8⼀GI/SURGERY/ID I Flashcards
newly diagnosis Type 1 DM should be screened with which 3 antibodies?
_________________
Why do we do this?
[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
Dx for Celiac disease - 4
________________
wt loss+ iron deficiency anemia + dermatitis herpetiformis = CELIAC!
“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!)
There are 4 Malabsorption syndromes - “_C_an Larry Control Stooling?”
Describe clinical features of Celiac disease (6)
“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
What are the 4 malabsorption syndromes?
_________________
Which 2 have [INC stool osmotic gap > 125]
Can Larry Control Stool?
[Celiac / Lactose intolerance = INC stool osmotic gap>125]
Chronic pancreatiits / SIBO
These cells are a/w ⬜
_________________
Describe the cp (5)
dx = atypical reactive lymphocytes
[EBV ⼀Infectious Mononucleosis]
_________________
- TIRED TEEN
- Fever
- exudative Tonsillitis
- cervical LAD
- HepatoSplenomegaly
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
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
Aside from STAT Laparotomy, name 3 other treatments used in perforated peptic ulcer?
- IVF
- IVAbx
- IVPPI
+ STAT Laparotomy
Serum Sickness etx
________________
What infection mimics this?
[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)
Having [1st degree relatives with CRC < 60 yo] modifies CRC screening schedule
Describe modified CRC screening (2)
[CScope at 40 yo (or 10y prior to relative’s age at their diagnosis)]
q5 years
What causes Necrotizing fasciitis in
_____ patients?
a. healthy?
_________________
b. DM (poor circulation)?
a. polymicrobial
_________________
b. GASP
Necrotizing fasciitis s/s (4)
- POOP
- swelling
- erythema
- fever
[DM = GASP] / [EE = polymicrobial]
s/s GERD (2)
_________________
management? (2)
-[reflux/heartburn]
-cough
_________________
[daily PPI8 wk trial] + [lifestyle ∆]
GERD = sx > 2x/week
alarm sx (odynophagia/dysphagia/GI bleeding/wt loss) = referral for EGD
dysphagia means difficulty ⬜
Describe the 2 types of dysphagia?
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
Describe the differences between the 2 types of Esophageal Cancer
UPPER esophagus = [SQC: (EtOH / smoking)]
_________________
lower esophagus = [ADC: (GERD / Barrett’s esophagus)]
normal range for
LDL
<100
normal range for
TAG
TriAcylGlycerides
<150
normal range for
HDL
50+
normal range for
TOTAL CHOLESTEROL
<200
________________
>240 = “HIGH”
how do you diagnose Acute Pancreatitis? -2
________________
how do you diagnose CHRONIC Pancreatitis?
Lipase and amylase
________________
[MRCP Pancreatic Calcifications (or CT Abdomen)]
cp for Chronic Pancreatitis -4
________________
dx = MRCP Pancreatic Calcifications
- 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)
Tx for CHRONIC Pancreatitis? -4
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)
Causes of CHRONIC Pancreatitis? -4
- EtOH
- Cystic Fibrosis (peds)
- Duct obstruction (CA/stones)
- autoimmune
Toxic Megacolon tx -3
[CTS if 2/2 IBD]
[Abx if 2/2 infectious colitis]
[Surgery if perforation]
________________
NO SULFASALAZINE OR OPIOIDS
Barrett Esophagus MOD
chronic gastric acid ➜ [lower esophagus metaplastic replacement of {normal stratified squamous epithelium} with {intestinal columnar epithelium}] ➜ INC risk for esophageal ADC
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
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
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
Which abx is best for intraabdominal infection?
Ampicillin-sulbactam
________________
(3rd Generation PCN and beta-lactamase inhibitor)
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
How does Peptic Ulcer Disease present? -3
GASsx GOE1 mo
1. [epiGastricepigastric pain postprandial]
2. [Abd fullness postprandial]
3. [Satiety early on]
________________
get stool antigen test for H Pylori
[GERD = (Cough + Reflux) > 2x weekly]
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)]}
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
- Aortic Stenosis (vW multimers are disrupted as they pass through turbulent space –> AVM)
- Von Willebran disease
- Renal disease
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]
(metanephrine & VMA) + (urine catecholamine 24h)+(dexamethasone suppression test)
_________________
SURGICAL RESECTION:
[radiographically malignant] vs [> 4cm] vs [functional (hormone secreting)]
Primary presenting complaint for Achalasia
Food AND Liquid dysphagia
Peptic Stricture
common complication of chronic GERD - in which healing from chronic ulcerative esophagitis ➜ stricturing of Esophagus ➜ progressive (solid then liquid) dysphagia
Lactose intolerance sx (3)
Lactose Intolerance Definitely Produces Flatulence
LactASE breaks down lactose ➜ glucose + galactose
- Diarrhea WATERY
- Periumbilical abd pain
-
Flatulence
* note: [MILK / ICE CREAM > > cheese / yogurt]*
Lactose Intolerance is a clinical diagnosis, but how is the diagnosis confirmed? (2)
worst with age, asian and african american
- L*actose Definitely Produces Flatulence
1. Lactose breath hydrogen test
2. [Symptom resolution with Lactose-restricted diet]
Name the single-item predictors of INC SEVEREITY in Acute Pancreatitis (5)
“HOBCO hurt the Pancreo”
= SEVERE ACUTE PANC
- BUN ≥20
- HCT >44%
- CRP >150
- Obesity
- Old age
What is OculoGlandular syndrome?
