esophagus

` INCISORS: cut 10 15 months

` BICUSPIDS: chop 15- 18 months
` MOLARS: grind 18 24 months
Pimary h fall ll by 8 d ` Pri teeth f out b age 8 and are
replaced by permanent teeth
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`
`
`
`

Masseter- closes
Temporalis- (closes) moves jaw forward and back
Medial Pterygoids (closes)
Lateral Pterygoids- (opens) lowers jaw

` Innervated by cranial nerve 5 (Trigeminal)mandibular V3

` Develop from first branchial arch
Tip of tongue rises >
Sides of tongue rise and fold medially >
Tip of tongue rises to hard palate >
Gravity begins bolus rolling >
When bolus approaches tracheahea, epiglottis
When bolus approaches trac epiglott
is
Closes off glottis >
Bolus rolls over epiglottis/touches the pharynx>
CN 9, 10 sense the bolus >
UES opens relaxes >
Bolus drops into esophagus
`

UPPER ESOPHAGEAL SPHINCTER

Voluntary
Skeletal muscle in upper 1/3 of esophagus
Constrictors of the pharynx
Stylopharyngeus yp y g

Develops from 4th pharyngeal arch

Innervated by
x CN 9(stylopharyngeus)
x CN10(all others)
` Nucleus Ambiguus: innervates the UESefferent vagus (motor CN 10)
` Dorsal motor nucleus: innervates the rest
of GI efferent vagus (motor CN 10)
` Primary peristalsis: requires vagus nerve

and Auerbachs plexus; begins just distal

to the UES only
` Secondary peristalsis: intrinsic to smooth
muscle; can begin anywhere in GI
UES
1 Peristalsis
- Vagus CN 10
- Auerbauch (VIP)
Nucleus
Ambiguous
2 Peristalsis
- Stretch from food
Dorsal motor nucleus
of CN 10 (Vagus)
LES Receptive
relaxation
No receptive
relaxation:
Achalasia
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Esophageal Pathology
` Choanal atresia: lack apoptosis /bluefeeding
` Esophageal atresia w/ distal TE fistula
Vomit on first feeding
Plummer
Vinson
UES
Syndrome
Iron deficiency
Strips of mucosal tissue- lack apoptosis
Risk of esophageal cancer
Young woman
Microcytic anemia
Schatzki rings:
-Intermittent
dysphagia

- Around LES
LES
` Zenckers: congenital
` Traction diverticula: occurs due to large bolus
Zenckers
Diverticulium Congenital it l
UES
LES
C
Traction
Diverticulium
Patients with a history of GERD > 5 years
(Screening for Barrettes esoph.-sq. to columnar)
Tx: PPIs, upper endoscopy every 2-3 years
Patients with long standing cirrhosis: screening for
varices
Tx: Propranolol- decreases risk of bleeding
` Abnormal esophageal acid exposure
` > 4 week trial of PPIs still having symptoms
Exclude l d GERD in ients ith h lained i d ` E GERD i pati wi unexpl
chest pain
` GERD symptoms with a negative upper
endoscopy
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` Best initial test for dysphagia
` Not the best test if the problem is due to an
obvious obstruction, then the best test is
upper endoscopy upper endoscopy
` Achalasia- bird beak
` Diffuse esophageal spasm- cork screw
` Diagnosis:
Dysphagia
Unexplained chest pain w/o mechanical obst.

Transducer d llaced d in hhagous dd ` T p i esop to recor

pressure
` Most accurate test for Achalasia, Esophageal spasm
` Diagnosis: GERD
` NGT placed at the esophageal junction
Dilute hydrochloric d hl i id is injected j d hrough h ` Dil h acid i i th
the NGT to reproduce the symptoms of GERD
` OLD TEST..PPIs and 24 hour pH monitor
` ALWAYS THE WRONG ANSWER !!!!!!!!!
Cardia
Fundus
FOOD
LES
Caudad
Region
Orad
Region
Body
Antrum
G cells
Pyloris
Duod
` Orad region- fundus and proximal portion of
the body
Thin muscle wall
` Caudad region distal portion of the body ` Caudad region - distal portion of t
he body
and the antrum
Thicker muscle wall
Region responsible for mixing the food
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` Receptive relaxation: relaxation of the lower
esophagous sphinctor and the orad region to

accept food into the stomach.

` Vagovagalagal reflexex- both afferent and efferent ` Vagov refl both afferent
and efferent
limbs of the reflex are carried in the vagus
nerve
Vagus
Afferent
Efferent
` Mechanoreceptors detect distension of
the stomach and relay this information
to the CNS via sensory neurons
` CNS then sends efferent information to
the smooth muscle wall of the orad
stomach, causing it to relax
from ` Neurotransmitter released f the
postganglionic vagal nerve fibers is VIP
` Vagotomy eliminates receptive
relaxation
VIP
` During fasting- periodic gastric contrations
occur MMC
migrating myoelectric complexes
diated d lin ` Med my Motil
` Occur ever 90 minutes
` Function to clear the stomach of any
residue remaining from a previous meal
` Takes approximately 3 hours to empty
` Rate must be regulated to provide adequate time to ` Rate must be regulated to
provide adequate time to
neutralize the gastric H+ in the duodenum
adequate time for absorption of nutrients
` Two factors slow or inhibit gastric emptying:
Fat and H+ in the duodenum
Fat- mediated by CCK (secreted by duodenum)
H+- mediated by reflexes of the enteric nerves (myenteric
plexus) ensures content is delivered to the duodenum

slowly
Four major components:
` Hydrochloric acid (HCL)- function is to reduce pH for
the conversion of pepsinogen to pepsin
` Pepsinogeninogen (inactive) Low pH converts it to the active ` Peps (inactive)
Low pH converts it to the active
form- pepsin for protein digestion
` Intrinsic factor-for the absorption of Vit. B12 in the
ileum (essential)
` Mucus- protects the gastric mucosa from HCL
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Glands of the Body of the Stomach
` Empty their secretory products via ducts
` Opening of the glands are called pits
` Lined with epithelial cells
Gastric
Lumen
Epithelial cells
Mucous cells
Parietal cells
Chief cells
HCL & Intrinsic factor
Pepsinogen
Glands of the Antrum of the Stomach
` Contain 2 cell type:
Mucus cells- mucus and HCO3 are
protective
G-cells (secrete gastrin into circulation)
Gastric
Lumen Epithelial cells
Mucous cells
G - cell Gastrin

