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176 Cards in this Set
- Front
- Back
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Why do clinicians order lab tests?
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Confirmation of clinical opinion
Screening Diagnosis Prev. abnormal result Monitoring Prognosis Establish baseline |
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Urinalysis
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Formation of urine begins with filtration of blood plasma through glomerular capillaries
In normal adults> 1 liter blood perfuses both kidneys per minute Tubules and collecting duct of each nephron modify this filtrate to produce excreted urine |
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U/A specimen collection
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**Diagnostic value depends on the quality of the sample
Midstream vs. catheterized specimen **50% of midstream collection in females will have significant perineal contamination (>10 epithelial cells/HPF) Risk of infection from cath: 1-3% **20% if elderly or debilitated |
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Urine clinistrip / dipstick test
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LENS RBP Kph
Leukocyte esterase Nitrates RBC’s / heme Specific gravity Protein Bilirubin Ketones pH |
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Leukocyte esterase
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Enzyme produced by neutrophils
**50-60% of pts with bacteriuria do not have pyuria (may be a later finding in acute UTI) - shows WBC, produced by neutophils shows enzyme is there = neutrophils are present |
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Nitrites
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Positive strip test for nitrites is highly suggestive for bacteriuria
Gram negative bacteria convert nitrate to nitrite Therefore a positive nitrite should raise suspicion of presence of gram neg bacteria; and specimen should be sent on for microscopic analysis |
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Blood
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Measures intact erythrocytes
Free hemoglobin from lysed RBC’s Myoglobinuria - break down of muscle; myoglobin may show + result **If reagent strips dip positive for blood but micro is neg; suspect myoglobinuria and test pt for rhabdomyolysis |
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Micro
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***
Urinary sediment Erythrocyte casts: glomerular nephritis Leukocyte casts: interstitial disease Fat laden histiocytes (oval fat bodies / macrophages) associated with nephrotic syndrome and proteinuria; seen in pts with nephropathies or non-glomerular renal dz Urate, phosphate, oxalate, cystine crystals: stone formers Uric acid crystals: gout |
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Cultures
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Not significant unless colonies are estimated to be **>10^3
Treat all pts presumptively for gram neg infection; send cultures on all resistant / recurrent infections |
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Blood Chemistries
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Provide information on metabolism, fluid balance,acid-base status, renal function
Basic serum electrolytes: Sodium: Na - Potassium: K+ Chloride: Cl – Carbon dioxide CO2 / bicarbonate HCO3 - |
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Anion Gap
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Electrolyte disorders common in pts with metabolic, renal disease, or hx of persistent vomiting/diarrhea
**Formula : Na+ - (HCO3- + Cl-) Normal anion gap **< 12-15 (depends on lab) |
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What's the normal anion gap?
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< 12-15
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Formula for anion gap
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Na+ - (HCO3- + Cl-)
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Sodium
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Normal 135 - 145
Major role is to hold water in the extracellular fluid space Serum Na content regulated by the kidneys in response to hormonal, neural, and vascular signals reflecting intravascular fluid volume Decreased Na: hypo-osmolarity Increased Na: hyper-osmolarity Exception: hypertonic hyponatremia |
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Normal range for Na+
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135-145
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Hypertonic Hyponatremia
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Extracellular osmotic substance accumulates causing water to shift from intracellular to extracellular space thus lowering serum sodium concentration
Caused by hyperglycemia or administration of mannitol - this is why diabetics egt dehydrated |
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**Sodium correction formula
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For every increase of 100 mg/dl in glucose above normal (100) multiply by 1.6 to add the corrected mEq of Na.
