosphorous Mg binds and excretes)
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What electrolytes effect cardiac system & clinical manifestations that occur?
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Low K- dysrhythmias
High K- dysrhythmias, cardiac arrest Low Ca- dysrhythmias High Ca- dysrhythmias Low Mg- dysrhythmias High Mg- bradycardia, dysrhythmias, cardiac arrest (resp. depression) High P- dysrhythmias (if Ca low) |
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What electrolytes effect neuro system & clinical manifestations that occur?
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High or low Na - confusion, lethargy
Low Na-coma, seizures Low K- lethargy Low Mg- seizures High Mg- lethargy Low P- confusion, stupor |
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What electrolytes effect neuromuscular system & clinical manifestations that occur?
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Low Ca- trousseau sign, chvostek sign, paresthesias, spasms, tetany.
High Ca- muscle weakness Low Mg- trousseau sign, chvostek sign, paresthesias, hyperactive DTR (deep tendon reflexes), tetany. High Mg- decrease DTR (deep tendon reflexes) Low P- trousseau sign, chvostek sign, paresthesias, spasms, tetany (if Ca low) |
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What electrolytes effect GI system & clinical manifestations that occur?
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Low sodium- anorexia
low potassium- polyuria low Phosphate- diarrhea High ca- constipation |
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Which electrolyte imbalances can occur as a result of laxative abuse?
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Low Mg and Low K
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Lines of Defense
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•Skin- Provide mechanical and chemical barriers that prevent microorganisms from gaining access to the body’s tissues
•Mucous Membranes- Same as skin^ •What is unique about the chemicals produced in the skin and intestinal wall? The skin produces antimicrobial peptides (defenses) that kill a wide variety of bacteria and fungi. Intestinal produce a bacteria peptide (crytocidins) that prevent bacteria from colonizing the intestinal wall. |
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Immunocompromise
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immune system that has been impaired by disease or treatment.
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White Blood cell changes in the presence of infection
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• Neutrophils- Infection will increase the # of neutrophils b/c they are trying to fight off the infection. Bands (immature neutrophils) cause a shift to the left; a decrease in neutrophils during prolong infection, will cause an increase in Bands.
• Eosinophils- responds to parasitic infection, associated w/ increase in # during allergic reactions and infection by intestinal parasites (trying to fight off the infection) • Basophils&Mast cells- typically related to seasonal allergies, get an increase during infection to fight off infection •Monocytes&Macrophages- plays a role in the healing process (surgical wounds), they sense any kind of invaders and serve as a protective mechanism to prevent infection before invaders come in, also secrete # of proteins that breakdown tissue or stimulate growth •Lymphocytes oT Lymphocytes- Made in bone marrow- have to go to the thymus to mature oB Lymphocytes- Made and mature in bone marrow. Both T and B lymphocytes communicate w/ chemical mediators to kill Infections and recruit neutrophils oNatural Killer Cells- Few lymphocytes that kill destroy tumor cells and viruses, do not depend on chemical mediators to fight off infections |
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Pathogenesis of autoimmune disorders
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Intrinsic
•Genetic •Rheumatoid Arthritis Extrinsic • Virus • Lupus Trigger (theories) •Viral infection • Trauma with exposure of sequestered tissue • Malfunction of regulatory T cells (thymus) |
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Types of Immunity
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Specific Adaptive
Acquired Passive Acquired Active |
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Specific Adaptive Immunity
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develops throughout life- development of specific antigens (body is exposed to an antigen and in response it turns into an antibody)
natural immunity- genetic B and T lymphocytes are the cellular mediators of specific adaptive immunity Humoral Immunity- the B lymphocytes recognize antigens and develop antibodies Cell-Mediated Immunity- the T lymphocytes recognize antigens on cell surfaces and develop antibodies |
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Acquired Passive Immunity
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immunity is transferred via plasma containing antibodies (body is not actively making antibodies, are given something to make them)
Maternal/fetal transfer- IgG and IgA Direct injection “serotherapy”- Administer of immunoglobulin (Hepatitis-effective immunoglobin) |
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Acquired Active Immunity
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the body develop antibodies in response to the presence of an antigen
Vaccination Exposure to an infectious disease (Chicken pox) |
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Inflammatory Process
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•Goal of inflammation is to establish environment so tissues can heal
