GI Portion Flashcards
GERD
what are 6 sxs?
1 thing to keep in mind about sxs?
- 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**
GERD
3 dx options
6 reasons of when it is not appopropriate to use the first line dx
- 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
what are the lifestyle changes a patient should make to relieve sxs of GERD?
5
- avoid eating 2-3 hours before bed
2. elevate head of bed
3. loose weight
- avoid acidic food, chocolate, peppermint, ETOH, coffee
- stop smoking
why is it important to treat GERD?
prevent cancer aka barrette esophagus because the damange from acid makes this more likely to occur
what is the emergency cocktail you give someone in the ED for heart burn?
- benadryl
- lidocaine
- maalox
what is the most common cause of esophagitits?
GERD, 50% of patients with GERD have esophagitits
gastroesophageal reflux disease
what is this?
population common in?
percent in US?
5 complications it can lead to
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
-
what is the pathway for txing GERD?
6
- lifestyle adjustments
- OTC antacids-2 weeks
- H2 receptor antagonists
- Proton pump inhibitors
**if these fail EDG**
- prokinetics
- surgical
esophagitits
what is this?
5 general causes?
4 sxs
inflammation of the esophagus, esp in immunocomprimised
- viral
- bacterial
- paraistic
- abx induced
- radiation or chest cancers
sxs;
- odyniaphagia
- dysphagia
- substernal chest pain
- oral thursh
esophagitis
herpes liabilis (HSV)
3 SXS?
2 DX?
1 TX
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!!!
ESOPHAGITIS
VARICELLA-ZOSTER
1 dx?
tx?
N/V fever chils
DX:
endoscopy: vesicles or confluent ulcers
Tx:
- usually resolve spontaneously but can cause necrotizing esophagitits
- ACYCLOVIR!!!!
barrett’s esophagus
how does this occur? what hcanges?
what are they at increased risk for? how much?
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
barettes esophagus
2 dx rules?
3 tx?
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
esophagitis
CMV
who does this occur in?
characteristics of ulcer? 2
3 sxs?
1 tx?
only occurs in immunocomprimised patients
CREEPING ULCER or can be GIANT ULCER
sxs:
odyniaphagia
persistent CP
hematememis
Tx:
IV GANCICLOVIR
esophagitis
candidia
who does it occur in?
3 complications?
1 dx?
1 tx?
occurs in immunocomprimised host
can cause complications:
- bleeding
- perforation
- stricture
dx:
endoscopy: small yellowwhite raised plaques
tx:
oral or IV fluconazole!!
esophageal cancer:
adenocarcinoma
where do you find this?
4 most important RF?
2 protective
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)
esophageal cancer
what are the two types?
frequency?
prognisis?
who is more common?
types:
- adenocarcinoma
- squamous cell carcinoma
prognosis typicaly poor, 5 year survival 10-13%
both appeare with equal frequency
males more common than females
esophageal cancer:
squamous cell carcinoma
prevalence?
location?
4 RF?
key point to remember?
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***
esophageal cancers
sxs
1 early
3 late
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***_
in esophageal cancer, when would you expect to see the weight loss and dysphagia?
when the lumen is less than 13 mm
esophageal cancer
2 DX
2 STAGE
dx:
- barium studies
- endoscopy
Staging:
- CT OF CHEST AND UPPER ABDOMENT
2. PET SCAN
where are adenocarcinomas and squamous cell esophageal cancers found?
adenocarcinoma: lower 1/3
squamous: middle esophagus
where is the most common stie for esophageal varices? why?
distal esophagus at gastroesophageal junction because veins are most superficial here!!
esophageal varices
6 sxs
3 dx
sxs:
1. hematemesis!!! over 50% stop bleeding spontaneously
- melena
- tachycardia
- hypotension
- syncope
- jaundice
DX:
1. emergent endoscopy
CBC
BUN/creatine
type and cross
esophageal varices
4 immediate tx options
- immediate tx-stop bleeding because mortaltiy approaches 75%
- visceral ligation- rubber band
- sclerotherapy
- balllon tamponade
esophageal varices
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
in esophageal cancer, when would you expect to see the weight loss and dysphagia?
when the lumen is less than 13 mm
esophageal cancer
2 DX
2 STAGE
dx:
- barium studies
- endoscopy
Staging:
- CT OF CHEST AND UPPER ABDOMENT
2. PET SCAN
where are adenocarcinomas and squamous cell esophageal cancers found?
