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84 Cards in this Set

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appendicitis
acute inflm of appendix
appendicitis
(etiology)
-fecalith obstruction
-twisting of appendix or bowel
-often no identifiable cause
appendicitis
(patho)
obstruction --> mucus drainage blocked --> increased lumenal pressure --> lumenal > venous pressure --> venous stasis --> ischemia --> mucosal ulceration --> bact invade wall
perforation --> damage to sterile body system
appendicitis
(mnfts)
acute abd pain (epigastric/umb --> RLQ)
vomiting, nausea, low grade fever, anorexia
appendicitis
(dx & tx)
dx: hx and px, u/s, CT, pain @ mcburney's point

tx: appendectomy to avoid risk of rupture (--> peritonitis?), antibiotics post-op
peritonitis
inflm of the peritoneum d/t bact infect or chem irritation (eg: perf ulcer, ruptured appendix...)

could be d/t normal flora outside of niche or excessive within niche
systemic effects of peritonitis
-altered perfusion (blood shunted to peritoneum)
-fluid shifts (increased HP)
-peristalsis ceases
-prob with ventilation d/t pain on movement of diaphagm
tx of peritonitis
-sx to fix perforation
-IV antibiotics
-fluid-elec replacement
-narcotics
inflm bowel disease (IBD)
crohn's + ulcerative colitis

et: unregulated immune response, genetic susceptibility, linked to HLA
crohn's disease
-affects sm+lg intestine, skip lesions
-all layers of bowel wall affected
-slow, nonagressive
-intermittent abd pain w/ chronic execerbations & remissions
-diarrhea & wt loss
crohn's disease
(dx & tx)
dx: hx & px, sigmoidoscopy, biopsy, stool sample

tx: decrease inflm, increase healing: nutritional supp, drugs (steroids, sulfasalazine), sx
ulcerative colitis
-affects colon & rectum, spreads proximally
-continuous lesions
-inflm, thickening, congestion, edema
-bloody diarrhea, abd cramping, wt loss
ulcerative colitis
(dx & tx)
dx: sigmoidoscopy, colonoscopy, biopsy, stool sample

tx: depends on severity, dietary modification, sx & drugs
IBS
-mobility disorder within intestine

et: unclear, linked to stress, anxiety, diet, lactose intolerence, etc
IBS
(patho & mnfts)
patho:
altered GI motility --> diarrhea, constipation, pain
identifiable triggers? --> inhibit mnfts

mnfts:
-abd pain/discomfort, constipation, diarrhea, mucoid stools, flatulence, n/v
IBS
(tx)
-exclude organic disease
-decrease stress
-diet (avoid triggering foods/chems)
-drugs: antispasmodics, metamucil
-serotonin link?
-probiotics?
hernia
-organ protrusion through retaining structure (usually within abd cavity)

weakened muscles + inc intra-abd pressure --> herniation
hiatal hernia
(sliding)
-95%
-upper stomach & GEJ slide through hiatus
-heartburn, reflux, substernal pain (50% asymptomatic)
hiatal hernia
(rolling/paraesophageal)
-GEJ remains below diaphragm
-all or part of stomach pass through hiatus
-chest pain, fullness after meals, dyspnea
tx of hiatal hernias
-behavioural: elevate HOB, do not bend down at waist after eating
-drugs for reflux (antacids, etc)
-sx in very serious cases
inguinal hernia
-intestine protrusion through inguinal canal (indirect: through existing opening, direct: through a muscle)
-requires sx
peptic ulcer
-ulcerative disorder of upper GI tract (stomach 30%, duodenum 80%)

stomach protection against acid:
-mucus barrier
-regulation of acid secretion
-regeneration of mucosal lining
-good perfusion to lining
peptic ulcer
(et/risks)
Helicobacter pylori infection, plus:
-excessive acid (HCl or biliary)
-NSAIDS/aspirin
-caffeine, smoking
-steroids, stress, alcohol
-chronic gastritis
peptic ulcer
(patho)
H.pylori --> inflm --> mucosal damage