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Hypotonic Hyponatremia
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Increased water intake;
psychogenic polydypsia or rapid consumption of large amount of beer ! Renal excreting capacity lags behind intake |
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Causes of Hyponatremia
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Normal water excretion:
- Psychogenic polydipsia - Massive beer drinking Impaired water excretion - Volume loss: diuretics, GI loss, bleeding * Edematous states: cirrhosis, CHF - Renal failure - Cortisol deficiency: adrenal / hypopituitary: - Severe hypothyroidism - SIADH |
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SIADH
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syndrome of inappropriate ADH
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Hypertonic Hyperosmolar
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Loss of water in excess of sodium
Loss through respiration, evaporation Dehydration often due to blunted thirst sensation in the elderly Failure of ADH coupled with thirst center in CNS |
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Causes of Hypernatremia
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Insensible water loss
- fever, hyperthermia, diaphoresis, loss of thirst sensation, burns, hyperventilation Neurogenic diabetes insipidus - Failure to secrete antidiuretic hormone Nephrogenic diabetes insipidus - Failure of the kidney to respond to antidiuretic hormone Osmotic diuresis - Sustained glycosuria, mannitol, prolonged high protein intake |
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Mannitol
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very strong diuretic
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Potassium
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Plays a vital role in intracellular ion exchange although we are only able to measure extracellular levels
Normal 3.5 - 5.0 Increased K+ considered a life threatening electrolyte abnormality |
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Normal K+ values
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3.5-5.0
over 6 is life-threatening |
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Hyperkalemia - EKG
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**Peaked T waves
Widened PR and QRS intervals Flattening / loss of P waves |
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Hypokalemia - EKG
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**U waves
flat or inverted T waves ST depression decreased QRS voltage |
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Hyperkalemia
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Levels > 6.0 can lead to myocardial irritability and fatal arrythmias
Falsely elevated K+ is very commonly due to breakdown of cells from improper blood sample collection (hemolysis) Renal failure Release of intracellular K+ into the extracellular space Metabolic acidosis, massive tissue breakdown, insulin deficiency |
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Hypokalemia
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True body loss vs. shift from extracellular to intracellular
Decreased dietary intake (of K+) Diarrhea / vomiting diuretics |
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Chloride
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Normal 98 – 109 mEq/l
Primarily extracellular Major role as anion companion to Na + Changes in Cl – generally reflect changes in other extracellular ions, especially bicarb |
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Hypokalemia
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True body loss vs. shift from extracellular to intracellular
Decreased dietary intake (of K+) Diarrhea / vomiting diuretics |
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Chloride
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Normal 98 – 109 mEq/l
Primarily extracellular Major role as anion companion to Na + Changes in Cl – generally reflect changes in other extracellular ions, especially bicarb |
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Normal Chloride values
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98 – 109 mEq/l
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** Bicarbonate
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***
CO2 / HCO3 normal 20-30 mEq/l Serum CO2 @ 5% higher then serum bicarbonate Therefore note that CO2 levels on electrolytes should be slightly higher than bicarb measured on ABG Bicarbonate is the major extracellular buffer Abnormalities in bicarb always represent disorders of the acid/base balance |
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** Blood Urea Nitrogen
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***
Normal 10 – 20 Urea is end product of protein metabolism BUN reflects effects of dietary protein, liver disease, tissue breakdown, reduced renal blood flow, renal pathology One half of normal renal function must be lost before BUN or creatinine become elevated If renal function is decreased enough to cause a rise in BUN / creatinine then a U/A will reveal proteinuria and abnormal urinary sediment BUN levels follow renal diuresis patterns Decreased renal blood flow = increased BUN Increased diuresis = decreased BUN Azotemia : elevated BUN BUN/creatinine ratio normally between 10-15 / 1 |
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Normal BUN levels
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10-20
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Normal BUN/Creatinine ratio
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10-15/1
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Prerenal Azotemia
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***
Inadequate renal perfusion of any cause Additional increase in BUN due to decreased perfusion of kidney (kidney’s response to underperfusion is to conserve water and Na+) Increased BUN/creatinine ratio |
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Causes of Prerenal azotemia
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***
CHF Hypotension (sepsis, MI, blood loss, over treatment with diuretics, dehydration, increased dietary protein intake, pt’s receiving hyperalimentation) Use of high dose steroids (increases urea production) Increased BUN / creatinine ratio |
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Renal Azotemia
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Retention of urea due to interstitial kidney disease with loss of renal function
Normal BUN / creatinine ratio |
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Postrenal Azotemia
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***
Increase in BUN due to OBSTRUCTION of urinary tract High BUN / creatinine ratio Slowing of urinary flow permits increased resorption of urea |
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Causes of Postrenal Azotemia
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***
Prostatic obstruction Renal lithiasis Hx of urologic surgery Neurogenic bladder Pelvic malignancies |
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Creatinine
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***
End product of metabolism of creatine, produced in liver and stored in muscle in the form of phosphocreatine; provides storage for high energy phosphate Daily muscle cell metabolism leads to renal excretion of 1 g creatinine/day SINGLE BEST CLINICAL TEST of RENAL FUNCTION Normal 0.6 – 1.2 mg/dl Increased creatinine represents loss of glomerular filtration **Any doubling of creatinine indicates that half of renal function is lost CRF pts may tolerate creat > 20 mg/dl; while ARF pt may not tolerate creat > 6 Decision to begin dialysis tx made on clinical symptoms rather than absolute #’s |
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Normal Creatinine levels
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0.6 - 1.2 mg/dl
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Complete Blood Count
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***
Most commonly ordered blood test Hematologic manifestation of disease Anemias Leukocytosis |
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Erythrocytes: RBC’s
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***
Mediate oxygen transport from lungs to tissues Densely packed with oxygen carrying protein hemoglobin RBC’s survive only 120 days in circulation MCV normal = 80-100 |
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Normal MCV
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80-100
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Hematocrit
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***
Defined as the proportion of blood volume occupied by erythrocytes Calculated value derived from the total erythrocyte count and the mean corpuscular volume (MCV) MCV is the factor by which a clinician can descriminate between types of anemia |
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Hemoglobin
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Hemoglobin is unique for its ability to carry and unload oxygen
Hgb concentration defines anemia World Health Organization: anemic if Males < 13 g/dL Females < 12g/dL pregnant < 11g/dL |
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Blood Smears
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***
Information on red cell size, morphology, variation, hypochromia Proportion of cell types % of immature circulating cells; i.e. bands, stabs Presence of precursor cells usually restricted to marrow (blasts, nucleated erythrocytes) Inclusion bodies ( Dohle, Heinz, Howell-Jolly) |
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** Dohle bodies
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Döhle bodies are intra-cytoplasmic structures composed of agglutinated ribosomes; they will increase in number with inflammation and increased granulocytopoiesis. If there are many neutrophils in the bloodstream containing Döhle bodies, these can be referred to as toxic neutrophils.
