Common learning
issues
Test 5
MOSBY’S
Arterial blood gases (p. 114-119)
• Monitor patients on ventilators, monitor critically ill
nonventilator patients, establish preoperative baseline
parameters, and regulate electrolyte therapy
• pH –log[H+]
• Acids normally found in blood: carbonic, dietary, lactic and
ketoacids
• Elevated indicates alkalosis
• Decreased indicates acidosis
• Normal pH: 7.35-7.45 (slightly larger range in infants and
children)
• pH (Venous): 7.31-7.41 - It is more acidic b/c it contains more CO2
Blood gases
• PCO2
• Measure of partial pressure of carbon dioxide in the blood
• Measure of ventilation (faster and deeper breathing removes
more CO2) PCO2 is a major medullary drive for respiration.
• 10% free floating in plasma, 90% carried by RBCs
• Respiratory component of acid-base determination
• Co2 and pH are inversely proportional
• Normal PCO2 = 35-45 mmHg (again infants and v. young children
wider range)
• PCO2 (venous) = 40-50 mmHg
• This is a measure of partial pressure, don’t confuse with HCO3concentration.
Blood gases
• HCO3- (or CO2 content) Concentration
• Measure of the metabolic component of the acid-base equilibrium
• Regulated by the kidney
• Directly proportional to pH (CO2 would be an indirect measure of
bicarbonate)
• In alkalosis kidneys excrete more into the urine to lower pH (compensating)
• Adult Normal HCO3-: 21-28 mEq/mL (infants lower)
• PO2
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Pressure of oxygen dissolved in plasma
Indirect measure of O2 content
Determines effectiveness of oxygen therapy
Determines the force of oxygen to diffuse across the pulmonary alveoli
membrane
Low if O2 diffusion difficulties (eg Pneumonia, shock lung, congestive failure)
Low if ventilation/profusion rations are off (under ventilated or over perfused
alveoli)
Normal PO2 = 80-100 mmHg (newborns less)
PO2 (venous) = 40-50 mmHg
Blood gases
• Oxygen saturation
• Percentage of hemoglobin saturated with oxygen
• As PO2 decreases so does saturation of hemoglobin (think about the sigmoidal shape of the
disassociation curve >75% stat, things are going very badly for the patient)
• Normal Adult/Child O2 saturation = 95%-100%
• Oxygen content
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The amount of oxygen in the blood
Nearly all of it is bound to hemoglobin
Arterial: 15-22 vol%
Venous: 11-16 vol %
• Base excess/deficit
• Amount of anions in the blood, bicarbonate being the largest. Also hemoglobin,
proteins, phosphates.
• Normal Base Excess = 0 +/- 2 mEq/L
• Negative base excess indicates metabolic acidosis (eg lactic acidosis)
• positive alkalosis (either metabolic or compensation to prolonged respiratory
acidosis)
• Alveolar to Arterial O2 difference
• Normally should be <10 mmHg
How to interpret ABG levels
• 1. Evaluation the pH
• If the pH is < 7.4
• If the pH is > 7.4
acidosis is present
alkalosis is present
• 2. Next look at the PCO2 (careful: text same, order different from book)
• A. If the PCO2 is high with acidosis = Respiratory acidosis (primary problem is with decreased
breathing eg drugs or lung disease)
• B. If the PCO2 is low with acidosis = Metabolic acidosis (with increased ventilation to blow off
of CO2)
• C. If PCO2 is high with alkalosis = Metabolic alkalosis (with compensatory retention of CO2,
down ventilation)
• D. If PCO2 is low with alkalosis = Respiratory alkalosis (Primary problem is hyperventilation)
• 3. Next look at the bicarbonate ion (HCO3-)
• Respiratory acidosis you would expect to see high HCO3- [kidneys compensating with
increased reabsorption]
• Metabolic acidosis you would expect to see a low HCO3- [lack of bicarb is part of primary
problem Ex: diabetes, renal failure]
• Metabolic alkalosis you would expect to see a high HCO3- [excess bicarb is part of primary
problem Ex: prolonged vomiting]
• Respiratory alkalosis you would expect to see a low HCO3- [kidneys decrease reabsorption to
compensate]
Blood Carbon Dioxide (p152 – 153)
• From peripheral venous blood
• Routinely obtained with CHEM 7 [DO NOT CONFUSE with
PCO2]
• Is an indirect measure of HCO3- (also measures the v. small
amounts of H2CO3 and dissolved CO2 in serum)
• HCO3- plays a major role in acid-base balance
• Levels of HCO3- are regulated by the kidneys
• Normal CO2 content = 23-30 mEq/L (mmol/L) [lower in kidsinfants]
• Diuretics can either increase or decrease this depending on
the class. [briefly ones that Increase: Loop diuretics Decrease:
thiazide diuretics + triamterene]
Blood Carbon Dioxide
Increases
• Severe vomiting
• b/c loss of acid in gastric secretions
• Hyperaldosteronism
• b/c aldosterone acts on intercalated
cells to stimulate proton secretion
that acidifies the urine and alkalizes
extracellular fluid
• COPD
• b/c compensatory increase for
chronic hypoventilation, PCO2 is
high
• Metabolic alkalosis
• Note: this is the definition of
metabolic alkalosis – an increase of
HCO3- anions in blood
Decreases
• Chronic diarrhea
• b/c loss of bicarb in lumen
• Chronic use of loop diuretics
• b/c increases loss of basic ions into
urine
• Renal failure
• b/c inability to alkalize extracellular
fluid
• Diabetic ketoacidosis &
Starvation
• b//c Ketoacids are neutralized by
bicarb and it lowers the amount in
serum
• Shock
• b/c lactic acid that builds up is
buffered by bicarb
• Metabolic Acidosis
• Note: this is the definition of
metabolic acidosis – a decrease of
HCO3- anions in blood
Blood chloride p164(
165*
pagesprovidedwereincorrect)
• Normal Cl- = 98-106 mEq/L (mmol/L) [Slightly wider range for
children]
• Performed in a CHEM 7
• Chloride is the major extracellular anion
• It’s primary purpose is to maintain neutrality (it often replaces
HCO3- intracellularly if bicarbonate is needed to buffer carbon
dioxide.