infection --> inc gastrin --> inc acid secretion
peptic ulcer
(mnfts & complications)
mnfts:
-burning, cramping abd pain relieved by antacids/ingestion of food
-severity depends on site, size, degree of damage
-nausea, vomiting

complications:
-hemorrhage d/t slow, continous bleeding
-perforation
-gastric obstruction
peptic ulcer
(dx & tx)
dx: hx & px, labs to test for h.pylori, endoscopy/barium swallow

tx: antibiotics for h.pylori (2) + drugs (H2 receptor antagonists: block acid sec, PPI: inhibit acid formation), sx, antacids
hepatitis
-inflm of liver d/t virus, bact, toxins (drugs)
-10% autoimmune
viral hepatitis
-several types of virus = several types of hepatitis (A, B, C, D, E, F, G)
-also can be triggered by EBV, CMV, rubella
-similar mnfts, but differ in virus, incubation, transmission, severity, carrier state
hep A
-mild
-no carrier or chronic state
hep B
-more severe
-10-15% progress to chronic
-carrier state possible
hep C
-80% progress to chronic
-carrier state
-remission & exacerbation of symptoms
-often leads to cirrhosis
hepatitis
(patho)
-similar in all types
-direct hepatocyte injury by virus
-immune mediated injury
-inflm, damage, necrosis of hepatocytes --> dec fxn
-vasculature & ducts damaged d/t inflm/edema
hepatitis
(mnfts)
3 phases:
prodromal: lethargy, anorexia, n/v, myalgia, abd pain, fever

clinical/icterus: 5-10 days post-prodromal, jaundice, pruritis, enlarged/tender liver

recovery: acute illness in remission

-acute mnfts subside in ~3 weeks
-full recovery takes up to 16 weeks
hepatitis
(tx)
-rest (dec energy demand = dec fnxal demand of liver)
-diet (sm meals, inc calories, dec fat)
-avoid alcohol & hepatotxic drugs
-antivirals (interferon, ribavirin) for hep C
-post exposure prophylaxis (gammaglobulins, vaccine)
cirrhosis
-end stage of liver disease: fibrosis & nodule formation d/t deposition of collagen fibres

linked to alcohol abuse
-hypersensitivity to alcohol
-alt liver fxn d/t liver busy processing alcohol
-metb of alcohol produces free radicals & H+
cirrhosis
(patho)
hepatocytes destroyed --> scar tissues --> vessels & ducts disrupted --> blood flow impeded --> portal HTN --> fluid shifts --> ascites

obstr bile flow --> bile stasis

decreased metb waste clearance
cirrhosis
(mnfts)
-variable: from asymptomatic to hepatic failure
-wt loss, anorexia, weakness, hepatomegaly, jaundice

-advanced: portal HTN, varices, ascites, GI bleeds, splenomegaly
cirrhosis
(tx goals)
-avoid complications (eg: hemorrhage)
-enhance liver fxn (eg: with diet)
-address cause (alcohol?)
portal HTN
-normal pressure is 5-10mmHg, HTN is 12mmHg and above
-causes can be pre, post, or intra hepatic
-mostly d/t cirrhosis
complications of portal HTN
-varices --> possible rupture
-ascites
-splenomegaly --> possible rupture
-portosystemic shunts form to relieve pressure
-hepatic encephalopathy
ascites
-massive 3rd spacing in peritoneal cavity
-d/t: cirrhosis & portal HTN, altered OP or HP, Na+ and H2O retention, R-sided heart failure (pooling of systemic blood)
-causes abd distension & dyspnea
ascites
(tx)
-paracentesis in severe cases
-plus a vol expander (albumin) to increase OP
-fluid/elec balance
-diuretics
portal HTN & ascites can result in...
...vascular collapse & hypovolemic shock
cholelithiasis
(et)
-to form a stone, there must be
1. change in composition of bile
2. prob with flow (stasis)
-inflm --> debris --> nuclei for stone
-genetic?
types of stones
1. cholesterol (80%)
-bile supersaturated with chol
2. pigment (20%)
-contain bilirubin & Ca+ salts
-assoc with hemolysis, cirrhosis
3. mixed stones
cholelithiasis
(mnfts)
-asymptomatic until stone migrates
-biliary colic: radiating, intermittent
-n/v?
cholelithiasis
(dx & tx)
dx: hx, scans (u/s)