adenocarcinoma: lower 1/3
squamous: middle esophagus
where is the most common stie for esophageal varices? why?
distal esophagus at gastroesophageal junction because veins are most superficial here!!
where is the most common stie for esophageal varices? why?
distal esophagus at gastroesophageal junction because veins are most superficial here!!
esophageal varices
6 sxs
3 dx
sxs:
1. hematemesis!!! over 50% stop bleeding spontaneously
- melena
- tachycardia
- hypotension
- syncope
- jaundice
DX:
1. emergent endoscopy
CBC
BUN/creatine
type and cross
esophageal varices
4 immediate tx options
- immediate tx-stop bleeding because mortaltiy approaches 75%
- visceral ligation- rubber band
- sclerotherapy
- balllon tamponade
esophageal varices
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
mallory weiss tear
1 dx?
2 tx?
DX:
ENDOSCOPY
TX:
-
stabliazation
- transfusion/gastric lavage if needed - control bleeding via endoscopy
**keep in mind most bleeding stops spontaneously and condition is usually benign**
mallory-weiss tear
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
most common location: gastroesophageal junction
RF:
alcholic
hiatial hernia
eating disorder BULEMIA
SXS:
- multiple bouts of vomiting and retching followed by PAINLESS HEMATEMESIS
- abdominal pain
***keep in mind the bleeding usually stops spointaneously as teh condition is usually benign**
esophageal ring
what is this?
sxs?
dx?
1 tx?
ring of tissue located at the gastroesophageal junction called
schatzkis ring
sxs:
- dysphagia with foods, but not typically liquds
DX:
barium esophagram
TX:
mechanical dilation with balloon
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
what are 6 RF for stomach neoplasms?
- genetic predisposition
- carcinogenic diet
smoked food/perserved food
- autoimmune gastritis
increased inflammation
- gastric adenomas
- polyps
- h. pylori, cofactor for some
what are the 5 common causes of PUD?
- NSAIDS
- H. pylori
- idiopathic
- hypersecretory states
- smoking
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?
- duodenal
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
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:
- ASA
- corticosteroids
- over 60
TX:
1. PPI or H2
***4 weeks duodenal***
***8 weeks gastric***
2. D/C NSAID
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!!!!!**
what is a RF for all ulcers?
smoking!
explain te patho of stomach ulcers caused by h. pylori?
- infection in body
- causes gastritis and chronic inflamation that overwhelms immune system
- causes mucosal breakdown
- creates gastric ulcer
PEPTIC ULCER DISEASE
2 sxs
3 dx
when do you use each?
1 think must do?
SXS
- epigastric like pain “hunger like” in 80-90%
- 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:
- endoscopy EDG TOC!
allow so for visulaization and also bx!!
- fecal antigen test (noninvasive)
- 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!
peptic ulcer disease
tx without h. pylori
2
3 for first
1 second
- antisecretory agents
A.PPIs 1st DOC-inhibit 90% acid secretion
ompreazole
lansoprazole
B. H2-inhibit histamine mediated secertion
C. OTC anti-secretory
- mucosal defense agents
2nd line can be used as adjunct for symptom relief
sacralfate, busmuth
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
Peptic ulcer disease
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
peptic ulcer disease:
Treatment for H. pylori
what is the tx regimen?
what must you do after tx and when?
2/3 abx, PPI, +/- bismuth
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***
in reccurent ulcers what must you do!?
rule out H. pylori and NSAID use
peptic ulcer disease:
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
peptic ulcer disease:
refractory ulcers
what is this caused by?
3 contributing factors
uncommon, contributed to non compliance with medication
Contirbutory factors:
- cigs
- NSAIDS
- failutre to eradicate H. pylori! MUST DO THIS
chronic pancreatitis
4 dx options
fat stranding
- amylase/lipase NORMAL
body gets used to working under these circumstances
- secretin stimulation test “gold standard” for early chronic pancreatitis dx
- plain xray films QUICK AND CHEAP-see calcifications
- CT SCAN-better at seeing calcifications but $$/rad
“arrowhead and fat stranding”
explain the pathophys of pacreatitis?
what are 2 theories that cause this?
