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Review GI system - Tubular - Non-tubular Esophagus only location in which involuntary skeletal muscle is found Two types of peristalsis Primary – initiated by swallowing Secondary – involuntary for continuation of food movement Esophagus narrowing where food can become trapped - Thoracic notch - As it passes Aorta arch - Enlargement of left atrium Proteins broken down in stomach Stomach churns food Pancreatic enzymes: lipase and amylase, bound by bile Choledochitis 1

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Review GI system- Tubular- Non-tubular

Esophagus only location in which involuntary skeletal muscle is found

Two types of peristalsisPrimary – initiated by swallowingSecondary – involuntary for continuation of food movement

Esophagus narrowing where food can become trapped - Thoracic notch- As it passes Aorta arch- Enlargement of left atrium

Proteins broken down in stomachStomach churns food

Pancreatic enzymes: lipase and amylase, bound by bile

Choledochitis

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History & Physical Exam History

o A M P L Eo O P P Q R S T o H I S T O R Y

Physical Examo Inspectiono Auscultationo Percussiono Palpation

History A M P L E

o Allergieso Medications – for what conditiono Past Medical Historyo Last Meal / LMPo Events of present illness

O P P Q R S To Onseto Provocative o Palliativeo Quality – character and typeo Radiation / Regiono Settingo Timing

H I S T O R Yo Hospitalizationo Injurieso Social history / Sugar diabeteso Tumors / Traumao Operationso Review of systemso Youth Dz

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Pic: Leg withpitting edema Cardiovascular disease or renal disease

Pic: Pair of hands withclubbing fingers aka: hypertrophic osteoarthropathy over production of bone by periosteum enlargement of terminal tufts may be due to poor O2 assoc. m/c withpulmonary disease

o also GI/GU disease

Pitting → graded 1 – 4 on how deep it pits & how long to return

Pic: Abdomen with LUQ mass/enlargement know where mass is coming from know organs in that area

Mass does not pulsate, does not move, gets larger on bearing downincisional hernia

Physical Examination Inspection

o Symmetry, size, shapeo Lumps, bumps scars, ecchymoses

Auscultationo Bowel sounds o Bruits

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Bulbous soft tissue expansion of finger tips

Inspection investigate asymmetry (eg hernia) ascites → m/c reason for ↑ size (in relation to rest of body) truncal obesity → Cushing’s stomach shape → should be flat (lateral), should be hour glass (A-P) tangential light → outlines shape withshadows m/c scars

o Cesarean – usually low (bikini line)o Cholecystectomy ( usually laparoscopic)o Appendectomy

Other causes of scarso Closed colostomyo Striaeo Splenectomyo Liposuction, GSWo Stab wound

Ecchymoses → bruises

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Percussiono Liver, spleen, diaphragm

Percussiono Liver, spleen, diaphragmatic excursiono LUQ

Tympanic → air in stomach Dull → eaten recently

o Spleen → dullo Liver → dullo rest of abdomen → resonanceo bowel obstruction → dull over obstruction

tympani above obstruction resonance distal to obstruction

Palpationo Organomegalyo Aneurysms

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Auscultationo Borborygmus → bowel sounds [5-35 (N)]

High pitched → use diaphragmo Appreciate change in pitch → eg.↑ pitch

means bowels are working hard to get past obstruction

o May also ↑ or ↓ in frequency No bowel sounds → obstruction

(late) ↑ bowel sounds → early

obstruction Late obstruction → vomit Adynamic bowel → due to blunt impact or post

operative → no bowel sounds Bruits → swishing noise

o Due to turbulence of bloodo m/c infrarenal AAA, renal artery stenosis

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Abdominal Exam Tips Comfortable room temp Pt gowned with abdomen exposed Groin uncovered with genitalia draped Bladder empty Start in non-tender quadrant Use Pt’s hand if ticklish Normal kidney is non-palpable

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Palpation Organomegaly Aneurysms Mass → where is it? Size? Borders? Pulsate? Pain? Firm/soft? Refer

pain? Mobile? Superficial/deep? Palpation start in non-tender quadrant, diagonal to area of pain Superficial → palpate in abdominal wall Deep → palpate in abdomen If mass disappears withabdominal contraction → intraabdominal mass Mass accentuation withabdominal contraction → abdominal wall mass Usually better if mass is mobile

o Benign → only in host tissueo Malignant → invade surrounding tissue, more inflammation,

causing CT formation = less mobile Palpation

Done after auscultation so as not to influence bowel sounds Palpation for pain If ticklish use pt’s hand What type of pain

o Sharp, dull, cramping Decrescendo, crescendo pain → luminal organs usually are the cause Organomegaly

o Usually liver/ spleeno Liver RUQ

Detoxifies Hormones Over 1000 functions

o Spleen LUQ Should not be palpable (unless extremely thin)

o Hepatosplenomegaly usually liver disease blood forming product disease’s

o m/c aneurysm → AAA (infrarenal) most are saccular rather than dissecting palpate with 2 fingers – one on either side of aorta

separation of fingers on pulsation shows lateral dilation = AAA pass

also palpate with 4 fingers on top of aorta thinner pt’s = more pronounced pulsation

not likely to rupture AAA on exam aorta N diameter max = 3.5 cm AAA → produces non-mechanical back pain

Pts are ortho, neuro, and mechanically intacto Abdominal rigidity – muscle tension to point “hard as desktop”

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Normal liver may be palpable 8–12 cm at mid-clavicular line A palpable spleen is enlarged

Abd Exam Tips Comfortable temp Gowned with ab & groin exposed

o Genitalia draped Empty bladder Strong/firm touch if ticklish N kidney not palpable M/c cause of hepatomegaly → alcoholism

Abdominal Regions 4 quadrants

o Rt uppero Lt uppero Rt lowero Lt Lower

9 Regionso R/L Hypochondriac 3 uppero Epigastrico R/L Lumbaro Periumbilicalo R/L Pelvico Suprapubic/Hypogastric 3 lower

Abd Regions 4, 6, 9 systems

o 6 = 4 quadrants and epigastric & hypogastric regions Epigastric

o Duodenum, pylorus, LL of liver, portion of pancreas, some transverse colon, some SI, aorta, celiac trunk, renal a.

o Many things can cause pain here LUQ

o Upper pole of kidney, adrenals, splenic flexure, spleen, tail of pancreas, lt renal a, abd aorta, splenic a

LLLo Desc Colon, sigmoid, lt common iliac, SI, lower kidney pole,

inferior mesenteric a, lt ovary, fallopian, uterus portion RLQ

o Ascending colon, SI, rt ovary, lower kidney, possibly some liver, appendix, cecum

RUQo Upper kidney, gall bladder, rt renal a, transverse colon portion,

biliary tree, head of pancreaso usually pain comes from a structure in that Q

Abdominal Exam Test Rebound tenderness

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o Peritonitis (Rovsing’s sign), push in quadrant with no pain, but pain is felt in different quadrant usually diagonally across.

o PN with recoil Palpation CVA Tenderness (Costal Vertebral Angle, on back where the

12th rib meets spine)o Kidney diseaseo AKA: Kidney Punch

Shifting Dullnesso Asciteso Fluid shifts in different positions

Psoas Signo Appendicitiso Resisted Rt hip flexion

Obturator signo Appendicitiso Resisted internal rt hip rotation

Abd Exam Test Rebound tenderness = peritonitis

o Push in Q catty-corner to pain (in non-tender Q)o Pain in area of complaint = +o Pain upon pressure = organ problemo Pain upon release = peritonitis

Rovsing’s signo For late stage appendicitis (RLQ)o Inflam. due to obstruction → can spread to peritoneum

Costovertebral angle tenderness (CVA)o Punch kidneyso Usually kidney disease – possible quadratus lumborum spasm

psoas sign/obturator sign → appendicitis possible

DX Imaging Barium swallow Barium enema CT scan with contrast MRI scan with contrast Endoscopy

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***EGD – Esophagus gastroduodenal ***Look up and know

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Abd Distention Mechanical Distention – Matter inside or outside the lumen

that physically obstructs the movement of material through the bowel

o Neoplasms (intraluminal / extraluminal)o Post operative adhesionso Abscesso Pregnancyo Herniaso Volvuluso Intussusception

Non-mechanical obstructiono Asciteso Excess gaso Traumao Infection peritonitis

Abd Distension SI, LI, stomach, liver, spleen ↑ size of an organ can cause ab distention m/c cause of distension is obstruction

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DX Imaging KUB (kidney-ureter-bladder) film

o Upright posture & supine positiono So fluid settles in diff. Areaso Looking for air/fluid levelso Mesenteric air/fluid → moves a loto Non peritoneal air/fluid → more fixedo See a lot of calcified lymph nodes in mesentery/omentum

[Higher Kv used – higher contrast – higher grays] Barium swallow

o Opaque on x-rayo Can watch in motion → checks functiono Can follow into duodenumo Can following into small bowelo Not a really good dx tool for small bowelo CO2 tablets withbarium to push barium to walls of bowel

CT scan withcontrasto IV iodineo Or barium

MRI withcontrasto IV usuallyo Not very useful with hollow organs

Endoscopyo Problem with this test → very technical, interpretive skill needed

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o due to intraluminal (m/c) mass or extraluminal

Mechanical Abd Distention Post operative adhesion can traverse a lumen Crohn’s → abscesses Appendicitis →abscesses Incarcerated hernia (can cause bowel strangulation) Volvulus - twisting of bowel

o Inverted U shape (or V-shape)o M/c sigmoid or cecal regiono Obstruction prone to volvuluso Fecal bolus may be twisted off

Intussusceptions → telescoping of bowel {c/cx adhesions, paralysis, ischemia, trauma}

Non-mechanical Abd Distention Ascites → m/c reason for abd distention

o m/c due to alcoholism (portal HTN) Gas Trauma [adynamic ileus - obstruction of the bowel due to paralysis of the

bowel wall, usually as a result of localized or generalized peritonitis or shock. – seat belt injuries most common cause

Infection Peritonitis

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Abd Pain Pattern Diffuse

o Visceral paino Organ involvement

Focalo Parietal paino Organ distentiono Peritonitis

Abd Pain Patterns Diffuse Focal → peritonitis

o Unless full blown → diffuse → entire peritoneum filled with bacteria

Abd Pain Burning

o PUD, GERD, confirmed with a nasogastric tube, worn for 24 hours to measure pH in middle and lower esophagus.

o Epigastric pain should also include cardiac workup, heartburn type pain can be a MI

Cramping (usually from organ distention)

o Biliary colic [typically from gallbladder disease], IBD, IBS, Mesenteric Ischemia

Colicky [very painful initially eventually becoming less to none painful.

o Renal stones, biliary colic, appendicitis Achy

o Constipation, appendicitis, AAA(saccular) Knife-Like(usually very serious)

o AAA (Dissecting / saccular rupture)o Pancreatitis

Sudden onseto Perforation [peptic ulcer perforates], obstruction

[ectopic pregnancy], pancreatitis, o Ruptured ectopic

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Usually not a sign of peritonitis

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Abd Pain Diffuse

o Early appendicitiso AAAo IBD – Inflammatory bowel disease [Crohn’s and

Ulcerative colitis – typically of the left colon]o Peritonitis – if diffuse peritonitis, if the peritonitis is

localized the so will the paino Traumao Obstruction

Epigastrico PUDo GB diseaseo Hepatic diseaseo Cardiac diseaseo Pancreatitis

RUQo Biliary tree diseaseo PUDo Pancreatitiso Renal diseaseo Cardiopulmonary disease

LUQo PUDo Pancreatitis – particularly of the tailo Splenic disease, Infectious mono, lymphoma,

leukemia, o Renal diseaseo Cardiopulmonary disease

RLQo Late appendicitis, pain will migrate to RLQo Crohn’s disease, most commonly affects distal ileumo Obstruction, cecal volvulus, overian cysts o Reproductive diseaseo AAA

LLQo Diverticulosis/it iso Obstruction, sigmoid vovulus o UC – Ulcerative colitis o Reproductive diseaseo AAA

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Periumbilicalo Obstructiono Early appendicitiso AAAo Mesenteric Thrombosis, thrombosis of one of the

mesenteric arteries, the more proximal the obstruction the greater the damage.

o PancreatitisAbd Pain

Nonspecific abd pain 35% - gastritis, heartburn, overeating

Acute appendicitis 17% Intestinal obstruction 15% -

especially with patients who have had previous surgery. Blount force trauma, common from a MVA seat belt

Urological disease 6% Gallstone disease 5% Colonic divertiucli 4% Abd trauma 3% Malignancy 3% Perforated Peptic ulcers 3% Pancreatitis 2% Ruptured AAA <1% IBD <1% Gastroenteritis <1% Mesenteric Ischemia <1%

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Abd Pain Burning – epigastric usually Cramping – usually from organ distention

o Early distention disease is usually not painfulo Organ capsule must be distended to cause paino usually in peristaltic organ

Colicky – crescendo/decrescendoo Usually indicate obstruction in hollow lumen

Eg. Renal/gall stones Achy – hardest to dx

o Anything from constipation to AAA Knife–like – usually serious → constant pain

o AAA, pancreatitis Sudden onset – usually serious

Organ pain usually is in it’s particular Q Always consider cardiac disease in someone withepigastric pain If diffuse pain – harder to determine cause

Appendicitis1. Diffuse or periumbilical pain2. Then localizes to RLQ – McBurney’s Point [a point between 1 1/2

and 2 inches superomedial to the anterior superior spine of the ilium, on a straight line joining that process and the umbilicus, where pressure elicits tenderness in acute appendicitis.]

