Cp Ii Internal Medicine Pre-Midterm

Front 1

How much of the pulmonary vascular bed must be occluded before reistance or pressure increases?

Back 1

~50%

Front 2

What mediators released b/c of platelets adhering results in the systemic phenomenon including bronchconstriction?

Back 2

histamine, serotonin, prostoglandins

Front 3

Common symptoms of pulmonary embolism?

Back 3

SOB, CP, cough, but often ASYMPTOMATIC

Front 4

Common compensatory feature seen in patients suffering from PE?

Back 4

hyperventilating, but overall there is not hallmark symptom

Front 5

What lab value is elevated in the presence of a clot?

Back 5

D-dimer

Front 6

How do you find DVT's?

Back 6

doppler ultrasound

Front 7

What are two findings on CXR that are highly suggestive of PE?

Back 7

Westermark's sign (enlarged left hilum, L lung hyperlucent) & Hampton's hump (infarct is opacified region)

Front 8

Common ABG findings in PE?

Back 8

resp. alkalosis + hypoxemia

Front 9

What imaging test is highly sensitive and specific for PE?

Back 9

Spiral CT

Front 10

What is the first step if you have any suspicion of DVT or PE?

Back 10

start on heparin or LMWH

Front 11

What lab do you use to monitor anticoagulation TX and what range is effective?

Back 11

INR: 2-3 is effective

Front 12

What is the minimum length of coumadin therapy post-PE?

Back 12

3 months

Front 13

When is it good to use to inferior vena cava filter to prevent future VTEs?

Back 13

bled on coumadin, or still clotted despite appropriate treatment

Front 14

Major complication of inferior vena cava filter?

Back 14

leg swelling

Front 15

What in-hospital patients are at highest risk of developing DVT/PE?

Back 15

orthopedic surgery

Front 16

What is the most common origin of DVTs?

Back 16

distal calf veins

Front 17

Virchow's Triad?

Back 17

hypercoagulability, venous stasis, vessel wall damage

Front 18

How many people have latent TB?

Back 18

1/3 of the world

Front 19

Three types of TB infection?

Back 19

primary infection, primary progressive, and reactivation infection

Front 20

Who is likely to get TB?

Back 20

greater innoculum, less defense

Front 21

Common pathological finding of TB?

Back 21

Ghon lesion (focus): organism reaches distal lung parenchyma

Front 22

When does reactivation normally occur in TB patients?

Back 22

months, years, decades later

Front 23

Common pathological finding in healing TB lesions?

Back 23

fibrosis, scarring, and calcium deposition

Front 24

Common clinical featues of active TB infection?

Back 24

weight loss, anorexia, fever, night sweats, cough, sputum, CP, hemoptysis

Front 25

CXR findings in TB primary progressive versus reactivation?

Back 25

primary: lower lobe infiltrate, reactivation: upper lobe infiltrate

Front 26

What TB test is a better diagnostically than mantoux?

Back 26

Quantiferon gold assay

Front 27

What is the regimen for treating LTBI?

Back 27

INH 300 mg daily for 9 mos

Front 28

What is the genetic defect of CF?

Back 28

CFTR mutation in >70% of cases (gene codes for transmembrane conductance regulator)

Front 29

What cells are affected by CF mutations?

Back 29

epithelial cells

Front 30

What organs (systems) are affected in CF?

Back 30

lungs, GI tract (pancrease too), sweat glands, reproductive glands

Front 31

What is the significance of CF PANCREAS

Back 31

clinical presentation: Chronic resp. disease, Failure to thrive, Polyps, Alkalosis (metabolic), Neonatal intestinal obstruction, Clubbing of fingers, Rectal prolapse, Electrolyte inc. in sweat, Aspermia, Sputum (stap and pseudomonas)

Front 32

What is the direct effect of a mutated CF gene?

Back 32

normal CFTR inhibits Na channel; mutated allows inc. Na absorption (and water) leaving airway surface liquid depletion (thick mucous)

Front 33

80% of CF pts. eventually become chronically infected w/ what?

Back 33

Pseudomonas aeruginosa

Front 34

Excluding pseudomonas, what are 3 common pediatric pathogens in CF pts.?

Back 34

S. aureus, H. influenza, and burkholderia cepacia

Front 35

Common neonatal GI problem seen in CF pts.?

Back 35

meconium ileus

Front 36

What is a common childhood clinical presentation of CF?

Back 36

failure to thrive

Front 37

What lab value is highly suggestive of CF?

Back 37

>70 meq/L Cl of sweat

Front 38

in the sweat chloride test, what range is considered positive

Back 38

60-165 meq/L Cl

Front 39

What is the primary cause of death in most CF pts?

Back 39

respiratory failure

Front 40

Hallmark of chronic bronchitis?

Back 40

Cough w/ chronic mucous hypersecretion

Front 41

Hypertrophy of what 2 things in CB?

Back 41

bronchial mucous glands and smooth muscle

Front 42

How do you estimate "pack-years" of smoking history?

Back 42

# packs/day x # years

Front 43

What lab value is increased in CB?

Back 43

hematocrit (polycythemia)

Front 44

What three types of drugs may improve bronchoconstriction associated with CB?

