Internal Diagnosis II (Infernal Die, Too) Larry Wyatt Get notes from bookstore

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look carefully at the points marked with (TQ) Organic – problems in the organs or body Inorganic – test all the organs and don’t know what’s wrong with the patient.

Treat your patients in a bio-psycho-social manner… Hx and Physical • History: AMPLE, HISTORY, OPPQRST: o Allergy, Medication, Past medical hx, Last menses/meal, Event of complaint (illness) o Hospitalizations, Immunizations, Sugar diabetes/Social Hx, Tumors/Trauma, Operations, Review of systems, Youth Illnesses. o Onset, Palliative, Provocative, Quality, Radiation/Region, Setting/Site/Severity, Timing • Physical exam: Inspection, Auscultation, Percussion, Palpation o Auscultation done 2nd to keep from altering sounds (bowel sounds, etc.) Pain in gut is primarily from distension. Most tumors are painless, until they grow enough to distend the organ (as they are encapsuled, in the serosa). The peritoneum is also pain producing, primarily due to inflammation.

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2 primary reasons for pain in the gut: o Distension. o Irritation/inflammation of the peritoneum. o Both shown in appendicitis.  At onset, pain in appendicitis is diffuse (caused by distension)  In 18-36 hours, the pain will migrate to the region of the appendix. Abdominal guarding begins.  If appendix ruptures – pain reduces substantially initially because the distension reduces.  However, within a few hours pain severely increases and generalized, and the abdomen becomes very rigid (muscle tension) as the pus and bacteria spread throughout the abdominal cavity (and abdominal sepsis begins).  Death CAN occur in this case. • Pitting Edema (of the leg) o Blood pooling on heel of the foot o Differential Dx:  Cardiovascular (most common) • Most likely CHF  Renal failure probably caused death (more common)  Hepatic (Maybe, but no jaundice present)  Renal dz  Thyroid dz

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Clubbing (right hand) o Findings:  White male  40’s  Swelling at DIP  Enlarged nails (no splinter hemorrhage) • Psoriasis has pitted nails o Enlargement of the terminal tuffs (seen on x-ray) o AKA: Hypertrophic Osteoarthropathy (digital clubbing)


Lung disease because of hypoxia (most common) Can be associated with GI and GU problems

A.M.P.L.E. - Allergies (wheat, soy, peanut, shellfish, iodine, meds) - Medications (what, how much, ? for, how long) - Past Medical “HISTORY” - Last Meal/Last Menstrual Period (1st day of mense) (onset) - Events of the present illness O.P.P.Q.R.S.T. - Onset (what cause, when, how long it takes) - Provocative (what makes it worse) - Palliative (what makes it better) - Quality (sharp, dull, aching, intermittent, cramping, cholicing) - Radiation/Region of pain (where does it hurt) - Setting (when – time)/Site (where is it located)/Severity - Timing (when does it happen and how long does it last) o Constant = 24/7/365 o Serious Large smooth dome-shaped mass in the LUQ Appears pale over lesion Have pt do a sit up so that abdominal muscles contract Incisional Hernia (past surgery) o Gets larger when she bears down and painful o Auscultation will hear bowel sounds o Feels like it is filled with air (like balloon) o Very mobile o When blood supply is lost to a hernia is call strangulation o Tender o Lateral debicutis o HISTORY - Hospitalization - Injuries/Immunizations - Sugar Diabetes - Tumors/Trauma - Operations - Review of Systems

Most Frequent Hernias

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Youth Illness

10-Day rule • Can only take X-ray’s first 10 days of cycle (starting at 1st day of menses) • Unless chance Mom’s life is in danger or severe morbidity • History [The History and Interviewing Process (06)] o Hospitalizations  When? What for? How long? What was outcome?  Recent surgery – mobilization/manipulation not recommended within 2 months. If doing sooner – call and discuss with their surgeon. o Injuries  When? What happened? What done? Outcome? o Sugar diabetes


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Tumors  Lipoma is the most common, benign tumor.  Most common malignant tumor is skin cancer (basal cell carcinoma or melanoma). o Operations  In-patient as well as out-patient. o Review of Systems o Youth Diseases  Measles, Mumps, Rubella, Diptheria, Pertussus, Tetanus and chicken pox. • Physical Examination (abdomen) o Inspection  Symmetry, size, shape • If abdomen is distended (besides obesity): fluid and gas (or combination) o Look for fluid wave, etc. to check for fluid. Can detect down to about 20 ml of excess fluid.  Puddle test – pt on all 4 for a few minutes.  Percuss on Pt and listen for sound as percuss. Tough to do. o Percussion notes for excess gas are higher than for fluid. There will also be a palpatory difference (fluid is less “squishy” and rebounds less than gas)  Lumps, bumps, scars, ecchymoses (bruising) • Hernias are common “bumps”, for example. • Large scars used to be common for abdominal surgery, but with endoscopic surgery, can’t tell just by incisions or what it was at this point. • Pt with scar always has to bear down to look for hernia. • Laprocholecystecomy, hysterectomy, appendectomy scars most common. o Auscultation

Insipidus or mellitus (NIDDM or IDDM) Look for increased adipose tissue in belly. Remember DM causes microvasculopathy and microneuropathy. • Hence these Pt’s have a lot of GI/GU problems, such as renal problems.

Bowel sounds (5-35/minute) (listen for about 1 minute) • AKA Borborygmi • Relatively high pitched  use diaphragm • Very high pitched and get faster than 35/minute  sign of obstruction • No bowel sounds  Paralytic (Adynamic illeus (blunt trauma, post operative) • Early bowel obstruction  Rapid sounds to force fecal bolus

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Late bowel obstruction  Shuts down and patient vomits (no bowel sounds) Adynamic Illeus  no bowel sounds b/c no peristalsis We percuss/palpate after auscultation to avoid altering bowel sounds. o But DO palpate, even if suspect AAA (TQ) Most bowel sounds come from the small bowel. (peristalsis) Not regular, hence Dr needs to listen for a full minute in each quadrant. Decreased bowel sounds – less peristalsis. (hypoactive bowel sounds) Increased bowel sounds – more peristalsis (hyperactive bowel sounds) o Oddly, in obstructions, there is initially a transient increase in bowel sounds, then it decreases as the bowel shuts down. o Prognosis is worse with decreased/absent bowel sounds. Adynamic/paralytic ileus – common after injury to the bowel, particularly after trauma, abdominal surgery, anesthesia.


 Bruits • • •

Normal vessels have a trilaminar flow. Disruptions to this flow cause microeddies, which generate the bruit sound. Renal arteries and abdominal aorta near the bifurcation into the common iliac are the most common sites for high pitched, stenotic bruits. • Occurs with aneurysm and stenosis • M/c in the aorta (infrarenal AAA) • Low pitched, rumbling bruits are usually found in aneurysms, such as aorta below the renal arteries and above the common iliacs. o Common. You will see them. o High pitched bruits = stenosis o Low pitched bruits = aneurysms. (possible TQ) • Venous hum is also possible to hear. o Obstruction of one of the major veins in the belly.  Ex: inferior vena cava (most common) • As with bowel masses (small bowel obstruction, large lymph node, etc.) or enlargement of the liver. o Not very pulsified, as in arterial problems. More constant, humming noise as the blood moves through the stenosis. Other noises • Friction rubs – rubbing noise o As in the liver with Pts with hepatitis. o As with abdominal adhesions, where portions of mesentery or small bowel are adhering to each other. o Listen over the liver (2nd most vascular structure in body next to the skin).


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Hemangiomas are VERY common (half the population) in the liver. Can have a noise like a venous hum, if the hemangioma is large and near the surface. Five Percussionary Notes 1. Flatness: muscular area • ex: thigh 2. Dullness: organs • ex: liver 3. Resonance: normal lung field 4. Hyper-resonance: abnormal lungs • Ex: emphysema, Pneumothorax 5. Tympany: normal abdominal • gastric air bubble

Percussion Liver, spleen, diaphragm 1. Size 2. Diaphragmatic Excursion 3. Note pitch  LUQ: Not eaten  tympanic (b/c air in the stomach) Eaten  dull 4. Spleen: dull 5. Liver: dull 6. Rest of the abdomen: tympany

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Bowel obstruction: dull  Tympanic: proximal  Dull: distal

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Palpation  Organomegaly • Cannot normally palpate either kidney or spleen (TQ) • Hepatosplenomegaly o Caused by sickle cell, etc.  Aneurysms • Palpate for tenderness, for guarding (voluntary), and for abdominal rigidity (involuntary). o Abdominal rigidity is textbook sign for peritonitis. • Also palpating for masses (are they tender? Mobile? Size? Shape? Contour? Pulsates (vascularity)? 1. Start in non-tender quadrant and go to tender quadrant 2. Superficial mass: in abdominal wall 3. Contraction of abdominal mm  Accentuated: in abdominal wall  If not in abdomen 4. If mobile: better than mass that is non mobile  Malignant masses do not move b/c not encapsulated and they invade other tumors and inflammatory tumor that makes scar tissue and makes more immobile  Benign tumors grow in the original tissue and do not invade Two types of abd organs: 1. Solid 2. tubular Palpation of organs 1. Liver 2. Spleen 3. Cholecystitis 4. Gallbladder – porcelain gallbladder (calcified wall) 5. Pancreas 6. Kidney 7. Duodenum Aorta 1. Lateral pulsation is not good, could represent AAA 2. 3.5 cm or less is normal size of aneurysm 3. AAA produce non-mechanical back pain

Abdominal Exam Tips o Comfortable room temp. o Pt gowned with abdomen exposed.  You can use 2 white towels to drape the abdomen (crosswise), exposing only the quadrant you are working on, which makes the Pt feel more comfortable. o Groin uncovered with genitalia draped. o Bladder empty (but not bowel – tricky TQ) o Start in non-tender quadrant.  Save the tender quadrant for last. (Pt gets used to the palpation that way.) o Use your hand over Pts’ hand if ticklish. o Normal kidney is non-palpable. (TQ) o Normal liver may be palpable (8-12 cm @ Mid Clavicle Line)  4 lobes (R, L, quadrate, and caudate)  Most common cause is alcoholism o A palpable spleen is enlarged. (Normally not palpable) (TQ)

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 Normally tucked up left of stomach and under left costal margin.  When it enlarged, enlarges into a mass medial and inferior. o In a chiropractors office – you ought to give an abdomen exam to someone with low back pain. o Remember that this is not necessarily an easy exam as it takes a lot of Pt involvement. o If a mass is palpable, have Pt bear down to help determine origin.  Hernias will usually protrude with valsalva maneuver. o When abdomen is involuntarily flex and is very hard  abdominal rigidity usually caused by peritonitis

• Abdominal regions
o 4 quadrants
• RUQ o o o o o o o Liver Right kidney Gallbladder Hepatic flexure Right renal artery Transverse colon Head of Pancreas Biliary tree (bile ducts) Biliary aa & vein Ascending colon Small intestine Right common iliac Right ovary Cecum Right fallopian tubes Appendix • LUQ o o o o o o o o LLQ o o o o o o o Stomach (fundus) Left kidney Spleen Splenic Flexure Left renal artery Transverse colon Tail of the pancreas Aorta

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• o RLQ o o o o

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Descending colon Small intestine Left common iliac vein Left ovary Inferior mesenteric artery Left fallopian tubes Sigmoid colon

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o 9 regions • Right Hypochondrium o Liver (R lobe) o Gallbladder o Hepatic flexure • •
Right Lumbar o Kidney (R) o Ascending colon Right Inguinal (Iliac) o Cecum o Appendix

Epigastric o Liver (L lobe) o Pancreas o Stomach (Antrum) o Transverse colon Periumbilical o Intestines o Aorta Suprapubic (hypogastric) o Bladder o Uterus

Left Hypochondrium o Stomach (Fundus) o Spleen o Splenic flexure Left Lumbar o Kidney (L) o Descending Colon Left Inguinal (Iliac) o Sigrnoid Colon

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o 6 regions • RUQ

• Liver Right kidney Gallbladder Hepatic flexure Right renal artery Transverse colon Head of Pancreas Biliary tree (bile ducts) Biliary aa & vein Ascending colon Lower portion of liver Ascending colon Small intestine Right ovary Right common iliac Cecum Appendix

o o o o o o o

Epigastric o Duodenum o Pylorus o Liver (left lobe) o Pancreas o Transverse colon o Aorta (Celiac trunk, renal aa. & veins)

LUQ o o o o o o

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Stomach (fundus) Left kidney Spleen Splenic Flexure Left renal artery Transverse colon Tail of the pancreas Descending colon

Suprapubi (hypogastric) o Bladder o Uterus

LLQ o o o o o o o

Sigmoid colon Descending colon Small intestine Left ovary Left common iliac vein Inferior mesenteric artery Left fallopian tubes

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• Abdominal exam tests

o Rebound tenderness (TQ)  Rovsing’s Sign: pain in the RLQ only
Peritonitis (Rovsing’s Sign) (classic sign) • (If appendicitis - Pain in RLQ. Appendicitis is a type of peritonitis, and is the most common organic source of rebound pain in the abdomen) • Highly suggestive of appendicitis, but not pa-thog-no-monic (indicative of a disease). Pt with recoil palpation (on rebound of organs back to their original position) 1. Push in an area where there is no pain and then quickly let go and pt will feel pain in a quadrant other than where you pushed (classic is appendix) 2. Peritonitis (Rovsing’s Sign – only on RLQ) → push in quadrant pain and hurt in same area (appendicitis) 3. Pain with recoil palpation  If pain in another quadrant then the test is positive • Peritonitis  If pain in RLQ and doing test in a LLQ than can be positive for appendicitis

o Costovertebral angle (CVA) tenderness (angle at junction of last rib and spine) (TQ)  Generally used to find retroperitoneal organs, such as the kidney.  Kidney disease  AKA: Kidney Punch Test  Also remember the quadratus lumborum muscle is there, and is prone to spasm.

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Shifting dullness  Done while palpation abdomen  Ascites  Fluid shifts as Pt moves in different positions. For small amounts of ascites called “Puddle Sign”  Pt on all fours for ~ 5-10 min  Start out to in and when run into dull mark  Move to different side and repeat  Will end up with outline of the “puddle”

Psoas sign  Appendicitis  Pain on resisted right hip flexion (supine)  Put knee and hip in flexion have pt try resist as Dr tries to extend leg  No particular practical clinical application. o

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Obturator sign  Appendicitis  Pain on resisted internal right hip rotation.  No particular practical clinical application.

May 15, 2006 (2nd Hour)
• Diagnostic Imaging (abdomen) o Barium swallow (Zenker’s diverticulum)


  follow through o

Uses barium sulfate  thick chalky substance Shows up very white on radiograph Can do upper GI study with a small bowel

Barium enema  Barium Dx not used much any more. Popular a few years ago, but now used only selectively, as endoscopy has become the preferred methodology.  Barium or barium with air  forces barium against the wall  Show endothelial wall in detail o CT scan with contrast  Computerized tomography.  Radiography, using X-ray.  CT scan in the bowel should be ordered with iodinated contrast. • Vascular tissues • (To differentiate blood vessels, nodes, and small bowel.) • Also tough to differentiate spleen from small bowel. MRI scan with contrast

Zenker’s diverticulum

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Endoscopy Most common, 80% of the time to investigate bowel complaints. Small endoscopes can even go into the pancreatic ducts. Typically used in either nasal or rectal insertion. (Not together, Some of the false negatives with an endoscopy are from user Hence if referring out, make sure the operator/physician

hopefully)  error. • is well practiced.

Esophagogastroduodenoscopy (EGD) (WHEW! Spelling bee word from hell…) (TQ)  From bottom Anoscopy, Rectoscopy, Sigmoscopy, Colonoscopy  Can be both diagnostic and therapeutic/operative (additional machinery for biopsy, microsurgery, electrocautery, etc. which can be done as an outpatient procedure.)  There are rigid and flexible endoscopes, with various lengths.

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 Ulcerative Colitis (UC), severe Crohn’s, or other conditions with fragile bowel are contraindications to the use of endoscopy. o KUB (Kidney Ureter Bladder)  X-ray of abdomen (upright and supine)  Cheapest and quick  Not a great tool  Helps see fluid lines  Helps see if a mass is moving around  M/c lesion: calcified lymph node • Follow lumbar or iliac chain • Can also find in mesentery and momentum Ultrasound  Quick and easy  Low resolution

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Common GI Signs/Symptoms o Abdominal distension o Abdominal pain o Anorexia (loss of appetite) o Belching, bloating, flatulence o Bleeding o Constipation/diarrhea o Nausea/vomiting o Heartburn/indigestion/dyspepsia o Hepatomegaly/splenomegaly o Hernias o Hiccoughs o Jaundice o Rectal pain/itching

Picture: - Black/Hispanic Female/20-30 - Valgus elbow - Very large umbilical hernia - Hernia is div into compartments - LR bulb is largest, LL, UR, and UL is smallest. - Well defined line separating LL and LR bulbs. - Purple variscosities at center. - Lighter skin on mass compare to natural skin. Pertinent negative: - No hair - Drainage - No color - No deformities

(Get .PDF from him on spine cancer from Australian journal)

May 16, 2006
• Abdominal Distension  Also called protruberant abdomen. Not caused by obesity. o 4 categories: 1. Excess fluid

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a. Most commonly from ascites (serous, serosanguinous, sanguinous, pustular)
2. KUB – “Kidneys Ureter and Bladder” – a flat plate X-ray of the abdomen, done both standing and supine (to look for fluid levels) (lateral view instead of standing if Pt cannot stand) Excess air a. Normally from excess gas, also from post-operative gas. b. Remember that gas will change position easily, and with the position of the Pt. c. Gas is either intraluminal (inside bowel) or extraluminal (outside bowel). A mass a. Abdominal hernia Organomegaly. a. Splenomegally b. Epatomegally b.

3. 4.

Mechanical Intestinal Obstruction  Neoplasm (intraluminal/extraluminal) • Ex: o Intraluminal:  colon cancer. o Extraluminal:  prostate cancer w/ lympadenopathy  uterine cancer  baby  hernia  abscess from appendicitis  ovarian tumor  uterian tumor/mass  Post-operative adhesions (TQ) • Adhesions are typical following abdominal surgery. (The bowel does not like to be manipulated during surgery). More diffuse adhesions may also form following peritonitis.  Abscess • Ex: o Peri-appendocoele abscess (appendix) o Sigmoid region (leading to diverticulitis, particularly in the elderly) o

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Crohn’s disease (RLQ) is also associated with abcesses. (m/c) Appendicitis (LLQ) Diverticulitis (LLQ)

Pregnancy Hernias  Volvulus (TQ) • A mesenteric portion of bowel twists on itself. • Occurs in areas like the caecum and sigmoid colon, in which at least one portion is already fixed in one portion, but not fixed in the other. • Could become ischemic and die.  Intusseception. (TQ) • Telescoping of the bowel inside itself. Most common in small bowel and in children. • Large bowel intusseception may occur in the large bowel with a mass or adhesion. Driven by peristalsis.

