1. What is another name for osteogenesis imperfecta? Brittle BoneDisease
2.
How is achondroplasia treated? Growth Hormone
3.
What factors increase the risk for osteoporosis?
4. What happens to bone when parathyroid hormone is increased?
·
1° is autonomous secretion
·
2° is underlying renal disease—problems w/Vit D synthesis
and activation leading to decrease in calcium absorption from the gut—chronic
renal failure include metabolic acidosis and aluminum deposition in bone
·
both cause
significant skeletal changes related to abnormal osteoclastic activity
·
increased
osteoclastic activity w/bone resorption
·
cortical and
trabecular bone is replaced by loose connective tissue eps subperiosteal
·
increased
numbers of osteoclasts and accompanying erosion of bone surfaces
·
"brown
tumor" of hyperparathyroidism—marrow space has
amounts of fibrovascular tissue; hemosiderin from episodes of hemorrhage;
collections of osteocytes and fibroblasts form a mass
5. What conditions are associated w/
6.
Osteomyelitis from salmonella is associated w/what
condition? Sickle Cell Disease
7.
Involucrum—seen in
Paget's disease (chronic osteomyelitis) large sequestra of acute infection after
repair reaction that induces osteoclast activation, fibroblastic proliferation,
and new bone formation—refers to the surrounding rim of reactive bone
Sequestrum—residual necrotic bone in chronic osteomyelitis
8.
What may cause osteitis deformans? (Paget's Disease)—infectious
etilogy; paramyxovirus-like particles and antigens have been identified w/in
osteoclasts; necleic acid sequencesof the canine distemper virus related to
measles virus have been identified; a slow viral infection that induces the
synthesis of IL-6 which recruits osteoclasts
9.
Benign and Malignant Bone Tumors
Benign
·
Osteoma
·
Osteoid osteoma
·
Osteoblastoma
·
Osteochondroma
·
Chondroma
Malignant
·
1° osteosarcoma
·
2° osteosarcoma
·
chondrosarcoma
Miscellaneous
·
Giant cell tumor
·
Ewing's tumor
10.
Who tends to get osteosarcoma?
·
Males are
affected more than females
·
1° is 10-20 yrs
· 2° is > 40yr
· From what cell type is it formed? Malignant mesenchymal neoplasmsin which the neoplatic cells produce osteoid
· Where does it tend to occur? 1° malignant tumor of bone, occur in 2nd decade of life, found in around the knee, specifically the distal femur and proximal tibia
· What is the name of that characterisitc periosteal elevation? Codman's Triangle
11. Study figure 21-13. Be able to differentiate OA and RA by features
·
Rheumatoid
arthritis
·
Inflammation
·
Pannus—highly
vascularized, inflammatory, reduplicated synovium that covers the articular
cartilaginous surfaces
·
Eroding
cartilage
·
Fibrous
ankylosis
·
Bony ankylosis
·
Osteoarthritis
·
Bony spur
·
No ankylosis
·
Subchondral cyst
·
Subchondral
sclerosis
·
Osteophyte
· Thinned and fibrillated cartilage
12.
What are the long term effects of gout on the body. Who gets it and what are tophi? Sickle
Cell anemia. Tophi—large, irregular
deposits of chalky white sodium urate and are deposited on the articular
cartilage and adjacent joint capsule.
Provoke a chronic granulomatous inflammatory reaction. Recurrent episodes of arthritis involve
increasing numbers of joints and eventually lead to permanent joint
deformity. Chronic tophi may cause
significnat additional soft tissue deformity.
Tophi are usually painless, despite the tendency of advanced lesions to
ulcerate. Acute urate nephropathy may
cause acute renal failure; chronic disease is associated w/recurrent episodes
of pyelonephritis and chronic renal failure.
13.
Identify the
characteristics of myasthenia gravis.
