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Med School Rotations > Internal Medicine Tips Tricks and Techniques Part II > Flashcards

Internal Medicine Tips Tricks and Techniques Part II Flashcards

1
Q

What are the two major classes of IBD

A

Ulcerative colitis;

Crohns disease

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2
Q

Where is the inflammation in ulcerative colitis

A

Limited to the colon and the rectum. Inflammation is limited to the mucosal lining.

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3
Q

Where is the inflammation in crohns disease

A

transmural inflammation in any part of the entire GI tract

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4
Q

What is the presentation of IBD

A

diarrhea;
weight loss;
abdominal pain

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5
Q

Crohns disease can also present with

A

fistula formation;
strictures;
abscesses;
bowel obstruction

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6
Q

How is IBD diagnosed

A

Endoscopy is the preferred method.
CT and MRI scans;
Serologic markers

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7
Q

What will differentiate crohns disease from UC histopathologically

A

UC: Chronic mucosal inflammation with crypt abscess and cryptitis;

Crohns: multinucleated giant cells and noncaseating granulomas in CD

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8
Q

What are the serologic markers used to distinguish UC from Crohns

A

CD: Anti-Saccharomyces cerevisiae antibodies;

UC: pANCA (perinuclear antineutrophil cytoplasmic antibodies)

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9
Q

How is treatment determined for IBD

A

Based on the severity of the symptoms

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10
Q

How is the severity of disease classified for IBD

A

Mild;
Moderate;
Severe

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11
Q

What defines mild to moderate disease

A

UC: less than 4 bowel movements with no rectal bleeding or anemia.;

CD: little to no abdominal pain

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12
Q

What are the medical treatment options for mild to moderate disease

A

5-ASA; Antibiotics for CD; Budesonide; Topical therapy (limited to left colon)

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13
Q

What are the 5-ASA used

A

Sulfasalazine; Mesalamine; Olsalazine

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14
Q

Name Mesalamine preparations used for IBD

A 
Asacol
Pentasa; 
Apriso; 
Balsalazide; 
Multimatrix delivery system mesalamine
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15
Q

What is budesonide

A

A synthetic corticosteroid with first pass liver metablism that limits systemic toxicity while retaining local efficacy from high affinity glucocorticoid receptors

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16
Q

What defines moderate to severe disease

A

CD: Patients that fail to respond to therapy with mild to moderate disease or those that develop significant weight loss, anemia, fever, abdominal pain or tenderness, and intermittent nauseas and vomiting without bowel obstruction.;

UC: Patients with more than 6 bloody bowel movements a day, fever, mild anemia, and elevated ESR

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17
Q

What are the medical treatments used for moderate to severe IBD

A

Glucocorticoids;
Immunosuppressive agents;
Anti-tumor necrosis factor alpha;
Natalizumab

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18
Q

What immunosuppressive agents are used in the treatment of IBD

A

6-Mercaptopurine;
azathioprine (6-M’s S-imidazole precursor);
Methotrexate

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19
Q

How does 6-Mercaptopurine work for IBD

A

causes preferential suppression of T=cell activation and antigen recognition and are useful in maintaining glucocorticoid induced remission in both UC and CD

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20
Q

What will help prevent toxicity caused by 6-mercaptopurine

A

Determination of thiopurine methyltransferase (TPMT) enzyme activity prior to initiation of therapy

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21
Q

How does methotrexate work for IBD

A

effective as a steroid sparing agent in CD but not UC.

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22
Q

What are the anti-tumor necrosis factor monoclonal antibodies for IBD

A

Infliximab;
Adalimumab;
certolizumab pegol

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23
Q

What are the adverse effects of using anti-TNFa

A

reactivation of a latent tuberculosis;

development of antibodies to infliximab and double stranded DNA

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24
Q

What is natalizumab

A

a humanized monoclonal antibody to alpha-4 integrin, a cellular adhesion molecule used for moderate to severe CD refractory to all other approaches including Anti-TNFa antibodies

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25
Q

What are the adverse effects of natalizumab

A

induce reactivation of JC polyoma virus causing progressive multifocal leukoencephalopathy.