Mucus, Pepsinogen, and HCO3` Mucus from goblet cells

` Prostaglandins (PGE2)
` HCO3: alkaline tide
Aspirin- i i irreversible ibl block k Cox 1 & 2 ` A i bl C 1 & 2
` NSAIDs - reversible inhibit COX
` Steroids
` COX 1 GI COX 2- Joints
` Misoprostyl- replace PGE
(Vasocon/Vasodilation- alprostadil)
` Cox 2 inhibitors ` Cox 2 inhibitors
Celecoxib- only one left
Rofecoxib- off the market
Valdecoxib off the market
(problem if on > 18 mo)- block
prostacyclins- inhibit platelet agg.
` Gastric ulcers due to lack of blood supply;
sympathetic output causes vasoconstriction
` CUSHINGS ULCER
` CURLINGS ULCER
` STRESS ULCER
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Regulation of H+ Secretion
` Is the most common cause of upper GI
bleeding in older children and adults
` Superficial erosions
`

Type A Gastritis (located in body)

A utoimmune etiology
A ntiparietal cell antibody
A trophic gastritis
A denocarcinoma risk Body

` Type B gastritis (located in antrum)

Due to a breakdown in barrier protection
NOT TOO MUCH ACID!
Associated with Helicobacter Pylori

` Gastric Ulcer
Pain is worse during the meal
Located in the antrum Located in the antrum
Associated with H. Pylori 70% of time
Associated with CANCER 20% of time
Endoscopy on ALL patients
` Duodenal Ulcers
Pain is worse 30 to 40 minutes after a meal and
also at night
Located in the second part of the duodenum
Associated with H. Pylori 95% of time
Cancer risk < 1%
Treat empirically with medication
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12
`Surgical indications:
I
ntractable pain- meds fail
H
emorrhage- massive UGB
H
emorrhage massive UGB
O
bstruction- Scarring
P
erforation- Retroperitoneal
R/O- CT
` Definition: a mass made of
undigestible materials
Most common type:yp Hair
Causes a gastric outlet obstruction
TX: endoscopy and removal
` SLIDING TYPE: 90%
Involve sliding of the fundus into the esophageal
hiatus

 MCC: obesity; restrictive lung disease

TX: conservative measures; medications;
x surgery( Nissan fundoplication)- no belch
High incidence of GERD
` ROLLING TYPE:
Due to a defect in the diaphragm
Requires surgery q g y
Risk of strangulation and infarction
` Rare
` Large RUGAL FOLDS on biopsy
Hyperplasia l i f blet lls ` H of gobl cell
` Cells ooze out proteins
Like nephrotic syndrome
Low albumin
` Hypertrophy of the pyloric muscle
` Presents at 3 to 4 weeks of life
` PROJECTILE vomiting J g
` Olive sign; string sign on Barrium;
` DX: ultrasound
` TX: correct fluids and electrolytes
pyloromyotomy
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` PROTEIN: no protein digestion in the mouth;
significant digestion in the stomach;
completed in the small bowel
` SUGARS: significant digestiong in the mouth;; it g
stalls in the stomach; completed in the small
bowel
` FATS: negligible digestion in the mouth; it
stalls in the stomach; completes in the small
bowel
Now we call it CHYME
` Secretin
` CCK

` Motilin
GIP ` GIP
` VIP
` Somatostatin
` Enterokinase
` Zymogens: inactive enzymes
` First trypsin activated by
enterokinase enterokinase
` Trypsin then activates all other
enzymes
`

Breaks alpha 1,4 glycosidic bonds

Lactose
Sucrose
Maltose
Alpha-dextrins p

Fructose is only sugar with its own transport system

`
`
`
`

Lactase
Sucrase
Maltase
Alpha-dextrinase

` Sucrase def is most common primary ` Sucrase def is most common primary
disacharidase deficiency
` Lactase def is most common secondary
disacharidase deficiency
First enzyme to disappear in gastroenteritis; last
one to return( in about 48 hours)
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` The most common severe abdominal pain
` Pain is mid-epigastric, boring through to the
back
` Children: MCC is (1)abdominal trauma
(2) infections
x Cocksackie B, Mumps virus
` Adults: MCC is (1) alcohol
(2) gallstones
` Phlegmon: inflamed pancreas with the
intestines wrapped around it

` Causes a severe ileus

` Severe dehydration ` Severe dehydration
`
x
x
x
x
x

Ransons criteria:
Age > 55 years
Blood sugar rises above 200
WBC > 16,000
LDH > 350
AST > 250

` Poor prognosis in first 24 hours if

Patient needs more than 6 liters of fluid
pO2 < 55 (ARDS)
Hemoglobin drops by 2 or more grams
Calcium drops to below 8
`

MANAGEMENT: (for ANY abdominal pain)

NPO
NG tube
IV normal saline IV normal saline
Meperidine
Abdominal x-ray

Hemorrhagic pancreatitis:
Bleeding into the retroperitoneal
Grey-Turner sign
Cullen sign Cullen sign

TX: subtotal pancreatectomy

` Pseudocyst: has no epithelial lining
Can become infected ( abscess)
Tx: connect it to skin or small bowel
Characterized by persistent high amylase
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` Virchows triangle
Bile Lecithin
Salts
Cholesterol
` RUQ colic (stone): pain comes in waves
` Murphys sign: cessation of inspiratory

effort with RUQ palpation

` 80% are madede of cholesterol (not seen on x-ray)-ray) ` 80% are ma of cholest
erol (not seen on x
` 20% are made of calcium bilirubinate (hemolytic
anemia) excess biliruben
` 90% get lodged in cystic duct (Alk phos normal)
` 10% get lodged in the common bile duct
` (Inc. Alk phos)
` 3 clues for common bile duct stone:
Pancreatitis
High alkaline phosphatase- common bile duct High alkaline phosphatase common bil
e duct
High WBC count and fever- pus backs up
` Dx: Ultrasound;
` HIDA scan (most specific)- injectable radioactive
- if an obstruction- non visualization of gall bladder
`

Management: like ALL abdominal pains ` Management: like ALL abdominal pains
NPO
NGT
IV
Opiates- meperadine (always start with)
ABD xray

` Stone in common bile duct

Surgery: ERCP (endoscopic retrograde
choleangopancreotophagraphy-pull it out by mouth;
Laporoscopic cholecystectomy- 90% of cases
Asymptomatic gallstones-ursodeoxycolic acid
(DM, OCP, pregnancy) and schedule for surgery (60 % will
progress)
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` Helps EMULSIFY fats
` Comes from Phosphatidylcholine
` Modified to make surfactant
` Bile acids:
Cholesterol go to the liver and forms
Cholic and Chenodeoxycholic acids Cholic and Chenodeoxycholic acids
which are conjugated to Glycine and
Taurine to form bile salts

