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

Internal Medicine Tips Tricks and Techniques Part I Flashcards

1
Q

What is the mechanism of Digoxin

A

Inhibits Sodium potassium ATPase

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2
Q

What are some common anti-arrythmic drugs

A

…

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3
Q

maxalt

A

rizatriptan

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4
Q

What is the treatment of bells palsy

A

steroids for anti-inflammatory.

Studies have not shown a decrease in symptoms when steroids are combined with acyclovir (up to date)

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5
Q

What is the SPIKES protocol

A
  1. SET up the Interview
  2. Assess the patients PERCEPTION
  3. Obtain the patients INVITATION
  4. Giving KNOWLEDGE and information to the patient
  5. Address the patients EMOTIONS
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6
Q

What is the antibiotic treatment for Cat Bites

A
  1. Monotherapy with a beta-lactam/beta-lactamase inhibitor, such as one of the following:
    a) Ampicillin-sulbactam
    b) Piperacillin-tazobactam
    c) Ticarcillin-clavulanate
  2. A third generation cephalosporin
  3. Metronidazole 500 mg IV every eight hours
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7
Q

What is the treatment for increased ammonia levels

A
  1. Lactulose (45-90grams QD) You want to create 2-3 soft stools per day with a pH less than 6. 2. Oral antibiotic such as Neomycin or rifaxmin
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8
Q

What does QHS mean

A

At bed time

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9
Q

What does QAC mean

A

with meals

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10
Q

What does QD

A

daily

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11
Q

What does QOD mean

A

every other day

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12
Q

efudex

A

fluorouracil topical

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13
Q

Lexapro

A

Escitalopram

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14
Q

Victoza

A

Liraglutide

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15
Q

What is liraglutide

A

activates glucagon-like-peptide-1 (GLP-1) receptor, increasing insulin secretion, decreasing glucagon secretion, and delaying gastric emptying (incretin mimetic)
Also helps with weight loss

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16
Q

Glucosamine Sulfate

A

A dietary supplement not a drug. Used to help prevent joint degeneration

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17
Q

Name the rapid acting insulin

A

Lispro,
Aspart,
Glulisine,
Onset in 15 - 30 minutes

Regular (30 minutes - 1 hour)

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18
Q

Name the intermediate acting insulin

A

NPH;

Onset in 1-2 hours

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19
Q

Name the long acting insulin

A

Glargine (onset in 4-6 hours)
Detemir (onset in 3-4 hours)

Used for basal insulin control

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20
Q

When should a sliding scale insulin be used

A

In patients with only intermittent minor BG elevations

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21
Q

How often should insulin be measured in patients taking insulin

A

at least 4 times per day;

Preprandially and at bed time

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22
Q

What is tested for when looking for ketones associated with DKA

A

b-hydroxybutyrate in the serum;

urine ketones are also often present

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23
Q

What are the big 3 that is used in the treatment of DKA

A

Fluids
Insulin
Potassium

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24
Q

If a patient has DKA and is hypotensive, how is their fluid load

A

greater 10% loss of fluids

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25
Q

What are major classes of T2DM

A 
Metformin, 
insulin secretagogues, 
DPP IV Inhibitors, 
GLP mimetics, 
TZD's,

All are effective with in days to weeks except TZD’s which may take weeks to months

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26
Q

First line treatment for T2DM

A

BG 200 combination therapy and possibly insulin

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27
Q

What are the insulin secretagogues

A 
SFU's, 
Non SFU's, 
Biguanides, 
a-glucosidase inhibitors, 
TZD's, 
DPP-4 Inhibitors, 
Bile Acid sequesterants, 
Dopamine receptor agonist, 
GLP agonist
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28
Q

What is the mechanism of SFU’s

A

Increase insulin secretion by binding to specific receptors in B cells. Must be taken 30 - 60 minutes before meals to prevent hypoglycemia

