GI Portion Flashcards
1
Q
A
2
Q
GERD
what are 6 sxs?
1 thing to keep in mind about sxs?
A
- heartburn, restrosternal and postprandial
substernal pain/discomfort most commong 30-60 minutes after a meal
worsens when laying down or recumbant
- regurgitation (vomit burp)
spontaneous reflux of sour bitter gastric contents in mouth
- dysphagia (discomfort)
cough at night from acid asipiraiton
- reccurent pneumonia
- sxs temp relieved with antacids
- can radiate to arm/jaw
***keep in mind sxs don’t correlate with dxs progression so can’t tell how much damage has been done**
3
Q
GERD
3 dx options
6 reasons of when it is not appopropriate to use the first line dx
A
- empirically first line unless (below)
- esphagogastroduodenoscopy(EGD) if high risk or tx has failed
a. over 50
b. weight loss
c. melena
d. odynophagia pain with eating
e. heavy alcohol or tabacco
f. non repsonsive to tx - modified/full barium swallow
4
Q
what are the lifestyle changes a patient should make to relieve sxs of GERD?
5
A
- avoid eating 2-3 hours before bed
2. elevate head of bed
3. loose weight
- avoid acidic food, chocolate, peppermint, ETOH, coffee
- stop smoking
5
Q
why is it important to treat GERD?
A
prevent cancer aka barrette esophagus because the damange from acid makes this more likely to occur
6
Q
what is the emergency cocktail you give someone in the ED for heart burn?
A
- benadryl
- lidocaine
- maalox
7
Q
what is the most common cause of esophagitits?
A
GERD, 50% of patients with GERD have esophagitits
8
Q
gastroesophageal reflux disease
what is this?
population common in?
percent in US?
5 complications it can lead to
A
most common dxs of esophagous 15-20% US, common in pregnancy
transient relaxation of lower esophageal spincter LES leading to gastric acid reflux that causees damange to esophagus and spincter and can lead to:
1. esphagitits- 50% will get this!!!
2. esophageal stricutre
3. barrettes esophagous
4. esophageal adenocarcinoma
- hiatial hernia
-
9
Q
what is the pathway for txing GERD?
6
A
- lifestyle adjustments
- OTC antacids-2 weeks
- H2 receptor antagonists
- Proton pump inhibitors
**if these fail EDG**
- prokinetics
- surgical
10
Q
esophagitits
what is this?
5 general causes?
4 sxs
A
inflammation of the esophagus, esp in immunocomprimised
- viral
- bacterial
- paraistic
- abx induced
- radiation or chest cancers
sxs;
- odyniaphagia
- dysphagia
- substernal chest pain
- oral thursh
11
Q
esophagitis
herpes liabilis (HSV)
3 SXS?
2 DX?
1 TX
A
N/V/ chills
herpetic vesicles on nose/lips
dx:
1. endoscopy showing small vesicles or superficial lesions
2. culture esophageal lesions
TX:
ACYCLOVIR 7-21 DAYS!!!
12
Q
ESOPHAGITIS
VARICELLA-ZOSTER
1 dx?
tx?
A
N/V fever chils
DX:
endoscopy: vesicles or confluent ulcers
Tx:
- usually resolve spontaneously but can cause necrotizing esophagitits
- ACYCLOVIR!!!!
13
Q
barrett’s esophagus
how does this occur? what hcanges?
what are they at increased risk for? how much?
A
metaplastic changes in which the stratified squamous** is replaced by the **columnar epithelium that is typically found in the duodenum….extens poximally from LES from repeated exposure to acid esp with GERD (thats why the cells change to this type because its the same exposure the duodenum gets)
increases risk for adenocarcinoma 5-10%
this change increases risk for neoplastic changes/cancer 40-100 times greater than general public
14
Q
barettes esophagus
2 dx rules?
3 tx?
A
DX:
EDG every 2 years with bx to check for neoplastic changes
if there is high risk dysplasia, consider surgrical resection
TX:
**more txing symtpoms unless surgical intervention**
- antacids
- H2 blockers OTCs
- PPIs
15
Q
esophagitis
CMV
who does this occur in?
characteristics of ulcer? 2
3 sxs?
1 tx?
A
only occurs in immunocomprimised patients
CREEPING ULCER or can be GIANT ULCER
sxs:
odyniaphagia
persistent CP
hematememis
Tx:
IV GANCICLOVIR
16
Q
esophagitis
candidia
who does it occur in?
3 complications?
1 dx?
1 tx?
A
occurs in immunocomprimised host
can cause complications:
- bleeding
- perforation
- stricture
dx:
endoscopy: small yellowwhite raised plaques
tx:
oral or IV fluconazole!!
17
Q
esophageal cancer:
adenocarcinoma
where do you find this?
4 most important RF?
2 protective
A
distal esophagus
RF:
- reflux over 20 years
- Barrettes esophagus-almost all cases
- obesisty
- caucasion males
- smoking increases risk (not main)
Protective effects:
- fiber
- NSAIDS (seems counterintuitive)
18
Q
esophageal cancer
what are the two types?
frequency?
prognisis?
who is more common?
A
types:
- adenocarcinoma
- squamous cell carcinoma
prognosis typicaly poor, 5 year survival 10-13%
both appeare with equal frequency
males more common than females
19
Q
esophageal cancer:
squamous cell carcinoma
prevalence?
location?
4 RF?
key point to remember?
A
prevalence is decreasing
middle esophagus
RF:
- smoking
- alchohol
- diet low in fruits and veggies
- achalasia increases risk 16 x
*** accounts for 90% of all squamous carcinoma in US***
20
Q
esophageal cancers
sxs
1 early
3 late
A
SXS:
early:
1. transient “sticking” of food that turns to PROGRESSIVE DYSPHAGIA
later:
- retrosternal pain/burning
2.iron deficient anemia -loss from chronic cancer, but not enough to notice hememensis or occult
3. tracheobronchial fistula
late complication where the esophageal wall infilates the stem bronchus causeing intractable coughing with frequent pneumonia
_***if this occurs person has less than four weeks to live***_
21
Q
in esophageal cancer, when would you expect to see the weight loss and dysphagia?
A
when the lumen is less than 13 mm
22
Q
esophageal cancer
2 DX
2 STAGE
A
dx:
- barium studies
- endoscopy
Staging:
- CT OF CHEST AND UPPER ABDOMENT
2. PET SCAN
23
Q
where are adenocarcinomas and squamous cell esophageal cancers found?
A
adenocarcinoma: lower 1/3
squamous: middle esophagus
24
Q
where is the most common stie for esophageal varices? why?
A
distal esophagus at gastroesophageal junction because veins are most superficial here!!
25
esophageal varices
## Footnote
6 sxs
3 dx
sxs:
**_1. hematemesis!!! over 50% stop bleeding spontaneously_**
2. melena
3. tachycardia
4. hypotension
5. syncope
6. jaundice
DX:
**1. emergent endoscopy**
CBC
BUN/creatine
type and cross
26
esophageal varices
## Footnote
4 immediate tx options
1. immediate tx-stop bleeding because mortaltiy approaches 75%
2. visceral ligation- rubber band
3. sclerotherapy
4. balllon tamponade
27
esophageal varices
## Footnote
what is this?
what causes this?
mortaltiy rate?
MOST COMMON CAUSE?
emergency!!!
