Aherrera Notes

Dr. Jaime Aherrera’s Internal Medicine Notes 2009

Aherrera Notes
Dr. Jaime Aherrera’s Internal Medicine Notes 2009

I. II. III. IV. V. VI. VII. VIII. IX. X.
Aherrera Notes | TAABLE OF CONTENTS

Basic Information Cardiology Endocrinology Gastroenterology Hematology Infectious Disease Nephrology Neurology Pulmonology Rheumatology

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Jaime Alfonso Manalo Aherrera, M.D.
Internal Medicine Notes 2009

WARD NOTES

1) MUST KNOW FORMULAS
I. DOPAMINE DOSAGE COMPUTATION
  Dopamine Drip – used primarily for stabilization of the Hypotensive Patient Formulation of Dopamine: o Dilute 200mg (1 Ampule) in 250cc D5W (Factor used: 13.3) o Drip at 2.5 – 10mcg/kg/min o Maximum Dose of 20mcg/kg/min (Dopa-Max) o If Double Strength: 2 Ampules in 250cc D5W (use 26.6)

Rate (ugtt/min) = . (mcg/kg/min) x body weight . 13.3  Dopamine Doses (from Harrisons p1453) DOSE < 2 mcg/kg per min 2-4 mcg/kg per minute > 5 mcg/kg per minute
o o o

Dose (mcg/kg/min) = .

(ugtt/min) x 13.3 body weight

.

MECHANISM OF ACTION
Stimulate DA1 and DA2 Receptors Stimulate B1-Receptors Effects on A1-Receptors overwhelm the Dopaminergic Receptors

EFFECT
Vasodilation of Splanchnic and Renal Vasculature Increase in Cardiac Output with little or no change in Heart Rate or SVR Vasoconstricion, leading to Increase in SVE, LV Filling Pressures, and Heart Rate

**NOTE: Dopamine is generally the 1st choice for Tx in situations where Modest Inotropy & Pressor Support are required
It is an Endogenous Catecholamine that stimulates B1, A1 Receptors, and Dopaminergic Receptors (DA1, DA2) in the heart and circulation Dopamine also releases Norepinephrine from nerve terminals, which itself stimulates A1 and B1 Receptors, thus raising Blood Pressure Most useful in treatment of heart failure patients who have Depressed Cardiac Output with Poor Tissue Perfusion

Example) Case on Septic Shock: Patient is a 45kg / F, given 2 amps of Dopamine in 250cc PNSS at a rate of 19uggts/min  In 1 Ampule of Dopamine = 200mg/amp Strength Factors:  In 1 Ampule of Dobutamine = 250mg/amp NOTE: 19ugtts/min = 19cc/hr

 

1 amp of Dopamine = 13.3 2 amps of Dopamine = 26.6

QUESTION: What is the Dose of Dopamine being given to the patient at a rate of 19uggts/min?: Dose Given (in mcg/kg/min) = Rate (in ugtt/min) x 26.6 = 19 uggt/min x 26.6 = 45 kg 45 kg 11.23 mcg/kg/min

ANSWER: 11.23mcg/kg/min is the dose given to the Patient at a rate of 19uggts/min (or 19cc/hr) Since we are giving 11.23mcg/kg/min, we have a Vasoconstricting Effect. This is what we want for a patient with Septic Shock. We can increase the ugtts/min if patient is still Hypotensive up to 34ugtt/min (20mcg/kg/min) for a 45kg patient (Dopa Max). If still No Response with Dopa Max, we can give LEVOPHED (Norepinephrine). In the computation, we used 26.6 because 2 ampules of dopamine were used for the patient. Recall the Action of Dopamine at Different Doses (Dr. Magno Notes): 1. At 1-5mcg = RENAL VASODILATOR  Exerts selective Renal and Mesenteric Vasodilation  Acts on Dopamine Receptors  Improve Renal Blood Flow and Urine Output 2. At 6-10mcg = INOTROPIC  Positive Inotropic Effect  Acts on Beta-1 Adrenergic Receptors  Increase Heart Rate 3. At 10-20mcg = VASOCONSTRICTOR  Peripheral Vasoconstriction  Acts on A-Adrenergic Receptors  Increase Systemic Vascular Resistance  Deleterious for CHF and Low Cardiac Output

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5 – 10mcg/kg/min o Maximum Dose of 20mcg/kg/min o If double strength: 2 Ampules in 250cc D5W (use 33. = 8.II. DOBUTAMINE DOSAGE COMPUTATION A.5ug/kg/min) but moderate Chronotropic Activity at Higher Doses III.6 body weight . Dobutamine Drip – selectively stimulates Beta-1 Adrenergic Receptors o Direct Inotropic Stimulation with Reflex Arterial Vasodilation o Afterload Reduction and Augmented Cardiac Output o BP remains constant. the concentration of Levophed will be 8mcg/cc (as computed above) 1) If Our desired dose to give patient is 2mcg/min (usual starting dose). what is the Rate? Step 1: Convert 2mcg/min to mcg/hour 2mcg/min x 60 mins  120mcg/hr Step 2: If we desire a dose of 120mcg/hr given a concentration of 8mcg Levophed per cc.000 mcg = 32mcg Noradrenaline per mL (Concentration of 4 Amps + 250cc D5W) 250cc 250cc Since we initially want to give a dose of 2 mcg/min . compute the rate: 120mcg/hr = 15 cc/hr or 15 ugtts/min 8mcg/cc 2) If our desired dose is 8mcg/min  480mcg/hr 480mcg/hr = 60 ugtts/min 8mcg/cc Example 2) We are using 4 ampules (8mg) in 250cc of D5W. If we mix 1 Amp with 250cc D5W. We want to give the patient a dose of 2mcg/min.000mcg = 8mcg Noradrenaline per cc (this is the concentration of 1 Amp + 250cc D5W) 250cc 250cc Drip of 2-8mcg Noradrenaline/min is equivalent to 15-60 ugtts/min Example: We are using 1 Amp (2mg) in 250cc D5W.2 mcg x 60 min = 120 mcg / hr min hr 120 mcg/hr = 4 cc/hr or 4 uggt/min 32 mcg/cc **NOTE: cc/hr is equal to uggts/min 3 . What is the rate? Concentration = 8 mg .6 C. (ugtt/min) x 16. Notes from Harrisons: Dobutamine has a Positive Inotropic Action and Minimal Positive Chronotropic Activity at Low Doses (2. Formulation of Dobutamine o Dilute 250mg (1 amp) in 250cc D5W (use 16. HR increases minimally o For patients with Chronic Refractory Heart Failure o NOT for Heart Failure resulting from Diastolic Dysfunction or High-Output State B.2) Rate (ugtt/min) = mcg/kg/min x body weight 16.6) o Drip at 2. NORADRENALINE (LEVOPHED) – Rounds  Each ampule has 2mg Noradrenaline per amp  Usual Starting Dose is at 2-4 mcg/min with a maximum of 15 mcg/min Noradrenaline (LEVOPHED) Drip: 2mg Noradrenaline in 2mL Ampule Usual Preparation: D5W 250mL + 1 Amp (2mg) Levophed to run at 15-60ugtts/min Concentration = 2mg = 2. Action of Dobutamine at Different Doses: o 0 – 10 mcg/kg/min = INOTROPIC EFFECT o 10 – 20 mcg/kg/min = VASOCONSTRICTION mcg/kg/min = .

III. COMMON FORMULAS USED A. General Formulas BMI = kg / m2
Underweight Normal Weight Overweight Obese I Obese II < 18.5 18.5 – 22.9 23 – 24.9 25 – 29.9 > 30

Ideal Body Weight: Females: 100 pounds + (5 pounds per inch over 5 feet) Males: 106 pounds + (6 pounds per inch over 5 feet) **NOTE: Divide 2.2 to convert to kilograms

B. Cardiac Output, Mean Arterial Pressure (MAP), Anion Gap, Osmolality, Etc. Cardiac Output Mean Arterial Pressure Heart Rate x Stroke Volume Systolic BP + (2 x Diastolic BP) 3
Normal Value: 70 – 100 mmHg

Urine Anion Gap Serum Anion Gap Urine Osmolality Plasma Osmolality

( Na + K ) – Cl Na – ( HCO3 + Cl ) ( SG – 1 ) x 40,000 [2 (Na + K)] + RBS (mmol/L) + BUN (mmol/L) or 2 (Na in mmol/L) + (Glucose in mg/dL / 18) + (BUN / 2.8) Normal Value is 280 – 300 mOsm/L Normal Value (from Harrisons) = 275-290 mosm/kg RBS: 1 mmol/L = 18 mg/dL

Effective Plasma Osmolality

2 Na + RBS in mmol/L or 2 Na + RBS in mg/dL 18

C. Adequacy of Urine Collection o M: 20-23mL/kg o F: 15-20mL/kg D. 24-Hour Urine Collection Adequacy
o o o Creatinine is produced at a constant rate and in an amount directly proportional to skeletal mass Creatinine Coefficient = 23mg/kg of IBW (men) and 18mg/kg of IB (women) If 24 hr urine creatinine is LESS than IBW x Creatinine Coefficient  INADEQUATE Collected Specimen Unpredictable when Serum Crea > 530umol/L

o

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IV. BUN / CREATININE RATIO; CREATININE CLEARANCE A. BUN / Crea Ratio (SI Units)

BUN:Crea Ratio = BUN x 247 Crea
Conversion Factor for Serum BUN: 1 mmol/L = 2.8 mg/dL B. Fractionated Urine Na (Best test to Diagnose if Renal or Prerenal)

Interpretation:  If < 10: Intrinsic Renal Cause  If 10-20: Doubtful Cause  If > 20: Pre-Renal Cause

FENa =

[ UNA x PCR ] x 100 [ PNA x UCR ]

Interpretation: <1 Pre-Renal >1 Renal (Oliguric ATN)

C. Creatinine Clearance (mL/min): Cockroft and Gault Equation

CreaClearance = . (140 – age) x weight in kg . 72 x Serum Crea in mg/dL

CreaClearance = . (140 – age) x weight in kg . 72 x (Serum Crea in umol/L / 88.4)

 IMPORTANT Notes: o If Female, multiply everything by 0.85 o If Creatinine is NOT in mg/dL, divide it by 88.4  Normal Creatinine Clearance o 100-125mL/min in Males o 85-105mL/min in Females  Staging of Chronic Kidney Disease (CKD) CKD STAGE DESCRIPTION Kidney damage with normal / increased GFT I Kidney damage with mildly decreased GFR II Moderately decreased GFR III Severely decreased GFR IV Renal Failure V GFR mL/min / 1.73m2 90 60 – 89 30 – 50 15 – 29 < 15 (for dialysis)

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V. ELECTROLYTES A. Calcium
1. Corrected Calcium (mg/dL)

[ (40 – Albumin in g/L) x 0.02 ] + Measured Ca2 in mmol/L OR ( 4 – Albumin in g/dL x 0.08 ) + Measured Ca2+ in mg/dL

A Fall in Serum Albumin of 1gm/dL is associated with a Fall of 0.8mg/dL in Total Calcium

   

LOW in Renal Failure, Hypoparathyroidism, Severe Hypomagnesemia, Hypermagnesemia, Acute Pancreatitis, Rhabdomyolysis, Tumor Lysis Syndrome, Vitamin-D Deficiency, Pseudohypoparathyroidism; Rarely due to Multiple Citrated Blood Transfusions, critically ill patients, Anti-Neoplastic Agents, Antimicrobials, Agents used to Treat Hypercalcemia Use with Hypocalcemia ONLY if Ionized Calcium cannot be measured Make sure that the alteration in Serum Calcium is NOT due to Abnormal Albumin Concentrations About 50% of Total Calcium is Ionized, and the rest is bound principally to Albumin When Serum Albumin Levels are REDUCED, a Corrected Calcium Concentration is calculated by adding 0.2mM (0.8mg/dL) to the Total Calcium Level for every Decrement in Serum Albumin of 1.0g/dL below the reference value of 4.1 for Albumin, and conversely for elevations in Serum Albumin
Example:  Present Total Calcium = 8mg/dL  Present Serum Albumin = 2.5g/dL (N: 4g/dL)  Corrected Ca2+ = (4 – 2.5) x 0.8 = 1.2  Corrected Total Calcium = 8 + 1.2 = 9.2 mg/dL

2. Hypocalcemia  Calcium Gluconate 10% Solution of 10mL/amp: 1-2amp Slow IV Push (10-15mins) with Cardiac Monitoring then incorporate 1amp Calcium Gluconate to present IV Fluids  Chronic Treatment:  Calcium Carbonate 500mg 1 tab BID-TID  Vitamin-D3 Supplements (Calcitriol 0.25mcg/cap OD-BID)  Treat Hypomagnesemia 3. Hypercalcemia  Hydrate: 0.9%NSS at 150-600cc/hr (up to 1-4 Liters in 24 hours)  Furosemide 20-40mg IV q8-12 hours  Bisphosphonates (Pamidronate 30-90mg/day as a single 24-hour Infusion for 3 Days)

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B. Sodium 1. Corrected Sodium

0.016 (RBS in mg/dL – 100) + Measured Na+ in mmol/L  Plasma Na+ Concentration FALLS by 1.4 mmol/L for every 100 mg/dL RISE in the Plasma Glucose Concentration

2. Hyponatremia: Sodium Deficit

( Desired Na – Actual Na ) x Body Weight in kg x 0.6
    Target Na+ = 125 – 135 mEq/L NOTE: 0.6 is Total Body Water NaCl 1 Tab = 17 mEq NaHCO3 GrX 1 tab = 7 mEq a. Sodium Correction  Time needed to Infuse = ( Desired Na – Measured Na ) / 0.5  Total # of L needed = Na Deficit / 154  Drip Rate = Total # of L needed / Time needed to Infuse  Give Patient 50% of Calculated amount of Na+ in the first 8 hours, and the other 50% in the next 16 hours (correct at a Rate NOT > 0.5meq/L/hr)

b. Sample Case for Hyponatremia  A 70-kg male has a Na+ Value of 105 mmol/L  We want to raise the plasma Na+ concentration from 105 to 115 mmol/L  Formula: Deficit in Plasma Na+ x Total Body Water (TBW)  [115 – 105] x 70 x 0.6 = 420 mmol  Plain NSS (PNSS) has 154 Na+ Content per Liter; therefore, we can give 2-3 L of PNSS in one day

3. Hypernatremia
a. Water Deficit

Water Deficit =

Plasma Na+ Concentration - 140 140 OR

x 0.6 x BW (kg)

Water Deficit = [ ( Actual Na – Desired Na ) ] x 0.6 x BW (kg) Desired Na


  

TBW is 0.6 mg/kg for MALES TBW is 0.5 mg/kg for FEMALES

Desired Na+ is 140 Total Body Water (TBW) in Hypernatremia is due to water loss Should be corrected SLOWLY over at least 48-72 hours, ideally with hourly Serum Na+ determination to target 0.5mmol/L/h, but NOT > 12mmol/L over the 1 st 24 hours b. Sample Case on Hypernatremia  A 50 kg woman with a Plasma Na+ Concentration of 160 mmol/L  Water Deficit = 2.9 L Water deficit should be corrected slowly over at least 48-72

160 – 140 x 0.4 x 50 kg = 2.9 L 140

hours. Safest route of administration of water is by mouth or via a nasogastric tube. Alternatively, 5% Dextrose in Water of Half-Isotonic Saline can be given IV

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and Plasma Na + Concentration should be raised by 1-2 mmol/L per hour for the first 3-4 hours or until seizures subside. to be diluted in Oral Feeding or Water **NOTE: Each Oral Dose should NOT exceed 20-40 meq K+ 2. Dysarthria.Measured K+) 0.4. Oral Route  Kalium Durule 0.  Osmotic Demyelination Syndrome (ODS): Risk of correcting Hyponatremia too rapidly – Flaccid Paralysis. and 2) To correct the underlying disorder  Rx: Plasma Na+ Concentration should be raised by NO more than 0. Water Excess Water Excess = Normal Na+ x TBW Actual Na+ .5-1.5 Target K is 3.5 mEq/L. 15cc + 20mEqs KCl.TBW Hyponatremia  Plasma Na+ Concentration < 135 mmol/L  Clinical Manifestations: Brain Swelling or Cerebral Edema  Stupor.5 mmol/L o Hyperkalemia = Plasma K+ Concentration > 5. leading to Contracted ICF Volume – Decreased Cell Volume is associated with an Increased Risk of Subarachnoid or Intracerebral Hemorrhage  Therapeutic Goals: Stop Ongoing Water Loss and to Correct the Water Deficit C. and Coma do NOT usually occur unless the Plasma Na+ falls below 120mmol/L of Decreases RAPIDLY  Goals of Therapy: 1) To raise plasma Na+ Concentration by restricting water intake and promoting water loss. replace 10-20 mEq KCl for every 0. then the excess within the next 3 days Sample Orders for Hypokalemia: 1.1 mEq/L Drop in K Maximum Drip: Max 10 mEqs / hr Central Line: Max 20 mEqs / hr Desired K is: 4.5 – 4. Dysphagia Hypernatremia  Plasma Na+ Concentration > 145 mmol/L  Clinical Features: Water shifts OUT of cells. requiring Oral Administration of K Administer as 10% Solution. Potassium o Hypokalemia = Plasma K+ Concentration < 3. Seizures.9 mEq/L If K is 2. Intravenous Route  Usual Concentration is 20-40 meq K+ in 1L Saline or Dextrose Solution  Ex) Add 20-60 meq KCl in 1L Plain NSS x 12 hours  If K+ Level is <2 and (+) ECG Abnormalities.0 mmol/L 1. 1/2 of the dose given within 24 hours.0 – 3.5 mEq/L for Non-Cardiac Causes.0 mEq/L for Cardiac Causes. It should be raised by no more than 12 mmol/L during the first 24 hours. requiring IV administration of K 3.27        x 100 Oral Kcl:  15cc: 10 mEqs  30cc: 20 mEqs Kalium Durule:  1 tab = 10 mEqs Desired K is 3.75gm (10 meq) TID PO x 2-3 days. Potassium Deficit (Desired K+ . use Glucose Free Solution 8 .0 mmol/L per hour and by LESS than 10-12 mmol/L over the first 24 hours  For Severe Symptomatic Hyponatremia: Treated with Hypertonic Saline. or  Oral KCl Solution 15-30cc TID (1gm KCl = 14meq K+.

OTHER CONVERSION FACTORS To mg/dL RBS: BUN: Crea: Ca2+: Bilirubin: Multiply by 18 Multiply by 2.5) Restrict Potassium Intake Kayexelate or Sorbisterit 20g.2.5-20mg/hr Salbutamol Nebulization Calcium Gluconate 10mL 1amp in 10% Solution Slow IV Push  Repeat after 10minutes if no improvement Glucose-Insulin  D50-50mL + 10 units Humulin R Slow IV stat.5-6. Goal is to Increase HCO3 to 10 mEq/L and pH to 7. so we usually give NaHCO3 GrX TID 9 . Hyperkalemia Mild (K <5.4    For correction of deficit.33 mEqs K 20 mEqs K 10 mEqs K 45 mEqs Na 7 mEqs Na Equivalents 1cc Oral KCl: 15cc Oral KCl: 1 K Durule (750mg): NaHCO3 50mL: NaHCO3 Gr X Tab: Regular requirement for NaHCO3 is 21mEq/day. administer 1/2 of computed value as Bolus.20 in Pure HAGMA.8 Divide by 88.5) D.5) Moderate (K = 5.4 Divide by 0. then remaining 1/2 as IV Drip Desired HCO3 of 15 – 18 if patient has Chronic Renal Disease For Severe Acidosis: < pH 7.25 Divide by 17.10 1. then q6 0 x 3 Doses  500mL 10% Dextrose + 10 Units Insulin over 30-60minutes  1L 10% Dextrose + 20 Units Insulin with 1/3 solution given in first 30 minutes and the remainder over the subsequent 2-3 hours Sodium Bicarbonate  1 amp Dilute in 100cc D5W Slow IV Push > 10 minutes  Fastest way to decrease Potassium (K+ shift in <15minutes) Severe (K > 6. or Kalmiate 1 Sachet in 50-150cc Water TID x 3 Doses (up to 4-5 Doses/day) Furosemide 40-80mg IV Stat or Drip 0.15 VI. Bicarbonate ( Desired HCO3 – Actual HCO3 ) x (Weight in Kg) x 0.

Elevated Gradient:  Shunting (ie. Normal Gradient (both reduce Alveolar Oxygenation):  Decrease in Inspired PO2  Hypoventilation 2. INTRAVENOUS FLUIDS IV SOLUTION D5W D10W 0. Pulmonary Edema)  Intracardiac Shunt  Vascular Shunt within Lungs 2. Intracardiac Shunt): Low PO2 is NOT correctable with Supplemental O2  V/Q Mismatch: Low PO2 is CORRECTED with Supplemental O2 Shunting VS V/Q Mismatch: 1.8) . Alveolar-Arterial O2 Difference (PAO2 – PaO2) or Alveolar-Arterial O2 Gradient (A-a Gradient) A – a Gradient PAO2 – PaO2 or ( FiO2 x 713) – (PCO2 / 0.9 NSS D5LR NM NR D50. Shunt:  Alveolar Collapse (Atelectasis)  Intraalveolar Filling (Pneumonia. TEMPERATURE CONVERSION  Degrees Fahrenheit to Degrees Celsius: C = (F – 32) x 5/9  Degrees Celsius to Degrees Fahrenheit: F = (C x 9/5) + 32 VIII. V/Q Mismatch:  Airway Disease (Asthma.VII. PULMONOLOGY FORMULAS A.9 NaCl D5NMK GLUCOSE 50 gm/L 100 gm/L 154 130 40 140 154 40 Na+ 154 109 40 98 154 40 Cl- K+ Ca2+ HCO3 4 13 5 30 3 28 50 gm/L 50 gm/L IX.PaO2 This formula is derived from:  Alveolar PO2 (PAO2) = FiO2 x (PB – PH2O) – PaCO2/R  In NORMAL Persons: PAO2 – PaO2 < 15 mmHg  Four Basic Mechanisms of Hypoxia: o Decrease in Inspired PO2 o Hypoventilation o Shunt o Ventilation/Perfusion (V/Q) Mismatch A-a Gradient: 1. COPD)  Interstitial Lung Disease  Alveolar Disease  Pulmonary Vascular Disease 10 .

29 374.8) Step II: Compute for AaO2 AaO2 = PaO2 PAO2 Step III: Compute for Desired FiO2 . we can use 60 11 .8 Step II: AaO2 = . x 100 = 36% .8) Desired PO2 = 80 – ( # of yrs > 60 y/o) = If < 60y/o = 104 – (0. Desired FiO2 Desired FiO2 [ ( Desired PO2 / PAO2 ) + ( PACO2 / 0.4 FiO2 = 60% O2 Sat = 90% Step I: PAO2 = (0. we can decrease FiO2 to 36% **NOTE: Instead of 80.8) ] x 100 713 Where: PAO2 = (FiO2 x 713) – (PCO2 / 0.8 Step III: FiO2 = .8) = 374.B. 60 .43 x age) Simplified Version (ER Rounds): Step I: Compute for PAO2 PAO2 = (FiO2 x 713) – (PCO2 / 0. we can use 80-100 o In COPD.therefore.4 / 0.8 713 . 109 . x 100 EXAMPLE: COPD Patient with the following values (ABG): pH = 7.8 713 . + 42.29 0. we used 60 – because patient has (+) COPD **NOTE: Desired PO2: o Instead of 80 (80 is usually used). + PCO2 AaO2 0. Desired PO2 . = 0.4 0.6 x 713) – (42.365 PCO2 = 42.4 PO2 = 109 HCO3 = 24.

**NOTE: In DM Patients.100 Kcal/day 1. we can give as much as 40 Kcal – 60 Kcal per kg Example: 70kg Patient If we use 30 Kcal/kg  Patient will need 2.9g/kg 3. OSTERIZED FEEDING TCR 1800 Kcal/day (for a 60kg patient) o CHO 270g/day o CHON 60g/day Divided into 6 Equal Feeding o Fats Rest 1:1 Dilution III.2) NUTRITION (DIET) I. COMPUTATION OF DIET IN NORMAL PATIENTS (Ambulant. TCR x 0.6 4 1gm / kg The Rest Subtract CHO + CHON from the TCR . we may go down to as much as 0. we can use 0. we give 3 meals + 2 snacks (to avoid Hypoglycemia) o If we want to Up Build Patients (for thin patients). etc) Total Caloric Requirement Ideal Body Weight x 35 Kcal (Kcal/day) CHO (g/day) CHON (g/day) Fats .6g/kg If patient has CKD and is on Dialysis. DM DIET TCR 1800 Kcal/day (for a 60kg patient) o CHO 270g/day o CHON 60g/day 3 Meals. 2 Snacks o Fats Rest No Simple Sugars Low Salt.100 x 0. Carbohydrates: 2. Proteins: 1gm x 70 = 70g/day If patient has CKD. Low Fat Diet Na <2g TC < 200mg Saturate Fats < 7% MUFA > PUFA If CBG >180: give HR 4‟u‟SC If CBG >250: give HR 6‟u‟SC CBG Monitoring pre-meals and at bedtime 12 . Fats REST II.6 315g/day 4 2.

25 times 1. then Increase by 2 units/kg/hr NO Change! Decrease by 3 Units/kg/hr STOP for 1 Hour.5 – 2. then Increase by 4 units/kg/hr 40 Units/kg/Bolus. ACUTE MYOCARDIAL INFARCTION  CKMB should be > 2x elevated (Normal is 16.3 33. the DTRs are usually disrupted II.3 / 37. Example Case: 60kg male with Massive MI o Give 80 „U‟/kg = 4.1. we are giving 1.8 ugtt/min o Monitor PTT and make necessary adjustments C.800 ‘u’ IV Bolus (initial push) o Then.5 times 2. Initial Therapy Warfarin = Monitor PT (INR) o Bolus = 60-80 U/kg Heparin = Monitor PTT o Infusion = 14-18 U/kg/hr aPPT (s) < 40 s 40 – 49 50 – 75 76 – 85 86 – 100 101 – 150 > 150 Bolus (H) 3000 0 0 0 0 0 0 Stop (min) 0 0 0 0 30 60 60 Rate Change (cc/hr) 22 1 No Change -1 -2 -3 -4 Rpt aPTT (hrs) 6 6 Next am Next am 6 6 6 aPTT < 1. therefore.8 cc/hr  10.0 times CHANGE 80 Units/kg/Bolus.5 – 3. therefore.0 times > 3. Atropine Toxicity T > 390C Flushing (-) Sweating Psychosis. HEPARIN DRIP COMPUTATION (Unfractionated Heparin) A. Restlessness III. maintain on Drip: Add 10.3) NOTES ON INHERITED PATIENTS I. ORGANOPHOSPHATE POISONING A.000 Units Heparin with PNSS to make 100cc o Infusion is at 18 „u‟/kg/hr. adjust the Heparin Dose by ADDING 2cc/hr (or 2ugtts/min) to the Baseline Drip D. Signs of GOOD Atropinization Dry Mucosa HR > 60 Hypoactive BS Pupils > 4mm B.25 – 1.5 times 1. then Patient is 33.080 Units per Hour (U/hr) o Give 10. there is 100 „u‟  Therefore.1 = 0. then Decrease by 3 Units/kg/hr B. 32 is already MI)  CKMB / CK Total should be > 5%  MI! IV. Example Case 2: PTT: Control is 37. Deep Vein Thrombosis o DVT Dose = 12 „u‟ UFH BID o DVT Prophylaxis Dose = 5 „u‟ BID 13 . GBS vs HYPOKALEMIC PERIODIC PARALYSIS  In Hypokalemic Periodic Paralysis = INTACT Deep Tendon Reflexes (DTR)  In GBS.9 times Give 80 Units/kg BOLUS Then INCREASE the Dose of heparin being given by 4 Units/kg/hr Computation: 4 x 60kg = 240 Units (therefore. we should ADD 240 units per hour) **NOTE: In 1 cc.

1300 U/h Infusion Rebolus with 5000 U and Increase Infusion by 100 U/h Increase Infusion Rate by 100 U/h No Change Decrease Infusion Rate by 100 U/h Stop Infusion for 30 minutes and Decrease Rate by 100 U/h at Restart Stop Infusion for 60 minutes and Decrease Rate by 200 U/h at Restart **NOTE: LMWH does NOT affect PTT 14 . 1000 U/hr 5000 U SC BID 10.000 U SC BID 10.5-2.5x 1.5x 1. MI 5000 U IV Bolus. 1000-1500 U/h Prophylaxis 5000 U SC q8-12h Acute Myocardial Infarction With Thrombolytic Tx With Mural Thrombus Unstable Angina Prophylaxis General Surgery Orthopedic Surgery Px with CHF.5x 1.5-2.0x 1.000 U SC BID < 1. 1000 U/hr 8000 U SC q8 + Warfarin 5000 U IV Bolus.5x LMWH DOSE AND SCHEDULE 100 U/kg SC BID 100 U/kg SC BID 100 U/kg SC BID 100 U/kg SC BID 100 U/kg SC BID Venous Thrombosis Pulmonary Embolism Treatment 5000 U IV Bolus.ANTICOAGULANT THERAPY WITH LOW-MOLECULAR WEIGHT AND UNFRACTIONATED HEPARIN (from Harrisons) CLINICAL INDICATION HEPARIN DOSE AND SCHEDULE TARGET PTT 2-2.5-2.5x 100 U/kg SC BID before & BID 100 U/kg SC BID before & BID 100 U/kg SC BID PTT at RECHECK Normal (27-35s) < 50s 50 – 60s 60 – 85s 85 – 100s 100 – 120s > 120s INTERVENTION 5000 U Bolus.5x 1.5x < 1.

may use DOUBLE Dose: D5W 90mL + Isoket 20mg in a Soluset  Drip of 5-25 ugtts/min is equivalent to 1-5 mg/hr E. D5W 90mL + Nicardepine 10mg in Soluset Concentration = 0. Omeprazole Drip o 80mg IV Bolus o 40mg + 100cc PNSS to run for 5 Hours (Continuous Drip) H. Electrolytes 1. Nicardepine Drip 1. D5W 250mL + Nicardepine 20mg Concentration = 0. Noradrenaline (LEVOPHED) Drip: 2mg Noradrenaline in 2mL Ampule D5W 250mL + 1 Amp Levophed at 15-60ugtts/min Concentration = 8mcg of Noradrenaline per mL Drip of 2-8mcg Noradrenaline/min is equivalent to 15-60 ugtts/min C.V. NaHCO3 Drip  150mg NaHCO3 + 250cc D5W x 240 2. Glyceryl Trinitrate (PERLINGANIT) Drip: 1mg/mL in 10mL Vials 1.1mg/mL Drip of 10-50ugtts/min is equivalent to 1-5mg/hr Maximum Dose = 15mg/hr NOTE: IV Infusion Site must be changed every 12 hours should a peripheral line be used B. KCl Drip (Correction)  Please incorporate 40 meqs KCl to 1L PNSS to run for 80 x __ Cycles  Repeat K+ Post-Correction J. If with CHF. MgSO4 Drip  2-4mg in 250cc D5W x 120 3.08mg/mL Drip of 15-67ugtts/min is equivalent to 1-5mg/hr OR 2. D5W 90mL + Isoket 10mg in a Soluset  Drip of 10-50 ugtts/min is equivalent to 1-5 mg/hr 2. Hydralazine (Apresoline) Drip D5W 250mL + Apresoline 2 Amps (20mg/amp) at 5-30ugtts/min (up to 60 ugtts/min) Maximum Daily Dose = 3. then 3mg in D5W 250cc x 120 3mg + 500cc PNSS x 42cc/hr (250mg/hr) I. If with CHF. Insulin Drip (Medicine Notes) 15 . NTG Drip o 10mg NTG in enough PNSS to make 100cc in Soluset x 10cc/hr o May increase or decrease by 2cc/hr to achieve Chest Pain-Free State G. Isosorbide Dinitrate (ISOKET) Drip 1. may use DOUBLE Dose: D5W 90mL + Perlinganit 20mg (2 Vials)  Drip of 5-25 ugtts/min is equivalent to 1-5 mg/hr F. OTHER DRIPS (A to E from Blue Book) A. D5W 90mL + Perlinganit 10mg (1 vial) in a Soluset  Drip of 10-50 ugtts/min is equivalent to 1-5 mg/hr 2.5mg/kg body weight per 24 hours D. Somatostatin Drip o 250mg IV Bolus.

0 unit/hr b.2 Unit/Kg IV Push b. Subcutaneous (SC) CBG < 80 80 – 180 181 – 200 201 – 300 > 300 ACTION Discontinue for 30 minutes. For Hyperkalemia (from Blue Book) – Glucose-Insulin Drip a. resume drip at 1 unit/hr. VIRCHOW‟S TRIAD: Encompasses the three broad categories of factors that are thought to contribute to thrombosis  The triad consists of: o Alterations in normal blood flow (Stasis) o Injuries to the vascular endothelium o Alterations in the constitution of blood (Hypercoaguability) VII. Loading Dose  CBG > 200 = 0. 50mL of 50% Dextrose in Water + 10 Units Insulin in 2-5 Minutes  Eg.1 Unit/kg/hr. For Hyperglycemia a.3 unit/hr No Change in Rate Increase Rate by 0. Intravenous (IV) CBG < 70 70 – 120 121 – 180 181 – 240 241 – 300 > 300 ACTION Discontinue for 30 minutes. METABOLIC SYNDROME (SYNDROME X. Heparin o See above discussion VI.6 unit/hr Increase Rate by 1.o o Formulation: Dilute 20 Units of Insulin in 100cc PNSS to concentration of 0. Mix D50-50 mL + 10 Units Humulin-R Slow IV Stat. INSULIN RESISTANCE SYNDROME)  Consists of a constellation of Metabolic Abnormalities that confer in Risk of Cardiovascular Disease and Diabetes Mellitus  Major Features include: NCEP:ATPIII 2001 CRITERIA for Metabolic Syndrome: Three or More of the following: o Central Obesity  Central Obesity: Waist Circumference > 102cm (M). Dobutamine. 500mL of 10% Dextrose + 10 Units Insulin over 30-60 Minutes  If Volume Overload is NOT a problem c.1 Unit/Kg IV Push  CBG > 300 = 0. Dosing Table a. 1000mL of 10% Dextrose + 20 Units Insulin with 1/3 of Solution given in the first 30 Minutes and the remainder over the subsequent 2-3hours 2.125 Unit/Kg IV Push  If DKA = 0. respectively.1 unit/cc) 1. > 88cm (F) o Hypertriglyceridemia  Hypertryglyceridemia: TG > 150mg/dL or specific medication o Low HDL Cholesterol  Low HDL Cholesterol: < 40 mg/dL and 50 mg/dL. re-measure in 30 minutes No Change in Rate Humulin-R 6 Units SC Humulin-R 8 Units SC Humulin-R 10 Units SC K.1 – 0.2 Unit/cc Standard Insulin Concentration is 1 Unit Regular Insulin per 10mL Saline (0. give 15-20mL of D50-50. titrate to desired Blood Glucose 3. give 15-20mL of D50-50. re-measure in 30 mins If > 100. Continue glucose infusion Decrease Rate by 0. Dopamine. or specific medication o Hyperglycemia  Hypertension: BO > 130 systolic or > 85 Diastolic or specific medication o Hypertension  Fasting Glucose > 100 mg/dL or specific medication or previously diagnosed T2DM 16 .3 unit/hr Increase Rate by 0. Maintenance Dose  0.075 – 0. then q6 hours x 3 Doses b.

2 D.2 2.2 B. Acute Respiratory Acidosis ∆HCO3 = 24 + [(∆PCO2 / 10) x 1] +/. Respiratory Acidosis 1. Chronic Respiratory Alkalosis ∆HCO3 = 24 – [(∆PCO2 / 10) x 4] +/. FORMULA A. Metabolic Acidosis Decrease in PCO2 = 40 – (∆HCO3 x 1. Metabolic Alkalosis Increase in PCO2 = 40 + (∆HCO3 x 0.2 2.75) +/. Respiratory Alkalosis 1.25) +/.4) ARTERIAL BLOOD GAS (ABG) Steps in Interpreting ABGs:  1) Check pH and Primary Disturbance  2) Check the Compensatory Mechanism  3) Check for presence of a Mixed Acid-Base Disturbance  4) For Metabolic Acidosis: Compute for Anion Gap (AG)  5) Note if with Good Oxygenation (should be > 90%) I.2 C. Acute Respiratory Alkalosis ∆HCO3 = 24 – [(∆PCO2 / 10) x 2] +/.2 17 . Chronic Respiratory Acidosis ∆HCO3 = 24 + [(∆PCO2 / 10) x 4] +/.

2 of 18.7 mmHg INCREASE in pCO2 for every 1 mEq/L RISE in HCO3 Acute: 1 mEq/L INCREASE in HCO3 for every 10mmHg RISE in pCO2 Chronic 3-5 mEq/L INCREASE in HCO3 for every 10mmHg RISE in pCO2 Decrease in pCO2 Acute: 2 mEq/L DECREASE in HCO3 for every 10mmHg FALL in pCO2 Chronic: 5 mEq/L DECREASE in HCO3 for every 10mmHg FALL in pCO2  Normal Values: pH pCO2 (mmHg) HCO3 (mEq/L) Anion Gap Cl (mEq/L) 7.4 = 264 mEq Deficit = Give half dose as IV Bolus. there should be a 1.2 mmHg DECREASE in pCO2 for every 1 mEq/L FALL in HCI3 0. then the remaining in Drip = Example: Give 100 mEq IV Bolus NOW.2 decreased  pCO2 = 18 decreased  HCO3 = 7 decreased A.25) = 40 – ([24 – 7] x 1.3 40 + 4 24 + 2 12 + 2 105 III. then the remaining 150 mEq as Drip IV. Formula for Metabolic Acidosis: Decrease in pCO2 = 40 – (∆HCO3 x 1.25 Decrease in PCO2 SAMPLE SCENARIO: If the Actual PCO2 is NOT within +/-2:  If pCO2 is 10  there may be Overcompensation.75  COMPENSATED!!!!! This means that for every decrease in HCO3.75 *NOTE: 24 is the desired HCO3. 7 is the actual HCO3 Since the Actual Decrease in PCO2 (18) is within +/. OXYGEN SATURATION > 80 Adequate Oxygenation 60 – 80 Mild Hypoxemia 40 – 60 Moderate Hypoxemia < 40 Severe Hypoxemia 18 . or a COMBINED Metabolic Acidosis AND Respiratory Alkalosis  If pCO2 is 25  UNCOMPENSATED! B. COMPENSATORY MECHANISMS DISORDER Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis  Acute < 2 weeks  Subacute 2-6 weeks  Chronic > 6 weeks Respiratory Alkalosis  Acute  Chronic PRIMARY DISTURBANCE Decrease in HCO3 Increase in HCO3 Increase in pCO2 COMPENSATORY RESPONSE 1.4 + 0. CASE: An 50/M. Compute for Bicarbonate Deficit: HCO3 Deficit = (Desired HCO3 – Actual HCO3) x weight x 0.II. post-intubation  pH = 7.25) = 18. intubated patient had the following ABG results. 60kg.4 = (18 – 7) x 60 kg x 0.

∆ AG >>> ∆ HCO3 INTERPRETATION:  Example: Na 140. Arginine -GI HCO3 Loss (Diarrhea) or Acid Gain -Impaired NH4 Excretion -Distal RTA (Type 1) -Diarrhea -Urinary Tract Obstruction VII. Metabolic Alkalosis – Respiratory Alkalosis  Key: PCO2 does NOT Increase as Predicted. HCO3 18. Metabolic Acidosis – Respiratory Acidosis  Key: High. pH 7. K 4. AG 20 PCO2 38. Normal-Anion Gap Metabolic Acidosis (NAGMA) o Renal o GI Losses Diseases with HAGMA: -Lactic Acidosis -Ketoacidosis  Diabetic  Alcoholic  Starvation -Toxins  Ethylene Glycol  Methanol  Salicylates  Propylene Glycol  Pyroglutamic Acid -Renal Failure (Acute and Chronic) Diseases with NAGMA -Renal HCO3 Loss (Proximal RTA Type 2) -Enhanced NH4 Excretion -Ingestion of HCl. K 3.5. pH is NORMAL INTERPRETATION:  Example: Na 140. HCO3 14. SOME EXAMPLES OF MIXED ACID-BASE DISORDERS FROM HARRISONS: A.0. ∆ Cl . K 3. AG 16 INTERPRETATION: PCO2 38. Mixed Acidosis – Respiratory Alkalosis  Key: High. HCO3 25.or Normal-AG Metabolic Acidosis  Prevailing PCO2 is ABOVE Predicted Value  Example: Na 14. pH 7. HCO3 42. HCO3 10. ANION GAP A.0. ∆ HCO3 . METABOLIC ACIDOSIS A.or Normal-AG Metabolic Acidosis INTERPRETATION:  Prevailing PCO2 BELOW Predicted Value Lactic Acidosis. Metabolic Acidosis – Metabolic Alkalosis  Key: Only detectable with High-AG Acidosis. K 3.0.42 2. NH.55 Liver Disease and Diuretics 4. Lysine. ∆ AG . Cl 88. pH 7. K 4.39 2. pH is HIGHER than Expected  Example: Na 140. AG 20 Uremia with Vomiting PCO2 40. AG 20 PCO2 24. Cl 110.V. Cl 102.42 B. Cl 91.0. Metabolic Acidosis – Metabolic Acidosis INTERPRETATION:  Key: Mixed High-AG – Normal –AG Acidosis. Cl.3 INTERPRETATION: Severe Pneumonia. High Anion Gap Metabolic Acidosis . pH 7. AG 10 COPD on Diuretics PCO2 67. HCO3 33. pH 7. Normal Anion Gap Metabolic Acidosis If: VI. Cl 95. pH 7. AG 15 Tx of DKA PCO2 25. Mixed Metabolic and Respiratory 1. Sepsis in ICU  Example: Na 140. High-Anion Gap Metabolic Acidosis (HAGMA) o Methanol o Uremia o DKA MUDPILES o Paraldehyde o Isoniazid o Lactic Acidosis o Ethanol o Salicylates B. Pulmonary Edema 3.20 19 .0. ∆HCO3 Diarrhea and Lactic Acidosis accounted for by combined change in ∆AG & ∆Cl Toluene Toxicity  Example: Na 135. Cl 106. Mixed Metabolic Disorders 1. K 4. Metabolic Alkalosis – Respiratory Acidosis  Key: PCO2 is HIGHER than Predicted. ∆ HCO3 If: = 1  Pure HAGMA < 1  HAGMA + NAGMA > 1  HAGMA + Metabolic Alkalosis = 1  NAGMA < 1  NAGMA + HAGMA > 1  NAGMA + Metabolic Alkalosis B.

645) 20 . 2008) 1) INTRODUCTION I. |I| + |aVF|  Where: o o o  Avf and I are integers derived by subtracting the Positive Deflection from the Negative Deflection The Avf in the numerator is an Integer. AXIS  Computation of Frontal Axis: Axis = .25 Mv in Limb Leads < 0. > 2mm Chest Leads II. 1500 . EJECTION FRACTION ON ECG Ejection Fraction = (QRS aVr x 2.44 (females) QTc < 0.12 sec QRS Duration 5 – 10 mm (0. # of Big Sq = . QT Actual .11 – 0.20 sec (up to 5 small boxes) PR Interval < 0.ECG TEACHING NOTES (PGH.64) + (Age x 0. # of Small Sq  Important Notes: o o o ST Depression: Ischemia Significant Q-Wave: > 25% of QRS ST Elevation: Infarction Significant ST-Segment Depression: > 1mm Significant ST-Segment Elevation: > 1mm Limb Leads. 300 .0 Mv) T Wave < 0.12 – 0. NORMAL VALUES < 0.48 (males)  Formula of Corrected QT-Interval (QTc) Corrected QT Interval = . then adjust the Axis by adding | 90 | Interpretation: Right Axis Deviation (RAD) Left Axis Deviation (LAD) Normal Axis Extreme Axis Deviation Read As: > 1000 < -300 -300 to 1000 -900 to 1800 III.1 Mv Terminal Negative Deflection in V1 0. NORMAL ECG Regular Sinus Rhythm (RSR) Normal Axis (NA) Within Normal Limits IV. √ R-R Interval  Computation of Heart Rate Rate = .12 sec P-Wave < 0. 90 x aVF . while the I and Avf in the Denominator are absolute values of integers If I is a Negative Integer.5 – 1.

Avf) PLUS LAE (Terminal Segment Of P-Wave > 1 Small Box (0. POOR R-WAVE PROGRESSION  In Leads V1-V3 (R-Wave < 3mm or 0.25Mv) in any of Lead II. Especially Lead II > 3mm (>0.5Mv)  read as To Consider Ischemia  ST-Segment Depression > 1mm (> 1Mv) in 2 or more contiguous leads  read as Ischemia **NOTE: Significant ST-Segment Depression > 1mm in at least 2 contiguous leads (Horizontal or Downsloping) III.12sec) 21 .5mm Amplitude (0. III or Avf P-Wave Widened > 3mm (> 0. ISCHEMIA  T-Wave Inversion > 5mm (> 0.12sec) especially Lead II. NON-SPECIFIC ST-T WAVE CHANGES  T-Wave Inversion < 5mm (< 0. III.2) SOME COMMON FINDINGS I.04 Sec) In V1 Or Widened PWave. OR Terminal Segment of P-Wave in V1 > 1 small box (>0.3Mv) AND Normal R-Wave in V4-V6  Do NOT Read as Poor R-Wave Progression in the following conditions: o Left Ventricular Hypertrophy o Left Bundle Branch Block o Wolff-Parkinson-White Rhythm o Anteroseptal Wall MI o Low-Voltage QRS Complexes **NOTE: NO Clinical Relevance: Do NOT Write: o Early transition / counterclockwise rotation o Persistent S V5-V6 or Persistent Posterobasal Forces IV.1 Mv)  Flattening of ST Segment without the presence of U-Waves **NOTE: Mention leads where ST-Segment changes and T-Wave inversions occur II.04 sec OR 0.5Mv)  ST Segment Depression < 1mm (< 0.5mm In Leads II. ATRIAL ENLARGEMENT Right Atrial Enlargement Left Atrial Enlargement P-Wave with 2.1Mv depth) Do NOT include Notching in Lead II as Criterion Bi-Atrial Enlargement RAE (Tall P-Waves > 2.

OR  Avl > 11mm **IMPORTANT Notes:  Cut-Off for LVH. Right Ventricular Hypertrophy RAD + R/S Ratio > 1 in V1 + R/S Ratio < 1 in V6 o o RAD is a Prerequisite Criterion for RVH An Upright V1 or Prominent R in V1 without RAD will NOT be signed out as RVH and need not be described D.0Mv) in Chest Leads Read as Low Voltage Complexes in Limb OR Chest Leads 22 .5Mv) VI. Sokolow-Lyon Criteria  [S in V1] + [R in V5 or V6] is Greater than 35mm (do NOT use S in V2).5Mv) in Limb Leads < 10mm (1. LOW VOLTAGE COMPLEXES  Chest Leads are more significant  QRS Complexes < 5mm (0. VENTRICULAR ENLARGEMENT A.V. Cornell Criteria  S in V3 + R in AvL  Female > 20mm  Male > 28mm B. Left Ventricular Hypertrophy 1. Left Ventricular Strain LVH by Voltage Criteria + Significant Asymmetric ST-Segment Depression with Broad-Inverted T-Wave Read as LVH with Strain. regardless of Age > 35mm  No need to Indicate “By Voltage” 2. Biventricular Hypertrophy Hypertrophy in presence of BBB: RAD + rsR Pattern in V1 (R-Wave Amplitude > 15mm or 1. Cannot Rule Out Concomitant Ischemia C.

Digitalis Effect o Seen in patients without Significant ECG Changes due to Organic Disease o Should describe Drug Effects in leads seen o Read as Scooping of ST-Segment Depression. Hyperkalemia o At least > 2 Contiguous Leads with Peaked T-Waves > 10mm (1.47 **NOTE: Use the Lead with the longest Absolute QT Interval without Prominent Q-Wave OR Largest Amplitude T-Wave A.0Mv) o Read as Peaked T-Waves. probably Digitalis Effect B. ELECTROLYTE ABNORMALITIES  Low Sensitivity of „U‟ Wave  „U‟ Wave Prominent + Normal T-Wave  Read as Prominent „U‟ Wave  Prominent „U‟ Wave + Flattened T-Wave  Read as T/C Hypokalemia  ST-Segment Depression + „U‟ Wave + Normal T-Wave  Read as Cannot R/O Ischemia.48 o Normal Value: Male < 0. Timing of MI Acute Significant ST-Elevation + T-Wave Inversion +/. NOT meeting the Criteria for LBBB or RBBB  LAFB  LPFB  Bifasicular Block  Trifasicular Block III.3) ABNORMAL ECG FINDINGS I. Prominent U Wave  Flattened T-Waves + Normal QRS-Complex  Read as Non-Specific ST-T Wave Changes QTc Computed to Adjust for Bradycardia (HR < 60bpm) or Tachycardia (HR > 100bpm) o Normal Value: Female < 0. BUNDLE BRANCH BLOCKS AND INTRAVENTRICULAR CONDUCTION DEFECT  LBBB  RBBB  Non-Specific Intraventricular Conduction Delay: Widened QRS without Repolarization changes.Q-Waves Old Significant Q-Wave + Isoelectric ST Segment + Upright T-Wave Age Undetermined ST-T Wave Change +/.Q-Wave not fulfilled by Criteria for Old and Acute MI B. EARLY REPOLARIZATION CHANGES  Embryonic R + ST-Elevation NOT fulfilling criteria for ST-Elevation in MI  Check morphology of ST-Segment if more convex rather than concave II. Non-Specific ST-T Wave Changes. MYOCARDIAL INFARCTION A. Definitions Significant ST-Segment Elevation > 1mm Limb Leads > 2mm Chest Leads 23 . T/C Hyperkalemia IV.

V4R RV Wall V. Avf Inferior Wall I. III.Significant Q-Wave C. Avf > 25% of the QRS Complex. INTERPRETING ECGs (Rounds) A. ST Elevation / Depression o ST Elevation = at least 2 small boxes in contiguous leads o ST Depression = at least 1 small box E. AvF Inferolateral Wall Almost All Leads Diffuse / Global / Massive Mirror Image V1. T-Waves o Peaked T-Waves = 10 boxes in chest leads. V2 Septal Wall V3. V4 Anterior Wall V5. 5 boxes in limb leads o If Inverted T-Waves = CANNOT rule out ischemia 24 . II. III.04 sec MYOCARDIAL WALL INVOLVED Posterior Septal Anteroseptal Anterior Lateral Anterolateral Massive Anterolateral Inferior D.2msec) Secondary AV Block I: There is prolonging PR-Interval. then Drop Beat Tertiary AV Block With AV dissociation (look for P-waves. or > 0. V6. Avl High Lateral V1. V6 Lateral Wall V1 – V3 Anteroseptal Wall V3 – V6. III. I. Q-Waves o 20% of R. Walls of Involvement LEADS V1 V1-V2 V1-V3 or V1-V4 V3-V4 V5-V6 V3-V6 V1-V6 II. Correspondence of Specific ECG Leads (from Medicine Notes) LEADS CORRESPONDING LV AREAS II. look for Q waves  DISSOCIATED!) The PR and QRS Waves are Independent from each other B.08 – 0. AV Block Primary AV Block Prolonged PR interval (More than 5 small squares or more than 0. AvL Anterolateral Wall V5. there is usually a Q-Wave C. Wide  OLD Infarct! o In aVr. V2 Posterior LV Wall V3R.12 o If Wider = Bundle Branch Block D. then Drop Beat II: There is a Regular PR-Interval. QRS o Normal = 0.

Indications for Permanent Pacemaker Insertion (Pacing) o Permanent Pacemaker Insertion should be implanted in the following conditions (Class-I Indications) 1. Classification Based on SYMPTOMS 1. Dyspnea. Some VT is associated with Reasonable Cardiac Output and may even be Asymptomatic  The heart usually tolerates this rhythm poorly in the medium to long term. Polymorphic Ventricular Tachycardia  Has beat-to-beat variations in morphology  This most commonly appears as a cyclical progressive change in cardiac axis referred to by its French eponym Torsades de Pointes (literally twisting of the points).  In some patients. hence. Digoxin for Tachycardia-Bradycardia Syndrome 4. Chest Pain 25 . Sustained Ventricular Tachycardia  If the rhythm lasts more than 30 seconds it is known as a sustained ventricular tachycardia (even if it terminates on its own after 30 seconds) C.VI. Monomorphic Ventricular Tachycardia  Means that the appearance of all the beats match each other in each lead of a surface electrocardiogram (ECG) 2. Sinus Node Dysfunction with Symptomatic Bradycardia. Ventricular Tachycardia can be classified based on its MORPHOLOGY: 1. this is due to Long-Term Essential Drug Therapy for which there are NO Acceptable Alternatives Eg. Carotid Sinus Stimulation causing Recurrent Syncope or Asystole > 3 seconds in the absence of any medication that depresses the Sinus Node or AV Conduction B. Pulseless VT  Associated with NO effective cardiac output. Complete Heart Block with:  (+) Symptoms due to the AV Block (eg. no effective pulse. with Symptomatic Bradycadia 3. B. and patients may certainly deteriorate to Pulseless VT or to VF VII. Heart Failure)  Asystole > 3 seconds by Holter Monitoring even if without symptoms  HR < 40 bpm even without symptoms (any escape rhythm < 40 bpm) 2. Syncope. Second Degree AV Block. three or more beats in a row on an ECG that originate from the ventricle at a rate of more than 100 beats per minute constitute a ventricular tachycardia 1. Permanent or Intermittent. VENTRICULAR TACHYCARDIA A. WOF: Pacemaker Syndrome o Neck vein engorgement. PACEMAKER A. Non-Sustained Ventricular Tachycardia  If the fast rhythm self-terminates within 30 seconds. Classification Based on Duration of the Episodes: o Technically. it is considered a non-sustained ventricular tachycardia 2. Dizziness. and is a cause of cardiac arrest  In this circumstance it is best treated the same way as ventricular fibrillation (VF) and is recognized as one of the shockable rhythms on the cardiac arrest protocol 2.

when T-Wave Inversion appears. ST-Segment Elevation disappears IX. OTHER NOTES (during rounds): A. ST Elevation in Pericarditis is Different from MI: In Myocardial Infarction. ECG of Pericarditis B. ECG FINDINGS OF PERICARDITIS  Diffuse ST-Segment Elevations = Concave Diffuse ST-Segment Elevation A.o This occurs when Atrium pumps against a Closed Mitral Valve  due to “Asynchronization” VIII.04 seconds (or 1 small box) duration 26 . it is CONVEX o In MI = ST-Segment Elevation WITH T-Wave Inversion o Difference = In Pericarditis. ECG Findings of Mitral Stenosis o LA-Enlargement = WIDE P-Wave o RAD o RVH B. Significant Q-Waves o 1) Q-Wave > 25% of R-Wave o 2) Q-Wave is > 0.

PSV    Usually initiated at a level adequate for full ventilator support (PSVMax) ie.5 and PEEP < 5cmH2O B. and Vital Capacity  Weaning Index: Ratio of Breathing Frequency to Tidal Volume (breaths per minute per liter). Inspiratory Pressure. Tidal Volume. Cooperative  PaCO2 > 60mmHg with FiO2 < 50%  PEEP < 5cm  PaCO2 and pH Acceptable  Spontaneous TV > 5mL  VC > 10mL/kg  MIP > 25cmH2O  RR < 30/min  Rapid Shallow Breathing Index (RBI) < 100  Stable Vital Signs following a 1-2 hour Spontaneous Breathing Trial A. and an SaO 2 > 90% can be achieved with an FiO2 < 0. Approaches to Weaning o o T-Piece and CPAP Weaning are best tolerated by patients who have undergone MV for brief periods and require little respiratory muscle reconditioning SIMV and PSV are best for patients intubated for extended periods likely to require gradual respiratory-muscle reconditioning 1. Alert.40. Weaning Index  Respiratory Drive and chest wall function are assessed by observation of RR.35 to 7. is both sensitive and specific for predicting the likelihood of successful extubation  If Ratio < 105 with patient breathing without mechanical assistance through an ET Tube. WEANING FROM MECHANICAL VENTILATION Indications for WEANING:  Mental Status: Awake. SIMV  Involves gradual tapering the mandatory backup rate in increments of 2 to 4 breaths per minute while monitoring blood gas parameters and respiratory rates  Rates > 25 / min on withdrawal of mandatory ventilator breaths generally indicate Respiratory Muscle Fatigue and the need to combine periods of exercise with rest  Exercise periods are gradually increased until a patient remains stable on SIMV at < 4 breaths per minute  A CPAP or T-Piece Trial can then be attempted before extubation 3. T-Piece and CPAP  Brief spontaneous breathing trials with supplemental O2  Initiated for 5mins/hour followed by a 1-h interval of rest  Trials are increased in 5 to 10 minutes/hour increments until patient can remain ventilator independent for periods of several hours  Extubation can then be attempted 2. intermittent periods of higher pressure support are alternated with periods of lower-pressure support to provide muscle reconditioning while avoiding diaphragmatic fatigue Gradual withdrawal of PSV continues until the level of support is just adequate to overcome the reistance of the ET Tube (~5 to 10cmH2O) 27 . Upper Airway Function must be Intact for a patient to remain extubated  If a patient can breathe on his own through an ET Tube but develops stridor or recurrent aspiration once tube is removed. Alveolar Ventilation is deemed adequate when:  Elimination of CO2 is sufficient to maintain arterial pH in the range of 7. successful extubation is likely 3. PSV is set slightly below the peak inspiratory pressures required by the patient during volume-cycled ventilation Level of pressure support is then gradually withdrawn in increments of 3-5cmH2O until a level is reached at which the RR increases to 25 breaths/min – At this point. Upper Airway Dysfunction or an abnormal swallowing mechanism should be suspected 2.MECHANICAL VENTILATION 1) BASIC INFORMATION I. Removal of Mechanical Ventilator support requires that a number of criteria be met 1.

ASSIST CONTROL MODE (Medicine Notes)  Each breath is assisted by the vent even if the RR exceeds the BUR  Parameters: VT.35 III. If the Following are Present. PFR/IFR. FiO2 – Start at 100% o If lungs are NORMAL (eg. Back Up Rate o 16-20 D. BUR.5mL/kg  O2 via Nasal Prong = # lpm x 0. the more work patient does) o Flow: Usually 2L 28 . Tidal Volume o o General: 8-10 mL/kg In ARDS: 6 mL/kg B. PEEP.4 + 20  VC < 10-15mL/kg  Inspiratory Force < 25cmH2O  FEV < 10mL/kg The primary indication for initiation of mechanical ventilation is Respiratory Failure. Sensitivity (Trigger) – 2 L o Pressure: (-) 1. start at 50% o DECREASED to tolerable % as fast as possible (doesn‟t have to be decreased by 10%) o Non-Toxic FiO2 = 50% (Golden Time to reach this is 4 hours) F. PEEP: o 5cm H2O C. Trauma patient). the ratio of the Respiratory Rate and Tidal Volume in Liters (f/V T) is < 105. Apnea  RR > 35  PaCO2 > 50 NOTES on FiO2:  PaO2 < 60  FiO2 at Room Air = 21%  TV < 3.0 cmH2O (the more negative. FiO2. Support can be discontinued and the patient extubated II.5 to 2. Sensitivity Flow Pattern A. Patient has passed the Screening Test and should undergo Spontaneous Breathing Trial o Stable Oxygenation (PaO2/FIO2 > 200) and PEEP < 5cmH2O o Cough and airway reflexes are intact o No Vasopressor Agents or Sedatives are being administered B. the patient can be EXTUBATED IV. Peak Flow Rate: o 40-60 mL o Asthma / COPD: Increase to allow more time to exhale o ARDS: Decrease to Prevent further injury E. SPONTANEOUS BREATHING TRIAL (Harrisons)  Consists of a Period of breathing through the Endotracheal Tube WITHOUT Ventilator Support (both Continuous Positive Airway Pressure [CPAP] of 5cmH2O & an Open T-Piece Breathing System can be used) for 30-120 mins A. Spontaneous Breathing Trial is Declared a FAILURE and STOPPED if any of the following occur: o 1) RR > 35/min for > 5mins o 2) O2 Saturation < 90% o 3) HR > 140/min or a 20% Increase or Decrease from Baseline o 4) Systolic BP < 90mmHg or > 180mmHg o 5) Increased Anxiety ot Diaphoresis If at the end of the Spontaneous Breathing Trial. of which there are 2 basic types:  VQ/VT > 0.6  Hypoxemic Respiratory Failure  To deliver High FiO2  Hypercarbic Respiratory Failure  Absent Gag  pH < 7. INDICATIONS FOR INTUBATION (Medicine Notes)  Impending Respiratory Failure.

