Gastrointestinal Flashcards
Study to order if pt presenting with dysphagia/regurg for solids AND liquids
Probably a motility disorder
Get barium swallow
Want to see how throat looks when pt swallows, aka the peristalsis function & motility
Study to order if pt is presenting with dysphagia - initially to solid foods only but now cannot tolerate liquids or soft foods either?
Order an EGD - you want to look at the tissues!
Think if a tumor was growing…initially huge chunks of stead would cause a problem but then as the tumor grew larger & obstructed more you’d have problems with soft foods & liquid too!
Study to order when identifying a motility disorder of the esophagus?
List motility disorders of the esophagus
Order a barium swallow - want to see the peristalsis (AKA MOTILITY) of the esophagus!
Achalasia (inc LES pressure 2/2 idiopathic loss of nerves)
Nutcracker esophagus (excessive pressure during peristalsis - manometry = inc pressure during peri)
Diffuse esopageal spasm - esophagram shows CORKSCREW - stabbing chest pain worse w/ hot or cold liquids/food
Gold standard dx achalasia
Manometry
Increased LES pressure > 40 mmHg
EGD of nutcracker will show?
NORMAL
Get manometry for dx - will show inc pressure during peristalsis
Barium swallow (esophagram) nutcracker esophagus?
NORMAL
Get manometry for dx - will show inc pressure during peristalsis
Initial study to order for dysphagia to solids
EGD
If looking for tissue abnl - ring/web, cancer (dysphagia for solids only) –> EGD
Initial study to order for dysphagia to both solids and liquids (at onset)
Barium swallow esophagram
If dysphagia to solids and liquids from onset then probably a motility disorder
For identifying abnormal motility disorder - make the SWALLOW - aka barrium swallow
Clinical presentation & Dx diffuse lower esophageal spasm
CP: Stabbing chest pain, worse w/ hot or cold liquids/foods
Dx: Barium esophagram - CORKSCREW
Drugs that lower the esophageal pressure
(and therefore used to treat disease - achalasia, nutcracker, diffuse esophageal spasm - 2/2 increased esophageal pressure)
CCB
Nitrates
Botox injections
Sildenafil
Diagnosis of nutcracker esophagus
Manometry - increased pressure during peristalsis
EGD and barium swallow will be NORMAL (will probs have already ordered at least a barium swallow to see why person is having difficulty swallowing liquids and solids)
Who gets eosinophilic esophagitis?
MC IN KIDS
ATOPIC PT (allergies, asthma, etc…lots of IgE!)
Dx of eosinophilic esophagitis
Dx:
EGD - can be normal
+/- multiple corrugated rings on the esopagus
+/- white exucates
Tx:
Remove foods that incite allergic response, inhaled ICS WITHOUT spacer - want to go to throat not lungs
MCC pill-induced esophagitis
Bisphosphonates
KCl
Iron pills
Bb, CCB
Hallmark of infectious esophagitis
ODYNOPHAGIA = PAIN
CMV = large superficial shallow ulcers - GANCYCLOVIR HSV = small deep ulcers - ACYCLOVIR Candida = linear yellow-white plaques - FLUCONAZOLE
What is the diagnostic test of choice for a evaluating a person with acute chron’s disease?
UGI series with small bowel follow thru
What is plummer-vinson syndrome?
It is the triad of:
- dysphagia
- esophageal webs
- iron-deficiency anemia
MC in Caucasian women 30-60
Can also have atrophic glossitis, angular cheilitis
What is an esophageal web?
Thin membranes in the mid-upper esophagus - may be congenital or acquired
What is a schatzki ring? What are they associated with?
It is a LOWER esophageal web/constriction at the squamocolumnar junction
MC a/w sliding hiatal hernias, but may be a complication of corrosive esophageal injury (chronic GERD = stricture)
CP Schatzki ring, esophageal web?
Dysphagia to SOLIDS (mainly) - liquid can get by the ring for the most part
Dx Schatzki ring, esophageal web?
Tx?
Barium esophogram (swallow) = diagnostic test of choice
Tx: Endoscopic dilation of the area if symptomatic without reflux
CP Boerhaave syndrome? Definitive diagnostic study?
