Definition of Infectious Diarrhea:

1) stool output

2) frequency

3) consistency

4) other

Definition of Infectious Diarrhea:

1) stool output >250g/24hr

2) frequency increased to >2-3 BMs/day

3) consistency loose or watery

4) other: urgent, fecal incontinence

virus

bacteria (or bacterial toxins)

parasites

ABX associated colitis

ABX associated colitis -

pseudomembranous colitis from overgrowth of c. difficile.

chronic diarrhea

infectious examples: c. difficile and parasites

Large Volume Diarrhea originating in the small bowel

(normally, of the 10L of fluid that enters duodenum, 85% is absorbed in the small intestines).

Arises from the disruption of the nml absorptive and secretory processes of the intestines.  Associated with mild periumbilical cramping and bloating. Characterized as large volume, watery, non-bloody diarrhea.

What is it?  Where does it usually occur?  Tissue invasion?

3 Causes of non-inflammatory diarrhea:

1) viruses - norwalk, rotovirus, enteric adenovirus

2) Parasites - giardiardiasis, cryptosporidium

3) bacteria -

a) preformed toxins: staph aureus, B. cereus, C. perfringens

b) enterotoxins: E. coli (ETEC), V. cholerae

Non - inflammatory diarrhea

Pt has bloody diarrhea.  Fecal leukocytes, blood culture positive, sigmoidscopy reveals hemorrhages and ulcers.

Dx and possible causes

Inflammatory diarrhea

causes:

1) viral - CMV (intestinal ulcers) in immunocompromised pts

2) protozoal - entamoeba histolytica

3) bacterial

a) cytotoxin producers: ETEC (hemolytic uremic syndrome), V. parahaemolyticus, C. difficile

b) direct mucosal invasion: Salmonella, shigella, C. jejuni, Y. entercolitica, STDs

General: fatigue, malaise, my/arthralgias, wt loss, appetitie change, mental status change

Skin: jaundice, pallor, edema, dryness

HEENT: URI, h/a, dizziness (postural)

Heart: palpitations

1) Diet: eating out, diet changes, raw/undercooked food

2) Sexual Hx: new partners, anal/oral sex

3) Home environment: dwelling (tight quarters?), pets

4) Occupation: food handler, daycare worker, animal handler

5) Travel/vacation

6) Hobbies: hunting, camping, hiking

7) Drugs, Meds (ABX within 6-8 wks), allergies (foods/meds)

1) Diarrhea >10d

2) Travel to endemic area

3) community water borne outbreak

4) HIV or homosexual male

leading cause of dehydrating gastroenteritis in infants and young children.

1) incubation pd

2) transmission

3) seasonal preference

4) most commonly seen in what age

5) tx and prevention

rotavirus:

1) incubation pd <48hrs

2) transmission fecal-oral

3) seasonal preference winter months

4) most commonly seen in what age 3mos-2yrs

5) tx and prevention vaccine available, supportive tx

Most common cause of gastroenteritis in older children and adults

1) incubation pd

duration

2) transmission

3) outbreaks seen in what populations?

4) tx

NORWALK VIRUS (norovirus)

1) incubation pd 12 hrs

duration 1-3 d

2) transmission fecal-oral, water, airborne?, raw shelfish consumption

3) outbreaks seen in what populations? military, school, cruises

4) tx supportive

Diarrhea Commonly seen in travel to undeveped countries (latin america, africa, middle east, asia), younger travelers, PPI users.

1) cause (80% of cases)

2) incubation pd

duration

3) stool presentation

4) tx and prevention

TRAVELLER'S DIARRHEA

1) cause (80% of cases) enterotoxigenic E Coli (ETEC)

2) incubation pd 2-10 days

duration 1-5 d (10% last > 1wk)

3) stool presentation >3 unformed stools daily, no blood or mucus

4) tx and prevention peel, cook, boil.  No milk, street food, local restaurants (very LAME)

4) tx and prevention

Enterotoxin-Associated Bacterial Food Poisoning:

1) etiologic agent

2) incubation

3) transmission

4) foods

1) etiologic agent staph aureus

2) incubation  1-6 hrs

3) transmission  food handlers during prep process

4) foods  foods prepared and cooled: ham, pork , canned beef, custard, cream, mayo

Enterotoxin- Assoc Bacterial Food Poisoning:

State bacteria and incubation pd.

1) ham, por, canned beef, custard, cream, mayo

2) rice, meat, sauce

3) spore producing, meat, poultry, pork cooked in bulk

1) ham, por, canned beef, custard, cream, mayo

Staph aureus, 1-6 hrs

2) rice, meat, sauce

Bacillus cereus, 6-24 hrs

3) spore producing, meat, poultry, pork cooked in bulk

Clostridium Perfringens, 8-24hrs

Abrupt onset of N/V/D, periumbilical cramping, RLQ pain, watery diarrhea with blood and mucus, fever/chills

Salmonella

incubation 8-24hrs, resolves 3-7 days

can invade sm & large intestines

usually self limiting

Protozoal infection of the upper sm intestines, most common protozoal infection in the US.

1) what form is infectious

2) transmission

3) population

GIARDIASIS

1) what form is infectious cyst

2) transmission food/water contamination, person-person, anal/oral sex

3) population campers - drinking from streams! Humans, dogs, cats, beavers can carry organism

The parasite is transmitted by environmentally hardy microbial cysts (oocysts) that, once ingested, exist in the small intestine and result in an infection of intestinal epithelial tissue. 

As well as watery diarrhea, there is often stomach pains or cramps and a low fever.

It is very rare to find blood or leukocytes in the diarrhea

If a pt is not menstruating and has an iron defienciency anemia (sideropenic anemia), what must you do?

Why???

A thorough GI evaluation

BECAUSE...

the most common upper GI cause of iron defienciency anemia is reflux esophagitis.

Risk assessment of an upper GI bleed is determined by the presence/absence of 5 clinical factors and ______ of a recent bleed.

The 5 clinical factors are:

Risk assessment of an upper GI bleed is determined by the presence/absence of 5 clinical factors and stigmata of a recent bleed.

Stigmata: scope the ulcer - is there a clot?  Is the clot red or black (red is more recent and worse).

The 5 clinical factors are: ¨CORE VANS¨

1. Age
2. Blood Volume - tilt test, black/red stool
3. Comorbidities
4. NSAID use
5. Recurrent Bleeding

1) Duodenal & Gastric Ulcers (PUD).

2) gastric erosions

3) esophagitis

4) duodenitis

1) ABCs (airway, breathing, circulation) - ORTHOSTATIC BP!

2) Hx and PE to determine risk - comorbidities, Rx/OTC, volume loss Sx

3) Locate site of bleed

4) Dx and therapeutic options

ROS - comorbidities

Rx/OTC Meds - NSAIDS

Sx of volume loss - orthostasis, syncope, BMs

tilt test (20 pulse incr/ 20 SBP drop/ 20% loss)

stool for blood (red is bad! black is not as bad)

1) CBC w/ platelets, protime

2) Electrolytes, BUN, creatinine

3) Type and HOLD (/cross)

4) ECG is >40y/o

-always give saline or ringers lactate...NEVER cut it with anything else.

-Transfusion goal is HgB of 9.5.  NEVER overtransfuse.

nl - 10:1

suspicious - 25:1

diagnostic - 50:1

1) you already know the source of the bleed

2) pt has liver disease

NGTs are risky, stressful for pt, and NOT accurate.

% of false negative rate of NG aspirates

1) duodenal ulcer

2) gastric erosion

3) gastric ulcer

1) duodenal ulcer 30%

2) gastric erosion 25%

3) gastric ulcer 20%

....NGT is wrong and shoes up with no blood (when there actually is a bleed).  So a negative result is not a very accurate result (esp in blood from your duodenum, B/C tube only goes to stomach).  Also, you stomach empties 90% of liquid (or blood) in 1 hr...so if the bleeding stops for a sec, beware of false negatives with NGT.

Medical Therapy in UPPER GI bleeds:

1) This pharma has shown clear benifit to upper GI bleeds if given by continous IV drip (80mg initially, then 8mg/hr)

2) This drug is #1 for pts with liver disease (variceal bleed).  If administered within the first 24hrs, it is as good as endoscopy.

1) This pharma has shown clear benifit peptic ulcer bleeds if given by continous IV drip (80mg initially, then 8mg/hr)

PPI (OMEPRAZOLE)

2) This drug is #1 for pts with liver disease (or esophageal variceal bleed).  If administered within the first 24hrs, it is as good as endoscopy.

