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Final review for Step 2 Ck > GI > Flashcards

GI Flashcards

1
Q

can you get pleural effusion in Boerrhave?

A

yes you can get pleural effusion in boeerhave

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2
Q

dx of Boeerhave?

A

Gastrografin water soluble gram or CT

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3
Q

Dx of esophagitis in HIV for CMV versus HIV versus candida?

A

Candida will have thrush and no odynophagia and just treat with PO fluconazole, versus CMV and HSV will have NO thrusth and will have odynophagia and NEED EGD to diagnose

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4
Q

Tx of CMV vs HSV esophagitis

A

Acyclovir (HSV) and gangciclovir (CMV)

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5
Q

Initial study for motility disorders?

A

Suggested when solid/liquids at same time are troublesome, not progressive, do a barium swallow and follow with manometry as definitive diagnosis. In achalasia, it mimics CA and EGD is needed after swallow to r/o cancer.

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6
Q

Other causes of Boeerhave other than vomiting?

A

Iatrogenic from instrumentation and procedures. Suspect with with acute chest pain, crepitus and emphysema and left pelrual effusion. Dx with contrast water-sol esophagram

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7
Q

What does a pill-induced esophagitis look like?

A

Circumferental ulceration that is sudden onset with pain and odynophagia + dysphagia. Commonly due to bisphosphonates, NSAID, KCl and tetracyclines

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8
Q

When do you see a cork-screw esophagus?

A

Diffuse esophageal spasm

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9
Q

What else is a concern in diffuse esophageal spasm?

A

Need to do a cario work-up.

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10
Q

Definitive test for diffuse esophageal spasm?

A

EKG/Cardio workup – barium swallow – manometry (Definitive) with simultaneous contractions

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11
Q

tx of diffuse esophageal spasm?

A

CCb, nitrates

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12
Q

What does barium swallow show for achalasia

A

LES tone is increased, birds-beak, Need EGD after then need to do manometry to make definitive diagnosis and remember the LES will not relax

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13
Q

tx of achalasia short term

A

NO2 and CCB or botulinum toxin

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14
Q

long term tx of achalasia

A

pneumatic balloon dilation, myotomy (Heller)

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15
Q

How is Zenker dx?

A

Dx Zenker with barium swallow showing outpouchings (false) diverticuli in the posterior UES of the cricopharyngeal muscle. Remember it can present as a mass

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16
Q

Tx of Zenker?

A

Surgery and removal of the false diverticuli is the treatment for Zenker

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17
Q

Dx of esophageal cancer

A

With alarm syx you go right to EGD (weight loss, pain, dysphagia, smoker) then stage it with CT

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18
Q

What causes stricture of esophagus?

A

GERD, radiation, sclerosis; it is circumferential narrowing. Dysphagia for solids not liquids more common

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19
Q

If someone has dysphagia progressive from solids to liquids, but has a history of radiation or esophageal surgery, how do you diagnose?

A

Suspect stricture, do barium swallow; if not, do EGD and suspect cancer. Alg 2212. These patients have increased risk of perforation from lesser diameter and can have barium swallow first to rule out stricture.

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20
Q

Dysphagia of solids AND liquids? Dx?

A

Means motility. Barium swallow. Progressive = mechanical obstruction = EGD and suspect CA

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21
Q

What is an odd, but common sign of perforation of esophagus?

A

Pleural effusion and look for wide mediastinum if quick XR done or Hamman sign with crunching on auscultation of the chest

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22
Q

Pill-induced esophagitis

A

CIRCUMFERENTIAL (viral would not cause this, does not contact whole mucsoa) ulcerations with normal surrounding mucosa on EGD

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23
Q

First line in diffuse esophageal spasms?

A

Calcium channel blockers

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24
Q

how does Diffuse eso spasm look on mano?

A

Multiple, simultaneous contraction

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25
Q

what is definitive dx for diffuse eso spasm?

A

like other motility disorders, manometry is definitive

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26
Q

achalasia tx short term

A

CCB and nitrates or botulinum

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27
Q

long term tx of achalasia

A

dilation and heller myotomy

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28
Q

how is zenker diagnosed?

A

Zenker is diagnosed with barium swallow

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29
Q

is manometry needed in zenker?

