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adenocarcinoma of the esophagus occurs in the setting of barrett changes. frequency of this cancer is on the rise. typically presents with dysphagia. long term survival is low
most common esophageal cancer in world (low in US) Common in asia
risk factors: smoking, alcohol, nitrosamines, lye strictures (scarring of esophagus)
dysplasia is common presenting symptom
treatment: surgery and radiotherapy (5 year survival=10%)
motor problems of the esophagus may cause dysphagia or dynophagia (painful swallowing).
potential cause: peripheral neuropathy (diabetes, alcohol) neurologic disease (stroke, ALS), systemic disease (sclerosis, amyloidosis, hypothyroidism)
LES loses ability to relax as a bolus of food travels down esophagus. peristalsis above LES is lost and esophagus bags out and is filled with food and liquid.
idopathic cause, clear loss of nerve body cells in myenteric nerve plexus of esophagus
trypamosoma cruzii in Latin America causes chagas disese (loss of ganglion cells in myenteric plexus)
break in mucosa of the stomach or duodenum, 1/10 ppl will develop an ulcer
risk factors: cigarette smoking and use of aspirin (NSAIDs), blood group O
treatment include: reducing acid (medication or surgery) or eradicating H. pylori infection with AB
what: erosions, hemorrhages and ulcers may be present.
cause: NSAIDs are most common cause. stress from trauma, critical illness, incapacitation
presentation: vague abdominal pain, severe hemorrhage, chronic bleeding (Fe anemia)
treat: acid suppression meds (histamine antagonist or proton pump inhibitor)
spectrum of problem rnges from mild chronic inflammation to severe atrophy.
autoimmune gastritis is diffuse inflammation in the body and fungus of stomach. associated with B12 anemia and severe achlorhydria. may lead to gastric cancer
tumors of UGI tract
runds horizontally across the mid abdomen and is surrounded by C shaped duodenum. lies deep to retroperitoneum. pancreatic duct drains into duodenum
exocrine pancreas: contain acinar cells which product digestive enzymes and bicarbonate
endocrine pancreas: islets cells which produce hormones (insulin and glucagon)
what: occurs when the acinar cells of exocrine become inflamed. spectrum is mild to severe hemorrhage and large scale necrosis of acinar cells
how: injury to pancreas causes zymogen granules (stored digestive enzymes) to become activated within pancreas cells
causes: alcohol, gallstones (also drugs trauma and viruses)
inflammation of pancreas causes fluid to collect in and around the gland (phlegmon)
over time, fluid collects (pseudocyst), which can pu pressur on the stomach/duodenum and cause obstructive symptoms.
pseudocyst can also become infected
pacreative necrosis: part of the land has completely died, potential site of infection (pancreatic abscess)
what: chronic inflammation in pancreas eventually leads to scar tissue formation (fibrosis), loss of cell function, and duct deformity. process can smolder almost unnoticed.
cause: alcohol, cystic fibrosis, inheritance, hypertriglyceridemia, idopathic
pts may develop pancreatic insufficiency.
exocrine insufficiency causes fat malabsorption induced diarrhea (steatorrhea) and secondary weight loss
endocrine insufficiency causes diabetes mellitus. calcium sones form in pancreatic duct leading to obstruction and pain. chronic pain is hte leading cause for pts to go to surgery
forth leading cancer in men and fifth in women
tends to occur later in life.
early symptoms are non-specific and imaging tests are insensitive
smoking is associated with higher incidence of pancreatic cancer. alcohol, chronic pancreatitis, high fat diet and exposure to certain chemicals also increase risk
pancreatic cancer is found in head of pancrease 60% of cases
presentation: painless jaundice, vague mid-epigastric pain with possible radiation to the back. tumor also can be associated to depression or recurrent thrombophlebitis
progression: obstructive jaundice, severe abdominal pain, weight loss, metastasis to liver, lung or peritoneum
allows for the absorption of water and electrolytes. colon begins as theileocecal valve enters into the sac like cecum. Vermiform appendix attaches to the base of the cecum. Taenia coli are three narrow bnds of longitudinal muscle tht run the length of the large intestine.
haustra are folds of circular muscle creating sac like segments along the colon
25% of the weight of the GI tract
includes kupfer cells, intraepithelial lympohcytes, peyer's patches in ileum, lymph notes outside the stomach
increase of stool volume or decrease in consistency. caused by large or small bowel problems
defined as volume of greater than 150-200ml per 24 hrs.