Somatostatin (OCTREATIDE)

What is the gold standard for upper GI bleed dx studies? (When should it not be used? - 4)

What study is contraindicated when diagnosing an upper GI bleed?

Endoscopy (95% accuracy)....don´t use:

1) unstable pt

2) peptic ulcer/minor bleeds

3) bleeding diathesis

4)Re-bleeding

FYI - bleeding diathesis is an unusual susceptibility to bleeding (hemorrhage) mostly due to a coagulopathy

Barium studies are CONTRAINDICATED - blocks scope and can leak and cause peritonitis if perforation.

1) H. pylori (50%)

2) NSAIDS + irritant (ETOH, smoking...)

Therapeutic endoscopy stops bleeding in

____ to ____% of bleeding ulcers and is highly cost effective

Therapeutic endoscopy stops bleeding in

85 to 95% of bleeding ulcers and is highly cost effective

SUMMARY - UPPER GI BLEED LECTURE

1) The most common cause of a hemodynamically significant “lower” GI bleed is an _______.

2) Peptic ulcers cause ___% of UGI bleeds.

3) 5 clinical factors determine risk (0-50%), they are...

4) The mainstay of medical treatment is....

5) Endoscopy provides ___% efficacy in dx and tx.

1) The most common cause of a hemodynamically significant “lower” GI bleed is an upper GI bleed.

2) Peptic ulcers cause 80% of UGI bleeds.

3) 5 clinical factors determine risk (0-50%), they are age, comorbidities, volume, recurrent, NSAID use.

4) The mainstay of medical treatment is IVF & tx of comorbidities.

5) Endoscopy provides >95% efficacy in dx and tx.

#1 ERCP - invasive

#2 MRCP

**CP=cholangiopancreatography

1) hepatocellular carcinoma...vaccination

2) Gastric cancer...eradication of H. pylori

3) esophageal adenocarcinoma - doubling in incidence q 7 yrs  -....screen for it

4) colon cancer...screen & polypectomy.

YOU MUST TEST EVERY PERSON WITH GI SX FOR BLEEDING! – 2 tests

YOU MUST TEST EVERY PERSON WITH GI SX FOR BLEEDING! – stool for occult blood and Hgb level

When do you use obstruction series? (2)

When does it give you information?

acute abdomen

distention/constipation

Only gives you information if there is gas in the bowels - otherwise useless.

Indications: dysphagia, dyspepsia, early satiety

Contraindications: Upper GI bleed (do EGD), severly ill (do EGD) pts, obstruction (do EGD or CT)

FYI:

Esophagogastroduodenoscopy (EGD) is an examination of the lining of the esophagus, stomach, and upper duodenum with a small camera

indications: diverticulitis, crohn's, constripation, screening

contraind: lower GI bleed, severly ill pt, obstruction

LFTS:

-for injury: hepatocellular & cholestatic

-for function: synthetic and metabolic

-indirect tests

-for injury:

hepatocellular - AST/ALT

if GGT incr, consider ETOH

Viral serology

cholestatic - ALP/GGT

do US/CT

MCRP/ERCP

CT for tumors

-for function:

synthetic - albumin, PT (**FYI - PTT is NOT liver)

metabolic - bilirubin total/direct

-indirect tests: chol, LDH, platelets

Uses of endoscopy (4):

1) stomach CA

2) GERD

3) Duod/Gastric ulcers

4) NSAID-induced gastropathy

GI Cancer Prevention:

1) Colorectal CA prevention (4)

2) Esophageal Adenocarcinoma prevention

1) Colorectal CA prevention:

-colonoscopy

-flexible sigmoidoscopy

-barium enema

-FOBT

2) Esophageal Adenocarcinoma prevention - endoscopic surveillance of Barrett's

FYI:

FOBT – fecal occult blood test

Barrett’s esophagus - refers to an abnormal change (metaplasia) in the cells of the lower end of the esophagus thought to be caused by damage from chronic acid exposure, or reflux esophagitis. The normal lining of the esophagus (squamous epithelium) is replaced by an intestinal-type lining (columnar epithelium).

Criteria for Chronic Constipation

1) within what time pd?

2) symptom onset how many months prior to diagnosis?

3) criteria within what % of cases

4) must include 2 or more of what criteria

1) within what time pd? 3 months

2) symptom onset how many months prior to diagnosis? sx onset at least 6 months prior to dx

3) criteria within what % of cases 25%

4) must include 2 or more of what criteria: straining, lumpy/hard stools, sensation of incomplete evacuation, sensation of anorectal obstruction, manual maneuvers, <3 defecations/wk

MS

spinal cord injury

parkinsons

DM

absorption

propulsion of contents

storage/expulsion of feces

part of autonomic nervous system responsible for integrating smooth muscle in GI tract, secretory cells, and blood lymph system.  2 neural networks:

• located between longitudinal and circular muscle layers and contols peristalsis and transit
• between the circular muscle and the mucosa and is involved in local control of epithelial cell function, blood flow, secretion and absorption

enteric nervous system

• located between longitudinal and circular muscle layers and contols peristalsis and transit - myenteric plexus

• between the circular muscle and the mucosa and is involved in local control of epithelial cell function, blood flow, secretion and absorption - submucosal plexus
  

1) submucosal plexus,

2) excitatory neurons,

3) local hormonal type cells (ACH at brunner's glands & goblet cells

1) nl transit constipation

2) slow transit constipation

3) aberrant visceral perception - unusually severe GI pain

4) combo of slow transit constipation & aberrant

Colonic Inertia

**

dilated colon or rectum

-primary problem suggests what cause?

-secondary problem is a result of ...

MEGACOLON

-primary: neurogenic cause

-secondary: later in life due to chronic fecal retention, increased compliance, elasticity, blunted sensation in rectum

Ca (Tums)

iron supplements

loperamide (a drug effective against diarrhea resulting from gastroenteritis)

NSAIDs

Red flag signs and symptoms calls a.....

what are some signs/symptoms

COLONSCOPY!

-new onset constipation in elderly

-severe/unresponsive to tx

-FH of colon CA or IBD

-positive FOBT

-unexplained anemia

-wt loss >10 lbs

pt education for constipation:

1) laxative use

2) diet

3) BM timing

-reduce laxative use

-incr fluid, fiber

-take time for BM, esp post-prandial and in morning (colonic activity highest)

Bisacodyl, Senna, castor oil, cascara are...

Lubiprostone (Amitiza) are...

Bisacodyl, Senna, castor oil, cascara are...stimulant laxatives

Lubiprostone (Amitiza) are...chloride channel laxatives in colon

Diverticulosis

incidence - age, gender, geographic region

30% by age 60, 65% by age 85

male:female = 1:1

westernized nations

pt presents with mild to mod aching abdom pan in LLQ.  Pt has rectal bleeding and diarrhea and/or constipaiton.  Low grade fever noted.  +FOCT.  CBC: mild leukocytosis.

Dx 

complications (4)

Management (diet, pharma, surgical)

Indications for emergency & elective surgery

Diverticulitis

Complications: fistula, abscess, peritonitis, bleeding

Managment:

clear liquids, broad spec ABX (metronidazole 500mg tid & cipro 500mg bid).  Colonoscopy 6-8 wks after complete resolution.

OR

20-30% pts require surgery: colon resection of fistula repair.

Indications for emergency surgery: abscess, peritonitis

Indications for elective surgical resection: recurrent episodes

Pt education:

for diverticulosis: diet and lifestyle

for diverticulitis: avoid what?

for diverticulosis: diet and lifestyle high fiber & exercise

for diverticulitis: avoid what? avoid fiber

IBD:

1)  mucosal ulceration in colon and rectum

2) patchy transmural inflammation in any part of GI tract, non circumfrential

3) microscopic inflammation of the colon

1) mucosal ulceration in colon and rectum Ulcerative colitis

2) patchy transmural inflammation in any part of GI tract, non circumfrential  Crohn's Disease

3) microscopic inflammation of the colon 

Microscopic colitis

 clinical sx:

1) RLQ abdominal pain, diarrhea, low grade fever, anorexia, wt loss

2) post.prandial cramps, distention, borborygmi, vomiting, wt loss (food avoidance)

Crohn's disease - inflammation

Crohn's - obstruction

Fistulization in Crohn's Disease: what type of fistula?

1) recurrent UTIs, pneumaturia

2) psoas abscess signs: back, hip, thigh pain; limp

3) drainage via scar

1) recurrent UTIs, pneumaturia  enterovesical

2) psoas abscess signs: back, hip, thigh pain; limp  retrperitoneal

3) drainage via scar  enterocutaneous

Confined perforation in crohn's: what condition does it mimic?

