Internal Medicine Tips Tricks and Techniques Part II Flashcards
1
Q
What are the two major classes of IBD
A
Ulcerative colitis;
Crohns disease
2
Q
Where is the inflammation in ulcerative colitis
A
Limited to the colon and the rectum. Inflammation is limited to the mucosal lining.
3
Q
Where is the inflammation in crohns disease
A
transmural inflammation in any part of the entire GI tract
4
Q
What is the presentation of IBD
A
diarrhea;
weight loss;
abdominal pain
5
Q
Crohns disease can also present with
A
fistula formation;
strictures;
abscesses;
bowel obstruction
6
Q
How is IBD diagnosed
A
Endoscopy is the preferred method.
CT and MRI scans;
Serologic markers
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
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)
9
Q
How is treatment determined for IBD
A
Based on the severity of the symptoms
10
Q
How is the severity of disease classified for IBD
A
Mild;
Moderate;
Severe
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
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)
13
Q
What are the 5-ASA used
A
Sulfasalazine; Mesalamine; Olsalazine
14
Q
Name Mesalamine preparations used for IBD
A
Asacol Pentasa; Apriso; Balsalazide; Multimatrix delivery system mesalamine
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
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
17
Q
What are the medical treatments used for moderate to severe IBD
A
Glucocorticoids;
Immunosuppressive agents;
Anti-tumor necrosis factor alpha;
Natalizumab
18
Q
What immunosuppressive agents are used in the treatment of IBD
A
6-Mercaptopurine;
azathioprine (6-M’s S-imidazole precursor);
Methotrexate
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
20
Q
What will help prevent toxicity caused by 6-mercaptopurine
A
Determination of thiopurine methyltransferase (TPMT) enzyme activity prior to initiation of therapy
21
Q
How does methotrexate work for IBD
A
effective as a steroid sparing agent in CD but not UC.
22
Q
What are the anti-tumor necrosis factor monoclonal antibodies for IBD
A
Infliximab;
Adalimumab;
certolizumab pegol
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
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
25
What are the adverse effects of natalizumab
induce reactivation of JC polyoma virus causing progressive multifocal leukoencephalopathy.
26
When is surgery an option for patients with IBD
```
patients with fistulas;
obstruction;
perforations;
abscesses;
bleeding
```
27
What are adverse outcomes of surgery for IBD
Short bowel syndrome;
| recurrence close to the resected margins is common with CD
28
Surgery for UC
a total colectomy may be curative
29
What defines nephrotic syndrome
Proteinuria >3.5 grams/d;
hypoalbuminemia;
hyperlipidemia
edema
30
What will biopsy show for nephrotic syndrome
will show injury along the filtration barrier;
thickening of the glomerular basement membrane
fusion of the podocyte foot processes
31
What is the general medical treatment for nephrotic syndrome
ACE inhibitors and ARBs to reduce intraglomerular pressure;
| Aggressive treatment of hypertension can also slow progression of renal disease
32
What bleeding disorders are often accompanied by nephrotic syndrome
hypercoaguable state and can predispose pt to thromboembolic events
33
Name the primary glomerular nephropathies
Minimal Change Disease;
Focal Segmental Glomerularsclerosis;
Membranous Nephropathy;
Membranoproliferative
34
What age groups are most commonly affect by MCD
children;
| second peak seen 50-60
35
How will MCD present
sudden onset proteinuria with hypertension and edema;
| Renal insufficiency is unusual
36
What are associated conditions of MCD
Hodgkins and solid tumors
37
How is MCD diagnosed
LM: Normal glomeruli;
Electron: shows effacement of the foot processes as the only abnormality
38
What is the treatment for MCD
oral prednisone for 1mg/kg/d for 8-16 weeks until remission.
