4 Flashcards
(500 cards)
1
Q
What is the most accurate test for Wegener granulomatosis?
A
The most accurate test for WG is a biopsy of the kidney or lung looking for granulomas. Biopsy of the nasal septum is less sensitive and has more false negative results.
2
Q
What is the treatment of Wegener’s granulomatosis?
A
Cyclophosphamide and steroids.
3
Q
What is Churg–Strauss syndrome?
A
Characterized by lung involvement, neuropathy, skin lesions, GI, cardiac, and renal involvement.
4
Q
What is the presentation of Churg–Strauss syndrome?
A
Fever, weight loss, malaise. Asthma, eosinophilia, atopic diseases. Elevated eosinophil, positive P–ANCA or antimyeloperoxidase. Most accurate test is lung biopsy: granulomas, eosinophils.
5
Q
What is the treatment of Churg–Strauss syndrome?
A
Glucocorticoids and cyclophosphamide.
6
Q
What is Goodpasture syndrome?
A
Idiopathic disorder of renal and lung disease characterized by a unique anti–basement membrane antibody. GP does not affect multiple organs or sites in the body other than the lung and the kidney.
7
Q
What are the clinical signs of Goodpasture syndrome?
A
Hematuria, proteinuria, hemoptysis, cough, dyspnea. Best test is anti–basement membrane Ab to type IV collagen. Lung or kidney biopsy shows hemosiderin macrophages and linear deposits.
8
Q
What is the treatment of Goodpasture syndrome?
A
Plasmapheresis and steroids. Cyclophosphamide.
9
Q
What is polyarteritis nodosa?
A
Systemic vasculitis of small and medium arteries of every organ exception lung. Renal involvement manifests as HTN, renal insufficiency, and hemorrhage due to microaneurysms. Biopsy.
10
Q
What is the treatment of polyarteritis nodosa?
A
Cyclophosphamide and steroids.
11
Q
What are the symptoms of polyarteritis nodosa?
A
Fever, weight loss, malaise. Involvement of skin, eyes, muscles, GI, heart, kidneys, and neurologic system. Abdominal pain and joint pain. Anemia and an elevated sedimentation rate.
12
Q
What is the treatment of polyarteritis nodosa?
A
Steroids and cyclophosphamide.
13
Q
What is Henoch–Schönlein purpura?
A
Systemic deposition of IgA, resulting in renal insufficiency, skin lesions, GI symptoms.
14
Q
What is the tetrad of Henoch–Schönlein purpura?
A
Tetrad of palpable purpura, arthralgias, abdominal pain, and renal disease. IgA deposited in walls of blood vessels. Biopsy is usually not performed. HSP most often resolves spontaneously.
15
Q
What is the treatment of Henoch–Schönlein purpura?
A
Treatment is supportive. Steroids can be used.
16
Q
What is IgA nephropathy (Berger disease)?
A
IgA nephropathy with mild hematuria that resolves spontaneously in 30%. About 40–50% of patients progress to end stage renal disease. Deposition of IgA only in kidney.
17
Q
What are the signs of Berger disease?
A
HTN. Usually an Asian patient under 35 years of age who has had a recent viral illness or pharyngitis, then develops hematuria 1–2 days later.
18
Q
How is Berger disease diagnosed?
A
The diagnosis is based on finding IgA deposited in the kidney on biopsy.
19
Q
What is the treatment of Berger disease?
A
Proteinuria is treated with ACE inhibitors or angiotensin receptor blockers (ARB).
20
Q
What are the causes of postinfectious glomerulonephritis?
A
Group A beta–hemolytic streptococci (S pyogenes) and other infections can cause postinfectious glomerulonephritis. Any infectious agent, including hepatitis B and C, CMV, staph endocarditis.
21
Q
What type of infection can cause post–streptococcal glomerulonephritis?
A
Poststreptococcal glomerulonephritis can occur with throat or skin infection with S pyogenes. Rheumatic fever only occurs after pharyngitis in 10–15% of patients with GABS pharyngitis.
22
Q
What are the signs of postinfectious glomerulonephritis?
A
Smoky, cola urine from hematuria, red cell casts, proteinuria. Periorbital edema and HTN. The best initial test is antistreptolysin (ASO) and the antihyaluronic acid. Complement low. Renal biopsy rarely.
23
Q
What is the treatment of postinfectious glomerulonephritis?
A
Treatment is management of fluid overload and HTN with diuretics. Resolves spontaneously. Antibiotics should be given to eradicate the organism from the pharynx.
24
Q
What are thrombotic thrombocytopenic purpura and hemolytic uremic syndrome?
A
TTP and HUS are two different varieties of the same disease of hemolytic anemia, uremia, and thrombocytopenia.
25
What are the causes of thrombotic thrombocytopenic purpura and hemolytic uremic syndrome?
TTP is associated with HIV, but it is most often idiopathic. HUS is more common in children and with E. coli 0157:H7 food poisoning.
26
What is the triad of hemolytic uremic syndrome?
HUS is a triad of hemolytic anemia, uremia, and thrombocytopenia.
27
What are the signs of thrombotic thrombocytopenic purpura?
TTP has anemia, uremia, and thrombocytopenia, and is also associated with fever and headache, confusion, seizures, focal deficit.
28
What are the laboratory findings in hemolytic uremic syndrome and thrombotic thrombocytopenic purpura?
Anemia is intravascular, and the blood smear shows schistocytes, helmet cells, fragmented red cells. LDH and reticulocyte count will be elevated and the haptoglobin decreased.
29
What is the treatment of thrombotic thrombocytopenic purpura and hemolytic uremic syndrome?
Plasmapheresis. Dipyridamole may preventing platelet aggregation in TTP. Antibiotics contraindicated in HUS; organism releases toxins. Administering platelets will worsen CNS and renal.
30
What is Alport syndrome?
Glomerular disease with anterior lenti conus (lens protrusion), and sensorineural hearing loss.
31
What is idiopathic rapidly progressive glomerulonephritis?
RPGN may occur with any glomerular disease. Idiopathic form is associated with crescent formation in the kidney, which is ANCA negative. Diagnosis is with renal biopsy.
32
What us the treatment of idiopathic rapidly progressive glomerulonephritis?
Treatment is with steroids and cyclophosphamide.
33
What is amyloid?
Amyloid is a proteinaceous material associated with chronic infectious or inflammatory conditions, such as rheumatoid arthritis, inflammatory bowel disease, or myeloma.
34
How does amyloidosis affect the organs?
Amyloid builds up in kidney, causing glomerulonephritis, accumulates in GI, nerves, muscles. Restrictive cardiomyopathy, rhythm disorders, heart block. Macroglossia, carpal tunnel, malabsorption.
35
How is amyloidosis diagnosed?
Biopsy of the involved organ, such as the kidney. Congo red testing shows green birefringence. Amyloidosis treatment consists of controlling the underlying disease. Melphalan and prednisone.
36
What is nephrotic syndrome?
Renal disease sufficient to cause proteinuria \>3.5 gm/24 h, hyperlipidemia, edema, and a low serum albumin.
37
What are the causes of nephrotic syndrome?
1/3 nephrotic syndrome associated diabetes, HTN, myeloma. Glomerulonephritis becomes nephrotic syndrome if massive proteinuria, low albumin. Nephrotic syndrome describes severity, not etiology.
38
What are the signs of nephritic syndrome?
Hyperlipiduria with droplets in shape of Maltese crosses in urinalysis. Hypercoagulability from urinary loss of anticoagulant proteins. Arterial or venous thrombosis.
39
How is nephrotic syndrome diagnosed?
High protein in urine, low protein in blood, edema, hyperlipidemia. 24–hour urine protein \>3.5 gm. A protein:creatinine ratio of \>3.5 on a single urine. The most accurate test is a renal biopsy.
40
What is the treatment for nephrotic syndrome?
Control the underlying disease. Steroids, cyclophosphamide, mycophenolate, azathioprine. ACE inhibitors or ARBs are used for all patients with proteinuria.
41
What are the causes of proteinuria?
Microalbuminuria is 30–300 mg/24 h. Mild amounts of proteinuria
42
What are the causes of hematuria?
Nephrolithiasis, cancer, bleeding disorders, trauma, cyclophosphamide (hemorrhagic cystitis). Cystitis or prostatitis. The red cells become dysmorphic in glomerular disease.
43
What is the cause of nitrites on urinalysis?
Gram–negative bacteria reduce nitrate to nitrite.
44
What is the significance of asymptomatic bacteriuria?
The isolated finding of bacteria in the urine in pregnant women should be treated. About 30% of pregnant women with bacteriuria progress to pyelonephritis.
45
What is the significance of hyaline casts in the urinalysis?
Dehydration. These casts develop as an accumulation of the normal amount of tubular protein. Hyaline casts may occur in normal persons.
46
What is the significance of red cell casts on the urinalysis?
Glomerulonephritis
47
What is the significance of broad, waxy casts in the urinalysis?
Chronic renal failure
48
What is the significance of granular casts in the urinalysis?
Also called dirty or muddy. They are associated with acute tubular necrosis and represent accumulated epithelial cells.
49
What is the significance of white cell casts in the urinalysis?
Pyelonephritis, interstitial nephritis.
50
What are the most common causes of end stage renal disease that require dialysis?
Diabetes and HTN. Glomerulonephritis is the etiology of about 15%, with cystic disease and interstitial nephritis, causing 4–5% each.
51
What are the indications for dialysis?
Life–threatening abnormalities that cannot be corrected, such as fluid overload refractory to diuretics. Acidosis, pericarditis, encephalopathy, neuropathies, hyperkalemia, persistent nausea, vomiting, bleeding.
52
What type of dialysis is used most frequently?
Hemodialysis is used in 85% of patients and peritoneal dialysis in 15%. The most common complication of peritoneal dialysis is peritonitis.
53
What is the cause of anemia in end–stage renal disease?
Decreased erythropoietin from the kidney. Treated with replacement of erythropoietin. The anemia of ESRD is normochromic and normocytic.
54
What is the cause of hypocalcemia/hyperphosphatemia in end–stage renal disease?
Loss of 1,25–dihydroxyvitamin D. Hyperphosphatemia is from inability of kidneys to excrete PO4. High PO4 contributes to low Ca by precipitating out in tissues in combination with the calcium.
55
What is the treatment of hyperphosphatemia in renal disease?
High phosphate levels are treated with phosphate binders, such as calcium carbonate or calcium acetate.
56
What is the treatment of hyperphosphatemia with hypercalcemia?
Sevelamer and lanthanum are phosphate binders. Used when calcium is high because of vitamin D. Aluminum–containing binders should not be used because associated with dementia and bone abnormalities.
57
What is osteodystrophy of end–stage renal disease?
Osteitis fibrosa cystica occurs because kidneys fail to produce 1,25 vitamin D. Low Ca leads to hyperparathyroidism, which removes Ca from bones. Controlled by increasing calcium levels.
58
What is the treatment of hypermagnesemia in renal insufficiency?
Magnesium accumulates because of decreased renal excretion. Treatment is restriction of magnesium intake.
59
What is the effect of end–stage renal disease on the cardiovascular system?
HTN, accelerated atherosclerosis, coronary artery disease. This is the most common cause of death for patients on dialysis. Goal BP is
60
What is the effect of end–stage renal disease on the immune system?
Increased infection because WBCs do not function in uremia. Infection is the second most common cause of death in dialysis patients. Most common organism is Staphylococcus.
61
What is the effect of end–stage renal disease on the coagulation system?
Bleeding occurs because uremic platelet dysfunction. Bleeding treated with desmopressin, which releases subendothelial von Willebrand factor and factor VIII, which increases platelet adherence.
62
What is the dietary treatment for severe renal disease?
Diet restricted in potassium, sodium, protein, magnesium, and phosphate.
63
What is hyponatremia?
Hyponatremia is defined as a low serum sodium
64
What is the formula for serum osmolality?
Serum osmolality is largely a function of the serum sodium level. Serum osmolality = (2 x sodium) + BUN/2.8 + glucose/18. When the glucose and BUN are normal, this equation becomes 2 x sodium + 10.