3. rebound tenderness will be positive4. Sudden relief of pain (rupture)5. Then extreme septic peritonitis → fatal

Most common cause of abd pain – idiopathic (1/3) Blown off by many doctors as gastritis or stomach flu

17% → appendicitis 15% → obstruction 6% → kidney/urological

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Patient over 40 presents with back pain, you should auscultate belly, and perform lateral lumbar film

November 6 th , 2000 74 year old female, woke with back pain, back pain progressed through the day. Daughter visited her, noted mother not feeling well, was lying on couch and not feeling well. Patient tried hot and cold packs to no avail, different positions did not ease pain.Lying on floor with feet and legs propped on couch toward end of day, found this helped and she finally got some sleep for first time that day. Short time later patient advised daughter she was “so tired” and went back to sleep. 15 minutes later she went into full arrest.Ambulance took her to hospital still under arrest.Later in day placed on ventilation, with suspected bleeding AAA.DNR given by son, patient pronounced late that night, early morning

Abdominal Aortic Aneurysm Focal widening > 3.5 cm > 60 yrs, M:F = 5:1 infrarenal (90%) Extension into iliac arteries (66%) Plain film mural calcifications (75-

90%) CT: perianeurysmal fibrosis (10%)

may cause urethral obstruction US: 98% accuracy in size

measurement Angiography: mural thrombus (80%) Complications

o Rupture 25% into retroperitoneum (usually lt) GI tract, IVC

o Peripheral embolizationo Spontaneous occlusion of aorta

AAA S/sx

o Most are asymptomatico Pulsating sensation in the abdomen o Abdominal pain (unchanged by position)o LBP (unchanged by position)o Bruito Radiating pain into legso Cold ↓ extremities, peripheral pulse losso Chocko Sudden death

Imaging

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o Plain films, 75% of the time seen on plain filmso MRI, CT

AAA Cannot find a position of comfort Non-mechanical lesion Wyatt’s mother → only had back pain, no abd pain Normal aorta → 2-2.5cm (average size according to Dr. Wyatt) See AAA → 75-90% on x-ray >3.5 cm = AAA 90% infrarenal , above common iliac a.

o can extend into c. iliac a. (2/3) Add 20-30% to size seen on x-ray = actual size of AAA If pt has AAA = most have coronary artery disease

o Chances are they have HTN and atherosclerosis Atherosclerosis

o Is a long-term vasculitis (inflammatory)o Not just fat/cholesterol depositiono Chronic inflammation → calcifies

Pt known to lose leg or atrophy due to embolization Rupture → STAT surgical emergency

[Picture – Normal aorta and a aortic aneurysm][Picture – Aortic dissection]

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Dissecting/Saccular Dissecting A – pts are very sick, usually dead in 8-10 hrs, usually not seen by

chiropractors Blood is in the wall of the artery, due to the pressure separating the of the

internal lumen. Saccular – m/c to see Dissecting – m/c in thoracic

o usually post traumatico doesn’t cause as much widening as saccularo harder to recognize on x-ray

AAA Most asymptomatic (3-5cm (small)) 3-5 cm

o Monitor 3, 6, 9 monthso At least once a yearo Advise patient to watch for belly pain, discoloration, numbness in the

legs, extremities become cold and or blue, get into doctors office ASAP 5-7 cm

o Patient runs must greater risk of rupture, when over 7cm have a 90% probability of rupture.

o only elective surgery if asymptomatic Blood if very irritating to peritoneum

o Leaking blood → focal pain Stent → inside vessel Graft → replaces vessel

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AAA TX

o 3.5 – 5 cm – careful observationo 5-7 cm – elective surgery (10% rupture/yr)o > 7 cm – non elective surgery (25% rupture /6 months)o symptomatic – non elective

Surgical procedureso Open laparotomyo Endoscopic stint placement

Less than50% withrupture surviveAnorexia Causes

o Infectiono Neoplasm (particularly malignant)o IBDo Constipationo GERDo PUDo Swallowing disorder

Anorexia Muscle wasting is visible, there is not enough protein in the body thus the

body begins to “digest” it’s own muscle Not the psycho case (nervosa) Unwillingness to eat:

o Flu, reflux, peptic disorders, loss of will to live GI problems or systemic disease Ex: liver CA (stage 4)

o Anorexia, cachexia (mm wasting), ascites

Belching, Bloating, Flatulence Aerophagia, the swallowing of air as you speak, eat, sleep

o Most common cause of belching, bloating, and flatulence

Insoluble carbohydrate ingestion Mal-absorption intolerance Lactose intolerance Diarrhea

Belching, Bloating, Flatulence Insoluble carbs

o Norm flora produce gaseso CO2, CH4, sulfur

Mal-absorption disordero Eg. Lactose intoleranceo Eg. Pancreatic insufficiency (fat mal-absorption)

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GI Bleeding Upper GI

o Esophageal variceso Esophageal CAo Esophagitiso PUD gastric CAo Hiatal Herniao Swallowed Hemoptysis

GI Bleeding Lower GI

o Mesenteric thrombosiso Meckel’s diverticulumo Volvulus / intussusceptiono Colon CAo Colonic Polypso IBD (Crohn’s, UC)o Diverticulosis/itiso Hemorrhoidso Anal Fissures

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GI Bleeding Upper GI vs Lower GI Divided by ligament of Treitz

o AKA – suspensory Ligament of duodenumo At duodenojejunal junctiono Helps maintain C-shape

Upper GI S/SX Hematemesis

o Acute ↑ GI bleed above stomacho Massive GI bleed into stomacho M/c cause → esophageal disease, m/c esophageal varices

Coffee ground emesis in gastric acids for some hours Can also B cause by esophageal varices Very common in alcoholics

Prostatitis PID – Pelvic Inflammatory DZ Endometriosis Esophageal CA

o Known for coffee ground emesis usually if any emesis Esophagitis

o Mechanical → eg. Swallowingo Infection

PUD → usually Coffee ground Swallowed hemoptysis

o Can be from pulmonary disease GI bleed scan

o Can see location of bleedsLower GI S/SX

Hematochezia – bright red blood/rectum (BRBPR)o 95% are from the colon downo usually not small bowelo m/c cause hemorrhoidso Blood streaked stool

Suggests that something within the bowel is bleeding and as the stool passes by it becomes streaked. (e.g. polyp)

Melena – black, tar-like stoolo Enzymes in GI turn blood blacko Chronic ↑ GI bleed – melena (or upper portion of ↓ GI)o Must have a lot of bleeding

Blood streaked stools - ↓ GI onlyo Bleeding in lumen

Occult blood in stoolso Only seen from a hemoccult, Guiac testo Suggest bleeding higher up o Reagent turns blue → + for bloodo Must have 3 tests to determine N or blood presenceo Associated with occult cancer

Lower GI Causes Meckel’s diverticulum

o Remnant of vitelline or omphalomesenteric duct Diverticulitis → m/c to cause pain & bleeding than diverticulosis

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Constipation/Diarrhea Constipation, obstipation - Intestinal obstruction; severe

constipation o Fecal impactiono Poor fiber intake (bulk helps hold water and is non-

digestible thus aids in maintenance of bowel) o Poor fluid intake (water)

Poor bowel hygiene, what kinds of food and fluids you intake.

o Colon cancero IBDo Psychiatric cause, anxiety or high stress creates a

pseudo fight or flight response to the bodyo Medicationso Hemorrhoidso Increased iron supplementations, seen common with

infants who have are consuming iron fortified formula.

Diarrheao Infection, most common cause for diarrhea, stomach

flu – viral gastroenteritis. Fungal infections of the bowel would be suggestive of immunosuppression, i.e. aids, or chemotherapy

o IBDo IBS, young females under high stress conditions o Stresso Colon CA, alternating constipation and diarrheao Psychiatric causeo Medications, antibiotics and parasympathomimetic o Lactose intolerance

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Constipation Decrease in volume of stool One of the most common conditions in the USA today

o Spinal manipulation has been shown to improve 50% of constipation cases. Mechanism is unknown.

Fecal impaction – dry & hardo Most severe form of constipation

Poor fiber & fluid intake & poor bowel hygiene → m/c cause

o Bowel hygiene – going to the bathroom when you have the urge

Gastrocolic reflex – reflex to defecate

Colon CA Can cause alternating constipation & diarrhea

Diarrhea Increase in stools volume (usually loose watery stools) results from parasympathomimetics m/c cause = infection, usually viral gastroenteritis IBD → Crohn’s & Ulcerative colitis IBS → usually alternates (constipation & diarrhea)

Nausea & Vomiting Infectious gastroenteritis Obstruction usually in the upper GI first Pregnancy, hormonal changes Severe pain (fight or flight) Cardiovascular disorder, so that the body will not have any

other activities to “concern” itself with. Meds PUD GI cancer Psychiatric disorders – anxiety and high stress

Nausea & VomitingNausea is the symptom of inclination to vomit

Autonomic reflux to many conditions Usually not GI Most common GI cause → gastroenteritis Usually proximal obstruction

Vomiting, the abdominal muscles contract, the stomach then tightens to the point that contents are expelled upwards due to the pyloric sphincter being stronger then the cardiac.

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Heart burn/ Indigestion Dyspepsia Gastritis – most common cause, large fatty meal GERD/Reflux Esophagitis – reflux esophagitis causes

permanent damage to the esophagitis Excess intestinal gas Gas entrapments (hepatic/splenic flexures)

Heart burn & Indigestion Hemorrhagic gastritis

o NSAID’s o Infection, vitamin deficiency

heart burn can B cause by cardiac reason or GI gastritis → spicy, fatty foods GERD → chronic heart burn & indigestion Reflux esophagitis → when GERD cause’s scarring, etc.

Hepatosplenomegaly Hepatomegaly

o Cirrhosiso Hepatitiso Pancreatic CAo Hepatobiliary CAo Cholangitiso Late right sided CHF, portal hypertension as a result

of vena cava hypertensiono Infectious Mono, an acute febrile illness caused by the Epstein-

Barr virus, a member of the Herpesviridae family; frequently spread by saliva transfer; characterized by fever, sore throat, enlargement of lymph nodes and spleen, and leukopenia that changes to lymphocytosis during the second week; the circulating blood usually contains abnormal, large lymphocytes that have a resemblance to monocytes, and there is heterophil antibody that may be completely adsorbed on beef erythrocytes, but not on guinea pig kidney antigen. Collections of the characteristic abnormal lymphocytes may be present not only in the lymph nodes and spleen, but in various other sites, such as the meninges, brain, and myocardium.