1) from terminal ileum

2) from sigmoid colon

Confined perforation in crohn's: what condition does it mimic?

1) from terminal ileum mimics appendicitis (RLQ)

2) from sigmoid colon  mimics diverticulitis (LLQ)

The most characteristic early lesions of ____________, as seen endoscopically, are discrete “punched-out” aphthae (upper left) with erythematous borders and relatively normal intervening mucosa

The sensitivity of colonoscopic surveillance for the detection of dysplasia or cancer in colitis is almost surely inadequate unless ___-quadrant biopsies are obtained approximately every ____ cm along the entire length of the colon from cecum to rectum.

The sensitivity of colonoscopic surveillance for the detection of dysplasia or cancer in colitis is almost surely inadequate unless four-quadrant biopsies are obtained approximately every 10 cm along the entire length of the colon from cecum to rectum.

Drug therapy for IBD:

1) first line in mild to moderate disease, can be used during pregnancy.  Localized anti-inflammatory, non-systemic.

2) good for sever diaseases, but immunocompromising and bad side effects (face swelling, acne)

3) this is good for fistulas but long term therapy may cause peripheral neuropathies.

1) first line in mild to moderate disease, can be used during pregnancy.  Localized antiinflammatory, non-systemic.

aminosalicylates

2) good for sever diaseases, but immunocompromising and bad side effects (face swelling, acne).

corticosteroids

3) this is good for fistulas but long term therapy may cause peripheral neuropathies.

metronidazole (flagyl)

6-mercaptopurine & azathioprine

6 months to work

ADV RXNS:

-hypersensitivity rxns (fever, rash, pancreatitis, hepatitis)

-bone marrow suppression

-opportunistic infections

-minimal rsk of lymphoma

INFLIXIMAB:

adv effects:

-immediate infusion rxns (anaphylaxis)

-serum sickness-like syndrome

-lupus-like syndrome

-infection (TB REACTIVATION)

-exsanguinating hemorrhage

-perforation

-cancer or dysplasia

-unresponsive acute disease

-free perforations

-massive hemorrhage

-cancer or dysplasia

-chronic high grade obstruction

PUD definition

1) location (preference and age group?)

2) diameter of ulcer

3) penetration of ulcer

4) three causes

5) risk of malignancy higher in which ulcer?

1) location (preference and age group?)

duodenal ulcers (25-55y/o) are five times more common than gastric ulcers (50s-70s y/o)

2) diameter of ulcer >5mm

3) penetration of ulcer

through muscularis mucosa

4) causes

H. pylori

NSAIDs

Acid hypersecretion (Zollinger-Ellison syndrome)

5) risk of malignancy higher in which ulcer?

gastric ulcers - must be biopsied

PUD:

H. pylori ulcer:

1)  association with what type of ulcer

2) recurrence rate

NSAID ulcer:

1) association with which ulcer

2) which drug is most ulceragenic?

H. pylori ulcer:

1)  association with what type of ulcer duodenal

2) recurrence rate 85%

NSAID ulcer:

1) association with which ulcer gastric

2) which drug is most ulceragenic? ASA

pt presents with episodic epigastric pain, even at night, relieved by food.

Labs:  Possible anemia, incr WBC, incr amylase

PE: possible mild epigastric tenderness, positive FOBT

PUD tx:

1) 2 drugs that decr acid secretion

2) 2 drugs that improve mucus barrier

3) therapy to eradicate H. pylori

PUD tx:

1) 2 drugs that decr acid secretion

PPI

H2 receptor antagonists

2) 2 drugs that improve mucus barrier

misoprostol

bismuth subsalicylate

3) therapy to eradicate H. pylori

3-4 abx + PPI

Zollinger-Ellison Syndrome (gastrinoma)

1) locations

2) 90% of pts usually develop...

3) Screen fasting gastrin level with what 4 cases?

1) locations

pancreas or duodenum

2) 90% of pts usually develop PUD of duodenum

3) Screen fasting gastrin level with what 4 cases?

-recurrent/non-healing ulcers

-large/multiple ulcers

-ulcer associated with diarrhea or hypercalcemia

-PUD w/o assoc NSAIDs or H. pylori

Gastritis

1) Erosive/Hemorrhagic Gastritis

-NSAIDs, EtOH, stress

**NSAID gastritis very common**

-Stress Gastritis: tx with IV H2 blockers, PPIs, bicarb, sucralfate

2) Nonerosive Gastritis

-H.pylori, Pernicious anemia

**H.pylori gastritis almost never diagnosed.  Risk of gastric CA, lymphoma

-Pernicious Gastritis: incr risk of gastric CA, small carcinoid tumors

2 alarm symptms of GERD

Dysphagia (difficulty swallowing)

and Odynophagia (painful swallowing)

SEND FOR ENDOSCOPY

GE reflux: effortless mov't of stomach contents into esophagus.  Occurs many times daily w/o injury or sx.

Reflux esophagitis: reflux causes sx and damage to esophagus.

2 GERD complications.

Who needs endoscopy?

General Tx:

-no food within ____hrs of bed

-no:

-prn:

-pharmas

-severe

Complications:

1) Barrett's Esophagus (pre-malignant) in 15% of pts.  Change from simple squamous to columnar cells in esoph

2) Peptic Stricture

Endoscopy:

-odynophagia/dysphagia

-persistant heartburn w/ tx

-Heme + stools

-longterm sx (>5yrs) to r/o Barrett's

-q 2-3 yrs with Barret's, to check for malignancy

General Tx:

-no food within 2 hrs of bed

-no: EtOH, chocolate, mint, caffeine, smoking

-prn:antacids

-pharmas: h2 blockers & PPIs

-severe: surgery

Liver function testing

Enzymes:

1) not specific to liver

2) raised in acute viral hep, specific.

3) mainly in bile duct cells

Non-enzyme:

4) measure chronic liver dysfunction

5) measures acute liver dysfunction

1) not specific to liver.                      AST

2) raised in acute viral hep, specific.  ALT

3) mainly in bile duct cells.               ALP

Non-enzyme:

4) measure chronic liver dysfunction Albumin

5) measures acute liver dysfunction  PT

non-enveloped, RNA virus, w/ replication in cytoplasm of hepatocyte.  Damage to hepatocyte occurs through immune response.  Interferon gamma helps clear virus.

Fecal-oral infection.  Community outbreaks due to contaminated food or water.

Which virus and name risk factors.

Serum Detection factors for acute and past exposures:

HAV

Risks:

-contact with infected person

-travel to low socioeconomic countries w/ unclean H2O

-MSM

-Street drug users

Detection:

-IgM anti-HAV during 1st wk and persist for months (ACUTE)

-IgG anti-HAV after 1 mnth and persist for years (PAST EXPOSURE AND IMMUNITY)

Acute, self limited.

Asx in children.

Adult sx from flu-like to fulminance.

Incubation: 15-49d

Fatigue, malaise, nausea, vomiting, anorexia, fever, RUQ pain, diarrhea in kids.  Within 1 wk, possible dark urine, acholic stools, jaundice peaks in 2 wks.

Hepatomegaly on PE, occasionally splenomegaly, cervical lymphadenopathy, rash, arthritis.

Avoidance of HAV:

1) heat food/water to....

2) chlorine bleach dilution:

3) prevention

Avoidance of HAV:

1) heat food/water to 185ºF

2) chlorine bleach dilution:1:100 dilution

3) prevention: vaccine - 1st dose 4wks before travel, not for children under 12 (use immune globulin).  Yes for chronic hep B/C pts.

-vertical

-horzontal: health care setting, needle sticks, children-children during play

-percutaneous: IVDU, tattoo, piercings

-sex

-blood transfusions/organ transplants

HBV serum indicators:

1) first evidence of infection, may persist after acute infection.

2) produced in response to above and confers protective immunity.  Detectable in pts who have recovered from natural infection and those immunized.

3) indicates acute hep B infection, can persist for >3ms

4) appears during acute infection, but persists with recovery or chronic HBV.

5) found ONLY in HBsAG positive blood.  Indicates high viral replication and infectivity.  Persistance >3ms suggest chronic HBV.

6) sensitive and precise measure of viral replication and infectivity.  May be at high level without HBeAg present b/c ¨pre-core mutation¨prevents synthesis of HBeAg.

1) first evidence of infection, may persist after acute infection.

HBsAg

2) produced in response to above and confers protective immunity.  Detectable in pts who have recovered from natural infection and those immunized.

Anti-HBs antibodies (antibody to HBsAg)

3) indicates acute hep B infection, can persist for >3ms

Anti-HBc IgM

4) appears during acute infection, but persists with recovery or chronic HBV.