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Some will relieve themselves, while others require surgical intervention. • Adhesions • Paralyzed persons (bowel doesn’t work as well) • Kid’s may be hypermobile bowel (not really sure though) • Trauma • Ischemia o Non mechanical obstruction of the bowel • Not a good nomenclature.  Ascites • Most common from alcoholic hepatitis (portal hypertension) (TQ) • World wide – m/c is Hep C  What cause Distented Abdominal • Water • Interstitial • Fecal • Urine • Blood • Pus  Excess gas • As from dietary sources.  Trauma • Pts involved in motor vehicle accidents (MVA) sometimes show this, as seat belts can shove into bowel during impact. Usually resolve within 24 to 48 hours.  Infection  Peritonitis.  Adynamic/paralytic ileus – will get distention of bowel. (TQ) • Ileus resulting from failure of peristalsis • Most commonly from surgery. As bowel tends to shut down for a short time after being handled during surgery. o Take KUB (kidney, ureters, bladder) x-ray as a start of diagnosing abdominal problems

May 17, 2006

Abdominal Pain Patterns o Diffuse  Visceral pain  Organ involvement – capsule being stretched  Ex: Appendicitis (initially)  Ex: Hepatitis (capsule being stretched) o Focal  Parietal pain.  Organ distension.  Ex: Peritonitis (late stage appendicitis) (TQ) [Photo: diastasis recti (splitting of the rectus abdominus)] o Burning

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PUD (pain upon defecation), GERD, dyspepsia (gastritis) • Do not ignore burning epigastric pain. (Possible cardiac involvement) • Can be caused by nicotine, alcohol, mint

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Cramping (usually from organ distension or peristalsis)  Biliary colic, IBD, IBS, mesenteric ischemia • Note: Men tend to have more active gastro-colic reflexes than women (When put fresh stuff in, not-sofresh stuff comes out. A useful bit of trivia to defend yourself from your wife’s pointed comments after a spicy meal.) • Note: Mesenteric infarct is supposed to be THE most painful condition in medicine. (Possible TQ)

Colicky  Renal stones, biliary colic, appendicitis. • Note: crescendo/decrescendo pain pattern in stone obstruction due to peristalsis waves (try, stop, try, stop, etc.) • Pain that goes up and down o Achy  Constipation, appendicitis (early), AAA (saccular) o Knife-like (usually very serious)  AAA (dissecting/saccular rupture), pancreatitis.  Pt’s will usually lie on their side in flexion (the fetal position) due to pain. o Sudden onset  Perforation, obstruction, pancreatitis, ruptured ectopic pregnancy, dissecting aneurysm • Abdominal Pain Patterns o Diffuse  Early appendicitis  AAA  IBD – Inflammatory bowel disease [Crohn’s and Ulcerative colitis – typically of the left colon]  Peritonitis – if diffuse peritonitis, if the peritonitis is localized then so will the pain  Trauma  Obstruction  Look for abdominal guarding (voluntary) and abdominal rigidity (involuntary) o Epigastric • Common region for abdominal pain, lots of different organs  PUD • (Peptic Ulcer Disease in this case) • Often described as “gnawing”, “chewing”, or “burning” type pain. • Usually duodenal disease.  Gall Bladder (GB) disease • Cholecystitis (inflammation) and cholelithiasis(gallstones production) o Commonly found together.  Hepatic disease • Particularly in left lobe of liver.  Cardiac disease (Red flag) • Referred pain to upper abdomen.  Pancreatitis • Pts assume the fetal position. • Severe pain radiating from abdomen to low back (Lumbar and thoracic spine) (TQ)  Gastritis  GERD  Dyspepsia o RUQ  Biliary tree disease o

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 o LUQ   

• Both intrahepatic and extrahepatic portions. • Liver, gall bladder and collecting ducts. PUD • Particularly involving the duodenum. Pancreatitis (head of pancreas can go that far over) Renal disease • Particularly the pole of the right kidney. • Renal cysts (uncomplicated) are the most common renal disease. o Usually only symptomatic if the cyst grows large enough to distend the renal capsule. Cardiopulmonary disease • Referred from heart or lungs (portal effusion, lower pneumonia) PUD • Usually from stomach. Pancreatitis Splenic diseases 1. Mononucleosis 2. Polycythemia vera (inc conc of hemoglobin in blood) 3. Sickle cell 4. other anemias, splenic artery aneurysm. o Splenic artery is a VERY tortuous, twisty artery as it moves laterally. Viewable on X-ray. Renal disease • Left kidney (higher than the right) Cardiopulmonary disease • More often causes LUQ pain than RUQ pain.

  o RLQ 

Late appendicitis • Once peritoneum is involved, focal pain.  Crohn’s disease (aka inflammatory enteropathy) • Chronic granulomatous disease of the GI tract, hence causes granulomas, effecting the entire thickness of the bowel wall (as opposed to UC). • Can affect any region of the GI tract. • Typically in the young (late teens to early 20’s) • Debilitating, sometimes requiring colostomy, etc. • Most commonly in distal portion of small bowel, beginning of large bowel.  Obstruction. • RLQ is a very common area, because is attached, and hence common for volvulus formation (coecle volvulus or sigmoid volvulus)  Reproductive disease • Ovaries, fallopian tubes, or uterus • Ex: Cancer, PID (if affect ovaries), endometriosis, fibroid tumors (leiomyomas – smooth muscle tumors) o Leiomyomas can be HUGE (largest on record was 350 lbs)  Pt can actually think they’re pregnant (TQ) o Can be calcified, looking like a ‘popcorn ball’ on PFXR. o Can interfere with menstrual cycle, fertility, etc. o Can also cause low back pain.

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o

VERY small chance of transformation to leiomyosarcoma, but VERY small. Normally benign. (TQ)  AAA o LLQ  Diverticulosis/itis • Diverticula are common with old age, most people get them. • 75% of patients over 70 has it Zenker's diverticulum is a diverticulum of the • Most often in the descending and sigmoid colon (local vasa recta – asymptomatic) mucous membrane of the oesophagus through a defect in the wall of • Referred pain to the low back. oesophagus.

• •

pulsion- occurs in area of weakness o pressure within esophagus causes area to push out Likely to cause Odynophagia (pain on swallowing) o A similar abnormality occurs in the intestines, but tends to be multiple. o Zenker's Diverticulum is solitary.

Obstruction • Sigmoid volvulus most often.  Colon cancer • More than ½ of colon cancers in the sigmoid/descending colon. • Alternating constipation/diarrhea. o Body has obstruction from tumor, floods bowel with water to remove it, resets, cycle repeats.  Ulcerative colitis (UC) • Causes superficial inflammation/ulceration (innermost layer) • But because of the number of vessels in this region, there is a LOT of bleeding. (an important differential from Crohn’s) • Late teens/early 20’s, with bloody diarrhea.  Reproductive disease  AAA o Periumbilical  Obstruction • Small bowel in this region. • Small bowel obstructions are usually intussceceptive.  Early appendicitis  AAA  Mesenteric thrombosis. • Lack of blood supply (embolism) in mesenteric arterial tree. • Again, supposedly the most painful condition in medicine. (Shoots a lot of holes in that labor and delivery guilt trip, eh? Sorry Mom.)  Pancreatitis. • Pt in fetal position, very painful. (So possible matching TQ is fetal position – pancreatitis) • Causes of Abdominal Pain o Most common cause of abdominal pain is non-organic. (TQ) Lot of musculoskeletal origin, believe it or not.  Non-specific abdominal pain – 35% Acute appendicitis – 17% (know this TQ) (most common source of organic abdominal pain) Intestinal obstruction – 15% Urologic causes – 6% Gallstone disease - 5% Colonic diverticular disease – 4% Abdominal trauma – 3%

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Abdominal malignancy – 3% Perforated peptic ulcer - 3% Pancreatitis – 2% Ruptured AAA - <1% Inflammatory bowel disease - <1% Gastroenteritis - <1% Mesenteric ischemia - <1%

[VBA dissection – REDFLAG: “The worst headache I’ve ever had.”]

May 22, 2006

Abdominal Aortic Aneurysm (TQ’s – particularly on the diameters, and what to do in each case) o Focal widening of a blood vessel (arteries or veins) o Focal widening >3.5 cm Diagnosed by seeing widening, usually on PFXR – as they tend to be atherosclerotic, calcified, and visible on X-ray. Typically > 60 years, M:F = 5:1  >40 years w/ backpain, do an abdominal exam. Intrarenal (90%) (infrarenal?)  Below renal arteries, but above common iliac arteries.  This is a good thing – if involved the renal arteries, would have a much higher mortality rate. Extension of aneurysm into iliac arteries (66%) Plain film: mural calcifications (75-90%) Best seen on a lateral lumbar spine film (TQ) • Can also see on A-P, but harder since overlaps the bony structures.  Aneurysm tends to be 25-30% larger on surgical excision than what is seen on PFXR (plain films underestimate size) – due to incomplete calcification (only see the calcification) CT: perianeurysmal fibrosis (10%), may cause ureteral obstruction.  The body is attempting to limit the expansion of the aneurysm, and this in turn might cause the ureteral obstruction. Abdominal UltraSound: 98% accuracy in size measurement. Angio: mural thrombus (80%) Complications:  Rupture (25%): 1. into retroperitoneum (usually left) 2. GI tract 3. IVC  Peripheral embolization.  Spontaneous occlusion of aorta. Growth rate varies.

o o

o o

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o o o

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Hence the treatment protocols vary until the aneurysm reaches 7 cm (at that point, chance of rupture is so high that surgery is non-elective)  Surgery generally not recommended until aneurysm is >5cm or the Pt becomes symptomatic. • [REDFLAG:Pt cannot find a comfortable position] (TQ) o Indicates an organic cause, not a mechanical problem. (possible AAA) o This is the Hallmark S/sx of AAA. (TQ)

• Two types of aneurysm: (picture) 1. Saccular (fusiform) aneurysm – “football shaped”
aneurysm.

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2.

Dissecting aneurysm

• Dissecting AAA o There is a separation between the interior and middle walls of the aorta (intima and media). o Can be traumatic or atherosclerotic. o When wall separates, the force of exiting blood causes increased widening of the separation. o Pt can easily exsanguinate (bleed out) without actually losing blood from vascular system.  The blood is trapped in the wall of the artery (between media and intima) o Mortality rate with AAA dissection is very high, unless they catch them very early. o Do NOT show up on PFXR (plain film X-ray). o Hallmark S/sx of AAA dissection.  “Tearing” abdominal pain.  Shock. o Odd trivia fact: Dissecting aneurysms used to show up most commonly in the aortic arch as a S/sx of tertiary syphilis. Now (with less cases of syphilis around) is most common in abdominal aorta.

Abdominal Aortic Aneurysm (AAA) (Picture) o S/Sx  Most are asymptomatic (since are between 3.5-5 cm, and not dissecting)  Pulsating sensation in the abdomen • On palpation, normal pulses A to P, lateral pulsation on palpation can be indicative of AAA. (TQ)  Abdominal pain (unchanged by position) (TQ)  LBP (unchanged by position)  Bruit (typically low pitched (blood flow slowed down)) • High pitched usually caused by stenosis.  Radiating pain into legs.  Cold Lower Extremities, peripheral pulse loss. • Dorsalis pedis and posterior tibial are most common pulses on the foot.  Shock • S/sx: cold clammy skin, pale skin, diaphoresis (sweating), pulse increases, BP drops • Quantifiable definition of shock: Systolic pressure of <90 mm Hg o In practice: poor perfusion of the vital organs. • 5 different kinds of shock: Hemorrhagic (hypovolemic) 1. anaphylactic shock – allergic reaction (bee sting) 2. insulin shock – excess insulin in blood (consulsions, potential coma) 3. osmotic 4. protein 5. septic shock – infected with bacteria 6. toxic (double check this) • Know that septic shock is a major risk with appendicitis (TQ) o Due to rupture and infect the intraabdominal cavity

17

o

o

o

 Sudden death. Imaging  Plain films • Maximal measurable normally is 3.5 cm. • Anything larger suggests aneurysm.  MRI, CT Treatment (big TQ) (Picture)  3.5-5 cm – careful observation • Tell Pt to avoid anything that might increase risk of trauma or intra-abdominal pressure. • Careful to absolute contraindications for adjustment. o Only in small size aneurysms. Perhaps mobilization only.  5-7 cm – elective surgery (10% rupture/yr)  >7 cm – non-elective surgery (25% rupture/6 mos)  Symptomatic – non-elective surgery.  If Pt is bleeding, condition is emergent. (well duh…) Surgical procedures  Open laparotomy  Endoscopic stent replacement.  <50% w/ rupture survive.

Anorexia • Anorexia – lack of appetite. o Anorexia nervosa – psychologic disease leading to wasting. o Self image problem (think they’re too fat) • Possible Causes o Infection. o Neoplastic (particularly malignant) o IBD o Constipation. o GERD o PUD (peptic ulcer disease) o Swallowing disorder. • [Picture: Old man with Anorexia, Cachexia, and Ascites] o Cachexia – wasting associated with disease and malnutrition. (possible TQ)  D/Dx: Possible end stage liver disease, endstage cancer, endstage AIDS Belching, Bloating, Flatulence • Eruptation – medical term for belching, at least according to Wyatt. o Sound is generated from the inverse flapping of the vocal chords. • Belching – gas from the top of GI tract. o Aerophagia, smoking, esophageal stricture (TQ) • Bloating – gas in the middle of the GI tract. o Extensive fullness in the abdomen • Flatulence – gas out the end of the GI tract. o Bacteria in the bowel produce CO2, HS, CH4, etc. o Carbohydrate ingestion. (TQ) • Possible causes:

18

o o o o o

Aerophagia (belching)  Primary cause. Natural part of eating, swallowing, chewing, talking, smoking, etc. Insoluble carbohydrate ingestion. (flatulence) Malabsorption syndromes Lactose intolerance. Diarrhea

May 23, 2006 (2nd Hour)
GI Bleeding • [Picture: Meckle’s scan] o Radionucleotide scan collecting in high blood flow areas. o Common usage to Dx appendicitis.


Ligament of Treitz differentiates the upper and lower GI tract (TQ) o This ligament suspends the last portion of the duodenum (suspensory ligament of the duodenum) and keeps it in a Cshaped loop (which enfolds the head of the pancreas). GI Bleeding can take a variety of different forms o Blood in Upper GI tract coming back up through oral cavity, blood appears in one of two forms: hematemesis or ‘coffeeground’ emesis. (TQ) o Type of blood seen in upper GI suggests type of bleeding. Hematemesis (vomiting blood) (not hemoptysis – from bronchial tree) – more acute type of bleeding (bright red blood) from GI tract (TQ)  Coffee-ground emesis – more chronic, slow type bleeding. • (looks darks and clumped, coagulated, like coffee grounds) • Gastric enzymes act on blood, denaturing proteins, which then coagulate. Can have a combination of both types of presentation, depending on pathology  Ex: Chronic condition that finally ruptures, etc.

o •

Upper GI Bleeding o Esophageal varices (most common)  Varicose veins (dilated veins) in the submucosal layer of the esophagus, usually in the lower portion of the esophagus.  Erosion occurs with long term passage of food over them.  Over time can progress to a massive bleed.  Usually due to alcoholic hepatitis and cirrhosis leading to portal and venous hypertension. o Esophageal CA  Long-standing, chronic bleed with coffee-ground presentation. o Esophagitis  Depending upon degree and cause, can have either coffee-ground (more common) or hematemesis presentations. o PUD (peptic ulcer disease)  More often coffee-ground presentation, but if erodes into a gastric/epiploic arteries, can present as hematemesis. o Gastric CA  Most often coffee-ground presentation, or mixed presentation. o Hiatal hernia o Swallowed hemoptysis Hemoptysis – “Coughing up blood” (TQ) • Remember that blood is VERY irritating to the GI tract, and will provoke emesis (vomit). Pt’s with Upper GI bleeds can present with signs of upper GI bleed in lower GI tract.

 

o

Melena (black tarry stools – occult blood) is usually a lower GI sign of an upper GI bleed. (TQ)

19

o

• Make sure pt. doesn’t have pulmonary condition. Blood streak stool – mix with blood Occasionally occult fecal blood. • Detectable through hemocult or FOB (fecal occult blood) testing (also called GUIAC). o False positives for GI bleed with PeptoBismol (contains the same enzyme as in GUIAC test) o Hence must have 3 separate positives on 3 separate occasions for true Dx. (TQ) Hematochasia – “Bright Red Blood Per Rectum” – abbreviated BRBPR (possible TQ)  

Most common cause: hemorrhoids (TQ)

Lower GI Bleeding  (causes are a TQ) o Mesenteric thrombosis  Said to be the most painful condition in medicine (mesenteric ischemia as a result)  (He’s said this often, possible TQ) o Meckel’s diverticulum  Blind fibrous tube associated with the ileum, as a development defect from the umbilicus. o Volvulus/intusseception.  Volvulus – twisting of bowel on itself.  Intusseception – telescoping of bowel.  Most common in sigmoid colon (?) and caecum. o Colon CA  Blood streaked stool or occult blood, not often hematochasia. o Colonic polyps o Inflammatory Bowel Diseases (Crohn’s, UC)  Common causes of hematochasia. o Diverticulosis/it is  Particularly in older patients. - (Helpful D/Dx – say if have 65 year old with rectal bleeding. Can D/dx from Crohn’s (which is most often in the young)) o Hemorrhoids Most common source of lower GI bleeding. (TQ) Are varicose veins in the rectum/colon. - Varices in the GI tract are the most common cause of GI bleeding, both upper and lower. - Upper most often due to alcohol induced portal hypertension. - (TQ) Lower GI usually due to poor bowel hygiene - Prevention: i. high fiber diet, lots of fluids, and “going when you need to go” (as the urge due to the gastrocolic reflex) Anal fissures  Cracks along the edge of the anus, as due to chronic constipation or inflammatory bowel diseases. 

o •

Hemoccult Testing (GUIAC) o Take home kit. o Stool sample (supplied by Pt), plus guiac reagent. o Blue is positive (remember possible false positive with PeptoBismol) o If the control strip doesn’t turn blue, it’s a bad strip. o Easy to do, but not often done by chiros.