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** Heinz bodies
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Heinz bodies are inclusions within red blood cells composed of denatured hemoglobin. They are named after Robert Heinz (1865-1924) a German physician, who in 1890 described these inclusions in connection with cases of **hemolytic anemia.
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** Howell – Jolly bodies
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Howell-Jolly bodies are spherical blue-black inclusions of red blood cells seen on Wright-stained smears. They are nuclear fragments of condensed DNA, 1 to 2 µm in diameter, normally removed by the spleen. They are seen in severe hemolytic anemias, in patients with dysfunctional spleens or after splenectomy.
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Malaria ring sign
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Plasmodium vivax
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Anemias
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Defects in production vs accelerated destruction
Microcytic Normocytic Macrocytic |
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Microcytic
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MCV < 80
Iron deficiency Thalassemia Hemolytic anemia |
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Normocytic
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MCV 80-100
Hemorrhage (acute) Chronic disease Bone marrow failure Lead poisoning |
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Macrocytic
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MCV > 100
Vitamin B12 deficiency Folate deficiency Hypothyroidism Severe liver disease |
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Leukocytes
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**
Normal 4.5 – 11 K WBC counts and differential most commonly ordered to help evaluate a pt with or to r/o bacterial infection Elevated neutrophil (PMN’s) count OR increase in the proportion of immature neutrophils is an important sign of bacterial infection (left shift) Evaluation of pts undergoing chemotherapy |
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normal leukocyte values
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4.5 – 11 K
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Platelet Count
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Measured on CBC
Formation of a platelet plug at the site of vessel injury is critical for effective hemostasis Normal 150-400 Thrombocytopenia = platelet ct < 100 < 50 at risk for severe bleeding from trauma < 10 risk for spontaneous cerebral hemorrhage |
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normal platelet count
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150-400
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Prothrombin Time
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**
When a blood vessel is injured, damaged cells release tissue thromboplastin which activates factors that set off the extrinsic pathway of coagulation PT measures the extrinsic coagulation cascade Normal 10-13 sec. Used to assess anticoag tx and Vit K deficiency |
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Partial Thromboplastin Time
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**
Exposure of subendothelial collagen to the plasma activates the intrinsic coag pathway Normal 25 – 42 sec Prolonged PTT implies a deficiency of any of the coag factors or presence of a circulating anticoagulant intrinsic pathway of coagulation a sequence of reactions leading to fibrin formation, beginning with the contact activation of factor XII, and resulting in the activation of factor X to initiate the common pathway of coagulation. common pathway of coagulation the steps in the mechanism of coagulation from the activation of factor X through the conversion of fibrinogen to fibrin. Coagulation pathway overview. |
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INR
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***
INR = patient PT / control PT normal INR range for pt on anticoags = 2 – 3 INR (International Normalized Ratio) now considered superior for monitoring anticoag tx |
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normal INR value
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1
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Differential for prolonged PT / PTT
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Prolonged PT ( extrinsic)
-Vit K deficiency -Coumadin effect -Factor VII deficiency -Liver disease Prolonged PTT (intrinsic) -Heparin effect -Lupus anticoagulant -Disseminated intravascular coagulation -Hemophilia A / B -Antibody to factor VIII / IX circulating anticoagulant |
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Liver Function Tests
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Bilirubin
Alanine Tranferase (ALT) Aspartate aminotransferase (AST) Ammonia |
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Bilirubin
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***
End product of heme metabolism derived from the breakdown of RBC’s Bilirubin is conjugated in the liver and secreted into bile Increased conjugated (direct) Intra/extrahepatic obstruction results in increased serum levels usually accompanied by bilirubinuria Increased unconjugated (indirect) bili; usually associated with hemolysis or congenital defects in bilirubin transport ( no assoc bilirubinuria) |
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Alanine Tranferase (ALT)
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Normal 3 – 35
Part of the enzyme system in the microsomal fraction of the hepatocyte Greatest concentration in the liver Specific: elevation of ALT typically only seen in pts with liver disease |
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normal ALT
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3-35
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Aspartate Aminotransferase (AST)
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***