Boerhaave = FULL THICKNESS rupture of DISTAL esophagus
CP: Retrosternal chest pain worse with deep breathing & swallowing, hematemesis
PE: Crepitus on chest auscultation due to pneumomediastinum
Dx: Definitive dx study = CONTRAST esophagram - positive = + leakage
Chest CT may be ordered first - shows pneumomediastinum, esophageal thickening
“Red wale” markings & cherry red spots are suggestive of what?
These are endoscopic esophageal variceal descriptions in which they are at very high risk of bleeding soon
When is a TIPS indicated in an esophageal varices bleed?
If bleeding despite endoscopic or pharmacologic treatment
C/I: Hepatic encephalopathy, infections
Mainstay of management to prevent rebleeds?
Nadolol
MOA: Decrease portal venous pressure with NON-selective beta blockers
Isosorbide
MOA: Long-acting nitrate (vasodilator) that reduces esophageal pressure
Type I hiatal hernia
“sliding” hernia = MC type (95%) - when GEJ comes loose & stomach w/ GEJ slide into the mediastinum (increases reflux)
Management: similar to GERD
Management of GERD
- Lifestyle modifications (elevation of HOB, avoid recumbency for three hours after eating, eating small meals, avoiding certain foods (fatty, spicy, citrus, chocolate, caffeinated), decrease ETOH intake, weight loss, smoking cessation
- “As needed” pharmacological therapy - OTC antacids, H2 blockers
- Initiation of scheduled pharmacological therapy - PPIs
**If alarm sx at any point (dysphagia, odynophagia, weight loss, bleeding) then order EGD
Alarm symptoms GERD
Dysphagia
Odynophagia
Weight loss
Bleeding
Gold standard GERD dx
24 hour ambulatory monitoring
Type II hiatal hernia
“rolling” hernia = when fundus of stomach protrudes thru diaphragm with GE junction remaining in anatomic location ….may lead to strangulation so ..
Tx = surgical repair of the defect to avoid complications
H. pylori triple thearpy
Clarithromycin
Amoxicillin
PPI
(CAP)
H. pylori quadruple therapy
Tetracycline
Metronidazole
PPI
Bismuth subsalicylate
Duodenal or gastric ulcers more common?
Duodenal 4x more common
All patients with a gastric ulcer need a ?
EGD w/ Bx to rule out malignancy
Alarm symptoms PUD
> 50 YO, dyspepsia, history of gastric ulcer, anorexia, weight loss, anemia, dysphagia
Follow up on gastric ulcer
ALL GU MUST BE FOLLOWED UP WITH ENDOSCOPY TO RULE OUT MALIGNANCY AND DOCUMENT HEALING!!!
Done 8-12 weeks after therapy initiation
Dyspepsia 2/2 duodenal ulcer - characteristics
Better w/ food
Worse 2-5 hours after eating
Worse at night
**Nocturnal sx clasically a/w duodenal ulcers
Gastric ulcers - characteristics of sx - onset
Food-provoked dyspepeia - bad pain soon after eating (30 min - 1 hr)
Weight loss (b/c afraid to eat)
Gold standard PUD dx
Endoscopy w/ bx
Causative factors, age, incidence, benign or malignant, pain worse or better with meals
Gastric vs duodenal - compare above characteristics
Duodenal:
- Cause - inc in DAMAGING factors (acid, H. pylori)
- Age - MC in younger pt (30-55)
- Incidence- 4x MC, BENIGN
- Pain BETTER w/ meals, worse 2-5 hours after meals
Gastric:
- Cause - decrease in mucosal protective factors (dec mucus, bicarb, prostaglandins, NSAIDs)
- Age - MC in OLDER pt (55-70)
- Pain WORSE w/ meals (& for 1-2 hrs after too)
- LESS common, 4% are MALIGNANT
What is the most important risk factor for gastric carcinoma?
H. pylori
MC type of gastric cancer
ADENOcarcinoma - gAstric
What is linitis plastica?