•Process- macrophages, such as the lungs or intestines, then these macrophages will be the first immune cells on the scene. They begin to digest the invading organism, and by presenting antigens (proteins from the destroyed bacteria), they stimulate other cells of the immune system into action. •Clinical Manifestations & Physiologic changes of each •Edema- swelling •Pain- dolor •Calor- heat, blood flow •Redness- erythemia |
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Active (acquired) immunity
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the body, exposed to an antigen, develops it’s own antibodies
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Passive immunity
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antibodies manufactured by someone else (or some animal) is given to another
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Types of Hypersensitivity Responses Type I
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Anaphylactic- severe Hypersensitivity, Life threatening (Bee sting or shellfish)
Rapid onset, wheezing, throat “closing,” tight chest, dyspnea, erythema (redness) with welts |
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Types of Hypersensitivity Responses Type II
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Tissue Specific (cytotoxic)- antibodies attack antigens of specific cells
o Involves activation of complement by IgA and IgM o Autoantibodies destroy own tissues or cells o Examples: Blood transfusion reactions, Autoimmune disorders, Graft rejection |
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Types of Hypersensitivity Responses Type III
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Immune Complex response
o Involves formation of antigen/antibody complexes that activate complement and cause inflammation o Ag/Ab complexes can cause tissue and organ destruction o Examples: Arthus reaction to improperly administered vaccine or repeated exposure to vaccine (continue invasion of antigens), persistent low grade infection (low grade bacteria infection), autoimmune process(antigens/antibodies buildup in tissues) |
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Types of Hypersensitivity Responses Type IV
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delayed response involving recognition of and response to foreign invaders by T-lymphocytes (not doing their job in response to foreign invaders)
o Examples: TB reaction, Poison Ivy o Clinical Manifestations: Red lesions w/ enduration(48 hrs), Urticaria |
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Acute infection
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Last 2 wks or less
• Clinical manifestations: pain, heat, redness, swelling |
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Chronic Infection
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Can go on for a long time- wks to months to years
• Example: arthroscopy for chronic knee pain |
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Anemia
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Decrease oxygen to tissues, S/Sx: increase respiration, increase heart rate, fatigue, decrease activity tolerance, pallor(pain)
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Types of Anemia
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• Hemolytic
o Sickle cell- defect in hemoglobulin, change the shape of RBCs- can not function o Thalassemia- destruction of RBC • Aplastic Anemia • Nutritional Anemia o B12 or Folate Deficiency Lack of intrinsic factor, AKA pernicious, Megaloblastic bone marrow cells (large and deformed) o Iron deficiency Anemia RBCs are mycrocytic in size, and hydrochromic in color MCHC , TIBC, and Ferritin/iron are decreased. Reticulocyte count (immature RBC) is increased |
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Aplastic Anemia: Etiologies & Clinical Manifestations
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o Etiology: decrease in functional bone marrow results in pancytopenia (decrease in WBC, RBC, and platelets)
o Clinical Manifestations: Insidious onset, weakness, fatigue, lethargy, pallor, dyspnea, fever, chills, infections, petechiae, bruising, nosebleeds |
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Nutritional Anemia (B12 or Folate deficiency): Etiologies & Clinical Manifestations
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Etiologies: genetic autoimmune disorder, chronic alcoholism, chron’s disease, severe gastric disease
Clinical manifestations: fatigue, parethesias, dementia, tachypnea (rapid breathing), arthralgia (joint pain) |
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Pernicuous anemia
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Nutritional Anemia (B12 or folate defieciency)
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Nutritional Anemia (iron deficiency): Clinical Manifestations
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Clinical manifestations:
mild anemia: hemoglobin- male(10-14) female(8-12); Moderate Anemia: hemoglobin- Male(8-10) Female(6-8); Severe Anemia: hemoglobin- Male(<8) Female(<6) Normal: Male (14-18)/Female (12-16) |
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Secretion and function of erythropoietin
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Hormone produced primarily by the kidney that stimulates bone marrow to produce erythrocytes
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Hematologic testing: CBC
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a complete blood count that gives important information about the kinds and numbers of cells in the blood, especially HCT (Hematocrit), WBC (Leukocytes), Platelets
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Hypercoagulation
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AKA: thrombophilia, may be defined as reduced capillary blood flow or a greater tendency than normal for blood to coagulate, or clot.