- inflammation of the pancreas causes damage to the acrinar cells
- the inactive proenzymes like trysinogen are activated early while still in the pancreas
- early activated lipases disolve the fat
- so the pancreatic enzymes start to DIGEST THE PANCREASE “EATS ITSELF”
theories:
- obstruction of the pancreatic duct due to stones
- failure of the two parts of the pacreas to fully join during development pancreatic divism
when dxing pancreatitis and looking at labwork, what test is most effective?
lipase
(this is better than amylase)
acute pancreatitis
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
acute pancreatitis
6 sxs
where is pain?
severity?
what makes worse/better?
pain with…?
two key signs you dont want to miss?
- epigastric radiates to back
- billiary colic PERSISTS DOESN”T GO AWAY
- worse SUPINE, BETTER LEANING FORWARD
- PAINFUL INSPIRATION, SHALLOW BREATHS
- TACHYCARDIA
6. hemmoragic pancreatitis
cullens sign: periumbical ecchymosis
grey tuner’s sign: flank eccymosis
acute pancreatitis
6 tx options?
what is the process dependent on?
mostly supportive
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
acute pancreatitis
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
chronic pancreatitis pathophysiology
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
chronic pancreatitis
what is the MC cause of this?
3 others?
NOT CAUSED BY WHAT?
what can this lead to?
- alcohol cause #1!!
***THIS IS NOT CAUSED BY GALLSTONES LIKE ACUTE**
- obstructive causes of spincter of oddi by neoplasms
- malnuitirion
- metabolic
chronic pain leads to opoid addiction! keep this in mind
chronic pancreatitis
4 sxs?
sxs:
- epigastric abdominal pain that radiates to the LEFT
- insufficiency of pancreatic function leads to
a. steatorhhea damages decreases lipase
b. diabetes once islets damaged
3. asymptomatic and found incidently
chronic pancreatitis
5 tx options
most important!!
2 drugs?
- _stop the alcoho_l!!
- controls sxs
a. pain control
b. prancreatic enzyme supplements viokase and pancrease
- endoscopic duct decompression
- surgical draingage of duct
- celiac plexsus nerve block
what are the two criteria used to identify the mortality with pancreatitis?
- Ranson’s criteria
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
- APACHE II score
**typically impatient ICU use**
over 8 is severe!!!
pancreatic cancer
what are thet wo tumor markers?
survival?
1 RF?
tumor markers:
- CA19-9 85%
- CEA 40-45%
5 year survival is only 4% really bad
only RF: chronic pancreatitis
pancreatic cancer
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
- whipple surgery-only at cancer specialties
- pallaitive care
pancreatic cancer
4 sxs?
toc? 1
sxs:
- painless jaundice is PC until prove otherwise
- virchows node-supraclavicular node
- trouseaus signs- recurring superficial thrombophlebitiscan be anywhere
- weight loss
TOC: CT scan dual phase helical
acute cholecystitis
2 dx tests? when to use?
2 labs?
TOC #1: US
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 $$$$$$$, so US becomes TOC******
Two elevated labs:
elevated gamma-glutamyl transpeptidase
elevated bilirubin
acute cholecystitis
what happens in this?
what is most likely to cause this?
leads to 3 things? possible worst case?
2 key sxs?
the cystic duct** becomes blocked **most commonly from gallstone!
less common:
cancer, sludge, infection
blockage causes distention and edema that cauess ischemia, necrosis, perforation and possible generalized sepsis
SXS
- RUQ/epigastric pain radiate to shoulder/scapula
- murphys sign (tenderness and pt stops inspiration on palpation)
acute cholycystitis
TXOC?
3 others?
TreatOT: TAKE IT OUT!! MOST COMMON!! via laproscopic cholecystectomy
- leave in if very mild
- drain it if patient too sick
- abx if elevated WBC
what are the four RF for cholithiasis?
- over 40
- obesity (or rapid weight loss)
- female/pregnant
- native american
“FEMALE, FAT, FORTY, FERTIL” 4, F’s
choledocholithiasis
where is the stone?
where does it come from?
where is pt?
sxs? 4
stone in the COMMON BILE DUCT
usually migrate from the gallbladder
patient very sick and likely in ICU!! compared to cholelithiasis
sxs:
asymptomatic in 30-40%
BILLARY COLIC
jaundice, pancreatitis
choledolithiasis
what are the two dx/tx options?
what must you keep in mind?