Diffuse thickening of the stomach wall w/ “leather bottle” appearance due to gastric cancer infiltration = WORSE type
Superficial spreading = best prognosis/type of gastric cancer
CP gastric cancer
EARLY SATIETY!!!
(tumor filling up stomach = full easier…duh)
Iron-deficiency anemia 2/2 small amt bleeding
Signs of mets gastric ca
Supraclavicular LN = VIRCHOW
Umbilical LN = sister mary joseph
Ovarian mets = krukenburg tumor
Left axillary LN = IRISH sign
Bilirubin metabolism - prehepatic, intrahepatic, posthepatic
Pre-hepatic -
Bilirubin produced by heme metabolism (2/2 RBC destruction). Heme degraded by macrophages in RES = green biliverdin to –> bilirubin (red/orange) -this unconjugated bilirubin is sent to liver for conjugation & excretion
Intrahepatic -
Hepatocytes conjugate the bilirubin w/ enzyme UGT. This conjugated bilirubin (d. bili) is now water soluble (for bile excretion)
Post-hepatic -
D. bili is mixed in with bile, transported thru biliary & cystic ducts to be stored in GB.
Conjugated bilirubin cannot cross intestinal wall. It is converted to urobilinogen which is oxidized by gut bacteria to stercobilin (give stool brown color), converted to urobilin in kidney & excreted in urine (give urine it’s color). Small amt converted back & reabosorbed for further use in biliary system (via enterohepatic circulation)
Therefore in disease where there is excess DIRECT (conjugated) bilirubin, it is excreted in the urine & stool –> if you have a biliary obstruction it prevents secretion of large portions of conjugated bilirubin from being excreted in stool which is normally given its brown color by the stercobilin. It stays in the blood, & goes to kidney where converted to urobilin –> The urinary excretion is not blocked so a lot of excretion from blood is shifted to urine = DARK urine & LIGHT stools in conjugated hyperbilirubinemia.
Why is dark urine & light-colored stool seen with conjugated (direct) hyperbilirubinemia?
In disease where there is excess DIRECT (conjugated) bilirubin, it is excreted in the urine & stool –> if you have a biliary obstruction it prevents secretion of large portions of conjugated bilirubin from being excreted in stool which is normally given its brown color by the stercobilin.
It stays in the blood, & goes to kidney where converted to urobilin –> The urinary excretion is not blocked so a lot of excretion from blood is shifted to urine = DARK urine & LIGHT stools in conjugated hyperbilirubinemia.
Urobilin is what gives urine its characteristic yellow color!
Why can you see dark urine with hemolysis (causes almost all cases of indirect (unconjugated) hyperbilirubinemia?
Because you have hemaglobinuria so the hemoglobin that’s being lysed from the RBC gets peed out in your urine…the dark urine is from that NOT from bilirubin
Increase bilirubin WITHOUT increased LFTs… = ?
Think inherited bilirubin metabolism disorders (Gilbert’s (dec UGT activity), or Crigler-Jajjar = NO UGT activity, dubin johnson - can’t excrete from hepatocyte)
Gilbert’s is v common!
Dubin johnson syndrome?
Isolated (mild - 2-5) conjugated hyperbilirubinemia (b/c hepatocytes can conjugate but not excrete the bilirubin how they’re supposed to = all conjugated bilirubin stuck in liver = dark
Dubin = DDD (3D’s)
Dubin
Direct
Dark liver
Indirect hyperbilirubinemia is 2/2?
Indirect = HemolysIIIIs & gIIIIIlbert’s!
Have I’s in them! Indirect starts w/ an I!
Cholestatic pattern of liver injury
Inc alk phos
Inc GGT
Inc bilirubin
Hepatocellular pattern of liver injury
Inc ALT & AST > others
ALT more sensitive for Liver dz
Which of the liver function tests is most sensitive for biliary injury?
GGT
But not specific
Increased ALP without increased GGT
Bone or gut issue not liver issue
Remember alk phos is also found in intestinal mucosa & bone
Inc ALT > 1000 AND + ANA…thinking?