A

zenker is not motility disorder, it is an outpouching so no confirmation with motility study is needed as it will likely be normal

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30
Q

how is zenker treated

A

zenker is treated with surgical excision of the diverticulum and myotomy

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31
Q

Is CT needed after EGD in eso or gastric cancer?

A

Yes, CT is always needed to stage after histologic diagnosis and determines prognosis and treatment

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32
Q

Duodenal ulcers are treated how?

A

Treat duodenal ulcers as if they are due to H/ pylori, as 90% are. Syx are better with food and wrose without food; need PPI + clarithro + amox (or gent if amox allergy)

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33
Q

ZE syndrome check for?

A

MEN1 parathyroid / PTH and pituitary dysfunction

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34
Q

Dxylose is absorbed when

A

When GI mucosa is normal, it does NOT need brush border to be absorbed (normal in lactose def), but it will be abnormal in Celiac, IBD, etc

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35
Q

Preferred diagnosis for Giardiasis?

A

Stool Ag (versus histolytica which is SERUM ag as it is systemic and no longer gut once RUQ syx start)

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36
Q

Tx for giardia

A

Dx with stool Ag then tx with metro

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37
Q

s/s of vit D deficiency?

A

May happen with chronic, malabsorptive diarrhea (DAKE) with low vit D, low Ca, HIGH PTH, and LOW PO4,3-

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38
Q

Tropical sprue s/s

A

endemic area for 1 month, most have malabsoprtion of the small gut

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39
Q

dx of tropical sprue

A

small gut biopsy, which is the reason they have malabsorption and megaloblastic anemia along with blunt villi and chronic inflammatory cells present

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40
Q

Dx for c. diff

A

stool studies + empiric metro

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41
Q

how is c. diff treated empirically?

A

metro and stool studies

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42
Q

unexplained leukocytosis in hospitalized patient on antibiotics (or not), think?

A

c. diff

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43
Q

Do you do I and D / aspiration of abscess from histolytica?

A

NO, DO NOT do I and D of histolytica in the RUQ as it is due to an abscess and not a cyst

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44
Q

how do you treat histolytic abscess?

A

Just use metro

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45
Q

How is histolytica dx?

A

Dx histolytica with BLOOD SERUM AG NOT STOOL AG (unlike giardia) because by the time there is RUQ pain it is an ascess and out of the gut

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46
Q

RUQ pain preceded by dysentary from a Mexican and mass seen on U/S, treat?

A

Get a serum Ag for histolytica (not stool) then do metro WITHOUT drainage of the ABSCESS and add praomycin or maromycin to get rid of larvae

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47
Q

Dx of EHEC?

A

Shiga-toxin stool assay

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48
Q

Cx of EHEC

A

Watch for microangiopathic hemolytic anemia and low PLT and rising Cr/BUN due to HUS

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49
Q

Do you treat EHEC?

A

NO! DO NOT TREAT EHEC it raises the risk for HUS

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50
Q

Abd pain and diarrhea without fever?

A

Abd pain and diarrhea without fever you suspect EHEC, versus C. diff which is healthcare associated and abd pain/diarrhea WITH fever

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51
Q

Salmonella associations (food and demographic?

A

Eggs and poultry + SCA osteomyelitis

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52
Q

Treat salmonella?

A

Yes with fluoroquinolones or TMPSMX

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53
Q

Tx shigella?

A

YES! treat shigella vs EHEC in which you do NOT treat

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54
Q

Whipple disease causes?

A

LAD, diarrhea (malab), fever, joint pain, heart block, weight loss, cough, dementia

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55
Q

Dx of Whipple

A

PAS + adn PCR, gram + bacillus

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56
Q

Small I overgrowth can cause?

A

malabsorption due to gut bacteria

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57
Q

what is diagnostic of bact small I overgrowth

A

Biopsy with 10^5 organisms or more; causes B12, calcium, iron def

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58
Q

Why is it a condition (small I overgrowth)

A

Usually not as many in small bowel due to higher acidity from gut

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59
Q

How do you treat small I overgrowth

A

Treat it with 7-10d of amox-clv and rifamixin and stimulate motility (metoclopramide and avoid narcotics as no movement allows bact to overgrow)

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60
Q

What nutrient def does Celiac commonly cause

A

Celiac commonly causes Iron Def as it is in the duodenum and early jejenum

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61
Q

Dx of Celiac?