_dilation of the submucosal veins that develop in pts with portal HTN_
patho: blood flow through the liver is diminished causing blood flow increase through the microscopic bood vessesl within the esophageal wall and the vessels _dilate_ _profoundly_, and then _continue to dilate until they are large enough to rupture_
patient acutely ill, _mortality rate 40-70%_
_MOST COMMON CAUSE OR PORTAL HTN IS CIRROSIS that causes this_
28
in esophageal cancer, when would you expect to see the weight loss and dysphagia?
when the lumen is less than 13 mm
29
esophageal cancer
## Footnote
2 DX
2 STAGE
dx:
1. barium studies
2. endoscopy
Staging:
1. **CT OF CHEST AND UPPER ABDOMENT**
**2. PET SCAN**
30
where are adenocarcinomas and squamous cell esophageal cancers found?
adenocarcinoma: lower 1/3
## Footnote
squamous: middle esophagus
31
where is the most common stie for esophageal varices? why?
distal esophagus at gastroesophageal junction because veins are most superficial here!!
32
where is the most common stie for esophageal varices? why?
distal esophagus at gastroesophageal junction because veins are most superficial here!!
33
esophageal varices
## Footnote
6 sxs
3 dx
sxs:
**_1. hematemesis!!! over 50% stop bleeding spontaneously_**
2. melena
3. tachycardia
4. hypotension
5. syncope
6. jaundice
DX:
**1. emergent endoscopy**
CBC
BUN/creatine
type and cross
34
esophageal varices
## Footnote
4 immediate tx options
1. immediate tx-stop bleeding because mortaltiy approaches 75%
2. visceral ligation- rubber band
3. sclerotherapy
4. balllon tamponade
35
esophageal varices
## Footnote
what is this?
what causes this?
mortaltiy rate?
MOST COMMON CAUSE?
emergency!!!
_dilation of the submucosal veins that develop in pts with portal HTN_
patho: blood flow through the liver is diminished causing blood flow increase through the microscopic bood vessesl within the esophageal wall and the vessels _dilate_ _profoundly_, and then _continue to dilate until they are large enough to rupture_
patient acutely ill, _mortality rate 40-70%_
_MOST COMMON CAUSE OR PORTAL HTN IS CIRROSIS that causes this_
36
mallory weiss tear
## Footnote
1 dx?
2 tx?
DX:
ENDOSCOPY
TX:
1. **stabliazation**
- transfusion/gastric lavage if needed
2. **control bleeding via endoscopy**
\*\*keep in mind most bleeding stops spontaneously and condition is usually benign\*\*
37
mallory-weiss tear
## Footnote
what is this?
what does it occur from?
who commonly seen in?
MC location?
3 RF?
2 sxs?
linear mucosal tear in the distal esophagus or gastric cardia from forceful _vomiting_ or retching, causing _hematemesis_ commonly seen in _alcoholics_
## Footnote
**most common location: gastroesophageal junction**
**RF:**
**alcholic**
**hiatial hernia**
**eating disorder BULEMIA**
**SXS:**
1. multiple bouts of vomiting and retching followed by **_PAINLESS HEMATEMESIS_**
2. abdominal pain
\*\*\*keep in mind the bleeding usually stops spointaneously as teh condition is usually benign\*\*
38
esophageal ring
## Footnote
what is this?
sxs?
dx?
1 tx?
ring of tissue located at the _gastroesophageal_ junction called
**_schatzkis ring_**
sxs:
1. dysphagia with **_foods, but not typically liquds_**
DX:
barium esophagram
TX:
mechanical dilation with balloon
39
in mallory weise syndrome what is somethign you want to do before releasing someone from hospital?
obtain occult negative stool to insure not bleeding still or hemmoraging
40
what are 6 RF for stomach neoplasms?
1. genetic predisposition
2. carcinogenic diet
_smoked food/perserved food_
3. autoimmune gastritis
_increased inflammation_
4. gastric adenomas
5. polyps
6. h. pylori, cofactor for some
41
what are the 5 common causes of PUD?
1. NSAIDS
2. H. pylori
3. idiopathic
4. hypersecretory states
5. smoking
42
3 locations of PUD?
which one is most common?
how long do they take to heel?
what do you need to keep in mind that is very important depending on location?
1. duodenal
## Footnote
a. **_MOST COMMON LOCATION!!_**
b. 90% heal in 4 weeks
2. pylorus
3. gastric
\*\*CAN BE MALIGNANT\*\*
\*\*must get bx at endoscopy time\*\*
a. take longer to heal 8 weeks!
b. increased length of tx
43
peptic ulcer disease
NSAIDS
cause?
why?
4 RF?
2 tx? length of time?
caused by long term NSAID use esp nonselective COX1 and COX2 blockers
_COX1 decreases prostaglandins_ which have a _protective effect on gastric mucosa_, it the lack of this **_impairs gastric mucous and HCO3 secretion_**
\*\*this is why COX2 selective are better option since decrease risk of bleeding\*\*
RF:
1. ASA
2. corticosteroids
3. over 60
TX:
**_1. PPI_** or H2
\*\*\*4 weeks duodenal\*\*\*
\*\*\*8 weeks gastric\*\*\*
**_2. D/C NSAID_**
44
peptic ulcer disease:
h. pylori
KEY?
characteristic?
acute/chronic characteristics?
what is key about this?!
**_nesscary cofactor for 75-90% of duodenal/gastric ulcers_**
characteristics:
PRODUCE UREASE
ACUTE:
a. infectious "gastroenteritis"
CHRONIC:
a. **_ASYMPTOMATIC_**
b. DIFFUSE SUPERFICIAL MUCOSAL INFLMMATION WITH POLYPS
\*\*ERRADIACATION IS ESSENTIAL OTHERWISE _85% WILL RECURR!!!!!\*\*_
45
what is a RF for all ulcers?
smoking!
46
explain te patho of stomach ulcers caused by h. pylori?
1. infection in body
2. causes **gastritis and chronic inflamation that overwhelms immune system**
3. causes **mucosal breakdown**
4. creates gastric ulcer
47
PEPTIC ULCER DISEASE
## Footnote
2 sxs
3 dx
when do you use each?
1 think must do?
SXS
1. _epigastric like pain "hunger like" in 80-90%_
2. _50% have relief by eating antacids within 2-4 hours_
\*\*physical exam is often unremarkable so need to watch for changes in pattern, indicating perforation or penetration\*\*
DX:
1. endoscopy EDG TOC!
allow so for visulaization and also bx!!
2. fecal antigen test (noninvasive)
3. c-urear breath test (noninvasive)
\*\*\*\*OPTIONS 2 AND THREE AT THE TOC FOR ACTIVE PUD AND PROOF OF ERADICATION\*\*\* _MUST D/C PPI 7-14 DAYS PRIOR OR MAY GET FALSE POSITIVIVE!_
48
peptic ulcer disease
tx without h. pylori
2
3 for first
1 second
1. _antisecretory agents_
A.**_PPIs_** 1st DOC-inhibit 90% acid secretion
**_ompreazole_**
**_lansoprazole_**
B. H2-inhibit histamine mediated secertion
C. OTC anti-secretory
2. _mucosal defense agents_
2nd line can be used as adjunct for _symptom relief_
**sacralfate, busmuth**
49
peptic ulcer disease:
post H. pylori tx tx
2 considerations
**DUODENAL f still large or bleeding post tx:**
_continue PPI for 2-4 weeks_
**GASTRIC if large ot blleding post tx:**
_continue PPI for 4-6 weeks_
50
Peptic ulcer disease
## Footnote
what this this?
