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Patho Final Exam Study Guide
Cell Response Cell Response to Stress/Adaptation may adapt by undergoing changes in size, number, and type; changes may lead to atrophy, hypertrophy, hyperplasia, metaplasia and dysplasia. Atrophy decrease cell size causing reduce oxygen consumption and other cellular functions. General causes: 1 Disuse : reduction in muscle use 2 Denervation : atrophy in muscles of paralyzed limbs 3 Loss of endocrine stimulation : in relationship with disuse atrophy 4 Inadequate nutrition and ischemia : cells decrease size and energy requirements due to lack of nutrition and oxygen. Hypertrophy increase cell size and with it an increase in the amount of functioning tissue mass. Pathogenic Hypertrophy: thickening of urinary bladder and myocardial hypertrophy. Hyperplasia increase in the number of cells in an organ or tissue. Occurs in tissues such as epidermis, intestinal epithelium, and glandular tissue. 2 types of PHYSIOLOGICAL HYPERPLASIA: 1 Hormonal hyperplasia : Breast and uterine enlargement during pregnancy, due to estrogen. 2 Compensatory hyperplasia : Regeneration of the liver that occurs after partial hepatectomy, or with the removal of a kidney. Most forms on NONPHYSIOLOGICAL HYPERPLASIA are due to excessive hormonal or the effects of growth factors on target tissues. Metaplasia Reversible change in which a cell type is replaced by another cell type, occurs in response to irritation and inflammation. Dysplasia deranged cell growth of a specific tissue, results in cells that varies in size, shape, and organization Strongly implicated as a precursor of cancer; reversible change Cellular Injury Reversible Although impairing cell function, does not result in cell death. Two patterns under microscope: 1 Cellular swelling : occurs with impairment of Na+/K+ pump, usually as a result of hypoxic cell injury 2 Fatty change : linked to intracellular accumulations of fat; reversible, usually indicates severe injury. Irreversible Cell death or necrosis can occur. Apoptosis (Programmed cell death): a form of cell death necessary to make way for new cells; NORMAL PROCESS IN THE BODY Necrosis: cell death and degradation; UNREGULATED death; cell swells and ruptures; inflammation results. Cells may undergo liquefaction, coagulation, infarction, or caseous necrosis Gangrene Large area of necrotic tissue; Three types: 1 Dry gangrene: lack of arterial blood supply but venous flow can carry fluid OUT of tissue 2 Wet gangrene : lack of venous flow lets fluid ACCUMULATE in tissue 3 Gas gangrene: Clostridium infection produces toxins and bubbles Cellular stressors Hypoxia : lack of oxygen in air, respiratory disease, ischemia, anemia, edema, or inability of cells
to use oxygen. Causes: ATP DEPLETION or “POWER FAILURE”; AEROBIC metabolism STOPS, less ATP is produced, Na+/K+ pump is impeded, cell swells up, lactic acid is produced due to ANAEROBIC metabolism. Heat and Cold : extremes of heat and cold cause damage to the cells Electricity : can cause extensive tissue injury and disruption of neural/ cardiac impulses Chemical agents : injures cell membrane, block enzymatic pathways, and disrupt osmotic/ionic balance Biologic agents : are able to replicate and continue to produce injurious effects Radiation : ionizing radiation, ultraviolet radiation, nonionizing radiation Nutritional imbalances : Nutritional excess/deficiency can predispose cells to injury Hypoxic and ischemic changes Hypoxia lack of oxygen supply to the tissue despite of good perfusion of blood. Ischemia Decreased blood supply to a body organ or part usually due to functional constriction or obstruction. ISCHEMIA commonly depends on blood flow through limited numbers of blood vessels and produces LOCAL TISSUE injury Stress and Disease Neuroendocrine response Locus Ceruleus : Central to the neural component of neuroendocrine response to stress; central integrating site for the ANS response to stressful stimuli Corticotropin-Releasing Factor : important endocrine regulator of pituitary and adrenal activity & a neurotransmitter involved in ANS activity, metabolism & behavior. Angiotensin II : mediates peripheral increase in vascular tone and renal retention of water and sodium. Other hormones: growth hormone, thyroid hormone, and reproductive hormones are responsive to stressful situations General Adaptation Syndrome (GAS): Involves 3 STAGES : 1 Alarm stage: stimulation of the SNS, resulting in release of catecholamines and cortisol 2 Resistance stage : body selects the most effective and economic channels of defense; cortisol levels present in first stage drop b/c they are no longer needed 3 Exhaustion stage : resources are depleted and signs of “wear & tear” or systemic damage appear SNS increased HR, increased contractility, vasoconstriction in skin, guts and kidneys, increased BP, pupil dilation, increased respiration, increase attention & arousal, intensified memory, dry mouth. Alpha: constrict vessels and sphincters, decrease output Beta 1: found on the heart, increase FORCE & CONTRACTILITY Beta 2: found on smooth muscle, vascular muscle, bronchioles; DILATE Epinephrine: Released from the adrenal medulla Norepinephrine: Released from postganglionic fibers Adrenal Cortical hormones (cortisol) found in adrenal cortex; alteration in glucose, fat, and protein metabolism; suppression of inflammatory & immune responses Adrenal Medulla Hormones (epinephrine) prolongation of fight or flight response; increased HR & BP, pupil dilation, dry mouth, increased blood coagulability. Coping Mechanisms: 1 Guided Imagery: scene visualization 2 Music therapy: listening to music to ease anxiety or stress 3 Massage therapy: manipulation of soft tissues to promote relaxation & relief of muscle tension
Clinical Manifestations initial manifestations usually reflect the function of site of involvement; tumor metastasizes, other body structures become affected produces generalized manifestations such as anorexia, cachexia, fatigue, and sleep disorders in late stages, cancer compresses blood vessels, obstructs lymph flow, disrupts tissue integrity, invades serous cavities, & compresses visceral organs Diagnostics methods used is determined by the location and type of cancer suspected. blood tests for tumor markers, cytologic studies and tissue biopsy, endoscopic examinations, ultrasound, x-ray studies, magnetic resonance imaging (MRI), computed tomography (CT), and positron emission tomography (PET) scans. Integumentary System Skin Ulcers Stages: One non-blanchable erythema (redness) of intact skin. Appearance: Redness and blue or purple hues in darker skin. Two partial-thickness skin loss (epidermis and/or dermis). Appearance: Its superficial looks like a blister or a shallow crater. Three full-thickness skin loss involving damage or necrosis of subcutaneous tissue. Appearance: a deep crater with or without undermining of adjacent tissue. Four full-thickness skin loss with extensive destruction, tissue necrosis, damage to muscle, bone, or supporting structures. (tendon or joint capsule) Risk Factors Elderly, Neurological deficits, Incontinence (urinary and fecal), Fractures, Lying on hard surface, wrinkled sheets, Chronic diseases, Malnutrition, Any kind of immobilization Wound Healing Depending on the damage to the tissue, healing occurs by primary or secondary intention. Primary: Sutured Surgical incision Secondary: Larger wounds, ex: burns and large surface wounds with greater loss of tissue and contamination. Phases of healing: Inflammatory prepares the wound environment for healing. It’s the release of histamine. Proliferative begins within 2 to 3 days of injury, it may last as long as 3 weeks. New tissue starts to fill the wound space. Fibroblasts synthesizes , secretes collagen and other elements needed for healing. Remodeling beings approx. 3 weeks after injury. Scar tissue is continuously remodeled and the scar becomes reoriented to increase the tensile strength of the wound. Scar shrinks so its less visible. Fun Fact: A wound can heal in the absence of neutrophils, but cannot heal in the absence of macrophages. Tissue Healing Granulation tissue glistening red, moist connective tissue fills the injured area while necrotic debris is removed. Nutrition proteins, carbs, fats, vitamins (A, C, K most important) and minerals. Malnutrition slows down healing. Oxygenation oxygen is vital for collagen synthesis and killing bacteria. Blood flow helps remove the resulting waste, toxins, bacteria, and other debris.