A

Anti-Endomysial IgA transglut (can be negative if IgA def ) to biopsy as definitive lesion

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62
Q

MCC of malabsorptoin?

A

Chronic pancreatitis due to alcohol

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63
Q

How is steatorrhea confirmed?

A

Fecal fat tests confrim steatorrhea with sudan stain on spot stool specimen

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64
Q

Person has foul smelling stools, loose and high volume, BMI19 with pain radiating to his back, what is the cause?

A

Alcohol most likely

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65
Q

Some fat-sol deficiencies in steatorrhea?

A

D, A, K, E

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66
Q

Why does Celiac affect Iron abs?

A

Earliest part of the gut is where it blunts villi in duod and jejenum where iron is absorbed

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67
Q

Lactose deficiency diagnosis?

A

Reducing substances in the stool with + Hydrogen breath test, low stool pH and osmotic diarrhea without steatorrhea (acidic due to fermentation products)

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68
Q

How is carcinoid diagnosed?

A

Carcinoid syndrome is due to serotonin which has breakdown product 5HIAA, diagnose it with 24 hour urine test of 5HIAA

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69
Q

s/s carcinoid

A

Wheeze, right valve issues, flushing, diarrhea and +5HIAA in urine

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70
Q

Carcinoid syndrome may cause what else?

A

Due to appendiceal and small bowerl 5HT3 secreting tumors, it uses up tryptophan to make it causing a niacin deficiency = pellagra

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71
Q

When is pellagra seen commonly

A

Malnutrition of niacin and serotonin syndrome

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72
Q

S/s of pellagra i/e in carcinoid syndrome?

A

The D’s: Dermatitis, dementia, diarrhea (hyperpigmentation comon)

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73
Q

Consider what in carcinoid sydrome?

A

Consider echocardiogram

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74
Q

Full dx of carcinoid

A

5HIAA – CT or MRI to locate – Octreoscan to detect mets

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75
Q

Carcinoid Tx before surgery for syx?

A

Octerotide treats carcinoid

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76
Q

Common met of carcinoid tumor

A

To liver, then you get syx

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77
Q

Big tip off for laxative (factitious) diarrhea?

A

Nocturnal diarrhea

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78
Q

How to diagnose factitious diarrha?

A

Diagnose factitious diarrhea wiht melanosis coli by dark brown discoloration of colon withlymph follicles shining through as pale patches. Their diarrhea will also be an extreme number of times a day with multiple hospitalization and no definitive diagnosis (3593)
(laxatives pigment GI tract)

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79
Q

What does IBS mucosa look like?

A

NORMAL mucosa

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80
Q

What are things suggesting something isn;t IBS

A

IBS has normal mucosa and alternating constipation and diarrhea, pain relieved with defecation, labs will be normal; won’t se rectal bleeding, noctunral diarrhea– functional disorder of the GI tract and NO ALARM SYX

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81
Q

What is a succession splash indicative of?

A

Bowel obstruction as food sloshes around between gas that is obstructed as a hollow viscus with gas

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82
Q

Tx of gastric outlet obstruction

A

NG tube, IVF, endoscopy is definitive

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83
Q

Diff between ileus and bowel obstruction on XR?

A

Ileus is both small and large bowel dilation and obstruction is dilation proximal to an obstructed lesion

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84
Q

Diverticulitis versus osis syx

A

itis is pain with fever and ifnectious syx and without bleeding and osis has bleeding that is painless

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85
Q

When do you see colovesicular fistula?

A

You see it with diverticular disease and consider in Crohn’s transmural inflammation; consider CRC as this may erode through bowel and follow-up with scope if high suspicion

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86
Q

dx colonovesicular fistula?

A

CT with oral/rectal contrast in bladder and thickened walls and get colonoscopy to excldue malignancy as these can erode too

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87
Q

Diagnosis of diverticulitis

A

AVOID SCOPE = perf; do CT

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88
Q

dx of diverticulosis

A

scope is definitive, do not scope in itits

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89
Q

Bright red blood per rectum in a young patient with pain and no alarm syx or family history?

A

Anoscopy in - office, if negative do a scope follow up

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90
Q

Do hyperplastic polyps need workup?

A

No

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91
Q

risks for polyp to cancer?