Anti-HBc IgG

5) found ONLY in HBsAG positive blood.  Indicates high viral replication and infectivity.  Persistance >3ms suggest chronic HBV.

HBeAg

6) sensitive and precise measure of viral replication and infectivity.  May be at high level without HBeAg present b/c ¨pre-core mutation¨prevents synthesis of HBeAg.

HBV DNA

HBV:

1) incubation pd

2) HBV window pd

3) 1st serological marker to appear in acute dz

4) serological marker indicating active replication

5) documents recovery from/immunity/vaccination

6) marker of reduced replication

7)marker of acute/recent infection

8) marker of current/past infection

1) incubation pd 2-3 months

2) HBV window pd During this 'window' in which the host remains infected but is successfully clearing the virus, IgM antibodies to the hepatitis B core antigen (anti-HBc IgM) may be the only serological evidence of disease.

3) 1st serological marker to appear in acute dz

HBsAg

4) serological marker indicating active replication

HBeAg

5) documents recovery from/immunity/vaccination

Anti-HBs

6) marker of reduced replication

Anti-HBe

7)marker of acute/recent infection

Anti-HBc IgM

8) marker of current/past infection

Anti-HBc IgG

general malaise, myalgia, arthralgia, fatigue, distaste for smoking, N/V, diarrhea or constipation, low grade fever, mild RUQ abdominal pain Jaundice after 5-10 days or never

- Mild hepatosplenomegaly

HBV Vaccine

1) prevents ____% of infections

2) Lasts up to _____years.

3) Routine vaccinations recommended for _____.

4) Indications:

HBV Vaccine

1) prevents 95% of infections

2) Lasts up to 15 years.

3) Routine vaccinations recommended for infants

4) Indications: IVDU, multiple sex partners, recently acquired STI, MsM, health professionals, household contact, correctional facilities, travelers to endemic countries, hemodialysis pts, pts recieving clotting factors.

Hepatitis C:

1) turns into chronic disease for over ___% infected.

2) leading indication for _______________in the U.S.

3) Strongest risk factor is history of ________.

4) list modes of transmission.

1) turns into chronic disease for over 70% infected.

2)leading indication for adult liver transplant in the U.S.

3) Strongest risk factor is history of IVDU.

4) list modes of transmission:

IVDU, blood transfusion b4 1985, promiscuity, 5% perinatally, tattoo/piercings

HCV Diagnostic Testing:

1) shows exposure to virus

2) confirmatory

3) highly sensative molecular testing

HCV Diagnostic Testing:

1) shows exposure to virus anti-HCV antibodies

2) confirmatory assays like RIBA-2

3) highly sensative molecular testing HCV RNA by PCR

Treatment involves PEG Interferon weekly SQ injections and Ribavirin tablets daily x 48wks in genotype I & IV, x24 wks in genotype II & III

Define Nonresponders

Define relapsers

Treatment for Chronic HCV

Nonresponder: detectable HCV RNA or less than 2 log drop in viral load after 12 wks of tx.

Relapsers: complete treatment then show a relapse of the virus after completion.

An RNA virus that causes hepatitis only with HBV. Progresses rapidly to cirrhosis.  Common in mediterranean areas and IVDU.

 Dx (serum dx?)

Hep D

anti HDV or HDV RNA in serum

Alcholic/viral hep

Fatty liver (NAFLD, NASH)

Autoimmune hep

Hemochromatosis (incr iron in blood)

Wilson Dz (decr copper excretion)

Alpha 1 antitrypsin def

Neoplasm

These are all diseases of _________ that can lead to ____________.

fats, inflammation and damage in the liver. 

What can it progress to and how do you differentiate btwn these stages?

How do you make the dx?

Risk Factors (4)

fats, inflammation and damage in the liver. 

Non-alcoholic fatty liver dz (NAFLD)

What can it progress to and how do you differentiate btwn these stages?

Non-alcholic steatohepatitis (NASH) progression in 2-5% pts.

Liver biopsy distinguishes NASH from NAFLD.

Risks:

obesity, DM, high TGs, severe wt loss

How do you make the dx?

Rountine AST, ALT labs are elevated.

major cause of cirrhosis of unknown etiology.  Usually asx, but possible fatigue, wt loss, weakness in advanced dz. 

Dx and tx

Dx: NASH

tx: weight loss, exercise, no ETOH/certain meds

Most common inherited liver disease in whites.  Sx begin middle age and lead to cirrhosis/liver cancer.

Dx and definition

Tx

Most common inherited liver disease in whites.  Sx begin middle age and lead to cirrhosis/liver cancer.

Dx and definition: Hemachromatosis: excessive iron in blood due to mutation of HFE gene

Tx: Phlebotomy

Autosomal recessive disorder.  Excessive absorption of Copper from small bowel, decr excretion from liver results in increased copper deposits in liver and brain.  Elevated serum ceruloplasmin & elevated urine copper.

Dx?

Occurs at what age?

Pathonomic sign, other clinical signs.

Dx? Wilson Disease

Occurs at what age? teens to 30 y/o

Pathonomic sign, other clinical signs.

Kayser-Fleischer: ring in eyes

Young pts with hepatitis/ splenomegaly

More common in women.  20% present with signs of decopensated cirrhosis.

+ HLA, +liver transaminases, +ANA, +smooth muscle antibody.

Dx and Tx

Autoimmune Hepatitis

tx: corticosteroids

insidious onset of weakness, fatigue, insomnia, muscle cramps, wt loss.

+/- abd pain, menstrual abnmlities, impotence, libido loss, sterility, gynecomastia, jaundice, hematemesis, varices, ascites, peripheral edema

Labs: anemia, PT/PTT changes, AST/ALT/bilirubin high, Alb low

In alcoholic hepatitis, AST is 2x greater than ALT.

  also GGT is elevated.

Formulas used to determine liver dz severity:

1) predicts mortality based on bilirubin, alb, INR, ascites, encephalopathy A/B/C

2) predicts prognosis for transplant, >14 is advanced liver dz.

1) predicts mortality based on bilirubin, alb, INR, ascites, encephalopathy A/B/C

Child-Pugh Score

2) predicts prognosis for transplant, >14 is advanced liver dz.

MELD score

Cachexia (¨wasting¨), weakness, wt loss, end stage cirrhosis.

Dx

what % of cases associated with cirrhosis

other risks

mortality rate

Dx: Hepatocellular Carcinoma

what % of cases associated with cirrhosis 80%

other risks: HCV, HBV

mortality rate: high

Cerebrovascular disease

Slide show

Storke

or

Cerebrovascular Accident (CVA)

-Definition

Transient Ischemic Attack (TIA)

1. Definition

2. whats the usual prognosis

3.What is the relationship of a TIA to CVA

4.whats another way to think of a TIA

1. what are the two main categories of a stroke

2.what % of strokes fall into each catagory

1. Most ischemic strokes  are  a result of?

2. About 1/4 of the ischemic strokes are a result of?

1-thrombosis with narrowing of the vessel and resultant platelet adhesion and clot formation

2-embolism with an emboli coming from a distal source (eg-Afib)

Ischemic Strokes

1-whats the largest and most commonly occluded of the intracerebral arteries

2-Which two arteries are uncommonly occluded artery

1-Middle cerebral artery infarct

2-Anterior cerebral artery infarct and Posterior cerebral artery infarct

1-What % of all CVAs are hemorrhagic

2- what % of all CVA's are Intracerebral hemorrhage
3- what % of all CVA's are Nontraumatic subarachnoid hemorrhages

Amaurosis Fugax

1-definition/ describe it

2-Cause

3-Treatment

1-A type of blindness described as a curtain being pulled down in front of one eye and the blindness is transient
Resolution of the episode is in the same fashion
“AKA”  fleeting blindness

2-Retinal emboli from ipsilateral internal carotid artery

3-CEA (carotid endarterectomy) or stenting of the carotid artery

MCA Syndrome

(Middle Cerebral Artery)

(This is the the most common area involved)

-How does this present, what and how is the body effected?

Motor or Sensory Deficit
- All Contralateral
Weakness
Numbness
Arm and Leg but arm usually affected more than leg
Face is variably affected

CVA With MCA Distribution

describe patients concentration, eyes and speech

1-What kind of symptoms can a Carotid Artery Obstruction cause

2-Critical Stenosis of carotid artery can cause

1-its an extracranial disease that causes TIA and CVA symptoms

 2-any of the Posterior Cerebral Artery (PCA) or Anterior Cerebral Artery (ACA) syndromes
eg-fugax
Transient Embolic obstruction of the ICA
-Easiest example of  Internal Carotid Artery (ICA) embolic disease  

Cerebellar Infarction

1-is an example of what?