Epstein Barr viruso Lymphoma, malignancy of the lymphocyteso Leukemia, malignancy of WBCs

Acute and chronic forms Effects younger and older individuals

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Hepatomegaly Inferior portion of liver becomes convex, the normal liver is

concave, when it becomes enlarged it losses that convex Most common cause → alcoholism → alcohol hepatitis =

cirrhosiso 70 to 80% of the livers parenchymal cells have to

be damaged in order to see alcohol hepatitis. Once damage reached 85 to 90% the liver cannot regenerate.

S/SX: Jaundice Yellow sclera Peripheral edema Bleeding tendencies Ascites

Hepatitiso Viral hep → most common is hep Co Alcoholic hepo Idiopathic hep

Pancreatic CAo Can block hepatic vesselso Obstruct common bile duct

Cholangitiso Inflammation of bile duct systemo Associate with a tri-ad – Charcot Triad

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SplenomegalyCauses:

Anemias Infectious mono HIV, affects T cells Leukemia Lymphoma Myeloma, cancer of bone marrow, cancer of plasmacytes,

multiple myeloma is the most common primary malignancy of bone

Polycythemia Vera, severe over production of red blood cells which results in thrombosis and

Splenomegaly Spleen cleans out dead RBCs Anemias → abnormal RBCs Reactive polycythemia

o Body makes more RBCs for O2 compensation in higher altitudes

Polycythemia verao Overproduction of RBCso Bruising, thrombocytosis

Hernia, a protrusion of a structure through the tissue normally containing it

Groino Inguinal (96%)

Direct Indirect

o Femoral (4%) Umbilical Incisional Hiatus, hernia of the stomach andisorderr

esophagus

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Hernia Examination in Men Fingertip at most dependent portion of scrotum Invaginate scrotal wall to external inguinal ring Gently insert finger into canal along spermatic cord Move finger lateral and cephalad Pt coughs, strains or performs Valsalva maneuver Findings

o Normal or no hernia You should feel nothing

o Inguinal hernia Small indirect hernia may slightly tap end of

finger Large direct hernia may be palpable as mass Direct inguinal hernia may be felt by pad of

fingero Spermatic cord tenderness (funiculitis) septic or

aseptic o Spermatic cord lipomao Hydrocele, smooth fluid filled sac located within the

scrotum

[Photo of large inguinal hernia causing right shift of the penis, with a large hernia auscultate and note any bowel sounds suggestive that the intestines are now contained within the hernia]

Hernias Indirect inguinal hernia

o Most common type, M=Fo Thru deeper (lateral)(internal) portion of inguinal

ring (entrance to canal)o Taps finger on examination

Direct inguinal herniao M > Fo > 40 yrso Through (superficially)(medial) external inguinal ring

(exit from canal)o Touches side of finger on examinationo Easily reduced, rarely enters scrotum

Femoral hernia (Femoral = Female)o Least common, elderly, F>M, 3:1o Through femoral ring/canal, compression can cause

neuro or vessel damageo Often asymptomatic (even strangulated) but can be

very painful. Can form a mass if large enough.

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In the older female you must consider lymphadenotomy via metastasis

Hiccoughs Transient

o High emotion, temp changeo Gastric distentiono Alcohol ingestion

Persistento Uremia, hyperventilation, IDDMo Meds (steroids, barbiturates)o General Anesthesiao Thoracic disorder (pneumonia, CA)o Gastric disorder (PUD, CA, GERD)

Hiccoughs Spasm of diaphragm May be cause by eating/drinking too fast or too much causing distention

on the diaphragm Intractable form → hiccoughs all your life Temp change → usually hot to cold Uremia → urea in blood irritates diaphragm Hyperventilation Diabetes Steroids and barbiturates Prostatectomy

Jaundice Direct Bilirubin (think liver and surrounding liver)

o Extrahepatic obstruction Calculi, neoplasm, stricture Metastatic CA, Pancreatic CA

o Hepatocellular disease Hepatitis Cirrhosis

o Meds (eg. Estrogen)o Jaundice of pregnancyo Itching is a common symptom of jaundiceo Bilirubin builds up in the body and deposited/stored

in the body, ie. Skin, eyes Indirect Bilirubin (think away from the liver)

o Hemolysis (breakdown or RBCs) Congenital anemias Acquired anemias

o Poor marrow productiono Neonatal jaundiceo Impaired conjugation from medications, some

medications interfere with the conjugation of bilirubin

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Jaundice Yellowing of skin

o Icterus → yellow sclera Direct Bilirubin deposition

o Cholelithiasis (gall stones) Earlier seen in eyes Usually eyes and trunk Indirect

o Classic congenital → sickle cello Neonatal jaundice → treated by placing baby under UV light

Rectal Pain & Itching Hemorrhoids Anal Fissures Fecal Impaction Prostatitis PID Endometriosis

Rectal Pain & Itching Most common cause → poor hygiene Pin worms → also common in children Hemorrhoids → rectal varicose veins Anal fissures → babies, diarrhea, constipation

GU S/SX CVA Pain Dysuria Polyuria Urethral Discharge Impotence Hematuria Oligoria/anuria Pelvic Pain Proteinuria Scrotal Swelling

GU S/SX Kidneys → electrolyte balance Micturition reflex → urge to urinate

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CVA Pain Nephrolithiasis Pyelonephritis Glomerulonephritis Renal CA Renal Abscess Spinal disorder

CVA Pain Lungs, kidneys, adrenals, liver on rt, stomach on lt Murphy’s punch M/c cause by kidney conditions Also spinal disorder → eg. Quadratus lumborum spasm 80% of renal stones → Ca based pyelonephritis → infection of renal pelvis glomerulonephritis → usually aseptic

o preceded by strep throato occurs if entire antibiotics are not taken

Renal abscess occurs in – diabetes, drug users, TB, chronic renal disease

Dysuria Cystitis Urethritis Vaginitis Prostatitis Chemical irritants Urethral Diverticulum Bladder CA

Polyuria[Excess production and voiding large amounts of urine; increased number of voids and /or volume of voids]

Cystitis/ Lower UTI Upper UTI DM DI {Triad – Polyuria, Polydipsia, Polyphagia} ADH

hormone; controls H2O loop Meds (Diuretic) CHF / HTN Anxiety Hypokalemia

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Urethral Discharge Prostatitis UTI Interstitial cystitis Vaginitis Gonococcal urethritis NGU (Chlamydia)

Urethral Discharge Discharge can be bloody, contain pus, have an odor

o The discharge occurs when not urinating Prostatitis → septic or aseptic

o Typically middle aged meno Microscopically could contain blood, exudate and or WBC

Interstitial cystitis → most common in diabeticso Due to immunosuppression and glucose in the urine

Vaginitis → most common type: yeast infection (candida) Gonococcal urethritis → the “clap” Most common STD → Chlamydia (in U.S.) most cases are

asymptomatic

Impotence Psychogenic DM Vascular insufficiency Meds Neurologic disease Systemic disease

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SHAPE \* MERGEFORMAT

Impotence Inability to obtain and or maintain an erection Erectile dysfunction, problem with ejaculation

o Can’t achieve or maintain erection Confined to males currently Most common cause → psychogenic (more than 80%)

o Due to stress and hormonal changeo Psychological treatment is usually the treatment of choice

Parasympathetic → erection Sympathetic → ejaculation Stressed males → sympathetic override, overrides parasympathetic

DM Micro vasculopathy – may cause impotence Neuropathy – may cause impotence Meds → parasympatholytics, sympathomimetics Neuro disease → cauda equina, para/quadriplegia Systemic disease → CA, etc. Prostatectomy → cut nerves

SHAPE \* MERGEFORMAT SHAPE \* MERGEFORMAT SHAPE \* MERGEFORMAT

Hematuria T.I.C.S.

o Trauma Renal damage Severe exercise

o Tumor Bladder CA Renal CA

o Infection Glomerulonephritis Pyelonephritis

o Calculi, stoneso Cystitis (Renal),o Surgeryo Sickle cell disease

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Hematuria 2 types: macro & microscopic (occult) Macro → usually more significant, Gross hematuria is when blood can be

seen with the naked eye. Painful types & painless types

o Painless types – worse prognosis usuallyo CA – tends to be ignored

Menstruation is the most common cause of hematuria, especially towards the end of her cycle. If microscopic levels found then wait couple of days and retest

Trauma Sever exercise → eg. Repetitive microtrauma (running cause bouncing of

the kidneys) Renal damage is possible, costal vertebral pain will present, is suspected,

request a UA, if UA is negative then consider musculoskeletal Cysts

Over 50% of population have these Usually small But can be acquired

Sickle Cell Anemia 3 main s/sx → ischemia, infarction, infection

Oliguria/anuria (Low urine output) Renal Failure Low fluid intake Strenuous exercise C H F

Oliguria/anuria Reduced/failure to urinate < 300 ml = anuria, absence of urine output < 600 ml = oliguria, decrease of urine output Most common cause of renal failure = DM

o TX: dialysis, transplant Kidney failure = uremia

o Affects BP, acid/base balance, electrolytes Low fluid intake = usually oliguria

o can only go with out fluid for 48-72 hrs sweat the most when sleeping (besides exercise) CHF can cause renal failure Pre-renal failure = m/c not enough blood going to kidneys Intrarenal failure = problem in actual kidney Postrenal failure =

obstruction past the kidneys

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Pelvic Pain Dysmenorrhea Fibroids (leiomyoma) Adhesions Cystitis Endometriosis, IBD, due to the sigmoid colons location

Pelvic Pain- referring anteriorly- Most common cause = constipation / intestinal gas (left side) Dysmenorrhea (Most common organic cause)

o Painful (outside normal, severe pain) during menseso Cause: thyroid problem, infection, pre menopause, fibroids,

endometriosis Fibroids

o Benign tumor of uterus (Uterina leiomyoma → smooth muscle tumor with fibrosis tissue interlaced)

o Found on plain films of lumbar spine – very commono Possible to become malignanto Can be very large

Adhesions post operative Cystitis → m/c cause = e. coli IBD → Crohn’s, Ulcerative Colitis

Proteinuria Nephritic syndrome Malignant HTN C H F DM, damages the kidneys Sickle Cell disease Idiopathic proteinuria, found in another wise healthy adult,

all other labs return normal, no physical signs. Some patient’s simply leak proteins without an underlying cause and the condition is self limiting

Pyelonephritis Pregnancy Myeloma, leukemia, lymphoma

o Make certain to review Bence-Jones Proteins

Proteinuria Protein not normally in urine because it’s too large Occurs with damage to basement membrane Malignant HTN → Increased BP, enough to cause tissue damage

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Scrotal swelling Testicular torsion Epididymitis Trauma, direct bruising Hernia, auscultation of the scrotum which reveals bowel

sounds Tumor, Testicular cancer one of the most aggressive of

cancers in regards to the speed it travels. Hydrocele Varicoceles

Scrotal swelling can be the scrotum or the contents of the scrotum

Scrotal Swelling Testicular torsion

o Spermatic cord & vessels twisto Jumping up and then landing helps to “untwist” the testicular

torsiono Testicular torsion is an emergent condition o

Varicocele → “bag of worms”, varicose veins Hydrocele → fluid filled, tubular cysts

ADDITIONAL NOTES:

Dysuria Painful urination (burn) Cystitis → bladder infection

o F > M, due to poor urinary hygiene (“holding it”)o M/c than urethra because shortero M/c → e. colio Then Proteus Moraliso TX: pure cranberry juice for 2 wks (boronic acid takes place of

antibiotics)o Anteverted bladder → not all urine is excreted

Urethritiso Most common cause → gonorrhea, o Secondary → chlamydiao Bladder and urethra CA can cause urethritiso Fungal → candida albicans

Vaginitis – infection of vagina or vaginal introitus (opening)o Due to poor hygieneo Most common fungal infection → yeast infection (candida

albicans Prostatitis

o 2 forms → septic / aseptico Septic → bacteriao Aseptic → autoimmune/antibody reactiono Cause pelvic and rectal pain, discharge from penis, o Capacitated → can be caused by stones → stasis backup

Chemical irritantso Latex on condoms

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o Medso Detergento Lubricantso Cologneo Douche

