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Medical Diagnosis > Lecture 8 (labs)-Exam 4 > Flashcards

Lecture 8 (labs)-Exam 4 Flashcards

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USMLE® Step 1 flashcards
1
Q
  • What is a BMP?
  • What does it provide important inform?
A

A test that measures eight different substances in your blood

Provides important information about:
* Electrolyte and fluid balance
* Kidney function
* Acid and base balance
* Blood sugar levels

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2
Q

What does a BMP include?

A
  • Sodium, potassium, carbon dioxide, chloride, BUN, Creatinine, glucose

Call out (CO2) salty (NaCL) bananas(K), on sugary (glucose) protein (creatinine) buns (bun)

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3
Q

What does cmp include?

A

Same as BMP but also includes albumin, bilirubin, liver function tests/LFT’s (ALP, ALT, and AST)

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4
Q

What can a BMP/CMP help you discover?

A
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5
Q
  • What is sodium? What is it involved in ? ⭐️
  • How it the cont/ between ECF and ICF maintained?
  • Sodium absoprtions occurs where?
  • Sodium is closely linked to what and what is it maintained by?
    *
A
  • Sodium is the major cation of extracellular fluid and essential nutrient involved in normal cellular homeostasis, regulation of fluid, and blood pressure
  • The concentration between ECF and ICF is maintained by the sodium-potassium pump activity
  • Sodium absorption occurs almost exclusively
    in the distal small bowel and colon
  • Sodium balance is closely linked to that of water and maintained by the kidney – VERY COMPLEX
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6
Q

When can sodium deficiency happen?

A

It can happen in pathologic conditions like severe adrenal insufficiency, sodium-losing kidney disease, extensive burns, chronic diarrhea/vomiting, DKA, or lung cancer (SIADH)

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7
Q

⭐️

What is hyponatremia?

A

low sodium

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8
Q

⭐️

What is the excess of salt called and recognized in what?

A
  • The excess of salt (hyper-natremia) is recognized causative factor of hypertension and cardiovascular disease
  • Also contributes to the development of chronic kidney disease, gastric cancer, calcium nephrolithiasis, and
    osteoporosis
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9
Q

FRACTIONAL EXCRETION OF SODIUM (FENa)
* Can be calculated by what?
* Used to determine what?
* Sensitivity and specificity found during testing of this theory/equation shows what?

A
  • Calculated by measuring creatinine and sodium levels in the blood and urine simultaneously
  • Used to determine tubular handling of sodium to define which issue the kidney is dealing with: pre-renal azotemia vs acute tubular necrosis
  • Sensitivity and specificity found during testing of this theory/equation shows has most utility in oliguric patients without CKD/diuretic use
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10
Q

What does the FENa <1% adn FENa >1% mean?

A
  • <1% indicated pre-renal azotemia
  • > 1% indicates tubular damage and intrinsic kidney injury aka ATN
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11
Q

What is pre-renal, intrinsic and post renal?

A
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12
Q

Potassium:
* Main what? What is it involved in?
* Where is it present?
* Absorbed why what?

A
  • The main intracellular cation in the body and is involved in membrane potential and electrical excitation of both nerve and muscle cells
  • Present in all body tissues
  • Absorbed in the small intestines
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13
Q
  • Postassium is maintained by what?
  • How is K mainly excreted in?
A
  • Maintained by the sodium/potassium pump (remember: intracellular concentration of K+ is higher than the extracellular concentration)
  • Ingested potassium is mainly excreted in the urine (approx. 80-90%)
  • The remaining 10-20% is excreted in feces and sweat
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14
Q

The potassium that is filtered by the kidney glomerulus is reabsorbed through the tubule
* What does high extraceullular K levels stimulate?
* When potassium is added as a preservative or as a supplement it is usually what?