A

> 2.5cm, villous/sessile adenoma

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92
Q

Most malignant polyp?

A

Villous >2.5cm

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93
Q

Person has FP, can you follow closely?

A

NO. IN FAP you DO NOT FOLLOW CLOSE – your recommended a proctocolectomy

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94
Q

What cancer is most common in HPNCC (lynch) other than bowel?

A

Endometrial, all women need endometrial collow up

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95
Q

C. diff high risk patient with negative PCR for stool toxins do what?

A

Do a scope to document pseudomembranous colitis

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96
Q

thumb printing on XR following procedure where BP drops in a patient with ASCVD and now abdominal pain and bloody stool?

A

Thumb printing on XR with the aforementioned think ischemic colitis

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97
Q

What marker for CRC?

A

CEA

98
Q

How is Mesenteric ischemic detected

A

Start with an U/S or a CT angiography

99
Q

In lower GI bleeds, what happens if scope doesn’t locate source of bleeding

A

Lower Gi bleed –NG tube– scope done – nothing found – Tn99 localization – then CT

100
Q

In the case of a GI bleed, first step?

A

In a GI bleed, do an NG tube then some sort of a scope either upper or lower

101
Q

IN a GI bleed that cannot be found with scope, then what?

A

Do a Tn99 scan after and THEN a CT to localize definitively

102
Q

In ISCHEMIC COLITIS, what do you start with

A

ischemic colitis you can start with SMA u/s and then do a CT

103
Q

Ischemic colitis, MC place and artery

A

Use u/s of splenic flexure for SMA and then consider IMA afterward

104
Q

Mallory weiss tears are due to what vasculature?

A

MW are due to submucosal arteries and sotp on their own 90% of time

105
Q

What type of rupture are varices?

A

Varices are GE junction veins due to portan HTN

106
Q

MW is vein or artery?

A

MW is artery

107
Q

Variceal is vein or artery?

A

Vein is variceal at GE junction

108
Q

Why is angiodysplasia Heyde associated with ESRD and aortic stenosis

A

Bleeding is more likley due to uremia consuming platelets and due to aortic stenosis turbulence causing microangiopathic anemia

109
Q

Urine bilirubin is what kind?

A

Only conjugated bilirubin is water soluble so only that can be found in the urine

110
Q

Someone has solely elevated Alk-phos, what needs to be ordered?

A

You need to image the liver with U/S

111
Q

What do you suspect with conj, bili elevated in the urine and no other lab findings?

A

Suspect DJ and rotor syndrome

112
Q

Gilbert is a defect in?

A

UDP conj and causes mild jaundice do to unconj bili

113
Q

Criggler is a defect in?

A

UDP conj bilir and more severe with kernicterus, pheno barb treats type II

114
Q

Dubin Johnson is a defect in ?

A

Conjugation excretion (it cannot be excreted) = jaundice and black liver

115
Q

Rotor is?

A

Same as DJ, cannot excrete bili, even milder no black liver

116
Q

Screening of CRC?

A

q10 with a scope, q5 sigmoid, at age 040 with cancer or 10 years beofre, less tan 5 years if polyp found that is precancerous

117
Q

What can TPN due to gallbladder?

A

TPN = less CKK = stasis = gallstones

118
Q

Person has high alk phospatase, what is next and how is it interpreted?

A

Do a U/S for intra vs extrahepatic cholestasis (intra is no CBD dilation)

119
Q

Why do UC get megacolon

A

UC get megacolon because the plexus is damaged and it distends and cannot maintain normal tone

120
Q

Biopsy of Crohns, classic lesion?

A

Non caseating granuloma in Crohn’s

121
Q

Biopsy of UC classic lesion?

A

Crypt abscess MORE COMMON in UC, non-caseating granuloma in Crohn’s

122
Q

Are fistulas in Crohn or UC

A

Fistula and tags and mouth to anus ulcers are in Crohn’s

123
Q

what IBD is skip lesions?

A

SKip lesions, fat creeping, cobblestoning, fistula, tags, oral ulcers are Crohn’s with non-caseating granuloma

124
Q

Dx of toxic megacolon in UC patient suspected?

A

DO an XR DO NOT do scope you will perf it

125
Q

Difference between acute cholecystis and biliary colic?