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Clotting disorders is also known as?
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hypercoagulability
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Thrombus
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pathological formation or clot inside a blood vessel or heart; stationary blood clot
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Embolus
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traveling blood clot, travels through/migrates in vascular system, impairs blood flow (very dangerous)
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Synthesis of red blood cells
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• Erythrocytes: carrying oxygen to tissues and removing carbon dioxide from tissues. AKA RBC
• Erythropoiesis: the process of red blood cell formation, almost exclusively produce in the bone marrow; The production of RBCs is triggered when the kidneys sense low oxygen tension and blood secretes the hormone erythropoietin and create RBCs |
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Diagnostic testing for clotting
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• Intrinsic Clotting: PTT (60-70 sec.) or APTT (30-40 sec.)
• Extrinsic Clotting: Prothrombin Time or INR (normal 11.0-12.5 sec.) |
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Down’s Syndrome
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Condition where you have an extra chromosome (chromosome 21) trisomy 21
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Human Genome Project
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• International project to map out all of the genes in the body. To try and find disease genes. Over 18,000 disease genes found.
• significance to healthcare because it can help find the cure for some diseases and prevention. |
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Genetic risk factors for autosomal dominant/recessive
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• likelihood of inheriting a disease that is autosomal dominant?
50% (1 affected parent)/75% 2 (both parents affected) • offspring being affected by an autosomal recessive disease? 25% (both parents carriers but don't have the disease)/50% (1 affected parent & other parent carrier) |
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Leukemia
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• Malignant disease of the bone marrow
• Characterized by increase in WBCs that infiltrate bone marrow, blood, organs, and tissues |
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Types of Leukemia
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• ALL (Acute lymphocytic leukemia)- proliferation of immature wbcs- infect all the functions they filterates
• AML (Acute milloid leukemia)- proliferation of granulocytes; rapid onset, patient can die w/o treatment, progression is fast • CLL (Chronic Lmphocytic leukemia)- proliferation of immature WBCs; over proliferation of lymphocytes, easier to treat, insidious onset- patient may not know they have symptoms • CML (Chronic myeloid leukemia) same ^ |
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Angiogenesis
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Process of forming new blood vessels
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Cancer warning signs
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C- change in bladder habits
A- a sore throat that does not heal U- unusual bleeding or discharge T- thickening of tissue/lump in breast or elsewhere in the body I- Ingestion or difficulty swallowing O- obvious change in wart or mole N- nagging cough or hoarse voice |
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PSA
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• Prostate specific antigen (Tumor marker) - substance found in the blood, urine, body tissue that can be elevated in the presence of cancer.
• Associated with prostate cancer |
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Benign
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tumor that does not metastasize, localized and well differentiated, insitu (don’t spread), doesn’t kill host
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Metastatic
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process whereby cancer cells escape their tissue of origin and initiate new colonies in distant sites
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Paraneoplastic syndrome
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• A disease or a symptom that is the consequence of the presence of cancer in the body
• This phenomena is mediated by humoral factors excreted by tumor cells or by an immune response against the tumor • Example: Hypercalcemia |
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Arteriosclerosis
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• General term for various pathologic processes the cause “hardening of the arteries”; Abnormal thickening and hardening of the vessel wall
• Pathogenesis: smooth muscle cells and collagen fibers migrate into the tunica intima causing it to stiffening and thicken, gradually the arterial lumen narrows and cause increase in blood pressure and tissue perfusion. |
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Atherosclerosis
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A form of arteriosclerosis, plaque: deposits of fatty substances, cellular waste products, calcium and other substances build up in the inner lining of an artery (Affects medium to large arteries)
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Aneurysm
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Localized dilation of blood vessel that can affect blood flow, a weak area in the vessel that may eventually rupture
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Where does an aneurysm commonly occur?