- MRCP magnetic resonance cholangiopacreatogprahy ONLY DX
- ERCP-endoscopic retrograde cholangioancreatography DX AND TX so GOLD STANDARD!!
****keep in mind contraindicated in pancreatitis/cholecystomy***
acute cholelithiasis
what are you 3 tx options and who are they appropriate for?
- cholecystectomy-MOST COMMON “it hurts
- leave in if doesn’t hurt UNLESS high risk to keep in
a. diabetics
b. sickle cell
c. Native americans with calfieiced “porcelain” stone - dissolve cholesterol stones with actigal, urodeoxycholic acid but $$$
acute cholithiasis
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%
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**
cholelithiasis
two types of stones?
percentage?
what do they look like?
1. cholesterol stones
MC-75% of stones!!
don’t show up on xray
- calcium bilirubinate/ca salts
25% of stones
pigmented black/brown sludge stones
celiac disease
what are 6 sxs that come with this?
explaination of the last?
- unintended weight loss
- persistently underweight
- sxs of poor nuitrition
- “failure to thrive in child”
- diarreah
-
dermatitis herpetiformis
a. intense itching
b. blisterning rashes
c. 10-15% of patients
celiac disease
what type of condition is this?
what is the patho of this and the specific component?
nickname?
autoimmune dx of SI
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”
celiac disease
what are the 3 dx options of this?
key thing to remeber?
- anti-tissue transglutaminase antibodies OR anti-endomysium IgA antibodies
- bx if small intestine and blood + for antibody
****if they have dermatitis herpetiform with + antibody skin bx, THEN NO NEED FOR INTESTINAL BX***
celiac disease
what are the 2 tx for this?
what about screening?
- gluten free diet
- wheat
- rye
- barley
2. abx for dermatitis herpetiformis
***make sure to screen if family hx using blood test for autoantibodies**
diverticula
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
diverticulosis
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
diverticulitis
what is this?
3 sxs?
2 tests?
inflammation of the pocuhes
- severe LLQ pain
- change in bowel habit
- constapation
Tests:
- CT TOC with IV and oral contrast
- WBCs
- barium enema
- colonoscopy
who is diverticulosa most common in?
2 percents?
western/industerialized societies
30% by 60
65% have by age 85
what are 3 RF for diverticulosa?
- connective tissue disorders
- low fiber diet
- too little exercise
what are the two conditions that make up inflammatory bowel disease?
- crohns disease
- ulcerative colitis
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?
- legions mouth to anus; spread out with healthy tissue between
2. transmural
3. RLQ pain MC
- fistulas, abscesses, fibrotic stricutres
- bleeding common
- weight loss common
- obstruction common
- perianal disease common
- can effect skin eyes joints liver
- large volume diarreah and mucous (trash bag)
what 2 are tests you want to do to look for crohns?
- anti-saccharomyces cervisial (ASCA)- 44% of crohns are pos
- colonoscopy TOC
what are the 4 tx options for crohns?
- 5-aminosalcyclics (5-ASA)
-mesalamine
-sulfasalazine
- corticosteroids
- cimzia-certolizumab
- humira-adalmumab
**surgery doesn’t work since it involves the entire GI tract**
ulcerative colitis
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?
- primarily localized in colon
2. LLQ
3. bleeding from rectum is most common
- urgency need of BM
4. potenital anemia due to blood loss
- lesions are continuous starting at the rectum and in mucosa only
- colon wall thin with continuous inflammation
- no granulomas
(weight loss/obstruction very rare with this)
which is more common crohns or ulcercerative colitis?
ulcerative colits 3x more likely
what do you use to dx ulcerative collitis?
colonoscopy
what are the 3 tx options for ulcerative collitis?
- 5-ASA
- sulfasalzine
- mesalamine - corticosteroids
- colonectomy CURE best choice
removal of colon
irritable bowel syndrome
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
irritable bowel syndrome
3 tx options?
4 medications tx options
- pt education and behavior/ emotional support
- dietary therapy
- pharm
a. antispasmotics
b. antidiarreals
c. psychotropic
d. serotonin receptor agonists
colorectal cancer
what are 3 risk factors?