·
Muscle
weakness—repeated contraction or stimulation
·
Ptosis (drooping
eyelids) and double vision
·
Difficulty
chewing and holding head upright
·
Speech w/nasal
quality
·
Respiratory
muscle leading to failure
14. What is the underlying defect in Duchene & Becker muscular dystrophy?
·
X-linked
hereditary muscular dystrophy
·
Caused by the
absence of structural protein termed dystrophin
·
Expressed in
muscles, brain and peripheral nerves
·
Impaired
contractile activity
15. What are the complications for cerebral edema
· Brain paenchymal edema
· Vasogenic edema—integrity of the normal blood-brain barrier is disrupted allowing fluid to escape from the vasculature into the interstitial space
· Cytotoxic edema—increase intrcellular fluid 2° to cellular injury (hypoxic-ischemic insult)
· Gyri are flattened
· Intervening sulci narrowed
· Ventricular cavities compressed
· Herniation may occur
· transtentorial (uncinate, mesial temporal) herniation—medial temporal lobe is compressed against the free margin of the tentorium cerebelli
· subfalcine (cingulate gyrus) herniation—unilateral or asymmetric expansion of the cerebral hemisphere displaces the cingulate gyrus under the falx cerebri
· tonsillar herniation—displacement of the cerebellar tonsils through the foramen magnum
16. What is the most common cause of infarcts, where do they tend to occur, and what is the significance of a transient ischemic attack?
· Caused by local cirulatory disturbances
· Most common form of cerebrovascular disease
· Account for 80% of cerebrovascular accidents (strokes)
· Cerebral atherosclerosis is the most common cause and factors that predispose to atherosclerosis (hypertension,diabetes mellitus, and smoking)
· Affects larger vessels like internal carotid, proximal middle cerebral, and basilar
· Blocked by thrombosis of an atherosclertoic arterial segment near carotid bifurcation or in basilar artery
· Emboli from the heart and proximal segment of carotid arteries
· Location and distribution of cerebral infarcts is influenced by a number of factors
· Site of arterial occulsion
· Time over which an occulsive event develops
· Presence or absence of arterial anastomoses (circle of Willis)
· Systemic perfusion pressure
· Transient ischemic attacks
· Self-limited episodes of vascular obstruction by atheromatous emboli and/or platelet-fibrin aggregates
· Predictor of subsequent infarcts
· Infarcts occur most commonly in areas supplied by branches of the middle cerebral artery
17. What type of aneurysm is associated w/hypertension? Where does bleeding occur w/rupture?
·
Most common
cause of spontaneous subarachnoid hemorrhage is rupture of a saccular aneurysm
·
The most common,
underlying cause of 1°
brain parenchymal hemorrhage
·
Abnormalities in
the vessel walls like acclerated atherosclerosis in large arteries, hyaline
arteriolosclerosis in smaller vessles, necrosis of arterioles
·
Minute
aneurysms—Charcot-Bouchard microaneurysms
·
Commonly in the
basal ganglion
18. What is an A-V malformation, cavernous angioma?
·
A-V malformation
·
Most common congential
vascular abnormalities in the brain
·
Significant
hemorrhage
·
Cerebral
hemisphere and middle meningeal artery
·
Spontaneous
hemorrhage
·
Saccular
aneurysms in 10% of AVMs
·
Cavernous
angiomas
·
Spontaneous
intracranial hemorrhage and seizures
·
Composed of ectatic,
thick-walled venous channels separated by dense fibrous stroma
19. Describe the differences b/w an epidural and subdural hematoma. Which is more dangerous, what are they associated w/and in what setting does brain atrophy effect either?
·
Epidural hematoma
·
Rupture of a
meningeal artery w/skull fracture
·
Middle meningeal
artery b/w dura matera dn squamous portion of temporal bone
·
Compress the
subjacent dura and flatten underlying brain parenchyma
·
Can cause uncal,
gyral, and cerebellar tonsillar herniation
·
Brain stem
compression
·
Death
·
A significant
number of patients w/epidural hematomas have a "lucid interval"
immediately after injury, followed by progressive loss of consciousness
·
Subdural
hematoma
·
Caused by
disruption of bridging veins from the surface of the brain to the dural sinuses
·
Rapid changes in
head velocity
·
Cause tears in
the delicate bridging veins as they penetrate the overlying dura mater
·
Occur most often
over cerebral convexities and vary from small hemorrhages to massive lesions
·
Acute or chronic
(clotted or liquefied blood clots)
20. What is the
result of diffuse axonal injury? Can
result in post traumatic dementia, hypoxic injury, and vegetative state.