Others Frequent Turning, Fluid Balance, Antibiotics, Flat, non-bulky dressings, Wound packing, Pressure mattresses Burns Thermal: exposed skin or mucous membranes to direct flame, hot liquids, or radiant energy Non-thermal sources : chemicals, electrical, radioactive Chemical: skin or mucous membranes have direct contact with chemical spills or inhalation of toxic gases Electrical: passage of electrical current through the body to the ground Ex: lightning; high- voltage sources; electrical devices Local & Systemic Responses minor burns heal with inflammatory response larger wounds heal with scar tissue formation loss of normal skin function; stress response; release of > cytokines; dysrhythmias (v-fib); alveolar and capillary membrane damage r/t inhalation of toxins; all body systems are affected First-degree outer layers of epidermis only, Partial thickness, No treatment required, No blisters for 24 hours, Palliative care with Aspirin/Tylenol and fluid intake, Heal within 3 to 10 days, Localized pain and erythema. Ex: Sunburn. Extensive first-degree burns on infants, the elderly, and persons who receive radiation therapy for cancer may require more care. Second-degree epidermis and dermis, deep full thickness burn, blisters arise within minutes, underneath is bright pink or red skin that is sensitive to temperature changes, air exposure, and touch. The blisters prevents loss of body water and superficial dermal cells. Excluding excision of large burn areas. It is important to maintain intact blisters after injury because they serve as a good bandage and may promote wound healing. These burns heal in approximately 1 to 2 weeks. Third-degree full-thickness Entire epidermis destroyed, Dry, leathery appearance. vary in color from waxy white or yellow to tan, brown, deep red, or black Requires hospitalization, Severe scarring, Fluid replacement, Narcotics, Contractures Extends into subcutaneous tissue, may damage muscle, bone, blood vessels. There is no pain because the nerve sensors have been destroyed. Fourth-degree Burn Severe tissue destruction, including muscle and bone; Permanent disfigurement Complications of Burns Fluid Imbalances during post-burn period capillaries reach maximal dilation and permeability r/t release of histamine, prostaglandins, and kinins Intravascular fluid shifts into interstitial space fluids are lost via evaporation 10 times normal rate causing Hypovolemic shock (“burn shock”) manifests as low cardiac output, hypotension, tachycardia, oliguria, massive edema (watch out for airway!) treat with large doses of isotonic fluid (Ringer’s Lactate) Respiratory system dysfunction injury commonly associated with burns is smoke inhalation and post burn lung injury. Signs of mucosal injury and airway obstruction often are delayed for 24 to 48 hours after a burn. Other pulmonary conditions, such as pneumonia, pulmonary embolism, or pneumothorax ,may occur secondarily to the burn. Hypermetabolic response stress of burn injury increases metabolic and nutritional requirements. characterized by increased oxygen consumption, increased glucose use, and protein and fat wasting. peaks at approximately 7 to 17 days after the burn, and tissue breakdown diminishes
Direct cell mediated cytoxicity: hepatitis Delayed type hypersensitivity: contact dermatitis (poison ivy), redness, induration, lesions, and urticaria. Hypersensitivity pneumonitis Positive TB: reddening and induration of >5mm at 72 hrs for immunosuppressed ppl or positive for TB HIV retrovirus selectively attacks CD4+ T lymphocytes; person with HIV infection is infectious even when asymptomatic Stage 1 Primary infection. Occurs shortly after infection, high viral load Symptoms: Fever, fatigue, malaise; Sore throat, night sweats; GI issues; Lymphoadenopathy (enlarged lymph), rash; 𝖳 viral replication and CD4+ cell count Stage 2 Latent Period, lowest viral load Symptoms: Asymptomatic of illness; CD4+ count drops progressively ; 200-499 cells/ᵤL; Risk for opportunistic infections; Inflammation in more than 2 areas for > 3 months Stage 3 AIDS phase , caused by HIV infection of cells, viral load increases, characterized by suppressed immune System and opportunistic infections, malignancies, wasting and CNS degeneration. Symptoms: Occurs when CD4+ cell count is less than 200 cells; without therapy can lead to death (2- years); Increased risk of infections caused by fungal, protozoal, bacterial, mycobacterial, and viral Respiratory: pneumocystis carinni pneumonia (PCP), pulmonary TB (can migrate anywhere in the body), Kaposi sarcoma GI: esophageal candidiasis, CMV infection, herpes simple virus, diarreah, gastroenteritis Nervous System: neurocognitive, HIV dementia, taxoplasmosis (cat poo) Malignancies: Kaposi sarcoma, non-hodgkins, lumphoma Diagnostic HIV tests
- ELISA enzyme-linked immunosorbent assay (ELISA) screens for HIV antibodies.
- Western blot test to confirm a positive Elisa test.
