York Midterm

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  1. What is ADHD?
    Attention Deficit Hyperactivity Disorder - affects one's ability to concentrate, be still and quiet or avoid impulses
  2. What are the three types of ADHD?
    • Hyperactive impulsive
    • Inattentive
    • Combined hyperactive
  3. What causes ADHD?
    Idiopathic mostly, genetic component, smoking and drinking in pregnancy, exposure to lead, CNS trauma or infection, artificial coloring, preservatives, prematurity, difficult neonatal course, hyperthyroidism
  4. What are the signs/symptoms of hyperactive ADHD?
    • Fidgetiness
    • Difficulty remaining seated in class
    • Excessive running or climbing
    • Difficulty in engaging in quiet activities
    • Excessive talking and blurting out answers before questions have been completed
    • Difficulty awaiting turns, interrupting and intruding on others
  5. What are the signs/symptoms of inattentive ADHD?
    • Failure to give close attention to detail
    • Difficulty sustaining intention in task
    • Failure to listen when spoken to directly
    • Filure to follow instructions
    • Difficulty organizing tasks and activities
    • Reluctance to engage in tasks
    • Losing utensils necesary for tasks or activities
    • Easy distractibility
    • Forgetfulness in daily activities
  6. Conditions that can coexist with ADHD?
    • Learning disability
    • Oppositional defiant disorder
    • Conduct disorder
    • Anxiety and depression
    • Bipolar disorder
    • Tourette syndrome
    • Bedwetting
    • Substance abuse
    • Sleep disorders
  7. Diagnosis of ADHD?
    Six or more symptoms are exibited, some symptoms must be present before the age of 7, symptoms must be present for at least 6 months, seen in two or more settings and not caused by another problem, must be severe enough to cause significant difficulties in many settings
  8. Treatment of ADHD?
    • Behavior modification techniques (structure, positive reinforcement, etc.)
    • Stimulant medications - ritalin, adderall
    • Diet changes - avoid artificial colors and preservatives, sugar reduction and gluten-free diet
  9. What is Addison's disease?
    body produces insufficient adrenal hormones such as corisol and often aldosterone as well, also known as hypocortisolism
  10. What causes Addison's disease?
    70% idiopathic, thought to be autoimmune, 30% granuloma, tumor amyloidosis or inflammatory necrosis of the adrenal gland or prescription drugs
  11. What is cortisol?
    A steroid hromone released by the adrenal glands in response to stress to increase blood sugar, and aid in fat, protein and carbohydrate metabolism
  12. What is aldosterone?
    A steroid hormone released by the adrenal glands that increases the reabsorption of sodium ions and water and the release of potassium ions
  13. Signs/symptoms of Addison's?
    • Changes in blood pressure or heart rate
    • Chronic diarrhea
    • Darkening of the skin or patchy skin color
    • Paleness
    • Unnaturally dark color is some places
    • Loss of appetite
    • Mouth lesions on the inside of a cheek
    • Salt craving
    • Slow, sluggish movement
    • Unintentional weight loss
    • Extremem weakness
    • Fatigue
    • Nausea and vomiting
  14. Diagnosis of Addison's?
    • Combination of history and low blood pressure readings
    • Blood tests may show decreased potassium, low sodium, low cortisol
    • Abdominal x-ray and CT scan
    • 17-hydroxycorticosteroids, 17-ketosteroids, 24-hour urinary aldosterone excretion rate, ACTH, Aldosterone, blood eosinophil count, CO2, potassium test, renin, urine cortisol
  15. Treatment/management of Addison's?
    • Replacement corticosteroids (glucocorticoids and mineralcorticoids) control symptoms
    • May increase in times of infection, injury and stress
    • Most never require hospitalization and lead normal lives
  16. What causes appendicitis? Frequency?
    Idiopathic (obstruction is a predisposing factor), most common abdominal surgery in childhood, frequency increases with age and peaks between 15 and 30
  17. Signs/symptoms of appendicitis?
    • Fever
    • Right lower quadrant pain (poorly localized in children younger than 2, perforation prior to surgery is common)