21. What are the CSF results in bacterial meningitis, viral meningitis?
·
Bacterial
(leptomeningitis)—turbid, contains predominantly neutrophils, protein is
elevated owing to increased vascular permeability and glucose levels are
markedly decreased b/c of impaired transport of glucose into CSF and metabolic
activity of neutrophils, Organisms visible in Gram stain
·
Viral—contains
predominantly lymphocytes; protein concentrations are elevated to a modest
degree; glucose levels are normal
22. What are some
examples of spongiform encephalitis? Creutzfeldt-Jacob disease, kuru,
Gerstmann-Straussler syndrome, fatal familial insomnia, scarpie and "mad
cow"; infectious prions are a modified form of a normal structural protein
found in the mammalian nervous system
23. What is the
most aggressive and least aggressive form of astrocytomas?
·
Most
aggressive—glioblastoma multiforme
·
Least
aggressive—pilocytic astrocytomas (kids)
24. What tumor arises w/in the central canal of the spinal cord? Ependymomas
25. What are psammoma bodies? Meningiomas; calcification; concentrically laminated, calcified granules
26. What is the most common demyelinating disease of the CNS? Multiple Sclerosis; waxing and waning neurologic abnormalities of CNS
27. What is confabulation and what condition is it associated w/? It is the filling in of gaps in memory with fictitious things or events that are believed to be true by the patient and is often associated w/ Wernicke-Korsakoff’s syndrome (thiamine deficiency) and specifically with Korsakoff’s psychosis.
28. What is the most common cause of dementia in the elderly? Alzheimer's disease
29. What is paralysis agitans, Lewy bodies, neurofibrillary tangles?
Paralysis agitans—idiopathic Parkinson's disease;
degenerative disorder involving the dopamine-secreting neurons of the
substantia nigra and locus ceruleus
Lewy bodies—concentrically laminated, eosinophilic, intracytoplamic inclusions
Neurofibrillay tangles—course, filamentous aggregates w/in the cytoplasm of neurons; found in the neocortex, hippocampus, basal forebrain and parts of brain stem
30.
What is the interest in b-amloid in Alzheimer's
disease? Deposition of amyloid, dervied from breakdown of a protein; prominent
component of both the neurofibrillary tangles and senile plaques found in the
brains of AD patients; present w/in the walls of cerebral blood vessels; can be
toxic to neurons in cell cultures
31.
Parkinson's disease—a
disturbance in motor function by rigidity, expressionless facies, stooped
posture, gait disturbances, slowing of voluntary movements, and a
characteristic "pill-rolling" tremor. Disturbance of dopaminergic pathways connecting the substantia
nigra to the basal ganglia
Guillan-Barre syndrome—one of the most common life threatening
diseases of the PNS; etiology is unknown, may develop after viral prodrome,
Mycoplasma infection, allergic reaction or surgical procedure—immunologic
basis; rapidly progressive, ascending motor weakness; death by failure of
respiratory muscles; segmental demyelination, inflammation of peripheral
nerves; CSF has
protein
Huntingtion's disease—hereditary, progressive, fatal disorder
involving the "extrapyramidal" motor system, characterized by
involuntary movements (chorea) and dementia—autosomal dominant; apparent in
adulthood; gain of function mutation; atrophy of the caudate nucleus, putamen
and globus pallidus
Amyotrophic lateral sclerosis—Lou Gehrig's disease—progressive degenerative
disorder involving the upper and lower motor neurons of he pyramidal system
w/muscle weakness, atrophy, and spasticity; loss of motor neurons in anterior
horns; fasciculations (small involuntary movements); hyperactive DTR and a
Babinski reflex
Alzheimer's disease—the most common cause of dementia in the
elderly, w/cerebrovascular disease accounting for most the remaining cases;
seinle dementia and presenile dementia; genetic factors; deposition of amyloid,
expression of specific alleles of apoprotein; neurofibrillary tangles; senile
plaques; amyloid core; amyloid angiopathy
32.