A

Cholecystitis is obstruction that isn’t moving with inflammation and colic is temporary obstruction that clears and does not cause inflammation (no fever, tenderness, pain resolves, WBC and liver counts normal)

126
Q

How is gallbladder emphysema treated?

A

Emergent chole and amp-sulbactam

127
Q

Best step for RUQ pain or odd LFTs?

A

U/S; after U/S do HIDA if equivocal and high suspicion

128
Q

Poor candidate for gall surgery?

A

Do ursodeoxycholic acid (but recur)

129
Q

Pain after chole “similar” to before? do what and fix how?

A

Do U/S and follow with ERCP/MCRP likely due to a stuck stone

130
Q

elevated alk phos and bilirubin levels do what?

A

Do a US of the gallbladder and suspect obstruction in CBD as high alk phos and leaking of bile suggests choledocholithisiasis and follow with ERCP

131
Q

Pancreatitis suspected, first test?

A

need to detect gallstones as it is a common cause of pancreatitis, so do a U/S in a person with acute pancreatitis and follow with ERCP if positive or unsure

132
Q

Calcified gallbladder

A

Porcelain gallbladder has high risk of adenocarcinoma, remove it even without syx.

133
Q

Risk of porcelain gallbladder?

A

Chronic cholecystitis

134
Q

If you see AST and ALT in the thousands, what is the cause

A

Think acute liver failure, which presents with AST ALT in the thousands and high INR, PT/PTT, bilirubin

135
Q

What is the antibody that distinguished infection from vaccination in asyx individual?

A

The antibody is the antiHBc which is the window AB in infected, but not in immunized

136
Q

First marker in HBV infection

A

HBsAg

137
Q

Window marker in HBV

A

HBcAg which is NOT in the vaccination and is unique to infected individuals (or antibodies against it)

138
Q

Hep a weird syx

A

aversion to cigarettes

139
Q

how is hep A treated

A

in hep A it self resolves IgA to close contacts

140
Q

Going abroad? MC travel acquired illness?

A

Hep A

141
Q

What is mixed cryoglobulinemia associated with

A

Mixed cryo = HCV screen and vice versa

142
Q

What other two things beside cyroglob are associated with HCV?

A

HCV is associated with membranoproliferative GN and porphoryia cutanea tarde

143
Q

If you see vesicles on the dorsum onf someones hands, IC deposits and purpura and low serum complement + membranoproliferative GN, think what?

A

HCV due to porphyria cutaneua tarda and cryoglobulinemia

144
Q

What vasculitis is associated with HBV

A

HBV has a PAN association (lungs spared)

145
Q

Autoimmune hep diagnosis?

A

ANA first then anti-SMC antibodies

146
Q

Chronic liver disease patients need what vaccination?

A

HAV and HBV in chronic liver disease. Infection of new virus and at high risk for fulminant liver failure

147
Q

What drugs are used to treat HBV

A

Treat HBV with entecarvir and tenofovir lowest resistance against them

148
Q

What do ALL HCV patients need before tx?

A

HCV patients need a liver biopsy to rule out other causes and types of liver disease and is the best way to assess response to treatment, weird time you jump right to the procedure and treat with IFN and ribavirin

149
Q

Why do you get liver biopsy in HCV

A

many have alternating levels of LFTs that do not correlate with severity and biopsy is best way to see severity

150
Q

Why do cirrhotic patients need U/S q6 months?

A

Cirrhotic patients get U/S q6 months because they are at risk of developing HCC

151
Q

A1 diagnosis and biopsy shows

A

Diastase resistance and PAS + along with elevated LFTs and early-onset emphysema

152
Q

Dx of a1 antitryp

A

GEnetic test

153
Q

Cirrhosis does what to HPA axis

A

Cirrhosis causes hypogonadism

154
Q

All new onset ascites needs?

A

TAP ALL NEW ONSET ASCITES just like all unknown pleural effusions

155
Q

Cause of the low libido, body hair, palmar erythema, small testes, ED in cirrhosis?

A

There is hyperestrogenism

156
Q

Cr >1.5 and Na in urine

A

Hepatorenal sydrome is due to renal hypoperfusion from splanchnic vasodilation and fluid shifts resulting in kidney damage that does not respond to IV bolus with high mortality rate, only transplant is curative

157
Q

How is hepatorenal treated?

