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GI Block 2 Cards > GI Block 2! > Flashcards

GI Block 2! Flashcards

1
Q

Anoscope is used to eval what?

A

Clinical eval of anal canal (is not for hemorrhoids fissures and lesions)

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2
Q

Sigmoidoscopy allows you to look where?

A

Further into Rectum at polyps

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3
Q

Flex Sigmoidoscope allows you to look and do what, where?

A

Take biopsy of large intestine from rectum to sigmoid colon with a light source
Reqs bowel prep

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4
Q

The left side of the colon contains what?

A

75% of cancers

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5
Q

Colonoscopy is?

A

Study of choice
100% of view of colon and distal small intestine(terminal ileum)
Uses a light source reqs bowel pre

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6
Q

CT Colonography is?

A

3D Image Eval of colon prox to lesion

Used for failed colonoscopy eval colon pros to lesion cancer screen in pts w contra to endoscope or refuse

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7
Q

Barium Enema is = to

A

Lower GI Series

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8
Q

Most common cause of C. Diff infxn?

A

Hosp Acq— Fecal to Oral or Contact of spores on surfaces(up to 5 months)

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9
Q

Risk factors for C.diff

A

ABX use
Hospitalization
Advanced Age

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10
Q

Medication induced C Diff. risks: Highest—Intermediate—Lowest

A

Highest—Clindamycin, Flouroq.,Cephalosporins
Int—Penicillin, Macrolide, Sulfonamide
Lowest—Tetracycline

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11
Q

C. Diff presentation

A

Green/fowl smelling, watery diarrhea, cramp lower abdomen

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12
Q

Fulminant colitis presentation

A

Fever Hemodynamic ABD Distention Pain and Tender and profuse and diminished diarrhea X 15 times a day

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13
Q

PE C.diff

A

Assess for systemic illness, fever, tachy, HYPOTN, dehydration,
Peritoneal signs, Rebound guarding

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14
Q

Stool Studies C.diff infxn

A

Glutamate Dehydrogenase (GDH)
Nuclei Acid Amp Tests(NAAT)
Rapid Enzyme Toxin Assay(EIA)
Cell Culture cytotoxic assay/toxigenic culture[GOLD STANDARD]

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15
Q

What is the initial screening study of C.diff

A

GDH/PCR

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16
Q

What confirms C. Diff/Active Toxin?

A

Rapid EIA to determine Toxin A or B

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17
Q

What test is used to determine C.diff vs Pseudocolitis?

A

Colonoscopy

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18
Q

Severity of infxn is determined by what criteria(3)?

A

NONSEVERE = WBC < OR EQUAL 15,000 w/ creatinine < 1.5

SEVERE = WBC > OR EQUAL 15,000 w/ creatinine > 1.5

FULM DZ = WBC > 30,000 ALBUMIN > 2.5 Lacatate/Creatinine HYPOTN/ SHOCK/ILEUS/MEGACOLON

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19
Q

First Line treatment for Pharmacotherapy for C. Diff (3)

A

Fidaxomicin
Vancomycin
Metronidazole

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20
Q

Fulminant Colitis TXM

A

Vancomycin and Metronidazole w surgery consult for colectomy

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21
Q

Recur TXM 1st recur

C diff infxn

A

Fadaxomycin + Vancomycin X 10 days

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22
Q

Recur TXM 2nd recur

C diff INFXN

A

Vancomycin by mouth 10 days

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23
Q

Recur TXM 3rd recur

A

Fecal transplant

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24
Q

Toxic megacolon occurs at what diameter dilation with what signs?

A

Signs of sepsis

Greater than 7cm

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25
Q

Describe the mucosa of Toxic MEGACOLON

A

Alt. Edematous submucosa

Hyperemic Mucosa

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26
Q

Dx for Toxic MEGACOLON studies =

A 
Radio graphic evidence on CT w 3 out of the 4 
1)	Fever 
2)	Tachy
3)	Neutro/Leuko over 10,500
4)	Anemia 
And 1 of the following 
1)	Dehydration 
2)	ALM 
3)	Electrolyte Disturbed 
4)	HYPOTN
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27
Q

Initial TXM of Toxic MEGACOLON

A

= support therapy + MED MGMT w/ early consult
IV Fluid
Pros. ABX [High Risk of Perf]

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28
Q

Diverticular indicates what abnormalities

A

Bleed or Diverticulitis

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29
Q

2 most common areas for diverticula

A

Sigmoid colon and Descending colon

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30
Q

What changes are often age related and seen with diverticula?

A

Collagen changes

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31
Q

What can also cause diverticula formation ?

A

Increased Intraluminal pressure (low fiber ABD colonic motility)

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32
Q

Asians Diverticular vs other population Diverticula

A

= Rt Side ascending colon

= Distal Left sided colon

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33
Q

Usual symptoms of diverticula

A

Usually ASX or hematochezia

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34
Q

Main diverticula treatment

A

Increase Fiber to decrease caliber of stool and increase bulk = decreased pressure

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35
Q

What should diverticula patients avoid?

A

NSAIDS and RED MEAT

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36
Q

Diverticulitis complicated vs uncomplicated

A 
Uncomplicated = Inflammation of colon diverticula 
Complicated = Inflammation of colon diverticula assoc w/ perforation, obstruction, or bleed
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37
Q

Sxs/ Presentation of Diverticulitis

A

LLQ
Low Grade Fever
NO HEMATOCHEZIA

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38
Q

Should you perform barium enema if you suspect diverticulitis?

A

NO

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39
Q

TXM of Mild Diverticulitis [ no peritoneal signs, PO tolerated, Mild sxs ]

A

Bowel Rest
Clear Liquids
Pain Mgmt / ABX 7-10 days

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40
Q

TXM of Severe Diverticulitis [ peritoneal signs, can’t tolerate PO, severe sxs ]

A 
NPO 
IV Fluids 
Pain mgmt 
NGT decompress 
IV ABX [ 5-7 days] 
PO ABX [ surgical consult ]
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41
Q

Acute ILEUS occurs when and where?

A

72 hours post op

Large Intestine

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42
Q

Acute ILEUS presentation

A

Continuous ABD discomfort + N/V

Distended Diffuse Abdomen

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43
Q

TXM Acute ILEUS

A 
Treat underlying cause 
D/C all drugs that decrease int. Motility 
NPO
Bowel Rest 
Acute ILEUS w significant issues TXM 
NGT
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44
Q

Pseudo Obstruct. Oglive syndrome is a functional obstruction where?

A

Right sided cecum to proximal colon

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45
Q

What can happen with progressive bowel dilation up to 6 days?

