8⼀GI/SURGERY/ID I Flashcards

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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

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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!)

Dermatitis herpetiformis (elbow, knee, butt, back)- celiac disease
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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

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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

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5
Q

These cells are a/w ⬜
_________________

Describe the cp (5)

A

dx = atypical reactive lymphocytes

[EBV ⼀Infectious Mononucleosis]​
_________________

  1. TIRED TEEN
  2. Fever
  3. exudative Tonsillitis
  4. cervical LAD
  5. HepatoSplenomegaly
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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
_________________​

  1. [SEVERE (shock, etc)]
  2. [Prolonged > 7 days]
  3. [patient at risk for severe progression (immunocompro/elderly)]
  4. [bacterial pathogen identified ➜ give low dose px to prevent transmission] ​
    _________________

SECCSY

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7
Q

Aside from STAT Laparotomy, name 3 other treatments used in perforated peptic ulcer?

A
  1. IVF
  2. IVAbx
  3. IVPPI

+ STAT Laparotomy

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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)

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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

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10
Q

What causes Necrotizing fasciitis in
_____ patients?

a. healthy?
_________________

b. DM (poor circulation)?​

A

a. polymicrobial
_________________

b. GASP​

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11
Q

Necrotizing fasciitis s/s (4)

A
  1. POOP
  2. swelling
  3. erythema
  4. fever
    [DM = GASP] / [EE = polymicrobial]
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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

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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

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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)]

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15
Q

normal range for

LDL

A

<100

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16
Q

normal range for

TAG

TriAcylGlycerides

A

<150

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17
Q

normal range for

HDL

A

50+

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18
Q

normal range for

TOTAL CHOLESTEROL

A

<200

________________

>240 = “HIGH”

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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)]

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20
Q

cp for Chronic Pancreatitis -4

________________

dx = MRCP Pancreatic Calcifications

A
  1. epigastric abd pain that radiates to back
  2. better with sitting up and leaning forward (positions other abd organs away from inflammed pancreas)
  3. worst with meals
  4. fat malabsorption (bulky foul stools)
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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)

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22
Q

Causes of CHRONIC Pancreatitis? -4

A
  1. EtOH
  2. Cystic Fibrosis (peds)
  3. Duct obstruction (CA/stones)
  4. autoimmune
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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

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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

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25
Q

Barrett Esophagus INC risk for developing ⬜

________________

How is this screened for? -3

A

esophageal ADC

________________

{[Sx(Chronic GERD|frequent sx) ≥5 years] + [≥2 risk factors(White/Obese/Male/Smoker/Hiatal Hernia)]}

= endoscopic screening

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26
Q

Why is chronic constipation a major risk factor for UTI?

A

Fecal retention ➜ rectal distension ➜ obstruct bladder emptying ➜ incomplete voiding ➜ stagnant urine ➜ promotes microbial growth ➜ UTI

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27
Q

Sulfasalazine is a ⬜ compound used for ⬜ maintenance

________________

Why should Sulfasalazine NOT be used acutely?

A

[5-AminoSalicyclic Acid] ; [IBD]

________________

[Sulfasalazine 5ASA] can precipitate IBD attacks if used acutely

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28
Q

Which abx is best for intraabdominal infection?

A

Ampicillin-sulbactam

________________

(3rd Generation PCN and beta-lactamase inhibitor)

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29
Q

Functional Abdominal Pain

________________

Tx?

A

chronic ( ≥2 mo) adolescent periumbilical abd pain, with no identifiable pathology, and self-resolves in a few hours

________________

tx = Symptom Diary

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30
Q

How does Peptic Ulcer Disease present? -2

A
  1. early satiety
  2. postprandial epigastric pain

________________

get stool antigen test for H Pylori

[GERD = (Cough + Reflux) > 2x weekly]

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31
Q

Why is [aAVM] a cause of upper AND LOWER GI bleed? (3)

(aAVM=angiodysplasia ArterioVenous Malformation)

A

-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)]}

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32
Q

In adults, what are the risk factors for developing Angiodysplasia - 3

This can occur ANYWHERE in the GI tract but most commonly occurs in R Ascending colon

A
  1. Aortic Stenosis (vW multimers are disrupted as they pass through turbulent space –> AVM)
  2. Von Willebran disease
  3. Renal disease
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33
Q

Patient with newly diagnosed “incidentaloma” / L adrenal mass found incidentally

What’s your first step?
_________________

When is surgical resection indicated? (3)​

A

[adrenal hormone mud labs]

(metanephrine & VMA) + (urine catecholamine 24h)+(dexamethasone suppression test)

_________________
SURGICAL RESECTION:

[radiographically malignant] vs [> 4cm] vs [functional (hormone secreting)]

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34
Q

Primary presenting complaint for Achalasia

A

Food AND Liquid dysphagia

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35
Q

Peptic Stricture

A

common complication of chronic GERD - in which healing from chronic ulcerative esophagitis ➜ stricturing of Esophagus ➜ progressive (solid then liquid) dysphagia

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36
Q

Lactose intolerance sx (3)

A

Lactose Intolerance Definitely Produces Flatulence

LactASE breaks down lactose ➜ glucose + galactose

  1. Diarrhea WATERY
  2. Periumbilical abd pain
  3. Flatulence
    * note: [MILK / ICE CREAM > > cheese / yogurt]*
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37
Q

Lactose Intolerance is a clinical diagnosis, but how is the diagnosis confirmed? (2)

worst with age, asian and african american

A
  • L*actose Definitely Produces Flatulence
    1. Lactose breath hydrogen test
    2. [Symptom resolution with Lactose-restricted diet]
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38
Q

Name the single-item predictors of INC SEVEREITY in Acute Pancreatitis (5)

A

HOBCO hurt the Pancreo

= SEVERE ACUTE PANC

  1. BUN ≥20
  2. HCT >44%
  3. CRP >150
  4. Obesity
  5. Old age
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39
Q

What is OculoGlandular syndrome?

A

Bartonella Henselae cat-scatch variation in which pt develops conjunctivitis + [iPL preauricular and cervical LAD]

most common complication of Cat Scratch Disease = lymph node suppuration

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40
Q

describe cp of Pyoderma gangrenosum (2)
_________________

Where does it come from?​ (2)

A

PAINFUL inflammatory [nodules/pustules/vesicles] ➜ PAINFUL ULCERS ​
_________________

neutrophilic dermatosis a/w IBD

Pyoderma Gangrenosum
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41
Q

normal range

Lipase

A

<160

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42
Q

⬜ occurs after acute pancreatitis in 10% of patients, and although sx depend on mass effect, presentation may include (⬜4)

A

[pancreatic pseudocyst IFC] ;

Abd pain / GI hemorrhage / ductal obstruction / [fistulization into adjacent organs]
_________________

tx = supportive –(if persist)–> endoscopic drainage

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43
Q

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?​

A

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

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44
Q

Why do [HIV patients with PCP] sometime additionally need CTS (in addition to abx)?
_________________

Which [HIV patients with PCP] should receive it?​

A

In Mod/Severe PCP, within first 2-3d of treatment, organism lysis ➜ potentially fatal inflammatory lung response ➜
_________________

add CTS if:​

  1. [(ALVeolar-arterial O2 ∆ ≥ 35) on ABG]​
    ________OR_________
  2. [(PaO2 < 70) on Room Air]
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45
Q

name the 3 most important goals in managing a brain-dead organ donor

A

MAINTAIN NORMAL “TV, B”

Temperature (or slightly hypOthermic)

Volume (IVF/desmopressin(synthetic ADH))

Blood pressure (pressors)

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46
Q

What is GGT used for?
_________________
gamma-glutamyl transpeptidase

A

Differentiates elevated ALP:

[⇪ALP and ⇪GGT] = LIVER origin

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47
Q

[Isolated Markedly elevated ALP (+/- ⇪ GGT)] indicates ⬜
_________________

what causes this?​ (2)

A

[infiltrative Liver disease]
_________________

  1. [granuloma (hepatic sarcoidosis, TB)]
  2. [metastatic CA]
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48
Q

In patients with [NAFLD/NASH], what is the single best predictor for liver-related death?