- genetic predisposition
- presence of adenomatous polyps)
3. diets high in fats and refined carbs that are low in plant fiber *industerialized world*
what does colonrectal cancer come from?
the progression of adenomatous polyp into malgnancy
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?
- tubular adenoma
MOST COMMON TYPE 65-80%
pedunculated, little cancer risk
- tubulovillous adenoma
10-25% of adenomas
22% risk of cancer
- vilous adenomas
40% RISK OF CANCER
only 5-10% so least common but most deadly
what is the least common but the most prognostic for cancer of the adenoma polyps?
vilous adenoma
*think vilian=evil*
what are the two tests that are reccomended annually to screen for colorectal cancer?
- guiac fecal occult blood test (gFOBT)
- immunochemical-based fecal occult blood test (iFBT)
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
- optical colonscopy-10 years
- flexible sigmoidoscopy-5 years
- CT colonography-10 years
colonrectal cancer
4 sxs
2 key dx
3 others
sxs:
- colic type pain
2. anorexia
3. thin appeareance
4. pallior/anemia
dx:
- xray: classic apple core/npaking ring appearance
- endoscopy with bx
- iron deficient anemia
- hypoalbuminemia
- occult blood in stool
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
what is the dentate line?
senstion?
divides the rectal mucosa from the squamous epithelium in the canal
above in anorectal canal: INSENSATE (no pain)
below in andoderm: SENSATE AND PAINFUL!!
anal fissure
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:
- passage or hard stool
- prolonged diarreah
lactose intolerance
what is this?
4 populations common in?
5 sxs? key 1?
difficulty digesting lactose from lack of lactulase
MOST COMMON IN:
- AFRICAN AMERICANS
- HISPANIC/LATINO
- ASIAN AMERICANS
- NATIVE AMERICANS
SXS:
- bloating
- pain
- increase passage of gas
- diarrhea and nausea
5. 2 hours post consumption of milk or dairy
lactose intolerance
1 dx?
1 tx?
dx:
hydrogen breath test
tx:
dietary avoidance
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!!
anal fissure
3 sxs?
what not to do?
sxs:
- “tearing” pain with BM since below dentate line
- hematochezia during BM
- SPREAD BUTTOCKS to examine
**NEVER DO RECTAL EXAM, TOO PAINFUL!..and cruel**
anal fissure
2 tx categories
4
1 (also, who not to do in)
- 90% heal without tx
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**
explain the pathophysiology of hemmoroids?
5
- anal canal is lined with “cushions” that are vascualr and connective tissue and make the hemmorrhoidal plexsus
- exist in 3 columns
- cushions encorge during defecation to profect the anal canal from abrasion
- 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
what are 6 RF for hemmoroids?
constapation
straining at stool
pregnancy
obesity
chronic liver disease
portal HTN
Internal hemmoroid tx categories
5
2
1-2 degree:
a. fiber
b. water
c. stool softner
d. anusol hydrocortisone
e. numbing agent nupercainal ointment
3-4 degree:
a. SURGICAL
b. EXCESIONALHEMMOIROIDECTOMY
internal hemmoroids
4 key sxs with these!
above the denate line!!
veins surrounded by mucosa
- PAINLESS, above denate
2. bright red bleeding with defecation
3. may prolapse and be palpable on DRE
4. bleed
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
external hemmoroids
whe do they occur/what are they covered in?
3 sxs
dx method?
1 tx?
below the dentate line and covered with andoderm
- usually don’t bleed
- may thrombose which is VERY painful
- cause pain, discomfort and most severe at time of defecation
dx
“either present or not”
tx:
- excision of outside of the mucotaneous junction leaving wound open hemroidectomy
acute hepatitis
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
- tylenol 45% of cases
- alcohol and drugs
- 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
viral infections account for what percent of hepatitis?
50% of all cases
hep a b c d e account for 95% of thse
hepatitis A
precentage?
virus type?
incubation?
transmission route? (3)
65% of all cases
RNAoccurs exclusively in liver cells
incubates 2-6 wks
transmission FECAL ORAL
- travel
- contanimated food and water
- close contact with infected individuals
hepatitis A
sxs?