tx: analgesics, prevent complications (pancreatitis, cholecystitis, perforation), sx, dissolving agents
acute pancreatitis
-inflm of the pancreas
-90% self-limiting, but can become fatal
-renal failure, ARDS
acute pancreatitis
(et)
-~70% linked to alcohol abuse
-also linked to gallstones (d/t obstr)
-others: hyperlipidemia, pancreatic trauma, drugs
-~10% idiopathic
acute pancreatitis
(patho)
-normally: presence of bile in duodenum activates panc enzymes that digest protein

-obstr bile flow --> premature activation of enyzmes d/t retrograde bile flow --> enzymes damage pancreas
(autodigestion, fat necrosiss, hemorrhage)
-alcohol? contributes bc it enhance secretion of pancreatic juices
acute pancreatitis
(mnfts)
-abrupt onset (eg:after a meal, after alcohol binge)
-severe abd pain: epigastric, radiates
-excessive 3rd spacing
-inc blood amylase & LIPASE d/t breakdown of pancreatic cells
acute pancreatitis
(tx)
-based on severity
-pain
-NPO (food activates enzymes, triggers symptoms)
-IV fluids/electrolytes
-sx
tracheo-esophageal atresia & fistula
-rare congenital defect (1:3000)
-fistula: abnormal passageway (trachea & esophagus not separate)
-atresia: blind-ending pouch (closure of esophagus)
-d/t foregut in weeks 4-8 gestation failing to form 2 separate fxning tubes (cause: teratogens)
-risk for aspiration
tx: emergency sx
goal: maintain patent airway
hirschsprung's disease
-genetic alteration on chr10, rare (1:5000)
-absense of ganglia in parts of colon --> no neural control, no peristalsis
-more common in sigmoid colon
-accum of contents --> colon distension --> abd distension
tx: sx to remove aganglionic segment
intussusception
-invagination of one part of ileum into another, often @ ileocecal valve

invagination --> obstr --> inflm --> edema --> ischemia
invagination --> obstr --> enlarged colon --> perforatoin --> peritonitis --> shock

tx: hydrostatic reduction if there is no risk of perf (by H2O soluble contrast medium & air pressure - so visualized on xray), sx
liver cancer
-primary or secondary/metastatic (more common)
-inc prevalence in men
liver cancer
(primary tumors)
1. hepatocellular carcinoma
-hepatocyte origin
-et assoc with chr liver disease
-hepB/C virus mutates host DNA
-environ agents (aflatoxins)
-usually a single mass
-tumor masked by mnfts of chr
liver disease
-poor prognosis
2. Cholangiocarcinomas
-cancer of bile duct epithelium
-assoc with chronic inflm
liver cancer
(metastatic tumors)
-often assoc with primary colon, breast, or lung cancer
-liver is a large, richly perfused organ... metastasis is more common
liver cancer
(mnfts)
-those of liver disease: hepatomegaly, ascites, abd pain
-anorexia, diaphoresis
-wt loss, fever
-90% of liver has to be neoplastic for hepatic insuff to show in blood tests
liver cancer
(tx)
-very poor prognosis
-if primary intervention (sx/radiation) fails, life expectancy is 3-6 mos
-care is supportive & palliatve
pancreatic cancer
-90% fatality rate in 1st year
-inc in males, african americans
-90% duct cell adenocarcinomas
-insidious onset, most have metastasized by dx
pancreatic cancer
(et, mnfts, tx)
et: unclear - link to: smoking, poor diet, diabetes, alcohol, hx chronic pancreatitis

mnfts: nonspecific - jaundice, wt loss, abd pain

tx: sx (primary), palliative (radiation, pain mgmt, etc)
diverticular disease
diverticulosis: mucosal layer of the colon herniates through muscularis layer
diverticulitis: inflm & perforation of diverticulum