A

Ischemia and or perforation risk

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46
Q

Symptoms and presentation of Oglive

A

Constant abdomen pain minimal ABD tenderness decreased bowel sounds
Fever peritoneal signs ischemia perforation

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47
Q

What needs to be ruled out when inspecting for Oglive

A

Mechanical obstruction / toxic megacolon / ILEUS

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48
Q

TXM of Oglive

A 
Less than12 cm dilation = Bowel rest 
Dec. Opiods 
NGT Rectal Tube decompress [most effective]
Enema if : FOS 
Ambulate 
Surger of greater than 12 cm dilation 
NO ORAL LAXATIVES
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49
Q

Most common place for colonic volvulus to twist

A

Sigmoid colon

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50
Q

Presentation of Colonic Volvulus

A 
Chronic Constipation 
Dysmotility 
High Fiber Diet 
Pain + Distention 
Previous surgery
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51
Q

Peritoneal signs and symptoms of Volvulus

A 
Fever 
HYPOTN 
TACHY 
Perforated perotinitis 
W/ insidious onset, constipation, Distention
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52
Q

What is a lab check for ischemia during volvulus work up

A

LACTATE

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53
Q

A sigmoid originating volvulus requires what?

A

Endoscopic depression

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54
Q

A right cecum originating volvulus reqs what?

A

Surgical resection = FIRST LINE

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55
Q

Common presentation of Crohns disease patient (4) =

A 
Young 
Chronic Diarrhea
RLQ pain 
Fatigue 
Low Grade Fever 
-ASX—Septic
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56
Q

Effects of Crohns on intestine?

A

Mouth to anus
Transmural
Any segment of GI
CANT Be CURED

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57
Q

Most common areas of bowel effected by Crohn’s disease? Least Common?

A 
Most = Skip Lesions of SB to colon (Ileocolic) 
Least = Upper GI
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58
Q

Hx of what things make you at risk for Crohns dz?

A 
Fam Hz
Tobacco 
ABX 
Jewish 
Gastroenteritis (Campy infxn + Salmonella infxn)
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59
Q

Hz of what types of diseases are assoc with Crohn’s disease?

A

Skin/joint/eye and other dz

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60
Q

Are Apthous ulcers common in Crohn’s disease or UC?

A

Crohn’s

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61
Q

What are immunomodulaters good for?

A

Reduces biologic antibodies that cause inflammatory symptom

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62
Q

What are examples of immunomod. Drugs?

A

Thiopurines + Methotrexate

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63
Q

Thiopurines are good for what?

A

Used in corticosteroid dependent pts to reduce recurrence of Abs w/ AntiTNF
*NoN HODgkin Lymphoma risk

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64
Q

Methotrexate is good for?

A

Combo w/ AntiTNF to decrease formation and risk of bone marrow suppression or hepatic fibrosis

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65
Q

What are biologics used for?

A

Suppress the physiologic response

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66
Q

What are examples of biologic therapies?

A

AntiTNF

AntiIntegrins

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67
Q

What is the job of AntiTNF

A

Prevent TNF stimulation of effector cells

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68
Q

What is the job of Antintegrins

A

Decrease circulation of leukocytes and reduce chronic inflammation

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69
Q

What needs to be ruled out when running labs for Crohn’s disease?

A

Celiac disease
Giardia
Decal Calprotectin (active inflammation)

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70
Q

Complications of Crohn’s disease

A

Abscess Obstructions Perianlal Diseae
CAXR
Fistulas

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71
Q

Four areas Crohn’s can cause fistulas

A

Skin
Bladder
SB
Vagina

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72
Q

First line diagnostic tech. For Crohn’s evaluation ?

A

Colonoscopy w biopsy

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73
Q

What can be the 2nd line study for Crohn’s disease eval?

A

CT or MRE/Capsule endoscope

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74
Q

IF UGI sxs present in Crohn’s disease what study should be done?

A

Upper Endoscope

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75
Q

Cutaneous manifestations of Crohn’s disease (3)

A 
Aphthous ulcers 
Erythema Nodosum (below the knee) 
Pyoderma Ganrenosum(Open sore inflammation]
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76
Q

Severity index of 150, 150-220, 221, 450, 450+

A 
150 = well controlled, remission 
150-220= mild active 
221-450= mod to severe w anemia 
450+= fulminant
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77
Q

When is endoscope required for Crohn’s disease

A

If Unintentional wt. loss observed

Index 221+ or mod-sever-fulminant

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78
Q

3 goals of therapy for Crohn’s disease

A

Control inflammation
Mx Control of sxs
Lifestyle modifications

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79
Q

Mild TXM of Crohn’s disease Right sided

A

Oral Budesonide

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80
Q

Mild TXM of Crohn’s disease left Sided

A

Prednisone or Prednisolone

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81
Q

If non response after mild TXM would should be given in Crohn’s disease?

A

Mesalamine or Sulfasalazine

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82
Q

Mod/Severe TXM Crohn’s

A

Oral pred./methyl prednisone

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83
Q

Severe TXM Crohn’s

A

Anti-TNF -1st Line Most Effective

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84
Q

Adding immunomodulators in severe Crohn’s disease treatment can cause what?

A

Higher rate of remission and increased risk of ADE’s

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85
Q

Fulminant TXM Crohn’s disease

A

IV Steroid [methylpredisolone]

+Oral Anti-TNF w/ inflammatory sxs

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86
Q

Criteria to admit for Crohn’s disease

A 
Int obstruction 
Abscess formation 
Infxn complications 
On immunomodul or Anti-TNF drugs 
Diarrhea/Dehydration/Wt Loss/ ABD Pain
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87
Q

How often should patients with Crohn’s disease receive colonoscopy

A

Every 8 years from Dx onset

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88
Q

What is characteristic of UC dz?

A

It is chronic, always presents w bloody diarrhea or nocturnal diarrhea LEFT SIDED
Age range around 15-30 years old

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89
Q

What is the Dx soc for UC

A

Flex Sigmoidoscope to prevent perforation

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90
Q

When are RADs performed for UC ?