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26
Q

When is surgery an option for patients with IBD

A 
patients with fistulas; 
obstruction; 
perforations; 
abscesses; 
bleeding
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27
Q

What are adverse outcomes of surgery for IBD

A

Short bowel syndrome;

recurrence close to the resected margins is common with CD

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28
Q

Surgery for UC

A

a total colectomy may be curative

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29
Q

What defines nephrotic syndrome

A

Proteinuria >3.5 grams/d;
hypoalbuminemia;
hyperlipidemia
edema

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30
Q

What will biopsy show for nephrotic syndrome

A

will show injury along the filtration barrier;
thickening of the glomerular basement membrane
fusion of the podocyte foot processes

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31
Q

What is the general medical treatment for nephrotic syndrome

A

ACE inhibitors and ARBs to reduce intraglomerular pressure;

Aggressive treatment of hypertension can also slow progression of renal disease

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32
Q

What bleeding disorders are often accompanied by nephrotic syndrome

A

hypercoaguable state and can predispose pt to thromboembolic events

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33
Q

Name the primary glomerular nephropathies

A

Minimal Change Disease;
Focal Segmental Glomerularsclerosis;
Membranous Nephropathy;
Membranoproliferative

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34
Q

What age groups are most commonly affect by MCD

A

children;

second peak seen 50-60

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35
Q

How will MCD present

A

sudden onset proteinuria with hypertension and edema;

Renal insufficiency is unusual

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36
Q

What are associated conditions of MCD

A

Hodgkins and solid tumors

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37
Q

How is MCD diagnosed

A

LM: Normal glomeruli;
Electron: shows effacement of the foot processes as the only abnormality

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38
Q

What is the treatment for MCD

A

oral prednisone for 1mg/kg/d for 8-16 weeks until remission.
Then tapered over the next 3 months

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39
Q

How will Focal Segmental Glomerulosclerosis present

A

nephrotic syndrome;
HTN;
Renal insufficiency

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40
Q

What are the associated conditions of Focal Segmental Glomerulosclerosis

A

Obesity;
HIV;
IV Drug use

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41
Q

How is FSGS diagnosed

A

Immunofluorescense shows staining for C3 and IgM in areas of sclerosis representing areas of trapped immune deposits

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42
Q

How is the prognosis for FSGS determined

A

the degree of interstitial fibrosis and tubular atrophy

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43
Q

What can be used to treat nephrotic syndromes if they are refractory to oral prednisone

A

cyclosporine;

cyclophosphamide

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44
Q

How will membranous Nephropathy present

A

nephrotic syndrome or heavy proteinuria while renal function is often normal

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45
Q

How is disease progression for Nephropathy

A

1/3 remit spontaneous;
1/3 ESRD;
1/3 intermediate course

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46
Q

What are the associated conditions with membranous nephropathy

A

SLE;
Viral hepatitis;
syphilis;
solid organ malignancy

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47
Q

How is membranous nephropathy diagnosed

A

kidney biopsy shows;
LM: thickening of the basement membrane;
Silver stain: “spikes”

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48
Q

Who receives treatment for membranous nephropathy

A

patients at higher risk for progression (reduced GFR, age >50, and HTN, and males);
Severe nephrotic syndrome (proteinuria >10g/d)

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49
Q

What is the primary cause of Membranoproliferative Glomerularnephropathy

A

Hepatitis C and frequently in association with cryoglobinemia

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50
Q

How is Membranoproliferative GN diagnosed

A

LM: mesangial proliferation and hypercellularity with lobularization of the glomerular tuft;
Silver stain: mesangial interpositioning appearance gives a double contour or “tram tracking appearance”

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51
Q

What are the compliment levels for Membranoproliferative GN

A

usually low

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52
Q

What is the treatment for membranoproliferative GN

A

treatment has not been shown to improve disease free survival, steroids may stabilize the disease in children.;
If renal function is rapidly declining in the presence of cyroglobulins, plasmapheresis may help stabilize the disease.

