Clin Lab Med Exam II Flashcards
Epithelial cells
contaminated specimen
Oval fat bodies
Nephrotic syndrome
Hyaline cast
Normal, most common
RBC cast
Glomerulonephritis
WBC cast
Acute pyelonephritis
Renal tubule cast
Acute tubular necrosis
Specific gravity (UA)
Acute kidney failure
Glucose (UA)
Diabetes
Ketones (UA)
Acidosis (DKA)
Protein (UA)
Kidney dz
Moderately increase Albumin (UA)
Early Kidney dz
Bilirubin/ Urobilinogen (UA)
Liver dz
Hemolysis
Biliary obstruction
Uric acid crystals
Hyperuricemia
Gout
Struvite crystals
Alkaline urine
Infection by urease producing bacteria
Hypokalemia
Low K
Causes: Vomiting/gastric suction Thiazide//loop diuretics Alkalosis Insulin
Kyperkalemia
Causes:
ACE-I, ARB
Aldosterone antagonist
K-sparing diuretics
Acidosis
Tx for Hyperkalemia
Insulin/Ca/Bicarb administration
Loop/Thiazide diuretics
Dialysis
Normal range of sodium
135-145
Solutes that determine ECF osmolality
Sodium
Glucose
Urea
Sx occur if osmolality is out of whack by this much
<265
>320
Substances that are active but not included in calculated osmolality (lead to Osmolol Gap)
Mannitol Other proteins Ethanol Methanol Ethylene glycol (antifreeze)
Tonicity
ability of all solutes to make Osmotic Driving Force that causes water mov from one compartment ot another
Examples of solutes unable to cross from ECF to ICF that influence tonicity
Sodium
Glucose
Mannitol
What is a substance that crosses freely and therefore does NOT contribute to tonicity?
Urea
Major determinant of the size of ECF volume
(Na) Sodium
Increase Na in ECF
Hypervolemia
Serum [Na+]
refers to amt of water relative to sodium in ECF
not the total body Na+ amt
Abnormal Serum [Na+] means
disorder of water regulation
not necessarily a messed up sodium level
Abnormal ECF volume
marker of abnormal (Na) sodium control
Causes of Hypovolemia
GI loss Renal loss (diuretics, Diabetes Insipidus) Skin loss (sweat, burn) Intestinal obstruction, pancreatitis, Rhabdo
Hypovolemia sx
Weakness Muscle cramps Decreased BP Postural hypotension Increased pulse
Causes of HYPERvolemia
Renal failure Nephrotic synd Primary Hyperaldosteronism Cushing's synd Liver dz Heart failure Pregnancy
3 main causes of HYPER volemia
Kidney failure
Liver failure
Heart dz
Signs of HYPERvolemia
Edema SOB Orthopnea (PND) JVD Hepatojugular reflux Crackles
Water retention influenced by:
Thirst
ADH
Salt retention influenced by:
RAAS
ANP
Catecholamines
Renal fx (GFR, BF)
Aldosterone actions
Increase Na absorption
Kicks K out of body
Severe Hyponatremia (sodium so low, in danger zone)
below 125
Most common electrolyte abnormality in hospitalized pts
Low sodium
Hyponatremia is assoc/ with
Pulmonary dz
CNS disorder
Signs of low sodium
HA, dizzy N/v Lethargy Weakness Confusion Severe: Hypoventilation, Resp arrest, Seizure, Coma, Death
Pseudohyponatremia
Falsely low serum sodium, <135 BUT osmolality is normal
Pseudohyponatremia (falsely low sodium) occurs with:
Hyperlipidemia
Hyperprotein
Redistributive or Hyperosmolar Hyponatremia
Osmotically active particles in the ECF are concentrating stuf out there and drawing water out of the cell as a result, diluting the Na concentration outside of the cell
Common cause of Redist/Hyperosmolar Hyponatremia (low sodium)