G. Sensitivity is generally set so that an Inspiratory Effort of 2cmH2O will trigger the Ventilation Since there is almost NO work involved by the Respiratory Muscles.Divinagracia Lecture) Indications for Mechanical Ventilation: 1. Muscle Atrophy starts within 6 hours 29 . ASSIST / CONTROL MODE (A/C MODE)  The Patient breathes at his OWN Rate and the Ventilator senses the Inspiratory Effort and delivers a Preset Tidal Volume with EACH patient effort  If patient‟s Respiratory Rate decreases past a Preset Rate. Worsening Physiological Parameters  Are of limited use since patients with Respiratory Insufficiency are unable to perform PFTs and their Respiratory Failure mandates immediate intervention  However in some cases especially in Neuromuscular Diseases. Muscle Tone is NOT well Maintained (Atrophy). the Ventilator delivers Tidal Breaths at the Preset Rate  EVERY BREATH is assisted A. Arterial Blood Gases (ABG)  Severe Hypoxemia (PO2 < 50) despite High-Flow Oxygen  Significant CO2 Retention (PCO2 > 50) 3. Advantages and Disadvantages ADVANTAGES Useful in Patients with Neuromuscular Weakness or CNS Disturbances The INITIAL Mode usually set upon advent of Mechanical Ventilation It totally Unloads (“rests”) the Respiratory Muscles requiring NO “Work” on the Patient‟s part DISADVANTAGES Tachypnea may result in Significant Hypocapnea and Respiratory Alkalosis Improper setting of Sensitivity to trigger the Ventilator may result in “fighting the ventilator” when sensitivity is set too low Increases Sensitivity may result in Hyperventilation. Flow Pattern: o Square Wave 2) BASIC MODES OF VENTILATION (Mech-Vent Work Shop: Dr. Clinical Assessment  Presence of Apnea. these parameters can be used as “warnings” that the patient will go into Respiratory Failure sooner rather than later: o 1) Vital Capacity < 15mL/kg o 2) Inspiratory Force < -25cm H2O o 3) FEV1 <10mL/kg TWO Main Modes of Ventilation:  Volume Cycled / Controlled: we set the Tidal Volume (ex. AC Mode)  Pressure Controlled Ventilation: we set the Peak Airway Pressure (Favorable in ARDS) I. Tachypnea (>40/min)  Respiratory Failure that cannot be corrected by any other means 2.

Square Wave  This provides a maximum peak flow throughout the Inspiratory Period  Fast Delivery  patients prefer it (but has higher pressures) c.22 2) Back-Up Rate: Number of Tidal Breaths Delivered per Min    Minimum number of breaths per minute Usually set 2 to 4 below the Spontaneous Rate and then the Effect on the patient of Decreasing Rate is noted (this can be adjusted depending on the desired PaCO2 or pH Ex) If set at 8.B. Sine Wave:  The maximum flow is at Mid Inspiration and resembles a Normal Spontaneous Tidal Breathing b. deliver the air SLOWER (so that Inspiration Time is Longer  more time to exchange  PO2 40-60 L/minute 5) Inspiratory Flow Pattern (IFP)  Square Wave  How do you deliver the Air? This is how flow is distributed throughout the Respiratory Cycle Normal Person: Sine Wave Wave Forms usually Available: a. Decelerating Wave  The flow is maximal at the Start and diminishes as Inspiration ends 6) PEEP   “Physiologic PEEP” of about 5cm H2O should be added regardless of FiO2 to prevent the Alveolar Injury due to the Shearing Effect of opening and closing the Alveoli Pressure at End Expiration (it is Positive) 5cm H2O 30 . Selection of Ventilator Settings for A/C Mode SETTING 1) Tidal Volume (VT)  How much volume will the Machine Deliver? USUAL VALUE 8-10 mL/kg of Ideal Body Weight 6mL/kg for ALI/ARDS 10-15mL/kg for Neuromuscular Dse 16 . patient will NOT breath below RR < 8 Faster RR =  Blow of CO2  PaCO2 and pH   3) Oxygen Concentration (FiO2)       Initial FiO2 should be 100% unless it is evident that a Lower FiO2 will provide adequate oxygenation We can start at 50% if Neuromuscular Disease (ex. MG) 100% 4) Inspiratory Flow Rate (IFR) How fast do we deliver the air? 60L/minute is FASTER than 40L/minute (Higher Flow Rates  Higher Peak Pressure) This is the Rate air is delivered to the patient to achieve the Tidal Volume set Rate needs to be HIGHER (80L/min) in COPD & Asthma An IFR LOWER than the patient demand will Increase the work of breathing and is a common cause of Patient-Ventilator Discordance (Fighting or Bucking the Ventilator) In Patients with Hypoxemia.

5cmH2O (Pressure Sensitivity) or 1 to 5 Liters (Flow Sensitivity) The MORE Sensitive (eg. Flow Sensitivity  Ex) If set at 1L. adjust to 1:3 o In ARDS. Should be Increased in ARDS -2. adjust to 1:1 o Ex) In COPD. Pressure Sensitivity  Ex) If set at –1.5cm or 1L). we Increase the IFR so that the IE Ratio will be 1:3 31 . 5cm or 5L). the patient has to exert a –1cmHg Pressure for the Vent to Deliver the Tidal Volume b. patient has to create a negative pressure  Advantage: Patients with COPD (difficult to empty lungs)  they will have LESS work  Sensitivity in PGH Mechanical Ventilators: o Turn knob Counterclockwise  becomes Less Sensitive o Turn know Clockwise  becomes More Sensitive  I:E Ratio: o Normal is 1:2 o In COPD.0cm or 2L Different for PGH Vents 7) Sensitivity   Ranges anywhere from –5 to –0. 0. the EASIER for the patient to Trigger the Ventilator which may lead to Hyperventilation The LESS Sensitive (eg. the HARDER for the patient to trigger the Ventilator which may lead to Increased Work of breathing and thus can cause Patient-Ventilator Desynchrony  a.

IFP. in AC Mode  ALL 20 will be Assisted A. with the Ventilator breath being timed or synchronized to patient effort o The Mechanical Ventilator breaths are limited to a preset number  Additional patient effort leads to Spontaneous Breaths made through a separate fresh gas system  Allows patient to take as many spontaneous breaths as he chooses around the Intermittent Synchronized Ventilator Breaths  The patient‟s contribution to Minute Ventilation depends on the number of Spontaneous Breaths and Inspiratory Effort Sample Case: SIMV Mode. BUR set at 12. FiO2. there is MORE WORK of Breathing The Increased Work of breathing results in Increased Oxygen Consumption which is deleterious in patients with Myocardial Insufficiency This mode is NOT useful in patients with Depressed Respiratory Drive or Impaired Neurologic Status B. Patients actual RR is 20  ONLY the 12 of 20 Breaths are Assisted in SIMV o 12 will Receive the COMPLETE TV set o 8 will Receive the TV. the patient gradually assumes the Bulk of Breathing DISADVANTAGES Even with the same Back-Up Rate as the A/C. SYNCHRONIZED INTERMITTENT MANDATORY VENTILATION (SIMV)  There are two separate circuits for contribution of Minute Ventilation o One circuit delivers Ventilator Breaths in a manned identical to A/C. A/C Mode VS SIMV: Assist Work of Breathing Can be Used for Weaning A/C MODE Total Almost NONE NO SIMV MODE Partial Variable YES III. PEEP  SAME of that in A/C C. IFR. RECENT MODALITIES OF MECHANICAL VENTILATION  1) Pressure Limited Ventilation o Pressure Support Ventilation (PSV) o Pressure Controlled Ventilation (PCV)  2) Combination of Volume-Cycled and Pressure-Limited Ventilation o SIMV with PSV  3) Inverse Ratio Ventilation o PCV with Inverse Ratio o A/C with Very Low Flow Rates 32 . Selection of Ventilator Settings for the SIMV Mode o Rate: Initial Rate should be Close to the Patient‟s Rate and then the Rate Decreased noting the effect on Patient Acceptance o VT. Advantages and Disadvantages ADVANTAGES Maintains Respiratory Muscle tone due to the continued use of the Inspiratory Muscles and thus prevents Disuse Atrophy There is Decreased Intrathoracic Pressure as compared to A/C which may lead to improved Hemodynamics Useful for WEANING because as the Back-Up Rate is Decreased.II. depending on the Patient‟s efforts  In CONTRAST.

21 PH2O = 47 PBREATH = 760 PaCO2 = Measured by Labs R = 0. PAO2-PaO2 Gradient PAO2 = FiO2 (Patm – PH2O) – (PaCO2 / R) Normal PAO2-PaO2 Gradient = 10 Increases by 5-6 per decade over 50 At Sea Level: FiO2 = 0. Desired FiO2 Desired FiO2 = (PaO2 Desired x FiO2 Known) PaO2 Known C. RESPIRATORY MONITORING  Gas Exchange o Carbon Dioxide and Ventilation o Oxygen  Lung and Chest Wall Mechanics o Pressure-Volume Relationships o Mean Airway Pressure o Auto-PEEP Effort  Breathing Effort  Ventilatory Drive and Breathing Pattern  Strength and Muscle Reserve II.3) OTHER NOTES IN MECHANICAL VENTILATION I. SOME FORMULAS: A. WEANING PARAMETERS AND STRATEGIES  Weaning: process of abruptly or gradually withdrawing Ventilatory Support when the cause of the Respiratory Failure is under resolution A. Weaning is NOT Synonymous with Extubation o Need for Mechanical Ventilation is NOT the same as the Need for Artificial Airway o Weaning Failure: inability to maintain adequate Respiration THROUGH an Artificial Airway o Extubation Failure: inability to maintain adequate Respiration AFTER removal of Artificial Airway Example: Desired FiO2 = 80 x 21% 50 33 . When should Weaning be Initiated? o Liberation from MV in the EARLIEST possible time without compromising the patient‟s safety and recovery is of prime importance to minimize the complications associated with MV and Intubation  Weaning: Shifting breathing workload from Machine to Patient  Spontaneous Breathing Trials: Testing the patient‟s ability to breath independently B. Minute Ventilation Minute Ventilation = Kg x 100 RR III.8 B.

Stable BP. Objective Measurements  Adequate Oxygenation  Stable Cardiovascular System (HR < 140.35  PaO2/FiO2 Ratio > 200  Normal PCO2 or back to Baseline for Chronic retainers with Normal pH 4. Pulmonary Gas Exchange  Minimal PO2 > 60mmHg with:  FiO2 < 0. Subjective Clinical Assessment  Resolution of Disease Acute Phase  M. Methods of Weaning: o T-Piece Weaning (abrupt and simple) o SIMV o Pressure Support Ventilation o Noninvasive Ventilation 34 . No (or Minimal Pressors)  Afebrile (T <380C)  No significant Respiratory Acidosis  Adequate Hemoglobin (Hgb > 8-10g/dL)  Adequate Mentation (arousable. Rapid Shallow Breathing Index (RSBI)  Overall has the BEST Combination of Sensitivity and Specificity among Weaning Indices  Threshold Value >105 RSBI = f (per minute) / VT (in Liters) D. believes Discontinuation possible  Adequate Cough 3.D. no continuous sedative infusion)  Stable Metabolic Status 2. Conditions which SHOULD be Met for Weaning o Resolution or Improvement of the cause of Respiratory Failure o Cessation of Sedative Drugs o Cessation of Neuromuscular Blocking Agents o Absence of Sepsis or marked Fever o Stable Cardiovascular Status o Correction of Electrolyte Disorders o Correction of Metabolic Disorders o No planned General Anesthesia o Adequate Gas Exchange o Adequate Respiratory Pump Capacity 1.C.4 with a PEEP level < 5cmH2O  PaO2/PAO2 > 0. GCS > 13.

an FiO2 of 100% can be used for up to 24 hours WITHOUT significant Lung Injury 35 .IV. OXYGEN DELIVERY  Low Flow: Nasal Cannula.5 for 2-7 days usually does NOT result in Toxicity  If needed. Nasal Cannula o FiO2 Increases approximately 2-4% / L o Flowrates >6 lpm do NOT augment the inspired gas o High Flows can dry the Nasal Mucosa o Humidification is recommended for Flow Rates > 4 lpm o Provides 23-45% of O2 o Maximum Flow Rates = 6 lpm B. Post Operative A. Face Mask. Simple Masks o Provides 31-61% O2 o Flow Rates = between 5-10 lpm o The reservoir is the space between the mask and the patient‟s face o Higher Potential FiO2 o Less than 5 lpm is NOT recommended o 5 lpm is needed to flush exhaled CO2 from the Mask V. OXYGEN TOXICITY  Injury to the Lung Parenchyma and Airway epithelium due to Cytotoxic Free Oxygen Radicals  Gas exchange abnormalities occur in 24-48 hours with 100% oxygen  FiO2 up to 0. Reservoir Mask  Indications: o PaO2 < 60mmHg or SaO2 < 90% o Acute Situation where Hypoxemia is suspected o Severe Trauma o Acute Myocardial Infarction o Short Term.

0-18.3-1.3 g/dL 3.42-1.022 4.0 mg/L 19-60 ug/dL < 20 IU/mL 75-110 mg/dL 7-20 mg/dL 0.4 ng/mL 0-0.06 0. fine.8-2.7 0.4-5.6-5.02 0 0. coarse.015 4-11 x 103/mm3 4-6 x 106/mm3 12.3-4.1-3.5 (-) 0/0-2/hpf 0-2/0-5/hpf hyaline.6-5.42-5.1 g/24hour 80-216 mmol/L 25-100 mmol/L 80-340 mmol/L 4. Albumin 7.370-0.02-0.LABORATORY WORK UPS AND ANTIBIOTICS 1) NORMAL LABORATORY VALUES (PGH VALUES) CBC Values WBC RBC Hgb Hct MCV MCH MCHC RDW-CV Platelets Neut% Lymph% Mono% Eo% Baso% Pro/Mye/Jv Stabs Blasts Reticulocytes 4-11x109/L 4-6 x 1012/L 120-180 g/L 0.2-0.2 pg/dL TSH 0.70-1.44 mmol/L 30-110 U/L 23-300 U/L 100-190 U/L M: 0-15 mm/h 0.2 mEq/L 100-108 mEq/L 8.9-6.30 microunits/mL Serum T3 70-200 ng//dL Serum T4 4.2-5.56 mmol/L 1.5.4 ug/L Small amounts Small amounts (-) Small amounts 0.52 mmol/L 0.41-2.0113  to convert to mg/dL  24 Urine Chemistry Total volume Creatinine Total protein Na+ K+ ClUric acid Ca++ 500-2000 cc 0.2-0.5-7.97 64-83 g/L 34-50 g/L 23-35 g/L 15-37 U/L 30-65 U/L 36-92 umol/L 0-17.25-4.0 ng/dL Free T3 2.3 mg/dL 0.2 mmol/L 100-108 mmol/L 2.65-0.0-0.0g/dL BLOOD CHEM Glucose BUN Creatinine Sodium Potassium Chloride Calcium Magnesium Phosphates Total protein Albumin Globulin AST (SGOT) ALT (SGPT) Alk phos Total bilirubin Dir bilirubin Ind bilirubin Urate Amylase Lipase LDH ESR CRP Ammonia RF Cardiac Enzymes CK-total CK-MB CK-MM Troponin I Cut Off for MI Lipid Profile HDL LDL Cholesterol Triglycerides  150-450 x 103/mm3 Thyroid Hormones Free T4 0.0 g/dL 0.540 % 80-100 fL 27-31 pg 320-360 g/L 11-16% 150-450 x 109/L 0.2 mmol/L 0.3 mg/dL 6.13-0.45 35-45 mmHg 90-100 mmHg 22-28 mEq/L 3.02-0. granular.5-2.1 mmol/L 2.0-0.7 umol/L 0.09 ng/mL > 0.37 mmol/L 35-60 mg/dL 40-145 mg/dL 160-200 mg/dL < 180 mg/dL HDL or LDL divided by 0.3 ng/mL 140-148 mEq/L 3.7-10.6-6.09 0.2 mg/dL 1.5 0.55/0.91-1.09 ug/L > 0.6-6.1 umol/L 0 .35-7.5-0. waxy 55-170 U/L 0-16 U/L 8-97 U/L 0-0.005-0.9 mg/dL F: 0-20 mm/h 11-35 umol/L RBC WBC Casts Crystals Epith cells Bacteria Mucus thr Yellow Clear/hazy 1.4 mg/dL 0.4 mmol/L 53-115 umol/L 140-148 mmol/L 3.6 – 1.4-8.1-0.00 mmol/L 0.2-3.0-11.4-13.016-1.70 g/L 0-0.00 umol/L 3.9 mmol/24hr 2.5 mmol/24hr 8.5 ng/L 0-4 ng/mL 0-35 U/mL 0-37 U/mL (-)Smoker: 0-3 ug/L (+)Smoker: 0-5 ug/L 36 .8-14 mmol/d < 100mg/d Varies with intake Cancer Markers AFP PSA CA 125 CA 19-9 CEA 0-8.0259  to convert to mg/dL TAG divided by 0.0 ug/dL ABG pH PCO2 PO2 HCO3 Urinalysis Color Transparency SG PH Sugar.12-2.8 mmol/L 4.9-1.04 0 0.

4-33.Phosphorus Amylase Microalbumin 22.25 U/L N: 0.03 g/d Microalbuminuria: 0.6 mmol/24hr 64.75-490.0-0.03-0.30 g/d Clinical Albuminuria: >0.3g/d 37 .

Give very slowly as IV infusion Alternate to Aminoglycosides in renal failure Use as reserve drug Gm (+) activity as good as Penicillin For Gm (-): may add Amikacin for Synergism Anaerobic activity as good as Metronidazole Very little activity against pseudomonas May cause GI upset ++ + ++ 1/2 ++ 1/2 + + +++ +++ +++ +++ ++ ++ 1/2 ++ 1/2 +++ + 1/2 ++ + + + 1/2 ++ ++ + For patients > 8 years old Tetracycline is cheaper. but given QID With Anti-Pseudomonas activity Amikacin with Anti-TB action + +++ - +++ + - ++ 1/2 ++ 1/2 ++ ++ ++ ++ +++ ++ ++ ++ +++ +++ +++ +++ + + ++ 1/2 ++ ++ ++ ++ IV drug Oral drug Cephalosporin with best Anaerobic coverage For multidrug resistant Typhoid Ceftazidime is best for Pseudomonas Cefotaxime is best for Meningitis These should be reserved for the very resistant strains 38 .aureus and Enterococcus.2) CLINICALLY USEFUL ANTIBIOTICS (from the Blue Book) DRUG Penicillins Penicillin Oxacillin PO/IV Flucloxacillin Amoxicillin PO. Ampicillin IV Co-Amoxiclav Ampi-Sulbactam Piperacillin / Tazobactam Glycopeptide Vancomycin Monobactams Aztreonam Carbapenems Imipenem-Cilastin Meropenem Ertapenem Macrolides Erythromycin Azithromycin Clarithromycin Dirithromycin Tetracycline Doxycycline Tetracycline Aminoglycosides Amikacin Gentamicin Tobramycin Netilmicin First Generation Cephalosporins Cephalexin PO Cefazolin IV Second Generation Cephalosporins Cefuroxime IV Cefuroxime Axetil PO Cefoxitin Third Generation Cephalosporins Ceftriaxone Ceftazidime Cefotaxime Fourth Generation Cephalosporins Cefepime Cefpirome Quinolones GRAM (+) +++ ++ ++ ++ ++ 1/2 ++ ++ +++ GRAM (-) ++ ++ 1/2 ++ ++ 1/2 ANAEROBES REMARKS Narrow spectrum penicillins Specifically used for Staphylococcus aureus Broad spectrum penicillin Good anaerobic coverage Good anaerobic coverage Use as reserve drug for Pseudomonas Reserve drug & most active for S.

Carbapenems (Meropenem) o Fourth Generation Cephalosporins (Cefepime and Cefpirome)  Drugs with Good Anaerobic Properties: o Clindamycin o Metronidazole o Chloramphenicol    Cefoxitin Meropenem Ampicillin-Sulbactam   Amoxycillin-Clavulanic Acid High Dose Penicillin  Drugs with Good Central Nervous System (CNS) Penetration in Meningitis: o Ceftriaxone  Ampicillin  Penicillin-G o Ceftazidime  Meropenem  Vancomycin o Cefuroxime  Ampicillin-Sulbactam o Cefotaxime  Ciprofloxacin o Chloramphenicol and Co-Trimoxazole have high diffusion to the CSF even WITHOUT Meningitis Drugs safe for patients with Liver Disease: o Aminoglycosides o Ampicillin o Amoxicillin o Cephalexin o Cefoxitin o Cefuroxime o Ofloxacin o Penicillin-G o Carbapenems  39 . Cefoperazone. Ticarcillin and Piperacillin o Monobactams (Aztreonam). Quinolones (Ciprofloxacin).Ciprofloxacin Norfloxacin Ofloxacin Fleroxacin Levofloxacin Moxifloxacin Others Co-Trimoxazole Co-Trimazine Chloramphenicol Clindamycin Metronidazole Rifampicin + +++ - Used for multidrug resistant Typhoid Fever Ciprofloxacin is best for Pseudomonas Norfloxacin is good for Severe UTI Moxifloxacin with better Anaerobic activity ++ +++ + ++ 1/2 ++ 1/2 ++ ++ ++ 1/2 ++ 1/2 ++ ++ 1/2 +++ ++ 1/2 + Drug of choice for Uncomplicated Typhoid “Above diaphragm” Anaerobes Good Gm(+) Activity “Below diaphragm” Anaerobes Used for pulmonary tuberculosis ADDITIONAL NOTES:  Drugs with Anti-Pseudomonas Properties: o Aminoglycosides (Tobramycin. Amikacin. Gentamicin) o Ceftazidime. Netilmicin.

Ceftizoxime o Cephalosporins with Best Anaerobic Coverage: CEFOXITIN. and should be given for < 7 days to avoid Nephrotoxicity. Ceftazidime. ESBL  Extended Spectrum Beta Lactamases  Mx: Carbapenems **NOTE: Use Penicillins. Anaerobic Coverage (ex. Creatinine is measured every 3 days. Two Organisms NOT Targeted by Cephalosporins  Enterococcus  Listeria monocytogenes 3. Other Cephalosporins also have some Anaerobic properties o Cefuroxime Axetil is given with Meals o Cefazolin is the Drug of Choice ONLY for Surgical Prophylaxis of abdominal operations & implant surgery On Aminoglycosides: o Aminoglycosides are given q 8-12 hours in 30 minutes by Slow IV or IM to avoid possible neuromuscular paralysis. Some Antibiotics to Target Pseudomonas  Ceftazidime  Piperacillin-Tazobactam  Carbapenems (Meropenem) EXCEPT Ertapenem 5. Netilmycin  Loading Dose = 2mg/kg  Maintenance Dose = 1.aureus o Resistance may develop easily when Rifampicin is used alone  NOTES ON ANTIBIOTICS 1. Ampicillin 40 . Methicillin Resistant Staphylococcus aureus (MRSA)  Give Vancomycin. lower the dose o Azithromycin is given 1 hour before meals Rifampicin o Aside from Anti-TB properties. HLARE  High Level Aminoglycoside Resistance Enterococcus  Mx: Vancomycin 7.5g OD = Gonorrhea  3g OD = Typhoid  2g BID = Meningitis 4. then shift to Oral Zivox (?) when MGH  General Rule: o If (+) with Bacteremia: 14 days o If (+) Solid Organ Abscess: 4-6 weeks 2. Cefaperazone may cause bleeding in predisposed patients o Cephalosporins that cross the Blood-Brain Barrier: Ceftriaxone.   On Cephalosporins o 4th Generation Cephalosporins have the same indications as 3rd Generation Cephalosporins and should remain as “reserved drugs” o The only two Third Generation Cephalosporins active against Pseudomonas are Ceftazidime and Cefoperazone. o Amikacin: Expensive but it is the most potent and least nephrotoxic  Loading Dose = 7. Rifampicin may be used synergistically with Oxacillin for S. IV o Gentamicin. If Pneumonia has + Aspiration)  Clindamycin  Metronidazole 6. Cefotaxime.5mg/kg/dose q 8hours IM. If with GI upset.5mg/kg  Maintenance Dose = 15mg/kg/day in 2 divided doses IM. Spectinomycin is used for Gonorrhea. They must have loading doses. IV o Gentamicin is the cheapest aminoglycoside. Streptomycin is used for PTB On Macrolides o Erithromycin is given with meals. Ceftriaxone Doses (double check):  2g OD = usual dose  2. Tobramicin.

qwertyuiopasdfghjklzxcvbnmqwertyui opasdfghjklzxcvbnmqwertyuiopasdfgh jklzxcvbnmqwertyuiopasdfghjklzxcvb nmqwertyuiopasdfghjklzxcvbnmqwer CARDIOLOGY tyuiopasdfghjklzxcvbnmqwertyuiopas dfghjklzxcvbnmqwertyuiopasdfghjklzx cvbnmqwertyuiopasdfghjklzxcvbnmq wertyuiopasdfghjklzxcvbnmqwertyuio pasdfghjklzxcvbnmqwertyuiopasdfghj klzxcvbnmqwertyuiopasdfghjklzxcvbn mqwertyuiopasdfghjklzxcvbnmqwerty uiopasdfghjklzxcvbnmqwertyuiopasdf ghjklzxcvbnmqwertyuiopasdfghjklzxc vbnmqwertyuiopasdfghjklzxcvbnmrty uiopasdfghjklzxcvbnmqwertyuiopasdf ghjklzxcvbnmqwertyuiopasdfghjklzxc vbnmqwertyuiopasdfghjklzxcvbnmqw ertyuiopasdfghjklzxcvbnmqwertyuiop Jaime Alfonso Manalo Aherrera.D. Internal Medicine Notes 2009 . M.

because of an inherited or acquired abnormality of cardiac structure and/or function.CONGESTIVE HEART FAILURE CONGESTIVE HEART FAILURE  Heart Failure is a clinical syndrome that occurs in patients who. Apoptosis. NYHA CLASSIFICATION OF CHF FUNCTIONAL CLASS DESCRIPTION Dyspnea occurs with Greater than Ordinary Physical Activity Dyspnea occurs with Ordinary Physical Activity Dyspnea occurs with Less than Ordinary Physical Activity Dyspnea may be present even at Rest GENERAL GUIDE Climbs > 2 flights of stairs with Ease Can climb 2 flights of stairs but with difficulty Can climb < 1 flight of stairs Dyspnea at rest I II III IV 2 . Minor Criteria o Extremity Edema D-P-V-T-H-E-N (the private hen) o Night Cough o Dyspnea on Exertion o Hepatomegaly o Pleural Effusion o Vital Capacity reduced by 1/3 from Normal o Tachycardia (>120bpm) C. a poor quality of life. Major Criteria o Paroxysmal Nocturnal Dyspnea P-R-I-N-C-E-S-P o Neck Vein Distention o Rales o Cardiomegaly o Acute Pulmonary Edema 1 Major + 2 o S3 Gallop o Increased Venous Pressure (>16cmH2O) o Positive Hepatojugular Reflux Minor Criteria B. develop a constellation of clinical symptoms (dyspnea & fatigue) and signs (edema and rales) that lead to frequent hospitalizations. which are responsible for maintaining Cardiac Output through increased retention of salt and water o 2) Increased Myocardial Contractility  LV Remodeling Changes: o o o o o Myocyte Hypertrophy Alterations in the Contractile Properties of the Myocyte Progressive Loss of Myocytes through Necrosis. FRAMINGHAM CRITERIA FOR DIAGNOSIS OF CONGESTIVE HEART FAILURE A. and a shortened life expectancy  Categorized into TWO Groups: o Systolic Failure: HF with a Depressed Ejection Fraction o Diastolic Failure: HF with a Preserved Ejection Fraction  Compensatory Mechanisms Activated in the Presence of Cardiac Injury and/or LV Dysfunction: o 1) Activation of the Renin-Angiotensin-Aldosterone (RAA) and Adrenergic Nervous Systems.5kg over 5 days Treatment II. and Autophagic Cell Death B-Adrenergic Desensitization Abnormal Myocardial Energetics and Metabolism Reorganization of the Extracellular Matrix with dissolution of the organized structural collagen weave and subsequent replacement by an interstitial collagen matrix that does not provide structural support to the myocytes o I. Major or Minor o Weight Loss ≥ 4.

as well B. Lead V1) Flattened or Inverted T-Waves Shortened QT Interval Prolongation of the PR-Interval compared with a Pretreatment Baseline. In the inferior and lateral leads). CANADIAN CARDIOVASCULAR SOCIETY CLASSIFICATION OF ANGINA FUNCTIONAL CLASS I II III IV DESCRIPTION Angina occurs with Greater than Ordinary Physical Activity Angina occurs with Ordinary Physical Activity Angina occurs with LESS than ordinary Physical Activity Angina may be present even at REST IV. HYPOKALEMIA. ECG Manifestations of the “Dig Effect” Include: o o o o o Depressed ST-Segments in leads where the main QRS Deflection is Positive (eg. a common side effect of diuretic therapy. so maintaining the desirable serum level of the drug is difficult.04 to 0. ECG Manifestations of Digitalis Toxicity include: o The same ST-Segment and T-Wave changes noted with the Dig Effect o Significant Prolongation of the PR-Interval o Supraventricular Dysrhythmias        Extreme Sinus Bradycardia Atrial Premature Complexes (APCs) Sinoatrial (SA) Block Junctional Premature Complexes (JPCs) Junctional Escape Rhythm Accelerated Junctional Rhythm Junctional Tachycardia Atrial Tachycardia with AV Block Ventricular Premature Complexes (VPCs) Ventricular Bigeminy Ventricular Tachycardia (VT) Ventricular Fibrillation Atrial Tachycardia with AV Block Second Degree AV Block Type I Third Degree AV Block Bidirectional VT (alternating Polarity of the QRS Complex) is associated with Poor Prognosis  o    Ventricular Dysrhythmias  o   Atrioventricular (AV) Block  o o o o E.III. Antidysrhythmic agents such as Quinidine and Amiodarone. POTENTIATES the Toxic Effects of Digitalis. Clues PE Suggesting Digitalis Toxicity as Verapamil. the STSegments gradually slope downward and look “scooped out” Elevated ST-Segments in leads where the main QRS Deflection is Negative (eg. the PR Interval often lengthens by 0.08 seconds (or more) D. Toxic Levels are associated with: o Potentially Life-Threatening Dysrhythmias o Heart Blocks o Etc Digitalis preparations have a narrow therapeutic range. Treatment of Digitalis TOXICITY Withholding further Digoxin Potassium Replacement Therapy (carefully AVOID Hypokalemia) Digoxin Antibody Fragments (Digoxin Immune Fab) Temporary Pacing Diphenylhydantoin (for treatment of Digitalis-Induced Ventricular Dysrhythmias) o 3 . are known to Increase Serum Digoxin Level o Change in visualization o Interruption in conduction system (bradycardia. branch blocks) C. CLUES SUGGESTING DIGITALIS TOXICITY  Digitalis glycosides are given to enhance myocardial performance in situations of chronic heart failure as well as to control many Supraventricular Dysrhythmias  NORMAL Serum Levels of Digoxin may produce subtle alterations in ECG called the Digitalis Effect A.

Cardiac Examination o An S3 (Protodiastolic Gallop) is most commonly present in patients with Volume Overload who have Tachycardia and Tachypnea. Jugular Venous Pressure (JVP) o Estimation of the Right Atrial Pressure o Two main objectives of the examination of the neck veins are inspection of their waveform and estimation of the central venous pressure (CVP) o Right Internal Jugular Vein is best for this purpose o Vertical distance between the top of the oscillating venous column and the level of the sternal angle is determined – generally. followed in turn by recurrence of Apnea D. DYSPNEA is observed only during exertion  Origin of Dyspnea = Multifactorial (Most Important: Pulmonary Congestion) A. but is usually present in patients with Diastolic Dysfunction Nice to Know:  Water-bottle Sign = Pericardial Effusion  Electrolytes that can cause arrhythmias = Potassium.7cm2 4 . usually 1-3 hours after patient retires o Cardiac Asthma: wheezing secondary to bronchospasm C. and often signifies Severe Hemodynamic Compromise o An S4 is NOT a specific indicator for HF. Magnesium Kussmaul’s Sign  An increase. resulting in Hyperventilation and Hypocapnia. in CVP during INSPIRATION  Most often caused by Severe Right Sided Heart Failure  Frequent finding in patients with Constrictive Pericarditis or Right Ventricular Infarction Mitral Stenosis  Normal Mitral Valve Orifice = 4-6cm2  Threshold for Surgical management of Mitral Valve Stenosis < 1. it is Less than 3cm (3cm + 5cm = 8cm blood) o Most Common cause of a high venous pressure is an Elevated Right Ventricular Diastolic Pressure **IMPORTANT Notes:  CVP = pressure within the right atrium  CVP is equal to [JVP + 5] E. Calcium. rather than the normal decrease. SOME SIGNS AND SYMPTOMS OF CHF  Cardinal Symptoms of HF: Fatigue and Shortness of Breath  In early stages. Orthopnea o Dyspnea occurring in the RECUMBENT position (later manifestation of HF than is exertional dyspnea) o Nocturnal Cough: frequent manifestation of this process o Relieved by sitting upright or by sleeping with additional pillows B. Paroxysmal Nocturnal Dyspnea o Acute episodes of severe shortness of breath and coughing that generally occur at night and awaken the patient from sleep. Abdominojugular Reflux o Done in patients suspected of having right ventricular failure who have normal CVP at rest o Palm of examiner‟s hand is placed over the abdomen. and firm pressure is applied for 10s or more o Normal Persons: maneuver does NOT alter the JVP significantly o Right Heart Function Impaired: Upper Level of venous pulsation usually INCREASES o Definition of a Positive Abdominojugular Test: An increase in JVP during 10s of firm midabdominal compression followed by a rapid drop in pressure of 4cm blood on release of the compression F. Cheyne-Stokes Respiration o Also referred to as Periodic Respiration or Cyclic Respiration o Common in advanced HF and is associated with Low Cardiac Output o Caused by a diminished sensitivity of the respiratory center to Arterial PCO 2 o There is an Apneic Phase.V. during which the arterial PO2 Falls and PCO2 Rises o These changes in the arterial blood gas content stimulate the depressed respiratory center.

Note on HDL VS LDL o If Decreased HDL but NORMAL LDL = we may give Fibrates to Increase HDL o If LDL is Increased. Abarquez Lecture) o Inotropy o Lusitropy (attenuates Growth and Collagen Factor) o Neurogenic o Preload & Afterload o Vagotonic o Less Apoptosis (has Anti-Apoptotic Events) VII. Pharmacologic Management o Diuretics (only agents that can adequately control fluid retention in advanced HF) o Preventing Disease Progression  ACE Inhibitors  B-blockers Effects of Digitalis (Dr.0113  convert to mg/dL 5 . Some Trials on Congestive Heart Failure o RALES: Randomized Aldactone Evaluation Study (Benefits of Spironolactone) o VHeFT: Vasodilators in Heart Failure B.VI. General Measures / Activity / Diet o Modest exercise o Salt Restriction (2-3g daily) o Fluid restriction (<2L/day) if with (+) Hyponatremia or difficult to control fluid retention despite high doses of diuretics and Na+ Restriction 2. Effects of Anti-Hypertensives: o Enalapril = Preload and Afterload o Hydralazine = Afterload o ISDN = Preload C. OTHER SIDE NOTES: A.0259  to convert to mg/dL  TAG divided by 0. Abarquez)  Diuretics (Spironolactone: Diuretic of choice because it also blocks aldosterone)  ACE Inhibitors / ARBS Caution in use of Beta-Blockers = may push patient into further congestion  Digoxin Management of HF with DEPRESSED Ejection Fraction (<40%) 1. we must address the LDL first! **CONVERSION Factor:  HDL or LDL divided by 0. TREATMENT FOR HEART FAILURE (Triple Therapy – Dr.

HYPERTENSION (from Harrisons)
CLASSIFICATION Normal Pre-Hypertension Stage 1 Hypertension Stage 2 Hypertension Isolated Systolic Hypertension SYSTOLIC (mmHg) < 120 120 – 139 140 – 159 > 160 > 140 DIASTOLIC (mmHg) And < 80 Or 80 – 89 Or 90 – 99 Or > 100 And < 90

 Clues for Secondary Hypertension: o Age of Onset < 20 or > 50 o (-) Family History o DBP > 110 – 120 o Sudden Increase in BP in a patient with Stable Stage I HPN o Poor BP Control, despite Good Compliance A. Hypertensive Urgency o Use ORAL Drugs first o ALA Hypertensive Crisis o Uncontrolled HPN with NO End-Organ Damage o Lower BP within 24 hours B. Hypertensive Emergency o Use IV Medications, stat o AKA Malignant Hypertension o WITH End Organ Damage (Papilledema, Encephalopathy, Eclampsia, etc) o Lower BP within 1 Hour

C. Treatment of Hypertensive Urgency / Emergency (Medicine Notes) 1. Oral / Sublingual
Nifedipine Captopril Clonidine 5-10 mg SL q30 mins, then 5-10mg PO or SL q6-8hours; OR 30mg/tab PO OD-BID (max 90mg/day) 25 mg/tab 1/2-1 tab SL q30 mins 75 mcg/tab SL q1 (max 700mcg) Initial 5mg/h; titrate by 2.5 mg/h at 5-15 min intervals Max: 15mg/h 5-10mg IV q3-6 hours (0.1-0.5mg/kg/dose, max 20mg/dose) Duration: 3-6 hours Especially for patients with concomitant CAD 1 amp (150mcg/amp) SC, IM or IV with patient supine Initial 0.3 ug/kg/min; usual 2-4 ug/kg/min; Max 10 ug/kg/min for 10mins

2. IV
Nicardipine IV Hydralazine ISDN IV Clonidine Nitroprusside IV

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Stages in the Evolution of Heart Failure (Recommended Therapy by Stage): STAGE A
At risk for heart failure, but without structural heart disease or symptoms of HF Patients with HPN, CAD, DM Or Patients using Cardiotoxins with FHx CM

STAGE B
Structural Heart Disease but without Symptoms of HF Patients with previous MI, LV Systolic Dysfunction, Asymptomatic Valvular Disease

STAGE C
Structural Heart Disease with Prior Current Symptoms of HF Patients with known Structural Heart Disease, Shortness of Breath and Fatigue, Reduced Exercise Tolerance

STAGE D
Refractory HF requiring Specialized Interventions Patients who have marked Symptoms at rest despite maximal therapy (eg. Those who are recurrently hospitalized or cannot be safely discharged from the hospital without specialized interventions)

Structural Heart Disease Therapy: Treat HPN Encourage smoking cessation Treat Lipid D/O Encourage regular exercise Discourage Alcohol Intake, Illicit Drug use ACE Inhibition

Symptoms of HF Develop

Refractory Symptoms of HF at Rest Therapy: All measures under Stage A, B, and C Mechanical assist devices Heart Transplant Continuous (not intermittent) IV Inotropic Infusions for Palliation Hospice Care

Therapy: All measures under Stage-A ACE Inhibitors in appropriate patients Beta-Blockers

Therapy: All Measures under Stage-A Drugs (Routine Use): -Diuretics -ACE Inhibitors -Beta-Blockers -Digitalis -Dietary Salt Restriction

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ISCHEMIC HEART DISEASE

ISCHEMIC HEART DISEASE
    Condition in which there is an Inadequate supply of blood and oxygen to a portion of the Myocardium IMBALANCE between Myocardial Oxygen Supply and Demand Most Common Cause: Atherosclerotic Disease of an Epicardial Coronary Artery sufficient to cause a regional reduction in Myocardial Blood Flow and inadequate perfusion of the Myocardium supplied by involved artery Obesity, Insulin Resistance, and T2DM are increasing and powerful risk factors for IHD

 Patients with IHD fall into Two Large Groups: o 1) Patients with Chronic Coronary Disease (CAD) who most commonly present with Stable Angina o 2) Patients with Acute Coronary Syndromes  Acute Coronary Syndromes is Composed of: o Unstable Angina and Non-ST-Segment Elevation MI o Acute Myocardial Infarction (MI) with ST-Elevation I. STABLE ANGINA PECTORIS  This episodic clinical syndrome is due to TRANSIENT Myocardial Ischemia  Males: 70% of all patients with angina pectoris  Typical History: Man older than 50y/o or Woman older than 60y/o who complains of chest discomfort usually described as heaviness, pressure, squeezing, smothering, or choking, and only rarely as frank pain  Levine‟s Sign: Hand placed over sternum with a clenched fist, to indicate a squeezing, central, substernal discomfort A. Clinical Presentation o Angina is usually crescendo-decresendo in nature, typically lasts 2-5 minutes, and can radiate to either shoulder and to both arms o Does NOT radiate to Trapezius Muscles (such a radiation pattern is more typical of Pericarditis) o Episodes of Angina typically caused by Exertion or Emotion, Relieved by Rest and Sublingual Nitroglycerin B. Electrocardiogram (ECG) o May be NORMAL (at rest) o ST-Segment and T-Wave changes – as well as LV hypertrophy and intraventricular conduction disturbances – are suggestive of IHD, they are non specific since they can also occur in Pericardial, Myocardial and Valvular Heart Disease C. Stress Testing o Most widely used for both Diagnosis of IHD and estimating prognosis involves recording the 12-Lead ECG before, during and after exercise

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II. MANAGEMENT OF STABLE ANGINA PECTORIS  1) Explanation of he Problem and reassurance about the ability to formulate a Treatment Plan  2) Identification & Treatment of aggravating conditions  3) Recommendations for adaptation of Activity as needed  4) Treatment of Risk Factors that will decrease occurrence of Adverse Coronary Outcomes  5) Drug Therapy for Angina  6) Consideration of Revascularization A. Dyslipidemia o Treatment of Dyslipidemia is Central when aiming for Long-Term Relief from Angina, reduced need for Revascularization, and reduction in MI and death o HMG-CoA Reductase Inhibitors (Statins): can lower LDL Cholesterol (25-50%), raise HDL Cholesterol, and Lower Triglycerides B. Pharmacologic Treatment 1. Drug Therapy
Nitrates Systemic Venodilation with concomitant reduction in LV End Diastolic Volume and Pressure, thereby reducing Myocardial Wall Tension and O2 Requirements Dilation of Epicardial Coronary Vessels Increased Blood Flow in Collateral Vessels Long Acting Nitrates B-Adrenergic Blockers Ca+ Channel Blockers None of the Long Acting Nitrates is as effective as Sublingual Nitroglycerin for the Acute Relief of Angina Reduce Myocardial O2 Demand by inhibiting the increases in HR, arterial pressure, and myocardial contractility caused by Adrenergic Activation Coronary Vasodilators that produce variable and dose dependent reductions in Myocardial O2 Demand, Contractility, and Arterial Pressure

**NOTE Beta-Blockers VS Ca2+ Channel Blockers  Beta Blockers have been shown to improve Live Expectancy following Acute MI (Ca+ Channel Blockers have not)  Ca2+ Channel Blockers are indicated in patients with:  Inadequate responsiveness to the combination of B-Blockers & Nitrates  Adverse Reactions to B-Blockers (depression, fatigue, sexual)  Angina and history of Asthma or COPD  Sick Sinus Syndrome or significant AV Conduction Disturbances  Prinzmetal‟s Angina  Sympomatic Peripheral Arterial Disease 2. Anti-Platelet Drugs
Aspirin Clopidrogel Irreversible Inhibitor of Platelet Cyclo-Oxygenase Activity, therefore interferes with Platelet Activation. Chronic administration of 75 to 325mg PO per day has been shown to reduce coronary events. Oral Agent that blocks ADP Receptor Mediated Platelet Aggregation

3. Other Therapies:  ACE-Inhibitors  Ranolazine **NOTE: NSAIDS should be AVOIDED! C. Coronary Revascularization
Percutaneous Coronary Intervention (PCI) Coronary Artery Bypass Grafting (CABG) Involves Balloon Dilatation usually accompanied by Coronary Stenting. Most common indication for PCI is Angina Pectoris, despite medical therapy, accompanied by evidence of Ischemia during a Stress Test For those with Three-Vessel IHD, Stenosis of the Left Main Coronary Artery

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usually lasting > 10 Minutes  2) It is Severe and of New Onset (ie. Non-ST-Elevation Myocardial Infarction (NSTEMI) o Clinical Features of Unstable Angina (UA) + evidence of Myocardial Necrosis – as reflected in Elevated Cardiac Biomarkers II. PATHOPHYSIOLOGY (Four Pathophysiologic Processes)  1) Plaque Rupture or Erosion with Superimposed Nonocclusive Thrombus (Most Common Cause)  2) Dynamic Obstruction (eg. left shoulder. Tachycardia. Sinus Tachycardia. Within the prior 4-6 weeks)  3) Occurs with a Crescendo Pattern (ie. Pale Cool Skin. Basilar Rales. but is reproducibly associated with Physical Exertion or Stress. S3 or S4. and is RELIEVED within 5-10 minutes by REST and/or Sublingual Nitroglycerin o UNSTABLE ANGINA is defined as Angina Pectoris or Equivalent Ischemic Discomfort with at least ONE of the Three Features:  1) Occurs at Rest (or with minimal exertion). Distinctly more Severe.UNSTABLE ANGINA & NSTEMI Unstable Angina  Angina Pectoris with at least ONE of THREE Features: o 1) Occurs at rest or with Minimal Exertion lasting > 10 minutes o 2) Severe and of New Onset o 3) Occurs with a Crescendo Pattern Non-ST-Elevation Myocardial Infarction (NSTEMI)  Clinical Features of Unstable Angina (UA) develops evidence of Myocardial Necrosis as reflected by Elevated Cardiac Enzymes  Clinical Features: o Chest Pain radiating to the Neck. or frequent than previously) B. Hypotension Criteria to Document AMI  1) Chest Pain  2) ECG Changes  3) Cardiac Enzymes I. Unstable Angina o STABLE Angina Pectoris is characterized by Chest or Arm Discomfort that may NOT be described as pain. Prolonged. Coronary Spasm as in Prinzmetal‟s Variant Angina)  3) Progressive Mechanical Obstruction  4) Secondary UA related to Increased Myocardial O2 Demand and/or Decreased Supply (eg. Anemia) III. and Left Arm o Dyspnea o Diaphoresis. and left arm. Epigastric Discomfort  PE: Unremarkable. CLINICAL PRESENTATION  Clinical Hallmark: CHEST PAIN – substernal region or sometimes epigastrium. severe enough to be considered painful  Anginal Equivalents: Dyspnea. or if (+) Large Area of Myocardial Ischemia or a Large NSTEMI: o Diaphoresis o Pale cool skin o Sinus tachycardia o 3rd & 4th heart sound o Basilar rales o Hypotension 10 . DEFINITION OF TERMS: A. radiates to neck. Left Shoulder.

Deep T-Wave Inversions (> 0. in patients WITHOUT a clear clinical history of Myocardial Ischemia. A panel of Cardiac Markers (eg. MINOR Troponin Elevations have been reported and can be caused by Congestive Heart Failure. could the Discomfort be due to an Acute Condition that Warrants Specific Treatment? o Pericarditis o Pneumonitis / Pleuritis o Herpes Zoster If Not. the presence of New ST-Segment Deviation. Goals are to:  Recognize or exclude MI (using Cardiac Markers)  Evaluate for Rest Ischemia (Chest Pain at rest. serial. unless they are New. DIAGNOSTIC PATHWAYS Four major diagnostic tools are used in the Diagnosis of UA/NSTEMI in the Emergency Department: History + ECG + Cardiac Markers + Stress Testing. could the Discomfort be due to another Treatable Chronic Condition? o Esophageal Reflux Esophageal Spasm o Peptic Ulcer Disease Gallbladder Disease o Other GI Conditions Cervical Disk Disease o Arthritis of the Shoulder or Spine Costochondritis o Musculoskeletal Disorders Anxiety State    11 . Cardiac Biomarkers o Patients with UA who have elevated Biomarkers of Necrosis such as CKMB and Troponin (a much more specific and sensitive marker of Myocardial Necrosis) are at INCREASED Risk for Death or Recurrent MI o Elevated Levels of these markers distinguish patients with NSTEMI from those with UA There is a direct relationship between the degree of Troponin Elevation and Mortality. DIAGNOSIS A. with imaging reserved for patients with abnormal baseline ECG. Troponin. in patients with an UNCLEAR History. If positive. could it be due to a Chronic condition likely to lead to Serious Complications? o Stable Angina o Aortic Stenosis o Pulmonary Hypertension If Not. even of only 0. patient is admitted. Small Troponin Elevations may NOT be diagnostic of an ACS V. CKMB) is drawn at baseline and 6 hours later. If patient has negative markers and no recurrence of pain. and 12-Lead ECGs are performed if the patient has recurrent chest discomfort. T-Wave changes are sensitive for Ischemia but less specific. DIFFERENTIALS FOR CHEST PAIN:  Could the Chest Pain be due to an Acute. is an important predictor of adverse outcome. Potentially Life-Threatening Condition that warrants Immediate Hospitalization? o Acute Ischemic Heart Disease o Aortic Dissection o Pulmonary Embolism o Spontaneous Pneumothorax If Not. he is admitted to the hospital and treated for UA/NSTEMI. If patient develops recurrent pain.IV. QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. or they may be False Positive Readings. he is sent for exercise treadmill testing. or Pulmonary Embolism. However.05 mV. Patients with a Low Likelihood of Ischemia enter the pathway and are observed in a monitored bed in the ED observation unit over a period of 6 hours. or has Positive Cardiac Markers. Patients at high or intermediate likelihood are admitted to the hospital. Myocarditis. Those with clearly atypical chest pain are sent home. ECG o ST-Segment Depression o Transient ST-Segment Elevation o T-Wave Inversion In patients with clinical features of UA. has ST-Segment or T-Wave Changes. or continuous ECGs)  Evaluate for significant CAD (using provocative stress testing) First step is to assess the likelihood of Coronary Artery Disease. Thus.3mV) B.

Invasive VS Conservative Strategy o High Risk Patients (Multiple Risk Factors): ST-Segment Deviation and/or (+) Biomarkers o Class I Recommendations for Use of an Early Invasive Strategy:  Recurrent Angina at rest / low level activity despite Rx  Elevated TnT or TnI  New. Medical Treatment o Bed rest with continuous ECG monitoring for ST-Segment Deviation and cardiac rhythm o Ambulation is permitted if patient shows NO recurrence of ischemia and does NOT develop a biomarker necrosis for 12-24 hours o Medical Therapy: Simultaneous Anti-Ischemic Treatment + Antithrombotic Treatment DRUG CATEGORY Nitrates CLINICAL CONDITION Administer IV when symptoms are not fully relieved with three sublingual nitroglycerin tablets and initiation of beta blocker therapy Unstable Angina WHEN TO AVOID Hypotension Patient receiving Sildenafil or other PDE 5 Inhibitor PR Interval (ECG) > 0.40 Agents. Coronary Arteriography is carried out within ~48 hours of admission. Anti-Ischemic Treatment o Bed Rest o Nitrates o Beta Blockers   Aspirin Clopidogrel D. and is associated with Transient ST-Segment Elevation (due to Focal Spasm of an Epicardial Coronary Artery)  Diagnostic Hallmark: Transient Coronary Spasm on Coronary Angiography 12 . rales. Anti-Thrombotic Therapy E.  Decreased BP followed by Coronary Revascularization (PCI or Coronary Artery Bypass  Sustained VT Grafting).VI. prior CABG VII. PRINZMETAL‟S VARIANT ANGINA  Ischemic Pain that occurs at rest.ST-Segment Depression  Recurrent Angina / Ischemia with CHF symptoms. but NOT usually with exertion. MANAGEMENT OF UA/NSTEMI A. MR  Positive Stress Test In this strategy. LONG TERM MANAGEMENT  Risk Factor Modification  Long Term Tx with Five Classes of Drugs have been shown beneficial: o Beta Blockers (anti-ischemic tx & reduce triggers for MI) o Statins (long-term plaque stabilization) o ACE Inhibitors (long-term plaque stabilization) o Antiplatelet Therapy (Aspirin + Clopidrogel for at least 9-12 months) VIII. Anticoagulation Therapy  Unfractionated Heparin (Mainstay)  LMWH Enoxaprin C. following treatment with Anti-Ischemic and Anti-Thrombotic  EF < 0.24s 20 or 30 Atrioventricular Block Heart Rate < 60bpm BP < 90mmHg Shock LV Failure with CHF Severe Reactive Airway Disease Pulmonary Edema Evidence of LV Dysfunction (for Diltiazem or Verapamil) Hypotension Respiratory Depression Confusion Obtundation Beta Blockers Ca2+ Channel Blockers Patients whose symptoms are not relieved by adequate doses of nitrates and Beta Blockers or in patients unable to tolerate adequate doses of one or both of these agents or in patients with variant angina Patients whose symptoms are not relieved after three serial sublingual nitroglycerin tablets or whose symptoms recur with adequate anti ischemic therapy Morphine Sulfate B. depending on the coronary anatomy)  PCI < 6 months.

Highly Specific  Increase after STEMI to levels > 20 times higher  Preferred Biochemical Markers for MI  Remain elevated for 7-10 days after STEMI QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. does NOT subside with cessation of activity (in contrast to angina pectoris) A. CLINICAL PICTURE  PAIN: Most Common Presenting complaint in patients with STEMI (heavy. LABORATORY TESTS IN CONFIRMING THE DIAGNOSIS:  ECG  Serum Cardiac Biomarkers  Cardiac Imaging  Non-Specific Indices of Tissue Necrosis and Inflammation A. squeezing. pallor.5 suggests. Molecular Markers in the Diagnosis of AMI (Blue Book) TESTS TIME TO PEAK DURATION DETECTION Troponin-T Troponin-I CK-MB 3-12 hrs 3-12 hrs 3-12 hrs 24 hours 24 hours 24 hours 5-14 days 5-10 days 2-3 days MOST COMMON SAMPLING SCHEDULE Once at least 12 hrs after chest pain Once at least 12 hrs after chest pain Every 12 hrs x 3. pericardial friction rub (transmural STEMI) B. including IM Injection  MB Isoenzyme of CK has advantage over Total CK that is not present in significant concentration in extracardiac tissue & therefore is more specific  CKMB Mass: CK Activity > 2. Temporal Stages of MI o Acute (first few hours – 7 days) o Healing (7 – 28 days) o Healed (> 29 days) II. 4th and 3rd Heart Sounds. dyskinetic bulging (in anterior infarct). Start at 6 hrs after chest pain Cardiac-Specific Troponin T and Troponin I:  Have amino acid sequences different from those of the skeletal muscle forms. Electrocardiogram o Initial Stage: Total Occlusion of an Epicardial Coronary Artery produces ST-Segment Elevation o Most patients initially presenting with ST-Segment Elevation ultimately evolve Q Waves  ECG Findings (from Medicine Notes): INTERPRETATION Hyperacute Acute MI Recent MI Undetermined Old MI Q WAVE (-) (-/+) (++) (++) (++) ST ELEVATION (-/+) (++) (++) (-) (-) T WAVE Peaked (-/+) Inverted Inverted Upright TIMING 0 – 6 hours 6 – 24 hours 24 – 72 hours 72 hrs – 6 wks > 6 wks B. restless. Creatine Phosphokinase (CK)  Rises within 4-8 hours and returns to normal by 48-72 h  An important drawback of Total CK measurement is its lack of Specificity for STEMI  May be elevated with Skeletal Muscle Disease or Trauma. crushing)  Similar to Angina.ACUTE MYOCARDIAL INFARCTION I. usually more Severe. Physical Findings: o Anxious. but is NOT diagnostic of a Myocardial rather than a Skeletal Muscle Source for the CKMB Elevation 13 . but occurs at REST. and Lasts Longer. diaphoresis o Anterior Infarction: Tachycardia + Hypertension o Inferior Infarction: Bradycardia + Hypotension o Precordium is usually quiet.

etc **NOTE: In Patients with 1st-Degree AV-Blocks (Relative Contraindication): o Look at PR Interval (Cut-Off is > 0.20s) o We can give Metoprolol if PR < 0. CONTRAINDICATIONS TO GIVING BETA-BLOCKERS (METOPROLOL)  Low Cardiac Output State  Evidence of CHF  Hypotension  AV Conduction Block (Relative Contraindication)  Asthma. the Inferior Wall is supplied by the Right Coronary Artery. radiating  Persistence of chest heaviness. relieved by rest. CASE: 57/M  CC: Chest Heaviness  HPI: Chest heaviness.24s 14 . treated. which also supplies the SA-Node  Hypotension IV. squeezing. DM  Social: Smoker. occasional alcoholic  Pertinents in the History: o Duration of his initial chest pain = 10 minutes (relieved by rest) o Duration of his second chest pain = 10 minutes (not relieved by rest)  Pertinents in the Physical Exam: o Crackles. (-) HPN. diaphoresis. midsternum. diffuse. 10/10. Cardiogenic Shock Class II 10-20% Mortality Rate Class III 35-45% Mortality Rate Class IV 85-95% Mortality Rate V.24s o We CANNOT give Metoprolol if PR > 0. shortness of breath  PMHx: PTB (1998). with exertion. Streptokinase o Initial Assessment: Acute Coronary Syndrome **QUESTION: Why are patients with Inferior Wall MI prone to Hypotension? o In 90% of patients. AvF (Inferior Wall Infarct) o Aspirin. (-) S3/S4  Initial Management and Labs o ECG revealed ST Elevation on Leads II. 5/10. KILLIP‟s CLASSIFICATION OF AMI CLASS Class I DESCRIPTION RISK OF MORTALITY (Blue Book) 0-5% Risk Mortality No Signs of Pulmonary or Venous Congestion (0-5% Mortality Rate) No Rales Normal Blood Pressure Moderate Heart Failure (+) Rales at the Lung Bases Normal Blood Pressure with Basal Congestion S3-Gallop Tachypnea or Signs of Right-Sided Heart Failure (Venous & Hepatic Congestion) Severe Heart Failure (+) Midbasal Rales (+) S3 and S4 Normal Blood Pressure Pulmonary Edema Shock with Systolic Pressure < 90mmHg & evidence of Peripheral Vasoconstriction Peripheral Cyanosis Mental Confusion and Oliguria Pulmonary Congestion Hypotension. sudden. bilateral to mid o Apex beat at the 6th ICS MCL. III.III.

then followed by daily administration of Aspirin in a dose of 75-162mg o Supplemental O2 (Nasal Prongs or Face Mask 2-4 L/min) o Goals in the ER:    Control of Cardiac Discomfort Rapid identification of patients who are Candidates for Urgent Reperfusion Therapy Triage of Lower-Risk Patients to appropriate location in the hospital Avoidance of inappropriate discharge of patients with STEMI  VII. therapy remains of benefit for many patients seen 3-6 hours after onset of infarction 1. PreHospital Care: 1. Management in the Emergency Department o ASPIRIN: rapid action is achieved by chewing 160-325mg tablet. we do Thrombolysis (Streptokinase) o Other modes of Reperfusion: Primary Percutaneous Coronary Intervention (PCI). INITIAL MANAGEMENT A. Major Elements of Prehospital Care:    Recognition of symptoms Rapid deployment of an emergency medical team capable of performing resuscitative maneuvers Expeditious transportation Expeditious implementation of reperfusion therapy  B. GOALS FOR MANAGEMENT OF ACUTE ST-ELEVATION MI (STEMI)  Reperfusion When ST-Segment Elevation of at least 2mm in 2  Relief of Chest Pain contiguous precordial leads and 1 mm in two adjacent  Anti-Platelets / Anti-Coagulants limb leads is present. Primary Goal in Management in STEMI = REPERFUSION o Ideally.VI. Primary Percutaneous Coronary Intervention  Usually Angioplasty and/or Stenting  Effective in restoring perfusion in STEMI when carried out on an emergency basis in the first few hours of MI Indications For Percutaneous Coronary Intervention (PCI)  Percutaneous Transluminal Coronary Angioplasty (PTCA) – alternative to Bypass Surgery  Fundamental Indication for PCI: o Presence of one or more Coronary Stenoses thought to be responsible for a Clinical Syndrome that warrant Revascularization o Approachable by Catheter-Based Techniques o With Risks and Benefits that compare favorably with those of Bypass Surgery 15 . Prognosis in STEMI is largely related to the occurrence of general classes of complications:   Electrical Complications (Arrhythmias) Mechanical Complications (Pump Failure) **NOTE: Most Out-of-Hospital Deaths from STEMI = due to Sudden Ventricular Fibrillation  Vast majority of deaths due to V-Fib occur within 24 hours of the onset of symptoms (over half occur in the 1st hour) 2. a patient should be considered a candidate for reperfusion therapy A. Relative CONTRAINDICATIONS to Thrombolysis (requires assessment of the Risk:Benefit Ratio)  Current use of Anticoagulants (International Normalized Ratio > 2)  Recent (< 2 weeks) Invasive or Surgical Procedure or Prolonged (>10min) Cardiopulmonary Resuscitation  Known bleeding diathesis  Pregnancy  Hemorrhagic Ophthalmic Condition (eg Hemorrhagic Diabetic Retinopathy)  Active Peptic Ulcer Disease  History of Severe Hypertension that is currently adequately controlled 3. Absolute CONTRAINDICATIONS to Thrombolysis  History of Cerebrovascular Hemorrhage at ANYTIME  History of a Non-Hemorrhagic Stroke or other Cerebrovascular Event within the PAST YEAR  Marked hypertension (a reliably detected SBP > 180mmHg and/or DBP > 110mmHg  Suspicion of Aortic Dissection  Active Internal Bleeding (excluding menses) 2. Bypass (CABG) o Golden Period for Thrombolysis: < 6 hours  Ideally initiated within 30 minutes of presentation (Door to Needle Time < 30 mins)  Although the reduction of mortality rate is more modest.

we can give Protamine Sulfate) VIII.5-2. In addition to diminishing or abolishing chest pain. IV Nitroglycerin should be considered if there is return of chest pain + ST segment or T wave shifts Very effective analgesic for the pain Control pain by diminishing O2 demand. Relief of Chest Pain o Nitrates o Morphine o B-Blockers Sublingual Nitroglycerin Avoid giving NSAIDS in the ACUTE Setting of Myocardial Infarction (AMI) Can be given up to 3 doses of 0. HOSPITAL PHASE MANAGEMENT Activity Patients should be kept at bed rest for the first 12 hours. patients should be increasing ambulation progressively to a goal of 185 m (600ft) at least 3x a day Nothing or only clear fluids (due to risk of emesis and aspiration) for the first 4-12 hours Use of stool softener. Reduce the risks of reinfarction & ventricular fibrillation Morphine IV Beta Blockers C. In the absence of complications. nitroglycerin can be capable of both decreasing Myocardial O2 Demand (by lowering Preload) and increasing Myocardial Oxygen Supply (by dilating infarct-related coronary vessels). Heparin: Anticoagulant  Binds Anti-Thrombin III and activates it (Antithrombotic)  Standard Antithrombin agent used in clinical practice is Unfractionated Heparin or UFH (an alternative to UFH is Low-Molecular-Weight Heparin / LMWH)  Heparin (Unfractionated Heparin or UFH): Initial Bolus 60-70 U/kg (maximum 5000 U) IV. By day 3. patients should be encouraged to resume an upright posture by dangling their feet over the side of the bed & sitting in a chair within the first 24 hours. additional mortality benefit occurs **NOTE: Risks of Heparin  Heparin Induced Thrombocytopenia (HIP)  Bleeding (if there is bleeding. followed by infusion of 12-15 U/kg per hour (initial maximum 1000 U/h) titrated to a PTT 1.B. patients are ambulating in their room with increasing duration and frequency.4mg at 5 min intervals.5 times control  When UFH is added to a regimen of Aspirin and a non-fibrin-specific thrombolytic (Streptokinase). We give Anti-Coagulants and Anti-Platelets for Secondary Prevention  It has no use in the Acute Ischemic Event  Secondary Prevention = Preventing complications or recurrence 2. By the 2nd and 3rd day. Many patients require sedation during hospitalization to withstand period of enforced inactivity Diet Bowels Sedation 16 . Anti-Platelets and Anti-Coagulation o Aspirin 80mg o Clopidrogel o Heparin 1.