2 causes?
1
3
size?
**break in the gastric or duodenal mucosa that _extends through the muscularis mucosa_ that comes from**
**1. _impaired normal mucosal defense factors_**
NSAIDS
**_2. defense factors overwhelmed by aggressive luminal factors_**
acid
pepsin
infection
greater than 5 mm in diameter
51
peptic ulcer disease:
## Footnote
Treatment for H. pylori
what is the tx regimen?
what must you do after tx and when?
2/3 abx, PPI, +/- bismuth
## Footnote
**_1. amoxicillin_** 1 g BID
**_2. clarithromycin_** 500 mg BID
**_3. HIGH DOSE 40 mg PPI_** BID
\*\*\*no reason shouldn't use quadrople therapy see in this pic\*\* KNOW BOTH
\*\*must confirm eradication with C-urea breath test or fecal antigen test
4 weeks post abx
2 weeks post PPI\*\*\*
52
in reccurent ulcers what must you do!?
rule out H. pylori and NSAID use
53
peptic ulcer disease:
## Footnote
COMPLICATIONS
PENETRATION/PERFORATION
results in?
2 sxs?
tx?
results in chemical peritonitis
a. severe generalized abdominal pain
b. _rigid abdominal rebound_
_TX:_
_1. laproscopic perforation closure_
_2. increased RX TX_
54
peptic ulcer disease:
refractory ulcers
what is this caused by?
3 contributing factors
uncommon, contributed to non compliance with medication
Contirbutory factors:
1. cigs
2. NSAIDS
3. failutre to eradicate H. pylori! MUST DO THIS
55
chronic pancreatitis
## Footnote
4 dx options
fat stranding
1. amylase/lipase **_NORMAL_**
## Footnote
body gets used to working under these circumstances
2. _secretin stimulation test "gold standard" for **early** chronic pancreatitis dx_
3. plain xray films QUICK AND CHEAP-see calcifications
4. CT SCAN-better at seeing calcifications but $$/rad
_"arrowhead and fat stranding"_
56
explain the pathophys of pacreatitis?
what are 2 theories that cause this?
1. inflammation of the pancreas causes damage to the **_acrinar cells_**
2. the inactive proenzymes like _trysinogen_ are activated early while still in the pancreas
3. early activated _lipases_ disolve the fat
4. so the _pancreatic enzymes_ start to DIGEST THE PANCREASE "EATS ITSELF"
theories:
1. obstruction of the pancreatic duct due to stones
2. failure of the two parts of the pacreas to fully join during development _pancreatic divism_
57
when dxing pancreatitis and looking at labwork, what test is most effective?
lipase
(this is better than amylase)
58
acute pancreatitis
## Footnote
5 labs tests?
TOC for dx?
LAB TESTS:
**_elevated cbc_** (infection)
**_elevated lipase_** (pancreas)
**_elevated LFT_**
**_elevated glucose_**
**_decreased calcium_**
TEST OF CHOICE FOR DX: **_CT SCAN!!!_**
scored A-E, A is good, E is bad
59
acute pancreatitis
## Footnote
6 sxs
where is pain?
severity?
what makes worse/better?
pain with...?
two key signs you dont want to miss?
1. **_epigastric radiates to back_**
2. **_billiary colic PERSISTS DOESN"T GO AWAY_**
3. **_worse SUPINE, BETTER LEANING FORWARD_**
4. **_PAINFUL INSPIRATION, SHALLOW BREATHS_**
5. _TACHYCARDIA_
**_6. hemmoragic pancreatitis_**
_cullens sign_: periumbical ecchymosis
_grey tuner's sign:_ flank eccymosis
60
acute pancreatitis
## Footnote
6 tx options?
what is the process dependent on?
mostly supportive
## Footnote
a. NPO 48-72 hours **_NO ALCOHOL_**
**_b. ERCP if presense of stone**_ _**on CT scan_**
b. maintain hydration
c. pain control
d. NG tube in extreme
e. abx if infectious
f. incision and drainage if infected/necrosis
61
acute pancreatitis
## Footnote
5 labs tests?
TOC for dx?
LAB TESTS:
**_elevated cbc_** (infection)
**_elevated lipase_** (pancreas)
**_elevated LFT_**
**_elevated glucose_**
**_decreased calcium_**
TEST OF CHOICE FOR DX: **_CT SCAN!!!_**
scored A-E, A is good, E is bad
62
chronic pancreatitis pathophysiology
## Footnote
what is this?
what should you think about when thinking of this?
what happens?
inflammatory disease of the pancreas
**_irreversible**_ _**changes occur_**
**_can lead to permanent loss of function_**
HINT: think necrosis fibrosis theory of alcoholic pancreatitis
alcohol to tissue damage to fibrosis to partial obstruction
63
chronic pancreatitis
## Footnote
what is the MC cause of this?
3 others?
NOT CAUSED BY WHAT?
what can this lead to?
1. alcohol cause #1!!
\*\*\*THIS IS **_NOT_** CAUSED BY GALLSTONES LIKE ACUTE\*\*
2. **_obstructive causes of spincter of oddi by neoplasms_**
3. **_malnuitirion_**
4. metabolic
chronic pain leads to opoid addiction! keep this in mind
64
chronic pancreatitis
4 sxs?
sxs:
1. **_epigastric abdominal pain_** that radiates to the **_LEFT_**
2. insufficiency of pancreatic function leads to
**_a. steatorhhea_** damages decreases lipase
**_b. diabetes_** once islets damaged
**3. asymptomatic and found incidently**
65
chronic pancreatitis
## Footnote
5 tx options
most important!!
2 drugs?
1. _stop the alcoho_l!!
2. controls sxs
a. **pain control**
**b. prancreatic enzyme supplements _viokase and pancrease_**
3. endoscopic duct decompression
4. surgical draingage of duct
5. celiac plexsus nerve block
66
what are the two criteria used to identify the mortality with pancreatitis?
1. Ranson's criteria
## Footnote
_Take home: higher numbers means more severe disease and increased risk of death_
-measured at time of admission and during first 48 hours
**6+=50% mortality**
2. APACHE II score
\*\*typically impatient ICU use\*\*
over **_8_** is severe!!!
67
pancreatic cancer
## Footnote
what are thet wo tumor markers?
survival?
1 RF?
tumor markers:
1. CA19-9 85%
2. CEA 40-45%
5 year survival is only 4% _really bad_
only RF: _chronic pancreatitis_
68
pancreatic cancer
## Footnote
what two lab findings supposrt this?
3 tx options?
LABS:
**_1. elevated direct bilirubin_**
**_2. elevated alkaline phosphatase_**
(significantly elevated in cancer)
**_TX:_**
**_1. chemo_**-poor respinse only reduces size to buy little time
2. _whipple surgery_-only at cancer specialties
3. **_pallaitive care_**
69
pancreatic cancer
## Footnote
4 sxs?
toc? 1
sxs:
1. _painless **jaundice** is PC until prove otherwise_
2. **_virchows node_-**supraclavicular node
3. **_trouseaus signs- recurring superficial thrombophlebitis_**can be anywhere
4. weight loss
TOC: _CT scan dual phase helical_
70
acute cholecystitis
## Footnote
2 dx tests? when to use?
2 labs?
