CPD II: liver

here is the section in the GI notes on liver diagnosis that i missed when we were in the thick of the semester...

liver dysfunction can manifest in many different body systems: liver failure or cirrhosis might cause generalized fatigue / anorexia / weight loss. an infection or inflammation of the liver might cause a fever. bad breath might result from abnormal methionine metabolism in late cirrhosis. bilirubin backup can appear as jaundice, or even pruritis. increased serum lipids might lead to xanthomas and xanthelasmas. improper estrogen / androgen metabolism might result in gynecomastia and testicular atrophy, as well as spider telangiectasias.

fatty liver is a fairly common dysfunction of the liver that afflicts about 25-30% of the population. it results from abnormal accumulation of fat droplets within the liver, which can ultimately lead to fibrosis, scarring, and cirrhosis. it is not directly caused by fatty food intake- other risk factors include diabetes and alcoholism. clinically, it might present as liver enlargement and slight elevation of liver enzymes. if steatosis progresses to fibrosis (and if alcohol is not involved), then non alcoholic steatohepatitis develops. this is more likely to occur in middle aged, obese, diabetic women who are on hormone therapy such as synthetic estrogen. like simple fatty liver, it might present simply as an enlarged liver and slightly elevated liver enzymes with no other symptoms, or might present with increased BP, palmar erythema, muscle aches/fatigue, muddy sclera.

hepatitis is inflammation and necrosis of the liver and infectious hepatitis can occur in several different flavors, hep A through E mostly. these all present with similar symptoms, including flu like symptoms, jaundice, RUQ pain, and have similar stages of development which include a prodromal phase with generalized symptoms. each variant has a particular mode of transmission: A and E are mostly via fecal oral, or oral/anal sexual practices. B and D are via unprotected sex or contaminated syringes, and C is mainly from contaminated syringes. all forms might present with an enlarged, tender liver and may have splenomegaly as well. labs that might aid in diagnosis: high ALT / AST, bilirubin, low albumin / platelets, normal WBC.

prolonged acute hepatitis can result in chronic inflammation which might lead to chronic hepatitis, which can come in several varities: lobular, persistent, and active (most likely to lead to failure/cirrhosis). presentation can be similar to acute, or nonspecific, or lupoid like symptoms. lab findings might be similar, with high ALT / AST, bilirubin, prolonged PT, decreased albumin, hyperglobulinemia, and presence of ANA in lupoid presenting patients. diagnosis is by liver biopsy and differential should consider wilson's disease if serum copper is elevated.

fulminant hepatic failure is defined as a combination of acute liver failure and encephalopathy that develops in less than 8 months with no prior history of liver dysfunction. it can be caused by a number of factors such as viruses, fatty liver, ischemia, toxin buildup. it might develop into coma, hypoglycemia, cerebral or GI hemorrhage, renal insufficiency-- despite this, the long term prognosis is excellent.

cirrhosis of the liver occurs after longstanding injury or inflammation of the liver from a variety of causes and is a combination of fibrosis, necrosis, regeneration, ultimately resulting in hepatocyte shrinking. it is most commonly caused by hep C, then alcoholism, then hep B and cryptogenic causes. if it is due to alcohol, the liver might feel both enlarged and with a bumpy edge. cirrhosis can present with clubbing, dupuytren's contracture, fetor hepaticus, pleural effusion, and dilated abdominal veins. additionally, because of restricted blood flow, it results in portal hypertension and can cause ascites and esophageal varices.

cirrhosis predisposes to formation of liver cancer, hepatocellular carcinoma. HCC can also be related to chronic alcoholism, childhood hep B infection, hep C (especially in japan and europe), HBV, hemocromatosis. prognosis is not good; usually leads to death within 6-20 months. it presents similarly to advanced cirrhosis and lab markers such as transaminases, alk phos, bilirubin, LDH are elevated. alpha fetal protein is elevated in 75% of cases and is a good way to predict for HCC.

liver tumors can also be benign, as in the case of hepatic adenoma- which is most commonly seen in women in their 30's on birth control pills. they would present asymptomatically, or with hepatomegaly if the tumor was big enough, or with RUQ pain if ruptured (rare). once oral contraceptives are stopped, prognosis is good.

finally, gilbert's syndrome is an autosomal recessive disorder in which bile pigment clearance from the liver is impaired, resulting in elevated bilirubin levels without outright liver damage. it might be triggered by dehydration, stress, menses, viruses, fasting, and might only present with mild jaundice and vague symptoms like abdominal cramping and fatigue. diagnosis is by excluding hemolysis by testing for normal LDH and CBC reports, and liver tests to confirm that liver function is normal (except for unconjugated bilirubin).

questions
how might the following symptoms be related to liver dysfunction?
1. fatigue / anorexia / malaise / weight loss.
2. fever.
3. fetor hepaticus.
4. spider telangiectasias.
5. jaundice.
6. pruritis.
7. xanthoma / xanthelasma.
8. gynecomastia / testicular atrophy.
9. hypoglycemia.
10. abdominal swelling.
11. behavioral changes.

fatty liver...
12. what are the top 3 causes of chronic liver disease?
13. what percentage of the population does fatty liver affect?
14. describe the general progression of pathogenesis from fatty liver to cirrhosis.
15. what are some etiological factors for fatty liver?
16. what are some diagnostic signs for fatty liver?

NASH...
17. how big a factor does NASH play in chronic liver disease?
18. what is the etiology of NASH?
19. describe the patient type that is at greatest risk for developing NASH.
20. many patients with NASH show an elevation of...
21. what is the clinical picture of a patient with NASH?

acute viral hepatitis...
22. what is hepatitis?
23. what are the four stages of presentation of infectious hepatitis?
24. what are the hallmarks of hep. A signs / symptoms?
25. when is the period of greatest infectivity in hep A and how long does it take for hep A to resolve?
26. what is the risk of complication for hep B and C?
27. Hep D requires...
28. where in the world is hep E most likely to be found?
29. how are hep A and E transmitted?
30. how are hep B and D transmitted?
31. how is hep C transmitted?
32. what are some PE signs for patients with infectious hepatitis?
33. what are some lab findings that can aid in the diagnosis of infectious hepatitis?
34. what are some potential complications of infectious hepatitis?

chronic hepatitis...
35. what is the etiology of chronic hepatitis?
36. what are three types of chronic hepatitis? which is the most serious?
37. what are the signs/symptoms of chronic hepatitis?
28. what are the lab findings expected to be found in chronic hepatitis?
29. if a patient has chronic hepatitis symptoms plus high serum copper, what should be considered as a DDX?
30. what is a way to differentiate between alcoholic and non alcoholic hepatitis by lab tests?

fulminant hepatic failure...
31. what is fulminant hepatic failure?
32. what are some etiologies for fulminant hepatic failure?
33. what are the signs/symptoms of fulminant hepatic failure?
34. what are the complications of fulminant hepatic failure?
35. what is the prognosis of fulminant hepatic failure?

cirrhosis...
36. what is cirrhosis?
37. what are the most common causes of hepatic cirrhosis?
38. what are the two presentations of a patient with hepatic cirrhosis?
39. what might the liver feel like for a patient with cirrhosis due to alcohol?
40. cirrhosis is the most common cause of...
41. why might cirrhosis have normal or low liver enzymes?
42. what markers might be elevated with liver cirrhosis?
43. what are some complications of cirrhosis?
44. what are two other potential causes of cirrhosis?

liver cancer...
45. HCC leads to death in...
46. what are some risk factors for HCC?
47. what is the median age of diagnosis of HCC in the US and europe?
48. how great of a risk factor for HCC is cirrhosis?
49. what percentage of HCC is related to alcohol use?
50. what is the most common cause of HCC in japan and europe?
51. what are the signs and symptoms for liver cancer?
52. what are some lab markers that would be increased in liver cancer?
53. which lab marker is elevated in 75% of HCC cases?

hepatic adenoma...
54. describe the patient type that is most likely to have a hepatic adenoma.
55. what are the signs and symptoms of hepatic adenoma?
56. what is the severity and prognosis of HA's?
57. what is a PE finding that hepatic adenoma might present with?
58. what is a ddx for HA and why?

gilbert's syndrome...
59. what is gilbert's syndrome?
60. how common is gilbert's syndrome?
61. what are the etiologies / triggers of gilbert's syndrome?
62. what is the clinical presentation of gilbert's syndrome patients?
63. what labs are performed to diagnose gilbert's and why?

answers
1. liver failure / cancer / cirrhosis.
2. infectious hepatitis or inflammation.
3. abnormal methionine metabolism; late stage of cirrhosis.
4. altered estrogen / androgen metabolism.
5. elevated bilirubin from decreased ability of liver to metabolize and excrete bilirubin.
6. elevated bilirubin levels again- skin is an elimination pathway.
7. increased serum lipids.
8. improper estrogen / androgen metabolism.
9. impaired gluconeogenesis.
10. ascites from portal hypertension.
11. hepatic encephalopathy.

12. hep C, alcohol, then hep B.
13. 25-30%.
14. fatty deposits in liver cause enlargement, leading to fibrosis and scarring, which eventually leads to cirrhosis.
15. diabetes, poor diet, heavy alcohol use.
16. enlarged liver, slightly elevated liver enzymes. confirmed by liver biopsy.

17. third most common reason for chronic liver failure after hep C and alcoholism.
18. no known specific cause.
19. middle aged, obese, diabetic woman taking hormones but doesn't drink alcohol.
20. ferritin.
21. asymptomatic, or
enlarged liver
palmar erythema
increased systolic BP
muddy sclera
muscle aches / fatigue

22. inflammation of the liver with patched or scattered necrosis affecting all acini.
23. viral replication (asymptomatic), prodrome (generalized symptoms), icteric (jaundice, darkened urine, RUQ pain), convalescence.
24. flu symptoms, abdominal cramps, jaundice.
25. 1-2 days before onset of jaundice, 2 months to resolve.
26. 10% of hep B and 80% of hep C patients can develop longstanding liver inflammation which might result in liver cirrhosis and failure.
27. hep B virus.
28. developing countries, rare in the US.
29. fecal/oral, contaminated food or water. high association with oral / anal sexual practices.
30. unprotected sex, contaminated syringes.
31. mostly contaminated syringes.

32. liver tender and enlarged, may see splenomegaly as well.
33. huge elevations of ALT / AST
hyperbilirubinemia
low platelets, albumin
normal WBC
34. post hepatitis syndrome, cholestatic hepatitis, fulminant hepatitis, chronic hepatitis.

