Exam 2 Flashcards
(102 cards)
1
Q
locations of pathology associated w/ GI symptoms
A
Primary GI
• Inflammatory +/- infectious
• Neoplasia
• Drug induced
Non-GI
• Metabolic (e.g. hyperthyroidism, DKA, Addison’s)
• Liver failure
• Kidney disease
Pancreatic
• Pancreatitis
• Exocrine pancreatic insufficiency
2
Q
First Steps in Diagnosing dog or cat w/ GI symptoms
A
- Minimum data base (CBC/Chem & urinalysis)
- Fecal
- Cats: T4 , FelV/FIV
- Dogs: cortisol +- ACTH stim
- Pancreatic Serum tests
- GI serum tests
3
Q
Anatomy of the pancreas & enzyme production
A
o Exocrine • Acinar cells • Secrete: trypsin (protien), pancreatic lipase (fat), pancreatic amylase (carb) o Endocrine • Secretes insulin & glucagon
4
Q
Stimuli for Pancreatic Secretion
A
o Acetylcholine from vagus N. stimulates digestive enzymes
o Cholecystokinin (CCK) from GI stimulates digestive enzymes
o Secretin from GI stimulates H2O & bicarb secretion
5
Q
Diagnosing Pancreatitis
A
o Inflammatory leukogram: neutrophilia, +- toxic neutrophils,
o +- stress leukogram: lymphopenia
o Erythrocytosis due to dehydration
o Possible anemia due to hemorrhage
o Hyperlipidemia (fatty serum)
o Hyperglycemia
o Azotemia (high nitrogen due to dehydration)
o Increased hepatic enzymes & hyperbilirubinemia
o Electrolyte abnormalities
o May have DIC (increased PT/PTT, increased D dimer, increased FDPs)
o High PLI & TLI
6
Q
Testing Amylase & Lipase
A
o Amylase: complex carbs -> maltose and glucose
o Lipase: triglycerides -> fatty acids and glycerol
o in other organs but highest conc. in pancreas & small intestine
o amylase decreased w/ corticosteroid use
o lipase increased w/ corticosteroid use
o inactivated by kidney -> renal disease can cause increased amy/lipase
o Limited diagnostic utility in dogs; suggestive if 3-4X high + no azotemia
o No diagnostic value for cats
7
Q
Pancreatic Lipase Immunoreactivity (PLI)
A
o Measurement of serum lipase derived only from the exocrine pancreas
o High Sensitivity and specificity
o Result of tests not affectd by GFR, gastritis, or corticosteroid use
o Magnitude of elevation no correlated w/ prognosis
o Spec or SNAP
8
Q
Spec PL Vs SNAP PL Vs TLI
A
- all are biochemical tests that measure presence / conc. of macromolecules in a solution through the use of an antibody or immunoglobulin
- Spec quantitative (numerical conc. of PL)
- SNAP qualitative (normal or abnormal amount of PL)
- TLI decreased w/ EPI, increased w/ acute pancreatitis
9
Q
Be able to contrast sensitivity and specificity of enzymes detecting muscle injury and pattern of elevation.
A
- Specificity: increases due specifically to muscle injury
- Sensitivity: increases even if muscle damage is minor
10
Q
Know what tests you should ask for to detect muscle injury.
A
- CK
- AST
11
Q
Know how to differentiate muscle injury from non-muscle disease processes.
A
- sometimes secondary to other diseases
- Cardiomyopathy -> aortic thromboembolism -> hypoxia of hind limb muscles -> Muscle necrosis -> high CK & AST
12
Q
Be familiar with other chemistry changes that can be seen with muscle injury.
