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Diabetes
Diagnostic Criteria (American Diabetes Association)
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
Diagnostic Criteria for Impaired fasting glucose (IFG)
IFG= fasting PG= 100-125 mg/dl.
impaired glucose tolerance (IGT)
Diagnostic Criteria
IGT= PG 140-199 mg/dl 2 hours after 75 gram oral glucose
metabolic syndrome = when 3 or more of following are present:
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
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
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
Initial Evaluation of a Patient with Diabetes (8)
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
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
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
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
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
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
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
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 %
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%
Pneumonia
Community acquired
?Likely microbiology?
?Suggested therapy?
S. pneum, H. Flu, Mycoplasma, Chlamydia, legionella, S. aureus, viruses—(no organism ID’d 40-60%)

Beta-lactam +/- Macrolide OR Quinolone
Pneumonia
ICU patient or Hospital Aquired
?Likely micro?
?SUggested therapy?
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
Bronchiectasis
?SUggested therapy?
(Pipercillin/tazobactam or imipenem or cefipine) + (macrolide or quinolone) + aminoglycoside
Blastomycosis

Histoplasmosis

Cyrtococcus
?Suggested therapy?
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
Candida albicans
?Suggested therapy?
PO - Fluconazole – especially used for Candida esophagitis

Topical - Miconazole, Clotrimazole, Ketoconazole

IV – Ketoconazole, 5-Flucytosine

Amphotericin B for deep seated, disseminated
Cholecystitis
?Microbiology?
?Therapy?
Coliforms and enterococci


Cefotetan (for mild to moderate infections)

Piperacillin/tazobactam (or ampicillin/sulbactam) + Gentamicin
Cholangitis
?Microbiology?
?Therapy?
Enterics, Enterococci, Anaerobes


Piperacillin/tazobactam (or ampicillin/sulbactam) + Gentamicin
Diverticulitis
?Microbiology?
?Therapy?
Enterics, Anaerobes


Cefotetan (for mild to moderate infections)

Clindamycin + Ciprofloxacin

Piperacillin/tazobactam (or ampicillin/sulbactam) + Gentamicin
Intra-abdominal peritonitis or abscess
?Microbiology?
?Therapy?
Enterics, Anaerobes, and Enterococci


Piperacillin/tazobactam (or ampicillin/sulbactam) + Gentamicin

Ceftazidime or Ceftizoxime

Imipenem

Clindamycin + Ciprofloxacin
Cystitis
?Microbiology?
?Therapy?
E. coli, Staphylococcus saprophyticus


TMP/SMX, Cephalexin, Augmentin, or Nitrofurantoin

Three day course; may resolve spontaneously without therapy.
Pyelonephritis
Community (no underlying GU disease
?Microbiology?
?Therapy?
E. coli, Proteus

Community (no underlying GU disease




TMP/SMX, Aminoglycosides, Ceftriaxone, or Ciprofloxacin
Pyelonephritis
Nosocomial (underlying GU disease)
?Microbiology?
?Therapy?
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
Neisseria gonorrhoeae, Chlamydia
?Therapy?
(Ceftriaxone 125 mg IM single dose or Ciprofloxacin 500 mg po single dose) plus Doxycycline 100 mg po bid X 7 days
Cellulitis (non-diabetic)

?Microbiology?
?Therapy?
Streptococcus, Staphylococcus


Nafcillin (oral dicloxacillin)

Clindamycin or cefazolin in non-anaphylactic penicillin allergy
.


Human/animal bites


Pasteurella multocida (cats), Streptococcus, Staphylococcu

?Therapy
Ampicillin/sulbactam IV or amoxicillin/clavulanate po

Do not use oral first-generation cephalosporins for Pasteurella
Osteomyelitis

Acute (hematogenous)
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
Osteomyelitis Diabetic foot or contiguous ulcer
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
Meningitis
Community
Age 18-50
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.
Meningitis


Age >50 or
Alcoholic or
Debilitated medical condition
Gram-negative aerobes, Strep. Pneumoniae, Listeria


Ampicillin + ceftriaxone
Sinusitis
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
Diptheria
Erythromycin
Disseminated N. gonorrhoeae
Ceftriaxone X 24-48h then switch to ciprofloxacin for 7 d
stigmata of chronic liver disease
§ Palmar erythema

§ Spider nevi

§ Ascites

§ Gynecomastia, etc.
Vitamin K-dependent clotting factors
II, VII, IX, X
PT or PTT prolonged if Vitamin K not absorbed?
PT
Cholestasis: then >30% correction with parenteral

Vit K
hepatocellular disease labs
§ Transaminases increase > 5x upper limit normal

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

normal
§ Cholestatic Disease
labs
§ Alkaline phosphatase increased 3-5 times upper

limit of normal with minimal elevation in

transaminases

§ Exception in cholestasis with cholangitis
Infiltrative Disease
labs
Alkaline phosphatase elevated disproportionately to
that of the bilirubin
Hepatitis C

initial test and confirmation
§ Initial test: serologic testing for Hep C antibody (sens. 92-97%)
§ Confirm by Hep C RNA by PCR (gold std)
Hepatitis B
labs
§ 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
Hepatitis A
labs
IgM hepatitis A antibody positive
Hemochromatosis
labs
Transferrin saturation (Fe/TIBC x100) >45%
Autoimmune Hepatitis
labs
§ 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
Wilson’s Disease
labs
§ 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)
Alpha-1-Antitrypsin
labs
§ Very uncommon

§ Lack of peak in alpha globulin bands in
SPEP.