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53
Q

Name the hepatotropic viruses

A 
HAV; 
HBV; 
HCV; 
HDV; 
HEV
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54
Q

What is the classification of HAV

A

RNA virus that belongs to the Picornavirus family

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55
Q

What is the most common cause of viral hepatitis world wide

A

HAV

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56
Q

How is HAV spread

A

fecal-oral route

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57
Q

What is the period of infectivity for HAV

A

2 weeks before symptoms through 2-3 weeks after symptoms

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58
Q

What are high risk conditions for HAV

A

anything to do with developing countries

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59
Q

How is the diagnosis made for HAV

A

detection of IgM anti-HAV antibodies

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60
Q

How is the recovery and immunity phase determined for HAV

A

detection of IgG anti-HAV antibody

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61
Q

What is the clinical presentation for HAV

A 
All are common but non specific: 
Malaise; 
fatigue;
pruritus; 
headache; 
abdominal pain; 
myalgias; 
arthralgias; 
nausea; 
vomiting; 
anorexia; 
fever
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62
Q

What is the treatment for HAV

A

no specific treatment, only supportive therapy

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63
Q

What can be used for preexposure prophylaxis

A

the HAV vaccine containing the single HAV antigen

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64
Q

What can be used for post exposure prophylaxis

A

Ig

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65
Q

What is the prognosis of HAV

A

almost all will resolve in 4-8 weeks

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66
Q

What is the classification of HBV

A

DNA virus that belongs to the hepadnavirus family

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67
Q

What phenotypes of HBV have been found in the US

A

All phenotypes; The most prevalent being A, B and C

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68
Q

What is the leading cause of HCC world wide

A

HBV attributes 60-80% of all cases

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69
Q

What percentage of liver transplants is due to HBV

A

5-10%

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70
Q

What causes liver damage following HBV

A

immune mediated

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71
Q

What are the modes of transportation for HBV

A

Parenteral or percutaneous routes; Sexual contact; Vertical transmission (mother to infant)

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72
Q

What is the incubation period after an HBV infection

A

30-160 days

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73
Q

What are the clinical phases of HBV

A

Acute hepatitis B;

Chronic Hepatitis B

  • Immune tolerant
  • Immune Active
  • Carrier state with low replication
  • Chronic HBeAg negative;

Resolution

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74
Q

What defines immune tolerant phase of HBV

A

high rates of viral replication, yet normal liver enzymes and low levels of inflammation and fibrosis

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75
Q

What define immune active phase of HBV

A

Characterized by elevated liver enzymes as a consequence of a vigorous immune response

76
Q

What defines Carrier state with low replication phase of HBV

A

low or undetectable levels of HBV DNA levels

77
Q

what defines the chronic HBeAg negative phase of HBV

A

patients harbor HBV variants with mutations that prevent the production of or have low expression of HBeAg

78
Q

What labs will indicate acute hepatitis

A 
abnormal: 
AST; 
ALT; 
ALP; 
total bilirubin
79
Q

What are the HBV antigens detected in the serum

A

HBsAg;

HBeAg

80
Q

What is the most accurate viral marker for HBV replication

81
Q

What genotypes of HBV have the highest response to IFN therapy

A

genotypes A and B

82
Q

Is liver biopsy beneficial for HBV

A

yes.

It can determine the grade (degree of inflammation) and stage (fibrosis)

83
Q

What are the medications used for HBV

A

Seven Agents in three main groups;

  1. Interferon based therapy;
    a. IFN-a;
    b. pIFN;
  2. Nucleoside analogs;
    a. lamivudine;
    b. entecavir;
    c. telbivudine;
  3. Nucleotide analogs;
    a. adefovir;
    b. tenofovir
84
Q

What are the first line treatment options for HBV

A

IFN-a;
pIFN;
Entecavir;
Tenofovir

85
Q

What drug groups are anti-viral resistance associated with for HBV

A

nucleoside and nucleotide analogs

86
Q

What is the classification of HCV

A

RNA virus that belongs to the flavivirus family

87
Q

What is the prevalence of HCV in the US

A

1.8%;
Genotype 1 makes up 70%;
Genotype 2 and 3 make up 20%

88
Q

What is the prophylactic treatment for HCV

A

does not exist

89
Q

What is the incubation period for HCV

A

15-150 days

90
Q

What are the symptoms of HCV

A 
All are common but non specific: 
Malaise; 
fatigue; 
pruritus; 
headache; 
abdominal pain; 
myalgias;
arthralgias; 
nausea; 
vomiting; 
anorexia; 
fever;

Fatigue is the most common. All may be subclinical until late when the symptoms are associated with advanced liver disease

