This document provides an overview of urine and body fluid crystal examination with a focus on morphological properties. It discusses the history of urine examination, routine urine analysis protocols and their limitations, normal and abnormal findings in urine sediment examination including red and white blood cells, casts, and crystals. It emphasizes the importance of urine crystal identification and differentiating various crystal types based on their morphological characteristics under both bright field and polarized light microscopy. The goal is to help pathologist consultants and prepare candidates for board examinations in clinical pathology.
A basic and worth information for diagnostic is urine microscopy. ideally it should be by the physician at his clinic to add and correlate diagnosis promptly. this will make physician confident in dealing with patients. it also help in follow up the consequences in some important glomerulopathies.
A basic and worth information for diagnostic is urine microscopy. ideally it should be by the physician at his clinic to add and correlate diagnosis promptly. this will make physician confident in dealing with patients. it also help in follow up the consequences in some important glomerulopathies.
An illustrative presentation on Microscopic examination of Urine for Medical, Dental, Pharmacology and Biotechnology students to facilitate easy- learning and self-study..
An illustrative presentation on Microscopic examination of Urine for Medical, Dental, Pharmacology and Biotechnology students to facilitate easy- learning and self-study..
Birefringence and Bragg grating control in femtosecond laser written optical ...Luís André Fernandes
PhD thesis presented at the University of Porto in December 2012.
The full thesis can be found here:
http://www.luisfernandes.org/thesis.php
http://books.google.pt/books/about/Birefringence_and_Bragg_grating_control.html?hl=pt-PT&id=iZFNRFl90d4C
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
2. Overview of laboratory examination for urine
and body fluid crystals with emphasis on
morphologic properties.
“Piss for path”: helpful information for
pathologist-clinical lab consultants. Inherent
limitation of urine examination.
Most importantly, enable board exam
candidates to rock the clinical path portion of
ABP examination. (continue our tradition of
near 100% passing rate for 1st time exam
takers).
3.
4. 5th century BC: Hippocrates described fluid intake
and urine output. DM urines taste sweet.
Byzantium and Middle Ages: Uroscopy, “piss
prophets” and pseudo-science (“Uromancy”)
1820’s: Richard Bright noted relationship
between edema and proteinuria. (archaic term
“Bright’s Disease”)
1837: Medical urine microscopy being taught in
Paris by Alfred Donné.
1844: Golding Bird publishes “Urinary Deposits”
and described urine casts in pts with “Bright’s
Dz.”
5. Sweet urine
I agree, it is sweet with a
fruity odor, which may
present ketone bodies.
Let’s pass it around so
everyone can get a sip.
pathology consults in Byzantium
Urine Wheel from
“Epiphaniae Medicorum”
6. NCCLS definition: “testing of urine with
procedures commonly performed in an
expeditious, reliable, and cost effective
manner…”
So routine UA protocols look for
- Physical : (color, transparency, odor, foam, spec
gravity)
- Chemical: (pH, protein, blood, nitrite, leuk
esterase, glucose, ketone, bilirubin, urobilinogen)
- Microscopic: (RBC, WBC, Epithelial cells, casts,
microrganisms, crystals)
7. Typically 96% water + 4 % solutes (of which
50% is urea, there is also creatinine).
Na,Cl,Ca,Mg,K,Phos, are also present in urine.
1st morning void (8hr specimen)
Random urine
Timed urine (24hr urine)
Double voided urine (glucose comparison blood vs. urine)
Mid-stream “clean catch” (for bacterial culture).
Catheterized urine
Suprapubic collectionl
8. Routine UA (room temp specimens) shall be
performed within 2 hrs of voiding. (CAP and
NCCLS requirement).
Refrigeration may reduce bacterial growth, but
may result in precipitation of amorphous urates
and phosphates (interfere with microscopy).
For 24hr urine collection, preservative maybe
required, depending on analyte of interest.
UA specimen in room temp >2hr should be
rejected. (refer to CAP checklist and local lab
policy for exceptions).