TOC #1: **_US_**
## Footnote
find gallstones and _wall thickening over **3 mm**_
TOC #2: **_HIDA nuclear med scan_** (cholescintigraphy) GOLD STANDARD and _BEST TEST_
\*\*\*\*not usually used since it is $$$$$$$, so US becomes TOC\*\*\*\*\*\*
Two elevated labs:
**_elevated gamma-glutamyl transpeptidase_**
**_elevated bilirubin_**
71
acute cholecystitis
## Footnote
what happens in this?
what is most likely to cause this?
leads to 3 things? possible worst case?
2 _key_ sxs?
the **_cystic duct**_ becomes blocked _**most commonly from gallstone!_**
less common:
cancer, sludge, infection
blockage causes distention and edema that cauess _ischemia, necrosis, perforation_ and possible _generalized sepsis_
SXS
1. RUQ/epigastric pain _radiate to shoulder/scapula_
2. _murphys sign_ (tenderness and pt stops inspiration on palpation)
72
acute cholycystitis
## Footnote
TXOC?
3 others?
TreatOT: TAKE IT OUT!! MOST COMMON!! via _laproscopic cholecystectomy_
2. leave in if very mild
3. drain it if patient too sick
4. abx if elevated WBC
73
what are the four RF for cholithiasis?
1. over 40
2. obesity (or rapid weight loss)
3. female/pregnant
4. native american
**"FEMALE, FAT, FORTY, FERTIL" 4, F's**
74
choledocholithiasis
## Footnote
where is the stone?
where does it come from?
where is pt?
sxs? 4
stone in the **_COMMON BILE DUCT_**
usually migrate from the gallbladder
patient very sick and likely in ICU!! compared to cholelithiasis
sxs:
asymptomatic in 30-40%
**_BILLARY COLIC_**
**_jaundice, pancreatitis_**
75
choledolithiasis
## Footnote
what are the two dx/tx options?
what must you keep in mind?
1. MRCP magnetic resonance cholangiopacreatogprahy ONLY DX
## Footnote
2. ERCP-endoscopic retrograde cholangioancreatography DX **_AND TX so GOLD STANDARD!!_**
\*\*\*\*keep in mind contraindicated in pancreatitis/cholecystomy\*\*\*
76
acute cholelithiasis
## Footnote
what are you 3 tx options and who are they appropriate for?
1. cholecystectomy-MOST COMMON "it hurts
## Footnote
2. leave in if doesn't hurt _UNLESS_ high risk to keep in
a. diabetics
b. sickle cell
c. Native americans with _calfieiced "porcelain" stone_
3. dissolve cholesterol stones with _actigal, urodeoxycholic acid_ but $$$
77
acute cholithiasis
## Footnote
what do you need to keep in mind about sxs?
how do they present? 3
dx TOC?
what do you need to keep in mind?
_asymptomatic in 50-60%_
## Footnote
symptomatic patients:
**biliary collic with _RUQ pain/epigastric areas_**
**_refers to back, scapula or R shoulder_**
DX:
TOC: transabdominal US
**_shows stone without wall thickening_**
\*\*_keep in mind not great for stones in common bile duct\*\*_
78
cholelithiasis
two types of stones?
percentage?
what do they look like?
**1. cholesterol stones**
MC-75% of stones!!
don't show up on xray
2. **calcium bilirubinate/ca salts**
25% of stones
pigmented black/brown sludge stones
79
celiac disease
## Footnote
what are 6 sxs that come with this?
explaination of the last?
1. unintended weight loss
## Footnote
2. persistently underweight
3. sxs of poor nuitrition
4. "failure to thrive in child"
5. diarreah
6. _dermatitis herpetiformis_
a. ***intense itching***
***b. blisterning rashes***
***c. 10-15% of patients***
80
celiac disease
## Footnote
what type of condition is this?
what is the patho of this and the specific component?
nickname?
autoimmune dx of _SI_
## Footnote
introlerance to **_gluten and the alpha-gliadin_**
gluten triggers immune response in turn causing damage to the small intestine
causes _nuitritional deficits secondary to absorption issues_
"celiac sprue"
81
celiac disease
## Footnote
what are the 3 dx options of this?
key thing to remeber?
1. anti-tissue transglutaminase antibodies OR anti-endomysium IgA antibodies
## Footnote
2. _bx if small intestine_ and blood + for antibody
\*\*\*\*if they have dermatitis herpetiform with + antibody skin bx, THEN NO NEED FOR INTESTINAL BX\*\*\*
82
celiac disease
## Footnote
what are the 2 tx for this?
what about screening?
1. gluten free diet
## Footnote
- wheat
- rye
- barley
2. abx for dermatitis herpetiformis
\*\*\*make sure to screen if family hx using blood test for autoantibodies\*\*
83
diverticula
## Footnote
what are these?
how are they formed?
sac-like protrusions in the colonic wall
**blood vessels penetrate the mucosal wall**
**internal layers penetrate through weak areas creating diverticula**
84
diverticulosis
## Footnote
what is this?
where does it most commonly occur?
what is important to know about this?
presentation?
2 things to avoid?
condition of having divericula
typically asymptomatic
MC in SIGMOID COLON, _account for 50% of all lower GI bleeds, bright red blood in rectum earliest finding MOST COMMON_
diet restricted in
seeds, strawberries
85
diverticulitis
## Footnote
what is this?
3 sxs?
2 tests?
inflammation of the pocuhes
1. severe **_LLQ_** pain
2. change in bowel habit
3. constapation
Tests:
1. **_CT TOC with IV and oral contrast_**
2. WBCs
3. barium enema
4. colonoscopy
86
who is diverticulosa most common in?
## Footnote
2 percents?
western/industerialized societies
## Footnote
30% by 60
65% have by age 85
87
what are 3 RF for diverticulosa?
1. connective tissue disorders
2. low fiber diet
3. too little exercise
88
what are the two conditions that make up inflammatory bowel disease?
1. crohns disease
2. ulcerative colitis
89
Inflammatory bowel disease
crohns disease
where are the lesions?
how deep are lesions?
where is the pain?
3 things that can occur as complications?
4 things that are common?
3 other things it can effect?
bowel appearance?
1. legions mouth to anus; spread out with healthy tissue between
_2. transmural_
**_3. RLQ pain MC_**
4. fistulas, abscesses, fibrotic stricutres
5. bleeding common
6. weight loss common
7. obstruction common
8. perianal disease common
8. can effect skin eyes joints liver
9. _large volume_ diarreah and mucous (trash bag)
90
what 2 are tests you want to do to look for crohns?
1. anti-saccharomyces cervisial (ASCA)- 44% of crohns are pos
## Footnote
2. _colonoscopy TOC_
91
what are the 4 tx options for crohns?
1. 5-aminosalcyclics (5-ASA)
## Footnote
**-mesalamine**
**-sulfasalazine**
2. corticosteroids
3. cimzia-certolizumab
4. humira-adalmumab
\*\*surgery doesn't work since it involves the entire GI tract\*\*
92
ulcerative colitis
## Footnote
where is this?
pain presents?
what is most common and worse?
what does person have increased?
what might they develop?
describe lesions and how deep?
what does the colon look like on colonscopy?
what are 3 things aren't present?
1. primarily localized in _colon_
**_2. LLQ_**
3**_. bleeding from rectum_** **_is most common_**
3. _urgency need of BM_
_4. potenital anemia due to blood loss_
4. lesions are continuous starting at the rectum and in mucosa only
5. _colon wall thin with continuous inflammation_
6. no granulomas
(weight loss/obstruction very rare with this)
93
which is more common crohns or ulcercerative colitis?
ulcerative colits 3x more likely
94
what do you use to dx ulcerative collitis?
colonoscopy
95
what are the 3 tx options for ulcerative collitis?