A
  • High extracellular potassium levels stimulate the release of aldosterone, which promotes increased distal tubular secretion of potassium into the urine
  • When potassium is added as a preservative or as a supplement it is usually potassium chloride, in fruits and vegetables it can be potassium citrate, potassium phosphate, or potassium sulfate,
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15
Q
  • What is hypokalemia?
  • What are midle, moderate to severe hypokalemia sxs?
A

Hypokalemia (K+ <than 3.6mmol/L)
* Affects up to 21% of hospitalized patients-usually because of use of diuretics and other medications
* Mild hypokalemia symptoms: constipation, fatigue, muscle weakness, and malaise
* Moderate to severe hypokalemia (K+ < 2.5mmol/L) symptoms: polyuria, encephalopathy in patients with kidney disease, glucose intolerance, muscular paralysis, and cardiac arrhythmias

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16
Q

⭐️

What are the severe hypokalemia sx? (think ekg)

A

Severe hypokalemia symptoms: life threatening because of effects on muscle contraction and cardiac function
* Typical electrocardiographic (ECG) features of hypokalemia include widespread ST depression, T wave inversion, and prominent U waves. Hypokalemia may present with different types of arrhythmia, such as premature ventricular contractions, ventricular fibrillation, atrial fibrillation, and torsade de pointes.

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17
Q

Rarely caused by low dietary intake, but can result from what (4)

A
  • diarrhea/vomiting, laxative use, repeated enemas, refeeding syndrome
  • diuretic use
  • Dialysis
  • lack of absorption with Crohn’s disease
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18
Q

Hyperkalemia:
* What happen in healthy people?
* What happens in patients with impaired urinary? In who?

A
  • In healthy people with normal kidney function, high dietary potassium intakes do not pose a health risk because the kidney secretes the excess in the urine
  • HOWEVER, patients with impaired urinary potassium excretion due to CKD or the use of ACEI/potassium sparing diuretics can develop hyperkalemia
  • ACEI/ARB and K+ sparing diuretics reduce urinary potassium excretion increasing extracellular concentrations
  • Can also occur in patients with DM Type I, CHF, adrenal insufficiency, or liver disease
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19
Q
  • Cellular injury can release large quantities of intracellular K into where?
  • What can this be due to?
  • Metabolic acidosis may cause what?
A
  • Cellular injury can release large quantities of intracellular K inot the extracellular space
  • Dt rhabdomyolysis, crush injury, excessive exercise, or other extracellular space
  • Metabolic acidosis may cause intracellular potassium to shift into the extracellular space without red cell injury– shock, DKA, sepsis
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20
Q

Mild hyperkalemia can be what? (sx)
* What is more imp? explain

A
  • Mild hyperkalemia can be asymptomatic, symptoms usually develop at higher levels>6/5mEq/L, but the rate of change is more important than the value
  • Chronic hyperkalemic patients may be asymptomatic at increased levels, but acute shifts can cause severe symptoms at a lower value
  • but severe hyperkalemia can caused muscle weakness, paralysis, paresthesia’s (burning/prickling sensation in extremities), and cardiac arrhythmia
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21
Q

Elevated potassium causes ECG changes in a dose- dependent manner, explain the changes?

A
  • K = 5.5 to 6.5 mEq/L ECG will show tall, peaked t-waves
  • K = 6.5 to 7.5 mEq/L ECG will show loss of p-waves
  • K = 7 to 8 ECG mEq/L will show widening of the QRS complex
  • K = 8 to 10 mEq/L will produce cardiac arrhythmias, sine wave pattern, and asystole
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22
Q

Chloride:
* lots or little?
* Key role in what?
* An abnormal chloride level usually signifies what?
* Chloride can be tested in what?

A
  • The second most abundant electrolyte in the serum
  • Key role in the regulation of body fluids, osmotic, metabolic
    electrical neutrality, acid-base status
  • An abnormal chloride level usually signifies a more serious underlying metabolic disorder (such as metabolic acidosis or alkalosis)
  • Chloride can be tested in sweat, serum, urine, and
    feces
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23
Q

Chloride:
* It is absorbed where?
* How is it excreted? What is there a close interrelationship between?

A
  • It is absorbed in the gut and then the chloride anions are freely transported in the blood
  • Renal excretion of chloride is coupled to that of sodium and potassium
  • There is a close interrelationship between sodium and chloride - excreted in similar amounts
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24
Q

How might a person get hypocholoremia?

A
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25
Q

Hypercholoremia:
* Chloride excess secondary to what?
* Usually caused by what? What are other conditions?

A
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26
Q

CO2/bicarb
* What is it know how?
* What does your blood do?
* Your kidneys also help with what?
* Bicarb works with what?

