8⼀GI/SURGERY/ID I Flashcards
1
Q
newly diagnosis Type 1 DM should be screened with which 3 antibodies?
_________________
Why do we do this?
A
[Anti-TissueTransGlutaminase(from anti🆃ED)= celiac disease]
[Anti-Thyroglobulin = thyroid disease]
[Anti-ThyroidPerOxidase = thyroid disease]
_________________
pts with DM1 have INC risk for other autoimmune conditions = must be screened at diagnosis
2
Q
Dx for Celiac disease - 4
________________
wt loss+ iron deficiency anemia + dermatitis herpetiformis = CELIAC!
A
“Celiac gluten-free… TWICED!”
[Anti-T.E.D. (IgA or IgG)]
➜ [DUODENAL BX FOR CONFIRMATION](GOLD STANDARD)
_________________
(TissueTransGlutaminase/Endomysial/DeaminatedGliadin)
(IgA test may result in false negative if concurrent IgA deficiency is present!)
3
Q
There are 4 Malabsorption syndromes - “_C_an Larry Control Stooling?”
Describe clinical features of Celiac disease (6)
A
“Celiac gluten-free… TWICED!”
- [Crypt hyperplasia / IEL / Villous atrophy]
- [INC Stool Osmotic Gap>125 a/w foul, flatulent, fatty, LARGE diarrhea with steatorrhea]
- [anEmia (microcytic iron deficiency anemia)]
- Weight loss
- Dermatitis Herpetiformis
- {[antiTED(IgA or IgG)] → duodenal bx} = Diagnostics
_________________
IEL = IntraEpithelial Lymphocytes
Tx = gluten-free diet
4
Q
What are the 4 malabsorption syndromes?
_________________
Which 2 have [INC stool osmotic gap > 125]
A
Can Larry Control Stool?
[Celiac / Lactose intolerance = INC stool osmotic gap>125]
Chronic pancreatiits / SIBO
5
Q
These cells are a/w ⬜
_________________
Describe the cp (5)
A
dx = atypical reactive lymphocytes
[EBV ⼀Infectious Mononucleosis]
_________________
- TIRED TEEN
- Fever
- exudative Tonsillitis
- cervical LAD
- HepatoSplenomegaly
6
Q
Why is primary management for BIDD primarily at-home supportive care with no abx?
_________________
When is antibiotic therapy for BIDD indicated? (4)
BIDD = Bloody Inflammatory Diarrhea Dysentery
A
healthy pts have self-limited BIDD
_________________
- [SEVERE (shock, etc)]
- [Prolonged > 7 days]
- [patient at risk for severe progression (immunocompro/elderly)]
- [bacterial pathogen identified ➜ give low dose px to prevent transmission]
_________________
SECCSY
7
Q
Aside from STAT Laparotomy, name 3 other treatments used in perforated peptic ulcer?
A
- IVF
- IVAbx
- IVPPI
+ STAT Laparotomy
8
Q
Serum Sickness etx
________________
What infection mimics this?
A
[Type 3 hypersensitivity reaction] involving INC circulating antibodies combining with antigens (Immune Complex) ➜ overload of normal clearance mechanisms ➜ activates complement = causes disease and
[SS fad (fever / arthritis diffusely / dermatitis)]
________________
Hepatitis B prodrome
(HBV also includes polyarteritis nodosa + glomerulonephritis)
9
Q
Having [1st degree relatives with CRC < 60 yo] modifies CRC screening schedule
Describe modified CRC screening (2)
A
[CScope at 40 yo (or 10y prior to relative’s age at their diagnosis)]
q5 years
10
Q
What causes Necrotizing fasciitis in
_____ patients?
a. healthy?
_________________
b. DM (poor circulation)?
A
a. polymicrobial
_________________
b. GASP
11
Q
Necrotizing fasciitis s/s (4)
A
- POOP
- swelling
- erythema
- fever
[DM = GASP] / [EE = polymicrobial]
12
Q
s/s GERD (2)
_________________
management? (2)
A
-[reflux/heartburn]
-cough
_________________
[daily PPI8 wk trial] + [lifestyle ∆]
GERD = sx > 2x/week
alarm sx (odynophagia/dysphagia/GI bleeding/wt loss) = referral for EGD
13
Q
dysphagia means difficulty ⬜
Describe the 2 types of dysphagia?
A
swallowing;
[Oropharyngeal upper dysphagia] = difficulty initiating swallowing (a/w coughing, drooling, aspiration) = nasopharyngeal laryngoscopy dx
_________________
[Esophageal Lower Dysphagia] = delayed sensation of “FOOD STUCK” in chest = EGD dx
14
Q
Describe the differences between the 2 types of Esophageal Cancer
A
UPPER esophagus = [SQC: (EtOH / smoking)]
_________________
lower esophagus = [ADC: (GERD / Barrett’s esophagus)]
15
Q
normal range for
LDL
A
<100
16
Q
normal range for
TAG
TriAcylGlycerides
A
<150
17
Q
normal range for
HDL
A
50+
18
Q
normal range for
TOTAL CHOLESTEROL
A
<200
________________
>240 = “HIGH”
19
Q
how do you diagnose Acute Pancreatitis? -2
________________
how do you diagnose CHRONIC Pancreatitis?
A
Lipase and amylase
________________
[MRCP Pancreatic Calcifications (or CT Abdomen)]
20
Q
cp for Chronic Pancreatitis -4
________________
dx = MRCP Pancreatic Calcifications
A
- epigastric abd pain that radiates to back
- better with sitting up and leaning forward (positions other abd organs away from inflammed pancreas)
- worst with meals
- fat malabsorption (bulky foul stools)
21
Q
Tx for CHRONIC Pancreatitis? -4
A
1st: stop Smoking/stop EtOH
2nd: small low fat meals with fat-soluble vitamin supplement
3rd: pancreatic enzyme supplement (i.e. low fecal elastase-1 level)
4th: Rx (TCA, NSAIDs, pregabalin)
22
Q
Causes of CHRONIC Pancreatitis? -4
A
- EtOH
- Cystic Fibrosis (peds)
- Duct obstruction (CA/stones)
- autoimmune
23
Q
Toxic Megacolon tx -3
A
[CTS if 2/2 IBD]
[Abx if 2/2 infectious colitis]
[Surgery if perforation]
________________
NO SULFASALAZINE OR OPIOIDS
24
Q
Barrett Esophagus MOD
A
chronic gastric acid ➜ [lower esophagus metaplastic replacement of {normal stratified squamous epithelium} with {intestinal columnar epithelium}] ➜ INC risk for esophageal ADC
25
Barrett Esophagus INC risk for developing ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
How is this screened for? -3
esophageal **ADC**
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
{[Sx*(Chronic GERD|frequent sx)* ≥5 years] + [≥2 risk factors*(White/Obese/Male/Smoker/Hiatal Hernia)*]}
**= endoscopic screening**
26
Why is chronic constipation a major risk factor for UTI?
Fecal retention ➜ rectal distension ➜ obstruct bladder emptying ➜ incomplete voiding ➜ stagnant urine ➜ promotes microbial growth ➜ UTI
27
Sulfasalazine is a ⬜ compound used for ⬜ **maintenance**
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Why should Sulfasalazine NOT be used acutely?
[5-AminoSalicyclic Acid] ; [IBD]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[Sulfasalazine 5ASA] can precipitate IBD attacks if used acutely
28
Which abx is best for intraabdominal infection?
Ampicillin-sulbactam
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*(3rd Generation PCN and beta-lactamase inhibitor)*
29
Functional Abdominal Pain
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Tx?
chronic ( ≥2 mo) adolescent periumbilical abd pain, with no identifiable pathology, and self-resolves in a few hours
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
tx = Symptom Diary
30
How does Peptic Ulcer Disease present? -3
**GAS**sx GOE1 mo
1. [epi**G**astricepigastric pain postprandial]
2. [**A**bd fullness postprandial]
3. [**S**atiety early on]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*get stool antigen test for H Pylori*
| *[GERD = (Cough + Reflux) > 2x weekly]*
31
Why is [aAVM] a cause of upper AND LOWER GI bleed? (3)
*(aAVM=angiodysplasia ArterioVenous Malformation)*
-aAVM...... can cause [SEVERE GI BLEED✳️] anywhere it occurs
-and (although aAVM mostly occurs in R ascending colon) it can potentially occur anywhere in the GI tract..which =
-aAVM is a cause of upper AND LOWER [SEVERE GI BLEED✳️]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
✳️= {in the setting of an [aAVM exacerbating RF *(Aortic stenosis|von willebrand dZ|renal dZ)*]}
32
In adults, what are the risk factors for developing Angiodysplasia - 3
## Footnote
*This can occur ANYWHERE in the GI tract but most commonly occurs in R Ascending colon*
1. Aortic Stenosis (vW multimers are disrupted as they pass through turbulent space --\> AVM)
2. Von Willebran disease
3. Renal disease
33
*Patient with newly diagnosed "incidentaloma" / L adrenal mass found incidentally*
What's your first step?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
When is surgical resection indicated? (3)
[adrenal hormone ***mud*** labs]
## Footnote
*(**m***etanephrine & VMA) + (**u**rine catecholamine 24h)+(**d**examethasone suppression test)
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*SURGICAL RESECTION:*
[radiographically malignant] vs [\> 4cm] vs [functional (hormone secreting)]
34
Primary presenting complaint for Achalasia
Food **AND** Liquid dysphagia
35
Peptic Stricture
common complication of chronic GERD - in which healing from chronic ulcerative esophagitis ➜ stricturing of Esophagus ➜ progressive (solid then liquid) dysphagia
36
Lactose intolerance sx (3)
*Lactose Intolerance* **D**efinitely **P**roduces **F**latulence
LactASE breaks down lactose ➜ glucose + galactose
1. **D**iarrhea WATERY
2. **P**eriumbilical abd pain
3. **F**latulence
* note: [MILK / ICE CREAM \> \> cheese / yogurt]*
37
Lactose Intolerance is a clinical diagnosis, but how is the diagnosis confirmed? (2)
## Footnote
*worst with age, asian and african american*
* L*actose **D**efinitely **P**roduces **F**latulence
1. Lactose breath hydrogen test
2. [Symptom resolution with Lactose-restricted diet]
38
Name the single-item predictors of INC SEVEREITY in Acute Pancreatitis (5)
"**HOBCO** *hurt the Pancreo*"
= SEVERE ACUTE PANC
1. **B**UN ≥20
2. **H**CT \>44%
3. **C**RP \>150
4. **O**besity
5. **O**ld age
39
What is OculoGlandular syndrome?
Bartonella Henselae cat-scatch variation in which pt develops **conjunctivitis** + [iPL preauricular and cervical **LAD]**
## Footnote
*most common complication of Cat Scratch Disease = lymph node suppuration*
40
describe cp of Pyoderma gangrenosum (2)
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Where does it come from? (2)
****_P_**AINFUL** inflammatory [nodules/pustules/vesicles] ➜ ****_P_**AINFUL** ULCERS
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
neutrophilic dermatosis a/w IBD
41
normal range
Lipase
\<160
42
⬜ occurs after acute pancreatitis in 10% of patients, and although sx depend on mass effect, presentation may include (⬜4)
[pancreatic pseudocyst IFC] ;
Abd pain / GI hemorrhage / ductal obstruction / [fistulization into adjacent organs]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*tx = supportive --(if persist)--\> endoscopic drainage*
43
# In a [HIV⊕] pt c/f PCP PNA
*HIV+ pt with high clinical suspicion for PCP PNA has an initial ⊝[induced sputum sample]*
Why is it important to obtain additional w/u in this patient, even despite an initial ⊝[induced sputum sample]?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Name the additional w/u that should be obtained next?
In 10% of ⊕PCP cases, PCP organism was unable to be identified from [induced sputum samples]
--(so if ISS negative **but high clinical suspicion**)--\>
[BAL via fiberoptic bronchoscopy]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*BAL= BronchoAlveolarLavage*
44
Why do [HIV patients with PCP] sometime additionally need CTS (in addition to abx)?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Which [HIV patients with PCP] should receive it?