osmotic diarrhea occurs when cars or minerals create an osmolar gap. water follows into the lumen to reduce the situation
secretory diarrhea may be secondary to toxins from infections bacteria or gut hormones
problem of large intestine.
causes: structual (tumor, adhesion), hormonal (hypothyroidism, diabetes), neurologic (hirschsprung disease)
most common cause is poor dietary fiber intake
inability to break down the disaccharide lactos causes diarrhea, gas and abdomial pain (sm intestine can only absorb simple sugars)
lactose (glucose-galactose) is found in dairy
generally all anials lose ability to make the brush border enzyme lactase around the time of weaning-sometimes this event doesn't occur and allows lactose to be consumed in large amounts
inability to absorb certain proteins found in most grains. leads to severe, chronic diarrhea containg large volumes of fat (steatorrhea) with associated weight loss, anemia or even death.
examingation of intestine shows flattening of normal folds and villi as well as inflammation
chronic inflammation of the bowel and often has a pattern of familial occurrence. there may be manifestations of IBD in systems outside of GI.
cause of IBD has not been determined. May be due to genetic susceptibility, immune dysregualtion, and environment
types: ulcerative colitis and crohn's disease
most commonly develops in young adults, peaking in incidence at age 30
disease of the lining or mucosa of the colon. may involve entire organ (pancolitis) or limitied to distal aspect (left sided colitis). pt may have involvement of rectum alone and never progress (ulcreative proctitis)
toxic megacolon: severe rapid progression of UC leading to microperforations, sepsis and death
microscopic characteristic: crypt abscess. over time raised islands of mucosa form (pseudopolyps)
often arises in adolescents and young adults. may be familial
may involve any part of GI tract (mouth to anus). often in terminal ileum and right side of colon.
no curative treatment. steroids, sulfasalzine and immunosuppressives (azathioprine) used. sometimes surgery (but chance for recurrence)
process is transmural, involveing the full thickness of the bowel wall in contrast to ulcerative colitis. early lesions are small round ulcers. granuloms are typicall found. skip lesions= area of involvement are interspersed between ormal appearing bowel
presentation is dependent on part of bowel involved. earlier, disease is non-specific and symptoms may include fever, abdominal pain, and diarrhea. partial obstruciton, malabsorption and bleeding also seen
formation of mucosal outpouchings of the lining of the large bowel. common in western world (1:3 over age 50). caused by low dietary fiber and higher pressures the colon akes to proel stool forward.
complications: diverticulitis (stool and bacteria become trapped in pockets leading to low grade infection and abscess formation) and bleeding (diverticula may rupture and lead to severe, painless, lower GI bleeding)
also known as vascular ectsia
common cause of lower GI bleeding (besides ruptured diverticula)
tufts of arterivenous malformations are most common in individuals over the age of 60. most common in right colon but may be found throughout bowel
over many years adenomatous polyps grow larger and develop changes in their microscipic struction from tubulous to villous in nature
the larger the polymp (>1-2cm) and more villous its histology, the greater the chance a focus of cancer will be found
adenoma-carcinoma hypothesis: reflects belief that polyps accumulate genetic mutations that eventually lead to cancer being formed
common in the west (low dietary fiber, high dietary fat)
risk factors: increased age, ulcerative colitis, prior history of colon cancer, hereditary polyposis syndromes
generally silent for majority of course. may cause subtle bleeding and screening should occur yearly after age 50
advanced colon cancer may cause gross bleeding, obstruction, performation, or a fistula
dukes A: tumors confined to the bowel wall (within muscular layer)
dukes B: cancer extends beyond the bowel wall
dukes C: implies lymph node involvement
dukes D: equals distant metastases
familial adenomaous polyposis (FAP): autosomal dominant gene, APC is due to specfic defect found on chromosome 5. gen has been identified and blood samples can be screened. thousands of polyps develop in the colon and colon cancer is inevitable by age 40
Hereditary non-polyposis colon cancer: relatively small # of polyps, but clustering of colon, pancreas, ovary and uterus cancers. defect in mis-match repair gene
a reduced transparency of the crystalline lens. either results from a change in color (brunescent or brown cataract), change in refractive index, or an increase in light scattering (opacificaiton)
A CATARACT IS NOT A FILM ON THE CORNEA
cataract is leading cause of blindness worldwide (even though reversible)
factors: age (most common), smoking, diabetes, trauma, inflammation of the eye exposure to sun /UV rays, corticosteroids
symptoms: normally slow and painless, decreased vision, glare, myopic shift (2nd sight)
becaue of the blocked aqueous fluid flow, there is an increaed intraocular pressure which damages the optic nerve and leads to vision loss.