Back 44

beta-agonists, anti-cholinergics, and methylxanthines (theophylline)

Front 45

What are common pathogens seen in acute exacerbations of CB?

Back 45

H. Flu (35-70%), S. pneumo, moraxella catarrhalis, and viral infections (1/3 of pts)

Front 46

What are the 3 cardinal symptoms of acute CB?

Back 46

worsening dyspnea, inc. sputum production, inc. sputum purulence (onset > 2 wks suggests worsening condition)

Front 47

When do you give antibiotics to a CB pt. ?

Back 47

2/3 cardinal symptoms

Front 48

Low risk CB treatment drugs?

Back 48

macrolide, 2nd cephalosporin, doxycycline

Front 49

High risk CB treatment drugs?

Back 49

amox-clavulanate, fluoroquinolones

Front 50

What part of the lungs is effected bronchiectasis and to what extent?

Back 50

bronchi dilation; may involve only one segment of lung or entire lung DEPENDING ON CAUSE

Front 51

What are the 2 prerequisites for developing bronchiectasis?

Back 51

1. infectious insult
2. impariment of drainage, airway obstruction, or defect in host defense

Front 52

What are 4 causes of DIFFUSE bronchiectasis?

Back 52

post-Infectious, Immunodeficiecy, Immune-mediated disease, congenital (Infancy) = 4 I's

Front 53

What is the most common cause of bronchiectasis?

Back 53

CF

Front 54

What are 4 findings on CT indicative of bronchiectasis?

Back 54

peribronchial thickening, dilated bronchioles, tram tracks, ring shadows

Front 55

What can corticosteroids positively affect in pts. w/ bronchiectasis?

Back 55

preserve FEV1 by decreasing inflammation

Front 56

Are mucolytics effective treatment of bronchiectasis?

Back 56

not enough evidence to support

Front 57

What is the most common bleeding disorder?

Back 57

thrombocytopenia

Front 58

What defines thrombocytopenia (lab value)?

Back 58

platelet count <100,000

Front 59

What is the best treatment for drug-induced thrombocytopenic purpura?

Back 59

discontinue and avoid the offending agent.... duh

Front 60

What are 5 commonly implicated drugs of drug-induced thrombocytopenic purpura?

Back 60

heparin, digitalis/digoxin, loop diuretic (furosemide) and H2 blockers

Front 61

What is an associated feature of antiphospholipid syndrome found on MRI?

Back 61

an unidentified bright object (UBO)

Front 62

What are the 2 main components of primary hemostasis?

Back 62

platelets and vascular endothelium

Front 63

What is an important question to ask in regards to clinical assessment of bleeding disorders?

Back 63

Have you had any bleeding problems related to medications before?

Front 64

What is normal PT?

Back 64

10-13 seconds

Front 65

What is the range of normal PTT?

Back 65

25-40 seconds

Front 66

Common findings in the history of pts. w/ idiopathic thrombocytopenic purpura?

Back 66

history of viral URI, IgG antibodies on platelet surface

Front 67

What is the common treatment for seevre ITP?

Back 67

prednisone (1-2 mg/kg/d)

Front 68

What are the 3 components of TTP?

Back 68

microangiopathic hemolytic anemia (MAHA), thrombocytopenia (<50,000), and fever

Front 69

What are the 5 components of hemolytic uremic syndrome (HUS)?

Back 69

TTP + renal failure + hepatic dysfunction

Front 70

What labs can help you distinguish early TTP from DIC?

Back 70

early in TTP, PT and PTT are normal, in DIC they would be abnormal

Front 71

Besides treating the underlying cause, how can one quickly treat TTP?

Back 71

plasmapheresis (100% life-saving)

Front 72

Pt. presents w/ large platelets, bleeding time of 20+ minutes, and mucocutaneous hemorrhaging. Diagnosis?

Back 72

Bernard-Soulier syndrome

Front 73

Inherited factor VIII deficiency. What disease?

Back 73

hemophilia A

Front 74

Inherited factor IX deficiency. What disease?

Back 74

hemophilia B

Front 75

Treatment for pt. w/ deficiency of Vit. K-dependent factors and liver disease?

Back 75

fresh frozen plasma

Front 76

What is the only (inherited) endothelial syndrome associated w/ hemostatic complications?

Back 76

hereditary hemorrhagic telangiectasia

Front 77

What is the pattern of inheritance and defective gene in hereditary hemorrhagic telangiectasia

Back 77

AD inheritance, defect in endoglin

Front 78

Chronic treatment for AT-III deficiency?

Back 78

warfarin for life

Front 79

Action of Protein C?

Back 79

inactivates factors V and VIII (dependent on Vit K)

Front 80

Action of protein S?

Back 80

cofactor for Protein C

Front 81

What is the action of vWF?

Back 81

allows platelets to bind to exposed collagen via glycoprotein receptors

Front 82

What substances are associated with the anticoagulant properties of intact endothelium?

Back 82

ADPase, NO, PGI2, heparan sulfate, tPA, and thrombomodulin

Front 83

What is required to turn a soft clot into a hard clot?

Back 83

calcium, XIIIa, and covalent cross-links between fibrin monomers

Front 84

What is the most common mutation leading to CF?

Back 84

CTT deletion (functionally deletes phenylalanine)
the F508 is where this takes place