A
  • Bicarbonate is also known as HCO3 – it’s a byproduct of your body’s metabolism.
  • Your blood brings bicarbonate to your lungs, it is exhaled as carbon dioxide
  • Your kidneys also help regulate bicarbonate- it is excreted and reabsorbed by your kidneys
  • Bicarbonate works with Na, K+, and CL to regulate your body pH – basically gives a rough estimate of your acid-base balance
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27
Q
  • Bicarb measures waht?
  • helps you diagnose what?
A
  • This value measures the total amount of carbon dioxide in the blood, which occurs mostly in the form of HCO3-
  • Helps to diagnose acidosis vs alkalosis
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28
Q

What are causes for high and low bicarb?

A
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29
Q

Blood urea nitrogen:
* What does it meaure?
* What is urea nitrogen the end product of?
* When amino acids are metabolized, nitrogen is formed into what?

A

Measures the amount of urea nitrogen in the blood
* Urea nitrogen is one of the significant end-products
of protein metabolism
* When amino acids are metabolized, nitrogen is formed into ammonia, which is highly toxic to cells. Ammonia is converted into urea through the urea cycle so the kidneys can excrete it.

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30
Q

BUN:
* What is it used to assess?
* When kidneys aren’t working correctly, what happens to BUN?
* urea production can vary independently of kidney function so BUN test alone is not what?

A

Used to assess kidney function
* When kidneys aren’t working correctly, BUN increases as less urea gets excreted in the urine
* However, urea production can vary independently of kidney function so BUN test alone not helpful to asses kidney health

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31
Q

What two levels can be used to determine renal failure?

A

BUN is combined with creatinine to create the BUN/creatinine ration which can help determine renal failure

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32
Q

What causes a high bun?

A
  • Impaired kidney function
  • High protein diet
  • Dehydration
  • Congestive heart failure – cardio-renal syndrome
  • Increased protein breakdown from things like GI bleeding, trauma, or corticoid therapy
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33
Q

What can cause a low bun?

A
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34
Q

Creatinine:
* What is the prinicple function of kidney? What are they crucial for?
* What is creatinine the product of? ⭐️

A
  • Principle function of kidney is formation of urine from filtered blood- it is the vehicle for excretion of toxic/waste products of metabolism (i.e creatinine, water, sodium, potassium, etc). Kidney’s are crucial for balancing the excretion amount based on variability of volume to preserve normal fluid, electrolyte and acid- base balance
  • Creatinine is the product of muscle creatinine catabolism
  • Daily around 1-2% of creatine in muscle is converted to the waste product, creatinine, which is then released from muscle cells to the circulation

The amount of creatinine produced varies with the subjects body muscle mass

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35
Q

Why and when should creatinine should be measured?

A
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36
Q

Creatinine is excreted primarily by what?
* What will happen with the creatinine levels when GFR goes down? ⭐️

A

Creatinine is excreted primarily by the kidneys- freely filtered by the glomerulus, THUS a decreased GFR will allow for less filtration resulting in increased levels of creatinine

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37
Q

What causes high and low creatinine levels?

A
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38
Q
  • What is creatinine clearance?
  • Both CrCl and GFR can be measured using what?
  • Creatinine clearance can be estimated using what?
  • What formula is used to predict CrCl
A
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39
Q
  • The BUN/Creatinine ratio is useful in what?
  • What does a increase or decrease in the rato cause?
A
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40
Q

What is the ratio of bun/creatinine ratio in chronic renal disease?

A

In most cases of chronic renal disease the ratio remains relatively normal.

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41
Q
A
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42
Q

What is prerenal, renal azotemia and postrenal azotemia due to?

A
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43
Q

Acute kidney injury (AKI) generally defined as what?
* What classification is used?

A
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44
Q

What is the rifle criteria?

A

Risk, Injury, Failure, Loss, and End-stage Kidney (RIFLE) Classification

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45
Q

Researchers around the world are discovering biomarkers that
can be detected in what for AKI?
* What is it used for?
* Created a clinical pathway to follow what?

A
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46
Q

GLOMERULAR FILTRATION RATE (GFR)
* What does it represent?
* The kidney receives what?
* What is the GFR?
* What are the two types?

A
  • GFR represents the flow of plasma from the glomerulus into Bowman’s space over a specified period and is the chief measure of kidney function
  • The kidneys receive 20-25% of the cardiac output with the blood entering individual glomerular tufts via the afferent arteriole and exiting through the efferent arteriole
  • GFR is approximately 120 ml per min
  • Estimated GFR vs measured GFR
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47
Q

What is the different between Estimated GFR vs measured GFR?