2-Patients often present after what happens to them?

3-What is this difficult to differentiate from

4-What study are these seen best with

Cerebellar Infarctrion

1-name 4 ways that this presents clinically

2-What may develop and how do we treat it

1-Headache, Truncal ataxia, Cranial Nerve findings, Dizziness

2-Cerebral edema may develop and surgical intervention to decrease ICP is possible in these cases

Posterior Circulation Syndrom

1-Vertebrobasilar Insufficiency or VBI refers to?

2-What is signifigant about the basilar artery?

3-THe Posterior Cerebral Artery is a branch of what artery?

VBI

1-Posterior circulation supplies what 3 areas

2-what's the deal with symptoms in this area and what can they be confused with?

1-Brainstem, Cerebellum and the visual cortex

2-Symptoms in this area are hard to find and appreciate and Can be confused with vertigo

VBI (Crossed neurologic deficits exist in posterior circulation strokes)

Wallenberg syndrome is an example

-Tell 5 things about this syndromke

Keep in mind, most times we are not worried about Wallenberg syndrome

The bigger clinical concern is dignosing a 75 yr old with vertigo and missing what?

What do these pt's need, if you suspect VBI

-Missing VBI, missing unstable angina of the brain

-These pt's need admission for an MRI

Basilar Artery Occlusion (posterior circulation)

Can result in what syndrome and describe what it looks like

Locked in Syndrome

-Severe Quadriplegia

-Coma (you better hope)

-Complete muscle paralysis except for upward gaze

 PCA Syndrome (Posterior cerebral artery) (Posterior Circulation)

1-the arteries that are effected branch from what artery

2-describe the clinical presentation by the pt

3-May be associated with what

1-Basilar artery

2-pt may be unaware of the clinical eficits, motor involvement is minimal, Light touch and pinprick may be diminished

3-May be overflow or part of watershed area of a large MCA infarct, so this may be another reason that this is hard to find cliniclly bc the main thing you notice is the MCA infarct

Lacunar Infarcts or Lacunes

1-Clinical presentation

2-what are the causes

3-Locations

4-how and in what population do we find Lacunar infarcts

5-Serve as a reminder to treat your patients progressively in regards to what 3 main chronic illnesses?

1-Pure motor or sensory deficits
May be no clinical deficits

2-Infarction of small penetrating arteries, Chronic hypertension

3-Pons, Basal Ganglia

4-Often found incidentally on CT scan
We will find more and more in the future
Found in elderly individuals

5-BP
DM
Cholesterol

ICH Stroke (Intracerebral Hemorrhage)

1-Definition

2-where does the bleeding happen and where does the blood not accumulate

ICH Hemmorhage

1-Clinical effects

2-Effects of increased IC pressure

1-Clinical Effects
May be indistinguishable from cerebral infarction

Can go down hill quickly in front of you
Depends upon location of bleed
Neurological deficits (Putamen)
Contralateral hemiparesis
Neglect
Aphasi

2-Effects of increased IC pressure
HA
Nausea
Vomiting
These often precede neurological deficits

Subarchnoid Hemmorhage (SAH)

1-what happens with an SAH

2-Causes

3-Diseases associated with aneurysms

1-SAH is blood that has leaked into  the subarachnoid space, it can be Non traumatic or Traumatic

(Focus here is on nontraumatic type
Less common than ICH)

2-Causes-80% of nontraumatic SAHs are caused by ruptured aneurysms

3-Diseases associated with aneurysms
HTN
AVMs
Lupus
Marfans
Congenital

Clinical Manifestations of  SAH

-is dx more h or p?

1-describe a + hx

2-describe a + physical exam

3-what tests for dx

Diagnosis is more history than physical

1-History-Worst HA of the patient’s life of Sudden onset and Maximal intensity within 1 minute, Worse with forward bending and coughing

2-Physical Exam-Difficult to obtain a good neuro exam, N/V and a lot of pain, Photophobia
Papilledema, Possible confusion, May have depressed level of consciousness, Ocular nerve palsies

3- Use a CT, but it may miss a small amount of blood so if you have a Negative CT scan and high clinical suspicion? do a LP (lumbar puncture)

H and P for general Cerebrovascular disease

1-General history

2-Diagnostic Studies

1-Previous CVAs
TIA history
Possible episodes of bleeding
Recent trauma
ask onset of symptoms
Stuttering vs. steady symptoms

2-Diagnostic Studies (Acute)
CT of the head without contrast
Most commonly used
Very good for fresh blood
Only shows infarct 24 to 36 hours out
MRI
More difficult to obtain
Difficult for unstable patients (time)
Better at picking up acute infarcts

TIA

1-what is it?

2-how do we work it up

Management

1-TIA

TIA
Full workup
If no bleeding on CT scan
ASA and Heparin

Check for Afib on EKG

1-Treatment

TPA is a clot buster
A lot of fights here
TPA vs.. no TPA
Depends where you are Depends when the patient came in or if pt Woke up with deficit?
Strict 3 hour window
Treatment
Go with the Romans
TPA - you need to be with experienced providers
A lot of risks
Neuroinvasive Radiologists
 Great way to go
Maybe just ASA and Plavix or Heparin

1-Meningitis

2-Encephalitis

3-Brain Abscess

Meningitis- An infection of the meninges and the underlying CSF

Encephalitis-Inflammation of the brain itself

Brain Abscess- Localized infection within the skull

Meningitis

1-Pathogenesis

2-Sources of bacteria

3-avg. age of dx in 1986 and 1995

1-Bacterial seeding from hematagenous source
Products of bacterial proliferation alter the blood brain barrier and allow dissemination

2-From nasal colonization
-Rarely from trauma or instrumentation
eg-Neurosurgical procedures
eg-Sinus fracture
-Rarely to the newborn via maternal transmission
-Impaired splenic function

3-Average age on diagnosis in 1986
15 months
Average age of diagnosis in 1995
25 years

Meningitis Etiology depends on age groups

1-Neonates

2-Infants and children past the neonatal age group

Immunizations for this age group

3-Young Adults

Immunizations for this age group

4-Adults

1-Neonates
Group B Streptococci, Listeria, Enteric gram negative pathogens E. Coli

2-Neisseria meningitis, Strep pneumoniae, Haemophilus influenzae

4 injections each of
Pneumococcal immunizations finished by 18 months
H. flu B finished by 18 months
These are the big reason that the avg. age is now 25 years for meningitis

3-Meningococcus
 Strep Pneumo
Meningococcal vaccine given around 11 to 12 years of age
Must be given prior to college 

4-Streptococcus pneumoniae(#1)
-Neisseria meningitidis
-Listeria Monocytogenes-1/4 of the cases in over 60 year olds
Above three cause most meningitis in adults but any organism can cause meningitis especially in immune compromised adults

Bacterial Meningitis

1-Clinical Manifestations

2-Most cases are obvious, name the 4 situations that are not

1-Fever, Stiff neck, Photophobia, Headache, Altered mental status
Seizures (up to 25% of the cases)

2-Subtle presentations
-Very young (8 weeks)
-Very old
-Immune compromised
-Viral meningitis

Labs

1-CSF

2-Opening Pressure

3-WBC's

1-Normal CSF is clear

it will be cloudy or perulent

2-Normal opening pressure < 170mm

Elevated opening pressure > 300mm

3-Normally <5 mononuclear cells
Mononuclear cells  are >1000/ul

Labs Meningitis

1-PMNs

2-CSF Glucose

3-CSF Protien

4-Gram stain blood vs csf

1-PMNs
Normally 0 percent
>80% in meningitis

2-CSF Glucose
 Normal > 40mg/dl)
Glucose- < 40mg/dl in meningitis

3-CSF Protein
 Normal < 50 mg/dl)
> 200 mg/dl in meningitis

4-Gram Stain is positive for an organism in meningitis whereas your spinal fluid should not grow out any organisms

1-ER management of Meningitis

2-Pharm Treatment

3-Complications of Meningitis

-Immediate

-Delayed

1-Need to see it ASAP, get the pt ABX w/in 30 minutes of seeing them, before tests, then maybe do a CT, Labs, blood cultures

2-Steroids have proven benefit
Decadron 10mg IV
-Antibiotics
Ceftriaxone 2 gms IV
Plus vanco if resistance likely
-Vancomycin plus chloramphenicol and rifampin for PCN allergic patients

3-Immediate-Septic shock, DIC, Coma, Seizures, Cerebral Edema, Septic Arthritis

Delayed-Deafness, Cranial Nerve Dysfunction, Recurrent Seizures, Paralysis, Subdural effusions, Hydrocephalus, Gangrene

1-Meningitis Prophylaxis is necesary for what groups

2-Prophylaxis Meds

1-For close contacts  or intensive exposures to  patients with suspected N. Meningitidis
-Respiratory droplet spread
Patient exposures
-Mouth to mouth
-Intubation

Community contacts (close)
-House mates
-Day care center mates
-Cell mates
-Kissing partners

2-Meds
Rifampin 600mg BID for 4 doses
Cipro 500mg for one dose
Rocephin 250mg for one dose

Aseptic Meningitis

-prognosis

-caused by?