LBBB = Manage like ST-Segment Elevation MI  NSTEMI = should NOT receive Thrombolytic Therapy 1) Thrombolysis  Greatest benefit initiated within 6 hours from the onset of symptoms  Benefit also observed when begun 12 hours  Associated with High Risk for ICH. Serum Electrolytes including Mg 2. ACE-Inhibitor  Patients with MI that is spontaneous or provoked in the days to weeks after AMI should undergo: o Elective Coronary Angio o Consider PTCA or CABG  However. PTCA **IMPORTANT Notes:  Acute MI. which occurs within 1st day of Therapy  Factors that Increase Risk for ICH: o Age > 65 y/o o BW < 70kg o Systemic HPN o Administration of Tissue Plasminogen Activator 2) Primary PTCA  May be performed as alternative to Thrombolytics  Provided that it can be accomplished promptly with prompt access to „E‟ CABG HOSPITAL MANAGEMENT 1. Urokinase o Improved Clinical Outcome with ALTEPLASE – IV at least 48 hours after administration of Alteplase **NOTE: High Dose IV Heparin – Recommended when PTCA was done d. reserve the said procedures for survivors who have preserved LV systolic function and spontaneous or provoke Ischemia 17 . ACC / AHA GUIDELINES FOR MANAGEMENT OF AMI (Medicine Notes) Initial Recognition and Management in the ER  Initial evaluation of the patient ideally should be accomplished within 10 minutes of his / her arrival at the ER  NO more than 20 minutes should elapse before an assessment is made At the ER.IX. Heparin Administration AFTER Thrombolysis shows: o Limited evidence of Benefit for Streptokinase. Medications: o Aspirin o IV Nitrates for 24-48 hours after hospitalization o ACE Inhibitors – should be continued in patients with impaired LV systolic function (EF < 40%) or CHF o On Admission: Lipid Profile. Thrombolytics o Streptokinase o Anisoylated Plasminogen Streptokinase Activator Complex (APSAC) o Urokinase c. this does NOT salvage myocardium nor reduce Reinfarction or Death  Thus. First 24 Hours  Confirm MI by Serial ECG and measurement of Cardiac Enzymes  Reinfarction and Death frequently occurs within the 1st 24 hours  Limit Physical Activities for at least 12 hours  Anxiety and Pain – appropriate Analgesics  Prophylactic Antiarrhythmias – NOT recommended in the 1st 24 hours of Hospitalization a. patient with Suspected MI should immediately Receive:  O2 Support  SL Nitrates (Defer if BP < 90 or HR < 50)  Adequate Analgesia (Morphine or Mependine)  ASA 160-325mg orally  12 L ECG must be done: o ST Segment Elevation (> 1mV in contiguous leads) o Presence makes patient a Candidate for Immediate Reperfusion Therapy by Fibrinolysis. B-Blocker. Increased Risk for Embolic Stroke: o Large Anterior Wall MI **Risk is reduced by Early Administration of Heparin o LV Mural Thrombus b. APSAC. After 1st 24 Hours  Continue ASA.

should be treated with:  Lidocaine  Procainamide  Amiodarone H. Beta-Blocker. RV Infarction and Dysfunction o Intravascular Volume Expansion and Inotropic Agent E. or symptom limited at 10-14 days o This is done to:  Assess patient‟s functional capacity and ability to perform test at home or work  Evaluate efficacy of patient‟s current medical regimen  Stratify risk for subsequent cardiac event B. VSD) X. PREPARATION FOR DISCHARGE A. leading to severe Pulmonary Congestion and Hypotension (eg. Monomorphic Ventricular Tachycardia o Direct Current Countershock if with associated angina and congestion o If NOT. Selected Dose of ACE-Inhibitors o Weight reduction o Diet – Low Fat and Cholesterol (Target LDL < 100mg/dL) o Smoking cessation o Formal Cardiac Rehab Program or engage in 20 minutes of exercise at least at level of brisk walking at least 3x per week 18 .Temporary Pacemaker Insertion (TPI)  Patients with: o Sinus Bradycardia. NOT amendable to PTCA  Mechanical Abnormality. Ventricular Fibrillation o Direct Current Countershock G. unresponsive to meds o Mobitz Type II 20 AV Block o 30 Heart Block o BBB o Newly Acquired BBB o R or LBBB in Conjunction with 10 AV Block Immediate Surgical Intervention:  Failed PTCA with Persistent Chest Pains or Hemodynamic Instability  Persistent or recurrent ischemia refractory to meds and NOT candidate for catheter intervention  Cardiogenic Shock and Coronary Artery. Pericarditis o Patients with Recurrent Chest Pain o Should receive High Dose ASA (650mg q4 to 6 hrs) o If caused by MI. Should undergo Stress-Testing Exercise o Submaximal at 4-7 day. Papillary Muscle Rupture. Long Term Management o Meds: ASA. MR. Atrial Fibrillation o Manifestation of extensive LV systolic dysfunction o Hemodynamic Compromise o Direct Cardioversion o DIGITALIS to Slow the Ventricular Response F. CHF o Should receive Diuretics and an Afterload Reducing Agent C. Symptomatic Bradycardia o Atropine XI. should be treated with:  IV Nitrates  Analgesics  Antithrombotics B. COMPLICATIONS (Medicine Notes) A. Cardiogenic Shock o Intra-Aortic Balloon Pump o E Coronary Angio  PTCA  CABG D.

Clinical:  Arthralgia (joint pains)  Fever 2. Major Manifestations Carditis (40-60%) Migratory Polyarthritis (75%) Syndenham’s Chorea (<10%) Erythema Marginatum Subcutaneous Nodules Pancarditis involving the pericardium.2 M „u‟ q 3-4 weeks RF without Carditis: 5 years until 30 y/o  Penicillin-V 250mg/cap BID RF with Mild Carditis: until 45 y/o  Erythromycin 250mg/cap BID RF with Mod-Sev Carditis: Lifetime III.RHEUMATIC HEART DISEASE RHEUMATIC HEART DISEASE I. ESR. ECG. 3 + 5 = 8) o Splitting of S2 (there is Delayed Closure of Pulmonic Valve)  Normal JVP = 3cm o Opening Snap  Normal CVP = 8cm o Low pitched rumbling Diastolic Murmur o o IV. Throat Swab CS. then taper  For Mod to Severe Carditis: Add Prednisone 1-2mg/kg/day x 2-3 weeks. Joints. knees. Laboratory Findings of:  Elevated Acute Phase Reactants (ESR / CRP)  Prolonged PR interval PLUS Supporting Evidence of Antecedent Group-A Strep Infection o (+) Throat Culture or Rapid Strep-Antigen Test o And/or Elevated or Rising Strep-Antibody Test 2 Major Criteria OR 1 Major and 2 Minor Criteria PLUS Evidence of Preceding Infection Management of Rheumatic Fever Diagnostics: include ASO Titer. Minor Manifestations 1. wrists. CRP. PERCUTANEOUS TRANSLUMINAL MITRAL VALVE COMISSUROTOMY (PTMC)  Right Atrium  Transluminal approach to Left Atrium  Mitral Valve (Creates a whole in the septum between the LA and RA) 19 . usually concentrated on trunk Found over extensor surfaces of joints B. PE OF A PATIENT WITH MITRAL STENOSIS (MS) A. the JVP reveals prominent a waves due to vigorous right atrial systole NOTE: JVP vs CVP o RV Tap (due to enlarged RV)  JVP is measured from Sternal Angle B. 2D Echo Treatment  For Infection: Pen-G or Ampicillin IV x 10 days  For Arthritis alone: ASA 75mg/kg/day x 2 weeks (when 1/2 dose – for 2-3 weeks)  For Mild Carditis: ASA 75mg/kg/day x 6-8 weeks. Inspection / Palpation Malar flush with pinched and blue facies In patients with sinus rhythm and severe pulmonary hypertension or associated tricuspid stenosis. myocardium. and endocardium Most often affecting the ankles. and other tissues A. continue both ASA and Prednisone until Normal ESR is reached  For Chorea: Dizepam tab PO Prophylaxis:  Penicillin-G 1. RHEUMATIC FEVER (JONE‟S CRITERIA)  Acute Rheumatic Fever (ARF) is a multisystem disease resulting from Autoimmune Reaction to infection with Group-A Streptococci (cardiac valvular damage may persist after other features have disappeared)  RF is a Hypersensitivity Reaction induced by Group-A B-Hemolytic Streptococcus  In RF. Auscultation  CVP is measured from Midclavicular Line o S1 is usually accentuated and slightly delayed  Difference of CVP from JVP is 5 (therefore. Antibodies against M-Proteins of certain strains of Streptococcus Cross-React with Tissue Glycoproteins in the Heart. elbows Involuntary jerking movements Evanescent macular eruption w/ round borders.

CNS hemorrhage. or Enterococci recovered from Two or More Blood Cultures o 2) Either Positive Echocardiography Study result for Infective Endocarditis: Oscillating Intracardiac Mass. but NOT Positive for Major Criterion III. Criteria for Infective Endocarditis o Two Major Criteria. RF o 2D Echo with Doppler. CBC.INFECTIVE ENDOCARDITIS INFECTIVE ENDOCARDITIS I. MINOR Criteria (Mnemonic: PF-VIME) o 1) Predisposing Heart Condition or Injected Drug User o 2) Febrile Syndrome o o o o 3) Vascular Phenomena: Arterial embolism. TEE B. DUKE‟S CRITERIA FOR INFECTIVE ENDOCARDITIS (IE) A. Treatment: Acute IE Subacute IE 1) NAFCILLIN or OXACILLIN 2g IV q4 or VANCOMYCIN 500mg IV q6 or 1g IV q12 x 4weeks 2) GENTAMYCIN 100-200mg IV. No Murmurs Prognosis Fatal in 6 weeks if Untreated SUBACUTE BACTERIAL IE Strep. Viridans. MANAGEMENT A. Staph aureus. false-positive VDRL test. but NOT Positive for Major Criterion 6) Echocardiogram: Suggestive of Infective Endocarditis. rheumatoid factor. or o One Major and Three Minor. U/A. (+) Murmurs Better Prognosis II. MAJOR Criteria o 1) Positive Blood Culture Results for Infective Endocarditis  Typical Organisms for Infective Endocarditis: Streptococci viridans. Strep bovis. HACEK Group. conjunctival hemorrhage. Acute Course Cardiac Pathology Normal cardiac valves. CLASSIFICATION OF INFECTIVE ENDOCARDITIS (IE) ACUTE BACTERIAL IE Pathogenic Organism Staph. or Roth spots 5) Microbiologic Evidence: Positive Blood Culture results. Osler‟s nodes. Crea. Janeway lesions 4) Immunologic Phenomena: Immune-complex Glomerulonephritis. Enterococci (Less Virulent) Low Grade Fever. Diagnostic o Blood CS x 3 Sites. then 80mg IV q8 x 3-5 days 1) PEN-G 2-4 M „u‟ IV q4 x 4 weeks or AMPICILLIN 2g IV q4 2) GENTAMYCIN 80mg IV q8 x 2 weeks 20 . Subacute Course Damaged Valves. Aureus (Virulent) Clinical Presentation High Fever. Abscess or New Dehiscence of Prosthetic Valve or New Valvular Regurgitation Or Persistently Positive Blood Culture Results: Microorganism consistent with IE recovered from One or more Blood Cultures drawn more than 12 Hours Apart C. or o Five Minor Criteria using definitions for these criteria as listed below o Possible Infective Endocarditis: findings consistent with Infective Endocarditis that fall short of the criteria listed above B.

OTHER CARDIOVASCULAR DISEASES CARDIAC TAMPONADE    Life Threatening Condition wherein Pericardial Effusion has compressed the Heart. Acute MI. impairing its Pumping Most Common Causes: Neoplasm. Iatrogenic I. Post-Pericardiostomy Syndrome. Uremia Other Causes: TB. Physical Examination o Hypotension o Elevated JVP (Neck Vein Engorgement) o Pulsus Paradoxus ( > 10mmHg decrease in SBP during Inspiration) o RR > 20. Three Principal Features o Increased Intracardiac Pressure o Limited Ventricular Filling o Decreased Cardiac Output B. CLINICAL FEATURES A. MANAGEMENT A. Idopathic Pericarditis. Orthopnea. Fatigue o Hepatic Engorgement C. Diagnostics 12-L ECG CXR 2D Echo (Diagnostic) Low Voltage QRS Complexes Electrical Alterans Cardiomegaly No Pulmonary Venous Congestion RV Collapse with significant Pericardial Effusion BECK’S TRIAD:  Hypotension  Engorgement of Neck Veins  Muffled Heart Sounds B. HR > 100 o Muffled Heart Sounds II. Bacterial. Treatment o Emergency Pericardiocentesis o Emergency Tube Pericardiostomy w/ Creation of Pericardial Window (recurrent cases / chronic cases / infectious cases) 21 . Symptoms o Dyspnea. Trauma.

etc)  Pericarditis related to Hypersensitivity or Autoimmunity II. Fungal. Cardiac Biomarkers o May have MODEST Increases in Serum Biomarkers of Myocardial Damage (CK and Troponin) B. ECG o ECG without Massive Effusion usually displays changes secondary to Acute Subepicardial Inflammation o Evolves through 4 stages: Stage 1 Widespread Elevation of ST Segments. arms or left shoulder. Pericardial Effusion with Cardiac Tamponade and Paradoxical Pulse (Chest Pain is an important. Pericardial Friction Rub. CT / MRI o Diagnosis of Pericardial Fluid or Thickening may be confirmed by CT or MRI III. involving two or three standard limb leads and V2 to V6. PERICARDIAL EFFUSION  Effusion is usually associated w/ Pain and/or the above mentioned ECG changes. Neoplasia. Uremia. Echocardiography o Most Effective Imaging Technique o Can identify accompanying Cardiac Tamponade D. referred to neck. TB. high pitched. Retrosternal. Left Precordial. with Upward Concavity. ST Segments return to normal. findings in Acute Myocardial Infarction:  ST Elevations CONVEX. changes in body position  Pain resembles an Acute MI  HOWEVER. with reciprocal depressions only in aVR & sometimes V1.PERICARDITIS   Acute Pericarditis – most common pathologic process involving the Pericardium Cardinal Manifestations: Pain. Elevated ST-Segments return to NORMAL within hours) C. scratching or grating (heard more frequently at end-expiration with patient upright & leaning forward) Etiologic Classification of Pericarditis:  Infectious (Viral. ECG changes. as well as with an enlargement of the Cardiac Silhouette  Can lead to Cardiac Tamponade  Ewart’s Sign: a Patch of Dullness and Increased Fremitus (and Egophony) beneath the angle of the Left Scapula (caused by compression of the base of the left lung by the pericardial fluid 22 . coughing. LABORATORY A. & only then. and reciprocal depressions are usually more prominent  QRS changes occur. and notching & loss of R-Wave amplitude  T-Wave are Inversions usually seen within hours BEFORE the ST-Segments have become Isoelectric  Sequential ECGs are useful in distinguishing Acute Pericarditis from AMI (in AMI. particularly development of Q waves. Myxedema. Pyogenic. pleuritic (consequent to accompanying pleural inflammation)  Pleuritic Chest Pain: Sharp and aggravated by inspiration. Trauma. other infections)  Non-Infectious (AMI. Aortic Dissection. do the T waves become inverted (Stage 3) Stage 3 T Waves become inverted Stage 4 ECG returns to Normal in Stage 4 (weeks or months after the acute onset) **NOTE: In contrast. Pericardial Pain may be relieved by Sitting Up and Leaning Forward and is intensified by lying supine  Pericardial Friction Rub (85%): may have up to 3 components per cardiac cycle. but not invariable symptom) I. CLINICAL PRESENTATION  Chest Pain: Severe. and is described as rasping. as well as PR segment depression Stage 2 After several days. Cholesterol. Chylopericardium. or later.

Cough. Diagnostics: Imaging Studies CXR CT Scan Widening of the Superior Mediastinum Pleural Effusion in 25% of cases Diminished or Absent Opacification of the Central Venous Structures Prominent Collateral Venous Circulation Most Reliable View of Mediastinal Anatomy NO Advantage over CT Scan MRI B. CHF. Emboli Endomyocardial scarring or myocardial infiltration resulting in restriction to Left and/or Right Ventricular Filling Disproportionate LV Hypertrophy. Surgery CARDIOMYOPATHIES Dilated Restrictive Hypertrophic Left and/or Right Ventricular Enlargement. CLINICAL PRESENATION  Neck and Facial Swelling (Periorbital)  Dyspnea. Pain. MANAGEMENT A. Chest  Distant or Unilaterally Absent Breath Sounds (sometimes normal breath sounds)  If Severe: Proprosis. Syncope  Symptoms are aggravated by bending forward or lying down II. Tracheal Obstruction  Neck Vein Engorgement is the one potentially Life-Threatening Complication  Visible collateral veins on chest wall  Cyanosis. typically involving Septum more than free wall. Glossal and Laryngeal Edema. Hoarseness. Nasal Congestion. impaired systolic function. Headaches. Decrease Venous Pressure (Diuretics. Oxygen) o Obtain Histologic Diagnosis o Other Modalities: Radiation. Treatment o Relieve Symptoms: Decreasing Cardiac Output. Arms. Dizziness. Obtundation III. PHYSICAL EXAMINATION Diagnosis of SVC Syndrome is CLINICAL. with or without an Intraventricular Systolic Pressure gradient. Hemoptysis  Dysphagia. Head Elevation. usually of a Non-Dilated LV Cavity 23 . Lethargy.SUPERIOR VENA CAVA SYNDROME   Clinical Manifestation of SVC obstruction causing severe decrease in venous return from head & neck & upper extremities 90% is secondary to malignancy (lung ca – 85%) I. Arrhythmias. Tongue Swelling. Chemotherapy. Low Salt Diet. Edema on Face. Epistaxis.

Second Heart Sound o Caused by the Closure of the Aortic and Pulmonic Valves (Diastole) o Indicates End of Systole (or beginning of Diastole) o Best heard at the BASE o SPLITTING is normally heard C. RENIN-ANGIOTENSIN-ALDOSTERONE AXIS VI. and therefore. ischemic. HEART SOUNDS A. dilated. Afterload RISES and limits Cardiac Output II. or both? Which valves are affected? Are they regurgitant and/or stenotic? Is there Pericardial involvement? Has there been a Myocardial Infarction? Is an arrhythmia present? Is there evidence of congestive heart failure or of myocardial ischemia? How strenuous is the physical activity require to elicit symptoms? IV. CONTROL OF CARDIAC PERFORMANCE AND OUTPUT  Extent of shortening of heart muscle. hypertensive. First Heart Sound (S1) o Coincides with the Closure of the Mitral Valve and Tricuspid Valve (Systolic Phase) o Best heard at the APEX o Start of Systole B. the stroke volume of the ventricle in the intact heart depend on three major influences: o The Length of the Muscle at Onset of Contractions (Preload) o The Tension that the Muscle is called upon to Develop during Contraction (Afterload) o The Contractility of the Muscle (extent and velocity of shortening at any given preload and afterload)  Laplace’s Law: When Myocardial Contractility becomes impaired and the ventricle Dilates. ACTIVATION OF NEUROHORMONAL SYSTEMS 24 . or inflammatory in origin? Which chambers are involved? Are they hypertrophied. Fourth Heart Sound (S4) o Coincides with LATE DIASTOLE or ATRIAL SYSTOLE (Atrial Contraction / Slow Ventricular Filling) o Best Heard before S1 o Occurs when diminished Ventricular Compliance Increases the Resistance to Ventricular Filling o Most Patients with an Acute MI and Sinus Rhythm have an audible S4 V.PHYSIOLOGY OF THE CARDIOVASCULAR SYSTEM I. ASSESSMENT OF CARDIAC FUNCTION  Cardiac Output and Stroke Volume may be depressed in Heart Failure  Ejection Fraction = ratio of Stroke Volume to End-Diastolic Volume (Normal is 67 + 8%)  Ejection Fraction is frequently depressed in Systolic Heart Failure. Third Heart Sound (S3) o Coincides with EARLY DIASTOLE or RAPID VENTRICULAR FILLING o It is caused by the Flow of Blood during Rapid Ventricular Filling o Best Heard after S2 o Suggestive of Heart Failure / Left Ventricular Failure D. CARDIAC DIAGNOSIS: 1) Underlying Etiology 2) Anatomic Abnormalities 3) Physiologic Disturbances 4) Functional Disability Is the disease congenital. even when the stroke volume itself is normal III.

signs of increased venous pressure including edema and JVP distention Dyspnea. Marfan Syndrome) Murmur of Aortic Insufficiency. AVP (ADH) is a powerful vasoconstrictor that increases permeability of renal collecting ducts. fever. QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. Tachycardia. These afferent signals to CNS also activate efferent SNS pathways that innervate the heart. RUQ. Hypotension Dyspnea.In Heart Failure QuickTim e™ and a TIFF (Uncom pres s ed) decom pres s or are needed to s ee this picture. or arms – frequently on left Similar to angina Similar to angina Unstable Angina Acute MI Aortic Stenosis Pericarditis Aortic Dissection As described for angina Retrosternal or toward Apex May radiate to left shoulder Anterior Chest. burning Similar to angina but often more severe Similar to angina but often more severe As described for angina Sharp Tearing or Ripping Sensation. rales. kidney. Epigastric Epigastric. Knifelike Pleuritc Pressure Pleuritic Pleuritic Burning Burning Burning. Pericardial Rub. leading to reabsorption of free H2O. cough. jaw. heaviness. may be retrosternal 25 . and aortic arch. may be episodic Abrupt Onset of unrelenting pain QUALITY Pressure. Tachypnea. tightness. Typical Clinical Features of Major Causes of Acute Chest Discomfort CONDITION Angina The  CO in HF results in an unloading of high pressure baroreceptors (circles) in the LV. Several Hours 10-60 mins Prolonged Prolonged Variable Variable Variable. and skeletal muscles ASSOCIATED FEATURES Precipitated by exertion. often with radiation to or isolated discomfort in neck. on the side of Embolism Substernal Unilateral. Pericardial Tamponade. often localized Lateral to Side of Pneumothorax Substernal. Pressure Aching Sharp or Burning Variable LOCATION Retrosternal. occasional rub Dyspnea. Decreased Breath Sounds on side of Pneumothorax Worsened by Postprandial Recumbency Relieved with food or antacids May follow meal Aggravated by movement May be reproduced by localized pressure on exam Vesicular Rash Situational factors may precipitate symptoms Often with anxiety / depression in Hx DURATION More than 2 and less than 10 mins 10-20 mins Variable (often > 30mins) Recurrent episodes as described for angina Hours to Days. exposure to cold. Substernal Epigastric. Substernal Variable Dermatomal Distribution Variable. may be fleeting Often lateral. Several Minutes to a Few Hrs Variable Variable Sudden Onset. psychologic stress S4 Gallop or MR murmur during pain Similar to angina but occurs with low levels of exertion or even at rest Unrelieved by nitroglycerin May be associated with evidence of heart failure or arrhythmia Late-Peaking Systolic Murmur radiating to Carotids May be relieved by sitting up and leaning forward (+) Pericardial Friction Rub Associated with HPN and/or underlying CT D/O (eg. shoulders. peripheral vasculature. often radiating to the back. This unloading leads to generation of afferent signals to CNS that stimulate cardioregulatory centers in brain which release AVP from posterior pituitary. or Loss of Peripheral Pulses Dyspnea. squeezing. between shoulder blades Pulmonary Embolism Pulmonary Hypertension Pneumonia or Pleuritis Spontaneous Pneumothorax Esophageal Reflux Peptic Ulcer Gallbladder Disease Musculoskeletal Disease Herpes Zoster Emotional / Psychiatric Abrupt Onset. carotid sinus.

M.qwertyuiopasdfghjklzxcvbnmqwertyui opasdfghjklzxcvbnmqwertyuiopasdfgh jklzxcvbnmqwertyuiopasdfghjklzxcvb nmqwertyuiopasdfghjklzxcvbnmqwer ENDOCRINOLOGY tyuiopasdfghjklzxcvbnmqwertyuiopas dfghjklzxcvbnmqwertyuiopasdfghjklzx cvbnmqwertyuiopasdfghjklzxcvbnmq wertyuiopasdfghjklzxcvbnmqwertyuio pasdfghjklzxcvbnmqwertyuiopasdfghj klzxcvbnmqwertyuiopasdfghjklzxcvbn mqwertyuiopasdfghjklzxcvbnmqwerty uiopasdfghjklzxcvbnmqwertyuiopasdf ghjklzxcvbnmqwertyuiopasdfghjklzxc vbnmqwertyuiopasdfghjklzxcvbnmrty uiopasdfghjklzxcvbnmqwertyuiopasdf ghjklzxcvbnmqwertyuiopasdfghjklzxc vbnmqwertyuiopasdfghjklzxcvbnmqw ertyuiopasdfghjklzxcvbnmqwertyuiop Jaime Alfonso Manalo Aherrera.D. Internal Medicine Notes 2009 .

8 0C 38. Abdominal Pain) Severe (Unexplained Jaundice) D. Tachycardia (Beats Per Minute) 99 – 109 110 – 119 120 – 129 130 – 139 > 140 2.9 – 39.3 0C 39. Cardiovascular Dysfunction 1. Radioiodine Therapy Iodinated Contrast Dye Condition associated with an Acute or Subacute Nonthyroidal Illness Nonthyroidal Surgery Infection. Nausea/Vomiting. Thermoregulatory Dysfunction (Temperature) 37. Congestive Heart Failure Absent Mild (Pedal Edema) Moderate (Bibasilar Rales) Severe (Pulmonary Edema) Atrial Fibrillation 3. CVA Pulmonary Embolism Parturition DKA Emotional Stress Trauma I.3 – 38. Psychosis.9 0C > 40. Extreme Lethargy) Severe (Seizure.8 – 38. Gastrointestinal-Hepatic Dysfunction Absent Moderate (Diarrhea.ENDOCRINE DISORDERS 1) THYROID STORM   Clinical presentation of Uncomplicated Thyrotoxicosis are generally present and accentuated in Thyroid Storm Known Precipitants of Thyroid Storm (associated with Rapid Rise in Thyroid Hormone Levels) o o o o o o o o o o o Thyroid Surgery Withdrawal to Therapy. Precipitant History Negative Positive 5 10 15 20 25 30 0 10 20 30 0 10 20 Scoring: < 25 Unlikely Storm 25 – 44 Impending Storm > 45 Highly Suggestive of Thyroid Storm 5 10 15 20 25 0 5 10 15 10 0 10 2 .0 0C B. BURCH AND WARTOFSKY‟S DIAGNOSTIC CRITERIA FOR THYROID STORM A.2 – 37. Central Nervous System Effects Absent Mild (Agitation) Moderate (Delirium.7 0C 37.2 0C 38. Coma) C.4 – 39.

Pathophysiology  No evidence that there is an Increased Production of T3 or T4 causing the Storm  Magnitude of Increase in Thyroid Hormones does NOT appear to be Critical  Increased Catecholamine Receptors (Key Role)  Decreased Binding to TBG (Increased Free T3/T4) 3. Surgery  Due to poorly prepared Thyroidectomy in Grave‟s Disease patient  Other conditions associated with a Rapid Rise in Hormone Levels:  Withdrawal of Antithyroid Drug Therapy  Radioiodine Therapy  Vigorous Thyroid Palpation  Iodinated Contrast Dyes  Salicylates (competes with Albumin Binding  Increase in Free Thyroid Hormone Levels)  Conditions associated with an Acute or Subacute Non-Thyroidal Illness  Infection  CVA  Trauma  DKA 2. Thyrotoxicosis VS Hyperthyroid o Thyrotoxicosis: Clinical Syndrome resulting from Cellular Responses to Excessive Thyroid Hormone (may be EXOGENOUS or ENDOGENOUS) o Hyperthyroid: Thyrotoxicosis that results from Increased Production of Thyroid Hormones from the Thyroid Gland itself (ENDOGENOUS) B.II. NOTES FROM LECTURE ON THYROID STORM A. usually with Grave‟s Disease of Toxic Multinodular Goiter o < 10% of Hospital Admissions for Thyrotoxicosis o Mortality Rate = 20-30% o Point of which Thyrotoxicosis transforms to Storm is controversial 1. Causes of Thyrotoxicosis: PRIMARY THYROTOXICOSIS Graves Disease Toxic Multinodular Goiter Toxic Adenoma Thyroid CA / Mets Struma Ovarii SECONDARY THYROTOXICOSIS TSH Secreting Pituitary Adenoma Thyroid Hormone Resistance Syndrome H-Mole THYROTOXICOSIS WITHOUT HYPERTHYROIDISM Leakage  Subacute Thyroiditis  Painless Thyroiditis  Suppurative Thyroiditis Thyrotoxicosis Factitia  Exogenous Thyroid Hormone  Diet Pills Other Causes of Thyroid Gland Destruction:  Amiodarone  Radiation  Infarction of Adenoma Ectopic Thyroid Gland Struma Ovarii (Thyroid Tissue in ovary) C. Trauma. Untreated or Partially Treated  Infection. Atypical Presentation  Suspect Hyperthyroid in patients with Fever and Atrial Fibrillation NOT controlled with appropriate Cardiac Management  Apathy and Coma  RARE Manifestation of storm 3 . Thyroid Storm o Extreme Accentuation of Hyperthyroidism. Precipitants of Thyroid Storm  Pre-Existing Thyrotoxicosis.

MANAGEMENT OF STORM Goals in Management:  1) Stop Synthesis of New Hormones within the Thyroid  2) Halt release of stored Thyroid Hormone from Thyroid Gland  3) Prevent conversion of T4 to T3  4) Control Adrenergic Symptoms associated with Thyrotoxicosis  5) control systemic Decompensation with Treatment  6) Treat Underlying cause Key Notes:  Thyroid Hormone Levels will Normalize after 4-Weeks (TSH  longer time to Normalize)  Some Tests done in the PGH Lab: o Total T4/T3 o Free T4/T3 o Tsh o Thyroglobulin Assay o Anti-TPO o TgAb Liver Function Tests:  In Thyroid Storm. DECREASE the Dose of PTU A. we give High Doses of PTU  Monitor Liver Function Tests. Key to Management = EARLY Recognition Grave’s Ophthalmopathy 4. Increased FT3  RAI  can Worsen Ophthalmopathy if still in  Decreased TSH the Active Phase (wait until Ophthalmopathy is  12 L ECG more stable before giving RAI)  Leukocytosis. Agranulocytosis  If Storm is resolving. Liver Function Tests should have a Decreasing Trend  If LFT‟s are still increasing. shift to the Left if (+) Infection  Mild Hypercalcemia  Liver Function Test Abnormalities  Hyperglycemia (Mild to Moderate) III. Inhibit New Hormone Production 1. Methimazole  20-25mg PO q6  Inhibit Hormone Synthesis 4 . Some Laboratory Findings:  90% will NOT go back to Normal  Increased FT4. Propylthiouracil (PTU)  Inhibits Thyroid Peroxidase (which is involved in organification and coupling)  Drug of choice because it inhibits Peripheral Conversion of T4T3 (in HIGH doses)  Given in Large Doses: 600-1000mg Loading Dose and 200-300mg every 6 hours – given orally or by nasogastric tube or per rectum Mechanism Of Action  Inhibit synthesis of thyroid hormones by inhibiting organification of iodine and coupling of the iodotyrosinases  Inhibit Peripheral Conversion of T4 to T3  Proposed to have direct effects on the immune system – producing a decrease in circulating thyroid-stimulating antibodies and restoration of normal suppressor cell activity 2.

Stable Iodide (SSKI)  Given 1 hour after PTU – it blocks the release of hormone from the gland (block the synthesis first before giving Iodine)  Wolff-Chaikoff Effect: One hour after the first dose of PTU. Esmolol (IV)  50-100 ug/kg/min D. Supportive o Acetaminophen 325-650mg PO/PRN q4-q6 o Hydrocortisone 100mg IV q8 (decreases T4 to T3 conversion. Diuretics)  Glucocorticoids to correct Relative Adrenal Insufficiency E. Propranolol  To reduce tachycardia and other adrenergic manifestations  60-80mg PO q4 or 80-120mg q6  High doses or Propranolol decrease T4T3 conversion  CAUTION is needed to avoid Acute Negative Inotropic Effects. Inhibit Hormone Release 1. Removal of T4 and T3 from the Serum: o Cholestyramine o Plasmapheresis o Hemodialysis o Hemoperfusion Deiodinase Activity 5 . as some patients develop a form of High-Output Heart Failure 2. Beta-Blockers: 1. but controlling the heart rate is important. Cardioselective Agents (for patients with Pulmonary Diseases)  Atenolol 500-200mg PO QID  Metoprolol 100-200mg  Nadolol 3. Others:  Lugol‟s Solution 4-8 Drops PO q6-8  Sodium Ipodate 1-3g PO QID  Iopanoic Acid 1g PO q8 Mechanism of Iodine:  Decreases Fractional Turnover of Thyroid Iodine and T4 Secretion Rate  Blocks Thyroid Hormone release C. or Ipodate or Iopanoic Acid (0. Vasomotor Stability) o Volume Depletion and Poor Nutrition:  IV Fluids / Electrolytes  Glucose 5-10%  Vitamins  Oxygen  Vasopressors  Treatment of CHF (Digoxin. Stable Iodide is given to BLOCK Thyroid Hormone Synthesis via the Wolff-Chaikoff Effect (the DELAY allows the Antithyroid Drug to prevent the excess Iodine from being incorporated into new hormone)  Administration: A saturated solution of Potassium Iodide (5 drops SSKI every 6 hours).5mg every 12h). Alternative Treatment Lithium Carbonate: o Lithium Carbonate 300mg PO q8 (mimics iodine)  Inhibits Coupling of Iodotyrosines  Inhibits release of Thyroid Hormones o Potassium Perchlorate 1g PO QID  Inhibit conversion of T4 to T3 by decreasing Type-1 o Cholestyramine 4g PO QID F.B. may be given orally **NOTE: Opposite of Wolff-Chaikoff = Jod Basedow (worsens) 2.

The converse state of T4 Toxicosis. Toxic MNG. including Lymphocytic and Postpartum variations Iodine Induced Hyperthyroidism Excessive Pituitary TSH or Trophoblastic Disease Excessive Ingestion of Thyroid Hormone SIGNS Tachycardia. HYPERTHYROIDISM  Consequence of Excessive Thyroid Hormone Action  Thyrotoxicosis is defined as a state of Thyroid Hormone Excess and is NOT synonymous with Hyperthyroidism (which is the result of excessive thyroid function) – however. In 2-5% of patients. Irritability. Proximal Myopathy Lid Retraction or Lag Gynecomastia A. Laboratory Examinations o o o o o Sensitive TSH Analysis: single best screening test for Hyperthyroidism T4 or Free T4 Triiodothyronine T3 Radioimmunoassay (RIA) or Free T3 Thyroid Autoantibodies – not routinely necessary Radioactive Iodine Uptake Thyroid Scan – done to help determine the cause of Hyperthyroidism o TSH level is suppressed and total and unbound Thyroid Hormone Levels are increased. Clinical Manifestations (Attributable to the effects of EXCESS Thyroid Hormones in the circulation) SYMPTOMS Hyperactivity. QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. 6 .2) HYPERTHYROIDISM / HYPOTHYROIDISM I. Moist Skin Muscle Weakness. Loss of Libido B. providing surplus substrate for Thyroid Hormone Synthesis. and Toxic Adenomas  Causes: o o o o o o o o Toxic Diffuse Goiter (Grave‟s Disease) Toxic Adenoma Toxic Multinodular Goiter (Plummer‟s Disease) Painful Subacute Thyroiditis Silent Thyroiditis. the major etiologies of Thyrotoxicosis are Hyperthyroidism caused by Grave‟s Disease. with elevated Total and Unbound T4 and Normal T3 Levels. is occasionally seen when Hyperthyroidism is induced by Excess Iodine. only T3 is increased (T3 Toxicosis). Atrial Fibrillation in the elderly Tremor Goiter Warm. Dysphoria Heat Intolerance and Sweating Palpitations Fatigue and Weakness Weight Loss with Increased Appetite Diarrhea Polyuria Oligomenorrhea.

Iodide  Inhibits Hormone Release  Decrease Vascularity of Thyroid Gland 4. unless Coexistent Thyroid Cancer  Common candidates include pregnant patients who are intolerant to medications or non-pregnant during definitive therapy. Thiocyanate 5. Radioactive Iodine Therapy  Yields quickest resolution of the Hyperthyroidism  Leads to Hypothyroidism and require lifelong Thyroid Replacement Therapy Pharmacology Notes (Med School) 1. Vocal Cord Paralysis 2. Methimazole  Inhibits Organification and Coupling (only) 3. Treatment (Surgical + Antithyroid Drugs + Radioactive Iodine) 1. Surgical Intervention  No uncommonly performed. Agranulocytosis  Indicated in patients with Graves Disease. PTU 50mg/tab  Dose: 50-150mg/tab PO q8 starting dose  Maximum Dose: 1200mg/day  Adverse Reactions: Rash.C. B-Adrenergic Antagonists  Reduces Activity of Thyroid Hormone on Target Tissues  Ex) Propranolol 6. Methimazole 5mg/tab  Dose: 10-20mg PO q8  Maximum Dose: 80mg/d b. but refuses Radioactive Iodine  Those with very large goiters  Pediatric patient  Complications: Hypoparathyroidism. elderly patients who require post treatment prior to radioactive iodine therapy C. Prophylthiouracil (PTU)  Inhibits Organification and Coupling  Inhibits Peripheral Conversion of T4 to T3 2. Radioactive Iodine  Damages the Gland thru Cytotoxic Effects  It is ONLY used for Hyperthyroid!!! NOT Hypothyroid!!! 7 . Anti-Thyroid Drugs a. Anion Inhibitors  Competitive Inhibitor of Iodide Transport Mechanism  Ex) Perchlorate.

but T4 is Inferior to TSH when used as a screening test. Cool Peripheral Extremities Puffy Face. and feet (Myxedema) Diffuse Alopecia Bradycardia Peripheral Edema Delayed Tendon Reflex Relaxation Carpal Tunnel Syndrome Serous Cavity Effusions B. 8 . hands. Autoimmune Disease (Hashimoto‟s Thyroiditis) and Iatrogenic Causes are most common (treatment of Hyperthyroidism)  Secondary Causes: Pituitary Disease. Weakness Dry Skin Feeling Cold Hair Loss Difficulty Concentrating and Poor Memory Constipation Weight Gain with Poor Appetite Dyspnea Hoarse Voice Menorrhagia (later Oligomenorrhagia or Amenorrhea) Paresthesia Impaired Hearing SIGNS Dry coarse skin. Circulating Unbound T3 Levels are NORMAL in 25% of patients. If the TSH is elevated. an Unbound T4 level is needed to confirm the presence of Clinical Hypothyroidism. Clinical Features (Descending Order of Frequency) SYMPTOMS Tiredness. Laboratory Examinations o TSH immunoassay o Free T4 o Thyroid Autoantibodies o Thyroid Scan o UTZ In Hypothyroid: Increased TSH IRMA. HYPOTHYROIDISM  Results from Undersecretion of Thyroid Hormone  Iodine Deficiency remains the Most Common Cause of Hypothyroidism worldwide  In areas of Iodine Sufficiency.II. NOT indicated QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. T3 measurements are therefore. Decreased FT4 A normal TSH Level Excludes Primary (but NOT Secondary) Hypothyroidism. Hypothalamic Disease A. because it will not detect Subclinical Hypothyroidism.

50mcg. Diffuse Non-Toxic (Simple) Goiter o When Diffuse Enlargement of the Thyroid occurs in the absence of Nodules and Hyperthyroidism. and Nodular Diseases can each lead to Goiter A. Toxic Multinodular Goiter o Presence of Functional Autonomy in Toxic MNG (in contrast to Non Toxic MNG) o Clinical Presentation: Subclinical Hyperthyroidism or Mild Thyrotoxicosis o Tx: Antithyroid Drugs often with B-Blockers can normalize Thyroid Function o Laboratory:  TSH is Low  T4 Level is normal or minimally increased  T3 is often elevated to a greater degree than T4 9 . Hypotension. Treatment 1. Autoimmune Disease. most Goiters are Asymptomatic o Pemberton’s Sign: refers to symptoms of faintness with evidence of facial congestion and external jugular venous obstruction when arms are raised above the head o Tx: Iodine or Thyroid Hormone Replacement induces variable regression of goiter in iodine deficiency o Levothyroxine can be started to suppress the TSH into Low-Normal. Non-Toxic Multinodular Goiter o Most are Asymptomatic – EUTHYROID o Thyroid Architecture is distorted. and 100mcg  Start usually with 25-50mcg/d – use Lower Dosages 12. GOITER AND NODULAR THYROID DISEASE  GOITER: “Enlarged Thyroid Gland”  Biosynthetic Defects.C. Levothyroxine Na 25mcg. Goal of Treatment:  Maintain Plasma TSH in the Normal Range. Monitor Plasma TSH q3-4 months 2.5-25mcg for patients > 60y/o and those with cardiac disease  Treatment for Life  WOF Adrenal Failure. Plan  Increase Dose by 25-50mcg every 4 weeks until patient is Euthyroid d. and multiple nodules can be appreciated C. Course:  Symptoms improve in weeks  WOF for heart failure from too aggressive therapy c. it is referred to as Diffuse Non Toxic Goiter (Simple Goiter or Colloid Goiter) o Thyroid Function is preserved. Primary Hypothyroidism a. nausea and vomiting b. Secondary Hypothyroidism  Monitor Serum T4 and other Pituitary Hormones  Give steroid replacement first prior to L-Thyroxine Treatment III. but detectable range B. Iodine Deficiency.

1 mmol/L (200 mg/dL). Note that Patients with DM are on the following drugs o Aspirin o Statins o Anti-Hypertensives **NOTE: Studies have shown benefits in using these drugs C.8 to 11.9 mmol/L (100-125 mg/dL) Diabetes Mellitus FPG > 7. give it 2 hours before meals **NOTE: Lispro / Aspart (Analogs) = when given SC.1 mmol/L (200 mg/dL) **NOTE: This is 2 hours after a 75-g Oral Glucose Load B. Criteria for the Diagnosis of Diabetes Mellitus:  Symptoms of Diabetes PLUS Random Blood Glucose Concentration > 11. Nice To Knows: o Metformin = CONTRAINDICATED in patients with Renal Insufficiency o Target Glucose in patients with Infection = 110-130 (?) o Human Biphasic Insulin  30% SHORT Acting + 70% INTERMEDIATE Acting  Short Acting = Onset of Action is after 30 minutes – therefore. CLINICAL FEATURES (Notes from Rounds) A. or  Two Hour Plasma Glucose > 11. DIAGNOSIS OF DM A.1 mmol/L (200 mg/dL) during an Oral Glucose Tolerance Test    Random is defined as without regard to time since the last meal Fasting is defined as No Caloric Intake for at least 8 hours Current Criteria for Diagnosis of DM emphasize that the FPG is the MOST reliable and convenient test for identifying DM in asymptomatic individuals 10 .0 mmol/L (126 mg/dL) 2. give it 30 minutes before meals  Intermediate Acting = Onset is after 2 hours – therefore.0 mmol/L (126 mg/dL).6 mmol/L (100 mg/dL) Impaired Fasting Glucose FPG = 5. give it IMMEDIATELY before meals.1 mmol/L (140 to 199 mg/dL) Diabetes Mellitus Glucose > 11. Based on Response to Oral Glucose Tolerance Test (OGTT) Impaired Glucose Tolerance 7. it acts IMMEDIATELY  Therefore.3) DIABETES MELLITUS I. Glucose Tolerance is Classified into THREE Categories Based on FPG: Normal FPG < 5.6–6. or  Fasting Plasma Glucose > 7. Diagnostic Criteria for DM is Based on the following Premises: o 1) Spectrum of Fasting Plasma Glucose (FPG) and the Response to an Oral Glucose Load (OGTT) o 2) DM is Defined as the Level of Glycemia at which Diabetes-Specific Complications occur. to AVOID Hypoglycemia  Ex) Lispro 30‟u‟ immediately before meals II. Symptoms of DM o Polyuria o Polydypsia o Unexplained Weight Loss **NOTE: Polyphagia was removed  Target BP if (+) DM: < 130/80 B. rather than on the deviations from a Population-Based Mean 1.

Carbohydrase Inhibitor  Acarbose  Miglitol 2. Non-Sulfonylureas  Repaglinide  Nateglinide C.III. Lipase Inhibitor  Orlistat 11 . 1/3 given pm)  Ex) In a 60 kg patient at a dose of 0.3 – 0. we can give HN 20 – 0 – 4 2. Insulin INSULIN PREPARATION Lispro (Rapid) Aspart (Rapid) Regular (Short) Isophane (Intermediate) Glargine (Long) Detemir (Long) ONSET OF ACTION 5-15 mins 5-15 mins 30-60 mins 2-4 hours 2-4 hours 3-8 hours PEAK 30-90 mins 30-90 mins 2-3 hours 4-10 hours Peakless Peakless DURATION 4-6 hours 4-6 hours 6-10 hours 10-20 hours 24 hours 1. Sulfonylureas  Gliclazide  Glibenclamide 2. Insulin Sensitizers (Enhance Insulin Sensitivity) 1.4 units/kg. Rapid Acting  Usually given 5 minutes before meals B. Short Acting  Humulin-R (Brand Name) = Regular Insulin  Usually given 30 minutes before meals  Ex) 4 „u‟ Pre-Breakfast 3. OVERVIEW OF SOME DRUGS USED: A. Intestinal Absorption Inhibitors 1. Biguanide  Metformin 2. Intermediate Acting  Humulin-N (Brand Name) = NPH or Humulin Isophane (Generic)  Given at a dose of 0. Insulin Secretagogues 1.5 units/kg SC (2/3 given am. Thiazolidinedione  Rosiglitazone  Pioglitazone D.

9-7. the Insulin Dose is usually higher because of Insulin Resistance B. include FBS. Stroke. Management of Diabetes 1. Nephropathy  Macrovascular: MI. HbA1c. Consider the Mechanism of Action of the Drug: PATHOPHYSIOLOGY OF DM Islet Cell Dysfunction (A and B)  A: Increased Glucagon  B: Decreased Insulin Non-Suppressable Hepatic Glucose Output (responsible for Fasting Hyperglycemia) Insulin Resistance High Carbohydrate Diet Decreased Incretin Levels / Activity  GLT  GIP DRUGS USED Sulfonylureas Meglitinides Insulin DPP-IV Inhibitors GLP-1 Analogues Metformin Thiazolidinediones Incretin Agents Metformin Thiazolidinediones A-Glucosidase Inhibitors DDP-IV Inhibitor GLP-1 Analogues Metformin 12 . LECTURE ON DIABETES MELLITUS A.2mmol/L) <180mg/dL (<10mmol/L) 110-150mg/dL (6-8.3mmol/L) **IMPORTANT NOTES:  According to AACE: HbA1c should be <6. HHS. Treatment Goals (according to ADA 2009) HbAIc Fasting / Preprandial Plasma Glucose Postprandial Plasma Glucose Bedtime Plasma Glucose <7 70-130mg/dL (3. Type 1 VS Type 2 CM o T1DM: Absolute Insulin Deficiency o T2DM: Relative Insulin Deficiency with Insulin Resistance o In T2DM.5  When monitoring Glucose. Retinopathy. Complications of DM: o Acute: DKA.IV. PAOD D. Hypoglycemia o Chronic:  Microvascular: Neuropathy.5: usually Diabetic already (not yet a recommendation) C. and Postprandial Glucose (PPG) E. Diagnosis of DM: o Recent Studies “suggest” that HbA1c > 6.

Renal Dysfunction. Liver Disease. Osteoporosis.2. Consider Side Effects (Two Most Common Side Effects = Hypoglycemia and Weight Gain) a. Consider MonoTx or Combination Tx or Insulin  Recent Studies show: Do Combination Therapy Earlier to achieve Goals earlier  Current Suggestions: HbA1c LEVELS 6 – 7% 7 – 10% MANAGEMENT Oral Monotherapy Combination Therapy  Oral + Oral  Oral + Basal Insulin  Biphasic Insulin Insulin > 10%  The following REQUIRE Replacement Therapy (Institute Insulin Therapy)  Type 1 DM  History of Pancreatectomy or Pancreatic Dysfunction  Wide fluctuations in Glucose (Brittle Diabetes)  History of DKA  Insulin use > 5 years  Diabetes > 10 years (because of Progressive B-Cell Destruction) 13 . but NOT advisable for elderly  it is prone to Hypoglycemia due to its Long Action b. Common Side Effects Insulin Sulfonylureas Metiglinides Thiazolidinediones  Hypoglycemia Weight Gain  Hypoglycemia Weight Gain Few Hypoglycemia Weight Gain No Hypoglycemia if MonoTx Weight Gain Edema. Abdominal Pain No Hypoglycemia if MonoTx Weight Loss No Hypoglycemia if MonoTx Headache. Nasopharyngitis Metformin Acarbose GLP-1 Agonist DP-IV Inhibitors **IMPORTANT Notes: -Reason for Weight Loss in DM (symptom of DM)  due to Lipolytic Actions in DM -Hypoglycemia in SU: o Glyburide > Glibenclamide > Glimepiride > Gliclazide > Glipizide o Glyburide is not available in the Philippines o Glibenclamide: used in the Philippines. CHF. etc 3. CHF  Glibenclamide: CKD  Some Drugs that can be used in CKD: Meglitinides. Acarbose. Flatulence. Heart Problem. Anemia No Hypoglycemia if MonoTx Weight Loss Lactic Acidosis (especially if with CKD. Hypoxia) No Hypoglycemia if MonoTx Weight Loss Diarrhea. Some Contraindications:  Metformin: Hypoxia.

Dysplipidemia. Evaluate at the Appropriate Time (based on Peak Effect) DRUG STARTED Sulfonylureas Meglitinide WHEN WILL DRUG TAKE EFFECT? 1-2 Weeks 1-2 Weeks WHEN TO MONITOR RESPONSE? (Clinical Monitoring) FPG at 2 Weeks HbA1c at 3 Months FPG at 2 Weeks HbA1c at 3 Months PPG at Initiation FPG at 2 Weeks HbA1c at 3 Months HbA1c at 3 Months PPG at Initiation FPG at 4 Weeks HbA1c at 3-6 Months FPG at 2 Weeks HbA1c at 3 Months PPG at Initiation Metformin Acarbose Thiazolidinediones DPPV-IV Inhibitors 2-3 Weeks 2-4 Weeks 1-2 Months 2 Weeks (?)  Annual Laboratories: o Lipid Profile o Liver Function Tests o Urine Albumin:Creatinine Ratio o Serum Creatinine / GFR o TSH in T1DM. Postprandial Plasma Glucose Fasting Plasma Glucose. Insulin INSULIN PREPARATION Lispro (Rapid) Aspart (Rapid) Regular (Short) Isophane (Intermediate) Glargine (Long) Detemir (Long) PRIMARY CONTROL Postprandial Plasma Glucose Postprandial Plasma Glucose Postprandial Plasma Glucose Fasting Plasma Glucose Fasting Plasma Glucose Fasting Plasma Glucose 5.4. Postprandial Plasma Glucose c. Monotherapy DRUG GROUP Sulfonylureas Meglitinides Metformin Thiazolidinediones Incretin Acarbose DDP-IV Inhibitor b. Consider Primary Effect of Drug (either Preprandial or Postprandial) a. and women > 50 o Dilated Eye Exam 14 . Suggested Regimen based on HbA1c If HbA1c is <7% Control Postprandial first 7-9% Control either Preprandial and Postprandial >9% Control Preprandial (fasting) first d. Combination Therapy Sulfonylureas + Metformin Sulfonylureas + Rosiglitazone Sulfonylureas + Acarbose Repaglinide + Metformin PRIMARY CONTROL Fasting Plasma Glucose Postprandial Plasma Glucose Fasting Plasma Glucose Fasting Plasma Glucose Postprandial Plasma Glucose Postprandial Plasma Glucose Postprandial Plasma Glucose Fasting Plasma Glucose Fasting Plasma Glucose Fasting Plasma Glucose.

not involving Tendon Capsule or Bone Superficial Wound. not involving Tendon Capsule or Bone with Infection Superficial Wound. Post-ulcer II: Dermal involvement III: Deep tissues (Muscle and bone) B. Joint Capsule (Gram Negative: Aminoglycosides Deep Ulcer with abscess. completely epithelialized with Infection and Ischemia I Superficial Wound. not involving Tendon Capsule or Bone with Infection and Ischemia II Wound Penetrating to Tendon or Capsule Wound Penetrating to Tendon or Capsule with Infection Wound Penetrating to Tendon or Capsule with Ischemia Wound Penetrating to Tendon or Capsule with Infection and Ischemia A: Non-infected. DIABETIC FOOT (NEUROISCHEMIC FOOT ULCER / NIFU) A. completely epithelialized Pre or Postulcerative Lesion. joint capsule or deep fascia without abscess / osteomyelitis Tendon. not involving Tendon Capsule or Bone with Ischemia Superficial Wound. Other Notes on Management  Approved Drugs for Management of Pre-Diabetes (Impaired Glucose Tolerance)  Acarbose  Metformin  TZD  If (+) Hypoglycemia  Stop SU: Glucose levels will normalize after 3-5 days If (+) Renal Disease. Non-ischemic B: Infected. Ischemic III Wound Penetrating to Bone or Joint Wound Penetrating to Bone or Joint with Infection Wound Penetrating to Bone or Joint with Ischemia Wound Penetrating to Bone or Joint with Infection and Ischemia Stage C Stage D I: Change in color. 1st Gen Cephalosporins Ulcer extends to ligament. Ampi-Sul. Pre-ulcerative. Glucose will normalize after 1 wk V. completely epithelialized with Ischemia Pre or Postulcerative Lesion. completely epithelialized with Infection Pre or Postulcerative Lesion. Wagner 0 I II III IV V No Open Lesion but may have deformity or cellulites Superficial Ulcer. or joint sepsis Bone (Anaerobic Coverage) Localized Gangrene (localized to forefoot or heel) Advanced Gangrene 15 . Non-ischemic C: Non-infected. University of Texas Grading: 0 Stage A Stage B Pre or Postulcerative Lesion. osteomyelitis. partial or full thickness Dermis only (Gram Positive: Cloxacillin.6. Ischemic D: Infected. tendon.