• Hypoclhloremia or hyperchloremia rarely occur alone and
usually correspond to sodium or bicarbonate changes.
Blood Chloride
Hypochloremia
• Signs and symptoms:
• Hyperexcitablity of nervous system and
muscles
• Shallow breathing
• Hypotension
• Tetany
• Causes:
• Over hydration
• SIADH
• Congestive heart failure
• Vomiting
• Chronic diarrhea
• Chronic respiratory acidosis
• Metabolic alkalosis (b/c chloride is driven into the
cell to compensate for the HCO3- that leaves the cell to
maintain blood pH)
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Salt-losing nephritis
Addison’s disease
Diuretic therapy
Hypokalemia
Aldosteronism
Burns (b/c sodium and chloride lost from burns can be
great)
Hyperchloremia
• Signs and symptoms:
• Lethargy
• Weakness
• Deep breathing
• Causes:
• Dehydration
• Excess normal saline infusion
• Metabolic acidosis
• Renal tubular acidosis
• Cushing syndrome
• Hyperparathyroidism
• Eclampsia (b/c chloride urinary excretion is
decreased)
• Respiratory alkalosis (b/c Chloride is
driven out of the cell in place of HCO3-)
Cholesterol (p166 – 167)
• Normal Findings:
Adult: <200 mg/dL
• Needed for production of steroids, sex hormones, bile acids, and cellular
membranes
• The main lipid associated with arteriosclerotic disease
• Metabolized by the liver
• 75% bound inside LDL and 25% is in HDL
• Main component of LDL (minimal in HDL and VLDL)
• Testing is typically part of a lipid profile (by itself is not an accurate predictor of
heart disease) [Ex: someone can have high cholesterol with high HDLs but low
LDLs]
• An Individual‘s cholesterol levels can vary daily by 15%. Positional changes affect
levels (15% decrease seen in lateral recumbent position, often seen in
hospitalized patients)
• Repeat tests should be done for abnormal values and an average will be
established
• Used to predict risk of CHD within the Framingham Coronary Prediction
algorithm (determines overall risk of ischemic event)
Cholesterol
• Increased levels:
• liver disease, pregnancy, oorophorectomy, postmenopausal status, familial hyperlipidemias or
hypercholesterolemias, hypothyroidism, uncontrolled diabetes mellitus, nephrotic
syndrome, xanthomatosis, hypertension, atherosclerosis, biliary cirrhosis, stress
• Drugs that increase levels:
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adrenocorticotropic hormone, anabolic steroids, beta-adrenergic blocking agents,
corticosteroids, cyclosporine, epinephrine, oral contraceptives, phenytoin, sulfonamides,
thiazide diuretics, and vit D
• Decreased levels:
• liver disease, malabsorption, malnutrition, acute myocardial infarction (6-8 weeks
following), advanced cancer, hyperthyroidism, cholesterol-lowering medication, pernicious
anemia, hemolytic anemia, sepsis, stress,
• Drugs that decrease levels:
• allopurinol, androgens, bile salt-binding agents, captopril, chlorpropamide, clofibrate,
colchicine, colestipol, erythromycin, isoniazid, liothyronine, MAO inhibitors, niacin, nitrates,
and statins
Blood Sodium (479 – 482)
• Blood Sodium (measured in a CHEM 7)
Adult/Ederly/children: 136-145 mEq/L (mmol/L)
Infant (134-150), and Newborn (134-144)
Critical: <120 or >160 mEq/L
• Major cation of the extracellular space (values as above; intracellular value of
only 5 mEq/L) Sodium salts are the major determinates of extracellular
osmolality.
• Dietary intake must be balanced with renal excretion. Sodium lost from sweat is
normally minimal.