Autoimmune hepatitis
+ANA
+ smooth muscle ab
+ Increased IgG
= Autoimmune issue
Labs for viral or toxic ACUTE liver injury
ALT> AST –> both very high
AST & ALT > 1000 –> think ACUTE viral hepatitis
Labs consistent with CHRONIC liver injury
Increased INR
Low albumin
Cholelithiasis - CP, RF, Dx, Tx
CP: Colicky, sudden onset, INTERMITTENT RUQ abd pain after big fatty meal, lasting 30 min - several hours
RF: Family history, native american = strongest factors. Also Fat, fair, female, forty, fertile etc
Dx: Ultrasound
Tx:
ASX –> observe
Symptomatic –> Elective cholecystectomy
Choledocolithiasis - CP, complications
Gallstone in CBD a/w ductal dilation
CP: ASX = MC (>50%) - may be incidental finding when doing studies for other reasons or during evaluation of abnormal LFTs on routine testing
Complications: Acute pancreatitis, acute cholangitis
Initial test ordered choledocolithiasis
Trans-abdominal US
Diagnostic test of choice choledocolithiasis
ERCP - dx & tx - extract the stone
Acute cholangitis - what is it? Etio
Biliary tract infection 2/2 obstruction in the CBC - MC due to GN organisms that ascend from the duodenum
E. coli MC, klebsiella, enterobacter species, anaerobes or enterococcus also common
Gold standard dx acute cholangitis
Cholangiography via ERCP
Management acute cholangitis
ABX:
Monotherapy - unasyn, zosyn
Dual - Cipro/flagyl, ceftriaxone/flagyl etc
Stone extraction:
Preferred via ERCP
Gold standard dx for acute cholecystitis
HIDA scan
+ HIDA = non-filling of GB
Management cholecystitis
NPI, IV fluids, ABX, cholecystectomy w/in 72 hours, laparoscopic preferred whenever possible
Who gets acute acalculous cholecystitis?
MC occur in the seriously ill (post op, ICU patients) 2/2 prolonged fasting, dehydration, TPN, GB stasis, burns, DM etc
It’s due to GB sludge not stones
Si of chronic cholescystitis -
Strawberry GB
Porcelain GB (premalignant condition)
Acute hepatic failure = what?
Rapid liver failure manifesting as hepatic encephalopathy with coagulopathy common
MCC acute liver failure
Acetaminophen overuse or overdose
Also drug reactions (Isoniazid, rifampin, pyrazinamide), viral hepatitis, budd-chiari (hepatic v. obs), Reye syndrome (ASA use during viral infection in kids) etc
Management of hepatic encephalopathy
Lactulose - converted to lactic acid, neutralized the ammonia
Rifaximin, neomycin - reduces GUT bacteria that produce ammonia in the GIT
Protein restriction (proteins are broken down into ammonia)
What is the only definitive treatment for acute liver failure?
Liver translplantation
Which viral liver infection is a/w spiking fevers?
Hepatitis A
CP viral hepatitis
Malaise, arthralgias, URI sx, anorexia (liver won’t let you eat if it’s sick!!!), N/V, abdominal pain, +/- acholic (clay) stools
CP fulminant hepatitis 2/2 acute viral hepatits
Encephalopathy Coagulopathy Jaundice Edema Ascites Asterixis Hyper-reflexia
MC source of Hep A
Asx children < 6 YO = mc source for adults
Also from drinking contaminated water/food during international travel b/c it spreads via FECAL oral route - just like Hep E
You can only catch Hep D if you have?
Hep B
Specifically HepB surface antigen (acute hep B infection) to allow dual Hep D entry
= Direct cytopathic effect = more severe hepatitis & faster progression to cirrhosis
Hep C labs in acute hep C infection
Use HCV RNA
HCV RNA will be positive w/in 6 weeks of infection
May have Anti-HCV ab –> but unlike Hep B, anti-HCV antibodies does not indicate cure (can have chronic Hep C if still positive for HCV RNA > 6 months)
Hep C labs indicating resolved infection
HCV RNA NEGATIVE
+/- Anti-HCV Ab
Hep C lavs indicating chronic hepatitis
HCV RNA positive for > 6 months
AND Anti-HCV positive
Even tho developed ab, your body couldn’t control & now you have a chronic Hep C infection (occurs in 80% of pt infected)
Screening for HCC
Via serum alpha-fetoprotein & US
First serologic evidence of Hep B infection
+ Hep B surface antigen
Hep B serologies consistent with distant resolved infection or vaccination?