Constipation/Diarrhea • Constipation – “reduction in the production of the volume of stool”. o Large, hard, and dry (brick)

20

Pt usually have fissures and tears More common in females. Most commonly due to poor bowel hygiene (see above). Look for change in bowel habits (normal defecation roughly every 36 hours.) Other causes  Fecal impaction  Poor fiber intake.  Poor fluid intake.  Colon CA • From obstruction. Tends to a constipation/diarrhea cycle.  IBD  Psychiatric causes  Meds • Particularly parasympatholytic drugs (  parasympathetics) or • Sympathomimetic (  sympathetics) drugs  Hemorrhoids • Pain particularly is part of this cycle, as hemorrhoids cause constipation and vice versa. o Tx:  Recommend gentle exercise.  Increase fluid intake (assuming no contraindications)  Increase fiber intake (if not due to inflammatory bowel disease)  Promotion of good bowel hygiene.  Laxatives (natural and prescription) • Avoid if possible, as Pts can become addicted to laxatives, even to the point of needing them to defecate at all. Diarrhea – “Overproduction of (watery) stool” o Infection. o o o o o Viral gastroenteritis (stomach flu and “Montezuma’s Revenge”) is the most common cause of diarrhea.  E. Coli (food poisoning)  Cholera Inflammatory Bowel Diseases (IBD)

o


o

IBS  

UC (LLQ) usually more often than Crohn’s (LRQ), since affects the distal portion of the colon. Accounting for far fewer cases are other forms of IBD: • Collagenous colitis • Lymphocytic colitis • Ischaemic colitis • Diversion colitis • Behçet's syndrome • Infective colitis • Indeterminate colitis Aka mucus colitis Supportive Symptoms of IBS: • Fewer than three bowel movements a week • More than three bowel movements a day • Hard or lumpy stools • Loose (mushy) or watery stools • Straining during a bowel movement • Urgency (having to rush to have a bowel movement)

21

• • • o o

Feeling of incomplete bowel movement Passing mucus (white material) during a bowel movement Abdominal fullness, bloating, or swelling

Stress  Part of the fight or flight syndrome, as the body shuts down all other non-essential functions. Colon CA From obstruction. Tends to a constipation/diarrhea cycle. (Obstruction leads to body flooding bowel with water to flush, the reset to normal, obstruction causes constipation, etc.) (possible TQ) Psychiatric causes Meds  Antibiotic  Laxative Lactose intolerance (TQ)

o o

o

But NOT lipase deficiency (trick TQ)

May 24, 2006
Nausea and Vomiting
• Nausea

o Def: The feeling of impending emesis (yacking, barfing, blowing chunks, praying to the porcelain bowl, ralphing,
spewing, hurling, Singing the College Frat Choir Song, etc.) Cool fact: There is some research supporting that acupuncture may be more effective than shams, and even some meds, in post-op nausea. Vomiting o Def: Emesis – the rapid, retrograde expulsion of stomach contents through the oro- and nasopharynx.  Regurgitation – wet burp  Aspiration – causes pneumonia These are both reflexes (usually defensive in some fashion) o Controlled in the emetic center in the base of the brain (targeted by the anti-emetic drugs) o

Possible causes: (picture of volvulus) o Infectious gastroenteritis – stomach flu (viral in nature) o Obstruction (bowel)  Has to be high in GI to lead to nausea and vomiting.  Lower usually results in distention, constipation, and only in severe, chronic cases leads to nausea and vomiting. • Know that post-stenotic narrowing occurs in a hollow lumen after obstruction (TQ) (post- or pre-stenotic??????) o Pregnancy o o

o o o o

 “Morning sickness” (hyperemesis gravidarum – nonstop vomiting) Severe Pain (and pain medications) Cardiovascular disorders  Angina, MI’s  Body cause vomiting because it doesn’t want to digest food  Vomiting control in the nervous center in the brain stem (emetic center) Meds PUD GI CA Psychiatric d/o

22

o Certain sights, sounds, SMELLS (have you ever BEEN in Deer Park?)
o Honestly almost anything in the GI tract, or almost anything in general (injuries, etc.) can cause nausea and vomiting. Intussuception (Picture) • Telescoping of bowel onto itself. • Sort of looks like a doughnut or bulls-eye on MRI. Heartburn, Indigestion (can be cause by cardiac disease) • Heartburn (pyrosis) o aka dyspepsia – burning pain in chest or epigastrum. • Indigestion o “Upset Stomach” • Possible causes o Gastritis – inflammation of stomach. Common ER diagnosis.  Alcohol, overeating o GERD/Reflux Esophagitis – most common cause of burning chest pain. o Excess intestinal gas (beer) o Gas entrapments (hepatic/splenic flexures) Hepatosplenomegaly • Both organs attached to the portal venous system. o Hence portal venous hypertension will cause enlargement of both. (TQ) o Hepatomegaly m/c is cirrhosis o Lymphoma and hematopoetic diseases tend to affect spleen more than liver. o Other diseases cause both. • Hepatomegaly o Measure by percussion, for example.  10-12 cm usually  Usually can’t palpate the liver border.  In LUQ o Inferior aspect of liver is concave – worry about hepatomegaly if flat or convex. o Magenblase – Ger. “ice cream cone”  Term for the gastric air bubble, right under the left hemidiaphragm.  Will shift down and inwards in a Pt with hepatomegaly. o Common causes:  Cirrhosis  Hepatitis  Most common form is alcoholic hepatitis/alcoholic cirrhosis in US (TQ)  Most common form of INFECTIOUS hepatitis is Hep. C in US o But Hep C is the most common cause worldwide.

 

Pancreatic CA – obstruction of common bile duct Hepatobiliary CA  Cholangitis  Inflammation of the biliary collecting duct  Late right sided CHF  Infectious mononucleosis (Epstein Bar – contagious)  Lymphoma  Leukemia Cause of pancreatitis to have hepatomegaly  compression of pancreomegaly on the common bile duct  incr. portal hypertension

23

Splenomegaly o Part of portal system o Physical filter o Common Causes  Anemias  Removal of abnormal RBC’s  Infectious mononucleosis  From Epstein Barr virus  HIV  Leukemia  Lymphoma  Myeloma  Polycythemia vera and reactive polycythemia (From TX and going snow ski in Colorado)  Increased red cell count (varying degrees)  Clots tend to be the complicating effect.

Hernias • An outpouching of material through a hole (natural or unnatural) • Types: o Groin (most common)

 
-

Inguinal (96%) males Direct (external) worse – acquired Thru weak fascia Indirect (more common) congenital Follow inguinal ring Femoral (4%) - women Umbilical – females (postpartum or gravid or multiparous) (picture) Incisional (2nd common) Hiatal (2nd common) Common locations (picture of hernia types on the body) o Epigastric  Dr. Wyatt has a small one here. o Umbilical

  o o o •

Indirect

Direct

Particularly in pregnant or multiparous females (TQ) If hernia enlarge during valsalva = umbilical hernia (mm contracts that opens the hole)  If hernia disappears during valsalva = intraabdominal o Inguinal  Present in scrotum. o Femoral  M/c in females. • Valsalva maneuver accentuates the hernia. • Hernia Examination in Men (most hernias occur in men) o Fingertip at most dependent portion of scrotum (portion hanging the lowest) o Invaginate scrotal wall to external inguinal ring.  Press up and slightly out into the ring. o Gently insert finger into canal along spermatic cord. o Move finger laterally and cephalad.

24

o

Pt coughs, strains, or performs valsalva maneuver

Pt turns head so that they don’t cough on the Dr. (it’s that simple, turning the head doesn’t change the outcome of the test) o Findings  Inguinal hernia • Small indirect hernia may slightly tap end of finger. • Large indirect hernia may be palpable as mass. • Direct Inguinal hernia may be felt on pad (side) of finger.  Spermatic cord tenderness (Funiculitis)  Spermatic cord lipoma  Hydrocele – water (fluid) in the scrotum; varicocele (bag of worm) • Types of Hernias

o

Indirect inguinal hernia

 Most common type, M=F  Through deep (lateral, internal) inguinal ring (entrance to canal)  Touches fingertip on examination.  Can be difficult to distinguish clinically from direct hernia.

o

Direct inguinal hernia

 M>F  >40 y/o  Though posterior wall of inguinal canal into superficial ring (exit)  Touches side of finger (pad) on examination (since comes through side of canal)  Easily reduced, rarely enters scrotum.

o

Femoral Hernia

 Least common, elderly, F>M (3:1)  Though femoral ring/canal  Often asymptomatic (even when strangulated), but can be very painful in cases. • Can remain asymptommatic until develop peritonitis, etc.

• o o • o

Strangulated hernia A hernia that has become cut off and lost its blood supply. Can lead to necrotic bowel. Mesh hernia repair Sutured mesh tends to patch the hole pretty well. o Like patching a tire (actually, the same tool and underlying process…sorta disturbing, ain’t it?) Hiccoughs • Hiccoughs occur when the glottis closes suddenly when the diaphragm suddenly contracts. • The closing of the glottis stops the air from going down into the lungs and produces the “hiccup” sound. • Transient o High emotion or temperature change. (hot to cold) o Gastric distension

25

o Alcohol ingestion Persistent o Uremia, hyperventilation, IDDM o Meds (steroids, barbiturates) o General anesthesia o Thoracic d/o (pneumonia, CA) o Gastric d/o (PUD, CA) o Causes suicide

Jaundice • Jaundice: abnormal buildup of bilirubin buildup in the body tissues, seen most obviously in sclera (icterus) and skin. o Seen first in sclera since is the “whitest” part of the body, and is among the thinnest. • [picture: bearded white, middle aged male with icterus and jaundice.] • Many also have bilirubinuria. • One side effect is severe itching (little known, but very Bilirubin is formed when red blood cells die and their hemoglobin is broken down within the macrophages to heme and globins. The heme common) (TQ) is further degraded to Fe2+, carbon monoxide and bilirubin via the • Conjugated form – convert into a usable form intermediate compound biliverdin. Since bilirubin is poorly soluble in • Direct Bilirubin (think of liver and surrounding) TQ water, it is carried to the liver and bound to albumin (protein; also o Extrahepatic obstruction found in egg whites). Bilirubin is made water-soluble in the liver by conjugation with glucuronic acid. Conjugated bilirubin, or  Calculi, neoplasm, stricture, cholangitis bilirubinglucuronide, moves into the bile canaliculi of the liver and (inflammation of collecting ducts) then to the gall bladder. When stimulated by eating, bile (including the  Metastatic CA, pancreatic CA conjugated bilirubin) is excreted into the small intestine. In the later o Hepatocellular disease (more common cause) portions of the small intestine (ileum) and the colon, about half of the  Hepatitis bilirubinglucuronide is converted into urobilinogen. Urobilinogen is either reabsorbed or converted by the presence of oxygen to • Alcoholic and otherwise (m/c stercobilin. The stercobilin and remaining bilirubinglucuronide are infectious type is Hepatitis C) excreted in the feces. These two metabolites of bilirubin are what give  Cirrhosis feces their characteristic brown color. Small amounts of urobilinogen o Meds (eg, estrogen) remaining in the blood are filtered by the kidneys, ending up in the o Jaundice of pregnancy (hormonal)  severe urine as urobilin. This bilirubin metabolite gives urine its characteristic yellow color. itching

• Indirect Bilirubin (BM) TQ o Hemolysis (RBC breakdown)
  o Congenital anemias (eg, sickle cell) Acquired anemias Poor marrow production Neonatal jaundice (treated by UV light exposure) Impaired conjugation from meds.

o
o

Rectal Pain and Itching • M/c due to hygiene • Hemorrhoids o m/c organic cause: dilated rectal veins (varicose veins of rectum), both internal/external • Anal Fissure (babies, people with chronic constipation/ diarrhea, anal sex, Crohn’s, UC, etc) • Fecal Impaction (constipation) • Prostatitis (causes anal itching) • Pelvic Inflammatory Disease (causes anal itching) • Endometriosis (causes anal itching)

26

[END GI MATERIAL] GU Signs and Symptoms • CVA (costovertebral angle) pain  kidney disease (stones) • Dysuria • Polyuria • Urethral discharge • Impotence • Hematuria • Oliguria/Anuria • Pelvic Pain • Proteinuria • Scrotal Swelling


• • •

Main parts of GU: kidney, ureter, bladder, urethra Functions: Rid of excess fluids, filter things out of the body that are water soluble Blood pressure is regulated by kidneys as well as electrolyte balance and acid/base balance (angiotension system) Micturition: reflex that tells you to pee Common congenital anomalies: renal cyst, double ureters, only one kidney/ureter

May 31, 2006
Costovertebral Angle (CVA) Pain
• • • Intrarenal failure – within the kidney Post renal failure – after/outside of the kidney
Nephrolithiasis o Kidney stones: Ca+ based – 80% – Murphy’s punch test: kidney infection Calcium oxalate – Mg inhibits oxalate precipitation (and VitA?), but Mg can cause the 2nd m/c type of kidney stones  Mg stones (CLD exam material concurrent with this section)(citrate inhibits Mg precipitation) Pyelonephritis - tubules (waxy casts) o Bladder infection going wild o Infection of renal pelvis – upper UTI o Most common from a poorly treated or untreated lower UTI (usually E.coli) Glomerulonephritis o Inflammation of the basement membrane of the glomerulus - aseptic inflammation, usually after strep pharyngitis Strep A infection m/c cause.  This is why Pt with strep throat must complete their antibiotic treatment (take all of them) o Often mistaken for kidney stone o D/dx? (question for Wyatt) Renal Cancer o AKA: hypernephroma (old term) – one of the fastest growing metastasis Renal abscess o People with chronic renal disease, diabetics (most common), IV drug users, patients with TB Spinal disorder o As from T12/L1 disc herniation Severe back pain can relate to quadratus lumborum o UA would rule out condition

• • • •

27

Dysuria

• Painful or difficult urination Cystitis (Urinary Bladder Infection) o Infasimatacis Cystitis  Air in the bladder wall o E. Coli most common bacteria to cause infection o Diabetics get cystitis a lot o More common in women  Urethra is shorter in women – shorter pathway for bacteria  Wiping from P to A instead of A to P  Holding the urge to pee o In the suprapubic region. Urethritis o Usually infectious o Causes: Gonorrhea (gonococcal urethritis), Chlamydia (M/C cause) (non-specific or non-gonococcal urethritis) Vaginitis o Inflammation of the vaginal introitus (opening)


• •

 Poor hygiene leads to Fungal Infection, m/c Candida Albicans (Yeast Infection) Prostatitis o Bacterial Prostatitis (Septic) o Aseptic Prostatitis  Both very painful  Can be caused by stones  Aseptic prostatitis can be a side effect of overuse (think Sailors on Shore leave)  Thought Keagel exercise may help prevent prostatitis Chemical Irritants o Latex on a condom, Meds, Laundry Detergents, Lubricants, Douche (common in female), Deodorant spray Urethral Diverticulum o Outpouching from a hollow viscus in the ureter (rarely urethra)  Can become infected and cause pain  Can be from high pressure in the system (such as a stone) or congenital weakness in the wall Bladder CA o Usually asymptomatic o Very aggressive

Polyuria • Excess/increased production of urine o Frequency, production, or both o Infection cause pain during urination leads to polyuria because to painful o Renal disorder cause both production(dilute concentration) and frequency o Too much fluid in the body (volume overload)  As from CHF (main cause of volume overload) • Know that clubbing hypertrophic osteoarthropathy (normally associated with CHF) is associated with GI disease, GERD, cardiac, and pulmonary disease (TQ). • Digital clubbing & cyanosis – CHF • Relative term compared to how much pt used to produce • Nocturia – getting up excessively at night to urinate o Usually with a sudden onset in someone who has not had to get up before. • Cystitis/ Lower UTI o Heightens micturation reflex

28

• •

• •

• •

Upper UTI Diabetes Mellitus o Glucose changes the osmolality of the blood o Patient pees a lot o Triad:  Polyuria  Polyphagia  Polydipsia  (Polyneuropathy)  (Polyvasculopathy) (There are actually 5P’s according to Wyatt) Diabetes Insipidus o Lack of anti-diuretic hormone which causes more diuresis (excess production of urine) o Or decreased sensitivity thereto. Meds (diuretics) o Blood pressure control, congestive heart failure (increase in volume lowers ejection fraction) o CHF – give lasik (? Is the generic name)  Polyuria at early stage  Oliguria at late stage b/c can’t get enough blood to the kidney Anxiety o Got to pee when you get nervous Hypokalemia and other electrolyte imbalances o Low serum potassium level o Be very careful if you see a Pt with increased K levels.

Urethral Discharge • Some abnormal fluid from the urethra when not urinating • Discharge can be: o bloody (sanguinous) o clear (serous) o serosanguinous (mixed) o pus (purulent) o Can have an odor

[picture: Gonococcal infection of the penis] (Not too pleasant to see first thing in the morning) • Things within the urethra, along its course, within the prostate gland, etc. can cause discharge. • Prostatitis o Bacterial Infection (septic and aseptic) o Prostatic fluid and/or WBC • UTI o Milky discharge (composed of pus) • Interstitial Cystitis o Most common in Diabetics o Affects interstitial rather than serous tissues • Vaginitis o Yeast infection  o Most commonly from Candida albicans • Gonococcal Urethritis o “The clap”


Historically, a “clap” on the male member was how it was treated. (OW! And ineffective to boot.) Pus, blood, or semen.

29

NGU- Non-gonococcal urethritis o Most commonly due to Chlamydia  M/C STD

June 1, 2006
Impotence (Erectile dysfunction, Ejaculatory dysfunction) - Inability in males to attain or sustain an erection. - Erectile process: o Autonomic NS controls erection o Parasympathetic controls or maintains erection o Sympathetic interference (stress) can prevent from getting erection  However sympathetic system promotes the ejaculatory process.  Mnemonic: “Point and Shoot” o Also remember that as we age the nervous system doesn’t work as well as it did. - Psychogenic o M/C cause of impotence (90%) o Stress  Sympathetic NS overloads the parasympathetic NS. o A side effect of the chronic stress lifestyle that predominates our culture. - Diabetes Mellitus (type I and type II) o M/C other than psychogenic (organic) o Poor blood supply o Micro neuropathies & Micro vasculopathies o 5 P’s – polyuria, polyphagia, polydipsia, polyneuropathy, polyvasculopathies - Vascular Insufficiency o Smokers o Also peripheral insufficiencies


-

LeReischies syndrome – presence of a saddle thrombus at the bifurcation of the common iliac arteries • Leads to poor blood flow to anything lower on the chain, including ischemic effects to the penis and other reproductive organs.

-

-

Medications o Parasympatholytic ( Parasymp) and Sympathomimetic (symp) medications. o Parasympathetic NS controls erection and sympathetic NS controls ejaculation Neurologic disease o Quadriplegic, Paraplegic o Cauda Equina Syndrome (as compressed from a low back injury – the loss of morning erection is one of the earliest signs) o Cancer, Chronic Heart Disease Systemic diseases Prostatectomy o Cut regional nerves innervating penis in about 10% of post surgical cases.

Hematuria – blood in the urine o Two types o Gross (macroscopic) o Microscopic – not seen by the naked eye. - M/C causes is menstruation - Painless has worse prognosis (CA, don’t notice, chronic) - “T.T.I.C.C.S.S.” o Trauma

30

  

o Tumor

Painful hematuria Renal damage (particularly in young people) Severe Exercise • Kidneys will bounce up and down. • Marathon runners frequently present with microscopic hematuria. • Football players clipped hard in the costovertebral angle. • Kidneys can even fracture obliquely in major trauma (MVA) • Intercourse or masturbation can cause hematuria in both sexes, both gross and microscopic.

o

o

o

o o

 Presents as painless hematuria  Bladder Cancer  Renal cell carcinoma Infection  Presents as painful hematuria  Any form of UTI can cause hematuria.  Bladder cystitis is most common  Glomerulonephritis: infectious and noninfectious types. • Secondary to strep throat  red casts  Pyelonephritis  white casts • Infection of the kidneys Calculi  Kidney stones • Calcified stones (gallstones m/c made with cholesterol) • Form b/c of stasis in system that slows the urine down  Happen more often in the summer due to dehydration (from excess perspiration) Cysts (renal)  Over 50% of population has at least 1 renal cyst at autopsy.  Epithelial lined from a couple mm across to 10-12 cm across.  Not the same as polycystic (causes still borne) disease.  Usually asymptomatic, but occasionally can rupture, resulting in hematuria. Surgery in the Urinary tract Sickle Cell Disease (Ischemia, Infarction, and Infection)  Due to abnormally shaped RBC

Oliguria/anuria • Reduced output of urine/absence of urine production (1200 ml/day) • < 100 ml/day = Anuria • < 600 ml/day = Oliguria • M/c cause of oliguria is dehydration, decrease fluid intake, diarrhea. • M/c cause of anuria is renal failure. • Renal failure = DM o TX: dialysis, transplant • Kidney failure = uremia o Affects BP, acid/base balance, electrolytes o Can be fatal if not treated. • Decreased fluid intake = usually oliguria o Can only go w/o fluid for 48-72 hrs (TQ) • Strenuous exercise • Sweat the most when sleeping (besides exercise) • CHF can cause renal failure

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• • •

Pre-renal failure = m/c not enough blood going to kidneys Intrarenal failure = problem in actual kidney Postrenal failure = obstruction past the kidneys

Pelvic Pain - Just the anterior soft tissue, not the bony structure. - M/c in women. - 80-90% of cases are undiagnosed. - M/c cause is inorganic (don’t know) - Treatment of pelvic musculature and joints can help non-organic pelvic pain (supported in urologic data) o A chiropractor hooked up with an Ob/Gyn to treat non-organic pelvic pain can make a mint. - M/c cause = constipation (left side) - Pelvis is triangle b/w both ASIS and pubic symphysis • Dysmenorrhea – m/c organic cause o Abnormally painful menstruation  (All periods are painful to some extent due to uterine contraction) o Cz: thyroid problem, infection, premenopause, fibroids, endometriosis • Fibroids o Benign tumor of uterus Uterine leiomyoma - smooth muscle tumor with fibrous tissue (TQ) Found on plain films of lumbar spine – very common • Look for a “popcorn ball” apperance in the region of the uterus. (TQ)  Can have dysmenorreha, infertility, pain, etc.  Very occasionally possible to become malignant (RARE: leiomyosarcoma) • Hence usually benign (TQ)  Can be VERY large (largest at 350 lbs in one Pt), and even can make women think they are pregnant (TQ) Adhesions after surgery Cystitis o Suprapubic region o M/c cause: E. coli Endometriosis o Abnormal deposition of ectopic endometrial tissue outside of the uterus IBD o Crohn’s, Ulcerative Colitis 

• • • •

Proteinuria • Not normally in urine because it’s too large • Occurs w/damage to basement membrane (in the glomerulus) • Malignant HTN: Increased BP, enough to cause tissue damage • Idiopathic proteinuria o Ok if everything else has been ruled out o Ok if it’s mild

Nephrotic syndrome - classically associated with proteinuria (waxy casts) o Post strept o Diffuse swelling associated with proteinuria o Associated with renal failure o Sicker than Pts with nephritic syndrome. o Nephritic syndrome secondary to glomerulonephritis o Nephrotic – non inflammatory, nephritic – inflammatory o But both allow proteinuria o The difference is not heavily hit on Exam 1.