35. all forms of infectious except for A and E.
36. persistent, lobular, active (most serious).
37. asymptomatic or
nonspecific
or present like acute hepatitis
hepatosplenomegaly
jaundice
lupoid symptoms
serious systemic illness symptoms: cutaneous, constitutional symptoms.
28. elevated AST, ALT, bilirubin, prolonged PT, decreased albumin, hyperglobulinemia, ANA.
29. wilson's disease.
30. strikingly high WBC count, and only moderate elevation of AST/ALT in alcoholic hepatitis.

31. liver failure and encephalopathy which develops in less than 8 weeks with no prior history of liver disease.
32. viral, fatty liver, ischemia, toxins.
33. symptoms of encephalopathy
symptoms of acute liver failure
ascites
hypoprothrombinemia
malnutrition.
34. cerebral hemorrhage
coma
hypoglycemia
Gi hemorrhage
renal insufficiency
35. 20% short term, excellent long term.

36. triad of parenchymal necrosis, fibrosis, regeneration from longstanding inflammation or injury.
37. hep C
alcoholism
hep B
"cryptogenic causes"
38. "well compensated"- asymptomatic
"decompensated":
clubbing
Dupuytren's contracture
fetor hepaticus
pleural effusion
dilated abdominal veins
[club dupuy fetor lungs stomach] [club deco- a contract for your feet, lungs, and stomach]
39. enlarged liver with bumpy, nodular edge.
40. ascites.
41. because of the shrinking and loss of functional hepatocytes.
42. bilirubin
transaminases
alk phos
PT
gamma globulin
43. GI hemorrhage
encephalopathy
renal failure
liver cancer
ascites
44. primary biliary cirrhosis, obstructive biliary cirrhosis.

45. 6-20 months.
46. asians, childhood hep B infection, cirrhosis, HBV, hemochromatosis.
47. 65 years old.
48. 80% of patients with HCC have preexisting cirrhosis.
49. 30%.
50. HCV.
51. present similar to advanced cirrhosis:
pruritis
jaundice
splenomegaly
varices
cachexia
ascites
[pj's vac]
52. transaminases
alk phos
bilirubin
LDH
AFP
[taable]
53. AFP.

54. 34 year old female who takes birth control pills.
55. asymptomatic.
56. benign and go away when OCP's halted.
57. RUQ mass or hepatomegaly.
58. cholecystitis because rupture can cause acute RUQ pain.

59. an autosomal recessive disorder that results in defective bile clearance from the liver which causes elevated bilirubin.
60. 3-5% population.
61. dehydration
stress
menstrual periods
viral infection
fasting
62. asymptomatic or nonspecific findings. may have mild jaundice.
63. CBC and LDH to rule out hemolysis, liver enzymes to rule out liver damage.

CPD II: gynecology week 2 cont'd

the second lecture of the second week of gynecology in CPD II: vaginitis, PID, GC/chlamydia.

here are some keywords for the different conditions:
BV: risky sexual practices, clue cells, thin white discharge. gardnerella.
candida: thick cottage cheese discharge, redder tissue.
atrophic: low estrogen, thin clear discharge, thin / dry walls, high pH, basal cells.
trichomonas: copious yellow / green, tender perineum, strawberry cervix.
cytolytic: overgrowth of lactobacillus. candida symptoms. atypical clue cells, baking soda.
PID: save the tubes in 36 hours! fever / discharge. high WBC's. inguinal lymphs. fitz-hugher-curtis.
GC: greenish yellow discharge, swelling of glands, 7-21 days prodrome, increased ESR/WBC/pH.
chlamydia: similar to GC. flourescent antibody test. increased pH.

questions
vaginitis...
1. what are the signs and symptoms of vaginitis?
2. when is vaginal discharge normal?
3. what effect does progesterone have on cervical discharge?
4. what are some common etiologies for vaginitis for children?
5. vaginitis in reproductive age women is usually from...
6. what is a factor that protects against bacterial overgrowth in the vagina?
7. what are some non infectious causes of vaginitis in reproductive age women?
8. what is the pathogenesis of vaginitis in menopausal women?
9. how might crohn's disease lead to a sequelae of vaginitis?
10. what is the most likely cause of vaginitis for symptoms that occur before vs. after menses?
11. what are some distinct morphological signs for vaginitis from candidia?
12. if the WBC count on a wet prep is below 50 per HPF, vaginitis is likely due to...
13. if the WBC count on a wet prep is above 50 per HPF, vaginitis is likely due to...
14. what is a differential diagnosis for vaginitis related to dermatology?

bacterial vaginosis...
15. what is a microscopic finding that can point to BV?
16. name some risk factors for bacterial vaginosis.
17. what are the potential complications for a woman with BV?
18. what are the criteria for diagnosis of BV?
19. the WBC count is usually...
20. what is the quality of the vaginal discharge in BV?

vaginitis due to candida...
21. what are some risk factors for candida infection?
22. what is the quality of the vaginal discharge in candida?
23. what are some other symptoms of a candida infection?
24. how does symptom severity relate to time during the menses cycle in a candida infection?
25. compared to other types of vaginitis, vaginal tissue with candida infection is generally more...
26. how is the diagnosis of candida vaginitis made?
27. if there is a candida infection without the positive sign in question 26, what does this indicate? how is this treated?
28. what are some ddx's for vaginitis due to candida?

atrophic vaginitis...
29. what is the cause of atrophic vaginitis?
30. what is the quality of the vaginal discharge and vaginal walls in atrophic vaginitis?
31. what is a differential diagnosis for atrophic vaginitis?
32. what is the pH of atrophic vaginitis?
33. what is seen on the wet prep for atrophic vaginitis?

trichomonas...
34. what are the signs / symptoms of a trichomonas infection?
35. what is the morphological sign on the cervix for a trichomonas infection?
36. what is the conventional treatment for a trichomonas infection?

cytolytic vaginosis...
37. what is cytolytic vaginosis?
38. what is a common cause of cytolytic vaginosis?
39. what are the signs / symptoms of cytolytic vaginosis?
40. what might be present in the wet prep of cytolytic vaginosis?
41. what is an effective and simple treatment for cytolytic vaginosis?

PID...
42. how long is the window of time before the uterine tubes might be irreversibly damaged by a PID infection?
43. what are the common etiologies for women under 35yo with PID?
44. what are the common etiologies for women over 35yo with PID?
45. what are some risk factors for PID?
46. what are the signs/symptoms for PID?
47. what are some PE findings for PID?
48. what are three main diagnostic criteria for PID?
49. what are some complications of PID?
50. what is fitz-huges-curtis syndrome?
51. what are the differential diagnoses of PID?

GC...
52. what is the quality of the discharge in a gonorrhea infection of the vagina?
53. what are some other symptoms in a gonorrhea infection?
54. how long does it take for symptoms to appear after exposure to GC?
55. what are the lab tests used to diagnose GC?

chlamydia...
56. what is the most common presentation of a chlamydia infection?
57. what is the test used to diagnose a chlamydia infection?

answers
1. abnormal vaginal discharge
irritation / swelling / pruritis
erythema
dysuria / dyspareunia
2. before ovulation due to high estrogen levels.
3. causes it to become thick and sticky, forming a plug in the cervix that can remain in place in conception occurs.
4. poor perianal hygeine
bath chemicals / soaps
foreign bodies
5. infection: trich, candida, or BV.
6. lactobaccilus (keeps pH low)
high estrogen levels (maintains wall thickness)
7. factors that raise pH in the vagina: semen, menstrual blood,
tight clothing
frequent douching
foreign bodies
8. lower estrogen levels leads to thinning of the vaginal wall which might lead to decreased lactobacillus which could lead to increased pH and greater vulnerability to infection.
9. through a fistula that connects the vaginal and the GI tracts.
10. before: chronic candida. after: BV.
11. paper cut-like fissures on the labia majora / minora.
12. normal flora imbalance.
13. staph, strep, ecoli, GC, chlamydia.
14. lichen sclerosis.

15. clue cells.
16. IUD's
risky sexual practices
uncircumcised male partner
17. PID if not pregnant
post partum, premature complications if pregnant
18. Amsel's criteria:
higher than 4.5 pH
fishy odor
gray/white discharge
clue cells
[your clue: 4.5 gray fishes]
19. below 50hpf.
20. thin, copious, white.

21. diabetes, antibiotics, pregnancy, chronic yeast infections, some contraceptives.
22. thick white cottage cheese discharge that adheres to vaginal wall.
23. pruritis, erythema, dryness
dyspareunia
24. symptoms increase before menses.
25. red.
26. the presence of hyphae / buds / spores on wet prep.
27. candida glabradae, as opposed to candida albicans. treat with boric acid.
28. contact / allergic / chemical irritation
paget's disease of the vulva

29. low estrogen levels due to menopause or primary ovarian insufficiency.
30. clear vaginal discharge, thin and dry vaginal walls.
31. erosive lichen planus.
32. greater than 6, because less lactobacillus.
33. increased WBC
decreased lactobacillus
increased parabasal cells
increased cocci

34. copious yellow / green discharge
tender perineal area
dysuria
35. "strawberry cervix".
36. antibiotics.

37. an overgrowth of the normal lactobacillus strain in the vagina.
38. increased stress.
39. similar to candida.
40. atypical clue cells.
41. baking soda.

42. about 36 hours.
43. STI, from GC and CT.
44. overgrowth of endogenous flora.
45. unsafe sex
age, economic factors
nulliparous
46. lower abdominal pain that radiates to the back / sternum
fever
discharge
abnormal bleeding
47. inguinal lymphadenopathy
fever
mucopurulent discharge
enlarged Skene's glands
easily friable, erythematous cervix
cervical motion tenderness
48. elevated wbc's on CBC
WBC's over 50hpf on wet prep
sed rate over 15mm/hr
49. fitz-hughes curtis
tuboovarian abscess
adhesions
infertility
hydrosalpinx
50. infective exudate leaving the fimbrae and travelling between liver and diaphragm.
51. endometriosis
adenomyosis
ectopic pregnancy
cysts

52. greenish mucopurulent discharge.
53. bartholin/skene gland swelling
urinary symptoms
54. 7-21 days.
55. increased ESR, WBC
increased pH
DNA probe

56. similar presentation to GC infection, or asymptomatic.
57. flourescent antibody testing, increased pH on wet prep.

CPD II: gynecology week 2- bleeding disorders

this lecture looked at some more disorders of the female reproductive tract: amenorrhea, dysfunctional uterine bleeding, PMS, PCOS, premature ovarian failure, and menopause.


questions
amenorrhea...
1. what are some signs that could indicate primary amenorrhea?
2. what are some signs in a reproductive age woman that could indicate secondary amenorrhea?
3. what are some general symptoms / signs to look for that could be correlated to amenorrhea?
4. obesity plus amenorrhea might suggest...
5. amenorrhea plus moon facies might suggest...
6. what is a maturation index and how might it help in the diagnosis of amenorrhea?
7. decreased DTR's might indicate...
8. what are the first two tests to perform on a patient with amenorrhea?
9. what are some other tests that might help with a diagnosis of amenorrhea?
10. hypothyroid is associated with amenorrhea and...
11. elevated TSH levels also cause the elevation of...
12. what can amenorrhea plus high FSH levels indicate?
13. what might amenorrhea plus low / low normal FSH levels indicate?
14. what might amenorrhea plus an elevation of free testosterone or DHEAS indicate?
15. if all the above tests are normal, what is the next diagnostic step?
16. what are the most common causes of secondary amenorrhea?