` Help EMULSIFY fats

` Cholestyramine
` Colestipol
` Side effects: need cholesterol to make
Estrogen E
Steroids
Malabsorption (diarrhea)
Fat for energy
Fat soluble vitamins
Cause gall stone
`
`
`
`

Micelle
Short chain fatty acids
Medium chain fatty acids
Long chain fatty acids

Chilomicrons i ` Chil
` VLDL
` IDL
` LDL
` HDL
LDL and B100
FOAM CELL
Atherosclerosis
Clathrin Pits
Symptoms:
70% Stenosis
FOAM CELL
Cholesterol Atheroma
Events:
90% Stenosis
` Metabolism of the lipoprotein is
defective
` Triglycerides, cholesterol or both can
be elevated
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` Predisposes to xanthelesma and
pancreatitis

` Defective metabolism of VLDL, IDL

or Chilomicrons
` Predisposes to early coronary artery
disease and xanthomas
` Defective metabolism of LDL
` TYPE 1: elevated chilomicrons
` TYPE 2A: elevated LDL
` TYPE 2B: elevated LDL & VLDL
` TYPE 3: elevated IDL
` TYPE 4: elevated VLDL
` TYPE 5: elevated VLDL & CHILOMICRONS
` STATINS: block HMG-CoA reductase
` Main side effects: myositis; hepatitis

Lovastatin
Provostatin Provostatin
Simvastatin Works best after 8pm
Atorvastatin
Cirivastatin
Valdestatin
Reduvastatin

` Cholestyramine- binds bile and blocks

reabsorption
` Colestipol
` Niacin : (-) VLDL
` Probucol
` Gemfibrozil : increases LPL
` Clofibrate
` Niacin
` Probucol
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`

Intravascular hemolysis
Vasculitis
Schistocytes
Low haptoglobin
Fibrin deposition in vessels

` Extravascular hemolysis

 Splenomegaly
Something is wrong
with RBC membrane
x Mcc: autoimmune Fibrin deposition in vessels
tear RBCs and platelets hemolytic anemia
` Direct hyperbilirubinemia: conjugated
` Indirect hyperbilirubinemia: unconjugated
`

INDIRECT ` INDIRECT
Low albumin
Gilbert syndrome
Criggler-Najjar syndrome
Type 1

DIRECT
Criggler-Najjar syndrome, type 2
Rotors syndrome
Dubin-Johnson syndrome Dubin Johnson syndrome

` Newborns: choledochal cyst; biliary atresia

` Children and adults: pancreatitis; gallstones;
sclerosing cholangitis; primary biliary
cirrhosis cirrhosis
` After age 40: pancreatic cancer
` The Ileum: in children
` The Sigmoid: in adults
`
`
`
`

Diverticulosis ` Diverticulosis
Diverticulitis
Volvulus
Intussusception

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` The last part of the small bowel
` An organ with NO known function
` Begins with pain around umbilicus
(visceral pain)
` Pain settles into RLQ ( McBurneys point)
somatic pain somatic pain
` Caused by a fecolith
` Management: like ALL abdominal pains
30% perforate in 24 hours

 Incidental appendectomies can be done

` The first part of the colon
` The largest part of the colon
` Cecal cancer has poor prognosis
` LAST chance to REABSORB fluids and
electrolytes
` Many Na-K pumps controlled by
aldosterone
` Haustration
` Mass movement ` Mass movement
` Watershed area: spleenic flexure
` Haustration
` Mass movement
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` Sits at a 90 degree angle with the
descending colon AND rectum
` Pubococcygeus muscle forms the
sling that holds the rectum at 90
degree angle
` Relax pubococcygeus muscle
` Rectum falls in line with sigmoid colon
` Gravity and distention start moving stool
down
` Once stool touches internal anal sphincter,
first d fecate f urge to def occurs
` Once stool touches external anal sphincter,
last urge to defecate occurs
` Relaxation of pelvic floor muscles relaxes
both sphincters
` NO sympathetic input to defecation
Duodenum Jejunum Ileum
Amino

Acids
FATS
Sugars
80
90
90
Iron
A,D,E,K,
B12
All else 90
90
100
`
`
`
`
`

Ca-carbonate
Aluminum hydroxide
Mg-hydroxide
Gaviscon
Sucralfate

h
`

`
`

PPI
Omeprazole
Esomeprazole
Pantaprazole
Robeprazole
lomeprazole
Bismuth
H-2 Blockers
Cimetidine
Ranitidine
Famotidine
Nizatidine

` Simethicone
` Loperamide
` Diphenoxylate
` Mineral oil
` Cisapride
` Metachlopramide
` Psillium
` Sorbitol
` Mg-citrate

` Phenophthalien
` Docussate sodium
` Sulfasalazine
` Sulfapyrazone
` Abetalipoproteinemia
` Ataxia telangiectasia
` Selective Ig-A def
Heavy hain i disease ` H ch di
` Celiac Sprue
` Tropical Sprue
` Necrotizing enterocolitis
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21
`
`
`
`
`

Irritable bowel syndrome

Spastic colon
Whipples disease
Toxic megacolon
Ischemic bowel

Crohns disease
Women
Transmural
Melena
Granulomatous
Creeping fat

Ulcerative Colitis
Men
Hematochezia
Mucosal
Starts in rectum > prox
Pseudopolyps Creeping fat
Cobblestoning
Skip lesions
From mouth to anus
Starts in ileum
Fistulas

Pseudopolyps
Continuous
HLA B-27
Sclerosing choolangitis
Toxic megacolon
Lead pipe colon
Colon cancer risk: 10%
at 10 years
x Begin annual colonoscopy
at 7 years
` Newborns: swallowed maternal blood

` Children: epistaxis
Adults: l iis ` Ad gastriti
` Massive UGI bleeding
Children: meckels diverticulum
Adults: Peptic ulcer disease
` Newborns: swallowed maternal blood
` Infants: anal fissure
Children: lyps ` Child pol
` Adults: IBD
` Elderly: Angiodysplasia
x Diverticulosis
x Cancer
` Newborns:
Choanal atresia
C-type esophageal atresia
Duodenal atresia
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`3 to 4 weeks old

Pyloric stenosis y
`4 to 6 months old

achalasia

achalasia
` 6 months to 2 years of age
intussusception
`2 years to 40 years

Adhesions

Adhesions

Internal hernias
`FIRST year of life

Hirschsprungsdisease Hirschsprung s disease

`1 year to 40 years

Adhesions Adhesions
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23
`After age 40