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
describe cp of Pyoderma gangrenosum (2)
_________________
Where does it come from? (2)
PAINFUL inflammatory [nodules/pustules/vesicles] ➜ PAINFUL ULCERS
_________________
neutrophilic dermatosis a/w IBD
normal range
Lipase
<160
⬜ 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
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
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:
- [(ALVeolar-arterial O2 ∆ ≥ 35) on ABG]
________OR_________ - [(PaO2 < 70) on Room Air]
name the 3 most important goals in managing a brain-dead organ donor
MAINTAIN NORMAL “TV, B”
Temperature (or slightly hypOthermic)
Volume (IVF/desmopressin(synthetic ADH))
Blood pressure (pressors)
What is GGT used for?
_________________
gamma-glutamyl transpeptidase
Differentiates elevated ALP:
[⇪ALP and ⇪GGT] = LIVER origin
[Isolated Markedly elevated ALP (+/- ⇪ GGT)] indicates ⬜
_________________
what causes this? (2)
[infiltrative Liver disease]
_________________
- [granuloma (hepatic sarcoidosis, TB)]
- [metastatic CA]
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)
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]
- {[ESRD (*uremia ➜ platelet dysfxn ➜ [1º hemostasis❌] →🩸
- [Aortic stenosis (*mechanical disruption during turbulent valvular flow ⬇︎ vWF → [1º hemostasis❌] →🩸= Heyde’s Syndrome
-
[von Willebrand disease]→ [1º hemostasis❌] →🩸 ___________________________x____________________________________
🩸= [(in setting of ⊕aAVM) may meet threshold for aAVM to bleed]}
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
What is the best test to evaluate Pancreatic Cyst?
_________________
what are all the indications for this modality? -7
Endoscopic Ultrasound with aspiration
_________________
- lymph node bx
- pancreas lesions
- liver lesions
- adrenal glandlesions
- bile duct lesions
- peritoneal fluid lesions
- pleural fl;uid lesions
indications for ERCP (4)
THERAPEUTIC
dilated Common Bile Duct
acute biliary pancreatitis
choleDocholithiasis
cholangitis
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
Acute diverticulitis presents as (⬜2)
_________________
How is it managed?
[LLQ TTP] + [CT focal bowel wall thickening +/- diverticula]
_________________
[Dyspepsia (GAS sx ≥1 mo)]
management
_________________
trial PPI = [PPI]4-8w
pulmonary ASPERGILLUS
What are the major risk factors? (4)
immunosuppression [transplants✳, neutropenia, chronic CTS, HIV/AIDS]
✳stem cell|organ
“bloody⼀chest ⼀cough”
pulmonary ASPERGILLUS
treatment (3)
“bloody⼀chest ⼀cough”
pulmonary ASPERGILLUS
diagnostics (4)
- [CT ground glass “halo sign” nodules]
- ⊕[Galactomannan]
- ⊕[β-D-glucan]
- [Sputum samplefor fungal stain & culture]
“bloody⼀cough ⼀chest”
pulmonary ASPERGILLUS
classic symptom triad
“bloody⼀chest ⼀cough”
- bloody = [bloody cough hemoptysis]
- chest = pleurtic chest pain
- cough = [bloody cough hemoptysis]
Oral Candidiasis
treatment (3)
_________________
AKA thrush
[topical Nystatin suspension🆚Clotrimazole troches]
–(if persist)–> [fluconazole PO]
_________________
be sure to watch for proper CTS inhaler usage
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
Why are [Hepatitis A vaccination] and [Hepatitis B vaccination] so important to a person with Hepatitis C?
if superimposed with HAV or HBV, chronic HCV causes rapid decompensation and liver failure
so vaccination to HAV and HBV are important
In terms of Hepatitis B,
how do you manage a healthcare worker s/p incidental occupational exposure?
Rhabdovirus Rabies
Tx? (2)
_________________
Prognosis? (3)
[Ig + Vaccine]-(only helpful BEFORE symptom onset)
_________________
UNIVERSAL FATAL WITHIN WEEKS ONCE SYMPTOMATIC
> Coma / Respiratory failure
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])
Hepatitis C screening is done via ⬜
_________________
A patient with a positive HCV screening indicates what 3 possibilities?
HCV Ab testing
_________________
- [ACTIVE INFECTION (obtain HCV RNA to determine acute vs chronic)]
- [Resolved Infection]
- False Positive
Spontaneous Bacterial Peritonitis is a serious complication of ⬜
_________________
Treatment? (4)
cirrhosis
_________________
[Paracentesis w/ascites labs(“Guts Can Never Totally Suck”) ]
➜[Albumin IV]
➜ {[CefoTaxime3ºCPN]
➜ [Fluoroquinolone px]
- 3ºCPN = 3rd gen cephalosporin*
Spontaneous Bacterial Peritonitis is a serious complication of ⬜
cirrhosis ( can → SBP)
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)]
- [hypOtensionw/SEVERE INFXN]
- [hypOTHErmiaw/SEVERE INFXN]
- [paralytic iLeusw/SEVERE INFXN]
What is the MELD score?
and how is it used?