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29
Q

What is contraindication for glyburide

A

Impaired renal function and used with caution in the elderly

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30
Q

Name the non SFU’s

A

Repaglinide,

Nateglinide

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31
Q

Name the biguanides

A

metformin

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32
Q

Name the a-glucosidase inhibitors

A

acarbose

miglitol

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33
Q

Name the thiazolidinediones

A

Rosiglitazone

Pioglitazone

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34
Q

Name the DPP 4 inhibitors

A

Sitagliptin
Saxagliptin
Vildagliptin

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35
Q

Name the bile acid sequestrants used in the treatment of T2DM

A

colesevelam hydrochloride

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36
Q

Name the dopamine agonist used in the treatment of T2DM

A

Bromocryptine Mesylate

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37
Q

Name the GLP Agonist

A

Exenatide

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38
Q

Name the amylin analogues

A

Pramlinitide acetate

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39
Q

What are the common side effects of SFU’s

A

hypoglycemia and weight gain

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40
Q

What are the common side effects of Non SFU’s

A

Hypoglycemia and weight gain

less severe than the SFU’s

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41
Q

What are the main adverse side effects of Biguanides

A

Diarrhea
nausea
abdominal pain or cramping
Lactic acidosis

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42
Q

What are the main adverse side effects of TZD’s

A

Weight gain, edema
CHF
anemia,
increased fractures in women

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43
Q

What are the main adverse side effects of sitagliptin

A

Angioedema,
Steven-Johnson syndrome,
URI

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44
Q

What are the main adverse side effects of saxagliptin

A

urticaria
facial edema
URI

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45
Q

What are the main adverse side effects of bile acid sequestrants

A

constipation

reduced absorption of some medications

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46
Q

What are the main adverse side effects of dopamine agonist

A 
Nausea
asthenia
dizziness
headache
constipation
diarrhea
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47
Q

What are the main adverse side effects of GLP agonist

A

Nausea
vomiting
GI distress
pancreatitis

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48
Q

What are the main adverse side effects of Amylin analogues

A 
Nausea
vomiting
diarrhea
headache
hypoglycemia
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49
Q

What is the mechanism of metformin

A

inhibits hepatic glucose output and stimulates glucose uptake in peripheral tissues

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50
Q

What is the mechanism of a-glucosidase inhibitors

A

Block polysaccharide and disaccharide breakdown and decrease postprandial hyperglycemia when administered with food.

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51
Q

What are the main adverse effects of the a-glucosidase inhibitors

A

gas
bloating
diarrhea
abdominal pain

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52
Q

What is the mechanism of the TZD’s

A

increase insulin sensitivity in muscle, adipose tissue and liver.

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53
Q

When is TZD’s contraindicated

A

compromised cardiac function NYHA Class 3 and 4

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54
Q

What is the mechanism of DPP 4 inhibitors

A

Blocks the enzyme that breaks down endogenous GLP, which is an incretin secreted from the intestinal L cells. Increased levels of GLP reduce BG concentration by inhibiting glucagon secretion from the pancreatic alpha cells and by stimulating insulin secretions

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55
Q

What is the mechanism for GLP agonist

A

peptides are structurally similar to GLP-1 but resist breakdown by DPP enzyme. Have a longer half life than native FLP 1 and reach higher blood and tissue levels

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56
Q

What is the treat of NKHS

A
  1. correct the fluid imbalance
  2. electrolyte replenishment (potassium)
  3. Gradual correction of hyperglycemia with fluid and insulin
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57
Q

What are some complications of NKHS

A

Thromboembolic events
cerebral edema
adult respiratory distress syndrome rhabdomyolysis

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58
Q

What is the problem with correcting hyperglycemic episodes too rapidly

A

osmotic encephalopathy

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59
Q

What is the main purpose of controlling BG in DM

A

prevention of chronic microvascular insufficiency

  1. Diabetic Retinopathy
  2. Diabetic Neuropathy
  3. Diabetic Nephropathy

Prevention of chronic macro vascular insufficiency

  1. CHD
  2. PVD.

Miscellaneous Complications

  1. Erectile Dysfunction
  2. Diabetic Foot Ulcers
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60
Q

What is heart failure

A

A clinical syndrome in which either structural or functional abnormalities in the heart impair its ability to meed the metabolic demands of the body

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61
Q

What are the two classes of heart failure

A

Systolic dysfunction

Diastolic dysfunction

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62
Q

What are the stages of heart failure

A
  1. Asymptomatic
  2. Mild symptoms (mild SOB/Palpitations with physical activity)
  3. Marked limitations in activity (walking 20-100 meters)
  4. Severe limitations (at rest)
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63
Q