Adhesions

Obstipation Obstipation

Diverticulitis

Cancer
GI
Management Management
` Measurement of radiolabeled carbon dioxide after
the oral ingestion of labeled urea
` H. pylori splits urea with urease
` Confirm eradication of H. pylori ` Confirm eradication of H pylori
` If ulcer is found on endoscopy, the test of choice
will be biopsy, not urea breath test
` Detect steatorrhea as a sign of fat
malabsorption
` Pick Sudan black stain when you see a patient
with chronic pale, greasy, malodorous with chronic pale greasy malodorous
diarrhea and no evidence of infection
` Suspect chronic pancreatitis in pts w/steatorrhea
` Trypsinogen levels are low from a burned out
pancreas
` Pick trypsinogen level only after Sudan black stain has ` Pick trypsinogen lev
el only after Sudan black stain has
confirmed a fat malabsorption
` Wheat or gluten (gliadin) antigens
` DX of celiac disease

` Small bowel biopsy is the most accurate test for

celiac disease
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` Differentiate between intestinal malabsorption and
chronic pancreatitis
` D-xylose is a sugar that should be absorbed if the small
bowel is intact
` Low urine levels of D-xylose- defective intestinal mucosa
( Celiac, tropical sprue and Whipples disease)
` Best initial test for Wilsons disease
` Unexplained hepatic and psychiatric abnormalities
with movement disorder
` Low ceruloplasmin levels = Wilsons disease
` Most accurate test is a liver biopsy
` Best initial test in the diagnosis of acute pancreatitis
` Lipase is more specific to the pancreas
` Amylase can be elevated from damage to the salivary y g y
glands, esophagus or small bowel
` Most accurate test for acute pancreatitis is abdominal
CT- indicator of the need for a pancreatic biopsy
` Best initial test for autoimmune hepatitis
` Young female with liver disease
` Liver biopsy most accurate test
` Best initital test for primary biliary cirrhosis
(PBC)
` Middle aged female with itching (pruritus) and
an elevated alkaline phosphatase with normal
158

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1
ENDOCRINOLOGY
Endocrinology, cont
Exocrine: secreted into a cavity (pancreas)
Paracrine: secreted, then works only in the vicinity
(somatostatin)
Autocrine: secreted by the cell it works on
(granulosa cells)
Apocrine ( merocrine) tip of cell is secreted with the
substance (sweat glands)
Holocrine: entire cell is secreted with the substance
(sweat glands of the arm pit and groin)
HORMONE
Name and where it comes from
Main stimulus
Main inhibitor
Where does it go? g
What is the main action?
What is second messenger?
Miscellaneous syndromes
HORMONES
STEROID HORMONES
Fat soluble
Nuclear membrane
receptorceptor
PROTEIN HORMONES
Water soluble
Cell membrane
receptorsceptors re
Affect DNA replication,
transcription and
translation
Work via proteins
NO second messengers
re
Work via second
messengers
ERYTHROPOETIN
Made by: renal parenchymal cells
Signal: hypoxia ( NOT anemia)
Inhibitor: increasedreased oxygen Inhibitor: inc oxygen
Where it goes: bone marrow

What it does: erythropoiesis

Second messenger: tyrosine kinase
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POLYCYTHEMIA
First.check erythropoietin
Normal erythropoietin:
Gaisbock syndrome;
Stress polycythemia;
Spurious (not real) ;
Due to loss of plasma volume
POLYCYTHEMIA
Increased erythropoietin: due to hypoxia
Acute hypoxia: tachypnea and dyspnea
Chronic hypoxia: clubbing
(angiogenengiogenen-new new vessels) (an vessels)
Restrictive LD; COPD;
RENAL CELL CARCINOMA- adults
Wilms tumor- children
POLYCYTHEMIA
Decreased erythropoietin:
You have a cancer !!!!!!!!
Bone marrow is actingg on its own
POLYCYTHEMIA RUBRA VERA
Essential thrombocythemia
(platelets>600000)
Angiotensin II
ACTH
ACTH
ADRENAL CORTEX
Zona Glomerulosa: ALDOSTERONE
Stimulus: hypovolemia; hyponatremia; hyperkalemia
Inhibition: hypervolemia
Where it goes: late DCT
What it does: stimulate synthesis of Na-K pumps
Second messenger: none
ALDOSTERONE, cont

Miscellaneous syndromes: (tumor)

Too much: CONNS SYNDROME
Hypernatremia
Hypokalemia (K freely filters out)
Alkalosis (K/H exchange)
Hypertension (3 H2O for every Na+)
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ALDOSTERONE, cont
Too little: ADRENAL INSUFFICIENCY
21 hydroxylase def
11 hydroxylase def
In adults:
Abrupt withdrawal of steroids
Autoimmune adrenalitis
21 Hydroxylase deficiency:
Decreased Aldosterone [mineral corticoid]
(Na+ wasting)- hypotension
Low cortisol tisol [Glucocorticoid] coco ticoid] Lo co [Gl
no feed ack y ACTH
Increased Androgensvirilization
11 Hydroxylase deficiency:
Excess 11-Deoxycorticosteroneretain salt HTN
Aldosterone decreased desmolase rate limiting
tep in the ththway- llosteric t i titivator- t AT-II II st i th pa all ac AT
(down regulated due to the HTN)
Low cortisol- no ACTH feed ack
Increased Androgen production- virilization
Zona Fasciculata
CORTISOL
Stimulus: stress; hypoglycemia
Inhi itor: hyperglycemia
Where it goes: everywhere >PERMISSIVE
What it does: up regulates ALL receptors during stress
Second messenger: none

CORTISOL
Physiologic affects
Proteolysis
Gluconeogenesis
( reakak down protein
Anti-inflammatory
Kills T-cells and
eosinophil
Inhi iti it macrophageacrophage ( re down protein
to make glucose)
Inh m
migration
Sta ilizes endothelium
Sta ilizes mast cells
Inhi its phospholipase-A
Cortisol, cont
Too little: Adrenal insufficiency ( Addisons )
Too much: CUSHINGS SYNDROME
Pituitary adenoma: Cushings disease (to much ACTH)
Small cell carcinoma: Cushings disease
Adrenal adenoma: Cushings syndrome
Disease affects one organ
Syndrome affects many organs
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4
Dexamethasone suppression test
Lo-dose: 0.5mg IV Q6 x 4
If suppression occurs
O esity O esity
Depression
Normal variant
Dexamethasone suppression test
Hi dose: 1 mg IV Q6 x 4
If suppression occurs
Pituitary adenoma
If suppression does NOT occur
Check ACTH levels:
High ACTH: SMALL CELL CARCINOMA
Low ACTH: ADRENAL ADENOMA
ZONA RETICULARIS
Testosterone
Stimulus:
Controls male external genitalia in utero

