Medicine Final

Front 1

Diabetes
Diagnostic Criteria (American Diabetes Association)

Back 1

1. Symptoms of DM & casual (PG=plasma glucose) PG ³200 mg/dl OR

2. Fasting PG ³126 mg/dl with or without symptoms OR

3. 2 hour PG >200 mg/dl after 75g oral glucose during OGTT

Front 2

Diagnostic Criteria for Impaired fasting glucose (IFG)

Back 2

IFG= fasting PG= 100-125 mg/dl.

Front 3

impaired glucose tolerance (IGT)
Diagnostic Criteria

Back 3

IGT= PG 140-199 mg/dl 2 hours after 75 gram oral glucose

Front 4

metabolic syndrome = when 3 or more of following are present:

Back 4

Abdominal Obesity
-Waist Circumference

--Men ≥102 cm (40 in)

--Women ≥88 cm (35 in)

Triglycerides


≥150 mg/dl

HDL Cholesterol


-Men ≤40 mg/dl

-Women ≤50 mg/dl

Blood pressure


≥130/ ≥ 85 mmHg

Fasting Glucose


≥110 mg/dl

Front 5

ADA Therapeutic Goals (2006) for diabetes
1 Avg fasting gluc
Avg peak postprandiol gluc
2 Avg bedtime gluc
3 HbA15
4 BP
5 Chol
6 LDL
7 HDL
8 Trig

Back 5

A. Avg. fasting glucose 90-130 mg/dl

Avg. peak postprandial glucose <180 mg/dl

B. Avg. bedtime glucose 100-140

C. HbA1c <7%, or as close to 6% (normal) as possible without hypoglycemia (ADA 2006 Guidelines)



HbA1C (%)


Avg. Glucose (mg/dl)

6.0


120

7.0


150

8.0


180

9.0


210

10.0


240



D. BP <130/80 (JNC VII)

E. Cholesterol <200 mg/dl

F. LDL <100 mg/dl

G. HDL >35 mg/dl

H. Triglycerides <200 mg/dl

Front 6

Initial Evaluation of a Patient with Diabetes (8)

Back 6

A. Serum creatinine and potassium

B. UA and urine microalbumin

C. EKG

D. Fasting lipid profile

E. HbA1c and fasting glucose

F. Dilated eye exam

G. Dietician consultation and diabetes education important- goal of reduced fat intake, reduced calorie intake to promote gradual sustained weight loss if obese

H. Exercise program to improve diabetes

Front 7

Sulfonylureas

A. Mechanism of action-
B. All are metabolized in the X and excreted Y

C. X range in potency and duration of action

D. Main side effect is X

E, Cheap, effective as monotherapy or in combination

Back 7

Sulfonylureas

A. Mechanism of action- stimulation of insulin secretion by beta cell by modulation of ATP dependant K+ channel (insulin secretagogue)

B. All are metabolized in the liver and renally excreted

C. Wide range in potency and duration of action

D. Main side effect is hypoglycemia

E, Cheap, effective as monotherapy or in combination

Front 8

Other Insulin Secretagogues: Repaglinide (Prandin), Natiglinide (Starlix)

A. Non-X molecular structure but same mechanism of action

B. Given QAC, up to 4x/day

C. Can be given to patients with X allergy

D. Should be held if patient skips meal

Back 8

Other Insulin Secretagogues: Repaglinide (Prandin), Natiglinide (Starlix)

A. Non-sulfonylurea molecular structure but same mechanism of action

B. Given QAC, up to 4x/day

C. Can be given to patients with sulfa allergy

D. Should be held if patient skips meal

Front 9

Metformin

A. Mechanism of action-
B. Metabolized in the X and X excreted

C. Given QPM supper or BID with breakfast and supper, principle side effects are X

D. Inexpensive; reduces Hba1c about X% with monotherapy. Does not cause hypoglycemia as monotherapy.

E. Does not promote weight gain- good for initial therapy

D. Contraindications:

1. Renal impairment Cr ³X (GFR <X ml/min)

2. Any hypoxic condition (i.e. decompensated CHF, severe lung disease)

3. History of lactic acidosis

4. Severe Liver disease or alcohol abuse

5. Severe infection

6. Must be held immediately prior to IV contrast administration and not restarted until 48 hours later and after renal function has been reassessed

