Medicine Flashcards
diabetic gastroparesis
Long standing DM -> autonomic neuropathy -> dysmobility dt a loss of ability to sense strech in GI tract
If diagnosis is clear (long standing diabetic, with sx of abdominal fullness, nausea, constipation, “bloating” and “splash” heard, can give erythromycin or metoclopramide
What is the Dxylose test for?
good for proximal small intestinal absorption deff btwn pancreatic insuff and celiac dz
NL: inc abs into blood (hi serum) inc excretion in urine (hi urine) and minimal fecal -> enz def
abl: dec levels and high fecal excretion -> impaired small int mucosa ie)celiac
What is pseudoalchalasia?
Narrowing of the distal esophagous secondary to causes other than denervation (real alchalasia) -> sx that look like alchalasia
ie) esophageal CA
* endoscope to r/o malignancy in all pt with suspected achalasia
In pt with typical GERD symptoms, when would you opt for endoscope study vs PPI tx?
Usually tx with PPI for 2 months monitor signs of improvement or refractory
UNLESS:
pt is >50 with sx >5yrs
alarm signs: disphagia, odynophagia, wt loss, anemia, GI bleeding, recurrent vomiting
and CA risk factors (tobacco use)
Pt with suspected diverticulitis, diagnostic
abdominal CT with oral and IV contrast
will show: inflammation in pericolic fat, presence of diverticula, bowel wall thickening, soft tissue masses. Pericolic fluid collections suggests abscess
*barium contrast enema, scope is contraindicated until performation is ruled out!!
Treatment for diverticulitis:
abx that will cover Ecoli and anaerobes that are present in the bowel:
*cipro + metronidazole
betalactam/beta-lactamase combos:
amoxicillin/clavulante, tic/clav, pip/tazo
Ertapenem (carbapenems)
SURGERY:
no response to med therapy
Freq recurrences of infection
Perforation, fistula formation, abscesses, strictures or obstruction
Toxic mega colon
sx
dx
tx
look for a pt with a history of IBD, acute worsening fever, abd distension, leukocytosis, hypotension, tachy
dx: abdominal xray
shows- colonic distension (>6cm dilation of right colon), w/manifestations of severe systemic tox
tx: conservative mgmt with bowel rest, NG suction
cortico+broad spect abx or abx targetted at cdiff
Treatment of IBD (Crohn and UC)
acute: steroids (budesonide or prednisone)
chronic maintenance of remission with 5-ASA derivatives (mesalamine)
w/lots of recurrences, can use azathioprine and 6-mercaptopurine to wean patients off steroids.
Perianal CD tx with cipro and metro
Fistuale and severe dz unresponsive to other meds can use anti-TNF (infliximab)
Surgery only when fistula and no response. UC can be cured with surgery via colectomy vs CD surgery only due for bowel obstruction; can recur at site
*colon cancer screening 8-10yrs after diagnosis or 12-15 if only in rectum/left colon. colonscopy with biopsies every 1-2yrs; prophylactic colectomy is advised if dysplasia is identified
Spontaneous Bacterial Peritonitis:
SBP
PMNS >250, protein <1, SAAG >1.1
Culture often positive for Ecoli or Kleb (most accurate)
- Reitan trail test (connect the pics) good to detect subtle mental status changes sometimes present in cirrhosis and SBP
- hypothermia, hypotension, paralytic ileus indicative of severe SBP
tx: empiric abx-third deg ceph-cefotaxime or ceftriazone (when cell count with >250 neutrophils), fluroquinolone for SBP
* all pt with SBP need lifelong prophlyaxis against recurrent
* ALL variceal bleeding with ascities needs SBP prophylaxis
SAAG values
<1.1: infection (except SBP), cancer, nephrotic syndrome
> 1.1: portal hypertension (SBP), CHF hepatic vein thrombosis, constrictive pericarditis,
Acalculous cholecystitis
Need high degree of clinical suspicion
Often due to cholestasis and GB ischemia leading to secondary infection by enteric organisms and resultant edema/necrosis of GB
DX- US shows GB wall thickening and distension, presence of pericholecystic fluid
tx: abx, percutaneous cholecystostomy, cholecystectomy with drianage of any abscess once pt improves
Wilsons Disorder
autosomal recessive
mutation at ATP7B -> hepatic copper accumulation; ends up leaking out of damaged hepatocytes and depositing in body
->hepatic, neurologic (>basal ganglia-parkinsonism, dysarthria, choreoathetosis, ataxia), psyc (personality changes, depression)
labs: dec ceruloplasmin, inc urinary Cu excretion, Kayser-Fleischer rings in eyes
tx: chelator (D-penicillamine, trientine), Zinc (interferes w/cu absorption)
Gallstone Ileus
mechanical obstruction of small bowel
sx: n/v, pneumobilia, hyperactive BS, dialted loops of bowels (dt obs)
mgmt of acute cholecystitis:
Supportive care- NPO, IB Abx, analgestics w/lapchole schedules after recover.
