Exam 2 part 2 Flashcards

1
Q

What are the symptoms of acute vs chronic pancreatitis?

A
  • Acute
    • Abdominal pain, distension, N/V
    • Great distress, profuse sweating, uncontrollable pain, syncope, rapidly developing shock
    • Sudden onset and occurs in pt w/history of gallstones or alcoholism
  • Chronic
    • Pain, exocrine pancreatic insuffiency (protein malabsorption)
    • Endocrine insuffiency - 70% have signs of diabetes, slow but steady destruction of islets of langerhans
    • Mild elevations or serum amylase and lipase
    • Alcohol abuse, epigastric pain, weight loss, bulky/fatty stools, numerous pancreatic calcifications
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2
Q

What happens to pancreatic tissue when there is blockage of biliary tract? (pathogenesis of acute hemorrhagic pancreatitis)

A
  • Answer: Auto-digestion
  • Tissue damage due to pancreatic digestive enzyme buildup (activation of Trypsinogen)
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3
Q

What are 80% of acute pancreatitis caused by?

A
  • Gallstones and alcohol
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4
Q

What condition would you find Mallory bodies in?

A
  • Seen in alcoholic hepatitis (micronodular cirrhosis)
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5
Q

How does alcohol affect liver function?

A
  • Doesn’t allow for peripheral FA’s to enter
  • Doesn’t allow for triglycerides to be broken down
  • High caloric content (leads to fatty liver - doesn’t allow for beta oxidation)
  • Alcholic hepatitis can be fatal
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6
Q

Match the following characteristics to the different hepatitis diseases:

  1. Benign - fecal/oral vector - picornavirus (like polio, cocksackie)
  2. Co-infection with Hep B
  3. DNA - (everything else is RNA)
  4. One used to be cause post-transfusion/non-A, non-B
  5. 20% of infected pregnant women develop heptaic necrosis
A
  1. Hep A
  2. Hep D
  3. Hep B
  4. Hep C
  5. Hep E
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7
Q

Which serologic test antibody would detect Hep B during the window period?

A

(Window period - where you have antigen present - but not enough anitbody reaction)

  • Order HBcAb (core antigen) - HBsAg and HbsAb will be negative during window period)
  • 3 phases of infection - incubation period, acute infection, and convalescent/recovery phase
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8
Q
  1. What is osteoporosis?
  2. Who is most likely to get it?
  3. What is pathophysiology?
A
  1. Loss of bone matrix
  2. Long bones and vertebral most commonly affected
  3. For women it’s related to decrease in estrogen levels, causes decrease in bone mass, etiology of osteoporosis is more hormonal thatn any other
  4. Changes in articular cartilage
  5. Prevalence and severity increases with age
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9
Q

What bone is most likely affected by fracture in osteoporosis? (in old age and postmenopausal women)

A

Weight bearing joints: hipts, kneew, and cervical spine

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10
Q

Which joint disease (osteoarthritis or gout) causes destruction of articular cartilage with underlying bone cysts/spurs?

A

Osteoarthritis

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11
Q

Within osteoarthritis - what are the definitions of:

  1. Eburnation?
  2. Fibrillation?
A
  1. Sclerosis of subchondral plate due to continued pressure
  2. Fibrillation - formation of vertical clefts, which shed cartilage into subchondral bone
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12
Q

What are the features of osteoarthritis througout the body?

A
  • When affects the toe, causes bunion
  • Affects cervical and lumbar vertebral bodies and hands
  • Bouchards vs Heberden’s nodules
  • Bone cysts - fill up with synovial fluid
  • Osteophytes - bone spurs
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13
Q

What are the definitions of pedagra and tophi?

A
  • Pedagra - foot seizure - the first symptom that occurs in Gout at big toe (tarsometatarsal joint)
  • Tophi - encapsulated urate crystals surrounded by macrophages, lymphocytes and giant cells
    • Can deposit in organs like the kidneys
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14
Q

What is the pathophysiology of gout?

A
  • 95% male, family history, unknown cause, but genetic and environmental factors
  • Hyperuricemia - uric acid crystal deposits in joints, subcutaneous tissue and kidneys
  • Big toe (most common area)
  • Alcohol exacerbates gout
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15
Q

Which environmental factors predispose development of lupus?

A
  • Young black adults - 10x women over men - familial
  • Malfunction of CD4+ T-cells, leading to polycolonal B-cell activation (autoimmune)
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16
Q

What parts of the body are most common involved with lupus?

A
  • Joints - most common manifestation
  • Face - erthematous rash - “butterfly rash”
  • Kidneys - Glomerulonephritis - IgG antibodies to ds/ss DNA
  • Serositis - pleuritis and pericarditis
  • Lungs - Pleural disease to pneumonia (deposition of immune complexes in alveolar septae with patchy acute inflammation)
  • Heart - pericarditis and all layers of heart
  • Brain - involvement of CNS is life-threatening
  • Spleen - Vasculitis and fibrosis of smaller arteries (onion skin pattern)
  • Note - no involvement with PANCREAS
17
Q

What is the most characteristic autoantibodies for lupus and drug induced lupus?

A
  • Lupus
    • Antinuclear antibodies - to dsDNA, RNA, nuclear proteins and Smith Sm antigen
  • Drug-Induced Lupus
    • Antibodies to histones (DS-DNA and to Sm antigen are unusual)
    • Procainamide (arrhythmias)
    • Hydralazine (hypertension)
    • Isoniazid (TB)
    • If you stop the above drugs - the signs/symptoms go away