9. Constituent Changes Mechanism
pH increase urea breakdown
cells decrease/disappear lysis
casts decrease/disappear dissolved
sugar decrease bacteria mediated
glycolysis
acetone decrease evaporation
acetoacetic acid decrease converted to
acetone
bilirubin decrease oxidized to
biliverdin
(yellow->green)
urobilinogen decrease oxidize to uribilin
(colorless ->orange)
Adopted from Ringsrud and Linne “Urinalysis and Body Fluids:
A Colortext and Atlas” 1st Ed.
10. Color: normal is pale yellow to straw colored.
if clear redhemoglobin
cloudy redRBCs
brownmyoglobin, hemoglobin, bilirubin
blackmelanin, homogentisic acid.
Foam: normal is small amt of white foam, if shaken.
if abundant foam proteinuria
yellow foambilirubin.
Specific Gravity: normal is 1.001 – 1.035 (water is 1.000)
spec grav is dependent on mass and amount of particles in
urine.
“spec grav” reported by reagent strips is actually a gestimation
by measures ionic concention (since most urine solutes are
ionized).
11. A refractometer can be used for more
accurate measurement of urine specific
gravity.
Usually, it doesn’t matter, but if there is
prominent glucosuria.
Spec grav by refractometer will be >1.035
yet
Spec grav by reagent strip will be WNL (b/c
glucose is not ionized).
12. Urine pH: normal is usually slightly acidic
(about pH of 6 but can range from 4.5 to 8 in
healthy population).
Other effects:
high protein diet, cranberries, morning void
more acidic urine.
Citrus fruits, postprandial, urine sample left
in room temp more alkaline urine.
13. Reagent strips are the most common way of
analyzing chemical properties of urine.
Reagent strips are simple and low cost with
relatively good shelf life, but they suffer from
- variable interpretation
- inadequate sensitivity for some analytes
- susceptible to interfering substances.
14.
15.
16. Urine is also been used to screen for
metabolic disease in babies.
But reagent strip (glucose oxidase reaction)
will only detects glucose.
Clinitest will detect reducing substances
(including glucose, galactose, fructose,
lactose, and pentose).
17. If regagent strip is negative (for glucose) but Clinitest is positive.
Additonal testing is needed to identify the specific non-glucose
reducing sugars.
Ascorbic acid, nalidixic acid, cephalosporins and probenecid in large
quantities may cause false positive results with Clinitest.
18. Most of the time, examination is performed
by lab instruments
This is an Iris iQ®200SPRINT™ Automated Urine Microscopy Analyzer.
By flow cell digital imaging, it can analye 101 samples/hr and reports RBC
WBC, WBC clumps, squamous epithelial cells, renal epithelial cells, urothelial
cells, hyaline casts, other casts, crystals (9 subtype), yeasts, bacteria, sperm
mucus, oval fat bodies, trichomans
But remember, without an astute human operator, even the
most advanced lab instruments is no more than a machine.
Auto “TAR” by lab techs will report out false results.
19. Urine microscopy are often unstained, so it will
look slightly different to us (anatomic focus
pathologists).
RBCs
Crenulated RBCs due to urine
hypertonicity
20. These pale RBCs have
“ghost cell” appearance.
This is due to loss of Hb
which occurs in hypotonic
urine specimen. This
doesn’t necessarily mean
patient is anemic.
21. These are dysmorphic RBCs (cytoplasmic blebs) and may mimic budding yeast.
Note the “Micky Mouse” morphology. Right hand side is differential interference
contrast microscopy which accentuates membrane distortion.
22. Dysmorphic RBCs are
associated with glomerular
hematuria. (glomerulonephritis)
But, elevated uric acid content
and hypotonicity can also show
similar morphologic changes.
23. WBCs
In fresh urine sample, the cytoplasmic
granules induce a sparkling appearance.
Squamous cells. Urothelial cells
(tadpole form)
24. Urine eosinophils
(to identify eos,
the urine needs
to be stained
with either
Wright Giemsa or
Hansel stain).