A

Only in severe cases (CT/MRE) to prevent going inside colon

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91
Q

Mild to mod distal UC sxs

A 
Less than 6 stools 
Mild Bleeding 
Tenesmus 
Mild Anemia 
HYPOTN
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92
Q

Mild to Mod distal UC TXM

A

Topical 5 ASA
Hydrocortisone enema
Budesonide foam
Oral 5 ASA

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93
Q

Mild to Mod proximal UC TXM

A

Oral + Topical 5 ASA

Oral sulfasalazine -Arthritis
[MUST TAKE W FOLIC ACID]

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94
Q

Refractory Mild to Mod TXM of UC

A

Prednisone + Budesonide (Oral Steroids)

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95
Q

If greater than 1 relapse TXM of UC =

A

Thiopurines and Anti-TNF

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96
Q

Moderate to Severe UC sxs

A

Greater than 6 stools a day
Bloody
Impaired nutrition
ABD pain

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97
Q

Mod to Severe UC TXM

A

Oral prednisone

Methlypredisone

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98
Q

Refractory Severe UC TXM

A

Anti-TNF

Anti-Intergrin

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99
Q

Fulminant UC sxs

A

Sepsis

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100
Q

Fulminant UC TXM

A

IV methlyprednisone

Oral Prednisone 3-5 days

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101
Q

Refractory Fulmminant UC TXM

A

IV anti-TNF

IV cyclosporine[immunosuppresant]

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102
Q

Can methotrexate or corticosteroids be used as mono therapy?

A

NO

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103
Q

If UC is mod to severe with corticosteroid then switch to what?
Thiopurines
[Azathiopurine or Mercaptopurine]

A

Thiopurines

[Azathiopurine or Mercaptopurine]

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104
Q

If UC is mod to severe with Anti-TNF therapy what should next TXM protocol be?

A

Continue Anti-TNFs

[Adalimumab or Golumumab or Infliximab]

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105
Q

What it’s the curative TXM for UC

A

Total proctolectomy w ileostomy

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106
Q

Microscopic Colitis consist of what

A

Chronic watery diarrhea w normal biopsy and inflammatory tissue

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107
Q

What can cause micro colitis?

What is a common sxs?

A

With chronic NSAID use

Wt. Loss

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108
Q

TXM of Micro colitis

A

D/C meds w sxs care : Loperamide , Bismuth subsc , Budesonide (6-8wks)

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109
Q

What is the age for average risk of colorectal CAXR and screening recommendation

A

45 years ASX

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110
Q

How often is the gFOBT test performed?

A

Stool sample [annual]

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111
Q

How often is the FIT test performed?

A

More specific[annual]

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112
Q

How often is the FIT DNA test performed?

A

Finds CAXR cells in stool [Every 3 years]

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113
Q

How often is the colonoscopy test performed?

A

Direct visualization and diagnostic of the entire colon [Every 10 years]

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114
Q

How often is the CT colongraphy test performed?

A

Visualization only/ NO DX[Every 5 years]

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115
Q

Capsule colonoscopy is performed how often?

A

Every 5 years

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116
Q

What is used to define prognosis after Dx of colorectal cancer?

A

CEA [carcinoembryologivcal antigen]

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117
Q

How often is the Flexible Sigmoidoscope test performed?

A

Every 10 years + Fit every year

Or 5 years

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118
Q

How often is Stool or serology DNA performed for colorectal CAXR

A

Every 3 years

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119
Q

If you have a relative with colorectal CAXR when should you be screened w/ colonoscopy?

A

Every 5 years 10 yrs younger than relative Dx or age 40 [Earliest]

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120
Q

How long does it take to develop Polyps / what are the risks?

A

5-10 years

No familial[non genetic risk]

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121
Q

3 classifications of polyps

A

Adenomatous
Serrated
Hamartomatous

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122
Q

What is the most common shape of polyp

A

Sessile

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123
Q

Common size of Adenomatous polyps?

A

5mm-1cm

Most Common TYPE!

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124
Q

What is the low risk-high risk adenomatous type?

A

Low= Tubular
More =Villous
High= Tubular-Villous

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125
Q

Serrated polyps include (2)

A

Hyperplastic skin tags and sessile polyps

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126
Q

Polyps is Syndrome =

A 
100-1,00s of polyps 
Genetic condition 
Confirmed by genetic testing 
Around 15 yes 
100% develop colorectal CAXR
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127
Q

TXM of polyposis syndrome

A

Colectomy @ 20 yrs old w colposcopy ID

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128
Q

Non-neoplasticism pedunculated cherry red, smooth polyps =

A

Hamartamous polyps

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129
Q

Cowden Dsiease has what two characteristics and increased risk of what?

A

Hamartamous polyps + Lipomas throughout GI tract

Increased risk of non GI CAXR

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130
Q

Non polyposis : LYNCH SYNDROME

A

Can cause colorectal CAXR w/o polyps

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131
Q

What other CAXR should be screened for in LYNCH SYNDROME

A

Ovarian + Endometrial and other CAXR’s

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132
Q

Demographic factors that lead to colorectal CAXR =

A

Male gender with increasing age

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133
Q

Right sided symptoms that could be Colon CAXR =

A

Pain/Mass RLQ, IDA, weakness, fatigue

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134
Q

Left Sided symptoms that could be Colon CAXR =

A

Change in bowel, stool streaked

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135
Q

Rectum symptoms that could be colon CAXR=

A

Hematochezia “ribbon stools” urgency to defecate, tenesmus

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136
Q

Apple core lesion leads you to suspect

A

Colon CAXR

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137
Q

Management of Colon CAXR

A

1st = Colonscopy

Then surgeon mgmt

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138
Q

Prognosis Grades for Colon CAXR I,II,III,IV,V

A 
I-	Greater than 90%
II-	70-85%
III-	Less than 4 positive Lymph nodes 
IV-	Greater than 4 positive Lymph nodes 
V-	5-7%
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139
Q

Blood flow from oxy/deoxy blood at hepatic portal vein travels where?

A 
Hepatic sinusoids 
Central Vein
Hepatic Vein 
IVC 
Right atrium of the heart
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140
Q

Where is bile formed and how much per day?

A

1L
Liver Hepatocytes
7.6-8.6 pH

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141
Q

Bilirubin Steps (1-5)

A

1) RBC B/D = unconjugated bili [insoluble]
2) Albumin carries uncon. Bili to the liver
3) Liver conjugates bili
4) Bili goes from gallbladder to intestine
5) When reqd bili is used for digestion

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142
Q

Components of LFT tests(6)

A

1) Albumin
2) Serum protein
3) ALP/ALT/AST/GGT
4) Bilirubin
5) Lactate Dehydrogenase
6) Prothrombin Time

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143
Q

What type of labs evaluate hepatocellular injury?

A

Serum ALT/AST

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144
Q

What labs eval cholestatsis blockage?

A

ALP/ ALK PHOS / GGT

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145
Q

Synthetic FXN Labs =

A

Decreased synthesis
Albumin
PT Time/INR
Platelets(WBC’s)

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146
Q

An AST : ALT ratio 1:1 = what?