A
48
Q

What is GFR used to stage what? List the stages

A
49
Q

Glucose:
* Can be meaursed how?
* What labs?
* How do we get the glucose in the bloodstream?

A
50
Q

HGBA1C
* What does glucose attach to?
* The glycated hemoglobin remains for how long?
* therefore what can be analysis?

A
  • Glucose molecules tend to attach to hemoglobin
  • The glycated hemoglobin remains for the life of the rest blood cell, approx. 120 days
  • Therefore analysis of the RBC and its glycated hemoglobin reveals the average blood glucose level
51
Q

For HGBA1C:
* What levels are normal, prediabetes and DM?

A
52
Q

HYPERGLYCEMIA
* What are the etiologies (4)

A
  • Inadequate insulin administration in patients with DM
    type I
  • Insulin resistance with or without diagnosed DM type II
  • Stress related experiences – surgery, critical illness
  • “dawn phenomena” – hormone surge between 4-5am
    that causes a spike in blood glucose levels
53
Q

What are the sx of hyperglycemia?

A
  • Polyuria – increased and frequent urination
  • Polydipsia – increased thirst
  • glucosuria
  • Blurred vision
  • Headache
  • Fatigue
54
Q

What can untreated and long term hyperglycemia cause?

A
55
Q

HYPOGLYCEMIA
* What is the etiology?

A
56
Q

HYPOGLYCEMIA
* What are the sx?

A
57
Q

Why do you need to treat hypoglycemia?

A
58
Q

What does a CMP include (not the BMP part)? What does each one of these do?

A
59
Q

Albumin:
* MC what?
* Represents what?
* Albumin is synthesized by what?
* Fuctions as what? ⭐️
* In clinical medicine, serum albumin has been advocated as a marker for an individual patients what? ⭐️

A
  • Albumin is the most abundant circulating protein found in plasma
  • Represents half of the total protein content of plasma in healthy human patients
  • Albumin is synthesized by liver hepatocytes and rapidly excreted into the bloodstream
  • Functions as a significant modulator of plasma oncotic pressure and transporter
  • In clinical medicine, serum albumin has been advocated as a marker for an individual patients nutritional status/frailty
  • It can also be used to give some insight into patients liver function or the ability to biosynthesize proteins and factors
60
Q

Alkaline phosphatases (ALP)
* What is this? Where does it originate from?
* We don’t know the full range of ALP’s function but contributes to what?

A
  • Alkaline phosphatases (ALP) is an enzyme found in the cytosol of liver cells and canalicular membrane of hepatocytes – over 80% of the ALP in serum originates from the liver and bone. Can also be found in GI and kidney
  • We don’t know the full range of ALP’s function but contributes to transporting nutrients and other enzymes in the liver, aiding the formation and growth of body, transporting fatty acids, phosphates and calcium in the intestines, regulating cell growth, death, and migration during fetal development
61
Q

Serum ALP levels exhibit age-related variations in healthy individuals
* When is it highest and lowest?

A

Highest during childhood and puberty due to bone growth and development and decrease as individuals age

62
Q

What can cause increase and decrease ALP?

A

Elevated levels can be cause to investigate possible:
* Cirrhosis
* Liver cancer
* Hepatitis
* Blockage in the bile ducts
* Bone metastasis
* Paget’s disease
* Vit D deficiency

Low levels can be caused by
* Zinc deficiency
* Hypothyroidism
* Wilson’s disease (build up of copper inside body
tissues)
* malnutrition

63
Q

Aspartate aminotransferase (AST)
* What is this?
* What is another name for AST?
* Damage to what causes release of AST?

A
  • Aspartate aminotransferase (AST) is an enzyme mostly found in the liver- can also be found in the kidney’s, heart, muscles
  • Another name for the AST enzyme is serum glutamic-oxaloacetic transaminase (SGOT)
  • Damage to hepatocytes can cause the release of AST into the blood
64
Q

⭐️

  • ALT levels occur in higher concent where?
  • If ALT level are normal but AST are high- would indicate
A

ALT levels occur in higher concentrations in the liver. If ALT level are normal but AST are high- would indicate the problem is outside the liver

65
Q

What can cause elevated AST and low levels AST?