Then tapered over the next 3 months
39
How will Focal Segmental Glomerulosclerosis present
nephrotic syndrome;
HTN;
Renal insufficiency
40
What are the associated conditions of Focal Segmental Glomerulosclerosis
Obesity;
HIV;
IV Drug use
41
How is FSGS diagnosed
Immunofluorescense shows staining for C3 and IgM in areas of sclerosis representing areas of trapped immune deposits
42
How is the prognosis for FSGS determined
the degree of interstitial fibrosis and tubular atrophy
43
What can be used to treat nephrotic syndromes if they are refractory to oral prednisone
cyclosporine;
| cyclophosphamide
44
How will membranous Nephropathy present
nephrotic syndrome or heavy proteinuria while renal function is often normal
45
How is disease progression for Nephropathy
1/3 remit spontaneous;
1/3 ESRD;
1/3 intermediate course
46
What are the associated conditions with membranous nephropathy
SLE;
Viral hepatitis;
syphilis;
solid organ malignancy
47
How is membranous nephropathy diagnosed
kidney biopsy shows;
LM: thickening of the basement membrane;
Silver stain: "spikes"
48
Who receives treatment for membranous nephropathy
patients at higher risk for progression (reduced GFR, age >50, and HTN, and males);
Severe nephrotic syndrome (proteinuria >10g/d)
49
What is the primary cause of Membranoproliferative Glomerularnephropathy
Hepatitis C and frequently in association with cryoglobinemia
50
How is Membranoproliferative GN diagnosed
LM: mesangial proliferation and hypercellularity with lobularization of the glomerular tuft;
Silver stain: mesangial interpositioning appearance gives a double contour or "tram tracking appearance"
51
What are the compliment levels for Membranoproliferative GN
usually low
52
What is the treatment for membranoproliferative GN
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.
53
Name the hepatotropic viruses
```
HAV;
HBV;
HCV;
HDV;
HEV
```
54
What is the classification of HAV
RNA virus that belongs to the Picornavirus family
55
What is the most common cause of viral hepatitis world wide
HAV
56
How is HAV spread
fecal-oral route
57
What is the period of infectivity for HAV
2 weeks before symptoms through 2-3 weeks after symptoms
58
What are high risk conditions for HAV
anything to do with developing countries
59
How is the diagnosis made for HAV
detection of IgM anti-HAV antibodies
60
How is the recovery and immunity phase determined for HAV
detection of IgG anti-HAV antibody
61
What is the clinical presentation for HAV
```
All are common but non specific:
Malaise;
fatigue;
pruritus;
headache;
abdominal pain;
myalgias;
arthralgias;
nausea;
vomiting;
anorexia;
fever
```
62
What is the treatment for HAV
no specific treatment, only supportive therapy
63
What can be used for preexposure prophylaxis
the HAV vaccine containing the single HAV antigen
64
What can be used for post exposure prophylaxis
Ig
65
What is the prognosis of HAV
almost all will resolve in 4-8 weeks
66
What is the classification of HBV
DNA virus that belongs to the hepadnavirus family
67
What phenotypes of HBV have been found in the US
All phenotypes; The most prevalent being A, B and C
68
What is the leading cause of HCC world wide
HBV attributes 60-80% of all cases
69
What percentage of liver transplants is due to HBV
5-10%
70
What causes liver damage following HBV
immune mediated
71
What are the modes of transportation for HBV
Parenteral or percutaneous routes; Sexual contact; Vertical transmission (mother to infant)
72
What is the incubation period after an HBV infection
30-160 days
73
What are the clinical phases of HBV
Acute hepatitis B;
Chronic Hepatitis B
- Immune tolerant
- Immune Active
- Carrier state with low replication
- Chronic HBeAg negative;
Resolution
74
What defines immune tolerant phase of HBV
high rates of viral replication, yet normal liver enzymes and low levels of inflammation and fibrosis
75
What define immune active phase of HBV
Characterized by elevated liver enzymes as a consequence of a vigorous immune response
76
What defines Carrier state with low replication phase of HBV
low or undetectable levels of HBV DNA levels
77
what defines the chronic HBeAg negative phase of HBV
patients harbor HBV variants with mutations that prevent the production of or have low expression of HBeAg
78
What labs will indicate acute hepatitis
```
abnormal:
AST;
ALT;
ALP;
total bilirubin
```
79
What are the HBV antigens detected in the serum
HBsAg;
| HBeAg
80
What is the most accurate viral marker for HBV replication
HBV DNA
81
What genotypes of HBV have the highest response to IFN therapy
genotypes A and B
82
Is liver biopsy beneficial for HBV
yes.