- Polymerase Chain Reaction (PCR) most accurate, most expensve Transmission Unprotected sexual activity; blood, semen, vaginal fluids, oral intercourse Contaminated blood; infected mother to child, breast milk, placenta, needles, blood transfusions Nursing Assessment Weight analysis, LOC, Reports of pain Skin; palpation of lymph nodes, VS, lung sounds, oral cavity, rectal and vaginal exam Systemic Lupus Erythematosus Chronic inflammatory multisystem, rheumatic, autoimmune disease. Characterized by vasculatis and malar “butterfly” rash. Common in females, African-Americans, Hispanics, Asians diagnosed in early 20’s Prognosis improves with early diagnosis and treatment, may affect connective tissue of any body organ Cause unknown; production of antibodies that attack self and non-self antigen. Defective elimination of B cells results in an increase production of antibodies that directly damage tissues or combine with antigen to form tissue-damaging immune complexes ANA (Antinuclear antibodies) test to determine lupus diagnoses Can attack musculoskeletal system, arthralgia and arthritis (joint aches), skin (Photosentitivity; UV, cones in eyes – Malar “butterfly” rash), cardiovascular system, lungs, kidneys (interstitial nephritis), the CNS, RBCs & platelets, Raynaud's phenomenon (Fingers/toes turn white/blue with cold temp or stress. Treatment Prevent loss of organ function, reducing exacerbations, minimizing disability from the disease process, and minimize sun exposure, apply protective lotion
HEMATOLOGIC DISORDERS
Pathology of Hemostasis
- Stage 1: vessel spasm reduces blood flow. Initiated by endothelial injury. ENDOTHELIN 1 most powerful vasoconstrictor
- Stage 2: platelet plug (thrombocytes) adhesion and aggregation - VON WILLEBRAND FACTOR ASPIRIN, PLAVIX & TICLID prevent aggregation THROMBOSIS: stationary clot EMBOLIST: traveling clot (usually results in PULMONARY EMBOLI STROKE) EXTERNAL BLEEDING: cardiovascular problems etc. Clotting factors synthesized in liver use vit. K: alcoholics lack vit. K severe GI bleeds MVC Normocytic: normal size; normal MVC Macrocytic: large size; high MVC Microcytic: small size; low MVC MCHC Normochromic: normal amount of Hb; normal MCHC Macrochromic: concentrated amount of Hb; high MCHC Microchromic: diluted amount of Hb; low MCHC Hypercoagulability Increased platelet function Diabetes Mellitus: if they develop CHF at risk for clots. Smoking and oral contraceptives directly correlated in developing clots Arterial Thrombi, Atherosclerosis, atrial fibrillation, blood clots arise from heart cause strokes, and murmurs Venous Thrombi: incompetent valves w/in veins Thrombocytopenia Platelet less than 100,000, most common cause of abnormal bleeding and loss of bone marrow function occurs Excessive consumption of platelet (DIC chews up platelets, usually occurs from sepsis) Excessive pooling of platelets in spleen Causes: dgrug induced Thrombocytopenia; Heparin Induced Thrombocytopenia (HIT); Patients allergic to heparin: platelets drop by more than 10%; Immune Thrombocytopenia Purpura (ITP) Signs and Symptoms mucus membranes bleeding: nose, mouth, GI, and uterine cavity. Occurs in small vessels Acute ITP most common bleeding disorder in children Chronic ITP most common in adults Excess destruction of platelets by body, platelet production decreased 1-3 days Petechiae (purplish red spots), Purpura (purple areas of bruising in large areas) DIC: Disseminated intravascular coagulation Not a primary disorder: complication of other disorders Bleeding and clotting at the same time, seen in septic pts or severe trauma, cancers, and hematologic conditions Treated w/ heparin as blood is transfused as well Post partum: amniotic emboli can occur along with DIC H1N1 also caused DIC in some pts Leukemia Malignant neoplasms, from precursor myeloid or lymphoid tissue cells. May infiltrate liver, spleen, lymph nodes and other tissues throughout the body enlarging these organs. Characterized by abnormal proliferation of immature WBC (leukocytes) and precursors that infiltrate the bone marrow, peripheral blood, body organs, and tissues.
Treatment chemotherapy; Bone marrow transplant ALL: lumbar puncture to assess CNS involvement AML treatment: massive amounts of chemotherapy given at one time (induction therapy) Hodkin Lymphoma replacement of normal cell by Reedsternberg cells , mutation of T- lymphocyte present in lymph node starts in single lymph node and spreads to neighboring lymph node. Eventually infiltrates liver, spleen, lungs, bone marrow, and ureters. 2 Categories:
1. Nodular lymphocyte predominant Hodgkin lymphoma, unique form that exhibits a nodular growth pattern 2. Classical Hodgkin lymphoma is characterized by clonal proliferation of typical mononuclear Hodgkin cells Unknown etiology, but exposure to carcinogens and viruses, genetics and immune mechanisms has been proved to be the involved. Common in early adulthood (15-40) and in older adulthood (>55); Most common in men Signs and Symptoms Painless enlargement of a single node or group of nodes; initial lymph above the diaphragm Chest discomfort with cough and dyspnea. Fever, night sweats Weight loss Pruritus (itching) Advance stages of HL: liver, spleen, lungs, digestive tract, and CNS are involved. Diagnostic Test presence of Reed Sternberg cells in biopsy CT scans of chest and abdomen. Thrombocytosis, leukocytosis, eosinophilia, elevated erythrocyte sedimentation rate (ESR), elevated alkaline phosphatase Non-Hodkin Lymphoma malignant transformations of either T or B cells during differentiation in peripheral lymphoid tissue. Originates outside the lymph and distributes rapidly. The NHLs are multicentric, spread early to several lymphoid tissues throughout the body specially liver, spleen, and bone marrow. linked to viral/bacterial infections, environmental agents, immunodeficiency, and autoimmune disorders MORE AGGRESSIVE , B cell malignancy affects T cells and macrophages DOES NOT HAVE REEDSTERNBERG CELLS Most common in men between 50 – 70 Common in pts. with HIV , chronic immunosuppressive therapy after organ transplantation, and with acquired or congenital immunodeficiency. Signs and Symptom Painless lymphodenopathy (cervical usually first, then axillary, and the inguinal) Fever, Night sweats Dyspnea Renal failure Weight loss Diagnostic Test and Treatments Lymph node biopsy and immunophenotyping to determine the lineage and clonality Bone marrow biopsy, blood studies, chest and abnormal CT scans, MRI Staging the disease is important to determine the treatment