65
What is the presentation of hyponatremia?
Neurologic symptoms range from mild confusion and memory loss to disorientation and obtundation to seizure or coma, depending on the severity.
66
What factor is associated with hyponatremic seizures?
Symptoms depend on rate of decline. Acute 15–20 point drop can result in a seizure or coma. If the level drops gradually, the patient can sustain an extremely low sodium. There should be no symptoms unless below 125.
67
What is the treatment of mild hyponatremia?
Mild asymptomatic hyponatremia should resolve with fluid restriction.
68
What is the treatment of moderate hyponatremia?
Moderate hyponatremia can be managed with normal saline administration combined with a loop diuretic such as furosemide. The saline provides sodium, and the loop diuretic causes a net free water loss.
69
What is the treatment of severe hyponatremia?
3% hypertonic saline. Severe symptoms do not occur unless Na
70
What is the maximum rate of correction of severe hyponatremia?
Hyponatremia can be corrected as rapidly as 2 mEq per hour if the patient is having seizures. Fludrocortisone is given for cerebral salt wasting disease.
71
What is pseudohyponatremia?
Na level is artificially low because of hyperglycemia. Na is decreased by 1.6 mEq/L for every 100 increase in glucose. Glucose load causes a transcellular shift of water. Hyperlipidemia causes low Na.
72
What hypervolemic states (increased ECF) are associated with hyponatremia?
There is a decrease in intravascular volume resulting in an increase in ADH secretion from the posterior pituitary in congestive heart failure; nephrotic syndrome and low albumin states; and cirrhosis
73
What is the cause of hyponatremia in renal insufficiency?
When renal failure becomes advanced, the impaired free water excretion will reduce the sodium level and result in hypervolemia.
74
What is the cause of hyponatremia in hypovolemic states?
Loss of sodium through body fluids and replacement with free water. Sweating and replacement only with free water causes the sodium level to drop.
75
What are the gastrointestinal causes of hyponatremia?
Vomiting, diarrhea, gastric suction; hypovolemia.
76
What are the causes of sodium loss through the skin?
Skin loss: burns, sweating with replacement with free water, cystic fibrosis.
77
How does renal failure cause renal sodium loss?
The kidney can lose the ability to reabsorb sodium in the proximal convoluted tubule as the kidney is damaged. Damaged tubules cannot reabsorb sodium and hypovolemia results.
78
How does adrenal insufficiency (Addison disease) cause hyponatremia?
Aldosterone reabsorbs sodium from the kidney. Without aldosterone, sodium is lost.
79
What are the causes of hypovolemic hyponatremia with a urine sodium
Dehydration, vomiting, diarrhea, sweating
80
What are the causes of hypovolemic hyponatremia with a urine sodium \>10?
Diuretics, ACE inhibitors, renal salt wasting, Addison disease, cerebral sodium wasting
81
What are the causes of euvolemic hyponatremia?
Psychogenic polydipsia with \>15–20 liters/d. Hypothyroidism. Diuretics: can be both hypovolemic and euvolemic. ACE inhibitors. Endurance exercise. Syndrome of inappropriate secretion of ADH.
82
What are the causes of syndrome of inappropriate secretion of ADH (SIADH)?
CNS infections, stroke, tumor, trauma, vasculitis, pain, pneumonia, TB, PE, asthma. Lung CA, pancreas CA. SSRIs, tricyclics, haloperidol, cyclophosphamide, vincristine, carbamazepine.
83
How is syndrome of inappropriate secretin of antidiuretic hormone diagnosed?
Neurologic symptoms; elevated urine osmolality and elevated urine sodium. If the urine osmolality is \>100 Osm/L in the presence of hyponatremia, the person has SIADH. Elevated ADH level.
84
What is the treatment of SIADH?
Restrict fluids. Give hypertonic saline for severe disease. Normal saline with a loop diuretic. For chronic disease, demeclocycline or lithium to inhibit the effect of ADH on the kidney tubule.
85
What are the insensible causes of hypernatremia?
Insensible losses: extrarenal loss of water without intake of hypotonic fluids; increased skin loss of water (sweating, burns, fever, exercise) or respiratory infections
86
What are the gastrointestinal causes of hypernatremia?
Osmotic diarrhea (e.g., lactulose, malabsorption), infectious diarrhea. Transcellular shift caused by Rhabdomyolysis or seizures can cause muscles to take up water and Na.
87
What are the renal causes of hypernatremia?
Nephrogenic diabetes insipidus (NDI), causing by renal disease, increased calcium, decreased potassium, lithium, demeclocycline, sickle cell disease, and others
88
What are the causes of central diabetes insipidus?
Idiopathic, trauma, infectious, tumor, granulomatous, hypoxic brain damage or neurosurgical brain injury. Idiopathic most common.
89
What types of osmotic diuresis can cause hypernatremia?
Osmotic diuresis: diabetic ketoacidosis (DKA), nonketotic hyperosmolar coma, mannitol, diuretics.
90
What are the signs of hypernatremia?
Lethargy, weakness, irritability, seizures, and coma are present with severe hypernatremia of any cause. Diabetes insipidus causes a dilute diuresis of 3–20 L per day.
91
How is central diabetes insipidus distinguished from nephrogenic diabetes insipidus?
Decrease in urine volume after administering ADH distinguishes central diabetes insipidus from NDI.
92
What is the treatment of acute hypernatremia?
IV isotonic saline. Correction should not be \>1 mEq every 2 h or 12 mEq/d. 1 mEq/h is acceptable if the patient is having seizures.
93
What are the complications of overly rapid correction of hypernatremia?
Complications of overly rapid correction include cerebral edema, permanent neurologic damage, or seizures.
94
What is the treatment of central diabetes insipidus?
Correct the underlying cause. Give vasopressin (ADH) subcutaneously, intravenously, intramuscularly, or by nasal spray.
95
What is the treatment of nephrogenic diabetes insipidus?
Correct underlying cause if possible. Diuretic or NSAIDs. NSAIDs function by inhibiting prostaglandins, which impair concentrating ability. NSAIDs will increase the action of ADH at the kidney.
96
What are the gastrointestinal causes of hypokalemia?
Gastrointestinal losses can be from vomiting, diarrhea, or tube drainage.
97
What types of transcellular shift can cause hypokalemia?
Increased entry into cells can be from alkalosis, increased levels of insulin, beta adrenergic, and the replacement of B12. Trauma causes increased beta adrenergic activity.
98
What are the causes of urinary potassium losses?
Diuretics. Increased aldosterone states, such as Conn, licorice, Bartter, or Cushing. Aldosterone is the most important regulator of potassium. Renal artery stenosis. Hypomagnesemia will cause potassium loss.
99
What is the presentation of hypokalemia?
Affects muscles and the heart. Weakness, paralysis, fatal arrhythmias, rhabdomyolysis. Potassium is necessary for ADH effect on the kidney, and hypokalemia causes nephrogenic diabetes insipidus.
100
What are the ECG signs of hypokalemia?
T–wave flattening and U–waves. A U–wave is an extra wave after the T–wave caused by Purkinje fiber repolarization.
101
What is the treatment of hypokalemia?
Correct the underlying cause. IV potassium maximum 10–20 mEq/h; do not use dextrose containing fluids, because dextrose causes increase insulin release and lower potassium.
102
What are the complications of excessively rapid repletion of potassium?
Fatal arrhythmia. Idioventricular rhythm, asystole.
103
How many mEq of potassium is needed to raise the potassium level by one point?
Very large amounts of potassium may be necessary to raise the body potassium level by 1 or 2 points. The total body requirement is to give 4–5 mEq per kg per point.
104
What are the causes of hyperkalemia related to movement of K+ from cells to extracellular fluid?
Pseudohyperkalemia: venipuncture, platelets \>1,000,000, WBC \>100,000. Acidosis. Insulin deficiency. Rhabdomyolysis, tumor lysis, seizures, exercise. Periodic paralysis: weakness, hyperK, family history.
105
What is the relationship between pH and potassium level?
H+ moves into cells, K+ out. For every 0.1–point decrease in the pH, the potassium level will increase by 0.7 points because of the transcellular shift.
106
What are the renal causes of hyperkalemia?
Renal failure. Hypoaldosteronism: ACE inhibitors, type IV RTA, adrenal enzyme deficiency; heparin. Primary adrenal insufficiency (Addison) or adrenalectomy. K–sparing diuretics. NSAIDs.
107
What is the presentation of hyperkalemia?
Muscular weakness can begin usually with K+ levels \>6.5.Abnormal cardiac conduction is the most common cause of death, hypoventilation.
108
How is hyperkalemia diagnosed?
ECG findings: peaked T waves, widened QRS, short QT, or prolonged PR interval.
109
What is the acute treatment of hyperkalemia?
Calcium chloride one ampule for membrane stabilization. Effect is immediate and short lived. Bicarbonate one ampule. Do not give in same IV line as calcium. Glucose one ampule and insulin, takes 30 min.
110
What is the non–acute treatment of hyperkalemia?
Furosemide, beta agonists. Cation exchange resin (Kayexalate) absorbs 1 mEq K+/gm. Given with sorbitol. Kayexalate can also be given as a retention enema. Dialysis.
111
What are the causes of distal renal tubular acidosis (type I)?
Sporadic. Also caused by Sjögren, SLE. Amphotericin, lithium, analgesics, cyclophosphamide. Nephrocalcinosis, sickle cell, chronic infection. Familial, chronic hepatitis.
112
What is the presentation of distal renal tubular acidosis (type I)?
Inability to concentrate H+ in urine. Urine pH is \>5.4. Secondary hyperaldosteronism and hypokalemia. Nephrocalcinosis and nephrolithiasis.
113
How is distal renal tubular acidosis (type I) diagnosed?
Acid load test; give ammonium, which should lower urine pH. With type I RTA, urine pH remains elevated. Bicarbonate
114
What is the treatment of distal renal tubular acidosis (type I)?
Oral bicarbonate is the treatment because bicarbonate reabsorption in the proximal tubule remains intact; potassium replacement.
115
What are the causes proximal (type II) renal tubular acidosis?
Fanconi, Wilson, amyloidosis, myeloma, acetazolamide, vitamin D deficiency, secondary hyperparathyroidism, hypocalcemia, heavy metals, hepatitis, SLE and Sjögren syndrome.
116
What is the presentation of proximal (type II) renal tubular acidosis?
Inability to absorb bicarbonate. Urine pH is basic. Hypokalemia and bicarbonate of 18–20, and malabsorption of glucose, phosphate, urate, amino acids. Bone lesions (osteomalacia and rickets).
117
How is proximal (type II) renal tubular acidosis diagnosed?
Patients are have a basic urine in the presence of acidemia.
118
What is the treatment of proximal (type II) renal tubular acidosis?
Give potassium; mild volume depletion will enhance proximal bicarbonate reabsorption. Thiazide diuretics and very large amounts of bicarbonates.
119
What are the causes of hyporeninemic/hypoaldosteronism (type IV renal tubular acidosis)?
An aldosterone deficiency of any cause or adrenal insensitivity to angiotensin II, diabetes (50%), Addison disease, sickle cell disease, renal insufficiency.
120
What is the presentation of hyporeninemic/hypoaldosteronism (type IV renal tubular acidosis)?
Usually asymptomatic hyperkalemia. Mild to moderate renal insufficiency. Hyperchloremic metabolic acidosis (nonanion gap).
121
How is hyporeninemic/hypoaldosteronism (type IV) diagnosed?
Presence of high urine sodium with oral salt restriction establishes the diagnosis.
122
What is the treatment of hyporeninemic/hypoaldosteronism (type IV)?
Administration of fludrocortisone. Fludrocortisone has a high degree of mineralocorticoid effect and is similar to administering aldosterone.
123
What is the relationship of serum bicarbonate and pCO2?
For every 1–point increase in the level of serum bicarbonate, there is a 0.7–point increase in pCO2. Dehydration results in increased aldosterone, which leads to metabolic alkalosis.
124
What are the causes of alkalosis from H+ ion loss?