Back 9

Metformin

A. Mechanism of action- main mechanism is reduction of hepatic glucose production, secondary mechanism of enhancing peripheral insulin action

B. Metabolized in the liver and renally excreted

C. Given QPM supper or BID with breakfast and supper, principle side effects are GI

D. Inexpensive; reduces Hba1c about 1-1.5% with monotherapy. Does not cause hypoglycemia as monotherapy.

E. Does not promote weight gain- good for initial therapy

D. Contraindications:

1. Renal impairment Cr ³1.4-1.5 (GFR <60 ml/min)

2. Any hypoxic condition (i.e. decompensated CHF, severe lung disease)

3. History of lactic acidosis

4. Severe Liver disease or alcohol abuse

5. Severe infection

6. Must be held immediately prior to IV contrast administration and not restarted until 48 hours later and after renal function has been reassessed

Front 10

a-Glucosidase Inhibitors

A. Mechanism of Action: X

B. Acarbose (Precose) and miglitol (Glyset)

C. Must be given at beginning of meals

D. Principle side effects are X, requires gradual dose titration

E. Acarbose can cause X elevation

F. X should be avoided in renal impairment

G. Contraindicated in infl;amatory bowel disease/malabsorption

H. not very potent- generally only lower A1c about X %

Back 10

a-Glucosidase Inhibitors

A. Mechanism of Action: inhibit dietary carbohydrate absorption

B. Acarbose (Precose) and miglitol (Glyset)

C. Must be given at beginning of meals

D. Principle side effects are GI, requires gradual dose titration

E. Acarbose can cause transaminase elevation

F. Miglitol should be avoided in renal impairment

G. Contraindicated in infl;amatory bowel disease/malabsorption

H. not very potent- generally only lower A1c about 0.25-0.5%

Front 11

Pneumonia
Community acquired
?Likely microbiology?
?Suggested therapy?

Back 11

S. pneum, H. Flu, Mycoplasma, Chlamydia, legionella, S. aureus, viruses—(no organism ID’d 40-60%)

Beta-lactam +/- Macrolide OR Quinolone

Front 12

Pneumonia
ICU patient or Hospital Aquired
?Likely micro?
?SUggested therapy?

Back 12

GNR including Pseudo, Klebsiella, Enterobacter, S aureus, Serratia

Ceftriaxone + (Macrolide or quinolone) OR Ampicllin/sulbactam + (Macrolide or quinolone) OR Pipercillin/tazobactam



60% of nosocomial pneumonias are gram-negative, 15% staph

Front 13

Bronchiectasis
?SUggested therapy?

Back 13

(Pipercillin/tazobactam or imipenem or cefipine) + (macrolide or quinolone) + aminoglycoside

Front 14

Blastomycosis

Histoplasmosis

Cyrtococcus
?Suggested therapy?

Back 14

For all three infections, Itraconazole if non-life threatening, Amphotericin B if life threatening or CNS disease

Fluconazole is used for chronic suppression of Cyrptococcus in HIV related disease

Front 15

Candida albicans
?Suggested therapy?

Back 15

PO - Fluconazole – especially used for Candida esophagitis

Topical - Miconazole, Clotrimazole, Ketoconazole

IV – Ketoconazole, 5-Flucytosine

Amphotericin B for deep seated, disseminated

Front 16

Cholecystitis
?Microbiology?
?Therapy?

Back 16

Coliforms and enterococci


Cefotetan (for mild to moderate infections)

Piperacillin/tazobactam (or ampicillin/sulbactam) + Gentamicin

Front 17

Cholangitis
?Microbiology?
?Therapy?

Back 17

Enterics, Enterococci, Anaerobes


Piperacillin/tazobactam (or ampicillin/sulbactam) + Gentamicin

Front 18

Diverticulitis
?Microbiology?
?Therapy?