    • Peritoneal irritation
    • Anorexia
    • Vomiting
    • Constipation
    • Diarrhea
  18. Diagnosis of appendicitis?
    • rectal exam - local mass or tenderness
    • repeated abdomen exams over several hours
    • Radiopaque fecalith is present in 2/3 of ruptured
    • Abdominal CT
  19. Treatment of appendicitis?
    • Exploratory laparotomy or laparoscopy
    • Postoperative antibiotic therapy if perforation or gangrene occurs
    • Single intra-operative dose of cefoxitin to prevent complications
    • Mortality rate is less than 1% during childhood
  20. What are duodenal ulcers?
    peptic ulcer in duodenum that erodes the lining of the duodenum
  21. Causes of duodenal ulcers?
    • Helicobacter pylori
    • Alcohol
    • Smoking
    • Caffeine
    • NSAIDs
    • Stress
    • Acid and pepsin
  22. Signs/symptoms of duodenal ulcers?
    • Gnawing or burning pain in the abdomen between the breastbone and the naval, tends to awaken patient at night
    • Pain often occurs between meals and in the early hours of the morning, may last a few minutes to a few hours
    • In neonates - perforation and hemorrhage may be first sign
    • Other less common symptoms: belching, poor appetite, nausea, loss of weight, vomiting, feeling tired
  23. Diagnosis of duodenal ulcers?
    • Upper GI series (barium x-ray)
    • Endoscopy
    • Blood, breath and stomach tissue tests to detect H. pylori
  24. Treatment of duodenal ulcers?
    • Lifestyle changes (avoid spicy, fatty or acidic foods)
    • H2-blockers - reduce stomach acid by blocking histamine
    • Acid pump inhibitors
    • Mucosal protective agents
    • Antibiotics
    • Surgery - vagotomy, antertomy and pyloroplasty
  25. What is hepatitis A?
    • Benign, self-limiting liver disease caused by a single-stranded RNA picornavirus
    • Mild, often asymptomatic
    • Virus is not toxic to heaptocytes, injury occurs from T cell-mediated response
  26. People at high risk for Hepatitis A (HAV)? (vaccine is recommended)
    • Sexual or household contact with infected person
    • Travel to countries where HAV is common
    • Men who have sex with men
    • Drug users (injecting and non-injecting)
  27. How is hepatitis A transmitted? How common is it?
    • Shed in stool for 2 to 3 weeks before and 1 week after onset of symptoms
    • Transmitted fecal-oral or in rare cases by blood
    • 33% of Americans have had an infection at some point
    • Mostly occurs in children
    • Occurs in epidemic worldwide
  28. Signs/Symptoms of Hepatitis A?
    • Most are asymptomatic
    • Anorexia and malaise
    • Hepatomegaly
    • Upper right hand quadrant tenderness
    • Dark urine
    • Fever just prior to jaundice
  29. Diagnosis of hepatitis A?
    IgM antibodies, increased ALT, AST, bilirubin and alkaline phosphatase
  30. Treatment of hepatitis A?
    Usually none, self-resolves, increase calorie intake, avoid hepatically metaboized drugs, lasts about 6 weeks, relapses may occur but no chronic infection (IgG antibodies protect against), fatal to only 0.1%
  31. What is hepatitis B? (HBV)
    • Benign, self-limiting liver disease caused by a partially double-stranded circular DNA
    • Does not integrate itself into DNA of host cell
  32. People at high risk for Hepatitis B? (vaccine is recommended)
    • Persons with multiple sex partners
    • Men who have sex with men
    • Sexual or household contact with infected person
    • Drug users (inject)
    • Hemodialysis patients
    • Infants born to infected mothers
    • Health care and public safely workers
  33. How is Hepatitis B transmitted? How common is it?
    • Transmitted by blood and body fluids
    • Highest rate in 20 to 49 year olds
    • 1 to 1.25 million chronically infected in US
    • 400 million affected worldwide
  34. Signs/symptoms of Hepatitis B?
    • Most asymptomatic (especially young)
    • Chronic malaise or fatigue
    • Possible urticaria, rash and arthralgias (serum sickness)