A

⊕HEPATIC FIBROSIS
_________________

[⊕HEPATIC FIBROSIS] ➜ Cirrhosis ➜ liver-related Death]. (Wt loss can reverse [HEPATIC FIBROSIS] if it occurs prior to Cirrhosis)

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49
Q

Angiodysplasias (AKA⬜ ) are defined as ⬜5.

Although only a small amount bleed, which conditions ⇪ Angiodysplasia bleeding? (3)

A

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]

Hematochezia mgmt

  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]}
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50
Q

pathophysiology of toxic shock syndrome

A

[exotoxin superantigens] (usually from Staph A) activate T cells widespread ➜ massive cytokine release

may require up to 20L per day of IVF resuscitation

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51
Q

What is the best test to evaluate Pancreatic Cyst?
_________________
what are all the indications for this modality? -7

A

Endoscopic Ultrasound with aspiration
_________________

  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
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52
Q

indications for ERCP (4)

A

THERAPEUTIC

dilated Common Bile Duct

acute biliary pancreatitis

choleDocholithiasis

cholangitis

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53
Q

HIV test is done on an opt [⬜ (in | out)] basis

What does this mean?

A

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

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54
Q

Acute diverticulitis presents as (⬜2)
_________________

How is it managed?

A

[LLQ TTP] + [CT focal bowel wall thickening +/- diverticula]
_________________

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55
Q

[Dyspepsia (GAS sx ≥1 mo)]

management

A

_________________

trial PPI = [PPI]4-8w

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56
Q

pulmonary ASPERGILLUS

What are the major risk factors? (4)

A

immunosuppression [transplants✳, neutropenia, chronic CTS, HIV/AIDS]

stem cell|organ

“bloody⼀chest ⼀cough”

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57
Q

pulmonary ASPERGILLUS

treatment (3)

A

“bloody⼀chest ⼀cough”

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58
Q

pulmonary ASPERGILLUS

diagnostics (3)

A

“bloody⼀chest ⼀cough”

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59
Q

pulmonary ASPERGILLUS

classic symptom triad

A

“bloody⼀chest ⼀cough”

  1. bloody = [bloody cough hemoptysis]
  2. chest = pleurtic chest pain
  3. cough = [bloody cough hemoptysis]
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60
Q

Oral Candidiasis

treatment (3)
_________________

AKA thrush

A

[topical Nystatin suspension🆚Clotrimazole troches]

–(if persist)–> [fluconazole PO]
_________________

be sure to watch for proper CTS inhaler usage

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61
Q

What should some patients be cautious of when they stop smoking? _________________

What can be done to mitigate this? (2)

A

[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

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62
Q

Why are [Hepatitis A vaccination] and [Hepatitis B vaccination] so important to a person with Hepatitis C?

A

if superimposed with HAV or HBV, chronic HCV causes rapid decompensation and liver failure

so vaccination to HAV and HBV are important

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63
Q

In terms of Hepatitis B,

how do you manage a healthcare worker s/p incidental occupational exposure?

A
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64
Q

Rhabdovirus Rabies

Tx? (2)
_________________

Prognosis? (3)

A

[Ig + Vaccine]-(only helpful BEFORE symptom onset)
_________________

UNIVERSAL FATAL WITHIN WEEKS ONCE SYMPTOMATIC

> Coma / Respiratory failure

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65
Q

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]?

A

[BATS (since U.S. dogs are immunized)] ; dogs
_________________

HYDROPHOBIA ( fear of drinking 2/2 [water-triggered pharyngeal spasms])

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66
Q

Hepatitis C screening is done via ⬜
_________________

A patient with a positive HCV screening indicates what 3 possibilities?

A

HCV Ab testing
_________________

  1. [ACTIVE INFECTION (obtain HCV RNA to determine acute vs chronic)]
  2. [Resolved Infection]
  3. False Positive
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67
Q

Spontaneous Bacterial Peritonitis is a serious complication of ⬜
_________________

Treatment? (4)

A

cirrhosis

_________________

[Paracentesis w/ascites labs(“Guts Can Never Totally Suck”) ]

➜[Albumin IV]

➜ {[CefoTaxime3ºCPN]

➜ [Fluoroquinolone px]

  • 3ºCPN = 3rd gen cephalosporin*​​​​
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68
Q

Spontaneous Bacterial Peritonitis is a serious complication of ⬜

A

cirrhosis ( can → SBP)

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69
Q

Spontaneous Bacterial Peritonitis is a serious complication of ⬜
_________________

clinical presentation? (6)

A

cirrhosis
_________________
1. Fever ≥37.8C

2. Abd pain

3. [AMS (abnl connect-the-dot test)]

  1. [hypOtensionw/SEVERE INFXN]
  2. [hypOTHErmiaw/SEVERE INFXN]
  3. [paralytic iLeusw/SEVERE INFXN]
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70
Q

What is the MELD score?

and how is it used?

A

MELD = Model for End stage Liver Disease = predicts 90-day survival in Liver Disease patients = ranks Liver Transplant List

_________________

MELDusesBICS to rank Liver Transplant List”

Bilirubin

INR

Creatinine

Sodium

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71
Q

What is Succussion splash?
_________________

What does it indicate?

A

audible epigastric splashing sound during sudden movement
_________________

delayed gastric emptying

2/2 gastroparesis vs intrinsic obstruction vs extrinsic obstruction

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72
Q

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?

A

[delayed gastric emptying] ; [intrinsic obstruction / EXtrinsic obstruction / gastroparesis] ; [EGD to r/o obstruction] ; [CT/MR enterography]
_________________

[scintigraphic gastric emptying study]⼀confirms gastroparesis

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73
Q

Diabetic gastroparesis often p/w ⬜
_________________

treatment? (2)

A

[delayed gastric emptying (succussion splash)]
_________________

[Fmeals] –(if persist)–> [metoclopramide]

[Fmeals : Finite(small), Freq, Fatless(low fat), FiberRICH(HIGH soluble fiber)]

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74
Q

cp of travelers’ diarrhea?
_________________

most common cause?

A

3d self limited ​[WATERY DIARRHEA + crampy abdP] 3 days post exposure
_________________

ETEC

EnteroToxigenic E Coli (commonly from developing countries’ street vendors)

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75
Q

Which 2 labs must be carefully monitored before and after starting TPN?

why?

A

Phosphate and K+ (from PTMK)
; [TPN contains dextrose ➜ insulin secretion ➜ insulin drives serum phosphate and serum K+ intracellular ➜ hypOphosphatemia] -this is a component of refeeding syndrome

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76
Q

Refeeding Syndrome etx

________________

How are alcoholics especially affected by this?

A

[Refeeding after severe starvation (think homeless/alcoholics)] ➜ surge of insulin ➜ [PTMK shift into intracell] ➜

VERY LOW PTMK
_________________

  1. [Phosphorous ⬇︎] = [rhabdomyolysis/ ⇪ CPK in EtOH] and/or HF
  2. Thiamine ⬇︎ = HF
  3. Mg⬇︎ = arrhythmias
  4. K+ ⬇︎ = arrhythmia
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77
Q

Refeeding syndrome can lead to the depeletion of serum Phosphorous and 3 other electrolytes such as ⬜

_________________
How is Phosphorous repletion administered?

A

PTMK

(Phosphorous/Thiamine/Mg/K)

_________________
ORAL Phosphorous repletion

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78
Q

Aside from IVF, which medication should be given promptly in Acute Variceal Hemorrhage?

A

Octreotide IV

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79
Q

Which 2 medications can be given to prevent Acute Variceal hemorrhage?

A

Nadolol 🆚 Propranolol

(general BBlocker [⬇︎portal system pressure] + band ligation +endoscopic surveillance)

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80
Q

what is charcot’s triad?

_________________

what is Reynolds pentad?

A
Acute Cholangitis

cholangitis dx =cholangitis siLx = cholangitis sxCharcot triad + cholangitis ixERCP/US/CT with Biliary Dilation + cholangitis LxCholestasis labs

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81
Q

acute Cholangitis is diagnostically confirmed and treated with ⬜ .

What is the initial diagnostic criteria for acute Cholangitis? (3)

A

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]

Acute Cholangitis

cholangitis dx =cholangitis siLx = cholangitis sxCharcot triad + cholangitis ixERCP/US/CT with Biliary Dilation + cholangitis LxCholestasis labs

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82
Q

nonpainful hematochezia

in patients > 40 yo should you make you s/f what diagnosis?