In Mod/Severe PCP, within first 2-3d of treatment, organism lysis ➜ potentially fatal inflammatory lung response ➜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
add CTS if:
## Footnote
1. [(ALVeolar-arterial O2 ∆ ≥ 35) *on ABG*]
\_\_\_\_\_\_\_\_OR\_\_\_\_\_\_\_\_\_
2. [(PaO2 \< 70) *on* *Room Air*]
45
name the 3 most important goals in managing a brain-dead organ donor
MAINTAIN NORMAL **"TV, B"**
**T**emperature (or slightly hypOthermic)
**V**olume (IVF/desmopressin*(synthetic ADH)*)
**B**lood pressure (pressors)
46
What is GGT used for?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*gamma-glutamyl transpeptidase*
Differentiates elevated ALP:
[⇪ALP **and ⇪GGT**] = LIVER origin
47
[Isolated Markedly elevated ALP (+/- ⇪ GGT)] indicates ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
what causes this? (2)
[infiltrative Liver disease]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
## Footnote
1. [granuloma (hepatic sarcoidosis, TB)]
2. [metastatic CA]
48
In patients with [NAFLD/NASH], what is the single best predictor for liver-related death?
**⊕HEPATIC FIBROSIS**
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*[**⊕HEPATIC FIBROSIS**] ➜ Cirrhosis ➜ liver-related Death]. (Wt loss can reverse [HEPATIC FIBROSIS] if it occurs prior to Cirrhosis)*
49
Angiodysplasias (AKA⬜ ) are defined as ⬜5.
Although only a small amount bleed, which conditions ⇪ Angiodysplasia bleeding? (3)
arteriovenous malformation ;
aAVM =
1. elderly
2. [cherry red lesions (on cscope)]
3. composed of [multiple aberrant *fragile* AVM in
4. [*(especially R Colon)*GI tract]
5. aberrancy ➜ [low threshold for [occult vs MASSIVE nonpainful GI Bleeding] i\ [any hemostasis❌]
| *[aAVM = angiodysplasia ArterioVenous Malformation]*
## Footnote
1. {[**ESRD** (*uremia ➜ platelet dysfxn ➜ [1º hemostasis❌] →🩸
2. [**Aortic stenosis** (*mechanical disruption during turbulent valvular flow ⬇︎ vWF → [1º hemostasis❌] →🩸= Heyde's Syndrome
3. **[von Willebrand disease]***→ [1º hemostasis❌] →🩸* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_x\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
🩸= [(in setting of ⊕aAVM) may meet threshold for aAVM to bleed]}
50
pathophysiology of toxic shock syndrome
[exotoxin superantigens] (*usually from Staph A*) activate T cells widespread ➜ massive cytokine release
*may require up to 20L per day of IVF resuscitation*
51
What is the best test to evaluate Pancreatic Cyst?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
what are all the indications for this modality? -7
Endoscopic Ultrasound with aspiration
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
## Footnote
1. lymph node bx
2. pancreas lesions
3. liver lesions
4. adrenal glandlesions
5. bile duct lesions
6. peritoneal fluid lesions
7. pleural fl;uid lesions
52
indications for ERCP (4)
***THERAPEUTIC***
## Footnote
dilated Common Bile Duct
acute biliary pancreatitis
choleDocholithiasis
cholangitis
53
HIV test is done on an opt [⬜ (in | out)] basis
What does this mean?
**OUT**
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Patients are informed that HIV test will automatically be performed UNLESS THE PATIENT SPECIFICALLY **OPTS OUT**
*patients have the right to refuse/ opt OUT HIV testing*
54
Acute diverticulitis presents as (⬜2)
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
How is it managed?
[LLQ TTP] + [CT focal bowel wall thickening +/- diverticula]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
55
[Dyspepsia (***GAS** sx ≥1 mo*)]
management
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
trial PPI = [PPI]4-8w
56
pulmonary ASPERGILLUS
What are the major risk factors? (4)
immunosuppression *[transplants✳, neutropenia, chronic CTS, HIV/AIDS]*
| ✳*stem cell|organ*
## Footnote
*"bloody⼀chest ⼀cough"*
57
pulmonary ASPERGILLUS
treatment (3)
## Footnote
*"bloody⼀chest ⼀cough"*
58
pulmonary ASPERGILLUS
diagnostics (4)
1. [CT ground glass *"halo sign"* nodules]
2. ⊕[Galactomannan]
3. ⊕[β-D-glucan]
4. [Sputum sample*for fungal stain & culture*]
## Footnote
*"bloody⼀cough ⼀chest"*
59
pulmonary ASPERGILLUS
classic symptom triad
*"bloody⼀chest ⼀cough"*
## Footnote
1. *bloody* = [**bloody** cough hemoptysis]
2. *chest* = pleurtic **chest** pain
3. *cough* = [bloody **cough** hemoptysis]
60
Oral Candidiasis
treatment (3)
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*AKA thrush*
[topical Nystatin *suspension*🆚Clotrimazole troches]
--(if persist)--\> [fluconazole PO]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*be sure to watch for proper CTS inhaler usage*
61
What should some patients be cautious of when they stop smoking? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
What can be done to mitigate this? (2)
[**WEIGHT GAIN** up to 30lb (Varenicline \> NRT = burpoprion)] is common after you stop smoking!
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Advise **overweight patients** ➜ [[reduced calorie diet ( ≥1200kcal/day)] and regular exercise] - *if ≤1200kCal/day ➜ smoking relapse*
*NRT = Nicotine Replacement Therapy*
62
Why are [Hepatitis A vaccination] and [Hepatitis B vaccination] so important to a person with Hepatitis C?
if superimposed with HAV or HBV, chronic H**C**V causes rapid decompensation and liver failure
so vaccination to HAV and HBV are important
63
In terms of **Hepatitis B**,
how do you manage a healthcare worker s/p incidental *occupational exposure*?
64
*Rhabdovirus Rabies*
Tx? (2)
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Prognosis? (3)
[Ig + Vaccine]-(*only helpful BEFORE symptom onset*)
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
**UNIVERSAL FATAL WITHIN WEEKS ONCE SYMPTOMATIC**
## Footnote
\> Coma / Respiratory failure
65
In the U.S., rhabdovirus rabies is acquired from ⬜ , but in the developing world rhabdovirus rabies is acquired from ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
What is the hallmark sign of [Rhabdovirus Rabies]?
[BATS (*since* *U.S. dogs are immunized*)] ; dogs
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
**HYDROPHOBIA** *( fear of drinking 2/2 [water-triggered pharyngeal spasms])*
66
Hepatitis C screening is done via ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
A patient with a positive HCV screening indicates what 3 possibilities?
HCV Ab testing
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
1. [ACTIVE INFECTION *(obtain HCV RNA to determine acute vs chronic)*]
2. [Resolved Infection]
3. False Positive
67
Spontaneous Bacterial Peritonitis is a serious complication of ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Treatment? (4)
cirrhosis
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[Paracentesis w/*ascites labs("**G**uts **C**an **N**ever **T**otally **S**uck") *]
➜[Albumin IV]
➜ {[CefoTaxime3ºCPN]
➜ [Fluoroquinolone *px*]
* * *
* 3ºCPN = 3rd gen cephalosporin*
68
Spontaneous Bacterial Peritonitis is a serious complication of ⬜
cirrhosis ( can → SBP)
69
Spontaneous Bacterial Peritonitis is a serious complication of ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
clinical presentation? (6)
cirrhosis
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
**1. Fever ≥37.8C**
**2. Abd pain**
**3. [AMS (abnl connect-the-dot test)]**
4. [*hypOtensionw/SEVERE INFXN*]
5. [*hypOTHErmiaw/SEVERE INFXN*]
6. [*paralytic iLeusw/SEVERE INFXN*]
70
What is the MELD score?
and how is it used?
**MELD** = **M**odel for **E**nd stage **L**iver **D**isease = predicts 90-day survival in Liver Disease patients = ranks Liver Transplant List
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
***"*****MELD***uses**BICS** to rank Liver Transplant List"*
**B**ilirubin
**I**NR
**C**reatinine
**S**odium
71
What is Succussion splash?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
What does it indicate?
audible epigastric splashing sound during sudden movement
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
delayed gastric emptying
## Footnote
*2/2 gastroparesis vs intrinsic obstruction vs extrinsic obstruction*
72
pt p/w [+ succussion splash] is c/f ⬜ which can be caused by (⬜3). Management for this starts with ⬜, and sometimes ⬜.
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
How is this diagnosis confirmed?
[delayed gastric emptying] ; [intrinsic obstruction / EXtrinsic obstruction / gastroparesis] ; [EGD to r/o obstruction] ; [CT/MR enterography]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[scintigraphic gastric emptying study]⼀***confirms gastroparesis***
73
Diabetic gastroparesis often p/w ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
treatment? (2)
[delayed gastric emptying (*succussion splash*)]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[*_F_*meals] --(if persist)--\> [metoclopramide]
## Footnote
[*_F_*meals : *_F_*inite(small), *_F_*req, *_F_*atless(low fat), *_F_*iberRICH(HIGH soluble fiber)]
74
cp of travelers' diarrhea?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
most common cause?
3d self limited [**WATERY DIARRHEA** + crampy abdP] 3 days post exposure
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
E*T*EC
## Footnote
*EnteroToxigenic E Coli (commonly from developing countries' street vendors)*
75
Which 2 labs must be carefully monitored before and after starting TPN?
why?
Phosphate and K+ (from **P**TM**K**)
; [TPN contains dextrose ➜ insulin secretion ➜ insulin drives serum phosphate and serum K+ intracellular ➜ hypOphosphatemia] -*this is a component of refeeding syndrome*
76
Refeeding Syndrome etx
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
How are alcoholics especially affected by this?
[*Refeeding* after severe starvation (think homeless/alcoholics)] ➜ surge of insulin ➜ [**PTMK** shift into intracell] ➜
VERY LOW **PTMK**
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
1. [**P**hosphorous ⬇︎] = [rhabdomyolysis/ ⇪ CPK in EtOH] and/or HF
2. **T**hiamine ⬇︎ = HF
3. **M**g⬇︎ = arrhythmias
4. **K**+ ⬇︎ = arrhythmia
77
Refeeding syndrome can lead to the depeletion of serum Phosphorous and 3 other electrolytes such as ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
How is Phosphorous repletion administered?
**PTMK**
## Footnote
*(**P**hosphorous/**T**hiamine/**M**g/**K**)*
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
**ORAL** Phosphorous repletion
78
Aside from IVF, which medication should be given promptly in Acute Variceal Hemorrhage?
Octreotide IV
79
Which 2 medications can be given to *prevent* Acute Variceal hemorrhage?
Nadolol 🆚 Propranolol
(*general BBlocker [⬇︎portal system pressure] + band ligation +endoscopic surveillance*)
80
what is charcot's triad?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
what is Reynolds pentad?
## Footnote
cholangitis dx =cholangitis siLx = cholangitis sxCharcot triad + cholangitis ixERCP/US/CT with Biliary Dilation + cholangitis LxCholestasis labs
81
acute Cholangitis is diagnostically confirmed *and* treated with ⬜ .
What is the initial diagnostic criteria for acute Cholangitis? (3)
ERCP (*provides life saving biliary drainage*);
Cholangitis sx
= *Charcot's triad*
Fever
Jaunndice
[RUQ abd pain 2/2 evidenced biliary obstruction]
| later f/b → [ERCP/US/CT with biliary Dilation] + [cholestasis labs]
## Footnote
cholangitis dx =cholangitis siLx = cholangitis sxCharcot triad + cholangitis ixERCP/US/CT with Biliary Dilation + cholangitis LxCholestasis labs
82
# nonpainful hematochezia
in patients \> 40 yo should you make you s/f what diagnosis?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
What causes this?