Back 18

Enterics, Anaerobes


Cefotetan (for mild to moderate infections)

Clindamycin + Ciprofloxacin

Piperacillin/tazobactam (or ampicillin/sulbactam) + Gentamicin

Front 19

Intra-abdominal peritonitis or abscess
?Microbiology?
?Therapy?

Back 19

Enterics, Anaerobes, and Enterococci


Piperacillin/tazobactam (or ampicillin/sulbactam) + Gentamicin

Ceftazidime or Ceftizoxime

Imipenem

Clindamycin + Ciprofloxacin

Front 20

Cystitis
?Microbiology?
?Therapy?

Back 20

E. coli, Staphylococcus saprophyticus


TMP/SMX, Cephalexin, Augmentin, or Nitrofurantoin

Three day course; may resolve spontaneously without therapy.

Front 21

Pyelonephritis
Community (no underlying GU disease
?Microbiology?
?Therapy?

Back 21

E. coli, Proteus

Community (no underlying GU disease




TMP/SMX, Aminoglycosides, Ceftriaxone, or Ciprofloxacin

Front 22

Pyelonephritis
Nosocomial (underlying GU disease)
?Microbiology?
?Therapy?

Back 22

E. coli, Pseudomonas, Enterococcus

Nosocomial (underlying GU disease)




Ampicillin + gentamicin or tobramycin

Piperacillin/tazobactam + tobramycin

Ciprofloxacin ± ampicillin

These drug combinations are for empiric coverage for Pseudomonas and Enterococcus

Patients who are septic require double gram-negative coverage

Front 23

Neisseria gonorrhoeae, Chlamydia
?Therapy?

Back 23

(Ceftriaxone 125 mg IM single dose or Ciprofloxacin 500 mg po single dose) plus Doxycycline 100 mg po bid X 7 days

Front 24

Cellulitis (non-diabetic)

?Microbiology?
?Therapy?

Back 24

Streptococcus, Staphylococcus


Nafcillin (oral dicloxacillin)

Clindamycin or cefazolin in non-anaphylactic penicillin allergy

Front 25

.


Human/animal bites


Pasteurella multocida (cats), Streptococcus, Staphylococcu

?Therapy

Back 25

Ampicillin/sulbactam IV or amoxicillin/clavulanate po

Do not use oral first-generation cephalosporins for Pasteurella

Front 26

Osteomyelitis

Acute (hematogenous)

Back 26

Staphylococcus aureus, Gram-negatives (less frequent)

Gram-negative osteomyelitis may occur in the setting of underlying gastrointestinal or genito-urinary tract infection


Nafcillin + rifampin

Nafcillin ± aminoglycoside

Ceftriaxone therapy may allow outpatient parenteral therapy

Cefazolin or clindamycin may be options for penicillin allergic patients

Front 27

Osteomyelitis Diabetic foot or contiguous ulcer

Back 27

Gram-negatives, Gram-positives, Anaerobes

Establish bacteriology with appropriate deep cultures (not superficial swabs) whenever possible


Piperacillin/tazobactam

OR
Ampicillin/sulbactam + aminoglycoside

Adequate surgical debridement is critical to overall success

Front 28

Meningitis
Community
Age 18-50

Back 28

Streptococcus pneumoniae, N. meningitis, Haemophilus influenza (1-3%)


Ceftriaxone (Add Vanc if Pneumococcal resistance locally)

Antimicrobial therapy should be initiated within 30-60 min of presentation.

Front 29

Meningitis


Age >50 or
Alcoholic or
Debilitated medical condition

Back 29

Gram-negative aerobes, Strep. Pneumoniae, Listeria


Ampicillin + ceftriaxone

Front 30

Sinusitis

Back 30

Acute


Strep. Pneumoniae, H. influenzae, Moraxella catarrhalis


TMP/SMX po or Cefuroxime po or Amoxicillin/clavulanate po




Chronic


Above plus anaerobes plus staph


Amoxicillin/clavulanate po

Front 31

Diptheria

Back 31

Erythromycin

Front 32

Disseminated N. gonorrhoeae

Back 32

Ceftriaxone X 24-48h then switch to ciprofloxacin for 7 d

Front 33

stigmata of chronic liver disease

Back 33

§ Palmar erythema

§ Spider nevi

§ Ascites

§ Gynecomastia, etc.