_________________

What causes this?

A

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)

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83
Q

What is the cause of rectal bleeding in internal and external hemorrhoids?

_________________

How do hemorrhoids present? (4)

A

Dilation of submucosal venous plexus ➜

  • small volume hematochezia covering the stool
  • perianal itching
  • mucus +/- mild fecal leakage
  • [Internal: NO pain / External: Painful]
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84
Q

pt s/p infectious mono 3 weeks ago, p/w persistent LAD

How do you manage persistent LAD?

A

pts with persistent localized LAD should be observed x 4 wks ➜ biopsy if persistent nodes fail to resolve after 4 wks

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85
Q

In an immunocompromised pt, EBV DNA in the CSF raises suspicion for what condition?

A

Primary CNS lymphoma

MRI: Solitary Weakly ring-enhancing mass in periventricular region

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86
Q

Dx for EBV infectious mono - 2

A
  1. [positive HAMSonly accurate during week 1 of sx 😟]
  2. Anti-EBV test

________________

HAMS = [Heterophile Antibody MonoSpotonly accurate during week 1 of sx 😟]
No sports for ≥3weeks because of splenomegaly!

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87
Q

Tx for EBV infectious mono - 3

A
  1. [self limited x weeks (fatigue x months)]
  2. NSAIDs
  3. No sports ≥3wks

________________

HAMS = [Heterophile Antibody MonoSpot]

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88
Q

From a lab perspective, how do you differentiate CMV from EBV?

A

CMV will have a [negative HAMS]

________________

HAMS = [Heterophile Antibody MonoSpot]

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89
Q

[T or F] Airway obstruction is a severe complication of [EBV infectious mononucleosis]

A

TRUE!

(give CTS if airway obstruction, severe infection, aplastic anemia or thrombocytopenia develops)

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90
Q

Diagnosis?

Treatment? -4

A

Acute Paronychia (Nailfold infection 2/2 gram positive skin flora)

_________________

NAIL tx
[Neosporin/TOP antiseptics]
[Abx TOP]
[I & D abscess]
[Lukewarm soaks]

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91
Q

Clinical triad of [Reiters Reactive Arthritis]

_________________

When do sx onset? resolve?

A

‘Can’t see, Can’t pee, Can’t climb a tree’

  • 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

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92
Q

Why should Chlamydia infection (symptomatic or asymptomatic) always be treated?

A

chronic Chlamydia may ➜ Reiters Reactive Arthritis

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93
Q

Patient presents with penis rash 2 weeks after having dysuria

diagnosis? | How do you confirm this? treat this?

A

[RReA ⼀[circinate Balanitis 2/2 chlamydia trachomatis]] ; [urine Chlamydia NAAT] ; [chlamydia abx + penile topical CTS]

RReA = Reiters Reactive Arthritis

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94
Q

Name the 3 classic symptoms of dyspepsia

A

indigestion GAS

Gastric (epigastric) pain/burning postprandial

Abd fullness postprandial

Satiety early on

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95
Q

dyspepsia

etx (4)

A

difficulty digesting food 2/2

[IDIOPATHIC functional] > [gastric ADC = HPylori ulcer = NSAID ulcer]

GAS sx GOE1mo

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96
Q

dyspepsia presents with what 3 sx ?

How long should these sx last for official dyspepsia diagnosis?

A

GAS = Gastric sx postprandial/Abd fullness postprandial/Satiety early on

_________________

GOE1 month

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97
Q

dyspepsia presents with what 3 sx ?

Upper GI endoscopy is indicated for dyspepsia [HIGH risk alarm features]

What are they? (7)

A

[GAS = Gastric sx postprandial/Abd fullness postprandial/Satiety early on] GOE1mo

_________________

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98
Q

how does biliary colic present? (4)

A
  • benign [RUQ or epigastric pain] with radiation to [back or R shoulder]
  • a/w [NV, diaphoresis]
  • <6h
  • +/- triggered by fatty meals

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99
Q

biliary colic

etx?

_________________

how is it diagnosed?

A

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

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100
Q

How do you workup patient with suspected uncomplicated Gallstones? (8)

A
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101
Q

What is Cholescintigraphy ?

A
  • 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
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102
Q

Chikungunya is a mosquito borne virus that causes ⬜ and ⬜​ ​

treatment? | prognosis?

A

[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]

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103
Q

[T or F] patients with Syphilis MUST have lumbar puncture if HA is present

Why or Why not?

A

TRUE _________________

any syphilis patient with any neuro ∆ require neurosyphilis r/o via neg [LP CSF VDRL] or neg [LP CSF FTA-ABS].

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104
Q

Tx for Neurosyphillis

A

[aPG 4MU]

[q4h]

[x 14 days]

________________

(aPG = aqueous PCN G - IV) / (MU = million units)

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105
Q

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

A

Doxycycline

  1. [Pregnancy (No DOXY for POXY)]
  2. refractory to initial (doxycycline)tx
  3. [3B5º neurosyphilis]3B5º requires {aPG 4MU q4h x 14d}
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106
Q

How do you know when a pt is fully cured from Syphilis?

A

4-fold ⬇︎in FTA Ab titer by 12 month mark AT THE LATEST

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107
Q

Name the specific signs of congenital syphilis - 3

A

“syphilis hurts the baby’s SKIN, NOSE & BONES!

  1. SKIN: Maculopapular palms/soles_rash that desquamates vs bullous
  2. NOSE: Rhinorrhea
  3. BONES: mulberry molars, long bone metaphyseal lucency
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108
Q

Describe the type of rash you’ll see with secondary syphilis

A

Diffuse Maculopapular rash starting at trunk and spreading to extremities TO INCLUDE PALMS AND SOLES

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109
Q

Why is RPR not reliable when a person first develops syphilis?

A

There is a possible [false negative RPR] early in infection - follow with FTA

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110
Q

Any RPR Titer greater than ___ is high syphilis titer (positive result)

A

1: 16
anything where they had to dilute it MORE than 16 times is HIGH RPR Syphilis titer

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111
Q

Tx for {CLUB} Syphilis :

[CV]⼀[Late latent ≥12 mo]⼀[Unknown duration]⼀[Ball•Gumma]

A

[BPG 2.4MU]

[q week]

[x 3 weeks]

________________

(BPG = BENZATHINE PCN G -IM) / (MU = million units)

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112
Q

Tx for {SEC} Syphilis :

[Secondary Systemic Sx]⼀[Early latent <12mo] ⼀[Chancre primary]

A

[BPG 2.4MU]

x 1

________________

(BPG = BENZATHINE PCN G -IM) / (MU = million units)

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113
Q

What other stages of Syphilis share the SAME TREATMENT as

[Early latent <12 mo] -2

A

[Chancre primary]

[Secondary Systemic sx]

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114
Q

Tx for Congenital syphillis

A

[aPG 50,000 u/kg/dose]

[q10h]

[x 10 days]

________________

(aPG = aqueous PCN G -IV) / (**MU = million units)

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115
Q

Positive syphilis serology but no symptom stage = ⬜

What sx make up ____ stage

Primary syphilis? -2

Secondary systemic?-3

Tertiary?-4

A

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

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116
Q

What is the Jarisch Herxheimer reaction?

_________________

How can it be prevented?

A

2 day long acute fever after initial syphilis treatment

_________________

THERE IS NO EFFECTIVE PREVENTION AT THIS TIME

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117
Q

How do you manage Dumping syndrome? (4)

A
  1. High protein diet
  2. low carb diet
  3. small meals
  4. frequent meals

goal is to DEC passage of food into small intestine

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118
Q

What are the 3 criteria for diagnosing Liver Failure?

A

ELI has Liver Failure!