Urethral diverticulumo Out pouching of hollow mucosao Can become obstructed and infectedo Can be due to bladder CAo Diabetics get recurrent cystitis and other infections all the timeo Air gets in wall of bladder → holds bacteria → bladder ruptures

→ death Polyuria – excessive urination production

o Cystitis/lower UTI (hurts to hold urine)o DM → micro neuropathy (vessels supplying bladdero Hypokalemia → osmotic pressure gradient

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Test Two Start Now

EXAM II

ESOPHAGUS- Propel food from the oral pharynx [not mouth] to the stomach- No real digestive functions- Can swallow standing on your head because of peristalsis- Lower 2/3 smooth involuntary muscle, Upper 1/3 striated

voluntary muscle (only voluntary smooth mm. In body)- Epiglottis keeps food from going into trachea- Primary Peristalsis (Reflex-initiated by swallowing)

o Initiated by swallowingo Propels food

- Secondary Peristalsis (peristalsis in lower 2/3)o Not initiated by swallowing, done so by the food

which is already in the esophaguso Propels food through lower esophagus

- Tertiary Peristalsis (Curling phenomenon; Cork screw appearance)

o Seen in the elderlyo No propulsion

Fibrillation of the esophagus; doesn’t cause any movement; is due to aging and breakdown of myenteric plexus/ usually seen in elderly

ESOPHAGEAL TUMORS- Where food gets stuck

1. Thoracic inlet2. Pharyngeal Esophageal Sphincter (Larynx)3. Aortic Knob (because of aorta uncoiling leaves an

indentation in the esophagus)a. When the aorta uncoils due to aging and

atherosclerotic Disease4. Left Atrium5. Cardiac Sphincter (lower esophageal)

Patients can usually with great accuracy point to the location where the bolus is “stuck”

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ESOPHAGEAL NEOPLASMS- Malignant tumors are most common (85-95%)- Leiomyoma is the most common benign tumor of the

esophagus(Fibroid in the uterus)o Sessile broad, wide baseo Pedunculated has a stalko Most are sessileo Most in lower esophagus (because of reflux)

- Most tumors occur in the lower esophaguso Due to reflux

- Squamous cell carcinoma is most common, squamous cells line the esophagus

- 7.6/100,000 cases in USA- 130/100,000 cases in China

o Because their diet is high of nitrites, smoked foods

- M:F 3:1- Most patients greater than 60 years of age- Most are asymptomatic because there is NO expansion

in the lumen, NO bleeding, not much pain, hematemesis or melena

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- Dysphagia is a late symptomo Leads to these being unknown until metastasis

- Patients don’t know they have usually until they become malignant

- Adenomas, lipomas, angiomas all possible in the GI tract. Think of the structures in the GI tract and the types of tumors associated with that type of tissue

- 9 out of 10 esophageal tumors are malignant o Esophageal tumors present very late

ESOPHAGEAL CANCER- Causes obstruction of the hollow lumen

- Etiologyo Alcohol abuse associated with 80-90% of cases

Cirrhosis Portal HTN Esophageal Varices CA

Higher incidence of reflux (irritating to epithelium)

Alcoholics are usually smokers Alcohol also irritates the esophagus itself

o Cigarette Smoking Cigarettes swallow nitrites [via salvia

and swallowing air]CAo Nitrate Ingestiono Chronic Achalasia, poor relaxation of the

proximal end Esophageal spasm (stenosis) Proximal end dilates; food gets stuck &

irritates and ferments Common sign is very bad breath

especially when they belch Swallow dysphagia regurgitation

o Chronic GERD/Barrett’s Esophaguso CA obstruction of hollow organregurgitation

- Differential Diagnosiso Achalasiao Diffuse Esophageal Spasm (DES)

Like the cold ice cream chest pain that is never ending and 10x worse

Pain lasts min to hours

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o Esophageal Rings Fibrocartilaginous ring that narrow the

esophagus Schatzki’s Upper esophageal ring Lower ring

o Scleroderma (Progressive Systemic Sclerosis, newest term)

Connective tissue disease Hardening of the interstitial tissues

narrowing and lack of peristalsis dysphagia

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ESOPHAGEAL CANCER - Physical Findings

o Dysphagia mc symptom usually asymptomatic until late stages of

CA motor problem – dysphagia with both

solids & liquids obstruction – dysphagia with solids early

& progresses to dysphagia with fluids CA cachexia occurs/wt loss just skin

& fato Weight Loss, suggestive that CA has

metastasized o Cervical Adenopathy

Virchow’s nodes Enlargement of supraclavicular

lymph node Common with GI malignancy Many times is first sign

o Hematemesis – vomiting of blood / Hemoptysis – spitting up blood

o Hoarseness Due to compression or destruction of

recurrent laryngeal in the mediastinum o Cough with clear sputumo Mets to liver, pleura, lungs with associated signs

and symptoms Mc presentation if mets to lung is

asymptomatic- Diagnostic Imaging

o Double contrast esophagramo (With a barium swallow the “shoulder” sign is

key 90 cutoff now use endoscopy instead get lung & ab CT/MRI to check for mets

o Esophagoscopyo Chest/abdominal CTo Abdominal MRI

Mediastinum lymph nodes would be involved with esophageal cancer if metastasis has occurred

- Laboratory Testso Done also to check for mets

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o CBCo Blood Chemistrieso Liver Enzymes, again looking metastasis, liver is

a common area for the metastasis to occur - Treatment

o Resection if no mets En bloc Resection during surgery to

see if they get all out Take out CA with normal tissue around it Lab makes sure clean tissue is found

around CA to ensure complete removal Only done if no mets

o Stomach/colon used for replacement

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o Radiation Therapy Targets rapidly changing/high turnover

cells CA cells Hair Gonads Bone marrow

Some divide too fast or too slow and are unaffected

Ex; renal cell CA outpaces chemo/radiation

Radiation not very effective with this cancer

o Chemotherapy- Prognosis

o Surgery 20-50% (all based on 5 year survival rate)

o Radiation 6-20% Have a node Not very effective again, due to

surrounding organs and tissueso Chemotherapy 15-80%

Kills cells that are in the S1 phase (immature cells) that are rapidly dividing

Hair, gonads, bone marrow are all affected because they turn over very rapidly

BENIGN ESOPHAGEAL TUMORS- Tumor Types

o Leiomyoma is most common Tumor in smooth muscle Found most commonly in the uterus

o Papillomao Fibrovascular Polyps hamartoma

Hamartoma overgrowth of normal tissue, made up of normal and fibrous tissue

- Very Rare

ESOPHAGEAL INFLAMMATION

ESOPHAGITIS- Reflux Esophagitis

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- Acute Ulcerative Esophagitis- Esophageal PUD- Crohn’s esophagitis- Infectious Esophagitis

o More commonly in immune suppressed patients- Chemical Esophagitis

REFLUX ESOPHAGITIS- Reflux of gastric contents with damage

o Contents reflux up through cardiac sphincter with force and through the lower esophageal sphincter

o Causing linear and nonlinear erosions of the esophageal lining

- Progression of GERD- Incompetent LES- Often associated with hiatus hernia

o Protrusion of the stomach through the hiatus- 30-60’ (minutes) post-prandial/reclining heartburn- NOT GERD GERD damage is reversible

o Is “GERD” gone wildo Permanent damage to esophagus o More severe thus causes strictures

- TX with Nexiumo GERD tx: Prilosec & Prevacido Due to incompetent lower esophageal sphincter

ACUTE ULCERATIVE ESOPHAGITIS- Seen in patients with PUD- Associated with frequent vomiting

o Alcoholics, chemotherapy patients, bulimics, etc.o Eventually leading to strictures, thus dysphagia

sets in depending on level of dysphagia as to weather solids and or liquids are involved

o Regurgitation is often involved Can lead to laryngitis

- Contracted fibrotic lower esophagus results

INFECTIOUS ESOPHAGITISInfection of the esophagus is rather unusual

- Immunosuppressed patientso AIDS

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o Malignancieso Diabeteso Burn patientso Transplant

(Long term corticosteroid treatment)- Organisms

o Herpes Simplexo Candida Albicans

Typically found in the vaginal region of females and faces of children

Pic: Candida Esophagitis, occurs especially with immunocompromised patients

o CMV (Cytomegalovirus), causes encephalitis in kids

- Dysphagia, Odynophagia (Painful swallowing), Chest Pain – more of a burning sensation instead of a crushing pain

- Treated with Antibodies

MECHANICAL ESOPHAGITIS- Swallowed object becomes lodged- Lodge at narrowed portions

o Laryngopharynxo Aortao Gastroesophageal junction o Left Atrium (not very often unless preexisting

CHF)- Objects include coins, pills, bone pieces

o 3 main groups that do this: Elderly, children, and insane

- Leads to ulceration, maybe perforationo Which can lead to mediastinitis

- Treated with an EGD, scope with surgical attachments on the end.

ESOPHAGEAL VARICESEnlarged tortuous veins in the esophagus, typically occurring in the lower 1/3 of the esophagus

- Varicose veins of the esophaguso Alcohol is the most common cause portal

hypertension (pressure increased in portal venous system, blood backs up)

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- Lower 1/3 submucosal veins involved- 1/3 of patients bleed

o Alcohol Cirrhosis Esophageal Varices Bleeding out

- Caused by portal HTN by hepatic cirrhosis- Highest mortality of any UGI bleed

o Peptic Ulcer Disease most common reason for UGI bleed

- Coffee ground emesis, hematemesiso Time depends on which you will see

- Treated with sclerotherapy, compressiono Compression Bougie balloon down the

lower esophagus and the balloon flattens out the varices

o Sclerotherapy inject hardening agent that hardens (sclerosis) the walls so they can no longer extend also used in peripheral vascular disease

- S/Sx o Pt has some pain and dysphagiao Symptoms are not extreme

ESOPHAGEAL DIVERTICULALocalized outpouching of tubular viscus

- Usually acquired (congenital forms are rare)- Two Types:

o Traction (extraesophageal) Mediastinal mass (inflamed lymph node

next to esophagus)that as it grows attaches to the esophagus as patient swallows and breaths it pulls on the wall months to years creates a weak spot that allows the outpouching

Something pulls on esophagus from the outside

Eg; an attached neoplasm Most common in middle

esophagus.o Because most lymph nodes

are in mediastinum their enlargement can cause them to become adherent to the esophagus

o Pulsion

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Weakness in the esophageal wall (where the vessels enter a lot of time) that eventually becomes weak and forms a diverticula

Occurs from a pushing out of a weak area of the esophageal wall where the small micro vascularity occurs to supply blood to the esophagus

Most common lower/upper esophagus.

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- Occur anywhere in esophaguso Middle esophageal are tractiono Upper/lower are pulsion

Lower just above the diaphragm Epiphrenic diverticula (just above diaphragm)

ZENKER’S DIVERTICULUM- Pulsion Type- Occurs at pharyngoesophageal junction

o Can be very large in size- Loss of upper esophageal sphincter laxity- Retains food- Signs/Symptoms

o Halitosiso Spontaneous Regurgitation

“Verp” – ½ vomit/ ½ burpo Nocturnal choking

The position they are in Recommended not to eat within a few

hours Neck mass Can sometimes see peristalsis in the

mass- Complications – 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, foul smelling sputum)

MISCELLANEOUS DIVERTICULA- Epiphrenic Diverticulum

o Occur in lower esophaguso Normally asymptomatic

- Middle Esophageal Diverticulumo Usually tractiono From mediastinal lymphadenitis

G.E.R.D.- GERD reflux esophagitis Barrett’s esophagus.