DUB...
17. what is dysfunctional uterine bleeding?
18. what is the most common age for DUB?
19. what is the etiology of DUB?
20. what are the signs / symptoms of DUB?
21. what are some tests that might aid in the diagnosis of DUB?
22. what is the salivary progesterone good for detecting?

dysmenorrhea...
23. what are the characteristics of primary dysmenorrhea?
24. what are the most common causes of secondary dysmenorrhea?
25. what are the signs and symptoms of dysmenorrhea?
26. how might primary and secondary dysmenorrhea be distinguished based on treatment?

PMS...
27. what are the theories of etiology for PMS?
28. diagnosis of PMS is made by...
29. what are some differential diagnoses of PMS?

PCOS...
30. how common is PCOS?
31. PCOS is characterized by...
32. what is a test that can aid in the diagnosis of PCOS?
33. what are the "cysts" in PCOS?
34. what are the possible sequelae for PCOS?
35. what are some common symptoms for PCOS?
36. what is a good lab test to diagnose PCOS?
37. what would be seen in the TVUS for a PCOS patient?
38. what is a hormone that further increases estrogen sensitivity in the uterus?

premature ovarian failure...
39. what is premature ovarian failure?
40. what are the etiologies for premature ovarian failure?
41. what are the signs / symptoms of premature ovarian failure?
42. what are labs that can aid in the diagnosis of premature ovarian failure?

menopause...
43. physiologic menopause occurs when menses stops for how long?
44. what is the average age for physiologic menopause in the US?
45. what is the hallmark symptom for the perimenopausal period?
46. describe the hormonal shifts that occur during the perimenopausal period.
47. what are some causative factors for premature menopause?
48. what is the most common reason that women with menopause seek treatment? what is the cause of this symptom?
49. what are some other common symptoms related to menopause?
50. if a patient comes in with symptoms of menopause, what is an important test to perform first?
51. what are the potential issues in menopause related to osteoporosis?
52. what are some factors that can increase a menopausal woman's risk for osteoporosis?
53. what are some tests to screen for the potential CV disease that might be associated with menopause?

answers
1. no signs of puberty before 13
menarche 16yo
2. negative pregnancy test, missed menses for over 3 months, have less than nine menses per year.
3. hypo or hyperthyroid symptoms
virilization (hypertrichosis, hirsuitism)
obesity
4. PCOS
5. Cushing's.
6. a microscopic assessment of (endometrial?) cells that looks at the stage of development of cells present which is an indication of the degree of estrogen influence. (superficial cells: high estrogen influence. basal cells: low estrogen influence)
7. hypothyroid.
8. thyroid panel and prolactin.
9. pregnancy test
CMP
CBC, sed rate
celiac panel
bone age
10. infertility.
11. prolactin levels.
12. primary ovarian insufficiency.
13. hypothalamic amenorrhea.
14. pituitary tumor, ovarian, adrenal tumor.
15. TVUS to see any structural abnormalities.
16. PCOS and hypothalamic.

17. abnormal bleeding in the absence of signs of structural abnormality, inflammation or pregnancy.
18. puberty and perimenopause.
19. related to anovulation, can be caused by PCOS or idiopathic.
20. polymenorrhea, menorrhagia, metrorrhagia.
21. thyroid panel
TVUS
progesterone test
EMB
22. good for detecting if patient is ovulating in general: test on day 21.

23. due to prostaglandin excess, pain related to excess contraction, begins in menarche and has consistent episodes.
24. structural abnormality: endometriosis, adenomyosis, fibroids.
25. colicky pain that begins 1-3 days prior to menses and lasts until 2-3 days after.
26. NSAID's and OCP's will alleviate symptoms of primary dysmenorrhea and not secondary dysmenorrhea.

27. fluctuations of estrogen / progesterone levels, increased sensitivity of tissues to E/P levels, fluid retaining effects of estrogen.
28. PMS journals.
29. thyroid disease
other hormonal disorders
affective disorders

30. 5-10% of women.
31. anovulation plus androgen excess symptoms.
32. test FSH/LH levels on day 3 of cycle, can be 1:3 instead of 3:1. high LH levels indicate chronic anovulation.
33. follicles that have not ovulated.
34. CV disease
diabetes
endometrial carcinoma
35. irregular menses
hirsuitism, acne, alopecia
mild to severe obesity
36. salivary hormone levels: estrogen, testosterone, progesterone, DHEA, cortisol
37. polycystic ovary; string of pearls morphology.
38. hyperinsulinemia.

39. premature menopause that results from insufficient estrogen production from ovaries despite high gonadotropin hormone levels.
40. autoimmune
chemotherapy / pelvic irradiation
congenital thymic aplasia
galactosemia
gonadal dysgenesis
41. amenorrhea plus estrogen deficiency symptoms.
42. high serum FSH combined with low serum estradiol.

43. one year.
44. 51.
45. increased menses frequency followed by oligomenorrhea.
46. estrogen and progesterone production decrease while testerone stays the same.
47. smoking, high altitude, malnutrition.
48. hot flashes, caused by low estrogen / high gonadotropin levels.
49. vaginal dryness / atrophic vaginitis / dyspareunia
neuropsychiatric changes
night sweats
urinary frequency or incontinence
Gi disturbances
musculoskeletal changes
decreased libido
50. thyroid function to rule out hypothryoid.
51. decreased estrogen levels causes increased bone resorption by osteoclasts which increases likelihood for fractures, etc.
52. alcohol/cigarettes
caucasian/asian race
family history of osteoporosis
GI malabsorption issues
53. lipid profile
glucose
BMI
inflammatory markers

CPD II: gynecology- pelvic pain, pelvic mass, abnormal bleeding

this week we began the gynecology section in CPD, taught by Dr. Windstar. we went over some of the anatomy and physiology from last year, then talked about diagnosis of various abnormalities: pelvic pain, pelvic mass, and abnormal bleeding disorders.

questions
introduction...
1. what is the characteristics of a normal menses in terms of color, how long the flow lasts, average blood loss?
2. what is menorrhagia?
3. how much blood does a saturated pad or tampon usually hold?
4. what is the connection between constipation and gynecological conditions?
5. what are rectoceles and cystoceles?
6. Skene's glands are palpated if what is suspected?
7. what are the 4 possible positions of the uterus?
8. what is the normal size of the uterus?
9. what is the normal size of a reproductive age ovary?
10. what is the normal size of a menopausal age ovary?
11. what is the most common place that endometriosis develops?
12. name three pregnancy tests.
13. what is the advantage to the serum qualitative test?
14. what is the serum quantitative test used for?
15. what is the normal pH of cervical secretions?
16. what is the most common imaging technique used when masses are suspected?

pelvic masses...
17. what are hematocolpos?
18. what is the most common benign neoplasm in women?
19. what are hydrosalpinges?
20. TVUS might be preferred over CT because...
21. what is the most common tumor marker elevated in ovarian cancer?

pelvic pain...
22. what are the four systems that must be assessed with the presentation of pelvic pain?
23. what might syncope or hemorrhagic shock suggest?
24. describe the quality of pelvic pain in adnexal torsion.
25. tenderness in the anterior abdominal wall might indicate...
26. describe the quality of pelvic pain in perirectal abscess.
27. what are some sources of pain that would require immediate referral to ER?
28. what are some concomitant symptoms that should always be asked when a patient presents with pelvic pain?
29. 70% of patients with chronic pelvic pain have...
30. what are some labs that would aid in the diagnosis of pelvic pain?
31. if source of pelvic pain cannot be determined with PE and labs, consider...

abnormal vaginal bleeding...
32. what is menorrhea?
33. what is polymenorrhea?
34. what is metrorrhagia?
35. what is oligomenorrhea?
36. what is amenorrhea?
37. how long after menopause does bleeding need to persist in order to be considered abnormal?
38. what are the common ages for anovulation and why?

what are the most common causes of abnormal vaginal bleeding for...
39. infants.
40. children.
41. women of reproductive age with syncope or hemorrhagic shock.
42. women of reproductive age with positive pregnancy test.
43. women of reproductive age with negative pregnancy test.

44. what are the labs and imaging tests that would aid in the diagnosis of abnormal vaginal bleeding?
45. what is a south american herb that can aid in estrogen imbalances?

female reproductive endocrinology...
46. how does weight affect onset of puberty?
47. how does blindness affect onset of puberty?
48. what is the most common cause of precocious puberty?
49. what is the average age of menarche in the US?
50. describe the levels of FSH and LH after birth and in early childhood.
51. what hormonal change triggers the beginning of the menstrual cycle?
52. what is the hormone that stimulates FSH and LH production and where is it produced?
53. what is the hormonal change that triggers ovulation?
54. corpus luteum makes which hormone?
55. why does body temperature rise during the luteal phase?
56. when do progesterone levels peak?
57. if implantation occurs, how long does the corpus luteum continue to produce progesterone?
58. what are the hallmarks of the endometrial proliferative stage? what stage of ovarian development does this correspond to?
59. what are the hallmarks of the endometrial secretory stage? what stage of ovarian development does this correspond to?
60. when during the lifetime is estrone (E1) highest? what demographic is it higher in?
61. when during the lifetime is estradiol (E2) highest? what is it produced by?
62. when is estriol (E3) highest? what is it produced by?
63. E3 is the breakdown product of...

amenhorrhea...
64. what is meant by primary and secondary amenhorrea?
65. what are causes of anovulatory amenhorrhea related to hypothalamic dysfunction?
66. what are causes of anovulatory amenhorrhea related to pituitary dysfunction?
67. what are causes of anovulatory amenhorrhea related to ovarian failure?
68. what are causes of anovulatory amenhorrhea related to other endocrine dysfunction?
69. what is ovulatory amenhorrhea?
70. what are examples of anatomical abnormalities that might cause ovulatory amenhorrhea?

answers
1. medium/dark red
3-7 days of bleeding
30mL blood loss
2. greater than 80mL blood loss during a cycle or bleeding for more than 7 days.
3. 5-15mL.
4. constipation can cause more estrogen to return from the GI back into the blood stream, via beta glucoronidase, causing an estrogen dominance state.
5. rectoceles are bulges of the posterior vaginal wall and cystoceles are bulges of the anterior vaginal wall due to wall laxity.
6. chlamydia.
7. retroverted, retroflexed, anteverted, anteflexed.
8. 6cm * 4cm.
9. 3 * 2 * 2cm.
10. 1 * 0.7 * 0.5cm.
11. pouch of douglas.
12. urine ßHCG
serum qualitative ßHCG
serum quantitative ßHCG
13. more specific and sensitive than urine.
14. miscarriage or ectopic pregnancy.
15. 3.5-4.5
16. ultrasound: transvaginal or abdominal.