| It can determine the grade (degree of inflammation) and stage (fibrosis)
83
What are the medications used for HBV
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
What are the first line treatment options for HBV
IFN-a;
pIFN;
Entecavir;
Tenofovir
85
What drug groups are anti-viral resistance associated with for HBV
nucleoside and nucleotide analogs
86
What is the classification of HCV
RNA virus that belongs to the flavivirus family
87
What is the prevalence of HCV in the US
1.8%;
Genotype 1 makes up 70%;
Genotype 2 and 3 make up 20%
88
What is the prophylactic treatment for HCV
does not exist
89
What is the incubation period for HCV
15-150 days
90
What are the symptoms of HCV
```
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
How long may it take before labs will show anti-HCV
up to 8 weeks post infection
92
Does the anti-HCV antibody imply immunity
NOPE
93
What are the medications for HCV
IFN;
| Ribavarin
94
With regards to HCV, what is RVR
rapid viral response;
| HCV RNA negative at 4 weeks of treatment
95
With regards to HCV, what is EVR
Early viral response;
| HCV RNA negative at 12 weeks of treatment
96
With regards to HCV, what is cEVR
no RVR, but HCV RNA negative at 12 weeks of treatment
97
With regards to HCV, what is pEVR
no RVR,
| detectable HCV RNA but >2log10 drop at 12 weeks of treatment
98
With regards to HCV, what is Slow responder
>2log10 drop at 12 weeks of treatment and HCV RNA negative at 24 weeks
99
With regards to HCV, what is partial responder
>2log10 drop at 12 weeks of treatment and HCV RNA positive at 24 weeks
100
With regards to HCV, what is relapse
HCV RnA negative at end of treatment but HCV RNA positive after treatment cessation
101
With regards to HCV, what is SVR
Sustained viral response; absence of HCV RNA 6 months post viral treatment
102
What is the prognosis of HCV
40% will have spontaneous remission while 60% will have chronic infection
103
What percentage of HCV pt's develop HCC
1-2%
104
What is HDV classification
considered a subviral particle resembling plant pathogens;
| Circular RNA genome
105
What is required for HDV infection and replication
HBV
106
What is the transmission of HDV
similar to HBV
107
What is a coninfection of HDV
simultaneous infection of HBV and HDV
108
What is a superinfection of HDV
HDV infection of a patient already infected with HBV
109
What is the treatment of choice for HDV
IFN-a
110
What is the classification for HEV
RNA virus that belongs to the hepeviridae family
111
What is the transmission of HEV
Fecal oral route
112
What is the fatality of HEV
high fatality rate in pregnant women in the second and third trimester
113
What is the treatment of HEV
supportive
114
What are the typical presentation of GERD
Esophageal symptoms;
Chest pain;
Extraesaphogeal symptoms
115
What are the esophageal symptoms associated with GERD
Heartburn and regurgitation
116
What are the extraesophageal symptoms of GERD
Cough;
Laryngitis;
Asthma;
Dental erosions
117
What other diseases should be considered in a differential of GERD
Eosinophilic esophagitis
- Infectious esophagitis
- Candida esophagitis
- HSV esophagitis
- CMV Esophagitis;
Chemical esophagits
118
How is the diagnosis made for GERD
Endoscopy;
Ambulatory pH;
Esophogeal manometry
119
What is the purpose for endoscopy when diagnosing GERD
to avoid misdiagnosis of alternate causes of esophageal symptoms
120
What are some warning symptoms of GERD
```
dysphagia;
odynophagia;
early satiety;
weight loss;
bleeding
```
121
What is the treatment for GERD
Antacids;
H-2 receptor antagonists;
PPI's
122
What is the most effective treatment for GERD
PPI's
123
What are the adverse effects of PPI's
bone demineralization; enteric infections; CAP;
| reduced circulating levels of B-12
124
What are some acid suppressive agents
```
Cimetidine;
Rantidine;
Famotidine;
Nizatidine;
Omeprazole;
Esomeprazole;
Lansoprazole;
Dexlansoprazole;
Pantoprazole
```
125
When is surgery indicated for GERD
Fundoplication is indicated for patients who have a continuous increase in medical dosage
126
Are there any lifestyle risk modifications for GERD
Yes, but they are unlikely to completely resolve symptoms. Recommendation is for lifestyle modifications in addition to Medical therapy.