Exogenous steroids. GI loss (vomiting, nasogastric suction). Renal loss (Conn syndrome, Cushing, ACTH overproduction, licorice, Bartter syndrome). Decreased chloride intake. Diuretics.
125
What are the causes of alkalosis from HCO3 retention?
Bicarbonate administration. Contraction alkalosis. Milk–alkali syndrome?
126
What is the cause of alkalosis from H+ movement into cells?
Hypokalemia.
127
What are the respiratory causes of alkalosis?
Hyperventilation, pulmonary embolus, sarcoid, anxiety, pain. Progesterone, catecholamines, hypoxia, cirrhosis, pregnancy, and salicylates.
128
What are the causes of acidosis (low pH) with a low anion gap?
Myeloma, low albumin level, lithium.
129
What is the formula for anion gap?
Anion gap = (Na + K) – (HCO3 + Cl) Normal: 8–14. Na+ and cations = HCO3– and Cl– and anions
130
What are the causes of a normal anion gap acidosis?
Diarrhea, renal tubular acidosis, ureterosigmoidostomy.
131
What are the causes of an increased anion gap acidosis?
Lactate (sepsis, ischemia). Aspirin. Methanol. Uremia. Diabetic ketoacidosis. Paraldehyde, Propylene glycol. Isopropyl alcohol, INH. Ethylene glycol (antifreeze), low calcium.
132
What are the causes of respiratory acidosis?
Hypoventilation, chronic obstructive pulmonary disease (COPD), Pickwickian, obesity, suffocation, opiates, sleep apnea, kyphoscoliosis, myopathies, neuropathy, effusion, aspiration.
133
What are the causes of nephrolithiasis?
1–5% of the population. Calcium oxalate stones in 70%. Calcium phosphate in 10%. Mg/Aluminum/phosphate (Struvite) 5%. Uric acid 5%. Cysteine 1%. Indinavir.
134
What are the causes of hypercalciuria?
Vitamin D intoxication with sarcoid and granulomatous disease. Familial. Idiopathic renal hypercalciuria. Hyperparathyroidism (10%). Multiple myeloma, metastatic disease to bone, hypercalcemia of malignancy.
135
What are the causes of hyperoxaluria?
Primary familial, enteric hyperoxaluria (chronic diarrhea causes excessive absorption of oxalate).
136
What complication may result from hypocitraturia?
Citrate binds calcium and prevents calcium absorption. Low citrate leads to increase in calcium absorption and kidney stones. Causes of hypocitraturia: renal tubular acidosis; chronic diarrhea, thiazides.
137
What are the causes of uric acid stones?
Uric acid stones are associated with diseases like gout, hematologic malignancies, and Crohn disease. Radiolucent on x–rays.
138
Infection with which organisms can cause struvite kidney stones?
Urinary infection with urease–producing organisms like Proteus, Staphylococcus, Pseudomonas, and Klebsiella causes a highly alkaline urine that produces struvite stones.
139
What is the presentation of nephrolithiasis?
Constant flank pain (not colicky), hematuria, and pain radiating to groin. Stones
140
How is nephrolithiasis diagnosed?
Ultrasound. Strain the urine. Serum and urine calcium. Helical (spiral) CT scan is the best test. No contrast needed for stones. Plain x–ray (80% yield) is rarely used. Intravenous pyelogram is not done.
141
What is the treatment of nephrolithiasis?
Analgesia, hydration, and bed rest. Shockwave lithotripsy for stones
142
What is the presentation of adult polycystic kidney disease?
Flank pain, hematuria (micro and gross), infections, and calculi. Genetic. Hepatic cysts (40–60%), colonic diverticula, HTN (50%), intracranial aneurysm (10–20%), mitral valve prolapse (25%).
143
How is adult polycystic kidney disease diagnosed?
Ultrasound and CT scan.
144
What is the treatment of adult polycystic kidney disease?
Management of complications (UTI, calculi, and hypertension).
145
What are simple renal cysts?
Very common; if smooth–walled with no debris in cyst, no treatment necessary. Cysts with irregular walls or debris inside should be aspirated to exclude malignancy. Dialysis causes cysts.
146
What is essential hypertension?
A systolic blood pressure of 140 mm Hg or a diastolic \>90 on multiple readings in the absence of a specific, identifiable underlying cause.
147
What is the criteria for hypertension in patients with diabetes or renal disease?
Any blood pressure above 130/80 mm Hg is defined as hypertension.
148
What is the treatment of stage 2 hypertension?
Patients with stage 2 hypertension (blood pressure \>160/100 mm Hg), should receive initial therapy with two medications.
149
What is the criteria for normal BP?
120/80 mm Hg.
150
What is the criteria for pre–hypertension?
Systolic 120–139. Diastolic 80–89 mm Hg.
151
What is the criteria for stage 1 hypertension?
Systolic 140–159. Diastolic 90–99 mm Hg?
152
What is the criteria for stage 2 hypertension?
Systolic \>160. Diastolic \>100 mm Hg.
153
What is a hypertensive emergency?
HTN with stroke, subarachnoid hemorrhage, encephalopathy, myocardial ischemia, retinopathy. Requires substantial reduction of blood pressure within one hour.
154
What are the symptoms of a hypertensive emergency?
Headache, dizziness, chest pain, dyspnea, blurred vision, and palpitations. Malignant HTN is defined as encephalopathy or nephropathy.
155
What are the long–term cardiac complications of hypertension?
Myocardial ischemia or infarction, congestive heart failure, left ventricular hypertrophy, aortic aneurysm, and dissection. S4 gallop, accentuated A2 heart sound, and prominent left ventricular impulse.
156
What are the long–term cerebrovascular complications of hypertension?
Transient ischemic attack (TIA) and stroke.
157
What are the long–term renal complications of hypertension?
Proteinuria, microscopic hematuria, and elevation of BUN/creatinine.
158
What are the long–term ocular complications of hypertension?
Retinopathy: Hemorrhages, exudates, arteriolar narrowing, and papilledema. Blurred vision, scotomata, and blindness.
159
What are the signs of secondary hypertension?
160
How is hypertension diagnosed?
Allow the patient to sit 5 min before BP measured. Should not diagnose HTN after only a single reading. Repeat the reading 3–6 times over several months before confirming diagnosis and initiating therapy.
161
What basic studies are obtained in the evaluation of hypertension?
Urinalysis for protein, glucose, and red blood cells. Hematocrit. Potassium to exclude hyperaldosteronism. Serum creatinine and BUN. ECG to evaluate for left ventricular hypertrophy. Glucose and lipid analysis.
162
What is the lifestyle modification for essential hypertension?
Weight reduction, sodium restriction, aerobic exercise, avoid alcohol. Low–fat, increased fiber. Severe HTN (diastolic \>100 mm Hg) should be start drug therapy with 2 medications.
163
What is the drug treatment of essential hypertension?
If DBP \>90 despite a 3–months nonpharmacologic, start antihypertensive. Diuretics are initial treatment. For stage 2 HTN, BP \>160/100, use a diuretic with an ACE/ARB/calcium–blocker or beta–blocker.
164
What medication should be added if a diuretic dose not control the patient's blood pressure?
If diuretics do not control BP, then add a beta–blocker, calcium–blocker, ACE inhibitor, or angiotensin–receptor blocker. beta–Blockers avoided in asthma, COPD, heart block, or depression.
165
What is the initial antihypertensive for diabetics?
Diabetics should be treated with ACEI or ARBs, which prevent nephropathy. BP goal in a diabetic is lower, at
166
What is the initial antihypertensive for patients who have ischemic heart disease?
After a myocardial infarction (ischemic heart disease), beta–blockers should be started.
167
What is the initial antihypertensive for patients with decreased left–ventricular systolic function?
Decreased left–ventricular systolic function (congestive heart failure or postmyocardial infarction) should receive ACE inhibitors and beta blockers.
168
Which antihypertensive should be avoided in African American patients?
African American patients are least effectively treated with ACE inhibitors.
169
What are the initial antihypertensive choices for pregnant patients?
Alpha–methyldopa, labetalol, hydralazine, or calcium blockers. ACE inhibitors and angiotensin–receptor blockers are contraindicated in pregnancy. Diuretics are relatively contraindicated.
170
What is a hypertensive emergency?
The acute onset of severe hypertension with severe and rapidly worsening symptoms of end–organ damage. This usually happens with a diastolic pressure \>120–130 mm Hg.
171
What are the neurologic manifestations of hypertensive emergencies?
Encephalopathy, headache, confusion, seizures, and subarachnoid or intracerebral hemorrhage.
172
What are the cardiac manifestations of hypertensive emergencies?
Chest pain, myocardial infarction, palpitations, dyspnea, pulmonary edema, jugular venous distension, and gallops.
173
What are the renal manifestations of hypertensive emergencies?
Nephropathy: Acutely progressive hematuria, proteinuria, and renal dysfunction.
174
What are the retinal manifestations of hypertensive emergencies?
Retinopathy: Papilledema, hemorrhages, and blurred vision.
175
What is the laboratory evaluation for hypertensive emergencies?
The laboratory evaluation is the same as with essential hypertension. CT scan of the head to exclude hemorrhage. ECG is as an initial test to exclude myocardial infarction.
176
What is the treatment of hypertensive emergencies?
Intravenous nitroprusside and labetalol are the two best agents. Nitroglycerin if myocardial ischemia. Enalaprilat is IV ACEI. Initial goal is to reduce BP by no more than 25% within the first 1 to 2 hours.
177
What is secondary hypertension?
HTN with underlying cause. 5% of cases of HTN are caused by an identifiable underlying cause. Renal artery stenosis is the most common of these causes.
178
Which patients should be screened for secondary hypertension?
Hypertension in the very young or very old (55)
179
What is the cause of renal artery stenosis?
Caused by arthrosclerotic disease in elderly persons and fibromuscular dysplasia in young women. Upper abdominal bruit is present in 50–70% of patients.
180
How is renal artery stenosis diagnosed?
Screening ultrasound. Captopril renogram measures the uptake of radioisotope before and after captopril. Positive test is decreased uptake (decreased GFR) after captopril. Arteriogram is the best method of diagnosis.
181
What is the treatment of renal artery stenosis?
Percutaneous transluminal angioplasty. If stenosis recurs, then the procedure should be repeated. If angioplasty fails, surgical resection. ACE inhibitors if angioplasty or surgery is not possible.
182
What is the cause of primary hyperaldosteronism (Conn Syndrome)?
Conn Syndrome is most commonly due to a unilateral adrenal adenoma. Bilateral adrenal hyperplasia is less common. Cancer is rare as a cause of hyperaldosteronism.
183
What are the symptoms of primary hyperadosteronism?
Hypertension in association with hypokalemia. Symptoms of hypokalemia such as muscular weakness and polyuria and/or polydipsia from a nephrogenic diabetes insipidus.
184
How is primary hyperaldosteronism diagnosed?
Elevated aldosterone levels in urine and blood.
185
What is the treatment of Conn syndrome?
Surgical resection of adenoma. Potassium sparing diuretics such as spironolactone in adrenal hyperplasia.
186
What is pheochromocytoma?
Pheochromocytoma is most often due to a benign tumor of the adrenal gland; 10% are bilateral, 10% are malignant, and 10% are extra–adrenal.
187
What is the presentation of pheochromocytoma?
Episodic hypertension with headaches, sweating, palpitations, and tachycardia. Pallor or flushing may also occur.
188
How is pheochromocytoma diagnosed?
Initial test is urinary vanillylmandelic acid (VMA), metanephrines, and free urinary catecholamines. Plasma catecholamine evaluation. CT and MRI scanning is used to localize tumor.
189
What is the treatment of pheochromocytoma?
Alpha–adrenergic blockade with phentolamine or phenoxybenzamine, followed by surgical removal.
190
What is the most common cause of Cushing disease?
Cushing Disease is commonly caused by ACTH hypersecretion by a pituitary adenoma. HTN in association with cushingoid truncal obesity, buffalo hump, menstrual abnormalities, striae.
191
How is Cushing disease diagnosed?
Dexamethasone suppression testing and 24–hour urine cortisol are the best initial tests.