17. accumulation of blood in the vagina due to imperforate hymen.
18. fibroids / leiomyomas.
19. uterine tubes filled with fluid due to blockage at the distal end.
20. because of the radiation from a CT.
21. CA-125.

22. gyn, GI, GU, MS.
23. ruptured ectopic pregnancy, ovarian cyst.
24. severe, colicky, unilateral pain which reaches peak intensity in seconds or minutes.
25. bladder / urethral pain due to a lower urinary disorder.
26. painful defecation, localized tender mass.
27. ectopic pregnancy
tubo-ovarian abscess
ovarian cyst rupture or torsion
appendicitis
bowel perforation
28. fever, chills, nausea, vomiting, dizziness, dyspnea, night sweats.
29. endometriosis.
30. UA
wet prep
CBC
pregnancy test
31. TVUS, laparoscopy.

32. see question 2.
33. menses that are too frequent (less than 21 days before menses).
34. bleeding that occurs not in relation to menses (including spotting).
35. infrequent menses (more than 35 days between menses)
36. no menses.
37. 6 months.
38. puberty and perimenopause due to the lack of progesterone.

39. in utero stimulation of endometrium via placental estrogens.
40. trauma, precocious puberty / premature menses, urethral meatus prolapse.
41. see question 23.
42. spontaneous abortion, ectopic pregnancy, gestational trophoblastic disease, endometritis.
43. hormonally related cause, or structural abnormality.

44. pregnancy, CBC, ferritin, TVUS, EMB, coagulation tests, vulvar biopsy, pap smear.
45. maca.

46. overweight girls have earlier puberty and underweight girls have later puberty.
47. earlier onset for unknown reasons.
48. hypothyroidism.
49. 12.5.
50. very high at birth but low in childhood.
51. drop in estrogen and progesterone.
52. GnRH, produced in the hypothalamus.
53. spike in LH.
54. progesterone.
55. because of the thermogenic effects of progesterone.
56. about day 21.
57. until the placenta takes over.
58. endometrial vascularization and proliferation, fertile mucous from cervix. corresponds to follicular phase.
59. stabilization and formation of secretory elements in endometrium. corresponds to luteal phase.
60. highest during menopause, obese women.
61. highest in childbearing years, produced by follicles.
62. pregnancy, placenta.
63. E1 and E2 in the liver.

64. primary: period never started. secondary: menses stop for over 3 months.
65. anorexia nervosa
excess exercise
66. galactorrhea
benign pituitary adenoma
67. autoimmune disorders
chemotherapy, pelvic irradiation
methyltrexate
68. cushing's
hypo/hyperthyroid
obesity
PCOS
69. a rare form of amenhorrhea that is marked by normal ovulation but abnormal anatomy.
70. acquired endometrial lesions
cervical stenosis
imperforate hymen
male pseudohermaphroditism
transverse vaginal septum
vaginal and uterine aplasia

CPD II: gall bladder disorders

this section in the GI lecture series went over the diagnosis of the various gall bladder pathologies; mainly biliary obstruction, acute cholelithiasis, and choledocholithiasis. gallstones are most commonly formed in older patients from high cholesterol levels, which causes the bile salts to precipitate out of solution. there biliary obstruction can cause pain that follows meals or wakes patients at night, plateaus for 3-4 hours, then subsides. it is a RUQ pain that often radiates around to the lower right scapula, and a positive Murphy's sign is helpful to diagnose gallbladder inflammation. imaging of the gallbladder via ultrasonography will show wall thickening and distention of the gall bladder, which should be monitored in patients periodically to determine efficacy of treatment. acute cholelithiasis presents as an unrelenting pain, mainly from the inflammation of the GB itself, as opposed to simply obstruction as in biliary obstruction. it can also be differentiated diagnostically by a low grade fever and a high WBC count. finally, choledocholithiasis is an obstruction of the common bile duct which may lead to cholangitis, obstructive jaundice, acute pancreatitis, and biliary pain.

questions
cholelithiasis...
1. what percentage of americans have gallstones?
2. what are gallstones formed by?
3. what are black gallstones associated with?
4. what are brown gallstones associated with?
5. what is the composition of cholesterol gallstones?
6. what is the cause of cholesterol gallstones?
7. how is the apoe4 gene related to gallstones?
8. what is the most common age of patients with gallstones?
9. gallstones are most prevalent in which demographic populations?
10. what type of diet is associated with formation of gallstones?
11. what are some hormonal factors associated with gallstones?
12. why does low progesterone facilitate gallstone formation?
13. what are some other risk factors associated with cholesterol gallstone formation?
14. what are some risk factors for pigment stones?
15. what are the "five F" predisposing factors for gallstones?

cholethiasis diagnosis...
16. what are three common clinical presentations for patients with gallstones?
17. how do the majority of patients with gallstones present?
18. describe the quality of the pain in a "biliary colic" presentation.
19. complicated biliary stones are similar to colic presentation, but with...
20. what percentage of people with mild gallstone symptoms have complications after 20 years?
21. describe the quality of pain in people with acute cholecystitis.
22. what is the difference in the source of pain with biliary colic vs. acute cholecystitis?
23. what is the location and radiation pattern of the pain from biliary colic or acute cholecystitis?
24. what are some PE findings of patients with biliary colic or acute cholecystitis?
25. what is the imaging technique of choice for gallstones?
26. what the criteria for diagnosing gallstones via ultrasonography?
27. what is the "HIDA scan"?
28. what are some possible differential diagnoses for gallstones?
29. what is the naturopathic treatment strategy for gallstones?
30. what is the "porcelain gallbladder" finding?
31. what is a complication of choledocholithiasis?

acute cholecystitis revisited...
32. what is acute acalculous cholecystitis? what percentage of childhood gallstones are of this type?
33. what are the triggers of acute cholecystitis?
34. what are the signs and symptoms of acute cholecystitis?
35. what are the PE findings for acute cholecystitis?
36. what are the lab findings for acute cholecystitis?
37. what are the imaging techniques used to diagnose acute cholecystitis?

choledocholithiasis...
38. what is choledocholithiasis?
39. what percentage of patients with choledocholithiasis are asymptomatic?
40. what are the 4 possible outcomes of choledocholithiasis?
41. what is a severe complication of choledocholithiasis and what is the prognosis?

answers
1. 10-20%.
2. cholesterol, bilirubin, calcium salts, proteins.
3. chronic hemolytic disorders, younger patients.
4. impaction of biliary tract.
5. 70-90% cholesterol, lecithin, bile salts.
6. inflammation of liver leads to high lipid levels, leads to high cholesterol content in the bile, leads to supersaturation of bile in cholesterol, leads to precipitation of bile salts.
7. a gene that is related to higher lipid levels which will lead to cholesterol gall stones as described above.
8. very uncommon in children, more in older people.
9. western caucasians, hispanic, native american, pima indian.
10. standard american diet or rapid weight loss diet programs.
11. high estrogen levels compared to progesterone, pregnancy, birth control pills.
12. by inhibiting gallbladder motility, leading to biliary stasis.
13. parenteral nutrition, cystic fibrosis, pancreatic insufficiency, vagotomy.
14. chronic hemolysis
alcoholic cirrhosis
increased age
infection
periampullary diverticulitis
15. fair, fat, forty, fertile female.

16. asymptomatic, biliary colic, "complicated".
17. 60-70% present asympatically.
18. colicky pain in the RUQ following meals. pain gradually increases over 15-30 minutes and lasts for several hours.
19. fever, increased WBC's.
20. 50%.
21. unrelenting.
22. BC: pain from obstruction of cystic ducts. AC: pain from inflammation of GB.
23. well localized RUQ, radiates around to right scapula.
24. RUQ tenderness/pain
abdominal guarding
tachycardia
fever (if acute cholecystitis)
positive Murphy's (if acute cholecystitis)
hypertension
25. ultrasonography.
26. gallbladder distention and wall hypertrophy, pericholecystic fluid, sonographic Murphy's sign.
27. biliary scintigraphy.
28. appendicitis
diverticular disease
IBS
pancreatitis
hepatitis
esophageal spasm
GERD
peptic ulcer
pneumonia
29. follow up and do reimaging to ensure thinning of GB walls. lifestyle modification.
30. calcification of GB walls.
31. pancreatic insufficiency.

32. inflammation of GB without gallstones. 50% of childhood cases.
33. fasting, stress, trauma, weight loss dieting.
34. RUQ pain radiating to lower R scapula
rebound tenderness
anorexia
nausea / vomiting
splinting of respiration
low grade fever
mild jaundice
35. positive Murphy's sign and palpable GB.
36. elevated WBC
shift to the left
mild elevation of transaminases
increased bilirubin and alk phos
increased amylase.
37. ultrasound, biliary scintigraphy.

38. obstruction of the common bile duct.
39. 10%.
40. cholangitis, obstructive jaundice, acute pancreatitis, biliary pain.
41. suppurative cholangitis, 50% mortality due to sepsis.