A
- Myoglobinuria (urine only tells you blood present; look at other bloodwork to identify hemoglobin, myoglobin, or intact RBCs)
- Hyperkalemia
- Hyperphosphatemia
- Hypocalcemia
13
Q
Explain the four basic mechanisms that lead to increased serum enzyme activity
A
Release from damaged cells
- Concentration of enzyme within the cell and/or intracellular distribution,
- enzyme half-life,
- number of cells damaged, severity
Increased production
- Inducers (drugs), neoplasia, hyperplasia, young patient
Decreased removal
- enzymes that are excreted by the kidneys will see increased levels with renal disease
Ingestion or absorption
14
Q
Correctly select and interpret the enzyme changes used for detection of muscle damage
A
CK
- Mostly muscle
- Specific, sensitive
- Short half-life
ALT
- Mostly liver
- Not very sensitive for muscle
AST
- Liver or muscle
- Longer half life than CK (rises more slowly than CK)
15
Q
Understand diagnostic sensitivity and specificity and explain how they influence our interpretation of assay results. Know your equations!
A
Sensitivity:
- will always detect positives but may falsely identify negatives as positive
- (true pos/(true pos+false neg)) X100
Specificity:
- Will always correctly identify negatives but will sometime incorrectly identify positives as negative
- (true neg/(true neg+false pos)) X100
16
Q
Understand positive and negative predictive values and prevalence and explain how they influence our interpretation of assay results. Know your equations!
A
Positive:
- Tells you what % of animals with a positive (abnormal) test result will actually have the disease
- (true pos/(true pos+false pos)) X100
Negative
- Tells you what % of animals with a negative (normal) test actually don’t have the disease
- (true neg/(true neg+false neg)) X100
17
Q
What are 3 phases of laboratory testing needed to ensure proper quality assurance?
A
- Pre-analytical: Sampling, transport/sample handling
- Analytical (Instrument measurement)
- Post-analytical: recording & interpreting data
18
Q
List 5 things that should be included in a quality control program
A
- Systematic monitoring of equipment operation
- System for monitoring reagent inventory
- Use of controls for external QC on some instruments-results can be plotted in a Levey- Jennings plot
- Written/computerized logs and documentation
- Proper training of ALL instrument users
19
Q
Identify and be able to discuss hepatic enzyme tests and know which are preferred for small versus large animals.
A
Small Animals
- ALT – hepatocellular injury
- ALP – cholestasis, isoenzymes
- GGT - cholestasis
Large Animals
- SDH – hepatocellular injury
- AST – hepatocellular injury and muscle injury
- GGT – cholestasis, colostrum
20
Q
Explain the similarities and differences between hepatocellular disease, biliary disease, and hepatic insufficiency. Identify laboratory data that indicate or suggest the presence of each.
A
Hepatocellular Dz
- enzymes in organelles/cytoplasm
- enzymes leak out through disruption of membrane
- enzymes in serum increase
Biliary Dz
- enzymes on membrane
- enzymes leak out due to disruption of bile flow
- elevated serum enzymes
Hepatic Insufficiency
- enzymes in organelles/cytoplasm
- too few functional hepatocytes to raise serum enzyme levels
21
Q
Know the 3 different processes in dogs that produce increased ALP
A
- Liver ALP:
cholestasis, drugs (dogs) - Bone ALP: bone growth
- Corticosteroids ALP (dogs only)
22
Q
Understand the explained hepatic function tests and know what test you would want to run in cases with suspected liver disease.
A
if no icterus, bile acids most important
Total Serum Bilirubin
- Hyperbilirubinemia: rate of bilirubin production exceeds liver’s ability to deal w/ it
- Any bilirubinuria in cats is SIGNIFICANT
Bile Acids
- More sensitive indicator of liver function than bilirubin
- Increase = decreased clearance from portal blood or cholstasis
Blood Ammonia
- Less sensitive than bile acids
- may perform if suspected hepatic encephalopathy
- Increase – portosystemic shunt, significantly decreased liver function, urea toxicosis (cows), ammonia producing bacteria (horses)
23
Q
Describe hematology or urinalysis abnormalities that may be associated with liver disease.