Mesenteric. Differential Diagnosis: but the degree of Hyperglycemia may be moderate (~300mg/dL or lower). Catecholamines.3 Normal Normal to Slightly High B.3 – 66.4) DIABETIC EMERGENCIES I. Pathophysiology o Results from RELATIVE or ABSOLUTE Insulin Deficiency combined with counterregulatory hormone excess (Glucagon. Serum Amylase and Transaminases may be elevated.6 (600 – 1200) 135 – 145 Normal Normal Normal Normal Moderately Increased 330 – 380 +/Normal to Slightly Decreased > 7. o Starvation Ketosis Urine Ketone reaction correlates poorly with Ketonemia. Volume Depletion. Plasma Glucose is usually elevated. Peripheral) Drugs (Cocaine) Pregnancy PHYSICAL FINDINGS Tachycardia Dehydration / Hypotension Tachypnea / Kussmaul Respirations Respiratory Distress Abdominal Tenderness (may resemble Acute Pancreatitis / Surgical Abdomen) Lethargy / Obtundation / Cerebral Edema Possibly Coma Symptoms / Signs of DKA usually develop over 24 hours Hyperglycemia  Glucosuria. Coronary. again raising suspicion for Intra-Abdominal Pathology. DKA vs HHS Glucose mmol/L (mg/dL) Na+ mEq/L K+ Mg2+ ClP Creatinine Osmolality (mOsm/mL) Plasma Ketones Serum Bicarbonate mEq/L Arterial pH Arterial PCO2 mmHg Anion Gap [Na-(Cl+HCO3)] DKA 13. Volume Depletion. Hyperkalemia.3 20 – 30 High HHS 33.8 – 7. Azotemia. Clinical Features of DKA SYMPTOMS Nausea / Vomiting Thirst / Polyuria Abdominal Pain Shortness of Breath PRECIPITATING EVENTS Inadequate Insulin Administration Infection (PNA / UTI / Gastroenteritis / Sepsis) Infarction (Cerebral. DIABETIC KETOACIDOSIS  DKA and Hyperglycemic Hyperosmolar State (HHS) are ACUTE Complications of Diabetes  DKA was formerly considered a Hallmark of DM Type 1  HHS is primarily seen in individuals with DM Type 2  BOTH disorders are associated with Absolute or Relative Insulin Deficiency. D. Ketone Body Laboratory evaluation of DKA shows an Increased Ion Gap Metabolic formation in the Liver Acidosis and Positive Serum Ketones.9 – 33. 16 . Complications of DKA o Lactic Acidosis o Arterial Thrombosis o Cerebral Edema Hyponatremia. and Acid-Base Abnormalities A. Cortisol and Growth Hormone) o BOTH Insulin Deficiency and Glucagon Excess are necessary for DKA to develop o Decreased Ratio of Insulin to Glucagon promotes Gluconeogenesis. but is usually o Alcoholic ketoacidosis Positive in DKA o Other Increased Anion Gap Acidosis o o o E. and Hyperosmolality are other findings.3 (250 – 600) 125 – 135 Normal to Increased Normal Normal Decreased Slightly Increased 300 – 320 ++++ < 15 mEq/L 6. Tachycardia Classic Signs: Kussmaul Respiration and a Fruity Odor of patient‟s breath (secondary to Metabolic Acidosis and Increased Acetone) C. Glycogenolysis.

1 units/kg/hour 11) Administer Intermediate or Long-Acting Insulin as soon as patient is eating. Increase 2 to 3 fold if NO response by 2-4 hours.3: Hold Insulin. CXR. glucose goal is 150 – 250 mg/dL.3 – 5: 20-30 meq K/L  If >5: Re-check Potassium q20 Potassium Drips:  Peripheral Line: Maximum Rate is 10 meq/hr (Maximum of 60meq/L)  Central Line: Maximum Rate is 20 meq/hr o o o o o o o 4) Replace Fluids: 2-3 L of 0. then 0. Na. fluid intake and output every 1-4 hours 9) Replace K+: 10 mEq/h when Plasma K+ < 5.5mEq/L. trauma. infarction.05 – 0.3mmol/L (3.3mEq/L).1 units/kg) or IM (0. and acidosis is resolved.45% Saline at 150-300mL/h.3units/kg). bicarbonate. pulse. Administer 40-80 mEq/h when Plasma K+ <3. If initial Serum K + is < 3. change to 5% Glucose and 0. ECG normal. cocaine)? Initiate appropriate workup for precipitating event (cultures. Cl. Criteria For Resolving DKA o Normalization of Serum Anion Gap o Normalization of Acidosis o (-) Ketones **IMPORTANT Notes:  Serum Ketones: B Hydroxybutyrate (which is converted to Acetoacetate)  Urine Ketones: Acetoacetate 17 .1 units/kg per hour by continuous IV infusion. phosphate) and Anion Gap every 4 h for first 24 hours 8) Monitor BP. measure electrolytes (especially K+. Phosphate) Acid-Base Status – pH.45% Saline at 100-200mL/h when Plasma Glucose reaches 250mg/dL (14mmol/L) 5) Administer Short-Acting Insulin: IV (0. HCO3. mental status. Urine Output) Notes on Potassium:  If < 3. Metabolic Acidosis) 2) Admit to Hospital.9% Saline over first 1-3 hours (10-15mL/kg per hour). Mg. (+) Serum Ketones.F. infection. Insulin Infusion may be decreased to 0. 0. Allow for overlap in Insulin Infusion and Subcutaneous Insulin Injection o G.5mEq/L or if Bicarbonate is given 10) Continue above until patient is stable. Bicarbonate. do NOT administer Insulin until the K+ is corrected to > 3.3mEq/L) 6) Assess patient: What precipitated episode (noncompliance. respirations. Intensive Care Setting may be necessary for frequent monitoring or if pH < 7. urine flow and normal creatinine documented.00 or Unconscious 3) Assess: Serum Electrolytes (K. pCO2.3mmol/L (3. ECG) 7) Measure capillary glucose every 1-2 h. Add 40meq K/L  If 3. B-Hydroxybutyrate Renal Function (Creatinine. Management of DKA o o o 1) Confirm diagnosis (High Plasma Glucose. subsequently.

Clinical Presentation: o Prototype patient: Elderly with Type 2 DM. before giving Insulin 2. and diminished Oral Intake that culminates in Mental Confusion. HYPERGLYCEMIC HYPEROSMOLAR STATE (HHS) A. exacerbated by inadequate fluid intake o Insulin Deficiency is only RELATIVE (probably) and less severe than in DKA C.6 (Ex. if there is NO Improvement. and an altered mental status o Notable ABSENT are symptoms of Nausea. concurrent illness such as MI or stroke. give 4. effectively inhibits Lipolysis and Ketogenesis B. 100cc X X = 45 cc / hour or 45 ugtts/min (which is equivalent to 9 U/hour) 3. Pathophysiology o Relative Insulin Deficiency and Inadequate Fluid Intake are the underlying causes of HHS o Hyperglycemia  Osmotic Diuresis  Volume Depletion.1 to 0. 20 U . we may: o 1) Start D5NR + 20 mEqs KCl x 10 Hours o 2) Start Fixed Dose of Insulin at HN 0. we give 9 Units/Hour . pneumonia & other serious infections o Results from Severe Dehydration and Hyperglycemia – clinical evidence of Severe Dehydration is the rule o Ketoacidosis is ABSENT because Residual Insulin Secretion. Gatchalian)  CASE: 60kg Patient comes in with a CBG of 500  1st thing to do is HYDRATE (up to 3 L can be given) – however. the difference is 200 If Difference is: > 75 50-75 < 50 Decrease by HALF MAINTAIN Dose Double Insulin Dose Ex) If we are giving 9 U/hr. and abdominal pain.4-0. with a several weeks history of Polyuria. though inadequate for Glycemic Control. sepsis. or Coma o PE: reflects profound Dehydration and Hyperosmolality and reveals Hypotension.5 U/hr 4. 9 U . Management o 1) Fluid Replacement o 2) Insulin Therapy o 3) Collection of Electrolyte Deficits 18 . Vomiting.15 U/kg  Maintain on a Drip at 0. Mix 20 U Insulin in 100cc PNSS)  Ex) In a 60 kg patient.6 „u‟ / kg / hr II. Insulin Regimen  Give a Bolus Dose of 0. RULE (Subjective for PGH)  If you get a CBG Value of LESS than 250 for 2-3 Consecutive Times. = . and the Kussmaul Respirations characteristic of DKA o Often precipitated by a serious. Adjusting Insulin  Monitor CBG every hour and get the difference  Ex) If CBG is 500. Hydration  Monitor CBG every 1 hour  We can give as much as 3 L. then decreases to 300 after one hour. Tachycardia.10 U/kg – range of 0. start Insulin 1. Weight Loss.MANAGEMENT OF DIABETIC KETOACIDOSIS (Dr. Lethargy.

qwertyuiopasdfghjklzxcvbnmqwertyui opasdfghjklzxcvbnmqwertyuiopasdfgh jklzxcvbnmqwertyuiopasdfghjklzxcvb nmqwertyuiopasdfghjklzxcvbnmqwer GASTROENTEROLOGY tyuiopasdfghjklzxcvbnmqwertyuiopas dfghjklzxcvbnmqwertyuiopasdfghjklzx cvbnmqwertyuiopasdfghjklzxcvbnmq wertyuiopasdfghjklzxcvbnmqwertyuio pasdfghjklzxcvbnmqwertyuiopasdfghj klzxcvbnmqwertyuiopasdfghjklzxcvbn mqwertyuiopasdfghjklzxcvbnmqwerty uiopasdfghjklzxcvbnmqwertyuiopasdf ghjklzxcvbnmqwertyuiopasdfghjklzxc vbnmqwertyuiopasdfghjklzxcvbnmrty uiopasdfghjklzxcvbnmqwertyuiopasdf ghjklzxcvbnmqwertyuiopasdfghjklzxc vbnmqwertyuiopasdfghjklzxcvbnmqw ertyuiopasdfghjklzxcvbnmqwertyuiop Jaime Alfonso Manalo Aherrera.D. Internal Medicine Notes 2009 . M.

000mm3 3. ongoing. hepatic encephalopathy). and Vascular Lesions I. or Hetastarch can be used  Blood should be used for volume replacement whenever possible and should be initiated as soon as it is evident that patient’s bleeding is massive. Correction of Coagulopathy  Discontinuation of offending anti-coagulants followed by infusion of FFP can be used to correct prolonged coagulation parameters  Protamine Infusion: 1mg antagonizes 100 units of heparin  Parenteral Vitamin-K (10mg SC or IM) for prolonged PT from Warfarin Tx or Hepatobiliary Disease  Platelet Infusion if Platelet Count < 50. Initial Resuscitation 1. CLINICAL PRESENTATION  Overt GI Bleeding: presents with passage of fresh or altered blood through the mouth or in the stool  Occult Bleeding: refers to (+) Fecal Occult Blood Test or Iron-Deficiency Anemia without visible blood in stool  Obscure Bleeding: refers to GI blood loss of unknown origin that persists or recurs after negative initial endoscopic evaluation (obscure bleeding can either be Overt or Occult) V.COMMON GASTROINTESTINAL DISEASES 1) UPPER GASTROINTESTINAL BLEEDING (UGIB)    Hemorrhage may develop from any gut organ Upper GI Bleeding presents with MELENA or HEMATEMESIS Lower GI Bleeding produces passage of Bright Red or Maroon Stools The Most Common Upper GI Causes of Bleeding are Ulcer Disease. or active variceal hemorrhage 2 . Other etiologies include Portal HPN. Malignancy. Alcohol. SOURCES OF BLEEDING  PUD (Duodenal and Gastric)  Gastritis (Stress. Tetracycline. Restoration of Intravascular Volume:  Isotonic Saline. TERMINOLOGIES  Hematemesis  Melena  Hematochezia  Occult GI Bleeding  Symptoms of Blood Loss or Anemia II. Liver & Renal Function Tests B. Airway Protection  Intubation to prevent aspiration should be considered in diminished mental status (shock. Drugs)  Esophagitis. MANAGEMENT  Antacids  H2 Blockers / PPI  AntBx: Metronidazole. Amoxicillin. Gastroduodenal Varices  Mallory-Weiss Tears  Angiodysplasia or Telengiectasia  Gastro-Esophageal Carcinoma  Hemophilia  Gastroduodenal Fistula  Bleeding Disorders (Leukemia. or severe enough that Colloid Infusion alone is NOT adequate for Tissue Oxygenation  Packed RBC Transfusion: should be continued until patient’s condition is hemodynamically stable and hematocrit reaches 25% or greater 2. Gastroduodenitis. Tears across the Gastroesophageal Junction. Duodenitis  Esophageal Varices. LR. massive hematemesis. and Esophagitis. Blood Type. Initial Evaluation o Intravascular Volume and Hemodynamic Status o Laboratory Evaluation (CBC. GENERAL CONSIDERATIONS IN OVERT BLEEDING A. Clarithromycin  Anticholinergics  Sucralfate  Bismuth  PGE2 IV. PT/PTT. Aplastic Anemia) III.

Balloon Tamponade Pharmacologic Prophylaxis with B-Adrenergic Antagonists  Shown to REDUCE Portal Pressure & lower risk of recurrent bleeding  Propranolol and Nadolol – reduce resting heart rate by 25% Hepatic Transplantation 3 . von-willebrand’s disease. DIC) Medications (warfarin. Color of Stool Can provide important clues NG Aspiration Useful in diagnosing Upper GI Bleeding Anoscopy/Sigmoidosocpy DRE may identify potential source of bleeding in anorectum B.5mL/min Emergent total colectomy may be a lifesaving maneuver for massive. heparin. coagulation disorders. this should be preceded by EGD to rule out rapidly bleeding upper source VII. liver disease. Melena. Fluid resuscitation & hemodynamic stability are essential prior to endoscopy. aspirin. vitamin-K deficiency. TIPS. thromboytics). Esophageal Varices  Variceal Ligation of Banding = Endoscopic Therapy of Choice (controls active hemorrhage)  Sclerotherapy (used less frequently because of complications)  TIPS / Transjugular Intrahepatic Portosystemic Shunt – to decompress the portal pressure  Shunt Surgery  Balloon Tamponade Gastric Varices  Octreotide Infusion or other pharmacologic therapy should be initiated early (as for Esophageal Varices)  Variceal Ligation or Banding – usually NOT successful  Sclerotherapy can be attempted. Hematochezia Important points in history include prior bleeding episodes. unlocalized lower GI bleed. THERAPY FOR SPECIFIC LESIONS Peptic Ulcer Disease (PUD) High Dose-Proton Pump Inhibitors (Omeprazole 40mg PO BID) reduces rate of recurrent bleeding & need for surgery. NSAIDs. Octreotide Infusion to reduce Portal Pressures acutely. Surgery for intractable or recurrent bleeding Risk Factors for increased morbidity & mortality:  Age > 60 y/o  More than one comorbid illness  Blood Loss > 5 units  Shock on Admission  Bright-Red Hematemesis with Hypotension Variceal Hemorrhage Coagulopathy Large (>2cm) Ulcers Recurrent Hemorrhage (within 72 hours) Requirement for Emergency Surgery ICU admission and Intubation for airway protection in patients who are actively bleeding from varices.VI. alcohol use. and bleeding tendencies:  History of emesis prior to GI bleed = suggest Mallory-Weiss Tear  NSAIDs and Aspirin  Hypotension and Hypovolemic Shock preceding bleed suggests Ischemic Injury to the gut  Radiation Therapy to prostate or pelvis suggests radiation proctitis  Prior Aortic Graft Surgery – possibility of Aortoenteric or Aortocolonic Fistula Precipitating Factors Abnormalities in coagulation (liver disease. Use of High Dose PPIs has documented utility in patients who are awaiting endoscopic treatment or in those whom endoscopy is contraindicated or postponed Therapeutic Endoscopy: advantage of immediate treatment & should be implemented in all patients early in the hospital course (within 24 hours). APPROACH TO PATIENT A. History & PE Degree of Volume Loss Level of Bleeding Etiology of Bleeding Patients with Lower GI Bleed have less hemodynamic compromise than those with Upper GI Bleed Hematemesis or Coffee-Ground Emesis. Further Evaluation and Therapy Esophagogastroduodenoscopy (EGD) Colonoscopy Tagged RBC Scanning Arteriography Surgery Preferred method of investigation and therapy of upper GI bleed All patients with acute Lower GI bleed from unknown source should undergo endoscopic evaluation of colon RBCs labeled with technetium 99m remain in circulation for as long as 48 hours and extravasate into the bowel lumen with active bleeding Allows rapid localization and potential therapy of GI bleeding when bleeding rates exceed 0.

vomiting. and abdominal distention Abdominal Pain (Major Symptom)  BORING and Steady in Character (in Epigastrium & Periumbilical Region)  Radiates to the Back (in 50% of Cases) or other Parts of the Abdomen (Chest. or CNS processes Prophylactic Therapy: Histamine-Receptor Antagonists and Sucralfate. especially those who require mechanical ventilation > 48 hours.0mg%)  GI Bleeding 4) > 3 Ransom Criteria (not fully utilizable until 48 hours) 5) Apache II Score > 8 (Cumbersome) o o o II. Sphincter of Oddi Obstruction o Drugs (MEAT-V) – Mercaptopurine. Common Causes of Acute Pancreatitis o Gallstones. Clinical Features o Steady and Boring Abdominal Pain. Azathioprine. Valproic Acid B. Flanks)  ACUTE in Onset (Sudden)  Lasts for Several Hours  Moderate to Severe **NOTE: It is Frequently more Intense when patient is SUPINE. Epigastric or Periumbilical in location. Proelastase. Post-Op. Tetracycline. radiating to the BACK o Pain is more intense when SUPINE o Relieved by sitting with the Trunk Flexed and Knees drawn up (Fetal Position / Prostration) o Associated with nausea. and relieved by Sitting 4 . burns. PPI’s 2) PANCREATITIS  Pathologic Spectrum varies from Edematous Pancreatitis (Mild & Self-Limited) to Necrotizing Pancreatitis (correlates with the Severity of the attack) I.Stress Ulcer Encountered in ICU setting. ACUTE PANCREATITIS  AUTODIGESTION: One of the pathogenic theories of pancreatitis – wherein pancreatitis results when Proteolytic Enzymes (Trypsinogen.8 mmol/L after IV-Administration Hypoalbuminemia  Severe Acute Pancreatitis: Risk Factors that Adversely Affect Survival in Acute Pancreatitis: o o 1) Associated with Organ Failure and/or Local Complications such as Necrosis 2) Clinical Manifestations  Obesity BMI > 30  Hemoconcentration (Hct > 44%)  Age > 70 3) Organ Failure  Shock  Pulmonary Insufficiecny (PO2 < 60)  Renal Failure (CR > 2. sepsis. Hypercalcemia o ERCP. Trauma.000 mm3 Hyperglycemia or FBS > 200 mg/dL Serum LDH > 400 units/mL Serum AST or SGOT > 250 units/mL AFTER 48 HOURS OF ADMISSION Fall in Hematocrit by > 10% Fluid Deficit of > 4000 mL Hypocalcemia (<8mg/dL) Hypoxemia (PO2 < 60mmHg) Increase in BUN to > 1. and Phospholipase-A) are activated IN the Pancreas. with coagulopathy. RANSON’S CRITERIA IN PANCREATITIS  POOR Predictive Power!  > 3 Factors at time of Admission (1) or during initial 48 hours (2) indicates an Increased Mortality Rate  These patients need closer monitoring in an ICU stting FIRST 24 HOURS Patients age > 55 y/o Leukocytosis or WBC > 16. Alcohol = MOST COMMON o HyperTriglyceridemia. Chymotrypsinogen. Estrogen. rather than in the Intestinal Lumen A.

ERCP. Ovarian  Macroamylasemia. Peritonitis. Irraiation Sialadenitis. Polyarteritis Nodosa Pain referred in Upper Abdomen Serum Lipase Level is NOT Elevated in DKA (however. esophagus. Approximately 85% of patients with acute pancreatitis have an elevated serum amylase level. Dissecting Aortic Aneurysm Serum Amylase & Lipase levels are widely used as Screening Tests for Acute Pancreatitis in patients with Abdominal Pain or Back Pain. Serum Amylase is often elevated in other conditions (because enzyme is found in many organs – pancreas. mild to moderate elevations of Amylase and/or Lipase are problematic in making a diagnosis of Pancreatitis. abdominal distention. In the absence of objective evidence of pancreatitis by abdominal UTZ. Values greater than THREE TIMES the upper limit of Normal virtually clinch the Diagnosis if Gut Perforation or Infarction is excluded. Esophagus. Physical Examinations o Distressed & anxious patient. Perforated / Penetrating Peptic Ulcer. xrays showing mechanical obstruction Evident in elderly debilitated patients with brisk leukocytosis. Cerebral Trauma. Tachycardia o Hypotension: which may be due to:  Hypovolemia 20 to exudation of Blood and Plasma CHON into retroperitoneal space  Increased formation and release of Kinin Peptides which cause Vasodilation and Increased Vascular Permeability  Systemic Effects of Proteolytic and Lipolytic Enzymes o Obstructive Jaundice due to Edema of the Head of the Pancreas o Erythematous Skin Nodules 2 0 to Subcutaneous Fat Necrosis o Bibasilar Rales. In Acute Pancreatitis. Amylase is elevated) Renal Colic. Signs of Organ Failure E. Ileus is usually absent. Angiography shows vascular occlusion SLE. Atelectasis. Choledocholithiasis. and bloody diarrheal. or pseudocyts formation. Differential Diagnosis = Any Disease with (+) Abdominal Pain Perforated Viscus (especially Peptic Ulcer) Acute Cholecystitis and Biliary Colic Acute Intestinal Obstruction Mesenteric Vascular Occlusion Connective Tissue Disorders with Vasculitis Pneumonia Diabetic Ketoacidosis Other Differentials Can usually identified by imaging studies or endoscopy Readily diagnosed by the presence of Free Intraperitoneal Air Pain of Biliary Tract in Origin is usually right-sided or epigastric than periumbilical. Levels return to normal within 3-5 days unless there is extensive pancreatic necrosis. Postoperative Hyperamylasemia Serum LIPASE may now be the Single Best Enzyme to measure for the diagnosis of Acute Pancreatitis.C. Diagnosis of Acute Pancreatitis o Any severe acute pain in abdomen or back should suggest Acute Pancreatitis o Diagnosis confirmed by a Threefold or Greater Elevated Level of Serum Amylase and/or Lipase o Strong Indicators include: Hemoconcentration (Hct > 44%). Chronic Liver Disease. Burns. Pleural Effusion o Hypoactive Bowel Sounds o Findings in Severe Necrotizing Pancreatitis:  Cullen’s Sign = Faint blue discoloration around umbilicus which occurs as the result of Hemoperitoneum  Turner’s Sign = blue-red-purple / green-brown discoloration of flanks due to tissue catabolism of Hemoglobin D. Maxilofacial Surgery  Tumor Hyperamylasemia: CA of Lung. Renal Transplantation. and is gradual in onset. Aortic Aneurysm. liver. Myocardial Infarction. UTZ is helpful in diagnosing Cholelithiasis and Cholecystitis Both Pancreatitis and Acute Cholecystitis can have elevated serum amylase Should be colicky pain. Breast. No single blood test is reliable for the diagnosis of Acute Pancreatitis in patients with Renal Failure. DKA. fallopian tube – and can be produced by various tumors – carcinomas of the lung. CT. Pregnancy. Serum Amylase is usually elevated within 24 hours of onset and remains so for 1-3 days. Ruptured Ectopic Pregnancy. Calculus. or EUS. small intestine. Low Grade Fever. 5 . breast. kidney.  Renal Insufficiency  Salivary Gland Lesions: Mumps. salivary glands. An Assay for Trypsinogen has a theoretical advantage over Amylase and Lipase determinations in that the pancreas is the ONLY organ that contains this enzyme. incomplete ductal obstruction. Intestinal Obstruction / Infarction. Drugs (Morphine)  Cholecystitis. ovary.

Aspiration Pneumonia  Cultures should be obtained and Broad-Spectrum Antibiotics should be administered 4. ARDS. Rupture (Pancreatic Ascites). marked Leukocytosis. Endoscopic Retrograde Cholangiopancreatography (ERCP)  Local Systemic G. which is frequently a Pseudocyst Can confirm clinical impression of Acute Pancreatitis. Infected Pseudocyst. Pseudocyst. Hypotension. ARDS  Cellular Injury & death result in liberation of bradykinin peptides. Oliguria. & histamine that can produce vasodilation. GI Hemorrhage. Encephalopathy 2. Lipase 3. Hyperbilirubinemia Elevated Serum Lactate Dehydrogenase (LDL) Levels > 8. Sonography 7. which results from isolated distention of Transverse Colon 4) Duodenal Distention with Air-Fluid Levels 5) A Mass. Ascites. usually involving the jejunum (Sentinel Loop) 2) Generalized Ileus with Air-Fluid Levels 3) Colon Cut-Off Sign.5umol or > 500 U/dL  POOR Prognosis Hypertriglyceridemia in 15-20% (Amylase and Lipase are normal in these patients) Hypoxemia ECG: ST-Segment and T-Wave Abnormalities. most notably: LUNG 5. Necrotizing Pancreatitis  Represents a severe form of Acute Pancreatitis. Fat Necrosis. Amylase                        Diagnosis of Pancreatitis is usually established by detection of an INCREASED Level of Serum Amylase (Salivary Gland Disease and Gut Perforation or Infarction should be EXCLUDED!) There is NO Definite Correlation between the Severity of Pancreatitis & Degree of Elevation After 48 to 72 hours. usually identified on Dynamic Dual-Phase CT Scanning with Contrast  Infected Pancreatic Necrosis: (+) Increasing Abdominal Pain. Hemorrhage. Complications: 1. Cholangitis. Endoscopic. Renal Failure  Due to Severe Intravascular Volume Depletion or Acute Tubular Necrosis 6 . Amylase tend to RETURN to NORMAL (even with continuing evidence of pancreatitis) Elevated Levels may remain for 7 to 14 days Three Fold Elevation of Serum Lipase is usually Diagnostic of Acute Pancreatitis Markedly Increased Levels of Peritoneal or Pleural Fluid Amylase (>1500nmol/L or > 5000U/dL) Leukocytosis (15. Hyperglycemia. Pseudocysts  Suggested by persistent pain or hyperamylasemia  Complications: Infection. Bacteremia  Mx for Infected Necrosis: CT-Guided Percutaneous Aspiration for GS/CS to Confirm 2. Infection  Sources of Fever: Pancreatic Necrosis. Pneumonia.000 per uL) Hemoconcentration in more severe disease (Hematocrit > 44%) Hyperglycemia. Pleural Effusion. Abscess. Other Findings: 4. Plain Films of the Abdomen in Acute Pancreatitis 5. Diagnostics: 1. Abscess. and edema with profound effects on many organs.F.000 – 20. vasoactive substances. even if Amylase is NORMAL Can indicate severity Useful in Acute Pancreatitis to evaluate the gallbladder Pancreas is enlarged in Acute Pancreatitis High resolution imaging of the Pancreatic Parenchyma and Pancreatic Duct with a trasducer fixed to an endoscope that can be directed onto the surface of the pancreas through stomach or duodenum May provide useful information on the status of pancreatic ductal system Necrosis. CT-Scan 6. Surgical Technique 3. Pulmonary Complications  Atelectasis. Hypocalcemia. DIC. Obstructive Jaundice Pleural Effusion. simulating Myocardial Ischemia 1) Localized Ileus. Obstruction of adjacent structures  Asymptomatic Non-Enlarging Pseudocyts < 6cm: followed clinically with serial imaging studies  Symptomatic / Complicated Pseudocysts: decompression by Percutaneous. increased vascular permeability. Endoscopic Ultrasonography (EUS) 8.

Aggressive Volume Repletion with IV Fluids  Serum Electrolytes. usually 3-7 days after treatment is instituted) 1. Narcotic Analgesics: For PAIN Relief Most Commonly used agent because it has the least effect on the Sphincter of Oddi Meperidine Morphine & Pantazocine It is the DOC because it does NOT cause Spasm of the Sphincter of Oddi) However. Urgent ERCP and Biliary Sphincterotomy  Within 72 Hours of presentation – can improve the outcome of Severe Gallstone Pancreatitis  Thought to result from reduced biliary sepsis. rather than being a true improvement of pancreatic inflammation 5. Ca2+. Nothing Per Orem (NPO)  NPO until they are free of pain and nausea  NG Suction is reserved for patients with Ileus or Protracted Nausea & Vomiting and is not routine (Nasogastric Suction to Decrease Gastrin Release from the Stomach and Prevent Gastric Contents from Entering the Duodenum)  When can we Start giving Food (Med School Notes)?  When patient is Stable already (+) Abdominal Sounds. it is Contraindicated in Renal Failure. Should be avoided if possible 3. Treatment = Supportive (Disease is Self-Limited & subsides spontaneously. Glucose levels should be monitored and supplemented 2.H. Indicators of Organ Failure Cardiovascular Pulmonary Renal GIT Hypotension (BP < 90mmHg) or Tachycardia ( > 130 beats/min) PO2 < 60mmHg Oliguria (<50ml/h) or Increasing BUN. Prophylactic Antibiotics  For SEVERE Pancreatitis (Nectrotizing Acute Pancreatitis) 7 . Creatinine Gastrointestinal Bleeding I. etc  Start with CARBOHYDRATES 4. Acid Suppression  May be necessary in severely ill patients with risk factors for Stress Ulcer Bleeding 6.

as distinct from the Reversible Changes noted in Acute Pancreatitis  Presence of histologic abnormalities. Classic Triad (seen in < 1/3 or Patients)  Pancreatic Calcification  Steatorrhea  Diabetes Mellitus 3. Marked Excretion of Fecal Fat  Corrected by Administration of Oral Pancreatic Enzymes 6. Management of Pain (Critical in Chronic Pancreatitis)  ABSTINENCE from Alcohol and Fatty meals  Use of Narcotics  Pancreatic Enzymes  Surgery  ERCP and Sphincterotomy – if (+) Pancreatic Duct Obstruction from stones. papillary stenosis 2.III. Treatment (Directed to TWO MAJOR Problems = Pain + Malabsorption) 1. including chronic inflammation. Intubation Test  Secretin Stimulation Test  Usually gives Abnormal Results when 60% or More of Pancreatic Exocrine Function has been lost 4. CHRONIC PANCREATITIS  Chronic Inflammatory Disease of the Pancreas – commonly seen with Chronic Alcohol Abuse  Characterized by Irreversible Damage to the Pancreas. Intermittent or Absent o WEIGHT LOSS o Abnormal Stools. Radiographic Hallmark = (+) CALCIFICATION throughout the Pancreas  Ultrasound  CT-Scan  ERCP C. structures. Clinical Features (Symptoms are IDENTICAL to Acute Pancreatitis) o PAIN = may be Continuous. Serum Trypsinogen Level  DECREASED  In the presence of Steatorrhea. Amylase and Lipase  They are NOT Elevated (in contrast to Relapsing Acute Pancreatitis) 2. Cobalamin Malabsorption  Corrected by the Administration of Oral Pancreatic Enzymes  40% of Patients have Cobalamin (Vitamin B12) Malabsorption 5. a Serum Trypsinogen Level < 10ng/mL = Diagnostic of Chronic Pancreatitis 7. Management of Malabsorption (Exocrine Insufficiency)  Pancreatic Enzyme Replacement  Supportive Measures  Diet should be Moderate in Fat (30%). Diagnosis 1. MALABSORPTION Signs of Malabsorption are Common in Chronic Pancreatitis B. fibrosis and progressive destruction in both Exocrine and eventually Endocrine Tissue A. and Low in CHO (40%)  Restriction of Long-Chain Triglyceride Intake can help Patients who DON’T respond satisfactorily to Pancreatic Enzyme 8 . High in protein (24%).

weight loss  Penetration (into adjacent organ): sudden onset of pain radiating to the back. round ulcer. ulcer crater beyond gastric wall. gastric folds into the base. Nausea. Anemia.3) PEPTIC ULCER DISEASE    Most Common Cause of UGIB Ulcer: Break in the Mucosal Surface > 5mm. direct & rebound tenderness  Gastric Outlet Obstruction: early satiety. with Depth into the Mucosa Burning Epigastric Pain exacerbated by Fasting and improved with Meals I. regular. decreased BS. Omeprazole (Lansoprazole) PLUS Clarithromycin PLUS Metronidazole OR Amoxicillin Quadruple Therapy Omeprazole (Lansoprazole) Bismuth Subsalicylate Metronidazole Tetracycline DOSE 2 tablets QID 250mg QID 500mg QID 400mg BID 500mg BID 500mg BID 20mg BID (30mg BID) 250 or 500mg BID 500mg BID 1g BID 20mg (30mg) daily 2 tablets QID 250mg QID 500mg QID 9 . Alarming Symptoms: Weight Loss. COMPLICATIONS  Hemorrhage: Most Serious  Perforation (intense pain. Early Satiety. and lack of appropriate response to Acid Suppression Benign: Smooth. DIAGNOSIS X Ray Double contrast upper GI series. Bismuth Subsalicylate PLUS Metronidazole PLUS Tetracycline 2. Ranitidine Bismuth Citrate PLUS Tetracycline PLUS Clarithromycin or Metronidazole 3. pylori  NO Single Agent is effective in eradicating the Organism  Combination Therapy for 14 days provides the GREATEST Efficacy  Goals in Treating PUD: o 1) Relief of Symptoms (Pain or Dyspepsia) o 2) Promote Ulcer Healing o 3) Prevent Ulcer Recurrence & Complications DRUG Triple Therapy 1. rigid abdomen. FEATURES  Epigastric Burning Pain  Bloatedness. High Amylase and Lipase (treatment is surgical) IV. epigastric fullness. TREATMENT PROTOCOLS FOR H. distensible gastric wall in the ulcer area Endoscopy Gastric Acid Analysis Primary Diagnostic Maneuver (usually with biopsy of the ulcer) Achlorydia usually in malignant III. nausea and vomiting of undigested food. collar of edema / Hampton’s line around the base. Vomiting. Bleeding. Insomnia  UGIB II.

Charcot’s Triad o Right Upper Quadrant Pain o Jaundice o Fever **NOTE: Seen in 70% of patients with Bacterial Cholangitis B. TREATMENT OF ACUTE CHOLANGITIS Mild (Grade I) Moderate (Grade II) Non responsive to medical management Severe (Grade III) Patients with acute cholangitis and organ failure Observation (Antibiotic. prevention of organ damage) Early Biliary Drainage Urgent Biliary Drainage **NOTE: Treatment for all = Treatment of ETIOLOGY 10 . CHARCOT’S TRIAD AND REYNOLD’S PENTAD A.4) ACUTE CHOLANGITIS I. Reynold’s Pentad o Right Upper Quadrant Pain o Jaundice o Fever o Altered Mental Status o Shock II. Analgesia.

5) COMMON CAUSES OF GI SYMPTOMS ABDOMINAL PAIN Appendicitis Gallstone Disease Pancreatitis Diverticulitis Ulcer Disease Esophagitis GI Obstruction Inflammatory Bowel Dse Functional Bowel D/O Vascular Disease Gynecologic Renal Stone NAUSEA & VOMITING Medications GI Obstruction Motor Disorders Functional Bowel D/O Enteric Infection Pregnancy Endocrine Disease Motion Sickness CNS Disease DIARRHEA Infection Poorly Absorbed Sugars Inflammatory Bowel Dse Microscopic Colitis Functional Bowel D/O Celiac Disease Pancreatic Insufficiency Hyperthyroidism Ischemia Endocrine Tumor GI-BLEEDING Ulcer Disease Esophagitis Varices Vascular Lesions Neoplasm Diverticula Hemorrhoids Fissures Inflammatory Bowel Dse Infectious Colitis OBSTRUCTIVE JAUNDICE Bile Duct Stones Cholangiocarcinoma Cholangitis Sclerosing Cholangitis Ampullary Stenosis Ampullary Carcinoma Pancreatitis Pancreatic Tumor 11 .

Regurgitation o Dysphagia:  Appears early  Occurs with BOTH Liquids and Solids  Worsened by Emotional Stress and Hurried Eating **NOTE: The presence of Gastroesophageal Reflux argues AGAINST Achalasia  In patients with Long-Standing Heartburn. but Cholinergic Neurons are also affected in Advanced Disease) A. in Achalasia. Chest Pain. owing to the loss of Inhibitory Neurons Endoscopy To exclude Secondary Causes of Achalasia. Duration. Primary Peristaltic Waves are Replaced by Simultaneous-Onset Contractions  These contractions may be of Poor Amplitude (Classic Achalasia) or of Large Amplitude and Long Duration (Vigorous Achalasia) CCK Test Cholecystokinin (CCK). particularly Gastric Carcinoma Barium Swallow Fluoroscopy Manometry 12 .6) OTHER GI DISEASES I. Consistency Esophageal Body shows an Elevated Resting Pressure In Response to Swallows. ACHALASIA  Motor disorder of the Esophageal Smooth Muscle in which the LES does NOT relax normally with swallowing. Primary VS Secondary o Primary Idiopathic Achalasia: Most of the patients (in the US) o Secondary Achalsia: May be caused by:  Gastric Carcinoma that infiltrates Esophagus  Lymphoma  Chagas’ Disease  Certain Viral Infections  Eosinophilic Gastroenteritis  Neurodegenerative Disorders B. cessation of Heartburn and appearance of Dysphagia suggest development of Achalasia on top of Reflux Esophagitis C. and the Esophageal Body undergoes Non-Peristaltic Contractions  Underlying Abnormality = Loss of Intramural Neurons (Inhibitory Neurons containing VIP and Nitric Oxide Synthase are predominantly involved. Diagnosis Chest X-Ray Absence of Gastric Air Bubble Tubular Mediastinal Mass beside the Aorta (sometimes) Air-Fluid Level in Mediastinum in Upright Position represents Retained Food in Esophagus Esophageal Dilatation Sigmoid Esophagus (in advanced cases) Normal Peristalsis is LOST in the Lower 2/3 of Esophagus Terminal Part shows a Persistent Beaklike Narrowing (represents Non-Relaxing LES) Basal LES Pressure NORMAL or ELEVATED Swallow-Induced Relaxation either does NOT occur or is Reduced in Degree. Paradoxically causes Contraction of the LES This paradoxical response occurs because. the Neurally Transmitted Inhibitory Effect of CCK is Absent. which normally causes a Fall in the Sphincter Pressure. Clinical Features o Main Symptoms: Dysphagia.

Campylobacter and Aeronomas Species. Yersinia  Severe Inflammation: Shigella Species. Nifedipine (10-20mg PO before meals) III. Clinical Features o Non-Peristaltic Patterns are dye to Dysfunction of Inhibitory Nerves o Histopathology: Patchy Neural Degeneration localized to Nerve Processes.coli. Enteroinvasive E. DIARRHEA  Loosely defined as Passage of Abnormally Liquid or Unformed Stools at an Increased Frequency  For adults: Stool Weight > 200g/d can be generally considered Diarrheal A.II. Clostridium perfringens  Enterotoxin: Vibrio cholerae. usually of Large Amplitude and Long Duration  An Esophageal Motility Pattern showing Hypertensive but Peristaltic Contractions has been called Nutcracker Esophagus A. Diagnosis of Diffuse Esophageal Spasm Barium Swallow The Normal Sequential Peristalsis below the Aortic Arch is REPLACED by Uncoordinated Simultaneous Contractions that produce the appearance of Curling or Multiple Ripples in the Wall.3 to 0. Entamoeba histolytica **REITER’s SYNDROME = Arthritis. Sacculations. Acute VS Chronic o Acute: < 2 Weeks o Persistent: 2-4 Weeks o Chronic: > 4 Weeks B. Aeromonas 2) Enteroadherent  Enteropathogenic and Enteroadherent E. Klebsiella pneumoniae. and Pseudodiverticula – the Corkscrew Wsophagus Barium Swallow is frequently Normal in DES and Mostly Normal in Related Disorders Manometry DES and other related disorders are Manometric Diagnoses Several Techniques to Provoke Esophageal Spasms:  Cold Swallows (produce Chest Pain but do NOT produce Spasm on Manometry)  Solid Boluses  Pharmacologic Agents (Edrophonium) – induce both Chest Pain and Motor Abnormalities C.coli. Ischemia. Enterotoxigenic E. Toxic Ingestions.coli 4) Invasive Organisms  Minimal Inflammation: Rotavirus and Norwalk  Variable Inflammation: Salmonella. Staphylococcus aureus.6mg) o Long-Acting Agents: Isosorbide Dinitrate (10-30mg PO before meals). etc 13 . Conjunctivitis  Salmonella  Campylobacter Reiter’s Syndrome may accompany or follow infections by  Shigella the following  Yersinia **NOTE: More than 90% of Acute Diarrhea are caused by INFECTIOUS AGENTS  Remaining 10% are caused by Medications. Urethritis. Vibrio parahaemolyticus.coli  Giardia organisms  Cryptosporidiosis  Helminths 3) Cytotoxin-Producers  Clostridium difficile  Hemorrhagic E. rather than the Prominent Degeneration of Nerve Cell Bodies seen in Achalasia (Diffuse Esophageal Spasm may progress to Achalasia) B. DIFFUSE ESOPHAGEAL SPASMS and RELATED MOTOR DISORDERS  Symptoms: Chest Pain and Dysphagia  Recognized by Manometric Features  DES: Characterized by Non-Peristaltic Contractions. Pathology of Causative Agents 1) Toxin-Producers  Pre-Formed Toxins: Bacillus cereus. Treatment = Agents that Relax Smooth Muscle o Sublingual Nitroglycerin (0.

1-1% Occasional (1-10%) – 90% of Neonates 0. Carrier State Young Adults (Sexual and Percutaneous) Babies.1 – 30% (+) Neonatal Infection Worse with Age. CLINICAL & EPIDEMIOLOGIC FEATURES OF VIRAL HEPATITIS A.1% Common: 50-70% chronic hepatitis. Debility Recombinant Vaccine Interferon (Immunomodulator). C33c.5-3. C22-3. Toddlers +++ +++ ++ Occasionally Severe 0. Hepatitis-A Virus Antigen (s) Antibodies Features Diagnosis Age Preference Transmission  Fecal-Oral  Percutaneous  Perinatal  Sexual Clinical  Severity  Fulminant  Progress to Chronicity  Carrier  Cancer  Prognosis Prophylaxis Therapy HAV Anti-HAV Early Fecal Shedding Acute Infection = IgM and Anti-HAV Previous Infection = IgG Anti-HAV Children. but More Common in Adults +++ +/+/Moderate 0.1% None None None Excellent Immunoglobulin Inactivated Vaccine NONE (No Specific Treatment – it is just Supportive) Blood-Borne Virus.LIVER DISEASES 1) VIRAL HEPATITIS I. NS5 Anti-HCV Blood-Borne Agent (formerly labeled as Non-A.2% + Moderate NONE Interferon + Ribavirin Some Points: There is NO Progression to Chronicity! No Carrier State! No Predisposition to Development of Hepatocellular Cancer B. Hepatitis-C Virus Antigen (s) Antibodies Features Diagnosis Age Preference Transmission  Fecal-Oral  Percutaneous  Perinatal  Sexual Clinical  Severity  Fulminant  Progress to Chronicity  Carrier  Cancer  Prognosis Prophylaxis Therapy Some Points: NO Vaccine Yet (because of the Several Subtypes!) Formerly labeled as Non-A NonB Hepatitis Most Common: Blood Transfusion Infection Complications and Sequalae  RARELY = Fulminant Hepatitis-C  Chronic Hepatitis-C 14 . 80-90% chronic infection 1. Hepatitis-B Virus Features Age Preference Transmission  Fecal-Oral  Percutaneous  Perinatal  Sexual Clinical  Severity  Fulminant  Progress to Chronicity  Carrier  Cancer  Prognosis Prophylaxis Therapy Some Points: It CAN Progress to CHRONICITY (especially if it is Transmitted Perinatally – from mother to neonate) There is a Recombinant Vaccine! Prognosis is WORSE with Age It is a DNA Virus (unlike Hepatitis-A) If we are Vaccinated = we will be (+) Anti-HBs C. Lamivudine (Antiviral) HCV. Non-B Hepatitis) Acute Diagnosis = Anti-HCV Chronic Diagnosis = Anti-HCV and HCV RNA Any Age. Young Adults +++ Unusual +/Mild 0. C100-3.

HDV Antigen Anti-HBs. Bile Young Adults (20-40 years) +++ Mild 1-2% None None None Good Unknown None  Summary of Some Differences: Incubation Onset Vaccination Transmission Therapy A 15-45 Acute IG. HDV-RNA HBV/HDV Coinfection: -IgM Anti-HBc and Anti-HDV HDV Superinfection: -IgG Anti-HBc and Anti-HDV Any Age (Similar to HBV) +++ + ++ Occasionally Severe 5-20% Common Variable +/Acute = Good Chronic = Poor HBV-Vaccine (None for HBV Carriers) Interferon +/- Complications and Sequelae  Fulminant Hepatitis  Mild Disease  Asymptomatic Carriers Diagnosis Age Preference Transmission  Fecal-Oral  Percutaneous  Perinatal  Sexual Clinical  Severity  Fulminant  Progress to Chronicity  Carrier  Cancer  Prognosis Prophylaxis Therapy E. Inactivated Feco-Oral None B 30-180 Insidious or Acute Recombinant Percutaneous (+++) Perinatal (+++) Sexual (++) Interferon Lamivudine C 15-160 Insidious NONE Percutaneous (+++) Sexual (+/-) Interferon Ribavirin D 30-180 Insidious or Acute HBV Vaccine Percutaneous (+++) Perinatal (+) Sexual (++) Interferon E 14-16 Acute Unknown Feco-Oral None 15 . Hepatocyte. Hepatitis-E Virus Antigen (s) Antibodies Features Diagnosis Age Preference Transmission  Fecal-Oral  Percutaneous  Perinatal  Sexual Clinical  Severity  Fulminant  Progress to Chronicity  Carrier  Cancer  Prognosis Prophylaxis Therapy HEV Antigen Anti-HEV Agent of Enterically Transmitted Hepatitis IgM/IgG Anti-HEV (assays being developed) Virus in Stool. Hepatitis-D Virus Antigen (s) Antibodies Features HBsAg. Anti-HDV Defective RNA-Virus – requires Helper Function of HBV (Hepadnaviruses) HDV Antigen present in Hepatocyte Nucleus Anti-HDV.D. Cytoplasm.

II. SIMPLIFIED DIAGNOSTIC APPROACH IN PATIENTS PRESENTING WITH ACUTE HEPATITIS (Medicine Notes) INTERPRETATION HBsAg IgM Anti HAV IgM Anti HBC Anti HCV Acute Hepa B + + Chronic Hepa B + Acute Hepa A + + Superimposed on Chronic Hepa B Acute Hepa A & B + + + Acute Hepa B + Acute Hepa A & B + (HBsAg below detection threshold) Acute Hepa B + (HBsAg below detection threshold) Acute Hepa C + III. COMMONLY ENCOUNTERED SEROLOGIC PATTERNS OF HEPATITIS-B INFECTION
INTERPRETATION Acute HBV Infection (High Infectivity) Chronic HBV Infection (High Infectivity) 1) Late-Acute or Chronic HBV Infection (Low Infectivity) 2) HBeAg-Negative (“Precore-Mutant) Hepatitis B (Chronic or, rarely, Acute) 1) HBsAg of one Subtype and Heterotypic Anti-HBs (Common) 2) Process of Seroconversion from HBsAg to AntiHBs (RARE) 1) Acute HBV Infection 2) Anti-HBc Window 1) Low Level Hepatitis B Carrier 2) Hep B in Remote Past Infection Recovery from HBV Infection 1) Immunization w/ HBsAg (Vaccination) 2) Remote Past Infection (?) 3) False Positive HBsAg Anti-HBs Anti-HBc HBeAg Anti-HBe

+ + +

-

IgM IgG IgG

+ + -

+

+ -

+ + +

+ IgM IgG IgG -

+/+/-

+/+/+/+/-

**NOTE: Anti-HBc Window = period wherein only the IgM Anti-HBc (Core Antigen) is POSITIVE!

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A. Genomic Structure of HBV o HBs = Surface Antigen o HBV-DNA = DNA Polymerase o HBc = Core Antigen o HBe = Envelope a. Antigen = HBsAg  HBsAg is detectable in > 95% of Patients with Acute Hepatitis-B  It is found in Serum, Body Fluids, Hepatocyte Cytoplasm b. Antibody = Anti-HBs  Appears following Infection  Protective Antibody! B. Scheme of TYPICAL Clinical and Laboratory for Hepatitis-B o Jaundice will come LATER than the Increase in ALT (unlike in Hepatitis-A) o (+) HBsAg IMPORTANT Notes:
When patient presents with Jaundice, look out for HBeAg, IgM Anti-HBc and HBeAg If after 6 months, the HBsAg is still present, then the Patient already has CHRONIC Hepatitis-B ALT Increase PRECEDES Jaundice

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1. Antigens and Antibodies  HBs  Anti-HBs  HBc  Anti-HBc (IgM; IgG)  HBe  Anti-HBe 2. Golden Period = 24-WEEKS  ALL the ANTIGENS must DECREASE in 24-Weeks – otherwise, it progresses to Chronicity!  Chronic Hepatitis = Persistence of Antigen (HBsAg) BEYOND 6-Months or 24 Weeks **Window Period = BOTH HBs and HBe Antigens are NEGATIVE  The only marker which is positive would be IgM Anti-HBc

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C. Complications and Sequelae 1. Serum-Sickness Like Syndrome  During the PRODROMAL PHASE  Signs and Symptoms:  Arthralgia / Arthritis  Rash  Angioedema  Hematuria, Proteinuria (5-10%) 2. Fulminant Hepatitis (90% will die)  Massive Hepatic Necrosis  It is a RARE Event  Signs and Symptoms = ENCEPHALOPATHY  Coma  Small Liver  Excessively Prolonged Prothrombin Time (PT) **Hepatic Failure with Encephalopathy:  SMALL Liver = Rapidly SHRINKING Liver Size  Rapidly Rising Bilirubin Level  Markedly Prolonged PT even as Transaminases FALL  Clinical Signs: o Confusion o Disorientation o Somnolence o Ascites & Edema **Terminal Events for Fulminant Hepatic Failure (Causes of Death)  Cerebral Edema (Most Common)  Brainstem Compression  GIT-Bleeding  Sepsis  Respiratory Failure  Cardiovascular Collapse  Renal Failure **NOTE: Mortality Rate > 80% 3. Chronic Hepatitis  There is an INCREASED Risk to develop Hepatocellular Carcinoma  95% of Patients with Hepatocellular Carcinoma will be Positive for Hepatitis-B **NOTE: Chronic if (+) HBsAg Persisting > 6 MONTHS 4. Increased Risk for Hepatocellular Carcinoma  Hepatitis-B = Most Common Cause of Hepatocellular Carcinoma

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D. Chronic Hepatitis-B (Antigens PERSIST > 6 Months) o Clinical and Laboratory Features, suggesting Progression from ACUTE to CHRONIC Hepatitis-B:  1) Lack and Complete Resolution of Clinical Symptoms of Anorexia, Weight Loss, Fatigue and Persistence of Hepatomegaly  2) Presence of Bridging or Multilobular Hepatic Necrosis on Liver Biopsy during Protracted, Severe Acute Viral Hepatitis  3) Failure of Serum Transaminase, Bilirubin and Globulin Levels to return to Normal within 6-12 months after Acute illness  4) Persistence of HBeAg beyond 3 months or HBsAg beyond 6 Months after Acute Hepatitis IMPORTANT Notes:
In Chronic Hepatitis B, HBsAg does NOT down (Anti-HBC may go down & be replaced by IgG)
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ALT may be Fluctuating – if it is Elevated, it may signify Activity

**NOTE: Chronic Hepatitis-B is (+) HBsAg Persisting > 6-MONTHS: 1. Active Chronic Hepatitis = TREAT!  (+) HBs Antigen  (+) HBeAg  ALT is Abnormal (Increased) **IMPORTANT Notes: o HBeAg = Marker for Infectivity! o Anti-HBe = Marker of Recovery! 2. Inactive Chronic Hepatitis  (+) HBs Antigen  (-) HBe Antigen  (+) Anti-HBe (Marker of Recovery)  ALT is NORMAL  We DON’T have to Treat – just Observe 3. Precore Type (Mutant Strain)  (+) HBs Antigen  (-) HBe Antigen  (+) Anti-HBe (Antibody)  ALT is ABNORMAL  We have to Treat!

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Spider angiomata IV. because in 1 beer = 12g) o WOMEN: 20-40 g/day for 10 YEARS III. HEPATOCELLULAR CARCINOMA  Most metastatic CA to the liver would come from the GI tract because of Hematogenous spread  Signs of Cirrhosis (CLD) = Palmar Erythema.2) CASE ON LIVER MASS   50/M with a chief complaint of Right Lower Lobe Liver Mass Dx: T/C Hepatocellular Carcinoma (HCCA) I. rule out a more serious pathology. Testicular Atrophy  Signs of Portal HPN = Caput medusae. before considering a benign one o Size of the mass would point to a malignancy B. Focal Nodular Hyperplasia o Considered because of the mass o However. Renal Cell Carcinoma o TRIAD: Hematuria + Flank Mass + Flank Pain o Not considered because these are absent in the patient 20 . Gynecomastia in males. NOTES ON LIVER DISEASES  Fatigue: Common symptom of liver pathologies  Jaundice: Common feature in Severe / Advanced cases  Importance of Digital Rectal Examination (DRE) in Liver Diseases: o Hemorrhoids would indicate portal hypertension o Melena would come from bleeding varices. ALCOHOLIC LIVER DISEASE  Pathology of Alcoholic Liver Disease comprises THREE Major Lesions o Fatty Liver o Alcoholic Hepatitis o Cirrhosis  The following contain ~12 g of Alcohol: o One Beer o Four Ounces of Wine o One Ounce of 80% Spirits  Threshold for Developing Alcoholic Liver Disease: o MEN: > 60-80 g/day for 10 YEARS (approximately 4 beers. due to portal hypertension II. Telangiectasia. DIFFERENTIALS A.

there must be 175cc of Fluid  Reactive Pleural Effusion: Pleural effusion on the right in cases of liver abscess. EXAMS TO EVALUATE LIVER FUNCTION  Albumin  Bleeding Parameters  Bilirubin **NOTE: ALT / AST are NOT markers of Liver Function! o They are Functions of HEPATOCELLULAR DAMAGE 21 . get AFP levels first o If AFP is > 200. because it would light up in the arterial phase  Highly Vascular Masses would suggest a Malignancy B. we would see Blunting of Costophrenic Angles. DIAGNOSTICS A. for pleural effusion to blunt the Costophrenic Sulci. Chest X-Ray o To check for any masses. Biopsy o Biopsy is NOT done in all cases of Hepatic Masses to avoid Invasive Procedure and its complications o If we do a biopsy.V. Triphasic CT-Scan (for Liver Masses) o Three Phases = Arterial + Venous + Plain o Done to see the vascularity of the mass. check PT/PTT E. Meniscus Sign  On CXR. treat as HEPATOCELLULAR CA!!!!  Read algorithm in harrisons D. etc o Pleural Effusion:  On CXR. pathologies. Dynamic UTZ) **NOTE: If the following are present. the mass is most probably MALIGNANT **NOTE: If the following are present. liver mass. AFP Levels o Before doing a biopsy. etc VI. there is NO need for a BIOPSY  1) Mass > 2cm detected by any imaging modality  2) Elevated AFP > 200  3) Features of Malignancy in Dynamic Scan (Triphasic CT. Dynamic Ultrasound C.

V. X depends on Vitamin-K Used to screen for dilation of Biliary Tree and to detect Gallstones & Cholecystitis in patients with right sided abdominal pain associated with Abnormal Liver Blood Tests Can detect and characterize Liver Masses. the blood clotting factors are made exclusively in HEPATOCYTES Useful for this purpose is the Serum Prothrombin Time (Factors II. Serum Globulins C. VII. Serum Levels may be NORMAL in Acute Liver Disease 2. while a Ratio of > 3:1 is Highly Suggestive of Alcoholic Liver Disease o The AST in Alcoholic Liver Disease is rarely > 300U/L and the ALT is often normal (a low level of ALT in serum is due to Alcohol Induced Deficiency of Pyridoxal Phosphate) 2. and Cysts Diagnostic Modality of Choice for Hepatocellular Carcinoma SCREENING Helical CT Scan with Contrast Useful in evaluation of Parenchymal Liver Disease Has the added feature of Contrast Enhancement to define space-occupying lesions (Abscess and Tumor) MRI Allows calculation of Liver Volume Similar information as the CT Scan. brain. 5’Nucleotidase. Tests that Measure Biosynthetic Function of the Liver 1. RADIOGRAPHIC EVALUATION Ultrasoonography 22 . Enzymes that Reflect Cholestasis  Alkaline Phosphatase. lungs. VII. Enzymes the Reflect DAMAGE to Hepatocytes  Aminotransferases (Transaminases) are sensitive indicators of Liver Cell Injury and are most helpful in recognizing Acute Hepatocellular Diseases such as Hepatitis  Includes: Aspartate Aminotransferase (AST) and Alanine Aminotransferase (ALT) o AST = found in the liver.VII. leukocytes. and -Glutamyl Transpeptidase – are usually elevated in Cholestasis B. but visualizes vessels without use of IV contrast Helpful in diagnosis of Benign Masses such as Focal Nodular Hyperplasia & Hamngioma VIII. Abscesses. skeletal muscle. X) Biosynthesis of Factors II. Serum Albumin  Frequently decreased in Chronic Liver Disease  Half Life is relatively long (~20 days) – therefore. Tests Based on Detoxification and Excretory Functions o Serum Bilirubin o Urine Bilirubin o Blood Ammonia o Serum Enzymes SERUM ENZYMES 1. cardiac muscle. and erythrocytes (in decreasing order of concentration) o ALT = found primarily in the LIVER  Any type of Liver Cell Injury can cause modest elevations in the Serum Aminotransferases  Aminotransferases > 1000 U/L occur almost exclusively in disorders associated with Extensive Hepatocellular Injury (Viral Hepatitis. Coagulation Factors o o o With the EXCEPTION of Factor-VIII. Toxin/Drug Induced Liver Injury)  Important Notes: o In most Acute Hepatocellular Disorders: ALT > AST o AST:ALT Ratio > 2:1 is suggestive. DIAGNOSTICS TO EVALUATE LIVER DISEASES A. Ischemic Liver Injury. pancreas. IX. kidneys.