no signs or symptoms in early stages
loss of peripheral vision in earlier stages
irreversible diminished visual acuity at end stages
response to poor blood glucose control that is seen eventually in most individuals with diabetes mellitus. Blindness can result from leakage of erum into the macular retina (diabetic macular edema)
Characterized by the growth of abnormal new vessels on retinal surface, which can bleed into retina or vitreous
sypmptoms: gradual vision loss, generalized blurring, areas of focal vision loss
blood vessels become damaged (from diabetes):
cotton wool spots
microaneurysms, which leak and impair vision
major cause of vision loss is macular edema
damaged blood vessels (from diabetes) lead to retinal ischemia, which decrease the blood and nutrient supply to the retina. New blood vessels from, which are very fragile and leak so vision is obscured
Major cause of vision loss is vitrous hemorrhage
frontal lobe: cognition, motor activity
parietal lobe: sensory input
temporal lobe: memory storage
occipital lobe: visual perception
hypothalamus: vital center for regulation of body temperature and blood circulation
right and left hemispheres
function: equilibrium and coordination
midbrain, pons, medulla
function: vital centers; respiration, heart rate, blood pressure
traversed by nearly all the nerves carrying information to and from the body
cervical: arms, diaphragm (respiration)
thoracic: chest abdomen
lumbo-sacral: legs, urinary bladder, rectum, reproductive organs
fibrous tissue covering the brain
dura: tough outer layer, separates cranial activity into compartments
pia-arachnoid: thin inner layer containing many blood vessels
cerebrospinal fluid: produced by choroid plexus, flows through the ventricles and is reabsorbed by special cells of pia-arachnoid
lateral ventricle with interventricular foramen (monroe)
third ventricle with cerebral (sylvian) aqueduct
forth ventricle with median aperture (magendie) and 2 lateral foramina (luschka)
cell body: in grey matter
axon: long, contained in white matter
myelin sheath: multiple lamellae of specialized cell membrane surround and insulate axon
high metabolic activity, high demand for glucose and O2
upper motor neuron: cell body in grey matter of frontal lobe, axon travels to brainstem/spinal cord to synapse with lower motor neuron
lower motor neuron: cell body in spinal cord grey matter, axon exits anterior nerve root to become peripheral motor nerve
pattern of atropy associated with neurogenic atrophy. small fibers with angular outlines occur together in groups in fascicles that may also have fibers of normal size and morphology or hypertrophied fibers.
eventually, adipose and fibrous tissue may replace lost muslce fibers (late phenomenon)
sex-linked, recessive disorder affects male children and produces a progressive course wiht proximal muscle weakness and atrophy and sometime pseudohyertrophy of the calf muscles.
caused by loss of contractile protein, dystrophin
progressive disease with uniformly fatal outcome around age 20
in a severed never soon after injury, axon distal to point of insult will undergo degeneration and fragmentation. Concomitantly, the myelin sheath surrounding the distal axon breaks down, although schwann cells remain
injuries that result in Wallerian degeneration: crush, stretch, penetrate, freeze
open injuries (penetrating wounds) commonly result in aberrant regenerative sprouting in the form of scar tissue buildup
note: closed injuries (crush, freeze) are more likey to regenerate with return to function
sudden onset of focal neuroligc deficit w/o regard for etiology. Normally due to embolism or spontaneous, massive hemorrhage.
Greatest incidence is between 40-80. more common in males. 3rd leading cause of death
Categories: infarcts, intraparenchymal hemorrhage, subarachnoid hemorrhage
onset of symptoms are usually sudden and reaches maximum intensity within a few minutes or a few hours.
Focal symptoms: paralysis, sensory loss, speech deficits related to site of damage
generalized symptoms: headache, vomiting, coma
necrosis of tissue secondary to ischemia/hypoxia. Some strokes are transient and reversible and do NOT result in infarct.
due to vascular occlusions
Cerebral infarcts are seen in pts without clinical stroke syndorme, because they are small and in non-critical location
embolus: occlusion of a vessel by any material (fragments of a clot, veetations from heart valve, etc) transported through the circulation from a distant site.
cerebral emboli are commonly the result of carotid or cerebral vessel thrombi (rarely atherosclerotic material breaks off and lodges distally)
disease of adults. aneurysms large than 1 cm are more likely to rupture (subarachnoid hemorrhage) than small aneurysms.
associated with hypertension, but there is no cause-effect relationship
associated with smoking
more common in women
most common location: juncture of the anterior communicating artery with anterior cerebral arteries.