192
What is the treatment of Cushing disease?
Surgical resection of the pituitary adenoma.
193
What is the clinical sign of coarctation of the aorta?
Hypertension greater in the upper extremities compared with the lower extremities.
194
What are the endocrinologic and renal causes of secondary hypertension?
Oral contraceptives, acromegaly, congenital adrenal enzyme deficiencies, glomerulonephritis, polycystic disease, diabetic nephropathy, pyelonephritis.
195
What are the commonly used thiazide diuretics?
Hydrochlorothiazide, chlorthalidone, metolazone, indapamide.
196
What are the names of the potassium sparing diuretics?
Spironolactone, amiloride, triamterene.
197
What are the indications for diuretics in hypertension?
Congestive heart failure, edematous states, African–American patients; least expensive.
198
What are the major side effects of diuretics?
Decreases in potassium and magnesium; increases in calcium, uric acid, glucose, LDL–cholesterol; gynecomastia.
199
What are the relative contraindications to diuretics?
Diabetes, gout, hyperlipidemia.
200
What are the two most commonly used beta–blockers for hypertension?
Metoprolol and atenolol are the most commonly used.
201
What are the specific indications for beta–blockers in hypertension?
Myocardial infarction or ischemic heart disease, supraventricular arrhythmias, migraine headaches, glaucoma, anxiety (resting tachycardia), congestive failure from diastolic dysfunction.
202
What are the major side effects of beta–blockers?
Bronchospasm, heart block, bradycardia, Raynaud phenomenon, depression, impotence, fatigue, decreased HDL, increased triglycerides, hyperglycemia.
203
What are the relative contraindications to beta blockers?
Asthma, COPD, atrioventricular conduction defects, congestive heart failure from systolic dysfunction; diabetes because of masking signs of hypoglycemia.
204
What are the names of the angiotensin converting enzyme (ACE) inhibitors?
Benazepril, captopril, enalapril, fosinopril, lisinopril, quinapril, ramipril, moexipril, enalaprilat (only IV form).
205
What are the specific indications for ACE inhibitors?
Diabetics with HTN to prevent nephropathy; BP goal in a diabetic is
206
What are the major side effects of ACE inhibitors?
Cough, angioneurotic edema, neutropenia, hyperkalemia, taste disturbances, anaphylactoid reactions. Less effective in African–American patients.
207
What are the absolute contraindications to ACE inhibitors?
Bilateral renal artery stenosis, pregnancy.
208
What are the names of the calcium channel blockers?
Amlodipine, diltiazem, felodipine, isradipine, nicardipine, nifedipine, verapamil.
209
What are the specific indications for calcium channel blockers?
Angina pectoris, supraventricular arrhythmia, migraine, Raynaud phenomenon, esophageal spasm.
210
What are the side effects of calcium–channel blockers?
Peripheral edema, constipation, heart block, reflex tachycardia.
211
What are the relative contraindications to calcium channel blockers?
Atrioventricular conduction defects, congestive heart failure from systolic dysfunction.
212
What are the angiotensin receptor antagonists?
Losartan, valsartan, irbesartan, candesartan, telmisartan
213
What are the indications for angiotensin receptor antagonists?
Patients who are intolerant to ACE inhibitors (because of cough).
214
What are the names of the central–acting sympatholytics?
Clonidine, guanabenz, guanfacine, methyldopa.
215
What are the side effects of central–acting sympatholytics?
Depression, fatigue, dry mouth, impotence, bradycardia, heart block, memory loss. Methyldopa causes hepatitis and Coombs–positive hemolytic anemia.
216
What is the criteria for an abnormal pulmonary flow rate?
120% of predicted is consistent with air trapping.
217
What is vital capacity?
The volume of gas exhaled with maximal forced expiration.
218
What is total lung capacity?
Volume of gas in the lungs after maximal inspiration.
219
What is residual volume?
Volume of gas remaining in the lungs after forced maximal expiration (unused space).
220
What is the formula for total lung capacity?
TLC = RV + VC or VC = TLC – RV
221
What is the purpose of measuring forced expiratory volumes (FEVs)?
FEVs determine degree of obstruction by comparing forced volume expired at 1 sec to the forced vital capacity. 80% of predicted is normal. It is decreased in patients with COPD or asthma. FEVs normal in restrictive.
222
What is the purpose of measuring carbon monoxide diffusing capacity (DLco)?
Lung diffusion testing determines how well oxygen passes from the alveolar space into blood. Diffusing capacity is reduced by emphysema, edema, consolidation, or fibrosis.
223
If pulmonary function tests show an obstructive pattern and decreased DLco, what is the diagnosis?
Emphysema.
224
If pulmonary function tests show a restrictive pattern and decreased DLco, what is the diagnosis?
Interstitial lung disease (intrapulmonary restriction) or mild left heart failure. Increased DLco may be seen in pulmonary hemorrhage caused by Goodpasture syndrome.
225
What is the methacholine challenge test?
Bronchoprovocation with methacholine is done to evaluate patients with cough or wheezing and who have a normal PFT; tests for asthma (bronchial reactivity).
226
What is the formula for oxygen delivery?
The most important factor in gas exchange is oxygen delivery (Do2) to the vital organs. Do2 = Cardiac Output x (1.34 x Hb x HbSat) + 0.0031 x PaO2
227
What are the two most important factors in maintaining the delivery of oxygen to the vital organs?
The two most important factors in the delivery of oxygen to the vital organs are the cardiac output and hemoglobin. In a critically ill patient, the hemoglobin and cardiac output should be kept near normal.
228
What is the formula for alveolar–arterial O2 gradient?
PAO2–PaO2 gradient is an assessment of oxygenation. The A–a gradient is valid on room air and increases with age. PAO2–PaO2 gradient = (150 –1.25) x pCO2 –PaO2orA – a = [150 – (1.25 x PaCO2) – PaO2]
229
What is the normal alveolar–arterial O2 gradient?
The normal gradient is between 5 and 15 mm Hg. It increases with all causes of hypoxemia except hypoventilation and high altitude.
230
What percentage of solitary pulmonary nodules are malignant?
One third of all solitary nodules are malignant. Calcification indicates benign. Popcorn calcifications are caused by hamartomas. Bull's–eye calcifications are caused by granulomas.
231
What is the first step in the evaluation of a solitary pulmonary nodule?
The first step in the evaluation of a pulmonary nodule is to look for a prior x–ray. Finding the same pulmonary nodule on an x–ray done years ago eliminates the need for further evaluation.
232
What is the approach to evaluation of a solitary pulmonary nodule if no prior x–ray is available and the patient is low–risk?
Low risk patients are
233
What is the approach to the evaluation of a solitary pulmonary nodule if no prior x–ray is available and the patient is high risk?
High–risk patients: \>50 smokers with a nodule, are likely to have bronchogenic cancer. Diagnostic procedure is open–lung biopsy and removal.
234
What are the causes of exudative effusions?
Pneumonia, cancer, and tuberculosis. An exudative effusion will cause unilateral effusions. Exudative effusions need further investigation.
235
What are the causes of transudative pleural effusions?
Heart failure, nephrotic syndrome, liver disease, pulmonary embolism, atelectasis.
236
What are the causes of exudative pleural effusions?
Parapneumonic effusions (pneumonia), malignancy (lung, breast, lymphoma), tuberculosis, pulmonary embolism, collagen vascular disease (RA, SLE), drug–induced, pancreatitis.
237
What is the diagnostic approach to pleural effusions?
Thoracentesis should be performed for new and unexplained pleural effusions when sufficient fluid is present. Observe pleural effusions when there is CHF, viral pleurisy, or recent thoracic or abdominal surgery.
238
What is the laboratory testing for thoracentesis fluid?
Lactate dehydrogenase (LDH) and protein. Measure serum LDH and protein. Calculate the ratios of effusion to serum for these measurements.
239
What is the Light criteria for exudative pleural effusion?
LDH of effusion \>200 IU/mL, LDH effusion/serum ratio \>0.6, and protein effusion/serum ratio \>0.5. If one criteria is met, it is an exudative effusion, and further evaluation is required.
240
What is the Light criteria for transudative pleural effusion?
All three are required: LDH of effusion
241
What kind of pleural effusion is associated with pulmonary embolism?
Pulmonary embolism can cause a transudate or exudate. A patient with a transudative effusion but no apparent cause may have a PE.
242
What is the management of parapneumonic effusions?
Thoracentesis to rule out an empyema (pus in the pleural space), which needs chest–tube drainage. Uncomplicated parapneumonic effusions respond to antibiotics alone.
243
What are the most common causes of malignant pleural effusion?
Lung cancer, breast cancer, and lymphoma. Cytologic examination is diagnostic.
244
What are the causes of hemorrhagic pleural effusions?
Hemorrhagic pleural effusion may be seen in mesothelioma (a pleural–based cancer associated with asbestos), metastatic lung or breast cancer, pulmonary thromboembolism (with infarction), and trauma.
245
What are the causes of lymphocytic predominant, exudative pleural effusions?
Caused by tuberculosis. Adenosine deaminase is elevated, and the PCR for tuberculous DNA is positive. Acid–fast stain and culture for Tb are positive in less than 30%. Pleural biopsy confirms diagnosis.
246
What amount of fluid is required for thoracentesis to be done safely?
If decubitus chest x–ray detects 1 cm or more of free–flowing fluid, the thoracentesis can be performed. If non–free fluid (loculated) an ultrasound–guided thoracentesis should be done.
247
What are the causes of respiratory compromise?
Airway obstruction (asthma, COPD, foreign object), parenchymal lung disease (bacterial or viral pneumonia, lung injury), heart failure, pulmonary embolism, opiates, myasthenia gravis.
248
What are the steps in treating respiratory compromise?
The first task is to ensure that the patient's airway is patent and that breathing is adequate. Administer supplemental oxygen.
249
What are the clinical manifestations of respiratory compromise?
Acute cough, fever, sputum suggest infection. Sudden dyspnea without fever suggests airway obstruction, cardiac disease, or thromboembolism. Chronic dyspnea is usually CHF, interstitial disease, COPD.
250
What are the physical signs of respiratory compromise?
Resp \>30 is severe respiratory compromise. Wheezing indicates asthma, COPD. Localized wheezing: foreign object, mass. Rales indicate pneumonia, interstitial disease, CHF. Consolidation: pneumonia, atelectasis.
251
What disorders are associated with respiratory compromise with a normal lung exam?
Normal lung examination may be seen in thromboembolic disease, Pneumocystis jiroveci, and disorders of central respiratory drive.
252
What are the most important laboratory tests in the evaluation of acute respiratory compromise?
An arterial blood–gas measurement is the most important initial laboratory test in determining the presence and severity of respiratory compromise.
253
What are the laboratory signs of acute respiratory failure?
Rise in pCO2 accompanied by a drop in pH. The bicarbonate level will decrease over 24 hours with renal compensation. Metabolic acidosis (lactic acidosis) in the presence of hypercapnia is an indication for ventilation.
254
What is the target O2 saturation in COPD exacerbations?
In the setting of acute–on–chronic respiratory failure, the administration of supplemental oxygen is often accompanied by a rise in PaCO2. The target range should be oxygen saturation 88–92%.
255
What is the significance of an elevated B–type natriuretic peptide?
An elevated BNP is seen in patients with left heart failure. Cor pulmonale and acute right ventricular failure (thromboembolism) may also cause a rise in the BNP.
256
What are the causes of respiratory failure with a clear chest x–ray?
Chest x–ray without parenchymal infiltrates accompanies respiratory failure due to thromboembolism, central respiratory depression, neuromuscular disease, and upper airway obstruction.
257
What are the chest x–ray findings in asthma and COPD?
Hyperinflation (hyperlucency). Focal infiltrates suggest bacterial, viral, or fungal pneumonia, aspiration, or pulmonary hemorrhage. Heart failure and ARDS present with diffuse edema.
258
What blood gas results indicate the need for mechanical ventilation in patients with an asthma exacerbation?
Respiratory acidosis and hypercapnia with asthma exacerbation requires ventilation. Indications for intubation include upper–airway injury, airway compromise, neurologic depression.