CPD II: pancreatic cancer and pancreatic insufficiency

pancreatic cancer is a disorder that is difficult to manage because of its often delayed diagnosis and high potential for metastasis. it most commonly afflicts males, older than 55 years, and can be caused by smoking, alcohol, high animal fat diets, diabetes, and some forms of chronic pancreatitis. it might manifest vaguely at first, with epigastric tenderness, fatigue, nausea, weight loss. pain radiating from the abdomen to the back might indicate retroperitoneal invasion of the splanchnic plexus. pancreatic cancer can also be associated with migratory thrombophlebitis, upper GI bleeding, and diabetes mellitus.

patients with pancreatic cancer might present clinically with epigastric tenderness, signs of jaundice, and significant weight loss. late stage patients might present with ascites, a palpable abdominal mass, and hepatosplenomegaly. the diagnosis of pancreatic cancer might be aided by CEA or alpha FP levels, a chem screen for liver/kidney function, and trypsin levels. additionally, the tumor markers CEA and CA19-9 might be present. ultrasound, CT, biopsy and MRCP (a type of MRI used to visualize the pancreas) are all used to diagnose pancreatic cancer.

pancreatic insufficiency is a functional disorder, much like hypochlorhydria is for the stomach. it is thus difficult to diagnose, sometimes determined by excluding other diagnoses. it can be caused by overeating, excess carbohydrates, excess caffiene, lack of raw foods, and other dietary factors. it might result in indigestion, gas/bloating, low blood sugar, and a "left scapula reflex". the indican test, heidelberg test, and fecal chymotrypsin are used to diagnose, and a CBC shows macrocytic RBC's. treatment strategies are to improve food hygeine and supplement with enzymes.

questions
pancreatic cancer...
1. what is the prognosis of pancreatic cancer?
2. how common is pancreatic cancer in males?
3. what is the gender and age that pancreatic cancer is usually found in?
4. what are the etiologies of pancreatic cancer?
5. initial symptoms are often...
6. what is a common problem with the diagnosis of pancreatic cancer?
7. describe the quality of pain experienced in pancreatic cancer?
8. radiation of the pain in pancreatic cancer to the back might indicate...
9. what is a clinical feature present in 90% of pancreatic cancer patients (besides abdominal pain)?
10. what are some of the complications of pancreatic cancer?

pancreatic cancer diagnosis...
11. what are some potential PE findings for pancreatic cancer patients?
12. what are some PE findings for patients with late stage pancreatic cancer?
13. what are some lab tests that might be useful in the diagnosis of pancreatic cancer?
14. what are two tumor markers useful in the diagnosis of pancreatic cancer?
15. CA 19-9 is not useful in diagnosing...
16. how specific is the CEA test for pancreatic cancer?
17. what are the imaging techniques used to diagnose pancreatic cancer?
18. what is an MRCP?
19. what are the conventional treatments of pancreatic cancer?

pancreatic insufficiency...
20. what is the etiology of pancreatic insufficiency?
21. approximately how much of the pancreas is functioning at the time of diagnosis of diabetes mellitus?
22. what are the signs and symptoms of pancreatic insufficiency?
23. describe the diagnosis of pancreatic insufficiency.
24. what are the labs used in the diagnosis of pancreatic insufficiency?
25. what are the treatment strategies for pancreatic insufficiency?

answers
1. 1-2% 5 year survival rate.
2. 4th most common cancer.
3. >55yo men.
4. smoking
age
diabetes
chronic pancreatitis
high animal fat / protein
coffee
alcoholism
5. nonspecific and subtle: fatigue, malaise, nausea, anorexia.
6. delayed diagnosis- 90% of cases already metastasized by the time diagnosis made.
7. midepigastric radiating to mid/lower back.
8. retroperitoneal invasion of the splanchnic nerve plexus by the tumor.
9. significant weight loss.
10. migratory thrombophlebitis, upper GI bleeding, DM, and abdominal masses.

11. midepigastric tenderness, significant weight loss, jaundice.
12. ascites, abdominal mass, hepatosplenomegaly.
13. CEA, alpha FP
chem screen for bilirubin and liver enzymes
trypsin, trypsinogen
14. CA (carbohydrate antigen) 19-9 and CEA (carcinoembryonic antigen).
15. early stage pancreatic cancer.
16. not very specific: many other conditions can lead to elevated CEA levels.
17. US, CT, biopsy, MRCP.
18. type of MRI used to see pancreas, ducts, and bile.
19. chemo/radiation, whipple procedure, painkillers.

20. caffiene
carbohydrates
overeating
lack of raw food
21. 7-9%.
22. indigestion
gas/bloating
left scapula reflex
low blood sugar
23. difficult to do because it is a functional disorder as in hypochlorhydria. may either be through symptoms or via exclusion.
24. indican test, heidelberg test, fecal chymotrypsin, CBC (increased MCV).
25. supplemental enzymes and improving food hygeine.

CPD II: stool appearance and pancreatitis

the first part of this lecture focused on the diagnosis of different GI disorders based on stool appearance. ribbon shape might indicate spasm/IBS, uterus malposition or enlargement, compression from a mass. pencil shaped: spasm/IBS and stricture. floating stools: malabsorption, cystic fibrosis. small and hard: dehydration, low fiber, delayed tract time, hypochlorhydria. large and hard: dehydration, hypotonic bowel. difficult to pass: hemorrhoids, anal fissure, dehydration, hypotonic bowel. loose but not watery: mild intestinal irritation and malabsorption. alternating constipation and diarrhea: poor diet, parasites, IBS. offensive stool odor: dysbiosis or food decay. very dark stool: melena, upper GI bleeding. light brown, clay, green, or bright yellow colors: gallbladder issues (obstruction, excess secretion).

the next section in the GI lecture covered pancreatic disorders: acute and chronic pancreatitis. acute pancreatitis causes severe abdominal pain which can feel like a knife stuck in the LUQ and cause extreme limitation of movement and even breathing. it is most commonly caused by heavy alcoholism (pain develops over a few weeks) in men and by biliary tract disease or obstruction (pain develops suddenly) in women. other etiologies might include NSAID use or hypertriglyceridism.

the diagnosis of acute pancreatitis is made through the history/physical and a few useful lab tests. besides the knife like LUQ pain, patients might present with fever, hypoactive bowel sounds, jaundice, dyspnea (because any movement will worsen the pain). additionally, cullens and grey-turner signs might be positive, which indicate retroperitoneal hemorrhage from pancreatic autodigestion. the lab tests most helpful are amylase, lipase, CBC and a chem screen; serum amylase levels are elevated soon after the onset of pain and return back to normal 2-3 days afterwards whereas urine amylase elevates 7-10 afterwards. CBC might show elevated hematocrit and leukocytosis, while a chem screen might show hyperglycemia, hypocalcemia, and elevated bilirubin/AST/ALT. treatment of acute pancreatitis generally involves 100% pancreatic rest and pain management, although 10% of patients will die regardless of treatment. the remaining 90% might recover within 2-3 weeks.

chronic pancreatitis is also caused mainly by long term alcoholism, and can also be idiopathic, or hereditary, or due to hyperlipidemia, protein malnutrition, cystic fibrosis, or biliary obstruction. patients with chronic pancreatitis might remain asymptomatic for 62 months (81 months for alcoholics), then develop severe epigastric/LUQ pain that may radiate to the back in a band like fashion and come in 2-3 hour episodes. the pain might be relieved slightly by lying in the fetal position on the left side, in contrast to acute pancreatitis, the pain of which is generally not relieved by anything.

in contrast to acute pancreatitis, the physical might not be very useful for diagnosis, although fundoscopy might reveal milky white retinal blood vessels from hyperlipidemia, and an abdominal exam might reveal pseuodocysts, which are inflammatory masses. amylase and lipase levels are only slightly elevated- the more useful tests are serum trypsin, calcium, and TG levels, as well as the bentiromide test, which measures the excretion of PABA in the urine (decreased in pancreatic insufficiency). ultrasound, chest xray, and CT all show calcification in 30% of patients. pancreatic function can also be measured via direct tests, or stimulating the pancreas with a secretogogue and measuring pancreatic output in the duodenum or directly via cannulation.

questions
stool diagnosis...
1. what might a ribbon shaped stool indicate?
2. what might a pencil shape stool indicate?
3. what might floating stools indicate?
4. what might stools that are small and hard indicate?
5. what might stools that are large and hard indicate?
6. what might stools that are difficult to pass indicate?
7. what might stools that are loose but not watery indicate?
8. what might be indicated from alternating constipation and diarrhea?
9. what might an offensive stool odor indicate?
10. what might a very dark stool color indicate?
11. what might a light brown or clay stool color indicate?
12. what might a greenish or bright yellow stool color indicate?

acute pancreatitis...
13. what is post prandial exocrine secretion stimulated by?
14. what is acute pancreatitis and what are its hallmark characteristics?
15. what are the common causes of acute pancreatitis in men and women?
16. what is the severity of alcoholism usually associated with acute pancreatitis?
17. what is the relationship between the size of gallstones and the risk of getting acute pancreatitis?
18. besides alcoholism and gallstones, what are some other etiologies for acute pancreatitis?
19. what are the signs and symptoms of acute pancreatitis?
20. what is the difference in the onset of pain for acute pancreatitis caused by alcoholism vs. gallstones?
21. what are the two typical pain patterns presented by patients with acute pancreatitis?
22. what might the pain from acute pancreatitis be alleviated by?
23. what might the pain from acute pancreatitis be worsened by?

acute pancreatitis diagnosis...
24. what are some PE findings that might be found from a patient with acute pancreatitis?
25. what do the cullen's and grey turner signs indicate?
26. what is a potential skin manifestation of acute pancreatitis?
27. which labs would be useful in the diagnosis of acute pancreatitis?
28. what might be found in the serum amylase test?
29. what might be found in the urine amylase test?
30. which amylase test would be ordered if the patient came in immediately after onset of pain vs. a few days after?
31. what is the advantage of the lipase test compared to the amylase test?
32. what does a lipase:amylase ratio of greater than 2 indicate?
33. what might be seen in a CBC of a patient with acute pancreatitis?
34. what might be seen in the chem screen of a patient with acute pancreatitis?
35. what is the imaging technique of choice in diagnosing acute pancreatitis?
36. what is the prognosis for patients with acute pancreatitis?
37. what are the treatment goals for patients recovering from acute pancreatitis?

chronic pancreatitis...
38. what is the mean age of diagnosis for chronic pancreatitis?
39. what is the bimodal age distribution for idiopathic chronic pancreatitis?
40. what are the etiologies for chronic pancreatitis?
41. what is the quality of the pain experienced in chronic pancreatitis?
42. how long do episodes of pain generally last?
43. how long on average might a patient with chronic pancreatitis remain asymptomatic? how does this vary if the patient is an alcoholic?
44. besides the abdominal pain, what are some other symptoms that a patient with chronic pancreatitis might present with?
45. what is the characteristic position that a patient with chronic pancreatitis assumes when undergoing a severe episode?
46. chronic pancreatitis may eventually lead to...

chronic pancreatitis diagnosis...
47. how useful is the PE in the diagnosis of chronic pancreatitis?
48. what might fundoscopy reveal?
49. what might be a finding in the abdomen of a chronic pancreatitis patient?
50. what signs might be present in an advanced case of chronic pancreatitis?
51. what are some lab tests that may aid in the diagnosis of chronic pancreatitis?
52. what is the bentiromide test?
53. at what extent of disease progression of chronic pancreatitis does steatorrhea occur?
54. what are two stool tests that might be helpful in the diagnosis of chronic pancreatitis?
55. what are some pancreatic function tests that can aid in the diagnosis of chronic pancreatitis?
56. what would be shown on an xray and ultrasound of a patient with chronic pancreatitis?
57. what would be shown on a CT scan of a patient with chronic pancreatitis?

answers
1. spasm / IBS, uterus malposition or enlargement, compression from a mass. [ribbon, spasm, IBS, uterus] [the uterus had a ribbon in it that caused it to spasm irritably]
2. spasm / IBS, stricture of colon. [pencil spasm stricture]
3. malabsorption, cystic fibrosis.
4. dehydration, low fiber diet, delayed tract time, hypochlorhydria.
5. dehydration, hypotonic bowel.
6. hemorrhoids, anal fissure, dehydration, hypotonic bowel.
7. mild intestinal irritation and malabsorption.
8. poor dietary habits / food allergies, parasites, IBS, liver/gallbladder irritation / dysfunction. [diet, parasites, IBS]
9. dysbiosis or food decay.
10. melena; upper GI bleeding.
11. lack of bile pigments, liver / gallbladder obstruction.
12. gallbladder problem; excess bile secretions/bile salt.