2% of all head injuries and represents one of the most acute medical emergencies
almost always results from laceration of the middle menigeal artery close to its point of entry into the skull throughthe foramen spinosum. Arterial blood then accumulates rapidly in epidural space
5% of all head injuries. may be nontraumatic. Usually not associated with a skull fracture and are not necessarily related to the severity of an injury.
Most common source is rupture of cortical veins at the point where they raverse the subarachnid space to enter the superior sagittal sinus
sudden onset with fever, severe headache, stiff neck, cloudng of conscousness, and if untreated, often coma and death
thick yellow, fibrino-purulent exudate over the convexity or base of brain
congestion of menigeal vessels, spreading of inflammatory cells along penetrating vessels into the brain tissue and brain edema
Perinatal period: E. coli, group B streptococcus
Infants and children: Haemophilus influenzae
Adolescents and young adults: Neisseria meningitis
Adults: stretococcus pneumoniae
features: 1) subacute, slow progressive clinical course with headaches and increasing cranial nerve deficits, 2) the location at the base of the brain of a sense whitish thickening of meninges, 3) the formation of granulomatous tissue, comprised of lymphocytes, macrophages and fibroblasts, 4) dilated ventircles due to partial outflow blockage of CSF by tissue reaction
lymphocytic infammatory infiltrate of meninges. Some viruses (ECHO and coxsackie viruses) elicit strictly meningeal response. Enteric viruses rach meninges via bloodstream. Aseptic menigitides are self-limited and do not require treatment.
clinical signs: headaches, anorexia, apathy
CNS virus is transmitted through saliva of rabid animal. Virus reaches CNS through peripheral nerves. Incubation time is 4-6wks.
Neurologic deficits: confusion, hyperirritability, pharyngeal spasms leading to dydrophobia, flaccid paralyses and coma.
Viral inflammation is most pronounced in deep grey matter, brainstem, spinal anterior horns and spinal ganglia (inclusion bodies= Negri bodies)
viruses have vertebrate hosts and moquito or tick vectors and human illnesses occurs in small epidemics. (La Crosse virus) attacks nerve cells of cerebral corte, the basal nuclei and brainstem.
pts show irritabiltiy, cnfusion, somnolence, stupor or coma
mechanical: pressure (mass, lesion, edema)
nutritional: B-12 deficiency, ponitin myelinolysis
toxin: heavy metals, organophasphate, isoniazid, hexachlorophene poisoning
infections: progressive multifocal leukoencephalopathy
vascular: ubcortical hyposica of oligodendroglia
allergic/autoimmune: multiple sclerosis
includes: Creutzfeldt-Jakob disease (CJD), new variant CJD (mad cow), and Kuru in humans and scrapies (sheep), bovine spongiform encephalopathy (mad cow), and chronic wasting disease (deer).
In general, rare, unusual, slowly progressive, fatal CNS diseases
infectious protein (prion) are conformational variant of normal proteins present abundantly in mammalian nerve cell membranes
typically starts in 50s or later.
features: failure of recent memory, disorientation, and confusion. Accompanied with loss of language, sensorimotor and perceptual capabilities. Depression, emotional and personality changes are common.
implicate Ach in memory functions. Drugs that increase Ach function enhance memory
the enzyme choline acetyl transferase can be measured and is a marker for Ach, in alzheimer's there is a profound DECREASE in cortical and hippocampal CAT
common group of sporadic degenerative diseases.
clinical features: mask-like facial expression, shuffling gait, pill-rolling tremor of the hands. Autonomic sysfunciton and dementia may be associated to parkinson's
Idiopathic: no cause specified (most common), lewy body (eosinophillic cytoplasmic inclusion in the neurons of substantia nigra and locus ceruleus)
Postinfections: occurs in ppl who had encephalitis
toxic: may follow carbon monoxide poisoning, manganese intoxication, phenothiazine toxicity or uses of MPTP.
motor neuron disease that may occur at any age buy rarely before the age of 20 or after age 70.
Clinical symptoms: muscle weakness (usually in distal extremities). weakness progresses to ivolve the whole body includng areas supplied by caranial nerve nuclei
noteworthy feature: fasciculations which are small vermiform movements under the skin or on the tongue. Small movements are attributed to irritation of dying neurons
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