Viral Meningitis

1-Clinical presentation

2-CSF Findings

-Opening pressure

-WBCs (Mononuclear)

-% of WBCs that are PMNs

-Glucose

-Protein

-Gram stain

Sick but clearly not bacterial meningitis
Fever
Stiff neck
Photophobia
Lymphadenopathy
No petechial rash

2-Opening pressure
Normal  is < 170 mm
Viral meningitis is 200 mm ( mildly elevated)
Bacterial meningitis is > 300 mm
WBCs (Mononuclear)
Normal is < 5/ul
Viral is < 1000/ul and usually < 500/ul
Bacterial > 1000/ul

% of WBCs that are PMNs
Normal 0%
Viral meningitis 1 to 50%
Bacterial meningitis > 80%
Glucose
Normal is greater than 40mg/dl
Viral meningitis > 40mg/dl
Bacterial meningitis < 40mg/dl

Protein
Normal is < 50mg/dl
Viral meningitis is < 200mg/dl
Bacterial meningitis is > 200mg/dl
Gram stain
Negative normally
Negative with viral meningitis
Positive with bacterial meningitis

Viral Encephalitis

1-what is it

2-clinical presentation

3-Consider in patients that look like viral meningitis but have

1-Viral Encephalitis is a viral infection of brain parenchyma producing a inflammatory response

2-Can occur with viral meningitis
HA
Photophobia
Fever
Meningeal irritation

Usually have some change in mental status here that is not present with viral meningitis
Seizures
Movement disorders

3-New psychiatric symptoms
Cognitive deficits
Aphasia
Amnestic syndrome
Confusional states

1-St Louis Encephalitis

2-(EEE) Eastern Equine Encephalitis
Risk for mortality in persons < 15 yrs and > 50 yrs of age

3-La Crosse Encephalitis
Worse in kids < 16 who live in wooded areas

4-West Nile Virus
Mostly elderly in the US
Worldwide more children are affected

1-St Louis Encephalitis
Mortality risk in the elderly

2-(EEE) Eastern Equine Encephalitis
Risk for mortality in persons < 15 yrs and > 50 yrs of age

3-La Crosse Encephalitis
Worse in kids < 16 who live in wooded areas

4-West Nile Virus
Mostly elderly in the US
Worldwide more children are affected

Brain Abscess

1-Incidence

2-Pathophysiology

3-Routes of access

1-Incidence
Progressively declined with the advent of modern antibiotics
2-Pathophysiology
Focal pyogenic infection

3-Routes of access
Hematagenous (OM)
Direct implantation (After Neurosurgery)
Penetrating trauma

Brain Abscess

1-who does this usually effect

2-Clinical presentation

3-what study do you need to dx

4-what is contraindicated after the dx is suspected

5-Tx

1-Often times are immune compromised patients

2-Typical signs of HA, Fever or Neck stiffness are often absent
Only present in < 50% of the cases

3-Need CT with contrast

4-LP is contraindicated once the diagnosis is suspected
5-Treatment-IV antibiotics
-Ceftriaxone is a great choice
-Bactrim plus chloramphenicol or Flagyl

Seizure

1-Definition

2-Partial vs. Generalized Seizures

1- an abnormal, sudden and excessive discharge of neurons in the gray matter that is delivered via the white matter or tracts to the affect organs

2-Generalized seizures
-Caused by diffuse involvement of the brain at the onset
-Simultaneously involves both hemispheres
-Accompanied by LOC

Partial seizures
-Caused by involvement of only a restricted part of the brain
-Partial because of only a part of the cerebral cortex is firing
-May also be called focal
-May become secondarily generalized

1-Primary Seizure

2-Secondary Seizure

1-Primary (epilepsy)
Recurring seizures without provocation
Idiopathic
Epilepsy is a disorder that occurs when there are recurrent seizures
Epilepsy is common, affecting between .5 and 2% of the population in the USA

2-Secondary to something
-More common than primary seizures
-May effect up to 10% of the population
Fever
ETOH or Benzo withdrawal
Hypoglycemia

CNS infections
Cocaine
Trauma
Malignancy
MS
Alzheimers

Primary seizure disorder

1-History

2- 3 ways they may recur

3- 4 Causes for cyclical recurrence

1-pt has it Lifelong, onset usually in childhood or teen years

2-May recur-Sporadically, Randomly or In a predictable fashion

3- Causes for cyclical recurrence- Sleep deprivation, Menses, Strobe lights, Certain music
Most common cause of recurrent primary seizures is medication noncompliance

Generalized Seizures

1-Causes

-any age group (2)

-adolescents (2)

Young Adults (6)

Elderly (2)

Any age group
-Infectious disease
-Neoplasms
Adolescents
-Epilepsy (No other reason)
-Trauma

Young Adults
Epilepsy
Post traumatic
Withdrawal
ETOH and Benzos
Tumors  in the > 30 yr old group

Elderly
Vascular disease is most common cause in >60 yr olds
Degenerative disorders, eg-Alzheimer's

Primary Generalized Tonic Clonic Seizures or Grand Mal Seizure

1-Age of onsetAge of onset
2-Frequency of seizures

3-Clinical

4-Tonic Phase

5-Clonic Phase

6-Post ictal state

7-Common associated clinical sequelae

8-Risk of recurrence in adults after a single non provoked seizure

1-Age of onset
Usually 5 to 20 years
Uncommon in infants
2-Frequency of seizures
80% of the time, patients have a single isolated seizure

3-Clinical
Sudden loss of consciousness, Phases, Tonic, Clonic, Flaccid coma, Post ictal

4-Tonic Phase
Patient becomes rigid, Apnea ensues, Phase lasts for less than 1 minute

5-Clonic Phase
-Immediately follows tonic phase
-Jerking of the body
Rhythmic
Symmetrical muscle grouping
Violent
Lasts 2 or 3 minutes

6-Post ictal state

Decreased level of arousal or consciousness, Disorientation, Amnesia, Headache
-Duration
Few minutes to hours

Should clear with time
Is variable from seizure to seizure
Can include Todd’s Paralysis-(Looks like a CVA)
Neurogenic pulmonary edema is a rare finding

7-Common associated clinical sequelae
Tongue biting- Usually lateral on the tongue
Urinary incontinence, Bowel incontinence, Petechiae on the upper chest wall
Posterior shoulder dislocation

8-Risk of recurrence in adults after a single non provoked seizure
14% at one year
29% at 3 years
34% at 5 years
Prognosis for spontaneous remission is fair
-Up to 1/4 of patients have side effects from antiepileptics

Primary Absence Seizures

1-Clinical characteristics

Absence (petit mal) Seizures

1-what are they

2-how do they present

Absence Seizures

1-Age at onset

2-Frequency

3-Duration of seizures

4-what is the only dx test for this

5-Prognosis for remission

-childhood

-juvenile

Age at onset
Begin in childhood
Childhood absence epilepsy-Typical onset from 4 to 8 years of age, Peak at age 6 to 7
Juvenile absence epilepsy-Typical onset 7 to 14 years, Peak at age 10 to 12 years

2-Frequency
May be hundreds per day that last only seconds
May be fewer that last a minute or two
3-Duration of seizures
Brief
Usually less than 30 seconds
No aura

4-DX test

EEG is the only diagnostic test for absence seizures

Background activity is normal
Typically have 3 Hz spike and wave complexes
5-Prognosis for remission
Childhood absence epileptics have remission rate of 80%
Juvenile absence epileptics have a remission rate of only about 1/3, Much more likely to progress to generalized tonic clonic seizures

Differential Diagnosis of Partial Seizures

4

Partial Complex Epilepsy

1-Causes

2-Treatment

3-what do they often start with

4-Motor Activity

5-Automatisms

6-Verbal

7-Describe Impairment to consciousness

8-Prognosis for spontaneous remission

9-Treatment

1-Causes
Partial complex epilepsy, Brain trauma, Encephalitis, Meningitis, Stroke, AVMs, Neoplasms