  1. Encephalopathy
  2. Liver injury evidence (transaminitis)
  3. INR GOE1.5
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119
Q

HDS Pt with HBV Surface antigen, and [HBV CoreIgM] has diagnosis ⬜

Explain the dispo for this patient

A

[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

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120
Q

Describe Serology for Hepatitis B -7

A

S - SEC - SCEb - Core - CEbSAb - CSAB - SAb

  • • unvaccinated pts acutely exposed to Hep should STILL get vaccinated in addition to the immunoglobulin*
  • • CSAB = RESOLVED HEP B INFECTION*
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121
Q

Most common side effects of [INH (isoniazid)] -2

A

Injuries to Nerves and Hepatocytes

_________________

Neuropathy (Pyridoxine B6 = tx/px)

Hepatitis - THIS IS SELF LIMITED AND RESOLVE WITHOUT INTERVENTION

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122
Q

The Hepatitis A vaccine is recommended for which groups - 3

A
  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

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123
Q

What 2 laboratory values are the best diagnostic test for [acute Hepatitis B infection]?

A

S - SEC - SCEb - Core - CEbSAb - CSAB - SAb

[SAg and CoreIgM]

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124
Q

HDS pt presents with [HBV SAg] and [HBV CoreIgM]; consist with diagnosis ⬜

Explain the management (3)

A

[acute HBV];

after [acute HBV] 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
Q

After acquiring [acute HBV], what is the risk of developing Chronic Hepatitis B?

A

5%

(based on age)

126
Q

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

A

> ≥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
Q

Sepsis is generally defined as ⬜-5

What is the clinical criteria for

Sepsis? -2

A

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
Q

For patients with Sepsis, [SIM⼀Sepsis Initial Management ( ⬜4 )] must be executed within ⬜ in order to ⬇︎ Mortality

A

SIMLBAF (Lactate/BCx/Abx/Fluids)

_________________

[first1-3H]

129
Q

What is the clinical definition of

Septic Shock? -2

A

{[Sepsis(infection + ≥2 organ system dysfxn)] + [refractory hypOtension(vasopressor, lactatemia]}

130
Q

What is gastroparesis? (3)

A
  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
Q

Describe the symptom triad for [Disseminated Gonococcal infection]

A
  1. [Several migrating asymmetric joint pain (or purulent monoarthritis)]
  2. Tenosynovitis ⼀pain with passive extension and/or TTP over flexor sheaths
  3. Dermatitis

note: dx = [+ gonorrhea urogenital NAAT]

132
Q

Stress Ulcers have multiple causes

What are the indications for (i.e. the major causes of) Stress Ulcer Prophylaxis? (10)

A

stress ulcer from {[GIVE_BS] ≥1| [sico] ≥2}

≥1

[GI bleeding or GI ulcer in last 12 mo]SHOCK

[INR>1.5(or [platelet<50K] or [PTT>2x normal control] ⼀coagulopathy)]

[Ventilator >48h]

hEad trauma

Burn severe

Spinal cord injury

  • ≥2*

sepsis

[iCU > 1wk]

cTS

[occult GI bleeding > 6d]

133
Q

Stress Ulcers have multiple causes

What 2 medications are used for Stress Ulcer Prophylaxis?

_________________

{ [GIVE_BS] ≥1| [sico] ≥2}

A

PPI > [H2 R Blocker]

stress ulcer? { [GIVE_BS] ≥1| [sico] ≥2}
134
Q

Stress Ulcers have multiple causes and require PPI px

How does [hEad trauma] cause stress ulcer?

_________________

{ [GIVE_BS] ≥1| [sico] ≥2}

A

Head trauma ➜ [INC gastrin secretion] ➜ [parietal cell acid secretion] ➜ stress ulcer

PPI > H2 R Blocker = px

135
Q

Stress Ulcers have multiple causes and require PPI px

How does [iCU > 1wk]Critical Illness cause stress ulcer?

_________________

{ [GIVE_BS] ≥1| [sico] ≥2}

A

[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
Q

Stress Ulcers have multiple causes and require PPI px

How does hypOtensive Shock cause stress ulcer?

_________________

{ [GIVE_BS] ≥1| [sico] ≥2}

A

hypotension ➜ gastric mucosa ischemia ➜ INC permeability ➜ stress ulcer

PPI > H2 R Blocker = px

137
Q

What are Spider Angiomas?

A

[Blanching bright red papules surrounded by outward radiating vessels]

(2/2 dilated central arterioles from cirrhosis)

138
Q

pts with [HIV and on HAART] often develop which metabolic condition?

Describe the features of this metabolic condition (4)

A

[HIV lipodystrophy DIVE]

Dyslipidemia

Insulin resistance

[Visceral obesity (lipoatrophy + buffalo hump)]

Elevated CVD risk

139
Q

pts with [HIV and on HAART] often develop which metabolic condition?

Due to [Elevated CVD risk] this condition causes, which medication should be initiated if these [HIV HAART] pts have [CVD10Y >7.5%]?

A

[HIV lipodystrophy DIVE]; RAPstatin

RAPstatin (Rosuvastatin or Atorvastatin or Pravastatin)

140
Q

Mngmt for Diverticulitis (4)

A
  • Colonic Bacterial Abx
  • NPO
  • IVF
  • rule out colon CA
141
Q

MOD of [AMBIC- Acute Mesenteric Bowel ischemic colitis]

A

[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
Q

[AMBIC - Acute Mesenteric Bowel ischemic colitis]

Sx (5)

A
  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
Q

[(AMBIC) Acute Mesenteric Bowel ischemic colitis]

Labs (4)

A
  • AMBIC* ⇪ WAHL products!
    1. WBC ⇪
    2. Amylase ⇪
    3. Hgb ⇪
    4. [LACTATE ⇪ ➜ metabolic acidosis]

________________

CTA revealing air & edema in bowel wall –> thickening = AMBIC

144
Q

[(AMBIC) Acute Mesenteric Bowel ischemic colitis]

Mngmt (6)

A
  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
Q

[(AMBIC) Acute Mesenteric Bowel ischemic colitis]

Dx (2)

A

[CT Angiogram (bowel wall thickening from air/edema)]

vs. [Mesenteric Angiogram]

_________________

146
Q

Diverticulitis Dx

A

CT revealing [bowel wall FREE AIR & edema]

147
Q

AMBIC and Acute Diverticulitis have similar clinical presentations

What main sx differentiates AMBIC from Acute Diverticulitis?

A

AMBIC = BLOODY DIARRHEA

Diverticulitis = nonbloody Diarrhea

148
Q

In addition to analgesia, what is the tx for acute Herpes Zoster? -2

A

[valacyclovir PO]7d < [rash 3 days old]\_≤\_[ZINC OXIDE CREAM]

________+________

analgesia

149
Q

[Primary Biliary Cirrhosis]

clinical features (4)

A
  1. {[intrahepatic bile duct] autoimmune obliteration with fibrosis ➜ [ALP ⇪ ⇪ ⇪]}etx
  2. {asx ➜ [Fatigue + Pruritus + (Xanthelasma HLD(from ⇪ cholesterol) + ⇪TOTALconjugated Bilirubin ]}sx
  3. [AMA]dx
  4. ={[UrsoDeoxyCholic Acid ➜ Liver Transplant(CURE)]}tx

AMA = Antimitochondrial Antibody

primary biliary cirrhosis
150
Q

In the U.S., water soluble vitamin deficiencies are 2/2 ⬜, ⬜ and ⬜

A
  • [chronic EtOH],
  • [restrictive diets (anorexia nervosa)],
  • [malabsorption syndrome]
151
Q

What are [Riboflavin B2] deficiency sx? (2)

A
  • Angular cheilitis
  • Stomatitis
[Angular cheilitis ⼀Riboflavin B2 deficiency]
152
Q

[Niacin B3] deficiency sx (4)

A

[Pellagra DDDD]

  1. Dementia
  2. [Dermatitisphotosensitive]
  3. Diarrhea
  4. Death
153
Q

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)

A

[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
Q

Most organizations recommend 2 step pre-employment testing for Tuberculosis. What does this mean?

Why is this done?

A

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
Q

After finishing their treatment regimen, when are patients with [active TB infection] considered no longer infectious?

A

after [3 consecutive negative [AFB sputum smears]]

_________________

[AFB=Acid Fast Bacilli] | 24h intervals and GOE 1 morning sample

Tuberculosis
156
Q

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]?

A

[PAC]14d –(if persistent/allergic/resistant)–> [PBMT]14d

_________________

  • [PAC = PPI + Amoxicillin + Clarithromycin]*
  • [PBMT = PPI + Bismuth(or diff abx) + Metronidazole + Tetracycline]*
157
Q

HPylori is a strong risk factor for developing which 3 conditions?