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
What is Succussion splash?
_________________
What does it indicate?
audible epigastric splashing sound during sudden movement
_________________
delayed gastric emptying
2/2 gastroparesis vs intrinsic obstruction vs extrinsic obstruction
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
Diabetic gastroparesis often p/w ⬜
_________________
treatment? (2)
[delayed gastric emptying (succussion splash)]
_________________
[Fmeals] –(if persist)–> [metoclopramide]
[Fmeals : Finite(small), Freq, Fatless(low fat), FiberRICH(HIGH soluble fiber)]
cp of travelers’ diarrhea?
_________________
most common cause?
3d self limited [WATERY DIARRHEA + crampy abdP] 3 days post exposure
_________________
ETEC
EnteroToxigenic E Coli (commonly from developing countries’ street vendors)
Which 2 labs must be carefully monitored before and after starting TPN?
why?
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
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
_________________
- [Phosphorous ⬇︎] = [rhabdomyolysis/ ⇪ CPK in EtOH] and/or HF
- Thiamine ⬇︎ = HF
- Mg⬇︎ = arrhythmias
- K+ ⬇︎ = arrhythmia
Refeeding syndrome can lead to the depeletion of serum Phosphorous and 3 other electrolytes such as ⬜
_________________
How is Phosphorous repletion administered?
PTMK
(Phosphorous/Thiamine/Mg/K)
_________________
ORAL Phosphorous repletion
Aside from IVF, which medication should be given promptly in Acute Variceal Hemorrhage?
Octreotide IV
Which 2 medications can be given to prevent Acute Variceal hemorrhage?
Nadolol 🆚 Propranolol
(general BBlocker [⬇︎portal system pressure] + band ligation +endoscopic surveillance)
what is charcot’s triad?
_________________
what is Reynolds pentad?
cholangitis dx =cholangitis siLx = cholangitis sxCharcot triad + cholangitis ixERCP/US/CT with Biliary Dilation + cholangitis LxCholestasis labs
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]
cholangitis dx =cholangitis siLx = cholangitis sxCharcot triad + cholangitis ixERCP/US/CT with Biliary Dilation + cholangitis LxCholestasis labs
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)
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]
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
In an immunocompromised pt, EBV DNA in the CSF raises suspicion for what condition?
Primary CNS lymphoma
MRI: Solitary Weakly ring-enhancing mass in periventricular region
Dx for EBV infectious mono - 2
- [positive HAMSonly accurate during week 1 of sx 😟]
- Anti-EBV test
________________
HAMS = [Heterophile Antibody MonoSpotonly accurate during week 1 of sx 😟]
No sports for ≥3weeks because of splenomegaly!
Tx for EBV infectious mono - 3
- [self limited x weeks (fatigue x months)]
- NSAIDs
- No sports ≥3wks
________________
HAMS = [Heterophile Antibody MonoSpot]
From a lab perspective, how do you differentiate CMV from EBV?
CMV will have a [negative HAMS]
________________
HAMS = [Heterophile Antibody MonoSpot]
[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)
Diagnosis?
Treatment? -4
Acute Paronychia (Nailfold infection 2/2 gram positive skin flora)
_________________
NAIL tx
[Neosporin/TOP antiseptics]
[Abx TOP]
[I & D abscess]
[Lukewarm soaks]
Clinical triad of [Reiters Reactive Arthritis]
_________________
When do sx onset? resolve?
‘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
Why should Chlamydia infection (symptomatic or asymptomatic) always be treated?
chronic Chlamydia may ➜ Reiters Reactive Arthritis
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
Name the 3 classic symptoms of dyspepsia
indigestion GAS
Gastric (epigastric) pain/burning postprandial
Abd fullness postprandial
Satiety early on
dyspepsia
etx (4)
difficulty digesting food 2/2
[IDIOPATHIC functional] > [gastric ADC = HPylori ulcer = NSAID ulcer]
➜ GAS sx GOE1mo
dyspepsia presents with what 3 sx ?
How long should these sx last for official dyspepsia diagnosis?
GAS = Gastric sx postprandial/Abd fullness postprandial/Satiety early on
_________________
GOE1 month
dyspepsia presents with what 3 sx ?
Upper GI endoscopy is indicated for dyspepsia [HIGH risk alarm features]
What are they? (7)
[GAS = epiGastric ∆ /Abd fullness postprandial/Satiety early on] GOE1mo
_________________
∆ = pain|burning
- ⊕fam hx gastric ADC
- odynophagia
- dysphagia
- IDA
- wt loss
- LAD
- [ age > 50]
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
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
How do you workup patient with suspected uncomplicated Gallstones? (8)
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
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]
[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].
Tx for Neurosyphillis
[aPG 4MU]
[q4h]
[x 14 days]
________________
(aPG = aqueous PCN G - IV) / (MU = million units)
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
- [Pregnancy (No DOXY for POXY)]
- refractory to initial (doxycycline)tx
- [3B5º neurosyphilis]3B5º requires {aPG 4MU q4h x 14d}
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
Name the specific signs of congenital syphilis - 3
“syphilis hurts the baby’s SKIN, NOSE & BONES!”