A
Hematology
- Mild-moderate anemia
- Target cells, ancanthocytes, microcytosis
Urinalysis
- Bilirubinuria / crystals
- Ammonium biurate crystals
24
Q
Understand how liver disease can cause increased hepatic enzymes, hypocholesterolemia or hypercholesterolemia, hypoglycemia, decreased BUN, hypoproteinemia with hypoalbuminemia, prolonged coagulation times, and ascites.
A
Hepatic enzymes:
- shows liver damage because lysis of hepatocytes releases enzymes
Hypoglycemia:
- liver isn’t performing gluconeogenesis
Hypoprotinemia, hypoalbumenia, Hypo/hypercholesterolemia, Decreased BUN
- decreased production by liver due to non functioning hepatocytes
Prolonged coag time:
- decreased production of clotting factors by liver due to non functioning hepatocytes
ascites
- due to portal hypertension
25
Basics of Liver Failure
- Liver Can’t clear toxins or process ammonia and bilirubin
- Inability to produce proteins, lipids, carbohydrates
- Serum enzymes may not be elevated in end stage
26
Exocrine Pancreatic Insufficiency (EPI) Basics & Causes
o failure of the acinar cells to produce pancreatic enzymes and HCO3-
o primary or secondary
```
Causes
o destruction of acini,
o Deficiency of CCK and secretin,
o Deficiency of enterokinase,
o Excessive secretion of HCl
```
27
Exocrine Pancreatic Insufficiency (EPI) Clinical Signs, Breed Disposition, Diagnosis
```
o Clinical Signs
• Weight loss
• Polyphagia
• Vomiting
• Greasy Ds
```
o Breeds
• Shepherds
• Collies
o Diagnosis
• Unremarkable CBC/Chem
• TLI is test of choice (TLI is decreased)
• Often occurs w/ SIBO
28
Tests for GI Disease
```
o cobalamin
o folate
o gastrin
o carb absorption (horses)
o fecal occult blood
o Alpha-1 Protease Inhibitor
```
29
Serum Cobalamin (B12)
* Requires intrinsic factor to be absorbed in ilium
* Decreased due to Distal small intestinal mucosal disease, EPI, Bacterial overgrowth
* Increased due to B12 supplement
30
Serum Folate (B9)
* Absorbed in proximal small intestine
* Decreased concentration: Mucosal disease in proximal small intestine
* Increased: SIBO, EPI, B9 supplement
31
When to evaluate Cobalamin & Folate
* Patients with suspected small intestinal disease (Once EPI & parasites excluded)
* intestinal malabsorptive abnormalities
* bacterial overgrowth
32
Gastrin Test
* Gastrin stimulates release of HCl in stomach
* Elevated gastrin = vomiting
* elevated due to: Neoplasia, ulcer, obstruction, renal failure, drugs, hepatobiliary dz
33
Carb Absorption test
* evaluate small intestinal function
* Oral D-xylose and D-glucose absorption test
* Sugar conc. measured at different time intervals
```
• Decreased absorption
=
o Delayed gastric emptying
o Vomiting
o bacterial overgrowth
o Rapid intestinal transit
o small intestinal dz
```
34
Fecal Occult Blood Test
* Identification of small intestinal bleeding
by detecting pseukoperoxidase activity of hemoglobin
* very sensitive
* False positives due to Diet, Iron supplementation, Contamination
* A repeatable negative result rules out bleeding into the GI tract
35
Alpha-1 Protease Inhibitor Test
* Test looks for pathologic protein loss in feces
* Shows protein loss in intestine or blood loss in intestine
* Take 3 fecal samples over 3 days
36
Bovine GI Content Analysis
o Rumen
• pH > 7 = ruminal alkalosis = decreased microbial fermentation
• pH < 5.5 = ruminal acidosis = carb overload & lactic acid accumulation
o Abomasum
• should have pH ~2-3
• pH can rise due to displacement or parasitisim
37