A
  1. PUD
  2. gastric ADC
  3. MALT lymphoma

_________________

tx = PAC14d–(prn)–> PBMT14d

158
Q

How is Misoprostol related to NSAIDs?

A

Misoprostol is a prostaglandin that inhibits gastric acid secretion and improves mucus defenses = prevents ulcers a/w NSAIDs

159
Q

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]?

A
  1. persistent symptoms
  2. HPylori associated ulcer on endoscopy
  3. HPylori associated MALT
160
Q

HPylori eradication confirmation is used in 3 High Risk situations

Name the 2 most common methods of [HPylori eradication confirmation]

A

GOE4w after completing [initial triple [PAC]14d ] ➜

  • urea breath test or
  • HPylori stool antigen test
    • *
  • tx = PAC14d–(prn)–> PBMT14d*
161
Q

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]

A

[PBMT]14d

[PBMT = PPI + Bismuth(or diff abx) + Metronidazole + Tetracycline]

162
Q

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

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
Q

In Tuberculosis dx,

Although TST and IGA have comparable accuracy, what are the 3 advantages IGA has over TST?

A

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))*

⚠️📺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
Q

What is the most common cause of asymptomatic isolated transaminitis?

_________________

What causes this?

A

NAFLD

_________________

insulin resistance (RF Obesity and DM)

dx confirmation = US revealing liver hyperechoic texture c/w steatosis

165
Q

Describe the clinical presentation of acute hepatitis from HAV (5)

A
  1. acute transaminitis in 1000s
  2. Fever
  3. Jaundice
  4. Abd pain
  5. Vomiting
166
Q

⬜ lab test is used to detect primary biliary cirrhosis

_________________

Recite clinical manifestations (6)

A

[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
Q

In patients with suspected [NAFLD (asymptomatic isolated transaminitis)], ⬜ is needed to confirm the diagnosis

A

[US revealing liver hyperechoic texture c/w steatosis]

168
Q

What are the guidelines for Colon Cancer Screening? -3

A
CRC Screening 2022
169
Q

What are the [ColoRectal Cancer screening options] available for otherwise normal patients(⊝UC, ⊝[FDR CRC or HR Polyp])? (7)

A

a. [cscope]q10y

CRC Screening 2022

b. [gFOBT]q1y
c. [FIT]q1y
d. [FIT-DNA]q1-3y
* * *
e. [CT colonography]q5y
f. [Flexible Sigmoidoscopy]q5y
* * *
g. [(Flexible Sigmoidoscopyq10y) + (FITq1y)]

170
Q

genetic testing to test for [hereditary colon cancer syndromes] (such as ⬜ and ⬜ ) is usually recommended for patients who have ⬜

A

[FAP (Familial Adenomatous Polyposis); [Lynch Hereditary Nonpolyposis CRC];

Strong family hx CA

171
Q

Small Intestinal Bacterial Overgrowth

how is Dx confirmed? (2)

_________________

SIBO can be a complication of ⬜ or ⬜

A

▶[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
Q

what abx are used to treat SIBO? -4

_________________

Small Intestinal Bacterial Overgrowth

A
  1. amox/clav
  2. rifaXimin
  3. fluoroquinolones
  4. metronidazole
    * SIBO = gram negative*
173
Q

SIBO

Management? (3)

A
  1. correct underlying cause (i.e. SSS)
  2. dietary modification
  3. abx(amp_sulf or amox_clav|rifaXimin|fluoroq|metronidazole)
174
Q

Loperamide MOA

A

[weak opioidmu R agonist] ➜ [slows intestinal motility] ➜ improves diarrhea

175
Q
  • 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
A

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
Q
  • 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

A

IRIS

_________________

[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
Q

Lyme Disease has 3 Clinical Symptom Stages: eL ➜ ED ➜ L

[eLLyme Disease] occurs ⬜ after bite from ⬜

What sx does this stage consist of? (5)

  • eL: early Localized*
A

(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)

Lyme Disease (Borrelia Burgdorferi)
178
Q

Lyme Disease has 3 Clinical Symptom Stages: eL ➜ ED ➜ L

[EDLyme Disease] occurs ⬜ after bite from a ⬜

What sx does this stage consist of? (5)

  • ED: Early Disseminated*
A

(weeks to mo) ; [Ixodes scapularis deer tick during blood feeding]

_________________

eL Lyme dx = clinical dx + empiric doxy if

Lyme Disease (Borrelia Burgdorferi)
179
Q

Lyme Disease has 3 Clinical Symptom Stages: eL ➜ ED ➜ L

[LLyme Disease] occurs ⬜ after bite from ⬜

What sx does this stage consist of? (3)

  • L: LATE*
A

(mo to years) ; [Ixodes scapularis deer tick during blood feeding]

_________________

eL Lyme dx = clinical dx + empiric doxy if

Lyme Disease (Borrelia Burgdorferi)
180
Q

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?

A

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

Lyme Disease (Borrelia Burgdorferi)
181
Q

Lyme Disease has 3 Clinical Symptom Stages: eL ➜ ED ➜ L

Tx for eLLyme disease

A

Tx eLLyme:

[⊕clinical dx?(erythema migrans, fv, HA, hx)] → give [empiric doxy]

Lyme Disease (Borrelia Burgdorferi)
182
Q

In pts with cystic fibrosis, pulmonary exacerbations are due to ⬜ and ⬜

________________

Name the empiric abx for each ? -5

A

MRSA → Vanc

Pseudomonas → [cephalosporin(cefePime|cefTAZidime) + aminoglycoside(amikacin|tobramycin))

183
Q

[meconium iLeus] indicates ⬜

________________

Describe MOD

A

Cystic Fibrosis

________________

lack of [aqueous HCO3 secretion] ➜ [inspissated (thickened) stool] that’s difficult to propel ➜ impaction in iLeum = [NARROW UNDERUSED MICROCOLON]

184
Q

A Contrast enema demonstrating microcolon is indicative of what condition?

_________________

etx?

A

Meconium iLeus 2/2 Cystic Fibrosis

_________________

[inspissated (thickened) meconium] accumulation obstructs terminal iLeum –> underused colon –> contracted microcolon

185
Q

Name the 6 major organ systems affected by Cystic Fibrosis and how they’re affected

A

LUNGS = Nasal Polyps, Digital Clubbing, Bronchiectasis, BronchiOlitis

186
Q

As long as the patient has normal GI function: …

[⬜ feeding]

is preferred over

[⬜ feeding]

A

Enteral ; {ParEnteral IV]

187
Q

In patients with normal GI function, [Enteral feeds] are more physiologic and have less complications than [⬜ feeds]

_________________

Describe clinical features of [Enteral feeds] (2)

A

[ParEnteral IV feeds];

ENTERAL FEEDS

  1. {[30 Kcal/kg/day] + [1g/kg ofprotein]} = standard composition
  2. gastrostomy tube can be placed surgically or perQ
188
Q

Most patients with Splenic Vein Thrombosis have hx of ⬜ . Why is this?

A

Pancreatits❌ (acute/chronic/CA); pancreatic inflammation damages splenic vein as the splenic vein runs along pancreas posterior surface ➜ splenic vein thrombosis

189
Q

What is the hallmark of Splenic Vein Thrombosis?

A

isolated [fundal gastric varices]

tx = splenectomy

190
Q

What is Budd-Chiari syndrome? (2)

A
  • 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
Q

What is hepatic veno-occlusive disease?

A

(in the setting of Bone Marrow Transplant) ➜ Occlusion of terminal hepatic venules (not veins) ➜ postsinusoidal portal HTN

192
Q

Ascitic Guts Can Never Totally Suck”

Ascites labs =[Gram stain & culture], Color, Neutrophils, Total Protein and SAaG

________________

How do you interpret Ascites fluid Neutrophils-3?