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• • • • • • • • • • •

Malignant HTN CHF Diabetes mellitus (know the 5 P’s) Sickle cell disease • 3 things that occur with sickle cell: Infection, Ischemia, Infarction Idiopathic proteinuria Pyelonephritis (m/c from UTI from E.coli) • Ascending infection from bladder Glomerulonephritis • Most commonly post-strep infection. (important point) Pregnancy (can be an early onset sign/risk for ecclampsia and pre-eclampisa) Myeloma • Pt’s produce Bence Jones proteins, which are small enough to naturally go through the glomerulus Leukemia Lymphoma

Scrotal Swelling (pictures) • Swelling of either scrotal sac or the growth of a mass that actually causes enlargement (as with hernias) • Testicular torsion o Spermatic cord & vessels twist on themselves (volvulus) o Can lead to infarction in the testicle – very painful (GREAT GOOGLY MOOGLY!) • Epididymitis o Epidydymis – storage system on the back of the testicle – so inflammation thereof. o Can occur from STD’s and other infections.

• •
• • • •

Trauma (m/c) o MVA, sport injuries. Infection (2nd m/c) o Mumps virus (Cox sackie virus) o Hernia Tumor o Testicular carcinoma • Very aggressive tumor, which can occur in relatively young men. Varicocele o “Bag of worms” palpation feel due to varicose veins in the pampiniform plexus Hydrocele o Dilated, cystic mass o Transilluminates easily. o Fluid filled, tubular cysts Swelling of the sack o allergies

Notes for Test One: Know which tumors arise from which tissues (as carcinoma from endothelial tissue) He likes comparisons. Maximal measurement for AA – 3.5 cm. Up to 5 cm, watch. Over 7 – chance of rupture in next 6 months. Symptoms of AAA (pt can’t find comfortable position, loss of lower limb pulses, low pitched bruits, etc.) 2 ways to check for ascites (fluid wave and…) Puddle sign (for small amounts of ascites) – pt on all 4’s. Draw filtration system (joking?) 40 questions, M/C, T/F

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[END TEST ONE] [Begin Exam 2 Material]
June 8, 2006 Esophagus
• Description in 5 words or less: Hollow, food propelling muscular tube • [picture: ESOPHAGOGASTRODUODENOSCOPY (EGD) of esophagus with varices (usually caused by alcoholic induced portal HTN) • First tubular viscus, begins as pharynx (pharngoesophageal junction) • Anatomy o Pharynx o Upper esophageal sphincter  Epiglottis o Esophagus o Lower esophageal sphincter at gastroesophageal junction.  Aka: Cardiac Sphincter • Normal Esophagus o 1° peristalsis Initiated by swallowing (scientific name: deglutition) – voluntarily initiated. • Soft palate, tongue assisted.  Propels food • Strong propagating propulsive wave o 2° peristalsis  Not initiated by swallowing – involuntarily initiated.  Propels food through lower esophagus o 3° peristalsis  Seen in elderly, abnormal  No propulsion – a feeble attempt at secondary peristalsis.  D/t degeneration of the nervous plexes and smooth muscle in the esophagus.  Similar to the fibrillation seen in a ventricular arrhythmia – just quivers. Esophageal Functions o Lower esophageal sphincter at level of diaphragm. o Esophagus contains smooth muscle.  Unique because it’s voluntary (almost the only instance of voluntary smooth muscle control) Esophageal Tumors o Normally not a very metabolically active area – purely propulsionary, no digestion occurs there. o As we age, the lower esophagus is exposed to years of reflux (everyone has it to some extent). o Of those that do occur, most tumors are found in the lower esophagus and 90% of them are malignant. Esophageal Neoplasms o Malignant tumors are the most common. (90%)

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o o o o

o

o o o o

High mortality rate, since are hollow organs and not well innervated (pain generation by a tumor) – hence pain only occurs when tumor grows beyond capsule or capsule is distended from tumor growth. S/sx usually only occur after 75% of the diameter of the lumen is occluded by growth.  Cost benefit must be done to determine whether or not it is prudent to screen EVERY Pt EVERY year for these tumors. • But costs are usually high (EGD’s) and these are rare, so the cost benefit is not good for yearly screening.  Fecal occult blood testing routinely done (as a general screen).  Also remember (takehome message from this class): any male over 40 with Iron deficiency type anemia has a malignancy until proven otherwise. Leiomyoma is the m/c benign tumor Most tumors occur in the lower esophagus Squamous cell carcinoma is m/c 7.6/100,000 in USA  But this rate has increased in the last 25 years or so. • D/t increasing popularity of BBQ’ing (or blackening) of food – the burning increases the nitrate concentration. (also a theory on acrylamide responsibility in smoked foods) 130/100,000 in China  D/t the processing of the foods in that area of the world – most smoking and pickling, which includes a lot of nitrates, which has a metaplastic effect on the esophageal epithelia. M:F 3:1 Most Pts >60 yoa. Dysphagia to solid and later fluid is due to esophageal dysfunctions Dysphagia to both fluid and solid is due to neurological condition 

Esophageal Carcinoma (Cancer) o Etiology  Alcohol abuse association w/ 80-90% of cases  Cigarette smoking • Aerophagia and swallowing saliva exposed to smoke, w/ all the oxidative radicals.  Nitrate ingestion. • Smoked or burned foods, pickled foods  Chronic achalasia • Poor relaxation of the lower esophageal sphincter (LES) • Spasm in LES, which closes – food just sits in the lower esophagus, with a fermenting effect in the static bolus, which in turn leads to damage. • Lead to bad breath  Chronic GERD • May or may not lead to Barrett’s esophagus o Dysplasia from squamous to columnar epithelia. o Associated with adenocarcinoma. o D/Dx (think S/sx of obstruction)  Achalasia (particularly in the elderly)  DES – Diffuse Esophageal Spasm • Think of chest pain when eating ice cream too fast – like that for hours on end. • Also a D/Dx for MI.  Esophageal rings • Congenital rings that narrow portions of the esophagus.  Scleroderma • Progressive systemic sclerosis (PSS) – connective tissue arthropathy, causing calcification in the digits. • Taut red skin (fingertips become pencil like, and may fall off, as well as the nose)

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o Stages of Malignancy:  Stage 1: Well contain within an organ  Stage 2: lymph node on same side  Stage 3: Lymph node on opposite side  Stage 4: Distant metastasis to another organ. o [picture: adenocarcinoma]
o Physical findings  Dysphagia (first for solids, then liquid) • Liquids can move around an obstructive mass early. o If liquid dysphagia right off the bat, think paralysis of some sort (or acute, massive obstruction).  Weight loss • Usually in late stage disease. [cachexia (wasting)]  Cervical adenopathy • Like a Virchow’s node (sentinel node in the left supraclavicular space for lymphadenopathy)  Hematemesisj(throw up blood)/hemoptysis (cough up blood)  Hoarseness • Damage from reflux • Extension of tumor into trachea, larynx, or recurrent laryngeal nerve (larynx innervation)  Cough w/ clear sputum  Mets from Esophageal cancer go to liver, pleura, lungs w/ associated S/sx • Since both drained by portal venous system.

70% of Pts with PSS have esophageal involvement – which becomes hard and inflexible.

June 12, 2006
o Diagnostic Imaging  Double contrast esophagram • Barium paste used. The bolus is then followed. • Looking for “shouldering” – a square cut off at the beginning of a lesion between it and the soft tissue. • This is now rarely used, normally an EGD is done (which also allows the obtaining of a biopsy.)  Esophagoscopy  Chest/abdominal CT  Abdominal MRI Laboratory tests  CBC  Blood chemistries  Liver enzymes. Treatment Resection if no mets – en bloc resection  Stomach/colon used for replacement  Radiation therapy  Chemotherapy. Prognosis  Surgery – 20-50% • Stage 1 or stage 2 • 50% effective  Radiation – 6-20%  Chemotherapy – 15-80%

o

o

o

36

Benign Esophageal Tumors o Tumor types  Sessile (broad based) or pedunculated  Leiomyoma is most common  Papilloma  Fibrovascular polyps o Very rare.

Esophagitis 1. Reflux esophagitis 2. Acute ulcerative esophagitis 3. Esophageal PUD 4. Crohn’s esophagitis 5. Infectious esophagitis 6. Chemical esophagitis 7. Mechanical esophagitis • Reflux esophagitis Reflux of gastric contents w/ permanent damage Progression of GERD

o
o

Possible progression to Barrett’s esophagus (squamous to columnar epithelial metaplasia) o Incompetent LES o Often associated with hiatal hernia (50-70%) o 30-60’ post-parandial/reclining heartburn. • Acute Ulcerative Esophagitis o Seen in Pts with PUD (tend to vomit a lot) o Contracted fibrotic lower esophagus results.

Results in stricture – mimics achalasia (nonrelaxation of the lower esophageal sphincter)

Infectious Esophagitis Immunosupressed Pts (picture)  AIDS  Malignancies and other chronic systemic illnesses.  Diabetes  Transplant – on anti-rejection drugs. o Organisms (3 primary) (picture)  Herpes simplex  Candida albicans  CMV (cytomegalovirus) o Dysphagia, odynophagia (painful swallowing), chest pain. o Treated with antibiotics.

o

Mechanical Esophagitis (picture of two safety pins stuck together) o Swallowed object becomes lodged. o Lodge at narrowed portions

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3 most common: Cardiac sphincter, thoracic inlet, at the aortic knob area • Also: Left atrial enlargement secondary to CHF impinges upon esophagus. o Objects include coins, pills, bone pieces o Leads to ulceration, maybe perforation. Miscellaneous Esophageal Conditions • Esophageal Varicies (picture) o Varicose veins of the esophagus o Lower 1/3 submucosal veins involved o 1/3 of Pts bleed o Caused by portal HTN by hepatic cirrhosis o 2nd to alcoholic o Highest mortality of any UGI bleed o Coffee ground emesis, hematemesis (or combo or neither) o Treated with sclerotherapy (via endoscope), compression (Balloon tamponade), rubber band ligation.

o 

Esophageal Diverticula Diverticula – out pouching of a hollow viscous.

Something either pushing from the inside or something pulling from the outside to pull the blind end pouch out.  Appendicitis is most common. o Usually acquired o Two types

 •

Traction (pulled from outside of viscus) When esophagus contracts during peristalsis and esophagus is has external adhesion cause traction. • Source from in the mediastinum, such as inflammation and subsequent fibrosis of lymph nodes (paraesophageal)  Pulsion (pushed from inside the viscus) • Pressure push on weak wall • Usually upper 1/3 of esophagus o Occur anywhere in esophagus  Middle esophageal are traction  Upper/lower are pulsion • Zenker’s Diverticulum (picture) o Pulsion type o Occurs at pharyngoesophageal junction o Loss of upper esophageal sphincter laxity. o Retains food o Can get large, to the point of looking like a gall bladder at the esophagopharyngeal junction. o S/sx

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  


be in incline)

Halitosis Spontaneous regurgitation Noctural choking The position they are in (Need to

Recommended not to eat within a few hours before bedtime  Neck mass • Can sometimes see peristalsis in the mass  Neck mass (particularly when eating) o Complications cause by regurgitation during sleep and laying on the stomach  aspiration (particulate matter into the lungs) • Causes abcess and bronchiectasis.  Aspiration (inhaling something that wasn’t there  Aspiration pneumonia – which has a high mortality rate)  Abscess (walled off chronic infection)  Bronchiectasis (chronic obstruction of the air flow that results in fluid build up  infection; 3 layered mucous (trilayers sputum), foul smelling sputum) Miscellaneous Diverticula - Epiphrenic Diverticulum o Occur in lower esophagus o Normally asymptomatic and small - Middle Esophageal Diverticulum o Usually traction o From mediastinal lymphadenitis

June 12, 2006 (2nd Hour)
G.E.R.D. - GERD  reflux esophagitis  Barrett’s esophagus.  Esophageal. CA  always rule out cardiac Disease first - Cough & bronchospasm or laryngitis from aspiration - Early satiety GERD  get “full” quickly - Chocolate  fat & caffeine contents cause GERD episode - Tobacco  when chemicals are swallowed - Commonly assoc. with hiatal hernia (>70%) - Nitroglycerin  will make anginal chest pain better o Makes GERD chest pain worse - Gastroesophageal Reflux Disease - Reflux of gastric contents into lower esophagus - Incompetent lower esophageal sphincter o Stuff from your stomach comes back up into the lower esophagus because the esophageal sphincter is not functioning correctly o Believes because of aging o Reflux Esophagitis  Barrett’s Esophagus  Squamous cell carcinoma o Heavier a person is the more chance they can have because increase in intra-abdominal pressure - Incidence o 60% of adults have heartburn o 80% of pregnant women have GERD - S/Sx o Heartburn (pyrosis) (burning pain the middle of the chest) o Dysphagia o Regurgitation

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-

-

-

-

 Sour taste in the mouth  Pt can also have excessive salivation (as a pseudo-Pavlovian response) o Can be confused with angina pectoris o Chronic cough  Refluxant comes up into larynx o Bronchospasm, due to irritation of the bronchi airway o Laryngitis (yes, from reflux – call it, “Mexican Food Induced Laryngitis”) o Early Satiety (Getting full fast) o Belching/Bloating Contributing Factors o Chocolate (caffeine and fat), Yellow Onions (particularly raw), Peppermint (oil), Garlic o Tobacco (nicotine and causes sphincter to relax), Alcohol (fat and causes sphincter to relax), Caffeine (anything caffeinated)  Spicy foods make the reflux more irritative, but doesn’t CAUSE reflux itself. o 70% of GERD suffers have a hiatal hernia (usually sliding type) o Beta Blockers (control BP and angina), Ca++ Channel Blockers, nitroglycerin  Causes dilation of lower esophageal sphincter (since are systemic smooth muscle relaxants and are not specific for cardiac muscle.) o Gastric Acid Hypersecretion Diagnosis o 24 esophageal pH monitoring o E.G.D. – final Dx for GERD o U.G.I o Manometry, (pressure measurement) to rule out diffuse esophageal spasms Treatment o Avoid triggers (diet modification) (most effective Tx honestly) o Proton pump inhibitors o H2-blockers (cimetidine – Prilosec ) o Antacids o Fundoplication  Reserved for pts with daily reflux (chronic intractable)  Stomach is wrapped around esophagus and sutured in place.  Three types • Nissen (complete) • Posterior (partial) • Anterior (partial) o Drink excessive amount of water, water helps to dilute the acid and provide weight to the stomach to pull the hiatal hernia down. Columnar epithelium in the Can result in esophageal strictures etc. if untreated. esophagus has a characteristic red
color and velvet-like texture (grossly indistinguishable from the normal lining of the stomach) that contrast sharply with the pale, glossy appearance of the adjacent squamous epithelium. Endoscopists recognize Barrett's esophagus when they see reddish epithelium extending above the anatomic gastroesophageal junction well into the distal esophagus. In this endoscopic photograph, the metaplastic columnar lining is seen tc extend up the esophagus in the form of flame-shaped tongues. The esophageal columnar epithelium also may take the form of a circumferential sheet, and islands of columnar mucosa occasionally are observed surrounded by squamous epithelium in the distal esophagus.

BARRETT’S ESOPHAGUS
Pre-malignant Associated with chronic reflux (5-10% incidence) Stratified squamous manifests to columnar epithelium, a precancerous condition Increased risk of adenocarcinoma o 30-50 times increased risk to develop adenocarcinoma of the esophagus o 500/100,000 people with Barrett’s esophagus will progress to adenocarcinoma. Dx o EGD, biopsy almost always accompanies an EGD

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o o o o

Biopsy Rx Laser Ablation Fundoplication Surgical Resection (En Bloc if area is large enough)

ESOPHAGEAL MOTOR DISORDERS
The Esophagus is a neural driven muscular system involved in Primary peristalsis (initiated by swallowing) and secondary peristalsis (initiated by presence of food bolus or liquid in pharynx) Possible disorders include: o Achalasia o Scleroderma o Diffuse Esophageal Spasms

ESOPHAGEAL ACHALASIA
Spasm (shut tight) of lower esophagus with pre-stenotic dilation which makes peristalsis ineffective (Inability of LES to relax, leading to storage of food product in the lower esophagus.) Chest pain can occur when peristalsis is attempted o Pain usually colicky Functional esophageal obstruction Inadequate relaxation of the LES Ineffective Peristalsis 1/100,000 incidence; 30-50 y/o S/Sx o Solid/liquid dysphagia, patient indicates they can feel the food sticking usually in the lower chest  Dysphagia for liquids and solids suggests a motor disorder.  Dysphagia for solids that PROGRESSES to liquids suggests an obstruction (growing). o Chest pain  D/dx for angina. o Vomiting of undigested food o Aspiration, can develop pneumonia, abcesses, bronchoastasis and die o May be confused with angina o Colicky type pain  Crescendo/decrescendo type pain  Stone, Ureters Etiology o Degeneration of myenteric plexus  Viral • Herpes Zoster • Measles Virus  Autoimmune o Not completely understood, true etiology not known Diagnosis o EGD with manometry o UGI

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o Tests to rule out other causes (eg: EKG for cardiac differential)  Especially with age group one wants to rule out MI Treatment o Medical  Smooth muscle relaxants (70% effective) • Nitrates • Calcium channel blockers • Botulinum toxins injection  Mechanical dilation (90% effective) • Bouginage (mechanical dilation by balloon)  Esophagomyotomy (90% effective), incise into the muscle (sphincter – draw back, reflux) Prognosis o Excellent with appropriate Rx o Long standing Disease increases risk of CA

SCLERODERMA Aka: progressive systemic sclerosis (PSS)
Means hardening of the skin and other tissues. o Primarily (most obviously) effects the skin, but is not limited to the skin o Tissue thickens and hardens  ANY connective tissue can be affected, even those holding in their teeth and vascular tissue. o Tends to onset in girls in their late teens to women in their early 20’s.  Runs a harsh course over 20-25 years. (not immediately fatal, but progressive difficulty). o Severe hardening of lips to point must be tube feed in late stages. o Tight, red, hard, fibrotic skin. o Fingers will come to a point, like a pencil and may tips may fall off. (a hallmark sign)  Radiographically, the distal tuft of finger is lost – with the bone of the phalanges coming right to the end of the finger with almost no soft tissue between bone and skin. • Flocculant calcifications in the para-articular distal fingertips.  Same applies to tip of nose. o Affects the esophagus in 3/4 of cases.  Hardening decreases peristalsis, leading to dysphagia, reflux, regurgitation Sometimes must replace the esophagus o Peristalsis is affected, thus difficulty in swallowing, reflux Kidneys are often affected as well Vessels become calcified, thickened and hardened Female > Male, Early teens to 20’s Smooth mm relaxants used if esophagus does not need replacing, patient receives temporary relief, usually do not work

The CREST syndrome is a variant of scleroderma. The acronym stands for Calcinosis, Raynauds’s phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasias. By definition, therefore, the full-blown syndrome always involves the esophagus. This slide illustrates the calcinosis (left panel) and Raynauds’s phenomenon (right panel) typical of CREST syndrome. [Reprinted from the Clinical Slide Collection on the Rheumatic Diseases, copyright 1991. Used by permission of the American College of Rheumatology.]