2-Treatment
Most forms are treated by medicine
Some forms resolve by adulthood
Some forms are amenable to surgery-Hippocampal sclerosis (adults), Cortical dysplasias, Low grade neoplasms

3-Often start with an aura which is unique to the part of the cortex affected
-Temporal lobe
Fear, déjà vu
Motionless stare
-Parietal lobe
Tingling or numbness
-Occipital lobe
Visual changes, seeing spots

Motor Activity
Temporal lobe-Often begin with a motionless state
Frontal lobe-Stereotyped tonic or clonic activity,
Arm posturing may occur contralateral to the side of the focus, Sustained head turning

5-Automatisms
Semi purposeful motor or verbal behaviors
Lip smacking
Chewing
Swallowing
Picking and patting
6-Verbal
Moaning

7-Impairment to consciousness
Decreased responsiveness
Decreased awareness
May not be total impairment of consciousness-(Patients are unaware of the seizure)

8-Prognosis for spontaneous remission is
Limited

9-Need lifelong treatment with anticonvulsants
Surgery if a identifiable lesion can be found or failure of 2 or more anticonvulsants

Status Epilepticus

1-presentation

2-Prognosis

3-Managment

4-Post Status Management

-Obvious in patients with tonic-clonic movements
-Seizure activity over an episode may lessen with treatment
-It may be difficult to decide if someone is still seizing
-Non convulsive status occurs when the patient is still seizing but you may be unaware of it clinically

-Mortality rate as high as 20%
-Neurologic and Mental sequelae may be high
-Prognosis is related to the amount of time that the patient spent in status

3-Management

ABC’s
IV Valium or IV Ativan
Ativan (Lorazepam) is the drug of choice
IV Ativan has a longer half life
Dilantin loading occurs next (18-20mg/kg)
Cardiac monitoring

4-Post Status Management

Oral drugs are started
Need EEG results
Patient needs a complete workup after the status episode

Diagnostic Studies of choice for neck pain

1) trauma (possible fracture)

2) disk disease

Diagnostic Studies of choice for neck pain

1) trauma (possible fracture) = CT

2) disease = MRI

Tx of non-specific neck pain in the absence of infection, malignancy, and neurological findings

tx: rest, analgesics, physical therapy

Whiplash injury:

Official name and tx (3)

Acute Cervical Musculotendinous Strain

tx:

analgesics, physical therapy,

gradual retun to full activity in encourages

Pt complains of pain along C6-C7, increased with coughing and sneezing, decreased reflexes of biceps and triceps, decreased sensation and muscle atrophy or weakness of the forearm.

Dx, Tx, what you do if traditional treatment fails, and when surgery is indicated.

Dx: herniated nucleus pulposus

Tx: <2days rest, NSAIDs, activity modification

If no response to tx after 4-6wks, do corticosteroid injections.

Surgery indicated for unremitting pain, progressive weakness and abnormality identified on MRI/CT myelography.

What population of adults experience low back pain?

What are some differentials for:

• Injury
• Degenerative
• Intra-Abdominal
• Metabolic
• Inflammatory
• Mechanical
• Nerve Root Compression
• Vascular
• Infectious
• Pelvic
• Tumors
• Psychosomatic

What population of adults experience low back pain? 80%

Differentials:

• Injury: paravertebral muscle strain/sprain, compression fracture
• Degenerative: OA, spinal stenosis
• Intra-Abdominal: peptic ulcer, pancreatitis, renal colic, appendicitis
• Metabolic: osteoporosis
• Inflammatory: RA, ankylosing spondylitis
• Mechanical: Hyperlordosis, lumbar scoliosis
• Nerve Root Compression: herniated intervertebral disc, sciatica, cauda equina (medical emergency!!)
• Vascular: aortic aneurysm
• Infectious: osteomyelitis, herpes zoster
• Pelvic: pelvic tumors, salpingitis
• Tumors: multiple myeloma, metastic tumors
• Psychosomatic: somatization, malingering

low back pain (4)

-ROS

-Past Medical History

ROS

-other joints affected

-systemic symptoms suggestive of RA

-mentrual hx

-weight loss, fatigue (r/o malignancy)

PMS

-CA

-HNP (herniated nucleus pulposus)

-RA

-OA

-Trauma

[image]

What is this test?

What does this differentiate in between.

Patrick’s Test: Evaluation of Sacroillac Joint Dysfunction

Differentiates between hip and lower back pain.

38 y/o with LBP with butt and leg pain which increases with Valsalva, along with numbness and tingling in toes & feet. Depressed reflexes. (+) straight leg raise, (+) sitting root test, muscle atrophy.

Dx:

Study of Choice for Evaluation:

Tx:

Dx: Disc Herniation

Study of Choice for Evaluation: MRI

Tx: max 2 days bedrest, NSAIDs, muscle relaxants, physical therapy, lumbar epidural steroids (for sciatica)

29 y/o UPS worker with LBP has decr ROM, tense/hard paraspinal muscles, absence of lordotic curve, no signs of neurological involvement

Dx:

Tx:

29 y/o UPS worker with LBP has decr ROM, tense/hard paraspinal muscles, absence of lordotic curve, no signs of neurological involvement

Dx: Lumbar sprain/strain

Tx: 2-4 days bedrests on hard bed, 48 hrs ice...then heat, NSAIDs, lumbar support, pt education,  Williams' Flexion/Mckenzie's Extension Exercises (see below)

Williams' Flexion:

[image]

[image][image]

McKenzie's Extension:

[image]

[image]

[image]

FYI

[image]

Pt c/o LBP at night, unrelieved by rest or laying supine.

Possible causes?

Cauda equina Syndrome

[image]

[image]

Ankylosing Spondylitis

[image]

21 y/o male presents with gradual onset of periods of diffuse LBP since he was 15.  Wakes up in the morning with profound morning stiffness.  He complains of transiet peripheral arthritis and anterior uveitis.

Labs: elevated ESR, (+) HLA-B27 in serum, (-) RF in serum.

Dx and Tx

Dx: Ankylosing Spondylitis

Tx: preserve motion, NSAIDs, rest, physiotherapy to maintain joint mov't

May result in fixed cervical, thoracic, or lumbar hyperkyphosis and restriction of chest expansion.

Radiograph shoes ¨bamboo spine¨

Narrowing of the spinal canal with compression of the nerve roots.

What is it and what is the most common cause?

Lumbar Spinal Stenosis

Most common cause: advanced DJD

65 y/o male c/o insidious back pain and extremity paresthesia with ambulation and extension, relieved by lying supine or with flexion of the spine.  Pt c/o of leg pain, numbness, and ¨giving way.¨

Pt's gait is unstable and wobbly.  ROM of spine causes pain with spinal extension.

Dx?

how do you confirm your dx?

tx?

Dx: Lumbar Spinal Stenosis

how do you confirm your dx: MRI confirms spinal stenosis

tx: wt loss/exercise, NSAIDs ,physical therapy, back exercises, lumbar epidural corticosteroid injections, surgery in select cases.

• Tenderness tests: superficial and diffuse tenderness and/or nonanatomic tenderness
• Simulation tests: these are based on movements which produce pain, without actually causing that movement, such as axial loading and pain on simulated rotation
• Distraction tests: positive tests are rechecked when the patient's attention is distracted, such as a straight leg raise test
• Regional disturbances: regional weakness or sensory changes which deviate from accepted neuroanatomy
• Overreaction: subjective signs regarding the patient's demeanor and reaction to testing

-Subdivisions of thoracic outlet syndrome (3). 

-Which is the most common (90% of cases)?

-Thoracic outlet syndrome results from irritation of ___  and ___ innervated nerves.

Neurogenic (most common, 90%), venous, arterial types.

-Thoracic outlet syndrome results from irritation of C8  and T1 innervated nerves.

Pt complains of vague burning over supraclavicular/anterior chest C8-T1 dermatome with paresthesias of the arm and ulnar nerve.

Pt was in MVA and taken to the hospital for whiplash 2 months ago.

obliteration of radial pulse on inspiration while turning the head away from the affected side

[image]

AND

reproduction of syx with rapid opening and closing of hand with arm 90º abducted at the shoulder and 90º flexed at elbow.

[image]

Both of these tests indicate what?  And what are the names of these tests?  What is the cornerstone of treatment?

THORACIC OUTLET OBSTRUCTION

(+) Adson's Test: obliteration of radial pulse on inspiration while turning the head away from the affected side

(+) Roos test: reproduction of syx with rapid opening and closing of hand with arm 90º abducted at the shoulder and 90º flexed at elbow.