    • Hepatomegaly
    • Upper right quadrant tenderness
    • Dark urine
    • Fever precedes jaundice
  35. Diagnosis of hepatitis B?
    • HBsAg
    • IgM anti HBc
    • Increased ALT, AST, bilirubin and alkaline phosphatase
  36. Treatment of hepatitis B?
    Usually self-limiting, lasts about 6 weeks, relapses may occur, increase calorie intake, avoid hepatically metabolized drugs
  37. Prognosis of hepatitis B?
    • Chronic infection in 90% of infants infected at birth, 6% in persons infected after the age of 5
    • Death occurs from chronic infections 15 to 25%
    • Possible outcomes:
    • 1. Acute heptatits with complete recovery
    • 2. Non-progressive chronic hepatitis
    • 3. Progressive chronic --> cirrhosis --> hepatocellular carcinoma
    • 4. Fulminant heptits with massive liver necrosis
    • 5. Asymptomatic carrier
  38. What is hepatitis C?
    • Major cause of liver disease
    • Acute progressive liver parenchymal infection that causes liver inflammation
    • Caused by positive-sense single-stranded RNA Flaviviridae virus
    • Many varieties because of poor fidelity of RNA replication, making a vaccine impossible
  39. People at high risk for hepatitis C?
    • Drug users who inject
    • Recipients of clotting factors made before 1987
    • Hemodialysis patients
    • Recipients of blood and/or solid organs before 1992
    • People with undiagnosed liver problems
    • Previous hepatitis B infection
    • Infants born to infected mothers
    • Health care and public safety workers
    • People having sex with multiple partners
    • People having sex with an infected partner
  40. How is hepatitis C transmitted? How common is it?
    • Transmitted via blood and body fluid
    • New infections have declined since 1980s
    • 3.9 million previous infections, 2.7 million chronic in US
    • 175 million carriers worldwide
    • Most infections due to illegal drug use
  41. Signs/symptoms of hepatitis C?
    • Asymptomatic in 75% when acute
    • Malaise
    • Anorexia
    • Fatigue
    • Upper right quadrant abdominal pain
    • Ascites
    • Dark urine
    • Jaundice
  42. Diagnosis of hepatitis C?
    • Anti-HCV antibody (ELISA)
    • Hepatitis C genotype (6 exist)
    • Elevated ALT and AST and bilirubin
  43. Treatment of hepatitis C?
    • Recombinant interferon-alpha (antiviral and immunomodulator) for 6 months
    • Frequently require liver transplant
    • Antiviral medication
    • Increase calorie intake
    • Avoid any hepatically metabolized drugs
  44. Prognosis of hepatitis C?
    • HCV antibodies do not give immunity to reinfection because of constatn mutation of virus
    • Strong immune responses invovling CD4+ and CD8+ cells in some will clear infection
    • Chronic infection in 75 to 85%
    • 20% cirrhosis
    • Death rate continues to increase
    • Infection returns after liver transplant
  45. What is hypothyroidism?
    Low T4 (thyroxine) , called cretinism in children (mental retardation and neuropsychological effects)
  46. What are the causes of hypothyroidism?
    • Dysfunction of the thyroid gland from inflammation or hashimoto's disease (chronic autoimmune thyroditis)
    • Sheehan syndrome (women bleeds severely during pregnancy or childbirth leading to destruction of the pituitary gland)
    • Pituitary does not produce enough TSH
    • Hypothalamus does not produce enough TRH
    • Amyloidosis (proteins deposited in tissue)
    • Sarcoidosis (inflammatory disease)
  47. How common is hypothyroidism? Who is at risk?
    • More common in females
    • Frequency increases with age (over 65)
    • 1 to 4% of population
    • Radiation therapy or radioisotope therapy
    • Autoimmune disorders
    • First-degree relative with thyroid problem
    • Amiodarone hydrochloride (given for heart arrythmias)