UTZ examination will demonstrate a cystic o Diagnosis: Confirmed by CT or UTZ mass in the liver. Etiology o Biliary Tract Disease (Acute Cholecystitis. multiple complex septations. Pyogenic Abscess o Result from hematogenous infection. RUQ Pain. often with multiple complex septations or B. PYOGENIC LIVER ABSCESS  70% MIXED Flora  Pyogenic Liver Abscess is MORE Toxic than an Amoebic Mass  Commonly caused by: Anaerobes. Anemia (Normo-Normo). Hypoalbuminemia. DIAGNOSIS  Single Most Reliable Laboratory Finding: Elevated Serum Alkaline Phosphatase  50% have elevated Bilirubin. weight loss. 50% of patients have Hepatomegaly. anorexia.3) LIVER ABSCESS   Liver is the organ most subject to the development of abscesses FEVER: Most Common presenting sign of Liver Abscess I. Jaundice II. E. Amebic Liver Abscess o Should be considered in patients from endemic areas o Diagnosis requires high index of clinical suspicion o Tx: Metronidazole. punch tenderness. Laboratory  Viscous Abscess contents that tend to plug the catheter  80% Elevated Alkaline Phosphatase  Associated Disease requiring surgery  33% Jaundice = Increased Bilirubin  Lack of a clinical response to percutaneous drainage in 4-7 days  40% = (+) Blood Culture 2. Clinical features o Fever. percutaneous aspiration with evaluation by GS/CS is essential to direct further antimicrobial & drainage therapy III. CLINICAL PRESENTATION  Right Upper Quadrant signs / symptoms: Pain. inhomogenous fluid characteristics  CT-Scan: Complex hypodense mass with peripheral enhancement  Ultrasound Guided Aspiration D. Diagnostic Procedures:  Ultrasound: Cystic mass. rebound tenderness  Chills. coli. In patients with a solitary dominant abscess. PYOGENIC VS AMEBIC A. Sizable Abscesses 1. vomiting. and 48% have elevated Aspartate Aminotransferase  Other Labs: Leukocytosis. nausea. Bacteroides. Chloroquine inhomogenous fluid characteristics. concomitant Bacteremia  On Radiography: (+) Elevation of the Right Hemidaphragm. Elevated AP In Pyogenic Abscesses. weight loss. UTZ): most reliable methods IV. Diagnosis  Presence of Multiple. MRI. hypoechogenic. abdominal pain from tender hepatomegaly o 50% of patients are jaundiced o Laboratory Studies: Leukocytosis. spread from intra-abdominal infection or ascending infection from biliary tract o Clinical Features: Fever. Cholangitis) o Appendicitis o Diverticulitis o Intrinsic Hepatic Lesion General Management o Undetermined (10%)  Drainage (Percutaneous or Surgical) = Mainstay of Therapy B. Treatment o Broad Spectrum Antibiotics = for Gram (-) Anaerobes o Aspiration = Percutaneous or Surgical Drainage o Drugs used for Empirical Therapy include the same ones used in Intraabdominal Sepsis and 2 0 Bacterial Peritonitis o Aerobic Gram (-) Bacilli and Anaerobes:  Broad Spectrum Penicillin: Ticarcillin / Clav 3. Klebsiella. Enterococcus. Streptococcus A.1g q4-6  Cefoxitin 2g q4-6 IV  Imipenem 500mg q6 IV  Meropenem 1g q8 IV  Combination: Ampicillin + Metronidazole + Ciprofloxacin  Empirical Therapy 23 . chills. Anorexia. Nausea Several Factors predicting Failure of Percutaneous Drainage o Tender Hepatomegaly (50%) (favors Surgical Intervention): C. guarding. Right Upper Quadrant Pain. CT findings will include a complex hypodense mass with peripheral enhancement. Chills. right basilar infiltrate. Staphylococcus aureus. right pleural effusion  Imaging Methods (CT.

Pulmonary Congestion. Abdominal Mass. HEPATOBILIARY TUBERCULOSIS A. Hx of Diarrhea – Jaundice is not common in Ameobic Liver Disease. in contrast to Pyogenic Liver Abscess (Med Notes)  Laboratory: Leukocytosis (50%). Fever. Splenomegaly D. Intestinal Amoebiasis (50%). TB-Liver. CT-Scan  Complex Hypodense Mass with Peripheral Enhancement 3. Chest X-Ray Findings  Pulmonary TB  Normal  Pneumonia. Pancreatitis. Common Bile Duct. Presentation o 1) Miliary Hepatic Tuberculosis (Disseminated) o 2) Focal or Nodular Tuberculosis = Single or Multiple Conglomerate Tubercles o 3) Tuberculosis of Bile Ducts (or Tubular Tuberculosis) B. RLQ)  Cervical Lymphadenopathy. Pancreatic Head Mass. Unspecified o Hepatomegaly: With Calcification (Liver Calcifications = MOST Common) or Without Calcification o Others: Contracted Gallbladder. Increased Serum Bilirubin. Sonographic Findings o Biliary Obstruction: Intrahepatic Duct. Hepatosplenomegaly B. Diagnosis 1. Pleuritic Pain. Fever. Cholelithiasis. Scrofuloderma. Physical Examination Findings  Jaundice = ALL Patients  Abdominal Tenderness (RUQ. Increased Transaminases. AMOEBIC LIVER ABSCESS  Etiology: Entamoeba histolytica – there is local proteolytic destruction of the liver parenchyma with focal infarction (invasion of the colonic mucosa into the portal system)  Clinical Features: RUQ Pain. Epigastric. It is indicated only if there is (+) Secondary Pyogenic Infection More than 90% respond to Metronidazole Tx. Aspiration Biopsy  “ANCHOVY PASTE” Fluid with TROPHOZOITES (when we Aspirate) 5. Abdominal Enlargement. Elevated Right-Hemidiaphragm **NOTE: We do NOT need a Pulmonary Tuberculosis to have a Diagnosis of Liver Tuberculosis! C.V. with Decrease in Pain and Fever within 72 hours Indications for Aspiration of Liver Abscess:  Need to rule out Pyogenic Abscess  No Clinical Response in 3-5 days  Threat of Imminent Rupture  Need to prevent Rupture of Left Lobe Abscess into Pericardium VI. Common Hepatic Duct. Chills. Abdominal Distention. Therapy = AMOEBICIDES: o METRONIDAZOLE 750mg PO or IV 5-10 days o Choloroquine C. Complications = CYST RUPTURE into the following: o Pleural Space o Lungs o Bowel o Retroperitoneum Aspiration & Drainage is rarely indicated. Ultrasound = COMPLEX MASS (Most Commonly seen)  Usually Solitary  RIGHT Lobe (90%) 2. Treatment of Hepatobiliary Tuberculosis o Anti-TB Therapy (12-18 Months Triple / Quadruple Treatment) o Surgery 24 . Normal Physical Examination. Gallium Scan  (+) Filling Defect 4. Portal Hypertension. Presenting Complaints o JAUNDICE (Most Common Complaint) o Abdominal Pain. Weight Loss C. Choledocholithiasis. Night Sweats. Clinical & Laboratory Features: A. Serologic Test  (+) in 95% of Case  Indirect Hemagglutination Gel Diffusion B. Cholecystitis. Fluid Wave. Increased Alkaline Phosphatase (80%) A.

Mild  in Alkaline Phosphatase Treatment: Surgical Aspiration / Decompression D. Occasionally = PAIN & FEVER (Secondary Bleeding. Abnormal Alpha Fetoprotein C. Jaundice & Nausea  Most Common Symptom = Abdominal Pain  Jaundice is usually due to obstruction of Intrahepatic Ducts by the underlying liver disease  Hepatomegaly = Most Common Physical Sign (50-90%)  Abdominal Bruits. PIVKA-2 and Antimitochondrial Ab should be measured. G-Glutamyl Transpeptidase) B. and the presence of Portal Vein Invasion accurately. Ferritin. Focal Nodular Hyperplasia o Typically benign. o Symptoms: RUQ Fullness. Peripheral Edema II. PTT. and Standard Liver Function Tests should be performed (including PT. Testicular Atrophy. Infection. Cold Spot  Abnormal Liver Function Test. Serologic Assays o A-Fetoprotein (AFP): Serum Tumor Marker in HCC o In a patient presenting with either a new hepatic mass or other indications of recent hepatic decompensation. III. AFP. CLINICAL FEATURES  Abdominal Pain. Wasting  Signs of Chronic Liver Disease: Jaundice. Radiology o UTZ Examination of liver is an excellent screening tool o Two Characteristic Vascular Abnormalities are:  1) Hypervascularity of the Tumor Mass (Neovascularization or Abnormal Tumor-Feeding Arteries)  2) Thrombosis by Tumor invasion of otherwise normal portal veins To determine Tumor Size and Extent. Lungs Laboratory Findings: Liver Function Tests are NORMAL. Weakness. ASYMPTOMATIC Disease Complications: Hemorrhage. causing acute problems. Rupture (+) Cyst: Pancreas. Gynecomastia. a Helical / Triphasic CT Scan of the Abdomen and Pelvis with Fast Contrast Bolus Technique should be performed to detect the vascular lesions typical of HCC. Surgery o Diagnosis:  CT Scan = Hepatic Mass. Intraabdominal Hemorrhage (25%) Biopsy is not Suggested due to Hypervascularity o Treatment: STOP Pill. Hemangioma o Most Common BENIGN Liver Tumor (5-7% Autopsy. Transaminases.4) TUMORS OF THE LIVER  Hepatocellular Carcinoma (HCC) is one of the most common malignancies worldwide I. together with subsequent delayed venous-phase imaging. Hepatic Adenoma o Usually in Women (Childbearing Age) – Common in Contraceptive Pill Use o They can cause pain and can bleed or rupture. Infection or Rupture) Polycystic Liver Multiple Cysts (Several mm to 10-15cm). CEA. Low potential for Malignant Change and a 30% risk of Bleeding. Vitamin B12. and usually no treatment is needed 25 . Splenomegaly. Weight Loss. Palmar Erythema. BENIGN TUMORS (found predominantly in women)  Hemangiomas Considerable effort has gone into differentiating these three entities radiologically. Weight Loss. Abdominal Fullness & Swelling. A. Women > Men) o Treatment is unnecessary unless their expansion causes symptoms B. APPROACH TO THE PATIENT A. Ascites (should be examined by cytology). Hepatic Cyst (Can be Multiple or Solitary): Problems = Bleeding and Infection Solitary Cyst RIGHT Liver Lobe Asymptomatic. The most  Adenomas useful diagnostic differentiating tool is a Triphasic CT-Scan performed with HCC fast Bolus  Focal Nodular Hyperplasia (FNH) Protocol for Arterial-Phase Imaging. Alk Phos. Albumin. Dilated Abdominal Veins. Spleen.

Breast. Weight Loss. Ovary  Lymphoma B. etc) A. TREATMENT (Depends on the Underlying Primary Source) o Radiotherapy. APPROACH TO PATIENTS WITH JAUNDICE  Yellowish discoloration of tissue resulting from the Deposition of Bilirubin 26 . Diagnosis o Laboratory:  Alkaline Phosphatase. Clinical Features o Hepatomegaly o Hepatic Bruit or Fruction Rub o Ascites (Bloody in 50%) o Non-Specific Symptoms (Malaise. Anorexia. Lungs. Treatment o NO Effective Treatment (Survival Rate < 6 months) o Surgery = 5-year Survival Rate < 10% o Radiotherapy & Chemotherapy = RARE Response V. Friction Rub. PRIMARY HEPATOCELLULAR CARCINOMA  80-90% of all Primary Liver Carcinoma  Most Commonly due to Cirrhosis prior to a Chronic Hepatitis-B  Incidence: 4x Men > Women A. Humoral Factors (Increased Androgen). Tyrosinosis (40% Risk). Clinical Features o Fever. Tumors Metastatic to the Liver: o Colon These three are predominantly the primary sites. Diagnosis o Liver Biopsy o CT or Ultrasound Guided Aspiration Biopsy D. Schistosomiasis (?). Primary Biliary Cirrhosis o Previous Hepatitis-B Infection  90-95% of Hepatocellular Carcinoma = (+) HBV Infection  60-70% of Hepatocellular Carcinoma = Chronic Hepatitis / Cirrhosis o Others: Mycotoxins. Clonorchiasis (?) B. Stomach. however. METASTATIC HEPATIC MALIGNANCY  It is MORE COMMON Than Primary Hepatocellular Carcinoma (MOST COMMON MALIGNANT Neoplasm)  Primary Source = Gastrointestinal Carcinoma (Colon. Jaundice C. Etiologic Factors o Chronic Liver Disease: Alpha-1 Antitrypsin Deficiency. RUQ Pain o Hepatomegaly. Abdominal Pain) o Clinical Deterioration or SUDDEN Increase in Transaminases in a STABLE Cirrhotic Patient C. Hemochromatosis. Chemotherapy o Hepatic Artery Infusion o Surgery VI. “Tumor Blush” o Liver Biopsy D. o Breast **Other Sources may be from:  GIT Carcinoma  Malignant Melanoma  Carcinoma of the Pancreas.IV. Kidney. metastatic tumors to the liver o Pancreas can originate from any organ primary.  Transaminases o Gallium Scan: Focal Filling Defects o Alpha Fetoprotein Elevation: 85-90% o Angiography: Hypervascularity.

Idosyncratic: Isoniazid Environmental Toxins (Vinyl Chloride) Wilson’s Disease Autoimmune Hepatitis QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. B. D. E  Epstein-Barr Virus  Cytomegalovirus  Herpes Simplex Alcohol Drug Toxicity  Predictable Dose Dependent: Acetaminophen  Unpredictable. C. 27 .Hepatocellular Conditions producing Jaundice: Viral Hepatitis  Hepatitis A.

CAUSES AND COMPLICATIONS OF CIRRHOSIS COMPLICATIONS OF CIRRHOSIS: Portal Hypertension (Gastroesophageal Varices.8 g/dL o Prolonged PT (INR > 1. Hep-C) Autoimmune Hepatitis Non-Alcoholic Steatohepatitis Biliary Cirrhosis  Primary Biliary Cirrhosis  Primary Sclerosing Cholangitis  Autoimmune Cholangiopathy Coagulopathy (Factor Deficiency. Hypersplenism. Alcoholic Hepatitis. Splenomegaly. and Nodular Regeneration of remaining Liver Parenchyma I. Thrombocytopenia) Malnutrition Hepatopulmonary Syndrome Cardiac Cirrhosis Inherited metabolic Liver Disease .000  AST / ALT Ratio > 1  Imaging (CT or UTZ) o Nodular Liver o Splenomegaly o Venocollaterals  Liver Biopsy: NOT always necessary if: o 1) Decompensated Cirrhosis (Variceal Hemorrhage.A1-Antitrypsin Deficiency .LECTURE ON LIVER CIRRHOSIS Additional Notes from Harrisons LIVER CIRRHOSIS     Characterized pathologically as IRREVERSIBLE Chronic Injury of the Hepatic Parenchyma Include extensive fibrosis in association with the formation of Regenerative Nodules Central Event leading to Hepatic Fibrosis: Cytokine-Mediated (tgf-B) Activation of the Hepatic Stellate Cells producing Fibrin Forming Type-1 Collagen Results from: o Hepatocyte Necrosis o Collapse of the supporting network with subsequent connective tissue deposition o Distortion of Vascular Bed.5 mg/dL  Portal Hypertension o Decreased Platelet Count: < 175. Portal Hypertensive Gastropathy. Ascites.Hemochromatosis .Cystic Fibrosis Cryptogenic Cirrhosis III. ALCOHOLIC CIRRHOSIS  Excessive chronic alcohol use can cause different types of Chronic Liver Disease: Alcoholic Fatty Liver. and Alcoholic Cirrhosis  Diagnosis requires an accurate history regarding amount and duration of alcohol consumption  Laboratory Tests can be completely normal in patients with Early Compensated Alcoholic Cirrhosis  In Advanced Liver Disease. etc) o 2) Liver/Spleen imaging diagnostic of Cirrhosis 28 . Neutropenia. Type 2) Hepatic Encephalopathy Portopulmonary Hypertension CAUSES OF CIRRHOSIS Alcoholism Chronic Viral Hepatitis (Hep-B.Wilson’s Disease . Thrombocytopenia) Bone Disease (Osteopenia. Osteomalacia) Hematologic Abnormalities (Anemia. Fibrinoysis. Ascites / SBP Hepatorenal Syndrome (Type 1. patient may be: LIVER ENZYMES: o Anemic from either Chronic GI Blood Loss AST / ALT >2 Alcoholic Liver Disease o Nutritional Deficiencies AST / ALT <1 Viral o Hypersplenism related to Portal Hypertension Alk Phos > Liver Enzymes Cholestatic o Direct Suppressive Effect of Alcohol on the Bone Marrow II. Osteoporosis. LABORATORY FINDINGS IN CIRRHOSIS (from the Lecture)  Liver Insufficiency: o Decreased Albumin: < 3.3) o Increased Bilirubin: > 1. Hemolysis.

8 x log(Bilirubin) V.5 30-35 4-6 1. Child Pugh Criteria for Hepatic Functional Reserve A Serum Bilirubin Serum Albumin Prothrombin Time Ascites Neurologic Disorder (mg/dL) (umol/L) (g/dL) (g/L) Seconds Prolonged INR < 2.0 > 51 < 3. MELD Score o Estimates the Risk of 3 month Mortality (higher the MELD score  likely to die in three months) o Three Laboratory Values used:  Serum Total Bilirubin  Serum Creatinine  INR 6.3 Poorly controlled Advanced Coma B.0 < 34 > 3.3 Easily controlled Minimal C > 3.IV.0 < 30 >6 > 2. COMPLICATIONS OF CIRRHOSIS Portal Hypertension Variceal Hemorrhage SBP Ascites Hepatorenal Syndrome Encephalopathy Jaundice Liver Insufficiency Encephalopathy 29 .0-3.5 > 35 0-4 < 1.0-3.0 34-51 3. HISTORY OF CHRONIC LIVER DISEASE Chronic Liver Disease Compensated Cirrhosis Decompensated Cirrhosis Death Compensated VS Decompensated: Presence of Complications!  Variceal Hemorrhage  Ascites  Encephalopathy  Jaundice VI.2 x log(Cr) + 3.4 + 9.7 None None B 2.7 – 2. SEVERITY OF LIVER DISEASE:  Child Turcotte Pugh  MELD Score A.8 x log(INR) + 11.

If SAAG is > 1. Mononuclear Variable If chylous. Fungal C. RBC Count > 50. Stain and Culture for AFB Positive Gram Stain. Fever.1 Unusual Pancreatic Ascites Turbid. may be blood stained A. > 25 Variable (15-53) < 25 (100%) SAAG (g/dL) > 1. Management of Ascites o Removal of > 1 L at a time (Paracentesis) may lead to Hypovolemia.VII. Culture Nephrosis Straw-colored or chylous < 1. Decreased Bowel Sounds. Chylous Turbid or purulent Straw-colored PROTEIN (g/L) < 25 (95%) > 25 (75%) > 25 (50%) If purulent. WBC.1 < 1. or Chylous Variable. Shock o Unless 10grams Albumin is replaced IV for each 1 L Ascitic Fluid removed 30 . cell block. INVESTIGATING ASCITES CONDITION Cirrhosis Neoplasm TB Peritonitis Pyogenic Peritonitis CHF GROSS APPEARANCE Straw colored or bile stained Straw colored. peritoneal biopsy Peritoneal Biopsy. Worsening of Hepatic Encephalopathy Diagnosis is likely when Ascitic Fluid has > 250 neutrophils/u/L E. per uL >10. Others: Amylase TAG Cytology Gram Stain or Culture pH < 7 Increased in Pancreatic Ascites Increased in Chylous Ascites Positive in Malignancy Bacterial Infections Bacterial Infection 3   Abdominal Pain & Distention. TB)  Infectious complication of Portal HPN-Related  Nephrotic Syndrome Ascites  Pancreatic or Biliary Ascites B. Hemorrhagic. mucinous.000u/L 1% < 250 (90%) Predominantly Mesothelial 20% > 1000 (50%) Variable Cell types 7% > 1000 (70%) Usually > 70% L Unusual Predominantly PMN Leukocytes 10% < 1000 (90%) Usually Mesothelial.000/mm = Hemorrhagic Ascites o Malignancy o TB o Trauma D. hemorrhagic.1 < 1.1g/dL (or 11 g/L)  Cause of Ascites is PORTAL HYPERTENSION with (97% Specificity):  Cirrhosis  Cardiac Ascites  Budd Chiari Syndrome Management of Ascites:  Portal Vein Thrombosis  Dietary Salt Restriction (2g Salt/day)  Veno-Occlusive Disease  Diuretic Therapy  Fatty Liver of Pregnancy  Paracntesis 2.1g/dL (or 11 g/L)  TIPS  Peritoneal Carcinomatosis Spontaneous Bacterial Peritonitis:  Infection (Peritonitis. If SAAG is < 1. ether extraction. Mononuclear < 250 Mesothelial.1 CELL COUNT RBC. SAAG: Serum to Ascites Albumin Gradient o Serum Albumin [minus] Albumin in Ascitic Fluid (Gradient) o The gradient correlates DIRECTLY with Portal Pressure 1. sudan staining  Amylase in Ascitic Fluid & Serum OTHER TESTS Cytology. Turbid.1 < 1. Absolute WBC Count (PMN) > 250/mm3 o Infection o When Mononuclear Cells are predominant: TB.1 > 1. Hemorrhagic. or chylous Clear. often >25 Variable.

Goal: 2-3 Stools per day. Impaired handwriting Asterixis. NH3 (Optional). II. Alkalosis. and III – but Negative on IV! o There will be NO Asterixis when patients is already in COMA o First Manifestation is the Reversal of the Sleep-Wake Pattern Treatment is multifactorial and includes management of the precipitating factors. Identify Precipitants and Correct Determine Electrolytes. BUN. Agitation. Ammonia levels are typically elevated in patients with hepatic encephalopathy. Hyponatremia. Diuretics o Miscellaneous: Infection. Babinski’s Sign. Aims of Treatment: o 1) Eliminate or Treat the Precipitating Factors o 2) Lower Blood Ammonia (and other Toxins): Decreases Absorption of Proteins and Nitrogenous Products from the Intestine D. Gut-derived neurotoxins are not removed by the liver because of vascular shunting and decreased hepatic mass get to the brain & cause symptoms. Mild Confusion. HEPATIC ENCEPHALOPATHY: Grading System for Hepatic Encephalopathy: GRADE 0 1 2 LEVEL OF CONSCIOUSNESS Normal Inverted Sleep Pattern. Irritable Disorientation from time. Constipation o Electrolyte and Metabolic Imbalance: Hypokalemia. Slow Responses Somnolent but can be aroused. Catharsis ensues. Sedatives. Sometimes hydration & correction of electrolyte imbalance is all that is necessary. amnesia. contributing to the elimination of waste products in the gut. Encephalopathy is more commonly seen in patients with chronic liver disease. Mainstay of Treatment (in addition to correction of precipitating factors) is to use Lactulose. inappropriate behavior Disorientation for place. Pathogenesis (Most Important): o SEVERE Hepatocellular Dysfunction and/or Intrahepatic & Extrahepatic Shunting of Portal Venous Blood into the Systemic Circulation BYPASSING the Liver (There is FAILURE to DETOXIFY the substances) B. Hypovolemia o Drugs: Narcotics. Incoordination. 1 to 4x daily until 4 stools/day)  Broad-Spectrum Antibiotics (eg. LACTULOSE 30-120mL. A. Approach to the Patient with Hepatic Encephalopathy. Dysarthria. Apraxia. Hypoactive Reflexes Asterixis. Superimposed Acute Liver Disease. Lactitol)  Neomycin  Metronidazole (250mg PO q8h) Portosystemic Encephalopathy is a serious complication of chronic liver disease and is broadly defined as an alteration in mental status & cognitive function occurring in the presence of liver failure. confused Coma PERSONALITY AND INTELLECT Normal Forgetful. Progressive Liver Disease. Hypoxia. which result in Colonic Acidification. Portal-Systemic Shunts C. Azotemia. Glucose   Protein Restriction Inadequate Response (?)  Laxative (eg. Surgery. or Metronidazole 250mg tid)  Inadequate Response (?)  Consider Liver Transplantation 31 . Neomycin 500-1000mg qid. decreased inhibitions.VIII. BUN (Blood Urea Nitrogen) Initial Evaluation: Exclude other Causes of Disordered Mentation. Creatinine. Hyperactive Reflexes. Excess Dietary Protein. Treatment of Hepatic Encephalopathy (Washington)  Treat Precipitating Factors  Dietary Protein Restriction (Controversial)  Non-Absorbable Disaccharide (Lactulose. Tranquilizers. Common Precipitants of Hepatic Encephalopathy: o Increased Nitrogen Load: Gastrointestinal Bleeding. aggressive Nil NEUROLOGIC ABNORMALITIES Normal Tremor. Restless Lethargic. Muscle Rigidity Decrebrate EEG ABNORMALITIES Normal Slowing Triphasic Waves Slowing Triphasic Waves 3 4 Slowing Triphasic Waves Slowing Delta Waves **NOTE: Asterixis is POSITIVE in Stage I.

VARICES  Gastroesophageal Varices: Most important complication of cirrhosis  Dilation of Coronary and Gastric Veins  Can lead to bleeding A. Atenolol  Non-Selective B-Blockers (B1 + B2): Propranolol.MANAGEMENT OF COMPLICATIONS (Lecture) I. Vasoconstrictors  Examples: Non-Selective B-Blockers. Pathophysiology Resistance to Portal Flow Increased Resistance to Portal Pressure Decreased Splanchnic Arteriolar Resistance Increased Splanchnic Flow (Increased Portal Blood Inflow) VARICES! o o o o Varices increase progressively by 7-8% per year Determinant of Severity of Varices = Severity of Liver Disease Everyone with Cirrhosis should be Endoscoped! Two Year probability of FIRST Bleed:  7% in Small Varices  30% in Large Varices B. Venodilators  ISMN (NOT used alone – usually combined with B-Blockers)  Mechanism: Decreases Intrahepatic Resistance to Decrease Portal Pressure AND Decreases Systemic Pressure to Decrease Portal Blood Inflow 3. Endoscopic Therapy  Sclerotherapy  Band Ligation 32 . Shunt  TIPS. Terlipressin. Esmolol Rationale for Use of Non-Selective B-Blockers:  If you Block the B2-Receptors in Vessels  Unopposed A1-Receptor Action  Constriction of Splanchnic Vessels  Increased Resistance Terlipressin:  Dose: 2mg q40 (very expensive)  BUT. Nadolol. Surgical Shunts  Mechanism: Decreases resistance to Portal Flow  Decrease Portal Pressure 4. Octreotide  Mechanism: Increases Splanchinc Arteriolar Resistance Note on Beta-Blockers:  Selective B-Blockers (B1): Metoprolol. there is increased survival 2. Principles in Treatment of Varices: 1. Vasopressin.

Sclerotherapy  Shunt: TIPS. B-Blockers did NOT prevent the development of Varices (Timolol actually increases adverse effects) Varices. Management of the Different Stages of Cirrhosis: STAGE MANAGEMENT No Varices Pre-Primary Prophylaxis: Prevention of Variceal Development  There is NO Specific Treatment  Recommendation: Repeat Endoscopy in 2-3 years (sooner if with Decompensated Liver Disease)  In studies. Surgical Shunts 3) TIPS (Transjugular Intrahepatic Portal Shunt)  Rescue treatment for recurrent Variceal Hemorrhage  Indicated in patients who re-bleed on Combination Endoscopic Management and Pharmacologic Treatment  Problem: Hepatic Encephalopathy (may be decreased by giving Lactulose) Recurrent Hemorrhage Secondary Prophylaxis: Prevent Recurrent Hemorrhage  1) B-Blockers Plus Endoscopic Variceal Ligation (BEST)  2) B-Blockers + ISMN or Endoscopic Variceal Ligation  3) TIPS / Shunt 33 . Vasopressin + Nitroglycerin  Endoscopic: Ligation. Somatostatin.C. but NO Hemorrhage Primary Prophylaxis: Prevention of First Variceal Hemorrhage 1) Small Varices  Recommendation: Repeat Endoscopy in 1-2 years  B-Blockers (?) – data are not clear 2) Medium to Large Varices  Recommendation: Beta-Blockers + Endoscopic Variceal Ligation Variceal Hemorrhage Treatment of Acute Variceal Hemorrhage: 1) General Management:  IV Fluids  Do NOT overtransfuse (this can actually increase Portal Volume  Increase bleeding)  Antibiotic Prophylaxis 2) Specific Treatment:  Pharmacologic: Terlipressin.

Differential Diagnoses: Hepatic Sinusoids SAAG > 1.5 Post-Sinusoidal HPN -Cardiac Ascites -Early Budd-Chiari -Venoocclusive 34 . Culture (SBP) o Albumin.II.5 Sinusoidal HPN: -Cirrhosis -Late Budd-Chiari Peritoneum SAAG < 1.1 Capillarized Sinusoid Ascites Protein < 2.1 Peritoneal Lymph Ascites Protein > 2. ASCITES  Cirrhosis: Most Common Cause of Ascites  Other Causes: Peritoneal Malignancy. Diagnostic Tap = 30-60cc o PMN Count. Peritoneal TB A.5 Malignancy TB Normal Leaky Sinusoid Ascites Protein > 2. Indication for Diagnostic Paracentesis o New Onset Ascites o Admission to Hospital o S/Sx of SBP o Renal Dysfunction o Unexplained Encephalopathi **NOTE: Contraindications: NONE!  Do we give FFP before Paracentesis? There are NO Recommendations!  Avoid the RIGHT side in Paracentesis (because these patients are usually maintained on Lactulose which causes Dilation of the Cecum)  LLQ is the better site (Lateral to the Inferior Epigastric Vessels) C. Heart Failure. Protein (Cirrhotic Ascites) o Glucose or LDH (Secondary Infection) o Amylase (Pancreatic Ascites) o Cytology (Malignant Ascites) B.

Gynecomastia 3) Large Volume Paracentesis (LVP) VS Diuretics in Uncomplicated Ascites  LVP: Faster resolution and Fewer Complications! Refractory Ascites LVP + Albumin (Mainstay) TIPS PVS Definition of Terms:  Diuretic-Intractable Ascites: Maximum doses of Diuretics could NOT be reached because of Side-Effects  Diuretic-Resistant Ascites: No response to Maximum Doses of Diuretics Volume Expanders:  Albumin  Dextran-70  Polygeline Albumin:  Decreases the Incidence of Post-Paracentesis Circulatory Dysfunction  Use Albumin if > 5L of Ascites is removed (if < 5 L. unless there is Hyponatremia (Na <125) 2) Diuretics  Should be Spironolactone-Based (Furosemide should NOT be used alone!)  Dose: Spironolactone 100-400mg/day Furosemide 40-160mg/day for Inadequate Weight Loss or if (+) HyperK +  Note:  Diuretics if Weight Loss < 1kg in the 1st week and < 2kg thereafter  Diuretics if Weight Loss > 0. or > 1kg/day in those with edema  Side Effects: Renal Dysfunction. Management of the Different Stages of Ascites: STAGE MANAGEMENT Portal Hypertension No Specific Therapy! Salt Restriction without Ascites Uncomplicated Ascites Definition: Ascites responsive to Diuretics in the absence of Infection & Renal Dysfunction Goal: to achieve Negative Sodium Balance 1) Salt Restriction  Effective in 10-20% of cases  2g salt/day (or 5.2g of Dietary Salt)  Fluid Restriction – NOT necessary.D.5kg/day in patient without edema. Hyperkalemia. Encephalopathy. may use Synthetic Expanders)  Dose: 6-8 g per Liter of Ascitic Fluid Removed Hepatorenal Syndrome Discussed in Another Lecture 35 . Hyponatremia.

but is NOT good in Diagnosis A. there should be a 25% decrease in the PMN count) C. Albumin (Plus Antibiotics) Indicated if: o BUN > 30 mg/dL o Creatinine > 1. Protein Restriction (?) o NOT necessary in Hepatic Encephalopathy o Do NOT restrict protein.0 o Bilirubin > 4 g/dL **NOTE. Mechanisms of Action of Lactulose o Colonic Acidification o Catharsis C. Constipation o TIPS o GI Bleeding o Sedation o Diuretics ( Serum K+. Precipitants of Hepatic Encephalopathy o Excess Protein. Plasma Volume  Azotemia) B. Early Diagnosis: Diagnostic Paracentesis o PMN Count > 250/mm3 o Done if Sx of SBP occur B. unless patient is in Stage IV 36 . Jaundice. Abdominal Pain A.III. Albumin is NOT indicated if (+) 100% Predicted Cure and Survival! D. HEPATIC ENCEPHALOPATHY  Ammonia Levels are NOT reliable – NOT necessary!  Clinical Diagnosis  Ammonia has good correlation with Severity. Pharmacologic Management o Antibiotics: 3rd Generation Cephalosporins. Quinolone (Ciprofloxacin) or B-Lactams (Co-Amoxiclav) o Usually Cefotaxime 2g q120 – 2g q60 o Duration: 5-10 days o Repeat Paracentesis in 48 hours if NO clinical Improvement with Antibiotics (no need to repeat if with Clinical Improvement – in repeat paracentesis. SPONTANEOUS BACTERIAL PERITONITIS (SBP)  Most Common Infection in Cirrhotic Patients  S/Sx: Fever. Infection. Prophylaxis for SBP: o Indicated for these Patients:  1) Cirrhotic with Active Variceal Hemorrhage  2) Patient Recovered from SBP (Long-Term) o Tx: Norfloxacin 400mg PO BID x 7 days IV.

Internal Medicine Notes 2009 .D. M.qwertyuiopasdfghjklzxcvbnmqwertyui opasdfghjklzxcvbnmqwertyuiopasdfgh jklzxcvbnmqwertyuiopasdfghjklzxcvb nmqwertyuiopasdfghjklzxcvbnmqwer HEMATOLOGY tyuiopasdfghjklzxcvbnmqwertyuiopas dfghjklzxcvbnmqwertyuiopasdfghjklzx cvbnmqwertyuiopasdfghjklzxcvbnmq wertyuiopasdfghjklzxcvbnmqwertyuio pasdfghjklzxcvbnmqwertyuiopasdfghj klzxcvbnmqwertyuiopasdfghjklzxcvbn mqwertyuiopasdfghjklzxcvbnmqwerty uiopasdfghjklzxcvbnmqwertyuiopasdf ghjklzxcvbnmqwertyuiopasdfghjklzxc vbnmqwertyuiopasdfghjklzxcvbnmrty uiopasdfghjklzxcvbnmqwertyuiopasdf ghjklzxcvbnmqwertyuiopasdfghjklzxc vbnmqwertyuiopasdfghjklzxcvbnmqw ertyuiopasdfghjklzxcvbnmqwertyuiop Jaime Alfonso Manalo Aherrera.

AVAILABILITY  Red Cell Products (Whole Blood. Malaria o Others: HTLV 1 & 2. etc (Plasma can transmit most infections) Platelet-Rich Plasma Plasma Derivatives 2 . Leukocyte Depleted Red Cells)  FFP  Cryosupernate  Cryoprecipitate  Platelets (Random Donor Platelets or Apheresed) III. Syphilis. CMV. PRBC. we can divide the units into Aliquots  Each unit should be tested for ABO and Rh Group o Tested in the Philippines: HIV 1 & 2. there are only TWO Conditions when we can Continue Transfusion: o Mild Allergic Reaction o Febrile Non-Hemolytic Reaction (continue when Fever subsides)  All Blood Units should be Infused within 4 Hours o If (+) Risks (such as Congestion).LECTURE ON RATIONAL BLOOD USE INTRODUCTION Whole Blood Red Cells Platelets Cryoprecipitate I. HBV. Washed RBC. Fibrinogen if stored for several days o Massive Blood Loss means Loss of >30% acutely  Most Common Fatal Hemolytic Transfusion Reaction: Clerical Error! o Donor should have Hgb > 125 o Risks: Early ( < 5 days) or Late ( > 7 days)  In Transfusion Reactions. KEY NOTES  There are only TWO Indications for Whole Blood Transfusion: o Massive Hemorrhage / Bleeding o Exchange Transfusion  Whole Blood: o No more Viable Platelets. HCV. ADVANTAGES OF COMPONENT THERAPY  Less volume transfused  Correct dose  Lower risk for immunologic transfusion reactions (Plasma = responsible for reactions)  Coagulation Factors are preserved  Decreased disease transmission  Unwanted Leukocyte and Platelet Aggregates eliminated  More patients can benefit II.

such as Fe deficiency) o 2) Symptomatic Anemia. Hgb: 84. PACKED RED BLOOD CELL (PRBC) A. Revised (Local) Guidelines for Adult BT of PRBC (~250cc): NVBSP Guidelines o 1) Hgb < 7 g/dL or Hct < 21% (If not due to a treatable cause. COPD. Lethargic o o D. Hemoglobinopathy. 1988) HEMOGLOBIN < 7 g/dL PRBC is Justified 6 – 10 g/dL > 10 g/dL MANAGEMENT Individualized – signs and symptoms of O2 Deprivation. CAD. no need for transfusion **NOTE: In Cancer Patients: Quality of Life is improved at Hemoglobin Level of 11 – 12 g/dL C. Sepsis 4) Patients receiving General Anesthesia. Current Standards (NIH Consensus Conference Report. MCH: 23. Do you transfuse?  Blood Loss in Elective Cholecystectomy: ~300-500cc  Most would opt to “Type and Screen” (if Blood Loss is < 500cc) – this means that there is no need for crossmatching yet.BLOOD PRODUCTS I. if:  a) Pre-Op Hemoglobin < 7 g/dL or Hct < 21%  b) Major Blood Letting Operation and Hemoglobin < 10 g/dL or Hct < 30% (Open Heart. Humans have Profound Capacity to Tolerate Anemia o Increase CO o Decrease Blood Viscosity o Redistribution o 2. Laminectomy)  c) Signs of Hemodynamic Instability or Inadequate O2 Carrying Capacity (Symptomatic Anemia) CLASS I Up to 750 mL Up to 15 % < 100 Normal Normal or Decreased 14 – 20 > 30 Slightly anxious CLASS II 750 – 1500 mL 15 – 30 % > 100 Normal Decreased 20 – 30 20 – 30 Mildly anxious CLASS III 1500 – 2000 mL 30 – 40 % > 120 Decreased Decreased 30 – 40 5 – 15 Anxious and confused CLASS IV > 2000 mL > 40 % > 140 Normal Decreased > 35 Negligible Confused. MCV: 65.23. Risks vs Benefits If (-) Cardiac / Neuro / Pulmo  patient can tolerate this level without transfusion Almost Never (more Harmful to transfuse) Sample Case: 32 year old female for Elective Cholecystectomy. Classification of Hypovolemic Shock according to Blood Loss Blood Loss (mL) Blood Loss (% BV) Pulse Rate Blood Pressure Pulse Pressure Respiratory Rate Urine Output (cc/h) CNS / Mental Status 3 . Hct: 0. regardless of Hemoglobin Level (usually < 10g/dL)  Dyspnea  Syncope  Postural Hypotension  Tachycardia  Chest Pain  TIA 3) Hgb < 7 g/dL or <21% with concomitant hemorrhage.3-DPG (change in affinity of Hgb to O2) B.

000 within 1 Hour and > 7. CONTRAINDICATIONS to Red Cell Transfusion: o Volume Expansion when O2 Carrying Capacity is adequate o Prophylaxis: No signs/symptoms of Anemia o Enhance General Sense of Well-Being o Promote Wound Healing F. Indications of “Prophylactic” Paracetamol / Anti-Histamines o Paracetamol: give only if (+) Febrile o Anti-Histamine: give only if (+) previous history of Allergy o Tx.000: Bleeding Time is Prolonged o At < 10.5 x 1010 Platelets/bag o Can carry Organisms (bacteria from the environment can go into the blood  induce Sepsis) B.000 – 10.000: Bleeding Time is > 30 minutes and NOT related to Platelet Count o At < 5. Give Leukocyte Depleted Products G.500 within 24 Hours Post-Transfusion Response 1 Unit increases PC by 5.000 – do NOT Transfuse yet Platelet Count will Increase in response to the Steroids  Dose and Response: POOLED / RANDOM DONOR PLATELETS 1 Unit / 10kg BW Dose SINGLE DONOR / APHERESIS PLATELETS 1 Pack (equivalent to 4-8 Units of RDP) Advantage: may reduce Infectious Disease Transmission by reducing the number of Donor Exposures Corrected Count Increment (CCI) > 10. PLATELET TRANSFUSION  Indications: Therapeutic and Prophylactic o Therapeutic: ex) Bleeding o Prophylactic: ex) Patient undergoing surgery (indications are controversial)  In Patients with Decreased Platelet Production: o At > 100. HUS. ITP o Heparin Induced Thrombocytopenia  Note on Dengue Hemorrhagic Fever: o If (-) Bleeding.000: Bleeding Time is NOT affected o At 10.E.000 cells/uL  Platelets are NOT useful in the following (these are due to Increased Platelet Destruction): o Drug Induced Thrombocytopenia o TTP. Random Donor Platelets (RDP) o Volume: 50 cc o Dose: 1 Unit / 10 kg Body Weight (ex: if 60kg. Single Donor Platelets (SDP) / Apheresed Platelets o Volume: 200 – 600 cc o Dose: 1 Apheresis Product / Transfusion Episode 4 . Transfusion of PRBC: o Give Blood Transfusion over 4 Hours after proper Blood Typing and Crossmatching o 1 Unit raises Hemoglobin by 1g/dL or Hematocrit by 3% II.000: Spontaneous Bleeding  Example: Case on ITP o Tx is Steroids o If Platelet Count is 12. NO Transfusion! A. give 6 units) o Content: > 5.

000 – give Prophylaxis (EXCEPT in Immune Mediated Diseases) o If Major Surgeries – maintain > 50. NOT responding to Antibiotics 5 . . CRYOPRECIPITATE TRANSFUSION  Indications: o Hemophilia-A with Bleeding or Anticipated o VonWB Disease o Fibrinogen Deficiency in DIC o Factor XIII Deficiency  Shelf Life: 1 year when Frozen at – 300C  Dose: In Pools of 6 Units each o Response: Increase Fibrinogen by 30-60 mg/dL V. but should be ABO Type-Specific o Pre-Medications NOT necessary CCI = Posttransfusion Count – Pretransfusion Count . x Body Surface Area Number of Platelets Transfused x 10 III. . FRESH FROZEN PLASMA (FFP) TRANSFUSION  Indication: Control or Prevention of Bleeding in Multiple Coagulation Defects o Liver Disease with Coagulopathy o Hemophilia o DIC o Reversal of Warfarin Effect  Dose: 4-7 Units for an Average Adult (15-20 mL/kg) o Response: Increase Coagulation Factors by about 2%  Shelf Life: 1 year when frozen at –300C IV. VII.000 o In Minor Surgeries – maintain > 30. . CRYOSUPERNATE TRANSFUSION  Indications: o Hemophilia-B o Factor II. . Some Generalizations: o If Platelet Count < 10. GRANULOCYTE CONCENTRATE TRANSFUSION  Indications: o Gram (-) Sepsis with ANC at < 500.000 o Cross Matching is NOT required prior to Platelet Transfusion. VII.

38-0.0 2.005 – 0.48 for Females (usually 0.45) **NOTE: Reticulocyte Index: Corrected Reticulocyte Count / 2 Interpretation:  LOW Retic Count = Marrow problem because of decreased production  HIGH Retic Count = Compensatory or Destruction or Blood Loss Absolute Reticulocyte Count = Patient’s Reticulocyte x Patient’s Reticulocyte 45 Corrected Reticulocyte Count = Absolute Reticulocyte Count Maturation Time (MT) MT is 1 1.BASIC HEMATOLOGY NOTES INTRODUCTION I.5 when Hct is 45% 35% 25% 15% Interpretation: CRC < 1% > 2% Hypoproliferative BM Hemolysis or 100. 0.5 for Males. Reticulocyte Count (0. SOME FORMULAS Hemoglobin: Hematocrit: Serum Fe: TIBC: Serum Ferritin M: 16 + 2 F: 13 + 2 M: 47 + 6 F: 40 + 6 50 – 150 mg/dL 54 – 64 mmol/dL M: 100 F: 30 A.015) o To know if with Marrow Problem or Anemia secondary to Hemodialysis or Blood Loss o Reticulocyte Count % = PGH Value x 100% o Corrected Reticulocyte Count:  Patient’s Reticulocyte Count x Patient’s Hct / Normal Hct x 1000  Normal Hct Values = 0.000mm2 Blood Loss 6 .5 2.4-0.

Normochromic Anemia (Reticulocytes are DECREASED) Aplastic Anemia.000 < 500 = NEUTROPENIC! 7 . Hypochromic = Iron Deficiency. Hypothyroidism. Normocytic or Macrocytic o Characterized by LOW Reticulocyte Count Microcytic Anemia Iron Deficiency Anemia Thalassemia Lead Poisoning Chronic Infection Macrocytic Anemia (Macrocytosis: MCV > 100Fl) Macrocytosis Reticulocytosis Liver Disease Down’s Syndrome Megaloblastic  Folic Acid Deficiency  B12 Deficiency C. Myelophthisic Anemia. Chronic Inflammatory Disease. Alcoholism. Aplastic Anemia  Normocytic. Pure Red Cell Aplasia. Myelodysplastic Syndromes  These are the Hypoproliferative Anemias associated with Marrow Damage  The have the following Characteristics: o Normochromic. Normochromic = Anemia of Chronic Disease o Anemia of Endocrine Failure = Mild Normocytic Normochromic Anemia o Anemia of Chronic Renal Failure = Normocytic. Absolute Neutrophil Count (ANC) (Neutrophils + Stabs) x WBC x 1. Hematology Formulas o MCH = Hgb/RBC o MCV = Hct (100)/RBC o MCHC = Hgb/Hct MCH = Hypo / Hyperchromic MCV = Micro / Macrocytic N: 27 – 31 N: 76 – 100 N: 330 – 390 Chromic Cytic IMPORTANT Notes:  Microcytic. Thalassemia. Liver Disease. Hemolysis. Myelodysplastic  Macrocytic = Megaloblastic Anemia.B.

RBC: Run x 4 hours D. HEMA CLEARANCE A. 500mL = 250g Iron III. FFP  FD  15cc/kg  2 Units q 12 (if you expect bleeding)  4 units FD 8 . Platelet o Volume: 50cc o Dose: 1 unit / 10 kg o Indication: PC < 10-20.II. X. Fresh Frozen Plasma (FFP) o Volume = 200Ml o Content: Normal Levels of all Coagulating Factors o Dose: 15mL/kg (each unit will raise factors by 3-5% or 10-15u/kg) o Indications:  PT INR > 1. Diphenhydramine 25-50mg PO/IV o In Non-Hemolytic Febrile Transfusion: Meperidine 25-50mg IV to prevent chills E. V. Cryoprecipitate o Volume: 15-20mL o Dose: Pool of 2 or 6 u (each unit Increase by 5-10%) – 1 bag/10kg BW o Pre-Med Tx: Paracetamol 500mg. TRANSFUSION THERAPY (Medicine Notes) A. Packed RBC (pRBC) o Indications:  1) Hgb < 7g/Dl or Hct < 21% in Hemodynamically STABLE Patients or without CVD  2) Hgb < 8g/Dl or Hct < 24% in UNSTABLE and CVD Patients % Increase: 1 Unit Prbc x 4 hours increases Hemoglobin by 10 B. Transfusion Threshold o NO Cardiac Disease: Hgb 70 o With Cardiac Disease: Hgb 80  100 **NOTE: How do you know if enough was transfused?  Check Symptoms B.000 in Bleeding Patients or undergoing Procedure  Massive Bleeding **NOTE: Given over 30 minutes. Platelet (50cc) Fast Drip o With Bleeding: < 100 T (NOT Purpura nor Petechiae) o W/O Bleeding: < 20 T C.000 (Prophylaxis)  If PC < 50. VII. NO Pre-BT Meds D.5x Normal  PTT > 5 sec of Upper Limit of Control  Active Bleeding  Coagulation Deficit of Factor II. XII  Reversal of Warfarin  TTP C. Whole Blood o Volume: 500Ml o Dose: 20mL/kg x 4 hours o Contains 1/2g of Fe per mL o Therefore.

INR  If > 1: means that blood is LESS Coaguable. High Molecular Weight Kininogen. Frequent Severe Bleeding  Severe Deficiencies of Factor VIII and IX 4. Heparin Interpreting PT 1. it is commonly used in the evaluation of patients with Liver Disease B. Variable. and also Prekallikrein. V. Prothrombin Time (PT) o PT assesses Factor I (Fibrinogen). VIII. SCREENING ASSAYS (from Harrisons)  Commonly used Screening Tests are: o PT o aPTT o Platelet Count A. X. Activity  > 70% = needed if you will do Invasive Procedures / Surgeries 9 . Protein Kinase 2. V. prone to bleeding. IX.IV. II (Prothrombin). but usually Mild Bleeding   Factor XI  Mild  in Factor VIII & IX 3. V. No Clinical Bleeding   Factors XII. ideal for ACS px  If < 1: coaguable blood 2. and X o Measures the time for clot formation of the citrated plasma after recalcification and addition of Thromboplastin o International Normalized Ratio (INR) is determined by: (PTPATIENT / PTNormal. High Molecular Weight Kininogen and Factor XII Prolonged PT:  Factor VII Deficiency  Vitamin-K Deficiency – Early  Warfarin Anticoagulation Prolonged aPTT and PT  Factor II. Activated Partial Thromboplastin Time (aPTT) o Assesses the Intrinsic and Common Coagulation Pathways: Factors XI. or X Deficiency  Vitamin-K Deficiency – Late  Direct Thrombin Inhibitors Prolonged aPTT: 1. Fibrinogen.Mean)ISI o INR was developed to assess Anticoagulation due to reduction of Vitamin-K Dependent Coagulation Factors. VII. II.

Laboratory Diagnosis o NORMOCYTIC. which is necessary for GPI Anchor  Without this Anchor. Clinical Course & Signs/Symptoms = Depends on SEVERITY o Anemia = Pallor. Treatment Washed Packed-RBC Transfusion Corticosteroids 15-30mg EOD Iron Replacement for IDA Heparin / Warfarin ATG 150mg/kg (Total) over 4-10 days Hematopoietic Stem Cell Transplant (HSCT) To Avoid further HEMOLYSIS To Control the Hemolysis Questionable – because if we give more Iron. Pathogenesis of Aplastic Anemia o Bone Marrow results from SEVERE Damage to the Hematopoietic Cell Compartment o In Aplastic Anemia = there is Replacement of the Bone Marrow by Fat (HYPOCELLULAR Marrow) C. we can promote Hemolysis If with History of Thrombosis For Marrow Hypoplasia Transplant II. WBC.COMMON HEMATOLOGIC CASES I. Pallor. Diagnosis o Clinical Symptoms = Ictericia. Treatment of Aplastic Anemia o HSCT (Hematopoietic Stem Cell Transplant) o Horse ATG 40mg/kg/d x 4 days or Rabbit ALG 3. Cell Membranes are Easily Destroyed (there are proteins which attach to this glycoprotein)  It is a DISTINCTIVE Disorder because it is an Intracorpuscular Defect acquired at the Stem Cell Level A. NORMOCHROMIC or MACROCYTIC RBC o Reticulocytopenia o Pancytopenia D. Thrombosis o PERIPHERAL CYTOPENIAS **NOTE: Other Findings (from the book)  Anemia is highly Variable  Hematocrit from < 20% to Normal  NORMOCHROMIC and NORMOCYTIC  Bone Marrow appears NORMOCELLULAR C. APLASTIC ANEMIA  PANCYTOPENIA with Bone Marrow HYPOCELLULARITY (Fats > Cellular Elements)  Acquired Aplastic Anemia = Abrupt Onset of Low Blood Counts in a previously Well Young Adult  Pancytopenia = it means DIMINISHED Amounts of RBC. Signs of Infections o (-) Organomegaly (in General) B. Platelets (all the blood elements) A.5mg/kg/d x 5 days o Cyclosporin 12mg/kg/d Orally o Androgens / Steroids / Growth Factors o Transfusions o Avoidance / Treatment of Infections o Removal of Suspected Etiologic Agent o Treatment for Severe & Very Severe = BONE MARROW Transplant 10 . Characterized by Three Common Manifestations: o Hemolytic Anemia o Venous Thrombosis o Deficient Hematopoiesis B. EF. Weakness o Bleeding = Most Common EARLY Symptom o Thrombocytopenia = Bleeding Diathesis o Leukopenia = Fever. PAROXYSMAL NOCTURNAL HEMOGLOBINURIA (PNH)  Main Defect = MUTATION in Pig-A Gene (in the X-Chromosome).

strong peripheral pulses. systolic flow murmur (Hemic) o Pale skin and mucous membranes 11 . Signs and Symptoms o Most often recognized by Abnormal Screening Lab Tests o Acute Leukemia: Always due to Blood Loss o 30% Loss of Blood Volume: Unable to compensate w/ Vascular Contractions and changes in Regional Blood Flow o 40% Blood Loss: will manifest signs and symptoms of Hypovolemic Shock o Hgb of 7-8 mg/Dl = Signs and Symptoms of Anemia will develop:  Bleeding  Easy Fatigability  Malaise  Fever  Weight Loss  Night Sweats C. Reticulocyte Count Reticulocyte Index < 2. Three Major Classes of Anemia o Marrow Production Defects (Hypoproliferative) o Red Cell Maturation Defects (Ineffective Erythropoiesis) o Decreased Red Cell Survival (Blood Loss / Hemolysis) Anemia  CBC.III. blood in stool. petechiae.5 Red Cell Morphology Normocytic Normochromic Hypoproliferative Marrow Damage *Infiltration / Fibrosis *Aplasia Iron Deficiency Decreased Stimulation *Inflammation *Metabolic Defect *Renal Disease Nuclear Defects *Folate Deficiency *Vitamin B12 Deficiency *Drug Toxicity *Refractory Anemia Reticulocyte Index > 2. lymphadenopathy. Physical Examination o Findings of infection. splenomegaly o Forceful heartbeat. ANEMIA (from Medicine Notes) A.5 Hemolysis / Hemorrhage Blood Loss Intravascular Hemolysis Metabolic Defect Membrane Abnormality Micro or Macrocytic Maturation Disorder Cytoplasmic Defects *Iron Deficiency *Thalassemia *Sideroblastic Anemia Hemoglobinopathy Immune Destruction Fragmentation Hemolysis B.

If the Reticulocyte Production Index is < 2 in the face of established Anemia.8-1. A reticulocyte count provides a reliable measure of red cell production In order to use the Reticulocyte Count to estimate marrow response.D. Hemoglobin of Patient / Expected Hemoglobin . Reticulocyte Count  Key to the initial classification of Anemia  < 2-3x the normal = Inadequate Marrow Response An accurate Reticulocyte Count is key to the initial classification of Anemia. Correction #1 for Anemia (Produces the Absolute Reticulocyte Count) Abs. and the relationship between the degree of shift. To correct for this effect. This provides an estimate of reticulocyte count corrected for anemia. two corrections are necessary. Expected Hgb for the Age and Gender Example: Person whose reticulocyte count is 9%.5/15) OR 9 x (23/45) = 4.25 2 12 . Hemoglobin of Patient . Hct 23% Absolute Reticulocyte Count = 9 x (7. seen in Fibrosis. Laboratory Examinations: 1. CBC  Hemoglobin. The correction is necessary because these prematurely released cells survive as reticulocytes in circulation for > 1 day. Hgb 7. Normally. Maturation Time Correction **NOTE: Maturation Time Correction varies from 1-3. the reticulocyte percentage (%) is multiplied by the ratio of the patient’s hemoglobin or hematocrit to the expected hemoglobin/hematocrit for age and gender of the patient. Calculation of Reticulocyte Production Index (Medicine Notes) 1.5g/Dl.5gm/Dl. Reticulocyte Count ranges from 1-2% and reflects the daily replacement of 0. but 2 is usually used Example: IN a person whose Reticulocyte Count is 9%. With anemia. thereby providing a falsely high estimate of daily red cell production. Peripheral Blood Smear  Anisocytosis = change in Cell Size  Poikilocytosis = changes in Cell Shape (suggests defect in maturation of RBC precursors in BM or fragmentation of circulating RBCs)  Polychromasia = Reticulocytes which are released Prematurely from the BM (slightly larger than normal and grayish blue). representing prematurely released reticulocytes. a further correction is required. Hct 23% Reticulocyte Production Index = 9 x 7. are referred to as shift cells. Ret Ct = Ret Count x . In order to convert the corrected reticulocyte count to an index of marrow production. Infiltration of BM by Malignant Cells 3. For this second correction. the peripheral blood smear is examined to see if there are polychromatophilic macrocytes present. Hgb 7. the % of reticulocytes may be increased while the absolute number is unchanged. a Defect in Erythroid Marrow Proliferation or Maturation must be present E. Hematocrit  Red Cell Indices  MCV (N: 90 + 8)  MCH (N: 30 + 3) Microcytosis: MCV < 80 Macrocytosis: MCV > 100 MCV and MCH reflect defects in Hemoglobin Synthesis 2. Correction #2 for Anemia (Produces the Reticulocyte Index) Reticulocyte Production Index = Retic Count x .5% 2. These cells.5 / 15 = 2. depending on whether some of the reticulocytes in circulation have been released from the marrow prematurely. The first correction adjusts the reticulocyte count based on the reduced number of circuloating red cells.0% of the circuloating red cell population.