A

[<250 = NO peritonitis]

________________

[≥250 = PERITONITISSBP vs PERITONITIS]

Neutrophils = PMN on CBC w/diff**

Ascitic Guts Can Never Totally Suck”

193
Q

Normal Range for ALT and AST is ⬜

________________

What etx’s would cause Aminotransferases to be > 1000! -5

A

8-20

194
Q

What’s an effective way to determine if Ascites is 2/2 Portal HTN ? -2

________________

Ascitic Guts Can Never Totally Suck”

A

SAaG = Serum to Ascites albumin Gradient

(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 Guts Can Never Totally Suck”

Ascites-Spontaneous Bacterial Peritonitis
195
Q

Pt presents with Ascites

What all do you order to analyze Ascites Fluid? -5

A

Ascitic Guts Can Never Totally Suck”

Ascites-Spontaneous Bacterial Peritonitis

  1. [Gram Stain & culture]
  2. Color
  3. [Neutrophils PMN on CBC w/diff]
  4. Total protein
  5. SAaG = Serum to Ascites albumin Gradient ([Serum albumin] - [Ascites albumin])
196
Q

Ascitic Guts Can Never Totally Suck”

Ascites labs =[Gram stain & culture], Color, Neutrophils, Total Protein and SAaG

________________

How do you interpret Ascites fluid Color -4?

A

Bloody = Trauma / CA / TB

Milky = chylous/pancreatic

Turbid = infection

Straw = benign

________________

Ascitic Guts Can Never Totally Suck”

Ascites-Spontaneous Bacterial Peritonitis
197
Q

Ascitic Guts Can Never Totally Suck”

Ascites labs =[Gram stain & culture], Color, Neutrophils, Total Protein and SAaG

________________

How do you interpret Ascites fluid Total Protein -8?

A

[<2.5 = Cirrhosis / nephrOtic syndrome / (SBP<1)]

________________

[≥ 2.5 = TB / Ovarian CA / R HF / budd-chiari / Fungal]

________________

Ascitic Guts Can Never Totally Suck”

Ascites-Spontaneous Bacterial Peritonitis
198
Q

Ascitic Guts Can Never Totally Suck”

Ascites labs =[Gram stain & culture], Color, Neutrophils, Total Protein and SAaG

________________

How do you interpret Ascites fluid [Serum-Ascites albumin Gradient]-8?

A

SAaG = Serum to Ascites albumin Gradient

(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 Guts Can Never Totally Suck”

Ascites-Spontaneous Bacterial Peritonitis
199
Q

⬜ 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)

A

ADENOMA ; [INC CRC ADC] = requires more frequent cscope surveillance

_________________

repeat colonoscopy interval
200
Q

⬜ 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)

A

ADENOMA ; [INC CRC ADC] = requires more frequent cscope surveillance

_________________

repeat colonoscopy interval
201
Q

⬜ 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)

A

ADENOMA ; [INC CRC ADC] = requires more frequent cscope surveillance

_________________

repeat colonoscopy interval
202
Q

⬜ 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)

A

ADENOMA ; [INC CRC ADC] = requires more frequent cscope surveillance

_________________

repeat colonoscopy interval
203
Q

⬜ 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)

A

ADENOMA ; [INC CRC ADC] = requires more frequent cscope surveillance

_________________

includes FAP (Familial Adenomatous Polyposis)

repeat colonoscopy interval
204
Q

⬜ 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)

A

ADENOMA ; [INC CRC ADC] = requires more frequent cscope surveillance

_________________

repeat colonoscopy interval
205
Q

⬜ polyps are the most common neoplastic colon polyp and are associated with ⬜

_________________

After Colonoscopy, patients with which findings require COLECTOMY? (2)

A

ADENOMA ; [INC CRC ADC] = requires more frequent cscope surveillance

_________________

HRPlymphovascular involvement

HRPCA extends to specimen margin

__________

High Risk Polyps with invasive malignancy:

repeat colonoscopy interval
206
Q

Why do pts with Crohn disease have ⬆︎ development of Kidney stones?

A

They have fat malabsorption which –> ⬆︎oxalate absorption –> Ca+Oxalate precipitation in the kidneys

207
Q

Endoscopic findings for Ulcerative Colitis

A

Continuous Friable mucosa with ulcers

208
Q

Pts with Ulcerative Colitis are at risk for _____ CA; What’s px for this?

A

Colorectal ;

8 years after diagnosis –> Screening Cscope with mucosal sampling q1-3years

209
Q

Which IBD condition are Pseudopolyps associated with?

A

Ulcerative Colitis

210
Q

[Ulcerative Colitis IBD] Sx (11)

A

U

L L

C C C C

E

R R

S

_____________________________

INFLAMMATORY BOWEL DISEASE- [Ulcerative Colitits]
211
Q

[Crohns IBD] Sx (11)

A

Crohns Can FCK GRT DCS

_____________________________

INFLAMMATORY BOWEL DISEASE- [CROHNS]
212
Q

describe

hepatic adenoma

________________

tx? -2

A

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
Q

Clinical features of Barrett Esophagus (4)

A
  1. [distal esophageal intestinal metaplasia**] that can →intestinal dysplasia → [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 ablationIF ⊕DYSPLASIA ONLY ]
214
Q

HPylori causes atrophic gastritis and [⬜ ADC], but not [⬜ ADC]

A

[gastric ADC];

[Barrett Esophagus/Esophageal ADC]

215
Q

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)

A

AAA

[Ammonia INC] , AMS, Asterixis

{precipitating event

most common= [hypOvolemia from diuretics given for ascites] > [hypOkalemiaconverts ammonium → ammonia] = [metabolic alkalosisDEC urinary ammonia excretion] = infxn }

→ [Ammonia INC]

  1. lactulose(DEC Ammonia)
  2. rifaximin(DEC Ammonia)
  3. correct precipitating event (IVF, abx, elyte )
216
Q

What are the major risk factors for [CRC ADC]? (4)

; minor? (4)

ColoRectal CA ADC

A
  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
Q

What are the protective factors for ColoRectal CA? (4)

A

a. fvf diet (fiber rich/vegetable/fruits)
b. exercise
c. NSAIDs
d. HRT

218
Q

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?

A

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
Q

Describe the path the parasympathetic CNS uses to coordinate with the [GI NS (i.e. ⬜ )] and activate peristalsis (3)

A

[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
Q

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)

A

[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
Q

What are the potential complications that cause [complicatedacute diverticulitis]? (4)

A

[complicated acute diverticulitis]

222
Q

What is the ___X___ of [Distal Esophageal Spasm]

a1. pathophysiology (3)
a2. How does this differ from Achalasia? (3)
* * *
b. how is diagnosis confirmed?

A

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 BeakNarrowed 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

Diffuse Esophageal Spasm
223
Q

What is the ___X___ of [Distal Esophageal Spasm]

c. symptoms (2)
d. treatment (2)

A

c.

  • solids & liquid stuck sensation”(worst with hot/cold food) = [COMPLETE dysphagia]
  • Intermittent cp
    • *
      d. CCB, [TCA if cp-predominant]
Diffuse Esophageal Spasm
224
Q

Pt p/w Hematochezia

How do you initially work this up? (4)

A
Hematochezia initial workup
225
Q

Pt p/w Hematochezia

When would Angiography be considered for these patients?

A
  • [Hematochezia⼀ persistent] → HDUS
  • [⊝EGD]

→ Angiography

Hematochezia initial workup
226
Q

The ⬜ separates [upper GI tract] from [lower GI tract].

BUN/Cr ratio ⬜ suggest [Upper GI Bleed].

Explain why Nasogastric aspiration can be problematic

A

[Ligament of Treitz] ;

> 20:1 ;

NGL aspirating +bile/-blood: [( iNGLO ) = No UGIB(but note: this may miss distal UGIB)]

227
Q

Explain the main sx discernment between Diverticulosis and Diverticulitis

In terms of workup, why is it important to discern the two?

A
  • osis=* [Hematochezia BRBPR] → [CSCOPE ✅]
  • ITIS= [(NO Hematochezia BRBPR)* + (LLQ TTP), FEVER…] → [CSCOPE c❌d]
228
Q

Achalasia

pathophysiology

A

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
Q

MOD for this finding

Dx?

A

[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
Q

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)

A

[( CiAMi ) chronic intestinal angina mesenteric ischemia]

Angiography > nonInvasive[CTA, MRA, US duplex]

_________________

c/s nonInvasive dx to localize obstructrion → angiography to resolve

231
Q

what is the tx for [CirrhosisAscites] - 3

Ascites 2/2 Cirrhosis

A
  1. Furosemide
  2. Na+ restriction
  3. Spironolactone

Tx:[(Furosemide/Na+ restriction/Spironolactone) –(REFRACTORY)–> TIPS].