• Aldosterone causes conservation of sodium through reabsorption in the kidneys
• Natriuretic hormone is stimulated by high sodium levels and decreases renal
absorption
• ADH controls the reasborption of sodium at the distal tubules of the kidney
(dilution or concentration)
• the 1st symptom of hyponatremia (signs begin <125) is weakness and may then
progress to (<115) confusion, lethargy, stupor, or even coma
Blood Sodium
• Causes of Hypernatremia:
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increased sodium intake
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Excess sodium in IV fluids
Increased dietary intake
Cause of Hyponatremia:
• decreased sodium intake
• increased sodium loss
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decreased sodium loss
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Cushing syndrome
Hyperaldosteronism
excessive free body water loss
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excessive sweating
thermal burns
diabetes insipidus
osmotic diuresis
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Drugs that may increase levels: anabolic steroids,
antibiotics, carbenicillin, clonidine, corticosteroids,
cough medicine, estrogens, laxatives, methyldopa,
and oral contraceptives
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Also recent trauma, surgery, or shock may cause
increased levels because renal blood flow is
decreased
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increased free body water
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Addison disease
Diarrhea
Vomiting
nasogastric aspiration
intraluminal bowel loss
diuretic administration
chronic renal insufficiency
excessive oral or IV H2O intake
Hyperglycemia
Congestive heart failure
peripheral edema
Ascites, peripheral edema, pleural effusion
Intraluminal bowel loss
SIADH – over secretion of ADH
Drugs that may decrease levels: ACE inhibitors,
captopril, carbamazapine, diuretics, haloperidol,
heparin, NSAIDs, sodium free IV fluids, sulfonylureas,
triamterene, tricyclic antidepressants, and vasopressin
Treatment of Hyponatremia: water restriction
Triglycerides (521 – 522)
Adult: Male 40-160 mg/dL
Female 35-135 mg/dL
Critical: >400 mg/dL
Children (yr)
Male (mg/dL)
Female (mg/dL)
0-5
30-86
32-99
6-11
31-108
35-114
12-15
36-138
41-138
16-19
40-163
40-128
• Produced in the liver using fatty acids and glycerol
• Transported by VLDL and LDL
• When levels are high, triglycerides are deposited in fatty tissues. Act as storage
of energy.
• Constitute most of the fat of the body
• Measured as part of a lipid profile
• Interfering factors:
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ingestion of fatty meals can cause elevated TG levels
ingesting alcohol causes increased VLDL levels, which increases TG
Pregnancy causes increased levels
Drugs causing increased TG levels: estrogen, oral contraceptives, cholestyramine
Drugs causing decreased TG levels: ascorbic acid (vit C), asparaginase, clofibrate,
fibrates, statins.
Triglycerides, pp. 521-522
• Increased levels:
• Ingestion of fatty meals, alcohol, pregnancy
• Glycogen storage disease
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Von Gierke disease (VLDL synthesis is increased and catabolism is decreased)
• Apoprotein CII deficiency
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(can’t activate LPL to unload the apoproteins so they accumulate in blood)
Hyperlipidemias, familial hypertriglceridemia
Hypothyroidism
High carb diet
Poorly controlled diabetes
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(VLDL synthesis is increased and catabolism is decreased)
• Nephrotic syndrome
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(the fall in oncotic pressure seems to stimulate the liver to produce VLDLs and LDLs)
• Chronic renal failure
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(insulin is excreted by the kidney, so in these patients insulin is high and it stimulates
lipogenesis)
• Decreased levels:
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Malabsorption
Malnutrition
Abetalipoproteinemia
Hyperthyroidism (catabolism of VLDLs increases therefore TGs blood levels fall)
Secretin-Pancreozymin (701702)
• This is a corroborative test used in the evaluation of Cystic Fibrosis. It is
indicated in children with recurrent respiratory tract infections,
malabsorption syndromes, or failure to thrive.
• Secretin and Pancreozymin are used to stimulate pancreatic secretions.
The duodenal contents are then aspirated and examined for pH,
bicarbonate, and enzyme levels.
• Secretin can be expected to stimulate pancreatic water and bicarbonate
secretion
• Pancreozymin can be expected to stimulate pancreatic enzyme (lipase,
amylase, trypsin, chymostrypsin) secretion
• Amylase is the most frequently measured enzyme
• Diminished values are suggestive of Cystic Fibrosis
• Due to the development of mucosal plugs pancreatic enzymes, bicarbonate
can not be secreted from the pancreas.
Sweat electrolytes (711-713)
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Children: sodium: <70 mEq/L (abnormal >90)
chloride: <50 mEq/L (abnormal >60)
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Sensitive and specific test used to diagnose Cystic Fibrosis
• does not measure the severity of the disease
Test is indicated in children with recurrent respiratory tract infections, chronic cough, early onset asthma, malabsorption issues, late
passage of meconuim stool, or failure to thrive
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CF patients will have increased sodium and chloride contents in their sweat
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Sweat, induced by electrical current (pilocarpine iontophoresis), is collected, and the sodium and chloride contents are measuredThe
• positive electrode is saturated with pilocarpine hydrochloride, a drug that induces sweating
• The negative electrode is saturated with a bicarbonate solution
• The electrical current flows for 5-12 mins
• Then paper disks with a paraffin airtight seal are placed over the test site for 1 hr. Then the paper is analyzed.