F.5x the Normal There is INCREASED Erythropoiesis: presence of Polychromatophilic Macrocytes in PBS 3. Red Cell Maturation Defects / Ineffective Erythropoiesis    Slight to Moderately Elevated Reticulocyte Production Index that is accompanied by either Macrocytic or Microcytic Red Cell Indices Marrow Morphology: E/G Ratio > 1:1 (Erythroid Hyperplasia) Has TWO Types:  Nuclear Maturation Defects (From Vitamin B12. Bone Marrow Examination Hypoproliferative Anemia Hemolytic Disease Maturation Disorder RETICULOCYTE PRODUCTION INDEX <2 >3 Decreased E/G RATIO 1:2 or 1:3 At least 1:1 Increased **NOTE: E/G Ratio or Erythroid / Granulocytic Ratio 1. Marrow Biopsy Serum Ferritin Acute or Chronic Inflammation In Mild to Moderate Deficiency  Serum Iron  Serum Iron  % Transferrin Saturation  % Transferrin Saturation N or  TIBC  TIBC  Ferritin  Ferritin **NOTE: Anemia of Chronic Disease  Cytokines  causes ANEMIA  This is in contrast to Anemia of Iron Deficiency 2. Hypoproliferative Anemia  Reticulocyte Production Index with little or no change in RBC morphology (Normocytic. Blood Loss / Hemolytic Anemia   13 . inadequate EPO stimulation in Renal Failure  Key Labs: Serum Iron. Folic Acid Deficiency. Normochromic)  At least 75% of all cases of Anemia  Majority due to Mild to Moderate Deficiency or Inflammation  Other Causes: Marrow damage. Drug Damage. Myelodysplasia)  Cytoplasmic Maturation Defects (Defects from Severe Iron Deficiency) RBC Production Indices > 2. Evaluation of Renal and Thyroid Function. TIBC.

or diaphoresis 2. Hematologic Findings  Anemia (can be severe) – Normocytic Normochromic  Decreased Erythropoiesis often results in a Reduced Reticulocyte Count  Decreased RBC survival by accelerated destruction  Active Blood Loss  Median Presenting Leukocyte Count is ~15. the Myeloid Lineage is virtually certain  Platelet Counts < 100. Leukopenia. Lymphadenopathy.HEMATOLOGIC MALIGNANCIES I. bone pain. drugs Classifications: WHO Classification + FAB Classification (see harrisons) 1. weakness. On Physical Examination  Fever.000u/L  Auer Rods: if present. Splenomegaly (common in ALL). ACUTE LEUKEMIA  Present with manifestations of CYTOPENIAS  Anemia: Fatigue and Dyspnea  Thrombocytopenia: Cutaneous or Mucosal Hemorrhages  Neutropenia: Fever and Infection  Leukemic Infiltration of organs: Lymphadenopathies. anorexia. Treatment: Induction + Postremission Management  Goal: to quickly induce Complete Remission (CR)  Once CR is obtained. Gingival Hyperplasia and Skin Nodules (common in AML) A. radiation. lymphadenopathy. Splenomegaly. evidence of Infection & Hemorrhage 3. Hepatomegaly. further therapy must be used to prolong survival and achieve cure B. weight loss. fever. or Leukocyte Dysfunction. nonspecific cough. headache. Clinical Presentation  Non-Specific Symptoms that begin gradually or abruptly and are the consequence of Anemia. Acute Lymphoblastic Leukemia o Characterized by predominance of Lymphoblasts o Occurs most often in children o Form of Acute Leukemia that is MOST Responsive to Therapy o o o Common in children – ALL is NOT a common Leukemia in Adults ALL cell origin is in the Lymphoid Line Most Common ALL Variant (75%) = B-Cell Lineage 14 . abnormal hemostasis. chemical and other occupational exposures. or Thrombocytopenia  Fatigue. Acute Myeloid Leukemia (AML) o 80% of adult Acute Leukemia o Characterized by predominance of Blasts (Myeloblasts and Early Promyelocyte) in the BM and PBS o o Etiology: Hereditary. Sternal Tenderness. Leuokcytosis.000/uL  Elevation of Serum Uric Acid (50%) 4.

left upper quadrant mass) 2. Peripheral Blood Lymphocytes o Increased Number of MATURE Lymphocytes (CD-5 B-Cells 95%) in Peripheral Blood & Bone Marrow o Males > Females 1. malaise. Infections 3. Symptomatic Organomegalies. CHRONIC LEUKEMIA  Characterized by Proliferation of Lymphoid or Hematopoietic Cells that are more mature than those of Acute Leukemia  Have a longer. Chronic Lymphocytic Leukemia (CLL) o Proliferation of neoplastic lymphoid cells (almost always B-Cells) with widespread infiltrations of BM. Important Cytopenias. PBS.000 to 200. Chronic Myeloid Leukemia (CML) o Neoplastic Clonal Proliferation of Myeloid Stem Cells o Characterized by reciprocal chromosomal translocation between chromosomes 1 and 2 – Philadelphia Chromosome o Marked Leukocytosis (50. Lymph Node. the disease is characterized by the inevitable transition from a Chronic Phase to an Accelerated Phase and on to Blast Crisis in a Median Time of 4 years 1.000) o Reduction in Leukocyte Alkaline Phosphatase activity in the Leukemic Leukocytes o Clinical Features:  Prominent Splenomegaly  Modestly Enlarged Liver and Lymph Nodes  Terminates in Accelerated Phase (BLASTIC CRISIS) with Increasing number of Blast Cells and Promyelocytes o o Diagnosis is established by identifying a Clonal Expansion of a Hematopoietic Stem Cell possessing a reciprocal translocation between Chromosomes 9 and 22 Untreated. Physical Examination  Minimal to Moderate Splenomegaly = Most Common  Mild Hepatomegaly 15 .Chemotherapeutic Agents  HSCT (for younger patients)  IVIG B. Treatment of Chronic Lymphocytic Leukemia  Indications for Treatment: Hemolytic Anemia. Disfiguring Lymphadenopathy. Marked Systemic Symptoms  Treatment / Management:  Chlorambucil + Prednisone  COP or CHOP  Mainstay of Treatment = Fludarabine +/.Lymphadenopathy Pallor. splenic enlargement (early satiety. Complications:  Warm Antibody Autoimmune Hemolytic Anemia (AIHA)  Hypoagammaglobulinemia and Increased Susceptibility to Bacterial Infection 2. Clinical Presentation  Clinical Onset of the Chronic Phase is generally insidious  Fatigue. less devastating Clinical Course than acute leukemia A. Signs of Bleeding. and weight loss.II. Clinical Features  Indolent Clinical Course  Generalized Lymphadenopathy and Moderate Hepatosplenomegaly   Asymptomatic or +/. Spleen and Liver o Incapable of producing into Antibody-Producing Plasma Cells o Often occurs in persons > 60 y/o o Presence of Smudge Cells in PBS o Leukemic Cells resemble Normal Mature.

nonclonal hematopoiesis. or platelet count < 100. Night Sweats.q11. we give Allopurinol AND we give NaHCO3 to Alkalinize the Urine III. Treatment  Goal of Tx: To achieve prolonged. nonneoplastic. Differential Diagnosis o Reactive Lymph Node Hyperplasia (as in INFECTIONS) o Undifferentiated Carcinoma E. cytogenetic clonal evolution. blood or marrow basophils >20%. Hereditary.2)  Originally. Mesenteric Lymph Nodes Blood. Hematogenous Spread In UNFAVORABLE Types Less Common Peripheral. goal is complete molecular remission and cure If Blasts > 20%  Blastic Crisis 10-20%  Accelerated Phase < 10%  Chronic Phase Hydroxyurea o Given as management – action of Leukocytes  Rupture o Problem: Ruptured WBCs may cause an Increase in Uric Acid Levels  therefore. Chemicals (Benzene Herbicides). which entails the eradication of any residual cells containing the BCR/ABL Transcript  Hence. Hodgkin’s VS Non-Hodgkin’s Lymphoma: Spread Extranodal Site Involvement Systemic Symptoms Involvement Cure HODGKIN’S LYMPHOMA Orderly Spread by Contiguity RARE Of Prognostic Importance Axial and Central Lymph Nodes POSSIBLE for All Types NON-HODGKIN’S LYMPHOMA Random. Weight Loss B. with increases in both immature and mature granulocytes  Platelet Counts are almost always elevated at diagnosis  Mild Normocytic Normochromic Anemia  Bone Marrow Cellularity is Increased (at diagnosis) – Increased Myeloid to Erythroid Ratio  Disease Acceleration: defined by development of increasing degrees of anemia unaccounted for by the bleeding or therapy. Immunodeficiency A. Prognosis o Hodgkin’s Lymphoma is BETTER than Non-Hodgkin’s Lymphoma o International Prognostic Index (IPI) for Non-Hodgkin’s Lymphoma (FIVE Clinical Factors):  Age 60 or Above  Serum LDH Levels ELEVATED  Performance Status  Ann-Arbor Stage III or IV  Extranodal Site Involvement 16 .3. LYMPHOMAS  Incidence: Males > Females (3:2)  Etiology: Viral (EBV).000/uL  Blast Crisis: defined as Acute Leukemia. or blood marrow blasts between 10-20%.22)(q34. durable. Diagnosis o Lymph Node or Extra-Nodal Mass BIOPSY o FNAB – (+) Limitations (very painful) o Histopathology = (+) REEDSTERNBERG CELL in Hodgkin’s Lymphoma o Immunohistochemistry D. with Blood or Marrow Blasts > 20% **NOTE: Cytogenic Hallmark of CML (90-95%) = t(9. Signs / Symptoms o Painless Enlarged Lymphadenopathy o With or Without Fever. this was recognized by the presence of a shortened chromosome 22 (22q-). designated as the Philadelphia Chromosome 4. Waldermyer’s Ring RARE in Low Grade Tumors C. Laboratory Hematologic Findings  Elevated WBC.

D. Internal Medicine Notes 2009 . M.qwertyuiopasdfghjklzxcvbnmqwertyui opasdfghjklzxcvbnmqwertyuiopasdfgh jklzxcvbnmqwertyuiopasdfghjklzxcvb nmqwertyuiopasdfghjklzxcvbnmqwer INFECTIOUS DISEASE tyuiopasdfghjklzxcvbnmqwertyuiopas dfghjklzxcvbnmqwertyuiopasdfghjklzx cvbnmqwertyuiopasdfghjklzxcvbnmq wertyuiopasdfghjklzxcvbnmqwertyuio pasdfghjklzxcvbnmqwertyuiopasdfghj klzxcvbnmqwertyuiopasdfghjklzxcvbn mqwertyuiopasdfghjklzxcvbnmqwerty uiopasdfghjklzxcvbnmqwertyuiopasdf ghjklzxcvbnmqwertyuiopasdfghjklzxc vbnmqwertyuiopasdfghjklzxcvbnmrty uiopasdfghjklzxcvbnmqwertyuiopasdf ghjklzxcvbnmqwertyuiopasdfghjklzxc vbnmqwertyuiopasdfghjklzxcvbnmqw ertyuiopasdfghjklzxcvbnmqwertyuiop Jaime Alfonso Manalo Aherrera.

adenopathy. Laboratory Findings o Leukopenia. Thrombocytopenia. DENGUE HEMORRHAGIC FEVER / DENGUE SHOCK SYNDROME  Usually with a background of Previous Exposure to another Serotype – the transient protection after Dengue Virus Infection is replaced within several weeks by the potential for Heterotypic Infection resulting in Typical Dengue Fever or – uncommonly – for ENHANCED Disease (Secondary DHF / DSS)  Macrophage Infection is CENTRAL to the pathogenesis of Dengue Fever and to the Origin of DHF / DSS A. retroorbital pain. Clinical Presentation o Sudden Onset of Fever. and all cause a similar clinical syndrome o Breeds near human habitation – relatively fresh water source such as water jars. SECOND infection with a Serotype of Dengue Virus different from that involved in the Primary Infection leads to Dengue Hemorrhagic Fever (HF) with Severe Shock o Incubation Period 2-7 Days B. nausea.5 inches from Volar Aspect of Antecubital o Hemorrhagic Manifestations (Petechiae + Tourniquet Test) Fossa o Leukopenia A. palatal vesicles and sclerae injection o Others: Anorexia. Microbiology o Aedes Aegypti = Principal Vector (All four distinct dengue viruses – Dengue 1-4 – have Aedes Aegypti as their principal vector. Pathogenesis Previous Infection with a Heterologous Dengue Virus Serotype  Production of Nonprotective Antiviral Antibodies  Bind to Virion’s Surface and through interaction with the Fc Receptor focus Secondary Dengue Viruses on the Target Cell  Enhanced Infection B. headache. maculopapular rash beginning on the trunk and spreading to extremities and face o Epistaxis and scaterred petechiae are often noted in uncomplicated dengue.COMMON INFECTIOUS DISEASES 1) DENGUE INFECTION I. and back pain along with the severe myalgia that gave rise to the colloquial desegnation “Break Bone Fever” o D1: Macular rash. discarded containers o In rare cases. cutaneous hypersensitivity. Induction of Vascular Permeability and Shock depends on Multiple Factors: o 1) Presence of Enhancing and Non-Neutralizing Antibodies o 2) Age (susceptibility to DHF/DSS drops after 12y/o) o 3) Sex (F > M) o 4) Race o 5) Nutritional Status (Malnutrition is Protective) o 6) Sequence of Infection (Serotype 1 followed by Serotype 2 is More DANGEROUS than Serotype 4 followed by Serotype 2) o 7) Infecting Serotype (Serotype 2 is MORE DANGEROUS) 2 . vomiting. DENGUE FEVER  Acute febrile illness with NO Identifiable Focus of Infection of 2-7 days Duration (sometimes Biphasic)  With Two or More of the following: o Headache Tourniquet Test:  Inflate cuff midway between Systolic and o Retro-Orbital Pain Diastolic for 5 minutes o Myalgia / Arthralgia  (+) If > 20 Petechiae in a 1 square inch area o Rash (Petechial) 1. and preexisting gastrointestinal lesions may bleed during the Acute Illness C. Serum Aminotransferase Elevation o Dx: IgM ELISA or Paired Serology during Recovery or by Antigen-Detection ELISA or RT-PCR during the Acute Phase II.

Hepatomegaly. Diagnosis o Virologic Diagnosis can be made by the usual means. and most patients respond promptly to close monitoring. GI Tract. Uncontrollable Bleeding – Fresh Whole Blood is indicated  If PT. Purpura  Bleeding from Mucosa.C. PTT. usually at the time of Defervescence Frank Shock is apparent. PTT are prolonged and with Thrombocytopenia. Ascites) 2. Rashes  Petechiae on Palate  Petechiae on Axillae GRADE 3 Grade 1 + 2 PLUS: Circulatory Failure  Rapid Weak Pulse  Narrowing Pulse Pressure  Hypotension  Cold. Diagnostics o CBC with PC. urinalysis. even if PC is LOW C.000 or 1-2 Platelets / OIF)  Evidence of Plasma Leakage due to Increased Capillary Permeability  Any Hematocrit > 40% of Rise of > 20% in Hematocrit for age and sex  A Drop in 20% Hematocrit following volume replacement treatment as compared to baseline  Signs of Plasma Leakage (Pleural Effusion. Therapeutics o Supportive Hydration o Optional Medications: H2-Blockers if with Abdominal Pain or GI Bleeding o Watch out for Complications:  If there is Frank. there is NO need to administer Platelet Transfusion. Ecchymosis. MANAGEMENT OF DENGUE HEMORRHAGIC FEVER A. Dengue Hemorrhagic Fever (DHF)  Fever or Hx of Fever lasting for 2-7 days  Hemorrhagic Manifestations such as:  (+) Tourniquet Test  Petechiae. Fresh Frozen Plasma Transfusion is indicated  If there is DIC. PT. and in some cases Severe Ecchymoses and GI-Bleeding Period of Shock lasts only 1 or 2 days. PLUS Signs of Circulatory Failure  Rapid and Weak Pulses  Narrow Pulse Pressure (< 20mmHg)  Hypotension for Age (< 60mmHg Systolic for < 5y/o and < 90mmHg Systolic for > 50 y/o)  Cold Clammy Extremities D. GRADING OF DENGUE (Medicine Notes) GRADE 1 Fever with Non-Specific Sx GRADE 2 Grade 1 PLUS: Hemorrhagic Manifestations:  (+) Torniquet Test  Easy Bruisability  Gum Bleeding  Epistaxis. Letharghy. Thrombocytopenia < 100. Pleural Effusions. oxygen administration. Petechiae) or Overt Bleeding in Absence of underlying causes Dengue Shock Syndrome: accompanied by Hemorrhagic Signs & results from Increased Vascular Permeability leading to shock Mild DHF / DSS More Severe Cases Restlessness. and infusion of Crystalloid or – in severe cases – Colloid 1. and this situation may result in a lack of Virus Specificity of the IgM and IgG Immune Responses o A secondary Antibody Response can be sought with tests against several Flavivirus Antigens to deminstrate the characteristic Wide Spectrum of Reactivity III. Cyanosis. Clinical Presentation of DHF o o Identified by detection of Bleeding Tendencies (Torniquet Test. Hemoconcentration are detected 2 to 5 days after onset of Typical Dengue Fever. Torniquet Test o Dengue Serology if Illness LONGER Than 4 days o Others: AST/ALT. Hematemesis or Melena  Thrombocytopenia (100. Prevention 3 . although Multiple Flavivirus Infections lead to a broad immune response to several members of the group. Dengue Shock Syndrome (DSS): All the criteria of DHF. Clammy Skin  Restlessness GRADE 4 Grade 1 + 2 + 3 PLUS Profound SHOCK Undetectable BP or Pulse IV. IV Sites or other sites. Ascites. CXR Monitor Platelet Count + Hematocrit Levels q12-24 hours B. with Low Pulse Pressure. Platelet Transfusion is indicated **NOTE: In the Absence of Bleeding.000/uL.

but yield is HIGHERST during the first 2 Weeks  Should be taken at least from different sites 2. Flagellar H-Antigen  Incubation Period: varies with the size of infecting dose and averages 10-20 days (range 3-55 days) I.2) TYPHOID FEVER  Gram (-) S. LABORATORY WORK-UP A. Stool Culture  (+) 2nd – 4th Week of Illness 3. lymph nodes and Peyer Patches of the Ileum  Transmitted to humans orally by contaminated food or water II. Hypochromia with Blood Loss o Neutropenia B. Clammy Skin Circumoral Cyanosis Seizures Hypotension or Narrowing Pulses All Patients suspected of having Complicated Typhoid Fever Intestinal Perforation GI Hemorrhages Peritonitis Pericarditis Hepatic and Splenic Abscesses DIC Myocarditis Meningitis III. Complete Blood Count (CBC) o Leukopenia / Leukocytosis o Thrombocytopenia o Normochromic Anemia. Culture of Appropriate Specimen 1. Surface V1 Antigen. typhi and S. Rapid Pulse Cold. CLINICAL MANIFESTATION NON-SPECIFIC SYMPTOMS PHYSICAL FINDINGS Chills Diaphoresis Anorexia Myalgia Cough Weakness / Malaise Sore Throat Dizziness Constipation / Diarrhea Abdominal Pain Abdominal Distention Persistent High Fever Relative Bradycardia Rose Spots (Rashes primarily trunk area) Abdominal Tenderness Hepatomegaly Splenomegaly Thyroid Psychosis / Encephalitis Epistaxis III. PATHOGENESIS  Hallmark: Invasion and Multiplication within the Mononuclear Phagocytic Cells in the liver. paratyphi  3 Major Antigenic Determinants: Somatic-O Antigen. Bone Marrow Culture  NOT likely done. spleen. but indicated in high suspicious cases with (-) Blood or Stool Culture  Can be done anytime during t he illness  Isolation Rate is around 90% 4 . Blood Culture  Gold Standard  Should be taken anytime during the illness. CRITERIA FOR ADMISSION (Medicine Notes) All Patients Suspected of Having Typhoid Fever with ONE or More of the Following: Persistent Vomiting or Unable to take Oral Fluids Severe Dehydration Spontaneous Bleeding Persistent Abdominal Pain Listlessness Changes in Mental Status Weak.

Presence of Severe Symptoms. Clinical Deterioration despite Conventional Therapy: (Empiric Therapy for Suspected Resistant Typhoid Fever) o Ceftriaxone (Rocephin) 3gm IV Infusion OD x 5-7 days. For COMPLICATED Cases. Or o Amoxicillin 4-5g/day in 3 divided doses x 14 days B. typhi = 4 oral doses (Ty21a) VII.IV. or Ceftriaxone may be used for Pregnant o Fluoroquinolones: Women and Children  Ciprofloxacin (Cibprobay) 500mg tab PO BID x 7-10 days  Ofloxacin (Inoflox) 400mg tab PO BID x 7-10 days  Pefloxacin (Floxin) 400mg tab PO BID x 7-10 days VI. Hepatic & Splenic Abscess.5 tabs BID x 14 days. Encephalitis 5 . Meningitis. LABORATORY FINDINGS (from Blue Book) IgM IgG (+) (-)  Acute Infection (+) (+)  Recent Infection (-) (+)  Equivocal: Past Infection or Acute Infection V. PREVENTION  Whole Cell Vaccine (Heat Killed) = 2 parenteral doses  Purified Vi Polysaccharide fro Capsule = 1 parenteral dise (ViCPS)  Attenuated S. TREATMENT A. Disseminated Intravascular Coagulation. Myocarditis. Or o Co-Trimoxazole Forte 1-1. UNCOMPLICATED Typhoid Fever: Conventional Therapy o Chloramphenicol 3-4g in 4 divided doses x 14 days. COMPLICATIONS:  Intestinal Perforation  GI Hemorrhage and Peritonitis may occur in the 3 rd to 4th Week of Illness  Pancreatitis.

CLINICAL MANIFESTATIONS A. Fish and Birds may also harbor these Microorganisms  Transmission of Leptospires: o Direct Contact with Urine.3) LEPTOSPIROSIS   MILD FORM = Leptospirosis may present as an Influenza-Like Illness with Headache and Myalgia SEVERE FORM (Weil’s Syndrome) = characterized by Jaundice. Abdomen) = IMPORTANT Feature of Leptospiral Infection 1. WATER is an Important Vehicle in their Transmission II. Nausea. but often present several months after the initial illness) 6 . Back. Immune Phase  Most Patients become ASYMPTOMATIC within 1-week  After an Interval of 1 to 3 days. which especially affects the Calves. Severe Headache. Chills. Myalgias  IMPORTANT Feature of Leptospiral Infection = MUSCLE PAIN. the Illness recurs in a number of cases  The Start of this Second (Immune) Phase COINCIDES with the Development of Antibodies  Symptoms are more VARIABLE than during the First (Leptospiremic) Phase  Fever is LESS Pronounced and Myalgias are LESS Severe than in the Leptospiremic Phase  NOTE: This is where we see the Inflammation Stages **An Important Event during the Immune Phase is the Development of Aseptic Meningitis:  Meningeal Symptoms usually DISAPPEAR within a few days. & Hemorrhagic Diathesis I. Iridocyclitis and Chorioretinitis = Late Complications that may persist for years (can become apparent as early as the third week. although other Wild Mammals. Vomiting. Renal Dysfunction. etc o Muscle Pain (Calves. EPIDEMIOLOGY  A ZOONOSIS with a worldwide distribution  Rodents (especially Rats) = Most Important reservoir. Blood or Tissue from an Infected Animal o Exposure to a Contaminated Environment o Human-to-Human Transmission is RARE! o Since Leptospires are Excreted in the Urine and can survive in water for many months. Anicteric Leptospirosis o Leptospirosis may present as an Acute Influenza-Like Illness with Fever. but may persist for weeks  Iritis. Back and Abdomen  Mental Confusion may be Evident  Pulmonary Involvement (is not Uncommon) = Manifested in most cases by COUGH and Chest Pain and in a few cases by Hemoptysis  MOST COMMON Finding on Physical Examination = FEVER with Conjunctival Suffusion  Mild Jaundice may be Present 2. Severe Headache. Dogs. Leptospiremic Phase  Acute Influenza-Like Illness = Fever. Chills.

after 4-9 days. Hemorrhagic Manifestations (seen in Weil’s Syndrome)  Common Manifestations = Epistaxis. Other Manifestations described in SEVERE Leptospirosis:  Rhabdomyolysis. however. and HIGH MORTALITY o Mortality = usually due to HEMORRHAGE! o Frequently (but NOT exclusively) associated with Serovar Icterohaemorrhagiae / Copenhageni o Serovar Icterohaemorrhagiae / Copenhageni = Causes the INFECTION (from RATS) o The onset of Illness is NO Different from that of Less Severe Leptospirosis. Hemorrhagic Diathesis. which can be profound and give an Orange Cast to the Skin.B. Dyspnea. Renal Failure  Develop during 2nd week of illness (respond to treatment if there is NO Hemorrhage)  Hypovolemia and Decreased Renal Perfusion = contribute to the Development of Acute Tubular Necrosis with Oliguria or Anuria  Dialysis is sometimes required. is usually NOT Associated with Severe Hepatic Necrosis  (+) Hepatomegaly & Tenderness in the Right Upper Quadrant (usually detected)  (+) Splenomegaly (in 20% of cases) **Findings in Weil’s Syndrome: 1. Pericarditis  Congestive Heart Failure. Adrenal or Subarachnoid Hemorrhage 4. Renal Dysfunction. Myocarditis. although a Fair Number of cases can be managed without Dialysis (Renal Function may be completely regained) 2. Purpura. Severe Leptospirosis (WEIL’S SYNDROME = Most Severe Form) o Characterized by Jaundice. and Blood-Stained Sputum  Sometimes = Hemoptysis or even Respiratory Failure 3. Petechiae. Jaundice as well as Renal & Vascular Dysfunction generally develop o NOTE: It has NO Biphasic Disease Pattern like that seen in Anicteric Leptospirosis! **Physical Examination and Other Findings:  The Jaundice of Weil’s Syndrome. Ecchymoses  RARE Manifestations = Severe GI-Bleeding. Chest Pain. Hemolysis. Cardiogenic Shock  Adult Respiratory Distress Syndrome  Multi-Organ Failure 7 . Pulmonary Involvement  Occurs frequently  Presents with Cough.

nevertheless. Low Titer Single (+). Korthof Medium B. A. High Titer Paired Sera. Others o Direct Darkfield Microscopy (Blood or Urine) – Usually results in Misdiagnosis and should NOT be used o Serology = Antibody Detection: Microagglutination Test (MAT). Chills. Hyaline or Granular Casts)  Anicteric Leprospirosis = Mild Proteinuria  Severe Leptospirosis = Renal Failure and Azotemia IV. Complement Fixation. Low Titer Single (+). and Vasodilation with Mild Hypotension 8 . High Titer Paired Sera. Headache.III. Increased Respiratory Rate. ELISA. consisting of Fever. For Severe Cases: IV Administration of Penicillin G. Ampicillin. TREATMENT  The Effectiveness of Antimicrobial Therapy for the Mild Febrile form of Leptospirosis is CONTROVERSIAL. Erythrocytes. Rising Titer CERTAIN 2 10 25 5 15 25 Scoring System:  (+) = Isolation of Leptospires from Culture  Presumptive: o A or A + B = 26 o A + B + C = 25  Suggestive o A or A + B = 20 – 25 o A + B + C = 20 – 25 A. a Jarisch-Herxheimer Reaction similar to that seen in other Spirochetal Diseases may develop o It is a Dramatic. LABORATORY DIAGNOSIS OF LEPTOSPIROSIS Isolation of Leptospires in Culture (+) Serology: Endemic Single (+). though usually Mild Reaction. NOT Endemic Single (+). Amoxicillin. treatment started after the first 4 days of illness is effective. Ampicillin. Microcapsule Agglutination Test (MCAT) o DNA Technology (eg. Tachycardia. Fletcher Medium. Increased Circulating Neutrophil Count. Doxycycline. PCR) C. Rising Titer (+) Serology. Renal Changes o Kidneys are Invariably Involved in Leptospirosis o Related Findings Range from:  Urinary Sediment Changes (Leukocytes. Culture Isolation o GOLD Standard o Isolated from Blood / CSF = during the First 10 days o Isolated from Urine = several weeks (beginning around the 1 st week) o Ellinghausen-McCullough-Johnson-Harris (EMJH) Medium. or Erythromycin is recommended o Pen G 1.5 M q6 1 week Jarisch-Herxheimer Reaction o After the start of Antimicrobial Treatment for Leptospirosis. but such Treatment is INDICATED for MORE SEVERE FORMS  Treatment should be initiated as EARLY as possible. or Amoxicillin should be considered o Amoxicillin 500mg QID PO o Ampicillin 500-750mg IV q6 B. IFA. In Milder Cases: Oral Treatment with Tetracycline. Myalgias. contrary to previous reports.

Plasmodium malariae  Of the 4 Species of Human Malaria. Plasmodium falciparum causes nearly ALL DEATHS and NEUROLOGICAL COMPLICATION  Transmission of P. the growing Malarial Parasite progressively consumes and degrades Intracellular Proteins. LIFE CYCLE OF MALARIA  In Humans. falciparum = Transmitted by the BITE of an Infected Anopheline mosquito (Anopheles flavirostris in the Philippines) II. principally HEMOGLOBIN Potentially Toxic Heme  Biologically Inert HEMOZOIN or Malarial Pigment Parasite also alters RBC membrane  Irregular Shape  More Antigenic & Less Deformable Result: Shortened RBC survival  9 . Plasmodium ovale. it is the Erythrocytic Cycle thats responsible for disease! o Erythrocytic Cycle = Responsible for the Development of the Disease o Schizonts Rupture & Merozoites are Released = causes PAROXYSM of Malaria Erythrocyte Changes in Malaria    After INVADING an Erythrocyte.3) MALARIA    Protozoan Disease transmitted by the Bite of Infected Anopheles Mosquitoes It is a Parasitic Infection caused by a Protozoan – Plasmodium spp It is presented with CYCLIC FEVER and CHILLS with SPLENOMEGALY leading to serious illness I. Plasmodium vivax. although Parasite undergoes development in the Liver. EPIDEMIOLOGY OF MALARIA  MOST IMPORTANT Parasitic Disease in Humans  Four Species of Malaria: Plasmodium falciparum.

Acute Renal Failure Acute Pulmonary Edema and Adult Respiratory Distress Syndrome (ARDS) 10 . Periodicity of Attacks ONLY if the Patient is UNTREATED  Periodicity = every 3 days. CEREBRAL MALARIA (MOST Life-Threatening)  COMA is a characteristic and ominous feature of Falciparum Malaria  Death Rate = 20% among adults. falciparum may NEVER become Regular) 2. Fluid and Electrolyte Disturbance. Vomiting. there is NO Neck Stiffness or Photophobia resembling Meningitis A. Metabolic Acidosis with Respiratory Distress. vivax. ovale MALIGNANT VS BENIGN TERTIAN  Malignant Tertian Malaria = severe w/ complications (Plasmodium falciparum)  Benign Tertian Malaria = mild (Plasmodium ovale. Other Features: o o o o o o Nausea. 4 days. 15% in children  Diffuse Symmetric Encephalopathy (Focal Neurologic Signs are UNUSUAL 2. Every 48-Hours for Plasmodium falciparum 3. it is NOT Significant B. Chills and Rigors) occur at REGULAR Intervals are relatively Unusual and suggest Infection with P. High Index of Suspicion o Travel to and Overnight Stay in Malarious Area (palawan) o Blood Transfusion in the past 6 months o Intravenous Drug Use **NOTE: Significant Travel History  Significant Exposure = at most. Others:    Severe Normocytic Anemia Hypoglycemia. etc (it does NOT occur if patient is Treated)  Eg. vivax) Cyclic Fever occurring every 72 Hours Includes Plasmodium malariae Quartan Periodicity C. Classical Malaria Paroxysm:  Cold Stage (Chills)  Hot Stage (Fever Spikes)  Sweating Stage **IMPORTANT Notes:  The CLASSIC Malarial Paroxysms (Fever Spikes. CLINICAL MANIFESTATIONS  Initial Symptoms: NON-SPECIFIC and NOT Reliable (Incubation Period = 8-40 days)  Headache may be SEVERE.III. vivax & ovale  Fever is IRREGULAR at First (P. and Orthostatic Hypotension Classic Malarial Paroxysms Anemia Splenic Enlargement Slight Enlargement of the Liver Mild Jaundice 1. Periodicity of Malaria: Tertian Periodicity Cyclic Fever occurring every 48 Hours Includes Plasmodium falciparum. Severe FALCIPARUM MALARIA 1. 1 Month (Incubation Period = as long as 30-45 days)  Ex) If patient had a History of Travel to Palawan 2 years ago.

 Crea. Normocytic Anemia o  ESR. TREATMENT   We Treat Malaria with COMBINATION Drugs – this is because of Chloroquine-Resistance Severe Malaria = DOC is QUININE (for Severe Malaria: Cerebral Malaria. vivax to PREVENT RELAPSE E. DIAGNOSIS A. Shock. ELISA. Thick and Thin Smears o GOLD STANDARD – Actual Demonstration of the Parasite in the Blood Smear o Thick Smear = for Quantification of Parasitemia o Thin Smear = for Species Identification B.  Ca2+. falciparum which did NOT respond to Adequate CQ + SP Treatment o It is NOT recommended for PREGNANT Women and children < 8y/o C. Haemoglobinuria High Fever. IHA) C. Artemether-Lumefantrin (Co-ArtemTM) o SECOND Line Drug o Given ONLY to Microscopically CONFIRMED P.  Muscle & Liver Enzymes.  Phosphate. give Quinine + Clindamycin D. Others o Rapid Diagnostic Tests o Serology (IFAT. CRP o Prolonged PT/PTT. Septicemia. First Line of Treatment = Chloroquine + Sulfadoxine / Pyrimethamine (CQ + SP) o First Line in the Drug Treatment of PROBABLE Malaria and CONFIRMED P. Abnormal Bleeding Jaundice.   IV. Metabolic Acidosis o  Plasma Glucose.  Na. Other Findings (Medicine Notes) o Normochromic.  HCO3. Plasma Viscosity. falciparum cases to PREVENT Transmission o Given for 14 days to CONFIRMED P. etc) A. falciparum provided that the Disease is NOT Severe B.  Urate.  Albumin o  Lactate. Hyperparasitaemia (>100. Chloroquine o Drug to be used in the Treatment of CONFIRMED P.  Bilirubin (DB & IB) D. vivax Circulatory Collapse. Severe Thrombocytopenia.  BUN.000 Ring Stage/uL) 11 . Quinine + Tetracycline / Doxycycline o THIRD Line Drug o Should be given to those who did NOT Respond to Co-ArtemTM o DRUG of CHOICE in the Treatment of SEVERE MALARIA! **IMPORTANT Notes:  Tetracycline and Doxycycline are CONTRAINDICATED for Pregnant Women and children < 8y/o  Instead. For Cerebral Malaria o Mean Opening Pressure at Lumbar Puncture is ~180mmHg of CSF o Normal or has slightly  Total Protein and Cell Count V. Primaquine o Given in single dose to CONFIRMED P.

patients would come for consult due to Signs of Liver Failure (Ascites.4) SCHISTOSOMIASIS   Endemic in 24-Provinces in the Philippines HIGHEST Prevalence of Infection in children 5-15 years of age I. Hepatomegaly. etc) 12 . CLINICAL ASPECTS  Main Pathology and Manifestations = due to Granulomatous Reaction to Eggs deposited in the Liver and other organs  Most Serious Consequence in the Liver is OBSTRUCTION of Intrahepatic Portal Branches leading to: o Portal Hypertension with Splenomegaly o Collateral Circulation o Ascites **IMPORTANT Notes: o End of Infection = LIVER CIRRHOSIS o Usually. EPIDEMIOLOGY  Schistosoma japonicum = MAJOR Species involved in Schistosomiasis (in the Philippines)  Snail Vector = Oncomelania quadrasi (Skin Penetration)  Transmission = requires CONTACT between Humans and other Animal Hosts with the Breeding Sites for Snails (there should be SKIN PENETRATION of the Cercaria!) II.

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Diagnosis: o Suggested by Normal Anion Gap Metabolic Acidosis with Urine pH > 5. EIGHT CLINICAL SYNDROMES OF UTI  Acute Uncomplicated Cystitis in Women  Acute Uncomplicated Pyelonephritis  Asymptomatic Bacteriuria  UTI in Pregnancy  Recurrent UTI (recurred > 2x Annually)  Complicated UTI (patients with Anatomic. URINALYSIS  NOT Recommended for Young Females presenting with Typical Symptoms of LOWER Urinary Tract Infection  ≥ 5 WBC / hpf  Routine Screening is NOT recommended for Diabetics. Treatment o NaHCO3 100mEq + 400cc H2O II. resulting in Hyperchloremic Acidosis with Hyperkalemia  Hyponatremic Hypoaldosteronism = MOST COMMON Cause of Type IV RTA  Treatment: Fludrocortisone 0. Kidney or Prostate  Growth of > 105 Organisms/mL of Urine = signifies INFECTION III. Bladder. Cancer Patients (taking Chemotherapy) III. Prostatitis. Uretha. Structural or Functional Abnormality)  UTI in Men (almost ALWAYS Complicated)  Catheter-Associated UTI 2 . TYPE-II RTA (PROXIMAL)  Hyperchloremic Acidosis  Bicarbonate Reabsorption in the Promximal Tubule is defective leading to Bicarbonaturia  Distinguished from Type-I by the ability to Normally Acidify Urine during Spontaneous or Induced Ammonium Acidosis  Treatment: NaHCO3 5-15 mmol/kg/day III.2mg/kg/day 2) URINARY TRACT INFECTIONS  Acute Infections of the Urinary Tract can be subdivided into TWO Categories: o Lower Tract Infections = Urethritis and Cystitis o Upper Tract Infection = Acute Pyelonephritis.COMMON RENAL (NEPHROLOGY) DISEASES 1) RENAL TUBULAR ACIDOSIS   Disorder of Renal Acidification out of proportion to the Reduction in GFR Characterized by Hyperchloremic Metabolic Acidosis with Normal Anion Gap I.1-0. and Intrarenal & Perinephric Abscesses I. CLINICAL FEATURES OF URINARY TRACT INFECTIONS:  UTIs exist when Pathogenic Microorganisms are detected in Urine.5 o (-) Bicarbonaturia B. Indwelling Foley Catheters. TYPE-1 RTA (DISTAL)  Distal Nephron does NOT lower Urine pH normally due to excessive back diffusion of H + Ions from the Lumen to the Blood  Chronic Acidosis: o Decreased Tissue Reabsorption of Ca2+ o Renal Calciuria (Increasing Osteoclast Activity)  Alkaline Urine o Decreased Urine Citrate Excretion A. TYPE-IV RTA  Distal Tubule Secretion of K+ and H+ ions are Abnormal.

3) ACUTE RENAL FAILURE    Syndrome characterized by Rapid Decline in GFR (hours to days) Diagnosed when Biochemical Screening of Hospitalized Patients reveals a Recent INCREASE in Plasma Urea and Creatinine Concentrations Frequent Clinical Features: Retention of Nitrogenous Waste Products. which occurs in the setting of Renal Hypoperfusion Prolonged Hypoperfusion  leads to Acute Tubular Necrosis (Ischemic) Clinical Features: thirst. ARF from obstruction requires:  Obstruction to Urine Flow between external urethral meatus and bladder neck  Bilateral Ureteric Obstruction  Unilateral Unreteric Obstruction with one functioning kidney SOME EXAMPLES Hypovolemia (GI losses. dry mucous membranes Intrinsic Can be conceptually divided based on the Predominant Compartment:  1) Ischemic or Nephrotoxic Tubular Injury  2) Tubulointerstitial Diseases  3) Diseases of the Renal Microcirculation & Glomeruli  4) Diseases of Larger Renal Vessels Urinary Tract Obstruction accounts for < 5% of hospital acquired ARF Because one kidney has sufficient reserve to handle generated nitrogenous waste products. Hyperkalemia. Abnormal Urinalysis Anemia. Scarred Kidneys ARF is often considered to be reversible. decreased skin turgor. orthostatic dizziness. decreased intake. Hyperphosphatemia Reversibility with Time II. ACUTE VS CHRONIC RENAL FAILURE   Kidney Size Carbamylated Hemoglobin Broad Casts on Urinalysis History of Kidney Disease. resulting in provound renal vasoconstriction 3 . tachycardia. etc) Low Cardiac Output Systemic Vasodilation Selective Intrarenal Vasoconstriction Hepatorenal Syndrome Ischemic Acute Tubular Necrosis Nephrotoxic ARF Post-Renal Bladder Neck Obstruction (Most Common)  Prostatic Disease  Neurogenic Bladder  Therapy with Anticholinergics  Hepatorenal Syndrome (HRS) o Unique form of Prerenal ARF that frequently complicates Advanced Cirrhosis as well as Acute Liver Failure o Kidneys are structurally normal but fail due to splanchnic vasodilation and arteriovenous shunting. HPN. orthostatic hypotension. Oliguria (UO < 400mL/d contributing to extracellular fluid overload). although a return to baseline serum creatinine concentrations postinjury might not be sufficiently sensitive to detect clinically significant irreversible damage that may ultimately contribute to CKD. TYPES OF RENAL FAILURE  Pre-Renal ARF: Diseases that cause Renal Hypoperfusion  Intrinsic ARF: Diseases that directly involve the Renal Parenchyma  Post-Renal ARF: Diseases associated with urinary tract obstruction TYPE Pre-Renal DESCRIPTION Most Common Form. and electrolyte and acid-base abnormalities First step in evaluating a patient with renal failure is to determine if the disease is Acute or Chronic Findings Suggestive of Chronic Renal Failure: o Anemia o Neuropathy o Renal Osteodystrophy o Small. Kidney Size may be Normal or Increased in some CKD:  Diabetic Nephropathy  Amyloidosis  Polycystic Kidney Disease  HIV Associated Nephropathy ACUTE KIDNEY DISEASE Normal Normal Absent Absent Often Present Usually Complete CHRONIC KIDNEY DISEASE Small High Present Present Usually Present Sometimes Partial I. reduced jugular venous pressure. Metabolic Acidosis.

No WBC (ACELLULAR) (+) Hyaline Casts (Fine Granular Casts) = Tamm Horsfall Protein Usually due to Obstructions. Approach to Patients with Azotemia 4 . Stones. Radiocontrast Exposure: Creatinine rises rapidly (within 24-48 hours)  Contrast Nephropathy: Peaks in 3-5 days  ATN. Atheroembolic: Peaks later – 7-10 days B. Atheroembolization. etc NORMAL RBC (this means that the RBC does NOT come from the Glomerulus) Muddy Brown Granular Cast = PATHOGNOMONIC Microscopic Hematuria Mild Tubular Proteinuria (protein is < 1 gram/day) Dysmorphic RBC (the RBC has to pass thru the Glomerulus  Distortion of Shape) (+) RBC Casts > 1g Proteinuria (Glomerular Proteinuria) WBC Casts.III. Serial Serum Creatinine Measurements o Prerenal ARF: Fluctuating Creatinine Levels that parallel changes in Hemodynamic Status o Renal Ischemia. Granular Cast Eosinophiluria (+) Broad Cast Broad Casts reflect Total Fibrosis and Dilatation of Tubules Post Renal ARF Acute Tubular Necrosis (ATN) Glomerulnephritis (GN) Allergic Interstitial Nephritis Chronic Kidney Disease (CKD) IV. DIAGNOSTICS A. URINALYSIS  Anuria suggests complete urinary tract obstruction but may complicate severe cases of Prerenal or Intrinsic Renal ARF  Findings in Urinalysis (from Med-School Notes) Prerenal ARF Low Volume Concentrated Urine (High Specific Gravity) No RBC. Prostatic Enlargement.

V. Ultrafiltration Hyponatremia Hyperkalemia Restruction of Enteral Free Water Intake Avoidance of Hypotonic IV solutions. Calcium Acetate.2) Administration of other bases (eg.Radiologic Findings:  UTZ: Useful to exclude Post-Renal  CT. and the cause of Intrinsic ARF is unclear Complications: ARF impairs renal excretion of Na. Aluminum OH) Calcium Carbonate or Gluconate (if symptomatic) Discontinue Mg++ Containing Antacids Treatment usually not necessary if < 890umol/L or < 15mg/dL Metabolic Acidosis Hyperphosphatemia Hypocalcemia Hypermagnesemia Hyperuricemia 5 . Forced alkaline diuresis for rhabdomyolysis. K. THAM) Dialysis Restriction of dietary phosphate intake Phosphate-Binding Agents (Calcium Carbonate. Sevelamer Hydrochloride. complications include:  Intravascular Volume Overload  Hyponatremia  Hyperkalemia  Hyperphosphatemia  Hypocalcemia  Hypermagnesemia  Metabolic Acidosis Uremic Syndrome: Develops because patients are unable to excrete nitrogenous waster products QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. including dextrose-containing solutions Restriction of Dietary K+ Intake Eliminate K+ supplements and K+-Sparing diuretics Loop Diuretics to promote K+ Excretion Potassium Binding Ion-Exchange Resins (eg. allopurinol for tumor lysis sx) Prevention and Treatment of Complications Intravascular Volume Salt and H2O Restriction Overload Diuretics. MANAGEMENT MANAGEMENT ISSUE Reversal of Renal Insult Ischemic ATN Nephrotoxic ATN THERAPY Restore systemic hemodynamics and renal perfusion through volume resuscitation and use of vasopressors Eliminate Nephrotoxic agents Consider toxin-specific measures (eg. and H2O and perturbs divalent cation homeostasis and urinary acidification mechanisms As a result. Sodium Polystyrene Sulfonate or Kayexelate) Insulin (10 units regular) and Glucose (50mL of 50% Dextrose) to promote Intracellular Mobilization Inhaled B-Agonist Therapy to promote intracellular mobilization Calcium Gluconate or Calcium Chloride (1g) to stabilize the Myocardium Dialysis Sodium Bicarbonate (maintain Serum HCO3 > 15mmol/L or Arterial pH > 7. MRI: Alternative  Retrograte / Anterograde Pyelography  Plain Film of Abdomen Renal Biopsy:  Reserved for patients in whom prerenal and postrenal ARF have been excluded.

Tx of comorbid conditions.Allopurinol. End-Stage Renal Disease (ESRD) or Stage 5 CKD o Irreversible Loss of Renal Function rendering an Individual PERMANENTLY dependent upon RRT o Represents a Clinical State or Condition in which there has been an Irreversible Loss of Endogenous Renal Function. forced Alkaline Diuresis. Radiocontrast Adjust doses and frequency of administration for degree of renal impairment VI.8 mg/dL VIII.4 4) CHRONIC RENAL DISEASE  CKD Encompasses a spectrum of different pathophysiologic processes associated with abnormal kidney function. CREATININE CLEARANCE (mL/min): Cockroft and Gault Equation Interpretation:  If < 10: Intrinsic Renal Cause  If 10-20: Doubtful Cause  If > 20: Pre-Renal Cause CreaClearance = . multiply everything by 0. (140 – age) x weight in kg . Rasburicase Nutrition Dialysis Choice of Agents Drug Dosing Protein and Calorie intake to avoid net negative nitrogen balance To prevent complications of ARF Avoid other Nephrotoxins: ACE Inhibitors / ARBs.85 o If Crea is NOT in mg/dL. divide it by 88. and frequently leading to End-Stage Renal Disease (ESRD) B. (140 – age) x weight in kg . slowing progression. 72 x Serum Crea in mg/dL CreaClearance = . ABSOLUTE INDICATIONS FOR DIALYSIS:  Symptoms or Signs of the Uremic Syndrome  Management of Refractory Hypervolemia. Aminoglycosides. CVD risk reduction Estimating progression Evaluating and Treating complications Preparation for kidney replacement therapy Kidney Replacement (if uremia is present) II III IV V Kidney damage with mildly decreased GFR Moderately decreased GFR Severely decreased GFR Renal Failure 60 – 89 30 – 50 15 – 29 < 15 (for dialysis) 6 . 72 x (Serum Crea in umol/L / 88. NSAIDs. or Acidosis VII.73m2 90 ACTION Diagnosis and Treatment.4)  IMPORTANT Notes: o If Female. resulting in the Inexorable Attrition of Nephron Number and Function. and a progressive decline in GFR I. of a Degree Sufficient to render the patient permanently dependent upon Renal Replacement Therapy / RRT (Dialysis or Transplantation) in order to avoid Life-Threatening Uremia  Staging of Chronic Kidney Disease (CKD) STAGE I DESCRIPTION Kidney damage with normal / increased GFT GFR mL/min / 1. Chronic Renal Disease o Pathophysiologic Process resulting to IRREVERSIBLE Reduction in Renal Mass and Function occurring MORE than 3 MONTHS o Pathophysiologic Process with Multiple Etiologies. BUN / Crea Ratio (SI Units) BUN:Crea Ratio = BUN x 247 Crea Conversion Factor for Serum BUN: 1 mmol/L = 2. Hyperkalemia. DEFINITION OF TERMS A.

and this results in Anemia. and typically corresponds to CKD Stages 3-5. especially chronic glomerular diseases An Accurate 24-Hour Urine Collection is the Gold Standard for measurement of Albuminuria Microalbuminuria refers to the excretion of amounts of Albumin too small to detect by urinary dipstick  The uremic syndrome and the disease state associated with advanced renal impairment involve more than renal excretory failure. Multiorgan System derangements become CLINICALLY MANIFEST II. and Abnormal Metabolism of carbohydrates. NOTES from Harrisons: o o o o C. Cardiovascular Abnormalities (leading cause of Morbidity and Mortality) o Ischemic Heart Disease o Congestive Heart Failure o Hypertension and LVH o Pericarditis (Pericardial Pain with respiratory accentuation. ETIOLOGY & EPIDEMIOLOGY   Most Frequent cause of CKD = Diabetic Nephropathy Hypertensive Nephropathy Progressive Nephrosclerosis The normal annual mean decline in GFR with age from the peak GFR (~120mL/min per 1. A host of metabolic and endocrine functions normally undertaken by the kidneys are also impaired. Uremia o Syndrome Reflecting DYSFUNCTION of all Organ Systems as a result of Untreated or Undertreated ARF or CRF o It is the Clinical and Laboratory Syndrome. involving hyperfiltration and hypertrophy of the remaining viable nephrons A. fats. In summary. Azotemia o LABORATORY Finding of an Elevated BUN and Creatinine o May or May NOT have Symptoms o Retention of Nitrogenous Waste as Renal Insufficiency develops D. such as fluid and electrolyte homeostasis and hormone regulation 3) Progressive systemic inflammation and its vascular and nutritional consequences II. CLINICAL ABNORMALITIES IN UREMIA        Fluid and Electrolyte Endocrine-Metabolic Neuromuscular Cardiovascular and Pulmonary Dermatologic Gastrointestinal Hematologic and Immunologic Chronic Renal Failure applies to the process of continuing significant irreversible reduction in nephron number. Bone Disease and Disorders of Calcium & Phosphate (PO4 Metabolism) Those Associated with:  HIGH Bone Turnover  HIGH PTH Levels Those Associated with:  LOW Bone Turnover  NORMAL PTH Levels Osteitis Fibrosa (classic lesion of secondary hyperparathyroidism) Osteomalacia Adynamic Bone Disease C.73m2) attained during the third decade of life is ~1mL/min per year per 1.73m2 at 70y/o Measurement of Albuminuria is also helpful for monitoring nephron injury and the response to therapy in many forms of CKD.73m2. fruction rub) 7 . Pathophysiology of CKD involves 2 Broad Sets of Mechanisms of Damage:  1) Initiating mechanisms specific to underlying etiology  2) Set of progressive mechanisms. and proteins. Fluid and Electrolyte. Acid-Base Balance o Sodium and Water Homeostasis o Potassium Homeostasis o Metabolic Acidosis B. reaching a mean value of 70mL/min per 1. Malnutrition. reflecting Dysfunction of all Organ Systems as a result of Untreated or Undertreated Acute or Chronic Renal Failure o Refers to more Advanced Stages of Progressive Renal Insufficiency when the Complex. including products of protein metabolism 2) Those consequent to the loss of other renal functions. the pathophysiology of the Uremic Syndrome can be divided into manifestations in three spheres of dysfunction: 1) Those consequent to the accumulation of toxins normally undergoing renal excretion.

EVALUATION OF CKD A. Excoriations (Calcium Deposition and Secondary Hyperparathyroidism) o Uremic Frost (White Sediments on the Skin) III. Initial Approach o Symptoms and overt signs of kidney disease are often absent until renal failure supervenes o Particular aspects in the history include: HPN. pericardial friction rub o The finding of Asterixis or a Pericardial Friction Rub not attributable to other causes usually signifies the presence of the Uremic Syndrome B. Nuclear Medicine Studies. sensory polyneuropathy. Pancreatitis G. CT or MRI Studies o Voiding Cystogram (for Reflux Nephropathy) D. Reduced Testosterone Level H. Neuromuscular Abnormalities o Central. abnormal urinalysis. Dermatologic Abnormalities o Pallor o Ecchymosis and Hematoma (defective Hemostasis) o Pruritus. with an Irreversible component of Scarring o Doppler Sonography. Laboratory Studies o Underlying cause / aggravating disease process and degree of renal damage and its consequences o A 24 hour urine collection may be helpful. PUD. Normochromic Type (Cause = Insufficient EPO-Production) o Abnormal Hemostasis  Prolonged BT  Decreased Activity of Platelet Factor-III  Abnormal Platelet Aggregation and Adhesiveness  Impaired Prothrombin Consumption E. problems with pregnancy o PE should focus on BP and target organ damage from HPN. edema. Endocrine-Metabolic Abnormalities o Glucose Metabolism: Plasma-Insulin is ELEVATED o Low Estrogen Level (Amenorrhea. as protein Excretion > 300mg may be an indication for therapy with ACE Inhibitors or ARBS C.D. Diverticulosis. Renal Biopsy is NOT advised because:  1) It is technically difficult and has a greater likelihood of causing bleeding and other adverse consequences  2) There is usually so much scarring that the underlying disease may not be apparent  3) The window of opportunity to render disease-specific therapy has passed 8 . Peripheral and Autonomic Neuropathy starting at STAGE-III CRD o Mild Disturbance in Memory and Concentration and Sleep Disturbances o Indication to Start RRT F. Imaging Studies o Renal Ultrasound: the finding of Bilaterally SMALL Kidneys supports the diagnosis of CKD of long-standing duration. Renal Biopsy o In a patient with Bilaterally Small kidneys. precordial examination. Inability to carry Pregnancy to Term o In Males: Oligospermia. Germinal Cell Dysplasia. DM. Gastrointestinal and Nutritional Abnormalities o Uremic Fetor: Urineferous Odor of the Breath due to breakdown of UREA to NH 3 in Saliva associated with a Metallic Taste o Gastritis. fundoscopy. asterixis. Hematologic Abnormalities o Anemia = Normocytic.

Slowing Progression of Diabetic Renal Disease o Control of Blood Glucose (Preprandial Glucose = 90-130mg/dL and HgbA1c < 7%) o Control of Blood Pressure and Proteinuria C. and elevated PTH and bone Alkaline Phosphatase levels suggests chronicity  Normochromic. APPROACH TO PATIENTS WITH PROTEINURIA  > 3 g per day = NEPHROTIC SYNDROME (Non-Selective Proteinuria)  In Early DM Patients = (+) Microalbuminuria 9 . Minimal Hematuria. and Hypertension Most Common Cause in Adults = Membranous Glomerulonephritis Most Common in Chilren = Minimal Change Disease Diabetic Nephropathy o Single Most Common Cause of Chronic Renal Failure in the US o Majority of patients with Diabetic Nephropathy have Type 2 DM III. NEPHRITIC SYNDROME  Hematuria  RBC Casts  Proteinuria  Hypertension  Edema  Deteriorating Renal Function II. Hypercholesterolemia. NEPHROTIC SYNDROME  Proteinuria > 3. MANAGEMENT OF CKD A. etc 5) NEPHRITIC / NEPHROTIC SYNDROME I.60 to 0. Edema. Managing Other Complications of Chronic Kidney Disease (CKD) o Medication Dose Adjustment o Preparation for Renal Replacement Therapy VI. ESTABLISHING THE DIAGNOSIS & ETIOLOGY OF CKD  Most Important Initial Step in evaluation of Elevated Serum Creatinine = to distinguish newly diagnosed CKD from Acute or Subacute Renal Failure (because the latter two conditions may respond to therapy specific to the disease)  Evidence of Metabolic Bone disease with Hyperphosphatemia. COMPLICATIONS OF HEMODIALYSIS  Hypotension = Most Common Acute Complication of Hemodialysis  High Output Cardiac Failure  Muscle Cramps  Anaphylactoid Reactions. Other Contraindications to Renal Biopsy: o Uncontrolled Hypertension o Active Urinary Tract Infection o Bleeding Diathesis o Morbid Obesity **NOTE: Ultrasound-Guided Percutaneous Biopsy is favored IV. Hypocalcemia.75g/kg/day) o Reducing Intraglomerular Hyperension and Proteinuria B.5 g/m+/24h  Hypoalbuminemia  Hyperlipidemia  Hypercoaguability  Edema  Nephrotic Syndrome classically presents with Heavy Proteinuria. Hypoalbuminemia.5cm in all but the smallest adults) favors CKD V. Slowing the Progression of CKD o Protein Restriction (intake of 0. Normocytic Anemia suggests that the process has been ongoing for some time  The finding of bilaterally reduced kidney size (<8.

10 .

Heparin)  Resistance to Aldosterone: Pseudohypoaldosteronism. chewing tobacco. burns  GI Loss: vomiting. Primary Na+ Loss (20 H2O Gain)  Integumentary Loss: sweating. Decreased K+ Secretion A. Clay Ingestion II. tube drainage. heat exposure. Primary H2O Gain (20 Na+ Loss)  Primary Polydipsia  Decreased Solute Intake (eg. Enhanced Cl.FLUID & ELECTROLYTE / METABOLIC DERANGEMENTS CAUSES OF HYPONATREMIA vs HYPERNATREMIA HYPONATREMIA I. Adrenal enzyme deficiency (21-Hydroxylase.Distal Delivery of Non-Reabsorbed Anions: Vomiting. NSAIDs. severe burns. Non-Renal  GI Loss (Diarrhea)  Integumentary Loss (Sweat) B. Liddle’s Syndrome. postobstructive diuresis. salt-wasting nephropathy. Normal Plasma Osmolality  Hyperlipidemia  Hyperproteinemia  Post-TURP B. Renal   Increased Distal Flow: Diuretics. HYPERKALEMIA HYPOKALEMIA I. DKA.Reabsorption (Chloride Shunt)  Gordon’s Syndrome  Cyclosporine 11 .Other: Amphotericin-B. Renal Failure II. Decreased Distal Flow (ie. Drugs (ACE inhibitors. Hypomagnesemia HYPERKALEMIA I. Redistribution into Cells A. Glucosuria. Pentamidine) B. exercise. hypoaldosteronism. thereby increasing solute-free water loss II. mechanically ventilated patients Na+ concentration of sweat decreases with profuse perspiration. Trimethroprim. Proximal (Type 2) Renal Tubular Acidosis. Bartter’s Syndrome) . Anabolic State  Vitamin B12 or Folic Acid (RBC production)  Granulocyte-Macrophage Colony Stimulating Factor (WBC production)  Total Parenteral Nutrition D. Primary Na+ Gain (Exceeded by 20 Water Gain)  Heart Failure  Hepatic Cirrhosis  Nephrotic Syndrome HYPERNATREMIA I. Increased Plasma Osmolality  Hyperglycemia  Mannitol II. Hypovolemia). obstruction. 20 Hyperaldosteronism (Malignant HPN. Nonrenal Water Loss  Evaporation from the skin and respiratory tract (insensible losses)  GI Losses: diarrhea (most common)  Increased Insensible Loss due to fever. nausea. Cushing Syndrome. Decreased Intake A. Pseudohyponatremia A. Other  Pseudohypokalemia  Hypothermia  Hypokalemic Periodic Paralysis  Barium Toxicity II. Impaired Na+ Reabsorption  Primary Hypoaldosteronism: Adrenal insufficiency. Osmotic Diuresis. nonoliguric acute tubular necrosis B. diarrhea  Renal Loss: diuretics. osmotic diuresis. 3BHydroxysteroid Dehydrogenase. Penicillin Derivatives . Hypoosmolal Hyponatremia A. fistula. Hormonal  Insulin  B2-Adrenergic Agonists (Endogenous or Exogenous)  A-Adrenergic Antagonists C. Tubulo-Interstitial Disease. carbenoxolone). Drugs (K+ Sparing Diuretics. Corticosterone Methyl Oxidase)  Secondary Hypoaldosteronism: Hyporeninemia. Renal Artery Stenosis. Increased Loss A. drugs  Syndrome of Inappropriate AVP Secretion  Glucocortidoid Deficiency  Hypothyroidism  Chronic Renal Insufficiency C. Congenital Adrenal Hyperplasia. Salt Wasting Nephropathies Increased Secretion of K+ . Glue-Sniffing (Toluene Abuse). apparent Mineralocorticoid Excess (Licorice. Renin-Secreting Tumors. IV Mannitol)  Diabetes Insipidus III. Primary Na+ Gain CAUSES OF HYPOKALEMIA VS. Starvation B. Acid-Base: Metabolic Alkalosis B. Renal Water Loss (Most Common Cause of Hypernatremia)  Drug Induced Diuresis  Osmotic Diuresis (Hyperglycemia.Mineralocorticoid Excess: 10 Hyperaldosteronism. Nasogastric Suction. Decreased Effective Circularing Arterial Volume) III. Beer Protomania)  AVP release due to pain.

Osmotic Diuresis. Abdominal and Chest Pain. diarrhea. Creatine Phosphate. K+ and its attendant anions are predominantly limited to the ICF and are necessary for Normal Cell Function II. Confusion) 12 . Nephrotic Syndrome). Rhabdomyolysis)  Increased Venous Capacitance: Sepsis A. Salt-Wasting Nephropathies  Renal Water Loss: Diabetes Insipidus (Central or Nephrogenic) 2.1) SODIUM & WATER    Water is the Most Abundant Constituent of the body. ECF Volume Contracted:  Extrarenal Na+ Loss: GI (vomiting. SODIUM BALANCE  Sodium is actively pumped out of cells by the Na-K-ATPase Pump  Result = 85-95% of Na+ is EXTRACELLULAR 2) HYPOVOLEMIA  True Volume Depletion – refers to a state of combined Salt and Water Loss exceeding intake. and Phospholipids) Solutes that are restricted to the ECF or the ICF determine the Effective Osmolality (or Tonicity) of that compartment. EXTRACELLULAR FLUID  Extracellular Fluid = Intravascular (Plasma Water) + Extravascular (Interstitial) Spaces  Major ECF Particles = Na+ and Anions (Cl. Likewise. a Minimum Urine Output of 500 mL/d is required for neutral solute balance **NOTE: Arginine Vasopressin (AVP. Total Body Na+ Content is a reflection of ECF Volume. Secreted by Posterior Pituitary o Net Effect: Passive Water Reabsorption along an Osmotic Gradient o Major Stimulus for AVP Secretion: HYPERTONICITY III. ECF Volume NORMAL or Expanded:  Decreased Cardiac Output: Muyocardial. Since Na+ is largely restricted to the ECF. comprising approximately 50% in Women and 60% in Men Total Body Water = 55-75% Intracellular Fluid + 25-45% Extracellular Fluid Osmolality: Solute or Particle Concentration of a fluid I. and since the maximal urine osmolality is 1200 mosmol/kg. etc). Ischemic Bowel. sweat. burns). Clinical Features o Most Symptoms: non specific and secondary to electrolyte imbalances and tissue hypoperfusion o More Severe Volume Contraction: End Organ Ischemia (Oliguria. leading to ECF Volume Contraction (loss of Na+ may be Renal or Extrarenal) Causes of HYPOVOLEMIA 1.and HCO3)  Major ICF Particles = K+ and Organic Phosphate Esters (ATP. Valvular or Pericardial Disease  Redistribution: Hypoalbuminemia (Hepatic Cirrhosis. about 600 mosmols must be Excreted per day.or Hypernatremia  Normally. Hypoaldosteronism. Pathophysiology o ECF Volume Contraction is manifest by a decreased plasma volume and HYPOTENSION o Hypotension: due to Decreased Venous Return (Preload) and diminished Cardiac Output B. Hemorrhage  Renal Na+ and Water Loss: Diuretics. WATER BALANCE  Normal Plasma Osmolality is 275 – 290 mosmol/kg  Disorders of water homeostasis result in Hypo. Skin/Respiratory (insensible losses. ADH) o Synthesized in the Supraoptic and Paraventricular Nuclei of Hypothalamus. Capillary Leak (Acute Pancreatitis.