Anemias Hemolytic Anemia Premature destruction of red blood cell; Retention of iron from hemoglobin destruction increase in Erythropoisis, normocytic and normochromic red cells Intrinsic: with in, defect of red cell membrane Extrinsic: defect outside (drugs, bacteria, toxins, trauma) Heart or valve malfunction Sepsis: microorganism can lead to RBC destruction Sickle cell decreased plasma oxygen hemoglobin S causes RBC to elongate, becomes rigid, with crescent sickled shape, cells clump together obstructing blood flow, or adhering to the vessel endothelium causing ischemia, thrombosis and possible tissue infarction. With normal oxygenation, sickled RBCs resume their normal shape. Common sites obstructed: abdomen, chest, bones, and joints caused by hypoxia, low environmental and/or body temperature, excessive exercise, high altitudes or inadequate oxygen during anesthesia, and stress. caused by blood viscosity, decreased plasma volume, infection, dehydration, and/or increased hydrogen ion concentration (pH/acidosis). Acidosis reduces affinity of hemoglobin for oxygen, increasing sickling. Repeated episodes of sickling and unsickling weaken cell membranes, causing them to hemolyze (breakdown) and be removed. Episodes can last 4-6 days. Acute chest syndrome: atypical pneumonia from pulmonary infarction characterized by infiltrates, shortness of breath, fever, chest pain, and cough Signs and Symptoms Strokes (another mayor complication) Retinal infarcts (blindness) Lung infarcts (pneumonia, acute chest syndrome) Pigment gallstones Avascular necrosis of femoral head Kidney infarcts (chronic kidney disease) Osteomyelitis Skin ulcers Pallor, Jaundice Fatigue and irritability. Diagnostic test hemoglobin electrophoresis : determines presence hemoglobin S, CBC. Treatement Folic acid supplements and analgesics Hydration therapy as well as scheduled transfusions decreases crisis episodes. During a crisis, hydration to improve blood flow, reduce pain, prevent renal damage, O 2 , IV (narcotics) Maintaining full immunization Hydroxyurea inhibits DNA synthesis, reduces pain crisis. Increases RBC levels, acts as an anti- inflammatory inhibiting the production of WBCs. Bone marrow or stem cell transplant; however risk of graft-versus-host disease. Gene therapy development future option. Megaloblastic Anemia impaired DNA synthesis results in enlarged RBC’s due to vitamin B12 (cobalmin) and folic acid deficiency causes pernicious anemia: inability to absorb vitamin B12 due to lack of intrinsic factor Macrocytic (Larger than normal cell size), Normochromic (normal concentration of Hb) Possibly destruction of the gastric mucosa, caused by the loss of parietal cells and
overproduction of RBC’s, WBC’s, and platelets increasing blood viscosity, volume, congestion of tissues (live and spleen) causing acidosis, clotting, and thrombi Absolute (PRIMARY) Polycythemia: most common in Caucasian men of European, jewish ancestry Neoplastic disease of bone marrow Thick, slow moving blood Secondary Polycythemia Physiologic increase in level of erythropoietin Compensatory response to hypoxia: High altitudes, chronic heart, lung disease and smoking GI Disorders GERD Gastric backflow into esophagus (reflux, heartburn or esophagitis) associated with weak or incompetent lower esophageal sphincter Delayed gastric emptying contributes to reflux, esophageal mucosal injury may occur Normally cleared and neutralized by esophageal peristalsis and salivary bicarbonate Chronic inflammatory disease of the antrum and body of the stomach H. pylori secretes urease which produces ammonia to buffer acidity of stomach; produces enzymes and toxins interfering with protection of the gastric mucosa against acid The severity of the heartburn is not indicative of the extent of the mucosal injury Related Risk Factors common problem in infants and children, occurs at least once a day in infants 0-3 months, by 6 months is less frequent Hiatal hernia Pregnancy Obesity; Poor dietary habits, high fat diet Esophageal structures or previous surgery Smoking Excessive caffeine intake Gastroparesis (delayed gastric emptying time) Vomiting, coughing, lifting or bending Signs and Symptoms Most frequent is heartburn; frequently severe, 30–60 minutes after meal; evening onset Belching and chest pain Dyspepsia (burning, pain in epigastric, radiates to throat, shoulder, or back) wheezing, chronic cough and hoarseness Diagnostic Test Radiographic studies with barium, esophagoscopy and ambulatory esophageal pH monitoring. pH probe test used to determine stomach pH (less than 4 = positive) H. pylori can be detected by C urea breath test Treatment Avoid large meals; eat sitting right up; foods that reduce esophageal pH(chocolate, fats, caffeine) Avoid recumbent position several hours after a meal; avoid bending for long periods Avoid alcohol use and smoking Sleep with the head elevated Lose weight if overweight Antacids, and inhibitors of gastric acid. Histamine-2 (H2) antagonist inhibits gastric acid production Treatment for h. pylori : PPI; Antibiotic therapy. Complication Produces a cycle of hyperemia, edema, and erosion of the mucosal surface of the esophagus. Barrett’s esophagus (combination of scar tissue, spasm, and edema).