Esophageal. CA always rule out cardiac Disease first

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- 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

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- Incompetent lower esophageal sphinctero Stuff from your stomach comes back up into the

lower esophagus because the esophageal sphincter is not functioning correctly

o Believes because of agingo Reflux Esophagitis Barrett’s Esophagus

Squamous cell carcinomao Heavier a person is the more chance they can

have because increase in intra-abdominal pressure

- Incidenceo 60% of adults have heartburno 80% of pregnant women have GERD

- S/Sxo Heartburn (pyrosis)o Dysphagiao Regurgitationo Sour taste in the moutho Can be confused with angina pectoriso Chronic cougho Bronchospasm, due to irritation of the bronchi

airway o Laryngitiso Early Satiety (Getting full fast)o Belching/Bloating

- Contributing Factorso Chocolate (caffeine and fat), Yellow Onions,

Peppermint, Garlico Tobacco (nicotine and causes sphincter to

relax), Alcohol (fat and causes sphincter to relax), Caffeine

o 70% of GERD suffers have a hiatal herniao Beta Blockers (control BP and angina), Ca++

Channel Blockers, nitroglycerin Causes dilation of lower esophageal sphincter

o Gastric Acid Hypersecretion- Diagnosis

o 24 esophageal pH monitoringo E.G.D. – final dx for GERDo U.G.I o Manometry, to rule out diffuse esophageal

spasms- Treatment

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o Avoid triggers (diet modification)o Proton pump inhibitorso H2-blockers (cimetidine – Prilosec )o Antacidso Fundoplication

Reserved for pts with daily reflux Stomach is wrapped around esophagus 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.

BARRETT’S ESOPHAGUS- Pre-malignant- Associated with chronic reflux (5-10% incidence)- Stratified squamous manifests to columnar epithelium,

a pre cancer action- 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 who have GERD

- Dxo EGD, biopsy almost always accompanies an

EGDo Biopsy

- Rxo Laser Ablationo Fundoplicationo Surgical Resection (En Bloc if area is large

enough)

ESOPHAGEAL MOTOR DISORDERS- Achalasia- Scleroderma- Diffuse Esophageal Spasms

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ESOPHAGEAL ACHALASIA- Spasm (shut tight)of lower esophagus with pre-stenotic

dilation which makes peristalsis ineffective - 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

o Chest paino Vomiting of undigested foodo Aspiration, can develop pneumonia and dieo May be confused with anginao Colicky type pain

Crescendo/decrescendo type pain Stone, Ureters

- Etiologyo Degeneration of myenteric plexus

Viral Herpes Zoster Measles Virus

Autoimmuneo Not completely understood, true etiology not

known

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- Diagnosiso EGD with manometryo UGIo Tests to rule out other causes (eg: EKG)

Especially with age group one wants to rule out MI

- Treatmento Medical

Smooth muscle relaxants (70% effective) Nitrates Calcium channel blockers Botulinum toxins injection

mechanical dilation (90& effective) Bouginage mechanical dilation

Esophagomyotomy (90% effective), incise into the muscle (sphincter – draw back, reflux)

- Prognosiso Excellent with appropriate RXo Long standing Disease increases risk of CA

SCLERODERMA - Aka: progressive systemic sclerosis (PSS)- Means hardening of the skin

o Primarily effects the skin, but is not limited to the skin

o Tissue thickens and hardenso Severe hardening of lips to point must be tube

feed- Sometimes must replace the esophagus

o Parastasis 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

- Multisystem disorder often affecting the esophagus o Lose ability to have peristalsiso Becomes very narrow and can develop strictureso EGD used to diagnose

- 75% have esophageal involvement- Fibrosis and inelasticity results

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- Signs & Symptomso Dysphagiao Esophageal reflux/regurgitationo S/Sx associated with scleroderma

- Diagnosis o EGDo UGI

- Reaction with smooth muscle relaxants- Etiology - unknown

DIFFUSE ESOPHAGEAL SPASM- Ice cream eating too fast is the same pain, “brain

freeze”- Pain lasts minutes to hours- Usually end up in the ER thinking they are having a

cardiac problem- Diffuse sustained contraction (spasm) of esophagus- Etiology unknown- Can be confused with angina pectoris- S/sx

o Substernal chest paino Dysphagia with pain, worsened by swallowing,

key differentiating featureo Regurgitation

- Dxo EGD (Esophagogastroduodenoscopy)o UGIo With barium swallow on x-ray appears as a cork

screwo Reaction with Ca++ channel blockers/nitrates

Causes patient to have reflux

DISEASES OF THE STOMACH- Gastric Tamponade (fluid around the heart ventricles

and atria can’t contract)o A pressure equilibrium develops outside the

heart as insideo Blood in the stomach from pillso Can lose 3-5 cc of blood per aspirin or other

NSAIDo Coated so that it will pass the stomach and be

absorbed in the small bowel

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GASTRIC ANATOMY- Stomach B12 absorption (intrinsic factor), storage, mixing, mineral absorption- Rugae increases surface area inside the stomach for production of HCl and pepsin

- GE Junctiono Gastroesophageal Reflux Disease

- Funduso Usually holds gas

Magenblase air in the stomach- Antrum- 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

- Curvatureso Lesser curvatureo Greater curvature

More metabolically active (because of where food sits)

- Estimated that 3 – 5 cc of blood is lost with each aspirin taken that is not buffered

EGD ANATTOMY- Normal antrum and pylorus (pictures)

GASTRIC PERISTALSIS

GASTRIC TUMORS

GASTRIC CANCER90% of tumors in the esophagus are malignant

- Occurs anywhere in the stomacho 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

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- 2 - 4X more common in 1st degree relatives- Male : Female 1.6:1- > 55 y/o- 7/100,000/year- Most common in blood group A- No symptom complex presented early in the Disease- Pic: 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 factorso Diet rich in additives (smoked, pickled)o Atrophic gastritis

Inflammatory disease of the stomach where there is atrophy of the rugae

Sequela : B12 deficiency pernicious anemia

o Pernicious anemiao Tobacco useo Hispanic, Japaneseo 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- DX

o Stool guaiac test test for bloodo Any male > 40 with anemia, has GI

malignancy until proven otherwise

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GASTRIC CANCER S/SX- Adenocarcinoma tends to mets to bone and organs- 18% survival

o but 50% survival if caught in stage 1o 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 antiacids

o Helps to differentiate from ulcers or reflux, both of which are often relieved by the use of antiacids

- Pain exacerbated by food- Pain relieved by fasting- Dysphagia

o With this tumor is near proximal stomach- Nausea and Vomiting- 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)- FOB, fecal occult blood test

o Will have black tarry stool if blood occurs in the stool

- Hemoglobin <12g/dl- Hematocrit <35- EGD- UGI (not done very often anymore)- CT/MRI for nodes mets

o 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%, due to the abundance of

glandular tissue, {adeno-, glandular}

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- Lymphoma 6%, malignancy of lymphocytes {mediastinum area is the most common area for a lymphoma}

- Gastric Sarcoma < 4%- Leiomyosarcoma < 1 %

GASTRIC CA TREATMENT- surgical resection, quit 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, research has shown this

treatment has very low benefit for gastric cancer. 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

- 18% 5 year survival rateo 57% with local Disease (stage I)o 19% with regional spread (stage II)o 2% with distal mets (staged III)

BENIGN GASTRIC TUMORS- Leiomyoma – fibroid tissue usually found in the uterus,

benign tumor of smooth muscleo Common tumoro Rarely symptomatico Only with obstruction

- Adenoma – benign tumor of glandular tissue, aka polyps

o Polypso 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 Most remain benigno Can obstructo Over 2cm, have malignant potential

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GASTRITIS- Erythema – reddening (aka injected)- Hemorrhage - Erosions - types

o erosiveo non-erosive, non-specifico specific

- s/sxo post-prandial (after eating) indigestion/paino Nausea and vomiting o bloating

- 50% have H. pylori (spiral shaped bacteria)

EROSIVE GASTRITIS- Etiology

o NSAID’so Alcohol(ism), portal HTN – venous congestion

decreases the removal of waste from the stomach blood supply.

o Stress from major illness (burns)- Hemorrhage also common with this Disease- Usually asymptomatic- Can produce pain, hematemesis, n/v- Diagnosed with EGD

NON EROSIVE, NON SPECIFIC (Common from over eating)

- H. pylori gastritiso Spiral gram (-) rodo Causes acute superficial mucosal Diseaseo S/sx

Nausea and vomiting Pain

- Atrophic gastritis

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o Associated with pernicious anemia – not producing enough intrinsic factor

o Autoimmune, achlorhydria (absence or reduction of HCl in stomach)

o Glandular hypertrophy and metaplasiao 3x increase gastric adenocarcinoma over the

general population

SPECIFIC GASTRITIS- Ménétrier’s Disease

o Giant fold gastritis (the rugae become very large)o Enlarged thickened gastric rugae

Get hypoproteinemia due to enlarged rugae

Cause’s edema, pleural effusions, etc.

o Severe protein loss Proteins are metabolized in stomach

o Hypoproteinemiao idiopathic

- Granulomatous gastritiso Crohn’s Disease (a chronic inflammatory

granulomatous bowel Disease), TB, sarcoidosis (idiopathic autoimmune disease that normally affects the lymph nodes of the chest, found primarily in young black males)

o Treat specific disorder- Phlegmonous gastritis

o Phlegmon – aggressive large abscesso Abscess from fungal, bacterial, parasitic infectiono Emergent gastrectomy and IV antibioticsTreatment is the removal of the stomach.Common among aids patients (immunosuppressed)

PEPTIC ULCER DISEASEDef: Ulceration of the stomach or duodenum “Ulcer Crater”

- ulcer a crater that penetrates the liningo typically < 1 cmo larger than 2 cm malignant potential

- Go through at least the mucosal layer- Malignant ulcer malignant tissue with an ulcer inside

of it

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- Normal acid production with lowered protection ulcers

- Normal protection with overproduction of acid ulcers

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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 secretiono 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

- Other ulcerogenic substanceso 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 out and helps with healthy cell turnover

Diabetics do not prone to ulcerso Normal cell renewal

Diabetics do not prone to ulcers Chemo patients

- 500,000/year- Duodenal : Gastric 2:1 - Predisposing factors

o High stress Increase histamine cause ↑ acid

production Activates sympathetics and shunt blood

away from stomacho Cigarette Smoking

Swallowed chemicalso NSAID use

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

Diabeticso Decreased bowel function,

high incident of PUD

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- H. pylori (produces urease) there is a inferred or coincidental correlation between H. pylori existence and ulcers

o Increases gastric acid secretiono 75% of patients are infected with H. pylorio 75% have recurrence in 1 year without

antibioticso 20% with recurrence with antibiotics

- NSAID useo 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

Gastric Bleeding (photo)Blood is very irritating to the stomach, thus bleeding in the stomach Signs and Symptoms

- Epigastric Paino Burningo Gnawingo Cramping

- Relieved by foods and or antacids (short term - pt. can become addicted)

o Gastric ulcers - eating makes it bettero Duodenal ulcers - eating makes it worse

- Pain is clustered (days-weeks)- Long symptom free periods (weeks-months-years)- Changes in pain

o If relapse and pain is worse this time May mean CA May mean ulcer may perforate

Differential Diagnosis- GERD- Reflux Esophagitis, most common condition confused

with PUD- Gastric CA, particularly if there is a change in the pain

pattern

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- Gastritis- Pancreatitis- Cholecystitis- Cardiac disease

Diagnostic Workup- Endoscopy

o Esophagogastroduodenoscopy (EGD), almost universally the means of diagnosis

o 95% accurate (5% due to human error)o Biopsy ALL lesionso Cancer / benign cannot be differentially

diagnosed by sighto Also biopsy for H. pylori

- Upper GIo BaSO4o Not as reliable as EGDo No biopsy capabilities

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LARGE GASTRIC ULCERPERFORATED DUODENAL ULCER

TREATMENT- Antibiotic therapy (clarithromycin – which is harsh on

the stomach lining)- Omeprazole- H+ pump inhibitors- Stop Smoking- Stop NSAID use- Diet Changes

o Bland Diet- Stress Reduction

o Because of sympathetic reactiono Valium (classic drug prescribed)

- Manipulation in conjunction with medical therapy has been proven beneficial to the patient

o Don’t use milk anymore because the sugar in it can help feed the bacterial and can actually make the ulcer work in the long run

COMPLICATIONS- GI Hemorrhage

o Most common (50% of all UGI bleeding)o 10-20% is bleeding clinically significant