Hyperglycemia
Hyperglycemia is often seen with
Hyponatremia
type: Hyperosmolar/Redistributive
Hypervolemic Hyponatremia
too much volume
too little Na
Cause of Hypervolemic Hyponatremia
too much fluid, too little sodium
Liver, Heart, or Kidney failure
Tx: diuretics, dialysis, fluid restrict
Hypovolemic Hyponatremia
low volume, low sodium
Check Urine Na
If urine Na >20 in Hypovolemic Hyponatremia
Cerebral salt wasting
Renal tubular acidosis
Diuretics (thiazide)
If urine Na <20 in Hypovolemic Hyponatremia
Vomiting/diarrhea
Third space loss (burn, pancreatitis)
Tx of Hypovolemic Hyponatremia (low everything)
Replace with fluids
Tx underlying cause
Euvolemic Hyponatremia
SIADH
Psychogenic polydipsia
Hypothyroid
Adrenal insuff
Tx of Euvolemic Hyponatremia
Fluid restriction
Tx underling cause
SIADH
too much ADH
retaining water
TOO MUCH ADH activity
Keeps water in
but lets Na out
Serum diluted
Urine concentrated
Determine cause of SIADH
CT/MRI head (CNS disorder)
CXR (lung tumor/inf)
Review pt meds
SIADH dx criteria (5 things)
- diluted plasma <275
- concentrated urine >100
- elevated urine Na >20
- euvolemic
- normal cortisol and thyroid levels
Dx Hyponatremia, First look at
Serum: Na, osmolality
Dx Hyponatremia, 2nd look at
Urine Na and osmolality
Dx Hyponatremia, 3rd look at
TSH, Serum Cortisol
When to admit a pt to hospital for Hyponatremia?
If sodium is below 125 OR symptomatic
Common use for tx of Chronic Hyponatremia
“Vaptans” and
Demeclocycline
Correcting Low Sodium
4-6 in first 24 hours
definitely less than 8
How often to check sodium when you are correcting levels
every 2 hours
CPM- Central Pontine Myelinolysis
Aka osmotic demyelination synd
Focal demyelination in the pons
Irreversible!
Sx of CPM- Central Pontine Myelinolysis
Dysarthria, dysphagia, seizures, AMS, quadriparesis, hypotension
1-3 days after over-correction
Hypernatremia
too little water relative to salt
>145
Clinical features of Hypernatremia d/t
brain shrinkage
Clinical sx of Hypernatremia (if any, often asymptomatic)
Thirst AMS, weakness Neuromusc irritability Focal neuro deficits Seizure/coma
Causes of Hypernatremia
GI loss (elderly or infants w diarrhea) Sweating, fever Renal loss Diuretics Osmotic diuresis
Vast majority of Hypernatremia are d/t:
Water loss
GI, skin, renal
Body’s normal response to Hypernatremia
Thirst and fluid intake
Diabetes Insipidus
dilute urine
concentrated blood
Losing a bunch of dilute water
(collecting ducts are impermeable to water and cannot reabsorb it)
Concentrated serum Na
Causes of DI
Central: impaired secretion of ADH
tx: desmopressin
Nephrogenic: lack of kidney response to normal amts of ADH
SIADH
too much ADH!
Diabetes Insipidus
not enough ADH or impaired response to ADH!
Tx of Nephrogenic DI
we want to get rid of Na
when kidneys aren’t responding to normal amts of ADH
- Thiazide diuretics (cause you to get rid of Na)
- Amiloride
- Chlorpropamide
- NSAIDs
Tx of Hypernatremia
Stop water loss
Replace water deficit
Hospitalize (if severe)
Water deficit
Normal TBW- current TBW
3 parts to UA
Gross examination
Dipstick
Microscopic analysis
What can cause urine to be red or red-brown
Beets and Rhubarb
What can cause urine to be brown-black?