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Base of the Brain (Circle of Willis), Aorta, thorax or abdominal area, but may develop anywhere.
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Types of Aneurysm
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True
False Dissecting |
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True Aneurysm
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• involves an out pouching of all three layers of a blood vessel: the intima the media, and the adventitia (less likely to rupture)
Saccular- one vessel effected Fusiform- both sides of vessel effected |
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False Aneurysm
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one tunica is left unaffected (blood escape and has layers to support it); muscle tissue and fascia often confine the leaking blood which enhances thrombus formation; usually caused by trauma rather than vessel disease
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Dissecting Aneurysm
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Tear in intima allows leaking and expansion of hematoma separates intima from other layers. Lethal b/c it could cause you arteries to burst which will be deadly.
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Varicose veins
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Valvular incompetence of the superficial veins cause by overstretching of the vein from excessive venous pressure
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Chronic Venous Insufficiency
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Inadequate Venous Return
• Can lead development of venous stasis ulcers; develop in areas where circulation is sluggish and blood return to the heart is slowed and not enough oxygen to site • Valvular incompetence of deep veins • Ankle is the most common site- blood is just sitting around and not able to get back to heart, and oxygenated blood is not able to reach site. |
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Hypertension
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Silent disease, degree and duration of elevated BP determine the manifestations and degree of target organ damage.
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Orthostatic Hypotension
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• A decrease in SBP (Systolic Blood Pressure) of greater than or equal to 20mmHg when standing; a drop in BP when change position from supine to standing
o Ex. 130/90 to 110/90 change in 20 |
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Coronary Artery Disease
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A narrowing of the coronary arteries resulting in decreased oxygen supply to the myocardium Etiology: Coronary atherosclerosis
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Prinzmetal angina
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Coronary artery vasospasm, chest pain due to vasospasm in coronary artery so you have a decrease oxygenated blood to heart = chest pain
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Myocardial Infarction
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Death of cells in the myocardium, r/t prolong or severe ischemia. Cell damage is irreversible (can not regenerate)
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Transmural infarction
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Type of MI, ischemic necrosis involves the full thickness of the affected muscle segment, extending from the endocardium through the myocardium to the epicardium.
Most serious b/c it involves all layers of the cardiac muscle. |
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Valvular stenosis
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Inability of valve leaflets to open and close properly (fail to open and close properly b/c become hard) Have an increase in afterload
Afterload means amount of resistance the ventricle must overcome to eject blood. |
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Depolarization of cardiac cells
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When the cell responds to an electrical stimulus
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Cardiomyopathy
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• Abnormality of heart muscle that leads to functional changes in the heart
• 3 Types: Dilated- all 4 chambers are dilated, decrease contractility and CO (most common) Restrictive- rigid ventricular wall create back pressure and right heart failure, reduced SV and CO. (least common) Hypertrophic- thickened ventricular muscle resulting in increase pulmonary and venous pressure, reduce CO (heart muscles getting bigger but fails over time b/c it’s overworked. |
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Pericardial effusion
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Accumulation of fluid within pericardial cavity, can progress to tamponade (medical emergency- can shut down the heart)
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Left sided heart failure
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Left ventricle has decreased ability to pump blood into systemic circulation and fluid backs up into pulmonary circulation (into lungs)
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Right sided heart failure
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• Right ventricle has decreased ability to pump blood to the lungs causing fluid backup into venous circulation (rest of the body)
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Atelectasis
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Collapse of the aveoli prevents exchange if CO2 and O2.
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Tension pneumothorax
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Air is sucked into the pleural space through the chest wall and can’t escape. This puts pressure on the heart and great vessels. Life threatening
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Asthma
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Lung disease characterized by acute, reversible episodes of airway obstruction
Pathogenesis: Inflammatory response causes bronchial smooth muscle spasm, vascular congestive, edema, and production of thick mucous |
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Aspiration pneumonia
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Lung inflammation resulting from introduction of foreign materials into the tracheobronchial tree (inflammation in lung due to what is aspirated in the lungs). Bacterial- inhaled bacteria in the lungs, Foreign body aspiration- blocking airway, Chemical- patient aspirates gastric contents
Aspiration means to inhale. |
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Flail chest
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• Multiple rib fractures interfere w/ generation of negative intrapleural pressures resulting in decreased lung expansion on inspiration
• Chest wall expands outward on expiration |
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What does ABG stand for?