- Produces narrowing of esophagus and causes dysphagia when lumen becomes constricted.
- Diagnosis: endoscopic evidence of abnormal mucosa, and intestinal metaplasia. Two types of esophageal cancer : adenocarcinoma (linked to gastroesophageal reflux and Barret
esophagus) and squamous cell carcinoma (attributed to alcohol and tobacco use). Peptic Ulcer Ulcerative disorder, upper gastrointestinal tract that’s exposed to acid-pepsin secretions Most common forms of peptic ulcer are duodenal and gastric ulcers Affects one or all layers of the stomach or duodenum. Superficial ulcers are called erosions Deep lesions extend through musculature, penetrate blood vessels causing hemorrhage, can cause perforation of the stomach wall or intestines Three main factors
1. Excessive acid : leads to a break or ulceration in mucosa of stomach or duodenum 2. Decreased mucus production : leaves mucosal cells unprotected from acid environment; hypoxia, shock, or severe burns can lead to injury of mucosa cells 3. Increased delivery of acid : irritated mucus layer because rapid movement of stomach content (dumping syndrome). The duodenum cannot keep up with it Gastric Ulcers Ingestion of medications (NSAID), tobacco, caffeine, alcohol, H. pylori infection, chronic bile reflux (bile backs up into stomach) and increased HCL. Occurs in older adults. Food aggravates pain Causes weight loss due to the aggravation by food No pain at hours of sleep Duodenal Ulcer Hypersecretion of pepsinogen, H. pylori infection. Occurs in early adults pain when stomach is empty. Weight gain Pain at hours of sleep; food and antacids relieve pain Related Factors H. pylori Aspirin and other NSAIDs Prior history of peptic ulcer Warfarin, Corticosteroid drugs Smoking (impairs healing) Zollinger/ellison syndrome Clinical Manifestations Burning, gnawing, cramp-like, rhythmic Pain in small area near midline in epigastrium near xiphoid May radiate below costal margins, into back or to right shoulder Complications Hemorrhage, perforation and penetration and gastric outlet obstruction. Bleeding may be sudden, severe, insidious producing only occult blood in stool (Melena). Diagnostic Test Bloodwork for electrolytes Laboratory findings of occult blood in the stools indicate bleeding. Test for presence of h pylori antibodies Endoscopy; X-ray studies with a contrast medium such as barium. Treatment Antibiotics to eradicate H. pylori Medications to relieve symptoms and healing the ulcer crater. Avoid aspirin and NSAID Inhibition of gastric acid
Gastroentoritis Caused by bacteria and/or acute infection (food poison) Dehydration & electrolyte imbalance Symptoms: nausea, diarrhea, vomiting, cardiac dysrhythmias b/c potassium loss Treatment: hydrate Irritable Bowl Syndrom (IBS) Reduced of intestinal motor & sensory function Diagnosed: history for pattern, abdominal assessment, persistent symptoms and abdominal pain RELIEVED WITH DEFECATION Treatment stress management, if constipated limit fiber and increase fluids. Drugs: antispasmodics, anticholinergic drugs to decrease motility Crohns Disease Recurrent, granulomatous type of inflammatory response, can affect any area of GI Slowly progressive, relentless and often disabling disease Most affected: distal small intestine (ileum) and proximal colon. More often lesions in ascending colon and terminal ileum Is a chronic inflammatory bowel disease (IBD) Cause is unknown, body’s immune system attacks and destroys healthy body tissues Local lesions: involves all intestinal wall layers; wall contains shallow long ulcers with long or short areas of stricture. Skip lesions: involve some areas of bowel but not all areas Involvement of submucosal layers causes Granuloma (tumor like growth), gives tissue a cobblestone appearance due to Ongoing chronic inflammation of the gastrointestinal tract. Malabsorption, also abscesses may develop, fistula between infected area , bladder or other area of intestine. Scar tissue may interfere w/ movement of chime, perforation or obstruction occurs. Risk Factors Genes/ family history; Jewish descents (higher risk) Women more than men. (20s-30s at risk) Environmental factors Hormonal Dietary antigen or microbial agent, smoking Allergy or immune disorder; Body reacts to normal bacteria in intestines. Complications fluid and electrolyte imbalance as well as dehydration due to diarreah Deficiency in absorption of folic acid, calcium and vitamin D Anal fissure, abdominal abscess, fistula, intestinal obstruction. Signs and Symptoms Intermittent diarrhea, colicky pain (usually in lower right quadrant) Exacerbation/remission Nausea, vomiting, weight loss caused by anorexia, loss of appetite. Low grade fever Malaise Urgency at night to defecate Joint pain/ swelling Tenesmus (pain passing stool) Swollen gums/ mouth ulcers Diagnostic Test Colonoscopy or sigmoidoscopy, eteroscopy Albumin level low, CBC (elevated WBC, low RBC, Hgb and Hct) Electrolyte (hypocalcemia) High ESR