What is an acoustic neuroma?
Schwannomas; from Schwann cells
and a little from fibroblasts; well-circumscribed masses attached to peripheral
nerves, cranial nerves or spinal nerve roots; the 8th cranial nerve
is a particularly common site well-demarcated masses in the angle b/w the
cerebellum and pons
33.
Which neuropathy presents w/a "glove & stocking"
distribution? Guillain-Barre (most common life threating peripheral nerve disease
34.
Recognize descriptions for the following:
Paraesophageal hernia—separate portion of the stomach, usually along the greater curvature, enters the thorax through the widened foramen
Sliding hernia—95% of cases; protrusion of the stomach above the diaphragm creates a bell-shaped dilation, bounded below by the diaphragmatic narrowing
Achalasia—failure to relax; incomplete relaxation of the lower esophageal
sphincter in response to swallowing 1) aperistalsis 2) partial or incomplete
relaxation of the lower esophageal sphincter w/swallowing 3) increased resting
tone of the lower esophageal sphincter
Mallory-Weiss syndrome—longitudinal tears in esophagus at
esophagogastric jxn; found in alcoholics
Barrett's esophagus—long standing gastroesophageal reflux,
replacement of the normal distal stratified squamous mucosa by abnormal
metaplasitc columnar epithelium containing goblet cells
Esophagitis—80% in Iran and high in China; origins include prolonged gastric
intubation, uremia, ingestion of corrosive or irritant substances, and
radiation or chemotherapy; overwhelming preponderance of cases in Western
countries are attributable to reflux of gastric contents (reflux
esophagitis) 1)decreased efficacy of
esphageal antireflux mechanisms 2)
inadequate or slowed esophageal clearance of refluxed material 3) sliding
hiatal hernia 4) increased gastric volume, contributing to the volume of
refluxed material 5) impaired
reparative capacity of the esophageal mucosa by prolonged exposure to gastric
juices
35.
What are the risk factors for carcinoma of the esophagus? Most
are squamous cell carcinomas; more incidence among blacks than whites
·
Long standing
esophagitis
·
Achalasia
·
Plummer-vinson
syndrome (esophageal webs, microcytic hypochromic anemia, atrophic glossitis)
·
Alcohol consumption
·
Tobacco abuse
·
Deficiency of
vitamins (A,C, riboflavin, thiamine, pyridoxine)
·
Deficiency of
trace metals (zinc, molybdenum)
·
Fungal
contamination of foodstuffs
·
High content of
nitrites/nitrosamines
·
Tylosis
(hyperkeratosis of palms and soles
36. Differentiate acute gastritis, peptic ulcers and chronic esophagitis by definition or clinical presentation.
Acute gastritis—acute mucosal inflammatory process, usually
of a transient nature; erosin—sloughing of the superficial mucosal epithelium
·
Heavy use of
nonsteroidal anti-inflammatory drugs—aspirin
·
Excessive
alcohol consumption
·
Heavy smoking
·
Treatment
w/cancer chemotherapeutic drugs
·
Uremia
·
Systemic
infections (salmonellosis)
·
Severe stress
(trauma, burns, surgery)
·
Ischemia and
shock
·
Suicide attempts
w/acids and alkali
·
Mechanical
trauma (nasogastric incubation)
·
After distal
gastrectomy w/reflux of bilious material
Peptic
ulcers—breach in the mucosa of the
alimentary tract that extends through the muscularis mucosa into the submucosa
or deeper; duodenum and stomach; chronic, solitary; 98% in first portion of
duodenum or stomach; need exposure to gastric acid and pepsin, very strong
causal association w/H. pylori infection
Chronic
esophagitis—10-20% of US population,
reflux of gastric contents, heartburn, regurgitation, usually over 40y/o;
bleeding, Barretts (malignancy); nausea and vomiting
37.