A

Ischemia

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147
Q

An AST: ALT ratio 2:1 = what?

A

AST MORE = Alcohol

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148
Q

An AST:ALT ratio 1:2 = what?

A

Hepatocellular damage

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149
Q

Examples of AST:ALT ration 1:2

A

Tylenol, viral hepatitis, Necrosis, Toxin induced hepatitis

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150
Q

Where is ALT specific origin?

A

Liver

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151
Q

Absorptive or Metabolism disease have what transaminase level predominant?

A

ALT

Celiac Dz, Autoimmune Dz, Alpha 1 Antitrypsin, Hemochromatosis

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152
Q

Alcohol related liver injury and cirrhoses predominant what transaminase level

A

AST

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153
Q

Dz Examples of Severe elevations of transaminase(3)

A

Wilsons
Acute Viral Hepatitis
Acute bile obstruction

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154
Q

Cholestasis means?

A

Liver not moving bile

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155
Q

ALP is specific for what organ and what issue?

A

Gallbladder scarring

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156
Q

GGT + AST:ALT 2:1 is suggestive of what?

A

Alcohol abuse

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157
Q

ALK phos greater than AST>ALT is = to what type of pattern?

A

Cholestatic pattern

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158
Q

Most common cause of hepatic portal HTN

A

Cirrhosis

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159
Q

Pressure gradient level measured for hepatic portal HTN include what? From low to high?

A

6-10 sub clinical
10-12 varices
12+ variceal bleed, Ascites

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160
Q

Budd Chiari syndrome is assoc with what type of hepatic damage

A

Post hepatic

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161
Q

Outflow obstruction of varices with decreased hepatic venous outflow

A

Budd Chiari

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162
Q

Budd Triad sxs

A

RUQ pain
Ascites
Hepatomegaly

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163
Q

Labs for Budd

A

Non specific

AST increased more than ALP

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164
Q

Study of choice for Budd syndrome

A

U/S

CT -views hepatic venous flow

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165
Q

What level of bili causes jaundiced skin and mucous membranes

A

7mg

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166
Q

Sclera conjunctiva jaundice is visualized at what level of bili

A

2mg

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167
Q

AST and ALT normal/Stool Color-Dark brown/Urine color-Normal acholuric/High Urobilinogen= What type of bili elevated?

A

Unconjugated

“Pre-hepatic”

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168
Q

Dark urine/Normal ish stool/Very high AST:ALT/2-3 times increased ALP = what type of bili elevated

A

Conjugated and unconjugated

“Hepatic”

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169
Q

High conjugated bili/Absent urobilinogen/increased bile salt/dark urine/clay colored stools/ increased AST:ALT/ALP 10/12X increased = what type of bili elevated?

A

Conjugated

“Post hepatic”

170
Q

ALP levels increased with more suspicion for what?

A

Obstruction

171
Q

Study of choice when eval jaundice =

A

U/S
MRI for lesions
ERCP MRCP

172
Q

ERCP =

A

Obstruction test
Endocholiagniography
View bile and pancreatic duct with stone removal

173
Q

MRCP =

A

MRI view non invasive

174
Q

Fulminant Acute Liver Failure signs =

A

8 wk development w/ INR greater than 1.5 f

175
Q

Subfulminant ALF includes what?

A

Hepatic encephalopathy

176
Q

Acute/Chronic ALF?

A

Acute Distention w/ pre-existing CLD

177
Q

Does Acute Liver Injury include AMS?

A

No alteration to level of consciousness

178
Q

ALF can be caused by what drugs (3)?

A

Acetaminophen
Mushrooms
(ABX/NSAIDS)

179
Q

Common symptoms of ALF

A

GI
Syst. Inflammation
Kidney dysfunction

180
Q

ALF Eval =

A

EMERGENCY

Perform Labs

181
Q

Management for ALF =

A

Supportive
N-acetylcysteine NAC for Tylenol induced OD

Activated charcoal for less than 4hrs since pain onset
Liver TXPL. Could be indicated

182
Q

Viral hepatitis has 4 stages =

A

1) Viral replication Phase
2) Prodromal Phase
3) Interim Phase
4) Convalescent Phase

183
Q

What time frame is important for Acute hepatitis?

A

Less than 6 months mostly self resolves

184
Q

What time frame indicated Chronic Hepatitis?

A

More than 6 months

185
Q

Acute Hep A Transmission and Presentation

A

Fecal to Oral

Fatigue 
N/V
Fever
Dark urine 
-Jaundiced eye/skin/uticuria/hepatomegaly
186
Q

Labs for Hep A standard diagnosis

A

IgM anti HAV = acute infxn

187
Q

IgG anti HAV =

A

Persistnat infxn W/ lifelong immunity

188
Q

LFT’s with AST>ALT and moderate elevation of bili + ALK phos = what type of hepatitis

A

A

189
Q

Main TXM for Hep A

A

Supportive

190
Q

Acute Hep B Transmission and Presentation

A

Body Fluid
Mild sxs w/ ab to Hep B
MOST COMMON INITIAL SXS – Fatigue

191
Q

Dx test for Acute Hep B =

A

HBcAG – Appears later but persists for LIFE

192
Q

HBsAg

A

Hep B in the Blood

[Not Acute or Chronic]

193
Q

AntiHBs

A

Immunity or Chronic

“You’ve got it, or you’ve had it! “

194
Q

IgM Anti-HBc means you have what?

A

Acute Hep B

195
Q

HBeAg means what is going on?

A

Viral replication and infectivity

196
Q

Antibody for HBeAg means what?

A

Chronic Hep B

197
Q

What’s is the diagnostic serology value that appears weeks later and persists for LIFE?

A

HBcAg

198
Q

What serology testing is used for monitoring Hep B Infxn?

A

HBV-DNA

199
Q

How should we manage an acute infxn with Hep B

A

DO serial testing for HBsAg to see if its has persisted (6months)
Should resolve at 16 weeks ~95%

200
Q

How should we manage chronic infxn with Hep B?

A

Serological molecular testing

Test for co-infxns

201
Q

TXM for Hep B

A

Supportive w Antivirals [Lamivudine]

202
Q

For mod to severe Hep B TXM=

A

Liver Transplant

203
Q

Transmission for HEP C virus

A

Blood transmission

Needle stick

204
Q

LFTS of Acture Hep C

A

ALT>AST

205
Q

What serology indicated exposure (Acute or Chronic) Hep C

A

Anti HCV

206
Q

What serology can show early and it’s the diagnostic confirmatory test for Hep C?

A

HEPC-RNA

207
Q

80% of presentation with Hep C = , the rest =?