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Arterial Blood Gas
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Normal ABGs
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pH: an indirect expression of the balance between CO2, which is regulated by the lungs, and HCO3 (Bicarbonate), a base that is regulated by the kidneys. Normal pH: 7.35-7.45
HCO3: body’s main base, it keeps the body from becoming too acidic. Normal range: 22-26 CO2: refers to the presence of dissolved carbon dioxide gas in the blood and is influenced by the lungs. Normal range: 35-45 |
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Causes of respiratory acidosis
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•Hypoventilation (delivery of air in alveoli is insufficient)
•Respiratory depression from diseases, poisons, anesthetics •Airway obstruction •Alveolar-capillary blockage •Inadequate mechanical ventilation •Inadequate chest expansion |
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Emphysema
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Destructive changes in the alveolar walls results in abdominal enlargement of alveolar sacs with loss of recoil “pink puffer”
S&S: minimal or absent cough Associated w/ chronic bronchitis |
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Pulmonary Embolism
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• Blockage of a pulmonary artery by fat, air, or thrombotic emboli
• Impact depends on size of emboli, degree of circulatory impairment, and underlying cardiopulmonary conditions |
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Acute Bronchitis:
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inflammation of the tracheobronchial airway accompanied by exudate formation and increased mucous production
Viral (most common), bacterial, fungal or chemical causes |
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Chronic Bronchitis:
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inflammatory response resulting in vasodilation, mucosal edema and fibrosis.
Associated w/ emphysema. Diagnosis: hypersecretion of mucous and recurrent productive cough lasting >3 months when other causes have been eliminated. (right sided heart failure) “blue bloater” |
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Hypoxemia
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low O2 concentration in the blood
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Hypoxia
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decrease oxygenation in tissues
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Hypercapnia
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excess CO2 in the blood
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Hypoventilation
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delivery of air to the alveoli is insufficient to provide adequate O2 and remove CO2
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Hyperventilation
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delivery of air to alveoli exceeds amount needed to meet metabolic needs for gas exchange
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Addison’s disease
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Adrenal insufficiency results in decreased levels of Cortisol, Aldosterone and testosterone
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Cushing’s disease
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Hypersecretion of Cortisol from the adrenal cortex; Classic symptoms: buffalo hump, truncal obesity, purple straie, moon space
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Hyperparathyroidism
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Hypersecretion of PTH (parathyroid hormone): increase absorption and reabsorption of Ca and increase phosphate excretion
Hypophosphatemia Hypercalcamia |
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Diabetes mellitus
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Disease that lead to high blood glucose (lack of or inadequate secretion of insulin)- insulin resistance
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Type I Diabetes
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Insulin dependent, juvenile onset, the body can not make insulin (lost of beta cells of the islets of Langerhans in the pancreas results in insulin deficiency
Underweight, Ketaoacidosis, Any age |
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Type II Diabetes
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Non insulin dependent, adult onset, situation of too little insulin or there is resistance- the is not responding (inadequate secretion of insulin or resistance to insulin results in hyperglycemia)
Overweight, Insulin secretion, adult onset |
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Pheochromocytoma
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Tumor of the adrenal medulla resulting in excessive secretion of catecholamines, results in hypertension
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Stroke
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General term used to describe cerebrovascular events that results localized brain infarction, “CVA” or “Brain Attacks”
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Decerebate posturing
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arms extended and wrists externally rotated, extension of legs and internal rotation of feet
Abnormal Posturing= Medical emergency |
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Decorticate posturing
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flexion of arms and wrist, extension of legs and internal rotation of feet
Abnormal Posturing= Medical Emergency |
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Paraplegia
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Inability to move lower body, both legs and usually the lower part of the trunk due to thoracic injury of the spinal cord
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Aphasia
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Decrease in vocabulary, attention span, and inability to use rules r/t language
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TIA
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Means: Transient Ischemic Attack
Brief or temporary episode of neurological symptoms as a result of ischemia. “Mini Stroke”, a warning for stroke; Common symptoms: vision problems, difficulty w/ speech, numbness in extremities, and loss of balance |
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Multiple Sclerosis