1. 5-ASA
- sulfasalzine
- mesalamine
2. corticosteroids
3. **_colonectomy CURE best choice_**
removal of colon
96
irritable bowel syndrome
## Footnote
what is this?
who most common in?
age?
pathogenIsis? 3 **causes**
**_dx of exclusion, no other cause_**
FUNCTIONAL BOWEL WITH MUCOSAL INFLAMMATION
women more than men
presents before age **_45_**
**_1. abnormal motiltiy_**
_2. **visceral hypersensitivity**_ lower visceral pain threshold
**_3. psychosocial interaction_**-emotional stress
97
irritable bowel syndrome
## Footnote
3 tx options?
4 medications tx options
1. pt education and behavior/ emotional support
## Footnote
2. dietary therapy
3. pharm
a. antispasmotics
b. antidiarreals
c. psychotropic
d. serotonin receptor agonists
98
colorectal cancer
## Footnote
what are 3 risk factors?
1. genetic predisposition
2. presence of _adenomatous polyps)_
_3. diets high in fats and refined carbs that are low in plant fiber \*industerialized world\*_
99
what does colonrectal cancer come from?
the progression of adenomatous polyp into malgnancy
100
what are the 3 types of adenoma polys? which is most common? which has higest risk of cancer? risk of cancer and prevalance for each?
1. tubular adenoma
## Footnote
**_MOST COMMON TYPE 65-80%_**
pedunculated, little cancer risk
2. tubulovillous adenoma
10-25% of adenomas
22% risk of cancer
3. **_vilous adenomas_**
**_40% RISK OF CANCER_**
only 5-10% so least common but most deadly
101
what is the least common but the most prognostic for cancer of the adenoma polyps?
vilous adenoma
\*think vilian=evil\*
102
what are the two tests that are reccomended annually to screen for colorectal cancer?
1. guiac fecal occult blood test (gFOBT)
## Footnote
2. immunochemical-based fecal occult blood test (iFBT)
103
what are the 3 screening tests that are reccomended for colorectal cancer? which is most reccomended? what age do you start?
age 50 to less than 10 years life expectancy
## Footnote
1. **_optical colonscopy_**-10 years
2. flexible sigmoidoscopy-5 years
3. CT colonography-10 years
104
colonrectal cancer
## Footnote
4 sxs
2 key dx
3 others
sxs:
1. **_colic type pain_**
**_2. anorexia_**
**_3. thin appeareance_**
**_4. pallior/anemia_**
dx:
1. xray: _classic apple core/npaking ring appearance_
2. endoscopy with bx
3. iron deficient anemia
4. hypoalbuminemia
5. occult blood in stool
105
rectal polyps
what are these?
why is it improtant to know type?
1 type concerned about?
why?
2 shapes?
small outcropping that grows in the rectum or colon
\*\*need to deterine the type since some are associated with carcinoma\*\*
_adenomas_
**_PREMALIGNANT POLYP_**
**_PRECURSOR TO COLORECTAL CANCER_**
**_sessile_**: flat and intimately attacted to mucosa
**_peduclated_**: round and attached be stalk
108
what is the dentate line?
## Footnote
senstion?
divides the rectal mucosa from the squamous epithelium in the canal
## Footnote
above in anorectal canal: INSENSATE (no pain)
below in _andoderm_: _SENSATE AND PAINFUL!!_
109
anal fissure
## Footnote
what is this?
where do these occur?
signicant stat?
2 causes?
**Tear in the andoderm of rectal canal**
90% are posterior along midline
**_most common cause of painful rectal bleeding_**
causes:
1. passage or hard stool
2. prolonged diarreah
110
lactose intolerance
## Footnote
what is this?
4 populations common in?
5 sxs? key 1?
**_difficulty digesting lactose from lack of lactulase_**
MOST COMMON IN:
1. AFRICAN AMERICANS
2. HISPANIC/LATINO
3. ASIAN AMERICANS
4. NATIVE AMERICANS
SXS:
1. bloating
2. pain
3. increase passage of gas
4. diarrhea and nausea
**_5. 2 hours post consumption of milk or dairy_**
111
lactose intolerance
## Footnote
1 dx?
1 tx?
dx:
## Footnote
hydrogen breath test
tx:
dietary avoidance
112
a kid with tearing pain with bowel movements and bright red blood when he or she whipes with toitlet paper
shuld mak eyou think of...
ANAL FISSURE!!
113
anal fissure
## Footnote
3 sxs?
what not to do?
sxs:
1. "tearing" pain with BM since below dentate line
2. hematochezia during BM
3. SPREAD BUTTOCKS to examine
\*\*NEVER DO RECTAL EXAM, TOO PAINFUL!..and cruel\*\*
114
anal fissure
## Footnote
2 tx categories
4
1 (also, who not to do in)
1. 90% heal without tx
## Footnote
a. bulk agents
b. stool softeners
c. sitz baths
d. hydrocortizone ointment Anusol
2. _surgical-lateral internal anal spincterotomy GOLD STANDARD if failure conservative_
\*\*can't do if patient incontinent\*\*
115
explain the pathophysiology of hemmoroids?
5
1. anal canal is lined with "cushions" that are **_vascualr and connective tissue and make the hemmorrhoidal plexsus_**
2. exist in 3 columns
3. **_cushions encorge during defecation_** to profect the anal canal from abrasion
4. when venous engorgement is increased with conditions like pregnancy, straining, and increased abdominal pressure it **prompts production of abnormal hemorrhoidal tissue** which can be symptomatic
116
what are 6 RF for hemmoroids?
constapation
straining at stool
pregnancy
obesity
chronic liver disease
portal HTN
117
Internal hemmoroid tx categories
## Footnote
5
2
1-2 degree:
## Footnote
a. fiber
b. water
c. stool softner
d. anusol hydrocortisone
e. numbing agent nupercainal ointment
3-4 degree:
a. SURGICAL
b. EXCESIONALHEMMOIROIDECTOMY
118
internal hemmoroids
## Footnote
4 key sxs with these!
above the denate line!!
veins surrounded by mucosa
1. **_PAINLESS, above denate_**
**_2. bright red bleeding with defecation_**
**_3. may prolapse and be palpable on DRE_**
**_4. bleed_**
119
what are the stages used to define internal hemmoroids?
**_first_**-bleed
**_second-_**bleed and prolapsed, spontanously reduce
**_third_**-bleed, prolapse, and require manual reduction
**_fourth degree_**-bleed/incarcerate
120
external hemmoroids
## Footnote
whe do they occur/what are they covered in?
3 sxs
dx method?
1 tx?
below the dentate line and covered with andoderm
1. usually don't **_bleed_**
2. may **_thrombose_** which is VERY painful
3. cause **_pain, discomfort and most severe at time of defecation_**
dx
"either present or not"
tx:
1. excision of outside of the mucotaneous junction leaving wound open **_hemroidectomy_**
124
acute hepatitis
## Footnote
what is the mortalty?
3 most common causes?
what are 4 sxs associated with this? **_KEY!!_**
**mortality 40-80%**
sudden onset deterioration of hepatocyte function causing coagulopathy
1. tylenol 45% of cases
2. alcohol and drugs
3. heptitis A and B
sxs:
**_1. jaundice_**
**_2. elevated transmidates AST/ALT_**
**_3. coagulopathy INR over 1.5_**
**_4. encepalopathy-alteration in mental status due to evelated ammonia_**
125
viral infections account for what percent of hepatitis?