13. CCK, cephalic stimuli, intestinal stimulation.
14. an acute inflammation of the pancreas associated with edema, swelling, autodigestion, necrosis, hemorrhage.
15. alcohol for men, biliary tract disease for women.
16. greater than 200mL a day for 5-15 years.
17. risk is inversely proportional to size.
18. hypertriglyceridemia, NSAID use, post ERCP.
19. severe LUQ pain that may radiate straight through back.
20. pain from gallstones develops suddenly, whereas pain from alcoholism develops over a few weeks.
21. the feeling of a knife stuck in the left ribcage, and pain in the left scapula that radiates from the front around the side.
22. supine position often alleviates pain.
23. coughing, deep breathing, movement.

24. fever
abdominal tenderness / guarding
hypoactive bowel sounds
jaundice
dyspnea
cullen's sign
grey-turner sign
25. hemorrhage: pancreas is autodigesting and leaking blood into skin.
26. erythematous nodules on extensor surfaces from focal subcutaneous fat necrosis.
27. lipase, amylase, CBC, chem screen.
28. 75% of acute pancreatitis cases have high serum amylase levels which may rise 2-12 hours after onset and remain elevated for 2-3 days.
29. elevated levels 7-10 days after serum amylase returns to normal levels.
30. serum amylase for immediately after onset, urine amylase for a few days afterwards.
31. more specific to the pancreas, and has a longer half life than amylase.
32. alcoholism or gall bladder dysfunction.
33. leukocytosis and elevated hematocrit.
34. hyperglycemia from decreased insulin
hypocalcemia from saponification of peritoneal fat
elevated bilirubin, ALT, AST.
35. abdominal ultrasound.
36. 10% die regardless of treatment, 90% recover within 2 weeks.
37. 100% pancreatic rest and pain management.

38. ~46yo.
39. one peak at 19.2yo, another at 56.2yo.
40. long term alcoholism
idiopathic
hereditary
cystic fibrosis
hyperlipidemia
protein malnutrition
pancreatic obstruction
[that idiot heretic hyped up pancreatic malnutrition]
41. severe, persistent pain often in the mid or LUQ which may radiate in a band to the back.
42. several hours.
43. 62 months, 81 months for alcoholics.
44. diarrhea, weight loss, steatorrhea.
45. lying on left side in the fetal position.
46. type II diabetes.

47. not very useful at all.
48. milky white hue in retinal blood vessels due to hyperlipidemia.
49. pseudocyst- inflammatory mass in abdomen.
50. signs of malnutrition: decreased subcutaneous fat, muscle wasting, sunken supraclavicular fossa.
51. serum amylase and lipase (slightly elevated), serum trypsin, calcium, and TG levels.
52. a test that measures the urinary excretion of PABA, which can indicate pancreatic insufficiency if lowered.
53. when 90% of the pancreas is destroyed.
54. fecal chymotrypsin and elastase.
55. direct tests (sensitive but invasive)
duodenal aspirate tests
pancreatic output tests
56. calcifications found in 30%.
57. calcifications and pseudocysts.

CPD II: bowel disorders

polyps are fleshy outgrowths of the intestinal mucosa that can be categorized as hyperplastic, adenoma, or "polyposis" syndromes, each with their own unique etiologies and morphologies. hyperplastic polyps are most common, making up about 90% of epithelial polyps, and are less than 5mm in diameter. they are asymptomatic, found via endoscopy, and are generally considered benign. adenoma polyps are precancerous and make up 10% of epithelial polyps and are from 1.5-10mm (most are smaller and the larger ones have a greater potential to be cancerous). polyposis syndromes are inherited conditions that result in a multitude of intestinal polyps that have a high chance of progressing to adenocarcinoma. for example, nearly 100% of patients with familial polyposis syndrome have adenocarcinoma by age 40. gardner's syndrome is another polyposis syndrome with osteomas, soft tissue tumors, and sebaceous cysts. peutz-jeghers syndrome is yet another with mucocutaneous pigmentation and polyps in the form of harartomas in the GI tract.

adenocarcinoma is a cancer that can affect the GI tract that is the third most common cancer, after lung and breast / prostate. in males it more commonly affects the rectum and in females the colon. etiological factors include diet low in fiber and high in animal protein, prolonged transit time, rancid oils / fats, while protective factors can include selenium, vitamin C and E, carotene, antioxidants. most patients present asymptomatically, or have a positive occult blood test, but late stage adenocarcinoma can result in a variety of symptoms including weight loss, malaise, anorexia, jaundice, and ascites. if adenocarcinoma is in the right colon, the patient might be more prone to developing anemia symptoms, bleeding, and vague abdominal discomfort. if adenocarcinoma is in the left colon, patients might develop diarrhea / constipation, tenesmus, hematochezia / occult blood. finally, adenocarcinoma of the rectum will cause blood with each bowel movement. diagnosis is usually missed on PE, but aided by CBC, livery enzyme tests, carcinoembryonic antigen tests, as well as a colonoscopy and double contrast barium enema.

hemorrhoids are clusters of vascular, connective, or musclar tissue that affects the epithelium of the anal canal. they are precipitated by laxity of rectal muscles or pelvic congestion- not surprisingly, 1/3 of truck drivers suffer from hemorrhoids. if the hemorrhoid is in the anal canal, patients would likely present with painless rectal bleeding, but may also have perianal itching/irritation/pain, or more acute pain if the hemorrhoid is thrombosed. external hemorrhoids are more prone to thrombosis and thus more acute pain which is triggered by exertion, diarrhea, etc. and can last 1-2 weeks or until the thrombosis is resolved, after which a skin tag remains where the hemorrhoid once was.

anal fissures are acute tears in the anal mucosa most commonly from either constipation or diarrhea. fistulas are new tracts that open up from the anal canal to the perianal or ischiorectal area (recall that this was a complication of crohn's), associated with leukemia, diverticulitis, foreign body reactions, actinomycosis, and chlamydia. fissures and fistulas cause throbbing pain that occurs most of the day, worsened with pressure from sitting, or movement, and especially from bowel movements. the draining of a fistula, or the formation of a new fistula tract may spontaneously resolve the pain.

a couple more anorectal disorders: pruritis ani is intense itching of the perianal area, usually brought on by allergies, pinworms, or dermatological disorders. proctalgia fugax is episodes of intense rectal pain that lasts seconds to minutes, with no symptoms in between episodes. it is associated with MS, low fiber diets and IBS, and is treated with kegel exercises.

questions
polyps...
1. what are the types of polyps?
2. how big are hyperplastic polyps?
3. what percentage of epithelial polyps are hyperplastic vs. adenomatous polyps?
4. what is the symptom picture and prognosis for hyperplastic polyps?
5. how big are adenomatous polyps?
6. how long do adenomatous polyps take to develop?
7. 90% of adenomatous polyps are...
8. polyposis syndromes are classified as...
9. polyposis syndromes always end up in...
10. what is familial polyposis?
11. what is gardner's syndrome?
12. what is peutz-jeghers syndrome?
13. what are some etiological mechanisms of polyps?
14. what is a type of skin lesion that is associated with polyps and how closely is it associated?
15. what is a type of medical procedure that can increase risk of polyps?
16. what are the signs and symptoms of polyps?
17. how is the diagnosis of polyps made?

adenocarcinomas...
18. how common is adenocarcinoma of the GI tract?
19. which parts of the GI tract does adenocarcinoma affect in males and females?
20. what are some etiological factors for adenocarcinoma?
21. what are some factors that might prevent adenocarcinoma?
22. what are the risk factors for adenocarcinoma?
23. what are the early signs and symptoms for adenocarcinoma?
24. what are the signs and symptoms for adenocarcinoma that develops in the right colon?
25. what are the signs and symptoms for adenocarcinoma that develops in the left colon?
26. what are the signs and symptoms for adenocarcinoma that develops in the rectum?
27. what are the signs and symptoms for late stage adenocarcinoma?
28. what are the best lab tests to perform for adenocarcinoma?
29. what are the imaging tests that can aid in the diagnosis of adenocarcinoma?
30. what are the differential diagnoses for adenocarcinoma?

hemorrhoids...
31. what are hemorrhoids?
32. hemorrhoids result from...
33. hemorrhoids are common in what occupation?
34. what is the imaging technique used to diagnose hemorrhoids and what does it find?
35. what are the treatments for hemorrhoids?
36. what are the signs and symptoms of internal hemorrhoids?
37. what are the signs and symptoms of external hemorrhoids?
38. describe the progression and quality of the thrombotic pain in external hemorrhoids.

anal fissures/fistulas...
39. what is an anal fissure?
40. 87% of people with anal fissures are between what ages?
41. what is the etiology of anal fissures?
42. what are anal fistulas?
43. what are anal fistulas associated with?
44. what are the signs and symptoms of anal fissures/fistulas?
45. describe the quality of pain with an anal fistula.
46. what are some differential diagnoses for anal fissures/fistulas?

pruritis ani, proctalgia fugax...
47. what is pruritis ani?
48. what are the most common etiologies for pruritis ani?
49. what is proctalgia fugax?
50. what condition in particular has a high incidence of proctalgia fugax?
51. what are some risk factors for proctalgia fugax?
52. what age group does proctalgia fugax usually affect?
53. describe the quality of pain in proctalgia fugax.
54. what is the treatment for proctalgia fugax?

answers
1. hyperplastic, adenomas, polyposis syndromes.
2. less than 5mm in diameter.
3. about 90% are hyperplastic, 10% adematous.
4. asymptomatic, found on endoscopy, benign on pathology report.
5. more than 10mm.
6. 5-10 years.
7. less than 1.5mm and have small potential for malignancy.
8. familial inherited (autosomal dominant), non familial.
9. colon cancer.
10. a rare hereditary disease that manifests in childhood with a colon carpeted with polyps, diarrhea / bleeding, and generally leads to carcinoma by age 40.
11. similar to familial polyposis, with osteomas, benign soft tissue tumors, sebaceous cysts.
12. similar to familial polyposis with more distribution and accompanied by mucocutaneous pigmentation and harartomas in stomach, colon, small intestine.
13. adaptative response to cigarette smoke, alcohol intake, ulcerative colitis.
14. 10-70% of individuals with skin tags have polyps.
15. irradiation of the pelvis.
16. asymptomatic, or bleeding (occult blood possible)
abdominal pain due to obstruction
change in bowel habits
watery diarrhea with large villous adenomas
17. barium x-ray, colonoscopy after routine exam.