Clinical assessment of renal function
o Evaluate creatinine and BUN on serum chemistry (estimation of GFR)
o Evaluate urine specific gravity
o Urinalysis: evaluate proteinuria and sediment changes
38
How to investigate glomerular function
o urea blood/serum nitrogen (BUN or SUN)
o creatinine
o SDMA
o clearance test
39
Urea Blood/Serum Nitrogen (BUN)
* Produced in liver from protein metabolism
* Expressed in terms of nitrogen content (BUN)
* More accurate term is serum urea nitrogen (SUN)
* Freely filtered through glomerulus with some tubular resorption
increase in BUN
• decreased GFR
• increased production due to GI bleeding or high protein meals
decreased BUN
• decreased production due to liver dysfunction
• increased excretion due to diuresis
40
Creatinine
* Freely filtered through glomeruli and not reabsorbed
* better estimate of GFR than BUN
* product of muscle metabolism
* Heavily muscled animals = mildly increased creatinine levels
* Will not significantly increase with muscle damage
* Increases in serum creatinine = Decreased GFR
41
Azotemia
Increase in Creatinine and/or BUN = decreased GFR, but not specific
• Prerenal Azotemia
• Renal Azotemia
• Post renal Azotemia
* If azotemia due to kidney disease = loss of 75% of kidney function
* Urine Specific Gravity is necessary to evaluate an azotemic animal!!
42
Pre-renal Vs Renal Vs Post-renal azotemia
Pre Renal Azotemia
• Most common
• Decreased renal perfusion
• Dehydration, cardiac dz, shock
Renal Azotemia
• Renal dz w/ at least 75% loss of function
• Due to infectious, toxins, renal amyloidosis, neoplasia, etc
Post Renal Azotemia
• Rupture bladder or ureters
• Causes obstruction -> no peeing -> resorption of creatinine or BUN
43
Symmetric dimethylarginine Test (SDMA)
* Product of protein methylation & released into circulation
* Excreted exclusively by kidneys
* Good estimate of GFR
* Increases earlier than creatinine (40% loss of kidney function)
44
Clearance Test
* Measures GFR or clearance of analytes thru kidneys
* Endogenous creatinine clearance
* Exogenous creatinine clearance
* Fractional excretion of electrolytes
* Not easily performed = rare in clinic
45
Urine Specific Gravity (USG)
o Measure conc. of solutes in urine using refractometer
o Affected by amount & size of molecules in urine
o Wide range of normal
o Compare USG to specific gravity of plasma conc. entering renal tubules (1.007-1.013)
46
Isothenuric Vs Hypersthenuric Vs Hyposthenuric Vs Gray range
Measure of Urine Conc.
Isosthenuric
• 1.007-1.013 = same as plasma ultrafiltrate
Hypersthenuric
• >1.025 (horse, cow)
• >1.030 (dog)
• >1.035 (cat)
Hyposthenuric
• <1.007
Gray range
• 1.014 to hypersthenuric
47
What does different combinations of azotemia and USG mean?
* Azotemia + hypersthenuria = poor renal perfusion = pre-renal azotemia
* Azotemia + isosthenuria = renal failure = renal azotemia
* Azotemia & variable USG = rupture or urinary tract obstruction = post renal azotemia
* Azotemia + hyposthenuria = functioning renal tubules but poor renal perfusion = pre-renal azotemia
48
Meaning of USG without azotemia
Hypersthenuria
• tubules functioning & urine concentrated
Isosthenuria
• normal in well hydrated animal OR
• indicate renal insufficiency
• USG will decrease before azotemia develops in most species with renal disease.
Hyposthenuria
• function of tubules because they are actively diluting.
• Can see w/ ADH abnormalities.
Grey Zone
• may be normal OR
• could indicate beginning renal insufficiency.