What are the classes of heart failure

A

A. No structural disease/ symptoms. Has risk factors
B. Abnormal LV systolic function
C. Structural heart dz and HF symptoms
D. Refractory heart failure symptoms to max medical management

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64
Q

What are the initial labs for suspected HF

A 
CBC
CMP
Fasting lipid profile
Urinalysis
Thyroid function
BNP (>400 to rule in <100 to rule out)
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65
Q

What is a concern when using vasodilators with HF patients

A

patients with a fixed cardiac output (aortic stenosis or HCM or with a predominately diastolic dysfunction)

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66
Q

What is the medical mainstays for HF treatment

A

Beta blockers
Vasodilators
Diuretics (for volume overload)

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67
Q

Why do ARB’s not cause cough and angioedema.

A

ACE’s will increase bradykinin while ARB’s will not.

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68
Q

How are ACE inhibitors excreted

A

through the kidneys… need to titrate the dose for renal insufficiency

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69
Q

How do nitrates reduce cardiac ischemia

A

decreasing ventricular filling pressures and by directly dilating coronary arteries

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70
Q

How does nitroprusside work

A

Primarily an arterial vasodilator with less potent vasodilatory properties

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71
Q

What diuretic is useful for patients with a low GFR

A

Metolazine

Its actions are are at the proximal as well as the distal tubule. It may be used in combination with a loop

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72
Q

What are some common side effects of loops

A 
hyperuricemia
hypocalcemia
ototoxicity
rash
vasculitis
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73
Q

Remeron

A

Mirtazipine

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74
Q

What is primary bilary cirrhosis

A

autoimmune disease of the liver marked by the slow progressive destruction of the small bile ducts (bile canaliculi) within the liver. When these ducts are damaged, bile builds up in the liver (cholestasis) and over time damages the tissue

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75
Q

Keflex

A

Cephalexin (1st generation cephalosporin)

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76
Q

Xenical

A

Orlistat

Inhibits gastric and pancreatic lipases, reducing fat absorption

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77
Q

Actos

A

Pioglitazone

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78
Q

Flexeril

A

Cyclobenzaprine

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79
Q

glucotrol

A

glipizide

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80
Q

Tikosyn

A

Dofetilide (anti arrhythmic: prolongs action potential during phase III)

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81
Q

What is a cox maze procedure

A

is a type of heart surgery for atrial fibrillation. May use a less invasive minimaze procedure too.

82
Q

Livalo

A

Pitavastatin (reduced myalgia than other statins)

83
Q

Tofranil

A

Imipramine (Tricyclic antidepressant)

84
Q

Penlac

A

ciclopirox topical

85
Q

Fioricet

A

butalbital + acetamenaphen + caffeine

86
Q

What are the major classes of valvular heart Disease

A 
Mitral Stenosis (MS) 
Aortic Stenosis (AS) 
Mitral Regurgitation (MR) 
Aortic Regurgitation (AR)
87
Q

What is the predominant cause of MS

88
Q

What is the pathophysiology of MS

A

increase in the transvalvular flow (CO) or decrease in diastolic filling time (tachycardia)

89
Q

What is the clinical presentation of MS

A

physical exam may have an:

  1. opening snap (OS)
  2. Mid diastolic rumble
90
Q

With regards to MS what does the OS-A2 time duration signify

A

the duration is inversely proportional to the severity.

The shorter the duration, the more severe the stenosis

91
Q

With regards to MS what does the duration of the murmur signify

A

The duration of the murmur is directly related to the severity of the stenosis.
The longer the murmur the more severe the stenosis

92
Q

What are some diagnostic testing for MS

A 
EKG
CXR
TTE (candidacy for PMBV)
Exercise testing with echo
TEE
Cath
93
Q

What will an EKG show for MS

A

ECG will have P-wave duration greater than 0.12 secs

94
Q

What are the findings for severe MS

A

Mean gradient > 10 mmHg
PASP > 50 mmHg
Valve area less than 1 square cm

95
Q

What is the treatment for MS

A

Medically - decrease Pulmonary HTN
AFIB - high risk of AFIB (30-40% of patients)
PMBV
Surgery