Eosinophiluria: Top 3 drug inducted acute intersitital nephritis,
hypersensitivity, parasitic infections. Also transplant rejection, RPGN,
Post infectious GN, eosphilic cystitis…etc.
The reagent strip will show ++WBC, but negative leukocyte esterase.
25. Oval Fat Bodies (renal tubular cells with fat
globules). Show maltese cross under cross
polarization. Associated with nephrotic
syndrome.
27. Spermatozoa in urine.
Some labs may not report it.
Considered “critical value” in
Pre-adolescent children and
vulnerable adults. Huge
medical-legal implication.
Need to be sure!
28. Now we turn our attention towards urinary casts (cylinders). Casts in
the urine mirrors that physiologic state of the kidney.
Casts are classified into 2 broad groups.
Acellular Casts Cellular Casts
- Hyaline - RBC
- Granular - WBC
- Waxy - RTE
- Fatty - Bacterial
29. Hyaline casts and granular casts are the only 2
types of cast that should be seen in normal
population.
Hyaline casts can be difficult to visualize by
bright field microscopy, but (fortunately) are also
clinically least important.
Vigorous exercise can increase hyaline cast in
urine. Granular casts are less commonly seen.
Hyaline casts are composed of
Tamm-Horsfall proteins. The
matrix contains few granular
material. Hyaline casts do not
polarize.
30. Granular casts are refractile and can have fine or coarse granules. The
granules are thought to derive from degenerative products of renal
tubular epithelium. Can be seen in both healthy population and in
patients with intrinsic renal disease.
31. Waxy casts are broad (>40um), often short, with sqare ends. They also
tend to show cracks and indentation. They from within dilated renal
tubules and are not seen in normal healthy population. Waxy casts are
associated with ESRD, and glomerulonephritis.
32. Fatty casts show surface fat globules and produce
maltese cross under polarization. They are seen in
nephrotic syndrome, ATN, and other renal dz.
33. RBC casts are rarely seen. RBCs are stuck
together in a matrix of Tamm-Horsfall protein.
But RBC casts are fragile and will degenerate after
voiding. Reddish appearance due to Hb. Seen in
acute glomerulonephritis, renal neoplasms, and
malignant HTN.
34. The so-called “Muddy Brown Cast.” There is usually a dirty background
composed of degnerated epithelial cells. A clinical nephrology buzzword in
1990’s, this has been equated to acute tubular necrosis(ATN).
The brownish pigment seen is either myoglobin or hemoglobin. This
But pts with ATN can also have non-pigmented casts in their urine.
So, this term is not endorsed by clinical laboratory community.
35. WBC casts: highly refractive, look for multilobed nuclei and
single WBCs in surrounding area. WBC casts are seen
pyelonephritis, interstitial nephritis, renal transplant
rejection, sepsis, lupus nephritis…etc.
36. Renal Tubular Epithelial (RTE) Casts: Mimics WBC
cast and at times can be difficult to
differentiated. So the term “Cellular Cast” can be
used to include both RTE and WBC casts.
RTE casts are seen in ATN, renal transplant
reject, heavy metal poisoning…etc.
37. Renal stones form because of undesired
phase change of a substance.
Normal urine is in a shifting state of
oversaturation. Small crystals are constantly
forming and dissolving.
Stones develop when there is an unstable
oversaturation which leads to precipitation.
Many different crystals have been described
in urine. We will mainly focused on ones that
are either clinically important or IMHO,
morphologically peculiar
38. Amorphous urate
and phosphate are
similar/essentially
identical under
light microscopy.
Difference are:
Amorphus urate: seen in pH <5.8, show birefringence in large clumps,
associated with dehyration, fever. But usually no significant
clinical implication.
Amorphus phosphate: seen in pH >6.3, no birefringence, clinically insignificant.
39. Alternatively,
urine can also be
spun and the
pellet is examined
macroscopically.
Urate is pink.
Phosphate is
white.
40. Triple phosphate/Struvite (Ammonium magnesium
phosphate) crystals. Left is the prototypical coffin lid
morphology. But, note that triple phosphate crystals
can be seen (less commonly) in “fern” form. These
crystals develop via biofilm produced by urease
producing bacteria.