- SKIN: Maculopapular palms/soles_rash that desquamates vs bullous
- NOSE: Rhinorrhea
- BONES: mulberry molars, long bone metaphyseal lucency
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
Why is RPR not reliable when a person first develops syphilis?
There is a possible [false negative RPR] early in infection - follow with FTA
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
Tx for {CLUB} Syphilis :
[CV]⼀[Late latent ≥12 mo]⼀[Unknown duration]⼀[Ball•Gumma]
[BPG 2.4MU]
[q week]
[x 3 weeks]
________________
(BPG = BENZATHINE PCN G -IM) / (MU = million units)
Tx for {SEC} Syphilis :
[Secondary Systemic Sx]⼀[Early latent <12mo] ⼀[Chancre primary]
[BPG 2.4MU]
x 1
________________
(BPG = BENZATHINE PCN G -IM) / (MU = million units)
What other stages of Syphilis share the SAME TREATMENT as
[Early latent <12 mo] -2
[Chancre primary]
[Secondary Systemic sx]
Tx for Congenital syphillis
[aPG 50,000 u/kg/dose]
[q10h]
[x 10 days]
________________
(aPG = aqueous PCN G -IV) / (**MU = million units)
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
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
How do you manage Dumping syndrome? (4)
- High protein diet
- low carb diet
- small meals
- frequent meals
goal is to DEC passage of food into small intestine
What are the 3 criteria for diagnosing Liver Failure?
ELI has Liver Failure!
- Encephalopathy
- Liver injury evidence (transaminitis)
- INR GOE1.5
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
Describe Serology for Hepatitis B -7
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*
Most common side effects of [INH (isoniazid)] -2
Injuries to Nerves and Hepatocytes
_________________
Neuropathy (Pyridoxine B6 = tx/px)
Hepatitis - THIS IS SELF LIMITED AND RESOLVE WITHOUT INTERVENTION
The Hepatitis A vaccine is recommended for which groups - 3
- Travelers going to countries where HepA is present
- Gay Men
- Chronic Liver Disease
_________________
Hepatitis A can cause SIGNIFICANT but benign TRANSAMINITIS so do not be alarmed by this
self limited to 1 month
What 2 laboratory values are the best diagnostic test for [acute Hepatitis B infection]?
S - SEC - SCEb - Core - CEbSAb - CSAB - SAb
[SAg and CoreIgM]
HDS pt presents with [HBV SAg] and [HBV CoreIgM]; consist with diagnosis ⬜
Explain the management (3)
[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]
After acquiring [acute HBV], what is the risk of developing Chronic Hepatitis B?
5%
(based on age)
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 ]
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] ]
For patients with Sepsis, [SIM⼀Sepsis Initial Management ( ⬜4 )] must be executed within ⬜ in order to ⬇︎ Mortality
SIMLBAF (Lactate/BCx/Abx/Fluids)
_________________
[first1-3H]
What is the clinical definition of
Septic Shock? -2
{[Sepsis(infection + ≥2 organ system dysfxn)] + [refractory hypOtension(vasopressor, lactatemia]}
What is gastroparesis? (3)
- [GPICC parasympathetic impairment] from (DM/Anticholinergic Rx / Vagus❌)]
- ➜ [gastric smooth m] dys-synchronous contraction ➜ delayed gastric emptying
- = [dyspepsia with succussion splash sx]
_________________
[GPICC] = [Gastric Pacemaker Interstitial Cells of Cajal]
Describe the symptom triad for [Disseminated Gonococcal infection]
- [Several migrating asymmetric joint pain (or purulent monoarthritis)]
- Tenosynovitis ⼀pain with passive extension and/or TTP over flexor sheaths
- Dermatitis
note: dx = [+ gonorrhea urogenital NAAT]
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}
≥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]
Stress Ulcers have multiple causes
What 2 medications are used for Stress Ulcer Prophylaxis?
_________________
{ [GIVE_BS] ≥1| [sico] ≥2}
PPI > [H2 R Blocker]
Stress Ulcers have multiple causes and require PPI px
How does [hEad 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
Stress Ulcers have multiple causes and require PPI px
How does [iCU > 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
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
What are Spider Angiomas?
[Blanching bright red papules surrounded by outward radiating vessels]
(2/2 dilated central arterioles from cirrhosis)
pts with [HIV and on HAART] often develop which metabolic condition?
Describe the features of this metabolic condition (4)
[HIV lipodystrophy DIVE]
Dyslipidemia
Insulin resistance
[Visceral obesity (lipoatrophy + buffalo hump)]
Elevated CVD risk
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%]?
[HIV lipodystrophy DIVE]; RAPstatin
RAPstatin (Rosuvastatin or Atorvastatin or Pravastatin)
Mngmt for Diverticulitis (4)
- Colonic Bacterial Abx
- NPO
- IVF
- rule out colon CA
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)
[AMBIC - Acute Mesenteric Bowel ischemic colitis]
Sx (5)
- periumbilical POOP
- hematochezia
- Rebound
- Guarding
- [NV ➜ hypOkalemia]
________________
- POOP = Pain Out Of Proportion*
- CTA revealing air & edema in bowel wall–>thickening = AMBIC*
[(AMBIC) Acute Mesenteric Bowel ischemic colitis]
Labs (4)
- AMBIC* ⇪ WAHL products!