    • Lithium and bipolar disorder
  48. Signs/symptoms of hypothyroidism?
    • Weakness
    • Fatiue
    • cold intolerance
    • Weight gain
    • Menstrual difficulties
    • Course, dry hair
    • Dry skin
  49. What can hypothyroidim lead to?
    • Arteriosclerosis
    • Poor peripheral circulation
    • Heart failure
    • Pernicious anemia
    • Megacolon
    • Bleeding tendencies
    • Iron deficiency anemia
    • Impaired fertility
    • Birth defects
  50. Diagnosis of hypothyroidism?
    • Low T3 and T4 levels
    • Increased (primary) or decreased (secondary) TSH
    • Signs and symptoms
  51. Treatment of hypothyroidism?
    • Levothyroxine - synthetic T4
    • Lifelong therapy is required
    • If not treated --> hypothermia, increased diastolic and decreased systolic blood pressure
  52. What is infectious mononucleosis? Who does it infect?
    • An acute viral infection caused by Epstein-Barr virus (herpes virus type 4)
    • Transmitted via saliva --> "kissing disease"
    • 80% of infected patients are carriers for life
    • Primarily affects young adults and children
    • Incidence varies seasonally amoung college students but not among general population
  53. Signs/symptoms of Mononucleosis?
    • Fever
    • Weakness
    • Sore throat
    • Swollen tonsils and lymph nodes
    • Night sweats
    • Skin rash
    • Loss of appetitie
    • Swollen, soft spleen
    • Headache
    • Hepatitis
    • Jaundice
    • Child - only a few symptoms
    • Adolescent and adult - all symptoms
    • Prodromal symtpms: headache, malaise, fever
  54. Complications of mononucleosis?
    • Splenic rupture
    • Aseptic meningitis
    • Encephalitis
    • Hemolytic anemia
    • Pericarditis
    • Guillain-Barre syndrome
  55. What can mononucleosis mimic?
    • Hepatitis
    • Rubella
    • Toxoplasmosis
    • Cytomegalovirus
    • Strep pharyngitis
  56. Diagnosis of mononucleosis?
    Increased WBC (lymphocytes and monocytes), 10% Downey cells, monospot test (heterophile antibody test)
  57. Treatment of mononucleosis?
    Bed rest, fluids, acetaminophen or ibuprofen, gargle warm salt water, prednisone (if severe), does NOT respond to antibiotics, avoid sports, splenectomy (if spleen ruptures), symptoms may linger for months but patients fully recover
  58. What is Jaundice?
    • Yellow Pigmentation of the skin and sclera and other mucomembranes caused by hyperbilirubinemia
    • Three types: Pre-hepatic (hemolytic), hepatic (hepatocellular), post-hepatic (cholestatic)
  59. Pre-hepatic jaundice?
    • anything that increased the rate of hemolysis
    • malaria, sickle cell anemia, thalassemia, hemolytic anemia
    • Lab tests: Increased Total bilirubin, Increased Unconjugated bilirubin, Increased Urobilinogen (urine), Dark urine
  60. Hepatic Jaundice
    • cell necrosis reduces the liver's ability to metabolize and exrete bilirubin leading to a build up of unconjugated bilirubin in the blood
    • Hepatitis, hepatotoxicity, alcohol liver disease, neonatal jaundice
    • Lab findings: vary (mix of pre and post)
    • Kernicterus - rare form of brain damge in newborn from excessive bilirubin is not associated with increased conjugated bilirubin
  61. Post-hepatic (obstructive) Jaundice
    • Interruption to the drainage of bile in the biliary system
    • Gallstones in the common bile duct, pancreatic head cancer, liver flukes (parasites), pancreatitis, ductal carcinoma, pancreatic pseudocysts
    • Lab findings: Increased total and conjugated bilirubin, dark urine, pale stool, conjugated bilirubin in the urine
  62. Signs/symptoms of jaundice
    • Yellowing of skin, sclera, other tissues
    • Dark urine
    • Nausea
    • Vomting
    • Anorexia
    • Malaise
  63. Diagnosis of jaundice
    • History
    • Abdominal exam
    • Blood and urine tests
    • Imaging - ultrasound (gallstones, tumor), CT (tumor), MRI (bile ducts)
    • Liver biopsy
  64. Treatment of Jaundice
    • Treat underlying cause: fluids, antibiotics and/or blood transfusions, surgery, phototherapy (neonates)