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o o o o o o o o -

Multisystem disorder often affecting the esophagus Lose ability to have peristalsis Becomes very narrow and can develop strictures EGD used to diagnose 75% have esophageal involvement Fibrosis and inelasticity results Signs & Symptoms Dysphagia Esophageal reflux/regurgitation S/Sx associated with scleroderma Diagnosis EGD UGI Tx with smooth muscle relaxants, but there is no cure. Etiology - unknown

DIFFUSE ESOPHAGEAL SPASM
o Diffuse sustained contraction (spasm) of esophagus Essentially an esophageal fibrillation. Ice cream eating too fast is the same pain, “brain freeze” So this is “Chest Freeze” Pain lasts minutes to hours Usually end up in the ER thinking they are having a cardiac

o

problem Etiology unknown Can be confused with angina pectoris o These people think they are dying. S/sx o Substernal chest pain o Dysphagia with pain, worsened by swallowing, key differentiating feature o Regurgitation Dx o EGD (Esophago-gastro-duodeno-scopy) o UGI o With barium swallow on x-ray appears as a cork screw Tx/Rx with Ca++ channel blockers/nitrates o But causes patient to have reflux

June 15, 2006
DISEASES OF THE STOMACH - Gastric Tamponade (fluid around the heart  ventricles and atria can’t contract)
o o o o A pressure equilibrium develops outside the heart as inside Blood in the stomach from pills Can lose 3-5 cc of blood per aspirin or other NSAID “Coated” so that it will pass the stomach and be absorbed in the small bowel

GASTRIC ANATOMY

43

o Stomach  B12 absorption (intrinsic factor), storage, mixing,
mineral absorption, protein breakdown o Rugae  increases surface area inside the stomach for production of HCl and pepsin , o GE Junction o Gastroesophageal Reflux Disease o Fundus o Usually holds gas

“Magenblase”  air in the stomach (in upper left stomach, near hemidiaphragm) at the fundus area o Antrum o Pylorus o Narrowed portion of the distal most aspect of the stomach o Pyloric Sphincter  b/w stomach and duodenum  help prevent outflow of gastric juices that could lead to PUD o Pyloric stenosis  prevents outflow, causes regurgitation o Curvatures  Lesser curvature  Greater curvature • More metabolically active (because of where food sits) • Also where most of the diseases of the stomach occur, for the same reasons. o Estimated that 3 – 5 cc of blood is lost with each aspirin taken that is not buffered o Layers to the stomach (4) o Mucosa, submucosa, muscle layer, serosa (inner to outermost)

EGD ANATTOMY
Normal antrum and pylorus (pictures) GASTRIC PERISTALSIS GASTRIC TUMORS

June 21, 2006
GASTRIC CANCER 90% of tumors in the esophagus are malignant Occurs anywhere in the stomach o With a greater occurrence in the greater curvature of the stomach due to the gravity of material to this area of greater metabolism Incidence of proximal CA is increasing in the US (almost logrhythmically) 2 - 4X more common in 1st degree relatives Male : Female 1.6:1 > 55 y/o

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-

7/100,000/year (not all that common) Most common in blood group A No symptom complex presented early in the disease Pictures: Linitis Plastica, an invasive form of gastric carcinoma , not a single tumor mass, the tumor cells spread throughout the entire stomach without causing a single tumor. o Aggressive, Infiltrated carcinoma  invades entire organ and cause thickening of entire organ - rarely found before stage 3 or 4 o S/SX  Cramps  Loss of appetite  Very low bleeding  No ulceration  Poor intrinsic factor production Risk factors o Diet rich in additives (smoked, pickled) (increased level of nitrates) o Atrophic gastritis  Inflammatory disease of the stomach where there is atrophy of the rugae  Sequela : B12 deficiency  pernicious anemia o Pernicious anemia o Tobacco use o Hispanic, Japanese o Polyps  Growth into lumen  Sessile and pedunculated  Usually premalignant mass (some benign) o H. pylori infection (PUD associated with H. pylori) o Barrett’s Esophagus o [picture: Linitus Plastica – thickened wall of the stomach leading to decreased pliability, d/t an invasive malignancy (non-focal mass, which instead invades whole thickness of the gastric wall)] DX o Stool guaiac test  test for blood o Any male > 40 with anemia, has GI malignancy until proven otherwise

GASTRIC CANCER S/SX
-

o
o

-

Adenocarcinoma tends to mets to bone and organs 18% survival but 50% survival if caught in stage 1 but usually not caught in stage 1 because there are not s/sx Chronic non-colicky (colicky pain crescendo decrescendo) epigastric

pain Anorexia Pain unrelieved by antacids o Helps to differentiate from ulcers or reflux, both of which are often relieved by the use of antacids Pain exacerbated by food o Opposite of gastric ulcer, where eating alleviates pain. (D/dx for gastric ulcer) Pain relieved by fasting

45

o o -

-

Dysphagia When this tumor is near proximal stomach (the fundus) Nausea and Vomiting From bleeding (coffee brown) Constipation Early Satiety  feeling full comes from hypothalamus [Picture] Ulcer mass greater than 1 cm in width, thus increasing the risk for gastric cancer dramatically When a tumor out grows it’s own blood supply the area becomes ischemic and ulcerates

GASTRIC CANCER DIAGNOSIS
Positive stool guaiac (blood to stool content) o FOB, fecal occult blood test  Will have black tarry stool if blood occurs in the stool Hemoglobin <12g/dl Hematocrit <35 EGD o Most produce a lot of blood. UGI (not done very often anymore) CT/MRI for nodes/mets o Spine, chest, and other places in the abdomen (liver) are most common, but can go anywhere.

-

Any male over the age 40 who is anemic has a GI malignancy until proven otherwise (blood loss from the malignancy)

GASTRIC CA PATHOLOGY
Adenocarcinoma 90% o Due to the abundance of glandular tissue, {adeno-, glandular} Lymphoma 6% o Malignancy of lymphocytes {mediastinum area is the most common area for a lymphoma} o Hodgekin o Non-Hodgekin lymphoma Gastric Sarcoma < 4% Leiomyosarcoma < 1 %

GASTRIC CA TREATMENT
Surgical resection, quite often an en bloc gastrectomy (resect until healthy tissue is found) Node resection (when larger then 1cm) Radiation non-beneficial (tumors are non-sensitivity to radiation) Chemotherapy non beneficial o Research has shown this treatment has very low benefit for gastric cancer. o Chemotherapy is designed to “attack” fast growing tissue.

GASTRIC CA PROGNOSIS
No S/sx until late in course, primarily due to the size of the hollow organ. It takes a rather large amount before it interferes with the function of the stomach. Therefore survival rates are typically low. 18% 5 year survival rate o 57% with local Disease (stage I)

46

o o

19% with regional spread (stage II) 2% with distal mets (staged III)

BENIGN GASTRIC TUMORS Leiomyoma – fibroid tissue usually found in the uterus, benign tumor
of smooth muscle o Common tumor o Rarely symptomatic o Only with obstruction o Usual in esophagus and stomach. (where smooth muscle is) o Symptoms usually only occur when the mass is in the pylorus (where it’s small), otherwise, they tend to be symptomless for the most part (as the mass of the organ is not altered by it.) Adenoma – benign tumor of glandular tissue, aka polyps o Polyps o Most of the stomach are hyperplastic (an adenoma with an increase in the number of cells – a reaction to chronic gastritis – a reaction to chronic inflammation) o Hamartoma – localized overgrowth of normal tissue.  Ex: osteoma in the skull.  Likewise, these GI overgrowths are qualified as Hamartomas o Most remain benign o Can obstruct o Over 2cm, have malignant potential.  If degenerate, to adenocarcinoma o More commonly in the small bowel (where the glandular tissue is) GASTRITIS - Gastritis is a “catch-all” term. o Most common emergency room Dx for abdominal pain. o Septsis (bacterial) or nonseptsis (non-bacterial) - Gastritis has: o Erythema – reddening o Hemorrhage o Erosions - Types o Erosive o Non-erosive, non-specific o Specific - S/sx o Post-prandial (after eating) indigestion/pain (dyspepsia) o Nausea and vomiting o Bloating - 50% have H. pylori (spiral shaped bacteria)

Atrophic gastritis – associated with anemia

EROSIVE GASTRITIS Etiology o NSAID’s  Gastric bleeding occurs frequently with all NSAIDs, but more frequently with the COX1 inhibitors than COX2.

47

 5 ml.

Each non-buffered aspirin reduces blood supply by 3-

Buffered: has a gelatinous coating that allows the drug to be broken down in the small bowel, as opposed to the stomach (gelatin as a carb is broken down in small intestine rather than the stomach). o Alcohol(ism) d/t portal HTN  Venous congestion decreases the removal of waste from the stomach blood supply. o Stress from major illness (burns, multi trauma from MVA) Hemorrhage also common with this Disease Usually asymptomatic Can produce pain, hematemesis, nausea/vomiting Diagnosed with EGD NON EROSIVE, NON SPECIFIC (Common from over eating) - H. pylori gastritis o Spiral gram (-) rod o Causes acute superficial mucosal Disease  Also purported to contributed to Peptic Ulcer Disease (PUD) o S/sx  Nausea and vomiting  Pain - Atrophic gastritis o Associated with pernicious anemia – not producing enough intrinsic factor o Autoimmune, achlorhydria (absence or reduction of HCl in stomach) o Glandular hypertrophy and metaplasia o 3x increase in gastric adenocarcinoma over the general population SPECIFIC GASTRITIS Ménétrier’s Disease o Giant fold gastritis (the rugae become very large, (friggin huge)) o Enlarged, thickened gastric rugae  Get hypoproteinemia due to enlarged rugae • Causes edema, pleural effusions, and other 3rd space fluid effusions,etc. • This causes an overload on the kidneys and heart, leading to heart and renal failure. o Severe protein loss  Proteins are metabolized in stomach o Hypoproteinemia o Idiopathic Granulomatous gastritis o Crohn’s Disease (a chronic inflammatory granulomatous bowel Disease) o TB o Sarcoidiosis  (idiopathic autoimmune disease that normally affects the lymph nodes of the chest, found primarily in young black males) o Tx: Treat the specific disorder Phlegmonous gastritis (nastiest you can ever have)

48

o o o o o o

Chronic abscess. Phlegmon – aggressive large abscess Abscess from fungal, bacterial, parasitic infection Emergent gastrectomy and IV antibiotics Treatment is the removal of the stomach. Common among AIDS patients (the immunosuppressed)

June 22, 2006
PEPTIC ULCER DISEASE Def: Ulceration of the stomach or duodenum  “Ulcer Crater” - Ulcer  an erosive crater that penetrates the lining of a hollow viscus o Most common in the stomach (and duodenum) o Typically < 1 cm o Larger than 2 cm  malignant potential - Go through at least the mucosal layer - Malignant ulcer  malignant tissue with an ulcer inside of it - Normal acid production with lowered protection  ulcers - Normal protection with overproduction of acid  ulcers Epidemiology (study of the incidence of the disease) - Imbalance between protection and damage, a decrease in the protective mechanism or an increase in the amount of HCl being produced – either case will lead to ulcerations of the stomach mucosa - Gastric chemical secretion o Helps digest proteins, damaging to lining with good protection  Hydrochloric acid  Pepsin o Stimulated by acetylcholine (acetylcholine production is increased with stress as is the HCl thus a double negative), gastrin, histamine, stomatostatin (buffers gastrin production) - Other ulcerogenic substances o Bile acids, reflux of bile into the stomach, thus the reason for their being found in the pyloric bulb o Pancreatic enzymes - Normal Protection o Good blood flow  Helps clear chemicals and helps with healthy cell turnover  Diabetics do not have good blood flow, and hence are prone to ulcers o Normal cell renewal Diabetics do not  prone to ulcers  Chemo patients - 500,000 new peptic ulcers are dx each year - Duodenal ulcers are more common than Gastric ulcers (2:1) Predisposing factors o High stress (anxiety)  Increase in histamine causes increased acid production  Activates sympathetics and shunt blood away from stomach o Cigarette Smoking  Swallowed chemicals  Also causes vasoconstriction (impair blood flow, etc.) o NSAID use

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 Irritating to the gastric mucosa – COX inhibitors stop prostaglandin production which stops blood flow to the stomach and inhibits protection to lining o Delayed gastric emptying  Food stays in stomach & irritates • Common in Diabetics o Decreased bowel function, high incident of PUD d/t the microneuropathies. - H. pylori (produces urease) there is a inferred or coincidental correlation between H. pylori existence and ulcers o Increases gastric acid secretion o 75% of patients are infected with H. pylori o 75% have recurrence in 1 year without antibiotics o 20% have recurrence in 1 year with antibiotics  Suspect that the H. pylori are the main etiologic agent.  Most likely, though, that the H. pylori really just makes the situation worse, as opposed to being the initial causative agent.  Wyatt suggests that H. pylori is a natural endogenous flora to the GI tract, but that it is opportunistic with impairment of the protection mechanisms of the stomach. - NSAID use o Cause decrease bicarbonate the base which counter acts stomach acid and pepsin, mucus and blood flow o Aspirin is most ulcerogenic, buffered aspirin helps protect stomach but still begins to break down in the duodenum thus the increase in ulcers in this area o 40x increased risk of PUD over the general population.  However chronic use of NSAIDs in the US may ACTUALLY be the reason that peptic ulcer disease has become so common in the US. - Peptic ulcers o Usually effect the mucosa and submucosa (about 1-2 mm deep) o But spares muscular layer in most cases.

But can if progresses, even to perforation.

Gastric Bleeding (photo)
Blood is very irritating to the stomach, thus bleeding in the stomach Signs and Symptoms - Epigastric Pain. o Usually described as:  Burning  Gnawing  Cramping - Relieved by foods and or antacids (in the short term - Pt can become addicted) o Gastric ulcers - eating makes it better o Duodenal ulcers - eating makes it worse ???? - Pain is clustered (days-weeks) - Long symptom free periods (weeks-months-years) - Changes in pain (RED FLAG) o If relapse and pain is worse this time, may mean 1 of 2 things:  May mean CA (or other malignancy)  May mean ulcer may perforate.

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Differential Diagnosis (other things that cause epigastric pain (burning, gnawing, etc.)) - GERD (esophagogastroduodenoscopy) - Reflux Esophagitis, most common condition confused with PUD - Gastric CA, particularly if there is a change in the pain pattern - Gastritis - Pancreatitis - Cholecystitis - Cardiac disease (don’t forget this one) Diagnostic Workup Endoscopy o Esophagogastroduodenoscopy (EGD), almost universally the means of diagnosis o 95% accurate (5% due to human error) o Biopsy ALL lesions o Cancer: benign vs. malignant cannot be differentially diagnosed by sight  More ragged the edge, the larger – the more likely is malignant. o Also biopsy for H. pylori Upper GI series o BaSO4 swallow, then X-ray results. o Not as reliable as EGD o No biopsy capabilities. o Not used much anymore. Treatment - Antibiotic therapy (clarithromycin – which is harsh on the stomach lining) - Omeprazole (Prevacid) - H+ pump inhibitors - Stop Smoking - Stop NSAID use - Stop/minimal antacid use o Not good in long term. Is addictive (gastric mucosa becomes so used to antacid, you have functionally altered it and decreased it’s effectiveness) o Also some risk of aluminum toxicity and hypercalcemia. - Diet Changes o Bland Diet o Don’t use milk anymore, because the sugar in it can help feed the bacterial and can actually make the ulcer worse in the long run.  Milk produce lots of mucous - Stress Reduction o Because of sympathetic reaction o Valium (classic drug prescribed) - Manipulation in conjunction with medical therapy has been proven beneficial to the patient COMPLICATIONS (“da stuff dat will bite you in da azz”) - GI Hemorrhage o Most common (50% of all UGI bleeding)  Ulcer is m/c  Varices is 2nd o 80% stop bleeding spontaneously

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10-20% is bleeding clinically significant  Cause sx and problems  Mortality rate is 6-10% of the 20% who do not stop bleeding spontaneously • Occult blood  don’t know it’s there • Some die because of vessel size that he ulcer is local to. o Anemia o Cancer - Perforation o 5% incidence o Usually on anterior wall  Because it’s thinner o Gastric contents now leaking into peritoneum. o These Pts will have a RAPID progression of symptoms. (They go quickly)  High morbidity rate. o Zollinger-Ellison should be considered - Gastric Outlet Obstruction o At pylorus or duodenal bulb o 2% Incidence o From tissue obstruction  scar tissue (fibrosis)  obstruction o S/sx: regurgitation, distension, pain, nausea and vomiting. o Zollinger-Ellison Syndrome Uncommon cause for PUD Occur because of Gastrin secreting tumors (gastrinoma) o Cause multiple peptic ulcers (literally hundreds of small ones) o Perforation is relatively common  Bleed outs common o 2/3 of gastrinomas are malignant  Will metastasize  Can lead to death o Hard to manage these cases due to the continuous production of gastrin from the tumor o o

June 26, 2006
HIATUS HERNIAS - Herniation of a portion of the stomach into the thoracic cavity (mediastinum) through diaphragmatic hiatus EPIDEMIOLOGY - 50% of patients over 50 - Female: Male (4:1) - Often associated with GERD (70%) - 90% with EGD esophagitis have a hernia (could be permanent damage) - Etiology unknown, age most likely culprit due to weakening of the sphincteric - May be congenital or post-traumatic - Bowel and stomach in the middle of the chest compressing the lungs and heart is termed a Bochdalek o The largest one

52

TYPES OF HERNIAS Sliding or rolling hiatus hernia (most common)
Fundus of stomach slide up the hiatus (sliding) Roling hernia - Sphincter remain the same where fundus role up next to it. Paraesophageal (AKA: Rolling Esophageal Hernia) Short Esophagus Intrathoracic Stomach o

o

SIGNS AND SYMPTOMS (same as reflux with the exception of the addition of borborygmi • Heartburn o Because also have GERD Dysphagia Regurgitation Chest Pain (burning) Postprandial fullness o After eating GI Bleeding Dyspnea o Most often with hiatal hernia, a useful d/dx from GERD. (possible TQ) o From impingement of the left lung. Hoarseness o Irritation of larynx from GERD Cough o Irritation and to keep stuff from going into the trachea Wheezing

-

SLIDING HIATUS HERNIA - Most common – the esophagus pull the fundus of the stomach up through the hiatus - AKA: Axial or Concentric Hernia - GE Junction/upper stomach herniates - Usually asymptomatic - Symptoms o Reflux o Burning Chest Pain o Regurgitation with recumbency /fatty meals o Episodic - Gas bubble above the diaphragm on x-ray (magenblase) PARAESOPHAGEAL HERNIA - Second most common - AKA: Rolling Hiatus Hernia - GE junction in normal position - Fundus herniates through diaphragm - Usually asymptomatic o A self containing condition, hence not as much GERD and reflux. - Should be surgically reduced - May become strangulated o Lead to ischemia (loss of blood supply)

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MISCELLANEOUS HERNIAS Short Esophagus Type o Variation of sliding hernia o Uncommon o Congenitally short esophagus or from surgery (enbloc resection from malignancy) Intrathoracic Stomach o Very rare o Entire stomach in chest o Incompatible with life Bochdalek o Gastric herniation into posterior mediastinum Incompatible with life o Tamponage – o Can’t breath DIAGNOSTIC WORKUP - Exclude other more serious conditions - EGD - UGI - Blood tests non-specific - Ex: On contrast PFXR, can see rugae above the hemidiaphragm DIFFERENTIAL DIAGNOSIS (similar to list for GERD) - PUD - Angina - Esophagitis - GERD - DES (Diffuse Esophageal Spasm) - Achalasia - Diverticulum - Esophageal Cancer TREATMENT - This is a common condition, remember. - Diet changes o Avoid caffeine, chocolate, mint, uncooked white onion, etc.… o Avoid drugs (Ca++ channel blockers), nitrates, etc. - Weight loss (most hiatal Pts are overweight) - Small meals (6 small meals is better than 3 large meals) o Keep metabolism up over a longer period of time. - Sleep with head elevated - Manipulation o Drink a glass of water and take a walk or jump up and down barefoot (remove shock absorbed) - Antacids, H+ pump inhibitors, etc.… - If all else fails, or sign of strangulation of the hernia, surgery for refractive disease o Fundoplication. COMPLICATIONS (similar to list for GERD, except for strangulation) - Erosive esophagitis - Ulcerative esophagitis

Diaphragmatic hernias are classified as Bochdalek's hernia (90%), hiatal hernia, and Morgagni's hernia. The parahiatal hernias are characterized by herniation through a small defect adjacent to the esophageal hiatus. They are rarely seen and may be associated with previous trauma.