A

ASX

Anorexia, Malaise, Fatigue

208
Q

Management of HEP C

A

25% spontaneously clearance, TREAT EVERYONE

209
Q

TXM for HEP C

A

Interferon (Antiviral)Ribavarin

210
Q

What drugs should be avoided when treating a HEP C patient

A

Tylenol

211
Q

What is the most common reason for liver transplant

A

HEP C infxn

212
Q

Prognosis of HEP C

A

Recover @ 3-6 months 55%-85% end up with chronic HCV

213
Q

What hepatitis conifers with HEP B

A

HEP D

214
Q

Route of Transmission for HEP D

A

IV Drug use routes similar to HBV

Outside US MOST COMMON

215
Q

What serology = presumptive for HEP D and could persist?

A

AntiHDV

216
Q

What serology confirms diagnosis for HEP D

A

HDV-RNA

217
Q

What Hepatitis is of concern in pregnant women?

A

HEP E

218
Q

HEP E transmission

A

Fecal to Oral transmission

219
Q

Confirmatory serology for HEP E virus =

A

IgM AntiHEV
IgG AntiHEV
HEP E Viral RNA

220
Q

Management of HEP E

A

Supportive

Severe cases = Ribavirin (Antiviral)

221
Q

Prognosis of HEP E

A

Can self resolve 4-6 weeks healing

Concerned w pregnant patients

222
Q

Chronic HBV, HCV, HDV, relations or reasons for disease.

A

HBV = alcohol related
HCV = non alcohol related steatohepatitis
HDV = Wilson’s disease , Alpha 1 antitrypsin DO, Celiac DZ
ALL CAN LEAD TO CANCER

223
Q

TXM management for Chronic Hepatitis

A

Inhibit viral replication- 1st Line = Pegylated Interferon Alfa-2A (PEG-IFN) X 48 weeks
2nd Line = Oral nucleoside analogs for 1-2 yrs [tenofovir, entecovir] = HIGH RELAPSE

224
Q

Chronic HEP C TXM

A

Decrease risk/sxs 1st Line = PREG-IFN + Ribavirin

2nd Line = DAA [glecaprenivir + pibrentasvin] EXPENSIVE BUT BEST

225
Q

Autoimmune HEP is common when? Presentation?

A

In women, following viral issues.

Can present ASX to fulminant

226
Q

Labs seen in autoimmune Hepatitis?

A

ALT HIGH
IgG Levels HIGH
ANA or pANCA

227
Q

Diagnostic study of choice for autoimmune Hep

A

Liver Biopsy, also assess severity

228
Q

TXM for Autoimmune Hepatitis

A

Prednisone + Azathioprine [decrease inflammation, liver enzymes, improve sxs]

229
Q

Most common cause of elevated Liver enzymes in the US

A

Steatosis [non alcohol]

230
Q

NAFLD is associated with what conditions?(3)

A

Insulin resistance
Obesity
Diabetes

231
Q

Difference between NAFLD and NASH

A 
NAFLD = Fat only 
NASH = inflammation + Scarring + Fibrosis + Fat.
232
Q

What can steatosis lead to?

A

Steaohepatitis
Cirrhosis
CAXR

233
Q

4 Risk factors for NAFLD

A

Obesity
Diabetes Type 2
Met. Syndrome
Hypertriglyceridemia

234
Q

Signs and sxs of NAFLD (3)

A

ASX
RUQ Pain
Jaundice

235
Q

Incidental labs of NAFLD

A

Inc ALT/AST

Inc ALP abnormal Liver images

236
Q

History of what two things leads you towards NAFLD

A

Met. Syndrome or Cirrhosis signs

237
Q

Alcoholic Liver Disease Labs

A

2X Inc of AST to ALT with Inc ALK PHOS
Serum bilirubin, albumin, PTT normal
Inc Glucose

238
Q

What diagnostic study is preferred for NAFLD

A

US

239
Q

What is diagnostic for NASH

A

Liver Biopsy

240
Q

NAFLD management (3)

A

Insulin and Glucose Control
Lipid Alerting Meds
Vitamin E

241
Q

Which gets pharmacologic thereby NASH or NAFLD

A

NASH

242
Q

Severe NASH TXM

A

Bariatric surgery or Liver TXPL prn

243
Q

3 associations with Alcohol Related Liver disease

A

Steatosis
Lobular Inflammation
Hepatic Elul are Injury

244
Q

Risk factors for Alcohol related Liver Disease

A

More than 7 beverages a week =Female
14 bevs = Male
Most significant at 30 bevs a week

245
Q

Alcoholic Related Steatosis definition

A

Fatty Liver First Stage-REVERSIBLE

246
Q

Alcohol Related Steatohepatitis definition

A

Clinical syndrome by jaundice

247
Q

ARLD Presentation

A

ASX—> Liver Failure

248
Q

Eval for alcohol use with ARLD with what?

A

AUDIT-C

249
Q

Labs for ARLD

A

AST 2X Greater than ALT w Inc. GGT

250
Q

RADS and confirmatory study for ARLD

A

US = preferred test to dx fatty liver disease, ARLD

Liver Biopsy for inflammation = hepatitis variant

251
Q

Management for ARLD

A

NO ALCOHOL
Manage commord’s
ICU w GI care

252
Q

Future use of alcohol does what for ARLD

A

Flares up the hepatitis and sxs

253
Q

Liver transplant is a consideration in ARLD when?

A

If they have stopped alcohol within the last 6 months+

254
Q

Most common hepatitis in the US vs Worldwide?

A

HEP C= US

HEP B= Worldwide

255
Q

Three stages of cirrhosis

A

Complicated
Complicated with varies
Decompress. (Variceal blood, Encephalopathy, Jaundice)

256
Q

Compensated cirrhosis presentation

A

ASX-> Anorexia , Wt loss, Fatigue

257
Q

Decompensated cirrhosis presentation

A

Jaundice
Pruritis
Upper GI Bleed
Clinical CLD

258
Q

The stigmata of chronic liver disease (5)

A 
Spider Angioma 
Jaundice Encephalopathy 
Asterixis 
Palmar Erythema 
Scleral Icterus
259
Q

Manifestations of cirrhosis stem from where?

A

Portal HTN

260
Q

Vital signs of cirrhosis patients

A

Dec BP

HTN-> Normotensive Wt Loss

261
Q

Cutaneous manifestations of cirrhosis

A

Clubbing
Terry nails
Muehrcke nails

262
Q

What is spider angioma

A

A vascular cirrhosis cutaneous manifestation that BLANCHES

263
Q

Endocrine manifestations of cirrhosis, Women vs Men

A

Women Chronic = Anovulation

Men = Gynecomastia

264
Q

Hepatic Encephalopathy = increased what?