96
Q

What is the survival with severe pulmonary HTN

A

mean survival is 3 yrs

97
Q

How common is AS

A

2% over age 65

4% over age 85

98
Q

What causes AS

A

Calcific/degenerative disease (most common in US)
Bicuspid
Rheumatic (most common world wide)

99
Q

What is the history in a patient with AS

A

Classic triad of:

  1. Angina
  2. Syncope
  3. HF
100
Q

What are the physical exam findings of AS

A
  1. Harsh crescendo/decrescendo murmur heart best at the apex
  2. Diminished or absent A2
  3. Opening snap suggest Bicuspid valve
  4. S4 reflects poor compliant ventricle
  5. Pulsus parvus et tardus (late peaking and diminished carotid upstroke in Severe AS)
101
Q

What diagnostic testing is used for AS

A
  1. EKG
  2. CXR
  3. TTE
102
Q

What findings signify severe AS

A

peak jet velocity > 4 m/s
Mean gradient > 40 mmHg
Valve area less than 1 square cm

Patients maybe asymptomatic until the valve area is less than 1 cm. Once symptomatic, average survival is 2-3 years with high risk of sudden death

103
Q

What is the treatment for AS

A

Only surgery… no medical treatment

Severe AS is a deadly disease

104
Q

What are the two types of MR

A

Organic - caused primarily by lesions to the valves and or chord tendonae;

Functional - caused primarily by ventricular dysfunction ussually with accompanying annular dilation

105
Q

What causes MR

A

DCM
Degenerative Dz
Ischemic (post infarct)
Rheumatic

106
Q

What is the presentation of a patient with MR

A

SOB
Palpitations
fatigue

107
Q

What are the physical exam findings of a patient with MR

A

Tachycardia
Systolic murmur usually at the apex
S2 maybe widely split due to an early A2

108
Q

What is the treatment for MR

A

Medically:
While awaiting treatment,
aggressive afterload reduction;

Percutaneous;
Surgery (repair is more common than replacement; no surgery for DCM)

109
Q

What are common causes of AR

A

Rheumatic
Calcification
Bicuspid

110
Q

What are the physical exam findings of AR

A

Tachycardia
Wide pulse pressure
Brief diastolic murmur heard best at Erb’s point
Austin Flint murmur (low pitch rumbling presystolic)

111
Q

What is the treatment for AR

A

Medical tx is limited (reducing HTN or antibiotics for infective endocarditis);

Surgery (the aortic root may need to be prepared at the same time as the valve)

112
Q

What are the common prosthetic valves

A

Bileaflet is the most common mechanical.

Anticoagulation is required for a mechanical replacement.

Bioprosthetic (bovine or porcine)

Homograft is rarely used

113
Q

What is CAD

A

Greater 50% luminal stenosis of any epicardial coronary artery

114
Q

What is the leading cause of morbidity and mortality in the western society

115
Q

What causes CAD

A

results from luminal obstruction by atheromatous plaque

116
Q

What percentage of stenosis is generally required to generate Angina

A

Greater 70% stenosis

117
Q

What are some risk factors for CAD

A 
HTN; 
DM (2-4 times greater incidence); 
Obesity; 
Dyslipidemia; 
Family history; 
Smoking
118
Q

When do we begin screening for CAD

A

Begins at age 20 and 5 year intervals (Framingham study)

119
Q

How do we prevent CAD

A

Screening;
High risk CV patients receive aspirin;
Statin for patients with elevated CRP;
Exercise (minimum of 30 minutes 5 days a week);

NOT INDICATED hormone replacement in postmenopausal women

120
Q

What are the two types of Angina

A

Typical and atypical

121
Q

What is typical angina

A

Includes all 3:
Substernal chest discomfort or heaviness;
precipitated by stress;
relieved by nitroglycerin

122
Q

What is atypical angina

A

Includes 2 of the 3.
Substernal chest discomfort or heaviness; precipitated by stress;
relieved by nitroglycerin;