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[End

Barrett’s esophagitis Stricture GI hemorrhage stomach material]

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Colon
1. Review normal anatomy and structure of the color Vermiform appendix 2. Cecum 3. Ascending colon 4. Hepatic flexure 5. Transverse colon 6. Splenic flexure 7. Descending colon 8. Sigmoid colon (8) o Rectum and anus are separate. 2 Functions: o Fluid control and storage of feces Review blood supply to colon o Superior mesenteric artery is larger than the inferior mesenteric artery  Superior mesenteric artery • Supply the right side  Inferior mesenteric artery • Supply the left side o Blood supply interruption  Mesenteric Thrombosis • Diabetics • Trauma causing vasocompression Sigmoscopes, anoscopes, and colonoscopes used to view the colon. o Used to be rigid, now are flexible. (… yaiiigghh!!) o Can view the haustra easily. (not that you WANT to…)  Increase surface area - Normal Colon (Pictures) o Normal transverse colon o Undissoved tablets o Normal cecum/appendix o Undigested berry o Normal vesels o Tapeworm Tapeworm (Taenia)– - S/SX abdominal pain, weight loss - Can grow to be 20-25 FEET long. - Pork (Taenia solis) and beef (Taenia sanguinatum) most common. - Can regrow if only partially removed. - Most Pts are asymptomatic, some are anemia, weight loss, etc. - EWW!

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June 26, 2006 (2nd hour)
INFLAMMATORY BOWEL DISEASE (IBD) 1. Irritable Bowel Syndrome (IBS) 2. Crohn’s Disease (agranulomatous) 3. Ulcerative Colitis 4. Antibiotic Associated Colitis 5. Bacterial Colitis (Food Poisoning) a. Ex: including from bubonic plague 6. Appendicitis IRRITABLE BOWEL SYNDROME aka: Mucous colitis, “spastic colon” 3 forms: o Diarrhea o Constipated o Mixed between the two Copious amounts of mucus produced, usually resulting in diarrhea. Alteration in normal bowel habits – constipation, diarrhea or a combination of the two Functional disorder o With minimal mucus production associated with 20% of general population affected (2 out of 10 are affected) F:M = 2:1 Begins in late teens/early adulthood 50% pts have psych problems (30% have an anxiety disorder) or are hyperactive Etiology unknown, but strong association with stress Commonly associated with stress S/sx o Crampy abdominal pain (severe, can double Pts over), low grade through the day up to the point that defecation is imminent, at which time the pain increases o Diarrhea  Up to 30 BM/day  Water/mucous in the stool o Bloating/abdominal distention, increased gas o Abdominal tenderness o Pain often relieved (temporarily) by BM o No blood in stool, important differential feature from Crohn’s and or ulcerative colitis o Sign and symptoms must be present for 3 months before dx  Remember this is episodic, and will come and go over a few days. o Hyperactive bowel sounds  Too much peristalsis. Major concern with this condition is maintaining the patients hydration level due to the condition being in the colon

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-

DIFFERENTIAL DIAGNOSIS (other inflammatory bowel diseases which cause cramp type pain and diarrhea) o Crohn’s Disease o UC o Diverticulitis o Colon CA  Alternating constipation and diarrhea. o PUD o Chronic pancreatitis  Colon does not react well to fatty stool. o Biliary Disease TX o High fiber diet – helps bulk up the stool and helps retain fluid o Fiber supplementation (psyllium) o Anti-spasmodics  Imodium  Lonotil  Bentyl • Parasympatholytics (block parasymps), usually working in 24 hours. o Eliminate stress o > 60% respond to Rx within 1 year o Fairly easily managed. o There are a number of natural anti-spasmotics. CROHN’S DISEASE - Chronic granulomatous inflammatory Disease (Picture of oral crohn’s dz) o Transmural (across the entire wall) GI inflammation o Causes granulomas – localized areas of necrosis.  “Lumpy, Bumpy Bowel Disease” – causes lots of lumps and bumps. - Regional enteritis (AKA for Crohn’s) o ½ of all Pts affected in the iliocecal region. - Debilitating, often requiring surgery - 1:1000 population o So fairly common. - Caucasians, Jews - Unknown etiology o Autoimmune is the current guess. - Affects young people o Teens to 20’s. - Pathophysiology o Location


    o

Anywhere in the GI (“Tongue to Bung”) 33% involve terminal ileum 50% involve distal ileum/proximal colon 20% involve colon only Can involve any portion of GI tract

Transmural Disease

59

 

 
  S/SX o o

Inflammation (granulation tissue) • Most common is TB Ulceration • But not as much bleeding as in UC (ulcerative colitis – which is hallmarked by bloody diarrhea, and important D/dx) Stricture Fistula (connection between 2 organs not normally connected) • Starts as an adhesion, then progresses. Abscess (walled off pocket of infection) (look for thickening and reddening of the wall in association with the inflammation) Crohn’s disease presents with a wide variety of signs and symptoms because its involvement is variable in both location and severity of inflammation

-

Abdominal distention/bloating Mass suggests abscess formation o “Crampy” abdominal pain (RLQ) o Hyperactive Bowel Sounds o Non-bloody/bloody diarrhea o Perianal fissures/fistulas o Bowel obstruction o Crohn’s arthropathy o Low grade fever, pallor o Weight loss, fatigue Diagnostic Evaluation o “Skip lesion” presentation. o CBC  Anemia  Decreased H&H o Electrolyte imbalance o Vitamin B12 deficiency o Endoscopy o UGI (Upper GI) o LGI (Lower GI) o The Pt Hx is very telling on this. Most commonly, there is one or a combination of the following clinical presentations: o Chronic inflammatory disease  Chronic relapsing inflammatory disease  This is the most common presentation  Often seen in patients with ileitis or ileocolitis  Patients report low-grade ever, malaise, weight loss, and loss of energy  There may be diarrhea which is non-blood y and intermittent  Cramping or steady pain in the right lower quadrant or periumbilical area  Examination reveals focal tenderness in the right lower quadrant o Intestinal obstruction  Narrowing of the small bowel may occur as a result of inflammation of fibrotic stenosis  Patients report postprandial bloating, cramping pains, and loud borborygmi o Fistulization with or without infection  Some patient develop sinus tracts that penetrate through the bowel and form fistulas to other areas

-

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o
o

Fistulas to the mesentery are usually asymptomatic (loose fatty CT that connect the bowel, organs) Fistulas from the colon to the small intestine or stomach can result in bacterial overgrowth with diarrhea, weight loss and malnutrition  Fistulas to the bladder or vagina produce recurrent infections Perianal disease (other presentation of Crohn’s): which usually includes anal fissures, perianal abscesses, and fistulas Extraintestinal manifestations  Oral aphthous ulcers  Increased prevalence of gallstones due to malabsorption of bile salts  Nephrolithiasis with urate or calcium oxalate stones 

-

Complications o Obstruction (common) o Abscess formation (common) o Fistula formation (inter-organ, skin) (common) o Perianal fissures o Colon carcinoma (Slightly increased risk, but not the same risk as in UC (substantially increased chance)  Patient’s with colonic disease are at a greater risk of developing colonic carcinoma Hemorrhage/shock  If fistulas/abcesses hit and disrupt a major artery or vein.  unusual in Crohn’s disease (except for Crohn’s colitis) Malabsorption - from bacterial over-growth in patients with fistulas Loss of haustration is the hallmark

o

o
o o D/DX

o UC (differentiated since UC has a lot of blood in the diarrhea) o IBS (more common differential, since this does not produce as much blood in the diarrhea)
o o

o
o o Tx o o o o

Infectious colitis (Yersinia pestis (bubonic plague), TB, Salmonella) Parasitic infection (amoebiasis) Ischemic colitis (tends to happen in older folks with atherosclerosis or diabetes mellitus) Diverticulitis Colon CA Nutritional supplementation Low residue diet with obstruction High fiber diet with diarrhea Medications  Sulfasalazine  Corticosteroids  Immunosuppressive drugs Monitor vitamin levels Surgery for obstruction, fistulae, etc. No specific treatment exists for Crohn’s disease, treatment is directed toward symptomatic improvement and controlling the disease process

o

o
o

June 28, 2006

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ULCERATIVE COLITIS (UC)
Epidemiology o Chronic superficial inflammation of the mucosal layer of the large bowel. o Occurs in descending and sigmoid colon (even the rectum) o Unknown etiology o Aka-idiopathic proctolitis o 100/100,000 incidence o Most common: 14 – 38 years o 15-20 % of pts require at least a partial colectomy (~1 out of 5 Pts) Presentation patterns o 70 % relapsing o 20 % chronic continuous o 10 % fulminate (Toxic Megacolon)  The large bowel becomes massively distended. • Can rupture, leading to peritonitis, sepsis, and possible death. o  o o S/sx Similar to Crohn’s disease, but in different location. Left, as opposed to Right in Crohn’s. Abdominal distention Abdominal pain/tenderness (LLQ, LUQ) o Bloody diarrhea (Hallmark sign of UC, more common and more severe than in Crohn’s) o Fevers o Dehydration  Because involves large bowel. o Extraintestinal manifestation  Liver Disease  Sclerosing cholangitis (see below) • Walter Peyton had this (football player)  Arthritis (like Crohn’s)  Ocular Disease (uveitis, iritis, conjunctivitis, etc.) DX workup o “Cobblestone” appearance on scoping. o Comprehensive H&P o Laboratory studies  CBC (anemia, elevated ESR)  SMAC (electrolytes, LFTs)  UA (dehydration) o Sigmoidoscopy o Double-contrast BE D/DX o Crohn’s Disease o Bacterial infection o IBS o Protozoal infection o Colon CA o Diverticulitis o Ischemic Bowel DISEASE

62

o o  o o o   o -

TX

Correct nutritional deficiencies May need “bowel rest” with TPN (Total Parenteral Nutrition) Totally fed by IV. Folate supplementation (decrease CA Risk) Low roughage diet during exacerbations Meds Sulfasalazme Corticosteroids Colectomy/colostomy (about 1 in 5 Pts) Complications [pictures] o Vesicocolic (colovesical) Fistula with Pneumaturia  Between bladder and bowel, with air sign in bladder on PFXR o Rectovaginal fistula

APPENDICITIS Vermiform appendix can be at a variety of positions on the caecum. Inflammation of appendix secondary to obstruction Clinical symptom complex o Periumbilical/diffuse pain (initially) o RLQ pain  12-24 hrs later  Sign of regional peritonitis  Rebound tenderness • Pain is on release of pressure, not on placing of pressure AND pain is in a different place than the point of pressure application (Rousing sign)  High fever o Can rupture  Within 36 hours of the pain moving to the RLQ, the appendix is usually enlarged enough to be at substantial risk of leaking and rupture.  Enlargement of the appendix can become HUGE. o May cause diffuse peritonitis o May result in abscess formation o Only in about 10-15% of the time AT BEST, appendicitis will remit on its own. Don’t take this risk. o If pain getting worse and worse, then gets better suddenly – usually a hallmark sign that the appendix has ruptured (rapid reduction of pressure on the serosa).  Within 12 hours, can get onset of sepsis, toxosis, and eventual death.

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DIVERTICULAR DISEASE Picture of X-ray Epidemiology o Herniation(s) of mucosa and submucosa through muscularis (at points at which vessels penetrate the GI wall) from low fiber diet o Occur because of poor bowel hygiene  (Low water intake, straining, “holding it too long”, low fiber in diet, etc.) o Occur at vasa recta (weakened area) o Diverticulosis is asymptomatic o Diverticulitis is symptomatic  Only when 1 or more of the ostia become obstructed are Sx present.  Can rupture and bleed (sometime asymptomatically) like appendicitis. o 30% of Pts over 40; 50% of Pts over 70 have diverticula (very common). o Most respond well to antibiotics o Up to 30% require surgery - S/sx o Diverticulosis exam is normal o LLQ pain most commonly. o Pain relieved with BM o Abdominal guarding  Voluntary contraction of abdominal mm, as opposed to abdominal rigidity, which is involuntary (d/t peritonitis) o Rebound tenderness suggests peritonitis o +/- small amount of blood in stool DIVERTICULAR BLEEDING - 70% occurs in right colon (don’t know why, when it mostly occurs in the left colon) - Bleeding is painless - Resolves spontaneously in 60% - Erosion of vessels from fecalith (fecolith?) - 15 – 20 % re-bleed within 5 yrs (deadly) Diagnostic workup o CBC (elevated WBC with diverticulitis) o Microcytic anemia o Barium enema (BE) o Sigmoidoscopy o Abdominal CT for abscess formation D/dx (you’ve seen this list before, as they all are D/dx for each other) o IBS o Crohn’s disease (which also has masses and abscesses) o UC o Colon CA o Ischemic Colitis o Infectious Colitis Tx o Good bowel hygiene  Increased dietary fiber  Increased fluids.

-

-

64

o o o o o

 Regular bowel habits (when you need to go) Avoid foods with residue (seeds and things that could obstruct the ostia of the diverticula) Regular exercise  Used for constipation too. Broad spectrum antibiotics  Makes Pt more regular. IV Antibiotics in severe cases Surgical resection/re-anastomosis

June 29, 2006
1Colorectal Cancer
• Almost impossible to tell just by looking if a polyp is benign or malignant. • Polyps can be found by DRE (digital rectal exam) depending on size and location. • Second leading cause of CA deaths in USA (secondary to lung CA) o 135K new cases/yr o 50K deaths/yr • 15% of all organ based cancers (except skin cancers) • Peak incidence in the 7th decade • Location o Descending colon – 40% o Rectosigmoid – 30% o Cecum/ascending – 25% o Transverse – 10%

Remember: any male over 40 with anemia must be assumed to have a GI CA until proven otherwise. o Remember that GI CA can present as alternating diarrhea/constipation o Digital Rectal Exams (DRE) – need to be done regularly as the Pt ages.

Risk Factors • Hereditary Polyposis syndromes o 100’s to 1000’s of polyps in their colon.  Pts usually have prophylactic colectomies – as they WILL develop malignancies.

65

o Familial polyposis  teens to 30's, pts have thousands of polyps o Gardner’s Syndrome  Colonic polyposis associated with osteomas in the skull. • Inflammatory bowel diseases • History of previous colorectal CA • 1st degree relative with colorectal CA • Age >40 • High fat, low fiber diet • Regional radiation therapy (eg. Female receives radiation for ovarian cancer - if the colon is in the port, the fast turnover of the epithelial cells makes them prone to damage from the radiation, due to the effect of radiation on fast growing tissue) [brain tumors can be treated with stereotactic radiation] Clinical Presentation Here is another example of polyposis with numerous small polyps covering the colonic mucosa. In this particular case, • Normally unremarkable there were osteomas of the skull, a periampullary o Normally only found after signs of bleeding (see below) adenocarcinoma, and epidermal inclusion cysts. Thus, this is • DRE finds 50% of tumors (polyps and colon cancer) a case of Gardner's syndrome. As with familial • Palpable abdominal mass (mets most likely not the colon cancer itself) adenomatous polyposis, the inheritance pattern is • Abdominal tenderness • Alternating constipation / diarrhea (blockage, attempt to flush, repeat) • Hepatomegaly (mets) • Rectal bleeding • Hematochezia • Melena • Blood streaked stool • Occult blood [blood mixed in with the stool] • Abdominal distension (picture of colon obstruction) o Obstruction o Initial symptom in 15% of patients  If gets to this point, probably already has metastasized, stage III or IV. • Pencil thin stools • Intusseception • Volvulus • Weight loss, suggest stage 3 or 4 carcinoma • Anorexia • Malaise Clinical Investigation • Anemia (microcytic) [Any male patient over 40 with rectal bleeding is to be considered positive for colon cancer](Ya think this is gonna be a TQ?) • Positive FOB test • Elevated CEA (carcinoid embryonic antigen) o Not as good for presence of colon CA, but good to monitor Pt response to treatment (Rx) • Elevated LFT’s (liver function tests) (usually indicating mets) • Colonoscopy • Double contrast BE • CT for staging

66

• •

CXR (chest X ray) o Chest is a common place for mets of colon cancer 25% have mets at presentation, they are in stage four of the cancer

Differential Diagnosis • Diverticular disease • Bowel stricture • Inflammatory bowel diseases • Adhesions • Mets • Extraluminal masses (ovarian mass) • AVMs (arterial/venous malformation) o Usually a congenital lesion, with a tumor like mass of arteries and veins. o Can present with alternating diarrhea/constipation, colorectal bleeding, etc. o Usually occur in younger Pts Cancer Staging (Picture of Apple core lesion) • Duke classification system (used almost universally for Colorectal CA Pts) o A - Confined to the mucosa-submucosa (essentially a carcinoma in situ) (best prognosis) o B - Invasion of muscularis (into vessels,  chance of spread) o C - Local node involvement (local spread) o D - Distant mets (liver, lung, brain)

[Look for “shouldering” on Ba Xray – the almost 90o cut off between edge of mass and normal tissue] Treatment • Surgical resection (often done for palliative reduction of S/sx, rather than curative reasons) o 70% are resectable at presentation (usually stages A and B) o 45% cured by primary resection • Radiation therapy (stages B & C) • Chemotherapy (stages B & C) o 5-fluoroucacil o Levamisole • FOB q 6 months • Colonoscopy q year x 2 years, then q 3 years o If they are clear. • Monitor CEA levels (Carcinoma Embryonic antigen) Prognosis • Duke A: >80% • Duke B: 60% • Duke C: 20% • Duke D: 3% Overall 5 year survival rate: 50% Pts usually are cachexic.