0 mmol/L  Occurs as a result of either K+ Release from Cells or Decreased Renal Loss  Most Serious Effect: Cardiac Toxicity  Potentially Fatal Hyperkalemia RARELY occurs unless the Plasma K + is > 7. HYPERNATREMIA: Plasma Na+ > 145 mmol/L  Hypernatremia is a state of HYPEROSMOLALITY  Majority of cases result from the LOSS of WATER  Clinical Features: As a consequence of Hypertonicity. ECG Changes: o Due to Delayed Ventricular Repolarization and do NOT correlate well with Plasma K + Concentration o Severe K+ Depletion: Increased Risk of Ventricular Arrhythmias o Hypokalemia also predispose to Digitalis Toxicity 1.5 mmol/L  May result from: Decreased Net Intake. Treatment o Calcium Gluconate: decreases membrane excitability o Insulin: causes K+ to shift into cells o IV NaHCO3: can also shift K+ into cells o B2-Adrenergic Agonists: promote cellular uptake of K o Loop and Thiazide Diuretics o Sodium Polystyrene Sulfonate (Cation-Exchange Resin) o Hemodialysis 13 . Seizures & Coma do NOT usually occur unless the Plasma Na + concentration falls < 120mmol/L or decreases rapidly II. Management o Correct K+ Deficit and Minimize ongoing losses II. HYPONATREMIA: Plasma Na+ < 135 mmol/L  Clinical Features: related to Osmotic Water Shift. ECG Changes o Earliest Finding: Increased T-Wave Amplitude (Peaked T-Waves) o More Severe Degrees of Hyperkalemia:    Prolonged PR Interval & QRS duration AV Conduction Delay Loss of P-Waves **NOTE: Progressive Widening of QRS Complex & merging with the T-Wave produces a Sine Wave Pattern  Terminal Event is usually Ventricular Fibrillation or Aystole B. HYPOKALEMIA: Plasma K+ Concentration < 3.3) HYPONATREMIA / HYPERNATREMIA I. Increased Net Loss  Clinical Features: Symptoms seldom occur unless the Plasma K+ Concentration is < 3 mmol/L A. specifically Brain Cell Swelling or Cerebral Edema (symptoms are primarily neurologic)  Stupor. HYPERKALEMIA: Plasma K+ Concentration > 5.5 mmol/L and is usually associated with: o o o Profound Weakness Absent P-Waves QRS Widening Ventricular Arrhythmias o A. leading to Increased ICF Volume. leading to a Contracted ICF Volume – a decrease in Brain Cell Volume is associated with an Increased Risk of Subarachnoid or Intracerebral Hemorrhage 4) HYPOKALEMIA / HYPERKALEMIA I. Severe K+ Depletion    B. water shifts OUT of cells. Early Changes:    Flattening or Inversion of T-Wave Prominent U Wave ST-Segment Depression Prolonged QU Interval Prolonged PR Interval Decreased Voltage Widening of QRS Complex  2. Shift into Cells.

these homeostatic mechanisms serve to restore Serum Ca2+ Levels to Normal. HYPERCALCEMIA A. Bisphosphanates  Inhibits activity of Osteoclasts. Collectively. Clinical Manifesations Mild Hypercalcemia (up to 11 – 11. hormone secretion. Hypercalcemia can present with ECG Changes: o o o C. anorexia. usually of the fingers. Nephrocalcinosis. Carpopedal Spasm. Bronchospasm. in turn. Laryngospasm. results in Increased Tubular Reabsorption of Ca2+ by the Kidney (2) and Resorption of Calcium from Bone (2) and also stimulates Renal 1. toes. Diuretics  Give Loop Diuretics  This will enhance excretion of Ca2+ -.25(OH)2D. personality changes. we Increase Calcium Excretion 2.5) HYPOCALCEMIA / HYPERCALCEMIA   Calcium Ion plays a critical role in normal cellular function and signaling. and circumoral regions. pancreatitis Decreased Renal Concentrating Ability – Polyuria and Polydipsia More Severe Hypercalcemia (>12-13 mg/dL) B. and Prolongation of QT-Interval II. or depression Peptic Ulcer Disease or Nephrolithiasis. 1.5 mg/dL Usually Asymptomatic and recognized only on routine Calcium Measurements Some may complain of vague Neuropsychiatric Symptoms Trouble concentrating. Stupor. Dialysis (In Severe Hypercalcemia. Complications of Hypercalcemia o o Arrhythmias Deposition of Calcium in Vessels. cardiac contractility. QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. I. PTH. make sure to hydrate the patient 4. in turn. Management (from Endorsements) 1. and is caused by Increased Neuromuscular Irritability  Chvostek’s Sign: Twitching of the Circumoral Muscles in response to gentle tapping of the facial nerve just anterior to the ear may be elicited  Trousseau’s Sign: Carpal Spasm may be induced by inflation of a BP cuff to 20mmHg above patient’s systolic BP for 3mins  Severe Hypocalcemia can induce Seizures. and blood coagulation Extracellular Ca2+ Concentrations are maintained w/in exquisitely narrow range thru a series of feedback mechanisms that involve: o o Parathyroid Hormone (PTH) Active Vitamin-D Metabolite 1.25(OH)2D Production (3). we improve perfusion to kidneys. refractory to the usual therapy) Bradycardia AV Block Short QT Interval C. thereby inhibiting RESORPTION 3. regulating diverse physiologic processes such as neuromuscular signaling. acts principally on the Intestine to Increase Calcium Absorption (4).when you give Diuretics. etc 14 . Increased Fracture Risk Lethargy.25(OH)2D) A decrease in ECF Ca2+ triggers an Increase in Parathyroid Hormone Secretion (1) via Activation of the Calcium Sensor Receptor on Parathyroid Cells.25-Dihydroxyvitmin-D (1. Coma GI Symptoms: nausea. or they may present with LifeThreatening Complications  Moderate to Severe Hypocalcemia: Paresthesias. HYPOCALCEMIA  May be asymptomatic if the decreases in Serum Ca2+ are relatively Mild and Chronic. constipation. IV-Hydration  Patients presenting with Hypercalcemia are volume-depleted already by ~2L  If we hydrate.

jittery. triamterene. WHIPPLE’S TRIAD  1) Symptoms consistent with Hypoglycemia  2) Low Plasma Glucose concentration measured with a precise method (Not a Glucose Monitor)  3) Relief of those symptoms after the Plasma Glucose Level is raised II. watch out for HYPERKALEMIA (especially in End Stage Renal Disease Patients) Potassium Homeostasis in CKD In CKD. tremors)  Late Phase: Patient is already Obtunded III. confusion. Glucose and Sugar-Containing Beverages)  IV Dextrose – Initial Bolus of 20-50mL 50% Dextrose should be given immediately. 15 . CLINICAL MANIFESTATIONS  Neuroglycopenic Symptoms of hypoglycemia are the direct result of CNS Glucose Deprivation  Symptoms: Behavioral changes. WE GIVE BLOCKING THERAPY  1) CaCO3 **NOTE: If Calcium x Phosphate x 12 is < 70 we can give CaCO3  If > 70. REMEMBER: 2-3-4-5  > 2x a night is Nocturia  > 3 L/day is Polyuria  < 400 mL is Oliguria  < 50 mL is Anuria Furosemide = Binds to ALBUMIN  Therefore. which is predominantly mediated by aldosterone-dependent secretory events in the distal nephron segments. ENDORSEMENT NOTES:  If there is Hypoglycemia. fatigue.0mmol/L) with symptoms that are relieved promptly after the glucose level is raised document Hypoglycemia I. tachycardia. catecholamines will ELEVATE (ex. seizure. ACE INHIBITORS AND CKD  For Diabetic Patients and those with Chronic Kidney Disease = choice of HPN is ACE Inhibitors or Angiotensin-II Antagonists to delay Diabetic Nephropathy  For End-Stage Renal Disease Patients: CAUTION on ACE-Inhibitors – use Calcium-Antagonists. eplerone. sweating. including alcohol The lower limit of the Fasting Plasma Glucose in NORMALLY 70mg/dL (3. we can give Bumetamide In Harrisons: Oliguria refers to a 24 hours urine output of < 500mL. Some medications can inhibit potassium entry into cells and renal K+ excretion. Diureticsm and Centrally Acting Agents  In giving ACE Inhibitors. palpitations.9mmol/L) Glucose Levels < 55mg/dL (3. do NOT give Furosemide in patients with Hypoalbuminemia  Instead. ARBs. and Anuria is the complete absence of urine formation (< 50mL) II. the decline in GFR is NOT necessarily accompanied by a parallel decline in urinary K + Excretion. TREATMENT OF HYPOGLYCEMIA  Readily absorbable Carbohydrates (eg. we DON’T given CaCO3. followed by Infusion of D5W (or D10W) to maintain Blood Glucose above 100mg/dL  Glucagon 1mg IM (or SC) NOTES ON RENAL ABNORMALITIES I. loss of consciousness. because we run the risk of Metastatic Calcification  2) NaHCO3  3) FeSO4 III. IN CKD. and if severe – death  Neurogenic (or Autonomic) Symptoms of Hypoglycemia are the result of the perception of physiologic changes caused by the CNS-Mediated Sympathoadrenal Discharge triggered by Hypoglycemia IV. The most important medications in this respect in clued ACE-Inhibitors. Spironolactone and other K+-sparing diuretics such as amiloride.6) HYPOGLYCEMIA    Most commonly caused by drugs used to treat DM or by exposure to other drugs.

Results from either:  1) Excretion of nonabsorbable solutes (eg. uremic fetor. SUGAR (IN URINALYSIS) Trace = 5mmol/L +1 = 15 +2 = 30 +3 = 60 +4 = 120 Polyuria > 3L/d. GI bleeding) Hematologic and Immunologic Disturbances (anemia. Glucose). 2 0 Hyperparathyroidism. pruritus.3 g/L  +2 = 1. vomiting. ALBUMIN (IN URINALYSIS)  Trace = 0. A 24 hour urine collection is needed for this evaluation.0 g/L  +4 = > 20 g/L 16 . etc) Dermatologic Disturbances (pallor. lymphocytopenia) VI. CRITERIA FOR INITIATING PATIENTS ON MAINTENANCE DIALYSIS  Presence of Uremic Symptoms  Presence of Hyperkalemia unresponsive to Conservative Measures  Persistent Extracellular Volume Expansion despite Diuretic Therapy  Acidosis Refractory to Medical Therapy  Bleeding Diathesis  Creatinine Clearance or Estimated GFR below 10 mL/min per 1. CHF. nausea. or  2) Excretion of water (usually from a defect in ADH production or renal responsiveness) V. Pulmonary Edema.2 g/L  +1 = 0. Osteomalacia) Neuromuscular Disturbances (fatigue. lethargy.73m2  Clinical Abnormalities in UREMIA (page 1763 for complete list) o o o o o o o Fluid and Electrolyte Disturbance Endocrine Metabolic Disturbances (Hyperuricemia.0 g/L  +3 = 3. hyperpigmentation. sleep disorders. uremic frost) Gastrointestinal Disturbances (anorexia.05 – 0. etc) Cardiovascular & Pulmonary Disturbances (Pericarditis. headache. ecchymoses.IV.

D.qwertyuiopasdfghjklzxcvbnmqwertyui opasdfghjklzxcvbnmqwertyuiopasdfgh jklzxcvbnmqwertyuiopasdfghjklzxcvb nmqwertyuiopasdfghjklzxcvbnmqwer NEUROLOGY tyuiopasdfghjklzxcvbnmqwertyuiopas dfghjklzxcvbnmqwertyuiopasdfghjklzx cvbnmqwertyuiopasdfghjklzxcvbnmq wertyuiopasdfghjklzxcvbnmqwertyuio pasdfghjklzxcvbnmqwertyuiopasdfghj klzxcvbnmqwertyuiopasdfghjklzxcvbn mqwertyuiopasdfghjklzxcvbnmqwerty uiopasdfghjklzxcvbnmqwertyuiopasdf ghjklzxcvbnmqwertyuiopasdfghjklzxc vbnmqwertyuiopasdfghjklzxcvbnmrty uiopasdfghjklzxcvbnmqwertyuiopasdf ghjklzxcvbnmqwertyuiopasdfghjklzxc vbnmqwertyuiopasdfghjklzxcvbnmqw ertyuiopasdfghjklzxcvbnmqwertyuiop Jaime Alfonso Manalo Aherrera. Internal Medicine Notes 2009 . M.

FT4. UPPER MOTOR NUERON LESION VS LOWER MOTOR NEURON LESIONS SIGN UPPER MOTOR NEURON LOWER MOTOR NEURON Atrophy None Severe Fasciculations None Common Tone Spastic Decreased Distribution of Weakness Pyramidal / Regional Distal / Segmental Tendon Reflexes Hyperactive Hypoactive / Absent Babinski’s Sign Present Absent MYOPATHIC Mild None Normal / Decreased Proximal Normal / Hypoactive Absent 2 . Common Etiologies of Delirium (page 160): o o o o o o o o o Toxins Metabolic Conditions Infections Endocrinologic Conditions Cerebrovascular Disorders Autoimmune Disorders Seizure-Related Disorders Neoplastic Disorders Hospitalization Terminal End of Life Delirium o B. Blood Culture  ECG. PE  CBC. SYNCOPE  Transient loss of consciousness & postural tone due to reduced Cerebral Blood Flow (associated with spontaneous recovery)  Causes of Syncope: o Disorders of Vascular Tone or Blood Volume o Cardiovascular Disorders (Obstructive Lesions. Mg2+. c-ANCA  Infectious Serologies: RPR. HIV  Lumbar Puncture  Brain MRI III. Initial Evaluation  History. and capacity to reason  Delirium: Acute confusional state A. Step-Wise Evaluation of a Patient with Delirium: 1. coherence. P)  Liver Function Tests including Albumin  Renal Function Tests 2. Cardiac Arrhythmias) o Cerebrovascular Disease II. Toxcology Screen  Brain Imaging  If suspecting a CNS Infection: Lumbar Puncture following Brain Imaging  If suspecting Seizure-Related Etiology: EEG 3. p-ANCA. First Tier Further Evaluation Guided by Initial Evaluation  Systemic Infection Screen: U/A and Culture. Electrolytes (including Ca2+.NEUROLOGIC SYMPTOMS 1) NERVOUS SYSTEM DYSFUNCTION I. Fungal & Viral. Folate. ABG. Thiamine  Endocrinologic: TSH. Complement Levels. CXR. CONFUSION AND DELIRIUM  Confusion: Mental and behavioral state of reduced comprehension. Second Tier Further Evaluation  Vitamin levels: B12. Cortisol  Serum Ammonia  Sedimentation Rate  ANA.

Seizures Lapse of consciousness is usually of longer duration & less abrupt in onset and cessation. (Petit Mal) Lasts for only a few seconds. the symptomatology is more complex and the seizure is termed Complex Partial Seizure B. The periods of relaxation progressively increase until the end of the Ictal Phase. tunneling of vision Posture at Onset Variable Usually erect Transition to Unconsciousness Often Immediate Gradual over seconds Duration of Unconsciousness Minutes Seconds Duration of Tonic or Clonic Movements 30 – 60 s Never more than 15 s Facial Appearance during event Cyanosis. but there is usually no post ictal confusion Sudden and brief muscle contraction that may involve one part of the body or the entire body. excessive salivation. secretions pool in oropharynx.2) SEIZURES I. bladder / bowel incontinence. which lasts no more than 1 minute. consciousness returns as suddenly as it was lost. lapses of consciousness without loss of postural control. Most common seizure type resulting from metabolic derangements. Post Ictal Phase: unresposinveness. diaphoresis. 3 . the clinical manifestations are considered relatively SIMPLE and the seizure is termed Simple Partial Seizures Complex Partial Seizures If Consciousness is IMPAIRED. Clonic Phase: After 10-20 sec. Respiration impaired. brief. Generalized Seizures o Arise from BOTH Cerebral Hemispheres simultaneously o Defined as bilateral clinical and electrographic events without any detectable focal onset Absence Seizures Sudden. muscular flaccidity. and the seizure is accompanied by more obvious motor signs that may include focal or lateralizing features) Generalized Tonic Clonic Seizures (Grand Mal) Primary generalized. Begins abruptly without warning. Initial Phase (Tonic Phase): Tonic contraction of muscles throughout the body. BP and papillary size. although some with vague premonitory symptoms in the hours leading up to the seizure. nausea. Patients gradually regain consciousness over minutes to hours (there is a period of postictal confusion) Atonic Seizures Myoclonic Seizures Sudden loss of postural muscle tone lasting 1 to 2 seconds. Frothing of Mouth Pallor Disorientation & Sleepiness after event Many minutes to hours < 5 minutes Aching of Muscles after event Often Sometimes Biting of Tongue Sometimes Rarely Incontinence Sometimes Sometimes Headache Sometimes Rarely II. Orthostatic Hypotension. CLASSIFICATION OF SEIZURES A. Marked enhancement of sympathetics leads to increased HR. tonic-clonic seizures are the main seizure type in ~10% of all persons with Epilepsy. Tonic phase evolves into the Clonic Phase. Cardiac Etiologies Premonitory Symptoms None or Aura (eg. cyanosis develops. Odd Odor) Tiredness. and there is NO postictal confusion Atypical Absence Have features that deviate both clinically and electrophysiologicaly from typical absence seizures (ex. Valsalva. Consciousness is briefly impaired. Produced by superimposition of periods of muscle relaxation on the tonic muscle contraction. SYNCOPE VS SEIZURES  The diagnostic dilemma encountered most often is the distinction between a Generalized Seizure and Syncope  Features that distinguish Generalized Tonic Clonic Seizure from Syncope include: FEATURES SEIZURE SYNCOPE Immediate Precipitating Factors Usually none Emotional stress. Partial Seizures o Seizures occur within Discrete Regions of the brain o Divided into: Simple Partial Seizures + Complex Partial Seizures Simple Partial Seizures If Consciousness is FULLY PRESERVED during the seizure.

Internal Medicine Notes 2009 . M.qwertyuiopasdfghjklzxcvbnmqwertyui opasdfghjklzxcvbnmqwertyuiopasdfgh jklzxcvbnmqwertyuiopasdfghjklzxcvb nmqwertyuiopasdfghjklzxcvbnmqwer PULMONOLOGY tyuiopasdfghjklzxcvbnmqwertyuiopas dfghjklzxcvbnmqwertyuiopasdfghjklzx cvbnmqwertyuiopasdfghjklzxcvbnmq wertyuiopasdfghjklzxcvbnmqwertyuio pasdfghjklzxcvbnmqwertyuiopasdfghj klzxcvbnmqwertyuiopasdfghjklzxcvbn mqwertyuiopasdfghjklzxcvbnmqwerty uiopasdfghjklzxcvbnmqwertyuiopasdf ghjklzxcvbnmqwertyuiopasdfghjklzxc vbnmqwertyuiopasdfghjklzxcvbnmrty uiopasdfghjklzxcvbnmqwertyuiopasdf ghjklzxcvbnmqwertyuiopasdfghjklzxc vbnmqwertyuiopasdfghjklzxcvbnmqw ertyuiopasdfghjklzxcvbnmqwertyuiop Jaime Alfonso Manalo Aherrera.D.

Zamboanga. give Primary Prophylaxis HR for 4 months or HE for 6 months If NOT a recent PPD converter.PULMONARY DISEASES 1) PULMONARY TUBERCULOSIS I. but currently exposed to a TB Case. CLASSIFICATION OF TB (ATS) CLASS DESCRIPTION ATS Class 0 No Exposure (-) PPD ATS Class 1 (+) Exposure (-) PPD TREATMENT BCG in high prevalence area If with recent exposure:  Give Primary Prophylaxis: HR for 4 months or HE for 6 months  Repeat PPD in 2 Months -if (+): Treat as Class 2 -if (-): Stop Primary Prophylaxis 70% of adult Filipinos are (+) for PPD. CXR with Minimal Infiltrates. Cavitary Lesions. Cavite. or High Community Resistance (eg NCR. TREATMENT REGIMEN FOR ATS CLASS 3 PATIENTS (TB ACTIVE) WHO TB PATIENTS ALTERNATIVE TB TREATMENT REGIMEN CATEGORY Initial Phase Continuation Phase I* New Smear-Positive PTB New Smear-Negative PTB w/ extended parenchymal involvement New cases of Severe Forms of Extra-Pulmonary TB II Sputum Smear-Positive: Relapse Treatment Failure Treatment after Interruption III ** New Smear-Negative PTB (other than in Category I) New Less Severe Forms of Extra-Pulmonary TB 2 HRZE 4 HR 2 HRZES and 1 HRZE 5 HRE 2 HRZE 4 HR * Give this regimen if with High Bacterial Load. II. give Streptomycin IM Alternate Days (60 Doses) instead of Ethambutol ** May give this cheaper regimen for Newly Diagnosed TB and those cases found in Low Community Resistance 2 . Davao. III Eg. AFB + 4 Smears. and are therefore naturally infected If with recent PPD Conversion. give primarily Prophylaxis as above If NOT a recent PPD converter and NO Family member has Active TB. Pampanga) If with Cavitary Disease. but NO Symptoms of Active Disease or Previously treated PTB Check previous CXR Reclassify patient into Class III or Class IV in 2-3 Months using Sputum Bacteriology or Serial X-Ray Changes II. may NOT give Primary Prophylaxis See Table Below ATS Class 2: TB Infection (+) Exposure (+) PPD (-) Target Organ TB Lesion ATS Class 3: PTB Active See Table Below ATS Class 4: Previous PTB Disease ATS Class 5: PTB Suspect ATC Class 3 patients are further subdivided into WHO Category I.

DOSAGE OF DRUGS DRUG H: Isoniazid (INH) R: Rifampicin (R) Z: Pyrazinamide (Z) E: Ethambutol (E) S: Streptomycin (S) CHILDREN 5 mg/kg/day 10-20 mg/kg/day 20-30 mg/kg/day 15-20 mg/kg/day 10-18 mg/kg/day ADULTS 300-400mg PO 450-600mg PO 1500mg/day PO 800-1000mg/day PO 1gram IM 3 . Indications of Active Disease o (+) AFB Sputum Smear (at least 2+) or (+) TB Culture o (+) Symptoms: Constitutional symptoms are more reliable than local symptoms o Increase in CXR Infiltrates (usually apical) B. NOTES FROM BLUE BOOK A. Extremely Drug Resistant Tuberculosis (XDRTB)  MDRTB Plus Resistance to Fluoroquinolones and an IV Aminoglycoside  NOTE: NO Effective Treatment regimen avilable IV. Multiple Drug Resistant Tuberculosis (MDRTB)  Infection with strain of M. Indications of Inactive Disease o Six Months interval with NO change in CXR infiltrates and NO constitutional symptoms o Preferable with History of Completed TB Therapy C. tuberculosis which shows in-vitro resistance to at least Isoniazid ad Rifampicin  Suspect in TB patients who are still Sputum Smear or Culture Positive despite 3 months of adequate Tx 2. Indications of Favorable Disease Response o Completion of prescribed treatment o Conversion of Sputum Smear and Culture to Negative o Resolution of Constitutional Symptoms o Resolution or Improvement of Local Symptoms D. Multiple Drug Resistant TB (MDRTB) and Extremely Drug Resistant Tuberculosis (XDRTB) 1.III.

or as soon as the TB symptomatic is identified o Second Specimen: very first sputum produced early in the morning immediately after waking up. It is collected by the patient according to instructions given by the DOTS facility staff o Third Specimen (Second Spot Specimen): collected when TB symptomatic comes back to the DOTS facility to submit the second specimen **NOTE: Pulmonary Nodule VS Mass: o Pulmonary Nodule is < 3 cm on CXR 4 .V. ALGORITHM FOR DIAGNOSIS OF PTB: CPM GUIDELINES (2008) TB SYMPTOMATIC (COUGH for 2 weeks of more) Three (3) Sputum Collection 2 or 3 Smear (+) Classify as SMEAR POSITIVE TB Only ONE (1) Smear Positive Collect another 3 Sputum Specimens Immediately At least ONE Smear Positive? Abnormal Findings on CXR Yes No Request for CXR Consistent with Active TB? Yes No Observation / Further Exam. If necessary Yes Classify as SMEAR NEGATIVE TB No Not Consistent with Active TB Consistent with Active TB Yes TB Diagnostic Committee No No Abnormal Findings on CXR All THREE (3) Smear Negative Refer to Physician (Symptomatic Tx for 2-3 wks) If Symptoms Persist. request for CXR  Collection of Sputum Specimens o First Specimen (Spot Specimen): collected at time of consultation.

Classification of TB Cases LOCATION OF SPUTUM SMEAR LESION EXAMINATION Pulmonary TB (PTB) Smear Positive DEFINITION OF TERMS 1. among others). Definition of Terms TB Symptomatic Any person with cough for two or more weeks with or without the following symptoms:  Chest and/or back pains not referable to any other musculo-skeletal disorders  Hemoptysis or recurrent blood streaked sputum  Significant weight loss  Other symptoms: Sweating. fatigue. or 2. A patient with at least 2 Sputum Specimens Positive for AFB. Formulation of Anti-TB Drugs o Fixed Dose Combination (FDCs) – two or more first line drugs are combined in one tablet o Single Drug Formulation (SDF) – each drug is prepared individually C. AND There is a Decision by a Medical Officer to Treat the Patient with Anti-TB Drugs Extrapulmonary TB 1. Joints & Bones. A Patient with one Sputum Specimen positive for AFB with Sodium Culture Positive for M. Genitourinary Tract. or A patient with Histological and / or Clinical Evidence consistent with Active TB and there is a Decision by a Medical Officer to Treat Patient with Anti-TB Drugs Smear Negative 2. Meninges. while on Treatment.VI. with or without Radiographic Abnormalities consistent with Active TB. AND There has been no Response to a Course of Antibiotics and/or Symptomatic Medications. A patient with at least one Mycobacterial Smear / Culture Positive from an Extra-Pulmonary Site (organs other than the Lungs = Pleura. Skin. who has been declared Cured or Treatment Completed. D. Lymph Nodes. and is Diagnosed with Bacteriologically Positive (Smear or Culture) Tuberculosis A patient who. ReRegister as “Other” for the next treatment  3) Chronic Case: a Patient who is Sputum Positive at the End of a Re-Treatment Regimen 5 . who was initially Registered as New Smear-Negative Case. turned out to be Smear Positive during Treatment. 2005 A. body malaise. Peritoneum and Pericardium. following Interruption of Treatment for Two Months or More A Patient who has been Transferred from another Facility with proper Referral Slip to continue Treatment All Cases who do NOT fit into any of the above definitions This Group includes:  1) Patient who is Starting Treatment again after Interrupting Treatment for more than 2 Months and has remained or became Smear-Negative  2) A Patient. or 3. shortness of breath A health worker‟s purposive effort to find TB cases who do not consult with personnel in a DOTS Facility Finding TB cases among TB symptomatics who present themselves in a DOTS facility Active Case Finding Passive Case Finding B. A patient with 1 Sputum Specimen Positive for AFB and with Radiographic Abnormalities consistent with Active TB as determined by a Clinician. NATIONAL TB CONTROL PROGRAM MANUAL OF PROCEDURES. (The Treatment Outcome of this case is “Treatment Failure”. Types of TB Cases o TB Cases shall be Categorized based on the History of Anti-TB Treatment o A thorough understanding on the Types of TB Cases is necessary in determining the correct Treatment Regimen TYPE New Relapse Failure Return after Default (RAD) Transfer-In Other DEFINITION OF TERMS A patient who has NEVER had Treatment for TB or who has taken Anti-TB Drugs for LESS than One Month A patient previously treated for Tuberculosis. is Sputum Smear Positive at 5 Months or Later during the Course of Tx A patient who returns to Treatment with Positive Bacteriology (Smear or Culture). Intestines. tuberculosis A Patient with at least 3 Sputum Specimens Negative for AFB with Radiographic Abnormalities consistent with Active TB.

Anemia. take HRZE for another month. SUMMARY OF TREATMENT MODIFICATION BASED ON T HE SPUTUM FOLLOW-UP RESULTS A. 10mg daily for prevention Arthralgia due to Hyperuricemia Pyrazinamide Give Aspirin or NSAID If symptoms persist. Ringing of Ear and Dizziness due to Damage of CN-VIII Oliguria or Albuminuria due to Renal Disorder Psychosis and Convulsion Thrombocytopenia. If Rifampicin. Shock Ethambutol Streptomycin Streptomycin Rifampicin Isoniazid Rifampicin Discontinue Ethambutol and refer to Ophthalmologist Discontinue Streptomycin and refer to MHO / CHO Discontinue Anti-TB Drugs and refer to MHO / CHO Discontinue Isoniazid and refer to MHO / CHO Discontinue Anti-TB Drugs and refer to MHO / CHO 6 . Pyrazinamide) symptoms subside. Category-I First 2 Months: HRZE If (-) 4 Months of HR o o If (+) Another 1 Month of HRZE If after 2 Months of HRZE you have Sputum Smear Negative. if you still have Sputum Smear Positive. go directly to 4 Months of HR BUT.VII. Discontinue Anti-TB Drugs and refer to MHO / CHO. Category-III First 2 Months: HRZ  4 Months of HR Sputum Smear is done at the end of 2nd Month WHAT TO DO? If (+) Another 1 Month of HRZE o VIII. consider Gout & give Allopurinol Flu-Like Symptoms (Fever. Muscle Pain) Rifampicin Give Anti-Pyretics Major Side Effects – Discontinue Taking the Medicines and refer to MHO / CHO immediately Severe Skin Rash (Hypersensitivity) Any Drug (especially Streptomycin) Discontinue Anti-TB Drugs and refer to MHO / CHO Jaundice due to Hepatitis Any Drug (especially Isoniazid. then go to HR for 4 Months. Category-II First 2 Months: HRZES 1 Month of HRZE If (-) 5 Months of HRE C. This makes the Intensive Phase 3 Months and a Total of 7 Months of Treatment B. resume treatment & monitor clinically Impairment of Visual Acuity and Color Vision due to Optic Neuritis Hearing Impairment. GUIDE IN MANAGING SCC DRUGS SIDE EFFECTS SIDE EFFECTS DRUGS RESPONSIBLE Minor Side Effects – Patient should be Encouraged to CONTINUE taking Medications Gastro-Intestinal Intolerance Rifampicin Give medication at bedtime Mild Skin Reactions Any kind of Drugs Give Anti-Histamines Orange / Red Colored Urine Rifampicin Reassure the patient Pain at Injection Site Streptomycin Apply Warm Compress Burning Sensation in Feet due to Isoniazid Give Pyridoxine (Vitamin B6) Peripheral Neuropathy 100-200mg daily for Treatment.

including nocturnal symptoms o 2) Minimal (Infrequent) Exacerbations o 3) Minimal need for PRN B2-Agonists. but does NOT meet the Criteria to be Classified as “Cured” of “Failure” Patient who DIES for any Reason during the Course of the Treatment Patient who is Sputum Smear POSITIVE at Five Months or LATER during the Treatment. T-Lymphocytes. OUTCOME OF TREATMENT Cured A Sputum Smear Positive Patient has COMPLETED Treatment and is Sputum Smear NEGATIVE in the Last Month of Treatment and on at least ONE Previous occasion Treatment Completed Died Treatment Failure Defaulter Transfer Out A Patient who has Completed the Treatment. Eosinophils. GINA CLASSIFICATION (Levels of Asthma Control) CONTROLLED Daytime Symptoms None (twice or less/week) Limitation of Activities None Nocturnal Symptoms (Awakening) None Need for Reliever None (twice or less/week) Lung Function Normal Exacerbation None PARTLY CONTROLLED > 2x / week Any Any More than twice/week < 80% Predicted > 1x / year UNCONTROLLED Three or more symptoms of Partly Controlled Asthma in any week One in any week 7 . and Neutrophils Monitoring Severity of Asthma: Peak Expiratory Flow Meter is practical and is recommended for use in both initial assessment and in monitoring severity of asthma I. Long-Acting B2 Agonist Plus Oral Steroids II. TREATMENT  Control of Triggers  Goals of Pharmacologic Treatment: Achieve CONTROL of Asthma o 1) Minimal (ideally none) chronic symptoms. ideally none o 4) No Limitations on activities.IX. A Sputum Smear Negative Patient initially who turned out to be Positive during Treatment Patient whose Treatment was Interrupted for Two Consecutive Months or More Patient who has been Transferred to another Facility with Proper Referral / Transfer Slip for continuation of Treatment 2) BRONCHIAL ASTHMA   Chronic inflammatory Disorder of the Airways. cells play a role: Mat Cells. including exercise o 5) Near Normal PEFR o 6) PEF Variability < 20% o 7) Minimal (or no) adverse effects from treatment III. CLASSIFICATION OF ASTHMA (ACCORDING TO SEVERITY)  Mild Intermittent  Mild Moderate Persistent  Severe Persistent PARAMETERS Mild Intermittent Daytime Symptoms Night Awakening Rescue B2-Agonist Use PEF or FEV1 Treatment needed to control Monthly Less than Monthly Less than Weekly > 80% of Predicted Occasional use of B2 Agonists CHRONIC ASTHMA SEVERITY Mild-Moderate Persistent Weekly Monthly to Weekly Weekly to Daily 60-80% of Predicted Regular use of Inhaled Corticosteroid and Long-Acting B2 Agonists Daily Severe Persistent Nightly Several Daily < 60% of Predicted Use of Combination of Inhaled Corticosteroids.

DRUGS USED TO TREAT ASTHMA A. dyspnea. Singulair) Zafirlukast (Accolate) Combined Corticosteroids and Long Acting Bronchidilators Leukotriene Receptor Antagonists B. Relievers o Reverse Airflow Obstruction and QUICKLY relieve its accompanying symptoms such as cough. Oral / Systemic  Salbutamol (Ventolin)  Procaterol (Meptin)  Terbutaline Sulfate (Bricanyl)  Terbutaline Sulfate. Guiafenesin (Bricanyl Expectorant Syrup) Short Acting Theophylline (Regular Formulations)  Neulin Tab  Brondil Tab Anti-Cholinergic Agents Combined Anti-Cholinergics and Short Acting B2 Agonists Ipratropuim Bromide (Atrovent) Ipratropium Bromide + Salbutamol (Combivent Metered Dose Inhaler) 8 . wheezing and chest tightness o Consists mainly of Short Acting Bronchodilators Short-Acting Bronchodilators Short Acting B2-Agonists 1.IV. Inhaled:  Salbutamol (Ventolin / Asmalin / Librentin Metered Dose Inhaler)  Procaterol (Meptin Air MDI)  Terbutaline Sulfate (Bricanyl Turbuhaler)  Terbutaline Sulfate (Bricanyl Metered Dose Inhaler) 2. Controllers: o Useful in achieving and keeping Persistent Asthma under control o They are also called Preventers o Include the following:  Anti-Inflammatory Agents (Corticosteroids)  Anti-Allergic Medications  Long Acting Bronchodilators Anti Inflammatory Agents (Corticosteroids) Inhaled:  Beclomethasone Dipropionate (Qvar Metered Dose Inhaler)  Budesonide (Budecort Turbuhaler / Primavent Metered Dose Inhaler) Oral / Systemic:  Prednisone (Orasone)  Methylprednisolone (Medrol) Long Acting Bronchodilators Long Acting B2 Agonist  Formoterol Fumarate (Inhaled)  Salbutamol (Oral / Systemic)  Bambuterol (Oral / Systemic) Long Acting Theophylline (Sustained Release Formulation)  Nuelin SR Formoterol and Budenoside (Symbicort Turbuhaler) Salmeterol and Fluticasone Montelukast Na (Kastair.

NOT to exceed 3-4x/day Add inhaled Ipratropium Bromide Step 3: Severe. If control is sustained for at least 3 months. B1.IV. A1. B1. Selective B2-Agonists SHORT ACTING Terbutaline Albuterol Levalbuterol Mataproterenol Pirbuterol B. Leukotriene Modifying Drugs o Zafirlukast o Montelukast o **NOTE: Epinephrine & Isoproterenol are not commonly used because of their effect on the Heart (B1 Receptors) LONG ACTING Salmeterol Bitolterol Formeterol Zileuton 9 . MANAGEMENT OF CHRONIC ASTHMA: HOME TREATMENT CLASSIFICATION CONTROLLER USED Step 1: Mild Intermittent NONE Step 2: Mild-Moderate Persistent Daily Medication: Inhaled Corticosteroids PLUS Long Acting B2 Agonists Daily Medication: Inhaled Corticosteroids PLUS Long Acting B2 Agonists (eg. CLASSIFICATION OF ANTI-ASTHMA DRUGS A. Seretide or Symbicort Inhaler) Oral Steroid > 7. compliance and environmental control  When to Step Down: Review treatment every 3-6 months. NOT to exceed 3-4x/day Consider Inhaled Ipratropium Bromide (Seretide or Symbicort Inhaler) Inhaled Short-Acting B2 Agonist. a gradual stepwise reduction in treatment may be started V. NOT > 3x/week Inhaled Short Acting B2 Agonist. B2 Agonists  Epinephrine  Ephedrine 2. A Rescue Course of prednisone may be needed at any time and any step  When to Step Up: If control is not achieved. B2 Agonists  Isoproterenol 3.5mg daily or alternate days RELIEVER USED Inhaled Short Acting B2 Agonist PRN Only. consider step up. Sympathetic Agonists: 1. Anticholinergics o Ipatropium Bromide o Atropine Methylnitrate D. But first review patient medication technique. Methylxanthines o Theophylline o Aminophylline o Anhydrous Theophylline o Theobromine o Caffeine C. Persistent Guide to Treatment Plan:  Patients should start treatment at the step most appropriate to the initial severity of the condition.

E. Beta Agonists o Stimulates the enzyme Adenylyl Cyclase to enhance cAMP o Increased cAMP causes BRONCHODILATION B. Glucocorticoids INHALED CORTICOSTEROIDS Beclomethasone Dipropionate Triamcinolone Acetonide Flunisolide Budesonide Fluticasone propionate F. BASIC MECHANISMS OF SOME DRUGS IN ASTHMA ATP Adenylyl Cyclase Bronchodilation (+) cAMP BRONCHIAL TONE Antimuscarinics Acetylcholine Adenosine Theophylline Bronchoconstriction A. Antimuscarinics (Muscarinic Antagonists) o Block the effects of Acetylcholine from causing Bronchoconstriction o Includes: Ipratropium and Atropine (+) (+) AMP Theophylline Phosphodiesterase Beta Agonists 10 . Cromolyn Sodium SYSTEMIC CORTICOSTEROIDS Prednisone Hydrocortisone Sodium Succinate VI. Theophylline o Inhibits Phosphodiesterase so that there is an accumulation of cAMP  BRONCHODILATION o Inhibits Adenosine from causing Bronchoconstriction o Disadvantage = lots of side effects C.

crackles) C. or o MDI plus Large Volume Spacer at 2-4 puffs q 20 minutes (cheaper and faster) B. Aminophyline o Only as Add-On Medication (if asthma still not controlled) o Acute Attack: Not controlled by N. Use of Accessory Muscles and Suprasternal Retractions PEF < 80% Personal Best or Predicted (if available)  INITIAL TREATMENT: Inhaled Short-Acting Beta-2 Agonist up to 3 Treatments in 1 Hour Alternative: Oral Short-Acting Beta-2 Agonist and/or Theophylline GOOD RESPONSE (Mild Exacerbation) No symptoms within 1 hr PEF > 80% predicted Sustained response for 4 hrs INCOMPLETE RESPONSE (Moderate Exacerbation) PEF 60-80% Predicted POOR RESPONSE (Severe Exacerbation) PEF < 60% Predicted Continue regular bronchodilator for 24-48 hrs Inhaled Short Acting B2-Agonist 2 puffs q3-4hr Alternative: Oral Short-Acting B2Agonist or Theophylline TID Add Oral Steroid (1mg/kg/day) Continue Beta-2 Agonist and/or Theophylline regularly Add Oral Steroid (1mg/kg/day) Repeat inhaled Beta-2 Agonist if available Consult Clinician Urgently for Instructions Contact clinician within 48hrs for follow up Immediate Transport to Hospital (ER) VIII. persistent purulence. then 100mg IV q4-6h x 4 doses or continuous if the condition warrants o More Stable: Start on Oral Steroids as soon as patients can safely swallow and taper off in 10-14 days D. Steroids o Acute Attack: Hydrocortisone (Solucortef) 250mg IV stat. Antibiotics o ONLY if with probable bacterial infection (fever. or o Ipratropium Bromide + Salbutamol (Combuvent) Nebulization 1 vial q6 hours.VII. Wheeze. Chest Tightness. MANAGEMENT OF ACUTE EXCACERBATIONS OF ASTHMA: HOME TREATMENT Assess SEVERITY: Clinical Features: Cough. MANAGEMENT OF ACUTE EXACERBATION OF ASTHMA: HOSPITAL CARE  Oxygen at 2-6 lpm via Nasal Canula  Avoid or Control Trigger Factors  Mneumonic: N-A-S-A A. or o Ipratropium Bromide (Atrovent) 1 Unit Dose vial TID-QID (less tachycardia). consider INTUBATION before Respiratory Fatigue sets in 11 . give Aminophylline Bolus at 5-6 mg/kg BW (if not maintained on Theophyllines) then Aminophylline Drip o More Stable: Shift to Long-Acting Theophylline If NOT controlled by N-A-S-A. A and S. Breathlessness. Nebulization o Salbutamol (Ventolin) Neb/Inhaler q3-6 hours (1 Nebule / 2-4 puffs).

CLINICAL SYNDROMES: Two Classic Types of COPD (from NMS)  Pink Puffers: Patients with EMPHYSEMATOUS. and use of accessory muscles On PE: Hyperresonant chest. indicating Air-Trapping Perfusion of Poorly Ventilated Areas of the Lungs (ie. they are Spared Severe Hypoxemia Chronic Bronchitis: Marked V/Q Mismatch. Areas with Low V/Q) results in an Increased Alveolar-Arterial Oxygen Tension (P(A-a)O2) Gradient and Hypoxemia A subpopulation of patients with Severe Airway Obstruction have chronically Increased Arterial PaCO 2. Functional Residual Capacity. Cyanosis) Severe Hypoxia. pursed-lip breathing. Pulmonary Function Testing o o Low. CLINICAL PRESENTATION      Chronic productive cough for many years. or marked reactive airway component) Tachypnea. Dyspneic. Chest Radiographs o o o B. but Metabolic Compensation (increased HCO3) maintains Arterial pH near normal During Acute Exacerbation of COPD  Worsening Airway Obstruction  Increased Dead Space Ventilation & Respiratory Fatigue  Rapid Rise in PaCO2  Acute Respiratory Acidosis o C. or Type-B COPD TYPE Pink Puffers PREDOMINANCE Emphysema AGE OF (+) SYMPTOMS Advanced Age (>60) SYMPTOMS Progressive exertional dyspnea Weight Loss Little / No Cough & Expectoration PULMONARY FUNCTION TESTING Mild Hypoxia. & Residual Volume may be Increased. disease is prominent in Upper Long Zones (except in A1-Antitrypsin Deficiency: basilar predominance) FEV1 and all other measurements of Expiratory airflow are Reduced FEV1 = Standard Way of objectively assessing the clinical course and response to therapy Total Lung Capacity. unlike asthma. Hypocapnia Decreased DLCO Mild Increase in Raw Little Improvement in Airflow after Treatment with Bronchodilators Blue Bloaters Chronic Bronchitis Young Age Chronic Cough & Expectoration Episodic Dyspnea Weight Gain Wheezing. does NOT fluctuate markedly  COPD includes Chronic Bronchitis and Emphysema I. Flattened Diaphragms Hyperlucent Lungfields with Bullae and diminished Vascular Markings (in Severe Emphysema) Often. Rhonchi Cor Pulmonale often develops (Edema. or Type-A COPD  Blue Bloaters: Patients with BRONCHITIC. Tussive. adventitious sounds Signs of Cor Pulmonale may be seen in severe or long-standing disease  II. obstructive sleep apnea. Hypercapnia Polycythemia Increased Raw Improved Airflow after treatment with Bronchodilators Relatively preserved Lung Volumes and DLCO   Emphysema: Proportional and Matched Losses of Ventilation and Perfusion  hence. decreased breath sounds. SOME DIAGNOSTICS: A. Arterial Blood Gases o o III. gastroesophageal reflux. followed by slowly progressive Breathlessness brought on with Decreasing amounts of Exertion Unusual in the absence of smoking Nocturnal Symptoms are UNUSUAL in COPD unless associated with comorbidities (cardiac disease.3) CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)  Syndrome of Chronic Dyspnea with Expiratory Airflow Limitation that. resulting in Severe Hypoxemia (which is worsened by Hypercapnia) 12 .

Non-Pharmacologic Therapies o Pulmonary Rehabilitation o Lung Volume Reduction Surgery (LVRS) o Lung Transplantation (COPD is the single leading indication for lung transplantation) QuickTime™ and a TIFF (LZW) decompressor are needed to see this picture. Sputum Little or NO Dyspnea Mild Symptoms NO Abnormal Signs > 80%  II: Moderate COPD   50 – 79%  Cough. add Long-Acting B2 Agonist or Oral Theophylline Consider Mycokinetic Agent Pulmonary Rehabilitation III: Severe COPD     Cough. Sputum Dyspnea on Mild Exertion Lung Hyperinflation Wheezing 30 – 49% As needed B2 Agonists For Continuous Symptoms:  Maintain on Tiotropium (Spiriva HandiHaler) Inhalation of 1 capsule daily For frequent exacerbations (>4x/yr):  Add inhaled Steroids of Long Acting B-Agonists  Eg. CLASSIFICATION AND TREATMENT OF COPD (from Blue Book) STAGE / SYMPTOMS & SIGNS 0: At Risk  Cough Sputum FEV1 as % PREDICTED NORMAL TREATMENT Smoking Cessation for everyone Reduce indoor pollution Reduce occupational exposure Flu vaccinations yearly As needed B2-Agonists  Eg. Terbutaline Sulfate (Bricanyl Turbuhaler) 250mcg/dose: 1 inh prn q2-6h Pulmonary Rehabilitation  I: Mild COPD    Cough. Formoterol & Budesonide (Symbicort Turbuhaler) 1-2 inhalations BID Pulmonary Rehabilitation IV: Very Severe COPD  < 30%  Dyspnea even at rest Chronic Respiratory Failure In addition to the above treatments:  Add long-term O2 Therapy at home  Consider surgical treatments like Lung Reduction Surgery and Bullectomy (removal of Bulla) V. Sputum Dyspnea on moderate exertion Continuous or intermittent Sx For intermittent Sx:  As needed B2 Agonists For Continuous Symptoms:  Maintain on Tiotropium (Spiriva HandiHaler) inhalation of 1 Cap daily If response is Unsatisfactory. THERAPY: A. Only 3 Interventions have been demonstrated to influence natural hx of COPD:    1) Smoking Cessation 2) Oxygen Therapy in Chronically Hypoxemic Patients 3) Lung Volume Reduction Surgery 13 . Nicotine Replacement Therapy o Bronchodilators (Symptomatic Benefit) o Anticholinergic Agens o Beta Agonists (Symptomatic Benefit) o Inhaled Glucocorticoids o Oral Glucocorticoids o Theophylline o Oxygen B. COPD VS ASTHMA (Med School Notes) Smoker or Ex-Smoker Symptoms under age 35 Chronic Productive Cough Breathlessness Night Time Awakening Significant Diurnal or Day to Day Variability COPD Nearly All Rare Common Persistent and Progressive Uncommon Uncommon ASTHMA Possible Often Uncommon Variable Common Common VI.IV. Pharmacotherapy o Smoking Cessation: Bupropion.

Maintenance of Adequate Gas Exchange: o Oxygen to achieve & maintain PaO2 55-60mmHg (88-90% Oxyhemoglobin Saturation) o Mechanical Ventilation in patients with Acute Ventilatory Failure B. Inhaled B2-Adrenergic Agonists o First Line Therapy for Rapid Symptomatic Improvement in patients with Acute Bronchoconstriction o Inhaled = most effective and safe o Ex) Metaproterenol. Lung Volume Reduction Surgery Lung Transplantation QuickTime™ and a TIFF (LZW) decompressor are needed to see this picture. but NO consistent Synergistic Bronchodilation is obtained with combination therapy o Combination of B2-Adrenergic Agonist and Anticholinergic Agent = provides Rapid Onset of the former PLUS the more prolonged Action of the latter D. SURGICAL CONSIDERATIONS    Non-Thoracic Surgery Lung Resection. QuickTim e™ and a TIFF (LZW) decom pres s or are needed to s ee this picture. 14 . Anticholinergic Agents (Ipratropium Bromide) o Have equivalent efficacy to B2-Adrenergic Agonists in treatment of Acute Exacerbations of COPD. Theophylline o Controversial F. Albuterol (q30-60 min. as tolerated) C. Terbutaline. Antimicrobial Therapy o Benefit of Antibiotic Therapy is seen in patients who have more severe underlying lung disease and in those who experience more severe exacerbations G. Glucocorticoids (Methylprednisolone 125mg IV q6h for 3 days) o Moderate improvement in clinical outcomes have been demonstrated o Use in hospitalized patients (role of glucocorticoids for Acute Exacerbations in outpatients is controversial) E.VII. Chest Physiotherapy o May improve clearance of secretions (>50mL/day) VIII. LONG TERM MANAGEMENT  1) Relief of Symptoms and Managing Acute Exacerbations  2) SLOWING Progression of Airflow Obstruction and Loss of Vital Capacity  Includes the Following: o o o o o o o o Smoking Cessation Optimal Bronchodilator Regimen (not established) Glucocorticoids Oxygen Therapy Pulmonary Hypertension and Cor Pulmonale Comprehensive Pulmonary Rehabilitation Program Influenza Vaccine and Pneumococcal Vaccine Psychoactive Drugs A1-Protease Inhibitor Augmentation Therapy o IX. MANAGEMENT OF ACUTE EXACERBATIONS A.

QuickTime™ and a TIFF (LZW) decompressor are needed to see this picture. QuickTime™ and a TIFF (LZW) decompressor are needed to see this picture. QuickTime™ and a TIFF (LZW) decompressor are needed to see this picture. NOTES FOR COPD (GOLD) QuickTime™ and a TIFF (LZW) decompressor are needed to see this picture. QuickTime™ and a TIFF (LZW) decompressor are needed to see this picture. 15 . QuickTime™ and a TIFF (LZW) decompressor are needed to see this picture. QuickTime™ and a TIFF (LZW) decompressor are needed to see this picture.X.

Goals of MV in Severe OAD o Restore Gas Exchange to stable baseline o Rest Ventilator Muscles / Reduce Work of Breathing until Primary Disease Process reverses or improves D. At Least TWO of: General Criteria for Acute Ventilatory Failure:  Moderate to Severe Dyspnea  Patient is Acutely Dyspneic. Contraindications to NIPPV in COPD  Frank Respiratory Arrest  Hemodynamic Instability  Inability to clear secretions or protect airways  Agitation or Uncooperativeness  Conditions that preclude placement of a Mask or achievement of a Proper Fit B. Mucus Plug)  Concomitant problems (Pneumonia. Pulmonary Embolism)  Complications (Pneumothorax. Non-Invasive Positive Pressure Ventilation (NIPPV) for ARF due to COPD o Patient receives air or air-O2 from a Flow Generator through a Full Facial or Nasal Mask o Enhance Ventilation by Unloading the Fatigued Ventilatory Muscles o Improve Gas Exchange by Increasing Alveolar Ventilation 1. Potential Deleterious Consequences of Severe OAD + MV: o Post-Hypercapnic Metabolic Alkalosis o Hypotension Secondary to Acute Hyperinflation o Alveolar Overdistention o Oxygen Toxicity  Acute Lung Injury o Cardiovascular o Ventilator Associated Pneumonia (VAP) C.XI. Right Mainstem Intubation 2. Monitoring Patients with Severe OAD on Mechanical Ventilation: 1. Peak Airway Pressure  PAP > 50cmH2O  associated with Barotrauma  If HIGH. Altered Mental Status  pH < 7. SaO2  Lowest possible FiO2 to maintain SaO2 > 92% or PaO2 > 60mmHg  Any further Increase in FiO2 will have little effect on SaO2 and Increases Risk of O2 Toxicity 5. suspect:  AF Obstruction (PEEPi. Auto-PEEP (PEEPi) / Dynamic Hyperinflation  Airflow obstruction prevents Complete Emptying of Alveolar Gas  End Expiratory PALV remains Positive  Consequences:  Decreased Venous Return  Promotes Barotrauma  Increased Work of Breathing 4. Secretions. Best Modes:  Arterial pH: significant Respiratory Acidemia  PSV  BiPAP  CPAP 3. pH. Bronchospasm. Atelectasis)  Patient-Ventilator Dyssynchrony  High Inspiratory Flow Rates  Small Size of ET  Kinks / Blocks along tubings. Plateau or Static Pressure  PPLAT > 30cmH2O  predicted of Barotrauma  Estimate of average End-Inspiratory Alveolar Pressure 3. PaO2. CHF. MECHANICAL VENTILATION FOR OBSTRUCTUVE AIRWAY DISEASES (ASTHMA & COPD) – Lecture A. PaCO2  COPD patients are Chronically Hypercapneic  Maneuvers that attempt to PaCO2 also Worsen Dynamic Hyperinflation & promote Barotrauma & Hypotension  Permissive Hypercapnea: Ignore PaCO2 as long as pH is acceptable 16 .35 or PaCO2 > 45  PaO2 < 50mmHg at Room Air  RR > 25  PaCO2 > 50mmHg 2.

FiO2  Achieve PaO2 > 60mmHg. and pulmonary mechanics F. Modes of MV of Patients with Severe OAD: 1. Assist Control Ventilation  Deliver breath with Preset Volume and Flow. Expiratory Time will Decrease and can become Shorter than T1 and can result in Inverse Ratio Ventilation Titrating the Level of Mandatory Breaths: consider NOT only the ABG but also the Patient‟s work of breathing and comfort NOT set IMV PSV 17 . Inspiratory Flow Rate (IFR)  Should be HIGH (60-100 L/min) – however High IFR can cause  Peak Airway Pressure  Barotrauma  If on A/C Mode at Low Flow Rates = the patient will NEED to Generate Inspiratory Effort against his own Pulmonary Impedance + that of the Ventilator. especially if Respiratory Drive is heightened or when Trigger Setting is NOT sufficiently sensitive  Risk for Hyperinflation 2. but NOT too sensitive that the MV Cycles inappropriately and results in Severe Respiratory Alkalosis  Consider the Effect of Auto-PEEP on Triggering: patients need to generate a negative pressure equal in magnitude to the Level of Intrinsic PEEP (Auto-PEEP) in addition to the Sensitivity Setting  Flow Triggering (instead of Airway Pressure Change Triggering). resulting in Increased Work of Breathing  High Inspiratory Flow Rate:  Helps satisfy the demands of Most Patients  Decreases the likelihood of DHI by Increasing Expiratory Time  allow more complete emptying of regions with Gas Trapping 4. NOT only for the Spontaneous Breaths but also for the Assisted breaths  largely due to Inability of the Respiratory Centers to adapt to Intermittent Unloading 3. Inspiratory Work and the Pressure-Time Product INCREASE progressively. Inspiratory Assistance continues until Inspiratory Flow Decreases  Tidal Volume is determined by Set Pressure Level. either when Trigerred by patient‟s Inspiratory Effort or to a Preset Backup Respiratory Rate  Excessive Patient Work occurs if Peak Flow Insufficient to meet Patient‟s Ventilatory Demands. Pressure Support Ventilation  Set a Level of Pressure (rather than Volume) to Augment each Spontaneous breath  Each breath is Patient-Triggered.E. Trigger Sensitivity  Set the Level of Sensitivity (usually –1 to –2) which will keep patient‟s Inspiratory Effort to a Minimum. Tidal Volume  Avoid Alveolar Overdistention  Set at 5-7 cc/kg  Provide enough pressure to ensure Inhaled Medication Delivery  NOT set in PSV 5. is available on Newer Ventilators. SpO2 > 92%  Lowest possible FiO2 to keep SpO2 > 92% 2. Synchronized Intermittent Mandatory Ventilation (SIMV)  Deliver Periodic Positive Pressure Breaths from the Ventilator at Preset Volume and Rate and also allow Spontaneous Breathing  As Ventilator Rate is Decreased. Ventilator Setting Strategies and Targets in Patients with Severe OAD: 1. Patient‟s Effort. can Decrease Inspiratory Effort by 30-40% during Triggering 3. Ventilator Rate A/C Mode Back up Rate of 4 Breaths per minute LESS than the Patient‟s Spontaneous Rate  to ensure that the MV will continue to supply adequate Volume in case of Sudden Decrease in Respiratory Center Output If with High Spontaneous RR.

Acute Hemodialysis and Ultrafiltration 4. Pharmacologic Morphine Sulfate Furosemide Nitroglycerin Inotropes Dilates pulmonary and systemic veins 2-5mg IV can be repeated 10-25min until effect is seen Potent Venodilators Initial Dose of 20-40mg IV. Methadone. Pathophysiology Increased Pulmonary Venous Pressure  Engorgement of Pulmonary Vasculature  CHF  Lungs become Less Compliant  Increased Resistance in Small Airways  Increased Lymphatic Flow and Intravascular Pressure  Interstitial Edema (net gain of fluid in the Extravascular Space)  Alveolar Edema (Outpouring of liquid that contracts both RBC and Macromolecules)  Progressive Acidemia. Treatment 1. Max dose of 200mg Venodilator Can potentiate the effect of Furosemide Dobutamine or Phosphatiesterase Inhibitors In patients with concomitant hypotension and shock 3. Precipitating Factors should be corrected II.4) PULMONARY EDEMA I. Hypercapnea  Respiratory Arrest o Manifested by Bilateral Wet Rales and Rhonchi o CXR: Diffuse Haziness of the lung fields with greater density in the Proximal Hilar Regions B. CARDIOGENIC PULMONARY EDEMA A. Right Heart Catheterization  Differentiates between Cardiogenic and Noncardiogenic causes of Pulmonary Edema 5. Morphine. Dextropropoxyphene  Protein Losing Enteropathy  Exposure to high altitudes – due to pulmonary venous constriction or pulmonary  Lymphatic Carcinomatosis arteriolar construction  Diffuse Pulmonary Infections  Neurogenic Pulmonary Edema – in patients with CNS disorders without preexisting LV  Aspiration dysfunction  Shock 18 . Supportive:  O2 Support – Raise the Arterial O2 Tension > 60mmHg 2. NON-CARDIOGENIC PULMONARY EDEMA  Severe Liver Disease  Nephritic Syndrome Other Forms of Pulmonary Edema:  Narcotic Overdose – parenteral Heroin.