1. WBC ⇪
2. Amylase ⇪
3. Hgb ⇪
4. [LACTATE ⇪ ➜ metabolic acidosis]
________________
CTA revealing air & edema in bowel wall –> thickening = AMBIC
[(AMBIC) Acute Mesenteric Bowel ischemic colitis]
Mngmt (6)
- O2
- IVF
- [Abx: CefTriaxone vs. (Levoflox + flagyl)]
- Pain control
- Heparin (if clot present)
- Laparatomy
[CTA: bowel wall thickening from air & edema]
[(AMBIC) Acute Mesenteric Bowel ischemic colitis]
Dx (2)
[CT Angiogram (bowel wall thickening from air/edema)]
vs. [Mesenteric Angiogram]
_________________
Diverticulitis Dx
CT revealing [bowel wall FREE AIR & edema]
AMBIC and Acute Diverticulitis have similar clinical presentations
What main sx differentiates AMBIC from Acute Diverticulitis?
AMBIC = BLOODY DIARRHEA
Diverticulitis = nonbloody Diarrhea
In addition to analgesia, what is the tx for acute Herpes Zoster? -2
[valacyclovir PO]7d < [rash 3 days old]\_≤\_[ZINC OXIDE CREAM]
________+________
analgesia
[Primary Biliary Cirrhosis]
clinical features (4)
- {[intrahepatic bile duct] autoimmune obliteration with fibrosis ➜ [ALP ⇪ ⇪ ⇪]}etx
- {asx ➜ [Fatigue + Pruritus + (Xanthelasma HLD(from ⇪ cholesterol) + ⇪TOTALconjugated Bilirubin ]}sx
- [AMA]dx
- ={[UrsoDeoxyCholic Acid ➜ Liver Transplant(CURE)]}tx
AMA = Antimitochondrial Antibody
In the U.S., water soluble vitamin deficiencies are 2/2 ⬜, ⬜ and ⬜
- [chronic EtOH],
- [restrictive diets (anorexia nervosa)],
- [malabsorption syndrome]
What are [Riboflavin B2] deficiency sx? (2)
- Angular cheilitis
- Stomatitis
[Niacin B3] deficiency sx (4)
[Pellagra DDDD]
- Dementia
- [Dermatitisphotosensitive]
- Diarrhea
- Death
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…
- NOT CONTAGIOUS ⼀pt can attend work/school without restrictions
- risk of conversion to [Active TB Infection] is low ➜
- ONLY immunocompro or congregant occupants need to consider [Latent TB infection] treatment
_________________
congregant occupant = occupies congregated areas (HealthcarePersonnel, inmates)
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
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
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 = PPI + Amoxicillin + Clarithromycin]*
- [PBMT = PPI + Bismuth(or diff abx) + Metronidazole + Tetracycline]*
HPylori is a strong risk factor for developing which 3 conditions?
- PUD
- gastric ADC
- MALT lymphoma
_________________
tx = PAC14d–(prn)–> PBMT14d
How is Misoprostol related to NSAIDs?
Misoprostol is a prostaglandin that inhibits gastric acid secretion and improves mucus defenses = prevents ulcers a/w NSAIDs
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]?
- persistent symptoms
- HPylori associated ulcer on endoscopy
- HPylori associated MALT
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 ] ➜
- urea breath test or
- HPylori stool antigen test
- *
- tx = PAC14d–(prn)–> PBMT14d*
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 = PPI + Bismuth(or diff abx) + Metronidazole + Tetracycline]
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
In Tuberculosis dx,
Although TST and IGA have comparable accuracy, what are the 3 advantages IGA has over TST?