A

Ammonia

265
Q

Scale of Hep. Encephalopathy. 0-4.

A 
0 = Normal 
1 = Mild confusion + asterixis 
2 = Lethargy w Inc Asterixis + Behavioral changes 
3 = Somnlence w decreased speech, marked confusion 
4 = Coma
266
Q

Symptoms that are for Hep Encephalopathy pathognemonic include

A 
Sleep Pattern Inversion = #1 
Personality changes 
Cognitive impairment 
Tremor 
Slurred speech 
Coma
267
Q

6 findings of Hepatic encephalopathy

A 
Bradykinesia 
Asterixis 
Dysarthria 
Heprflexia
Ataxia 
Nystagmus
268
Q

Treatment for hyperammonemia

A

Lactulose = absorb and metabolize(decrease the amount) ammonia

269
Q

Pre/Probiutics can help heperammonemia by what?

A

Building up gut bacteria to help with absorption

270
Q

Labs for Cirrhosis

A

AST inc more than ALT

271
Q

Management of cirrhosis

A

GI

Treat the cause of the complication including portal HTN

272
Q

Child Turcotte Pugh Score shows what

A

Relative Dz severity of trauma , with classes that relate to prognosis

273
Q

Model for End stage Liver Dz (Mild) shows what

A

History to predict surgical survivability

274
Q

Hepatotoxic substance induced toxic liver injury(TLI) is most often caused by what?

A

Acetaminophen

275
Q

What two drugs have a potentiation effect for TLI ?

A

Tylenol + Alcohol

276
Q

Direct Hepatotoxic rxns are what?

A

Predictable
Dose related
Universally susceptible

277
Q

Indirect Hepatotoxic rxns are what?

A

Drug exacerbating

W/ existing Liver Dz

278
Q

What hepatotoxic rxn us unpredictable and sporadic

A

Idiosyncratic rxns

279
Q

Two types of Cholestasis patterned injury

A

Non Inflammatory = drug induced

Inflammatory = Drug induced inflammation of portal areas

280
Q

Medication for hepatitis can cause what?

A

Acute or Chronic Hepatitis

D/C that agent

281
Q

1st line TXM for Acetaminophen poisoning

A

N-acetylecystine NAC

D/C agent

282
Q

Acute liver failure and organ failure can be due to what?

A

Acetaminophen hepatotoxicity

283
Q

What does primary biliary cholangitis refer to?

A

Inside the Liver bile stasis

284
Q

PBC is what kind of dz?

A

Autoimmune destruction of the bile ducts = cholestasis

T Lymph mediated

285
Q

Females w Aut immune D/O’s are at most risk for what?

A

PBC

286
Q

Findings with PBC

A

Progressive sxs , ASX hepatomegaly
Fatigue
Pruritis
Xanthamatous Lesion of skin or tendons

287
Q

Late stage sxs of PBC

A

Jaundice , Steatorrhea, Portal HTN, cirrhosis , Liver Failure

288
Q

Labs for PBC

A

Increased Lipids
Cholestatic Pattern = Inc ALK PHOS , Inc Bill , Small inc ALT/AST
AMA
ANA

289
Q

TXM for PBC

A

Ursodeoxycholic ACID

To slow slow progression to liver TXPL

290
Q

Hemochromatosis = accumulation of what?

A 
Iron – Hemocidrin 
Liver
Pancreas 
Heart 
Pituitary 
Kidney 
Adrenals 
Testes
291
Q

Hemochromatosis w Alc Abuse makes you at risk for what?

A

Cirrhosis

Liver Failure

292
Q

Labs for hemochromatosis

A 
Inc plasma Iron 
Inc serum ferritin 
Inc AST/ALK PHOS 
(Outside liver indications) 
Hemocidrin
293
Q

Suspect Hemochromatosis you do what test?

A

Genetic testing

294
Q

Colors the skin turns for hemochromatosis

A 
Grey = Iron 
Bronze = Melanin
295
Q

Diagnostic test for hemochromatosis

A

Biopsy

296
Q

1st line TXM for hemochromatosis, 2nd, 3rd?

A 
1st = phlebotomy 
2nd = chelation defoaxamine meds
3rd = Liver TXPL
297
Q

Wilson’s disease is a build up of what leading to what in female vs males?

A

Copper
Female = Liver Failure sxs
Male = Neuro psych sxs , dysarthria, incoordination
Psych symptoms

298
Q

Pathognomonic for Wilson’s disease

A

Kayser Fliescherr Rings at the cornea and scleral jxn

299
Q

Labs for Wilson’s disease

A

Clinical dx = DECREASED ceruloplasmin protein
Increased urinary copper [MOST COMMON FINDING]

Inc copper in the liver

300
Q

Confirmatory test for Wilson’s?

A

Molecular analysis genetic defect in chromosome 13

301
Q

TXM for Wilson’s disease

A

Chelation with a D penicillin [ hard on the kidneys ]
2nd = Triantine $$$[better]
3rd = Zinc [absorption and excretion of copper]

302
Q

What is the DOC for pregnant,ASX, or good Mx therapy after chelation in patients with Wilson’s disease

A

Zinc

303
Q

Explain Pyogenic abscess

A 
Invasion of 
1)	Bile Duct 
2)	Hep. Artery 
3)	Portal Vein 
Traumatic impact of bacteria into the ABD wall
304
Q

Clinical Presentation of pyo hep abscess

A

Fever
Jaundice
+blood culture

305
Q

What complication can cause Pyo Abscess

A

Ascending cholangitis

306
Q

Cavernous hemangioma is what?

A

BENIGN Cluster of capillaries in the liver

Incidental / unless large

307
Q

Hepatocellualr carcinoma is associated with what?

A

Cirrhosis

Hep B/C

308
Q

Labs for hep. CAXR?

A

Leukocytes is CBC
Alpha Fetoprotein
Sudden sustained increase of ALK PHOS

309
Q

Dx and TXM for hep. CAXR?

A 
Dx= Liver biopsy 
TXM= Surgery resection
310
Q

What should you screen for if hep. CAXR?

A

Alpha fetoprot. + U/S every 6 months
Cirrhosis pts
Chance of HBV /HCV
Fam Hx of HCC

311
Q

Cholelithiasis = what?