Cause sx and problemso 80% stop bleeding spontaneouslyo Mortality rate is 6-10% of the 20% who do not

stop bleeding spontaneously Occult blood don’t know it’s there

o Anemiao Cancer

- Perforationo 5% incidenceo Usually on anterior wall

Because it’s thinnero Zollinger-Ellison should be considered

- Gastric Outlet Obstructiono At pylorus or duodenal bulbo 2% Incidenceo From tissue obstruction scar tissue (fibrosis)

obstruction

Zollinger-Ellison Syndromeo Uncommon cause for PUD

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o Occur because of Gastrin secreting tumors (gastrinoma)

o Cause multiple peptic ulcerso Perforation is relatively common

Bleed outs commono 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

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- 90% with EGD esophagitis have a hernia- 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

TYPES OF HERNIAS- Sliding (most common)- Paraesophageal (AKA: Rolling Esophageal Hernia)- Short Esophagus- Intrathoracic Stomach

SIGNS AND SYMPTOMS (same as reflux with the exception of the addition of borborygmi

Heartburno Because also have GERD

- Dysphagia- Regurgitation- Chest Pain (burning)- Postprandial fullness

o After eating- GI Bleeding

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- Dyspnea- 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 Refluxo Burning Chest Paino Regurgitation with recumbency /fatty mealso 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- Should be surgically reduced- May become strangulated

o Lead to ischemia (loss of blood supply)

MISCELLANEOUS HERNIAS- Short Esophagus Type

o Variation of slidingo Uncommono Congenitally short esophagus

- Intrathoracic Stomacho Very rareo Entire stomach in chesto Incompatible with life

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DIAGNOSTIC WORKUP- Exclude other more serious conditions- EGD- UGI- Blood tests non-specific- Will find rugae above the hemidiaphragm

DIFFERENTIAL DIAGNOSIS- PUD- Angina- Esophagitis- GERD- DES (Diffuse Esophageal Spasm)- Achalasia- Diverticulum- Esophageal Cancer

TREATMENT- Diet changes

o Avoid caffeine, chocolate, mint, etc.…o Avoid drugs (Ca++ channel blockers)

- Weight loss- Small meals- Sleep with head elevated- Manipulation- Antacids, H+ pump inhibitors, etc.…- Surgery for refractive disease

COMPLICATIONS- Erosive esophagitis- Ulcerative esophagitis- Barrett’s esophagitis- Stricture- GI hemorrhage

Colon- Review normal anatomy and structure of the color- Review blood supply to colon

o Blood supply interruption Mesenteric Thrombosis

Diabetics Trauma causing vasocompression

- Colonoscopes used to view the colon

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Tapeworm –- S/SX abdominal pain, weight loss-

INFLAMMATORY BOWEL DISEASE- Irritable bowel syndrome- Crohn’s Disease- UC- Antibiotic Associated Colitis- Bacterial Colitis (Food Poisoning)- Appendicitis

IRRITABLE BOWEL SYNDROME- aka: Mucous colitis, spastic colon- 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, 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 gaso Abdominal tendernesso Pain often relieved (temporarily) by BMo No blood in stool, important differential feature

from Crohn’s and or ulcerative colitis o Sign and symptoms present for 3 months before

dxo Hyperactive bowel sounds

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- Major concern with this condition is maintaining the patients hydration level due to the condition being in the colon

- D/DX (other diseases which cause cramp type pain and diarrhea)

o Crohn’s Diseaseo UCo Diverticulitiso Colon CAo PUDo Chronic pancreatitiso Biliary Disease

- TXo High fiber diet – helps bulk up the stool and

helps retain fluido Fiber supplementation (psyllium)o Anti-spasmodics

Imodium Lonotil Bentyl

o Eliminate stresso > 60% respond to RX within 1 year

CROHN’S DISEASE- chronic granulomatous inflammatory Disease- regional enteritis (aka for Crohn’s)- debilitating, often requiring surgery- 1:1000 population- Caucasians, Jews- Unknown etiology- Affects young people- Pathophysiology

o Location 33% involve terminal ileum 50% involve distal ileum/proximal colon 20% involve colon only Can involve any portion of GI tract

o Transmural DISEASE Inflammation (granulation tissue) Ulceration Stricture Fistula

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abscess- S/SX

o Abdominal distention/bloatingo Mass suggests abscess formationo Crampy abdominal pain (RLQ)o Hyperactive Bowel Soundso Non-bloody/bloody diarrheao Perianal fissures/fistulaso Bowel obstructiono Crohn’s arthropathyo Low grade fever, palloro Weight loss, fatigue

- Diagnostic Evaluationo CBC

Anemia Decreased H&H

o Electrolyte imbalanceo Vitamin B12 deficiencyo Endoscopyo UGIo LGI

- Presentation Patternso Chronic inflammatory Disease (mc)o Intestinal obstruction from stricture abscesso Fistula formationo Perianal diseaseo Extraintestinal

- D/DXo UCo IBSo Infectious colitis (yersinia, TB, Salmonella)o Parasitic infection (amoebiasis)o Ischemic colitiso Diverticulitiso Colon CA

- TXo Nutritional supplementationo Low residue diet withobstructiono High fiber diet with diarrheao Medications

Sulfasalazine Corticosteroids Immunosuppressive drugs

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o Monitor vitamin levelso Surgery for obstruction, fistulae, etc.

- Complicationso Obstructiono Abscess formationo Fistula formation (inter-organ, skin)o Perianal fissureso Colon carcinomao Hemorrhage/shocko Malabsorptiono UC

- Epidemiologyo Chronic superficial inflammationo Unknown etiologyo Aka-idiopathic proctolitiso 100/100,000 incidenceo mc 14 – 38 yearso 15-20 % of pts require colectomy

- Presentation patternso 70 % relapsingo 20 % chronic continuouso 10 % fulminate (toxic megacolon)

- S/SXo Abdominal distentiono Abdominal pain/tenderness (LLQ, LUQ)o Blood diarrheao Feverso Dehydrationo Extraintestinal

Liver Disease Sclerosing cholangitis Arthritis Ocular Disease (uveitis, iritis)

- DX workupo Comprehensive H&Po Laboratory studies

CBC (anemia, elevated ESR) SMAC (electrolytes, LFTs) UA (dehydration)

o Sigmoidoscopyo Double-contrast BE

- D/DXo Crohn’s Diseaseo Bacterial infection

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o IBSo Protozoal infectiono Colon CAo Diverticulitiso Ischemic Bowel DISEASE

- TXo Correct nutritional deficiencieso May need “bowel rest” with TPNo Folate supplementation (decrease CA Risk)o Low roughage diet during exacerbationo Meds

Sulfasalazme corticosteroids

o ?

Crohn’s Disease

One-third of the cases involve only the distal small bowel (ileitis)

Half the cases involve the distal small bowel and proximal colon (ileocolitis)

In 20% of the cases only the colon is involved Crohn’s disease is a transmural process that can result in:

Inflammation Ulceration Stricturing (narrowing) Fistula formation Abscess formation

Crohn’s disease presents with a wide variety of signs and symptoms because its involvement is variable in both location and severity of inflammation

Most commonly, there is one or a combination of the following clinical presentations:

Chronic inflammatory disease o This is the most common presentationo Often seen in patients with ileitis or ileocolitiso Patients report low-grade ever, malaise,

weight loss, and loss of energyo There may be diarrhea which is non-blood y

and intermittent

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o Cramping or steady pain in the right lower quadrant or periumbilical area

o Examination reveals focal tenderness in the right lower quadrant

Intestinal obstruction o Narrowing of the small bowel may occur as a

result of inflammation of fibrotic stenosiso Patients report postprandial bloating,

cramping pains, and loud borborygmi

Fistulization with or without infection Some patient develop sinus tracts that penetrate

through the bowel and form fistulas to other areas 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 car 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

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Complications Abscess Obstruction Fistulas Perianal disease Carcinoma – Patient’s with colonic disease are a t a

greater risk of developing colonic carcinoma Hemorrhage – unusual in Crohn’s disease (except for

Crohn’s colitis) Malabsorption – from bacterial over-growth in

patients with fistulas

No specific treatment exists for Crohn’s disease, treatment is directed toward symptomatic improvement and controlling the disease process

APPENDICITIS- Inflammation of appendix secondary to obstruction- Clinical symptom complex

o Periumbilical/diffuse paino RLQ pain

12-244 hrs later Sign of regional peritonitis Rebound tenderness High fever

o Can ruptureo May cause diffuse peritonitiso May result in abscess formation

DIVERTICULAR DISEASE- Epidemiology

o Herniation of mucosa and submucosa through muscularis from low fiber diet

o Occur at vasa recta (weakened area)o Diverticulosis is asymptomatico Diverticulitis is symptomatico Most respond well to antibiotics o Up to 30% require surgery

- S/SXo Diverticulosis exam is normalo LLQ pain mco Pain relieved with BMo Abdominal guarding

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o Rebound tenderness suggests peritonitiso +/- small amount of blood in stool

DIVERTICULAR BLEEDING- 70% occurs in right colon- bleeding is painless- resolves spontaneously in 60%- erosion of vessels from fecalith- 15 – 20 % re-bleed within 5 yrs

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- Diagnostic workupo CBC (elevated WBC with diverticulitis)o Microcytic anemiao BEo Sigmoidoscopyo Abdominal CT for abscess formation

- D/DXo IBSo Crohn’s DISEASEo UCo Colon CAo Ischemic Colitiso Infectious Colitis

- TXo Increased dietary fibero Regular exerciseo Broad spectrum antibioticso IV Antibiotics in severe caseso Surgical resection/re-anastomosis

Colorectal CancerMissing first slide

Risk Factors Hereditary polyposis syndromes

o Familial polyposis, teens to 30's, pts have thousands of polyps

o Gardner’s Syndrome 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 epitheal 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 sterotactic radiation]

Clinical Presentation Normally unremarkable DRE finds 50% of tumors

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Palpable abdominal mass (mets most likely not the colon cancer itself)

Abdominal tenderness alternating constipation / diarrhea Hepatomegaly (mets)

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Rectal bleeding Hematochezia Melena Blood streaked stool Occult blood [blood mixed in with the stool]

Abdominal distensiono Obstructiono Initial symptom in 15% of patients

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]

Positive FOB test Elevated CEA (used for Rx response) Elevated LETS Colonoscopy Double contrast BE CT for staging CAR (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

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Cancer Staging Duke classification system A - confined to the mucosa-submucosa B - invasion of muscularis C - Local node involvement D - distant mets (liver, lung, brain)

Treatment Surgica resection

o 70% are resectable at presentationo 45% cured by primary resection

Radiation therapy (stages B & C) Chemotherapy (stages B & C)a

o 5-fluoroucacilo Levamisole

FOB q 6 months Colonoscopy q year x 2 years, then q 3 years CEA levels (Carcinoma Embryonic antigen)

Prognosis Duke A >80% Duke B 60% Duke C 20% Duke D 03%

Overall 5 year survival rate 50%

Colon Polyps- 50% patients have polyps

o hyperplastico adenomaso lipomaso leiomyomas

- Sessile / pedunculated- 25% patients with colon cancer have polyps

Signs / Symptoms- most are asymptomatic- rectal bleeding most common- cramps- abdominal pain- obstruction- anal polyps may prolapse

Diagnosis

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- DRE- Endoscopy- Double contrast BE

Treatment- Careful observation (hyperplastic, lipoma)- endoscopic surgery- open laparotomy

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 US1. lung CA2. colorectal CA3. Breast CA

o Most common CA is skin CAo 135,000 new cases/yearo 50,000 deaths/yr.o 15% of all cancers (except skin cancers)o peak incidence in the 7th decadeo Location

Lower colon – 40% rectosigmoid - 30 % cecum / ascending – 25 % transverse – 10%

- 2 types of CA can occur o adenocarcinomao squamous cell CA – Most common with HPV

(condylomata)- Risk factors

o Hereditary polyposis syndromes Familial polyposis Gardner’s syndrome

Polyposis & osteoma in skullo Inflammatory bowel Disease

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o H/o previous colorectal CAo 1st degree relative with colorectal CAo age > 40o high fat, low fiber dieto regional radiation therapy

- Clinical presentationo Normally unremarkableo DRE finds 50% of tumorso Palpable abdominal mass (mets)o Abdominal tendernesso Alternating constipation/diarrheao Hepatomegaly (mets)