IGA has…
- no [BCG vaccine] false positives
- no need for a return visit to measure induration
- 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])] 📺
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
Describe the clinical presentation of acute hepatitis from HAV (5)
- acute transaminitis in 1000s
- Fever
- Jaundice
- Abd pain
- Vomiting
⬜ lab test is used to detect primary biliary cirrhosis
_________________
Recite clinical manifestations (6)
[AMA (AntiMitochondrial Ab)] ;
T-cells & AMA destroy _intra_hepatic bile duct ➜
- [cholestatic elevated ALP]
- jaundice
- pruritus
- RUQ abd pain
- Wt Loss
- [Xanthelasma (from INC blood cholesterol deposition)]
In patients with suspected [NAFLD (asymptomatic isolated transaminitis)], ⬜ is needed to confirm the diagnosis
[US revealing liver hyperechoic texture c/w steatosis]
What are the guidelines for Colon Cancer Screening? -3
What are the [ColoRectal Cancer screening options] available for otherwise normal patients(⊝UC, ⊝[FDR CRC or HR Polyp])? (7)
a. [cscope]q10y
b. [gFOBT]q1y
c. [FIT]q1y
d. [FIT-DNA]q1-3y
* * *
e. [CT colonography]q5y
f. [Flexible Sigmoidoscopy]q5y
* * *
g. [(Flexible Sigmoidoscopyq10y) + (FITq1y)]
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
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]
what abx are used to treat SIBO? -4
_________________
Small Intestinal Bacterial Overgrowth
- amox/clav
- rifaXimin
- fluoroquinolones
- metronidazole
* SIBO = gram negative*
SIBO
Management? (3)
- correct underlying cause (i.e. SSS)
- dietary modification
- abx(amp_sulf or amox_clav|rifaXimin|fluoroq|metronidazole)
Loperamide MOA
[weak opioidmu R agonist] ➜ [slows intestinal motility] ➜ improves diarrhea
- 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]
- 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
_________________
[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
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*
(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 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*
(weeks to mo) ; [Ixodes scapularis deer tick during blood feeding]
_________________
eL Lyme dx = clinical dx + empiric doxy if ⊕
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*
(mo to years) ; [Ixodes scapularis deer tick during blood feeding]
_________________
eL Lyme dx = clinical dx + empiric doxy if ⊕
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
Lyme Disease has 3 Clinical Symptom Stages: eL ➜ ED ➜ L
Tx for eLLyme disease
Tx eLLyme:
[⊕clinical dx?(erythema migrans, fv, HA, hx)] → give [empiric doxy]
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))
[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]
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
Name the 6 major organ systems affected by Cystic Fibrosis and how they’re affected
LUNGS = Nasal Polyps, Digital Clubbing, Bronchiectasis, BronchiOlitis
As long as the patient has normal GI function: …
[⬜ feeding]
is preferred over
[⬜ feeding]
Enteral ; {ParEnteral IV]
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
- {[30 Kcal/kg/day] + [1g/kg ofprotein]} = standard composition
- gastrostomy tube can be placed surgically or perQ
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
What is the hallmark of Splenic Vein Thrombosis?
isolated [fundal gastric varices]
tx = splenectomy
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)
What is hepatic veno-occlusive disease?
(in the setting of Bone Marrow Transplant) ➜ Occlusion of terminal hepatic venules (not veins) ➜ postsinusoidal portal HTN
“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?
[<250 = NO peritonitis]
________________
[≥250 = PERITONITISSBP vs PERITONITIS2º ]
Neutrophils = PMN on CBC w/diff**
“Ascitic Guts Can Never Totally Suck”
Normal Range for ALT and AST is ⬜
________________
What etx’s would cause Aminotransferases to be > 1000! -5
8-20
What’s an effective way to determine if Ascites is 2/2 Portal HTN ? -2
________________
“Ascitic Guts Can Never Totally Suck”
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”
Pt presents with Ascites
What all do you order to analyze Ascites Fluid? -5
“Ascitic Guts Can Never Totally Suck”
- [Gram Stain & culture]
- Color
- [Neutrophils PMN on CBC w/diff]
- Total protein
- SAaG = Serum to Ascites albumin Gradient ([Serum albumin] - [Ascites albumin])
“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?
Bloody = Trauma / CA / TB
Milky = chylous/pancreatic
Turbid = infection
Straw = benign
________________
“Ascitic Guts Can Never Totally Suck”
“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?
[<2.5 = Cirrhosis / nephrOtic syndrome / (SBP<1)]
________________
[≥ 2.5 = TB / Ovarian CA / R HF / budd-chiari / Fungal]
________________
“Ascitic Guts Can Never Totally Suck”
“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?
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”
⬜ 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
_________________
⬜ 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
_________________
⬜ 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
_________________
⬜ 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
_________________
⬜ 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)
⬜ 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
_________________
⬜ 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
_________________
HRPlymphovascular involvement
HRPCA extends to specimen margin
__________
High Risk Polyps with invasive malignancy:
Why do pts with Crohn disease have ⬆︎ development of Kidney stones?
They have fat malabsorption which –> ⬆︎oxalate absorption –> Ca+Oxalate precipitation in the kidneys
Endoscopic findings for Ulcerative Colitis
Continuous Friable mucosa with ulcers
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
Which IBD condition are Pseudopolyps associated with?
Ulcerative Colitis
[Ulcerative Colitis IBD] Sx (11)
U
L L
C C C C
E
R R
S
_____________________________
[Crohns IBD] Sx (11)
Crohns Can FCK GRT DCS
_____________________________
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])
Clinical features of Barrett Esophagus (4)
- [distal esophageal intestinal metaplasia**] that can →intestinal dysplasia → [Esophageal ADC (note: LOW RISK < 1% if dysplasia absent)]
- [(Chronic GERD>5y), (>50 yo), (White), (Obese)]risk factors
- **[Red Velvety Columnar Epithelium (with goblet cells)] replaces [pale shiny stratified squamous epithelium] in distal esophagus
- Tx: = [endoscopic surveillance + (PPI)lifelong]] + [endoscopic ablationIF ⊕DYSPLASIA ONLY ]
HPylori causes atrophic gastritis and [⬜ ADC], but not [⬜ ADC]
[gastric ADC];
[Barrett Esophagus/Esophageal ADC]
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
[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]
- lactulose(DEC Ammonia)
- rifaximin(DEC Ammonia)
- correct precipitating event (IVF, abx, elyte )
What are the major risk factors for [CRC ADC]? (4)
; minor? (4)
ColoRectal CA ADC
- FAP
- FAM HX(esp if family < 60 yo at their dx)
- UCIBD
- BLACKrace
- etoh
- smoking
- obesity
- red meat
What are the protective factors for ColoRectal CA? (4)
a. fvf diet (fiber rich/vegetable/fruits)
b. exercise
c. NSAIDs
d. HRT
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
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
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
What are the potential complications that cause [complicatedacute diverticulitis]? (4)
[complicated acute diverticulitis]
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 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
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]
- *
Pt p/w Hematochezia
How do you initially work this up? (4)
Pt p/w Hematochezia
When would Angiography be considered for these patients?