+ Hep B surface ANTIBODY
Serologies consistent with successful Hep B vaccination
+ Hep B surface ANTIBODY
Negative for Ab to core, envelope
Negative for all actual antigens (surface, envelope antigen)
Hep B serologies consistent with acute Hep B infection
Hep B surface antigen +
aCute infection: IgM against Hep B Core (Anti-HBc)
Chronic Hep B infection categorized as?
Hep B surface antigen positive for > 6 months
Presence of Hep B envelope antigen a sign of ?
Active viral replication & increased infectivity
Present > 3 months = high likelihood of developing chronic HBV
(only 10% of adults do but 90% of perinatally acquired Hep B –> chronic)
Labs consistent with chronic replicative Hep B
Anti HBs negative
Anti Hbe negative
HbsAg +
HbeAg +
Anti Hbc + (IgG)
Basically your immune system sucks & didn’t make antibodies to anything it was supposed to. So all antigens still positive (except core b/c not acute inf anymore) and all antibodies are negative
Labs consistent with chronic non-replicative hepatitis
HbsAg +
HbeAg -
Anti-Hbc + (IgG)
Anti-Hbe +
Anti-Hbs -
HbsAg -
Anti-HBs -
Anti-HBc IgM +
HbeAg -
Anti-Hbe -
Window period
Anti - core IgM = first antibody to appear
HbsAg+
Anti-Hbs -
Anti-Hbc + (IgM)
HbeAg +/-
Anti-Hbe +/-
aCute hepatitis
Anti-Hep B core IgM antibodies AND
Hep B surface antigen positive
**Establishes infection & infectivity
If it is replicating already then Hep B envelope antigen will be positive & if body has made Ab to that then anti- Hbe will be as well - depends on when serologies were ordered & how fast immune system reacts
HbsAg -
Anti-Hbs +
Anti-Hbc + (IgG)
HbeAg -
Anti-Hbe -
Recovery (resolved)
Antibodies to the surface antigen and core without any actual active viral antigens present in blood = body controlled the infection & killed every viral particle with those antigens
HbsAg -
Anti-Hbs +
Anti-Hbc -
HbeAg -
Anti-Hbe -
Immunization
Antibodies to surface w/o antibodies to core b/c vaccine doesn’t contain any core viral material only surface
HbsAg +
HbeAg -
Anti-Hbc + (IgG)
Anti-Hbe +
Anti-Hbs -
Chronic non-replicative hep b
Remember this is after 6+ months of labs staying like this b/c > 6 months = chronic hep b by definition
HbsAg +
AntiHbs -
Anti-Hbc + (IgM)
HbeAg +
Anti-Hbe -
Chronic replicative Hep b
Remember this is after 6+ months of labs staying like this b/c > 6 months = chronic hep b by definition
Prevention of Hep B
Vaccin given @ 0, 1, & 6 months
Hepatic vein obstruction known as? MC in who? Primary vs secondary?