Increasee in appetite Increas in appetite

Aggression and violence
Increases li ido and RBC count
Stimulated y ACTH
Second messenger: none
TESTOSTERONE
DHT: made in testes y 5 alpha reductase
Leads to secondary male characteristics at
pu erty.
Responsi le for hair growth Responsi le for hair growth
Too much leads to hair loss, especially in the
middle and front of scalp
Male patterned aldness
FENESTERIDE locks 5 alpha reductase
FLUTAMIDE locks DHT receptors
ADRENAL MEDULLA
Epinephrine:
Stimulus: stress/hypoglycemia
Inhi ition: hyperglycemia
Where it goes: liver and adrenal cortex
What it does: gluconeogenesis;
glycogenolysis
Second messenger: c-AMP
Misc. syndromes
Pheochromocytoma or Neuro lastoma
An excess of NE and Epi
Intermittent palpitations, HTN, diaphoresis and headache
Neuro lastoma:
hypsarrythmiarrythmia (dancingancing eyes)) hypsa (d eyes
opsoclonus (dancing feet)
Dx: measure urinary VMA and metanephrines
( dopamine > HVA)
Phentolamine- short acting alpha locker for diagnosis
Tx: phenoxy enzamine (longer acting, not specific)
162
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5
Pheochromocytoma or Neuro lastoma
Difficult to differentiate enign from malignant
on iopsy; they look alike
Neuro lastoma is MOST common a dominal
mass in children
Pheochromocytoma
10% are malignant
10% are ilateral

10% are in children

10% are familial
10% are metastatic at diagnosis
Pheochromocytoma
24 hr urine collection
Metanephrine
Vanillyl mandelic Acid (VMA)
Catecholaminestecholamines Ca
If elevated CT or MRI
If CT or MRI find nothing:
meta-iodo- enzyl-guanidine (MIBG) scinigraphy
(NE analogue that concentrates in the adrenals)
Stress Hormones
Epinephrine:
immediately
Glucagon: within 20
minutes
Cortisol:rtisol: within 2 to 4
Insulin: within 30 min
ADH: within 30 min
Insulin pushes the
itnto lls d Co within 2 to 4
hours
GH: after 24 hours
THESE PRODUCE THE
SUGAR
sugar i cell and
ADH normalizes the
osmolarity
Pancreatic Hormones
Glucagon: from ALPHA cells
Insulin: from BETA cells
Somatostatin: from DELTA cells
Pancreatic Polypeptide: from F cells
Glucagon
From: pancreatic alpha cells ( 1 receptors)
Stimulus: hypoglycemia and stress
Inhi ition: hyperglycemia
Where it goes: adrenal cortex, liver, and
dipose tissue adi ti
What it does: gluconeogenesis (raises
sugar), glycogenolysis (glycogen), lipolysis
(fat), and ketogenesis
Second messenger: c-AMP
Misc. syndromes

Glucagonoma
Pancreatic tumor
High glucose; high lipids; and high
ketones
Related to MEN I ( Wermers)
Hormone responsi le for KETOACIDOSIS
in type 1 dia etes
163
4/29/2008
6
cells of the pancreas lnsulin
From: pancreatic islet cells cells
( 2 and 2 receptors)
Stimulus: hyperglycemi

Inhibition: hypoglycemi

Where it here t BRICKLE Wh it goes: everywh except BRICKLE
Wh
t it does: incre
se
ll
n
bolic
processes
Second messenger: tyrosine kin
se
Misc syndromes
Insulinom
vs Nessidiobl
stosis
INSULINOMA
Seen prim
rily in

dults
C
uses hypoglycemi

Me
sure high h insulin li
NESSIDIOBLASTOSIS
seen prim
rily in
inf
nts
c
uses
hypoglycemi
ypoglycemi
M hi i

nd high C-peptide
Dx: c
t sc
n
Tx: remove surgic
lly
h
me
sure high insulin

nd high C-peptide
Tx: subtot
l
p
ncre
tectomy
Som
tost
tin
From: p
ncre
tic DELTA cells
Stimulus: insulin
nd gluc
gon
Inhibition: low insulin
nd gluc
gon
Where Wh it goes: p
r
crine
Wh
t it does: inhibits insulin
nd gluc
gon
Second messenger: c-AMP
Misc. syndromes

Som
tost
tinom

Usu
lly
p
ncre
tic tumor
Severe constip
tion
Dx: c
t sc
n
Tx: surgery
P
ncre
tic Polypeptide
NO KNOWN FUNCTION!
Wh
t t is the ly know ith Wh i th onl k org
n with no
known function?
164
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7
GI
HORMONES
GI Hormones
Stom
ch
G
strin
Duodenum
Secretin
CCK
Motilin Motilin
GIP
VIP
Som
tost
tin
Secretin
From: duodenum
Stimulus: low pH
Inhibition: high pH
Where it goes: p
r
crine (p
ncre
s &
g
llbl
dder)
llbl
dder) g
Wh
t it does: stimul
tes production
nd
secretion of bic
rbon
te ions from p
ncre
s
& GB
Second messenger: c-AMP
Misc. syndromes: none
CCK
From: duodenum
Stimulus: food, especi
lly f
ts
Inhibition: high pH
Where it goes: p
ncre
s (digestive enzymes)

nd g
llbl
dder (bile)
Wh
t it does: prim
rily f
t
nd protein
digestion
Second messenger: IP3/DAG
Misc. syndromes: none
GIP
From: duodenum
Stimulus: glucose
Inhibition: high pH
Where it tic islet l t lls Wh it goes: p
ncre
ti i cell

Wh
t it does: enh
nces insulin secretion

Second messenger: c-GMP
Misc. syndromes
GIP Syndromes
Dumping Syndrome: seen
fter Bilroth ll
procedure
Incre
sed osmotic lo
d dumped Into duodenum
C
uses osmotic di
rrhe

C
n
lso c
use postpr
ndi
l
l (re
ctive)e
ctive) C
n
lso c
use postpr
ndi (r
hypoglycemi

C
uses insulin resist
nce over time (type 2
di
betes)
165
4/29/2008
8
Som
tost
tin
From: duodenum
Stimulus: duoden
l hormones
Inhibition: high pH
Where it goes: p
r
crine
Wh
t it does: purely inhibitory
Second messenger: c-AMP
Misc. syndromes: som
tost
tinom