Diverticulosis
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Within 1 of the outpouches of the colon wall (*AKA diverticula*), at the point of weakness (where the vasa recta penetrates the circular muscle layer) , the penetrating artery becomes increasingly exposed as it herniates thru muscular layers ➜ **erosion or trauma to overlying mucosa of that penetrating artery** ➜ brisk bleeding (*melena if in R colon*)
83
What is the cause of rectal bleeding in internal and external hemorrhoids?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
How do hemorrhoids present? (4)
Dilation of submucosal venous plexus ➜
- **small** volume hematochezia covering the stool
- perianal itching
- mucus +/- mild fecal leakage
- [Internal: NO pain / External: Painful]
84
*pt s/p infectious mono 3 weeks ago, p/w persistent LAD*
How do you manage persistent LAD?
pts with *persistent* localized LAD should be observed x 4 wks ➜ biopsy if persistent nodes fail to resolve after 4 wks
85
In an immunocompromised pt, **EBV DNA in the CSF** raises suspicion for what condition?
Primary CNS lymphoma
## Footnote
*MRI: Solitary **Weakly** ring-enhancing mass in periventricular region*
86
Dx for EBV infectious mono - 2
1. [positive **HAMS***only accurate during **week 1** of sx 😟*]
2. Anti-EBV test
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*HAMS = [Heterophile Antibody MonoSpot**only accurate during **week 1** of sx 😟*]
*No sports for ≥3weeks because of splenomegaly!*
87
Tx for EBV infectious mono - 3
1. [self limited x weeks (fatigue x months)]
2. NSAIDs
3. No sports ≥3wks
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*HAMS = [Heterophile Antibody MonoSpot]*
88
From a lab perspective, how do you differentiate CMV from EBV?
CMV will have a [**negative** *HAMS*]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*HAMS = [Heterophile Antibody MonoSpot]*
89
[T or F] Airway obstruction is a severe complication of [EBV infectious mononucleosis]
TRUE!
*(give CTS if airway obstruction, severe infection, aplastic anemia or thrombocytopenia develops)*
90
# Diagnosis?
Treatment? -4
Acute Paronychia (Nail**fold** infection 2/2 gram positive skin flora)
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
**NAIL** tx
[**N**eosporin/TOP antiseptics]
[**A**bx TOP]
[**I** & D abscess]
[**L**ukewarm soaks]
91
Clinical triad of [Reiters Reactive Arthritis]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
When do sx onset? resolve?
*'Can't see, Can't pee, Can't climb a tree'*
## Footnote
* Can't see (conjunctivitis / ANT uveitis)
* Can't pee (urethritis / [circinate balanitis ⼀penile nonpainful coronal lesions])
* Can't climb a tree (LE asymmetrical oligarthritis, [keratoderma blenorrhagica ⼀waxy yellow papules on palms/soles])
-onset within 4w of GU/GI infxn ➜ resolves after 4mo
92
Why should Chlamydia infection (symptomatic or asymptomatic) always be treated?
chronic Chlamydia may ➜ Reiters Reactive Arthritis
93
# Patient presents with penis rash 2 weeks after having dysuria
diagnosis? | How do you confirm this? treat this?
[RReA ⼀[circinate Balanitis 2/2 chlamydia trachomatis]] ; [**urine** Chlamydia NAAT] ; [chlamydia abx + penile topical CTS]
*RReA = Reiters Reactive Arthritis*
94
Name the 3 classic symptoms of dyspepsia
indigestion **GAS**
**G**astric (*epigastric*) pain/burning postprandial
**A**bd fullness postprandial
**S**atiety early on
95
# dyspepsia
etx (4)
*difficulty digesting food* *2/2*
## Footnote
[IDIOPATHIC functional] \> [gastric ADC = HPylori ulcer = NSAID ulcer]
*➜ **GAS** sx GOE1mo*
96
# dyspepsia presents with what 3 sx ?
How long should these sx last for official dyspepsia diagnosis?
**GAS** = **G**astric sx postprandial/**A**bd fullness postprandial/**S**atiety early on
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
GOE1 month
97
# dyspepsia presents with what 3 sx ?
Upper GI endoscopy is indicated for dyspepsia [HIGH risk alarm features]
What are they? (7)
[**GAS** = epi**G**astric ∆ /**A**bd fullness postprandial/**S**atiety early on] GOE1mo
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
| ∆ = pain|burning
## Footnote
- ⊕fam hx gastric ADC
- odynophagia
- dysphagia
- IDA
- wt loss
- LAD
- [ age > 50]
98
how does biliary colic present? (4)
* *benign* [RUQ or epigastric pain] with radiation to [back or R shoulder]
* a/w [NV, diaphoresis]
* \<6h
* +/- triggered by fatty meals
99
# biliary colic
etx?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
how is it diagnosed?
If [gallstones (*shadowed* echogenicity)] or [sludge (*bare* echogenicity)] get stuck in cystic duct, episodal gb contraction ➜ episodal [RUQ/epigastric pain with R shoulder/back radiation \< 6h] = biliary colic
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
TAUS
*TAUS = TransAbdominal US*
100
How do you workup patient with suspected uncomplicated Gallstones? (8)
101
What is Cholescintigraphy ?
* uses technetium-labeled HIDA to evaluate cystic duct, CBD and ampulla in patients with suspected cholecystitis but negative TAUS*
*AKA HIDA scan*
*alternative dx for cholecystitis*
102
# Chikungunya is a mosquito borne virus that causes ⬜ and ⬜
treatment? | prognosis?
[high fever \> 39C] / [severe symmetrical polyarthralgia (BL hands/BL wrist/BL ankles)]
tx = [self limited to 1 wk = supportive]
pgn = [70% develop chronic arthralgia = MTX]
103
[T or F] patients with Syphilis MUST have lumbar puncture if HA is present
Why or Why not?
TRUE \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
any syphilis patient with any neuro ∆ require neurosyphilis r/o via neg [LP CSF **VDRL**] or neg [LP CSF **FTA-ABS**].
104
Tx for **Neuro**syphillis
[aPG 4MU]
[q4h]
[x 14 days]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*(aPG = aqueous PCN G - IV) /* *(MU = million units)*
105
# PCN G(BPG vs aPG) is the first line tx for Syphilis
The alternative tx to Syphilis is \_\_\_\_
When is it indicated to desensitize and still give PCN G(BPG vs aPG) to a [PCN allergic patient]?-3
Doxycycline
1. [Pregnancy (No DOXY for POXY)]
2. refractory to initial (doxycycline)tx
3. [3B5º neurosyphilis]*3B5º requires {aPG 4MU q4h x 14d}*
106
How do you know when a pt is fully cured from Syphilis?
**4**-fold ⬇︎in FTA Ab titer by 12 month mark AT THE LATEST
107
Name the specific signs of congenital syphilis - 3
*"syphilis hurts the baby's **SKIN, NOSE & BONES!**"*
## Footnote
1. SKIN: Maculopapular palms/soles_rash that desquamates vs bullous
2. NOSE: Rhinorrhea
3. BONES: mulberry molars, long bone metaphyseal lucency
108
Describe the type of rash you'll see with secondary syphilis
Diffuse Maculopapular rash **starting at trunk and spreading to extremities TO INCLUDE PALMS AND SOLES**
109
Why is RPR not reliable when a person first develops syphilis?
There is a possible [false negative RPR] early in infection - follow with FTA
110
Any RPR Titer greater than ___ is high syphilis titer (positive result)
1: 16
*anything where they had to dilute it MORE than 16 times is HIGH RPR Syphilis titer*
111
Tx for {**CLUB**} Syphilis :
[**C**V]⼀[**L**ate latent ≥12 mo]⼀[**U**nknown duration]⼀[**B**all•Gumma]
[BPG 2.4MU]
[q week]
[x 3 weeks]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*(BPG = BENZATHINE PCN G -IM) /* *(MU = million units)*
112
Tx for {**SEC**} Syphilis :
[**S**econdary Systemic Sx]⼀[**E**arly latent \<12mo] ⼀[**C**hancre primary]
[BPG 2.4MU]
x 1
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*(BPG = BENZATHINE PCN G -IM) /* *(MU = million units)*
113
What other stages of Syphilis share the SAME TREATMENT as
[Early latent \<12 mo] -2
[Chancre primary]
[Secondary Systemic sx]
114
Tx for **Congenital** syphillis
[aPG 50,000 u/kg/dose]
[q10h]
[x 10 days]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*(aPG = aqueous PCN G -IV) /* *(**MU = million units)*
115
# Positive syphilis serology but no symptom stage = ⬜
What sx make up ____ stage
Primary syphilis? -2
Secondary systemic?-3
Tertiary?-4
Latent ;
1Aº = [Chancre primary]
1B: [CNS invasion (asx vs meningovascular vs 👁️vs🦻)] --> *3B2*
2Aº = diffuse rash / condylomata LATA
2B= early latent = asx
2C = late latent = asx
3A = lifetime latent
3B1= CV
#3B2= NEURO
#3B3= BALL GUMMA
3º = Neurosyphilis / CV aortitis
116
What is the Jarisch Herxheimer reaction?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
How can it be prevented?
2 day long acute fever after initial syphilis treatment
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
THERE IS NO EFFECTIVE PREVENTION AT THIS TIME
117
How do you manage Dumping syndrome? (4)
1. High protein diet
2. low carb diet
3. small meals
4. frequent meals
*goal is to DEC passage of food into small intestine*
118
What are the 3 criteria for diagnosing Liver Failure?
**ELI** has Liver Failure!
1. **E**ncephalopathy
2. **L**iver injury evidence (*transaminitis*)
3. **I**NR GOE1.5
119
# HDS Pt with HBV Surface antigen, and [HBV CoreIgM] has diagnosis ⬜
Explain the dispo for this patient
[Acute Hepatitis **B** infection] ; Because acute HBV is not likely to deteriorate into LIVER FAILURE, and usually resolves spontaneously ➜
-[outpatient supportive care and follow up] \> [Hospitalization only for HIGH RISK\*]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*HIGH RISK = HDUS, high fever, many comorbidities*
120
Describe Serology for Hepatitis B -8
S - **S**E**C** - SCEb - Core*m* - CEbSAb - CSAB - Core*G* - SAb
## Footnote
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*unvaccinated pts acutely exposed to HBV should STILL get HBV vaccination in addition to the HBV immunoglobulin*
* * CSAB = RESOLVED HEP B INFECTION*
121
Most common side effects of [INH (isoniazid)] -2
**I**njuries to **N**erves and **H**epatocytes
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
**N**europathy (Pyridoxine B6 = tx/px)
**H**epatitis - THIS IS SELF LIMITED AND RESOLVE WITHOUT INTERVENTION
122
The Hepatitis A vaccine is recommended for which groups - 3
1. Travelers going to countries where HepA is present
2. Gay Men
3. Chronic Liver Disease
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Hepatitis A can cause **SIGNIFICANT but benign TRANSAMINITIS** so do not be alarmed by this
self limited to 1 month
123
What 2 laboratory values are the best diagnostic test for [acute Hepatitis B infection]?
S - **S**E**C** - SCEb - Core - CEbSAb - *CSAB* - SAb
[**S**Ag and **C**oreIgM]
124
# HDS pt presents with [HBV SAg] and [HBV CoreIgM]; consist with diagnosis ⬜
Explain the management (3)
[acute HBV];
*after [acute H**B**V] initial dx:*
a. [Transaminase normalize ≤2mo]
b. [HBV(SAg and DNA) clear ≤6mo --(*AND IF NOT)* = [Chronic HBV-5% chance ( ➜ Liver Failure)]
c. so…[Monitor & **Obtain HBV serology at 6 mo mark** to assess progression]
125
After acquiring [acute HBV], what is the risk of developing *Chronic* Hepatitis B?