1 (time)
7 after sxs
SXS
- 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
- arthralgias
- hepatomegally
hepatitis A
3 dx findings
tx
DX:
- anti-hep A IGM and IGG
- LFTS
- increase AST/ALT over 1000
- increased bilirubin 5-10 x
TX: selflimiting supportive
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
who gets vaccinated for hep A? 4
Harvix
travelers
miliary personnel
lab workers
immunocomprimised
when you think of raw shellfish think..
hep A!
hepatitis B
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:
- perianatal
- sexual
- blood containing med equiment
*******causes 80% of hepatocellular carcinoma=fatal!!!!*****
what type of hepatitis can lead to hepatocellular carcinoma?
HEPATITIS B!! vaccines for this mandated
what are the categories of hepatitis B?
3
immunity
- vaccination
- natural infection
actue infection
chronic infection
- active
- chronic
surface=
core=
envelope=
surface=immunity (vaccine or exposure)
core=exposed to virus
envelope=present infection with active replication
acute hepatitis B
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
- elevated AST/ALT
- elevated bilirubin
TX:
- supportive
**many will seroconvert to HBsAB and HBeAB meaning they develop immunity on their own!!**
- high calorie diet
chronic hepatitis B
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:
- tenofovir DOC
- entecavir DOC
***both of these are lifelong drugs!!!***
- interferone alpha 6 months
hepatitis prevention and vaccination
2
- recombinant hepatitis vaccine
- hep B immune globulin (exposued)
what is key to know about hepatitis D?
transmission?
RNA coinfection with HEP BE IS REQUIRED!!!
HBsAg
transmission: sexual contact
hepatitis C
what is this?
3 RF/transmission?
virus type?
age?
most common chronic blood borne infection in the US
- injection drug use/cocaine
- sexual contact
- transfusion
RNA virus, 30-49 y/o
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
hepatitis C
3 tx options?
when do you start tx?
2 main options?
how long is the tx?
- supportive first since can clear on their own
- avoid hepatotoxic drugs
- **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
what do you want to check when txing someone for hep C?
viral load after 12 weeks to confirm cure
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!!!
what is interesting about hep G?
if coinfected with HIV, helps reduce the HIV replication
HEP E
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
cirrohosis
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
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
cirrhosis
5 tx
- alcohol abstinence
- vitamin supp
- nuitrional supp
- BB for portal HTN
- CURE IS TRANSPLANT!!!
what MUST you do for someone with cirrhosis?
_*****must screen for alpha fetal protein and imaging ever 6 months***_
***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
hepatitis B envelope antigen (HBeAg): NEEDS TREATMENT, current infection
cirrhosis
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
hepatocellular carcinoma (HCC)
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
4-6 months from time of dx
5 year survival is 25%
SXS:
- painless jaundice
- weight loss
- hepatomegaly
dx
- triple phase CT or MRI
- percutaneous bx of lesions!!! TOC
3. Alpha fetoprotein tumor marker is PATHOPNEUMONIC
hepatocellular carcinoma
4 tx
- surgical ressection
- chemo
- portal vein embolizations
- transplant if small and localized
appendicitis
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
- umbilicus progresses to RLQ pain
- pain to palpation
appendicitis
5 physical tests to do to confirm?
2 tests to do to confirm suspicion?
TESTS:
- rovsings sign
- obturatory sign
- psoas sign
- mcburneys
- rebound tenderness
- CT-inflammation
- surgical consult
appendicitis
what is the tx for this?
what is the controversy concerning this?
surgical tx is standard of care
*****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***
obstruction
5 causes
explain last 3
4 sxs
- tumor
- foreign body
- paralytic ileus-trauma, surgery, infection, metbaolic disease with DM
4. volvulus-twisting of intesinte
5. intusssception-telescoping of intestine
sxs;
- severe abdominal cramping
- inability to pass stool
- increased bowel sounds first, then decreased
- abdominal swelling, distention
obstruction
3 dx
3 tx
- abdominal xray
- CT
- barium enema
tx:
- NG tube (relieve pressure)
- relieve obstruction
- surgery often needed
what are four complications from obstruction?
tissue death
perforation
sepsis
death
fecal impaction
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
pilonidal cyst/disease
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
pilonidal cyst/disease
4 key sxs?
1 tx otpion? why?
- fluctuant mass with erytmatous “halo”
- purluent d/c
3. NO ANAL PAIN OR DEFECATION ISSUES
- 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!!!
Intestinal obstruction
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
intestinal obstruction
2 dx with 3 key findings?
2 tx options?