Biliary dz
Alkaptonuria
Malignant melanoma
Maple syrup urine dz and Phenylketonuria
Amino acid disorder
Normal pH for Urine
4.5-8.0
Urine is water containing dissolved:
Urea, Na, and Cl (some other stuff)
Normal Spec Gravity of Urine
1.003-1.035
Spec Grav reflects kidney’s ability to
Concentrate and dilute the urine
In kidney dz, Spec Grav may be fixed at
1.01
“Isothenuria”
Urine volume normal
500-2000
Olig: <500
Anuria: <100
False negatives for Glucose in urine
Absorbic acid
ASA
Ketones
product of incomplete fat metabolism, occur when carbs diminished
Ketones in urine
Acidosis
DKA, rapid weight loss, fasting, starvation, pregnant
Albumin
indication of Renal endothelial dysfx
Early sign of kidney dz
False positive Albuminuria test
Pyridium can cause false positive
Limit to Albuminuria test
Low levels: 30-300 usually not detectable with dipstick
Alb to Cr ratio used for screening for Kidney Damage in high risk pts
Diabetes
HTN
Cardiovascular dz
Persistently positive dipstick for protein should:
also have Albuminuria quantified
Blood in urine can mean 3 things:
RBC
Hemoglobin
Myoglobin
False negative to blood can be d/t
Ascorbic acid
High power field
WBC
RBC
Low power field
Casts
RBC
> 3 in urine is abnormal
If sediment is red
Hematuria (RBC)
If supernatant is red, do a dipstick heme
if negative, red color is d/t something else
If supernatant is red, do a dipstick heme
if positive, centrifuge again and determine color
Clear: myoglobin
Red: hemoglobin
WBC
lobed nuclei
refractile cyto granules
> 5 is abnormal
10-20 suspicious
20 probably UTI
Tubular and transitional epithelial cells
tubular degeneration if high numbers
Oval fat bodies
“Maltese cross”
Nephrotic syndrome
“Maltese cross”
seen by Polarized light microscopy
Nephrotic synd
Where are casts formed?
Distal tubule or Collecting duct
Red cell casts
Glomerulonephritis
White cell casts
Pyelonephritis
Renal tubular casts
Acute tubular NECROSIS
Cystine crystals
“sisteine chapel genetically caused stones”
rare Genetic cause of kidney stones
Struvite
Urease producing bacterial infection
Calcium oxylate
kidney stones
crystals that cause Kidney stones
Cystine (rare genetic)
Calcium oxylate
Regulation of Renal K excretion occurs in
Distal nephron
Too much K
Hyperkalemia
Serum level >5
Causes of too much K
Hyperkalemia
Pseudo
Inadequate kidney excretion
Redistribution
Excess administration
Aldosterone leads to low K levels
so anything that antagonises Aldosterone will —> too much K (Hyperkalemia)
Causes of Hyperkalemia (too much K)
Aldosterone antagonist
K sparing diuretic
ACE-I/ ARB
Adrenal insuff (Addison’s dz)
Congenital Adrenal Hyperplasia
Renal tubular dysfx
When to clinical features of Hyperkalemia generally appear?
7 or greater
“It’s
A F A C T”
A F A C T
Arrhythmia
Flaccid paralysis
Asc muscle weak
Conduction abn
T waves (tall and peaked)
Tx for Too much K
Hyperkalemia
ER/ICU if >6.5 Correct levels (rapid or slow)
Rapid correction of Hyperkalemia
IV Calcium Chloride
Maneuver to shift K from ECF to ICF
Birmingham lecture
treat for too much K
Sodium bicarb IV
D50W + Insulin IV
Slow correction of Hyperkalemia
Loop or thiazide diuretic
Hemodialysis
Med cause of too much K
ACE-I and ARBs
K-sparing diuretic
Aldo Antag
Tx of Hyperkalemia
Thiazide or Loop diuretic
Not enough K
Hypokalemia
<3.5
When does low K become dangerous?
below 3.0
Causes of Not enough K
Hypokalemia
Inadequate intake
GI tract loss
Kidney loss
Redistribution
When does a person usually suffer from Hypokalemia d/t inadequate intake?