259
What are the signs of pulmonary embolism in ICU patients?
Dyspnea, tachypnea, hypoxemia.
260
What complication may result from gastric aspiration?
Aspiration, which may precipitate respiratory failure directly or through the development of pneumonia or acute respiratory distress syndrome.
261
What are the risk factors for aspiration?
The risk factors for aspiration include impaired consciousness and upper airway instrumentation (nasogastric tubes). Respiratory depression from opiates.
262
What is acute respiratory distress syndrome?
Diffuse inflammatory response of lungs within 24 hours of the onset of severe illness or injury. Tachypnea and hypoxemia. Diffuse pulmonary infiltrates of noncardiogenic pulmonary edema.
263
22–year–old with asthma, wheezing after URI. Resp 28, pulse 120; afebrile. Oxygen by nasal cannula is administered. What should be the next treatment?
Beta–Agonist (albuterol) by nebulizer.
264
What is asthma?
Inflammatory hyperreactivity of the respiratory tree, resulting in reversible airway obstruction. Mucosal inflammation, bronchial musculature constriction, excessive mucus; episodic pattern.
265
What factors precipitate attacks in intrinsic asthma?
Occurs in 50% of asthmatics who are nonallergic. Attacks are precipitated by infections, irritants, cold air, exercise, emotional upset. Prognosis is poor.
266
What is the pathophysiology of extrinsic asthma?
Extrinsic (allergic, atopic) asthma results from sensitization. IgE elevated. Family history. Precipitated by allergens and accounts for 20% of asthma. Allergic rhinitis, urticaria, eczema. Prognosis good.
267
What are the most common stimuli that cause asthma exacerbations?
Respiratory infections with respiratory syncytial virus in young children, rhinoviruses in adults. Aspirin, coloring agents such as tartrazine, and beta–adrenergic antagonists.
268
What are the signs of asthma?
Tachypnea, tachycardia, prolonged expirations, diffuse wheezing. Use of accessory muscles, diminished breath sounds, hyperresonance, intercostal retraction.
269
What are the signs of poor prognosis in asthma?
Poor prognostic factors include fatigue, diaphoresis, pulsus paradoxus, inaudible breath sounds, decreased wheezing, cyanosis, bradycardia.
270
What are the arterial blood gas findings in acute asthma?
In the acute phase, PaCO2, increase in pH, and normal or low PaCO2. In severe asthma or status asthmaticus there will be a decreased PaCO2, increased PaCO2, and decreased pH.
271
What is the significance of a normal PaCO2 in acute asthma?
A normal PaCO2 may indicate respiratory muscle fatigue in acute asthma.
272
What are the chest x–ray findings in asthma?
Chest x–ray shows hyperinflation. Acute infection may be visible as the cause of an acute attack.
273
What are the pulmonary function test abnormalities in asthma?
PFTs show obstructive pattern that reverses with bronchodilation. PFTs may be normal because asthma is episodic; in this case a provocative challenge may be performed with methacholine or cold air.
274
What is the treatment of acute exacerbations of asthma?
beta–Adrenergic agonist inhalers (albuterol, terbutaline). Inhaled beta–adrenergic agonists are preferred. Side effect is tremor. beta–Adrenergic agonists terminate 70% of asthmatic attacks.
275
What are the indications for salmeterol?
Salmeterol is a long–lasting (12 h) type of albuterol that is effective in nocturnal cough variant and exercise–induced asthma. Salmeterol has no benefit in acute episodes.
276
What diseases may be adversely affected by beta–agonists?
beta–Adrenergic agonists must be used with caution in cardiovascular disorders, hypothyroidism, diabetes mellitus, hypertension, and coronary insufficiency.
277
What is the role of theophylline in the treatment of asthma?
Aminophylline and theophylline are only modest bronchodilators. Sometimes of benefit for nocturnal cough. Improve contractility of diaphragm. Not routinely used in asthma because no added benefit.
278
What are the indications for ipratropium and tiotropium in the treatment of asthma?
Anticholinergics (ipratropium, tiotropium) are especially beneficial with heart disease when beta–adrenergic agonists may be dangerous. Slow to achieve bronchodilation (\>90 min), medium potency.
279
What is the role of supplemental oxygen in the treatment of acute asthma exacerbations?
Supplemental oxygen, by nasal cannula or mask, should be given immediately for acute asthma exacerbation. Always maintain an oxygen saturation above 90%.
280
When should antibiotics be given to patients with an exacerbation of asthma?
Antibiotic treatment should be considered in patients with purulent sputum and chest x–ray infiltrates consistent with bacterial pneumonia.
281
What medication is used for long–term control of asthma?
Corticosteroids reduce airway inflammation. Used in acute exacerbations in short bursts for 10–14 days, along with bronchodilators.
282
What are the side effects of systemic corticosteroids?
Oral candidiasis, weight gain, HTN, glaucoma, cataracts, diabetes, muscle weakness, and osteoporosis.
283
What is the role of mast cell stabilizers in the treatment of asthma?
Cromolyn and nedocromil. Used for prophylaxis, and exercise and allergic asthma. Adults will benefit less than children. Cromolyn is first–line chronic treatment in children.
284
What is the mechanism of the leukotriene modifiers?
Inhibit 5–lipoxygenase, the enzyme of leukotriene production, or competitively antagonize LTD4. Zileuton is the only leukotriene inhibitor. The LTD4 receptor antagonists are zafirlukast and montelukast.
285
What is the role of leukotriene modifiers in the treatment of asthma?
This group of drugs is approved for severe asthma resistant to maximal doses of inhaled steroids. Leukotriene modifiers are not first–line drugs.
286
What is the treatment of mild asthma?
Mild asthma: Inhaled, short–acting bronchodilators as needed (albuterol inhaler).
287
What is the treatment of moderate asthma?
Inhaled steroids. Children with mild symptoms benefit from cromolyn, along with inhaled beta–agonists as needed. Nocturnal symptoms, despite short–acting beta agonists, will benefit from salmeterol.
288
What is the treatment of severe asthma?
Inhaled steroids daily, inhaled long–acting beta agonists (salmeterol), inhaled short–acting agonists for breakthrough symptoms, along with antileukotriene drugs (montelukast) and oral steroids.
289
What is the most common cause of chronic obstructive pulmonary disease?
Cigarette smoking; 10–15% of smokers develop COPD. 90% of COPD patients are cigarette smokers. COPD symptoms usually begin after at least 20 pack–years of tobacco exposure.
290
What is alpha–1 antitrypsin deficiency?
Rare hereditary autosomal recessive disease which can cause emphysema and liver abnormalities.
291
What are the physical signs of emphysema?
Distant breath sounds will be heard on auscultation.
292
What are the physical signs of chronic bronchitis?
Rhonchi and wheezes. Right heart failure (cor pulmonale) and clubbing.
293
What are the chest x–ray findings in chronic bronchitis?
Increased pulmonary markings can be seen?
294
What are the chest x–ray findings in emphysema?
Hyperinflation with diaphragm flattening, small heart size, and increase in retrosternal space. Cor pulmonale in COPD is caused by chronic pulmonary HTN.
295
How is COPD diagnosed?
Reduction in FEV1/FVC ratio and FEF 25. RV and TLC are increased. Emphysema will has decreased DLco; chronic bronchitis has normal DLco. After a bronchodilator the FEV1/FVC increase.
296
What are the complications of chronic obstructive pulmonary disease?
Hypoxemia with nocturnal desaturation. Erythrocytosis. Pulmonary HTN, cor pulmonale and right HF. Ventilatory failure and CO2 retention in early chronic bronchitis and end–stage emphysema.
297
What is the treatment of chronic obstructive pulmonary disease?
Anticholinergic agents (ipratropium bromide and tiotropium) are the first–line drugs in COPD via MDI. Anticholinergic agents can be used synergistically with beta2–adrenergic agonists in COPD.
298
What medication is given if chronic obstructive pulmonary disease remains symptomatic after treatment with ipratropium?
beta2 agonists (albuterol) are used after anticholinergic. Beta–agonists are not first–line agents in COPD because many have heart disease. Inhaled corticosteroids are not used routinely in COPD.
299
What is the role of theophylline in the treatment of COPD?
Theophylline is used if beta2 adrenergics and anticholinergics are not effective.
300
What medications interact with theophylline?
Increased theophylline clearance is seen in smokers, rifampin, phenytoin, phenobarbital. Decreased theophylline clearance is seen with erythromycin, ciprofloxacin, or H2–blockers (cimetidine, ranitidine).
301
What are the indications for home oxygen in patients with COPD?
Home O2 is given to patients with hypoxemia (PaO2 90%. Cor pulmonale will benefit from home oxygen when PaO2
302
What immunizations should be given to patients with chronic bronchitis or emphysema?
All patients with COPD should receive the pneumococcal vaccine (Pneumovax) every 5 years and the influenza vaccine yearly. H. influenzae vaccine if they were not previously immunized.
303
What are the most common causes of COPD exacerbations?
Viral lung infections. Other: bacterial infections, heart failure, myocardial ischemia, pulmonary embolism, lung cancer, esophageal reflux disease, and beta–blockers.
304
What is the initial management of COPD exacerbation?
Measure O2 saturation. Arterial blood gas determination of hypercapnia and hypoxia. Chest x–ray to identify pulmonary infiltrates pneumonia. Pulmonary edema indicates heart failure.
305
What is the laboratory evaluation of COPD exacerbations?
Check theophylline levels. CBC for elevated WBCs and polycythemia; ECG may reveal atrial fibrillation, that may precipitate heart failure and exacerbate COPD.
306
What are the indications for mechanical ventilation in COPD?
Intubation and mechanical ventilation for decreased consciousness, cyanosis, or hemodynamic instability, persistent hypoxemia.
307
What is the role of antibiotics in patients with COPD exacerbations?
Beneficial in exacerbations. Second–gen macrolides (clarithromycin, azithromycin), extended–spectrum fluoroquinolones (levofloxacin, moxifloxacin), cephalosporins (2nd/3rd gen), amoxicillin–clavulanate.
308
What medications are used to treat exacerbations of COPD?
O2 supplementation titrated to \>90% saturation. Inhaled bronchodilators are the most effective. In acute COPD exacerbations, use albuterol and anticholinergics (ipratropium) simultaneously.
309
What medications should be avoided in patients with COPD?
There is no benefit to intravenous aminophylline. Avoid opiates and sedatives that may suppress respiratory system.
310
What is the role of corticosteroids in the treatment of COPD?
Corticosteroids may be given intravenously or orally because the efficacy is similar. 60 mg prednisone is continued for 2 weeks. Severe exacerbation is treated with IV methylprednisolone.
311
What is bronchiectasis?
Permanent dilation of small– and medium–sized bronchi from destruction of bronchial elastic and muscle. Can be caused by tuberculosis, fungal infections, abscess, cystic fibrosis, immotile cilia syndrome.
312
What are the clinical signs of bronchiectasis?
Chronic cough, hemoptysis, copious, foul–smelling sputum, sinusitis, immune deficiencies. Wheezes, crackles. Recurrent pneumonias with gram–negative bacteria, especially Pseudomonas. Polycythemia.
313
How is bronchiectasis diagnosed?
Chest x–ray: advanced cases may show 1– to 2–cm cysts and crowding of the bronchi (tram–tracking). High– resolution CT scan of the chest detects bronchiectasis.
314
What is the treatment for bronchiectasis?
Bronchodilators, chest physical therapy, postural drainage. TMP–SMZ, amoxicillin, amoxicillin/clavulanate when sputum production increases. A different antibiotic each time.
315
What bacterial coverage is required in the treatment of bronchiectasis?
Symptoms should be treated IV for gram–negative bacteria (quinolones, ceftazidime, aminoglycosides. Surgical therapy with localized bronchiectasis or massive hemoptysis.
316
What vaccines are indicated for patients with bronchiectasis?
Yearly vaccination for influenza and vaccination for pneumococcal infection with a single booster at 5 years.
317
What are the complications of bronchiectasis?
Complications hemoptysis, amyloidosis, cor pulmonale, and visceral abscesses.