50% of all cases
hep a b c d e account for 95% of thse
126
hepatitis A
## Footnote
precentage?
virus type?
incubation?
transmission route? (3)
**65% of all cases**
**RNA**occurs exclusively in liver cells
**incubates 2-6 wks**
transmission **_FECAL ORAL_**
1. travel
2. contanimated food and water
3. close contact with infected individuals
127
hepatitis A
## Footnote
sxs?
1 (time)
7 after sxs
SXS
1. prodrome, flu like
_most infectious here 12-21 days_
_2. icteric phase_
**1. dark urine appeares first (bilrubinuria)**
**2. pale stool follows**
**3. jaundice 70-85%**
**4. abdominal RUQ pain 40%**
**5. _prurits, indicates bilirubin_**
6. arthralgias
7. hepatomegally
128
hepatitis A
## Footnote
3 dx findings
tx
DX:
1. anti-hep A IGM and IGG
2. LFTS
- increase AST/ALT over 1000
- increased bilirubin 5-10 x
TX: selflimiting supportive
129
what are 5 prevention methods for hepatitis A?
improvement in hygiene and sanitation
cooking food
avoidance of water foods and endemic areas
avoidance of raw shellfish
immunization
130
who gets vaccinated for hep A? 4
Harvix
**travelers**
**miliary personnel**
**lab workers**
**immunocomprimised**
131
when you think of raw shellfish think..
hep A!
132
hepatitis B
## Footnote
what type of virus?
what percent of people have it and who?
3 transmission pathways?
**_KEEY THING TO KNOW ABOUT THIS_**
DNA virus
1/3 of population infected, majority immigrants or 1st gen
transmission:
1. perianatal
2. sexual
3. blood containing med equiment
**_\*\*\*\*\*\*\*causes 80% of hepatocellular carcinoma=fatal!!!!\*\*\*\*\*_**
133
what type of hepatitis can lead to hepatocellular carcinoma?
HEPATITIS B!! vaccines for this mandated
134
what are the categories of hepatitis B?
3
**immunity**
- vaccination
- natural infection
**actue infection**
**chronic infection**
- active
- chronic
135
surface=
core=
envelope=
surface=**immunity (vaccine or exposure)**
core=**exposed to virus**
envelope=**present infection with active replication**
136
acute hepatitis B
## Footnote
what is the breadown for how they present? (%)
1 key dx? 2 supportive?
tx2? why?
70% are subclinical (no jaundice or aniteric)
30% get icteric hepatitis
dx
**_1. HBcIGM for dx_**
2. elevated AST/ALT
3. elevated bilirubin
TX:
1. supportive
\*\*many will seroconvert to HBsAB and HBeAB meaning they develop immunity on their own!!\*\*
2. high calorie diet
137
chronic hepatitis B
## Footnote
three phases of this?
3 tx options and length of time?
initial phase:
**positive HBeAG**
immune clearance phase
**HBsAg, HBeAG**
**elevated ALT**
**inflammation on liver bx**
inactive carrier
tx:
1. tenofovir DOC
2. entecavir DOC
\*\*\*both of these are lifelong drugs!!!\*\*\*
3. interferone alpha 6 months
138
hepatitis prevention and vaccination
## Footnote
2
1. recombinant hepatitis vaccine
2. hep B immune globulin (exposued)
139
what is key to know about _hepatitis D_?
transmission?
RNA coinfection with **_HEP BE IS REQUIRED!!!_**
**_HBsAg_**
transmission: sexual contact
140
hepatitis C
## Footnote
what is this?
3 RF/transmission?
virus type?
age?
**_most common chronic blood borne infection in the US_**
## Footnote
1. injection drug use/cocaine
2. sexual contact
3. transfusion
RNA virus, 30-49 y/o
141
what percent of people proceed to the chronic state? what are two things you are at increased risk for?
80% proceed to the chronic state
HIGH RISK OF CIRRHOSIS AND HEPATOCELLULAR CARCINOMA
142
hepatitis C
## Footnote
3 tx options?
when do you start tx?
2 main options?
how long is the tx?
1. supportive first since can clear on their own
2. avoid hepatotoxic drugs
3. \*\*most wait **_6 months_** for posisble clearance before starting antiviral therapy\*\*
- harvoni (sofosbuvir/ledipasvir)
- daklinza (daclatasvir)
\*\*12-24 weeks tx depending tx naive and if cirrhosis\*\*
\*\*some regimens still include ribaviran, but not all of them\*\* NO INTERFERON
143
what do you want to check when txing someone for hep C?
viral load after **_12 weeks_** to confirm cure
144
what is cool about treating hep C?
IT IS CURABLE!!! nearly 100!!!!!
there is no vaccine and no post exposure immunoglobulin **_THEREFORE YOU WANT TO SCREEEN!!!_**
145
what is interesting about hep G?
if coinfected with HIV, helps reduce the HIV replication
146
HEP E
## Footnote
2 places you find this?
transmition
_AT RISK POP?_
North Africa
South Asian
fecal oral
self-limiting
***issues in pregnacy!!! EXTREMELY SEVERE!!!! esp in third trimester 20% mortality!!!!!! KEY***
147
cirrohosis
## Footnote
4 sxs of compensated?
7 sxs of decompensated?
_compensated sxs:_
ammenorreah
impotence
gynecomastica
**_hematemesis as present features in 15-25% (esophageal varices)_**
_decompenstated_:
**1. spider angiomas**
**2. muscle wasting**
**3. palmar erythema**
**4. dilated superficial veins of abdomen**
**5. ascities**
**6. portal HTN**
**7. encepalopathy**
148
cirrohsis
5 labs
3 tests
LABS:
low platelets
**_prolonged PT_**
moderate elevations enzymes
**_elevated bilirubin_**
**_low serum albumin_**
**_1. abdominal US WITH DOPPLER_**
- nodular appearing liver +/- hepatosplenomegaly
2. LIVER BX! TOC to confirm, determine staging
149
cirrhosis
## Footnote
5 tx
1. alcohol abstinence
2. vitamin supp
3. nuitrional supp
4. BB for portal HTN
5. _CURE IS TRANSPLANT_!!!
150
what MUST you do for someone with cirrhosis?
_**\*\*\*\*\*must screen for alpha fetal protein and imaging ever 6 months\*\*\***_
151
\*\*\*what are the **_2_** test results you want to keep in mind when looking at hepatits infection\*\*\*
**_hepatitis B surface antibody (HBsAB)=_**IMMUNITY--ONLY PRESENT IN VACCINATED PEOPLE
## Footnote
**_hepatitis B envelope antigen (HBeAg)_**: NEEDS TREATMENT, current infection
152
cirrhosis
## Footnote
what is this?
2 classifications?
**chronic end stage dxs of the liver marked by _degeneration of cells_ from inflammation resulting in _fibrous thickening of tissue_**
4 stages of fibrosis and cirrhosis is the last
**_compensated_**: although fibrotic can still preform functions
**_decompensated_**: fibrotic with loss of essential function
155
hepatocellular carcinoma (HCC)
## Footnote
what is this strongly associated with?
5 year survival?