232
Q

what is the tx for Hepatic Encephalopathy - 2

A
  1. Lactulose
  2. Rifaximin
233
Q

Hepatic hydrothorax presents as ⬜ in patients with ⬜. Treatment consist of ⬜2. Explain MOD

A

[R transudative pleural effusion]; [CirrhosisAscites]

Tx:[(Furosemide/Na+ restriction/Spironolactone) –(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
Q

Acute Cholangitis

a. etx
* * *
b. cp (5)

A

a. biliary tree obstruction → ascending infection
b. [RUQ pain + Jaundice + fever= charcot’s triad+AMS, hypOtension = Reynold Pentad]

Acute Cholangitis

cholangitis dx =cholangitis siLx = cholangitis sxCharcot triad + cholangitis ixERCP/US/CT with Biliary Dilation + cholangitis LxCholestasis labs

235
Q

Acute Cholangitis

a. how is it diagnosed? (3)
* * *
b. treatment (2)

A
  1. ERCP/US/CT: Bile Duct Dilation
  2. ⇪cholestasis labs ( ⇪ Direct Bilirubin/ ⇪ ALP/ ⇪ LFTs-mildly)
  3. Charcot’s triadRUQx, Jaundice, Fever

_________________

Acute Cholangitis

  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
Q

⬜ is responsible for [Cirrhosis sequelae].
List sx of [Cirrhosis sequelae] (4)

A

hyperestrogen;

  1. Palmar erythema
  2. spider angioma
  3. loss of sexual hair
  4. testicular atrophy
237
Q

Screening for Barrett’s Esophagus [via ⬜] is indicated if patient has ⬜ or more risk factors.

Name the 7 risk factors for Barrett’s Esophagus

A

[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]
Barrett esophagus mgmt
238
Q

Patients with ⬜ or more Barrett’s Esophagus risk factors should be screened for it with ⬜

How should you manage Barrett’s Esophagus if screening is ⊕? -3

A

2 ; [upper GI EGD]

239
Q

prior to medium/high risk procedures, interrupting ⬜ is necessary to DEC surgical bleeding

________________

which patients do require bridging prior to surgery? -4

A

[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
Q

What is Bile Salt-Induced Diarrhea?

________________

tx?

A

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
Q

⬜ is a risk factor for developing Eosinophilic Esophagitis (which is triggered by ⬜)

cp? -4

________________

Tx?3

A

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
Q

dx for Acute Cholecystitis -2

________________

What if this method is inconclusive?

A

Ultrasound showing

[cholelithiasis]

+

[gallbladder wall thickening] OR [sonographic Murphy sign]

________________

➜ HIDA (if above inconclusive)

243
Q

Charcot Triad consist of [⬜3] and indicates ⬜

________________

Describe this disease

A

[Fever + Jaundice + RUQ pain] = Acute Cholangitis = [bile duct gallstone obstruction] ➜ impaired biliary drainage ➜ ascension and infection of enteric bacteria in biliary duct

________________

cholangitis dx =cholangitis siLx = cholangitis sxCharcot triad + cholangitis ixERCP/US/CT with Biliary Dilation + cholangitis LxCholestasis labs

244
Q

Pt presents with Fever, Jaundice and RUQ pain

Management? -2

A

[ERCP biliary decompression/drainage - within 48h]

+

enteric abx

________________

dz = Acute Cholangitis

245
Q

organisms most commonly associated with

intraAbdominal -2

A

E coli

Bacteroides fragilis

246
Q

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

A

brisk UPPER ; EGD

________________

hematochezia (BRBPR) is usually a/w lower GI bleed but BRISK upper GI bleeds also cause hematochezia

247
Q

SBP

patient p/w ascites

How do you diagnose Spontaneous Bacterial Peritonitis?

Ascites
A

Ascitic Guts Can Never Totally Suck”

_________________

labs from Ascitic fluid_revealing:

⊕[GramStain & Culture](often gram negative)

⊕[Color: Turbid]

⊕[Neutrophils PMN on CBC w/diff] ≥250

⊕[Total protein < 1]

⊕[SAaG ≥1]

248
Q

⬜ is a common cause of AKI in patients with Cirrhosis, but is a diagnosis of exclusion

what’s the tx for this? -3

A

[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
Q

How is smoking related to surgery?

A

smoking cessation ≥4 weeks prior to surgery ⬇︎ pulmonary complication risk postop

PFT, ABG, etc. preop will not help

250
Q

Why are patients undergoing [major surgery with extensive transfusions] at ⇪ risk of developing [Hyperactive Deep Tendon Reflexes]?

A

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
Q

What is gallstone pancreatitis?

________________

Management for gallstone pancreatits? (mild vs severe)

A

pancreatitis (epigastric abd pain/NV/cholic/⇪ lipase) in the setting of [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
Q

Name the 12 Absolute Contraindications to Organ Donation

A
253
Q

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

A

OFFICIAL CLINICAL DEATH =[BS_HL dead.]

_________________

{ [Brain] [brainStem] [Heart] [Lungs] } = NO activity = dead.

254
Q

[Boerhaave Esophageal Perforation] MOD

________________

Delay of surgical intervention leads to what complication

A

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
Q

Name the differentiating sx between [Mallory Weiss tear] and [Boerhaave Esophageal Perforation]

A

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
Q

cp for [Perforated gastric ulcer] -3

A

-acute severe abd pain with
-[free air under diaphragm on upright CXR]
-HDUS= SURGICAL EMERGENCY

257
Q

[Boerhaave Esophageal Perforation] dx (2)

A

[esophaGography] vs. [water soluble contrast CT]

258
Q

⬜ infections develop in up to 50% of patients with acute variceal bleeding.

Management?

A

BACTERIAL (SBP/PNA/UTI) ;

( [Ceftriaxone IV x 7 days] prophylaxis)

259
Q

the primary tx for all Hernia is what?

A

surgery
_________________
complications: incarceration vs strangulation

260
Q

s/s of Compartment Syndrome -6

A

[Pain (especially with Passive stretch)]

Paresthesia

Poikliothermia
_________________

Paralysis

Pulselessness

Pallor

261
Q

What are the 2 lab features of [Subclinical hypOthyroidism]?

________________

[Subclinical hypOthyroidism] is usually not treated. What are the 4 exceptions?

A

[⇪ TSH] with [normal T4 Thyroxine]

________________

  1. antiThyroid antibodies (antiTPO)
  2. abnormal lipid profile
  3. hypOthyroidism sx
  4. ovulatory/menstrual dysfunction
262
Q

clinical definition of Rectal Prolapse
_________________

When is surgery indicated? -3

A

[when rectal tissuemucosal|FULL thickness[14] slides thru anus[15]]
_________________
🔨[Rectal Prolapse COMPLETELY] or

🔨[Rectal Prolapse w incontienence] or

🔨[Rectal Prolapse w constipation]

RECTAL PROLAPSE

🔨=surgery

263
Q

what’s management of

partial SBO (*air in distal colon on XR*)? -2
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

COMPLETE SBO?

A

partial SBO = [conservative x 24h] –(sx persist)–> [XLAP]
_________________

COMPLETE SBO = XLAP

_________________
conservative = IVF / NG suction / electrolyte correction

264
Q

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] ?

A

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
Q

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

A

45 ; 10
_________________

266
Q

Dumping Syndrome MOD

________________

Dumping Syndrome Sx(5)

A

rapid emptying of hypertonic stomach contents into small intestine (usually after gastrectomy or RYGB) –> DDUMP

________________

Diarrhea

Diaphoresis

[Umbilical ABD Pain]

M (N)ausea

Palpitations

worst after eating and better at night

“avoid DDUMPafter RYGB plus give [F, D, C and Bx3]”

267
Q

[SIBO - Small Intestinal Bacterial Overgrowth] MOD
_________________

clinical features of SIBO (6)

A

(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
_________________

Stinky flatulence / [Intestinal lack of TTP OR Fever] / [bloating | b12 deficiency | ⊕breath LactuLOSE test] / [Oasis WATERY Diarrhea]

_________________

[NO abd pain (CDiff has diffuse abd pain)]

[NO fever (CDiff has FEVER)]

268
Q

How do you manage a patient presenting after accidentally swallowing a sharp fish bone?