Test MUST be done multiple times to be useful as a diagnostic tool
In normal individuals, sweat produced at the bottom of a sweat duct is rich in sodium and chloride, but as it moves through the duct, the
chloride (followed by sodium)is transported through the cells lining the duct out of the sweat. This leaves behind water.
In CF patients, the epithelial lining cells in the sweat ducts fail to take up the electrolytes, leaving a high sodium and chloride content
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A screening test to detect chloride levels can be done by pressing paper containing silver nitrate against the child's hand for several
seconds. A positive test occurs when the child leaves a white powder, "heavy" handprint on the paper. Positive screens are followed up
by iontophoresis
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Other conditions that can have abnormal sweat tests include:
• G6PD deficiency
• Adrenal hypofunction
• Glycogen storage diseases
A cold room or dehydration can alter results. Adolescents going through puberty can have variable results and are not measured
accurately.
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Urine Osmolality (980-981)
Urine Osmolality
• 12-14 hr fluid restriction: >850 mOsm/ kg H2O
• Random specimen: 50-1200 mOsm/ kg H2O (depending on fluid intake)
• This test is an accurate determination of the kidney's concentration
capabilities
• Also used to evaluate ADH abnormalities and fluid and electrolyte
balance
• Measures the number of dissolved particles in the urine
• Most commonly measured by determining the freezing point
• More exact measurement of urine concentration than specific gravity
• because specific gravity depends on the weight and density of particles,
temperature, and requires correction for presence of glucose or protein
• Urine osmolality is more easily interpreted when the serum osmolality is
simultaneously measured
• Normal ratio of urine to serum osmolality of 1:3
Urine Osmolality
• Increased levels:
• SIADH
• ADH is inappropriately secreted despite factors normally would inhibit its secretion. As a
result, large quantities of water are reabsorbed by the kidney. (Low serum, high urine)
• Shock
• The normal response minimizes the loss of free body water. The kidney therefore absorb
all the free water possible.
• Hepatic cirrhosis and CHF
• These illnesses are associated with water retention because of reduced perfusion of the
kidneys.
• Paraneoplastic syndromes associated with carcinoma
• Ectopic secretion of ADH.
• Decreased levels:
• Diabetes insipidus
• Insufficient secretion of ADH in context of high serum osmolality, kidneys have
diminished concentrating ability (high serum, low urine)
• Excess fluid intake
• Renal tubular necrosis
• Severe pyelonephritis
• When kidneys are damaged the concentrating ability can be diminished
Blood Culture and Sensitivity
(p 747-749)
• Bacteremia can be intermittent and transient, except in endocarditis or
suppurative thrombophlebitis.
• Episodes of bacteremia are usually accompanied by chills and fever.
Blood drawn at times with these signs increases the likelihood of
yielding bacteria on culture.
• Draw at least 2 samples from 2 different sites. This helps eliminate
growth that may occur as a result of contamination. When both cultures
grow the infecting agent, bacteremia exists and is a result of that
organism.
• If the patient is currently receiving antibiotics, resin can be added to the
culture medium to negate the antibiotic effect in the culture.
• Cultures ideally are drawn before initiating antibiotics.
• Blood drawn from IV catheters are frequently contaminated. Only draw
blood from these in cases of suspected catheter sepsis to help identify
the causative organism.
• Most organisms require 24hrs to grow. 48-72 hours are required for
growth and identification of the organism. Anaerobic organisms may
take longer to grow.
Sputum Culture and Sensitivity
(p 802-804)
• Indicated in patients with persistent productive cough, fever,
hemoptysis, or a chest x-ray picture compatible with a pulmonary
infections.
• A gram stain is the first step in analysis
• The sample is then plated on several plates, bacteria that grow is
later identified. Preliminary reports usually after 24 hours.
• After 1-3 days of growth drug sensitivity testing is performed to
identify the most appropriate antibiotic treatment. Cultures require
at least 48 hours for completion.
• Antibiotic plugs (small infused disks) are put onto the plate. The ring
of inhibited growth around the disk indicates that the bug is sensitive
to that drug.
Note: culture for Mycobacterium tuberculosis (TB) take 6-8 weeks.
Stool culture (p896-898)
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Usually performed on patients with unrelenting diarrhea, fever and abdominal bloating. Especially if patient has
traveled outside the USA, has been drinking well water, or has been receiving prolonged course of antibiotics.
The normal stool flora can become pathogenic is bacterial overgrowth occurs as a result of antibiotics or
immunosuppression.
Most common bacteria in stool: (in no particular order)
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Pathogenic Bacteria:
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Enterococcus
Escherichia coli
Proteus
Pseudomonas
Staphylococcus aureus
Candida albicans (fungus)
Bacteroides
Clostridium
Salmonella
Shigella
Camplylobacter
Yersinia
Pathogenic E. coli, Clostridium, and Staphylococcus
Common parasites in stool:
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Ascaris (hookworm)
Strongyloides (tape worm)
Giardia (protozoans)
Cryptosporidium (esp in AIDs patients)
Note C. difficile normal in stool, problem when overgrown. H. Pylori can be found in stool, usually better cultured from
stomach or determined by serologic blood test.