    • Will usually disappear if underlying cause is treated
    • If secondary to cirrhosis may develop kidney or liver failure
    • If secondary to cancer, five year survival rate is 30 to 40%
  65. What is lyme disease?
    • Bacterial infection from Borrelia burgdorferi
    • Primary reservoir is the white-footed mouse, other mammals may be hosts
    • Named after Lyme, Conn. where it was first discovered
    • 3 stages: Early localized, Early disseminated and Late
  66. What causes lyme disease?
    • transmitted to humans though the deer tick
    • Children and young adults that live near or visit wooded areas are most susceptible
    • Occurs mostly in summer or early fall
  67. Signs/symptoms of lyme disease?
    • 1st and most common: erythema migrans (red rash) at tick bite (75% in early localized stage)
    • Early Disseminated stage: Flu-like symptoms, spreads to different systems (heart, brain, joints), fibromyalgia-like symptoms
    • Late stage: Arthritis, inflammation
  68. Diagnosis of lyme disease?
    • Case history of tick bites or wooded areas
    • Can be difficult to diagnosis if rash is not present
    • Lab test: ELISA and IFA (immunofluorescent assay) are done for late stage only
  69. Treatment of lyme disease
    • Early stages: Antibiotics for at least 21 days
    • Late stages: Antibiotics and probenocid (increases the time the antibiotic stays in the blood) for at least 30 days, if neurological symptoms then intravenous antibiotics, may have residual symptoms (1/3rd)
    • NSAIDs and joint aspiration for joint inflammation
  70. What is malignant melanoma?
    the most serious type of skin cancer, occurs in melanocytes, found mainly on the skin, also on the oral and genital mucosa and conjunctiva, can metastasize via lymph or blood or to adjacent tissue
  71. What are the 4 types of malignant melanoma?
    • Lentigo Maligna melanoma (5 to 15%) - older population, face or sun-exposed areas, begins benign
    • Superficial spreading melanoma (67%) - women's legs and men's torso, asymptomatic lesion invaded by atypical melanocytes
    • Nodular melanoma (10 to 15%) - anywhere on body, asymptomatic, grows rapidly
    • Acral-lentiginous melanoma (5 to 10%) - most common form in blacks, on palmar plantar or subungual (beneath the nail)
  72. Incidence and contributing factors to malignant melanoma?
    • 60,000 diagnosed per year, 8400 deaths per year
    • Idiopathic but heredity, hormonal factors, sun exposure and fair skin contribute, rare in blacks
    • 50% grow from an existing mole
    • Precursor can be a dysplastic nevi (atypical mole)
  73. Signs/symptoms of malignant melanoma
    • Asymmetery of lesion
    • Borders are irregular
    • Color is not the same throughout
    • Diameter is >6mm (size of a pencil eraser)
    • Inflammtion, bleeding or itching
  74. Diagnosis of malignant melanoma
    Biopsy - excise small lesion and incise larger lesions, include material from the full depth of the lesion and the edges, if spreads prognosis is poor
  75. Four stages of malignant melanoma and treatment
    • Stages I and II: localized primary melanoma (deep excision is best, also cryotherapy, radiation is less effective), survival rate depends on thickness of tumor, mucosal melanomas are poor prognosis
    • Stage III: metastasize to local lymph nodes (excision of lymph nodes also, 5 year survival rate is 25 to 70%)
    • Stage IV: metastasize beyond the lymph (usually inoperable, chemotherapy, 5 year survival rate of 10%)
  76. What is multiple myeloma?
    Proliferation of plasma cells with replacement of bone marrow causing osteroporosis, hypercalcemia, anemia, renal disease and infection
  77. What is produced in excess in marrow plasmacytomas of mulitple myeloma?
    • 55% produce IgG
    • 20% produce IgA
    • 1% produce IgD
    • 40% of IgG and IgA patients have bence jones proteinuria
    • 80% have "M" spike
  78. Causes of multiple myeloma
    Idiopathic, >50 years, may be associated with Kaposi's sarcoma, more common in males and blacks
  79. Signs/symptoms of multiple myeloma
    • Unexplained deep, boring pain especially in back or thorax, worse at night
    • Renal damage/failure
    • Increased susceptibility to bacterial infections
    • Pathological fractures and vertebral body collapse, leading to spinal cord compression (paraplegia)
    • Weakness and fatigue from anemia
    • CRAB (increased Calcium, Renal failure, Anemia, Bone lesions)
  80. Diagnosis of multiple myeloma
    • serum "M" protein with: clusters of marrow plasma cells, osteolytic lesions and/or bence jones proteinuria
    • (note: 20% show monoclonal light chains instead of "M" spike)
    • X-ray - diffuse osteoporosis and "punched-out" lesions
    • Normocytic, normochromic anemia, increased ESR, increased serum creatinine and uric acid
    • Proteinuria
  81. Treatment of multiple myeloma
    • Pamidronate for skeletal complications - decreased pain and increases life span)
    • Analgexics and localized radiotherapy
    • Prednisone for hypercalcemia
    • Hydration for renal failure
    • Blood transfusion for anemia
    • Chemotherapy to reduce "M" protein
  82. Prognosis of multiple myeloma
    • Median survival is 2.5 to 3 years, good management improves the quality and duration of life
    • Decreased life expectancy if: high "M" protein levels, diffuse bone lesions, hypercalcemia, anemia or renal failure