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An autoimmune disorder of the CNS where myelin and nerve axons in the brain and spinal cord are destroyed; Pathogenesis: loss of myelin sheath (refers to scars/ plaques that form in the brain and spinal cord as a result of demyelination)
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Alzheimer’s disease
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Most common type of dementia (progressive decline in cognitive function); chronic, progressive form of dementia, usually occurs after age 65 but can occur as early as age 40
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Seizures
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Uncontrolled discharge of neurons of the cerebral cortex interferes w/ normal function
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Types of Seizures
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Partial (Simple or Complex)
Generalized (Absense, Clonic, Tonic, Myoclonic, Tonic-Clonic) |
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Partial Seizure
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Only one part of brain affected
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Simple Seizure
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Partial seizre w/ no impairment of consciousness, limited to one part of body
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Complex Seizre
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Partial seizure w/ impaired consciousness, characterized by involuntary, repetitive movement, can be in more than one part of body
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Generalized Seizure
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entire brain is affected
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Absence seizure
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Generalized seizure w/ brief lapse of consciousness that may involve staring, blinking, eye rolling, arm movement; more common <20
AKA (petit mal) |
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Clonic seizure
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Generalized seizure w/ jerking of muscle groups w/ some changes in LOC
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Tonic seizure
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Generalized seizure w/ stiffening of muscle group, may or may not involve changes in LOC
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Myoclonic seizure
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Generalized seizure w/ single jerk of muscle group, doesn’t involve change in LOC
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Tonic-Clonic seizure
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Generalized seizure w/ stiff phase followed by jerking phase w/ change or loss of LOC
AKA (grand mal) |
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GERD (Gastroesophageal Reflux)
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•Backflow of gastric contents into the esophagus through the lower esophageal spincter.
Pathogenesis: alteration of the lower esophageal sphincter. Clinical Manifestations: Heartburn (most common), regurgitation, chest pain, Dysphagia |
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Peptic Ulcer Disease
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•Disease where ulcers are located in stomach, esophagus, or duodenum
Etiology: H pyloric bacteria, Clinical Manifestations: epigastric burning. Gastric: pain more likely after a meal and can radiate to the back and flank; Duodenal: pain occurs on an empty stomach, can radiate to back or thorax, pt may get relief w/ food or antacids |
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Hiatal Hernia
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Condition where part of the stomach protrudes above the diaphragm into the medial stinal cavity
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Types of Hiatal Hernia
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Sliding- cause by weakened esophageal muscle, part of the stomach and lower esophageal sphincter protrudes above diaphragm w/ peritonitis
Paraesophageal: parts of the stomach roll up above the diaphragm but not the gastro-esophageal junction or the lower esophageal sphincter |
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Cholecystitis
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• Acute inflammation of the gall bladder
Pathogenesis: obstruction of cystic duct Clinical manifestation: Right upper quadrant pain, abdominal tenderness, and fever |
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Intestinal Obstruction & Signs & Symptoms
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• Partial or complete blockage of the intestinal of the lumen; 90% in small intestine but can occur in large intestine
•Signs& Symptoms: Crampy abdominal pain that comes and goes (intermittent) Nausea Vomiting or diarrhea Inability to have a bowel movement or pass gas Swelling of the abdomen (distention) Abdominal tenderness Fever |
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Types of Intestinal Obstruction
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Mechanical: cause by some type of blockage such as adhesions, fecal impaction, tumor, inflammation or restrictions.
Functional: caused by lost of compulsive compactability, AKA Illus, no peristalsis going on system just stop |
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Hepatitis
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•Inflammation of the liver
most commonly cause: Viral; other causes: Cytomegalovirus, Epstein Barr |
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Chron's Disease
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chronic inflammation of bowel anywhere in GI Tract (destruction of the mucous immune system, inflammation extending through all layer of the intestinal wall), most commonly affects the illum and colon
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Chron's Disease: Clinical Manifestations
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N/V, abdominal pain (right lower quadrant pain w bowel inflammation), increase in WBCs, decrease in appetite- weight loss, increase in # of stool (foul smelling)
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Diverticulitis:
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when bacteria becomes trap into the diverticuli pouches and inflammation become infected
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Diverticulitis: Clinical Manifestations
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Acute or acute abdominal pain, fever, tachycardia, diarrhea or constipation, increase in WBC.