A

Hepatorenal is treated with midodrine and octreotide + norpeinpehrine to constrict the splanichic circulation, otherwise liver must be trasnplanted. IV bolud will still show decreaseing urine output.

158
Q

What is a way to treat hepatic hydrothorax

A

hepatic hydrothorax is transudative and can be treated with fluid restriction and diuretics, but TIPS is curative

159
Q

Everytime you see ascites you need a tap, but how do you evaluate the cause?

A

You do serum alb - ascitic alb and >1.1 =portal HTN and

160
Q

SAAG > 1.1

A

Portal HTN

161
Q

SAAG

A

Not portal related

162
Q

What is the stepwise approach for ascites tx?

A

Tx ascites with water and salt restriction, then add spironolactone because it decreases antiandrogen syx and blocks Na reabsorption, then add furosemide, then tap ascitic fluid 2-4x daily

163
Q

How come you have to be careful with diuresis in ascites?

A

There is transudate and hydrostatic edema in ascites and the patients are volume deplete, ease into diuresis as this prevents hepatorenal syndrome which is why the last step of tx is tapping it rather than more diuresis

164
Q

When do you suspect SBP?

A

In ascites when a patient has fever, any abd pain or altered mentorium

165
Q

How is SBP diagnose

A

PMN >250

166
Q

HOw is SBP treated

A

Treat empirically with third generation cephalosporins (e.coli and klebsiella)

167
Q

How does heptarenal present?

A

It is due to lack of perfusion to kidneys from splanchinic VASODILATION and storage of blood from portal hypertension resulting in decreased urine output and rising Cr and down GFR in the absence of proteinuria/extreme acute hypoperfusion event

168
Q

Tx o hepatorenal syndrome

A

Will not respond to IVF and urine output will be still low, they will third space. Octreotide and Epi and midodrine can constrict splanchnic and improve flow to kidneys, but only cure that reduces mortality is liver transplant

169
Q

Urine lab indicating hepatorenal syndrome?

A

They have very very low urine sodium (

170
Q

Body labs for hepatorenal sydrome/cirrhosis

A

They have very dilute sodium and low potassium. There is decreased perfusion to kidneys activating RAA and increasing sodium reabsorption and K+ excretion along with HCO3 absorption

171
Q

First step in Tx of bleeding varices?

A

Control blood as surgery is prepped with IVF + OCTREOTIDE

172
Q

After IVF and octreotide as first step for varcies then what?

A

IVF and octreotide for variceal bleed – then sclerotherapy;

173
Q

Tx of varices is IVF + octreotide then EGD with sclerotherapy, what if that doesn’t work?

A

Then do a balloon tamponade and follow with TIPS. If it works, initiate BB and follow up for band ligation in 1-2 weeks. If they have a rebleed to EGD again and follow up with TIPs

174
Q

Who gets primary sclerosing cholangitis?

A

Primary sclerosing cholangitis = UC patients

175
Q

What is the defect in primary sclerosing cholangitis?

A

The defect in primary sclerosing cholangitis si fibrosis and stricturing intra and extra hepatically

176
Q

What is the histologic sign of primary sclerosing cholangitis

A

Onion skinning

177
Q

What is definitive tx for PSC

A

PSC is treated definitively with liver transplantation

178
Q

How is PSC diagnosed?

A

U/S does NOT diagnose it usually, requires a cholangiogram with ERCP, MRCP to see the beading

179
Q

Diagnosis of PSC after a U/S in a UC patient with high alk phosphatase is negative?

A

YOU NEED To diagnose PSC in a UC patient with cholangiogram ERCP/MCRP because U/S cannot detect it.

180
Q

A patient has primary biliary cirrhosis confirmed with anti-mitochondrial Ab, what treatment without s/s of cirrhosis?

A

Ursodeoxycholic acid slows progression, if cirrhotic syx/ they need a liver transplant

181
Q

Where is the defect in PBC

A

PBC is in middle aged women and intrahepatic

182
Q

Why does it matter that PBC is intraheptic

A

U/S will not detect intrahepatic duct changes, similar to PSC in US which is intra and extra, but U/S cannot detect it. Diagnose with anti-mito Ab here and in PSC you need cholangiogram with ERCP and MRCP

183
Q

What is NAFLD

A

It is mild liver elevations due to fatty steatosis not form alcohol in obese, DM patients

184
Q

how is NAFLD treated?