Immediate chole if perf or gangrene
Differential for pruritus in pregnancy:
Intrahepatic cholestasis of pregnancy, pruritic urticarial papules and plaques of preg
Intrahepatic cholestasis: marked pruritus, elevated total bile acids and/or aminotransferases
PUPPP: develops in 3rd trimester, red papules w/striae sparing around umbilicus, sometimes extremities (rare to find in soles, face), no liver lab abnl
Hepatic adenomas:
benign epithelial tumors most common in young/middle age women
RF: oral contraceptives, anabolic androgen use, pregnancy
Dx: clinical pres + US showing well demarcated HYPERECHOIC lesion
Contrast CT can show early peripheral enhancement. Needle bx not rec dt risk of bleed
tx: surgical excision
long term complications: progressive growth, rupture, malignant transformation
US findings of focal nodular hyperplasia:
imaging shows inc arterial flow, +/- central scar
Diagnosis of acute pancreatitis:
req 2 of the following: acute onset of severe epigastric pain radiating to back, increased amylase or lipase >3X upper limit of normal, characteristic abd imaging: focal/diffuse pancreatic enlargment contrast ct
*LIPASE is more useful and sensitive esp for alcoholics because it RISES EARLIER than amylase and STAYS elevated for LONGER (8-14days)
Differential for solid liver mass:
focal nodular hyperplasia, adenoma regenerative nodules, hepatocellular CA, liver mets (most common)
emphysematous cholecystitis
life threatening acute cholecystitis that occurs more in immunocompromised pt dt infection of GB with gas forming bacteria (clostridum, some ecoli)
*emergent cholecystectom, abx
Postcholecystectomy syndrome
persistent abdominal pain/dyspesia similar to pre-cholecystectomy.
DT: retained stone in common bile, biliary dyskinesai, extra bili..
mgmt: endo US, ERCP, MRCP
hepatic hydrothroax
pleural effusion (transudative!) thought to occur dt small defects in the diaphragm, permitting peritoneal fluid to pass into pleural space, more common in right dt less muscular hemidiaphgram.
tx: salt restriction, diuretic, therapeutic thorocentesis
What is one clue that could help distinguish biliary cause of RUQ vs pain due to dysfunction of sphincter of Oddi?!
dysfunction of sphincter of oddi is any process (surg, pancreatitis..) that causes dyskinesis and stenosis of SOD -> obstruction of bile, function biliary DO mimicing a structual lesion
BUT: opioids contract the sphincter and MAKE PAIN WORSE instead of better
dx: SOD manometry
Tx: sphincterotomy
Biliary tree antibiotics to consider:
with no surgery involved, primary involve gram negative rods and anaerobes
Cipro + metro
Ampicillin-gent + metro
Pip/tazo (if skin flora is considered)
treatment of choice for choledocholithiasis and ascending cholangitis:
ERCP, emergent for ascending cholangitis then cholecystectomy
When would glucocords be used in the setting of liver dysfunction?
Can benefit alcoholic hepatitis and autoimmune hepatitis but not acute liver failure (liver failure without underlying liver disease)
most common cause of death in acute liver failure is cerebral edema (coma and brain stem herniation)
When would you delay an appendectomy vs immediate?
If patient is presenting with acute appenditicitis and classical symptoms, okay for immdiate appendectomy to prevent appendiceal rupture.