Normal 10 – 40 Found in the cytosol and mitochondria of hepatocytes Present in large concentration in liver, heart, skeletal tissue Less specific than ALT for liver disease Significant elevation in pts with massive hepatic necrosis |
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normal AST
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10-40
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AST vs ALT
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**
In most cases of liver disease ALT and AST will be elevated but the ratio of ALT : AST > 1 In alcoholic hepatitis and massive hepatic necrosis the ratio of ALT : AST < 1 (AST will be higher) |
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Alkaline Phosphatase
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Monophosphate concentrated in hepatocytes, bone, gut, lung
Normal serum value 25 – 100 Increased alk phos significant for obstruction anywhere in the biliary tract elevated alk phos in pulmonary, renal, splenic infarction / inflammation, carcinoma, osteoblastic activity |
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normal values of Alk Phos
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25-100
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Ammonia
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Elevated NH3 is an indicator of severe hepatic parenchymal damage
Useful in identifying cases of hepatic encephalopathy Normal range 30-70 ug/dl |
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normal range of Ammonia
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30-70 ug/dl
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Increase Phosphorous
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A-HIV
Imminent renal failure Hypoparathroidism Acromegaly Vitamin D intoxication |
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Decreased Phosphorous
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Primary hyperparathyroidism
Mg deficiency Vitamin D deficiency |
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Elevated Calcium
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Hyperparathyroidism
Presence of malignancy Thyrotoxicosis Vitamin D intoxication Sarcoidosis |
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Decreased Calcium
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Renal disease
Vitamin D deficiency Hypoparathyroidism Mg deficiency |
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Increased Magnesium
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Renal failure
Iatrogenic ingestion Adrenal insufficiency |
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Decreased Magnesium
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Decreased intake
Diarrhea Alcoholism Hyperthyroidism SIADH diuretics |
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Normal Albumin values
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3.5 - 5.0
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Albumin
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Normal 3.5 - 5.0
Most abundant protein found in blood plasma; 40-60% of total protein Decreased in : Primary liver disease Tissue damage / inflammation Malnutrition Malabsorption syndrome Renal failure |
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Cardiac Markers
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***
Creatinine kinase CK, CK-MB Troponin |
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CK
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CK level elevation from cardiac muscle, skeletal muscle, CNS injury
***CK-MB specific for cardiac injury Rises 4-6 h; returns to baseline in 36-48 h; troponins may remain elevated for as long as 10 days. |
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Troponin
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Troponin : cardiac regulatory protein that controls the calcium mediated interaction of actin and myosin;
release into serum is related to the degradation of actin and myosin filaments in the area of myocardial damage. ***Troponin is more specific than CK-MB and is the preferred marker for the diagnosis of myocardial injury Rises 4-6 hours after MI ; at least two serial serum levels 6 hours apart are REQUIRED to r/o acute MI in all pts. |
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PLEURA
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A semipermeable membrane composed of mesothelial cells, connective tissue, blood vessels and lymphatics.
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Visceral Pleura
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covers the lung parenchyma
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Parietal Pleura
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adheres to the inner surface of the thoracic cavity; covering the chest wall, diaphragm, and mediastinal structures
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Pleural Space
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The visceral and parietal pleura are separated by a narrow space that is normally filled with 20-30 ml of pleural fluid.
In disease states, the pleural space may fill with air, blood, or fluid. Flows from parietal pleura capillaries into the visceral pleura where it is reabsorbed. Movement of pleural fluid influenced by hydrostatic and oncotic pressures. Hydrostatic forces that filter water out of the vessel are balanced by osmotic forces that reabsorb water back into the vessel |
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PLEURAL FLUID
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Pleural fluid acts as a lubricant allowing the visceral pleura covering the lung to slide easily along the parietal pleura lining the thoracic cavity during respirations.
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Volume of Pleura Fluids
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20-30 ml
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Classifications of Pleura Fluid
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Exudate vs. transudate
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Where does Pleural fluid originates from?
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the systemic vessels of both the parietal and visceral pleural membranes.