Stool Culture
• Tape test:
• Tests for Pinworms (Enterobius)
• Clear tape in patient’s perianal region at night before bedtime.
Remove it in the AM before patient leaves bed. Female worm
lays eggs at night around this region.
• Press sticky side directly onto a glass slide.
• Can take up to 6 weeks to isolate.
• Parasitic enterocolitis:
• These organisms can be grown on a special culture plates. Can
also be detected in smears of stool.
Urinalysis (p1000-1016)
• Normal:
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Appearance: clear
Color: amber yellow
Odor: aromatic
pH: 4.6-8.0 (avg 6.0)
Protein: 0-8 mg/dL
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50-80 mg/24 hr (at rest)
<250 mg/24 hr (during
exercise).
Specific gravity: Adult 1.0051.030 (usually, 1.010-1.025)
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Elderly: values decrease with
age
Newborn: 1.001-1.020
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Leukocyte esterase: negative
Nitrites: none
Ketones: none
Bilirubin: none
Urobilinogen: 0.01-1
Crystals: none
Casts: none
Glucose: Fresh sample – none
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24 hr spec – 50-300mg/24hr
WBCs: 0-4 low power field
RBCs: <2
RBC casts: none
Urinalysis
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Indications: used as part of routine diagnostic and screening evaluations
can give info on kidneys, performed on essentially everyone
If UTI is suspected a clean-catch specimen is obtained and divided. Half
is sent to UA the other half is cultured.
Laboratory:
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Appearance: should be clear, cloudy indicates WBC, RBC or bacteria. Can
also be cloudy due to some food.
Color: color indicates concentration (urochrome) of urine and varies with
specific gravity. Dilute is straw colored and concentrated is deep amber.
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abnormal color may indicate bleeding from kidney (dark red) bleeding from
lower UT (bright red)
Dark yellow indicates urobilinogen or bilirubin
Pseudomonas could cause green urine
Beets cause red urine, rhumbarb causes brown urine
Porphyria can cause wine-colored or even dark brown urine
Chart on p 1002 goes over common drugs that change urine color.
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Ex (most commonly mentioned from all sources): Rifampin= red/orange urine
UA
• Odor: normal odor caused by presence of volatile acids.
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Diabetic ketoacidosis have strong, sweet smell of acetone
UTI causes foul odor
Fecal odor could be a fistulas
Long standing if breaks down and begins to smell like ammonia
Some food have characteristic urine odors
Genetic disease: Maple syrup urine disease and Phenylketouria
• pH
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Kidneys help maintain normal pH homeostasis. They assist in in
acid-base balance by resorbing sodium and excreting hydrogen.
Alkaline urine: indicates alkalemia, bacteria, UTI or citrus fruits or
vegetables, common after eating
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Alkaline causes calcium carbonate, phosphate and magnesium
phosphate stones
Acidic urine: dehydration, high meats and cranberries,
UA
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Protein
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Indicates if glomerular membrane is intact like in glomerularnephritis, protein then seeps
into urine and can lead to hypoproteinemia which decreases capillary oncotic pressure
causing edema called nephrotic syndrome
Proteinuria indicates renal disease or preeclampsia
Indicates complications of DM, glomerularnephritis, amyloidosis, multiple myeloma
Most commonly lost protein is albumin
Over 24 hour period if protein lost is >3000mg/24hrs patient has nephrotic syndrome.
Compared to creatinine to control for other factors such as hydration status
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Specific gravity
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Normal protein/creatinine ration is less than 0.15
High indicates concentrated urine
Low is dilute urine
Weight of urine compared to that of pure water
Chronic diseases associated with low specific gravity measure of hydration status
Dehydration causes it to be really high
Leukocyte esterase
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Positive indicates UTI. Tests form WBCs in urine.
UA
• Nitrites
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Screening for UTI, bacteria produce reductase converting nitrates to
nitrites
• Ketones
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Poorly controlled diabetes and hyperglycemia, massive fatty acid
catabolism
• Bilirubin and urobilinogen
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Conjugated bilirubin is water soluble, indicates disease affecting
bilirubin affecting bilirubin metabolism after conjugation or defects
in excretion indicate previously suspected liver disease, gallstones,
or drug toxicity
• Crystals
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Indicate renal stone formation is imminent
Can be with high serum uric acid levels
Parathyroid causes high phosphate and calcium crystals
Urinanalysis: Casts
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Casts
Rectangular clumps that form renal distal and collecting tubules, pH must be acidic and urine
concentrated. Always indicate renal origin.