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Colon Polyps
50% patients have polyps o Hyperplastic o Adenomas  Of concern for degradation to adenocarcinoma.  DRE’s and FOB testing encouraged. o Lipomas  Common. o Leiomyomas (smooth muscle tumors)  Longitudinal strips of smooth muscle transversing the colon. Sessile / pedunculated 25% patients with colon cancer have polyps There is also Familial Adenomatous Polyposis (FAP) (see above)

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Signs / Symptoms - Most are asymptomatic. - Rectal bleeding is most common Sx (most in recto-sigmoid region) o Hematochezia (BRBPR) Familial Adenomatous Polyposis (FAP) - Cramps - Abdominal pain - Obstruction - Anal polyps may prolapse - Generally polyps are small, but the larger they get, the higher the chance of malignant degeneration. - Cannot tell by external observation whether a polyp is malignant or benign o Which is why most are removed and biopsied to tell. Diagnosis - DRE (digital rectal exam) (aigh!) - Endoscopy - Double contrast BE Treatment - Careful observation (hyperplastic, lipoma) - Endoscopic surgery - Open laparotomy

END OF TEST II MATERIALS
SIGMOID DIVERTICULITIS TX - ↑ dietary fiber - Broad spectrum antibiotics - Reg. Exercise - IV antibiotics in severe cases - Surgical resection/re-anastomosis TUMORS OF THE COLON - Colorectal CA o 2nd leading cause of CA deaths in US 1st Lung CA 2nd Colorectal CA 3rd Breast CA Most common CA is skin CA

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135,000 new cases/year 50,000 deaths/yr. 15% of all cancers (except skin cancers) o Peak incidence in the 7th decade o Location  Lower colon – 40%  rectosigmoid - 30 %  cecum / ascending – 25 %  transverse – 10% 2 types of CA can occur o adenocarcinoma o squamous cell CA – Most common with HPV (condylomata) Risk factors o Hereditary polyposis syndromes  Familial polyposis  Gardner’s syndrome • Polyposis & osteoma in skull o Inflammatory bowel Disease o H/o previous colorectal CA o 1st degree relative with colorectal CA o age > 40 o high fat, low fiber diet o regional radiation therapy Clinical presentation o Normally unremarkable o DRE finds 50% of tumors o Palpable abdominal mass (mets) o Abdominal tenderness o Alternating constipation/diarrhea o Hepatomegaly (mets)  Mets usually to liver (stage 4 colorectal Ca) • Liver drains all of GI o Rectal bleeding  Hematochezia  Melena  Blood streaked stool o Abdominal distention  Obstruction  Initial sx in 15% o Pencil thin stools o Intussusceptions o Volvulus o Wt loss o Anorexia o Malaise o Colon CA can cause lumbar & sacral back pain Clinical investigation o Anemia (microcytic) o Positive FOB test o Elevated CEA (used for RX response) o Elevated LFTs o Colonoscopy o o o

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o Double contrast o CT for staging o CXR o 25% have mets at presentation D/DX o Diverticular Disease o Bowel stricture o Inflammatory bowel Disease o Adhesions o Mets o Extraluminal masses (ovarian) o AVMs (Arterial venous malformations) Cancerous staging o Duke Classification system  A – confined to the mucosa – submucosa  B – Invasion of muscularis  C – local node involvement  D – Distant mets TX o Surgical resection  70% are respectable at presentation  45% cured by primary resection o radiation therapy (Stages B & C) o chemotherapy (stages B & C )  5-flourouracil  levamisole o FOB (fecal occult blood) every 6 months

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 Guaiac test  finds occult blood in feces Colonoscopy every year x 2 years, then every 3 years CEA level  Carcinogenic embryonic antigen Prognosis o Duke A – 80 % o Duke B – 60% o Duke C – 20 % o Duke D – 3 % o Overall 5 yr. survival rate – 50 %
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COLON POLYPS - Most non-inflammatory CA arise from polyps - 50 % patients have polyps o Hyperplastic o Adenomas o Lipomas o leiomyomas - sessile/pedunculated - 25% pts with colon CA have polyps - S/SX o Most are asymptomatic o Rectal bleeding mc o Cramps o Abdominal pain

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Obstruction Anal polyps may prolapse DRE Endoscopy  Complicated with severe inflammation disease  May perforate bowel  Do BE instead Double contrast BE Careful observation (hyperplastic, lipoma) Endoscopic surgery Open laparotomy

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[End Exam 2 Material]

July 10, 2006
Test Three and Final Small Bowel Diseases - Usually result in some form of malabsorption CELIAC SPRUE - AKA: Gluten enteropathy non-tropical sprue o Antigen mediated rxn. - Gliadin protein fraction in gluten o Wheat o Rye o Barley o Oats - Gluten intolerance - 50-500/100,000 people - Incidence ↑ during 1-36 months - F>M o Mc to find in a child - Clinical Presentation o May be normal presentation o Weight loss o Dyspepsia (indigestion) o FTT in children (failure to thrive) o Bloating o Diarrhea o Pallor/fatigue (anemia) o Angular cheilosis (Vit B def.) o Osteomalacia (malabsorption of Vit D) o Dermatitis - Lab tests o Iron ↓ anemia o Folic acid ↓ o B 12 ↓ o Antigliadin IgA and IgG antibodies elevated

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Small bowel biopsy  Show villi atrophy  Signs of inflammation IBS (mc d/dx)  More mucous in IBS stools  Age 20 - 40 Laxative abuse  Yes, Pts can become addicted to laxatives. Intestinal Parasites Tropical Sprue Lymphoma  Always include as D/Dx Gluten Free Diet Iron supplementation Folate supplementation B12 supplementation Good Px w/ diet

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WHIPPLES DISEASE - Caused by bacteria, Tropheryma whippelii (gram +) - Multisystem Disease - Aka: intestinal lipodystrophy o Poor digestion of fats. - Uncommon disease - 30-60 yr. olds - M>F - Clinical Presentation o Irregular folds (giant) in the small bowel, and thickening of the wall. o Malabsorption  Diarrhea  Bloating/cramps  Anorexia  Weight loss / fatigue  anemia o Extra intestinal Sx  Arthritis • Can be peripheral or sero-negative o Similar to UC and Crohn’s which both can have arthritis Sx.  Pleuritic chest pain (localized pain)  Pericarditis  Osteomalacia - Pathology o Bacteria never been able to cultured  Cannot find an agar to culture it in, must be cultured in human tissue. o No human to human transmission. o o D/dx o

 Mode of transmission unknown. Appearance of bacterium can change (overall morphology: longer/shorter, thicker/thinner, etc.) Response to antibiotics confirms Dx
Celiac sprue

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Lymphoma Crohn’s disease  Consider this on just about all small bowel D/dx.  Crohn’s has more inflammatory symptoms than Whipple’s, but is included because of the extraintestinal Sx, particularly the arthritis. Short bowel syndrome  Take portion of bowel out  Get malabsorption Pancreatic insufficiency  Fatty stools Lactose intolerance

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Trimethoprim Sulfamethoxazole Treat Vitamin deficiencies. Iron supplementation. Pts respond well to antibiotics.  Prognosis very good, once antibiotics have been administered.

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LACTOSE INTOLERANCE - Can have a transient form in people that are ill - 1 in 6 of all people have it - Have malabsorption symptoms o But vitamin deficiencies are usually not as bad - Insufficient concentration of lactase - Results in fermentation of lactose - Aka: “milk intolerance” o Thickening agent o Sweetener - 50 million are affected (about 18% of the population) - > 85% Asian American affected - > 60 % African American affected - < 25% Caucasians affected - There can be conditional lactose intolerance. o Pts presenting with food poisoning or occasionally other infections, can have a transient lactose intolerance after an illness for a couple of days to a week or so. o Common in infants and children. o Take them off milk for a few days, then gradually add it back in. (for infants, but them on pedialyte in the intermediate.) - Clinical presentation o May be normal o Bloating o Diarrhea o Cramping o Abdominal pain o Flatulence - DX workup o Hydrogen Breath test  Ingest 50 gm of lactose  Rise in breath hydrogen to > 20 ppm in 90 min after lactose administration. o Exclude other disease o Imaging studies not indicated (sorry Dr. Fritsch)

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IBS IBD Pancreatic insufficiency Sprue, Celiac Disease (gluten intolerance) Lactose free diet  Milk  Bread  Candies  Cold cuts  Commercial sauces Read labels LactAid tablets Ca2+ supplementation (since don’t drink milk) Excellent prognosis – easily treatable, if inconvenient.

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MECKEL’S DIVERTICULUM - Of the small bowel - Remnant of vitelline (omphalomesenteric) duct. o Duct that used to feed the fetus o Right before the cecum at the ileum. - Most commonly misdiagnosed as appendicitis o Because of its location - Even looks like an appendix at the end of the ileum (as opposed to the ileocecal region) o About 12 cm long (~4 inches). o Some of them contain gastric mucosa – which can have ulcers, which in turn can bleed and perforate. Risk of feces in mesentery. - Congenital lesion o 2% of Population o Failure of obliteration of vitelli intestinal o Duct connecting interesting 2 yolk sac o Most common anomaly of SI - Found w/in 3 ft of IC valve - Less than 12 cm (4 inches) in length - Complications o Bleeding o Obstruction o Diverticulitis (contains gastric mucosa) perforation - RX w/diverticutomy MESENTERIC ISCHEMIA - Most painful condition in medicine o Very painful, high mortality rate. - Pancreatitis is pretty painful as well. - Most painful procedure in med is bone marrow test. - More proximal obstruction of artery, the higher the risk of mortality. - Occurs as a result of either superior mesenteric arterial or venous occlusion o Less commonly from the inferior mesenteric artery (which largely affects small bowel) - Affects the bowel from 2nd part of duodenum 2 transverse colon - 50% embolic, 25% atheromatous, 10% venous occlusion - Overall mortality is approx. 90% o Usually within a few hours.

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DX features o Nothing highly suggestive o Central abdominal pain, out of proportion  Arterial obstructions appear more acute, venous appear more chronic. o KUB may be normal  KUB: Kidney, Ureter, Bladder – plain film X-ray of the abdomen. o Look for in diabetics, alcoholics, people with long standing systemic diseases.

GENITOURINARY DISEASES • Up to 75% of kidney tissue can be destroyed before affecting renal function. • Surviving on one kidney is not difficult. • Normal congenital anomalies include pelvic kidneys (unascended), Horseshoe shaped kidney (1 big one), agenesis of kidney, urethra diverticula or bifurcations, etc. • Polycystic disease is the most common disease of the kidney. Usually benign. URINARY TRACT INFECTIONS - Can present w/ back pain - Female UT in close proximity to bacteria From anus - Normal urinary tract is sterile - M/c bacterial infection in humans o Upper Respiratory Tract Infections m/c viral infection - Women more prone to infections o Shorter tract (urethra)  Bacteria doesn’t have to travel as far o Hygiene (very important)


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Lower UTI o Urethritis  Most commonly from chlamydia. o Cystitis  Infection of urinary bladder  Most commonly from E. coli. o Lower UTI will eventually move retrograde up to the kidneys, resulting in an Upper UTI. - Upper UTI o Pyelonephritis  Kidney Infections (Pyelo = pelvis) Pathophysiology - 100,000 bacteria/ml is threshold for pathology (UTI diagnosis) o B/w 10,000 – 100,000 is contaminated - Must have a certain amount of bacteria in a certain volume of urine to dx a UTI o 10,000 – 100,000 ml = contaminated specimen o > 100,000/ml = UTI → become symptomatic - Some patients are symptomatic with less - Neonates- most commonly in boys from anomalies (boys get more anomalies than girls) o “Neonates” - 30 days old or less - Prechool- most commonly in girls, from hygiene - Adults- most commonly in women from hygiene - Four pathways o Ascending form urethra o Lymphatic spread

Wiping A to P, not P to A • E. coli from the anal region to the ureter, which then travel up and multiply in the bladder.

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Hematogenous spread Direct extension  Pelvic abscess from ovary or uterus Diabetics have sugar in urine that bacteria can feed off of and therefore are more prone to UTI’s (Infra somatic cystitis  air in wall of bladder from aerobic bacteria) Pregnancy → higher risk d/t incomplete emptying or obstructed ureters Risk factors o Neurologic disease o Diabetes o Renal failure o Pregnancy Pathogens o E. Coli o Proteus Mirabilis Defense Mechanisms o Low pH o Normal Micturition  Detrusor mm contracts  Trigone muscle relaxes o High Osmolarity o o

LOWER UTI - Presentation inconsistent o Some asymptomatic, some just have urgency, some have extreme pain - Testing (?) - Polyuria (increase in Urinary frequency), with minimal quantity - Dysuria (painful urination) - Urgency - Urge incontinence - Suprapubic pain aka hypogastric region - Hematuria (menstruation most common caused, bladder infection most common pathogenic cause) o Gross  Patient will see blood in toilet o Microscopic  If the infection is mild to moderate PYELONEPHRITIS - More common in immunocompromised patients, diabetics, and other constitutional illnesses. - Usually secondary to a UTI - Patient will be positive for a kidney punch - Fever, more prevalent then with a UTI - CVA (costovertebral angle) pain - Radiating pain into groin o Anterior and inner thighs, males will refer to the ipsilateral testicle - Chills o Fever, night sweats - Malaise o Fatigue - Vomiting - Diarrhea Clinical testing - Clean catch UA o Wipe w/alcohol pad → start urination → stop → catch → mid-steam urine → stop before urination is complete

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Urine Culture & Sensitivity, by culturing you are able to determine the type of bug and degree of activity level and then the sensitivity to antibodies so as to determine treatment plan CBC o Elevated WBC, anemia (mild) KUB (kidney, ureter, bladder) (a plain film Xrayof the abdomen) Ultrasound IVP (Intravenous Pyelogram) o Outlines renal substance o Uses iodine, as it’s cleared by the renal system (not GI, respiratory, or biliary system) CT scan o For tumors or abscess Cystoscopy Retrograde pyelography (obstruction) o Dye from urethra up (via catheter) and stops where infection is o 2 check for stones o Surplanted now as a technique by Ultrasound.

[Ok, guys, you are NOT going to like the slides on this section…] Non-gonococcal Urethritis - NGU is the most common STD o More than gonorrhea or syphilis. o NGU twice as common as gonorrhea (the clap) - Chlamydia is the most common bug - Often asymptomatic (~25%), especially in women o Which is why the spread can occur so quickly and broadly. - Symptoms o Dysuria o Whitish discharge from urethra meatus. o Meatal edema • Treatment w/ antibiotics Gonorrhea • “The Clap” - That’s how they used to treat it….no really. • Neisseria gonorrhoeae • Urethra is most common sight of infection - Can have Gonococcal urethritis, Gonococcal cervicitis, Gonococcal opthalmia, and Bartholin’s abcesses • Contraction rates(single intercourse) - 20% for males - 80% for females, will tear up the cervix and cause sterility if not aggressively treated • Can be mistaken for Candida albicans infection, due to the itching. • Symptoms - Dysuria - Urethral discharge - Urethral itching • Treatment w/ antibiotics

Herpes Simplex -HSV II infection affecting ~20% of adults -Spread through direct contact

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Can be infectious, even if no direct lesions are present. -Causes blisters/ulcers around genitals Blisters release clear fluid which contains high levels of the infected agent -May also infect the eye, skin, other organs -No cure, only symptom control Acylovir and Valtrex

Genital Warts -

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Condylomata acuminata Caused by a form of HPV Represents 1/3 of cases of STDs, 20 million people Most people are exposed at some point in life

Treated with antiviral creams, cryotherapy, laser Will reoccur

[Now back to less disturbing slides] Urolithiasis (Kidney stones)

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Calculus in the urinary tract Aka- renal colic, when in the active state Types of stones o Calcium (70%) o Uric acid (8%) – in gout Pts predominantly. o Struvite (15%) o Cystine (3%) – in Pts with homocystienuria. Large enough stones (3-4mm) are large enough to lodge in the ureter, and coincidentally, are about the size necessary for visualization on PFXR. Can have a “Stag Horn calculus” – looks like a stag’s horn in the calculi of the renal pelvis. o Pt has calcium metabolism problems. - Obstructive uropathy. 250K-750K /year M: F = 4:1 Incidence is highest in summer (dehydration decreases ability to clear precipitates) Hydronephrosis (water in the kidney) results from obstructed ureters, blocking outflow. o Will only show up on venous pyelogram (IVP), as opposed to a retrograde pyelogram, which will not detect it. Signs/symptoms o Acute colicky CVA, flank, low back pain. - “Renal Colic” – crescendo/decrescendo pain presentation. • Occurs as a peristaltic wave passes a stone in the ureter as it is propelling urine to the bladder. o N/V (nausea and vomiting) o Referred pain to testes/vulva/groin o FCNS (Fever, Chills, Night Sweats) suggests infection Diagnostic work-up

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UA (hematuria) (gross or microscopic) Plain film radiography Renal Ultrasound IVP (intra venous pyelogram) L1/L2 disc herniation (pain in the same areas) Pyelonephritis Cystitis Diverticulitis PID

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Increased fluid intake, low calcium diet (contraindicated if an obstruction exists) - “Just let them pass” o Uteroscopic stone removal o Extracorporeal shockwave lithotripsy - High-energy ultrasound. Pt is usually sedated. 50% pass within 48 hrs 50% recurrence rate without Rx

Glomerulonephritis - Autoimmune inflammation of glomerulus - Synonyms - Post-infectious GN Usually after strep infection o o Acute nephritic syndrome - Deposition of various immune complement precipitates after infection into glomeruluar basement membrane. Can lead to renal damage/failure. o Remember that failure only occurs after destruction of 75% of kidney. - Epidemiology o 50% affect < 13 y/o o Most common cause of chronic renal failure (~25%), these individuals wind up on dialysis - Most common cause of renal failure from diabetes mellitus. o Post group A beta strep infection mc o Collagen vascular disease (SLE) o Idiopathic Proteinuria - Normal adult excretes ~150 mg/day of short and long chain proteins (0 - +2 on a UA dipstick) o 3.5% prevalence (idiopathic) in normal adults - Perform 3 separate tests o You must not assume that finding protein equates the “normal” amounts excreted. You must rule out all possible causes. o If positive again, then follow up a third time. o Negative- Dx “transient functional proteinuria” - Causes o IDDM o Nephrotic syndrome o Amyloid o Lymphoma o NSAID use o Orthostatic proteinuria (only occurs when Pt is upright)

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Nephritic Syndrome - Secondary to GN - Signs/symptoms o Edema (periorbital, scrotal), due to loss of protein o HTN, damage to kidneys which help regulate HTN o Hematuria (d/t damage to basement membrane) o Proteinuria - Will result in renal failure if continues for any period of time. Nephrotic Syndrome - Most common cause is membranous GN - Signs/symptoms o Peripheral edema, protein loss o Ascites o HTN, o Pleural effusion o Hypoalbuminemia o Hyperlipidemia / hypercholesterolemia o 1/3 of pts have DM, SLE, amyloidosis, or scleroderma Many of these patients end up on dialysis. These patients are placed very low on the transplant list due to DM, they are poor surgical candidates and the DM is not reversible, thus damage to the new organ is inevitable

Acute Renal Failure Sudden decrease in renal function Inability to maintain fluid/electrolyte balance Inability to eliminate wastes Signs/symptoms o Obnoxious bouts of nausea and vomiting o Oliguria / anuria (very important to monitor intake and output of fluids) o Altered sensation, electrolyte influenced (ex: uremic neuropathy, etc.) Laboratory findings o Elevated BUN/creatinine (creatinine levels are very specific for renal function)  Remember that BUN can also be associated with liver disease. o Electrolyte imbalance o Anemia, platelet dysfunction 3 divisions of acute renal failure: o I. Pre-renal failure (most common cause)  Secondary to inadequate renal perfusion • Hypovolemia (hypovolemic shock) • CHF • Strokes • Sepsis o II. Intra-renal/Intrinsic renal failure  Renal disease • GN, drug toxicity (NSAID’s), ATN (acute tubular necrosis), microvasculopathy from DM. o III. Post-renal/Obstructive (least common) renal failure  Outlet obstruction, outflow obstruction is going to cause pressure build up in the renal system • Benign Prostatic Hyperplasia (BPH)(most common cause), prostate CA

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• • • • Chronic Renal Failure -

Ureteral stones (as in repeated stone producers) Intra-abdominal mass Metstatic lesions in the abdomen. Bilateral renal vein occlusion

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Progressive decrease in renal function >250,000 dialysis pts/year o These are the Diabetics you see on dialysis. Signs/symptoms o Pallor, ecchymosis - Bleed easy. o Edema o HTN o Depression o Fatigue o N/V o Pruritus (urea makes the patient itch) Etiology o DM (37%) [Also the most common reason for dialysis in the US] o HTN (30%) - DM and HTN make up 2/3 of the cases of renal failure (TQ) o GN (12%) o Polycystic kidney disease - Look for this in women with polycystic ovarian or polycystic breast disease. o Drug toxicity o Obstructive uropathy o Renal artery stenosis - From trauma and external mass, artery is obstructed, yada yada… Laboratory findings o Elevated BUN/creatinine o Proteinuria, RBC casts o Electrolyte imbalances