VIP
From: duodenum (from Auerb
chs
plexus)
Stimulus: duoden
l hormones
Inhibition: high pH
Where it goes: p
r
crine
Wh
t it does: purely Inhibitory to
ll
duoden
l hormones
Second messenger: c-AMP
Misc. syndromes
Vipom

Usu
lly
p
ncre
tic tumor
WATERY or secretory di
rrhe

Dx: c
t sc
n Dx: c
t sc
n
Tx: surgery
G
strin
From:
ntrum of stom
ch
Stimulus: high pH
Inhibition: low pH
Where it goes: p
riet
l
riet
l cells of the Where it goes: p cells of the
stom
ch (mostly in the body of stom
ch)
Wh
t it does: production of HCL
nd
intrinsic f
ctor (for
bsorbing VIT B12)
Second messenger: c
lcium
Misc. syndromes
G
strinom

Usu
lly
p
ncre
tic tumor

Zollinger-Ellison syndrome
G
strinrin levels
re high
ll the timee G
st levels
re high
ll the tim
C
n be p
rt of MEN-1 syndrome
ANP ( B-type n
triuretic peptide )
From: right
trium
Stimulus: high volume (stretch of right Atrium)
Inhibition: low volume
Where it goes: kidney
Wh
t it does: dil
tes the
fferent ren
l
rtery;
inhibits
ldosterone
Second messenger: nitric oxide
Misc. syndromele
ds to polyuri
, nocturi

nd
hypon
tremi
in right
tri
l distention
166
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9
PTH
VITAMIN D
CALCITONIN
CALCIUM
METABOLISM
PTH
Superior p
r
thyroids: 4th ph
rynge
l pouch
Inferior p
r
thyroids: 3rd ph
rynge
l
rch
Stimulus: low c
lcium; high phosphorus
Inhibition: high c
lcium; low phosphorus
Wherere it goes:s: (1) osteocl
stseocl
sts of bone (2)l
te2)l
te Whe it goe (1)
ost of bone (
DCT
Wh
t it does:
(1) stimul
te osteocl
stic
ctivity
(2) incre
ses secretion of phosphorus
(3)
ctiv
tes 1-
lph
hydroxyl
se
PTH, cont
Second messenger: c-AMP
Misc. syndromes
PTH Syndromes
HYPO-PARATHYROIDISM
Prim
ry: due to thyroidectomy
Pseudo: d tor tt king; hort t 3rd P recept no worki sh 3rd

nd 5th digit
Pseudopseudo
HYPOPARATHYROIDISM : only
difference is th
t c
lcium is norm
l
PTH Syndromes
HYPER-PARATHYROIDISM

Prim
ry: due to p
r
thyroid
denom
;

MCC of isol
ted hyperc
lcemi
in
dults
Second
ry: due to ren
l f
ilure
Ren
l Osteodystrophy
Osteitis Fibros
Cystic
- fibrous tissue
Osteopeni
- low density
Osteom
l
ci
- nutrition
Osteosclerosis- tr
um

Vit
min D
From: skin > liver > ren
l
Stimulus: low c
lcium; low phosphorus
Inhibition: high c
lcium; high phosphorus
Where it goes: (1) kidney
nd (2) GI
Wh
t it does: (1) production of C
-ATP
se
nd
(2) production of CBP ;(3) stimul
tes
osteobl
stic
ctivity
Second messenger: none
Misc. syndromes
167
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10
Vit
min D syndromes
Deficiency: Osteom
l
ci
in
dults; Rickets in
children
Excess: highg c
lcium; highg phosphorusp p
C
lcitonin
From: p
r
follicul
r cells
Stimulus: high c
lcium
Inhibition: low c
lcium
Where it goes: bone
Wh
t it does: inhibit osteocl
stic
ctivity
Second messenger: c-AMP
Misc. syndromes
MEN Syndromes
MEN 1: pituit
ry
denom
s, p
r
thyroid

denom
s,
nd p
ncre
tic
denom
s
(Wermer syndrome)
MEN 2: medull
ryedull
ry c
rcinom
m
of thyroidyroid (highigh MEN 2: m c
rcino o
f th (h
c
lcitonin), pheochromocytom
, plus or minus
p
r
thyroid
denom
( Sipple syndrome)
MEN 3: men 2 with neurom
/g
nglioneurom
but

minus p
r
thyroid
denom

Bisphosphon
tes
Inhibit osteocl
stic
ctivity like c
lcitonin
Second line drugs for osteoporosis
Very corrosiveve in thee GI Very corrosi in th GI
C
uses osteonecrosis (if received vi
IV)
Stored in bone for up to 20 ye
rs
i.e. etidr
n
te; el
ndron
te; ibondr
n
te,
residron
te
Hypoth
l
mic Hormones
Pituit
ry Hormones
Prol
ctin:
Stimul
te PRL rele
se- nipple
stimul
tion
Inhibit PRL rele
se- DA
168
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11
Dop
mine Agonists
L-Dop
/C
rbidop

Bromocriptine- old (stop l
ct
tion)
Selegyline- MAO type B, incre
ses extr
cellul
r
dop
mine
Am
nt
dine-
ntivir
l (influenz
A)
(-) prol
ctin- c
nt l
ct
te
N/V CTZ
Movement disorders- gross motor
Dop
mine Blockers (D-2)
Phenothi
zines
Chlorprom
zine
Prochlorper
zine (Comp
zine):
nti-N/V
Prometh
zine
Fluphen
zine Fluphen
zine
Thiorid
zine- pigment retinop
thy
Thiox
nthenes
Thiothixene- long
cting (>30 d
ys)
Dop
mine Blockers (D-2)
Butyrephenones
H
loperidol-
ntipsychotic- schizophreni
, psychosis
Droperidol -
ntimetic
Atypic
ls: i l block k D-4 4 ttors At bl D recep

Used for neg
tive symptoms

Used when pt h
s h
d extr
pyr
mid
l side effects
Cloz
pine-
gr
nulocytosis
Onl
z
pine- wt. g
in
Resperidone- neuroleptic
nesth.
(fever, muscle stiffness)
Pituit
ry Tumors
Nonfunction
l (chromophobic)
denom
s: most
common pituit
ry tumor
Prol
ctinom
: most common function
l pituit
ry
tumor t
ALL pituit
ry tumors
ssoci
ted with high prol
ctin
levels
High PRL > g
l
ctorrhe

nd
menorrhe

Hypothyroidism
Cretinism- Mom
nd fetus- hypo
Iodine deficiency
H
shimotos dise
se
DeQu
rv
ins dise
se- Virus (p
inful)-self limiting
Lymphocytic thyroiditis (postp
rtum )
Riedels Strum
- c
psule c
ncer (woody)
Tx: Thyroxine(T-4) or L-Thyronine (T-3)
Hypothyroidism:
3 T4 TSH TRH
2 T4 TSH TRH
1 T4 TSH TRH
169
4/29/2008
12
Hyperthyroidism
Gr
ves Dise
se (
utoimmune) < 50 y/o TSH

ntibody
Plummers Syndrome: toxic multinodul
r goiter
> 50 y/o one
re
hot (iodine t
keup)
Tx: prop
nolol
Propylthiour
cil- blocks peroxid
tion
Methim
zole- block peroxid
tion
I-131- destroy the tissue
Thyroxine- repl
cement