Non cardiac chest pain will only have 1 of the 3

123
Q

How do we quantify angina chest pain

A

Canadian cardiovascular Society classification system;
CCS 1 - angina with strenuous activity;
CCS 2 - Angina with moderate activity (>2 blocks);
CCS 3 - Angina with mild activity (<2 blocks);
CCS 4 - Angina with any activity or at rest

124
Q

What symptoms will be presented with CAD

A 
Angina; 
dyspnea; 
Diaphoresis; 
nausea; 
vomiting; 
dizziness
125
Q

Female patients or CKD or DM will present with what symptoms of CAD

A

Minimal or atypical symptoms;
dyspnea;
epigastric pain;
nausea

126
Q

What is the diagnostic testing used for CAD

A 
Stress testing; 
Excercise stress testing; 
Myocardial perfusion imaging 
Echocardiography imaging with stress; 
MRI
127
Q

What is the bruce protocol

A

3 minute stages of increasing treadmill speed and incline.

BP, HR and ECG are monitored through the study and recovery period

128
Q

What is the duke treadmill score

A

Exercise stress test:
Minutes exercised - (5 X maximum ST segment deviation) - (4 X angina Score);

0= no angina; 
1 = angina that is not stress limiting; 
2 = test limiting angina;

total score >5 use medical therapy;
total score -10 to 4 further testing; total score <-10 coronary angiography

129
Q

What is the gold standard for CAD diagnosis

A

Coronary angiography

130
Q

What is the major goal for treatment of patients with stable angina

A

prevent MI, cardiac death and to reduce symptoms

131
Q

What are the medical treatment goals for CAD

A

improve myocardial oxygen supply, reducing myocardial oxygen demand, controlling exacerbating factors, and limiting the development of further atherosclerotic disease

132
Q

What are the medical treatment options for CAD

A 
Aspirin; 
B blockers; 
Calcium channel blockers (avoid short acting DHP's); 
Nitrates; 
Ace Inhibitors; 
Ranolazine; 
Cholesterol lowering agents (Statins)
133
Q

What is ranolazine

A

a novel antianginal agent that does not depend upon reductions in HR or BP. Its exact mechanism of action is unknown:
however, it appears to have effect on cardiomyocyte metabolism and sodium ion channel function.

134
Q

When should coronary revascularization be attempted

A

after 2 and preferably 3 antianginal agents have failed

135
Q

When is PCI or CABG indicated

A

Angina refractory to medical therapy; Angina and reduced LV function; Severe activity limiting angina (CCS 3 and CCS 4);
Angina in the presence of left main or severe three vessel CAD

136
Q

What type of revascularization is preferred in diabetic patients

137
Q

What are the alternative procedures for CAD for patients that are unable to have PCI or CABG surgery

A

Transmyocardial laser revascularization;

Therapeutic angiogenesis

138
Q

What is COPD

A

expiratory airflow limitation that is not fully reversible

139
Q

What are two conditions largely associated with COPD

A

Emphysema;

Chronic Bronchitis

140
Q

What is the pathology of emphysema

A

enlargement of the distal airways, destruction of the acinus and absence of associated fibrosis

141
Q

What is the pathology of chronic bronchitis

A

productive cough on most days for at least 3 consecutive months per year for at least 2 consecutive years in the absence of other lung disease that could account for the symptoms.

142
Q

When should you suspect an a-1-antitrypsin deficiency

A

minimal smoking;
early onset COPD;
family history of lung disease;
lower lobe predominant emphysema

143
Q

What are the main pathophysiologic processes associated with COPD

A
  1. Inflammation;
  2. Imbalances of proteinases;
  3. oxidative stress;
  4. apoptosis
144
Q

Where are the pathophysiologic changes found in COPD

A

central airways;
peripheral airways;
lung parenchyma;
pulmonary vasculature

145
Q

What are the common symptoms of a patient with COPD

A 
dyspnea; 
cough; 
sputum production; 
wheezing; 
Weight loss often occurs in end stage COPD
146
Q

What are the physical exam findings of a patient with COPD

A 
prolonged breath sounds (>6 secs on a maximalforced expiration); 
Decreased breath sounds; 
use of accessory muscles; 
Chest hyperresonance to percussion; 
Expiratory Wheezing
147
Q