18. 3rd most common cancer after lung, prostate/breast.
19. females: colon. males: rectum.
20. low fiber diet
high animal protein (grain fed animals that don't exercise)
prolonged transit time
rancid oils / fats
[fiber, fat, animal, transit]
21. selenium, vitamin C, vitamin E, carotene, antioxidants. [sell the vitamins to the anti carrot people]
22. over 40 years old
familial polyposis
low cholesterol with standard american diet
crohn's / ulcerative colitis
septicemia from strep bovis infection
[AC 40 familial SAD inflammatory septicemia] [ack- 40 sad families with toilets on fire?!?]
23. asymptomatic, or positive occult blood.
24. microcytic / hypochromic anemia symptoms
vague abdominal discomfort or palpable mass (later)
bleeding
[anemia, vague pain, bleeding]
25. diarrhea / constipation
tenesmus with BM
pain due to obstruction
hematochezia or positive occult blood
[diarrhea, tenesmus, pain, blood]
26. blood with each bowel movement.
27. weight loss, malaise, anorexia, jaundice, ascites.
28. CBC, liver enzymes, CEA, occult blood.
29. sigmoidoscopy / colonoscopy, double contrast barium enema.
30. diverticula, ischemic colitis, IBD, benign polyps, hemorrhoids.

31. clusters of vascular tissue, connective tissue, and musclar tissue.
32. laxity of rectal musculature, pelvic congestion/stagnation
33. 1/3 truck drivers.
34. anoscope reveals bluish color from veins.
35. lancing or sclerosing via electrodes.
36. bleeding with BM
perianal itching / irritation / pain
acute pain from thrombosed hemorrhoid or spasm
37. pain from thrombsed hemorrhoid
skin tags
38. thrombosis results from exertion, straining, diarrhea, or other event, pain lasts 7-14 days and resolves when thrombosis resolves.

39. an acute tear in the mucosa of the anal canal.
40. 20-60.
41. hard stool
chronic diarrhea
constipation
childbirth
cathartics
intercourse or examination
STD's
[poop cccc sex]
42. opened perianal or ischiorectal absesses that drain spontaneously.
43. leukemia, diverticulitis, foreign body reactions, actinomycosis, chlamydia.
44. burning/cutting rectal pain
pain / blood / spasm with BM
mucoid discharge
pruritis
45. throbbing pain throughout most of the day that is made worse by sitting, moving, BM, coughing and might resolve spontaneously with draining of abscess or formation of new fistula.
46. diverticular disease
foreign bodies
herpes simplex
hidradentis suppuritiva
HIV
inflammatory bowel

47. intense perianal itching
48. allergies, pinworms, dermatologic disorders
49. benign anorectal pain, thought to be associated with spasm of anal sphincter.
50. MS.
51. low fiber
IBS
52. 50% are 30-60.
53. sudden onset pain localized to rectum that lasts seconds to minutes, asymptomatic between episodes.
54. kegel exercises.

CPD II: GI malabsorption disorders

malabsorptive disorders of the intestine are categorized within this lecture into three categories: disorders related to insufficient digestive elements (such as lactase insufficiency), tropical sprue, celiac sprue. tropical sprue afflicts those who visit certain tropical countries and is thought to be related to infection by an unknown organism perhaps associated with an underlying nutritional deficiency. tropical sprue begins as foul, bulky stools characteristic of fat malabsorption, then progresses to systemic manifestations of malabsorption: weight loss, weakness, glossitis, stomatitis, cheilosis, hyperpigmentation, dry skin. a CBC might show megaloblastic anemia and a chem screen might show decreased levels of serum protein, calcium, phosphorous, cholesterol, prothrombin, HCl, but normal pancreatic function. decreased urine and serum levels in the D-xylose test is also used to diagnose tropical sprue.

gluten enteropathy is a general condition that involves a reactivity to gluten that afflicts up to 1/3 of the US population. of this subset, 5% have a more serious condition called celiacs which results in inflammation of the intestinal lining that leads to villous atrophy and malabsorption. traditionally a disease that afflicted young children, celiacs is now more commonly diagnosed in mid age adults- in particular those from western european, indian, south american, north african countries. there have been some hereditary factors identified such as certain allelles that are present in celiacs patients in the HLA-DQ2 and DQ1 genes, but for the most part the etiological mechanisms are unclear. celiacs patients might present with diarrhea / constipation, abdominal distention (in infants and children due to oncotic pressure changes resulting from low albumin levels), anemia / fatigue, hair loss, aphthous ulcers, dermatitis herpetiformis. lab tests of celiacs patients might show anemia of various types with an increased RDW, AST alkaline phosphatase with low albumin / plasma protein levels. other tests that can be performed are biopsy after gluten ingestion, and testing for IgA to gliadin, endomysial, tissue transglutaminase. two severe complications of celiacs that might arise are malignancy and osteoporosis.

the third major malabsorptive disorder that we learned about is lactase deficiency, the enzyme that digests lactose into glucose and galactose. this disorder is widespread and affects about 3/4 of the world's population, with a higher prevalence in native american, asian, and african american races. lactase deficiency can be congenital (very rare), primary (due to an inherent lack of production), or secondary (due to an acute illness or injury such as gastroenteritis or chemotherapy). it might result in a range of symptoms, from mild abdominal discomfort to severe diarrhea upon lactose ingestion. lactase deficiency is best diagnosed with the hydrogen breath test, which would measure abnormally high levels of hydrogen in the breath after ingestion of lactose. another method is simply to eliminate lactose from the diet and observe for change of symptoms.

questions
tropical sprue...
1. what is the etiology of tropical sprue?
2. what is the first stage of symptoms for tropical sprue?
3. what is the second stage of symptoms for tropical sprue?
4. what does a PE for tropical sprue patients reveal?
5. a CBC for tropical sprue patients might show...
6. what would stool analysis for a tropical sprue patient show?
7. what would a chem screen for a tropical sprue patient show?
8. what is the D-xylose absorption test?

gluten enteropathy and celiacs disease...
9. what is celiacs disease?
10. what is the difference between gluten enteropathy and celiacs?
11. why do babies with celiacs have big bellies?
12. what are the factors that increase susceptibility to a negative reaction with gliadin?
13. what are regions of the world associated with celiacs?
14. what percentage of americans have gluten enteropathy?
15. what percentage of americans have celiacs?
16. what are the symptoms of celiacs for infants?
17. what are the symptoms of celiacs for children?
18. what are the symptoms of celiacs for adults?
19. what percentage of patients with dermatitis herpetiformis has celiacs?
20. what will lab tests show for a celiacs patient?
21. what are the histological findings for a celiacs patient?
22. what is the definitive diagnosis for celiacs disease?
23. what are the IgA tests used to diagnose celiacs?
24. how specific is the diagnostic finding of tissue transglutaminase IgG?
25. what are some diseases associated with celiacs?
26. what are two important complications associated with celiacs?

lactase deficiency...
27. what is lactose intolerance?
28. how much of the world's population has lactase deficiency?
29. what are the different types of lactose intolerance?
30. what are two factors that can cause secondary lactose intolerance?
31. what are the signs and symptoms of lactase deficiency?
32. what is the lab test that can diagnose lactase deficiency?
33. what is another method for diagnosing lactase deficiency?

answers
1. idiopathic, or nutritional deficiency, infection.
2. bulky, pale, foul stools from fat malabsorption.
3. weight loss, flatulence, cramps, pallor, weakness, irritability.
4. signs of vitamin deficiency:
glossitis, stomatitis, cheilosis, hyperpigmentation, dry skin, abdominal distention, tenderness, edema, weight loss.
5. megaloblastic anemia.
6. fat malabsorption.
7. decreased:
serum protein
calcium
phosphorous
cholesterol
prothrombin
HCl
...and normal pancreatic function
[pcpcphp]
8. a test in which 25mg D-xylose is ingested orally, followed by 5 hour urine level measurement and 1 hour serum level measurement.

9. an immune related inflammation of the intestines related to gliadin which leads to loss of vili and malabsorption.
10. gluten enteropathy is a broader term than celiacs, referring to any condition that reacts to gliadin.
11. low albumin levels lead to changes in oncotic pressure which causes fluid to leak out into tissues.
12. some hereditary factors have been identified such as HLA-DQ2 and DQ1 genes, but precise mechanism is basically unknown.
13. western europe, india, south america, north africa,
14. 30%.
15. about 1/133.
16. diarrhea
abdominal distention
failure to thrive
anorexia, vomiting
psychomotor impairment
[diarrhea, distention, thrive, anorexia, impairement] [the infant's diarrhea impaired his intended to thrive on anorexia]
17. diarrhea / constipation
anemia
loss of appetite
secondary dentition
may have abdominal distention
[basically same as infants + secondary dentition?]
18. diarrhea / constipation
anemia / fatigue
dyspepsia / abdominal pain / weight loss

hair loss
aphthous ulcers
dermatitis herpetiformis

angular chelitis

cardiomyopathy
osteoporosis
weakness
[dad had a cow]
19. 75-90%.
20. anemia / increased RDW
increased AST, alkaline phosphatase
low albumin / plasma protein, cholesterol
21. villous atrophy is the characteristic finding.
22. ingest gluten and do a biospy.
23. anti gliadin IgA, anti endomysial IgA, anti tissue transglutaminase IgA
24. 100% specific.
25. type 1 diabetes, autoimmune thyroid disease
26. osteoporosis and malignancy (enteropathy associated t cell lymphoma)

27. a deficiency in lactase in the brush border resulting in an inability to digest lactose.
28. approximately 75%.
29. congenital (very rare), primary (due to inherent lactase production deficit), secondary (acute illness or injury)
30. acute gastroenteritis and chemotherapy.
31. ranges from minor abdominal discomfort to severe diarrhea in response to lactose, nausea
32. hydrogen breath test: measuring hydrogen breath levels after lactose ingestion.
33. eliminating lactose containing foods from the diet and observing change in symptoms.