THE
END
170
6/25/2008
1
Rheum
tologygy
Steps to ev
lu
te
p
tient
First Step: Distribution
Poly
rticul
r symmetric Mono
rticul
r
rthritis
Oligo
rticul
r
symmetric Migr
tory
rthrop
thyPoly
rticul
r symmetric
Rheum
toid
rthritis (RA)
SLE (sp
res joint destruction)
Vir
l
l (HepHep. B, EBVV, CMV, B19) Vir ( B EB CMV B19)
First Step: Distribution
Poly
rticul
r symmetric:
Mono
rticul
r
rthritis
Oligo
rticul
r
symmetric
Migr
tory
rthrop
thy
Mono
rticul
r
rthritis
OA
Gout
Septic
rthritis
First Step: Distribution
Poly
rticul
r symmetric:
Mono
rticul
r
rthritis:
Oligo
rticul
r
symmetric:
Migr
tory
rthrop
thy:
171
6/25/2008
2

Oligo
rticul
r
symmetric joint

Spondylo
rthrop
thies
First Step: Distribution
Poly
rticul
r symmetric:
Mono
rticul
r
rthritis:
Oligo
rticul
r
symmetric:
Migr
tory
rthrop
thy:
Migr
tory
rthrop
thy
Rheum
tic fever
Gonococc
l
rthritis (dissemin
ted)
Lyme dise
se
P
in move
round the body
Second step:
Acute or Chronic
Osteo
rthritis
Septic
rthritis
Cryst
l induced
Third step:
Is there
ny evidence of systemic
symptoms?
Lungs: L
Kidney:
CNS:
Skin:
Hemotologic:
Fourth step:
Any evidence of infl
mm
tion?
OA:
RA:
172
6/25/2008
3
Infl
mm
tion
ssoci
tion
Morning stiffness > 1hr

 Red,, w
rm,, tender

Erythem
tous joint
Incre
sed ESR
nd CRP
CASE 1
72 y/o wom
n
presentsesents with leftft pr with le
knee p
in.
Mono
rticul
r
OA (chronic)
Septic (
cute)
Cryst
l induced (
cute)
CASE 2
30 y/o fem
le
presentsesents with wristt, pr with wris
MCP
nd PIP
swelling
nd p
in.
Poly
rticul
r
SLE
Vir
l
RA
CASE 3
32 y/o m
le presents with
knee swelling
fter you h
d
seen him for left wrist p
in
the d
y before which h
s
now resolved.
173
6/25/2008
4
Migr
tory
rthrop
thy
GC GC
Rheum
tic fever
Lyme dise
se
C
se 4
25 y/o fem
le presents
compl
ining of right
knee p
in
nd swelling

nd left hip p
in.
Oligo-
rthrop
thy
Spondylo
rthrop
thy (Reiters)
Test in
Rheum
tologictologic Rheum

dise
ses

Test:
Joint Aspir
tion: whenever there
is fluid in
joint, you need to

spir
te
te it
spir it
Exception: Contr
indic
tion
Test:
Joint Aspiration: whenever there is fluid
in a joint, you need to aspirate it

Exception: Contraindication
Bleeding disorders
Anticoagulants with leeding diathasis
Cellulitis overlying

174
6/25/2008
5
Test:
Always order the 3 Cs and a
gram stain
1.
2.
3.
WBC ranges
OA / Traumatic arthritis
Inflammatory (RA, Gout)
Septic arthritis
Crystals:

OA / Traumatic arthritis
RA
SLE SLE
Gout
Pseudo gout
Septic

Anti-Nuclear Anti odies (ANA)

Anti odies against part of the
nucleus
10% of normal people have + ANA
High AB titer
Anti-Nuclear Anti odies (ANA)
97% of SLE patients have a + ANA

Sifo hhe llts ack k S if t test resu come

negative, assume they dont have
SLE
If you think the patient may have
SLE, what is your first step in
management?
If positive, order
175
6/25/2008
6
A

association
SLE (60%), lupus nephritis
SLE (30%)
Drug induced lupus
Neonatal lupus, Sjogrens
Sjogrens
CREST
Mixed connective tissue dz.

Rheumatoid Factor (RF)

Anti odies against anti odies
Fc portion of IgG
Increase with age
Anti-Neutrophilic Cytoplasmic
Anti odies (ANCA)
Anti odies against certain
proteins in the cytoplasm of
neutrophils.
(c) ANCA:
(p) ANCA:
Diseases:

Rheumatoid Arthritis
Systemic Lupus Erythematosus
Scleroderma (SSc)
Sjogren Syndrome

Rheumatoid Arthritis
Chronic inflammatory disease
Target- Synovium
Symmetric distri ution
Potential to destroy cartilage and
erosion

one

Rules of 6:
Morning stiffness > 1 hr - for at least 6 weeks
Swelling of wrist, MCP, PIP 6 weeks
Swelling of at least 3 joints- 6 weeks
Symmetric joint swelling 6 weeks
176
6/25/2008
7
Extra-articular manifestations
Damage to tendon and ligaments
Boutinniere deformity- PIP flexion, DIP extension
Swan neck deformity- PIP extension, DIP flexion
Rheumatoid nodules- vasculitis
Caplan syndrome- rheumatoid nodules in lungs
La s for RA
RF
Anemia
ESR
X-ray:
Synovial fluid analysis
Mgt. for RA
Old Tx:
NSAIDS > Steroids > Methotrexate (2yrs later)
NEW TX: Startart with MTX NEW TX: St with MTX
after 1 week add prednisone for 1 week
only use for flare-ups
Antimalarial- hydroxychloroquine- MTX ackup
CASE 5
Patient with RA presents
with a swollen painful calf.
Diagnosis?
Alentoaxial Su luxation in RA
C1, C2
Dx:X: ray / CT Dx X-ray / CT

 Must rule out efore surgery

Systemic Lupus Erythematosus (SLE)
Systemic disease
Tissue and multiple organ damage
anti odies and immune complexes