5%
(based on age)
126
# Normally, positive TST = induration ⬜ mm and at minimum indicates ⬜
▶Explain how the BCG vaccine affects the TST? (2)
▶▶How do you mitigate this?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*TST= Tuberculin Skin Test*
> *≥15 mm ; ⊕[Latent TB infection]*
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
▶ [BCG Vaccine] sensitizes Host to Tuberculin ➜ up to 20 mm *artificially* robust induration when given TST later (even if pt never had TB) ➜ **INC False Positive TST**
▶..BCG Vaccine effect wears off after 15 years ➜ Host becomes less sensitized to tuberculin after 15y =
▶▶LTBI screening: [**TST (***BCG vaccine in past 15y?***)IGA** ]
127
# Sepsis is generally defined as ⬜-5
What is the _clinical criteria_ for
Sepsis? -2
**SEVERE** **INFECTION(GramPOS > gramneg)** that (2/2 dysregulated immune response) → life-threatening:
▶SIRS,
▶[proinflammatory and anti-inflammatory *widespread* tissue injury],
▶distributive shock
▶end-organ system dysfxn
* * *
infection
+
[≥2 organ system dysfxn](defined as acute [SOFA ∆ ≥2] ]
128
For patients with Sepsis, [*SIM⼀Sepsis Initial Management* ( ⬜4 )] must be executed within ⬜ in order to ⬇︎ Mortality
*SIM*LBAF (*Lactate/BCx/Abx/Fluids*)
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[first1-3H]
129
What is the clinical definition of
Septic Shock? -2
{[Sepsis(infection + ≥2 organ system dysfxn)] + [refractory hypOtension(vasopressor, lactatemia]}
130
What is gastroparesis? (3)
1. [**GPICC** parasympathetic impairment] from *(DM/Anticholinergic Rx / Vagus❌)*]
2. ➜ [gastric smooth m] dys-synchronous contraction ➜ delayed gastric emptying
3. = [dyspepsia *with succussion splash* sx]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*[GPICC] = [Gastric Pacemaker Interstitial Cells of Cajal]*
131
Describe the symptom triad for [Disseminated Gonococcal infection]
1. [**S**everal migrating asymmetric joint pain (or purulent monoarthritis)]
2. **T**enosynovitis ⼀pain with *passive* extension and/or TTP over flexor sheaths
3. **D**ermatitis
*note: dx = [+ gonorrhea urogenital NAAT]*
132
# Stress Ulcers have multiple causes
What are the indications for *(i.e. the major causes of)* Stress Ulcer Prophylaxis? (10)
*stress ulcer from {[**GIVE**\_**BS**] ≥1| [**sico**] ≥2}*
## Footnote
*≥1*
[**G**I bleeding or GI ulcer in last 12 mo]SHOCK
[**I**NR\>1.5(or [platelet<50K] or [PTT>2x normal control] ⼀coagulopathy)]
[**V**entilator \>48h]
h**E**ad trauma
**B**urn severe
**S**pinal cord injury
* * *
* ≥2*
**s**epsis
[**i**CU \> 1wk]
**c**TS
[**o**ccult GI bleeding \> 6d]
133
# Stress Ulcers have multiple causes
What 2 medications are used for Stress Ulcer Prophylaxis?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*{ [**GIVE**\_**BS**] ≥1| [**sico**] ≥2}*
PPI \> [H2 R Blocker]
134
# Stress Ulcers have multiple causes and require PPI px
How does [h**E**ad trauma] cause stress ulcer?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*{ [**GIVE**\_**BS**] ≥1| [**sico**] ≥2}*
Head trauma ➜ [INC gastrin secretion] ➜ [parietal cell acid secretion] ➜ stress ulcer
*PPI \> H2 R Blocker = px*
135
# Stress Ulcers have multiple causes and require PPI px
How does [**i**CU \> 1wk]Critical Illness cause stress ulcer?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*{ [**GIVE**\_**BS**] ≥1| [**sico**] ≥2}*
[INC uremia & bile salts (INC by virtue of critical illness)] reflux in the stomach ➜ both disrupt protective glycoprotein ➜ [INC gastric mucosa permeability] ➜ stress ulcer
*PPI \> H2 R Blocker = px*
136
# Stress Ulcers have multiple causes and require PPI px
How does hypOtensive Shock cause stress ulcer?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*{ [**GIVE**\_**BS**] ≥1| [**sico**] ≥2}*
hypotension ➜ gastric mucosa ischemia ➜ INC permeability ➜ stress ulcer
*PPI \> H2 R Blocker = px*
137
What are Spider Angiomas?
[*Blanching* bright red papules **surrounded by outward radiating vessels**]
(2/2 dilated central arterioles from cirrhosis)
138
# pts with [HIV and on HAART] often develop which metabolic condition?
Describe the features of this metabolic condition (4)
[HIV lipodystrophy **DIVE**]
## Footnote
**D**yslipidemia
**I**nsulin resistance
[**V**isceral obesity (lipoatrophy + buffalo hump)]
**E**levated CVD risk
139
# pts with [HIV and on HAART] often develop which metabolic condition?
Due to [**E**levated CVD risk] this condition causes, which medication should be initiated if these [HIV HAART] pts have [CVD10Y \>7.5%]?
[HIV lipodystrophy **DIVE**]; *RAP*statin
## Footnote
*RAPs*tatin (Rosuvastatin or Atorvastatin or Pravastatin)
140
Mngmt for Diverticulitis (4)
- Colonic Bacterial Abx
- NPO
- IVF
- rule out colon CA
141
MOD of [AMBIC- Acute Mesenteric Bowel ischemic colitis]
[IMA low blood flow state + underlying nonocclusive atherosclerosis] ➜ inadequate [Left Descending Colon] and [Sigmoid Colon] arterial perfusion --\> Ischemia = [periumbilical POOP with hematochezia]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*CTA revealing thickened bowel wall 2/2 [bowel wall free air & edema](also seen in diverticulitis)*
142
[AMBIC - Acute Mesenteric Bowel ischemic colitis]
Sx (5)
1. periumbilical **POOP**
2. hematochezia
3. Rebound
4. Guarding
5. [NV ➜ hypOkalemia]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
* POOP = Pain Out Of Proportion*
* CTA revealing air & edema in bowel wall--\>thickening = AMBIC*
143
[(AMBIC) Acute Mesenteric Bowel ischemic colitis]
Labs (4)
* AMBIC* ⇪ **WAHL** *products!*
1. **W**BC ⇪
2. **A**mylase ⇪
3. **H**gb ⇪
4. [**L**ACTATE ⇪ ➜ metabolic acidosis]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*CTA revealing air & edema in bowel wall --\> thickening = AMBIC*
144
[(AMBIC) Acute Mesenteric Bowel ischemic colitis]
Mngmt (6)
1. O2
2. IVF
3. [Abx: CefTriaxone vs. (Levoflox + flagyl)]
4. Pain control
5. Heparin (if clot present)
6. Laparatomy
*[CTA: bowel wall thickening from air & edema]*
145
[(AMBIC) Acute Mesenteric Bowel ischemic colitis]
Dx (2)
**[CT Angiogram (bowel wall thickening from air/edema)]**
vs. [Mesenteric Angiogram]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
146
Diverticulitis Dx
**CT** revealing [bowel wall FREE AIR & edema]
147
*AMBIC and Acute Diverticulitis have similar clinical presentations*
What main sx differentiates AMBIC from Acute Diverticulitis?
AMBIC = **BLOODY DIARRHEA**
Diverticulitis = nonbloody Diarrhea
148
In addition to analgesia, what is the tx for acute Herpes Zoster? -2
[valacyclovir PO]7d \< [rash 3 days old]_\__*_≤\__*_[ZINC OXIDE CREAM]_
\_\_\_\_\_\_\_\_**+**\_\_\_\_\_\_\_\_
analgesia
149
# [Primary Biliary **Cirrhosis**]
clinical features (4)
1. {[intrahepatic bile duct] autoimmune obliteration with fibrosis ➜ [**ALP ⇪ ⇪ ⇪]**}etx
2. {asx ➜ [Fatigue + Pruritus + (Xanthelasma HLD*(from ⇪ cholesterol)* + ⇪*TOTAL*conjugated Bilirubin ]}sx
3. [AMA]dx
4. ={[UrsoDeoxyCholic Acid ➜ Liver Transplant(CURE)]}tx
| *AMA = Antimitochondrial Antibody*
150
In the U.S., water soluble vitamin deficiencies are 2/2 ⬜, ⬜ and ⬜
* [chronic EtOH],
* [restrictive diets (anorexia nervosa)],
* [malabsorption syndrome]
151
What are [Riboflavin B2] deficiency sx? (2)
- Angular cheilitis
- Stomatitis
152
[Niacin B3] deficiency sx (4)
[Pellagra **DDDD**]
1. **D**ementia
2. [**D**ermatitisphotosensitive]
3. **D**iarrhea
4. **D**eath
153
# A patient has [(⊕TST|IGA) but no TBsx and no CXR findings] = ⬜ diagnosis
Based on this diagnosis, what can you tell them about their diagnosis? (3)
[Latent TB Infection] is…
1. **NOT CONTAGIOUS** ⼀pt can attend work/school without restrictions
2. risk of conversion to [Active TB Infection] is low ➜
3. _ONLY_ immunocompro or congregant occupants need to consider [Latent TB infection] treatment
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*congregant occupant = occupies congregated areas (HealthcarePersonnel, inmates*)
154
Most organizations recommend 2 step pre-employment testing for Tuberculosis. What does this mean?
Why is this done?
people with an initial negative TST have to repeat their TST in 1-3 wks
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
…this is because people exposed to TB in the past might have desensitized reaction (DEC production of TNFα, IFNγ, IL8) on their TST ➜ false negative TST
155
After finishing their treatment regimen, when are patients with [active TB infection] considered no longer infectious?
after [3 consecutive **negative** [AFB sputum smears]]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*[AFB=Acid Fast Bacilli] | 24h intervals and GOE 1 morning sample*
156
# treatment for HPylori is typically ⬜
What tx do you give if [initial therapy failed] or [patient is resistant or allergic to one of the drugs]?
[**PAC**]14d --(if persistent/allergic/resistant)--\> [**PBMT**]14d
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
* [PAC = **P**PI + **A**moxicillin + **C**larithromycin]*
* [PBMT = **P**PI + **B**ismuth(or diff abx) + **M**etronidazole + **T**etracycline]*
157
HPylori is a strong risk factor for developing which 3 conditions?
1. PUD
2. gastric ADC
3. MALT lymphoma
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*tx = PAC14d--(prn)--\> PBMT14d*
158
How is Misoprostol related to NSAIDs?
Miso**pros**tol is a **pros**taglandin that inhibits gastric acid secretion and improves mucus defenses = prevents ulcers a/w NSAIDs
159
# HPylori eradication confirmation is used in 3 High Risk situations
HPylori has high rates of treatment failure and so HPylori eradication confirmation should be implemented in what [3 *HIGH RISK* situations]?
1. persistent symptoms
2. HPylori associated ulcer on endoscopy
3. HPylori associated MALT
160
# HPylori eradication confirmation is used in 3 High Risk situations
Name the 2 most common methods of [HPylori eradication confirmation]
GOE4w after completing [initial triple *[PAC]14d* ] ➜
## Footnote
- urea breath test *or*
- HPylori stool antigen test
* * *
* tx = PAC14d--(prn)--\> PBMT14d*
161
# HPylori eradication confirmation is used in 3 High Risk situations
What tx is given if [initial HPylori tx]*(PAC*14d*)* fails? -4
| *fail = [⊕Urea breath test] 🆚 [⊕HPylori Stool Antigen test]*
[**PBMT**]14d
*[PBMT = **P**PI + **B**ismuth(or diff abx) + **M**etronidazole + **T**etracycline]*
162
a. HealthcarePersonnel should determine pre-employment TB baseline using what 2 options?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
b. How do you apply this to anyone who've received the BCG vaccine in the past?
c. Explain why
a.
- TST
- IGA
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
b. { **TST (***BCG vaccine in prior 15y?***)IGA** }
c. \*\*📺(*pts previously exposed to TB mycobacterium _may_ have either [future robust TB immunity] and/or [future waning TB immunity] at time of TST*📺 ⚠️
▶Those with [future ***ROBUST*** TB immunity*(at time of TST )*] can ➜
BCG vaccine can sensitize Host to tuberculin … so if Host receives TST later ➜ [up to 20 mm *artificially* *robust* induration] even if patient's never had TB infxn ➜ **false positive TST** = [use IGA for BCG vaccine recipients] instead
163
# In Tuberculosis dx,
Although TST and IGA have comparable accuracy, what are the 3 advantages IGA has over TST?
