Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
35 Cards in this Set
- Front
- Back
|
Squamous epithelial cells in urine
Normal? Appearance |
Normal
Pale with big cytoplasm |
|
|
Non-squamous epithelial cells in urine?
Normal? Source? |
Normal
From bladder |
|
|
WBC in urine?
normal? |
normal if 1-2/hpf, if >3/hpf abnormal
|
|
|
Eosinophils in urine
Normal? |
Not normal
|
|
|
RBC
Normal? Source? |
Not normal if >5
Can come from anywere along urinary tract Determine location based on presence of casts |
|
|
Hyaline casts in urine
Form from what? |
Presence of albumin
|
|
|
Granular casts in urine?
Seen when? |
Plasma proteins embedded in Tamm-horsfall proteins
Seen in heavy proteinuria, not dz specific |
|
|
How to ID granular casts?
|
stain with anti-albumin AB
|
|
|
Dysmorphic RBC in urine
|
Seen in bleeding from glomerulus --> RBC cast
|
|
|
Where do casts come from?
|
Casts must come from kidney, regular RBC can come from anywhere!
For casts, blood collects after passing through glomerulus, and casts form in DCT |
|
|
Where do WBC casts come from? When are they seen
|
Kidney
Commonly seen in interstitial dz (pyelonephritis) |
|
|
When are tubular epithelial casts seen?
|
Acute renal failure, secondary to ATN
|
|
|
Calcium oxalate crystal appearance?
Clinical presentation |
Envelope shaped kidney stones
Unilateral flank pain (Can be normal in low #) |
|
|
Triple phosphate crystals appearancE? Clinical presentation?
|
Coffin shaped
Seen in pts with chronic UTI w/ alkaline urine (Urea secreting organisms make the urine more alkaline) |
|
|
Uric acid crystal appearance? Treatment?
|
Lemon drop shaped
Precipitates in acidic urine Treat with alkaline to dissolve crystals |
|
|
Cause of cystine crystals?
|
Seen in hereditary cystine defect
Tubules can't resorb cystine |
|
|
Pulmonary causes for respiratory acidosis
|
Asthma
COPD Pneumonia Pulmonary edema PE |
|
|
Non-pulmonary causes for respiratory acidosis
|
Decreased central drive (drugs, stroke, sleep apnea)
Decreased neural linkage Muscle weakness Thoracic cage dysfunction |
|
|
Acute phase of compensation for respiratory acidosis
|
Make H2Co3 (from high PCO2) whcih can't be buffered with HCO3-, so use intracellular buffering mech
CO2 diffuses into cell and combines with H20 and dissociates into HCO3- and H+. Proton is buffered intracellularly by Hb via histadine side group For each increase in 10 mmHg PCO2, serum HCO3- increases 1 mEq/L |
|
|
What is the chronic phase of compensation for respiratory acidosis
|
HCO3- production by kidneys and increased H+ excretion
|
|
|
How long does it take for acute phase compensation to start working for resp acidosis? Chronic phase?
|
Minutes to hours
Hours to days |
|
|
What are the pulmonary causes for respiratory alkalosis?
|
Pneumonia
Pulmonary edema/CHF Interstitial dz Asthma |
|
|
What are hte non-pulmonary causes for respiratory alkalosis
|
Sepsis
Liver dz CNS d/o Salycilate intoxication Pregnancy High altitude |
|
|
What is the compensation for respiratory alkalosis?
|
Decreased HCO3 from H release from IC buffers
Incresaed cellular lactate production HCO3-/Cl- exchange at RBC |
|
|
Causes of metabolic alkalosis?
|
H+ loss (vomiting, NG suction)
Renal loss (mineralocorticoid excess) H+ movement into cells (hypokalemia) HCO3- retention (from giving NaHCO3) Contraction alkalosis/diuretics |
|
|
What are the 2 phases of metabolic alkalosis?
|
The part that initiates the alkalosis
The part that maintains the alkalosis |
|
|
What causes the maintaining of metabolic alkalosis
|
Decreased filtration (renal failure)
Increased HCO3- resorpption (volume depletion, hypokalemia, aldosterone excess, Cl- deficit) |
|
|
How do you correct metabolic alkalosis?
|
Eliminate source of excess HCO3- resorption or H+ loss
Replete volume (isotonic saline) |
|
|
How do patients compensate for metabolic alkalosis
|
Hypoventilation, can only do this until pCO2 = 60. Won't breathe any slower than that! At this point, hypoxemic drive takes over
|
|
|
How do you assess a patient in metabolic alkalosis?
|
Use urine Cl to determine if pt is volume depleted or not
Cl is better than Na b/c sometimes patient may excrete increased Na so it becomes unreliable (although this is not the norm) If urine Cl <10 = volume depletion Urine Cl NOT RELIABLE IN PATIENTS TAKING DIURETICS!!! |
|
|
What is the normal value of anion gap?
|
10
|
|
|
What are causes of non-anion gap metabolic acidosis?
|
SEvere diarrhea (GI loss of HCO3)
RTA Carbonic anhydrase inhibition NH4Cl intake Ureterosigmoidoscopy |
|
|
Causes of anion gap metabolic acidosis
|
Methanol
Uremia Diabetic ketoacidosis Paraldehyde Iron, isoniazid (INH) Lactic acid Ethanol, ethylene glycol Salicylates |
|
|
Why does giving HCO3 to a pt in metabolic acidosis not work?
|
You can alter the pH with HCO3, but you are not treating the underlying cause of the acid-base d/o
This won't help the arrhythmias, CNS disturbances, etc |
|
|
What are the most common causes for non-anion gap metabolic acidosis?
|
GI loss of HCO3-
RTA |