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Appendicitis
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Inflammation of the vermiform appendix
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Appendicitis: Clinical Manifestations/Symptoms
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Pain in right lower quadrant (Mac Burnnes point- halfway b/t umbilicus and right iliac crest), N/V, anorexia, diarrhea, rebound tenderness, fever.
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Jaundice
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Yellowish discoloration of body tissues, (alteration in Bilirubin metabolism and alteration of flow of bile) Symptom, not a disease!
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Types of Jaundice
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o Hemolytic (pre-hepatic jaundice): Increase breakdown of RBC, increase in unbound Bilirubin and the liver can’t handle the increase. Seen w/ Sickle Cell crisis or blood transfusion reaction.
o Obstructive (post-hepatic jaundice): Obstruction of the flow of bile from the liver. Bilirubin is a pigment of bile and there is an increase of bound and unbound Bilirubin doesn’t enter the intestines so it is not excreted. Seen w/ common bile duct obstruction and Cholelithiasis. o Hepatocellular (hepatic jaundice): Alteration in liver function. Liver can’t take Bilirubin from the blood and conjugate it and excrete it. Seen w/ hepatitis or liver sclerosis. |
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Hepatitis transmission
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• Hepatitis A: virus spread by oral fecal route (associated with improper food precautions, contaminated water, poor hand washing when preparing food
• Hepatitis B: virus spread by parenteral contact w/ infected blood (needle stick etc) • Hepatitis C: virus spread by intravenous drug and blood transfusion (highly unlikely) |
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Signs of fractures
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•Local pain
•Local bleeding •Local swelling •Deformity or dislocation •Symptoms of associated nerve damage: (Numbness & Paralysis) •Loss of pulse below fracture |
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Stress Fracture
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failure of one cortical surface of the bone, caused by repeated movement or bone stress, common injury in athletes (running, etc)
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Complete Fracture
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fracture line disrupts bone continuity through the entire thickness of the bone
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Incomplete Fracture
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(greenstick) usually seen in children (more flexible, growing bones) incomplete break in bone w/ the intact side of cortex flexed, bone continuity is not disrupted
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Open Fracture
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bone is broken and external wound leads to the fracture site, greater risk for infection
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Closed Fracture
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fragments do not extend through mucous membranes or skin is not broken
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Linear Fracture
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split bone along length (longitudinal)
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Comminuted Fracture
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consist of more than one fracture line and more than two bone fragments, may be shattered or crushed, associated w/ soft tissue damage and multiple bone fragments
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Spiral Fracture
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result of rotational forces and cause bone to separate in the form of a S shape around the bone
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Oblique Fracture
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results from rotational force but the fracture is along an oblique course
(45 degree angle) and does not rotate around the entire bone |
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Transverse Fracture
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fracture occurs in a straight line @ approximately 90 degree angle to the longitudinal axis of the bone
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Onset of Rheumatoid Arthritis
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• Degenerative joint disease; chronic, progressive destruction of cartilage in joints
• Joint pain more in the morining |
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Gout
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• Disease caused by inflammatory response due to too much uric acid
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Fracture Healing Process
Step 1 |
• Hematoma formation (1-3 days)
1. Hematoma forms at fracture site 2. Size depends of the damage at site. 3. Hematoma offers stability to fracture ends 4. Aseptic inflammation occurs at the fracture site. |
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Fracture Healing Process
Step 2 |
• Fibrocartilage formation (3 days 2 weeks)
1. Healing continues w/ formation of granular tissue containing blood vessels, fibroblasts and osteoblasts. 2. Hematoma provides foundation for reparative tissue and bone healing. |
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Fracture Healing Process
Step 3 |
• Callus formation (2-6 weeks)
1. Callus forms after granular tissue matures. 2. If stage is delayed or interrupted final stage can’t occur. |
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Fracture Healing Process
Step 4 |
• Ossification (3 weeks to 6 months)
1. Occurs as the space in the bone is bridged and fracture ends are united. 2. Callus slowly replaced by trabecular bone along lines of stress and unnecessary callus reabsorbed. |
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Fracture Healing Process
Step 5 |
• Consolidation and remodeling (6 weeks to 1 year)
1.Occurs as medullary canal is re-established. 2. Bone resorbed & deposited along stress lines as bone reshapes to meet mechanical requirements. |