A
66
Q

Alanine aminotransferase (ALT)
* What is it?
* Plays a crucial role in what?
* An increase in ALT is often the first sign of what?

A
  • Alanine aminotransferase (ALT) is an enzyme that is found mostly in the liver
  • Plays a crucial role in metabolism
  • An increase in ALT is often the first sign of a liver problem and is often elevated before other symptoms appear
67
Q

What causes high and low ALT

A
68
Q

Bilirubin
* Derived from what?
* RBC destruction primarily happens where?
* Excreted where? ⭐️

A
  • Derived from when red blood cell naturally break down (cycle 120 days)
  • RBC destruction primarily happens in the spleen, Hgb is released and metabolized to biliverdin and finally to bilirubin
  • Excreted in stool as bile
69
Q
  • What causes elevated bilirubin concentration? ⭐️
  • When do you jaundice?
A
  • Major manifestation of obstructive biliary tract disease is an elevated bilirubin concentration
  • Once the total bilirubin exceeds 2-3 mg/dL you get clinical signs of jaundice
70
Q
  • When you get a CMP it will give you the total bilirubin, but you also need to know how much?
A

unconjugated (“indirect”) bilirubin vs conjugated (“direct”) bilirubin

71
Q

What is the pathway of bilirubin?

A
  • Bilirubin enters the circulation as unconjugated and is insoluble in water. It gets bound to Albumin which helps transport it to the hepatocytes AKA bilirubin created from red cell breakdown
  • Inside the hepatocyte the molecule are conjugated to bilirubin making it water soluble (conjugated bilirubin) AKA bilirubin once it reaches the liver and undergoes chemical change prior to excretion
  • Conjugation is mandatory to render bilirubin aqueous soluble and facilitate its secretion and excretion into bile
  • Pathologic elevations of conjugated bilirubin can lead to bilirubin excretion in the urine (uncommon) – yellow-brown, green-brown color
  • Conjugated hyperbilirubinemia signifies the presence of either liver or biliary disease
72
Q

If the concentration of either conjugated or unconjugated bilirubin rises, what happens?

A

the skin and sclera can develop jaundice (icterus). If it’s really high it can make your skin itch

73
Q

Conjugated or unconjugated:
* Which can be measured? Which one needs to be calculated?

A
74
Q

What are the causes of hyperbillrubinemia?

A
  • Your RBC’s are breaking down at an usual rate (hemolytic disease)
  • Your liver isn’t breaking it down or clearing it appropriately (liver disease)
  • There’s a problem along the pathway that gets bilirubin out of your liver and into your stool (bile duct/gallbladder issue)
  • Medications
75
Q

Hyperbilirubinemia: Your RBC’s are breaking down at an usual rate (hemolytic disease):
* Explain

A
76
Q

Hyperbilirubinemia: Your liver isn’t breaking it down or clearing it appropriately (liver disease)
* Explain

A
  • Cirrhosis, hepatitis ,Gilberts syndrome, Wilson disease,Crigler-Najjar syndrome
77
Q

Hyperbilirubinemia: There’s a problem along the pathway that gets bilirubin out of your liver and into your stool (bile duct/gallbladder issue)
* Explain

A
  • Gallstones, cholecystitis ,cholangitis, cholelithiasis
  • This can cause clay colored stool
78
Q

How do some medications cause hyperbilirubinemia?

A

Some antibiotics, antimalarials, MAO inhibitors, morphine, oral contraceptives

79
Q

Unconjugated hyperbilirubinemia arises in one of the three major pathophysiologic conditions or a combination of them:

A
80
Q

Conjugated hyperbilirubinemia is usually secondary to what?

A

hepatocellular disease or cholestasis (intra-hepatic and extra-hepatic)

81
Q

What are the sx of low bilirubin and what are the causes?

A
82
Q
A
83
Q

LACTASE DEHYDROGENASE (LDH)
* An important enzyme in what pathway?
* Serves as what?
* What are conditions that increase LDH?
* Non specific marker of tissue turnover – provides what?
* RBC’s contain their own LDH protein- so hemolysis causes what?

A
84
Q

Urine:
* Urine output important in monitoring what?
* Typical UOP in adults is what?
* Normal urine should be what color?