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parietal vessels
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The (intercostal microvessels) are thought to be of primary importance because they are closer to the pleural space and have a higher filtration pressure than the bronchial parietal vessels
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Pleural liquid reabsorption
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initially reabsorbed by the microvessels; the remaining fluid exits the pleural space via the lymphatic stomata in the parietal pleura.
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Classic findings of Pleural effusion
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diminished breath sounds.
dullness to percussion. decreased tactile fremitis. |
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Clinical Presentation of Pleural Effusion
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Depends on the cause of effusion and timing of accumulation.
Asymptomatic. Pleuritic chest pain, dyspnea, cough. PE – classic findings: diminished breath sounds, dullness to percussion, decreased tactile fremitis |
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Diagnostic Approach to Pleural Effusion
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Radiographic findings:
blunting of costophrenic angle on upright film. lateral decubitis with affected side down will demonstrate movement of fluid toward dependent area of thorax. loculations: fluid trapped in small cavities caused by pleural adhesions |
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Thoracentesis
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Diagnostic and therapeutic.
no more than 1000-1500 ml should be removed at one time-- to avoid reexpansion pulmonary edema |
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how do you differentiate btwn transudative and exudative effusions
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protein and LDH levels
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Criteria for Dx:
Exudative Effusions |
Must meet one of the following criteria:
pleural fluid protein/serum protein > 0.5 pleural fluid LDH/serum LDH > 0.6 pleural fluid LDH > 200 IU / L |
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Exudative Effusions
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result primarily from pleural and lung inflammation (resulting in a capillary protein leak) or from impaired lymphatic drainage of the pleural space.
Examples: Neoplastic disease Infectious Pulmonary Emboli Gastrointestinal disease Collagen Vascular disease Postcardiac injury syndrome Drug induced Radiation therapy Hemothorax Asbestos exposure |
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Transudative Effusions
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Conditions of increased serum oncotic pressure or increased serum hydrostatic pressure
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Causes of transudative effusions
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Congestive Heart Failure
Cirrhosis Nephrotic Syndrome Myxedema – caused by severe hypothyroidism Uremia Pulmonary Emboli - note: both exudative & transudative |
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Treatment of Pleural Effusions
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Therapeutic or diagnostic thoracentesis.
Treatment of underlying etiology. Pleurodesis – do if pt’s gets recurrent pleural effusion fuses space so they don’t get fluid collections (inject tetracycline) |
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PNEUMOTHORAX
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Defined as air in the pleural space; between the lung and the chest wall
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types of pneumothorax
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Spontaneous (primary or secondary);
Traumatic; Iatrogenic |
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Primary Spontaneous PNEUMOTHORAX
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Usually occurs in young thin males who are otherwise healthy;
Incidence: 1/100,000 females, 7/100,000 males; usually results from rupture of an air containing space (bleb) at or just below the visceral pleura rupture not related to exertional activity or trauma |
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Secondary Spontaneous PNEUMOTHORAX
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occurs as a complication in patients with underlying lung disease;
Incidence: 2/100,000 females; 6/100,000 males; more serious than primary due to danger of decreased pulmonary function in a patient with an already compromised pulmonary state |
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Secondary Spontaneous PNEUMOTHORAX
Etiologies |
COPD
Asthma Pulmonary Infarction Sarcoidosis Carcinoma Tuberculosis Cystic Fibrosis Marfan’s Syndrome Interstitial Lung Disease |
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PNEUMOTHORAX
Clinical Findings |
Acute onset of sharp, localized chest pain and dyspnea; cough, nonproductive;
hypoxemia |
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PNEUMOTHORAX
Physical Exam |
negligible findings on small pneumos;
absence or reduction of breath sounds; decreased tactile fremitis; hyper-resonance to percussion; shifting of trachea to contralateral side (large pneumo) pleural line on chest xray |
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PNEUMOTHORAX
Treatment |
Observation
Supplemental Oxygen Aspiration Tube Thoracostomy Pleurodesis Pneumothorax which occupies under 20% of the pleural cavity usually resolves spontaneously and requires no therapeutic interventions. Pneumothorax over 20% usually requires a thoracostomy tube. |
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Traumatic Pneumothorax
Penetrating trauma |
wound allows air to enter the pleural space directly through the chest wall.
If visceral pleura is penetrated, air enters the pleural space from alveoli |
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Traumatic Pneumothorax
Nonpenetrating trauma |
increased alveolar pressure and rupture secondary to chest compression
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Tension Pneumothorax
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Occurs when intrapleural pressure exceeds atmospheric pressure throughout inspiration and expiration.