A

Gallstones in the gallbladder

Effects women more than men

312
Q

5F’s of gallstones

A 
Fat 
Fair
Forty
Familial  
Fertile
313
Q

What is the make up of solid stones

A

Calcium or bilirubin

314
Q

5 protective factors for gallstones

A 
Coffee 
Physically Active 
High fiber, Low carb 
Statins 
Unsaturated Fats
315
Q

Common sxs of gallstones

A

Colicky pain that is episodic at RUQ
Pain w High fat meals
Middle of the night pressure

316
Q

Common sxs of gallstones

A

Colicky pain that is episodic at RUQ
Pain w High fat meals
Middle of the night pressure

317
Q

TXM for cholesterol gallstones

A

Ursodeoxycholic acid (bile salt)

318
Q

Who is indicated for surgery when treating gallstones?

A

Cholecystectomy for symptomatic patients and cholelithiasis

319
Q

Define acute cholecystitis

A

InflaMMATION of the gallbladder w thickened wall
Due to impaction by stone or sandy obstruction[acalculous]

RUQ Pain —> Shoulder
Fever (LOW GRADE)
Palpable GB

320
Q

Is Jaundice common w Acute cholecystitis?

A

NO

The ROCK is not @ ampulla of vadar its higher up

321
Q

Positive Murphy sign?

A

Sudden exhale w pain

322
Q

Where does the pain localize in acute cholecystitis

A

Infra-scapular region

“Pos Dx choelcystitis”

323
Q

Does acute cholecystitis have a cholestatic pattern?

A

NO

324
Q

Labs for AC

A

CBC Inc WBC Inc 12,000-15,000
Serum bilirubin mild elevation
ALK PHOS / AST ALT non specific elevation
Mild elevation of Amylase

325
Q

Rads for AC in order for preference

A

1st US = RUQ, study of choice
2nd HIDA SCAN = Obstruction Check
3rd CT = perforation gangrene check

326
Q

2 complications of AC

A

Gangrenous cholecystitis

Chronic Cholecystitis

327
Q

Gangrenous chole?

A

Necrotic perforation. Ischemia
Continuous RUQ pain
Abscess
Obese patients/DM/Elderly

328
Q

Chronic Chole?

A

Result from repeat episodes of acute chole irritation by STONES
Can become —> porcelain gallbladder

329
Q

Management for AC

A

Admit
NPOR Pain control (Morphine + Merperidine)
SURGERY[curative] or IV ABX[w high recurrence rate]

330
Q

When does perforation usually occur with AC?

A

48-72hours

331
Q

Choledocholithiasis is a stone where?

A

Common bile duct origination = gallbladder

Post Hepatic obstruction

332
Q

Charcots Triad?

A

RUQ pain
Fever/Chills
Jaundice

333
Q

PE eval for what with Choledoco?

A

Sepsis
Hemodynamic status
AMS

334
Q

What study helps decide if there is a stone?

A

MRCP

335
Q

What study is good for ID and TXM of stones?

A

ERCP

336
Q

Lab pattern for choledoc?

A 
Cholestatic pattern 
Inc ALK PHOS > AST/ALT 
Serum bilirubin 
Inc WBC’s 
Amylase -2nd to pancreatitis
337
Q

Dx evidence for choledoc?

A

Charcots Traid
Or
2/3 Charcots + Imaging positive or + elevated liver levels(w Cholestatic Pattern)

338
Q

Alcohol related liver dz and cirrhosis have what liver enzymes levels

A

AST-predominates more than 5X normal

339
Q

Chronic hep, acute viral hep, steatosis, hemochromatosis, Wilson’s dz have what liver enzymes levels?

A

ALT-predominates more than 5X normal

340
Q

Acute cholecystitis duct obstruction, budd chairi presents with what liver enzymes levels?

A

ALT/AST greater than 15X normal

341
Q

PBC, Primary sclerosis cholangitis, cystic fibrosis, and hep masses are examples of what on the US

A

US= Normal bile ducts

Hepatic obstructions

342
Q

Common bile duct stone, biliary structure worms flukes and CAXR cause what on US?

A

US = Dilated bile ducts

Bile Duct Obstructions

343
Q

Management for Choledoc?

A

GI ERCP TXM

344
Q

Within what time frame should you perform ERCP

A

12-24 hours

345
Q

Within what time frame should you remove the gallbladder after ERCP

A

72 hours

346
Q

Complications of choledoc?

A

Cholangitis w fever shock jaundice

Pancreatitis

347
Q

What is Acute Cholangitis AKA?

A

Ascending Cholangitis

Acute superlative Cholangitis

348
Q

What is present with Acute cholangitis?

A

Charcots Triad + AMS/HYPOTN

349
Q

What is Reynolds Pentad

A

Suppurative Cholangitis w evidence of sepsis

350
Q

Definition of Cholecystitis =

A

Gallstone + Fever/Pain

351
Q

Def of Choledoc?

A

Gallstones + Jaundice

352
Q

Cholangitis Def?

A

Gallstones + Jaundice + Higher Fever

353
Q

Suppurative Cholangitis def?

A

Gallstone + Jaundice + AMS + HYPOTN

354
Q

Primary sclerosing cholangitis is what type of response?

A

Immune response common in MEN

Intestinal endotoxins causing inflammation w IBD (UC)

355
Q

What decreases the risk for Primary sclerosing cholangitis?

A

Smoking and Coffee

356
Q

What is the Dx study of choice for Primary sclerosing cholangitis?

A

MRCP

Look for bile duct dilations b/w strictures

357
Q

Is there an obstructive stone with Primary sclerosing cholangitis?

A

NO

358
Q

TXM for PSC?

A 
Duct dilation stent placement 
Cholecystectomy [treatment for stenosis] 
Colectomy 
Liver TXPL 
9-20 yrs survival rate
359
Q

What should management be for PSC?

A

Annual MRCP/PET

CA19-9 (Nonspecific)

360
Q

What does PSC have a risk for?

A

Bile CAXR and Colon cancer

361
Q

PBC is associated with what type of cancer?

A

Liver

362
Q

Biliary cancer commonly presents with what?

A

Painless jaundice
Dilated biliary tract
Pruritis

363
Q

What is courvoisier sign?

A

Jaundice w profound and palpable GB

Mets progress or ascites

364
Q

Labs for Biliary CAXR

A

ALK Phos> Obstructive pattern (potential mass?)

365
Q

Study of choice to ID Mass in biliary CAXR

A

MRCP

366
Q

The sphincter of Odii is controlled by what?

A

The ampulla of vadar

367
Q

What is increased in acute pancreatitis?

A

Inc pancreatic enzymes (amylase Lipase)

368
Q

What type of cells are injured in acute pancreatitis?

A

Acinar cells

369
Q

Most common cause of biliary tract dz?