91
Q

How long may it take before labs will show anti-HCV

A

up to 8 weeks post infection

92
Q

Does the anti-HCV antibody imply immunity

93
Q

What are the medications for HCV

A

IFN;

Ribavarin

94
Q

With regards to HCV, what is RVR

A

rapid viral response;

HCV RNA negative at 4 weeks of treatment

95
Q

With regards to HCV, what is EVR

A

Early viral response;

HCV RNA negative at 12 weeks of treatment

96
Q

With regards to HCV, what is cEVR

A

no RVR, but HCV RNA negative at 12 weeks of treatment

97
Q

With regards to HCV, what is pEVR

A

no RVR,

detectable HCV RNA but >2log10 drop at 12 weeks of treatment

98
Q

With regards to HCV, what is Slow responder

A

> 2log10 drop at 12 weeks of treatment and HCV RNA negative at 24 weeks

99
Q

With regards to HCV, what is partial responder

A

> 2log10 drop at 12 weeks of treatment and HCV RNA positive at 24 weeks

100
Q

With regards to HCV, what is relapse

A

HCV RnA negative at end of treatment but HCV RNA positive after treatment cessation

101
Q

With regards to HCV, what is SVR

A

Sustained viral response; absence of HCV RNA 6 months post viral treatment

102
Q

What is the prognosis of HCV

A

40% will have spontaneous remission while 60% will have chronic infection

103
Q

What percentage of HCV pt’s develop HCC

104
Q

What is HDV classification

A

considered a subviral particle resembling plant pathogens;

Circular RNA genome

105
Q

What is required for HDV infection and replication

106
Q

What is the transmission of HDV

A

similar to HBV

107
Q

What is a coninfection of HDV

A

simultaneous infection of HBV and HDV

108
Q

What is a superinfection of HDV

A

HDV infection of a patient already infected with HBV

109
Q

What is the treatment of choice for HDV

110
Q

What is the classification for HEV

A

RNA virus that belongs to the hepeviridae family

111
Q

What is the transmission of HEV

A

Fecal oral route

112
Q

What is the fatality of HEV

A

high fatality rate in pregnant women in the second and third trimester

113
Q

What is the treatment of HEV

A

supportive

114
Q

What are the typical presentation of GERD

A

Esophageal symptoms;
Chest pain;
Extraesaphogeal symptoms

115
Q

What are the esophageal symptoms associated with GERD

A

Heartburn and regurgitation

116
Q

What are the extraesophageal symptoms of GERD

A

Cough;
Laryngitis;
Asthma;
Dental erosions

117
Q

What other diseases should be considered in a differential of GERD

A

Eosinophilic esophagitis

  • Infectious esophagitis
  • Candida esophagitis
  • HSV esophagitis
  • CMV Esophagitis;

Chemical esophagits

118
Q

How is the diagnosis made for GERD

A

Endoscopy;
Ambulatory pH;
Esophogeal manometry

119
Q

What is the purpose for endoscopy when diagnosing GERD

A

to avoid misdiagnosis of alternate causes of esophageal symptoms

120
Q

What are some warning symptoms of GERD

A 
dysphagia; 
odynophagia; 
early satiety; 
weight loss; 
bleeding
121
Q

What is the treatment for GERD

A

Antacids;
H-2 receptor antagonists;
PPI’s

122
Q

What is the most effective treatment for GERD

123
Q

What are the adverse effects of PPI’s

A

bone demineralization; enteric infections; CAP;

reduced circulating levels of B-12

124
Q

What are some acid suppressive agents

A 
Cimetidine; 
Rantidine; 
Famotidine; 
Nizatidine; 
Omeprazole; 
Esomeprazole; 
Lansoprazole; 
Dexlansoprazole; 
Pantoprazole
125
Q

When is surgery indicated for GERD

A

Fundoplication is indicated for patients who have a continuous increase in medical dosage

126
Q

Are there any lifestyle risk modifications for GERD

A

Yes, but they are unlikely to completely resolve symptoms. Recommendation is for lifestyle modifications in addition to Medical therapy.