Pleural pressure becomes positive causing lung compression, mediastinal shift, and diaphragmatic depression |
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Tension Pneumothorax
Clinical Findings |
Sudden deterioration in patient’s cardiopulmonary status;
patient appears distressed; Rapid, labored respiration; Cyanosis; profuse diaphoresis; marked tachycardia hypoxemia |
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Iatrogenic Pneumothorax
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CAUSED by US:
Transthoracic needle; aspiration; subclavian needle stick; thoracentesis; transtracheal biopsy; pleural biopsy; positive pressure ventilation; CPR |
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What is Interstitial Lung Disease?
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Chronic lung disorder:
Characterized by (PIS) parenchymal damage> inflammation > scarring or fibrosis. Scarring within interstitium causing restrictive defect. Clinical: Cough: chronic (>3 wk), dry & SOB; May be rapid or gradual onset; Course unpredictable |
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ILD Pathophysiology
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1. Begins with parenchymal injury, followed by inflammatory response, collagen deposition, alveolar compromise.
2. Development of restrictive defect: reduction in forced vital capacity; ventilation-perfusion mismatch caused by inflammation and fibrosis of gas-exchanging surfaces (can’t perfuse tissues well). 3. Progressive dyspnea, accompanied by dry cough |
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ILD Common Manifestations
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Cough
Dyspnea Hemoptyisis (often from sinuses or below vocal cords) |
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Chronic cough etiologies
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ABC PPG:
Asthma; Bronchiectasis; Chronic bronchitis – more than 3 episodes in 6 mo; Postinfectious; Postnasal drip; GERD. ABC'S: aspiration Bronchogenic CA Chronic interstitial pneumonia Sarcoidosis |
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Differential Diagnosis ILD
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Environmental:
Silicosis; asbestosis; organic dusts Mining, metal dusts, moldy hay, hypersensitivity exposure Protein sensitivity; animal exposures. Drugs: radiation; chemo; Hydralazine, nitrofurantoin, amiodarone – cause idiopathic rxns. Connective Tissue: SLE; RA; Scleroderma; Polymyositis |
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History for ILDs
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environmental
occupational drug use arthritis |
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PE of ILDs
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nonspecific lung findings;
consolidation vs hyper-resonance. |
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Diagnostic Testing for ILDs
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Oxygen saturation (pulse oximetry);
ABGs - arterial blood gases; Pulmonary function: - Spirometry; - Lung volume measurements; Radiographs (CXR); Bronchoscopy; Bronchoalveolar lavage; CT; labs; Lung biopsy; |
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Pulmonary Function Tests
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Spirometry:
Can distinguish obstructive from restrictive; Provides quantification of the degree of dysfunction; PFT’s classify the degree of impairment |
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Chest X-ray - ILD
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The correlation between radiographic abnormality of the chest and physiologic dysfunction is variable;
****Reticular and nodular opacities are the hallmark; honeycombing: late finding; ***Symmetric hilar adenopathy – widening of mediastinum (Sarcoid) |
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CT Imaging
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CT offers insight into anatomic changes, but does not help evaluate the degree of physiologic impairment.
High resolution shows more subtle interstitial changes |
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Ground glass appearance - CXR
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Ground glass pattern less common
-more favorable finding |
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Reticular pattern - CXR
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most common finding for ILD
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ILD Lab Studies
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Routine labs of limited value:
Rheumatologic; disease/vasculitis; ANA, RF; Antineutrophil cytoplasmic; antibodies (ANCA); Antiglomerular basement membrane (anti-GBM); C-Reactive Protein & Fibrinogen: Increased in restrictive lung disease ; C-reactive protein increased in response to acute and chronic infections; Fibrinogen is an acute phase reactant |
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Differential Diagnosis ILD
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Primary Lung Diseases:
- Sarcoidosis - alveolar Filling Disease - Goodpasture’s syndrome - alveolar hemorrhage - Lupus; Other: - Idiopathic pulmonary fibrosis; - Scleroderma (pulmonary fibrosis); - Wegener’s Granulomatosis - Lymphocytic Interstitial Pneumonia |
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Treatment for ILD
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Corticosteroids;
Immunizations; Oxygen; avoid exposures/meds/tobacco; Lung transplant |