IGA has…
1. ***no*** [BCG vaccine] false positives
2. ***no*** need for a return visit to measure induration
3. ***no** [*2 step negative confirmation]\*\*
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
\*\*📺(*pts previously exposed to TB mycobacterium _may_ have either [future robust TB immunity] and/or [future waning TB immunity] at time of TST*📺 ⚠️
▶▶Those with [future ***waning*** TB immunity*(at time of TST )*] can ➜ negative 1º TST [but since this may activate anamnestic immunity] ➜ require 2 weeks later a 2º TST (which may then be positive). HCP require 2-part negative TST (2wk apart))*
## Footnote
⚠️📺*pts previously exposed to TB mycobacterium can have _either_ [future robust TB immunity( which can → [false⊕ TST] i\previous BCG vaccine)] and/or [future waning TB immunity( which can→ [false**⊝** 1ºTST] which →req [2º ⊝TST confirmation for employment screening])]* 📺
164
What is the most common cause of asymptomatic isolated transaminitis?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
What causes this?
NAFLD
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
insulin resistance (RF Obesity and DM)
*dx confirmation = US revealing liver hyperechoic texture c/w steatosis*
165
Describe the clinical presentation of acute hepatitis from HAV (5)
1. acute **transaminitis in 1000s**
2. Fever
3. Jaundice
4. Abd pain
5. Vomiting
166
⬜ lab test is used to detect primary biliary cirrhosis
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Recite clinical manifestations (6)
[AMA (AntiMitochondrial Ab)] ;
T-cells & AMA destroy **_intra_hepatic bile duct ➜**
1. [cholestatic elevated ALP]
2. jaundice
3. pruritus
4. RUQ abd pain
5. Wt Loss
6. [Xanthelasma (from INC blood cholesterol deposition)]
167
In patients with suspected [NAFLD (*asymptomatic isolated transaminitis*)], ⬜ is needed to confirm the diagnosis
[US revealing liver hyperechoic texture c/w steatosis]
168
What are the guidelines for Colon Cancer Screening? -3
169
What are the [ColoRectal Cancer screening options] available for otherwise normal patients(⊝UC, ⊝[FDR CRC or HR Polyp])? (7)
a. [cscope]q10y
## Footnote
* * *
b. [gFOBT]q1y
c. [FIT]q1y
d. [FIT-DNA]q1-3y
* * *
e. [CT colonography]q5y
f. [Flexible Sigmoidoscopy]q5y
* * *
g. [(Flexible Sigmoidoscopyq10y) + (FITq1y)]
170
genetic testing to test for [hereditary colon cancer syndromes] (such as ⬜ and ⬜ ) is usually recommended for patients who have ⬜
[FAP (Familial Adenomatous Polyposis); [Lynch Hereditary Nonpolyposis CRC];
Strong family hx CA
171
# Small Intestinal Bacterial Overgrowth
how is Dx confirmed? (2)
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
SIBO can be a complication of ⬜ or ⬜
▶[Carbohydrate breath test *(measures PO hydrogen and methane - present if SIBO gut bacteria ferment the carbohydrate \<90m after given to patient)*] vs
▶ [Jejunal aspirate & cx *(measures bacterial load)*]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[Roux-en-Y gastric bypass] **;** [Systemic Sclerosis Scleroderma]⼀*smooth m fibrosis and atrophy ➜ alters intestinal motility➜ allows [gram negSIBO]*
172
what abx are used to treat SIBO? -4
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*Small Intestinal Bacterial Overgrowth*
1. amox/clav
2. rifaXimin
3. fluoroquinolones
4. metronidazole
* SIBO = gram negative*
173
# SIBO
Management? (3)
1. correct underlying cause (i.e. SSS)
2. dietary modification
3. abx(amp_sulf or amox_clav|rifaXimin|fluoroq|metronidazole)
174
Loperamide MOA
[weak opioidmu R agonist] ➜ [slows intestinal motility] ➜ **improves diarrhea**
175
* newly diagnosed HIV⊕ pt presents 3 weeks after starting HAART for first time, with fever and respiratory sx*
* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_*
a. Explain what is likely causing this reaction
b. Treatment? -2
**IRIS**
* [Immune Reconstitution Inflammatory Syndrome] is [fever/respiratory sx] that present several weeks after initiating HAART ⼀2/2 robust immune recovery.*
* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_*
b. self-limited = [symptomatic tx (NSAID \> CTS) only if severe]
176
* Newly diagnosed HIV⊕ pt, s/p recent initiation of HAART, now with [active TB infection] but is improving with TB treatment.*
* Despite this, suddenly pt starts to get worst again p/w worsening fever and respiratory sx*
* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_*
List and explain the likely Diagnosis
**IRIS**
## Footnote
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*[Immune Reconstitution Inflammatory Syndrome] is [fever/respiratory sx] that present several weeks after initiating HAART ⼀2/2 robust immune recovery.*
Immune Reconstitution Inflammatory Syndrome
177
# Lyme Disease has 3 Clinical Symptom Stages: eL ➜ ED ➜ L
[**eL**Lyme Disease] occurs ⬜ after bite from ⬜
* * *
What sx does this stage consist of? (5)
* * *
* eL: early Localized*
(days to 4 weeks) ; [Ixodes scapularis deer tick *during blood feeding*]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*eL Lyme dx = clinical dx + empiric doxy if* ⊕ *(since early Borrelia burgdorferi serology has high false negative rate)*
178
# Lyme Disease has 3 Clinical Symptom Stages: eL ➜ ED ➜ L
[**ED**Lyme Disease] occurs ⬜ after bite from a ⬜
* * *
What sx does this stage consist of? (5)
* * *
* ED: Early Disseminated*
(weeks to mo) ; [Ixodes scapularis deer tick *during blood feeding*]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*eL Lyme dx = clinical dx + empiric doxy if* ⊕
179
# Lyme Disease has 3 Clinical Symptom Stages: eL ➜ ED ➜ L
[**L**Lyme Disease] occurs ⬜ after bite from ⬜
* * *
What sx does this stage consist of? (3)
* * *
* L: LATE*
(mo to years) ; [Ixodes scapularis deer tick *during blood feeding*]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*eL Lyme dx = clinical dx + empiric doxy if* ⊕
180
# Lyme Disease has 3 Clinical Symptom Stages: eL ➜ ED ➜ L
Which Clinical Symptom Stage of Lyme Disease is diagnosed clinically, and why?
* * *
How are the other 2 Clinical Symptom Stages of Lyme Disease diagnosed?
*early Localized --* eLLyme dx =
clinical dx + empiric doxy if ⊕ (since **early** Borrelia burgdorferi serology has high false negative rate 2/2 not yet developed humoral response)
* * *
EDLyme and LLyme = [Borrelia Burgdorferi *ELISA ➜ Western Blot*] (then give Doxy vs CefTriaxone(if severe) )
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*Enzyme Linked ImmunoSorbent Assay*
181
# Lyme Disease has 3 Clinical Symptom Stages: eL ➜ ED ➜ L
Tx for eLLyme disease
Tx **eL**Lyme:
[⊕clinical dx?(erythema migrans, fv, HA, hx)] → give [empiric doxy]
182
In pts with cystic fibrosis, pulmonary exacerbations are due to ⬜ and ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Name the empiric abx for each ? -5
**MRSA →** Vanc
* * *
**Pseudomonas →** [cephalosporin(cefePime|cefTAZidime) + aminoglycoside(amikacin|tobramycin))
183
[meconium iLeus] indicates ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Describe MOD
Cystic Fibrosis
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
lack of [aqueous HCO3 secretion] ➜ [inspissated (thickened) stool] that's difficult to propel ➜ impaction in iLeum = **[NARROW UNDERUSED MICROCOLON**]
184
A Contrast enema demonstrating microcolon is indicative of what condition?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
etx?
Meconium iLeus 2/2 Cystic Fibrosis
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[inspissated (thickened) meconium] accumulation obstructs terminal iLeum --\> underused colon --\> contracted microcolon
185
Name the 6 major organ systems affected by Cystic Fibrosis and how they're affected
**L**UNGS = Nasal Polyps, Digital Clubbing, Bronchiectasis, BronchiOlitis
186
As long as the patient has normal GI function: …
[⬜ feeding]
is preferred over
[⬜ feeding]
Enteral ; {ParEnteral IV]
187
In patients with normal GI function, [*Enteral* feeds] are more physiologic and have less complications than [⬜ feeds]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Describe clinical features of [*Enteral* feeds] (2)
[*ParEnteral* IV feeds];
**_ENTERAL FEEDS_**
1. **{[30** **Kcal/kg/day****] + [1****g/kg of*****protein*****]}** = standard composition
2. gastrostomy tube can be placed surgically or perQ
188
Most patients with Splenic Vein Thrombosis have hx of ⬜ . Why is this?
Pancreatits❌ (acute/chronic/CA); pancreatic inflammation damages splenic vein as the splenic vein runs along pancreas posterior surface ➜ splenic vein thrombosis
189
What is the hallmark of Splenic Vein Thrombosis?
isolated [fundal gastric varices]
## Footnote
*tx = splenectomy*
190
What is Budd-Chiari syndrome? (2)
- acute: thrombosis of [intrahepatic veins | intrahepatic IVC | suprahepatic IVC] that ➜ RUQ pain, hepatomegaly, jaundice and rapidly developing ascites
* * *
- chronic: budd chiari eventually ➜ cirrhosis and portal HTN *(Gastroesophageal varices, splenomegaly)*
191
What is hepatic veno-occlusive disease?
(in the setting of Bone Marrow Transplant) ➜ Occlusion of terminal hepatic **venules** (not veins) ➜ postsinusoidal portal HTN
192
"*Ascitic ***G**uts **C**an **N**ever **T**otally **S**uck"
*Ascites labs =[**G**ram stain & culture], **C**olor*, ***N**eutrophils, **T**otal Protein and **S**AaG*
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
How do you interpret Ascites fluid **N**eutrophils-3?
[\<250 = NO peritonitis]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[≥250 = PERITONITISSBP vs PERITONITIS2º ]
* * *
Neutrophils = PMN on CBC w/diff\*\*
"*Ascitic* **G**uts **C**an **N**ever **T**otally **S**uck"
193
Normal Range for ALT and AST is ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
What etx's would cause Aminotransferases to be **\> 1000**! -5
8-20
194
What's an effective way to determine if Ascites is 2/2 Portal HTN ? -2
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*"Ascitic ***G**uts **C**an **N**ever **T**otally **S**uck"
**SAaG** = **S**erum to **A**scites **a**lbumin **G**radient
(Serum albumin - Ascites albumin)
* * *
[SAaG \<1.1] = [Ascites(no Portal HTN)] = (nephrOtic syndrome , Ovarian CA, TB, pancreatic)]
* * *
[**SAaG ≥1.1**] **= [ASCITES(****⊕****PORTAL HTN)] =(CIRRHOSIS/ BUDD-CHIARI/ R HF/ SBP)!]**
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
"*Ascitic ***G**uts **C**an **N**ever **T**otally **S**uck"
195
*Pt presents with Ascites*
What all do you order to analyze Ascites Fluid? -5
"*Ascitic ***G**uts **C**an **N**ever **T**otally **S**uck"
## Footnote
1. [**G**ram Stain & culture]
2. **C**olor
3. [**N**eutrophils PMN on CBC w/diff]
4. **T**otal protein
5. **SAaG** = **S**erum to **A**scites **a**lbumin **G**radient (*[**S**erum albumin] - [**A**scites albumin]*)
196
"*Ascitic ***G**uts **C**an **N**ever **T**otally **S**uck"
*Ascites labs =[**G**ram stain & culture], **C**olor*, ***N**eutrophils, **T**otal Protein and **S**AaG*
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
How do you interpret Ascites fluid **C**olor -4?