49
Kidney requirements for concentration of urine
o Sufficient nephrons
o ADH present
o Ability of tubules to respond to ADH
o High osmolarity of renal interstitial fluid
50
Extra-renal causes of abnormal USG
Lack of ADH secretion
• Pituitary (central) diabetes insipidus
Lack of response of the tubules to ADH
• Hypercalcemia, Pyometra, etc
Loss of medullary concentration gradient
• Prolonged hyponatremia due to Diuretics or Hypoadrenocorticism
• Diuresis (e.g.fluids, Diabetes Mellitus..)
• Hepatic insufficiency
• Hyperthyroidism
51
Ways to collect urine
Midstream catch
• Easy but contamination occur
Manual
• Not easy
• Can traumatize bladder
Catheterization
• Decreased contamination
• Can cause trauma
Cystocentesis
• Preferred method in small animals
• Decreased contamination but may have RBCs
52
Urobilinogen
* formed from bilirubin
* May see increase w/ increased bilirubin = Hemolytic disease or liver disease
* usually not diagnostically helpful
53
Tests for protein in urine
* SSA Test
* protein creatinine ratio (UPC)
* Microalbumin test
54
SSA Test
```
o Use to confirm (+) protein on dipstick
o Performed on supernatant
o Picks up proteins other than albumin
o No false + in alkaline urine
o If positive & urine sediment normal, a quantitative test is recommended
```
55
Protein Creatinine Ration (UPC)
o Quantitatively evaluates proteinuria
o Used on urine w/ no cystitis or overt blood
o Disregards urine dilution
o Urine microprotein / urine creatinine = UPC
o Normal = <0.5
56
Microalbumin Test
o Most sensitive test for urine albumin
o P.O.C. and ELISA tests available
o Detects urinary albumin >1 mg/dL - <30 mg/dL
o Used on urine w/ no cystitis or overt blood
57
Proteinuria
o If persistent associated w/ increased morbidity/ mortality
o Pre-glomerular/Renal
o glomerular / renal
o Post glomerular/renal
58
Proteinuria: Pre-glomerular/Renal
Vs glomerular / renal
Vs Post glomerular/renal
o Pre-glomerular/Renal
• Abnormal plasma content of protein (Bence Jones proteins- multiple myeloma, hemoglobin, myoglobin)
o Glomerular/Renal
• Abnormal renal handling of normal proteins
o Post glomerular/renal
• Most common!
• Entry of protein into urine after urine enters renal pelvis
• Due to inflammation or hematuria
59
3 elements to assess w/ proteinuria
Localize
• Exclude extra-renal, pre-renal, and post renal causes
• Rule in other causes of proteinuria with clinical signs
Persistence
• Evaluate over multiple days
Magnitude
• Need to look for persistance
• need a quantitative test!
60
Nephrotic Syndrome
• Severe proteinuria -> nephrotic syndrome
```
Characterized by
• Proteinuria
• Hypoalbuminemia
• Hypercholesterolemia
• Edema
• lose anti-thrombin & start to throw clots = death
• +/- azotemia
```
61
Define balottement
fluid wave in abdomen
62
Blood on dipstick
* Should be negative
* If (+) = RBCs, hemoglobin, or myoglobin
* Look at sediment exam, hematology/chem, serum color, ammonium sulfate, & history to figure out (+)
* IMHA dog will have red urine & plasma
63
Ketones on dipstick
* Should be (-)
| * If (+) consider: negative energy balance or diabetes
64
Bilirubin on dipstick
* Should be (-) (except dogs in small amounts)
* If (+) consider: cholestasis, hemolysis
* Use ictotest (more sensitive) to confirm (+)
65
Glucose on dipstick
* Should be (-)
| * If (+) consider: hyperglycemia (renal threshold) or renal tubule dysfunction
66
Urine Sediment Exam
* 10x objective (LPF)
* 40x objective (HPF) – used to look at cells
* RBCs & WBCs should be <5