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Scleroderma Progressive Systemic Sclerosis
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Rare disease characterized by diffuse thickening of skin, organ fibrosis;
Telangiectasia and pigment changes; Etiology: autoimmunity, fibroblast disregulation; occupational exposure to silica 90% have Raynaud’s @ 165,000 in US |
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Scleroderma
Systemic features |
Dysphagia;
Hypomotility of GI tract; Pulmonary fibrosis; Cardiac & renal involvement; Localized vs systemic |
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Scleroderma
Localized features |
linear scleroderma;
No organ involvement; Benign |
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Scleroderma
Systemic, Diffuse |
20%;
Rapid progression of organ disease & death |
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Scleroderma
Systemic, Limited |
80%;
**CREST Syndrome - Calcinosis cutis (Ca deposits in skin); - Raynaud’s; - Esophageal involvement; - Sclerodactyly (affecting the digits); - Telangiectasia |
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CREST S/Sx
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Skin tightening limited to hands and face;
Lower risk of renal involvement; Higher risk of pulmonary hypertension; Overall better prognosis |
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Scleroderma
Laboratory |
Mild anemia, may be hemolytic;
Increased ESR; Hypergammaglobulinemia; Proteinuria; ANA frequently positive; Scleroderma antibody |
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Scleroderma
Prognosis |
increased mortality among patients with systemic sclerosis;
- scleroderma patients with severe ILD had a nine-year survival rate of approximately 30 percent; - patients with scleroderma who did not have severe ILD had a nine-year survival rate of 72 percent. The most rapid decline in forced vital capacity (FVC) occurred within the initial three years. |
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Scleroderma
Treatment |
Symptomatic & supportive;
D-Penicillamine - immunomodulatory agent that inhibits the formation of collagen crosslinks. used for over four decades, but its efficacy remains uncertain. No role for systemic steroids; Cyclophosphamide may improve severe lung disease; methotrexate associated with the development of pneumonitis and, rarely, pulmonary fibrosis, (chemo-like tx); Not recommended in the treatment of SS-associated ILD. Lung transplantation option for patients with severe systemic sclerosis associated interstitial lung disease (ILD) that is not responsive to pharmacologic interventions. |
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Sarcoidosis
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Multi-organ disease of unknown cause;
Abnormal immunological response; granulomatous inflammation in affected organs: Lungs (90% of patients), lymph nodes, eyes, skin, liver, spleen, salivary glands, heart, nervous system |
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Sarcoidosis - who gets it
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Third or fourth decade, female> male
**African American > caucasian ** 1 in 2,500 to 1 in 10,000 |
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Sarcoidosis: Clinical presentation
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Cough, dyspnea of insidious onset, chest discomfort
Malaise, fever, organ related c/o; Labs: leukopenia, eosinophilia, inc ESR, hypercalcemia (10%) , hypercalciuria (20%) *** CXR: Bilateral symmetric hilar and paratracheal adenopathy, diffuse reticular infiltrates |
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Sarcoidosis: Dx & Treatment
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Diagnosis by transbronchial lung biopsy or needle node biopsy;
90% response to moderate maintenance corticosteroids; Must rule out other granulomatous diseases: TB, berylliosis |
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Sarcoidosis Stages
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Stage 0: Normal CXR
Stage I: Hilar and mediastinal lymph node enlargement Stage II: Lymphadenopathy and parenchymal disease Stage III: Parenchymal disease only Stage IV: Pulmonary fibrosis Clinical staging is based on the CXR |
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Goodpasture’s Syndrome
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Ideopathic, recurrent alveolar hemorrhage ;
Associated with rapidly progressive glomerulonephritis |
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Goodpasture’s Syndrome - who gets it
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Commonly in men in 30s and 40s
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Goodpasture’s :
Clinical Presentation |
Usual presenting symptom is hemoptysis;
Dyspnea, cough, hypoxemia and diffuse bilaterial alveolar infiltrates typical; Iron deficiency anemia – hemorragic dz; Microscopic hematuria |
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Goodpasture’s :
Radiologic Features |
Radiologic Features:
Nodules, solitary or multiple, may cavitate Bilateral alveolar infiltrates Localized air space disease Reticulonodular interstitial disease Adenopathy Pleural effusions |
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Clinical manifestation of Goodpasture's syndrome
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characterized by the combination of glomerulonephritis and diffuse alveolar hemorrhage accompanied by anti-glomerular basement membrane (GBM) antibodies in serum or tissue.