Budd-chiari syndrome
Mc in women in 20’s-30s
primary - hepatic vein thrombosis (MC)
secondary - hepatic vein or IVC occlusion (exogenous tumor suppression)
Classic triad budd-chiari
- Ascites
- Hepatomegaly
- RUQ abd pain
Dx budd-chiari - screening
Ultrasound
Gold standard dx budd-chiari
Venography
performed if HIGH suspicion and negative non-invasive testing
Tx budd chiari
Shunts (tips)
Balloon angioplasty w/ stent (if stenotic or obstruction of ivc = hepatic v occ)
Pharmacologic - anticoagulation - if acute thrombus < 4 weeks, not involving the IVC
Manage ascites - diuretics, low sodium, paracentesis
HCC dx, tx
Ultrasound
Inc alpha-fetoprotein
Tx: Surgical resection
AVOID FNA to prevent seeding
Cirrhosis definition
Irreversible liver fibrosis with nodular regeneration 2/2 chronic liver disease
Si/sx hepatic encephalopathy
AMS - confusion, lethargy (ammonia)
Asterixis
Fetor hepaticus (sweet musty odor)
Inc ammonia levels
General sx & physical exam severe liver cirrhosis
Sx: Fatigue, weakness, weight loss, anorexia
Si: Spider angiomas Palmar erythema Ascites Caput medusa Gynecomastia Muscle wasting Jaundice Bleeding Dupuytren's contractures
CHILD-PUGH staging parameters
0-3 points for each - values listed + 3 points
Total bili > 3 Serum albumin < 2.8 PT INR > 2.3 Ascites moderate - severe Hepatic encephalopathy Grade III-IV
5-6 pt = class A = 100% 1 yr 85% 2yr survival 7-9 pt = class B = 81% 1-yr, 57% 2-yr 10-15pt = class C = 45% 1-yr, 35% 2-yr
Anti-mitochondrial antibody is hallmark in which disease?
Primary biliary cirrhosis
= Idiopathic AI d/o intrahepatic sm bile ducts
Primary biliary cirrhosis -what is it? MC in? Sx? hallmark? tx?
Idiopathic AI d/o intrahepatic sm bile ducts
MC In middle-aged women (40-60)
Fatigue = 1st sx, then pruritis, RUQ, hepatometaly, jaundice
Dx: Hallmark = Anti-mitochondrial antibody, labs w/ cholestatic pattern
Tx =
- Ursodeoxycholic acid - dec progression
- Cholestyramine & UV light for pruritis
Primary sclerosing cholangitis = what? MC in who? A/w with which disease?
AI progressive cholestasis 2/2 diffuse fibrosis of intrahepatic AND extrahepatic ducts
MC in YOUNG MEN 20-40 YO …notice whereas PBC is MC in middle-aged WOMEN…
PSC = UC –> MC a/w IBD - esp ULCERATIVE COLITIS. Inc risk of cholangiocarcinoma.
Dx ERCP, labs w/ cholestatic pattern
Tx: Liver transplant = definitive, stricture dilation to relieve sx, meds not beneficial
Kayser-flescher rings?
COPPER deposits in eye 2/2 wilson’s disease = rare autosomal recessive mutation = inadequate bile excretion of copper
Wilson’s disease? What? Dx, Tx
What:
Rare autosomal recessive mutation =
inadequate bile excretion of copper = abnormal deposits in brain, cornea, kidney (Wilson BRA-CO-KI = his name)
CP: Parkinson-like sx 2/2 basal ganglia cCu deposition, personality & behavioral changes, liver disease, corneal deposits
Dx: Decreased ceruloplasmin, inc urinary copper excretion
Tx:
- D-penicillamine (chelates copper) - also chelateds vitmain B6 (pyridoxine), so give to prevent depletion
- Zinc
Ransons criteria used for? Parameters?
Deciding whether to admit someone w/ acute pancreatitis
Glucose > 200 Age > 55 LDH > 350 AST > 250 WBC > 16
0-2= severe pancreatitis unlikely, 2% mortality
> 3 = severe pancreatitis likely, 15% mortality
MCC chronic pancreatitis in kids
Cystic fibrosis
Remember pancreatic insufficiency = one of three MC clinical manifestations of CF - pancreatic duct gets clogged = loss of exocrine function
MC pancreatic cancer
CP
PE
Dx
Tx
Ductal adenocarcinoma, most in head
pAncreatic = Adenocarcinoma
painless jaundice, wieght loos = CP
Pruritis 2/2 inc bile salts in skin, anorexia, acholic stools, dark urine (CBD obs)
PE - courvosier’s sign – palpable NON-dtender distende gallbladder a/w jaundice
Dx - CT scan = initial TOC. ERCP most sensitive test.