  83. What is multiple sclerosis?
    • patchy demyelination with reactive gliosis (proliferation of astrocytes in damaged areas of the nervous system, leads to a glial scar) in the spinal cord, optic nerve and white matter of the brain,
    • affects the ability of the nerve cells to communicate with each other
    • inflammatory disease in which fatty myelin sheaths around the axons are damaged
    • Episodic attacks that initially resolve but leave residual neurological deficits
  84. Causes of multiple sclerosis
    • Idiopathic but many theories
    • Autoimmune: Abnormal immunoglobulins, inflammatory response of lymphocytic and mononuclear cells
    • Viral: Epstein Barr
    • Nutritional: Vitamin D deficiency
    • Genetic: HLA-DR2 (broad antigen serotype)
  85. Incidence of multiple sclerosis
    400,000 people in US (1 in 700), affects women more, higher incidence further from the equator (temperate latitudes)
  86. Signs/symptoms of multiple sclerosis
    • Partial or complete loss of vision, usually in one eye at a time, often with pain during eye movement (optic neuritis)
    • Numbness or weakness in one or more limbs
    • Double vision
    • Tingling or pain in parts of the body
    • Electric shock sensations
    • Tremor
    • Unsteady Gait
    • Dizziness
    • Worsened in high temperatures
  87. Diagnosis of multiple sclerosis
    • Decreases in the function of two different parts of the CNS at two different times
    • Lumbar puncture - elevated IgG in CSF
    • MRI - detects lesions
    • Nerve function study (abnormal EEG in 1/3 of patients)
    • Neuro exam - reduced function including abdominal nerve reflex, decreased motor, decreased sensory, abnormal pupil response, decreased visual acuity, rapid eye movements
  88. Treatment of multiple sclerosis
    • No known cure
    • Control symptoms
    • Physical, speech and occupational therapy
    • Good nutrition, adequate rest
    • Interferon (immune modulating therapy)
    • Methotrexate (immune suppressor)
    • Diazepam (relieves spasms)
    • Steroids to reduce severity of attacks
    • Cholinergic drugs (minimize urine frequency and urgency)
    • Antidepressants
  89. Prognosis of multiple sclerosis
    • Varies, chronic and incurable
    • Most people continue to function with minimal loss of ADL's for 20 years
    • Best prognosis for women, people who were young when the disease started, infrequent attacks, limited evidence of disease on MRI
  90. What is myasthenia gravis?
    chronic autoimmune neuromuscular disease (autoimmune "channelopathy"- disease caused by disturbed function of ion subunits or the proteins that regulate them) from antibodies block acetylecholine receptors causing weakness
  91. Causes and incidence of myasthenia gravis
    • Autoimmune
    • Men > 50, women 20 to 40 and around 70
    • 10% of infants whose parents have the disease are born with transient neonatal myasthnia --> respiratory difficulties, hypotonia, poor suckling
    • 14 to 20 per 100,000 in US (36,000 to 60,000 cases)
  92. Signs/symptoms of myasthenia gravis
    • Bilateral weakness of eye muscles is first noticeable symptom
    • Dysphagia
    • Slurred speech
    • Ptosis
    • Diplopia
    • Waddling Gait
    • Shortness of breath
    • Dysarthria
    • Weakness in neck, limbs
    • Not being able to maintain posture
    • Problems chewing
    • Altered speech
    • Loss of facial expression
  93. Diagnosis of myasthenia gravis
    • Mild cases are often missed as weakness is the only symptom
    • Case history, neuromuscular exams
    • Acetylcholine receptor antibodies elevated
    • Anti-MuSK in 35% of those who do not have the acetylcholine receptor antibodies
    • Edrophonium chloride temporarily relieves symptoms
    • Nerve conduction studies
    • EMG
    • MRI
    • CT
    • Pulmonary function tests
  94. Treatment of myasthenia gravis
    • Anticholinesterase (long-term therapy)
    • Immunosuppressive drugs (prednisone)
    • Thymectomy - 50% success rate
    • Plasmapheresis
    • Intravenous immunoglobulins (IVIG)