Treatment: physical therapy (with special attn to breathing a posture)

Pain over the deltoid, exacerbated by abduction and internal rotational.

Tests are positive for:

(+) pain elicited with abduction against resistance.

(+) pt winces with forward flexion of upper extremity.

Dx

Test names

tx

Supraspinatus Tendinitis

ADSON'S TEST: (+) pain elicited with abduction against resistance.

ROOS TEST: (+) pt winces with forward flexion of upper extremity.

tx: ice for 24-48hrs, rest of overhead use, physical therapy

[image]

Supraspinatus

[image]

anterior shoulder pain with direct palpation to biccipital tendon.

(+): pain with resisted supination with elbow flexed at 90º.

Dx

Test name

tx

[image]

Bicipital tendonitis

(+) Yeargason's Sign: pain with resisted supination with elbow flexed at 90º.

tx: ice for 24-48hrs, rest of overhead use, physical therapy

1) pain when wrist is extended against resistance, tenderness over lateral humeral epicondyle.  What is this and what tendons/muscles are involved.

2) tenderness over the medial humeral epicodyle and increased pain with tasks that require grasping and squeezing  (flexing the wrist against resistance). What is this and what tendons/muscles are involved.

3) is #1 or #2 more common?

1) pain when wrist is extended against resistance, tenderness over lateral humeral epicondyle.  Lateral Epicondylitis (Tennis Elbow) involves the common tendon to the extensor muscles of the wrist and hand.

2) tenderness over the medial humeral epicodyle and increased pain with tasks that require grasping and squeezing  (flexing the wrist against resistance). Medial Epicondylitis (Golfers Elbow) inolves the common flexior pronator.

3) is #1 or #2 more common: lateral epicondylitis is more common

pt presents with weakness and clumsiness of L hand with numbness of digits 1, 2, 3 , and lateral half of 4.  Symptoms increase with typing and awake her from her sleep.

Name 3 diagnoistic tests and your dx.

Also what is the tx?

CARPAL TUNNEL SYNDROME

[image]

Phalen's Test

[image]

Tinel's Test

[image]

Compression Test: compress over carpal tunnel

treatment: modify activity, splint 2-6wks, NSAID

50 y/o white male pt c/o gradual progression of tightness of digits 4 & 5nodular cord-like thickening of one or both hands, digits 4 & 5.

[image]

Dx and what type of injection can you use for tx?

Dupuytren's Contracture Disease

[image]

highest incidence in white males ages 40-60

Treatment: triamcinolone

Inflammation of the synovium-like cellular membrane overlying the bony prominences, can be secondary to trauma, infection, arthritic conditions.

1. What is this?
2. Where are the most common sites? (6)
3. Will respond to what tx?
4. How do you distringuit from arthritis (3)?
5. Most common sites if secondary to infection and dx/tx for this.

1. What is this? Bursitis
2. Where are the most common sites? (6) subdeltoid, olecranon, ischial, trochanteric, semimembranous-gastrocnemius (Baker's Cyst), prepatellar bursae
3. Will respond to what tx? local heat, rest, NSAIDs, local corticosteroid injections
4. How do you distringuit from arthritis (3)? begins abrubtlly and unilaterally usually, ROM usually okay to an extent, will respond to tx above
5. Most common sites if secondary to infection and dx/tx for this. olecranon, prepatellar.  Aspiration may reveal S. aureus infection and WBCs, tx with antibiotics.

[image]

college-aged female athlete c/o of anterior knee pain.  She has a hx of patella alta & recurrent patellar subluxion.  Pain and instability is felt when climbing or descending stairs.

PE reveals no swelling, by creptiance on movement.  Quad tone and strength is decreased.  Pain with flexion of knee.  Pain is reproducible with compression of patella as pt contracts quads.

Overuse Syndrome of the Knee (often in runners):

Subtypes:

1) pain medial and inferior to the knee joint over the medial tibia

2) pain along lateral side of knee

3) anterior knee pain, pain at tendon insertion into inferior pole of patella, common in basketball/volleyball players

Treatment?

Overuse of the Knee Syndrome Subtypes:

1) Anserine Bursitis: pain medial and inferior to the knee joint over the medial tibia

2) Iliotibial band syndrome and popliteal tendonitis:  pain along lateral side of knee

3) Patellar tendonitis: anterior knee pain, pain at tendon insertion into inferior pole of patella, common in basketball/volleyball players

Treatment: ice, discontinue activity, strengthen quads, physical therapy, NSAIDs

Meniscal Injury

[image]

A pop or shift in the knee with immediate injury suggests what type of injury?

Specifically, cases with the following signs suggest:

1) positive bulge sign and lachman's test.  Tx: RICE

2) positive drawer sign

3) laxity with valgus stress

4) laxity with varus stress

A pop or shift in the knee with immediate injury suggests what type of injury?

Ligamentous Instability/Rupture

[image]

Specifically, cases with the following signs suggest:

1) ACL: positive bulge sign and lachman's test.

2) PCL: positive drawer sign.

3) MCL: laxity with valgus stress.

4) LCL: laxity with varus stress

[image]

Valgus stress

[image]

Ankle sprain (defined as when joint is carried through ROM greater than normal without dislocation or fracture) is classified into 3 grades...describe them:

-damage to ligament

-tenderness

-edema

-joint laxity

-ecchymosis

-radiograph findings

[image]

****what type of fracture should you look for in grade III ankle sprains?***

I: stretching/microscopic tearing of ligament.  LOcal tenderness, minimal edema, no laxity, radiograph nml.

[image]

II: severe stretching/partial ligament tearing.  Tenderness, mild edema, mild ecchymosis, slight laxity.  Stress radiograph reveals loss of ligamentous function.

[image]

III: complete ligament rupture. marked tenderness, edema, ecchymosis, laxity, deformed joint.  Radiograph shows abnormal bony relationship.  ***look for 5th metatarcil fracture***

[image]

Lateral collateral ligaments, esp anterior talofibular ligament complex

[image]

Plantar Fasciitis - constant strain on the plantar fascia at its insertion into the medial tubercle of the calcaneus.

[image]

pt c/o severe pain in bottom of feet in the morning which subsides with minutes of ambulation.  Pt stands alot in flip flops for her job.  Pain increases with dorsiflexion of toes. Radiograph reveals large plantar calcaneal spur.

Dx and Tx.

Dx: Plantar Fasciitis

[image]

Tx:  stop prolonged standing, use arch support, NSAIDs, direct injection of corticosteroid + lidocaine into sole.

A disc herniation compresses the nerve above or below that spinal segment.  Give example.

[image]

above.

L4 disc herniation refers to the L3/L4 disc

• Pain: lower back, hip, posterolateral thigh, anterior leg
• Numbness: anteromedial thigh and knee
• Weakness and atrophy of quadriceps
• knee reflex diminished

• Pain: over sacro-iliac joint, hip, lateral thight and leg
• Numb: lateral leg, web of big toe
• Weakness in dorsiflexion of big toe and foot, difficultly walking of heels, possible foot drop
• Minor atrophy and reflexes ok

• Pain: over sacro-iliac joint, hip, posterolateral thigh and leg to heel
• Numbnes: back of calf, lateral heel, foot and toe
• Weakness: plantar flexion of foot and great toe, difficulty walking of toes
• Atrophy of gastrocnemius and soleus
• Diminished ankle jerk

• Pain: lower back, thights, legs, perineum.  May be bilat.
• Numbness: thights, legs, feet, perineum.  May be bilat.
• Variable paralysis/paresis of legs
• Possible bladder/bowel dysfuntion
• Ankle jerk diminished or absent

-Traction or displacement of large intracranial veins of dural envelope

-Compression, traction, intrinsic disease of cranial/spinal nerves

-Menigeal irritation/raised increased Intra-cranial pressure

...can all cause...

Worse headaches in younger years and decrease in incidence over lifetime, primarily occuring in women.  Sometimes beginning with aura (spots, field cuts, speech cuts, hearing loss), then followed by throbbing pain (bilat or unilat).

Assoc sx: N/V, photophobia, phonophobia

Headaches occuring primarily in men (30-50 y/o), occuring during REM sleep.  Pts c/o unbearable pain, unilateral, in eye/face, upon awaking.

Precipators: EtOH, sleep deprivation

Managment of Headaches

1- for the symptoms (2)

2-Prophylaxis (5)

3-Non pharmacologic measures (2)

Managment of Headaches

1- for the symptoms (2)

NSAIDs, 5-HT agonists, analgesics

2-Prophylaxis (5)

CCB, B-blockers, SSRIs, antidepressants, anti-seizure meds

3-Non pharmacologic measures (2)

stress management, biofeedback