Remem er: you can have all the criteria for

SLE, ut if the ANA is negative, the patient
does not have lupus
177
6/25/2008
8
Organs involved with SLE

CNS: confusion, personality change

Skin:
Kidney:
Lungs:
Hematologic:
Immune:
Bone:

Diagnosis of SLE
Best screening test ANA
Specific A s associated
Complement levels (C3,C4,CH50)
Active lupus
Lupus nephritis
Case 6
26 y/o female, admitted for
confusion. Hx. SLE and was recently
tappered off prednisone (10 pp p (
mg/day). Pt was fine a couple of days
ago. PE- no focal deficits.
DDx?
Pregnancy and SLE
Fertility rates:
Spontaneous a ortions and still irths
DOC Mgt.:
Exacer ation (flare up) DOC:
All pregnant women with SLE need to e

screened:
Mgt. SLE
NSAIDs for arthritis
Antimalarials: Chloroquine
Steroids: for major organ involvement
Cytotoxins: Azathioprine
Cyclophosphamide
Drug induced lupus
Limited form of lupus due to a drug
No major organ involvement
Dx: rash + anti-histone anti odies
(complement normal)
Mgt: Discontinue offending drug
178
6/25/2008
9
Scleroderma (SSc)
Chronic multisystem disease
Thickening of the skin
Raunaud phenomenon
Visceral organg involvement
GI: esophageal dysmotility, hypomotility of small
intestine
Pulmonary
Renal
CREST syndrome
Limited form of scleroderma
Symmetrical skin thickening
C
R R
E
S
T
Anti-centromere anti odies
Sjogren Syndrome
Chronic auto-immune disease
Xerostomia and dry eyes

 Lymphoproliferative disease- Malignant lymphoma

Bilateral parotid enlargement
Itchy eyes, sand under their eyes
Keratoconjunctivitis sicca
Spondyloarthropathies
Ankylosisng spondylitis
Reactive Arthritis
Psoriatic Arthritis
Enteropathic arthropathy
Ankylosing spondylitis
Inflammatory disorder of axial skeleton and peripheral
joints
Rare after age 40
90% of patients + HLA-B27
Young male 20s, chronic lower ack pain, morning
stiffness > 1hr, get etter with exercise
Cervical spine involvement- late stage of the disease
Extra-articular manifestations AS
Cardiac:
Spine:
Eyes:
Skin:
Mgt: NSAIDs, Physical therapy, Exercise
179
6/25/2008
10
Reactive Arthritis:
Complication of an infection somewhere in
the ody.
Non-Gonococcal urethritis:
1. 1.
2.
Infectious diarrhea:
1.
2.

3.
Reactive Arthritis Mgt.
NSAIDs
Anti ioticsti iotics (prompt)ompt) An (pr
Psoriatic Arthritis
DIP joint
Nail pitting
Sausage shaped digits
Enteropathic Arthropathy
Ulcerative colitis
Crohns disease
Skin lesions:
Pyoderma gangrenosium
Erythema Nodosum
Osteoarthritis (OA)
Target- articular cartilage
Hypertrophy of one
NOT an inflammatory disease
MC joint affected?
2nd most common joint affected?
Joint involved with the greatest disa ility?
Osteoarthritis (OA)
Target- articular cartilage
Hypertrophy of one
NOT an inflammatory disease
MC joint affected? Knee
2nd most common joint affected?
Joint involved with the greatest disa ility?
180
6/25/2008
11
Two forms of OA:
Idiopathic

Secondary (cause)
Arthropathies - gout
Endocrine dz
Desosition dz
Mechanical factors

Association with OA

 Joint pain with exercise

Relieved

y rest

Morning stiffness (< 20- 30 min)

Slow, progressive, irreversi le
NO systemic manifestations
La s with OA
CRP and ESR : Normal
X-ray: Osteophytes
Unequal joint space
Bouchards nodules (PIP)
He erdens nodules (DIP)
Mgt. with OA
Non- pharmacological
Correct poor posture
Weight reduction
Physicalysical therapyerapy Ph th
Drug therapy
First drug- Acetaminophen (contra: use i uprofen)
Add Capsaicin
Orthopedic surgery and joint
arthroplasty
Unsatisfactory medical Tx
Quality of lifee decreasedeased Quality of lif decr
Crystal Induced Arthropathies
Monosodium urate (MSU)
Calcium phrophosphate (CPPD)
Calcium oxylate (CaOx)
Calcium hydroxyapatite (CaHA)
181
6/25/2008
12
Gout:
Acute Monoarthritis
Tophi:
Metaatarsophalangeal joint (first toe):

 First episode:
Red, tender, warm
Predispose to Gout:
Excess ETOH
Trauma
Infection
Diuretics: Hydrochlorthiazide, Furosemide
Anti-TB meds: Pyrazinamide
Etham utol
Diagnosis of Gout:
It is made with fluid analysis of synovial fluid
MSU crystals
Negative i Birefringent f i N Bi
Needle shape crystals
WBC 5,000-50,000
Mgt. Acute Gouty Arthritis
NSAIDs
Indomethacin 50 mg 3 x day
Colchicine: 0.6 mg every hr until symptoms
resolve
Steroids: intraarticular or oral (elderly)
Chronic Hypouricemic Therapy
Low urine levels of uric acid
Usually life long therapy
Follow uric acid levels here !!!
Pro enecid- under secretors
Allopurinol- over producers
Pseuod-gout:
CPPD crystal formation
Elderly and pre-existing joint damage
May present acute like gout
Knee most common joint affected
182
6/25/2008
13

Diagnosis of pseudo-gout
Arthrocentesis:
Rhom oid crystals
+ Birefrengent
X-ray: linear radiodense deposits in joint
menisci Condro- calcinosis
Mgt: same as acute gout
Septic Arthritis
MCC gonorrhea
70% of cases > age 40
Elderly- Staph aureus (pre-existing joint
destruction)
Mgt. Septic Arthritis
Non-GC: (older) Staph aureus
GC (younger) sexually active
Both WBC > 50,000 and negative crystals
Staph aureus- IV Vancomycin
GC- IV Ceftriaxone
Therapeudic arthrocentesis
THE END THE END
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REPRODUCTIVE
ENDOCRINOLOGY
Menstrual irregularities
The num er one reason an adult woman
goes to see a doctor
The num er one reason a teenage female
misses work or school (dysmenorrhea)
Dr. Naegle Naegles Rule
Assumed that a womans menstrual cycle
lasts 28 days long
Allows us to calculate the EDC
Begin with the last first day of menses, go
forward 9 months or go ackward 3 months,