318
What is interstitial lung disease?
Group of heterogeneous diseases of chronic inflammation and fibrosis of interstitium and lung parenchyma. The worst prognosis is with idiopathic pulmonary fibrosis and interstitial pneumonitis.
319
What is the pathophysiology of interstitial lung disease?
Inflammation and scarring of the interstitium that disrupts normal gas exchange the area in and around the small blood vessels and alveoli.
320
What are the clinical signs of interstitial lung disease?
Exertional dyspnea and nonproductive cough. Coarse crackles, pulmonary HTN (increased pulmonic sound, right heart failure), and clubbing.
321
What are the chest x–ray findings in interstitial lung disease?
Reticular (branching) or reticulonodular pattern (ground–glass appearance). PFTs show intrapulmonary restrictive pattern.
322
What are the causes of interstitial lung disease?
Idiopathic pulmonary fibrosis, sarcoidosis, pneumoconiosis, occupational; autoimmune; hypersensitivity pneumonitis; eosinophilic, Wegener, hemosiderosis, bronchiolitis obliterans, lymphangioleiomyomatosis.
323
What is the diagnostic evaluation of interstitial lung disease?
High–resolution CT scan and, eventually, biopsy via bronchoscopy or open lung biopsy.
324
55–year–old man with exercise intolerance. Dyspnea on exertion; nonsmoker. Resp 25, JVD, crackles, clubbing, pedal edema. Diffuse reticular disease. What is the diagnosis?
Idiopathic pulmonary fibrosis.
325
What is idiopathic pulmonary fibrosis?
Inflammatory lung disease of unknown origin that causes lung fibrosis and restrictive lung disease. Only the lung and has no extrapulmonary manifestations except clubbing.
326
What is the age of onset of idiopathic pulmonary fibrosis?
IPF occurs in patients in the fifth decade of life, with an equal distribution between men and women.
327
What are the clinical signs of idiopathic pulmonary fibrosis?
Progressive exercise intolerance and dyspnea. Coarse dry crackles.
328
What are the radiographic findings in idiopathic pulmonary fibrosis?
Reticular or reticulonodular disease. CT shows ground–glass appearance. A restrictive intrapulmonary process on PFTs. Bronchoalveolar lavage will show increased macrophages.
329
What is the treatment for idiopathic pulmonary fibrosis?
Treatment with steroids with or without azathioprine will benefit 20% of patients; 80% progress to fatal lung fibrosis. There is a 20 to 40% five–year survival.
330
A 29–year–old woman, painful erythematous papules. Joint swelling, pain. Fever, symmetric swelling of knees, PIP and MCP joints, and 3 cm papules over the anterior legs. What is the diagnosis?
Sarcoidosis
331
What is sarcoidosis?
Systemic disease, characterized by noncaseating granulomas in the lung and other organs. Increased incidence of sarcoidosis among blacks and patients 20–40 years.
332
What are the clinical signs of sarcoidosis?
Sarcoidosis can involve any organ system. Hilar adenopathy in an asymptomatic patient. Erythema nodosum, arthritis. Fever, parotid enlargement, uveitis, facial palsy. Lung involvement in 90%.
333
What are the chest x–ray findings in sarcoidosis?
Hilar adenopathy, reticulonodular parenchyma, or honeycombing with fibrosis.
334
What are the laboratory findings in sarcoidosis?
Hypercalcemia or hypercalciuria caused by vitamin D produced by macrophages. Elevation in ACE in 60%. Increased LFTs in 30%. Skin anergy; PFT restrictive pattern. Uveitis and conjunctivitis in \>25%.
335
How is sarcoidosis diagnosed?
Lung biopsy shows noncaseating granulomas.
336
What is the prognosis in sarcoidosis?
Eighty percent of patients with lung involvement from sarcoidosis remain stable, or the disease resolves. Twenty percent of patients develop progressive disease with end–organ compromise.
337
What is the treatment for sarcoidosis?
Trial of steroids. Mandatory for uveitis, sarcoidosis involving the CNS, and hypercalcemia.
338
What are the pneumoconioses?
Occupational lung diseases in which inhalation of fibers initiate an inflammatory process that leads to fibrosis. Appears 20–30 years after exposure to mining of gold, silver, lead, copper.
339
What is the pathology of pneumoconioses?
Macrophages engulf offending agents, causing inflammation and fibrosis of the lung. Respiratory insufficiency.
340
What are the signs of pneumoconioses?
Dyspnea, shortness of breath, cough, sputum production, cor pulmonale, and clubbing. PFTs show a restrictive pattern with a decreased DLco. Hypoxemia with an increased PAO2–PaO2 gradient.
341
What are the chest x–ray finding in pneumoconiosis?
Small irregular opacities, interstitial densities, ground glass appearance, and honeycombing.
342
What is asbestosis?
Lung disease caused by inhalation of asbestos fiber in mining, milling, foundry work, shipyards, or the application of asbestos to pipes, brake linings, insulation, and boilers.
343
What are the signs of asbestosis?
Exertional dyspnea and reduced exercise tolerance, cough and wheezing, chest wall pain, and respiratory failure.
344
What are the chest x–ray findings in asbestosis?
Pleural thickening, pleural plaques, and calcifications of the diaphragm. Pleural effusions and the interstitial lung process associated with asbestosis usually involves the lower lung fields.
345
What cancer is most commonly associated with asbestosis?
The most common cancer associated with asbestosis is bronchogenic carcinoma (adenocarcinoma or squamous cell). Mesotheliomas are also associated with asbestos.
346
How is asbestosis diagnosed?
Lung biopsy shows barbell–shaped asbestos fiber.
347
What is silicosis?
Lung disease caused by inhalation of silica dust during mining, quarrying, tunneling, glass and pottery making, and sandblasting.
348
What are the signs of silicosis?
Exertional dyspnea, cough, wheezing.
349
What are the chest x–ray findings in silicosis?
Nodules (1–10 mm) throughout the lungs, most prominent in the upper lobes. Eggshell calcifications.
350
What percentage of miners contract coal miner's lung/coal worker's pneumoconiosis?
12% of all miners.
351
What is the presentation of coal worker's pneumoconiosis?
Coal worker's pneumoconiosis presents with exertional dyspnea, cough, wheezing.
352
What are the chest x–ray findings in coal worker's pneumoconiosis?
Small round densities in parenchyma, upper half of the lungs.
353
What are the laboratory abnormalities associated with coal worker's pneumoconiosis?
Increased IgA, IgG, C3, antinuclear antibodies, and rheumatoid factor are seen in coal worker's pneumoconiosis.
354
38–year–old woman with sudden onset of shortness of breath and pleuritic chest pain; oral contraceptives. Respirations 28, pulse 110. Mild hypoxemia (7.52/70/25/90%). Chest x–ray is normal. What is the diagnosis?
Pulmonary embolism
355
What are the high–risk factors for embolism and DVTs?
Surgery, cancer, CHF, travel. Lupus anticoagulant, nephrotic syndrome (loss of antithrombin III), OCPs (smoker). Factor V Leiden mutation; protein C, S, antithrombin III deficiency. Pregnancy.
356
What are the symptoms and signs of pulmonary embolism and deep vein thrombosis?
Sudden onset of dyspnea (shortness of breath) and tachypnea. Thigh or calf swelling. Pleuritic chest pain, hemoptysis. Increased respiratory rate with tachycardia; increased pulmonic sound (P2).
357
What patients are considered to be high–risk for pulmonary embolism?
Patients with one risk factor and consistent symptoms and no alternative diagnosis. Low–risk patients have no risk factors, atypical symptoms, and an alternative diagnosis (eg, pneumonia).
358
What are the arterial blood gas findings in pulmonary embolism?
Hypoxemia with an elevated A–a gradient. The A–a gradient may be normal.
359
What are chest x–ray findings in pulmonary embolism?
Usually normal. Other nonspecific findings include atelectasis and pleural effusion. Westermark sign is the loss of vascular markings. Hampton hump is a wedge–shaped infiltrate caused by pulmonary infarction.
360
What diagnosis should be considered in all patients with dyspnea and normal chest x–ray?
Pulmonary embolus should be considered in all patients with dyspnea and normal chest radiography.
361
What are the ECG signs of pulmonary embolism?
Right heart strain: large S wave in lead I and deep Q in lead III with T–wave inversion in the same lead. The most common finding is sinus tachycardia. The ECG excludes acute pericarditis and myocardial ischemia.
362
What diagnostic tests are used to diagnose pulmonary embolism?
Spiral CT is initial test for PE. Ventilation–perfusion scan is a nuclear test. Pulmonary embolus will cause perfusion defects. Angiogram is most accurate test, but risk of pulmonary artery rupture is 1%.
363
What diagnostic tests are used to diagnose deep vein thrombosis?
Compression or duplex ultrasound. Venogram is rarely done. MRI.
364
What is the role of D–dimer testing in evaluating thromboembolic disease?
D–dimer is the most sensitive test for PE. Indicates fibrin degradation from thromboembolism, surgery, infection, trauma, pregnancy, DIC. Normal test means no thrombus; only be used to rule out PE.
365
What is the diagnostic approach to suspected pulmonary embolism?
CXR, then spiral CT. Normal CT and normal D–dimer in low–risk excludes PE. Normal CT and normal Doppler ultrasound in low–risk excludes PE. If tests are negative, but high risk, angiogram is done.
366
What treatment should begin to patients suspected of having a pulmonary embolism or deep vein thrombosis?
All patients should be on anticoagulation while completing diagnostic evaluations. Heparin should always be started before sending that patient for CT or V/Q scan.
367
What is the treatment of pulmonary embolism?
Give oxygen and start heparin immediately while the diagnostic evaluation is being completed. LMWH or unfractionated heparin for 7–10 d. Warfarin should be started with heparin and continued for 6 mo.
368
What is the mechanism of action of low molecular weight heparin?
LMWH inactivates factor Xa but has no effect on thrombin (no need PTT). Dosing is based on weight QD or bid. LMWH is equal to unfractionated heparin in DVT and PE.
369
What are the advantages of low molecular weight heparin over unfractionated heparin?
Less hemorrhage or heparin–induced thrombocytopenia.
370
What is heparin–induced thrombocytopenia?
Heparin–induced thrombocytopenia (HIT) is a common complication of heparin 5 days after starting in 5%. Associated more with thrombotic events than bleeding. Stop heparin when platelets decrease.
371
What is the cause of recurrent pulmonary embolism despite treatment with heparin?
Consider heparin–induced thrombocytopenia in a patient with recurrent pulmonary embolism or DVT despite heparin.
372
What is the treatment of heparin–induced thrombocytopenia?
HIT is treated with the new anticoagulants (argatroban, lepirudin).
373
What are argatroban and lepirudin?
Anticoagulants that are used in patients who can not use heparin.
374
What is the mechanism of warfarin?
Warfarin inhibits the vitamin K–dependent factors (II, VII, IX, and X). Factor VII has the shortest half–life of all the affected factors.
375
What test is used to assess the anticoagulant effect of warfarin?
PT is monitored to assess the warfarin anticoagulant effect. INR is used to control for variability in PT. Warfarin should be titrated to an INR of 2–3.
376
What complication occurs when warfarin is given to patients with protein C deficiency?
Rare procoagulant effect that occurs in preexisting protein C deficiency. Warfarin causes transient hypercoagulable state and diffuse thrombosis. Risk reduced by starting heparin and warfarin simultaneously.
377
What are the contraindications to anticoagulation?
Anticoagulation is contraindicated in patients with recent neurosurgery or eye surgery.
378
What is the anticoagulant treatment of patients who have had recent neurosurgery or eye surgery?
An inferior vena cava filter (Greenfield filter) should be used to prevent further embolism in these patients.
379
Want is the anticoagulation method for pregnant patients with deep vein thrombosis?
Warfarin is contraindicated in pregnant patients. LMWH for 6 months is the best alternative with injections once or twice a day.
380
What is the indication for thrombolytics in patients with pulmonary embolism?
Thrombolytics (tPA) for hemodynamically unstable (hypotension, right heart failure) or for massive DVT to prevent the postphlebitic syndrome.