Stool cultures CT scan of abdomen Barium enema (reveals characteristics skip lesions) or upper GI series Treatement No cure, treatment focuses on preventing complications. Promote healing and maintain adequate nutrition. Surgery, resection of damage bowel, drainage of abscesses, or repair fistula tracts. Fluid replacement to correct dehydration, TPN (total parenteral nutrition) may be added. Give low residue, low fat, high protein, and high calorie diet. lifestyle management to reduce stress Ulcerative Colitis Nonspecific inflammation of the colon, mucosa disease, can be cured by colectomy Confined to the rectum and colon , Its an Chronic inflammatory bowl disease (IBD) Begins in rectum, spreads proximally affecting mucosal layer , can extend to submucosal layer may feature small hemorrhages and abscesses, inflammation is confluent and continuous, leads to formation of crypt abscesses; may become necrotic; ulcerations are fibrotic in later stages Pseudopolyps develop Related Factors Causes uncertain; virus or bacterium may trigger ulcerative colitis. Possible that inflammation may come from an autoimmune reaction Heredity or stress. Complications Intestinal obstruction , dehydration, fluid and electrolyte imbalances, malabsorption, iron- deficiency anemia Diarrhea for days/months , stools contain blood and mucous, nocturnal diarrhea. Fecal incontinence Anorexia, weakness, fatigue Risk for : Toxic megacolon , cancer of the colon Abdominal pain, nausea and vomiting, urge to defecate Risk Factors usually before age of 30; can occur at any age Whites have a higher risk Family history Stress Diagnostic Test Physical exam and medical history CBC (low RBC, Hgb, Hct) Negative Stool Test Biopsy Sigmoidoscopy; Colonoscopy/ risk perforatin with severe disease Barium Enema X-Ray Computerized Tomography (CT) Scan Treatment Medication Therapy to reduce symptoms Bulk free diet and a well- balanced nutritious diet Avoid caffeine, lactose Surgical Procedures Monitor intake and output, administer iv fluids as ordered Pancreatitis Reversible inflammatory process of pancreatic acini (functional units of exocrine pancreas) Auto-digestion of tissue by inappropriately activated pancreatic enzymes Begins with trypsin, trypsin activates other digestive enzymes causing pancreatic injury
Signs and Symptoms Weight loss Hepatomegaly Splenomegaly Late manifestations related to portal hypertension and liver cell failure. Jaundice; abnormally high levels of bilirubin (>2.0) Fetor hepaticus (musty sweet breath) Vascular spiders, esophageal varices (enlarged veins) Anemia: chronic blood loss Hepatic encephalopathy (inability to get rid of ammonia) Symptoms: ALOC, confusion, Hepatorenal syndrome Hepatitis acute chronic inflammation of the liver caused by virus known as Hepatotropic virus chronic alcoholism, drug toxicities, and autoimmune disorders. Malaria, infectious mononucleosis, salmonellosis, & amoebiasis. 5 Types: A, B, C, D, E Hepatitis A: up to a month incubation period
- Contracted by the fecal–oral route for lack of hand hygiene
- Contaminated food or water
- Most common in children to spread
- Having sex with someone who has the virus
- Not chronic, Hep-A vaccine Symptoms: fever, malaise, nausea, anorexia, abdominal discomfort, dark urine and jaundice (can last for 2 months or more) Hepatitis B: up to 6 months incubation period
- Enters liver, invades cells and begins to multiply and this causes inflammation
- Sexual contact (unprotected sexual intercourse,blood , saliva , semen or vaginal secretions)
- Sharing needles or accidental needle sticks
- Mother to child: during childbirth
- Hep-B vaccine Symptoms: fever, fatigue, abdominal pain, nausea and vomiting, joint pain, jaundice, and clay colored stool Hepatitis C: 2-26 weeks incubation period
- Transmitted via Blood /serum
- Patient w/ organ transplants
- Via Unprotected sex
- Patients who undergo dialysis are in contact with blood.