Bloody = Trauma / CA / TB
Milky = chylous/pancreatic
Turbid = infection
Straw = benign
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
"*Ascitic ***G**uts **C**an **N**ever **T**otally **S**uck"
197
"*Ascitic ***G**uts **C**an **N**ever **T**otally **S**uck"
*Ascites labs =[**G**ram stain & culture], **C**olor*, ***N**eutrophils, **T**otal Protein and **S**AaG*
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
How do you interpret Ascites fluid **T**otal Protein -8?
[\<2.5 = Cirrhosis / nephrOtic syndrome / (SBP\<1)]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[≥ 2.5 = TB / Ovarian CA / R HF / budd-chiari / Fungal]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
"*Ascitic * **G**uts **C**an **N**ever **T**otally **S**uck"
198
"*Ascitic ***G**uts **C**an **N**ever **T**otally **S**uck"
*Ascites labs =[**G**ram stain & culture], **C**olor*, ***N**eutrophils, **T**otal Protein and **S**AaG*
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
How do you interpret Ascites fluid [**S**erum-Ascites albumin Gradient]-8?
**SAaG** = **S**erum to **A**scites **a**lbumin **G**radient
(Serum albumin - Ascites albumin)
* * *
[SAaG \<1.1] = [Ascites(no Portal HTN)] = (nephrOtic syndrome , Ovarian CA, TB, pancreatic)]
* * *
[**SAaG ≥1.1**] **= [ASCITES(****⊕****PORTAL HTN)] =(CIRRHOSIS/ BUDD-CHIARI/ R HF/ SBP)!]**
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
"*Ascitic ***G**uts **C**an **N**ever **T**otally **S**uck"
199
⬜ polyps are the most common *neoplastic* colon polyp and are associated with ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
After Colonoscopy, patients with which findings undergo repeat Colonoscopy in **10 years**? (2)
ADENOMA ; [INC CRC ADC] = *requires more frequent cscope surveillance*
*\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_*
200
⬜ polyps are the most common *neoplastic* colon polyp and are associated with ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
After Colonoscopy, patients with which findings undergo repeat Colonoscopy in **7-10 years**? (2)
ADENOMA ; [INC CRC ADC] = *requires more frequent cscope surveillance*
*\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_*
201
⬜ polyps are the most common *neoplastic* colon polyp and are associated with ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
After Colonoscopy, patients with which findings undergo repeat Colonoscopy in **3-5 years**? (2)
ADENOMA ; [INC CRC ADC] = *requires more frequent cscope surveillance*
*\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_*
202
⬜ polyps are the most common *neoplastic* colon polyp and are associated with ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
After Colonoscopy, patients with which findings undergo repeat Colonoscopy in **3 years**? (5)
ADENOMA ; [INC CRC ADC] = *requires more frequent cscope surveillance*
*\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_*
203
⬜ polyps are the most common *neoplastic* colon polyp and are associated with ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
After Colonoscopy, patients with which findings undergo repeat Colonoscopy in **1 year**? (1)
ADENOMA ; [INC CRC ADC] = *requires more frequent cscope surveillance*
*\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_*
***includes FAP (Familial Adenomatous Polyposis)***
204
⬜ polyps are the most common *neoplastic* colon polyp and are associated with ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
After Colonoscopy, patients with which findings undergo repeat Colonoscopy in **6 _months_**? (1)
ADENOMA ; [INC CRC ADC] = *requires more frequent cscope surveillance*
*\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_*
205
⬜ polyps are the most common *neoplastic* colon polyp and are associated with ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
After Colonoscopy, patients with which findings require COLECTOMY? (2)
ADENOMA ; [INC CRC ADC] = *requires more frequent cscope surveillance*
*\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_*
HRP**lymphovascular involvement**
HRP**CA extends to specimen margin**
\_\_\_\_\_\_\_\_\_\_
**H**igh **R**isk **P**olyps with invasive malignancy:
206
Why do pts with Crohn disease have ⬆︎ development of Kidney stones?
They have fat malabsorption which --\> ⬆︎oxalate absorption --\> Ca+Oxalate precipitation in the kidneys
207
Endoscopic findings for Ulcerative Colitis
Continuous Friable mucosa with ulcers
208
Pts with Ulcerative Colitis are at risk for _____ CA; What's px for this?
Colorectal ;
8 years after diagnosis --\> Screening Cscope with mucosal sampling q1-3years
209
Which IBD condition are Pseudopolyps associated with?
Ulcerative Colitis
210
[Ulcerative Colitis IBD] Sx (11)
U
L L
C C C C
E
R R
S
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
211
[Crohns IBD] Sx (11)
**C**rohns **C**an **FCK GRT DCS**
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
212
describe
hepatic adenoma
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
tx? -2
**ASX** (incidentally found) [liver lesion ≤5 cm with peripheral enhancement] in young females on OCP
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
d/c OCP ➜ (surgery if sx/[large lesion \> 5cm])
213
Clinical features of Barrett Esophagus (4)
1. [distal esophageal intestinal metaplasia\*\*] that can →intestinal **dys**plasia → [Esophageal ADC (*note: LOW RISK \< 1% if dysplasia absent*)]
2. [(Chronic GERD\>5y), (\>50 yo), (White), (Obese)]risk factors
3. \*\*[**Red Velvety Columnar Epithelium (with goblet cells)**] replaces [pale shiny stratified squamous epithelium] in distal esophagus
4. Tx: = [endoscopic surveillance + (PPI)lifelong]] + [endoscopic ablation**IF ⊕DYSPLASIA ONLY **]
214
HPylori causes atrophic gastritis and [⬜ ADC], but not [⬜ ADC]
[gastric ADC];
* * *
[Barrett Esophagus/Esophageal ADC]
215
Hepatic Encephalopathy is a neurocognitive disorder largely characterized by which 3 sx?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Although multifactorial in origin, explain what typically is the cause? -4
and how to treat it? (3)
**AAA**
[**A**mmonia INC] , **A**MS, **A**sterixis
* * *
_{precipitating event_
most common= [hypOvolemia from diuretics given for ascites] \> [hypOkalemiaconverts ammonium → ammonia] = [metabolic alkalosisDEC urinary ammonia excretion] = infxn }
→ [**A**mmonia INC]
* * *
1. lactulose(DEC Ammonia)
2. rifaximin(DEC Ammonia)
3. correct precipitating event (IVF, abx, elyte )
216
What are the major risk factors for [CRC ADC]? (4)
; minor? (4)
| *ColoRectal CA ADC*
1. **FAP**
2. **FAM HX(esp if family < 60 yo at their dx)**
3. **UCIBD**
4. **BLACKrace**
5. etoh
6. smoking
7. obesity
8. red meat
217
What are the protective factors for ColoRectal CA? (4)
a. fvf diet (fiber rich/vegetable/fruits)
b. exercise
c. NSAIDs
d. HRT
218
Most celiac patients experience symptomatic improvement within ⬜ of eliminating dietary gluten. After diet elimination, the most common cause of persistent/recurrent celiac symptoms is ⬜. How do you mitigate this?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
How does serologic studies correlate with Celiac diagnostics?
2 weeks; continued gluten intakeinadvertent vs poor compliance; diet diary
* * *
After dietary gluten elimination, [Anti-**TED**] should [⬇︎ 50% first 8 weeks] and [normalize within 12 months]. If this does not occur → upper endoscopy to evaluate for refractory sprue vs other dx
219
Describe the path the parasympathetic CNS uses to coordinate with the [GI NS (i.e. ⬜ )] and activate peristalsis (3)
[myenteric and submucosal plexus];
* * *
[Medulla(dorsal vagal nucleus)]→
[Vagus CN10]parasympathetic fibers →
[esophagus / stomach / small intestine / proximal colon] → INC peristalsis
*commonly disrupted by MS, DM and surgical vagotomy*
220
In [*uncomplicated* acute diverticulitis], pts s/p appropriate [*initial* tx with (\_\_*3*\_\_)], but whom still fail to improve after 3 days are c/f ⬜, and need what mgmt *secondarily*?
* * *
This is followed by what management *thirdly*? (2)
[Analgesics, Liquid diet, *( +/- abxPO)*] ; [*complicated* acute diverticulitis]
* * *
**REPEAT [I&O CONTRASTCT ABD/PELVIS]** to evaluate for [*complicated* acute diverticulitis]
* * *
If repeat CT shows:
⊕Diverticular abscess (fluid collection on CT) =[percutaneous drainage and IVabx]--*(weeks later)*--\> c/s elective partial colectomy
⊝Diverticular abscess (or any other diverticular complications) = [IVabx(until clinical improvement or alt etx)]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
abx = Cipro + Metronidazole
221
What are the potential complications that cause [***_complicated_***acute diverticulitis]? (4)
[*complicated* acute diverticulitis]
222
# What is the \_\_\_X\_\_\_ of [Distal Esophageal Spasm]
a1. pathophysiology (3)
a2. How does this differ from Achalasia? (3)
* * *
b. how is diagnosis confirmed?
a1.
[Distal Esophageal Spasm(uncoordinated [premature simultaneous contractions) ]
[nml(⊕LES relaxation)] ⼀
[2/2 impaired inhibitory neurons]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
a2.
- Achalasia = degeneration of [Myenteric Auerbach Plexus ganglia]*functional > [Chagas Trypanosoma cruzi]* →**[failed(⊝)LES relaxation)]** = [*Bird's Beak*Narrowed distal esophagus] on esophagogram
- Achalasia = **[failed(⊝LES relaxation)]** vs
- DES =[nml(⊕LES relaxation)]
* * *
b. *dx=esophageal manometry: (distal esophagus [premature simultaneous contractions] with [nml distal sphincter relaxation]*
| *_A_chalasia* _A_int relaxing vs _D_ES _D_oes too much contracting
223
# What is the \_\_\_X\_\_\_ of [Distal Esophageal Spasm]
c. symptoms (2)
d. treatment (2)
c.
- "**solids & liquid *stuck* sensation"(worst with hot/cold food)** = [**COMPLETE** dysphagia]
- Intermittent cp
* * *
d. CCB, [TCA if cp-predominant]
224
# Pt p/w Hematochezia
How do you initially work this up? (4)
225
# Pt p/w Hematochezia
When would Angiography be considered for these patients?
- [Hematochezia⼀ *persistent*] → HDUS
- [⊝EGD]
→ Angiography
226
The ⬜ separates [upper GI tract] from [lower GI tract].
BUN/Cr ratio ⬜ suggest [Upper GI Bleed].
Explain why Nasogastric aspiration can be problematic
[Ligament of Treitz] ;
\> 20:1 ;
NGL aspirating +bile/-blood: [( iNGLO ) = No UGIB*(but note: this may miss **distal **UGIB)*]
227
Explain the main sx discernment between Diverticulosis and Diverticulitis
* * *
In terms of workup, why is it important to discern the two?
* osis=* [Hematochezia BRBPR] → [CSCOPE ✅]
* ITIS*= [(*_NO_ Hematochezia BRBPR)* + (LLQ TTP), FEVER…] → [**CSCOPE c❌d]**
228
# Achalasia
pathophysiology
At the LES, [lymphocyte and eosinophil] infiltration of its [MAP's **inhibitory neurons**]→ loss of NO for LES relaxation → constant LES constriction =
[dysphagia to solids AND liquids] + [*Birds Beak ⼀*Dilated Proximal Esophagus]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*LES: Lower Esophageal Sphincter |MAP: Myenteric Auerbach Plexus | NO:Nitric Oxide*
229
MOD for this finding
* * *
Dx?
[constant LES constriction (from LES MAP inhibitory neuron lymphocytic infiltration)] → stasis of [solids AND liquids] → obstruction sequelae(air fluid level, regurgitation, delayed emptying)---(eventually)→ proximal esophagus smooth m weakens, Dilates = [*Bird Beak*(barium swallow)]
* * *
Achalasia
230
*pt p/w chronic crampy epigastric pain exacerbated with meals⼀s/p negative CT, abd US, PPI trial, EGD*
Likely dx?