381
What is postthrombotic syndrome?
Most common complication of DVT, occurring in up to two–thirds. Destruction of the valves. Pain, edema, hyperpigmentation, and skin ulceration. Compression stockings prevent the postthrombotic syndrome.
382
What is the duration of anticoagulation for noncomplicated proximal deep vein thrombosis?
6 months. In patients with thrombophilias (hypercoagulable states), lifelong anticoagulation is with warfarin if there have been two or more episodes of thrombosis.
383
Why should protein C or protein S levels not be checked during acute thrombosis?
Both warfarin and acute clot formation cause lower protein C and S.
384
What disorders should be suspected in patients who develop recurrent thrombosis while on anticoagulants?
Heparin–induced thrombocytopenia or cancer–related thrombosis. Place an inferior vena cava filter or use the hirudin derivative anticoagulants. IVC filters are associated with clot formation around the filter site.
385
What is the management of distal deep vein thromboses?
Below–the–knee DVT is not a cause of pulmonary embolism unless extend to proximal veins. Monitor for extension to the proximal veins by serial ultrasound or anticoagulation for 3 mo.
386
What is fat embolism syndrome?
Fat embolism is a rare type of embolism that occurs 3 days after long bone fracture (femur fracture). It may rarely occur after CPR. Acute dyspnea, petechiae (neck and axilla), and confusion.
387
What is the treatment of fat embolism syndrome?
The treatment is supportive (no anticoagulation).
388
A 50–year–old man with gram–negative sepsis severe dyspnea. Crackles; ABG shows hypoxemia and hypercarbia. Diffuse alveolar densities. What is the diagnosis?
Acute respiratory distress syndrome
389
What is acute respiratory distress syndrome?
Increased permeability of alveolar–capillary membrane, edema, hypoxemia caused by sepsis, trauma, DIC, drug overdose, inhalation of toxins, Goodpasture, SLE, drowning, bypass surgery.
390
What are the signs and symptoms of acute respiratory distress syndrome?
Dyspnea, increased respiratory rate, diffuse crackles, and rhonchi.
391
What are the chest x–ray findings in acute respiratory distress syndrome?
Diffuse interstitial or alveolar infiltrates; whiteout of both lung fields.
392
What are the blood gas findings in acute respiratory distress syndrome?
Decreased PaO2 and increased or normal PaCO2. Swan–Ganz catheter findings will reveal normal cardiac output and normal capillary wedge pressure, but increased pulmonary artery pressure.
393
What is the treatment for acute respiratory distress syndrome?
Mechanical support with increased positive end–expiratory pressure and permissive hypercapnia. Mortality rate 70%.
394
What is sleep apnea?
Cessation of airflow (\>10 seconds) that occurs at least 10–15 times per hour during sleep. Oxygen saturation decreases. Daytime somnolence. Systemic HTN. Pulmonary HTN and cor pulmonary.
395
What is obstructive sleep apnea?
Airway closure despite adequate ventilatory effort. Usually obese and have abnormal airways. Treatment is weight loss and nasal continuous positive airway pressure.
396
What is the central sleep apnea?
Central sleep apnea occurs in
397
How is sleep apnea diagnosed?
Polysomnography (sleep studies).
398
64–year–old man with headache and blurry vision. Neck vein distension and darker coloration over his face and neck. Confusion. Right upper lobe lung mass. Hypercalcemia. What is the diagnosis?
Bronchogenic carcinoma
399
What is the leading cause of cancer death in men and women?
Bronchogenic carcinoma is the leading cause of cancer death in men and women. 5–year survival rate for small cell cancer is 5% and non–small cell cancer is 8%.
400
What is the most common cause of bronchogenic carcinoma?
90% of bronchogenic carcinoma are directly related to smoking. 2 most common bronchogenic lung cancers are adenocarcinoma (40%) and squamous cell carcinoma.
401
What are the characteristics of squamous cell carcinoma?
Squamous cell carcinoma is centrally located. Cavitary lesions. Usually metastasizes by direct extension to hilar node and mediastinum. Hypercalcemia from the secretion of a PTH–like substance.
402
What are the characteristics of small cell carcinoma?
Central, rapidly growing, early metastasis to liver, adrenals, brain, bone. Associated with Eaton–Lambert syndrome (weakness), and paraneoplastic syndromes. Most common cause of venocaval obstruction syndrome.
403
What are the characteristics of large–cell carcinoma?
Peripherally located. Metastasize late in the course of disease.
404
What are the characteristics of adenocarcinoma?
Peripheral lesion metastasizes to liver, adrenals, brain, bone. Bronchioalveolar carcinoma is a subtype of adenocarcinoma; low–grade, may be caused by asbestos.
405
What are the symptoms of lung cancer?
Cough (74%), weight loss (68%), dyspnea (58%). Hemoptysis, chest wall pain, and post–obstructive pneumonia. Hoarseness indicates a nonresectable bronchogenic carcinoma.
406
How is lung cancer diagnosed?
Sputum cytology. Bronchoscopy for centrally located lesions. If there is a high degree of suspicion for carcinoma and the bronchoscopy results are nonspecific, a biopsy must be done.
407
What is the clinical evaluation of benign solitary pulmonary nodules?
75% of solitary nodules are benign. Benign nodules
408
What is the management of solitary pulmonary nodules in low–risk persons?
If a patient is at low–risk for carcinoma, follow–up CT scans are indicated. In a high–risk patient the lesion should be removed.
409
What is the significance of bull's–eye lesions and popcorn bull lesions on chest x–ray?
Bull's–eye lesions are seen in granulomas, popcorn ball lesions are seen in hamartomas.
410
What are the symptoms that suggest an unresectable lesion?
Wt loss \>10%, bone pain, extrathoracic metastases, CNS, superior vena cava syndrome, hoarseness, mediastinal adenopathy, TV
411
What is the treatment of small cell carcinoma?
Resectable lesions are treated with VP16 (etoposide, platinum). Non–small cell lesions are treated with chemotherapy and radiation therapy or cyclophosphamide, Adriamycin, and platinum. Effusions can be sclerosed.
412
67–year–old man dyspneic after cholecystectomy. Resp 24, pulse 100. Fever and decreased breath sounds in left lower lobe. Leukocytosis of 27,000. What is the diagnosis?
Atelectasis
413
What is atelectasis?
Collapse of part or the entire lung. Most commonly postoperative; caused by poor inspiration or lack of coughing, mucous plug, tumor, or foreign body.
414
What are signs of atelectasis?
Tachycardia, dyspnea, fever, hypoxemia. Tracheal deviation caused by volume loss. Diaphragm elevation . Mediastinal shift. Lobe will appear to be densely consolidated and smaller.
415
What is the treatment for atelectasis?
Induce deep breathing and stimulate coughing. Incentive spirometry and pulmonary toilet. Bronchoscopy with subsequent removal of mucous plugs.
416
After determining that the unresponsive patient is truly unresponsive, what is the next step?
Call for help. After calling for help, position the patient on a firm, flat surface, and roll the patient so that he is face up. Open the airway by performing the chin lift or jaw–thrust maneuver.
417
After opening the airway of an unresponsive patient, what is the next step?
After opening the airway, assess the patient's breathing by looking, listening, and feeling for air movement. If there is no air movement, then perform two rescue breaths with about two seconds per breath.
418
After delivering two rescue breaths to a non–breathing patient, what is the next step?
Check to see if there is a pulse by feeling for at least 5–10 seconds at the carotid artery.
419
If a patient has no pulse, what is the next action that should be taken?
If no pulse, perform chest compressions at a rate of 100 per minute, push hard and push fast: Provide 30 compressions and then two ventilations, regardless of whether one or two rescuers is present in adults.
420
What is the compression to ventilation ratio for CPR on a child?
In children, perform 30 compressions and 2 ventilations if one rescuer is present, and give 15 compressions and 2 ventilations if two rescuers are present.
421
What are the causes of asystole?
Ischemia and severe underlying cardiac disease. Metabolic derangements, drug overdose, trauma.
422
How is asystole diagnosed?
Asystole should always be confirmed by observing the rhythm in more than one lead on the ECG.
423
What is the treatment for asystole?
1 mg epinephrine IV q3–5min. Atropine 1 mg IV q 3–5min (max 0.04 mg/kg). Bicarbonate if cause of asystole is acidosis, or if the cause is tricyclic or aspirin overdose, hyperkalemia, or DKA. Pacing for very slow bradycardia.
424
What are the H's and T's of the causes of arrhythmias?
Hypoxia, Hyper/Hypokalemia, Hypothermia, Hypoglycemia, Hypovolemia, Trauma, Toxins (overdose), Tamponade, Tension pneumothorax, Thrombosis (coronary and pulmonary)
425
What are the ECG signs of ventricular tachycardia?
Ventricular tachycardia (VT) is a wide complex tachycardia with an organized, uniform sawtooth pattern on the ECG. There are no P–waves visible.
426
What are the causes of ventricular tachycardia?
Ischemia, MI, anatomic cardiac disease. Quinidine, tricyclics, phenothiazines. Long QT syndromes. The dysrhythmia originates from an ectopic focus in the myocardium or from the AV node.
427
What are the ECG characteristics of ventricular tachycardia?
The slowness of the conduction produces the slower and wider complexes on the ECG. The rate varies between 160–240 beats per minute.
428
What is the ECG appearance of torsade de pointes VT?
Torsade is a form of VT in which the morphology varies with an undulating amplitude, making it seem to twist around a point. Associated with hypomagnesemia.
429
What is the treatment of torsade de pointes VT?
Magnesium is most useful for torsade.
430
What is the presentation of ventricular tachycardia?
VT lasting more than 30 seconds is referred to as sustained VT. Symptoms include lightheadedness, hypotension, congestive heart failure, syncope, and death.
431
What is the treatment for unstable ventricular tachycardia?
Requires immediate synchronized cardioversion if hypotension, chest pain, altered mental, or CHF. A lower dose of electricity, starting at 100 J, can be used at first for monomorphic VT. Synchronized.
432
What is the management of ventricular tachycardia without a pulse?
Immediate synchronized cardioversion. VT without serious hemodynamic compromise can be treated with amiodarone. If there is no response, then lidocaine or electrical cardioversion is used.
433
What is the long–term therapy for ventricular tachycardia?
Long–term therapy is most effective with beta–blockers. VT producing sudden death or VT that is sustained through initial drug therapy requires placement of an implantable cardiac defibrillator.
434
What is pulseless electrical activity?
Loss of pulse with some type of electrical activity. Caused by hypovolemia, tamponade, tension pneumothorax, PE, MI, hypoxia, hypothermia, potassium disorders, acidosis, tricyclics, digoxin, beta–blockers, Ca–blockers.
435
What is the treatment for pulseless electrical activity?
CPR while determining the cause. Epinephrine. Atropine if there is bradycardia. Bicarbonate is useful if a known acidosis caused the arrest or in a prolonged resuscitation, or hyperkalemia.
436
What are the atrial dysrhythmias?
Atrial fibrillation, flutter, supraventricular tachycardia. Ectopic focus in atrium or re–entry at AV. Atrial dysrhythmias have normal conduction in ventricles. QRS normal and narrow. A normal P is not present.
437
What are the causes of supraventricular tachycardia?
Re–entrant around AV node. A–fib is most commonly caused by HTN, enlarged atria. Hyperthyroidism, pheochromocytoma, caffeine, theophylline, alcohol, cocaine, digoxin, pericarditis, PE, surgery, trauma, ischemia.
438
What percentage of cardiac output is attributable to the atria?
In normal heart, only 10% of cardiac output is from atria. In a person with a dilated or postinfarction heart, or in significant valvular disease, the contribution is 30–40%, in which case more severe symptoms arise.
439
What are the symptoms of supraventricular tachycardia?
Asymptomatic to palpitations, lightheadedness, hypotension, disorientation, CHF, syncope. Rate–related symptoms are unlikely if the heart rate is
440
How is supraventricular tachycardia diagnosed?
ECG and may need a 24–72 hour Holter monitor to detect brief paroxysms of the dysrhythmia not seen on the ECG.