What is the relationship b/w stomach ulcers and Helicobacter
infection? What is the most important
in allowing an ulcer to develop? H. pylori is present in virtually all
duodenal ulcers and about 70% of those w/gastric ulcers; only 10-20% of
individuals worldwide infected w/H. pylori actually develop peptic ulcers; must
have breach in mucosa; imbalance b/w the gastoduodenal mucosal defenses and the
countervailing aggressive forces that overcome such defenses
38.
What is linitis plastica?
What is the different appearance of ulcerative carcinoma and a benign
peptic ulcer? Gastric wall is extensively infiltrated by malignancy. It has a rigid and thickened stomach—leather
bottle stomach (breast and lung may have similar appearance)
·
Ulcerative
carcinoma—large w/irregular, heaped-up margins; extensive excavation of the
gastric mucosa w/a necrotic gray area in the deepest portion Fig 15-17
·
Peptic
ulcer—small ulcer w/sharply punched-out appearance. The margins are not elevated.
The ulcer base shows a small amount of blood, but is otherwise
clean.
39. Differentiate b/w Crohn's disease and ulcerative colitis. What are skip lesions, pseudopolyps? Which is a granulomatous disease? Chronic relapsing disorders of unknown origin; idiopathic inflammatory bowel disease
Crohn's disease—granulomatous disease that may affect any portion of
the GI tract form esophagus to anus but most often involves the small intestine
and colon; skip lesions have affected area followed by an unaffected area in a
scattered pattern; viewed as a systemic disease w/predominant GI involvement
1)
sharply delimited
and typically transmural involvement of the bowel by an inflammatory process
w/mucosal damage
2)
the presence of
nancaseating granulomas in 40-60% of cases
3)
fissuring
w/formation of fistulae
4)
mesenteric fat
"creeping fat" that wraps around the bowel surface
Ulcerative colitis—nongranulomatous disease limited to the colon;
ulceroinflammatory disease affecting the colon but limited to the mucosa and
submucosa except in the most severe cases.
Begins in the rectum and extends proximally in a continuous fashion. Can
be considered a systemic disease (ankylosing spondylitis). Pseudopolyps—w/severe disease, there is
extensive and broad-based ulceration of the mucosa in the distal colon or
throughout its lenth—isolated of islands of regenerating mucosa bulge upward
1. no well-formed granulomas
2. no skip lesions
3. mucosal ulcers do not extend below the
submucosa w/little fibrosis
4. mural thickening does not occur; serosal
surface is normal
5. greater risk for carcinoma
40. Bowel Obstruction
1. hernia—weakness in wall of peritoneal cavity
w/protrusion. Segments of viscera
frequently intrude and become trapped in them (external herniation)
2. intestinal
adhesions—surgical procedures,
infections endometriosis or peritonitis can form fibrous bridges than may
create loops and trap viscera
3. intussuception—telescoping of proximal segment of bowel
into the immediate distal segment. In
children, may occur spontaneously.
Adults usually have a point of attachment (tumor) that
"sling-shots" the proximal bowel forward
4. volvulus—twisting of bowel loop or ovary blocking
venous outflow and arterial supply.
Infarction and obstruction may follow.
5. Toxic megacolon—rare—extensive erosion and exposure of neural plexus to fecal material—neuromuscular function shuts down, colon progressively swells and becomes gangrenous—seen w/Ulcerative Colitis
6. Hirschesprung Disease—Congenital Megacolon—caudad migration of neural crest are arrested during descent before reaching the anus—aganglionic segment which lacks both Meissner's and Auerbach's plexi—functional obstruction and progressive distention of the colon proximal to the affected segment
7. Peutz-Jeghers syndrome—non-neoplastic polyps—uncommon hamartomatous polyps that occur as part of the rare autosomal dominant—melanotic mucosal and cutaneous pigmentation—increased risk of both intestinal and extraintestinal malignancies
8. Diverticulitis—blind pouch leading off the alimentary tract, lined w/mucosa, that communicates w/the lumen of the gut; taeniae coli are muscular bands of the colon which can lead to muscular defects; seen in 60+ Westerners from consumption of refined, low fiber diet leading to smaller stools and difficulty passing it through
9. Meckel's
diverticulum—most common and innocuous
of these anomalies; failure of involution of omphalomesenteric duct, leaving a
persistent blind ended tubular protrusion; seen in ileum; composed of all
layers of the normal small intestine; asymptomatic; bacterial growth that
depletes vit B12 leading to condition similar to pernicious anemia
41.