Tx: whipple
Tumor markers for pancreatis cancer
CEA
CA 19-9 (p looks like a P)
Ovarian is CA-125 (5 looks like an O)
Painless rectal bleeding in 2 YO boy
Meckel’s diverticulum
Management = surgical excision if sx
First line imaging SBO
Plain films - KUB will show air fluid levels in a step ladder pattern
First line imaging paralytic ileus
Plain ABD radiograph - uniformly distended lops of small and large bowel
Celiac dz - CP, dx
CP:
1. Malabsorption - diarrhea, abd pain, distension, steatorrhea, growth delays
- Dermatitis herpetiformis (pruritic, papulovesicular rash on extensor surface, neck, trunk & scalp)
Dx:
+ endomysial IgA Ab
+ transglutaminase Ab
Definitive dx celiac
Small bowel biopsy
Test of choice lactose intolerance
Hydrogen breath test
Mc sites of a volvulus?
Sigmoid colon
Cecum
Initial TOC volvulus
Endoscopic decompression of the bowel
Characteristics of IBS - typical pt, diagnostic criteria
Pt: Young woman, early 20s
Dx criteria:
Recurrent abd pain on average at least 1x/week in the last 3 months with at least 2/3:
- Pain is related to defecation
- Pain onset a/w change in stool frequency
- Onset a/w change in stool form
NO BLOOD NO ANOREXIA NO WEIGHT LOSS NO NOCTURNAL SX (if nocturnal sx then IBD not IBS) NO family hx CRC, IBD, celiac sprue
Tx: Lifesytle changes - no smoking, dec fat & processed food, sleep, veggies
Diarrhea sx - dicyclomine (antispasmodic) or antidiarrheal - loperamide
Constipation sx - prokinetics, bulk-forming laxatives, saline or osmotic laxatives, lubiprostone
Management of chronic mesenteric ischemia
Bowel rest, surgical revascularization (angioplasty w/ stenting or bypass)
Dx was via angiogram
Definitive dx acute mesenteric ischemia
Angiogram
Ishcemic colitis 2/2?
Low perfusional states - shock, shunting blood from organs = areas of ischemia in colon (watershed)
CP: LLQ pain (if sigmoid ischemic) w/ bloody diarrhea
Tx: Restore perfusion (IVF)
Toxic megacolon definition, causes
Non-obstructive extreme colon dilation (>6cm)
Seen in :UC, chron’s pseudomembranous colitis, infectious, colitis, ischemic colitis etc
Tx: bowel decompression, bowel rest, NGT, ABX, fix electrolytes
UC/CD a/w which rheumatological d/o? Skin d/o?
Seronegative spondyloarthropathies, aknylosing spondylitis
Erythema nodosum (also in sarco)
Right sided colon ca presentation
change in bowel habits
+FOBT
Anemia
Diarrhea
Left-sided colon ca
Present LATER (left colon = bigger) Large bowel obstruction \+ change in stool diameter Hematochezia
CRC Tx - localized vs mets
Local - surgical resection
Dx colon ca, labs
Colonoscopy w/ bc = Dx TOC
elevated CEA, Iron-def anemia
Elevated CEA = ?
COLON cancer - monitored during treatment too
CRC = CEA
Indirect inguinal hernia is lateral or medial to the inferior epigastric artery?
LATERAL
Originates at weak spot in the INTERNAL (deep) part of the inguinal ring/canal & travels down thru ring & patent process vaginalis into the scrotum
Direct inguinal hernia is lateral or medial to the inferior epigastric artery?
MEDIAL
Originates due to weakness in the floor of the inguinal canal - plows thru hesselbach’s triangle
Anal fissure
Longitudinal paper-cut like tear in anoderm = anal pain at rest exacerbated by BM assoc w/ anal bleeding
Hx anal pain brought on by BM that lasts hours-days afterwards,, assoc w/ some bleeding, confirmed by PE
Dx hemorrhoids
PE and/or anoscopy, DRE
CP Anal abscess
Diffuse, tender, erythematous, indurated and fluctuant area within/near the buttocks
Pain is CONSTANT, can have problems sitting, NOT a/w BM (unless along wall)
CP Anal fistula, MCC
MCC:
Non-healing (chronic) anorectal abscess of anal crypt gland in 40 YO M
CP:
Non-healing anorectal abscess following I&D
Intermittent rectal pain worse w/ BM sitting, activity
Malodorous perianal drainage, perianal skin excoriated/inflamed
May feel palpable cord leading to opening
Tx Anal abscess/fistula
I&D followed by WASH
Warm-water cleansing
Analgesics
Sitz baths
High-fiber diet
PKA common in? CP? Dx? Tx?