441
What is the origin of narrow complex tachycardias?
Narrow complex tachycardia is always atrial in origin (QRS
442
What is the treatment for supraventricular tachycardia?
Hypotension, confusion, CHF, chest pain require synchronized cardioversion. If stable, use vagal maneuvers such as carotid sinus massage, Valsalva, ice water. If vagal maneuvers are not effective, give IV adenosine.
443
What drugs are used to slow the ventricular rate in supraventricular tachycardias?
For atrial fibrillation, atrial flutter, and in SVT after the failure of adenosine, slow the heart rate with calcium–channel blockers (such as diltiazem or verapamil), beta–blockers, or digoxin.
444
What are the contraindications for verapamil?
Severe left ventricular dysfunction and low EJECTION FRACTION. Beta–blockers are contraindicated in reactive airway disease.
445
What is the best treatment approach for atrial fibrillation?
Rate control to
446
What are the medications that convert atrial fibrillation to sinus rhythm?
Procainamide, amiodarone, ibutilide, sotalol, quinidine, propafenone, and dofetilide can convert a minority to sinus. Elective cardioversions should be preceded and followed by several weeks of Coumadin.
447
What is the treatment of atrial fibrillation that cannot be converted with antiarrhythmics?
If medications can not convert to sinus, then attempt electrical cardioversion. Preceded and followed by several weeks of anticoagulation if AF present \>48 h. Transesophageal echo can exclude a clot.
448
What is bradycardia?
Heart rate
449
What is the presentation of bradycardia?
Hypotension and decreased cardiac output. Mobitz–type I second–degree block is characterized by progressive P–R lengthening, whereas in Mobitz–type II, the P–R interval remains constant.
450
What is the treatment for asymptomatic bradycardia?
Asymptomatic bradycardia, first–degree block, Mobitz–type I (Wenckebach) second–degree block need no therapy.
451
What is the treatment for symptomatic bradycardia?
Symptomatic bradycardia is treated with atropine and pacemaker. Mobitz–type II second–degree block and third–degree block pacemaker. Dopamine or epinephrine if hypotension.
452
Which toxins cause miosis?
Clonidine, barbiturates, opiates, cholinergics, and pontine stroke.
453
Which toxins may cause mydriasis?
Sympathomimetics and anticholinergics.
454
Which toxins may cause dry skin?
Anticholinergics
455
Which toxins may cause profuse sweating?
Cholinergics, sympathomimetics.
456
What are the indications for gastric lavage?
Lavage is only useful within first hour after ingestion (usually not done). Contraindicated with acids or alkalis. If altered mental, lavage should be preceded by intubation. Large bore oropharyngeal hose (eg, an Ewald tube).
457
What are the indications for activated charcoal administration?
The main therapy for toxin ingestion is activated charcoal administration every 2–4 h to block absorption and accelerate the removal of toxins. Not effective for hydrocarbon or for metals such as iron.
458
What are the indications for whole bowel irrigation?
Large–volume pill ingestions in which the pills can be seen on x–ray. Gastric tube is placed and 1–2 L/h of GoLYTELY (polyethylene glycol) until the bowel movements run clear.
459
What medications should be given first to any patient with altered mental status or coma?
Naloxone, dextrose, and thiamine should be given first to any altered mental status or coma. Naloxone has no adverse effects and is immediately effective. Dextrose prevents permanent brain damage from hypoglycemia.
460
What are the substances or drugs that may require dialysis for removal?
Ethylene glycol poisoning, lithium overdose, methanol poisoning, aspirin overdose, theophylline overdose.
461
What amount of acetaminophen will cause serious toxicity?
140 mg per kg of acetaminophen causes serious toxicity. For a 70–kg person, 7–10 grams will cause toxicity. Fatalities can occur above 12–15 grams.
462
What is the presentation of acetaminophen overdose?
Nausea, vomiting from gastritis. At 24–48 h, there is subclinical elevation transaminases, bilirubin. At 48–72 h, liver damage, nausea, jaundice, abdominal pain, encephalopathy, renal failure, death.
463
What is the treatment of acetaminophen overdose?
Large acetaminophen ingestions warrant – acetyl cysteine. Nomogram based on drug level is necessary to determine risk of toxicity. Elevated AST is more common than ALT. Bilirubin, PT indicate hepatic necrosis.
464
What elimination measures are used for acetaminophen overdose?
Gastric emptying should not be used because it will delay NAC as a. Activated charcoal is given in repeated doses. When more than 24 hours have elapsed since ingestion, there is no therapy that can prevent toxicity.
465
What are the common causes of methanol ingestion?
Methanol paint thinner, Sterno, solvents, and windshield washer solution.
466
What is the most common source of ethylene glycol ingestion?
Ethylene glycol is most often found in antifreeze.
467
What is the pathophysiology of alcohol toxicity?
All alcohols are metabolized by alcohol dehydrogenase, which metabolizes methanol to formaldehyde and formic acid. Ethylene glycol is metabolized partially to oxalic acid and oxalate, which leads to kidney damage.
468
What is the presentation of ethanol, methanol, ethylene glycol, and isopropyl alcohol toxicity?
Methanol causes visual disturbances, including blindness. Ethylene glycol causes renal failure, oxalate crystals, stones. Isopropyl alcohol can only be distinguished by drug level or by non–anion gap acidosis.
469
What are the laboratory signs of isopropyl alcohol ingestion?
Isopropyl alcohol results in ketonuria and ketonemia with little to no metabolic acidosis (without evidence of an increased anion gap).
470
How is toxicity from the alcohols diagnosed?
Specific levels. Ethylene glycol has oxalate crystals in urine, increasing BUN/creatinine, hypocalcemia. Ethylene glycol and methanol cause metabolic acidosis with anion gap.
471
What is the treatment for ethylene glycol and methanol intoxication?
Fomepizole (Antizol) is an IV alcohol dehydrogenase inhibitor. Fomepizole inhibits the production of toxic metabolites without leading to intoxication.
472
What are the symptoms of carbon monoxide poisoning?
Dyspnea, tachypnea, and shortness of breath. Headache, nausea, and dizziness occur early. Confusion, syncope. Chest pain, arrhythmia, and hypotension.
473
What is the laboratory evaluation of carbon monoxide poisoning?
Carboxyhemoglobin levels. Metabolic acidosis is caused by the failure of carboxyhemoglobin to release oxygen to tissues. The pO2 will be normal. CPK is elevated. Pulse oximetry is not helpful.
474
What is the treatment of carbon monoxide poisoning?
100% oxygen administration. Hyperbaric oxygen in severe cases with CNS abnormalities or chest pain.
475
What are the common sources of acid ingestions?
Toilet, drain, swimming pool, and metal cleaners. Common alkali ingestions are lye, dishwasher detergents, hair relaxers, and oven cleaners.
476
What is the presentation of acid or alkali ingestion?
Oral pain, drooling, odynophagia, abdominal pain. Esophageal injury with subsequent stricture formation from acid or alkali ingestion. Gastric perforation. Alkali is more destructive than acid.
477
What is the treatment of acid or alkali ingestion?
Wash out the mouth with large volumes of cold water. Irrigate ocular exposures with saline or water. Do not induce emesis with either acids or alkaline ingestion because emesis can worsen the injury.
478
What conditions predispose to digoxin toxicity?
Poisoning is more common with renal failure. Hypokalemia predisposes to toxicity because potassium and digoxin bind to the same site on the sodium–potassium ATPase pump.
479
What is the presentation of digoxin toxicity?
Nausea, vomiting, diarrhea, anorexia, blurred vision, color vision, hallucinations. Bradycardia, PVCs, VT, arrhythmias. Paroxysmal atrial tachycardia is most common. HyperK from inhibition of Na+/K+ ATPase. Digoxin level.
480
What is the treatment of digoxin toxicity?
Repeated charcoal. Digoxin–antibodies (Digibind) for arrhythmias. Potassium correction. Phenytoin, lidocaine for ventricular arrhythmias. Pacemaker for bradycardia or block refractory to atropine.
481
What are the signs of opiate intoxication?
Death from acute respiratory acidosis. Analgesic and euphoric effects, pupillary constriction, constipation, bradycardia, hypothermia, hypotension. Opiates can be rapidly reversed by naloxone.
482
What is the mechanism of cocaine?
Cocaine blocks the re–uptake of norepinephrine at synapse.
483
What is the presentation of cocaine toxicity?
Alpha–adrenergic stimulation, HTN, hemorrhagic stroke, subarachnoid hemorrhage, MI, arrhythmia, seizures, death. Metabolic acidosis, rhabdomyolysis, hyperthermia. Pulmonary edema.
484
What is the treatment for cocaine toxicity?
Benzodiazepines control agitation. Alpha/beta agents, such as labetalol, or alpha–blockers, such phentolamine, for HTN. Pure beta–blockers, propranolol, should be avoided.
485
What are the signs of benzodiazepine overdose?
Somnolence, dysarthria, ataxia, stupor. Rarely cause death from respiratory depression. Most deaths from benzodiazepine are co–ingestion with ethanol or barbiturate. Flumazenil is not used because seizures.
486
What are the signs of barbiturate overdose?
Death from respiratory, CNS depression. Hypothermia, loss of tendon reflexes, corneal reflexes, coma, flat EEG. Withdrawal may result in seizures. Bicarbonate can increase the urinary excretion of phenobarbital.
487
What are the signs of hallucinogen ingestion?
Marijuana, LSD, mescaline, peyote, psilocybin can cause delirium, bizarre behavior, flushed skin, dry mouth, dilated pupils, urinary retention. PCP may cause seizures. Treatment is benzodiazepines.
488
What are the symptoms of lead toxicity?
Adults: Abdominal pain, anemia, renal disease, headache, memory loss. Children: Abdominal pain, anemia, lethargy, seizures, coma; mental retardation.
489
What are the laboratory signs of lead toxicity?
Blood lead levels \>10 mcg/dL. Lead lines are densities seen at the metaphyseal plate of the bones of children. Anemia and azotemia.
490
What is the treatment of lead overdose?
Chelation with calcium EDTA, dimercaprol (BAL), penicillamine, or succimer.
491
What are the signs of mercury toxicity?
Interstitial pneumonitis; tremors, excitability, memory loss, delirium, insomnia; nausea, vomiting, pain, bleeding.
492
What is the treatment of mercury toxicity?
Organic mercury is in paints and cosmetics. Treatment is oral chelation with succimer or dimercaprol.
493
What is the presentation of salicylate overdose?
Nausea, vomiting, gastritis, tinnitus. Stimulate respiratory centers to hyperventilation; salicylates directly toxic to lungs, causing edema. Hyperthermia, confusion, coma, seizures, encephalopathy.
494
What are the laboratory abnormalities in salicylate overdose?
Salicylates interfere with Krebs cycle and lead to metabolic acidosis. Salicylates cause lactic acid production with metabolic acidosis, an elevated anion gap and compensatory respiratory alkalosis.
495
How is salicylate overdose diagnosed?
Aspirin level. Elevated anion gap metabolic acidosis. Respiratory alkalosis early. An elevated prothrombin time and hypoglycemia.
496
What is the treatment for salicylate overdose?
Within the first hour after ingestion, gastric decontamination may be attempted. Charcoal and increase alkalization of the urine along with aggressive fluid resuscitation.
497
What is the pathophysiology of tricyclic antidepressant overdose?
Tricyclic antidepressants have anticholinergic and sodium channel blocker effects. Cardiac and CNS toxicities.
498
What is the presentation of tricyclic antidepressant overdose?
Anticholinergic dry mouth, tachycardia, dilated pupils, and flushed skin. Dysrhythmia, widening QRS, resulting in VT, and first–degree conduction blocks; confusion, seizures.
499
How is tricyclic antidepressant overdose diagnosed?
Serum drug levels, ECG: sinus tachycardia; prolongation of PR, QRS and QT.
500
What is the treatment for tricyclic antidepressant overdose?
Charcoal is the primary treatment in the acute setting. Any sign of cardiac toxicity should lead to the immediate use of bicarbonate, which protects the heart.