127
What are the lifestyle modifications for GERD
Elevation of the head in bed;
no food 2-3 hours before sleep;
Avoiding trigger foods;
Smoking cessation
128
What is Peptic Ulcer Disease
mucosal breaks in the stomach and duodenum when corrosive effects of acid and pepsin overwhelm mucosal defense mechanisms
129
What is responsible for 50% of PUD
H. Pylori, a spiral gram negative urease-producing bacillus
130
Can chronic NSAID and aspirin users develop PUD
yes, about 15-25% will develop PUD
131
What are the main causes of PUD
H. Pylori;
NSAIDs;
Gastrinoma
132
Does cigarette smoking effect risk of PUD
doubles the risk
133
How is PUD diagnosed
```
Endoscopy (gold standard);
Barium studies;
Serum H. pylori antibody testing;
Stool H. Pylori antigen testing;
Rapid Urease assay;
carbon-labeled urea breath test
```
134
What is the most accurate non invasive test for diagnosis of PUD
Carbon labeled breath test
135
What is the medical treatment for PUD
```
Acid suppression:
PPI;
H2 Receptor Antagonist;
Triple therapy;
Sucralfate;
Antacids (symptomatic relief)
```
136
What are adverse effects with Cimetidine therapy for PUD
impairs metabolism of many drugs including
warfarin anticoagulants,
theophylline, and
phenytoin
137
What medical treatment protocol is used for treatment of H. Pylori induced PUD
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
When is GI bleeding more commonly associated with PUD
when the ulcer is are close to the pyloric channel
139
What is Zollinger Ellison syndrome
a gastin secreting, non-B islet cell tumor of the pancreas or duodenum. MEN-I associate in 25%
140
When is pancreatitis associated with PUD
results when there is penetration in to the pancreas, most commonly seen with ulcers in the posterior wall of the duodenal bulb.
141
How often are duodenal ulcers malignant
almost never.
142
What is Rheumatoid Arthritis
a systemic disease of unknown etiology that is characterized by symmetric inflammatory polyarthritis, extra-articular manifestations, and serum RF
143
What is the clinical criteria for diagnosis of RA
```
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
Rheumatoid nodules are most commonly present where
on extensor surfaces
145
What is more specific than Rheumatoid Factor for diagnosis of Rheumatoid arthritis
Anti-CCP (cyclic citrullinated peptide)
146
What is the treatment for RA
DMARD's (disease modifying anti rheumatic drugs)
147
What is the initial treatment for moderate to severe RA
Methotrexate
148
What is the initial treatment for mild RA
Hydroxycholorquine or Sulfasalazine
149
What is Methotrexate
a purine inhibitor and folic acid antagonist
150
What are the treatment options for RA if the initial treatment fails
leflunomide; TNF blocker; Abatacept
151
When is rituximab indicated as a treatment option for RA
Approved for patients who have failed TNF therapy
152
What is rituximab
a monoclonal antibody directed against the B-cell surgace molecule CD20
153
What is abatacept
a fusion protein comprising the CTLA4 molecule and the Fc portion of IgG1. It blocks selective costimulation of T-cells
154
What are the TNF inhibitors used in RA
Etanercept;
infliximab;
Adalimumab
155
What is leflunomide
A pyrimidine inhibitor that has been approved for the treatment of RA
156
What is the interleukin inhibitor that is available for RA
Anakinra
157
What is the mechanism for Anakinra
Recombinant IL-1 receptor antagonist that block the proinflammatory and immunomodulatory actions of IL-1
158
Can NSAIDs be used for treatment in RA
yes, but as an adjunct to DMARDs
159
What is the use of steroids for RA
provides symptomatic relief in conjunction with DMARDs
160
What are some associated complications of RA
Sjogrens disease;
Felty syndrome;
irreversible joint damage with in first 3 years of Dx
161
What is felty syndrome
Triad of RA, splenomegaly, granulocytosis
162
Osteoarthritis is also known as ...