Mets usually to liver (stage 4 colorectal Ca)

Liver drains all of GIo Rectal bleeding

Hematochezia Melena Blood streaked stool

o Abdominal distention Obstruction Initial sx in 15%

o Pencil thin stoolso Intussusceptionso Volvuluso Wt losso Anorexiao Malaiseo Colon CA can cause lumbar & sacral back pain

- Clinical investigationo Anemia (microcytic)o Positive FOB testo Elevated CEA (used for RX response)o Elevated LFTso Colonoscopyo Double contrasto CT for staging o CXRo 25% have mets at presentation

- D/DXo Diverticular Diseaseo Bowel strictureo Inflammatory bowel Diseaseo Adhesions

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o Metso Extraluminal masses (ovarian)o AVMs (Arterial venous malformations)

- Cancerous stagingo Duke Classification system

A – confined to the mucosa – submucosa B – Invasion of muscularis C – local node involvement D – Distant mets

- TXo 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

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o FOB (fecal occult blood) every 6 months Guaiac test finds occult blood in feces

o Colonoscopy every year x 2 years, then every 3 years

o CEA level Carcinogenic embryonic antigen

- Prognosiso Duke A – 80 %o Duke B – 60%o Duke C – 20 %o Duke D – 3 %o Overall 5 yr. survival rate – 50 %

COLON POLYPS- Most non-inflammatory CA arise from polyps- 50 % patients have polyps

o Hyperplastico Adenomaso Lipomaso leiomyomas

- sessile/pedunculated- 25% pts with colon CA have polyps- S/SX

o Most are asymptomatico Rectal bleeding mco Crampso Abdominal paino Obstructiono Anal polyps may prolapse

- DXo DRE o Endoscopy

Complicated with severe inflammation disease

May perforate bowel Do BE instead

o Double contrast BE- TX

o Careful observation (hyperplastic, lipoma)o Endoscopic surgeryo Open laparotomy

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Test Three and Final

Internal DX Test # 3 Notes(In class notes)

3/24/03Small Bowel Diseases- Usually result in some form of malabsorption

CELIAC SPRUE- aka: Gluten enteropathy non-tropical sprue- Gliadin protein fraction in gluten

o Wheato Ryeo Barleyo 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 B normal presentationo WT ↓o Dyspepsia (indigestion)o FTT in children (failure to thrive)o Bloatingo Diarrheao Pallor/fatigue (anemia)o Angular cheilosiso Osteomalaciao dermatitis

- Lab testso Iron ↓ anemiao Folic acid ↓o B 12 ↓o Antigliadin IgA/IgG ↑o Small bowel biopsy

Show villi atrophy Signs of inflammation

- D/DXo IBS (mc d/dx)

More mucous in IBS stools Age 20 - 40

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o Laxative abuseo Intestinal Parasiteso Tropical Sprueo Lymphoma

- TX/PXo Gluten Free Dieto Iron supplementationo Folate supplementation

WHIPPLES DISEASE- Cz by bacteria- Men 30 - 60- Multisystem Disease- Tropheryma whippelii (gram +)- Aka: intestinal lipodystrophy- Uncommon disease- 30-60 yr. olds- M > F- Clinical Presentation

o Malabsorption Diarrhea Bloating/cramps Anorexia Wt ↓ / fatigue anemia

o Extra intestinal Arthritis

Can be peripheral or sero-negative Pleuritic chest pain (localized pain) Pericarditis osteomalacia

- Pathologyo Bacteria never culturedo No human 2 human transmit iono Response 2 antibiotics confirms dx

- D/DXo Celiac sprueo Lymphomao Crohn’s diseaseo Short bowel syndrome

Take portion of bowel out Get malabsorption

o Pancreatic insufficiency Fatty stools

o Lactose intolerance

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- TX/PXo Antibiotics

LACTOSE INTOLERANCE- Can have a transient form in people that are ill- 1 in 6 pts 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- 50 million R affected - > 85% Asian American affected- > 60 % African American affected- < 25% Caucasians affected - Clinical presentation

o May B normalo Bloatingo Diarrheao Crampingo ABD paino Flatulence

- DX work ↑o Hydrogen Breath test

Ingest 50 gm of lactose ↑ in breath hydrogen > 20 ppm in 90 min

o exclude other diseaseo imaging studies not indicated

- D/DXo IBSo IBDo Pancreatic insufficiencyo Sprue

- TX/PXo Lactose free diet

Milk Bread Candies Cold cuts Commercial sauces

o Read labelso LactAid tabletso Ca ++ supplementationo Excellent prognosis

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MECKEL’S DIVERTICULUM- Remnant of vitelline (omphalomesenteric) duct- Mc misdiagnosed as appendicitis- Congenital lesion

o 2 % of Populationo failure of obliteration of vitelli intestinalo duct connecting interesting 2 yolk saco mc anomaly of SI

- Found w/in 3 ft of IC valve- ↓ 12 cm in length- Complications

o bleeding o obstructiono diverticulitis (contains gastric mucosa)

perforation- RX w/diverticutomy

MESENTERIC ISCHEMIA- Most painful condition in medicine- More proximal obstruction of artery → higher mortality- Occurs as a result of either superior mesenteric arterial

or venous occlusion- Affects the bowel from 2nd part of duodenum 2

transverse colon- 50% embolic, 25% atheromatous, 10% venous

occlusion- Overall mortality is approx. 90%- DX features

o Nothing highly suggestiveo Central abd pain out of proportiono KUB may B normal

3/25/03GENITOURINARY DISEASESURINARY 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

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o Shorter tract Bacteria doesn’t have to travel as far

o Hygiene Wiping A to P NOT P to A

- Lower UTIo Urethritis o Cystitis

Infection of urinary bladder- Upper UTI

o Pyelonephritis Kidney Infections (Pyelo = pelvis)

PATHOPHYSIOLOGY- 100,000/ml is threshold

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 UTIo 10,000 – 100,000 ml = contaminated specimeno > 100,000/ml = UTI → become symptomatic

- Some patients are symptomatic with less- Neonates- m/c in boys from anomalies

o 30 days old or less- Preschool- m/c in girls from hygiene- Adults- m/c in women from hygiene- Four pathways

o Ascending form urethrao Lymphatic spreado Hematogenous spreado 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 factorso Neurologic diseaseo Diabeteso Renal failureo Pregnancy

- Pathogenso E. Colio Proteus Mirabilis

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- Defense Mechanismso Low pHo Normal Micturition

Detrusor mm contracts Trigone muscle relaxes

o High Osmolarity

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LOWER UTI- Presentation inconsistent

o Some asymptomatic, some just have urgency, some have extreme pain

- testing- Urinary frequency, with minimal quantity- Dysuria- Urgency- Urge incontinence- Suprapubic pain- Hematuria (menstruation most common caused,

bladder infection most common pathogenic cause)o Gross

Patient will see in toileto Microscopic

If the infection is mild to moderate

PYELONEPHRITISMore common in the immunocompromised population

(diabetic)Usually secondary to a UTIPatient will be positive for a kidney punch

- Fever, more prevalent then with a UTI- CVA pain- Radiating pain into groin

o Anterior and inner thighs, males will refer to the ipsilateral testicle

- Chillso Fever, night sweats

- Malaiseo 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

- 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

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o Elevated WBC, anemia (mild)- KUB (kidney, ureter, bladder) (a plain film of the

abdomen)- Ultrasound- IVP (Intravenous Pyelogram)

o Outlines renal substance- CT scan

o For tumors or abscess- Cystoscopy- Retrograde pyelography (obstruction)

o Dye from urethra up and stops where infection iso 2 check for stones

Non-gonococcal Urethritis- NGU is most common STD- NGU twice as common as gonorrhea (the clap)- Chlamydia is most common bug- Often asymptomatic(~25%) especially in women- Symptoms

o dysuriao whitish dischargeo meatal edema

Treatment w/ antibiotics

Gonorrhea- Neisseria Gonorrhoeae - Urethra is mc sight of infection- Contraction rates(single intercourse)

20% for males 80% for females, will tear up the cervix and cause

sterility if not aggressively treated- Symptoms

dysuria urethral discharge urethral itching

- Treatment w/ antibioticsHerpes Simplex- HSV II infection affecting ~20% of adults- spread through direct contact- 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

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symptom controlGenital Warts- Condylomata acuminata- Cause by 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 Urolithiasis (Kidney stones) calculus in the urinary tract

- aka- renal colic, when in the active state- types of stones

o calcium(70%)o uric acid(8%)o struvite(15%)o cystine(3%)

- 250k-750K /year- M:F 4:1- Incidence is highest in summer(dehydrate)- Signs/symptoms

o acute colicky CVA/flank paino n/v (nausea and vomiting)o referred pain to testes/vulva/groino FCNS suggests infection

- Diagnostic work-upo UA(hematuria)o plain film radiographyo renal USo IVP (intra venous pyelogram)

- DDxo pyelonephritiso cystitiso diverticulitiso PID

- Rxo increased fluid intake, low calcium diet

(contraindicated if an obstruction exists)o uteroscopic stone removalo extracorporeal shockwave lithotripsy

- 50% pass within 48 hrs- 50% recurrence rate without

RxGlomerulonephritisautoimmune inflammation of glomerulus

- synonymso post-infectious GNo acute nephritic syndrome

- epidemiologyo 50% affect < 13 y/o

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o Most common cause of chronic renal failure (~25%), these individuals wind up on dialysis

o post group A beta strep infection mco collagen vascular disease(SLE)

o idiopathic

Proteinuria- normal adult excretes ~150 mg/day short and long chain

proteins (0 - +2 on a UA dipstick)o 3.5% prevalence in normal adultso perform 3 separate testso You must not assume that finding protein equates

the “normal” amounts excreted. You must rule out all possible causes.

- positive again-follow up- negative-dx transient functional proteinuria- Causes

o IDDMo Nephrotic syndromeo Amyloido Lymphomao NSAID useo Orthostatic proteinuria (only when upright)

Nephritic Syndrome- secondary to GN- signs/symptoms

o edema(periorbital, scrotal), due to loss of proteino HTN, damage to kidneys which help regulate

HTNo hematuriao proteinuria

Nephrotic Syndrome- Most common cause is membranous GN- signs/symptoms

o peripheral edema, protein losso asciteso HTN, o pleural effusiono hypoalbuminemia

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o hyperlipidemia / hypercholesterolemiao 1/3 of pts have DM, SLE, amyloidosisMany 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 Failuresudden decrease in renal function

- inability to maintain fluid/electrolyte balance- inability to eliminate wastes- signs/symptoms- obnoxious bouts of nausea and vomiting - oliguria/anuria (very important to monitor intake and output

of fluids)- altered sensation, electrolyte influenced - laboratory findings- elevated BUN/creatinine (creatinine levels are very specific

for renal function)- electrolyte imbalance- anemia, platelet dysfunction Pre-renal failure(most

common cause )o inadequate renal perfusion

hypovolemia CHF Strokes sepsis

- Intrinsic renal failureo renal disease

GN, drug toxicity, ATN- Post-renal(least common)

o outlet obstruction, outflow obstruction is going to cause pressure build up in the renal system

Benign Prostatic Hyperplasia (most common cause), prostate CA

ureteral stones bilateral renal vein occlusionChronic Renal

Failureprogressive decrease in renal function

- >250,000 dialysis pts/year- signs/symptoms

o pallor, ecchymosiso edemao HTNo depressiono fatigueo n/v

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o pruritus, urea makes the patient itch- Etiology

o DM(37%) [also the most common reason for dialysis in the US]

o HTN(30%)o GN(12%)o polycystic kidney diseaseo drug toxicityo obstructive uropathyo renal artery stenosis

- Laboratory findingso elevated BUN/creatinineo proteinuria, RBC castso electrolyte imbalances

Renal Cysts- fluid-filled epithelium-lined cavities- found on 50% of autopsies- rarely symptomatic- simple cysts are ~70% of all renal masses- Polycystic renal disease

o mc hereditary disease in the USAo 50% have renal failure by age 60o repeated UTIs, large kidneys, flank paino 50% pts also have liver, pancreas cystsRenal