3 sxs? 1 key
3 dx methods
**one key think you want to order**
associated with **_cirrhosis_**
## Footnote
4-6 months from time of dx
5 year survival is 25%
SXS:
1. _painless jaundice_
2. weight loss
3. hepatomegaly
dx
1. triple phase CT or MRI
2. **_percutaneous bx of lesions!!! TOC_**
**_3. Alpha fetoprotein tumor marker is PATHOPNEUMONIC_**
156
hepatocellular carcinoma
## Footnote
4 tx
1. surgical ressection
2. chemo
3. portal vein embolizations
4. _transplant_ if small and localized
157
appendicitis
## Footnote
what is this?
MC cause?
2 risks?
3 presentations?
**inflammation of the appendix causing leakage of cecum contents and blockage** _MC common due to fecalith_
RISK OF SEPSIS AND DEATH IF RUPTURES
SXS:
**1. sudden onset of abdominal pain**
2. **_umbilicus progresses to RLQ pain_**
3. pain to palpation
158
appendicitis
## Footnote
5 physical tests to do to confirm?
2 tests to do to confirm suspicion?
TESTS:
1. rovsings sign
2. obturatory sign
3. psoas sign
4. mcburneys
5. _rebound tenderness_
6. CT-inflammation
7. surgical consult
159
appendicitis
## Footnote
what is the tx for this?
what is the controversy concerning this?
surgical tx is standard of care
## Footnote
\*\*\*\*\***abx in recent studies conclude that 80% could be txed IV but 25% required emergency removal of appendix within first year post op....SO NOT IDEAL\*\*\***
160
obstruction
## Footnote
5 causes
explain last 3
4 sxs
1. tumor
2. foreign body
3. **paralytic ileus-trauma, surgery, infection, metbaolic disease with DM**
**4. volvulus-twisting of intesinte**
**5. intusssception-telescoping of intestine**
sxs;
1. severe abdominal cramping
2. inability to pass stool
3. **_increased bowel sounds first, then decreased_**
4. **_abdominal swelling, distention_**
162
obstruction
## Footnote
3 dx
3 tx
1. abdominal xray
2. CT
3. barium enema
tx:
1. NG tube (relieve pressure)
2. relieve obstruction
3. surgery often needed
163
what are four complications from obstruction?
tissue death
perforation
sepsis
death
164
fecal impaction
## Footnote
what is this and when typcailly does it occur?
2 key sxs?
PE? 1
TX 3
large mass of dried hard stool _typically after chronic constapation_
SXS:
_1. sudden watery diarreah in patient that has had cronic constapation_
_2. straining with passage of liquid or small stool_
PE:
DRE shows hard mass or dry stool in vault
TX:
**_1. removal manually_**
**_2. prevention with stool softeners, colase, bulk (fiber) and H20_**
**_3. high fiber diet_**
165
pilonidal cyst/disease
## Footnote
what is this?
what does it look like?
location?
who is it in? age? KEY!!!!!!
common, _congenital abnormality_
_"opening of a sinus tract that may conttain a **tuft of hair**"_
location:
midline, post sacral intergluttal fold superoir to anus
**ALMOST ALWAYS MEN 20-30, _always under 40_**
167
pilonidal cyst/disease
## Footnote
4 key sxs?
1 tx otpion? why?
1. **_fluctuant mass with erytmatous "halo"_**
2. purluent d/c
_3. NO ANAL PAIN OR DEFECATION ISSUES_
4. painful but in gluteal area
Tx:
**_1. MOST LIKELY SURGERY with secondary closure (leaving open) vs ID with abx_**
HIGH RATE OF RECURRANCE SO SURGERY IS BETTER OPTION TO GET DEEPER TRACTS!!!
168
Intestinal obstruction
## Footnote
what are the differences between the presentation of L intestine and small intestine?
2
4
what likely causes each?
2
3
Large intestine
**_distention and pain_**
D/T intussceptions, volvulus, neoplasm
Small Intestine
**_abdominal pain, distention, vomiting, high pitched bowel sounds that become silent!_**
D/T hernias and adhesions
169
intestinal obstruction
## Footnote
2 dx with 3 key findings?
2 tx options?
DX:
1. Xray
2. CT
**_distended proximal colon_**
**_air fluid levels_**
**_multiple dilated loop of bowel_**
TX:
1. **_laparotomy with or without colostomy if perforated_**
**_2. nasogastric suction_**
URGENT SURGERY IF TOTAL OBSTRUCTION SUSPECTED
170
what are the two groups of polyps?
1. imflammatory polyps/psuedopolyps **benign**
2. adenomas **premalignant**
(tubular, tubulovillous, villous)
171
of the colon adenomas "premalignant" explain the 3 different types?
malignancy potential goes up from tubular to vilous
## Footnote
1. **_tubular_**
least malignant, most commonly **pedunculated**
2. **_tubulovillous_**
more commonly **pedunculated**
3. **_villous_**"villous think villian"
more commonly **_sessile, highest potentiall for maligancy_**
172
what is the number one cause of iron deficient anemia? what are 3 other causes?
1. **blood loss! need to find the cause!!**
**2. malignancy! need to think about this**
3. dietary, vegan!! less common
4. poor iron absorption/ trauma
173
explain how B12 is absorbed and which conditions effect these stages?
B12 is bound to intrinsic factor that prevents it from being absorbed until it reached the ilieum
**chrons disease, ilium ressection effect:** where it is absorbed
**gastric surgery, pernicious anemia, gastritis effect:** where intrinsic factor is made
\*\*\*both of these cause B12 deficiency either in its protection or its absorption!\*\*\*
174
what cells produce intrinsic factor that are important for the absorption of B12? where are they located?
parietal cells in the stomach
gastritis PUD can prevent this from working
no intrinsic factor, no absorption
175
what are three things can cause poor absorption of B12 for anemia?
alcoholism
fish tapeworm
elevated LDH
176
what are the 3 treatment options for B12 deficient anemia?
1. **life long vitamin B supplement IM monthly (1000 ug)**
**2. cyanocobalasmin nasal spray**
\*\*\*neuro symptoms are reversible if treated within 6 months\*\*\*
177
explain the schillings test and what it tells you?
**tells you which there is a B12 deficiency**
Normally, give B12 IM injection so the body is saturday, then give oral B12 radioative, it will be absorbed by the body and AT LEAST 10% excreted in the urine since it isn't needed. This means uptake is normal and working!!
if pernicious anemia or imparied absorption: **LESS than 10% in the urine since not absorbed or partially from bowel**
if give intrinsic factor and see B12 in the urine then absorption has improved: **pernicious anemia**
if no B12 in the uring after intrinsic factor then: **problem with absorption** **in illium, not intrinsic factor**
178
Vitamin B12 deficient anemia
## Footnote
what size and color at these RBC? what factor sets this appart from folate deficient anemia and what are the 5 presentations? what are the 6 things that can cause this and where are the two general sections of the GI system that are effected? what are the 4 important lab results that point to this?