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Hyaline
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Cellular
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Granular
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Conglomerations of degenerated cells
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After exercise and renal disease, result from disintegration of cellular material into granular particles
within a WBC
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Some diseases epithelial cells desquamate into renal tubule fatty droplets become free oval fat bodies or
incorporated into proteins associate with nephrotic syndrome or nephrosis, fatty emboli or bone
fractures
Fatty
Waxy
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Conglomerations of protein, proteinuria
Cell, hyaline, renal failure or further degeneration of granular casts, associated with chronic renal disease
and renal failure or diabetic nephropathy, malignant hypertension, and glomerularnephritis
Epithelial
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Shed from bladder from tumor, infection, or polyps
Tubule epithelial casts indicate glomerulonephritis
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Five or more indicate UTI involving bladder, kidneys, or both
Inflammatory nephritis, glomerulonephritis
pyelonephritis
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Bladder, urethral, and ureteral disease, tumor, trauma stones infection, glomerloneprhitis, renal infarct,
goodpasture, vasculitis, sickle cell, interstitial nephritis, tubular necrosis, pyelonephritis
WBC
RBC
Urinalysis: quick associations
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Bilirubin: Jaundice, hepatitis, fecal contamination of sample
Blood: Stones, BPH, infection, Foley cath
Glucose: DM, pancreatitis, steroids
Ketones: Starvation, high fat diet, diabetic ketoacidosis,
vomiting, diarrhea, aspirin overdose
• Leukoesterase: UTI
• Leukoesterase plus nitrates: 75% of UTI
• Neither LE or nitrates: 92% not UTI
• Protein: Renal failure, CHF
• Glucose, Ketones, Leukoesterase and bilirubin in urine is never
normal
Arteriography (p1039-1043)
• Injection of radiopaque contrast material (usually iodinated
CO2 can be used and an alternative) into arteries, blood
vessels can be visualized to determine arterial anatomy,
vascular disease or neoplasms.
• Catheter femoral or brachial artery and injected while x-ray
films are being obtained.
• Can see:
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Blood flow dynamics
abnormal blood vessels
vascular anomalies
Normal and abnormal vascular anatomy
Tumors
Arteriography
• Digital subtraction angiography (DSA)
• Allows bony structures to be removed from images, this enables better visualization of
arteries especially the carotid and cerebral arteries
• Renal Angiography
• Differentiate cysts from hypervascular cancers (Highly vascular tumors can produce a “blush”
of contrast material)
• Evaluate blood flow dynamics
• Adrenal Angiography
• Hyperplasia, benign or malignant neoplasms can be detected
• Risk of hemorrhage leading to adrenal insufficiency
• With pheochromocytomas risk or hypertensive crisis
• Cerebral Angiography
• Injected into carotid or vertebral arteries
• To ID: Aneurysms, occlusions, stenosis, AVMs, vascular and non-vascular tumors, abscesses,
hematoma
• Lower-Extremity Angiography
• Allows identification and location of occlusions within the abdominal aorta and lowerextremity arteries. Also Aneurysmal dilations, arterial trauma such as intimal tearing, emboli.
• Some vasculitis show up as characteristic “beading”
Note that iodinated contrast is nephrotoxic
DRUGS TO KNOW
Drug
Uses
Side effects
Contraindications
Therapeutic
considerations
Captopril
Pg 349
Class: ACE inhibitor
Mech: decreases conversion
of AT I to AT II decreasing
arteriolar vasoconstriction,
aldosterone synth, renal
proximal tubule NaCl
reabsorp. and ADH release.
Also inhibit degradation of
the vasodilator, Bradykinin
Indications:
•
Hypertension
•
Heart failure
•
Diabetic Nephropathy
•
Myocardial Infarction
• Angioedema (more
frequent in black
patients)
• Agranulocytosis
• Neutropenia
• Cough
• Edema
• Hypotension
• Rash
• Gynecomastia
• hyperkalemia
• History of angioedema
• Bilateral renal artery
stenosis
• Renal failure
• pregnancy
• Given as active drug
and processed to
active metabolite
• Cough and
angioedema caused by
bradykinin action
• Hyperkalemia risk
increased when used
with potassiumsparing diuretics
• First-dose hypotension
more common in
patients with bilateral
renal stenosis
Furosemide
Pg 351
Class: Loop diuretic
Mech: reversibly and
competitively inhibit
Na+/K+/Cl- co-transporter in
apical membrane of thick
ascending limb
Indication:
• Hypertension
• Acute pulmonary edema
• Edema from heart failure,
hepatic cirrhosis, or renal
dysfunction
• Hypercalcemia
• Hyperkalemia
•
•
•
•
• Co-admin with
aminoglycosides increases
ototoxicity and
nephrotoxictiy
• Sulfonamide derivative
• Front-line therapy for
listed indications
• Can counteract
hypercalcemic and
hyperkalemic states
•
•
•
•
•
Hypotension
Pancreatitis
leukopenia
Volume contraction
alkalosis
Hypokalemia
Hyperuricemia
Hypomagnesemia
Hyperglycemia
Glycouria
Drug
Uses
Side effects
Contraindications
Therapeutic
considerations
Cefazolin
Class: Cephalosporins
have a six-membered
accessory ring attached to the
Beta-lactam ring.