- [Hematochezia⼀ persistent] → HDUS
- [⊝EGD]
→ Angiography
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)]
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]
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
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
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
what is the tx for [CirrhosisAscites] - 3
Ascites 2/2 Cirrhosis
- Furosemide
- Na+ restriction
- Spironolactone
Tx:[(Furosemide/Na+ restriction/Spironolactone) –(REFRACTORY)–> TIPS].
what is the tx for Hepatic Encephalopathy - 2
- Lactulose
- Rifaximin
Hepatic hydrothorax presents as ⬜ in patients with ⬜. Treatment consist of ⬜2. Explain MOD
[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]
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]
cholangitis dx =cholangitis siLx = cholangitis sxCharcot triad + cholangitis ixERCP/US/CT with Biliary Dilation + cholangitis LxCholestasis labs
Acute Cholangitis
a. how is it diagnosed? (3)
* * *
b. treatment (2)
- ERCP/US/CT: Bile Duct Dilation
- ⇪cholestasis labs ( ⇪ Direct Bilirubin/ ⇪ ALP/ ⇪ LFTs-mildly)
- Charcot’s triadRUQx, Jaundice, Fever
_________________
- Enteric Abx
- [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
⬜ is responsible for [Cirrhosis sequelae].
List sx of [Cirrhosis sequelae] (4)
hyperestrogen;
- Palmar erythema
- spider angioma
- loss of sexual hair
- testicular atrophy
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
- [chronic GERD > 5y]
- Male
- White
- Hiatal hernia
- central obesity
- smoker
- [FDRwith BE or EAC]
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
2 ; [upper GI EGD]
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
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)
⬜ is a risk factor for developing Eosinophilic Esophagitis (which is triggered by ⬜)
cp? -4
________________
Tx?3
ATOPY (asthma/food allergy/eczema) ; food antigens
- dysphagia
- reflux/regurgitation
- epigastric abd pain
- [eosinophilic esophageal linear furrows on endoscopy]
__________________
elimination diet | PPI | [Topical CTS (fluticasone spray)]
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)
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
________________
cholangitis dx =cholangitis siLx = cholangitis sxCharcot triad + cholangitis ixERCP/US/CT with Biliary Dilation + cholangitis LxCholestasis labs
Pt presents with Fever, Jaundice and RUQ pain
Management? -2
[ERCP biliary decompression/drainage - within 48h]
+
enteric abx
________________
dz = Acute Cholangitis
organisms most commonly associated with
intraAbdominal -2
E coli
Bacteroides fragilis
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
SBP
patient p/w ascites
How do you diagnose Spontaneous Bacterial Peritonitis?
“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]
⬜ 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
How is smoking related to surgery?
smoking cessation ≥4 weeks prior to surgery ⬇︎ pulmonary complication risk postop
PFT, ABG, etc. preop will not help
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]
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
Name the 12 Absolute Contraindications to Organ Donation
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.]
_________________
{ [Brain] [brainStem] [Heart] [Lungs] } = NO activity = dead.
[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
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)]
cp for [Perforated gastric ulcer] -3
-acute severe abd pain with
-[free air under diaphragm on upright CXR]
-HDUS= SURGICAL EMERGENCY
[Boerhaave Esophageal Perforation] dx (2)
[esophaGography] vs. [water soluble contrast CT]
⬜ infections develop in up to 50% of patients with acute variceal bleeding.
Management?
BACTERIAL (SBP/PNA/UTI) ;
( [Ceftriaxone IV x 7 days] prophylaxis)
the primary tx for all Hernia is what?