Is clubbing a feature of COPD

A

NO;

presence should prompt an evaluation for other conditions, especially lung cancer

148
Q

What are treatment options for smoking cessation

A
  1. Nicotine replacement;

2. Nonnicotine pharmacotherapy

149
Q

What are the nicotine replacement options

A
  1. transdermal patch
  2. Oral (chewing gum, lozenges, inhaler)
  3. Nasal Spray
150
Q

What are the non-nicotine pharmacotherapy options

A
  1. Bupropion ER (Zyban)

2. Varenicline (Chantix)

151
Q

What diagnostic testing is used in the diagnosis of COPD

A

Pulmonary function testing

152
Q

How is the severity of COPD scaled

A

GOLD classification (Global strategy for diagnosis, management and prevention of COPD)

153
Q

What is required for the diagnosis of COPD

A

expiratory airflow limitation on spirometry, defined as a forced expiratory volume in the first second/forced vital capacity (FEV1/FVC) to be less than 0.70

154
Q

What are the stages in the GOLD classifications

A 
All stages have FEV1/FVC ratio less than 0.70;
Stage I - Mild: FEV1 > 80% predicted; 
Stage 2 - Moderate: 50 - 79% predicted;
Stage 3 - Severe: 30-49% predicted; 
Stage 4 - Very Severe: <30% predicted
155
Q

What labs should be ordered to monitor COPD

A

ABG;
bicarbonate;
CBC

156
Q

What is significant with a CBC for COPD

A

polycythemia may reflect a physiologic response to chromic hypoxemia and inadequate supplemental oxygen use.

157
Q

What is the only proven chronic medical therapies proven to increase survival in COPD

A

smoking cessation and the correction of hypoxemia with supplemental oxygen

158
Q

What is the stepwise approach to COPD therapy

A

Mild:
smoking cessation,
vaccination, and
short acting B agonist prn;

moderate:
all mild + long acting bronchodilators and
pulmonary rehabilitation;

severe:
all moderate + inhaled corticosteroids if repeated exacerbations.
Oxygen if needed;

Very severe:
all severe + considerations for surgical treatment

159
Q

Name the short acting beta agonist used for COPD

A

Albuterol;
Levalbuterol (Xopenex);
Pirbuterol (Maxair)

160
Q

Name the long acting beta agonist used for COPD

A

Salmeterol (Serevent);
Formoterol (Foradil);
Arformoterol (Brovana)

161
Q

Name the anticholinergics used for COPD

A

Ipratropium (Atrovent);

Tiotropium (Spiriva)

162
Q

What should be accompanied with an inhaled bronchodilator

A

proper use of an MDI (metered dose inhaler)

163
Q

Are steroids indicated for COPD

A

Yes.;
Inhaled corticosteroids;
Systemic corticosteroids are used in patients with severe disease that are not responding to other therapies

164
Q

How is the use of supplemental oxygen determined

A

A room air resting ABG is the gold standard for determining supplemental O2;

PaO2 < 55 mmHg; SaO2 < 80%; SaO2 < 92% and (pulmonary HTN, Polycythemia, or HF)

165
Q

How will the CBC indicate polycythemia

A

hematocrit > 55%

166
Q

How is a lung transplant indicated in COPD

A

BODE score

167
Q

What is an acute exacerbation of COPD

A

increased dyspnea, often accompanied by increase cough, sputum production, sputum purulence, wheezing, chest tightness or other symptoms and signs in the absence of other pathology

168
Q

When is hospitalization indicated for COPD

A

significant increase in symptom severity;
significant comorbidities;
failure to respond to initial medical management;
insufficient home support

169
Q

When is the ICU indicated for COPD

A 
invasive mechanical ventilation; 
hemodynamic instability; 
severe dyspnea; 
mental status changes; 
persistent worsening hypoxemia, hypercapnia or respiratory acidosis
170
Q