**macrocytic/megloblastic anemia, normochromic**
can occur from **vegan diet, bariatric gastric surgery (_MOST COMMON WAY TODAY)_, ilium resection, chrons disease, pernicious anemia (no intrinsic factor), gastritics**
neurologic symptoms, stocking glove paresthesia, loss of position, vibratory sense, balance, glottitis
On lab exams find:
_1. antibodies for intrinsic factor_
_2. MCV \>103_
_2. serum b12 low_
_4. multinucleated neutrophils!!! 5-6 lobes_
Tx: oral supplement or cyanocobalamin nasal spray
179
explain what falls under the two categories of uncomplicated UTI (2)
and
complicated UTI? (6)
**uncomplicated UTI**
- acute cysitits
- acute pyelonephritis
**complicated UTI**
1. something that makes the more likely to fail treatment
- obstruction
- anatomic abnormality
urologic dysfunction
- MDR uropathogen
2. pregnant
3. elderly
4. children
5. males
6. recurrent
180
Complicated UTI
Pregnancy
what are 3 things its assocaited with?
do you screen?
if positive what must you do (2)?
what is one really key thing to remember about UTI and pregnant women?
associated with preterm birth, low birth weight, prenatal mortality
screen in 1st trimester with UC
**_admit them since dangerous with baby_**
always check urine culture if asymptomatic because the bacteria in the urine can cause the things under A, if + treat with abx
**_if they get 2+ positive tests with greater than 100,000 positive tests they they will be on suppressive abx for the remainder of the pregnancy_**
181
Complicated UTI
eldery
what are two groups of peopel that are esp susceptible?
what are three things that contribute to the first?
**postmenopausal women**
1. bladder/uterine prolapse
2. loss of lactobacilli in vaginal flor allos for E. coli to take over
3. diabetes (sugar)
**benign prostatic hypertrophy**
182
complicated UTI
children
who is this more common in?
3 symptoms?
what is the DOC?
how long do you treat for, two options?
white children more common than black children
**fever, hematuria, abdominal pain**
**DOC: 2nd-3rd line cephalosporin**
_7-14 days_ if febrile
_5 days_ if immune competent and afebrile
183
complicated UTI
males
what are two risk factors?
urethra length?
unusual for men 15-50
RF: **uncircumcised, anal intercourse**
antibacterial material in prostatic fluid
**18-20 cm urethra**
184
who are UTIs most common in?
what is the most common route of infection?
what are most from?
what isthe pathogenisis of this and what does it RARELY come from?
**30:1 ratio women to men** because women have a significantly short urethra
route of infection: ascending from the urethra
UTI most commonly from _uncomplifcated acute cystitis_
pathogenisis:
1. colonization of vaginal introitus by uropathogens from fecal flora ascend from urethra into bladder **CYSTITIS**
2. uropathogens ascend from bladder to kidney via ureters
RARELY CAUSED BY SEEDING OF BACTERIA
185
what are 5 RF for UTI?
female sex
frequent sexual intercourse
diaphragm/spermicide use
delayed post-coital micturition (not urinating after intercourse)
hx of UTI
186
what are four bacteria that cause UTI and which is by far the most common? what percent?
**e.coli most common 75-95%**
proteus mirabilis
klebsiella pneumoniae
enterococcus
187
what are the difference in symptoms for
cystitis (6)
vs
pyelonephritis? (5)
cystitis:
## Footnote
1. dysuria or burning while urination
2. increased frequency/urgency
3. suprapubic pain/discomfort
4. hematuria
5. voiding small amounts
6. AFEBRILE
pyelonephritis
1. FEBRILE
2. chils
3. flank pain
4. costovertebral tenderness
5. CBC with left shift
188
what 3 lab tests are important to do when diagnosiing a UTI?
what do you find on each?
**1. UDIP**
_+ leukocyte esterase (product of baceteria)_
_+ nitrites (conversion of nitrates to nitrites via bacteria)_
_+WBC_
_+WBC casts (**INDICATES KIDNEY ORIGIN!\*\*\***)_
**2. hematuria**
**3. culture greater than 100,000**
189
what are the DOC fo acute cystitis (4) vs pyelonephritits (2)?
what do you need to note?
**_acute cystitis_**
_DOC1: TMP-SMX_
DOC2: CIPRO
DOC3 if pregnant/allergic: Nitrofurantoin
\*\*\*add _pyridium_\*\*\*
**_acute pyelonephritis_**
_DOC1: ciprofloxacin_
DOC2: TMP-SMX
\*\*\*\*\*NOTE THE DOC FOR FOR THESE TWO ARE DIFFERENT!!!\*\*\*\*\*
190
what is the DOC for an inpatient with UTI/pyelonphritis?
CIPROFLOXACIN!!
others:
fluoroquinolone, amp+gentamycin, ceftriaxone
191
what is the most common nosocomial infection in the US? what is the tx protocol with this?
cathertized associated UTI
## Footnote
_if asymptomatic don’t need to treat with abx_
screen urine 48 hours after removing catheter
192
recurrent UTIs
## Footnote
what are the two definitions of this?
what should you consider?
what about in women with decrease in lactobacillis?
_3 or more episodes per year confirmed UC_ OR _2 UTIs in last 6 months_
## Footnote
consider self treatment at first sign (urine cup for UC)
vaginal estrogen in women since they have a decrease in lactobacillus
193
in _asymptomatic bacteremia_ who do you treat (3) and who do you not treat (3)? \*key!\*
**_treat:_**
1. pregnant
2. before urologic procedures
3. after renal transplant
**_DONT TREAT_**
1. diabetics
2. elderly
3. patients with spinal cord injury or indwelling urethral catheter
194
do you tx UTI empirically while waiting for culture?
YES! then adjust abx as appropriate! :)
195
testicular torsion
## Footnote
what is this and what are you at risk for?
who is most likely to get this? esp?
emergency? 3 sxs?
testes is anormally twisted in the spermatic cord thus comprimising arterial blood flow and venous drainage which leads to **testicular ischemia**
most common in _prepubertal and post pubertal 12-18 year old males_, esp with those who had _crytorchidism_ or late decent of the testes
UROLOCIAL EMERGENCY!!
SXS:
1. **_negative prehns sign-no relief with elevation of the scrotiom_**
**_2. unilateral, swollen, retracted testicle_**
**_3. absent cremaster reflex_**
197
testicular torsion
## Footnote
2 dx?
3 tx?
DX:
1. clinically
2. doppler US shows decreased blood flow
TX:
1. NSAIDS
2. surgical detorsion and orchiopexy (make teste descended)
\*\*\*GOAL: GET THIS ALL DONE WITHIN 6 hours!!!\*\*\*
198
cryptochidism
## Footnote
who does this occur in?
what is this?
2 RF?
consequences if not fixed?
1 PE finding?
1 Tx option
**one or more undescended testes that don't move into the scrotal sac, which remain in the _abdomen or stuck in the inguinal canal_**
\*\*those born prematurely or are small for gestational age have he highest risk of effect\*\*
**consequences:**
**1. infertility**
**2. testicular torsion**
**3. maligancy**
PE:
1. absence of palpable testicle, or palpable within the inguinal canal
TX:
1. **_SURGERY! by age 1 to prevent risk of infertility_**
199
what does having cryptorchidism increase your risk for?
increases risk of malignancy in undescending testis is 4-10 times greater than gerneral population
200
explain what falls under the two categories of uncomplicated UTI (2)
and
complicated UTI? (6)
**uncomplicated UTI**
- acute cysitits
- acute pyelonephritis
**complicated UTI**
1. something that makes the more likely to fail treatment
- obstruction
- anatomic abnormality
urologic dysfunction
- MDR uropathogen
2. pregnant
3. elderly
4. children
5. males
6. recurrent
201
phenylketonuria
what is this?
what happens in this?
screened for in?
TX? 2 key things?
inability to metabolize phenylalanine protein
## Footnote
accumulates in CNS and causes retardation and movement disorders
Screened at birth, if not dx by 3 irreversible damage
TX:
**_low phenylalanine diet and tyrosine supplementation_**
\*\*MUST PROTEIN RESTRICT TO LIVE\*\*