Degenerative joint disease
163
What is osteoarthritis
deterioration of articular cartilage with subsequent formation of reactive new bone at the articular surface
164
Who is prone to Osteoarthritis
Predominately the elderly but can occur at any age especially with joint trauma or congenital malformation
165
What is initial treatment option for osteoarthritis
Acetaminophen because most patients are elderly and often have decreased renal function
166
What is second line for treatment of Osteoarthritis
NSAIDs or selective cox2 inhibitor
167
Can steroids be used for the treatment of osteoarthritis
Intra-articular glucorrticoid injections are often beneficial but should not used more often than every 3-6 months.;
Systemic steroids should be avoided
168
Can anything be used to help with cartilage regeneration
Glucosamine sulfate;
| Chondroitin sulfate
169
What is an alternative analgesic agent for osteoarthritis
Tramadol
170
What is the mechanism of tramadol
Mu opiod aganist
171
How is synvisc used for the treatment of osteoarthritis
Synthetic and naturally occurring hyaluronic acid derivative administered intra-articularly. Reduce pain and improve mobility in select patients
172
What options are available for severe pain and deformity
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
What is SLE
Systemic Lupus Erythematosus; a multisystem disease of unknown etiology that primarily affects women of childbearing age.
Women:Men 9:1
174
What is required to diagnose SLE
```
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
What comorbidities are associated with SLE
accelerated coronary and peripheral vascular disease
176
What are the medical treatments for SLE
NSAIDS;
Hydroxychloroquine;
Glucocorticoid therapy;
Immunosuppressive therapy
177
What role does NSAIDs have for SLE
controlling arthritis, arthralgias, fever, mild serotosis
178
What caution is with NSAID use and SLE
Hepatic and renal toxicities appear to be increased in SLE
179
When is glucocorticoid therapy indicated in SLE
Life threatening manifestations of SLE;
| Debilitating manifestions of SLE
180
What is the dosage and tapering of glucocorticoid therapy for SLE
Prednisone 1-2mg/kg; after disease is controlled, begin to tapered slowly.;
Reduce no more than 10% every 7-10 days.
181
When is immusupressive therapy indicated for SLE
Life threatening manifestations of SLE;
| inability to reduce corticosteroid therapy or severe corticosteroid side effects
182
What are immunosuppressive treatment options for SLE
Cyclophosphamide;
Azathiprine and mycophenolate mofetil are used for steroid sparing agents;
Rituximab
183
How is the outcome of renal transplants of pts with SLE
the same as other patients with different chronic renal disease
184
What is drug induced lupus
```
Sudden onset;
Male:female is 1:1;
Primarily a MSK manifestation;
+ANA and +Anti-Histone antibodies;
-DS DNA and Anti-SM
```
185
What is the treatment for drug induced lupus
Remove the drug and relief is noticed in a few weeks
186
What drugs are associated with drug induced lupus
```
Procainamide;
Hydralazine;
minocycline;
diliazem;
Penicillamine;
INH;
quinidine;
methyldopa;
ANTI-TNF;
IFN-a
```