If they are already on Thiazide or Loop diuretic which enhances K excretion
Common cause for K los
GI loss
Upper GI: vomiting, NG suction (this causes Alkalosis which promotes Renal K loss, further worsening the problem)
Too much Aldosterone function can lead to
Low K
Hypokalemia
(i.e. Hyperaldosteronism and Cushing’s syndrome)
Redistribution causes of Low K
Alkalosis
Insulin administration
B-adrenergic agonists
Hypokalemia sx
U CRAMP
U CRAMP with low K
U waves
Cramp Rhabdo and Resp failure Anorexia, n/v Musc weakness Paralysis
Having a hard time correcting low K?
check Mg level
Rapid correction of Low K
Cardiac monitor
IV Potassium Cl
(check K every 2-4 hrs)
Slow correction of Low K
orally
Causes of Hypokalemia
vomiting/gastric suction
Thiazide/loop
Alkalosis
Insulin
Alkalosis causes
Low K
KOH dissolves host cells and bacteria, sparing:
Fungi and elastin
Tzank Prep
Herpes Virus
Giemsa or Wright stain
Giant multinucleated cells
What is more commonly used to diagnose HSV than Tzanck smear?
Immunofluorescencse
India Ink
Cyrptococci
large capsules that exclude the ink
Dark field microscopy
thin bacteria
T. pallidum (Syphilis)
Diagnosing Syphilis (T. pallidum) We use dark field microscopy bc Syphilis is
cannot be cultured
gram (-) but too thin for staining
Dark stain reveals spirochetes
Extra testing for Syphilis (other than dark field)
Veneral Dz Research Lab (VDRL):
- CSF test
- Fluorescent Trep Antibody Absorption FTA-ABS
ALSO
Rapid Plasma Reagin (RPR)
-serum
Extra testing for Syphilis
VDRL (venereal)
RPR (rapid plasma)
Latex agglutination
CSF for Meningococcal
also serum, saliva, urine
Latex agglutination
detects pathogen specific antibodies/antigens
ELISA
Enzyme Linked Immunoassay
Detects antibodies in serum
(used for many body fluids)
May need to repeat testing bc it takes up to 2 wks for some immune responses to kick in
IFA
Indirect Immunofluorescence Assay
Detects antibodies
Primary test for ANA
NAAT/PCR
Detects small quantities of bacterial/viral DNA or RNA
faster than ELISA
AFD Acid Fast Bacilli stain
Tuberculosis
rapid and cheap
(mycobacterial culture is most sensitive and spec)
Only types of sterile C&S
CSF, pleural, pericardial, peritoneal, or synovial fluids
MIC Minimum Inhibitory Concentration
Lowest conc of Abx to inhibit the growth of an organism- achieved through microdilution
Intermediate results on Antimicrobial sensitivity mean
Organism is inhibited by MAXIMAL recommended Abx dose
Blood culture results
Prelim: 24 hours
Identification of org: 48-72 hours
When should blood cultures be repeated within 48 hrs of starting Abx?
Staph Aureus bacteremia Endocarditis Infection site w/limited penetration Persistent leukocytosis Prosthetic vascular grafts Pacemaker Resistant pathogens Unknown source of original bacteremia
Bacteremia
infection specifically in the blood
Thoracocentesis
Aspirate fluid from PLEURAL space
Paracentesis
Aspirate fluid from ABDOMINAL cavity
Transudative effusion
Intact vascular wall
d/t Pressure differences
Transudative effusion usually d/t
CHF
Liver cirrhosis
Nephrotic synd
Is further testing usually needed for fluid from Transudative effusions?
NO
Exudative effusion
D/t inflammation and Vascular wall DAMAGE
Common causes of Exudative effusion
Infection
CA
Inflammatory disorder (RA, Lupus)
Trauma
Does fluid from exudative effusion usually require further testing?