A

EMERGENT FLEX ENDOSCOPY
_________________
any sharp object in esophagus must be removed emergently with flex endoscopy

269
Q

patients with large TBSA burns have high mortality rates

How do you determine if burn patients require hospice? -3

A

[revised Baux score] =

[age + TBSA (+17 if inhalation injury present)] > 140= poor survival pgn

→ pt will likely need HOSPICE

270
Q

How do you differentiate cp of duodenal ulcer vs gastric ulcer
_________________

Whats the tx for HPylori Ulcer -7

A

[DEC = D​uodenal] <–(EPIGASTRIC PAIN AFTER MEAL)–> [GETS WORST = Gastric]

_________________

[PAC]14d –(if persistent/allergic/resistant)–> [PBMT]14d

_________________

  • [PAC = PPI + Amoxicillin + Clarithromycin]*
  • [PBMT = PPI + Bismuth(or diff abx) + Metronidazole + Tetracycline]*
271
Q

After Triple Therapy, what 3 clinical elements warrants CONFIRMATION of H Pylori eradication?
_________________

How is eradication confirmation done? -2

A

duodenal ulcer | ongoing dyspepsia | MALT lymphoma
_________________

([Urea Breath test] or [Fecal Antigen test])

x 4 weeks after Triple Therapy

272
Q

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?

A

45 ; 10
_________________

COLONOSCOPY STAT

(follow ⊕FlexSigmoidoscopy with STAT Colonoscopy to scan entire colon for proximal colon adenomas and advanced neoplasia)

273
Q

In patients with SEVERE malnutrition, which route of administration is the preferred method of rehydration? why?
_________________

A

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
Q

What is Chronic Exertional Compartment Syndrome?

A

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
Q

describe Autoimmune hepatitis
_________________
lab findings (2)

\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
 diagnostic labs (2)
A

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
Q

How are the results of the D-xylose test interpreted? -2

_________________

How does Rifaximin play a role in this?

A

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
Q

What type of diarrhea is associated with [decreased stool osmotic gap < 50]

A

Secretory

these are larger volume diarrhea that occurs during fasting or sleep

278
Q

What type of diarrhea is associated with [INCREASED stool osmotic gap > 125]

A

Osmotic

ex: Lactose intolerance

279
Q

What are the laboratory findings for Lactose intolerance? - 5

Lactose intolerance is most commonly seen in Asians

A
  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
Q

There are 4 Malabsorption syndromes

Describe clinical features of Lactose Intolerance (4)

A
281
Q

There are 4 Malabsorption syndromes

Describe clinical features of Chronic Pancreatitis (2)

A
282
Q

what are the sx of Viral gastroenteritis (3)
_________________

it is transmitted via ⬜ with which 2 viruses?

A

[WATERY DIARRHEA +/- vomiting]

Abd pain

[+/- Fever]
_________________

283
Q

tx for Viral gastroenteritis (3)

A

self-limited

  1. oral rehydration (mild)
  2. IV REHYDRATION (SEVERE)
  3. [Regular Limited Lipid(fat)/ Simple Sugardiet as tolerated]
284
Q

The major side effects of [INH Isoniazid] for TB are peripheral neuropathy and ⬜.

How do you manage each side effect?

A

[HEPATITIS]

(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
Q

Porcelain Gallbladder is often asymptomatic and found incidentally. What is it?
_________________

Why is it clinically significant?

_________________
What’s the management? -2

A

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
Q

In neonates, how might Cystic Fibrosis present? -4

A

Meconium iLeus = inspissated GI secretions obstruct meconium excretion in distal iLeum ➜

[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
Q
  • List Main differences between Esophageal SQC and Esophageal ADC :*
  • Location
  • What risk factors are associated with each?
A

[eSQC = UPPER esophagus = Tobacco , EtOH]

[eADC = lower esophagus = GERD/Barrett’s]

288
Q

What is the TRIAD PRIORITY for managing [Brain-Dead Organ Donors] ?

A

MUST MAINTAIN NORMAL PET w IVF / Desmopressin

Pressure

Euvolemia

Temperature (or mild hypothermia)

289
Q

What Lipase level is c/f Acute Pancreatitis in Adults?

A

GOE 1,000

290
Q

What Lipase level is c/f Acute Pancreatitis in kids?

A

GOE 7 x upper limit of nl for that age group

291
Q

What supplements will pts s/p RYGB (Gastric bypass Surgery) require? - 6

Roux-en-Y Gastric Bypass
A

“avoid DDUMPafter RYGB plus give [F, D, C and Bx3]”

Fe

D3cholecalciferol

Ca+

B1Thiamine

B9Niacin

B12Cobalamin

292
Q

Why does compartment syndrome cause kidney damage?

A

compartment syndrome –> myoglobin release –> [myoglobin heme] is nephrotoxic

293
Q

Compartment Syndrome Dx- 2

A
  1. [Direct Compartment Pressure > 30]
  2. [delta pressure(diastolic BP - Direct) < 20]
294
Q

Which part of the Esophagus is [Esophageal ADC] located?

A

LOWER

a/w Barrett’s and GERD

295
Q

Which part of the Esophagus is [Esophageal SQC] located?

A

UPPER

a/w SMOKING AND EtOH

296
Q

What is [Enteropathy associated T cell Lymphoma (EATL)] ?

A

Jejunal CANCER from [NON-COMPLIANT CELIAC DISEASE]

similar sx to celiac but long standing

297
Q

describe pathology for Crohn disease

A

Transmural GI inflammation

Crohns Can FCK GR🅃 DCS

298
Q

What type of diarrhea is associated with INCREASED stool osmotic gap > 125

A

Osmotic

ex: *“Can Larry –“*Celiac, Lactose intolerance

299
Q

What are the laboratory findings for LactOse intolerance? - 5

LactOse intolerance is most commonly seen in Asians and AA

A

LactOse Intolerance =
1. = {INC Stool Osmotic Gap>125 a/w [LARGE OASIS (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

Definitely Produces Flatulence”

LactOse Intolerance is most commonly seen in Asians and African Americans

300
Q

generally describe distinguishing sx for these 4 conditions

Celiac

[Irritable Bowel Syndrome]

[Inflammatory Bowel Disease]

Lactose Intolerance -2

A

Celiac(TWICED) = {INC 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

________________

LactOse Intolerance = {INC Stool Osmotic Gap>125 a/w [LARGE OASIS (WATERY) DIARRHEA]}postprandial + postprandial flatulence, Asian=RF

301
Q

Where is the intestinal enzyme lactase located?

A

Duodenal brush border

________________

LactOse intolerance Definitely Produces Flatulence

302
Q

[MASSIVE Rectal Bleeding in Adults] ddx -3

A
  1. Diverticulosis (L colon)
  2. Ulcerative Colitis
  3. [angiodysplasia AVM (R colon)]
303
Q

[MASSIVE Rectal Bleeding in Adults] with active hemorrhaging dx -2

A
  1. radionuclide scintigraphy
  2. Angiography
304
Q

Why is Nasogastric tube placement helpful in patients with hematochezia?

A

helps discern UGI Bleed from LGI Bleed

10% of hematochezia come from the upper GI tract

305
Q

Why is BUN elevated in [Profuse Rectal Bleeding]? (4)

A

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
Q

Indication for [Blood Transfusion (pRBC)] -2

A
  1. Hb < 7

OR

  1. [Cardiac Patients Hb < 8]
307
Q

Tx for active & brisk [Angiodysplasia hematochezia] -5

A
  1. MOST ANGIODYSPLASIA RECTAL BLEEDING STOPS SPONTANEOUSLY
  2. endoscopic coagulation (if #1 fails) ➜
  3. arterial embolization by catheterization (if #2 fails) ➜

➜ 4. subtotal colectomy

  1. aortic valve replacement (if aortic stenosis)(Heyde’s syndrome)

.

do not use vasopressin

308
Q

Heyde’s Syndrome

A

[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
Q

Why should Raloxifene be d/c before surgery?

A

SE = DVT/PE