NR 507 Week 7 quiz
Anorexia Nervosa - ANS --restriction of energy intake leading to low body weight
-intense fear of gaining weight
-disturbance in the way one's body weight or shape is experienced
complications:
dysphagia, constipation, apoptosis of liver cells, slowed gastric emptying, dysrhythmias,
long QT interval, sudden cardiac death, anemia, thrombocytopenia, leukopenia, delayed
response to infection, osteoporosis, stress fractures, decreased bone formation
\Bulimia Nervosa - ANS -- binge eating followed by purging, misuse of laxatives,
diuretics, excessive exercise, fasting
-usually once a week for at least 3 months
Complications:
Persistent acid reflux, chronic induced vomiting, tooth erosion, inflamed vocal cords,
hoarse voice, parotid gland enlargement, hypokalemic metabolic acidosis, diarrhea,
hemorrhoids, rectal prolapse, hyperphosphatemia
\Causes of elevated LFTs - ANS -- High aminotransferases and lactate dehydrogenase
(LDH)= hepatocellular injury, hypoxic and primary liver injury
- Obstruction of bile canaliculi or ducts resulting in regurgitation of bile back into the
hepatic sinusoids and into circulation= elevated bilirubin levels.
-prothrombin time= hepatitis and chronic liver disease
\Changes with osteoarthritis (DJD) - ANS -- Degeneration and loss of/poor repair of
articular cartilage- loss of smooth, frictionless joint
-Chondrocytes of articular cartilage become damaged d/t atypical load bearing as well
as genetic/biochemical factors.
-Cartilage loses glistening appearance, becomes yellow-grey/brown, surface area flakes
off and deeper layers develop longitudinal fissures (fibrillation).
-cartilage becomes thin/absent, exposing subchondral bone (becomes sclerotic, may
have cysts).
-pressure builds in cysts until their contents move into synovial cavity, breaking through
articular cartilage on the way.
-as cartilage erodes, cartilage-coated osteophytes may grow out from the bone and
alter the bone contours and joint anatomy.
-spurlike bony projections enlarge until small pieces, joint mice, break off into synovial
cavity causing synovitis and joint effusion.
, -joint capsule becomes thick and adheres to deformed underlying bone (limits
movement).
-*Loss of proteoglycans from articular cartilage*
-elevated Stromelysin and collagenase enzymes
-water content increased, reducing strength
\Characteristics of duodenal ulcers - ANS --20-50yo
-positive family hx (men and women)
-average stress
-increased ulcerogenic drugs
-no cancer risk increase
- H Pylori present (95-100%)
-increased parietal cell mass, acid production and serum pepsinogen
-no gastritis
-*pain* upper abd, intermittent, antacid and food relief, nocturnal pain common
-pattern of remission and exacerbations for years
\Characteristics of gastric ulcers - ANS --Less common than duodenal ulcers
-Usually caused by H. Pylori infection (60-80%) (treat with Atb)
-between 50-70yo both men and women
-neg family history
-increased stress/cancer
-normal or decreased parietal cell mass/acid production
-increased gastrin
-normal pepsinogen
-associated gastritis
-*pain* upper ABD, intermittent, antacid relief, food causes pain
-chronic without pattern of remission and exacerbation
\Chronic DM complications
Microvascular overview - ANS --Blindness, cataracts
-Kidney failure
-neuropathies
occlusion of capillaries and thickening of capillary basement membrane, endothelial cell
hyperplasia, thrombosis, and pericyte degeneration.
Hypoxia and ischemia in eye, kidney, and nerves
\Complications of DM
Macrovascular - ANS --Unrelated to the severity of the disease, (more related to
duration)
-Stroke
-CHF
Anorexia Nervosa - ANS --restriction of energy intake leading to low body weight
-intense fear of gaining weight
-disturbance in the way one's body weight or shape is experienced
complications:
dysphagia, constipation, apoptosis of liver cells, slowed gastric emptying, dysrhythmias,
long QT interval, sudden cardiac death, anemia, thrombocytopenia, leukopenia, delayed
response to infection, osteoporosis, stress fractures, decreased bone formation
\Bulimia Nervosa - ANS -- binge eating followed by purging, misuse of laxatives,
diuretics, excessive exercise, fasting
-usually once a week for at least 3 months
Complications:
Persistent acid reflux, chronic induced vomiting, tooth erosion, inflamed vocal cords,
hoarse voice, parotid gland enlargement, hypokalemic metabolic acidosis, diarrhea,
hemorrhoids, rectal prolapse, hyperphosphatemia
\Causes of elevated LFTs - ANS -- High aminotransferases and lactate dehydrogenase
(LDH)= hepatocellular injury, hypoxic and primary liver injury
- Obstruction of bile canaliculi or ducts resulting in regurgitation of bile back into the
hepatic sinusoids and into circulation= elevated bilirubin levels.
-prothrombin time= hepatitis and chronic liver disease
\Changes with osteoarthritis (DJD) - ANS -- Degeneration and loss of/poor repair of
articular cartilage- loss of smooth, frictionless joint
-Chondrocytes of articular cartilage become damaged d/t atypical load bearing as well
as genetic/biochemical factors.
-Cartilage loses glistening appearance, becomes yellow-grey/brown, surface area flakes
off and deeper layers develop longitudinal fissures (fibrillation).
-cartilage becomes thin/absent, exposing subchondral bone (becomes sclerotic, may
have cysts).
-pressure builds in cysts until their contents move into synovial cavity, breaking through
articular cartilage on the way.
-as cartilage erodes, cartilage-coated osteophytes may grow out from the bone and
alter the bone contours and joint anatomy.
-spurlike bony projections enlarge until small pieces, joint mice, break off into synovial
cavity causing synovitis and joint effusion.
, -joint capsule becomes thick and adheres to deformed underlying bone (limits
movement).
-*Loss of proteoglycans from articular cartilage*
-elevated Stromelysin and collagenase enzymes
-water content increased, reducing strength
\Characteristics of duodenal ulcers - ANS --20-50yo
-positive family hx (men and women)
-average stress
-increased ulcerogenic drugs
-no cancer risk increase
- H Pylori present (95-100%)
-increased parietal cell mass, acid production and serum pepsinogen
-no gastritis
-*pain* upper abd, intermittent, antacid and food relief, nocturnal pain common
-pattern of remission and exacerbations for years
\Characteristics of gastric ulcers - ANS --Less common than duodenal ulcers
-Usually caused by H. Pylori infection (60-80%) (treat with Atb)
-between 50-70yo both men and women
-neg family history
-increased stress/cancer
-normal or decreased parietal cell mass/acid production
-increased gastrin
-normal pepsinogen
-associated gastritis
-*pain* upper ABD, intermittent, antacid relief, food causes pain
-chronic without pattern of remission and exacerbation
\Chronic DM complications
Microvascular overview - ANS --Blindness, cataracts
-Kidney failure
-neuropathies
occlusion of capillaries and thickening of capillary basement membrane, endothelial cell
hyperplasia, thrombosis, and pericyte degeneration.
Hypoxia and ischemia in eye, kidney, and nerves
\Complications of DM
Macrovascular - ANS --Unrelated to the severity of the disease, (more related to
duration)
-Stroke
-CHF