YES
Normal values for Pleural fluid (around lungs) AND Peritoneal fluid (around abdomen)
50 mL
Clear, serous, light yellow
NO RBC
WBC <300
Parapneumonic effusion (exudative) most common causes
Bacterial PNA
Lung abscess
Bronchiectasis
Second most common cause of Parapneumonic effusion (exudative)
Lung CA
Breast CA
Lymphoma
Hemothorax (exudative) effusion
RBCs in pleural space
>100,000
Main causes: trauma, CA, PE
PE can cause either
transudative or exudative effusion
Chylous effusion (exudative)
Lymphatic duct disruption or impairment
Cloudy, milky
+Triglycerides and lipids
Causes of Chylous effusion (exudative)
Trauma
CA to induce lymphoma
CXR before Thoracocentesis
PA, lateral, lateral decubitus
Ensure fluid is accessible by needle
Check for fluidy (lays out when person lies down)
Parapneumonic effusion should be sampled if it meets any of the following
Layers out >25 mm
Loculated
Assoc w thickened parietal pleura on CT
Clearly delineated by US
Contra for Thoracocentesis
Significant thrombocytopenia
Rules for Thoracocentesis
Do not remove >1L
Do not perform bilaterally
Pleural fluid- Transudative features
Protein ratio <0.5
LDH <0.6
Others: WBC <300, glucose levels equal, ph 7.4-7.4
Pleural fluid- Exudative features
Protein ratio >0.5
LDH ratio >0.6
Others: WBC >500, Glucose serum, pH lower
Pleural fluid analysis
Gross app, cell count, gram stain, protein, glucose, amylase, cytology, CEA carcinoembryonic, cultures, AFB
Why would pleural fluid have a pH of <7.3?
infection
esoph rupture
CA
Why would amylase be elevated in pleural fluid?
pancreatitis
esoph rupture
CA
Eisonophilia in pleural fluid
Parasite
CA
TB
Causes of Ascites
Liver cirrhosis
Alc Hepatitis
Acute Liver failure
Gold standard for dx Peritoneal Effusion
US
Abdominal paracentesis indication
New onset Ascites
with or without:
Fever, abd tender, AMS, hypotension, periph leukocytosis, worsening kidney fx, trauma, severe cirrhosis
Abdominal paracentesis contra
Coag abnormalities
Small amt fluid
Previous abd surgery
Massive ileus w bowel/distension
Peritoneal fluid- Transudative features
Albumin gradient >1.1
Peritoneal fluid- Exudative features
Albumin gradient <1.1
LDH ratio >0.6 regarding Peritoneal fluid
Bowel perforation
CA
Infection
Amylase elev with peritoneal fluid
Pancreatic
Bowel perforation
CA
Esoph rupture
Ammonia with peritoneal fluid
Ruptured or strangulated bowel
Bilirubin in peritoneal fluid
Bowel or biliary perforation
Urea/Cr
Possible bladder rupture
trauma
Spontaneous bacterial peritonitis SBP
IMP to recognize and tx d/t high Mortality
Pts with Hepatic cirrhosis and Ascites
Sx: ACUTE ONSET fever, chills, abd pain, rebound tender
Labs: exudative effusion
Pericardial normal values
<50 mL
Clear, straw colored
NO RBC OR WBC
Overall diagnostic approach for Pericardial effusion
CBC, CMP, Trop, Thyroid fx, ANA/ESR/CRP, EKC, CXR, US, MRI or CT
Pericardiocentesis only if necessary
When to do pericardiocentesis
Pericardial effusion with TAMPONADE
If fluid needed for dx and may change tx
Contra to pericardiocentesis
Coagulopathy
Uncooperative pt
CSF located b/w
Pia and Arachnoid mater
in the Subarachnoid space
Lumbar puncture indications categories
Infection
CA
Multiple Sclerosis
Cerebral/Subarachnoid Hemorrhage
Subcategories of infection indications for LP
Meningitis
Encephalitis
Abscess
Neurosyphilis
Contraindications to LP
Increased intracranial pressure
Vertebral degenerative joint dz
Infection near LP site
Pts on anticoags
IDSA guidelines to do CT before LP!!!!