Cell Carcinomaadenocarcinoma- Malignant transformation of renal tubular cells- aka-hypernephroma (name no longer used because the

name does not suggest malignancy) - 1:10,000 people/yr- 50-70 y/o- male : female 2:1- etiology

o familialo 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%)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

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o HTN (20-40%) – sudden hypertensive changes are a red flag

o Weight loss (30-35%)- Classic Triad (5-10%)hematuria {differentiate runners who

classically suffer fro hematuria}o flank paino abdominal mass

- Treatmento Nephrectomy – complete removal of the kidneyo Radiotherapy -o Chemotherapy (5% response rate)

- Prognosiso Stage I ~90%o 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

o Stage III ~20%o Stage IV ~5%Prostate

Diseasesprostatitis- 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 traumaProstatitisMen over 50

- may be aseptic or septic (infectious or noninfectious)- Signs/symptoms

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 paino urethral dischargeo fever

- Dx made by culture and stain of prostate secretions- Anti-biotics if infectious

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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 symptomso hesitancy, decreased caliber and force of streamo double voiding, post-void dribblingo 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 Cancerhas 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) mc pop. in world- Clinical presentation

o Generally asymptomatico bone pain/fx may be initial presentationo outflow obstructiono mass on DRE(10% have normal DRE) DDxBPH

- prostatitis- prostate stonesDiagnosis- elevated PSA (may be normal in 20%)- elevated acid phos (extracapsular extension)- biopsyTreatment (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 tumorso Epididymitiso Incarcerated herniao Orchitis – caused by mumps viruso Hydrocele – an obstructive disease where there

is enlargement of the epididymis

Testicular Torsion- Clinical Findings

o Sudden hemi scrotal pain (10% are painless)o Swelling o Nausea and vomitingo Afebrile – no fevero 30% patients report previous episode of pain

- Dx based on H and P- Surgical derotation with suture fixation

Epididymitis- Septic/traumatic inflammation of epididymis- >600k visits per year- occurs in sexually active men- DDX

o Orchitiso Testicular torsiono Hydrocele / varicocele

- Agentso N. gonorrhoeaeo C. trachomatis

- Clinical presentationo Tender scrotal swellingo Erythemao Dysuriao Urethral dischargeo Fever

- RXo Ice packs with scrotal elevationo Analgesicso Antibiotics

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- Pxo Usually self limited

Hydrocele- fluid collection in the scrotal space- if congenital, associated with inguinal hernia- in adults

o infectiono tumoro trauma

- Clinical presentationo Scrotal enlargement / pain / radiating to backo Transillumination

- Rxo None if asymptomatic

Orchitis- infection of the testicle- usually viral (mumps/coxsackie B virus)- occurs in post-pubertal males- Clinical presentation

o testicular pain / swellingo may be bilateralo inguinal lymphadenopathy, especially in a

relatively young maleo history of mumpso Rx- observation if viralo may lead to sterilityTesticular

Cancerseminoma(most common), teratoma, choriocarcinoma

- 2-3/100k/yr- mc in young adults(30-40)- Clinical presentation

o scrotal masso does not illuminateo 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- mc 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 hematuriao painless microscopic hematuriao frequency, urgency – due to bladder becoming

filled with the masso mets causes pain in distant organ (eg, back

pain)- Diagnosis

o H&P History and physical examinationo UA, cystoscopy – and endoscopic procedure for

the bladder- Rx- chemo, radiations, TURP, cystectomy- Px- dependent on cell type and gradeLiver

FunctionAnatomyo four lobes – right, left, caudate and quadrateo Weighs – 3 lbs

- Blood Supplyo 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

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- 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?)o alcoholic hepatitiso drug-induced hepatitiso toxic hepatitis(carbon tetrachloride, benzene)o leptospirosiso toxoplasmosis

o EBV, CMV, HIV, HIV

Hepatitis A- caused by HAV (RNA virus)- fecal-oral route, close family contacts- 9-45/100,000/yr

o institutionalized childreno day care centerso male homosexualso exposure to imported apeso undercooked mussels, clams, oysters

- highly contagious- represents 33% of viral hepatitides in USAmc 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 hepatitideso viral illness w/ liver involvement(CMV, EBV)o non-viral hepatitides

- Clinical presentationo often asymptomatic(25% adults, 90% <2 y/o)o anorexia, malaiseo hepatomegaly (87%), RUQ tendernesso splenomegaly rare (9%)o jaundiceo dark urine(bilirubinuria)o fever variable (precedes jaundice)

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- Workupo LFTs (Liver Function Test)o HAV antibody

- Laboratory testso ALT/AST(often > 8x normal)o Bilirubin (usually 5-15x normal)o Alkaline phosphatase (1-3x normal)o albumin, prothrombin normalo WBC most often normalo 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- acute disease lasting < 6 wks- rarely prolonged(3-5 mos), no carrier state- Treatment

o avoid hepatically metabolized drugso IV fluid replacement for vomiting (rare)o steroids not normally helpfulo follow-up as outpatiento Overall do not over tax the liver, no alcohol

- Pxo <0.1% fatality rateo 60% w/ fulminant recovero evidence of previous disease in 40% of adults

Hepatitis B- acute viral hepatitis(aka 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 userso homosexual maleso hemodialysis and hemophilic ptso health care workerso neonates/infants

- mc in 20-45 y/o- DDx

o other viral hepatitides

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o other viral illness w/ liver involvemento non-viral hepatitides

- Clinical presentation of acute diseaseo most often anicteric and asymptomatico anorexia, malaise, n/vo serum sickness(hives, rash, arthralgia)o hepatomegaly, splenomegaly(uncommon)o jaundice, bilirubinuria, +/- feverClinical

presentation of chronic disease(1-2%)o similar to acute HBVo asymptomatic chronic active carrier (have active

virus in the system, patient is asymptomatic and contagious)

o hepatic decompensationo cirrhosiso hepatocellular CA

- Laboratory testso HBsAgo elevated ALT/ASTo hyperbilirubinemiao elevated alk. phos.

- Treatmento IV fluids for dehydration (increased vomiting over

Hep A)o treat for hepatic failure, if presento avoid hepatically metabolized drugs (including

alcohol)o steroids not helpfulo interferon for chronic caseso antiviral agents

- famciclovir- lamivudine

o liver transplant- prevention

o avoid high-risk behaviorso testing blood supplyo hepatitis B vaccine

- high risk groups(90% effective)- childhood vaccination

- HBV hyperimmune globulino given after needle sticko given after birth w/ infected momo given after sexual exposure

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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 hemophiliacso IV drug userso occupational needle stickso hemodialysismale=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 onseto milder that HAV/HBVo RUQ tendernesso hepatomegalyo jaundice o dark urine(bilirubinuria)o many are anicteric asymptomatic(75%)

- 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 antibodyo LFTso biopsy for complications

- Rxo avoid meds metabolized by livero otherwise acute Rx is non-specifico follow-up for complicationso Interferon may be helpful in relapses

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- acute disease lasts <6 wks- no vaccine- immune globulin injections are not helpful

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 alcoholismo viral hepatitis(especially HBV and HCV)

- other causeso drugs(Tylenol), chronic CHF, hemochromatosis,

amyloidosis- Clinical Presentation

o early- weakness, fatigability, disturbed sleep- muscle cramps, weight loss

- advancedo anorexia, weight losso n/v, hematemesis, due to esophageal variceso jaundiceo hepatomegaly, asciteso amenorrhea, due to cholesterol production

interferenceo impotence in menSkin lesionso spider nevio palmar erythema(alcohol abuse)o glossitis, cheilitiso ecchymosis

- CNS damageo Asterixis (intermittent lapse of body position)o tremoro delirium

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o dysarthria, slurred speecho coma

- Laboratory findingso macrocytic anemiao abnormal LFTso decreased albumino leukopenia

- Rxo avoid hepatotoxic medso treat disease that caused cirrhosis

o treat complications(ascites, varices, CHF))

Primary Biliary Cirrhosis- autoimmune disease- destruction of intrahepatic bile ducts- mc in females(95%)- 40-60 y/o age group- associated w/ PSS, SLE, Sjögren’s Synd., RA, and other

connective tissue arthropathies - SSx

o Fatigue (extreme fatigue)o prurituso ~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 colchicineo ursodiolo liver transplant

- Px-o asymptomatic- 10-16 yrs from time of diagnosiso symptomatic- 7 yrs from time of diagnosis

Hepatic Tumors- Benign

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o Hemangioma- Most common benign liver tumor- Vascular tumor- Asymptomatic- Found incidentally

o Adenoma- Rare solitary or multiple tumor- Usually asymptomatic- Found in steroid abusers, OCA users

- Malignanto Hepatocellular Carcinoma (old term Hepatomas)o Cholangiocarcinomao Metastasis (Most common cause liver

malignancy), colon cancer is the most common malignancy which mets to the liver

Hepatocellular CA- malignant tumor of hepatocytes- associated with:

o chronic liver diseaseo cirrhosiso HBV, HCVo hepatotoxins(ETOH, steroids)

- Clinical presentationo weight loss, anorexiao asciteso hepatomegalyo 33% are asymptomatic

- Diagnostic evaluationo elevated AFP in ~90% (alpha-fetoprotein – this

protein non-specific)o elevated LFTso MRIo Ultra Sound/CT-guided biopsy

- Treatmento dependent on size of lesion/metso resectiono chemotherapy

- Px is 20-30% following resection

Cholangiocarcinoma- Intrahepatic bile duct malignancy- Rare in USA and Europe – more common in Asia

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- 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 skino femaleo obesityo ~40 y/oo OCA useo 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 paino refers to right shouldero 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-goodCholecystitis (inflammation of the gallbladder)acute

and chronic forms- 95% associated with gallstones- mc in same groups as cholelithiasis- Clinical presentation

o RUQ pain/tendernesso pain radiating to right shouldero Murphy's signo Fever (~33%)o Jaundice (25-50%)o fever, chills, n/vDiagnostic workupo Ultrasound

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o MRI/CT to rule out more ominous causes- Treatment

o laparoscopic cholecystectomy (lap chole)o open cholecystectomyo broad-spectrum antibiotics

- Prognosiso Excellento 1% complication rate with lap chole

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 ptsDiagnostic workup

o Ultrasoundo ERCP endoscopic retro( if US is inconclusive)

- Treatmento biliary decompression

- ERCP(maybe w/ stent placement)- percutaneous transhepatic biliary

drainageo broad-spectrum antibiotics

- Prognosis is excellent- Chronic disease associated w/ porcelain gallbladder, a

premalignant condition Primary Sclerosing Cholangitisdiffuse inflammation leading to stricture

- most common in males age 20 – 40commonly associated with UC

- Assoc

o Clinical is progress jaundice, indigestiono Malaise, purity, anorexia

- Poor Pxo Most require liver transplant within 10 years

- Think Walter PattonGallbladder CancerAdenocarcinoma most common- asymptomatic unless disease is advanced

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- usually found during surgery for stonesweight loss, anorexia

- palpable gallbladder, RUQ pain- associated with stones in 80%- porcelain GB also assoc.- poor prognosis

Pancreatic Disease- Acute pancreatitis- Chronic pancreatitisPancreatic CancerAcute

Pancreatitismost often secondary to biliary disease- enzymes released into pancreas- S/Sx

o severe abdominal/back paino fetal positiono n/vo mild jaundiceo shock – as a reaction to the pain

- lipase and amylase levels increased- CT/MRI for DxTreatment

o IV hydrationo NPOo NG suctiono pain controlo treat complications

- Prognosiso 5-10% mortality associated with the shocko worse in older, sicker patientsChronic

Pancreatitisrecurrent pancreatitis- male : female 5:1- S/Sx

o recurrent epigastric/back paino abdominal tenderness/guardingo weight losso 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

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- 2nd mc tumor of GI system (colon cancer is #1)- m : f 2:1- mc in head of pancreas, carcinoma in the tail will not cause

jaundice, because it does not block the duct.- S/Sx

o jaundiceo abdominal paino weight loss, anorexia, nauseao biliary obstruction S/Sx(head tumor)

- CT/MRI are best imaging procedures- Poor Px from early mets

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