Front 34

Vitamin K-dependent clotting factors

Back 34

II, VII, IX, X

Front 35

PT or PTT prolonged if Vitamin K not absorbed?

Back 35

PT
Cholestasis: then >30% correction with parenteral

Vit K

Front 36

hepatocellular disease labs

Back 36

§ Transaminases increase > 5x upper limit normal

§ Alkaline phosphatase usually < 2-3x upper limit of

normal

Front 37

§ Cholestatic Disease
labs

Back 37

§ Alkaline phosphatase increased 3-5 times upper

limit of normal with minimal elevation in

transaminases

§ Exception in cholestasis with cholangitis

Front 38

Infiltrative Disease
labs

Back 38

Alkaline phosphatase elevated disproportionately to
that of the bilirubin

Front 39

Hepatitis C

initial test and confirmation

Back 39

§ Initial test: serologic testing for Hep C antibody (sens. 92-97%)
§ Confirm by Hep C RNA by PCR (gold std)

Front 40

Hepatitis B
labs

Back 40

§ Initial tests: HepB surface Ag, Hep B surface Ab, Hep B core

antibody

§ Surface Ab and core Ab positive indicates immunity

§ Surface Ag and core Ab positive indicates infection

§ Hepatitis B e antigen, Hep B e antibody, and Hep B virus DNA

represent viral replication

Front 41

Hepatitis A
labs

Back 41

IgM hepatitis A antibody positive

Front 42

Hemochromatosis
labs

Back 42

Transferrin saturation (Fe/TIBC x100) >45%

Front 43

Autoimmune Hepatitis
labs

Back 43

§ Young to middle-age women (4:1 female: male)

§ Elevated transaminases in absence of other causes of
chronic hepatitis

§ Serum protein electrophoresis is useful screening test

§ > 80% of patients will have hypergammaglobulinemia

§ ANA

§ Anti-smooth muscle antibodies

§ Anti-liver-kidney microsomal antibodies

§ Liver biopsy is essential to confirm the diagnosis

Front 44

Wilson’s Disease
labs

Back 44

§ Initial screening test: serum ceruloplasmin (low)

§ Can check 24-hr urine for quantitative assessment of

copper excretion if ceruloplasmin normal but suspect

disease (>100 ug/day suggest’s Wilson’s)

§ Low uric acid b/c these patients RTA and low uric acid
in urine

§ Confirm diagnosis with liver biopsy (>250 ug/gram of

liver dry weight)

Front 45

Alpha-1-Antitrypsin
labs

Back 45

§ Very uncommon

§ Lack of peak in alpha globulin bands in
SPEP.

§ Can measure serum levels directly

Front 46

ast and alk phos in gallstone disease

Back 46

§ AST is elevated first in gallstone disease
because it leaks out of cells.

§ Alkaline phosphatase has to be

synthesized, and so it rises after AST.

Front 47

An increase in alkaline phosphatase out

of proportion to other LFTs suggests XXX, and should be further
investigated by YYY

Back 47

An increase in alkaline phosphatase out

of proportion to other LFTs suggests an

infiltrative process, and should be further
investigated by liver biopsy.

Front 48

Transaminase levels in the 1,000-10,000
range are seen in the presence of

XXXX or YYYY.

Back 48

Transaminase levels in the 1,000-10,000
range are seen in the presence of

ischemic injury or toxins.

Front 49

Nuchal rigidity

Back 49

the patient cannot place his/her chin upon their chest

Front 50

• Brudzinski’s sign

Back 50

Place the pt supine

Hold the thorax down upon the bed

Attempt to flex the neck

With meningeal irritation, it causes involuntary hip flexion

Front 51

• Kernig’s sign

Back 51

Place the patient in a supine position

Flex the hip and knee to 90o

With the hip immobilized, attempt to extend the knee

In meningeal irritation, the attempt is resisted and results in pain in the hamstring muscles

Front 52

Goal LDL for diabetics or known CAD patients

Back 52

Goal LDL <100 for diabetics or known CAD patients

Front 53

Goal LDL for those with 2 or more risk factors

Back 53

Goal LDL <130 for those with 2 or more risk factors (see above).