A

Stones and Alcohol

370
Q

What type of bite can lead to acute pancreatitis?

A

Scorpion

371
Q

Sxs of Acute Pancreatitis?

A

Abrupt onset / epigastric pain boring radiation to the back
Episodic
Hurts worse:
When walking around and laying down

372
Q

What ultimately causes pancreatitis?

A

Backflow pressure build-up

373
Q

What two signs are assoc with acute pancreatitis?

A

Cullen sign-umbilical
Grey Turner sign= Flank bruise
Hemorrhagic pooling of blood

374
Q

Hx of what lines up with pancreatitis?

A 
Boring biliary colic pain
To the back pain 
Stones Hx
Distended Abdomen 
Low grade Fever (101/102F)
375
Q

Explain when you would perform MRCP for AP?

A

Older than 40 years old to exclude malignancy if no stones on U/S

376
Q

Labs for Acute Pancreatitis (AP)

A

Amylase and Lipase[stays longer, best]
ALK PHOS>AST/ALT
Hyperlipidemia

377
Q

The Atlanta classification is good for what?

A

Present Transient or Persistent organ failure classification

378
Q

Severity index is good for what in AP?

A

Fluid collections and ability to cause pancreatic necrosis

379
Q

What age is at risk for AP via Ranson criteria?

A

Over 55 yrs

380
Q

What elevated labs are indicative points on ranson criteria for AP? (4)

A

WBC
Blood glucose
Lacatae dehydrogenase
Aspartate aminotransferase

381
Q

What liver enzymes is specific to the pancreas?

A

AST

382
Q

Hematochezia @ greater 10%, BUN increase by 5mg/dL, pO2 less than 60mmHg, base deficit greater than 4MEq/L ABD fluid sequestration greater than 6000 mL is a point on the ranson criteria for AP at what time?

A

48hours

383
Q

TXM of mild AP

A 
Pancreatic “rest” 
NPO
Aggressive early fluids  
NGT 
Pain control [meperdine = preferred]
                      [morphine = irritates sphincter of odii ; SOME]
384
Q

TXM of Severe AP

A

Admit to ICU
Early surgery consult
IV fluids
NPO

385
Q

Why are IV fluids given in severe AP?

A

To maintain intravascular volume and urine output

386
Q

Necrotizing pancreatitis is treated with what?

A

ABX + team of specialists

387
Q

AP complications (4)

A

1) Sterile or Infxn Necrotizing Pancreatitis
2) Intravascular volume depletion
3) Acute resp distress syndrome (ards w cardiac dysfunction)
4) 100% progress to chronic

388
Q

What do 80% of chronic pancreatitis patients develop?

A

DM

W/ permanent structural damage

389
Q

Most common risk for chronic pancreatitis?

A

Alcoholism

390
Q

S/sxs of chronic pancreatitis (CP)?

A

LLQ pain + Epigastric Pain ; anorexia + streatorrhea

391
Q

How does CP present with exocrine deficiency?

A

Fat Malabsorption

392
Q

Labs for CP include (4)?

A

Amylase / Lipase
ALK PHOS
Stool study = Fecal Fat
Pancreatic FXN tests

393
Q

What is the most sensitive imaging study for CP?

A

ERCP

394
Q

Pancreatic tissue sampling gold standard for diagnosis and NOT SCREEN of CP?

A

ERCP

395
Q

Explain a direct pancreatic fxn test

A

Secretin FXN Test
Give a meal or secretagogue to analyze duodenal fluid
Diagnostic for EARLY chronic pancreatitis if the imaging is piss poor

396
Q

TXM for CP?

A

GI referral
NO ETOH
Non opiodal pain controls
Pancreatic enzyme supplementation

397
Q

Main complications of CP (3)

A

DM
Cholestatic liver enzymes
Pancreatic CAXR

398
Q

CLIN presentation of exocrine pancreatic insufficiency

A

Patients w ABD pain chronic diarrhea and steatorrhea

399
Q

Endo and Exo labs fir exocrine insufficiency

A

Endo = serum glucose decrease and trypsinogen decrease

Exo = fecal fat and secretin stimulation on pancreatic fxn tests

400
Q

Pancreatic CAXR is highly what?

A

Lethal

401
Q

Sx of pancreatic CAXR

A

ABD pain
Courvoiser sign [non tender, palpable gallbladder]
LUQ pain depending on tail vs head

402
Q

LABS for pancreatic CAXR

A

Non specific
Amylase /Lipase
Bilirubinemia
CA-19-9

403
Q

RADS 1st study for pancreatic CAXR

A

CT

404
Q

2nd study and monitor studies for known Pancreatic CAXR?

A

EUS/MRCP/ERCP/PET

405
Q

TXM for pancreatic CAXR

A

Surgical resection = TXM of Choice

406
Q

If resectable what is the TXM protocol for a pancreatic CAXR mass?

A

Endo stent of bile duct

407
Q

What part of the pancreas is going to present with obstructive jaundice symptoms if affected?

A

Head

408
Q

What part of the pancreas is going to present without obstructive symptoms if affected?

A

Tail

409
Q

Inflammation of the appendix can result in what 3 things? (3)

A

Rupture
Abscess
Gangrene

410
Q

What are two potential causes for appendicitis?

A 
Luminal obstruction (Fecalitch)
Distention of bacterial growth
411
Q

What happens to blood flow if a fecalith is present?

A

Loss of flow distal to the fecalith
Leading to infxn and inflammation
Then perforation

412
Q

How will a patient with appendicitis lay?

A

Lies still

413
Q

What is the characteristics spot of tenderness with appendicitis?

A

McBurney’s point

414
Q

What is the obturator or sign?

A

Pain with passive flex ion of the internally rotated right hip

415
Q

Where is McBurney’s point?

A

Between ASIS and UMB.

416
Q

What is the length of thickness suspect for inflammation or calcified appendicolith?

A

2mm

417
Q

TXM for appendicitis?

A

Pain mgmt = morphine
Surgical consult win 24 HOURS [TXM of Choice]
Other countries = ABX

418
Q

What ABX can treat appendicitis?

A

Cephalosporins

+ Metronidazole

419
Q

Complications of untreated appendicitis?

A

Abscesses [trasnmural w pus]
Gangrene [transmural w necrosis]
Perforation
Recurrence after TXM (38%)

420
Q

At what time frame is a patient at risk for appendicitis perforation?

A

36 hours

421
Q

What signs should make you concerned for appendicitis perforation?

A

Pressure
Pain
Release! [Decreased Pain] = PERFORATION

GI Block 2 Cards (1 decks)

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