In >90% of patients with Goodpasture's syndrome, anti-GBM antibodies can be detected in the serum . Only 2% of the patients develop diffuse alveolar hemorrhage without clinically evident renal disease. Typically, young male smokers are affected by Goodpasture's syndrome. |
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Goodpasture’s Syndrome:
Treatment |
Combination immunosuppressive drugs: Methylprednisolone, cyclophosphamide;
Plasmapheresis; Occasionally long-term remissions |
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Wegener’s Granulomatosis - who gets it
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Idiopathic;
Rare: 1 in 50,000; Male: female 3:2; Most common in whites; Age range 3 months to 75 years; Mean onset age 40-45yo; 82% mortality in 1 yr w/o treatment if renal involvement |
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Wegener’s Granulomatosis: pathophysiology
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Pathologic lesions-three types:
1. Aseptic necrotizing granulomatous lesions in mucosa of respiratory tract; 2. Systemic vasculitis of small arteries & veins; 3. Focal necrotizing glomerulonephritis-late sign of progressive disease from inflammatory changes in glomeruli |
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Wegener’s Granulomatosis: Classification
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Variants:
1. Classic - Multiple organs; most extreme form; 2. Limited - One organ or only kidneys; no vasculitis; May resolve or rapidly progress to classic form 3. Granulomatous Lesions - involve multiple organs; may evolve to classic |
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Wegener’s Granulomatosis: Symptoms
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Insidious (years) or acute;
Chronic sinusitis/upper airway most common; Less often pulmonary symptoms (50% presenting, 85% during course); Arthralgias, fever, skin rash, weight loss |
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Wegener’s Granulomatosis: Diff Dx
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Granulomatous disease, SLE, polyarteritis, other vasculitides;
Infectious, neoplastic, autoimmune disorders; High index of suspicion with patients presenting with nonspecific or nonresolving physical complaints |
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Wegener’s Granulomatosis: Dx
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Tissue biopsy:
Demonstrating vasculitis and granulomas; Laboratory: Leukocytosis, normocytic-normochromic anemia, thrombocytosis, elevated ESR, C-reactive protein with immune complexes - Kidney involvement: - - Urine: hematuria & RBC casts; Imaging: Sinus and chest x-rays to rule out active disease CT: extent of inflammatory changes, soft-tissue and bony destruction; MRI: to define soft-tissue abnormalities |
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Wegener’s Granulomatosis
Treatment |
Daily high-dose corticosteroids until active disease abated;
Low-dose cyclophosphamide (Cytoxan)[chemo agent] until 1 year after remission; Morbidity and mortality associated with treatment |
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Wegener’s Granulomatosis
Prognosis |
Remission 75-95% with early recognition and treatment
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Lymphocytic Interstitial Pneumonitis
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uncommon disease entity characterized by infiltration of the interstitium and alveolar spaces of the lung by lymphocytes, plasma cells, and other lymphoreticular elements
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Lymphocytic Interstitial Pneumonitis - who gets it
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adults - rare; LIP occurs most commonly in women (2 to 1 female to male ratio), usually between the ages of 40 and 70 years (median age 56 years).
children (esp with AIDS) - increasing |
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LIP Etiology
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Up to three fourths of patients have a serum protein abnormality.
autoimmune etiology for LIP given its association with autoimmune processes . A possible infectious (especially viral) etiology for LIP is suggested by its marked increased incidence in persons infected with the HIV virus, especially children reports of improvement with antiviral therapy alone . The Epstein-Barr virus (EBV) has been associated with lymphoproliferative disorders in immunosuppressed populations. post-transplant ; lymphoproliferative disorder has a strong relationship to the EB virus. |
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LIP Clinical Presentation
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slow progression:
Cough - 71%; Dysnpea - 61% Weight loss (16 percent); Fevers (10 percent) ; Pleuritic chest pain (6 percent); Fatigue ; Arthralgias |
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LIP PE
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Lung exam - rales;
Digital clubbing - 10%, cyanosis - rare. Other findings often depend upon the presence of another underlying disease process and include: hepatosplenomegaly, lymphadenopathy, parotid gland enlargement, and arthritis |
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LIP CXR
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varied radiographic appearance - basilar reticular opacities or as a nodular process.
alveolar spaces become involved, and a mixed pattern of interstitial and alveolar opacities appears. Nodular disease appears to be more common in patients with HIV. Honeycomb changes may be seen in endstage disease |
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LIP CT
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Ground-glass attenuation, centrilobular nodules, and interstitial thickening are frequently seen.
Lung cysts are common in patients with LIP, Pleural thickening and effusions are rare in LIP, as are hilar and mediastinal lymphadenopathy, which suggest an underlying malignant process. |
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LIP PFT’s
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Pulmonary function testing characteristically shows reduced lung volumes and diffusing capacity with preserved airflow.
Marked gas exchange abnormalities and hypoxemia also occur |
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LIP Treatment
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Corticosteroid therapy alone or in combination with other agents has been used to treat symptomatic patients with LIP
efficacy has not been established in a controlled trial. Treat for 6 mos – 1 year. Antiviral agents has shown limited success in children with HIV-associated LIP |
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Summary Health Maintenance for Interstitial Lung Dzs
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Smoking cessation;
Immunizations: DPT, polio, MMR, H flu b, varicella, Influenza, Pneumococcal; Screening for early detection; CXR after pneumonia in smokers or > 40yo; hx of TB Pulmonary rehabilitation |