What is the most
common cell type of colon cancer? What
is a napkin ring lesion? Where is it
typically found? How does the
presentation w/right colon cancer differ from left colon cancer? Adenocarcinomas; When carcinomas in the
distal colon are discovered, they tend to be annular, encircling lesions that
produce so-called napkin ring constrictions of the bowel narrowing the lumen;
Shift towards right colon cancer; can't be detected by digital or
proctosigmoidoscopic examination; left-sided lesions—occult bleeding, changes
in bowel habit, or crampy LLQ (left lower quadrant) discomfort; cecal and right
sided lesions are found do to fatigue, weakness, and iron deficiency anemia
42. What is the
significance of iron deficient anemia in the older male? It almost always
means GI cancer.
43. What dietary
factors are implicated in colon cancer?
44.
What is the most important prognostic indicator of colorectal
cancer? favorite metastatic sites: regional lymph nodes, liver, lungs and bone;
25%-30% of cases are beyond surgical cure at dx—extent of the tumor at the time
of diagnosis
45.
Define
a.
fetor hepaticus—characteristic
body odor variously described as "musty" or "sweet and
sour";related to the formation of mercaptans by the action of GI bacteria
on the sulfur containing aa methionine, and shunting of splanchnic blood from
the portal into the systemic circulation
b.
ascites—excess fluid in
peritoneal cavity; detectable at 500mL; serous fluid w/albumin; involves one or
more 1)sinusoidal hypertension; percolation of hepatic lymph flow into
peritoneal cavity; renal retention of Na+ and water
c.
spider angiomas—spider
telangiectasia—radial array of some-what dilated subcutaneous arteries and
aterioles about a central core; they may pulsate; liver cirhosis; impaired
estogen metabolism and consequent hyperestrogenemia
d.
caput medusa—abdominal
wall collaterals that appear as dilated subcutaneous veins extending form the
umbilicus toward the rib margins—hallmark of portal hypertension
46. Clinical Consequences of Liver Disease
|
Characteristic Signs |
Hepatitisatic
dysfxn |
|
|
Jaundics and cholestasis |
|
|
Hypoalbuminemia |
|
|
Hyperammonemia |
|
|
Fetor hepatitisaticus |
|
|
Palmar erythema |
|
|
Spider angiomas |
|
|
Hypogonadism |
|
|
Gynecomastia |
|
|
Weight loss and muscle wasting |
|
|
Portal hypertension
form cirrhosis: |
|
|
Ascites |
|
|
Splenomegaly |
|
|
Hemorrhoids |
|
|
Caput medusa |
|
Life-threatening Complications |
Hepatitisatic failure |
|
|
Multiple organ failure |
|
|
Coagulopathy |
|
|
Hepatitisatic encephalopathy |
|
|
Hepatitisatorenal syndrome |
47.
What is the most common cause of cirrhosis? What are typical causes of death of
cirrhosis? Alcoholism; mechanism of death is progressive liver failure,
complications to portal hypertension; hepatocellular carcinoma
48.
Define
a.
hepatic failure—hepatic
destruction; end point of progressive damgae to the liver; loss of 80-90% of
hepatic function; findings include jaundice, hypoalbuminemia, hyperammonemia,
fetor hepaticus; it is life threatening; death multiple organ system failure
esp respiratory w/pneumonia and sepsis and renal failure
b.
fulminant hepatitis—hepatic
insufficiency that progresses from onset of syptoms to hepatic encephalopathy
w/in 2-3 wks; viral hepatitis accounts for 50-60%; drugs and chemical account
for 25-30%; loss of liver substance; complete destruction of hepatocytes
c.
acute hepatitis—any of
the hepatitis viruses can cause; 4 phases 1) incubation period 2) symptomatic
preicteric 3)symptomatic icteric 4)
convalescnce; hepatocyte injury is diffuse swelling (ballooning degeneration),
cholestasis (bile plugs in canaliculi and brown pigmenation of hepatocytes);
fatty change in unusual except in HCV
d.