A
  • Urine output important in monitoring volume status and kidney function
  • Typical UOP in adults 0.5-1.5mL/kg/hr–differs due to weight of patient
  • Normal urine should be straw colored – gets color from urobilin
85
Q
  • What is oliguria? what are causes?
  • What is polyuria? What are the causes?
  • What is hematuria?
  • What is malodorous urine?
A
86
Q

What is a urinalysis?

A

examination of the physical, chemical and microscopic contents of urine

87
Q

Urinalysis:
* Urine samples collected from what void?
* Urine should be examined within when?
* Can obtian urine via what?
* Completed where?
* Can also use what?

A
88
Q

Urinalysis:
* What are the three components?

A
89
Q

Urine color:
* amber color
* Brown/black (tea)
* Dark yellow
* Green/blue
* Orange
* Rink/pink

A
  • amber color: Bile pigments
  • Brown/black (tea): Bile pigments, metronidazol, nitrofurantoin
  • Dark yellow: Concent. specimen (dehydration, exercise)
  • Green/blue: asparagus, biliverdin, methylene blue, pseudomonal UTI
  • Orange: phenazopyridine, rifampin
  • Rink/pink: hematuria, hemoglobinuria, menstrual contamination
90
Q

CLARITY of urine:
* Normal:
* Associations of clarity?

A
  • Normal: Clear or translucent
  • Associations: Bacteria, fecal contamination, mucus, squamous and non- squamous epithelial cells), pyuria
91
Q

SPECIFIC GRAVITY
* what does it indicate?
* What can raise the urine specific gravity?

A
  • The urine specific gravity is important because it indicates the kidney’s capacity to dilute or concentrate urine
  • The presence of glucose, protein, or blood in the urine can raise the urine specific gravity
92
Q

What causes high and low specific gravity?

A
  • High: Contrast media, dehydration, decreased renal blood flow (shock, heart failure, renal artery stenosis)
  • Low: Diabetes insipidus, acute tubular necrosis, intravenous (IV) radiopaque contrast media
93
Q

pH:
* Provides insight into what?
* Normally urine is what? ⭐️
* Alkaline urine is most commonly caused of what?

A
  • Provides insight into tubular function
  • Normally urine is slightly acidic because of metabolic activity
  • Alkaline urine is most commonly caused from a bad sample that wasn’t run in the appropriate time frame
94
Q

What are causes of high and low values of urine pH?

A
  • High Values (alkaline): Stale/old urine specimens (most common
  • Low Values (acid): Cranberry juice, dehydration, diabetes mellitus, diabetic ketoacidosis
95
Q

Proteins in urine:
* What type of finding?
* Proteinuria= _
* What is albumin?
* Most proteins are what in the renal system?

A
  • A critical finding, occurs when you have albumin in your urine
  • Proteinuria=Albuminuria
  • Albumin- an important protein found in blood that has many roles – repairing tissue, fighting infection, etc. – BUT NOT usually found in urine
  • Most proteins are reabsorbed and metabolized by the proximal tubule cells –if your kidneys are damaged than albumin can “leak” through the filters and into your urine
96
Q

Proteinuria can be classified into what (2)? Explain each one

A

Proteinuria can be classified into a transient or persistent
* Transient – benign – seen with heavy exercise
* Persistent – can occur when proteins aren’t normally filtered pass by a damaged glomerular capillary or when excessive concentrations of small proteins in plasma are filtered and the reabsorption capacity of the tubular cell is surpassed – this is seen in rhabdomyolysis and multiple myeloma

97
Q

RBC’S in urine
* Can either see with what?
* What is normal?
* What is associations?

A
  • Can either see with the naked eye or need a dipstick test to identify
  • Normal: Negative (usually) or less than or equal to 5 RBCs per mL (lab-dependent value)
  • Associations: Hematuria: glomerulonephritis, pyelonephritis, tumors
98
Q

What are the causes of hemoglobinuria and myogloburia?

A
  • Hemoglobinuria: Hemolytic anemias, RBC trauma, strenuous exercise, transfusion reactions, severe burns, infections (i.e., malaria)
  • Myoglobinuria: Muscle trauma eg, rhabdomyolysis, prolonged coma, convulsions, drug abuse, extensive exertion, alcoholism/overdose, muscle wasting diseases
99
Q

What can cause false positive and negative RBCs in urine?