-often multiple diverticula, generally in sigmoid colon

et: increased in western society: indicates poor bowel habits, lack of fibre, decreased physical activity contribute
diverticular disease
(patho/mnfts)
patho:
circular bands of muscle in colon contract --> lumen constricted --> increased pressure causes herniations

mnfts:
osis: often asymptomatic, abd discomfort, change in bowel habits, bloating, flatulence
itis: LLQ pain/tenderness, n/v, fever, elevated WBC
diverticular disease
(complications)
-perforation --> peritonitis
-hemorrhage
-bowel obstruction
-fistulas
diverticular disease
(dx & tx)
dx: hx, presenting mnfts, scans (CT, u/s)

tx: prevent symptoms & complications by inc bulk in diet, bowel retraining, acute diverticulitis NPO & broad spectrum antibiotic, hospitalization, sx
cleft lip
-failure of maxillary & median nasal processes to fuse during weeks 5-8 gestation
-ranges from small notch in upper lip to total separation involving teeth & gingiva
-more prevalent in boys
-1:700
cleft palate
-failure of palatal processes to close during weeks 9-12 gestation
-midline opening, may involve hard palate, soft palate, or both
-often occurs with cleft lip
-more prevalent in girls
-1:1000-2000
cleft lip & palate
(et)
-genetic
-2x higher in japanese, rare in african american
-teratogens: viral infect, folic acid deficiency
cleft lip & palate
(dx & tx)
dx: sonogram in utero, inspection at birth

tx: surgical repair (lip 2-10 weeks, palate 6-18 months), early repair to avoid nutritional probs, followup with a pedodontist, fetal sx?
pyloric stenosis
-hypertrophy or hyperplasia of muscles surrounding pyloric sphincter, causing difficulty in stomach emptying
pyloric stenosis
(et)
-unknown, linked to genetics
-higher in 1st born white males
-1:150 for males, 1:750 females
pyloric stenosis
(mnfts)
-vomiting after feeding (projectile)
-dehydration
-alkalosis
pyloric stenosis
(dx & tx)
dx: presence of pyloric mass, more prominent with feeding --> vomiting, sonogram, endoscopy

tx: surgical/laparoscopic repair, management of symptoms
gastro-esophageal reflux
-neuromuscular disturbance in which the gastro-esophageal sphincter & lower esophagus are lax, allowing easy regurgiation of gastric contents into esophagus
gastro-esophageal reflux
(et & mnfts)
et: assoc with hiatal hernia, high risk in infants with cerebral palsy or other neuro problems

mnfts: vomiting after feeding (effortless & not projectile), irritability, apnea
gastro-esophageal reflux
(dx & tx)
dx: hx, determine px of secretions, endoscopy, barium swallow

tx: formula thickened with rice cereal, feed upright/keep upright for 1hr, H2 receptor antagonist/PPI, sx?
colorectal cancer
-3rd most common cancer
-severity divided into 4 stages
stage I colorectal cancer
-mucosal/submucosal involvement
-90-100% 5 year survival
stage II colorectal cancer
-lymph-negative, muscularis propria involvement
-80% 5 year survival
stage III colorectal cancer
-lymph-positive, serosa involvement
-30-50% 5 year survival
stage IV colorectal cancer
-metastatic
-<30% 5 year survival
colorectal cancer
(et & mnfts)
et: unknown, but linked to age, fam hx, hx of IBD, polyposis, diet high in fat & low in fibre

mnfts: insidous, often no early symptoms, bleeding, change in bowel habits, urgency or incomplete emptying, pain
colorectal cancer
(dx & tx)
dx: DRE (digital rectal exam) to detect neoplasms, occult blood tests, sigmoidoscopy, colonoscopy

tx: sx is the only effective primary tx, sometimes with pre-op radiation
chemo & radiation are used as palliative