Mech: Beta-lactams inhibit
transpeptidase by forming a
covalent (“dead-end”) acyl
enzyme intermediate
Indication:
• Proteus mirabilis
• E. Coli
• Kiebsiella pneumoniae
• Pseduomembranous
enterocolitis
• Leukopenia
• Thromobocytopenia
• Hepatotoxicty
• Nausea
• Vomiting
• Diarrhea
• Rash
• Hypersensitivity to
cephalosporins (rarely
crose-react with
penicillins)
• First-generation
cephalosporins
• Relatively good Grampositive coverage
• Sensitive to many betalactamases
•
•
•
•
• Co-admin with tizanidine
• Hypersensitivity
• Resistance: thru
chromosonal mutations in
genes that encode type II
tops, or thru alterations in
expression of membrane
porins and efflux pumps that
determine drug lvls in
bacteria
• Bacteriostatic at low conc.
• Bactericidal at high conc.
First Aid:
1st Gen
Cephalosporins
Gram (+) and
“PEcK”
• Skin and soft-tissue
infections
• Surgical prophylaxis
Ciprofloxacin
pg596
Class: Quinolones: inhibitor
of topoisomerase
Mech: inhibit bacterial type
II topoisomerases; causing
dissociate of Top II (DNA
gyrase) from cleaved DNA,
leading to double stranded
breaksand cell death
Indication:
• Gram (-) infections
• Common Upper Resp
Infections
• UTI
• GI infections
•
•
•
•
Cartilage damage
Tendon rupture
Periph. Neuropathy
Increased Intracranial
pressure
Seizure
Severe hypersensitivity
reaction
Rash
GI disturbance
(Nausea/ Vomiting,
diarrhea)
Drug
Uses
Side effects
Contraindications
Therapeutic
considerations
Metronidazole
Class : Nitroimidazole
Mech: activated by
enzymes in parasites and
anaerobic bacteria to
form reduced cytotoxic
compounds (ROS) that
damage microbial
proteins, membranes,
and DNA.
Indication:
• Anaerobic bacteria
• Amebiasis
• Giardiasis
• Trichomoniasis
•
•
•
•
Leukopenia
Thrombocytopenia
Ototoxicity
Disulfiram-like effect
with alcohol
gastrointestinal
disturbance
Handache,
Neuropathy
Metallic taste
Vaginitis
• Hypersensitivity to
metroniazole or other
nitromidazole agents
• Hypersensitivity to
parabens (gel formulation)
• First trimester of pregnancy
• Concomitant alcohol
administration leads to
disulfiram-like reaction
• Active against E.
histolytica trophozoites
in tissues, but much
less active against
intraluminal ameba
• Individuals with
invasive amebiasis are
typically treated first
with mitronidazole and
then with a second
agent such as
iodoquinol or
paromomycin
Class: alpha2 adrenergic
agonist
Mech: selectively activate
central alpha2-adrenergic
auto-receptors to inhibit
sympathetic outflow from
CNS
Indication:
• Hypertension
• Opioid withdrawal
• Cancer pain
•
•
•
•
•
Bradycardia
Hypotension
Heart failure
Hepatotoxicity
(side effects related
to depressed
sympathetics and
increased vagal
response)
• Not listed
• Used for HTN and
symptoms of opioid
withdrawal
From first aid
(used for anaerobes
below the diaphragm)
Pharm 1-liners
(DOC for
pseudomembranous
enterocolitis – C. diff)
Clonidine
Pg 144
•
•
•
•
•
Drug
Uses
Side effects
Contraindications
Therapeutic
considerations
Linezolid
Class: Oxazolidinones
Mech Exact mechanism remains
uncertain
Indications:
• Gram-postive bacterial infections
Especially
• vancomycin-resistant enterococcus
• Methicillin-resistant S. aureus
(MRSA)
• S. agalactiae
• S. pneumoniae (including multidrug
resistant strains)
• S. pyogenes
• Nosocomial pneumonia
• Complicated diabetic foot infections
• Myelosuppression
• Peripheral
neuropathy
• Optic neuropathy
• Gastrointestinal
disturbances
• Headache
•
• Linezolid is available in
both oral and IV
formulations
Cisplatin
Pg 696
Class: Directly modify DNA structure
Mech: Platinum compound that crosslinks intrastrand guanine bases
Indications:
• Genitourinary
• Lung cancer
• Nephrotoxicity
• Myelosuppression
• Peripheral
neuropathy
• Ototoxicity
• Electrolyte
imbalance
• Severe bone marrow
depression
• Renal or hearing
impairment
• Can be injected
intraperitoneally for
treatment of ovarian
cancer
• Co-administration of
amifostine can limit
nephrotoxicity
Etoposide
aka VP-16
Pg 691 & 697
Class: Antineoplastic agent:
Topoisomerase inhibitor
Mech: bind topoisomerase II and DNA,
trapping the complex in its cleavable
state
Indications:
•
Lung cancer
•
Testicular cancer
•
Leukemia
• Heart failure
• Myelosuppression
• Alopecia (hair
loss)
• Rash