A

Diet and exercise

185
Q

Are statins ok in NAFLD?

A

YES! Statins are ok in NAFLD, tell them to lose weight

186
Q

What is NAFLD related to?

A

NAFLD is related to insulin resistance

187
Q

Is NAFLD related to alchol

A

NO, NAFLD is NON ALCOHOLIC

188
Q

Why is NAFLD related to insulin resistance?

A

More insulin resistance, more release of FFA which are taken up by the liver

189
Q

Do you biopsy hepatic adenoma?

A

do not biopsy hepatic adenoma, follow with AFP and U/S to make sure no transformation

190
Q

What is the marker to follow benign adenoma with?

A

AFP and U/S

191
Q

Hepatic adenoma, who gets it and how is it treated and what is C/I?

A

hepatic adenoma in OCP and anabolic steroid use and is followed with AFP and U/S to make sure it does not transform, DO NOT biopsy it due to hemorrhage, just complete resection if becomes worrisome

192
Q

Main risk for cholangiocarcinoma (cancer of biliary tress)

A

main risk of cholangiocarcinoma is primary sclerosing cholangitis as found in UC patients

193
Q

Multiple liver lesions (mets) where do you look first to find primary tumor?

A

Colon.

194
Q

AFP and RUQ pain think?

A

Liver cancer. AFP is associated with liver cancers

195
Q

Biggest risk for Hemochromatosis

A

Risk of HCC

196
Q

HCC is associated with hemochromatosis true of false

A

TRue! HCC has 20-200x increase risk in hemochromatosis

197
Q

Syx of hemochromatosis

A

bronze skin, hepatic LFT elevation, small testes, DM evidence, herat failure and arthropathy with hepatomegaly

198
Q

What weird syx do hemochromatosis patients get

A

They get chondrocalcinosis of joints confused with pseudogout, along with small testes and bronze skin and high risk of HCC

199
Q

What genes are associated in hemochromatosis

A

HFT and H63D

200
Q

Dx of hemochromatosis

A

First do iron studies (otherwise wasted gene test) then test for HFE and H63D and if negative, but suspicion high, then you do liver biopsy

201
Q

What is another name for Wilson disease?

A

Hepatolenticular degeneration

202
Q

How is Wilson diagnosed?

A

Dx with low ceruloplasmin, high copper (or high copper excretion) and Kayser Fleisher rings with slit lamp, biopsy liver only if unceratin

203
Q

How is Wilson treated

A

Wilson is treated with trienterene or penicilaamine vs hemochromatosis with phlebotomy and deferoxamine

204
Q

Gastrinoma is diagnosed after EGD with multiple ulcers and gastrin level >1000, what if gastrin is less/equivocal? (between 110 and 1000)? Note: if gastrin >1000 and stomach pH

A

Then do secretin stimulation test to see if the levels drop, if they do not, check stomach pH

205
Q

For beta cell tumor, what do you need to order?

A

Order insulin levels, blood sugar, C peptide and sulfonylurea levels (remember sulfonylureas cause incresaed C peptide it is endogenous as well)

206
Q

How is bleeding treated in someone with cirrhosis?

A

Cirrhotic patients cannot make their clotting factors so you treat it with FFP which replaces all those factors

207
Q

Most significant risk of pancreatic CA?

A

Smoking most consistent reversible factor

208
Q

What drug is a common cause of pancreatitis

A

Alc and stones are mCC (Get U/S) but anti-seizure meds like valproic acid cause pancreatitis

209
Q

MCC of chronic pancreatitis?

A

MCC is alcohol abuse of CHRONIC pancreatitis, mCC reversible for pancreatic cancer is cigarettes

210
Q

Is imaging needed to diagnose pancreatitis?

A

NO IMAGING IS NOT NEEDED TO DIAGNOSE PANCREATITIS. Just n/v with radiating pain and get a lipase level. Consider U/S d/t high risk of stones causing it.

211
Q

How is pancreatitis diagnosed?