Common in BLONDE, blue-eyed with FAIR skin
CP:
Vomiting, mental delays, irritability, convulsions, eczema, inc DTR
Screening:
PKU heel stick at birth
Dx:
Urine w/ mousy odor
Tx:
Lifetime dietary restriction of phenylalanine (found in milk, cheese, nuts, fish, chicken, meats, eggs, legumes, aspartame in sodas
Vitamin A involved with which bodily functions?
Vitamin A involved in: Vision, immune function, embryo development, hematopoiesis, skin & cellular health (epithelial cell differentiation)
VISION, SKIN, IMMUNE SYSTEM
CP Vitamin A def
CP: Xerophthalmia Night blindness Poor wound healing Dry skin Poor bone growth
squamous metaplasia in conjunctiva, resp epithelium, urinary tract
BITOT’s SPOTS on eyes = white spots on conjunctiva due to squamous metaplasia of the corneal epithelium
Vitamin C (ascorbic acid) def RF
Diet lacking raw citrus & green veggies, smoking, alcoholism, elderly, malnourished
Vitamin C CP
= SCURVY = 3 H’s
Hyperkeratosis - hyperkeratotic follicular papules surrounded by hemorrhage
Hemorrhage - vascular fragility due to abnormal collagen production w/ recurrent hemorrhages in gums, skin & joints, impaired wound healing
Hematologic - anemia, glossitis, malaise, weakness, increased bleeding time
Vitamin D def children
Rickets = soft bones = bone bending (Bowed legs), fx, costochondral thickening (rachitic rosary), dental problems, muscle weakness, developmental delay
Tx Ergocalciferol (vitamin D2)
Vit D def adult
Osteomalacia
Diffuse bony pain
Muscle weakness
Fractures
LOOSER LINES - radiolucencies on xray
Tx Ergocalciferol (vitamin D2)
B1 deficiency - 3 big clinical manifestations
ETOH = MCC
CP:
- BERIBERI
- Dry = CRAN = muscle cramps/wasting, Reflexes impaired symmetrically, ANorexia, Neuropathy (peripheral, paresthesias)
- Wet = HOHF, dilated CMP - Werkicke’s encepholapthy TRIAD - AGO - Ataxia, global confusion, ophthalmoplegia (paralysis or abnl of ocular mu)
- Korsakoff’s dementia - irreversible - short term memory loss (50 first dates), confabulation
Riboflavin def
Ribovlafin = B2
Def = Oral-ocular-genital syndrome
Oral = lesions of mouth, magenta-colored tongue, angular cheilitis, pharyngitis
Ocular = photophobia, corneal lesions
Genital = scrotal dermatitis
Noticing a pattern here with b vitamins…if have to then guess a mucosal membrane issue or nervous system issue or skin issue…
Niacin def
Niacin = B3
Def = PELLAGR - 3D;s= diarrhea, dementia, dermatitis
Noticing a pattern here with b vitamins…if have to then guess a mucosal membrane issue or nervous system issue or skin issue…
Pyridoxine def
Pyridoxine = B6 def
Etio: isoniazid, OCP
B6 def = PERIPHERAL NEUROPATHY, seizures, headache
Stomatitis, cheilosis, glossitis, glaky skin, anemia
Noticing a pattern here with b vitamins…if have to then guess a mucosal membrane issue or nervous system issue or skin issue…
B12 def - etio, CP
Etio - pernicious anemia, strict vegans, malabsorption (ETOH, chron, atrophic gastritis (dec IF prod)
CP: Neurologic sx similar to neurosypalis 2/2 degeneration of posterior cord - loss of proprioception (clumsy, stumbling around, flap feet, looks like neurosyphilis)
Macrocytic, megaloblastic anemia
Tx IM (malabsorptive issues) or oral B12 (dietar issues)
Shillings test tells the difference