127
Q

What are the lifestyle modifications for GERD

A

Elevation of the head in bed;
no food 2-3 hours before sleep;
Avoiding trigger foods;
Smoking cessation

128
Q

What is Peptic Ulcer Disease

A

mucosal breaks in the stomach and duodenum when corrosive effects of acid and pepsin overwhelm mucosal defense mechanisms

129
Q

What is responsible for 50% of PUD

A

H. Pylori, a spiral gram negative urease-producing bacillus

130
Q

Can chronic NSAID and aspirin users develop PUD

A

yes, about 15-25% will develop PUD

131
Q

What are the main causes of PUD

A

H. Pylori;
NSAIDs;
Gastrinoma

132
Q

Does cigarette smoking effect risk of PUD

A

doubles the risk

133
Q

How is PUD diagnosed

A 
Endoscopy (gold standard); 
Barium studies; 
Serum H. pylori antibody testing; 
Stool H. Pylori antigen testing; 
Rapid Urease assay; 
carbon-labeled urea breath test
134
Q

What is the most accurate non invasive test for diagnosis of PUD

A

Carbon labeled breath test

135
Q

What is the medical treatment for PUD

A 
Acid suppression: 
PPI; 
H2 Receptor Antagonist; 
Triple therapy;
Sucralfate; 
Antacids (symptomatic relief)
136
Q

What are adverse effects with Cimetidine therapy for PUD

A

impairs metabolism of many drugs including
warfarin anticoagulants,
theophylline, and
phenytoin

137
Q

What medical treatment protocol is used for treatment of H. Pylori induced PUD

A

TRIPLE THERAPY;
Two antibiotics and a PPI;

Patients previously exposed to a macrolide antibiotic should be treated with a regimen that does not include clarithromycin

138
Q

When is GI bleeding more commonly associated with PUD

A

when the ulcer is are close to the pyloric channel

139
Q

What is Zollinger Ellison syndrome

A

a gastin secreting, non-B islet cell tumor of the pancreas or duodenum. MEN-I associate in 25%

140
Q

When is pancreatitis associated with PUD

A

results when there is penetration in to the pancreas, most commonly seen with ulcers in the posterior wall of the duodenal bulb.

141
Q

How often are duodenal ulcers malignant

A

almost never.

142
Q

What is Rheumatoid Arthritis

A

a systemic disease of unknown etiology that is characterized by symmetric inflammatory polyarthritis, extra-articular manifestations, and serum RF

143
Q

What is the clinical criteria for diagnosis of RA

A 
4 out of 7 of the following (the first 4 present for 6 weeks) 
Morning stiffness >60 minutes; 
Arthritis of three or more joint areas; 
Arthritis of hand joints; 
Symmetric arthritis; 
Rheumatoid nodules; 
Serum RF; 
X-ray changes (erosions or decalcifications)
144
Q

Rheumatoid nodules are most commonly present where

A

on extensor surfaces

145
Q

What is more specific than Rheumatoid Factor for diagnosis of Rheumatoid arthritis

A

Anti-CCP (cyclic citrullinated peptide)

146
Q

What is the treatment for RA

A

DMARD’s (disease modifying anti rheumatic drugs)

147
Q

What is the initial treatment for moderate to severe RA

A

Methotrexate

148
Q

What is the initial treatment for mild RA

A

Hydroxycholorquine or Sulfasalazine

149
Q

What is Methotrexate

A

a purine inhibitor and folic acid antagonist

150
Q

What are the treatment options for RA if the initial treatment fails

A

leflunomide; TNF blocker; Abatacept

151
Q

When is rituximab indicated as a treatment option for RA

A

Approved for patients who have failed TNF therapy

152
Q

What is rituximab

A

a monoclonal antibody directed against the B-cell surgace molecule CD20

153
Q

What is abatacept

A

a fusion protein comprising the CTLA4 molecule and the Fc portion of IgG1. It blocks selective costimulation of T-cells

154
Q

What are the TNF inhibitors used in RA

A

Etanercept;
infliximab;
Adalimumab

155
Q

What is leflunomide

A

A pyrimidine inhibitor that has been approved for the treatment of RA

156
Q

What is the interleukin inhibitor that is available for RA

157
Q

What is the mechanism for Anakinra

A

Recombinant IL-1 receptor antagonist that block the proinflammatory and immunomodulatory actions of IL-1