CPD II: ischemic colitis, irritable bowel, appendicitis, diverticulitis

this lecture is a continuation of intestinal disorders, specifically focusing on inflammatory bowel diseases. ischemic colitis is the first disorder we covered, and is an inflammation of the mucosa and submucosa of the intestine that results either from insufficient perfusion (CHF) or an occlusive event (atherosclerosis), and accordingly is associated with elderly, smokers, and those who live sedentary lifestyles. acute cases, generally from occlusive events, present with sudden onset lower left abdominal pain, rectal bleeding, fever / hypotension, and peritoneal signs. chronic cases of ischemic colitis present with rectal bleeding as well, but have longer periods of vague abdominal pain, diarrhea, and generally a spared rectum, similar to crohn's. IC might present similar to diverticulitis or CA if there is frank blood.

irritable bowel syndrome is an extremely common disorder that contributes to 50% of all gastroenterologist visits. patients can be any age, and are more typically female. IBS can be the result of many different factors, and the exact etiological mechanism is unclear and oftentimes heavily influenced by emotional factors such as stress. other potential etiologies are: food allergy, abnormal transit profile, local histamine sensitization, epigenetics. diagnosis of IBS is made by the "rome III" criteria: lower abdominal pain for 3 days for 3 months in a row which is relieved by defecation and was accompanied at the onset by a change in stool frequency or appearance. diagnosis is also made by excluding "alarm signs" which might indicate a more serious, acute condition: onset after 50, severe diarrhea, nocturnal symptoms, severe weight loss, hematochezia, and positive family history for organic GI disease. the physical exam might be unremarkable, or reveal tenderness over the course of the colon. lab tests are generally only useful for excluding other diagnoses.

appendicitis is an inflammation of the appendix, which can be caused by fecaliths, lymphoid hyperplasia, parasites, and presents as epigastric pain that migrates to the right lower quadrant accompanied by weight loss and vomiting (which generally occurs after the onset of pain, as opposed to intestinal obstruction). there are a number of physical exam tests which can diagnose appendicitis with varying success, such as mcburney's, rovsing, obturator, cough, markle signs. a CBC might show WBC levels above 10,000 and neutrophilia above 75%.

diverticula present similarly to appendicitis in that they both cause localized lower abdominal pain-- but on opposite sides. diverticula are relatively common outpouchings of the colon caused by any factor that increases the intraluminal pressure of the colon, such as a low fiber diet or constipation. the sigmoid colon is particularly vulnerable to diverticula and thus typically pain is in the lower left quadrant of the abdomen.

while diverticula by themselves can be asymptomatic, inflammation and infection can result in diverticulitis, a more acute and serious condition which might even lead to perforation. patients with diverticulitis might have had a recent history of recurrent UTI's or pneumaturia, and present with severe LLQ pain, fever, altered bowel habits, and nausea/vomiting. complications of diverticula are manifold and can be detected by the symptoms that result: a vaginal fistula would result in feculent vaginal discharge. diffuse peritonitis would result in severe generalized abdominal pain. perforation would cause back or lower extremity pain, absent bowel sounds, and a high grade fever. lower GI bleeding might appear suddenly, be accompanied by an urge to defecate, and stop spontaneously. hemorrhoids or anal fissures might result in pain with defecation. diverticulitis is diagnosed by history, PE, and sigmoidoscopy imaging-- take note that barium xray should not be used in acute cases due to the danger of perforation.

questions
ischemic colitis...
1. what is ischemic colitis?
2. the morphology of ischemic colitis is similar to...
3. what are the risk factors for ischemic colitis?
4. what are the two etiological mechanism for ischemic colitis?
5. what is the clinical presentation of an acute case of ischemic colitis?
6. what is the clinical presentation of a chronic case of ischemic colitis?
7. what are the ddx's of ischemic colitis?
8. what are the imaging techniques used to diagnose ischemic colitis?

irritable bowel syndrome...
9. how common is IBS?
10. what is the age and gender that most commonly suffers from IBS?
11. what are the postulated etiological mechanisms for IBS?
12. what are the the "alarm symptoms" diagnostic criteria for IBS and what are their significance??
13. what is the primary symptom for the rome III criteria for diagnosis of IBS?
14. what must the primary symptom of the rome III criteria be associated with?
15. what is the clinical picture of patients with IBS?
16. what are some PE findings for patients with IBS?
17. how useful are labs in diagnosing IBS?
18. IBS can be confidently diagnosed by...
19. what are some naturopathic treatment strategies for IBS?

appendicitis...
20. what is the most common age of appendicitis sufferers?
21. what are the different etiological mechanisms for appendicitis?
22. what are fecaliths?
23. what is the "classic" history / symptom picture of an appendicitis patient and how often does it actually occur?
24. if vomiting occurs in a case of appendicitis, is it more likely to occur before or after the onset of pain?
25. duration of symptoms is typically...
26. what symptoms can be caused by appendicitis near the bladder?
27. what PE finding may male infants and children present with and why?
28. what are the tests one can perform in a PE that can diagnose appendicitis?
29. what are the expected CBC findings for a patient with appendicitis?
30. what are the imaging studies that can diagnose appendicitis?
31. what are the possible differential diagnoses for appendicitis?
32. what are some differential diagnoses for appendicitis in children?

diverticula...
33a. what are diverticula?
33b. what percentage of 60 and 80 year olds have diverticula?
34. what percentage of people with diverticula are asymptomatic?
35. which part of the GI tract is most prone to diverticula?
36. what are some factors that can increase intraluminal pressure?
37. what are some possible symptoms for diverticula?

diverticulitis...
38. what is diverticulitis?
39. what are some risk factors for diverticulitis?
40. what are some main differences and similarities between diverticulitis and appendicitis?
41. what are some signs / symptoms of diverticulitis?
42. patients with diverticulitis might have a recent history of...
43. what is a complication of diverticulitis related to the female reproductive tract?
44. if diverticulitis is accompanied by diffuse peritonitis, it might present as...
45. if diverticulitis is accompanied by perforation, it might present as...
46. if diverticulitis is accompanied by lower GI bleeding, it might present as...
47. describe the characteristics of blood flow from diverticulitis with GI bleeding.
48. diverticulitis with discomfort / pain upon defecation suggests...
49. in a case of diverticulitis, what sign would indicate an inflammatory bowel disease?
50. what would be involved in the PE for diverticulitis?
51. what might be the PE findings for diverticulitis that has led to perforation?
52. what is the imaging test used to diagnose diverticulitis?
53. what is an imaging test that might be dangerous to perform during an acute case of diverticulitis and why?
54. what are the conventional and naturopathic treatments for diverticulitis?

answers
1. an inflammatory bowel disease that results from ischemia of the mucosa and submucosa.
2. crohn's.
3. over 60, smokers, sedentary.
4. either decreased perfusion from insufficient cardiac output or occlusive disease such as atherosclerosis.
5. sudden onset lower left abdominal pain
rectal bleeding
fever / hypotension / tachycardia
peritoneal signs
[lower left, blood, fever, peritoneum] [i see you left perry's blood in the lower left freezer]
6. vague abdominal pain / tenderness
rectal bleeding
diarrhea
sparing of rectum
[vague, blood, diarrhea, spare] [i see you vaguely spared the bloody diarrhea]
7. diverticulitis, CA.
8. abdominal plain film, CT.

9. up to 50% of gastroenterologist visits are because of IBS.
10. any age, 70% females.
11. abnormal transit profiles
local histamine sensitization
food sensitivities
epigenetic effect (3-5%)
underlying emotional component.
12. part of the diagnosis of IBD by identifying symptoms that would be indicative of a more acute disorder:
onset after 50
severe diarrhea
nocturnal symptoms
unintentional weight loss
hematochezia
positive family history for organic GI diseases
[50, diarrhea, night, weight loss, blood, family] [HBS 50th anniversary: i had diarrhea that night, lost a lot of weight and blood, and called my family]
13. recurrent abdominal pain at least 3 days a month for 3 months in a row.
14. relief with defecation, onset associated with change in stool frequency, form, or appearance.
15. crampy abdominal pain
constipation, diarrhea, or alternating
increased mucous production
flatulence, nausea, anorexia
anxiety / depression / stress
[cramp, alternating, mucous, various, emotional]
16. may be asymptomatic, or increased bowel sounds and tenderness
17. only useful in excluding other conditions.
18. identifying typical symptoms, doing a complete PE, and excluding alarm features.
19. food hygiene and diet, stress reduction, fiber, probiotics, cell salts.

20. late teens.
21. obstruction from fecaliths, lymphoid hyperplasia, parasites.
22. a hard mass of feces formed from fecal debris and calcium.
23. 50% of cases have anorexia / weight loss with epigastric pain that is followed by RLQ pain.
24. nearly always follows onset of pain.
25. 48 hours, longer in elderly.
26. "irritative voiding symptoms", hematuria, pyuria.
27. hemiscrotum from migration of inflamed appendix or pus through patent processus vaginalis.
28. mcburney's point, rovsing sign, obturator / psoas sign, cough sign, Markle sign, rectal/vaginal tenderness.
[mburney, rovsing, obturator/psoas, cough, Markle, ass] [mr. burns's remarkable cough obstructed my roving ass]
29. WBC above 10,000
neutrophilia above 75%
30. abdominal CT, ultrasound.
31. pelvic inflammatory disease, acute gastroenteritis, pancreatitis, crohn's, cholecystitis, pyelonephritis, IBS.
32. volvulus, intussusception, acute gastroenteritis.

33a. outpouchings of the colon.
33b. 30%, 80%.
34. 90%
35. sigmoid colon.
36. low fiber diet
refined carbs
constipation
dehydration
corticosteroids
[fiber, refined, constipation, water, steroids] [divert the refined fiber-water; i have constipation on steroids right now]
37. if not asymptomatic, then LLQ pain, constipation, rectal bleeding if erosion.

38. inflammation of one or more diverticuli, leading to complications such as abscess, obstruction, fistula.
39. same as diverticula.
40. looks almost identical to appendicitis, except doesn't generally appear in children, and appears on the LLQ instead of RLQ.
41. LLQ pain- steady, severe, deep
fever
altered bowel habits
nausea/vomiting
dysuria, pyuria
[LLQ, fever, altered, nausea, pyuria] [look- a fever altered my nausea of pies via diversion!]
42. pneumaturia / recurrent UTI's.
43. fistulas with the vagina might result in feculent vaginal discharge.
44. severe, generalized abdominal pain.
45. back or lower extremity pain.
46. bright red or wine colored stool.
47. sudden onset, urge to defecate, massive flow, stopping spontaneous.
48. hemorrhoids or anal fissures.
49. history of weight loss, mucous in the stools.
50. checking abdomen for localized tenderness / rebound tenderness / guarding
vitals for hemodynamic stability, low grade fever
51. diffuse tenderness, absent bowel sounds, high grade fever.
52. sigmoidoscopy shows narrowing and inflammation.
53. barium xray, might cause perforation.
54. conventional: Cipro. naturopathic: hot vinegar pack, then treat like infection (similar to appendicitis treatment)