§ Can measure serum levels directly
ast and alk phos in gallstone disease
§ 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.
An increase in alkaline phosphatase out

of proportion to other LFTs suggests XXX, and should be further
investigated by YYY
An increase in alkaline phosphatase out

of proportion to other LFTs suggests an

infiltrative process, and should be further
investigated by liver biopsy.
Transaminase levels in the 1,000-10,000
range are seen in the presence of

XXXX or YYYY.
Transaminase levels in the 1,000-10,000
range are seen in the presence of

ischemic injury or toxins.
Nuchal rigidity
the patient cannot place his/her chin upon their chest
• Brudzinski’s sign
Place the pt supine

Hold the thorax down upon the bed

Attempt to flex the neck

With meningeal irritation, it causes involuntary hip flexion
• Kernig’s sign
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
Goal LDL for diabetics or known CAD patients
Goal LDL <100 for diabetics or known CAD patients
Goal LDL for those with 2 or more risk factors
Goal LDL <130 for those with 2 or more risk factors (see above).
Calculate TIMI risk score
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.
MI management
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.
Secondary prevention/treatment of chronic CAD:
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.
[H+] =
[H+] = 24 X pCO2/[HCO3-]
estimate [H+]
40 (pH of 7.40) by 1 nEq/L in the correct direction for each 0.01 change in pH from 7.40
If a primary respiratory disturbance is present, determine whether it is acute or chronic by comparing pH and pCO2
Acute pH = 0.08 x {(measured pCO2-40)/10}; chronic 0.03 X ….
AG =
AG = Na+ - (Cl- + HCO3-) = 10 (+/- 2) mEq/L
albumin and anion gap
For each 1 g/dl drop in albumin below 4 g/dl, subtract 2 from normal AG range
Winter’s Formula (to calculate pCO2)
pCO2 = {1.5 x [HCO3-]} + (8 +/- 2)
Corrected [HCO3-] (if AG)
= [HCO3-] + AG - 12; = [HCO3-] + [Delta]AG
[Delta]AG
AG - 12
If Delta/Delta < 1
AG metabolic acidosis + non-AG metabolic acidosis
If Delta/Delta = 1-2
typical AG metabolic acidosis
If Delta/Delta > 2
AG metabolic acidosis + metabolic alkalosi
how do nsaids cause prerenal state?
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
How do ACEIs cause prerenal state
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
The most common cause of hospital- or ICU-acquired ARF
Acute Tubular Necrosis(ATN)
Causes of acute tubular necrosis
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)
A group of diseases characterized by interstitial inflammation
Acute Interstitial Nephritis(AIN)
A nephritic pattern classically includes
hypertension and an active urine sediment (dysmorphic RBCs, RBC casts, WBCs) with variable proteinuria
Nephrotic disorders present with
edema, hypoalbuminemia, and massive proteinuria
The three main categories of disease processes that present as RPGN include
(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
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%.
urine sodium is often greater than 50 mmol/L with a FENa of greater than 2-3%.
FENa is defined as the ratio of
sodium clearance (cna) to creatinine clearance (cCr).
FENa (%) =
= (UNa x Pcr)/(PNa x UCr) x 100
renal lab effect: gi bleeding
inc BUN
renal lab effect: corticosteroids
inc BUN
renal lab effect: cimetidine
increased creatinine d/t decreased tubular secretion
renal lab effect: tmp/smx
increased creatinine d/t decreased tubular secretion
renal lab effect: cephalosporines
increased creatinine d/t decreased tubular secretion
renal lab effect: rhabdomyolysis
increased creatinine…d/t incraeased release from muscle
renal lab effect: ketones
increased creatinine, d/t interference w/ Jaffe rx
renal lab effect: cefoxitin
increased creatinine, d/t interference w/ Jaffe rx
oliguria def
<400 mL/24 h bc minimum for daily nitrogenous waste
anuria def
<40-100 ml/day
4 causes anuria
complete obstruction, arterial occlusion, severe atn, bilateral renal vein thrombosis
asthma classic triad of symptom
shortness of breath, cough and wheezing.
astha HEENT exam
: increased nasal secretion, mucosal swelling and nasal polyps
Asthma: The most useful clinical indicators that have been shown to correlate with objective findings
pulsus paradoxus and accessory muscle use
Chronic bronchitis is a clinical diagnosis defined by
productive cough that occurs on most days for at least 3 months of the year, for 2 consecutive years
Seven Killer Causes of Chest Pain
1. Acute MI; 2.Tension PTX; 3. Aortic Dissection; 4.Tamponade; 5.PE; 6.Pneumonia; 7.Ruptured Esophagous (Borhave’s)
coronary artery disease 8 risk factors
# Smoking # High LDL # Low HDL # HTN # Obesity # DM # Post-menopausal # Hyperhomocyteinemia
Beck's triad of tamponade
Jugular venous distention, hypotension, and muffled heart sounds) Kussmaul sign: JVD elevation during inspiration.
Lights criteria
LDH effusion/serum >0.6; Protein effusion/serum > 0.5; LDH > 2/3 upper limit normal for serum
outpatient tx for comm aq pneumonia; no commorbid or risk fx for resistant or for gram neg
macrolide (azithro or clarithro) daily 7 days; doxy as second line
com aq pneumonia and risk fx, commorbid
b lectam and macrolide; or quinolone
inpatient pneumonia, non icu
IV B lactam & macrolide: OR fluoroquinilone alone