DX:
- Xray
- CT
distended proximal colon
air fluid levels
multiple dilated loop of bowel
TX:
- laparotomy with or without colostomy if perforated
2. nasogastric suction
URGENT SURGERY IF TOTAL OBSTRUCTION SUSPECTED
what are the two groups of polyps?
- imflammatory polyps/psuedopolyps benign
- adenomas premalignant
(tubular, tubulovillous, villous)
of the colon adenomas “premalignant” explain the 3 different types?
malignancy potential goes up from tubular to vilous
- tubular
least malignant, most commonly pedunculated
- tubulovillous
more commonly pedunculated
- villous“villous think villian”
more commonly sessile, highest potentiall for maligancy
what is the number one cause of iron deficient anemia? what are 3 other causes?
- blood loss! need to find the cause!!
2. malignancy! need to think about this
- dietary, vegan!! less common
- poor iron absorption/ trauma
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!***
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
what are three things can cause poor absorption of B12 for anemia?
alcoholism
fish tapeworm
elevated LDH
what are the 3 treatment options for B12 deficient anemia?
- life long vitamin B supplement IM monthly (1000 ug)
2. cyanocobalasmin nasal spray
***neuro symptoms are reversible if treated within 6 months***
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
Vitamin B12 deficient anemia
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
explain what falls under the two categories of uncomplicated UTI (2)
and
complicated UTI? (6)
uncomplicated UTI
- acute cysitits
- acute pyelonephritis
complicated UTI
- 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
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
Complicated UTI
eldery
what are two groups of peopel that are esp susceptible?
what are three things that contribute to the first?
postmenopausal women
- bladder/uterine prolapse
- loss of lactobacilli in vaginal flor allos for E. coli to take over
- diabetes (sugar)
benign prostatic hypertrophy
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
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
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:
- colonization of vaginal introitus by uropathogens from fecal flora ascend from urethra into bladder CYSTITIS
- uropathogens ascend from bladder to kidney via ureters
RARELY CAUSED BY SEEDING OF BACTERIA
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
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
what are the difference in symptoms for
cystitis (6)
vs
pyelonephritis? (5)
cystitis:
- dysuria or burning while urination
- increased frequency/urgency
- suprapubic pain/discomfort
- hematuria
- voiding small amounts
- AFEBRILE
pyelonephritis
- FEBRILE
- chils
- flank pain
- costovertebral tenderness
- CBC with left shift
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
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!!!*****
what is the DOC for an inpatient with UTI/pyelonphritis?
CIPROFLOXACIN!!
others:
fluoroquinolone, amp+gentamycin, ceftriaxone
what is the most common nosocomial infection in the US? what is the tx protocol with this?
cathertized associated UTI
if asymptomatic don’t need to treat with abx
screen urine 48 hours after removing catheter
recurrent UTIs
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
consider self treatment at first sign (urine cup for UC)
vaginal estrogen in women since they have a decrease in lactobacillus
in asymptomatic bacteremia who do you treat (3) and who do you not treat (3)? *key!*
treat:
- pregnant
- before urologic procedures
- after renal transplant
DONT TREAT
- diabetics
- elderly
- patients with spinal cord injury or indwelling urethral catheter
do you tx UTI empirically while waiting for culture?
YES! then adjust abx as appropriate! :)
testicular torsion
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:
- negative prehns sign-no relief with elevation of the scrotiom
2. unilateral, swollen, retracted testicle
3. absent cremaster reflex
testicular torsion
2 dx?
3 tx?
DX:
- clinically
- doppler US shows decreased blood flow
TX:
- NSAIDS
- surgical detorsion and orchiopexy (make teste descended)
***GOAL: GET THIS ALL DONE WITHIN 6 hours!!!***
cryptochidism
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:
- absence of palpable testicle, or palpable within the inguinal canal
TX:
- SURGERY! by age 1 to prevent risk of infertility
what does having cryptorchidism increase your risk for?
increases risk of malignancy in undescending testis is 4-10 times greater than gerneral population
explain what falls under the two categories of uncomplicated UTI (2)
and
complicated UTI? (6)
uncomplicated UTI
- acute cysitits
- acute pyelonephritis
complicated UTI
- 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
phenylketonuria
what is this?
what happens in this?
screened for in?
TX? 2 key things?
inability to metabolize phenylalanine protein
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**