• GI disturbance
• hypersensitivity
• Class breakdown:
• Antineoplastic->
topoisomerase
inhibitors->
epipodophyllotoxin
• Action is specific to
late S and G phases of
cell cycle
Hypersensitivity to
linezolid
Drug
Uses
Side effects
Contraindications
Therapeutic
considerations
Vancomycin
pg614
Class: Inhibitor of murein
polymer synthesis
Mech: Bind to D-Ala-D-Ala
terminus of the murein
monomer and inhibit PGT
preventing addition of
murein units to the growing
chain
Indication:
• MRSA (IV admin)
• Serious skin infections
involving staph or strep
(IV admin)
• C. Difficile
enterocolitis(oral)
•
•
•
•
•
Neutropenia
Ototoxicity
Nephrotoxicity
Anaphylaxis
“Red-man syndrome”
(flushing and
erythroderma)
• Drug fever
• Hypersensitivity rash
• Co-admin with Gentamycin
• Solutions containing
dextrose in patients with
known corn allergy
• Increased nephrotox
with aminoglycosides
• “red-man syndrome”
can be avoided by
slowing infusion rate or
preadministering
antihistamines
• Resistance: arises thru
acquisition of DNA
encoding enzymes that
catalyze formation of
D-Ala-D-lactate
• Used for Gram (+) rods
and cocci
• Gram(-) rods are
resistant
Methicillin
Pg 615
Class: Penicillins: inhibitors
of polymer cross-linking
Mech: Beta-Lactams inhibit
transpeptidase by forming a
covalent (“dead-end”) acyl
enzyme intermediate
Indication:
• Skin and soft tissue
infections or systemic
infection with Blactamase- producing
methicillin-senstive S.
aureus
• All side effects listed are
for the other drugs in
this class
• Hypersensitivity to
penicillins
• Beta-lactamase
resistant
(staphlococcal)
• Narrow-spectrum
antibacterial activity
• Gram (+) only
• Is a hydrophobic
substance
• Penicillins have a 5membered ring
attached to the betalactam ring
For boards this drug is
important because of the
resistance of MRSA.
Methicilin is actually quite
toxic (acute interstital
nephritis) and rarely used
clinically.
• MRSA has the gene
mecA which changes the
binding site.
Drug
Uses
Side effects
Contraindications
Therapeutic
considerations
Trimethoprim
Pg 579
Class: Antimicrobial
dihydrofolate reductase
inhibitor
Mech: folate analogue;
competitively binds
microbial DHFR to
prevent regeneration of
tetrahydrofolate from
dihydrofolate
Indications:
• Urinary Tract Infection
• Stevens-Johnson
syndrome
• Leukopenia
• Megaloblastic anemia
• Rash
• pruritus
• Megaloblastic anemia due
to folate deficiency
• Used with medication
below to limit
resistance
development
•
Excreted unchanged
into urine
Class: Antimircrobial
dihydropteroate synthase
inhibitor
Mech: PABA analogue
that competitively inhibit
microbial
dihydropteroate synthase
and thereby prevent the
synthesis of folic acid
Indications:
•
Pneumocystis carinii
pneumonia
(CD4<200)
•
Shigellosis
•
Traveler’s diarrhea
•
UTI
•
Granuloma inguinale
•
Acute otitis media
•
• Infants less than 2 months
old
• Pregnant women at term
• Breastfeeding
• Megaloblastic anemia due
to folate deficiency
• Co-administration with
PABA
• Used with medication
above to limit
resistance
development
• Indications listed for
TMP/SMX
combinations
• Compete with bilirubin
for binding sites on
serum albumin and can
cause kernicterus in
newborns; can also
cause brain damage
•
“Bactrim” =
Trimethoprim/
Sulfamethoxazole
Sulfamethoxazole
Pg 579
•
“Bactrim” =
Trimethoprim/
Sulfamethoxazole
TMP/SMX is an
acceptable
appreivation
•
•
•
•
•
•
•
•
Kernicterus in
newborns
Brain damage in
newborns
Crystalluria
Stevens-Johnson
syndrome
Agranulocytosis
Aplastic anemia
Hepatic failure
GI disturbance
rash
Mietzner guide to
bacterial tests
Directly from his powerpoint
Catalase Test
Differentiates
-Streptococci (-) from Staphylococci (+)
-Clostridia (-) from Bacillus (+)
4/16/2013
• Detects the presence of catalase, and enzyme the converts
hydrogen peroxide to water and oxygen. The liberated oxygen
causing bubbles.
Catalase Test
Cocci
4/16/2013
Gram Positive
Rod
Catalase Test
Positive
Negative
Staphylococcus
Positive
Negative
Bacillus
Streptococcus
Clostridia
COAGGULASE Test
4/16/2013
• Detects the presence of coagulase. This enzyme acts with a
plasma factor to convert fibrinogen to a fibrin clot
• Used to differentiate Staphylococcus aureus (pos) from
Staphylococcus epidermidis (neg)