A

2/3: Acute pain radiating to back, high lipase, or imaging with U/s – imaging is NOT required

212
Q

Pancreatic CA marker

A

Pancreatic CA marker is CA19-1

213
Q

How is pancreatic pseudocyst diagnosed

A

it is a non-epithelial fibrous capsule that may present with pain and a mass, observe for 6 weeks then drain if no resolution. Diagnosis with US, a CT iS NOT NEEDED

214
Q

Pancreatic pseudocyst dx with CT or U/s

A

U/S if possible

215
Q

Is screening recommended in pancreatic CA

A

NO SCREENING RECOMMENDED FOR PANCREATIC CA

216
Q

what screening is rx for pancreatic ca

A

NO SCREENING FOR PANCREATIC CA REGARDLESS OF HISTORY IN ASYX PATIENT

217
Q

When do you suspect zinc def

A

Suspect in TPN/bowel resection/Crohn/IBD patients with hair loss, skin lesions, foot tastes bad, and pustular bullae on the skin

218
Q

What causes pellagra

A

Niacin def

219
Q

when does niacin cause a disease

A

niacin causes pellagra and shares a precursor with serotonin so high serotonin means less tryptophan and less niacin synthesis

220
Q

s/s of niacin def (pellagra)

A

pellagra is niacin deff and presents with dermatitis, dementia and diarrhea in setting of serotonin syndrome

221
Q

What drug causes pellagra

A

INH causes pellagra

222
Q

INH causes what nutritional deficiency

A

prolonged INH can cause pellagra

223
Q

What disease is associated with vanishing ducts in the hepatic system

A

ductopenia intrahepatic is due to primary biliary cirrhosis

224
Q

what disease is associated with ductopenia

A

vanishing ducts is associated with primary biliary cirrhosis

225
Q

When else does ductopenia happen

A

ductopenia is due to an immune response and happens after bone marrow transplant, liver transplant or in patients with primary biliary cirrhosis

226
Q

Pallor in an old person first guess?

A

NSAIDs/ASA or iron deficiency anemia from bleeding get CBC and iron studies and scope if no NSAIDs and deficient

227
Q

Duodenal ulcer treatment?

A

Better with eating, suspect H. pylori, as they are involved in 90% of cases. Treat with triple therapy, not just PPI

228
Q

A patient has elevated alkaline phosphatase with normal LFTs and high bilirubin, what is considered as a next diagnostic step?

A

This reflects cholestasis and obstruction and RUQ U/S needs consideration (especially with s/s of jaundice/iceterus or elevated bilirubin, don’t forget Paget’s as well). If Alk phosph was high and AST and ALT were high, you would consider hepatitis, hemochromatosis, toxins, alc, ischemia, etc

229
Q

DJ syndrome and treatment?

A

Benign, conjugated hyperbilirubinemia with grossly black liver (Rotor is less intense form) and look at urine uroporphyinogen levels to confirm, no tx needed.

230
Q

How is Zenker treated?

A

Zenker is treated with surgical excision, commonly they have a mass and regurgitation – barium swallow first and confirm with mano.

231
Q

Who gets Zn def?

A

TPN patients

232
Q

what are s/s of Zn def?

A

Periorbital rash, hair loss, food/taste aversion, TPN, skin lesions and impaired wound healing

233
Q

Does NAFLD cause fibrosis?

A

Yes, up to 40%

234
Q

How is NAFLD treated?

A

Exercise and statins are ok too

235
Q

What are NAFLD labs like

A

Exclude alc and mild elevation in AST and ALT and ratio~1

236
Q

Urine is dark and dipstick shows bilirubin, interpret as what?

A

CONJUGATED BILIRUBIN can be renally excreted, not unconjugated

237
Q

PBC treatment as soon as diagnosed?

A

As soon as PBC diagnosed start ursodeoxycholid acid

238
Q

if someone has high alk phosphatase and nos/s of jaundice, first step?

A

yGGT, then if high you know its liver, if not = Paget. After you find it is liver = RUQ U/S

239
Q

hemochromatosis genes?

A

HFE

240
Q

How is cholangitis treated?

A

Treated wtih ERCP and broad-spec antibiotics

241
Q

s/s of cholangitis

A

RUQ pain, jaundice, fever, hypotension, mental status changes

242
Q

Pancreatic cancer is associated with what antigen?

A

CA19-9 = pancreatic CA

Final review for Step 2 Ck (12 decks)

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