Associated with staghorn calculi, UTI, vericoureteral
reflux.
41. Calcium oxalate: Left side is the classic “square
envelope” (large 8 faced bi-pyramids). Right side is
the monohydrate with “dumbbell” and oval shapes,
which can cluster into microlith.
Calcium oxalate crystals form in pH <5.4 and is
associated with oxalate stones, ethylene glycol
poisoning, oxaluria, s/p ileal resection, Crohn’s Dz.
dihydrate form (Weddellite) monohydrate form (Whewellite)
42. 2/3 of all renal calculi are calcium oxalate
stones.
S/P small bowel resection leads to
malabsorption of fat. Ca selectively binds fat
and leave free oxalate in the colon to be
absorbedoxalate goes to the kindey and
stones develop.
Ethylene glycol ingestionmetabolized to
glycoaldehydeglycolic acidglyoxylic
acidoxalic acidadd Ca to form calcium
oxalate (more crystals in monohydrate form).
43. Uric acid crystals: has many morphologic appearance; most commonly
rhomboid plates, but also hexagonal, barrel, clubs/short rode/blade (not
illustrated).
More about uric acid cystals in joint fluid examination section
45. While hexagonal form of uric acid is less
common, it mimics cystine crystals.
They can be differentiate by polarized light and
cyanide nitroprusside test.
Uric acid hexagons show
Polychromasia.
Nitroprusside negative.
Cystine crystals lack
polychromasia
Nitroprusside positive.
46. Cholesterol crystals: overlapping rectangular plates
Associated with nephrotic syndrome, chyluria.
Should also be accompanied by oval fat bodies and
fatty casts.
Radiologic dye can mimic cholesterol crystals.
47. Leucine crystals: concentric rings, like tree’s
annual rings. Very rare. Seen in severe liver
disease.
48. Tyrosine crystals: tufts of fine silky needles.
Seen in severe liver dz, tyrosinemia.
49. sulfonamide crystals: “sheafs of
wheat”
ammonium biurate crystals: “thorn apples”
Seen in prolonged storage of urine. No
clinical significance
ampicillin crystals
50. Should be examined with compensated
polarized light microscopy.
Also consider other clinical laboratory values
(e.g. cell count)
First, lets review compensated polarized light
microscopy.
51. Don’t always expect clinical hx when an
orthopod ask you to look at a joint fluid.
52. Since I barely recall being awake during undergrad
physics, this is my fraudulent technician’s version of
polarized microscopy.
Most illumination transmits light waves whose electric
field vectors vibrate in all perpendicular planes with
respect to the direction of propagation. With
polarized light, filtration is used to restrict vibration
to a single plane.
http://www.olympusmicro.com
53. Crystals can be either
- isotropic: index of refraction is equal in all
directions.
- anisotropic: refraction differs when light
enters at non-equivalent axis.
http://www.olympusmicro.com
54. When placing anisotropic crystals between cross polarization. From the
left, polarized light (P) enter the anisotropic crystal and is refracted into
2 component waves. This light then passes through the analyzer (A).
One component wave is now “retarded.”
After passing through the analyzer, light interference between 2
component waves acquire a spectrum of color under usual bright field
microscopy.
http://www.olympusmicro.com
55. In this case, light reflections from outer- and inner-
surfaces of the bubble (separated by a few micros)
interfere with each other and result in this colorful display.
56. Above is a Michel-Levy chart used to quantify
birefringence. The most sensitive area for
detection of birefringence is approx 550nm (1st
order red). With slight change in retardation,
there will be a dramatic color shift into either
blue or yellow.
This is achieved by using a red compensator.
57. From: Bullough- Orthopedic Pathology 5th ed.
arrow is the “slow wave”
“U PAY PEB”
Urate PArallel Yellow, PErpendicular Blue
61. Now the fun parts, lets walk over to the core
lab and get some hands on experience with
operating a compensated polarized light
microscope.
Questions?