chronic hepatitis—symptomaic,
biochemical or serological evidence of continuing or relapsing hepatic disease
for more than 6 months w/histologically documented inflammation and necrosis;
Wilson's disease, a1-antitrypsin
deficiency, chronic alcoholism, drugs, and autoimmunity; findings include
spider angiomas, plamar erythema, mild hepatomegaly, hepatic tenderness, and
mild splenomegaly
49. Hepatitis A, B, C
|
|
Hepatitis A |
Hepatitis B |
Hepatitis C |
|
Agent |
Icosahedral capsid, ssRNA |
Enveloped dsDNA |
Enveloped ssRNA |
|
Classification |
Picornavirus |
Hepadnavirus |
Flavivirus |
|
Transmission |
Fecal-oral |
Parenteral; close personal contanct |
Parenteral; close personal contact |
|
Incubation period |
2-6 |
4-26 |
2-26 |
|
Fulminant hepatitis |
<0.5% |
<1% |
Rare |
|
Carrier state |
None |
0.1-1% |
0.2%-1% |
|
Chronic hepatitis |
None |
5-10% of acute infections |
>50% |
|
Hepatocellular carcinoma |
No |
Yes |
yes |
50. What are the risk factors for hepatocellular carcinoma? #1 is hepatits B viral infection, hepatocarcinogens in food (primarily aflatoxins), and chronic liver disease
51.
What are the most common type of gallstone, which is visible
on x-ray, how often are they symptomatic?
What leads to ductual obstruction?
Cholesterol stones containing
crystalline cholesterol monohydrate are the most common; need sufficient
calcium carbonate to be seen on x-ray; brown stones contain calcium soaps and
can be seen on x-ray; >80% are asymptomatic (<20% a symptomatic);
52. Define
a.
cholelithiasis—gallstones
b.
cholecystitis—inflammation
of gallbladder
c.
cholangitis—acute
inflammation of the wall of the bile ducts; almost always due to bacterial
infection of the normally sterile lumen
53. What are the diseases of endocrine pancreas? The exocrine?
Enodcrine—diabetes mellitus (b
cells) and islet cell carcinomas (hyperinsulinism, hypergstinemia,
Zollinger-Ellison syndrome, endocrine neoplasia
Exocrine—acute and chronic pancreatitis, carcinoma of the pancreas
54.
acute pancreatitis—acute
onset of abdominal of abdominal pain resulting form enzymatic necrosis and
inflammation of the pancreas; elevation of pancreatic enzymes in blood and
urine; fat necrosis; acute hemorrhaic pancreatitis
chronic pancreatitis—repeated bouts of mild to moderate pnacreatic
inflammation w/continued loss of pancreatic parenchyma and relplacement by
fibrous tissue; distinction b/w acute and chronic whether the pancreas was
normal before a symptomatic attack or is already chronically damaged
55.
In what portion of the pancreas is carcinoma most likely to
arise? Exocrine portion; 60% in the head, 15% in body, 5 % in tail; 20%
throughout the entire gland
56.
Difference b/w adult onset and juvenile onset diabetes
|
|
Type
I—Juvenile—insulin dependent |
Type
II—Adult—non-insulin dependent—80-90% of cases |
|
Clinical |
Onset <20yrs; normal weight; decreased blood insulin; anti-islet antibodies; ketoacidosis common |
Onset >30yrs; obesity; normal or increased blood insulin; no anti-islet cell antibodies; Ketoacidosis rare |
|
Genetics |
50% conconrdance in twins |
60%-80% concordance in twins |
|
Pathogenesis |
Autoimmunity, immunopathologic mechanisms, severe insulin deficiency—dependent upon insulin treatment |
Insulin resistance—insulin sensitivity of target tissue decreases, serum levels of insulin may be elevated; decrease in # of insulin receptors and postreceptor signaling by insulin is impaired |
|
Islet cells |
Insulitis early; marked atrophy and fibrosis; severe b-cell depletion |
No insulitis; focal atrophy and amyloid deposits; mild b-cell depletion |