158
Q

Can NSAIDs be used for treatment in RA

A

yes, but as an adjunct to DMARDs

159
Q

What is the use of steroids for RA

A

provides symptomatic relief in conjunction with DMARDs

160
Q

What are some associated complications of RA

A

Sjogrens disease;
Felty syndrome;
irreversible joint damage with in first 3 years of Dx

161
Q

What is felty syndrome

A

Triad of RA, splenomegaly, granulocytosis

162
Q

Osteoarthritis is also known as …

A

Degenerative joint disease

163
Q

What is osteoarthritis

A

deterioration of articular cartilage with subsequent formation of reactive new bone at the articular surface

164
Q

Who is prone to Osteoarthritis

A

Predominately the elderly but can occur at any age especially with joint trauma or congenital malformation

165
Q

What is initial treatment option for osteoarthritis

A

Acetaminophen because most patients are elderly and often have decreased renal function

166
Q

What is second line for treatment of Osteoarthritis

A

NSAIDs or selective cox2 inhibitor

167
Q

Can steroids be used for the treatment of osteoarthritis

A

Intra-articular glucorrticoid injections are often beneficial but should not used more often than every 3-6 months.;

Systemic steroids should be avoided

168
Q

Can anything be used to help with cartilage regeneration

A

Glucosamine sulfate;

Chondroitin sulfate

169
Q

What is an alternative analgesic agent for osteoarthritis

170
Q

What is the mechanism of tramadol

A

Mu opiod aganist

171
Q

How is synvisc used for the treatment of osteoarthritis

A

Synthetic and naturally occurring hyaluronic acid derivative administered intra-articularly. Reduce pain and improve mobility in select patients

172
Q

What options are available for severe pain and deformity

A

Surgery: Total hip or knee replacement relieves pain and increases function in select patients;
Laminectomy reserved for patients with severe disease with intractable pain or neurologic complications

173
Q

What is SLE

A

Systemic Lupus Erythematosus; a multisystem disease of unknown etiology that primarily affects women of childbearing age.
Women:Men 9:1

174
Q

What is required to diagnose SLE

A 
4 or More of the 11 criteria (DOPAMIN RASH): 
Discoid Rash; 
Oral Ulcers; 
Photosensitivity 
ANA + antibodies (Smith or Double DNA); 
Malar Rash; 
Immunologic Diseases; 
Neurological (seizures and psychosis); 
Renal Dysfunction (proteinuria); 
Arthralgias; 
Serositis; 
Hematologic disorders
175
Q

What comorbidities are associated with SLE

A

accelerated coronary and peripheral vascular disease

176
Q

What are the medical treatments for SLE

A

NSAIDS;
Hydroxychloroquine;
Glucocorticoid therapy;
Immunosuppressive therapy

177
Q

What role does NSAIDs have for SLE

A

controlling arthritis, arthralgias, fever, mild serotosis

178
Q

What caution is with NSAID use and SLE

A

Hepatic and renal toxicities appear to be increased in SLE

179
Q

When is glucocorticoid therapy indicated in SLE

A

Life threatening manifestations of SLE;

Debilitating manifestions of SLE

180
Q

What is the dosage and tapering of glucocorticoid therapy for SLE

A

Prednisone 1-2mg/kg; after disease is controlled, begin to tapered slowly.;
Reduce no more than 10% every 7-10 days.

181
Q

When is immusupressive therapy indicated for SLE

A

Life threatening manifestations of SLE;

inability to reduce corticosteroid therapy or severe corticosteroid side effects

182
Q

What are immunosuppressive treatment options for SLE

A

Cyclophosphamide;
Azathiprine and mycophenolate mofetil are used for steroid sparing agents;
Rituximab

183
Q

How is the outcome of renal transplants of pts with SLE

A

the same as other patients with different chronic renal disease

184
Q

What is drug induced lupus

A 
Sudden onset; 
Male:female is 1:1;
Primarily a MSK manifestation; 
\+ANA and +Anti-Histone antibodies; 
-DS DNA and Anti-SM
185
Q

What is the treatment for drug induced lupus

A

Remove the drug and relief is noticed in a few weeks

186
Q

What drugs are associated with drug induced lupus

A 
Procainamide; 
Hydralazine; 
minocycline; 
diliazem; 
Penicillamine; 
INH; 
quinidine; 
methyldopa; 
ANTI-TNF; 
IFN-a

Med School Rotations (26 decks)

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