What symptoms will Asthma patients have

A

paroxysms of cough;
dyspnea;
chest tightness;
wheezing

171
Q

What are the mechanisms that asthma classified

A

based on the level of impairment;
Risk;
responsiveness to treatment

172
Q

How is asthma classified on initial assesment

A 
Intermittent (Day 2 week, night 3-4 month);
Moderate Persistant (daily, >1 week); 
Severe persistent (continous during day, and night)
173
Q

how is asthma control staged

A

Well controlled (similar to intermittent);
not well controlled (similar to mild persistent);
very poorly controlled (similar to severe persistent)

174
Q

What is the leading chronic illness among children

A

Asthma (20-30%)

175
Q

What are some factors that contribute to the development and persistence of asthma

A

Severe viral infection early in life, particularly RSV and rhyinovirus

176
Q

What is the pathophysiology of asthma

A

Characterized by airway obstruction, hyperinflation, and airflow limitations resulting from:
chronic airway inflamation by activated eosinophils;
Bronchial smooth muscle contraction;
epithelial damage;
airway remodeling

177
Q

What are the physical findings of asthma

A

wheezing;
prolonged expiratory phase;
During respiratory distress peak airflow <25%

178
Q

How is asthma diagnosed

A

Severe distress or FEV1 < 40% predicted;
PaO2 < 60 mmHg;
PFT with improvement of >12% after bronchodilator;
heightened airway responsiveness to a methacholine;
challenge (drop in FEV1 of 20%)

179
Q

How is the severity of asthma exacerbation classified

A

Mild: PEF or FEV1>70%;
moderate: PEF or FEV1 40-69;
Severe: PEF or FEV1 <25%

180
Q

How do treat asthma

A

Initiate treatment at the highest level that occurred over the last 2-4 weeks.
Recheck every 3 months to step down treatment as necessary

181
Q

What are the primary step wise treatment options for asthma control

A 
PRN: Short acting bronchodilators; 
Step 1: None; 
Step 2: Low dose ICS; 
Step 3: Low dose ICS +LABA; 
Step 4: Medium dose ICS + LABA; 
Step 5: High dose ICS + LABA; 
Step 6: Add OCS to step 5
182
Q

What are some alternative treatment options for asthma control

A 
Leukotriene modifiers; 
Cromolyn sodium; 
Anti IgE therapy (omalizumab); 
Methylxanthines;
IV Mag sulfate; 
Inhaled heliox
183
Q

What are the leukotriene modifiers

A 
Leukotriene receptor antagonist (LTRA's):
Montelukast; 
zafirlukast; 
5-lipoxygenase inhibitor; 
zileuton
184
Q

When should a LTM be considered for initial therapy

A

patients with aspirin sensitive asthma or for individuals who cannot master the use of an inhaler

185
Q

What are side effects of SABA

A

tremor; anxiety; tachycardia; decrease in serum potassium and magnessium;
mild lactic acidosis;
prolonged QT

186
Q

What are side effects of ICS

A

oral thrush and systemic effects;

patients should be instructed to rinse their mouth after use.

187
Q

What are the side effects of LTM

A

churg-straus vasculitis;

Ziuleten can cause a reversible hepatitis

188
Q

How do patients monitor their asthma at home

A

max PEF;
Green is 80-100;
Yellow is 50-79;
Red is <50

189
Q

What is the sign called of a clinched fist over the heart

A

Levines sign. A symbol of ischemic chest pain

190
Q

What is tissue connecting the septum to the wall of the right ventricle

191
Q

What are the two major classes of IBD

A

Ulcerative colitis;

Crohns disease

192
Q

Where is the inflammation in ulcerative colitis

A

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

193
Q

Where is the inflammation in crohns disease

A

transmural inflammation in any part of the entire GI tract

194
Q

What is the presentation of IBD

A

diarrhea;
weight loss;
abdominal pain

195
Q

Crohns disease can also present with

A

fistula formation; strictures; abscesses; bowel obstruction

196
Q

How is IBD diagnosed

A

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

197
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

198
Q

What are the serologic markers used to distinguish UC from Crohns

A

CD: Anti-Saccharomyces cerevisiae antibodies;
UC: pANCA (perinuclear antineutrophil cytoplasmic antibodies)

199
Q

How is treatment determined for IBD

A

Based on the severity of the symptoms

200
Q

How is the severity of disease classified for IBD

A

Mild;
Moderate;
Severe

Med School Rotations (26 decks)

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