Bronchial Asthma. Drug Therapy (eg. Interstitial Lung Disease. CAUSES OF CHRONIC COUGH:  Intrathoracic: COPD. Gastroesophageal Reflux. QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture.5) INVESTIGATING AN SPN  SPN: Solitary Pulmonary Nodule QuickTime™ and a TIFF (LZW) decompressor are needed to see this picture. Cystic Fibrosis  Extrathoracic: Postnasal Drip. Central Bronchial Carcinoma. Endobronchial TB. Left Heart Failure. Bronchiectasis. ACE Inhibitors) 19 .

increased tactile fremitus on Left  Crackles. Fibrinogen 2. Prothrombin Time (PT)  Tests the Extrinsic and Common Coagulation Pathways  Prolonged Time = deficiency / dysfunction in Factor V. DIAGNOSTICS A. OTHER SYMPTOMS (ROS): A. Congestive Heart Failure FC II. easy fatigability. Partial Thromboplastin Time (PTT)  Tests the Intrinsic and Common Coagulation Pathways  Prolongation = deficiency / dysfunction of factor V. Screen for other Organ Systems. as a site of Possible Metastasis o Breasts (Most Common CA for age group) o GI System (changes in stools. as a part of the Metabolic Syndrome C. anorexia. XII. undocumented fever. Blurring of Vision o Flame Shaped Hemorrhages = consistent with HYPERTENSION o Diplopia = “nagdadalawa ang paningin” B. Prothrombin. No Clubbing in Extremities o Elicit because “Pulmonary Mass” IV. no cough II. XI. CASE: 71/F With Chief Complaint of DOB  Hypertensive. wheezes on Right A. Polyuria o In patients presenting with Pulmonary Mass. Dyslipidemia. Fibrinogen 20 . history of PTB  Admitted due to Pleural Effusion prob 20 to Left Pleural Mass S/P Thoracentesis (no malignant cells)  Symptoms: Dyspnea. there is shifting of trachea to right o On Lateral: there is NO effusion in the POSTERIOR GUTTER (most dependent portion) B. Prothrombin. back pain. Colon Carcinoma (2nd most common CA):  Right Side = sometimes ASYMPTOMATIC  Left Side = decreased caliber of stools 2. abdominal pain) o Liver (history of jaundice) 1. PHYSICAL EXAMINATION  Decreased breath sounds. Shifting Dullness o Can also be done in the chest / lungs o To differentiate fluid from solid B. X. IX. weight loss. Gynecologic Carcinomas (3rd most common CA)  Ask for gynecologic complaints III. VIII. Notes on PT / PTT 1. Bronchoscopy C. Chest X-Ray (AP/L) o Findings: the mass is causing an Obstructive Atelectasis to the LEFT. X. VII. significance of Polyuria = Paraneoplastic Syndrome o Patient may also be diabetic.6) CASE ON PULMONARY DISEASE I.

CLASSIFICATION (2004): Management-Oriented Risk Stratification of CAP in Immunocompetent Adults CAP Any of the following: 1. pleural effusion. Suspected aspiration 6. Shock or signs of Hypoperfusion -Hypotension -Altered mental status -Urine output < 30mL/hr YES HIGH RISK CAP 2. GI.7) COMMUNITY ACQUIRED PNEUMONIA   Pneumonia is an infection of the Pulmonary Parenchuma Results from the Proliferation of microbial pathogens at the alveolar level & host‟s response to those pathogens I. abscess. Uncompensated COPD. Renal Failure on Dialysis. Unstable comorbid conditions* 7. Temp > 400C or < 350C 4. RR > 30 / min 2. Hematologic. PaO2 < 60mmHg or Acute hypercapnea (PaCO2 > 50mmHg) NO NO LOW RISK CAP MODERATE RISK CAP Outpatient LOW RISK CAP Stable Vital Signs  RR < 30/min  PR < 125bpm  SBP > 90mmHg  DBP > 60mmHg No or Stable Comorbid Conditions No evidence of Extrapulmonary Sepsis No evidence of Aspiration Chest X-Ray:  Localized infiltrates  No evidence of Pleural Effusion nor abscess  NOT progressive within 24 hours In Patient MODERATE RISK CAP Unstable Vital Signs:  RR > 30/min  PR > 125bpm  Temp > 400C or < 350C Unstable Comorbid Condition Uncontrolled DM. Extrapulmonary evidence of sepsis 5. progression of lesion to > 50% of initial within 24 hours YES Any of the following: 1. CXR: Multilobar. Progressing Neurologic Disease. Endocrine Suspected Aspiration Chest X-Ray:  Multilobar Infiltrates  Pleural Effusion or Abscess  Progression of findings to >50% in 24h 21 . CHF Class II-IV. Unstable CAD. PR > 125 / min 3. Active Malignancies. Decompensated Liver Disease Intensive Care HIGH RISK CAP Any of the clinical features of Moderate Risk CAP plus any of the following: 1) Shock or Signs of Hypoperfusion  Hypotension  Altered Mental State  Urine Output < 30mL/hr 2) Hypoxia (PaO2 < 60mmHg) or Acute Hypercapnea (PaCO2 > 50mmHg) Chest X-Ray: * As in Moderate Risk CAP Evidence of Extrapulmonary Sepsis Hepatic.

influenzae C. pneumoniae M. influenzae Amoxicillin C. pneumoniae OR M. MANAGEMENT OF CAP (from 2004 guidelines) – see updated 2010 guidelines when available POTENTIAL PATHOGENS EMPIRIC THERAPY Low Risk CAP S. pneumoniae M. pneumoniae Previously Healthy: H. Serology IV. Diagnostics o Gram Stain and Culture of Sputum o Blood Cultures o Antigen Tests. DIAGNOSIS A. catarrhalis Gram (-) Enteric Bacilli Legionella pneumophilia Anaerobes (with risk of aspiration) S. aureus P. pneumoniae M. catarrhalis Alternative: CoTrimoxazole Gram (-) Enteric Bacilli With Stable Comorbid Illness: Co-Amoxiclav or Sultamicillin OR 2nd Generation Cephalosporins OR Extended Macrolides Moderate Risk CAP S. IV Antipneumonococcal FQ With Risk for P. pneumoniae Extended Macrolides M. Pulmonary Embolism. aeruginosa IV Non-Pseudomonal B-Lactam With or Without B-Lactamase Inhibitor PLUS Macrolide OR Antipneumococcal Fluoroquinolones (FQ) No Risk for P. Heart Failure. CRITERIA IN HARRISON‟S 17TH EDITION: CURB-65 CRITERIA  C: Confusion Scoring System:  U: Urea >7mmol/L  0: Outpatient  R: Respiratory Rate >30/min  2: In-Patient  B: Blood Pressure (Systolic <90 or Diastolic <60)  >3: In-Patient ICU  65: Age >65years old 22 . influenzae C. Differential Diagnosis of Pneumonia o Infectious o Non-Infectious (Acute Bronchitis. catarrhalis Gram (-) Enteric Bacilli Legionella pneumophilia Anaerobes (with risk of aspiration) S. Radiation Pneumonitis) B. pneumoniae M. aeruginosa IV Pseudomonal B-Lactam with or without B-Lactamase Inhibitor PLUS IV Macrolide or IV Antipneumococcal FQ With or Without Aminoglycoside or IV Ciprofloxacin High Risk CAP **NOTE: Respiratory Quinolones (because they cover Pneumococcus) o Levofloxacin o Gatifloxacin o Moxifloxacin III. PCR. aeruginosa: a. pneumoniae H. IV Non-Pseudomonal B-Lactam with or without BLactamase Inhibitor + IV Macrolide b. Acute Exacerbations of Chronic Bronchitis. pneumoniae H.II.

or o Moxifloxacin (400mg IV q24h). or o Ertapenem (1g IV q24h) B. up to 1g IV q12h) 23 . pneumoniae H. catarrhalis S. EMPIRICAL ANTIBIOTIC TREATMENT OF HEALTH CARE ASSOCIATED PNEUMONIA (Harrisons) A. Imipenem (500mg IV q6h or 1g IV q8h). marcescens E.5g IV q6h). PLUS 3.8) HOSPITAL ACQUIRED PNEUMONIA I. pneumoniae S. aeruginosa Enterobacter spp Acinetobacter spp K. Patients without Risk Factors for MDR Pathogens: o Ceftriaxone (2g IV q24h). coli Other Enteric Gram (-) Bacteria S. or Meropenem (1g IV q8h). EARLY VS LATE ONSET HAP EARLY ONSET (≤ 5 days in Hospital) S. or  Piperacillin / Tazobactam (4. or o Ampicillin / Sulbactam (3g IV q6h). A Second Agent Active Against Gram-Negative Bacterial Pathogens:  Gentamicin or Tobramycin (7mg/kg IV q24h) or Amikacin (20mg/kg IV q24h). influenzae M. PLUS 2. A Beta-Lactam:  Ceftazidime (2g IV q8h) or Cefepime (2g IV q8-12h). aureus OTHERS Anaerobic Bacteria Legionella Candida spp Influenza A and B RSV **NOTE: Organisms we deal with in Asia are DIFFERENT from the US / Europe II. aureus Enteric Gram (-) Bacteria LATE-ONSET (> 5 days) P. An Agent Active Against Gram-Positive Bacterial Pathogens:  Linezolid (600mg IV q12h) or  Vancomycin (15mg/kg. or Levofloxacin (750mg IV q24h). or  Ciprofloxacin (400mg IV q8h) or Levofloxacin (750mg IV q24h). Patients with Risk Factors for MDR Pathogens 1. Ciprofloxacin (400mg IV q8h).

Differential Count. Dyspnea Dullness on Percussion Decreased or Absent Tactile Fremitus Decreased Breath Sounds Tracheal Deviation Pleural Rub B. Exudative  Local factors are altered  Ex) Bacterial Pneumonia. bronchiectasis o Empyema = Grossly purulent effusion o If free fluid separates the lung from the chest wall by > 10mm  THORACENTESIS! o Factors indicating need for procedure more invasive than Thoracentesis (increasing order of importance)      Loculated Pleural Fluid Pleural Fluid pH < 7. Malignancy. Total Protein. Transudative  Systemic factors that influence the formation and absorption of pleural fluid is altered  Ex) LV Failure. PLEURAL EFFUSION  Excess quantity of fluid in the pleural space  Decreased pleural fluid removal by the lymphatics  Excess pleural formation from the interstitial spaces of the lung. Pulmonary Embolus 2.2 Pleural Fluid Glucose < 3.00 and 0. Transudative Effusions meet NONE)  Pleural Fluid Protein / Serum Protein > 0. Pulmonary Embolus. Transudative and Exudative Pleural Effusion 1. Viral Infection. C&S  Bottle 3: Cytology and Cell Block (obtain 200cc of Fluid or more to increase yield) D. Transudative VS Exudative a.3mmol/L (<60mg/dL) Positive Gram Stain or Culture of Pleural Fluid Presence of Gross Pus in the pleural space C. the difference between the Albumin Levels in the Serum and the Pleural Fluid should be measured  If > 12g/L (1.15 units lower than Arterial pH o 24 . parietal pleura.6  Pleural Fluid LDH > 2/3 Normal upper limit for Serum LDH If one or more of the Exudative Criteria are met and the patient is clinically thought to have a condition producing a Transudative Effusion. LDH (5-10mL EDTA)  Bottle 2: AFB. Gram Stain. Cirrhosis b. or peritoneal cavity A. lung abscess.5 L every 24 hours Send Specimen:  Bottle 1: Cell Count.5  Pleural Fluid LDH / Serum LDH > 0. Parapneumonic Effusion o Associated with bacterial pneumonia.2g/dL) = TRANSUDATIVE! 3.9) PLEURAL EFFUSION AND PNEUMOTHORAX I. Thoracentesis o o o Usual Site: 8th ICS L PAL Maximum Drainage = 1. Indications for Chest Tube Insertion o o o 1) Gross Pus on Thoracentesis 2) Presence of Organisms on Gram Stain of the Pleural Fluid 3) Pleural Fluid Glucose < 50mg/dL 4) Pleural Fluid pH below 7. Light‟s Criteria (Exudative Effusions meet at least ONE. Symptoms / Signs of Pleural Effusion        Intercostal Pain (Inflammation of Parietal Pleura) Cough.

Rheumatoid Pleuritis. Transudative Pleural Effusion  Congestive Heart Failure  Cirrhosis  Pulmonary Embolization  Nephrotic Syndrome  Peritoneal Dialysis  Superior Vena Cava Obstruction  Myxedema  Urinothorax 2. etc)  Collagen Vascular Diseases (SLE. Pancreatic. Indications for Chemical Pleurodesis: Talc or Tetracycline Pleurodesis o o o 1) Recurrent Pleural Effusion 2) Malignant Pleural Effusions 3) Secondary Pneumothorax including Iatrogenic Pneumothoraces 4) Patients with Poor Surgical Risk Differential Diagnoses of Pleural Effusions: 1.E. Exudative Pleural Effusions  Neoplastic Diseases  Infectious Diseases (Bacterial. TB. etc)  Post-Coronary Artery Bypass Surgery  Asbestos Exposure  Sarcoidosis  Uremia  Meigs‟ Syndrome  Yellow Nail Syndrome  Drug-Induced Pleural Disease  Trapped Lung  Radiation Therapy  Post-Cardiac Injury Syndrome  Hemothorax  Iatrogenic Injury  Ovarian Hyperstimulation Syndrome  Pericardial Disease  Chylothorax o QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. Fungal. 25 . Viral)  Pulmonary Embolization  GI Diseases (Esophageal Perforation.

Secondary Pneumothorax o Most are due to Chronic Obstructive Pulmonary Disease. Traumatic Pneumothorax o Can result from both Penetrating and Non-Penetrating Chest Trauma o Should be treated with Tube Thoracostomy. which results in Decreased Venous Return to the heart and reduced Cardiac Output o Diagnosis is made by Physical Examination:  Enlarged Hemithorax with NO Breath Sounds  Hyperresonance to Percussion  Shift of Mediastinum to the Contralateral Side o Must be treated as a Medical Emergency o A large bore needle should be inserted into the Pleural Space through the 2 nd Anterior Intercostal Space – if large amounts of gas escape from the needle after insertion. the diagnosis is confirmed 26 . Small Cystic Spaces that lie within or immediately under the visceral pleura o Occur almost exclusively in Smokers. Primary Spontaneous Pneumothorax o Occurs in the absence of Underlying Lung Disease o Usually due to Rupture of Apical Pleural Blebs. unless they are very small o Iatrogenic Pneumothorax: due to Transthoracic Needle Aspiration. Thoracentesis. which suggests that these patients have subclinical lung disease o Initial Recommended Treatment: Simple Aspiration o Thoracoscopy and Thoracotomy with Pleural Abrasion is almost 100% successful in preventing recurrences B. Insertion of Central IV Catheters D. PNEUMOTHORAX   Presence of Gas in the Pleural Space Spontaneous Pneumothorax: Occurs WITHOUT antecedent Trauma to the Thorax A.II. but Pneumothoraces have been reported with every lung disease (pneumothorax with lung disease is more life-threatening) o Nearly all should be treated with Tube Thoracostomy o Most should also be treated with Thoracoscopy or Thoracotomy with Stapling of Blebs & Pleural Abrasion C. Tension Pneumothorax o Occurs during Mechanical Ventilation or Resuscative Efforts o The positive Pleural Pressure is life-threatening both because Ventilation is severely compromised and because the Positive Pressure is transmitted to the Mediastinum.

RBBB. Syncope C. CLINICAL PRESENTATION A. they embolize to the Pulmonary Arterial Circulation or. Physical Examination o Tachypnea. S-Waves at precordial leads  V/Q Scan: Interpreted as Normal. Pneumothorax 27 . Pericardial or Pleural Disease  Acute Coronary Syndrome / Myocardial Ischemia  Congestive Heart Failure  Axiety  Pneumonia.10) PULMONARY EMBOLISM   When Venous Thrombi dislodge. PATHOPHYSIOLOGY:  Anatomic Dead Space INCREASES because breather gas does NOT enter gas exchange units of the lung  Physiologic Dead Space INCREASES because ventilation to gas exchange units exceeds Venous Blood Flow through the pulmonary capillaries  Other Pathophysiological Abnormalities: o Increased Pulmonary Vascular Resistance (due to vascular obstruction) o Impaired Gas Exchange o Alveolar Hyperventilation o Increased Airway Resistance o Decreased Pulmonary Compliance II. Intermediate or High Probability of PE  Pulmonary Angiography: Gold Standard for Diagnosis 2. Costochondritis. Tachycardia o Increased P2 o Inspiratory Crackles / Rales NOTES from BLUE BOOK: 1. to the Arterial Circulation through a patent foramen ovale or ASD Most Common Gas Exchange Abnormalities: o Hypoxemia (Decreased Arterial PO2) o Increased Alveolar-Arterial O2 Tension Gradient (represents inefficiency of O2 Transfer across lungs) I. paradoxically. High Index of Suspicion o Presence of DVT o Hypercoaguable State o Pathologic Fractures o Long Bone Fractures o Post-Partum Period B. Load P 2  ABG may show Respiratory Alkalosis. Dyspnea o Pleuritic Chest Pain. Diagnosis of Pulmonary Embolism:  Clinical setting & high index of suspicion  On PE: Increase JVP but Clear Lungs. Symptoms: o Unexplained Breathlessness o Cough. Diagnosis of Deep Vein Thrombosis (as source of Emboli)  Duplex Ultrasound of the Lower Extremities (Non-Invasive)  Ascending Venography: Gold Standard Differentials:  Dissecting Aortic Aneurysm  Acute Bronchitis  Bronchogenic CA  Pericarditis. COPD  Pleurisy: “Viral Syndrome”. Musculoskeletal  Rib Fracture. Hypoxemia  ECG: Transient RAD. Low. Asthma.

Elevation of D-Dimer indicates endogenous although often clinically ineffective thrombolysis. Non-Imaging Diagnostic Modalities: 1. Plasma D-Dimer (ELISA) Normal Value: < 500ng/mL  Useful RULE-OUT Test. Expected ABG  Mild Respiratory Alkalosis  Hypoxemia The most common gas exchange abnormalities are Hypoxemia (Decreased Arterial PO2) and an Increased AlveolarArterial O2 Tension Gradient. ECG in Pulmonary Embolism  Most Cited Abnormality (in addition to Sinus Tachycardia) = S1-Q3-T3  S-Wave in Lead I  Q-Wave in Lead III This finding is relatively SPECIFIC. Arterial Blood Gases LACK diagnostic utility for Pulmonary Embolism. it is NORMAL in > 90% WITHOUT DVT QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. neither the room air Arterial PO2 nor calculation of the Alveolar-Arterial O2 Gradient can reliably differentiate or triage patients who actually have PE at angiography.III. even though both the PO 2 and PCO2 often decrease. Anatomic dead space increases because breathed gas does not enter gas exchange units of the lung. Among patients suspected of PE. Elevated Cardiac Biomarkers predict increase in major complications and mortality from PE 3. The sensitivity of D-Dimer is > 80% for DVT and > 95% for PE. Levels increase in patients with:  Myocardial Infarction  Pneumonia  Sepsis  Cancer  Postoperative State  Second o Third Trimester Pregnancy Troponin Levels increase in RV Microinfarction. but INSENSITIVE  Inverted T-Wave in Lead III  Most Frequent Abnormality: T-Wave Inversion in Leads V1 to V4 28 . which represents the inefficiency of O2 Transfer across the lung.  It is NORMAL in > 95% of patients WITHOUT Pulmonary Embolism (PE)  In patients with low clinical suspicion of DVT. The quantitative plasma D-Dimer Enzyme-linked Immunosorbent Assay (ELISA) rises in the presence of DVT or PE because of plasmin‟s breakdown of fibrin. 2. DIAGNOSTICS A. QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. D-Dimer is NOT Specific. Physiologic dead space increases because ventilation to gas exchange units exceeds venous blood flow through the pulmonary capillaries.

Invasive Diagnostic Modalities 1. Pulmonary Angiography: GOLD STANDARD  Can detect as small as 1-2mm Embolus  (+) Intraluminal Filling Defect in Pulmonary Circulation 2. Immediate Parenteral Anticoagulation  Unfractionated Heparin. Primary Therapy VS Secondary Prevention o Primary Therapy: consists of Clot Dissolution with Thrombolysis or removal of PE by Embolectomy o Secondary Prevention: Anticoagulation with Heparin & Warfarin or placement of an Inferior Vena Cava Filter B. 97% Specificity  Principal imaging Test for the Diagnosis of PE  CT Scanners can image small peripheral emboli  RV Enlargement on chest CT indicates a fivefold likelihood of death within the next 30 days compared with PE patients with Normal RV size on chest CT 4. Chest CT Scan: 60% Sensitivity. Echocardiography  NOT a reliable diagnostic imaging tool for acute PE because most patients w/ PE have normal echocardiograms  McConnell’s Sign: Hypokinesis of the RV Free Wall with Normal Motion of the RV Apex (which is the BestKnown Indirect Sign of PE) C. at least 1 day apart. or  Enoxaparin 1mg/kg BID with normal renal function 2. V/Q Lung Scan (Lung Scanning)  Segmental Perfusion defect with Normal Ventilation  Key Diagnostic Test – second-line diagnostic test for PE  High Probability of PE: defined as 2 or more segmental perfusion defects in presence of Normal Ventilation 5.B. target 2. Chest X-Ray (Multidetector-Row Spiral CT)  May be NORMAL or Near Normal  Some Signs:  Westermark’s Sign: Decreased Vascularity  Hampton’s Hump: Wedge-Shaped Density above Diaphragm in outer 2/3 lung field  Palla’s Sign: Enlarged Right Descending Pulmonary Artery  Knuckle’s Sign: Abrupt tapering / termination of Vessels 3. to achieve aPTT 2-3 times the upper limit of the laboratory normal. Non-Invasive Imaging Modalities 1. consider Intubation  Embolectomy  Thrombolytics A. Magnetic Resonance (MR) Contrast Enhanced  MR Venography is an excellent imaging modality to diagnose DVT 6.0  Continue parenteral anticoagulation for a minimum of 5 days and until 2 sequential INR values. TREATMENT  Give O2 at 2-4 lpm via NC. Contrast Phelbography  Venous Ultrasonography has virtually replaced contrast phlebography as the Diagnostic Test for suspected DVT IV. Bolus and continuous infusion. return in the target range 29 . Warfarin Anticoagulation  Usual Start Dose is 5-10mg  Titrate to INR. Venous Ultrasonography  UTZ of DVT: relies upon loss of vein compressibility  A Normal Venous UTZ does NOT exclude Pulmonary Embolus (PE) 2. Risk Stratification ANTICOAGULATION OF VTE: 1.0 – 3.

VII. Prothrombin is standardized with INR.5x) Low Molecular Weight Heparin (LMWH) Warfarin Ex) Initial Bolus of 80 units/kg. long term anticoagulation with Warfarin (Vitamin-K Antagonist) – Warfarin requires 5-7 days to achieve a therapeutic effect Unfractionated Hepatin (UFH) Anticoagulates by binding to and accelerating the activity of Antithrombin III. or Fondaparinus with Warfarin for at least 5 days can counteract the early procoagulant effect of unopposed warfarin Initiated at a dose of 5mg. Fibrinolysis o Successful fibrinolytic therapy rapidly reverses right heart failure o Thrombosis usually:  Dissolves much of the anatomically obstructing pulmonary artery thrombus  Prevents continued release of serotonin and other neurohormonal factors that exacerbate pulmonary hypertension  Dissolves much of the source of thrombus in the pelvic or deep leg veins. IX.0-3. LMWH.0) – continue for 3 months **NOTE: Protamine Sulfate = Administer if there is Life-Threatening or Intracranial Hemorrhage due to UFH / LMWH Duration of Hospital Stay: Acute PE Patients.000 „u‟ IV bolus. thus preventing additional thrombus formation and permitting endogenous fibrinolytic mechanisms to lyse clots Achieve a Target aPTT 2-3 times the upper limit (~aPTT 60-80s) 5000-10. followed by initial infusion rate of 18 units/kg per hour Exhibit less binding to plasma proteins and endothelial cells No monitoring or dose adjustment needed Enoxaparin 1mg/kg BID and Tinzaparin 175 unigs/kg OD Vitamin-K Antagonist prevents carboxylation activation of Factors II. then infusion of 1000-1500 „u‟/h (maintain PTT 1. PREVENTION OF VENOUS THROMBOEMBOLISM  Prophylaxis for Medically Ill Patients: Mini-UFH or LMWH o Mini-UFH: 5000 units SC twice or three times a day o LMWH: Enoxaparin 40mg OD 30 . Fondaparinux o Parenteral drugs are continued as a transition or bridge to stable.C. a Pentasaccharide.5 (2. Other Management: o Inferior Vena Caval (IVC) Filters Indications: 1) Active Bleeding that precludes anticoagulation 2) Recurrent Venous Thrombosis despite Intensive Anticoagulation o o o o o   Maintaining Adequate Circulation (for patients with Massive PE and Hypotension = 500-1. LMWH. LMWH. Target INR = 2.000mL normal saline) Pulmonary Embolectomy Pulmonary Thromboendarterectomy Emotional Support Prevention of Posphlebitic Synrdome (compression stockings) V. or Warfarin Administration VI.0) Warfarin 5-10mg PO 3 days before stopping heparin (maintain PT INR 2. X Full effect requires 5 days. PREVENTION (Medicine Notes)   Coumadine x 6 months IVC Filter (for patients with Absolute Contraindications to Anticoagulants) DVT Prophylaxis Compression Stockings and Pneumatic Compression Devices may complement mini-dose UFH. D. who traditionally have required 5-7 day hospital stays for IV heparin as a bridge to warfarin.5-2. Anticoagulation (Medicine Notes) o Foundation for successful treatment of DVT and PE o Immediately effective anticoagulation is initiated with a parenteral drug: UFH. even if the Prothrombin Time becomes elevated more rapidly Overlapping UFH.0 – 3. can be considered for abbreviated hospitalization if (+) excellent prognosis Duration of Anticoagulation: Patients with PE following surgery or trauma ordinarily have a low rate of recurrence after 3-6 months of anticoagulation. thereby decreasing the likelihood of recurrent PE **IMPORTANT Notes:  Preferred Fibrinolytic Regimen is 100mg of Recombinant Tissue Plasminogen Factor (tPA) on IV infusion over 2 hours E.

Inflammation  Fibrosis 31 . Epithelial Hyperplasia. CAUSES OF ARDS DIRECT LUNG INJURY Pneumonia Aspiration of Gastric Contents Pulmonary Contusion Near-Drowning Toxic Inhalation Injury INDIRECT LUNG INJURY Sepsis Severe Trauma  Multiple Bone Fractures  Flail Chest  Head Trauma  Burns Multiple Transfusions Drug Overdose Pancreatitis Post-Cardiopulmonary Bypass III. Consolidation  Cellular Necrosis. Clinical Syndrome of: o Severe Dyspnea of rapid onset o Hypoxemia o Diffuse Pulmonary Infiltrates B. ACUTE LUNG INJURY (ALI) VS ACUTE RESPIRATORY DISTRESS SYNDROME OXYGENATION ALI ARDS PaO2 / FiO2 < 300mmHg PaO2 / FiO2 < 200mmHg ONSET Acute Acute CHEST XRAY Bilateral alveolar or interstitial infiltrates ABSENCE OF LEFT ATRIAL PRESURE PCWP < 18mmHg or No clinical evidence of Increased Left Atrial Pressure IV.11) ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) I. DEFINITION A. THREE PHASES OF ARDS  Exudative (Day 0-7)  Proliferative (Day 7-21)  Fibrotic Three Compartments in ARDS Lung: 1) Normally Aerated / Hyperaerated 2) Poorly Aerated (Ground Glass) 3) Non-Aerated  (+) Shunting Pathology: Severe Injury to the Alveolocapillary Unit: Alveolocapillary Leak  Permeability Pulmonary Edema (Protein Rich Edema Fluid) Surfactant Disruption Hyaline Membrane Formation Alveolar Collapse. Definition: o Acute Onset o Bilateral infiltrates on CXR o PCWP < 18mmHf or Absence of LAH II.

Avoid Alveolar Overdistention  Low Tidal Volume (6-8mL/kg)  Control Plateau Pressure to be below UIP 2.V. Use Sufficient PEEP  To prevent significant Shearing or Cyclic Atelectasis to be above LIP 3. Partial Liquid Ventilation o Spontaneous Breathing Trial 32 . Other Ventilatory Strategies: o Prone Positioning o Recruitment Maneuvers o Pressure VS Volume Limited Mode o High Frequency Ventilation o Inverse Ratio Ventilation o ECMO.3 aside from Increasing the Respiratory Rate  Contraindications to Permissive Hypercapnea:  Increased ICP  Active Myocardial Ischemia  Hypotension and/or Severe LV Failure with Catecholamine Dependence  Pulmonary Hypertension with Acute RV Failure  Severe Metabolic Acidosis B. Goals in ARDS: Protective Mechanical Ventilation:  To accomplish Effective Gas Exchange  To minimize further Lung Damage & facilitate Healing Aim to PROTECT the Lung:  Decrease Tidal Volume  Give PEEP A. MANAGEMENT OF ARDS Some Notes:  Mortality: mostly due to Sepsis or Multiple Organ Failure  Primary Pulmonary cause / AHRF Causes < 20% of ARDS Mortality  Impaired Lung Compliance = Hallmark of ARDS QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. Lung Protective Ventilation (LPV) 1. Permissive Hypercapnea  This is a consequence of Low Tidal Volume (but we allow this)  Beneficial effect of Permissive Hypercapnea is still controversial  Safety of a very High PaCO2 is NOT proven  Usually well-tolerated – the ARDSNet used NaHCO3 when pH<7.

12) RESPIRATORY FAILURE    A Condition in which the Respiratory System FAILS in one or both of its Gas Exchanging Functions Ie. and PCO2 is HIGH!) b. ACUTE VS CHRONIC RESPIRATORY FAILURE A. etc III. Acute Respiratory Failure o SUDDEN o Leads to Life-Threatening Respiratory Insufficiency B. Oxygenation of. Chronic Respiratory Failure o Gradual WORSENING of Respiratory Function leads to Progressive Impairment of Gas Exchange o Metabolic Effects are PARTIALLY Compensated by Adaptations of other Systems II.3)  There is Acute Respiratory Acidosis (Ph is LOW. CLASSIFICATION BASED ON ONSET AND CATEGORY A.60 a. Chronic  Develops over Several Days or Longer  Ex) Milder Pneumonia The Central & Peripheral Nervous Systems. there may be Compensation in Chronic Respiratory Failure (Ph may even normalize) 2. GENERAL CRITERIA FOR ACUTE RESPIRATORY FAILURE     Patient is Acutely Dyspneic PaO2 < 60mmHg (Breathing Room Air) PaCO2 > 45mmHg Arterial Ph shows Significant Respiratory Acidemia (Acute) **NOTE: Many Patients with ARF do NOT Fulfill all FOUR Components of this Definition o MUST SHOW AT LEAST TWO OF THE FOUR CRITERIA o ABG is very Important in the Diagnosis 33 . we see Respiratory Alkalosis in people who Hyperventilate HYPOXEMIA constitutes the Primary Disturbances in ALVEOLAR Disturbances. Acute VS Chronic: 1. Acute  Develops in Minutes to Hours  Ex) Severe Pneumonia **NOTE: FiO2 = Fraction of Inspired Oxygen (Oxygen delivered to the Patient) b. Chronic  Develops over Several Days or Longer  However. Hypercapneic Respiratory Failure = PaCO2 > 45mmHg (due to HYPOVENTILATION) a. Respiratory Muscles & Chest Wall and Airways constitute the “RESPIRATORY PUMP: HYPERCAPNEA = Hallmark of Respiratory Pump Failure  Hypoventilation  Decreased VA  Accumulation of CO2 & Respiratory Acidosis  Just in comparison. and CO2 Elimination from Mixed Venous (Pulmonary Arterial) Blood Findings in Respiratory Failure: o HYPOXEMIA = PO2 < 60mmHg at Sea Level (inadequate blood oxygenation) o HYPERCARBIA = PCO2 > 45 mmHg (excess of circulating CO2) I. Hypoxemia Respiratory Failure = PaO2 < 60mmHg when FiO2 > 0. producing Respiratory Failure  Pulmonary Edema  Pneumonia. Acute  Develops in Minutes to Hours with ACIDEMIA (Ph < 7.

multiple BT. Lung Hemorrhage  Ex) In a Vehicular Accident. Clinical Description a. the absence of Left Atrial HPN. there may be Pulmonary Contusion & Decreased Perfusion  This leads to Hypoxemia and V/Q Mismatch 4. Reduced Strength  Impaired Neuromuscular Transmission (Myasthenia Gravis. GB Syndrome. Emphysema 2. Alveolar Hemorrhage) 1. pneumonia. gastric aspiration. TYPES OF RESPIRATORY FAILURE A. therefore.IV. Phrenic Nerve Injury)  Respiratory Muscle Weakness (Myopathy. Pulmonary Edema  Cardiogenic (Increased Hydrostatic Pressure)  Non-Cardiogenic (ARDS Secondary to an Acute Lung Injury) 2. Pneumonia. Increased Overall Load in the Respiratory System: Increase in Resistive Loads Loads due to Reduced Lung Compliance Bronchospasm Alveolar Edema Atelectasis Intrinsic Positive and Expiratory Pressure Pneumothorax Pleural Effusion Abdominal Distention Pulmonary Embolus with Increased Dead Space Fraction. TYPE 2: Acute Hypoventilatory Respiratory Failure o Due to alveolar hypoventilation and results in the inability to eliminate CO 2 effectively o PCO2 > 45mmHg o Hypoventilation leads to a Problem in CO2 Elimination (Hypercarbia and Respiratory Acidosis) 1. there is Accumulation of Secretions in the Alveoli  This leads to V/Q Abnormalities (Ventilation-Perfusion Mismatch)  Decrease in Ventilation. pancreatitis B. near drowning. Diminished CNS Drive:  Drug Overdose. and profound shunt physiology  Occurs in sepsis. ARDS  Defined by Diffuse Bilateral Airspace Edema seen by CXR. Amyotrophic Lateral Sclerosis. Brain Stem Injury  Sleep disordered breathing  Hypothyroidism b. Pneumonia  In Pneumonia. there will be “Hypoxemia” 3. Electrolyte Derangements. Mechanism = Decreased Alveolar Ventilation (VA) – there is Hypoventilation (RR < 10/min)  Decrease in CNS Drive = Central Lesion  Decrease Neuromuscular Coupling: Ex) Respiratory Muscle Fatigue  Increased Load in Respiratory System: Ex) Bronchospasm in Asthma. TYPE 1: Acute Hypoxemic Respiratory Failure o Occurs when alveolar flooding and subsequent intrapulmonary shunt physiology occurs o Hypoxemia = PO2 < 60mmHg o Mechanism = Problem is in the Lungs itself o Etiology = Air Space Flooding (consequence of Pulmonary Edema. COPD. Sepsis Loads due to Reduced Chest Wall Compliance Loads due to Increased Minute Ventilation Requirements 34 . Fatigue) c.

C. Peaked P Waves RAD with RVH Cardiomegaly. TYPE 3: Perioperative Respiratory Failure o Occurs as a result of Lung Atelectasis (occurs so commonly in the Perioperative Period) o Mechanism = ATELECTASIS o Etiology = Decreased Functional Residual Capacity (FRC) w/c lead to Collapse of Dependent Lung Units o Clinical Description (they cause a Decreased FRC)  Supine Position / Obese  Ascites (Difficulty in Lung Expansion)  Upper Abdominal Incision  General Anesthesia  Airway Secretions D. Physical Examination: RV-Failure Signs o Neck Vein Engorgement o RV Heave o Increased O2 o Systolic Murmur (TR) o Hepatomegaly o Dependent Edema II. Hypovolemic. MANAGEMENT A. Easy Fatigability. Clinical Manifestations: o Acute (see Pulmonary Embolism) o Chronic: Productive Cough. Weakness B. Management o Oxygen (Vasodilates Pulmonary Arteries. or Respiratory Gas Exchange o Acute: Pulmonary Thromboembolism o Chronic: Severe COPD o Acute on Chronic: COPD + Infection & Worsening Hypoxemia I. decreasing Resistance and Pulmonary Pressure) o Treat Infection. Pulmonary Vasculature. RV Form Enlarged Pulmonary Conus Diagnostic Allows measurement of RV Thickness VS LV B. remove secretions o Diuretics (Caution in Loop Diuretics – it causes Metabolic Alkalosis and Decreases Pulmonary Drive) o Bronchodilators (Theophylline) 35 . Septic o Clinical Description  Myocardial Infarction (Cardiogenic Shock)  Hemorrhage (Hypovolemic Shock)  Dehydration (Hypovolemic Shock)  Endotoxemia (Septic Shock) 12) COR PULMONALE  RV Enlargement 20 to a Disease process which Primarily involves the LUNGS. Diagnostics 12-L ECG CXR 2D Echo Tall. Exertional Dyspnea. TYPE 4: Shock o Mechanism = HYPOPERFUSION o Etiology: Cardiogenic. SYMPTOMS / SIGNS A.

13) TYPICAL CHEST EXAMINATION FINDINGS: CONDITION Normal Consolidation or Atelectasis (with Patent Airway) Consolidation or Atelectasis (with Blocked Airway) Asthma Interstitial Lung Disease Emphysema Pneumothorax Pleural Effusion PERCUSSION Resonant Dull Dull Resonant Resonant Hyperresonant Hyperresonant Dull FREMITUS Normal Increased Decreased Normal Normal Decreased Decreased Decreased BREATH SOUNDS Vesicular (at lung bases) Bronchial Decreased Vesicular Vesicular Decreased Decreased Decreased VOICE TRANSMISSION Normal Bronchophony. Whisphered Pectoriloquy. Egophony Decreased Normal Normal Decreased Decreased Decreased ADVENTITIOUS SOUNDS Absent Crackles Absent Wheezing Crackles Absent or Wheezing Absent Absent of Pleural Friction Rub 36 .

qwertyuiopasdfghjklzxcvbnmqwertyui opasdfghjklzxcvbnmqwertyuiopasdfgh jklzxcvbnmqwertyuiopasdfghjklzxcvb nmqwertyuiopasdfghjklzxcvbnmqwer RHEUMATOLOGY tyuiopasdfghjklzxcvbnmqwertyuiopas dfghjklzxcvbnmqwertyuiopasdfghjklzx cvbnmqwertyuiopasdfghjklzxcvbnmq wertyuiopasdfghjklzxcvbnmqwertyuio pasdfghjklzxcvbnmqwertyuiopasdfghj klzxcvbnmqwertyuiopasdfghjklzxcvbn mqwertyuiopasdfghjklzxcvbnmqwerty uiopasdfghjklzxcvbnmqwertyuiopasdf ghjklzxcvbnmqwertyuiopasdfghjklzxc vbnmqwertyuiopasdfghjklzxcvbnmrty uiopasdfghjklzxcvbnmqwertyuiopasdf ghjklzxcvbnmqwertyuiopasdfghjklzxc vbnmqwertyuiopasdfghjklzxcvbnmqw ertyuiopasdfghjklzxcvbnmqwertyuiop Jaime Alfonso Manalo Aherrera.D. Internal Medicine Notes 2009 . M.

etc)  Antinuclear Antibody  Serositis  Hematologic Disorder CLASSIFICATION CRITERIA FOR THE DIAGNOSIS OF SLE (Harrisons): CRITERIA Malar Rash Discoid Rash Photosensitivity Oral Ulcers Arthritis Serositis Renal Disorder Neurologic Disorder Hematologic Disorder Immunologic Disorder Antinuclear Antibodies REMARKS Fixed Erythema. Sensitivity is ~75%) 2 . and/or Anti-Phospholipid An Abnormal Titer of ANA by Immunofluorescence at any point in time in the absence of drugs known to induce ANAs If > 4 of these Criteria. the diagnosis is likely to be SLE (Specificity is ~95%. well documented.5g/d or 3+. Pyuria. or Cellular Casts Seizures or Psychosis without other causes Hemolytic Anemia or Leukopenia. Headaches. Stroke. observed by Physician Non-Erosive Arthritis of 2 or more Peripheral Joints. Swelling or Effusion Pleuritis or Pericarditis documented by ECG or Rub or Evidence of Effusion Proteinuria > 0. are present at any time in a patient’s history. Flat or Raised. or Thrombocytopenia in the absence of offending drugs Anti-ds DNA. over the Malar Eminences Erythematous Circular Raised Patches with Adherent Keratotic Scaling and Follicular Plugging. with Tenderness. Anti-Sm. Hematuria. etc)  Renal Disorder (Albuminuria. Atrophic Scarring may occur Exposure to Ultraviolet Light causes Rash Includes Oral and Nasopharyngeal Ulcers. or Lymphopenia. ACR CRITERIA FOR SLE  Discoid Rash We ONLY need FOUR out of the ELEVEN to make a  Oral Ulcers Diagnosis of SLE  Photosensitivity  Arthritis  Malar Rash  Immunologic Disorder  Neurologic Disorder (Seizures.COMMON RHEUMATOLOGIC CASES 1) SYSTEMIC LUPUS ERYTHEMATOSUS  Autoimmune Disease in which organs and cells undergo damage mediated by Tissue-Binding Autoantibodies and Immune Complexes I.

Pulmonary Hypertension Most Common Pulmonary Manifestation = PLEURITIS with or without Pleural Effusion  May respond to NSAIDs if MILD  Glucocorticoid Therapy if Severe Hemolytic Anemia. Hepatitis Seizures.II. Psychosis Stroke Most Common Manifestations of Diffuse CNS Lupus = Cognitive Dysfunction Inflammation of all the Linings of the Heart: Pericarditis. Inflammatory Myositis Pancreatitis. METHYLPREDNISOLONE (rounds)  MPPT: Methylprednisolone Pulse Therapy Drip  Usually. Pulmonary Hemorrhage. Etc FROM HARRISONS:  Methylprednisolone Sodium Succinate IV (approved for Lupus Nephritis): Used for SEVERE Disease at a Dose of 1g IV qd for 3 days 3 . Panniculitis. Endocardial (Libman-Sacks Endocarditis). Raynaud’s Phenomenon Most Frequent Cardiac Manifestation = PERICARDITIS Pulmonary Pleuritis. Retinitis Hypocomplementemia (Low C3 and C4 Levels). Vasculitis Arthritis. Normocytic) Conjunctivitis. Thrombocytopenia. Myocardial. Elevated ESR and CRP Azotemia. Osteonecrosis. Fatigue. Pneumonitis. Scleritis. Bowel Vasculitis. Accelerated Atherosclerosis. CLINICAL FEATURES OF SLE Constitutional Fever. Albuminuria. Uveitis. Pulmonary Embolism. dose is 500-1000mg 4-6 hours given 1 dose/day for 3 days (check harrisons)  This therapy is given in patients with SLE in Activity: o Carditis o Nephritis o Anemia. Lymphopenia. Alopecia. Weight Loss Mucocutaneous Musculoskeletal Gastrointestinal CNS Cardiovascular Discoid LE. Persistent Pyuria (not infection related) Nephritis = the Most SERIOUS manifestation of SLE  Nephritis is usually ASYMPTOMATIC in Most Lupus Patients Hematologic Eyes Laboratory Abnormalities Renal III. Leukopenia. Prolonged PTT Most Frequent Hematologic Manifestation = ANEMIA (Normochromic. Subacute Cutaneous LE. Renal Failure. Hematuria.

fatigue  Potential Retinal Toxicity B. MANAGEMENT OF SLE (from Medicine Notes) For Arthritis For Active SLE (CNS. Quinacrine)  Reduce dermatitis. particularly for arthritis / arthralgias  TWO Major Issues – CAUTION with NSAIDS  SLE patients are at increased risk for NSAID-Induced Aseptic Meningitis. and renal dysfunction  All NSAIDS (particularly COX-2 Inhibitors) may increase risk for MI 2. arthritis.5-1mg/kg of daily Prednisolone or equivalent o Evidence that glucocorticoid therapy is life-saving comes from studies – survival is better in people with DPGN treated with high dose daily glucocorticoids (40-60mg Prednisone daily for 4-6 months) o Currently. doses are tapered as rapidly as the clinical situation permits (usually to a maintenance dose of 5-10 mg Prednisone V. Conservative Therapies for Management of Non-Life Threatening Disease o Sx: Fatigue. Pain. followed by 0. Thereafter. maintained on dose of 10-20mg MPPT 500-1000mg/am in D5W 50cc x 6h X 3 doses in 3 days (Severe SLE with Organ Damage) Cyclophosphamide 2-3mg/kg/day Cyclophosphamide IV Pulse Therapy 500-1000mg in D5W 500cc x 6h (give Metoclopromide 2 tabs before the drip) – for life threatening SLE Sunscreens Hydrocortisone 200mg BID + Betamethasone 0. Life Threatening SLE: Proliferative Forms of Lupus Nephritis o Mainstay for any Inflammatory Life-Threatening or Organ-Threatening Manifestations of SLE = SYSTEMIC GLUCOCORTICOIDS (0. NSAIDs  Useful analgesics / anti-inflammatories.5-2mg/kg per day PO or 1000mg of Methylprednisolone Sodium Succinate IV Daily for 3 days. Antimalarials (Hydroxychloroquine. high doses are recommended for much shorter periods (recent trials of interventions for severe SLE employ 4-6 weeks of these doses).05% Ointment Coumadine PO For Photosensitivity For Skin Lesions For Thrombosis 4 . but WITHOUT Major Organ Involvement o Management is directed to suppression of symptoms o Mainstay: Analgesics and Antimalarials 1. Renal. HPN.IV. Chloroquine. (+) Autoantibodies of SLE. Hema) Diclofenac Na 50mg/tab BID Prednisone 5mg/tab PO 40-60mg/day. MANAGEMENT OF SLE (Harrisons) A. elevated serum transaminases.

ankle. elbow. metacarpophalangeal. and feet. or Proximal Interphalangeal Joint o d) Symmetric Arthritis: Simultaneous involvement of the same joint areas on BOTH sides of the body o e) Rheumatoid Nodules: Subcutaneous Nodules over bony prominences. weight loss) or extraarticular disease (vasculitis. Criteria o a) Morning Stiffness: Stiffness in and around the joints lasting 1 hour before Maximal Improvement o b) Arthritis of Three or More Joint Areas: At least 3 Joint Areas. observed by a physician simultaneously. and vague musculoskeletal symptoms until the appearance of Synovitis becomes apparent  Specific symptoms usually appear gradually as several joints. episcleritis. especially those of hands. knee. not just bony overgrowth. wrist. Criteria b-e must be observed by a physician IV. The 14 possible joint areas involved are right or left proximal interphalangeal. Morning Stiffness of > 1 hour duration II. and metatarsophalangeal joints o c) Arthritis of Hand Joints: Arthritis of Wrist. LABORATORY FINDINGS  Rheumatoid Factors (RF): Autoantibodies Reactive with the Fc Portion of IgG – found in more than 2/3 of adults with the disease and have classically been used to evaluate patients with RA  Normochromic. become affected in a Symmetric Fashion  Signs and Symptoms: Pain. aggravated by movement. extensor surfaces. generalized weakness. have Soft Tissue Swelling or Joint Effusions.2) RHEUMATOID ARTHRITIS   Chronic multisystem disease of unknown cause – systemic disease of unknown etiology Characteristic Features: Persistent Inflammatory Synovitis. THERAPY GOALS  1) Relief of Pain  2) Reduction of Inflammation  3) Protection of Articular Structures  4) Maintenance of Function  5) Control of Systemic Involvement Medical Management:  NSAIDs or Selective COX-2 Inhibitors  Glucocorticoids for: o 1) Symptomatic relief while waiting for a response to a slow-acting immunosuppressive or immunomodulatory agent o 2) Persistent Synovitis despite adequate trials of NSAIDs and immunosuppressive or immunomodulatory agents o 3) Severe constitutional symptoms (fever. Metacarpophalangeal Joint. usually involving Peripheral Joints in a Symmetric Distribution I. knees. CLINICAL MANIFESTATIONS  Onset: RA is a chronic polyarthritis which begins insidiously with fatigue. usually greatest after periods of Inactivity. is the Most Common Manifestation of established RA  Generalized Stiffness. wrists. Guidelines for Classification: o Four of Seven Criteria are required to classify a patient as having Rheumatoid Arthritis (RA) o Patients with Two or More Clinical Diagnoses are NOT Excluded B. CRITERIA FOR THE DIAGNOSIS A. anorexia. and Tenderness  PAIN in affected joint. Swelling. or juxtaarticular regions observed by a physician o f) Serum Rheumatoid Factor: Demonstration of abnormal amounts of Serum Rheumatoid Factor by any method for which the result has been positive in less than 5% of normal control subjects o g) Radiographic changes: Typical changes of RA on Posteroanterior Hand and Wrist radiographs that must include erosions or unequivocal bony decalcification localized in or most marked adjacent to the involved joints Criteria a-d must be present for at least 6 weeks. pleurisy)  Immunomodulatory and Immunosuppressive Agents o Methotrexate (initial choice for moderate to severe RA) o Hydroxychloroquine or Sulfasalazine 5 . Normocytic Anemia is frequently present in Active RA  ESR is increased in nearly all patients with Active RA  Synovial Fluid Analysis: presence of Inflammatory Arthritis Labs Requested for RA:  ERC / CRP  RF  CBC  Renal  ALT (for MTX Therapy)  Urinalysis  Synovial Fluid Analysis III.

000-30. Surgical Drainage or Arthroscopic Lavage & Drainage Indications:  1) Septic Hip  2) Joints in which either the anatomy. Fungi. or by direct inoculation during surgery. or loculation of pus prevent adequate needle drainage  3) Septic Arthritis with coexistent Osteomyelitis  4) Joints that do not respond in 4-6 days to appropriate Tx and repeated arthrocenteses  5) Prosthetic joint infection 6 . ACUTE BACTERIAL ARTHRITIS A. Microbiology o Infants: Group-B Strep. Rheumatoid. Repeated Arthrocenteses  Should be performed daily or as often as necessary to prevent reaccumulation of fluid  Arthrocentesis is indicated to: o 1) Remove destructive inflammatory mediators o 2) Reduce intra-articular pressure and promote antimicrobial penetration into the joint o 3) Monitor response to therapy by documenting sterility of synovial fluid cultures & decreasing Leukocyte Count 5. Spirochetes. Pathogenesis o Bacteria enter the joint from the bloodstream. animal or human bite. Usual presentation is with fever and an acute monoarticular arthritis. and other Non Infectious Inflammatory Arthritides Mycobacterial and Fungal Contains < 180 Cells (predominantly Mononuclear Cells) Cell Counts averaging 100. large amounts of tissue debris. Gonococcal Arthritis causes one-half of all septic arthritis in otherwise healthy.000 cells/uL 10. Neisseria gonorrhoeae. sexually active young adults General Principles of Treatment: 1.000/uL (25. Gram (-) Enteric Bacilli. aureus o Young Adults & Adolescents: N.000-250. and S. and Viruses also infect joints) Acute Bacterial Infection typically involves a Single Joint or a Few Joints Subacute or Chronic Monoarthritis or Oligoarthritis suggests Mycobacterial or Fungal Infection Approach to Patients with Infectious Arthritis: o ASPIRATION of SYNOVIAL FLUID – an essential element in the evaluation of potentially infected joints o Ultrasonography or Fluoroscopy may be used to guide aspiration of difficult to localize effusions Normal Synovial Fluid Acute Bacterial Infections Crystal Induced. Hospitalization  Indicated to ensure drug compliance and careful monitoring 3.3) INFECTIOUS ARTHRITIS     Staphylococcus aureus. and other bacteria are the MOST COMMON Causes of Infectious Arthritis (various Mycobacteria. gonorrhea (most commonly implicated organism) o S. or trauma o Hematogenous Route: Most Common Route in all age groups B. injection.000/uL) with > 90% Neutrophils < 30. IV Antimicrobials  Provide good serum and synovial fluid drug concentrations  Oral or Intra-Articular Antimicrobials are NOT appropriate as initial therapy 4. Joint Fluid Examination  Includes Gram Stain and Culture – mandatory to make a diagnosis and to guide management  Joint Fluid Leukocyte Count: useful diagnostically and as a baseline  Cultures of Blood and other extra-articular sites of infection also should be obtained 2. although multiple joints may be affected by hematogenous spread of pathogens Nongonococcal Infectious Arthritis in adults tends to occur in patients with previous joint damage or compromised host defenses.000-50. In contrast. from a contiguous site of infection in bone or soft tissue.000/uL with 50-70% Neutrophils & the remainder Lymphocytes **NOTE: Definitive Diagnosis of Infectious Process: o Identification of Pathogen in Stained Smears of Synovial Fluid o Isolation of Pathogen from Cultures of Synovial Fluid and Blood o Detection of Microbial Nucleic Acids and Proteins by PCR-Based Assays and Immunologic Techniques I.aureus accounts for most Non-Gonococcal Isolates in Adults of all ages Infectious Arthritis is generally categorized into Gonogoccal and Nongonococcal Disease.

90C  Inflamed. On Gram Stain:  Gram (+) = we will see 65-75% Staph / Strep  In 30-50%. knee. Late Infection  Bone Erosions  Joint Space Narrowing Culture other Fluids Peripheral WBC Acute Phase Reactants X-Ray of the Joint III. Cervix.000-20. True Gonococcal Septic Arthritis o True Gonococcal Septic Arthritis is LESS Common than the Diffuse Gonococcal Infection (DGI) Syndrome and always follows DGI. wrists.II. Bursitis. Culture of Synovial Fluuid:  > 90% Culture (+) for Staphylococcus aureus Blood CS will be (+) 50% for Staph Elevated with a Leftward Shift ESR / CRP = HIGH 1. Gram smears confirm presence of large numbers of Neutrophils  Total Protein and Lactate Dehydrogenase in synovial fluid are elevated. ankle. more frequently.000 leukocytes/uL and can be obtained with ease o Gonococcus is only occasionally evident in Gram-Stained Smears o Cultures of Synovial Fluid are Positive in < 40% of cases o Blood Cultures are almost always Negative 7 . and Acute Osteomyelitis. muscle spasm.000 1. hands.3 – 38. should be distinguished from Septic Arthritis by their greater range of motion and less-than-circumferential swelling  Labs: (+) Blood Cultures in 50-70% of S. which may produce a similar clinical picture. serosanguinous. GONOCOCCAL ARTHRITIS  Accounted for up to 70% of Infectious Arthritis  Consequence of Bacteremia arising from Gonococcal Infection or. Swollen Joint  Cellulitis. Glucose Level is Depressed Synovial Fluid Turbid WBC Count > 100.000 leukocytes/uL B. Small numbers of papules that progress to hemorrhagic pustules develop on the trunk and the extensor surfaces of the distal extremities o Migratory Arthritis and Tenosynovitis of the knees. we will have NOTHING on Gram Stain (don’t automatically rule this out)  Gram (-) Bacilli = 30-50% 2. which is unrecognized in 1/3 of patients o A single joint (hip. and usually contains only 10. Synovial Fluid is turbid. or frankly purulent. and decreased range of motion  (+) Fever 38. Early Infection  Soft Tissue Swelling  Joint Space Widening 2. NON-GONOCOCCAL BACTERIAL ARTHRITIS  90% present with involvement of a Single Joint – most commonly the KNEES (less frequently the hip)  (+) Moderate to Severe Pain that is uniform around the joint.aureus infections. from asymptomatic gonococcal mucosal colonization of the Urethra. effusion. Chills. or Pharynx A. Rash. and Blood Cultures are Positive in < 45% o Synovial Fluid may be difficult to obtain from inflamed joints. and ankles are prominent o Cutaneous Lesions and Articular Findings = due to immune reaction to circulating gonococci and immune complex deposition in tissues o Cultures of Synovial Fluid are consistently NEGATIVE. or wrist) is usually involved o Synovial Fluid has > 50. and Articular Symptoms. feet. Diffuse Gonococcal Infection (DGI) o Most Common Manifestation: Fever.

Gram (-) in Smear  Cefotaxime 1g q 8h  Ceftriaxine 1-2g q 24h 3. Staphylococcus:  4 Weeks DURATION 2. Pseudomonas  At Least 2 Weeks B. MEDICAL MANAGEMENT: Objectives = Relief of Pain + Prevention of Disability  Acetaminophen (dose up to 1000mg up to QID) – initial pharmacologic treatment  Low-Dose NSAIDs or Selective COX-2 Inhibitors  Glucosamine Sulfate 1500mg/day  Intra-Articular Glucocorticoid Injections  Tramadol  Topical Capsaicin II. Suspect Pseudomonas  Add Aminoglycoside. Penicillin Sensitive Pneumo / Strep:  2 Weeks on Penicillin-G 2m u q4h 3. DIAGNOSIS  Difficulty in isolation of Gonococci from Synovial Fluid and Blood  Specimens for culture should be obtained from potentially infected mucosal sites  Cultures and Gram-Stained Smears of Skin Lesions are occasionally Positive  All specimens for culture should be plated onto Thayer-Martin Agar directly or in special transport media at the bedside and transferred promptly to the microbiology laboratory in an atmosphere of 5% CO 2. with subsequent formation of reactive new bone at the articular surface I. Gram (+) in Smear  Oxacillin or Nafcillin 2g q4h 2. Enteric Gram (-)  3-4 Weeks 2nd /3rd Generation Cephalosporin IV. or  Quinolone IV/PO 5. Penicillin-Resistant  Cefotaxime / Ceftriaxone for 2 Weeks 4. the 7-day course of Tx can be completed with an oral agent such as Ciprofloxacin (500mg BID) 4) OSTEOARTHRITIS  OA or Degenerative Joint Disease – characterized by deterioration of articular cartilage. Once local and systemic signs are resolving.IV. ADJUNCTIVE MEASURES: Non-Pharmacological Measures  Brief periods of rest for the involved joint relieve pain 5) GOUTY ARTHRITIS    90% due to Uric Acid UNDER Excretion 10% due to Uric Acid OVER Production Ex) Beer  BOTH Under and Over! 8 . as generated in a candle jar V. or  3rd Generation Cephalosporin 1. TREATMENT A. Gonococcal Septic Arthritis o CEFTRIAXONE 1g IV or IM q 24 h:  7 days If with Resolution and if Isolate Sensitive  7 day additional Ciprofloxacin 500mg bid po Ceftriaxone (1g IV or IM every 24 hours) to cover possible Penicillin-Resistant Organisms. Non-Gonococcal Septic Arthritis EMPIRICAL 1.

malalignment of articulating structures. the arc of measurable movement Range of through which the joint moves in a single plane Motion Loss of full movement. or damage to periarticular supportive structures Inflammation of the entheses (tendinous or ligamentous Enthesitis insertions on bone) Epicondilytis Infection or Inflammation involving an Epicondyle QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. Definition of Terms: A Palpable (less commonly audible) vibratory or Crepitus crackling sensation elicited with joint motion Alteration of joint alignment such that articulating Subluxation surfaces incompletely approximate each other Abnormal displacement of articulating surfaces such that Dislocation the surfaces are not in contact For diarthrodial joints. QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. 9 .More on Rheumatologic Diseases: Algorithm for the Diagnosis of Musculoskeletal Complaints: Sites of Hand or Wrist Involvement & Diseases QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. may result from Deformity bony hypertrophy. resulting from a fixed resistance Contracture caused either by tonic spasm of muscle (reversible) or to fibrosis of periarticular structures (permanent) Abnormal shape or size of a structure.

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