- **No vaccine
- Associated with liver cancer, failure and cirrhosis** Symptoms: fatigue, weight loss, anorexia, Jaundice Hepatitis D: 30 days incubation period
- Via Blood/serum
- Symptoms similar to Hepatitis A
- Can become chronic
- Hep-B vaccine to prevent Hepatitis E: 40 days incubation period - Contracted primarily by the fecal–oral route for lack of hand hygine
- High mortality rate
- No vaccine
- Severe infections develop Hormone disorders Tertiary: abnormality in stimulation from the hypothalamus Secondary: abnormality in stimulation from the pituitary
Primary: abnormality in the gland Adrenal Cortex Hypofunction Addison’s Disease → destruction of adrenal glands due to trauma, infection, hemorrhage into gland, AIDS, drugs, cancer, or sudden stress resulting in chronic adrenocortical hormones insufficiency and decreased production of cortisone, aldosterone, and androgens
- Hyperpigmentation from ↑ACTH levels causing bronze pigment. (lack of feedback inhibition) Mineralocorticoid deficiency (aldosterone) : cause low NA+, low Cardiac Output, high K+; Dehydration (Water follows solute causing Hypovolemia and hypotension) Weakness, fatigue; CV collapse; orthostatic pressure Glucocorticoid deficiency: Hypoglycemia; Lethargy, weakness; Fever; GI symptoms Addisonian Crisis → acute cortisol insufficiency during stress (ex: surgery and pregnancy) or when corticosteroid therapy is abruptly stopped, can cause circulatory collapse, shock, and death. immediate IV glucocorticoid replacement and fluids with Na+^ (isotonic solution 0.9% Na+CL) Signs and Symptoms → Neurological (neurosis, depression); Cardiovascular (hypotension, EKG changes: Peaked T- wave due to Hyperkalemia); Musculoskeletal (weakness, fatigue); Integumentary (hyperpigmentation of skin) GI (diarrhea, nausea, vomiting, anorexia); Reproductive (decreased libido, little pubic hair); Metabolic increased K+, hyponatremia, hypoglycemia, weight loss) Nursing Management → Monitor for signs of dehydration; Maintain high Na+, Low K+^ diet
- Teach client to carry medical alert identification Mineral and glucocorticoid replacement Adrenal Cortex Hyperfunction Cushing syndrome → hypercortisolism causing an increase in glucogenesis (glucose synthesis)
- Primary cushing: caused by adrenal tumor (increases cortisol)
- Secondary cushing: disorder of pituitary or hypothalamus (increases ACTH)
- Iatrogenic cushing: most common cause of cushing, results by long term glucocorticoid therapy Signs and Symptoms → Neurological (psychosis, loss of memory, depression, poor concentration); Cardiovascular (HTN, dysrhythmias); GI (peptic ulcers); Musculoskeletal (muscle weakness and wasting, osteoporosis, “buffalo” hump , abdominal obesity ); Integumentary (ecchymosis, hirsutism, abdominal purple striae , poor wound healing, thin skin, acne); Renal (glycosuria, polyuria, polydipsia, renal calculi); Reproductive (decreased libido, impotence, amenorrhea, male characteristics in females); Metabolic (High Na+, low K+, edema, moon face , weight gain) Nursing Management → monitor for Addisonian crisis caused by drug therapy
- Priority nursing diagnoses: excess fluid volume; risk for infection; risk for injury; activity tolerance; anxiety; deficient knowledge; risk for impaired skin integrity monitor I&O’s and cardiac rhythm Disorders of the Thyroid Hyperthyroidism hyperfunction of thyroid gland leading to high levels of TH circulating in the body causing an increase in metabolic function. Disorder: Grave’s disease, Adenomas, Thyroid Storm, and Iodine containing agents