A
  • False-positive: Dehydration, exercise, hemoglobinuria, menstrual blood, myoglobinuria
  • False-negative: Captopril, elevated specific gravity, acid urine, proteinuria, vitamin C
100
Q

WBC in urine

  • What does high levels of WBCs indicate?
  • What can sterile pyuria lead to?
  • Can be attributed to what?
A
101
Q

URINE CULTURE SENSITIVITY AND SUSCEPTIBILITY MIC
* Gold standard for what?
* Urine culture may not be necessary as part of the evaluation of outpatients with what?
* However, urine cultures are necessary for outpatients who have what?

A
  • Urine culture is the gold standard for diagnosing a UTI
  • Urine culture may not be necessary as part of the evaluation of outpatients with uncomplicated UTIs
  • However, urine cultures are necessary for outpatients who have recurrent UTIs, experience treatment failures, inpatients who develop UTI, or have complicated UTIs
102
Q

However, urine cultures are necessary for outpatients who have recurrent UTIs, experience treatment failures, inpatients who develop UTI, or have complicated UTIs
* Why?

A
  • It helps to document infection and is necessary for determination of the identity of the infecting microorganism(s) and for antimicrobial susceptibility testing.
  • This is particularly true because of the increased incidence of antimicrobial resistance
103
Q
  • What is MIC?
  • How is it determined?
  • A lower MIC value indicates what?
A
104
Q

GLUCOSE
* Glycosuria occurs when?
* Helps identify who?
* What is normal?
* Associations?
* What can cause false + and -

A
105
Q

Ketones: can also see these in the urine with those patients that are what?

A

Ketones: can also see these in the urine with those patients that are poorly controlled DM – diabetic ketoacidosis
* Can also see in patients that are placing themselves in a state of ketoacidosis for diet purposes

106
Q

BILIRUBIN in urine
* There no bilirubin where?
* What are associations?
* What are false neg and positive?

A
107
Q

Urobilinogen in urine:
* What is urobilinogen?
* What are associations with high and low levels?
* What can cause false + and -?

A
108
Q

Nitrates in urine:
* What are products originating from?
* What is normal?
* What are associations?
* What can cause a false positive?
* What can cause a false neg?
* What do you need to rememeber?

A
109
Q

LEUKOCYTE ESTERASE
* What is it?
* What is normal?
* What is associations?
* What can cause false neg and postive?

A
110
Q

Cells in urine: What are they normally and what are they associated with?
* RBC?
* WBC?
* Eosinophil?
* Epithelial cell?
* Bacteria, fungi or parsites

A
111
Q

Casts:
* Casts are composed of what?
* They origninate where?
* It is normal to see what?
* They can dissolved within what?

A
  • Casts are composed of trapped contents of tubule lumen and Tamm- Horsfall mucoprotein
  • They originate in the lumen of the distal convoluted tubule with pH alterations or long periods of urinary concentration or stasis
  • It is normal to see a few under normal physiological conditions
  • They can dissolve within 10-30 minutes so prompt testing is mandatory
112
Q

What is they normally in urine and what are they associated with?
* Red Blood Cell Casts
* White Blood Cell Casts
* Epithelial Cell Casts
* Granular Casts

A

RBC:
* Normal: Absent
* Associations: Glomerulonephritis

WBC:
* Normal: Absent
* Associations: glomerulonephritis,

Epithelial cells:
* Normal: Absent
* Associations: Acute tubular injury/necrosis and glomerulonephritis

Granular
* Normal: Absent
* Associations: Glomerular

113
Q

What is they normally in urine and what are they associated with?
* Waxy Casts
* Fatty Casts

A

Waxy (broad) Casts - pathologically significant
* Normal: Absent
* Associations: Advanced renal failure (dilated tubules with decreased flow)

Fatty Casts
* Normal: Absent
* Associations: Heavy proteinuria (nephrotic syndrome

114
Q

Crystals:
* End products of what?
* The presence of them is not necessarily what?

A
  • End products of metabolism are found highly concentrated in urine and can precipitate in the form of crystals
  • The presence of them is not necessarily pathologic although several types are associated with certain diseases
115
Q
  • What does triple phosphate (struvite) show? WHat is it associated with?
A

Triple Phosphate (Struvite)
* “Coffin lid” appearance crystals
* Normal: Absent
* Associations: Alkaline urine, decreased urine volume, UTI from urease-producing bacteria (Proteus, kleb)

Medical Diagnosis (16 decks)

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