    • Most lead normal lives with treatment
  95. What is Pelvic inflammatory disease (PID)?
    Inflammation of the uterus, fallopian tubes and other reproductive organs
  96. Causes of PID?
    • Primary organisms: Chlamydia trachomatis, Neisseria gonorrhoeae
    • Other: Haemophilus influenzae, other enteric organisms
    • Sexually transmitted infections
    • Mostly in nonwhites and those who smoke or douche, sexually active females in childbearing years
  97. Signs/symptoms of PID
    • Slow onset of bilateral lower abdominal and suprapubic pain that begins during or soon after menstruation
    • Tender, bilateral adnexal masses (masses in the adnexa of the uterus, which is the space occupied by the uterus, fallopian tubes and ovaries)
    • Movement of cervix produces pain
    • Fever
    • Vaginal discharge (foul smelling)
    • Tenderness outside the RLQ
    • May lead to: scarring, infertility, ectopic pregnancy, chronic pelvic pain
    • Fitz-Hugh-Curtis syndrome - failure to treat PID leads to ascending infection to the liver
  98. Diagnosis of PID
    • Case history
    • Elevated WBC
    • Culdocentesis and gram staining of cervical discharge
    • Ultrasound for any masses
    • Laparoscopy
  99. Treatment of PID
    • Antibiotics
    • Pain medication
    • Bed rest
    • Avoid intercourse
    • Surgery in severe cases
    • Prognosis is good with treatment if no complications (ex. infertility) have occured
  100. What is ulcerative colitis?
    • Inflammatory, usually chronic condition of the mucosa of the colon (type of IBS)
    • Produces edema (leading to mucosal friability - crumbliness) and ulcerations
    • Begins in the rectum and sigmoid colon and extend upward into colon, rarely affects small intestine
    • Mild, localized to fulminant disease that causes perforation
    • Usually not progressive, flare-ups and remissions occur, increased risk of colon cancer
  101. Causes of ulcerative colitis?
    • Idiopathic - possible abnormal immune response to food or bacteria such as E.coli
    • Stress increases the severity but is not a cause
    • Young women 15 to 30, and those 50 to 70, Jewish
    • 10 to 100 per 100,000 (<0.1%) of US
    • More common in nonsmokers and former smokers
  102. Signs/symptoms of ulcerative colitis
    • Recurrent attacks of bloody diarrhea with remissions, may have as many as 15 to 20 liquid, bloody stools daily
    • Spastic rectum and anus
    • Abdominal pain
    • Irritability
    • Weight loss
    • Weakness
    • Anorexia
    • Nausea and vomiting
  103. Complications of ulcerative colitis
    • Anemia
    • Colon cancer
    • Nutritional deficiencies, Anal fissure
    • Perirectal abscess
    • Hemorrhage
    • Joint inflammation
    • Mouth ulcers
    • Liver disease
    • Ankylosing spondylitis
  104. Diagnosis of ulcerative colitis
    • Case history, endoscopic findings, sigmoidoscopy (mucosal friability, pinpoint hemorrhages, thick inflammatory exudates)
    • Decrease potassium, magnesium, hemoglobin, albumin
    • Increased WBC, ESR and C-reactive protein
  105. Treatment of ulcerative colitis
    • Control inflammation, replace nutritional losses and blood volume, prevent complications
    • Sulfasalazine (anti-inflammatory and antimicrobial)
    • Immunomodulators
    • Steroids
    • Bed rest
    • IV fluids
    • Iron supplements or blood transfusion
    • No diet has been found to help
    • Surgery (25%) Proctocolectomy - remove all colon
    • Lifelong but with proper management most can leave normal lives
Card Set
York Midterm
Flashcards for York's midterm in quarter 9 (case 1)
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