surgery
_________________
complications: incarceration vs strangulation
s/s of Compartment Syndrome -6
[Pain (especially with Passive stretch)]
Paresthesia
Poikliothermia
_________________
Paralysis
Pulselessness
Pallor
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]
________________
- antiThyroid antibodies (antiTPO)
- abnormal lipid profile
- hypOthyroidism sx
- ovulatory/menstrual dysfunction
clinical definition of Rectal Prolapse
_________________
When is surgery indicated? -3
[when rectal tissuemucosal|FULL thickness[14] slides thru anus[15]]
_________________
🔨[Rectal Prolapse COMPLETELY] or
🔨[Rectal Prolapse w incontienence] or
🔨[Rectal Prolapse w constipation]
🔨=surgery
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
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)]
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
_________________
Dumping Syndrome MOD
________________
Dumping Syndrome Sx(5)
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]”
[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
_________________
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)]
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
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
How do you differentiate cp of duodenal ulcer vs gastric ulcer
_________________
Whats the tx for HPylori Ulcer -7
[DEC = Duodenal] <–(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]*
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
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)
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
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
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]
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
- Celiac disease (D-xylose will be LOW in the urine because it can’t be reasbsorbed in the small intestine because of villous atrophy)
- 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**
What type of diarrhea is associated with [decreased stool osmotic gap < 50]
Secretory
these are larger volume diarrhea that occurs during fasting or sleep
What type of diarrhea is associated with [INCREASED stool osmotic gap > 125]
Osmotic
ex: Lactose intolerance
What are the laboratory findings for Lactose intolerance? - 5
Lactose intolerance is most commonly seen in Asians
- [INC stool osmotic gap(osmotic diarrhea) > 125]
- [⊕hydrogen breath test (indicates intestinal bacterial carbohydrate catabolism)]
- [⊕reducing substances in stool]
- acidic stool pH
- NO [fatty stool steatorrhea]
Lactose Intolerance is most commonly seen in Asians
There are 4 Malabsorption syndromes
Describe clinical features of Lactose Intolerance (4)
There are 4 Malabsorption syndromes
Describe clinical features of Chronic Pancreatitis (2)
what are the sx of Viral gastroenteritis (3)
_________________
it is transmitted via ⬜ with which 2 viruses?
[WATERY DIARRHEA +/- vomiting]
Abd pain
[+/- Fever]
_________________
tx for Viral gastroenteritis (3)
self-limited
- oral rehydration (mild)
- IV REHYDRATION (SEVERE)
- [Regular Limited Lipid(fat)/ Simple Sugardiet as tolerated]
The major side effects of [INH Isoniazid] for TB are peripheral neuropathy and ⬜.
How do you manage each side effect?
[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]
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)
In neonates, how might Cystic Fibrosis present? -4
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
- 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]
What is the TRIAD PRIORITY for managing [Brain-Dead Organ Donors] ?
MUST MAINTAIN NORMAL PET w IVF / Desmopressin
Pressure
Euvolemia
Temperature (or mild hypothermia)
What Lipase level is c/f Acute Pancreatitis in Adults?
GOE 1,000
What Lipase level is c/f Acute Pancreatitis in kids?
GOE 7 x upper limit of nl for that age group
What supplements will pts s/p RYGB (Gastric bypass Surgery) require? - 6
“avoid DDUMPafter RYGB plus give [F, D, C and Bx3]”
Fe
D3cholecalciferol
Ca+
B1Thiamine
B9Niacin
B12Cobalamin
Why does compartment syndrome cause kidney damage?
compartment syndrome –> myoglobin release –> [myoglobin heme] is nephrotoxic
Compartment Syndrome Dx- 2
- [Direct Compartment Pressure > 30]
- [delta pressure(diastolic BP - Direct) < 20]
Which part of the Esophagus is [Esophageal ADC] located?
LOWER
a/w Barrett’s and GERD
Which part of the Esophagus is [Esophageal SQC] located?
UPPER
a/w SMOKING AND EtOH
What is [Enteropathy associated T cell Lymphoma (EATL)] ?
Jejunal CANCER from [NON-COMPLIANT CELIAC DISEASE]
similar sx to celiac but long standing
describe pathology for Crohn disease
Transmural GI inflammation
Crohns Can FCK GR🅃 DCS
What type of diarrhea is associated with INCREASED stool osmotic gap > 125
Osmotic
ex: *“Can Larry –“*Celiac, Lactose intolerance
What are the laboratory findings for LactOse intolerance? - 5
LactOse intolerance is most commonly seen in Asians and AA
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
generally describe distinguishing sx for these 4 conditions
Celiac
[Irritable Bowel Syndrome]
[Inflammatory Bowel Disease]
Lactose Intolerance -2
Celiac(TWICED) = {INC Stool Osmotic Gap>125 a/w [LARGE STEATORRHEA DIARRHEA]}foul, flatulent, FATTY
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iBS = [smoderate diarrhea with recurrent abd pain (bowel habit ∆s )]
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IBD = Bloody diarrhea, fever, fatigue
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LactOse Intolerance = {INC Stool Osmotic Gap>125 a/w [LARGE OASIS (WATERY) DIARRHEA]}postprandial + postprandial flatulence, Asian=RF
Where is the intestinal enzyme lactase located?
Duodenal brush border
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LactOse intolerance Definitely Produces Flatulence
[MASSIVE Rectal Bleeding in Adults] ddx -3
- Diverticulosis (L colon)
- Ulcerative Colitis
- [angiodysplasia AVM (R colon)]
[MASSIVE Rectal Bleeding in Adults] with active hemorrhaging dx -2
- radionuclide scintigraphy
- Angiography
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
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
Indication for [Blood Transfusion (pRBC)] -2
- Hb < 7
OR
- [Cardiac Patients Hb < 8]
Tx for active & brisk [Angiodysplasia hematochezia] -5
- MOST ANGIODYSPLASIA RECTAL BLEEDING STOPS SPONTANEOUSLY ➜
- endoscopic coagulation (if #1 fails) ➜
- arterial embolization by catheterization (if #2 fails) ➜
➜ 4. subtotal colectomy
- aortic valve replacement (if aortic stenosis)(Heyde’s syndrome)
.
do not use vasopressin
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
Why should Raloxifene be d/c before surgery?
SE = DVT/PE