P A N I C S
Papilledema AMS Neuro def Immunocomp CNS dz hx Seizure within past week
Try to draw two separate blood cultures immediately if CNS infection is concern
before starting Abx if possible
CSF normal values
Clear Pressure <20 RBC and WBC 0-5 Protein 15-45 Glucose 50-75 LDH <40
Xanthochromia (yellow) CSF
Bilirubin
indicating lysis of RBC
Decreased pressure (hypovolemia)
dehyrdation
shock
nasal fracture w dural tear
Increased ICP
infection
intra-cranial bleed
tumor
hydrocephalus
Neutrophilia in CSF
Bacterial/TB meningitis
Abscess
Subarach bleed
Tumor
Macrophage in CSF
Fungal/ TB meningitis
Subarach bleed
Brain INFARCTION
Lymphocytosis in CSF
VIRAL, SYPHILIS, Fungal, or TB meningitis
Multiple Sclerosis
Guillian Barre synd
Multiple Sclerosis and Guillian Barre Syn
Lymphocytes in CSF
Eisonophilia in CSF
Parasitic meningitis
Allergic rxn
Xanthochromia usually present with
Subarachnoid hemorrhage
but beware it takes 2-4 hours to occur
Oligoclonal gamma globulin bands in CSF
Multiple Sclerosis
Lymphocytes in CSF and
Ologiclonal gamma
Multiple Sclerosis
What to order with CSF analysis
everything with others PLUS:
Lactic acid
VDRL
Is Lactic Acid elevated in viral meningitis?
NO
only in bacterial/fungal
Glutamine in CSF
Hepatic failure
CRP C-reactive protein
bacterial meningitis
Syphilis test
VDRL or FTA-ABS
Toxoplasmosis eval for CSF
Geimsa/Wright stain
also used for herpes
CSF Tubes
1: Chemistry- Protein and glucose
2: Microbio- Gram stain, Acid fast stain, C&S, PCR
3. Heme- Cell count and diff
4. Hold
Intracellular ions
K
phosphate and organic ions
protein
Extracellular iions
Mainly Na
Cl also
Types of IVF
Crystalloids
Colloids
Blood
Types of Crystalloids (most commonly used)
Isotonic (often- dehydration and hypovolemia)
Hypertonic (emergency)
Hypotonic (maintenance)
Dextrose (sugar)
What is used for IV boluses in dehydration and hypovolemia?
CRYSTALLOIDS
NS (0.9%)
Lactated Ringer
Plasmalyte
Life threatening hyponatremia
CRYSTALLOID
Hypertonic 3% NS
life threat low Na with water excess
Caution: CPM
Maintenance fluids
CRYSTALLOIDS
Hypotonic
NOT good for replacing volume deficits like dehydration or hypovolemia
Hypoglycemia
CRYSTALLOIDS
D5W/Dextrose
Colloids
more likely to expand Vascular compartment
Used when crystalloids fail to sustain plasma volume d/t low osmotic pressure
Colloids use (not often)
Pt with burn or peritonitis can’t hold onto the Crystalloid fluid given
DexTRAN and Hetastarch
Colloids, not often used
Operation room
Types of COLLOIDS
Albumin
DexTRAN
Hetastarch
Albumin (a Colloid)
Liver dz
Peritonitis
Burn
“third spacing”
PRBCs
used WITH Crystalloids to expand intravascular volume
What fluids can you bolus?
NS, LR, Plasma lyte, PRBCs
Hypovolemia (dehydration or acute blood loss)
What incriments do we bolus?
250mL,500mL, 1L
Maintenance IVD
maintain water and electrolyte balance in someone who isn’t eating/drinking normally
What is generally used for Maintenance fluid?
D5/0.5 NS with 20 meq KCl
Maintenance IVF
“Kg method” for Normal adult patients
1500 for basically everybody, then once past 20kg, add 20 ml/kg/day
Children require less sodium than adults
Use 0.25 instead of 0.5 NS
NEVER BOLUS
K-containing IVF
Parkland formula
Burn patients
How much total fl to give them?
% burns x weight x 4 mL
8 hours: give 1/2 total amt
8 hours: 1/4
8 hours: 1/4
Parenteral means
not into mouth
into blood in this case
When to consider TPN for adults vs children with anticipated or current inadequate energy intake by mouth
adults 7-10 days
children 3-7 days
Diuretics cause you to
lose K
ACE-I
ARBs cause you to
retain K
too much K