Front 54

Calculate TIMI risk score

Back 54

1) Age >65y, 2) >3 traditional risk factors for CAD, 3) known CAD with stenosis >50%, 4) ST segment deviation, 5) positive cardiac enzymes, 6) ASA use in the past week, 7) 2 episodes of severe angina in past 24 hours.



Score: 0-2= low risk, medical management

3-4= intermediate risk- go to cath lab

5-7= high risk, go to cath lab ASAP.

Front 55

MI management

Back 55

T- thrombolytics within 6 hours, ok to use before 12 hours. PTCA- within 90 minutes of arrival, OK within 24 hours.

H- Heparin- Lovenox has better data on outcomes, but lasts 12 hours, not reversible.

A- ASA 325mg chewable on arrival, Plavix load for patients not getting CABG (bypass), Abciximab or other GP IIb/IIIa inhibitor if TIMI score >3.

N- nitrates until chest pain free

K- check and correct potassium

S- relieve stress (Ativan)

M- Morphine for chest pain until chest pain free.

O- oxygen

M- metoprolol, aim for HR 60 bpm.

Front 56

Secondary prevention/treatment of chronic CAD:

Back 56

A- ASA 81mg po qd, Plavix for those with stents, ACE inhibitors for all post MI patients or ARB if intolerant to ACE.

B- B-blockers!!! Long acting are best, and BP control, goal <130/80 but really as low as possible.

C- Cholesterol reduction/use statins first, and Cigarette smoking cessation.

D- Diet and diabetes control.

E- exercise program 30 min to 75% of Max HR 3-4 times per week.

Front 57

[H+] =

Back 57

[H+] = 24 X pCO2/[HCO3-]

Front 58

estimate [H+]

Back 58

40 (pH of 7.40) by 1 nEq/L in the correct direction for each 0.01 change in pH from 7.40

Front 59

If a primary respiratory disturbance is present, determine whether it is acute or chronic by comparing pH and pCO2

Back 59

Acute pH = 0.08 x {(measured pCO2-40)/10}; chronic 0.03 X ….

Front 60

AG =

Back 60

AG = Na+ - (Cl- + HCO3-) = 10 (+/- 2) mEq/L

Front 61

albumin and anion gap

Back 61

For each 1 g/dl drop in albumin below 4 g/dl, subtract 2 from normal AG range

Front 62

Winter’s Formula (to calculate pCO2)

Back 62

pCO2 = {1.5 x [HCO3-]} + (8 +/- 2)

Front 63

Corrected [HCO3-] (if AG)

Back 63

= [HCO3-] + AG - 12; = [HCO3-] + [Delta]AG

Front 64

[Delta]AG

Back 64

AG - 12

Front 65

If Delta/Delta < 1

Back 65

AG metabolic acidosis + non-AG metabolic acidosis

Front 66

If Delta/Delta = 1-2

Back 66

typical AG metabolic acidosis

Front 67

If Delta/Delta > 2

Back 67

AG metabolic acidosis + metabolic alkalosi

Front 68

how do nsaids cause prerenal state?

Back 68

NSAIDS inhibit the enzyme cyclooxygenase which leads to a decrease in prostaglandins. the body would normally maintain GFR by dilating the afferent glomerular arteriole via prostaglandins and constricting the efferent arteriole via angiotensin II

Front 69

How do ACEIs cause prerenal state

Back 69

ACE inhibitors inhibit the production of angiotensin II. the body would normally maintain GFR by dilating the afferent glomerular arteriole via prostaglandins and constricting the efferent arteriole via angiotensin II

Front 70

The most common cause of hospital- or ICU-acquired ARF

Back 70

Acute Tubular Necrosis(ATN)

Front 71

Causes of acute tubular necrosis

Back 71

Injury to tubules can be ischemic (50% of cases) or toxic (35% of cases). (e.g. aminoglycocides, amphotericin, methotrexate), IV contrast agents, pigments (myoglobin, hemoglobin)