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Osetoarthritis
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Destruction of cartilage joints
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Characteristics of Osetoarthritis
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Commonly affects weight barring joints: hands, wrist, neck, lower back, hip, knees, ankles, feet
Commonly w/ increase age and obesity Have pain stiffness, swelling, tenderness, limited ROM, muscle wasting Joint pain more symptomatic at the end of the day |
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Compartment syndrome
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• Syndrome resulting from trauma to soft tissues caused by swelling w/in the unyielding structure of neoelastic tissues
• Occurs w/ severe muscle trauma |
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Compartment Syndrome: Clinical Manifestations
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6 p’s: parathesia- numbness and tingling in toes, pain- not relieve w/ pain medication, pallor, pressure, paralysis, pulsiness
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Polyuria
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Excessive urination
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Anuria
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• Severe decrease or lack of urine output
Less than 100 ml in 24 hrs associated w/ acute renal failure |
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Oliguria
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Urine output less than 400 ml in 24 hrs associated w/ acute renal failure
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Clinical changes w/ glomerulonephritis
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Alteration in structure and function of glomerular capillary circulation
•Primary Effects just the kidney • Secondary Occurs from some other disease, result of medication, diabetic neuropathy Hematuria, decrease in GFR |
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Incontinence
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not control where and when to go to the bathroom
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Stress incontinence
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due to increased abdominal pressure like laughing, coughing, and sneezing
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Urge incontinence
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ppl know when they have to go but have an urgency
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Mixed incontinence
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combo of stress and urgency, most common in women
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Overflow incontinence
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usually some obstruction and urine starts to leak from bladder when bladder is full
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Functional incontinence
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can not get to the bathroom when needed to get there (mobility problems are most common cause)
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Renal Calculi
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Concentration of crystals of material that form in the pelvis of kidneys
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Renal Calculi Risk Factore
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o Increased concentration of solutes-dehydration (increase risk of stones)
o Abnormal urine pH (increases risk of stones) o Low urine volume o Hypercalciuria High levels of calcium in urine or blood predisposes to urinary stones o Genetic predispositio 10-15% of people will develop renal stones |
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Hematologic Tests
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Serum Creatinine
BUN GFR |
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Serum Creatinine
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end product of muscle metabolism changes when there is a decrease in GFR; normal 0.5-1.5
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BUN
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end product of protein metabolism, increase when something is wrong w/ kidneys
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GFR
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assessing renal function- part of the nephron where filtration takes place Average GFR is 125 ml/min
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Renal Failure
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Decrease blood flow to kidneys
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Acute Renal Failure
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o (Temporarily and potentially reversible, primary cause is ischemia)
symptoms: decrease urine output, elevated BUN and serum creatinine |
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Chronic Renal Failure
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o (decrease in kidney function or kidney damage for 3 months or longer)
Symptoms: increased BUN, decrease GFR, loss of nephrons (decrease renal reserve 70% lost, renal insufficiency 75-90% lost, |
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Pyelonephritis
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Inflammation/infection of the kidneys
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Factors increasing risk for pyelonephritis
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Pregnancy, increasing age, gender (female), obesity, sickle cell trait, diabetes mellitus, urinary obstruction, glucocorticoids, radiation, or cytotoxic chemotherapy
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UTI (urinary tract infection)
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AKA Cystitis
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Cystitis
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inflammation of the bladder lining (urothelium)
Women @ higher risk b/c have short urethra (short distance between the urethra and rectum) Unidirectional flow, acidic pH, and regular voiding can decrease bladder infection |