How do you confirm diagnosis? (4)
[( CiAMi ) chronic intestinal angina mesenteric ischemia]
* * *
Angiography \> nonInvasive[CTA, MRA, US duplex]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*c/s nonInvasive dx to localize obstructrion → angiography to resolve*
231
what is the tx for [*Cirrhosis***Ascites**] - 3
| Ascites 2/2 Cirrhosis
1. Furosemide
2. Na+ restriction
3. Spironolactone
## Footnote
Tx:[(**F**urosemide/**N**a+ restriction/**S**pironolactone) --*(REFRACTORY)*--\> TIPS].
232
what is the tx for Hepatic Encephalopathy - 2
1. Lactulose
2. Rifaximin
233
Hepatic hydrothorax presents as ⬜ in patients with ⬜. Treatment consist of ⬜2. Explain MOD
[R transudative pleural effusion]; [*Cirrhosis***Ascites**]
Tx:[(**F**urosemide/**N**a+ restriction/**S**pironolactone) --*(REFRACTORY)*--\> TIPS].
peritoneal ascites passes thru diaphragm (mostly R since it's thinner with more porous defects) into R pleural Lung. Thoracentesis only temp since hydrothorax will reoccur so tx = [FNS→ TIPS]
234
# Acute Cholangitis
a. etx
* * *
b. cp (5)
a. biliary tree obstruction → ascending infection
b. [RUQ pain + Jaundice + fever*= charcot's triad*+AMS, hypOtension = Reynold Pentad]
## Footnote
cholangitis dx =cholangitis siLx = cholangitis sxCharcot triad + cholangitis ixERCP/US/CT with Biliary Dilation + cholangitis LxCholestasis labs
235
# Acute Cholangitis
a. how is it diagnosed? (3)
* * *
b. treatment (2)
1. **ERCP/US/CT: Bile Duct Dilation**
2. ⇪cholestasis labs *( ⇪ Direct Bilirubin/ ⇪ ALP/ ⇪ LFTs-mildly)*
3. Charcot's triadRUQx, Jaundice, Fever
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
## Footnote
1. Enteric Abx
2. [ERCP within 24-48h(*for to drain bile duct*)]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
cholangitis dx =cholangitis siLx = cholangitis sxCharcot triad + cholangitis ixERCP/US/CT with Biliary Dilation + cholangitis LxCholestasis labs
236
⬜ is responsible for [Cirrhosis sequelae].
List sx of [Cirrhosis sequelae] (4)
hyper**estrogen**;
1. Palmar erythema
2. spider angioma
3. loss of sexual hair
4. testicular atrophy
237
Screening for Barrett's Esophagus [via ⬜] is indicated if patient has ⬜ or more risk factors.
* * *
Name the 7 risk factors for Barrett's Esophagus
[upper GI EGD]; ≥2
* * *
1. [chronic GERD \> 5y]
2. Male
3. White
4. Hiatal hernia
5. central obesity
6. smoker
7. [FDRwith BE or EAC]
238
Patients with ⬜ or more Barrett's Esophagus risk factors should be screened for it with ⬜
## Footnote
How should you manage Barrett's Esophagus if screening is ⊕? -3
2 ; [upper GI EGD]
* * *
239
prior to medium/high risk procedures, interrupting ⬜ is necessary to DEC surgical bleeding
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
which patients do require bridging prior to surgery? -4
[anticoagulation 1-3 days before surgery]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
pts on warfarin must be bridged to [Enoxaparin LMWH] if they are CHADS VASC ≥7, recent stroke, mechanical valve or moderate risk
240
What is Bile Salt-Induced Diarrhea?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
tx?
5-10% of patients after [cholecystectomy vs short bowel syndrome] have ⇪ [secondary bile acids] into the large intestine ➜ INC diarrhea
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Cholestyramine
([*bile salt-binding resin] that sequesters excess bile salts in the intestine*)
241
⬜ is a risk factor for developing Eosinophilic Esophagitis (which is triggered by ⬜)
cp? -4
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Tx?3
ATOPY (*asthma/food allergy/eczema*) ; food antigens
1. dysphagia
2. reflux/regurgitation
3. epigastric abd pain
4. [eosinophilic esophageal **linear furrows** on endoscopy]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
elimination diet | PPI | [Topical CTS (*fluticasone spray*)]
242
dx for Acute Cholecystitis -2
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
What if this method is inconclusive?
*Ultrasound showing*
[cholelithiasis]
+
[gallbladder wall thickening] OR [sonographic Murphy sign]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
➜ HIDA (*if above inconclusive*)
243
Charcot Triad consist of [⬜3] and indicates ⬜
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Describe this disease
[Fever + Jaundice + RUQ pain] = **Acute Cholangitis** = [bile **duct** gallstone obstruction] ➜ impaired biliary drainage ➜ ascension and infection of enteric bacteria in biliary **duct**
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
## Footnote
cholangitis dx =cholangitis siLx = cholangitis sxCharcot triad + cholangitis ixERCP/US/CT with Biliary Dilation + cholangitis LxCholestasis labs
244
*Pt presents with Fever, Jaundice and RUQ pain*
Management? -2
[ERCP biliary decompression/drainage - *within 48h*]
+
enteric abx
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*dz = Acute Cholangitis*
245
*organisms most commonly associated with*
intraAbdominal -2
E coli
Bacteroides fragilis
246
Large volume Hematochezia should make you suspicious for (⬜ upper|lower) GI bleed , which should be evaluated with ⬜ after IVF
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*Hematochezia = Bright Red Blood Per Rectum*
*brisk* UPPER ; EGD
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*hematochezia (BRBPR) is usually a/w lower GI bleed but **BRISK** upper GI bleeds also cause hematochezia*
247
# SBP
*patient p/w ascites*
How do you diagnose Spontaneous Bacterial Peritonitis?
"*Ascitic ***G**uts **C**an **N**ever **T**otally **S**uck"
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*labs from Ascitic fluid\_*revealing:
⊕[**G**ramStain & Culture](often gram negative)
⊕[**C**olor: Turbid]
⊕[**N**eutrophils PMN on CBC w/diff] ≥250
⊕[**T**otal protein \< 1]
⊕[**S**AaG ≥1]
248
⬜ is a common cause of AKI in patients with Cirrhosis, but is a diagnosis of exclusion
what's the tx for this? -3
[HepatoRenal Syndrome (➜preRenal AKI)] = dx of exclusion]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
1st: [IVF bolus challenge] ➜
(if BP response = preRenal AKI from intravascular volume depletion)
(if **no** BP response [and pt has Cirrhosis]) = HepatoRenal ➜ 2nd: ([Midodrine + Octreotide] + Albumin )
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*Octreotide= somatostatin analog / Midodrine= Αlpha 1 agonist*
249
How is smoking related to surgery?
smoking cessation ≥4 weeks prior to surgery ⬇︎ pulmonary complication risk postop
## Footnote
*PFT, ABG, etc. preop will not help*
250
Why are patients undergoing [major surgery with extensive transfusions] at ⇪ risk of developing [Hyperactive Deep Tendon Reflexes]?
major surgery require massive blood transfusions, which has large amts of citrate (to anticoagulate blood) ➜ this [citrate chelates free serum calcium] ➜ hypOcalcemia ➜ [HYPERACTIVE Deep Tendon Reflexes]
251
How does [gallstone pancreatitis] present?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Management for [gallstone pancreatits]? *(mild vs severe)*
pancreatitis(epigastric abd pain/NV/cholic/⇪lipase) i\ [cholelithiasis with no EtOH or ⇪TAG]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[mild (no organ dysfxn)] = cholecystectomy within 7 days of inflammation resolution
SEVERE = cholecystectomy **AS SOON AS INFLAMMATION RESOLVES**
252
Name the 12 Absolute **Contraindications** to Organ Donation
253
*During _Vital_ Organ Donation, the donator not being “Officially Clinically Dead” is an absolute contraindication to continuing Organ Donation*
What does it mean to be “Officially Clinically Dead”? -4
OFFICIAL CLINICAL DEATH =[**BS**\_**HL** *dead.*]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
{ [**B**rain] [brain**S**tem] [**H**eart] [**L**ungs] } = *NO activity* = *dead*.
254
[Boerhaave Esophageal Perforation] MOD
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Delay of surgical intervention leads to what complication
repeat vomiting ➜ [distal 1/3 **full** thickness esophageal tear] ➜ release of gastric content into sterile mediastinum
= **Fatal Mediastinitis** presenting as [ACUTE RETROSTERNAL CHEST PAIN (+/- L pleural effusion c/b PTX or Pneumomediastinum)]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Fatal Mediastinitis within 24H
255
Name the differentiating sx between [Mallory Weiss tear] and [Boerhaave Esophageal Perforation]
*both have NV➜ hematemesis*
MW: [**partial***_m_ucosal* thickness esophageal tear]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
BEP: [**FULL** thickness esophageal tear] | [Perforation sx (fever/retrosternal cp/ L pleural effusion)]
256
cp for [*Perforated* gastric ulcer] -3
-acute severe abd pain with
-[**free air under diaphragm** on upright CXR]
-HDUS= SURGICAL EMERGENCY
257
[Boerhaave Esophageal Perforation] dx (2)
[esophaGography] vs. [water soluble contrast CT]
258
⬜ infections develop in up to 50% of patients with acute variceal bleeding.
Management?
BACTERIAL (SBP/PNA/UTI) ;
( [Ceftriaxone IV x 7 days] prophylaxis)
259
the primary tx for all *Hernia* is what?
surgery
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*complications: incarceration vs strangulation*
260
s/s of Compartment Syndrome -6
[**P**ain (especially with *P*assive stretch)]
**P**aresthesia
**P**oikliothermia
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
**P**aralysis
**P**ulselessness
**P**allor
261
What are the 2 lab features of [Subclinical hypOthyroidism]?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[Subclinical hypOthyroidism] is usually not treated. What are the 4 exceptions?
[⇪ TSH] with [normal T4 Thyroxine]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
1. antiThyroid antibodies (antiTPO)
2. abnormal lipid profile
3. hypOthyroidism sx
4. ovulatory/menstrual dysfunction
262
clinical definition of Rectal Prolapse
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
When is surgery indicated? -3
[**when rectal tissue***mucosal|FULL thickness**[14]* **slides thru anus***[15]*]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
🔨[Rectal Prolapse COMPLETELY] or
🔨[Rectal Prolapse w incontienence] or
🔨[Rectal Prolapse w constipation]
## Footnote
*🔨=surgery*
263
what's management of
```
partial SBO (*air in distal colon on XR*)? -2
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
```
COMPLETE SBO?
partial SBO = [conservative x 24h] --(sx persist)--\> [XLAP]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
COMPLETE SBO = XLAP
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*conservative = IVF / NG suction / electrolyte correction*
264
Typically, [CRC Colonoscopy screening] starts at age ⬜ --and if normal--\> repeats every ⬜ years
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
How does this differ for patients who have either [high risk adenomatous polyps] or [First Degree Relatives with CRC] ?
45 ; 10
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*HR: 40 ; 5*
*IF HIGH RISK: [*Cscope at 40 yo (or 10y prior to age FDR received dx) (which ever is first)]
then [Repeat every 5 years (or 10 if FDR diagnosed \> 60 yo)]
265
Typically, [CRC ADC screening] starts at age ⬜ --and if normal--\> repeats every ⬜ years (for colonoscopy)
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
How does this differ for patients who have Ulcerative Colitis -2
45 ; 10
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
266
Dumping Syndrome MOD
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Dumping Syndrome Sx(5)
rapid emptying of **hyper**tonic stomach contents into small intestine (usually after gastrectomy or RYGB) --\> **DDUMP**
**\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_**
**D**iarrhea
**D**iaphoresis
[**U**mbilical ABD Pain]
**M** (N)ausea
**P**alpitations
*worst after eating and better at night*
## Footnote
*"avoid **DDUMP**after _RYGB_ plus give [**F, D, C** and **Bx3**]"*
267
[SIBO - Small Intestinal Bacterial Overgrowth] MOD
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
clinical features of SIBO (6)
*(**SIbbbO**)*
[surgeryRoux-en-Y vs dysmotilitySSS] ➜ blind loop of small intestine that (especially if partially obstructed by intraabd adhesion) allows gram neg bacterial overgrowth ➜ mucosal inflammation and damage to brush border enzymes ➜*(**SIbbbO**)* sx
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
**S**tinky flatulence / [**I**ntestinal lack of TTP OR Fever] / [**b**loating | **b**12 deficiency | ⊕**b**reath LactuLOSE test] / [**O**asis WATERY Diarrhea]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[_NO_ abd pain (*CDiff has diffuse abd pain*)]
[_NO_ fever (*CDiff has FEVER*)]
268
How do you manage a patient presenting after accidentally swallowing a sharp fish bone?