Front 72

A group of diseases characterized by interstitial inflammation

Back 72

Acute Interstitial Nephritis(AIN)

Front 73

A nephritic pattern classically includes

Back 73

hypertension and an active urine sediment (dysmorphic RBCs, RBC casts, WBCs) with variable proteinuria

Front 74

Nephrotic disorders present with

Back 74

edema, hypoalbuminemia, and massive proteinuria

Front 75

The three main categories of disease processes that present as RPGN include

Back 75

(1) anti-GBM disease, (2) immune complex-mediated diseases, and (3) pauci-immune (i.e., a necrotizing glomerulonephritis without immune deposits detected, such as Wegener's or microscopic polyangiitis). Glomerular crescents are a common feature

Front 76

in ATN the damaged renal tubule cells fail to reabsorb sodium normally and the spot urine sodium is often greater than X mmol/L with a FENa of greater than Y%.

Back 76

urine sodium is often greater than 50 mmol/L with a FENa of greater than 2-3%.

Front 77

FENa is defined as the ratio of

Back 77

sodium clearance (cna) to creatinine clearance (cCr).

Front 78

FENa (%) =

Back 78

= (UNa x Pcr)/(PNa x UCr) x 100

Front 79

renal lab effect: gi bleeding

Back 79

inc BUN

Front 80

renal lab effect: corticosteroids

Back 80

inc BUN

Front 81

renal lab effect: cimetidine

Back 81

increased creatinine d/t decreased tubular secretion

Front 82

renal lab effect: tmp/smx

Back 82

increased creatinine d/t decreased tubular secretion

Front 83

renal lab effect: cephalosporines

Back 83

increased creatinine d/t decreased tubular secretion

Front 84

renal lab effect: rhabdomyolysis

Back 84

increased creatinine…d/t incraeased release from muscle

Front 85

renal lab effect: ketones

Back 85

increased creatinine, d/t interference w/ Jaffe rx

Front 86

renal lab effect: cefoxitin

Back 86

increased creatinine, d/t interference w/ Jaffe rx

Front 87

oliguria def

Back 87

<400 mL/24 h bc minimum for daily nitrogenous waste

Front 88

anuria def

Back 88

<40-100 ml/day

Front 89

4 causes anuria

Back 89

complete obstruction, arterial occlusion, severe atn, bilateral renal vein thrombosis

Front 90

asthma classic triad of symptom

Back 90

shortness of breath, cough and wheezing.

Front 91

astha HEENT exam

Back 91

: increased nasal secretion, mucosal swelling and nasal polyps

Front 92

Asthma: The most useful clinical indicators that have been shown to correlate with objective findings

Back 92

pulsus paradoxus and accessory muscle use

Front 93

Chronic bronchitis is a clinical diagnosis defined by

Back 93

productive cough that occurs on most days for at least 3 months of the year, for 2 consecutive years

Front 94

Seven Killer Causes of Chest Pain

Back 94

1. Acute MI; 2.Tension PTX; 3. Aortic Dissection; 4.Tamponade; 5.PE; 6.Pneumonia; 7.Ruptured Esophagous (Borhave’s)

Front 95

coronary artery disease 8 risk factors

Back 95

# Smoking # High LDL # Low HDL # HTN # Obesity # DM # Post-menopausal # Hyperhomocyteinemia

Front 96

Beck's triad of tamponade

Back 96

Jugular venous distention, hypotension, and muffled heart sounds) Kussmaul sign: JVD elevation during inspiration.

Front 97

Lights criteria

Back 97

LDH effusion/serum >0.6; Protein effusion/serum > 0.5; LDH > 2/3 upper limit normal for serum

Front 98

outpatient tx for comm aq pneumonia; no commorbid or risk fx for resistant or for gram neg

Back 98

macrolide (azithro or clarithro) daily 7 days; doxy as second line

Front 99

com aq pneumonia and risk fx, commorbid

Back 99

b lectam and macrolide; or quinolone

Front 100

inpatient pneumonia, non icu

Back 100

IV B lactam & macrolide: OR fluoroquinilone alone