* can see casts
* can see crystals
67
Urinary Casts
* Formed in tubules by sloughing of cells
* Can be normal in small numbers
* When excessive = tubular necrosis
* Granular (concern)
* Fatty (rare)
* Hyaline (horses & insignificant)
68
7 Types of Crystals
* Magnesium ammonium phosphate (struvite)
* calcium carbonate
* urate
* calcium oxalate
* cystine
* cholesterol
* bilirubin
69
Magnesium ammonium phosphate crystals (struvite)
o rectangular
o May be normal
o Associated w/ neutral or alkaline urine
o Can form calculi
70
Calcium Carbonate Crystals
o round
o Normal in horse
o Associated w/ alkaline urine
o No clinical significance
71
Urate Crystals
o Thorny round shape
Ammonium biurate
• Associated w/ slight acidic, neutral or alkaline urine
• Yellow/brown
```
Amorphus urates
• Associated w/ acidic urine
• Yellow/brown
• Common in dalmations
• Associated hepatic dz
```
72
Calcium oxalate crystals
Dehydrate:
o square
monohydrate:
o flat & oblong
o ethylene glycol poisoning
73
Cystine Crystals
o Hexagonal
o Amino acid problem
o Formed in acidic urine
74
Bilirubin Crystals
o Reddish-orange needles
o Normal in concentrated dog urine
o High numbers = abnormal bilirubin metabolism
75
Why use Modified Water deprivation test & what should you test first?
Use when no azotemia, no dehydration, PU/PD & USG <1.020
Test these first:
• CBC/Chem & U/A to rule out underlying metabolic abnormality, cystitis, etc
• Bile acids to exclude hepatic insufficiency
• Urine culture +/- ACTH stimulation test to rule out
Hyperadrenocorticism
76
Method for Modified Water deprivation test
* Slowly limit water intake over a few days (modified) ->
* Take USG, body weight, hydration status, BUN/Creatinine ->
* remove water and re-evaluate parameters every 1-2 hours
Stop if:
o Urine concentrates (>1.030)
o Animal becomes dehydrated or azotemic
o Body weight decreases 5%
Results:
o If animal concentrates - primary polydipsia problem
o If animal doesn’t concentrate
-> Give ADH.
• Response to exogenous ADH = pituitary diabetes insipidus
• No response to ADH = Nephrogenic cause
77
Renal Dz
* refers to any lesion of the kidney
| * Can progress to renal failure
78
Acute Kidney Injury (AKI)
* sudden renal injury ranging from mild nephron loss to acute renal failure.
* IRIS* staging system used to denote severity
79
AKI Grading Criteria
* Grade I: non-azotemic; other evidence of kidney injury
* Grade II: mild AKI
* Grade III-V: moderate to severe AKI leading to renal failure
80
Late Stage AKI / Renal Failure
* Not seen as commonly as chronic kidney disease
* Sudden onset
* Oliguria or anuria
* Usually looking for toxic or infectious cause (ethylene glycol)
81
Stages of Ethylene Glycol Toxicity
Stage 1
• 30 min to 12 hours post ingestion
• CNS signs, PU/PD, vomiting
Stage 2
• 12-24 hours
• Tachypnea and tachycardia from developing metabolic acidosis
```
Stage 3
• 24-72 hours (dogs)
• 12-24 hours (cats)
• Acute renal failure
• vomiting, oliguria, anuria
```
82
Symptoms of Ethylene Glycol Toxicity
```
Early Abnormalities (1-6 hours)
• Decreased bicarbonate (TCO2)
• Increased anion gap
• Increased osmolal gap
• Possible hypocalcemia
• Crystalluria (calcium oxalate monohydrate)
```
```
Late Abnormalities (24-72 hours)
• Azotemia (seen as early as 12 hours in cats)
• Isosthenuria
• Hyperphosphatemia
• Hyperkalemia
```
83
Chronic Renal Failure (CKD)
* Common
* structural or functional abnormalities of kidneys present for 3 months or longer w/ late stage leading to renal failure.