EMERGENT FLEX ENDOSCOPY
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*any sharp object in esophagus must be removed emergently with flex endoscopy*
269
*patients with large TBSA burns have high mortality rates*
How do you determine if burn patients require hospice? -3
[revised Baux score] =
* * *
[age + TBSA (+17 if inhalation injury present)] **\> 140**= poor survival pgn
→ pt will likely need HOSPICE
270
How do you differentiate cp of duodenal ulcer vs gastric ulcer
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Whats the tx for HPylori Ulcer -7
[**D**EC = **D**uodenal] \<--(EPIGASTRIC PAIN AFTER MEAL)--\> [**G**ETS WORST = **G**astric]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[**PAC**]14d --(if persistent/allergic/resistant)--\> [**PBMT**]14d
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
* [PAC = **P**PI + **A**moxicillin + **C**larithromycin]*
* [PBMT = **P**PI + **B**ismuth(or diff abx) + **M**etronidazole + **T**etracycline]*
271
After Triple Therapy, what 3 clinical elements warrants **CONFIRMATION** of H Pylori eradication?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
How is eradication confirmation done? -2
duodenal ulcer | ongoing dyspepsia | MALT lymphoma
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
([Urea Breath test] or [Fecal Antigen test])
x 4 weeks after Triple Therapy
272
Typically, [CRC Colonoscopy screening] starts at age ⬜ ---and if normal--\> repeats every ⬜ years
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
How do you manage a patient who instead underwent flexible sigmoidoscopy and was positive for adenomatous polyps?
45 ; 10
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
**COLONOSCOPY STAT**
(**follow ⊕FlexSigmoidoscopy with STAT Colonoscopy** to scan entire colon for proximal colon adenomas and advanced neoplasia)
273
In patients with SEVERE malnutrition, which route of administration is the preferred method of rehydration? why?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
**ORAL** --(if oral insufficient)--\> NG --(if pt in shock)--\> [IV 10 cc/kg over 30m]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
IV rehydration in chronic malnourishment may cause fluid overload ➜ HF
274
What is Chronic Exertional Compartment Syndrome?
muscular volume expansion during endurance exercise ➜ INC pressure within fascial compartment **of BL lower leg**➜ chronically impairs tissue perfusion .
alleviated with rest and nml activity
*TX = elective fasciotomy*
275
describe Autoimmune hepatitis
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
lab findings (2)
```
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
diagnostic labs (2)
```
autoimmune progressive parenchymal liver damage of young women that may ➜ cirrhosis and liver failure in 6 mo
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[⇪ALT and ⇪AST +/- ALP] and [normal bilirubin level]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[ANA] / [AntiSmooth Ab]
276
How are the results of the D-xylose test interpreted? -2
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
How does Rifaximin play a role in this?
**In patients with** [**fatty stool steatorrhea**]...
It differentiates between
1. **Celiac disease** (D-xylose will be LOW in the urine because it can't be reasbsorbed in the small intestine because of villous atrophy)
2. **Pancreatic insufficiency** (D-xylose will be HIGH because absorption occurs normally and pancreatic enzymes never break down D-xylose
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
\*\*Small Intestine Bacterial Overgrowth can digest D-xylose before it has the chance to be reabsorbed --\> Falsely low D-xylose. Rifaxmin abx prevents this\*\*
277
What type of diarrhea is associated with [decreased stool osmotic gap \< 50]
Secretory
## Footnote
*these are larger volume diarrhea that occurs during fasting or sleep*
278
What type of diarrhea is associated with [INCREASED stool osmotic gap \> 125]
Osmotic
## Footnote
*ex: Lactose intolerance*
279
What are the laboratory findings for Lactose intolerance? - 5
*Lactose intolerance is most commonly seen in Asians*
1. [INC stool osmotic gap*(osmotic diarrhea)* \> 125]
2. [⊕**hydrogen breath test (indicates intestinal bacterial carbohydrate catabolism)**]
3. [⊕reducing substances in stool]
4. acidic stool pH
5. NO [fatty stool steatorrhea]
*Lactose Intolerance is most commonly seen in Asians*
280
There are 4 Malabsorption syndromes
Describe clinical features of Lactose Intolerance (4)
281
There are 4 Malabsorption syndromes
Describe clinical features of Chronic Pancreatitis (2)
282
what are the sx of Viral gastroenteritis (3)
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
it is transmitted via ⬜ with which 2 viruses?
[**WATERY DIARRHEA** +/- vomiting]
Abd pain
[+/- Fever]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
283
tx for Viral gastroenteritis (3)
*self-limited*
## Footnote
1. oral rehydration (mild)
2. IV REHYDRATION (SEVERE)
3. [Regular *Limited Lipid(fat)/ Simple Sugar*diet as tolerated]
284
The major side effects of [INH Isoniazid] for TB are peripheral neuropathy and ⬜.
How do you manage each side effect?
[HEPATITIS]
## Footnote
**(*****measure LFTs** now then q 3 mo ➜ dc INH if LFT [≥5x baseline] or [≥3x baseline with sx] )*
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
***supplement** INH **with [PYRIDOXINE B6]** (INH outcompetes ([pyridoxine B6] - a cofactor in synthesizing synaptic NTS) so giving more [pyridoxine B6]) ➜ prevents*
[peripheral neuropathy]
285
Porcelain Gallbladder is often asymptomatic and found incidentally. What is it?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Why is it clinically significant?
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
What's the management? -2
gallbladder wall calcification (*punctate vs curvilinear*) 2/2 chronic cholelithiasis
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
INC risk for GALLBLADDER CANCER if *punctate* *calcification*
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[prophylactic Cholecystectomy (if +sx or +*punctate calcification*)
286
In neonates, how might Cystic Fibrosis present? -4
**Meconium iLeus** = inspissated GI secretions obstruct meconium excretion in distal iLeum ➜
## Footnote
[**DILATED SMALL BOWEL LOOPS with NARROW UNDERUSED MICROCOLON**]
[**Bilious** emesis]
[R ground glass mass AXR (from iLeum air mixing with iLeum meconium)]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*AXR = Abdominal XRay*
*ASK ABOUT FAM HX OF RECURRENT SINUS INFECTIONS*
287
* List Main differences between Esophageal SQC and Esophageal ADC :*
- Location
- What risk factors are associated with each?
[eSQC = **UPPER** esophagus = Tobacco , EtOH]
[eADC = lower esophagus = GERD/Barrett's]
288
What is the TRIAD PRIORITY for managing [Brain-Dead Organ Donors] ?
MUST MAINTAIN NORMAL **PET** w IVF / Desmopressin
## Footnote
**P**ressure
**E**uvolemia
**T**emperature (or mild hypothermia)
289
What Lipase level is c/f Acute Pancreatitis in Adults?
GOE 1,000
290
What Lipase level is c/f Acute Pancreatitis in kids?
GOE 7 x upper limit of nl for that age group
291
What supplements will pts s/p RYGB (Gastric bypass Surgery) require? - 6
*"avoid **DDUMP**after _RYGB_ plus give [**F, D, C** and **Bx3**]"*
## Footnote
**F**e
**D**3cholecalciferol
**C**a+
**B**1Thiamine
**B**9Niacin
**B**12Cobalamin
292
Why does compartment syndrome cause kidney damage?
compartment syndrome --\> myoglobin release --\> [myoglobin heme] is nephrotoxic
293
Compartment Syndrome Dx- 2
1. [Direct Compartment Pressure \> 30]
2. [delta pressure(diastolic BP - Direct) \< 20]
294
Which part of the Esophagus is [Esophageal ADC] located?
LOWER
a/w Barrett's and GERD
295
Which part of the Esophagus is [Esophageal SQC] located?
UPPER
a/w SMOKING AND EtOH
296
What is [Enteropathy associated T cell Lymphoma (EATL)] ?
**Jejunal CANCER** from [NON-COMPLIANT CELIAC DISEASE]
## Footnote
*similar sx to celiac but long standing*
297
describe pathology for Crohn disease
**T**ransmural GI inflammation
## Footnote
**C**rohns **C**an **FCK GR🅃 DCS**
298
What type of diarrhea is associated with INCREASED stool osmotic gap \> 125
Osmotic
## Footnote
*ex: *"**C**an **L**arry --"***C**eliac, **L**actose intolerance*
299
What are the laboratory findings for LactOse intolerance? - 5
## Footnote
*LactOse intolerance is most commonly seen in Asians and AA*
Lact**O**se Intolerance =
1. = {INC Stool Osmotic Gap>125 a/w [LARGE _**O**ASIS (WATERY)_ DIARRHEA]}*periumbilical abdP postprandial + Flatulence postprandial, Asian=RF*
2. ⊕reducing substances in stool
3. **⊕LactOse hydrogen breath test (indicates intestinal bacterial carbohydrate catabolism)**
4. acidic stool pH
5. NO steatorrhea
| *"**D**efinitely **P**roduces **F**latulence"*
## Footnote
*LactOse Intolerance is most commonly seen in Asians and African Americans*
300
*generally describe distinguishing sx for these 4 conditions*
## Footnote
Celiac
[Irritable Bowel Syndrome]
[Inflammatory Bowel Disease]
Lactose Intolerance -2
Celiac*(TW**I**CED)* = {**I**NC Stool Osmotic Gap>125 a/w [LARGE _STEATORRHEA_ DIARRHEA]}*foul, flatulent, FATTY*
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
iBS = [smoderate diarrhea with recurrent abd pain (bowel habit ∆s )]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
IBD = Bloody diarrhea, fever, fatigue
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Lact**O**se Intolerance = {INC Stool Osmotic Gap>125 a/w [LARGE _**O**ASIS (WATERY)_ DIARRHEA]}*postprandial + postprandial flatulence, Asian=RF*
301
Where is the intestinal enzyme lactase located?
Duodenal brush border
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
*LactOse intolerance* **D**efinitely **P**roduces **F**latulence
302
[**MASSIVE** Rectal Bleeding in Adults] ddx -3
1. Diverticulosis (L colon)
2. Ulcerative Colitis
3. [angiodysplasia AVM (R colon)]
303
[**MASSIVE** Rectal Bleeding in Adults] with active hemorrhaging dx -2
1. radionuclide scintigraphy
2. Angiography
304
Why is Nasogastric tube placement helpful in patients with hematochezia?
helps discern UGI Bleed from LGI Bleed
10% of hematochezia come from the upper GI tract
305
Why is BUN elevated in [Profuse Rectal Bleeding]? (4)
1: blood leaks into GI tract ➜
2: . [blood catabolized into Nitrogenous products] in GI tract ➜
3: [GI tract Nitrogenous products] is absorbed back into circulation ➜
4: elevated BUN
306
Indication for [Blood Transfusion (pRBC)] -2
1. Hb \< 7
OR
2. [Cardiac Patients Hb \< 8]
307
Tx for **active & brisk** [Angiodysplasia hematochezia] -5
1. **MOST ANGIODYSPLASIA RECTAL BLEEDING STOPS SPONTANEOUSLY** ➜
2. endoscopic coagulation (if #1 fails) ➜
3. arterial embolization by catheterization (if #2 fails) ➜
➜ 4. subtotal colectomy
5. aortic valve replacement (if aortic stenosis)(Heyde's syndrome)
.
*do not use vasopressin*
308
Heyde's Syndrome
[Aortic Stenosis = narrowed calcified valve] ➜ turbulent passage of [von Willebrand Factors] forces interaction with platelets ➜ actually DEC vWF ➜(in setting of ⊕aAVM) may meet threshold for nonpainful aAVM bleed
309
Why should Raloxifene be d/c before surgery?
SE = DVT/PE