BUT if sx for >5 days, likely has a phlegomon with an absecess that is walled off..thus 1) manage conservatively with IV abx, bowel rest and delayed appendectomy weeks later
Niacin deficiency sx
Vitamin B3 deficiency -> 3D symptoms: dermatitis, diarrhea, dementia
endogenously synthesized from tryptophan
developing - high corn diets
developed- impaired intake (elderly, chronic dz, etoh), carcinoid syn, hartnup dz, prolonged isoniazid therapy
Diverticulitis management:
Stable? outpatient ok with bowel rest, oral abx, obs
Elderly, immunosupr, high fevers, significant leukocytosis or comorbidities: inpatient, IV Abx
Complicated with abscess (t showing rim-enhacning perisigmoid fluid collection), perf, obstruction, fistula w/fluid <3cm -> IV abx, obs
> 3cm of fluid -> CT guided percutaneous drain
worsening/no improvement by day 5 -> surgical drain an debriedment
Eval of suspicion of pancreatic CA:
When pancreatic CA is suspected,
If jaundiced: US to r/o CA of pancreatic head
If not jaundiced: abdominal CT, to RO malignancy of body or tail
What type of ulcer can make you suspect gastrinoma?
Ulcers distal to duodenum, in jejunum suggestive of excess gastric acid that cannot be fully neutralized early.
Other clues is ulcers refractory to PPIs,
dx with gastrin >1000
what electrolyte abnl to expect with diarrhea
hypokalemia dt loss of K in stool, increase chloride -> metabolic alkalosis
if patient is using laxative with mag -> hyper mag
melanosis coli - dark brown discoloration of the colon with pale patches of lymph follice could be indicative of laxative use. Laxative diarrhea is more freq, more likely to have nocturnal movment, abd cramping
What is the stool osmotic gap:
290 -2(stool Na + K)
>125 –> osmotic diarrhea (stool pH is acidic in lactase def dt the fermentation products, no steatorrhea), milk of mag, carbohydrate/fat malabs
50-125 undetermined, but look at other clues.
<50 secretory diarrhea, (carcinoid, VIPoma, gastrinoma, ETEC..)
Zinc deficiency:
hypogonadism, impaired taste, impaired wound healing, alopecia, skin rash with perioral involvement
What meds can cause acute pancreatitis?
anti-seizure meds (>valproic acid), diuretics (lasix, thiazide), drugs for IBD (suulfasalazine, 5-ASA), immunosup agents (AZATHIOPRINE), HIV-rel meds (didanosine, pentamidine), abx (metro, tetracy)
usually mild. CT showing sweating of pancreas with prominent peripancreatic fluid and fat stranding
tx: supportive, fluids, electrolyte replacement
Toxic megacolon DX
Subset of pt with UC can develope inflammation of the smooth muscle layer which transforms into muscular paralysis and colonic dilation.
Total or segmenta, nonobstructive colonic dilation. Severe bloody diarrhea, systemic findings, esp within 3 yrs of diagnosis
DX: thick haustra not extending into lumen + >3: fever (100.4), pulse >120, WBC >10,500, anemia
tx: IVF, broad abx, bowel rest; if 2/2 IBD, could use steroids IV
Surgery last ditch
Dumping syndrome
Gi and vasomotor (palpatations, diaphoresis) symptoms
common postgastrectomy
loss of the normal action of the pyloric sphincter dt injury or surgical bypass, leading to rapid emptying of hypertonic gastric contents into the duodenum and small intestines -> fluid shift from intravascular space to the small intestines -> hypotension, stimulation of autonomic reflexes, vasoactive peptides
tx: dietary modification, should diminish over time
Angiodysplasia
cause of PAINLESS GI bleed, dt dialted submucosal veins and AV malformations
increase after age 60, higher incidence in pt with renal disease, vWd, aortic stenosis (dt acquired vW factor def as trasverse teh valve)
dx: endoscope, but many times missed
tx: if asymptomatic, no need to tx. if anemia or gross bleed, ca be treated with endo cautery
small bowel vs colon ischemia etiology:
what will a colonoscopy show for ischemic colitis?
small bowel ischemia more likely dt atheroembolic or thrombic events..
Ischemic colitis more likely due to lack of blood flow at watershed areas (SMA/IMA), rectosigmoid jxn btwn sigmoid artery and superior rectal artery
colonoscopy can show: pale mucosa with petechial bleeding, bluish hemorrhagic nodules or cyanotic mucosa w/hemorrhage