* IRIS staging system used to denote severity
* Impaired urine conc. & increased SDMA before azotemia
* PU/PD
* isosthenuria, azotemia, anemia, (hypercalcemia in horses)
84
PU/PD
Primary polydipsia
o psychogenic, hepatic or neurologic disease
Primary polyuria
o Osmotic
o Lack of ADH
o Primary nephrogenic diabetes insipidus
o Secondary nephrogenic diabetes insipidus
o Medullary washout
85
Renal Failure
* functional renal tissue is inadequate to maintain health.
* IRIS staging can be used to indicate severity.
* Generally both azotemia and inappropriate renal concentration (check USG) are noted.
86
Uremia
• clinical signs associated with severe renal disease (eg, vomiting)
87
Proper Sample Collection for Acid-Base Evaluation
Heparinized syringe
Arterial better than venous sample
Avoid air exposure
• increases pH
Record temperature
• CO2 drops 2mmHg & O2 drops mmHg every 1C below 37C
Evaluate ASAP!
88
Organs involved in acid base balance
Lungs
• remove H+ & CO2 (acids)
kidneys
• add HCO3 (base)
• remove H+ (acid)
89
Systemic Approach for Evaluating Acid-Base Disorders
o Acidemia or alkalemia?
o Respiratory or metabolic?
o Compensatory response?
Subclassify
• Is metabolic acidosis titrational or secretional?
• Is it a mixed acid-base disturbance?
90
Secretional V Titrational Metabolic Acidosis & relation to anion gap
Secretional
• HCO3 loss -> decreased HCO3, normal anion gap, increased Cl-
• Diarrhea, Renal loss, Excess salivation
Titrational
• Acid accumulation -> decreased HCO3, increased anion gap
• Lactic acidosis, ketoacidosis, uremic acids, toxins
91
Basics to remember for inflammatory & stress leukograms
o inflammatory: neutrophelia +/- L shift & tox change
| o stress: lymphopenia
92
Start w/ pH and figure out respiratory or metabolic acidosis or alkalosis
o low pH = acidemia ->
o high pCO2 -> resp acidosis
o low HCO3 -> met acidosis
o high pH = alkalemia ->
o low pCO2 -> resp alkalosis
o high HCO3 -> met alkalosis
93
paradoxical aciduria
cows can have metabolic alkalosis w/ acidic urine
Must have
o hypovolemia
o hypochloremia
o hypokalemia
94
Calculate Anion Gap
anion gap = (Na) – (Cl + HCO3)
| TCO2 = (HCO3 + CO2)
95
Causes of respiratory alkalosis
```
Extrathoracic
• PO2 is normal
• Fear
• Pain
• Anxiety
```
Intrathoracic:
• PO2 decreased
• Pulmonary disease
• Airway obstruction/mal function
96
Causes of respiratory acidosis
```
• Severe pulmonary disease
• CNS disease that decreases
respiratory rate
• Airway obstruction
• Pleural effusion/masses
• Neuromuscular disorders
```
97
Hypernatremia
Hypotonic fluid losses
• GI: vomiting, diarrhea
• Renal: Diabetes insipidus
• polyuria
Pure water deficits
• Primary hypodipsia
• Water unavailable or unable to drink
Gain of solute
• Salt poisoning (ruminants)
• Iatrogenic causes
98
Hyponatremia
* Hypoadrenocorticism
* Diarrhea
* Renal disease
* Dietary salt deficiency
* Diabetes mellitus
* 3rd space loss
* False decrease with lipemia or hyperproteinemia
99
Hyperkalemia
* decreased urinary excretion
* marked exercise or metabolic acidosis
* pseudo due to thrombocytosis or hemolysis
100
Hypokalemia
* anorexia
* insulin or metabolic alkalosis
* GI or renal loss
* sweating or burns
101
Hypochloremia
* chronic vomiting
| * aggressive diuretic therapy
102
Hyperchloremia
* fluid therapy
| * small bowel Ds