Renal Cysts - Fluid-filled epithelium-lined cavities - Found on 50% of autopsies - Rarely symptomatic - Simple cysts are ~70% of all renal masses o So unlike esophagus or stomach, masses in kidney are usually benign (possible TQ) - Polycystic renal disease o M/c hereditary disease in the USA o 50% have renal failure by age 60 o Repeated UTIs, large kidneys, flank pain o 50% pts also have liver, pancreas cysts Renal Cell Carcinoma - Adenocarcinoma - Malignant transformation of renal tubular cells - A.k.a.: "Hyper-nephroma" (name no longer used because the name does not suggest malignancy)

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o Accurately describes how fast it grows and metastasizes (“blow out” mets, similar to blow out mets in bone.) 1:10,000 people/yr 50-70 y/o Male: female = 2:1 No S/sx until late in the disease progression. Etiology o Familial (genetic predisposition, particularly in 1st degree relatives) o Smoking, obesity, diuretics, Tylenol {chronic long term use} Signs/symptoms {often the tumor is very asymptomatic for long periods prior to its discovery} o Hematuria (50-60%)  About ½ microscopic and ½ macroscopic hematuria. o Abdominal mass (25-45%), found on individuals who are relatively thin or found rather incidentally o Anemia (20-40%) o Flank pain (35-40%) - there is no major distention of the capsule thus no pain. o HTN (20-40%) – sudden hypertensive changes are a red flag o Weight loss (30-35%) o Classic Triad (5-10%) for adenocarcinoma of kidney. o o o Treatment o o o Prognosis o o Hematuria {differentiate runners who classically suffer from hematuria} Flank pain Abdominal Mass Nephrectomy – complete removal of the kidney Radiotherapy Chemotherapy (5% response rate) Stage I ~90% Stage II ~75%  Good prognosis in stage I and II but because the tumor is typically asymptomatic during this stage it is not found during these stages Stage III ~20% (once it mets, px really becomes bad) Stage IV ~5%

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Prostate Diseases
Prostatitis Benign prostatic hyperplasia Prostate carcinoma Prostate specific antigen o Normal 0-4 ng/ml (nanograms) o Elevated in:  BPH  Prostate CA (not 100% accurate)  Post-rectal examination  Prostate trauma

Prostatitis - Men over 50 - May be aseptic or septic (infectious or noninfectious) - Signs/symptoms

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o Dysuria (painful urination and in the case the pain is deep inside the pelvis) o Polyuria (because they don’t want to urinate thus they urinate a little at a time) o Pelvic/ back pain o Urethral discharge o Fever - Dx made by culture and stain of prostate secretions - Antibiotics if infectious Benign Prostatic Hyperplasia - Benign overgrowth of the prostate - Generally begins in periureteral area - 80% of men by age 80 - Medical /surgical intervention in 20% men by age 75 - TURP (TransUrethral recession prostatotomy) is the 10th mc surgical in USA(>400k/yr) - 10-30% w/ BPH have an occult CA - Clinical presentation o Enlarged prostate on DRE (loss of sulcus) o Poor correlation between size and symptoms o Hesitancy, decreased caliber and force of stream o Double voiding, post-void dribbling o nocturia DDx prostatitis Prostate CA Urethral stricture - Dx workup PSA Protease secreted by epithelial cells Elevated in ~40% pts w/ BPH UA Ultrasound to ensure to hidden masses - Treatment Avoid caffeine Avoid medications (cold and allergy drugs) Medications TURP Stents Laser Coils - Prognosis is good (>70%) Prostate Cancer Has surpassed lung CA as most common cause of CA in men 100,000 new cases/yr; 30,000 deaths Uncommon <50; 80% new cases >65 y/o Average age at dx is 72 Black males (1 in 9) m/c population in the world Clinical presentation o Generally asymptomatic o Bone pain/fx may be initial presentation

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Outflow obstruction Mass on DRE (10% have normal DRE)

DDx - BPH - prostatitis - Prostate stones Diagnosis - Elevated PSA (may be normal in 20%) - Elevated acid phos (extracapsular extension) - Biopsy Treatment (chemo, rad, prostatectomy) Px depends on stage (~90% w/ stage I) Testicular Torsion - Twisting of spermatic cord

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Leads to testicular ischemia / infarct 1:4000 incidence 70% occur between 1 – 18 y/o DDX o Testicular tumors o Epididymitis o Incarcerated hernia o Orchitis – caused by mumps virus o Hydrocele – an obstructive disease where there is enlargement of the epididymis

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Testicular Torsion - Clinical Findings o Sudden hemi scrotal pain (10% are painless) o Swelling o Nausea and vomiting o Afebrile – no fever o 30% patients report previous episode of pain - Dx based on H and P - Surgical de-rotation with suture fixation Epididymitis - Septic/traumatic inflammation of epididymis - >600k visits per year - Occurs in sexually active men - DDX o Orchitis o Testicular torsion o Hydrocele / varicocele - Agents o N. gonorrhoeae o C. trachomatis - Clinical presentation o Tender scrotal swelling

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Erythema Dysuria Urethral discharge Fever Ice packs with scrotal elevation Analgesics Antibiotics Usually self limited

Hydrocele - Fluid collection in the scrotal space - If congenital, associated with inguinal hernia - In adults o Infection o Tumor o Trauma - Clinical presentation o Scrotal enlargement / pain / radiating to back o Transillumination - Rx o None if asymptomatic Orchitis Infection of the testicle Usually viral (mumps/coxsackie B virus) Occurs in post-pubertal males Clinical presentation o Testicular pain / swelling o May be bilateral o Inguinal lymphadenopathy, especially in a relatively young male o History of mumps o Rx- observation if viral o May lead to sterility

Testicular Cancer seminoma (most common), teratoma, choriocarcinoma 2-3/100k/yr M/c in young adults(30-40) Clinical presentation o Scrotal mass o Does not illuminate o Not painful (even less than normal testicle) o Pain from mets is more common Workup (70% have elevated hCG/AFP) Rx o Surgical resection, chemo, radiation Px o 70-85% for early stages

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Bladder Cancer - Range from low-grade to high-grade - Cell types o Transitional cell (93%) o Squamous cell (6%) o Adenocarcinoma (1%) - 54,000 new cases/yr; 12,000 deaths - 4(F)-10(M)% of all cancers - M/c over age 60 - 25% result from occupational exposure o Dye, textile, rubber tire, petroleum workers - 15-65% associated w/ smoking - Clinical presentation o Gross painless hematuria o Painless microscopic hematuria o Frequency, urgency – due to bladder becoming filled with the mass o mets causes pain in distant organ (eg, back pain) - Diagnosis o H&P History and physical examination o UA, cystoscopy – and endoscopic procedure for the bladder - Rx- chemo, radiations, TURP, cystectomy - Px- dependent on cell type and grade (high grade indicates how fast grows) Liver Function - Anatomy o Four lobes – right, left, caudate and quadrate o Weighs – 3 lbs - Blood Supply o Hepatic artery (oxygenated blood) (20%) o Hepatic portal vein (nutrients) 80% o Hepatic veins (drain liver) o Holds 1 pint of blood - Only organ that can regenerate - 75% damaged before failure - Over 500 functions - Produces bile - Produces plasma proteins - Produces cholesterol - Converts glucose to glycogen - Stores iron - Converts ammonia to urea (one of the reasons that BUN levels can be elevated in the liver as well as the kidney - Clears drugs - Blood clotting - Normal portal venous pressure = 5-10 mm Hg (a relatively low pressure system)

Hepatitis
Liver inflammation Types o Viral (A, B, C, D, E, X?)

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o o o o o

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Alcoholic hepatitis Drug-induced hepatitis Toxic hepatitis (carbon tetrachloride, benzene) Leptospirosis Toxoplasmosis EBV, CMV, HIV, Most common is alcoholic, and viral Most common is C typeHIV

Hepatitis A - Caused by HAV (RNA virus) - Fecal-oral route, close family contacts - 9-45/100,000/yr o Institutionalized children o Daycare centers o Male homosexuals o Exposure to imported apes o Undercooked mussels, clams, oysters - Highly contagious - Represents 33% of viral hepatitides in USA M/c in 2-5 y/o(day care) and age >50 Infants may be non-jaundiced Neonates have subclinical infection Incubation 15-45 days (aka Short incubation Hepatitis) Rarely causes fulminant hepatitis Rarely transmitted thru infected blood DDx o Other hepatitides o Viral illness w/ liver involvement (CMV, EBV) o Non-viral hepatitides Clinical presentation o Often asymptomatic (25% adults, 90% <2 y/o) o Anorexia, malaise o hepatomegaly (87%), RUQ tenderness o splenomegaly rare (9%) o Jaundice o Dark urine (bilirubinuria) o Fever variable (precedes jaundice) Workup o LFTs (Liver Function Test) o HAV antibody Laboratory tests o ALT/AST (often > 8x normal) o Bilirubin (usually 5-15x normal) o Alkaline phosphatase (1-3x normal) o Albumin, prothrombin normal o WBC most often normal o Hepatitis A IgM Imaging studies not normally useful No such thing as chronic hepatitis A it is an acute disease whose course rarely exceeds 8 weeks

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Acute disease lasting < 6 wks Rarely prolonged (3-5 mos), no carrier state o o o o o Avoid hepatically metabolized drugs IV fluid replacement for vomiting (rare) Steroids not normally helpful Follow-up as outpatient Overall do not over tax the liver, no alcohol <0.1% fatality rate 60% w/ fulminant recover Evidence of previous disease in 40% of adults

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Px o o o

Hepatitis B - Acute viral hepatitis (a.k.a. serum hepatitis) - Uncommon chronic form (5-10%) - 4000-5000 deaths/yr from chronic HBV - Incubation 30-180 days - DNA virus - 200-300k new acute cases/yr (300 deaths) - At risk populations (blood transmission) o IV drug users o Homosexual males o hemodialysis and hemophilic pts o Health care workers o Neonates/infants M/c in 20-45 y/o DDx o Other viral hepatitides o Other viral illness w/ liver involvement o Non-viral hepatitides Clinical presentation of acute disease o Most often anicteric and asymptomatic o Anorexia, malaise, n/v o Serum sickness (hives, rash, arthralgia) o hepatomegaly, splenomegaly (uncommon) o Jaundice, bilirubinuria, +/- fever Clinical presentation of chronic disease (1-2%) o Similar to acute HBV o Asymptomatic chronic active carrier (have active virus in the system, patient is asymptomatic and contagious) o Hepatic decompensation o Cirrhosis o hepatocellular CA Laboratory tests o HBsAg o Elevated ALT/AST o hyperbilirubinemia o Elevated alk. phos.

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Prevention o o o

IV fluids for dehydration (increased vomiting over Hep A) Treat for hepatic failure, if present Avoid hepatically metabolized drugs (including alcohol) Steroids not helpful Interferon for chronic cases Antiviral agents - famciclovir - lamivudine Liver transplant

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Avoid high-risk behaviors Testing blood supply Hepatitis B vaccine - High risk groups (90% effective) - Childhood vaccination HBV hyperimmune globulin o Given after needle stick o Given after birth w/ infected mom o Given after sexual exposure

Hepatitis C - Viral infection of the liver with HCV - Non-A, non-B RNA virus - Intermediate incubation (15-150 days) - Most common cause of non-alcoholic liver disease in US (40%) - Epidemiology o Transfused hemophiliacs o IV drug users o Occupational needle sticks o hemodialysis Male = female 18-39 y/o mc Clinical presentation Gradual symptom onset Milder that HAV/HBV RUQ tenderness Hepatomegaly Jaundice Dark urine (bilirubinuria) Many are anicteric asymptomatic (75%) Male = female 18-39 y/o mc Clinical presentation o Gradual symptom onset o Milder that HAV/HBV o RUQ tenderness o Hepatomegaly o Jaundice o Dark urine (bilirubinuria) o Many are anicteric asymptomatic (75%)

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Immunity after infection is incomplete Fulminant acute disease is rare (0.1%) Persistent infection is common (50-70%) Results in chronic hepatitis Cirrhosis develops in 20-50% Hepatocellular CA develops in 50% DDx (other inflammation hepatic diseases) Diagnostic workup o Acute hepatitis c antibody o LFTs o Biopsy for complications Rx o Avoid meds metabolized by liver o Otherwise acute Rx is non-specific o Follow-up for complications o Interferon may be helpful in relapses Acute disease lasts <6 wks No vaccine Immune globulin injections are not helpful

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Alcoholic Hepatitis - Most common form of hepatitis - Most common cause of cirrhosis - SSx similar to other hepatitis x flu-like Sx - Hepatomegaly - Splenomegaly more common than viral - Ascites Hepatic Cirrhosis Caused by hepatocellular injury Results in fibrosis ad nodular regeneration Micronodular, macronodular, mixed forms 9 deaths/100k people/yr in us(#11 death) Most common causes o Alcoholism o Viral hepatitis (especially HBV and HCV) Other causes o Drugs (Tylenol), chronic CHF, hemochromatosis, amyloidosis Clinical Presentation o Early - Weakness, fatigability, disturbed sleep - Muscle cramps, weight loss Advanced o Anorexia, weight loss o N/V, hematemesis, due to esophageal varices o Jaundice o Hepatomegaly, ascites o Amenorrhea, due to cholesterol production interference o Impotence in men

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Skin lesions o Spider nevi o Palmar erythema(alcohol abuse) o Glossitis, cheilitis o Ecchymosis CNS damage o Asterixis (intermittent lapse of body position) o Tremor o Delirium o Dysarthria, slurred speech o Coma Laboratory findings o Macrocytic anemia o Abnormal LFTs o Decreased albumin o Leukopenia Rx o Avoid hepatotoxic meds o Treat disease that caused cirrhosis o Treat complications (ascites, varices, CHF))

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Primary Biliary Cirrhosis - Autoimmune disease - Destruction of intrahepatic bile ducts - M/c in females (95%) - 40-60 y/o age group - Associated w/ PSS, SLE, Sjögren’s Synd., RA, and other connective tissue arthropathies - S/Sx o Fatigue (extreme fatigue) o Pruritus o ~50% are asymptomatic o Hepatosplenomegaly, jaundice later on Laboratory tests o Anti-mitochondrial antibodies (98% specific), almost pathognomonic for this disease o Abnormal LFTs Rx o Methotrexate, a commonly used chemotherapy agent, which helps control the over growth of cell in the bile duct o Colchicine o Ursodiol o Liver transplant Pxo Asymptomatic- 10-16 yrs from time of diagnosis o Symptomatic- 7 yrs from time of diagnosis

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Hepatic Tumors - Benign o Hemangioma - Most common benign liver tumor

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- Vascular tumor - Asymptomatic - Found incidentally Adenoma - Rare solitary or multiple tumor - Usually asymptomatic - Found in steroid abusers, OCA users Hepatocellular Carcinoma (old term Hepatomas) Cholangiocarcinoma Metastasis (Most common cause liver malignancy), colon cancer is the most common malignancy which mets to the liver

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Malignant o o o

Hepatocellular CA - Malignant tumor of hepatocytes - Associated with: o Chronic liver disease o Cirrhosis o HBV, HCV o Hepatotoxins(ETOH, steroids) - Clinical presentation o Weight loss, anorexia o Ascites o Hepatomegaly o 33% are asymptomatic Diagnostic evaluation o Elevated AFP in ~90% (alpha-fetoprotein – this protein non-specific) o Elevated LFTs o MRI o Ultra Sound/CT-guided biopsy Treatment o Dependent on size of lesion/mets o Resection o Chemotherapy Px is 20-30% following resection

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Cholangiocarcinoma - Intra-hepatic bile duct malignancy - Rare in USA and Europe – more common in Asia - Presents as a liver mass - Associated with liver fluke infestation – more common in Asian culture - Slow progression to metastasis

Gallbladder Diseases
Cholelithiasis - Gallstones - Affects 20,000,000 Americans - Predisposing factors (Female, forty, fat, flatulence, fair skin) o Fair skin o Female o Obesity

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o ~40 y/o o OCA use o DM ~20% chance of developing biliary colic, passage of gallstones Pts are asymptomatic unless passing a stone S/sx o Colicky RUQ pain o Night pain o Refers to right shoulder o Lasts mins to hours depends on the amount of time is takes for the gallbladder to push the stone through 75% of stones contain cholesterol Ultrasound is imaging procedure of choice Rx-cholecystectomy, ESWL, dissolution (substances which will dissolve gallstones) Px-good

Cholecystitis (inflammation of the gallbladder) Acute and chronic forms 95% associated with gallstones M/c in same groups as cholelithiasis Clinical presentation o RUQ pain/tenderness o Pain radiating to right shoulder o Murphy's sign o Fever (~33%) o Jaundice (25-50%) o Fever, chills, n/v Diagnostic workup o Ultrasound o MRI/CT to rule out more ominous causes Treatment o Laparoscopic cholecystectomy (lap chole) o Open cholecystectomy o Broad-spectrum antibiotics Prognosis o Excellent o 1% complication rate with lap chole

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Cholangitis - Inflammation of bile ducts - Complication of cholelithiasis(~1%) - Occurs during 7th decade and older - Clinical presentation o Charcot's Triad - Fever/chills - RUQ pain - Jaundice o Bilirubinuria - All S/Sx present in 50-85% of pts Diagnostic workup

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o o Treatment o

Ultrasound ERCP endoscopic retro (if US is inconclusive)

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Biliary decompression - ERCP (maybe w/ stent placement) - percutaneous transhepatic biliary drainage o Broad-spectrum antibiotics Prognosis is excellent Chronic disease associated w/ porcelain gallbladder, a premalignant condition

Primary Sclerosing Cholangitis - Diffuse inflammation leading to stricture - Most common in males age 20 – 40 Commonly associated with UC Assoc o Clinical is progress jaundice, indigestion o Malaise, purity, anorexia Poor Px o Most require liver transplant within 10 years Think Walter Patton

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Gallbladder Cancer Adenocarcinoma most common - Asymptomatic unless disease is advanced - Usually found during surgery for stones Weight loss, anorexia Palpable gallbladder, RUQ pain Associated with stones in 80% Porcelain GB also assoc. Poor prognosis

Pancreatic Disease
Acute pancreatitis Chronic pancreatitis Pancreatic Cancer

Acute Pancreatitis - Most often secondary to biliary disease - Enzymes released into pancreas - S/Sx o Severe abdominal/back pain o Fetal position o N/v o Mild jaundice o Shock – as a reaction to the pain - Lipase and amylase levels increased - CT/MRI for Dx Treatment

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o o o o o Prognosis o o

IV hydration NPO NG suction Pain control Treat complications 5-10% mortality associated with the shock Worse in older, sicker patients

Chronic Pancreatitis - Recurrent pancreatitis - Male: female = 5:1 - S/Sx o Recurrent epigastric/back pain o Abdominal tenderness/guarding o Weight loss o Foul-smelling stools, that are chalky white in color and float - Associated with alcoholism/biliary disease - Major DDx is pancreatic CA - KUB may reveal calcifications - 50% pts die w/in 10 yrs(malignancy) Pancreatic Carcinoma - adenocarcinoma - 2nd mc tumor of GI system (colon cancer is #1) - Male: Female = 2:1 - M/c in head of pancreas, carcinoma in the tail will not cause jaundice, because it does not block the duct. - S/Sx o Jaundice o Abdominal pain o Weight loss, anorexia, nausea o Biliary obstruction S/Sx(head tumor) - CT/MRI are best imaging procedures - Poor Px from early mets • o [test material?]

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