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276 Cards in this Set
- Front
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How can you tell if a patient w/ signs of HAC does not just have DM
|
There should be glucosuria w/ DM
|
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What are 3 other dzs that can cause adrenal fxn testing abnormalities, besides HAC
|
Uncontrolled DM
Liver dz Renal failure |
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What is the most Sp test for HAC
|
ACTH Stim
|
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What is the most Se test for HAC
|
LDDST
|
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T/F: ACTH is a good test for IDing iatrogenic HAC
|
True
It can also be used to monitor therapy |
|
What does a high resting cortisol level mean in an ACTH stim test
|
?
|
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What is considered a + result for ACTH stim
|
Post-ACTH cortisol value > reference range
|
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T/F: A drawback to the LDDST is the # of false -s you can have
|
False
The problem is it is not very Sp, and there are many false +s |
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What is considered a positive result for LDDST
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Cortisol > 1ug/dL (or the RI) at any point in the test (3hrs, or 8hrs)
|
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What is meant by "rebound" LDDST results
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Cortisol suppresses to <50% of baseline at 3hrs, but jumps back up at 8hrs
Consistent w/ PDH |
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T/F: A patient w/ a positive LDDST has HAC
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False
You must look at the big picture; + LDDST alone is not definitive! |
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What does it mean if the Cortisol is high before ACTH, but w/in post-ACTH RI after giving ACTH
|
? Inconclusive; do LDDST
|
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If, after therapy for HAC the Cortisol values normalize, but there is no clinical response, what does that mean
|
Likely not HAC to blame for the signs
Do other diagnostics to find out reason for signs |
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How is the Se for Urine Cortisol:Creat
|
Very good
But, unacceptable Sp Requires 2nd confirmatory test |
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What are 4 ways to tell b/t PDH and ADH HAC
|
HDDST
Endogenous ACTH Abd U/S LDDST (if rebounds) |
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How often does Cortisol suppress in HDDST testing of PDH cases
|
75-85% cases
|
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T/F: There is no suppression of cortisol in HDDST testing if a case of ADH
|
True
|
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What can you conclude about the source of the HAC problem if there is no cortisol suppression in a HDDST
|
Nothing
There is 50:50 chance of ADH or PDH "Failure to suppress is ambiguous" |
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What is, reportedly, the most reliable test for differentiation of ADH from PDH
How is it interpreted |
Endogenous ACTH
<10 pg/mL = ADH >45 pg/mL= PDH In b/t those values, ? |
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What is a + HDDST
|
Post-dexamethasone Cortisol <50% of baseline at any time during the test
Do NOT use RIs for this test, use the patient's baseline |
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What is the caveat for the use of U/S to tell b/t ADH and PDH
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Both adrenal glands must be visualized
|
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What is atypical HAC
|
Dog has signs of HAC, but normal or low cortisol [ ]s
|
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What causes atypical HAC
|
Adrenal tumors making a hormone other than cortisol
OR PDH w/ excessive production of 2 or more cortical Hs other than cortisol |
|
How do you dx atypical HAC
|
ACTH Stim, but measure progesterone, 17-OH progesterone, +/- estradiol
(in addition to cortisol) |
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How do you tx atypical HAC
|
Like any other case of HAC
|
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What are the two protocols for use of Mitotane (Lysodren) in tx of HAC
|
"Old Standby"- selective destruction of cortex; must monitor erll
Alternative- wipe out cortex via high dose for 25d, with H replacement starting at day 3; may be cheaper and have fewer complications |
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Why might the "alternative" Lysodren protocol end up actually costing more than the "traditional" protocol
|
Supplemental tx may add up!
|
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What determines which method you should use when txing HAC w/ Mitotane
|
The owner, and their ability to "regulate" via clinical signs, etc.
|
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How does Ketoconazole work for HAC? SEs?
|
Enzyme inhibition blocks production of Cortisol
Works in 75% PDH cases Can be hepatotoxic |
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What does L-deprenyl work on for tx of HAC
|
Only the region of pituitary under influence of DA (pars intermedia)
SO, reduces cortisol in only 15-20% cases (i.e. if have pars distalis tumor, will not decrease cortisol) But, does improve signs in 83% of cases! |
|
What is Trilostane, and what are the benefits of it vs. Mitotane
|
Enzyme inhibitor
If wrong dx, can stop drug w/ "no harm, no foul" 89% have good response Rarely can cause permanent HYPOadreno and death, but considered as safe as Mitotane |
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How should tx of HAC w/ Trilostane be started
|
Start once daily and adjust based on signs and [cortisol]
But, some need BID, and it may be best to start them that way b/c safer |
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What are potential SEs of Trilostane
|
Lethargy
Decrease appetite Can die, rarely |
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How soon after starting Trilostane should you do an ACTH
|
10-14, 30, and 90 days after start tx (do 4-6hrs after dose)
Want post-ACTH results w/in normal PRE-ACTH range |
|
How should you adjust Trilostane based on ACTh results
|
If post-ACTh cortisol <0.7, stop pill for 2days, and then re-start at lower dose (w/ another ACTh in 10-14days)
If post-ACTH >4.3, increase dose by 25-50% If b/t 0.7 and 4.3, and clinical control seems adequate, leave alone |
|
What is mean survival of HAC dogs on Trilostane
|
661 days
|
|
What txs can be used for ADH
|
Sx
Mitotane Ketoconazole (helps 80%) Trilostane |
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What should you do before doing sx for ADH HAC
|
Tx medically to stop the HAC before do sx (then replace steroids post-op)
|
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What is the px for PDH HAC tx'd w/ Mito or Trilo
|
1yr- 70% still alive*
2yr- 50% still alive* 4yr- 20% still alive* * may have died from other causes * |
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What is the breakdown of tumor type in ADH HAC
|
40% adenomas
60% AC (1/2 of are inoperable) |
|
T/F: It is recommended that you refer for adrenalectomy in ADH
|
True
There can be many complications |
|
Why do IV fluids and Abx result in temporary improvement in cases of HypoAC
|
Rebalances electrolytes temporarily
|
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T/F: Addison's is often a waxing/waning dz
|
True
|
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What are the 2 most impt DDx for HypoAC, and which is the hardest to tell it apart from
|
Acute oliguric/anuric RF***
Post-renal uremia ***= hardest to tell from |
|
What should be your diagnostic plan for HypoAC
|
CBC/Chem/UA
ECG (look for bradycardia w/ sinoventricular rhythm) Basal cortisol ACTH stim |
|
How does a Basal Cortisol test aid in dx of HypoAC
|
If result >2, can R/O
If <1, likely has HypoAC Gray area in b/t |
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What is unqique about the leukogram of a patient in hospital w/ HypoAC
|
There is no stress leukogram, despite being chronically ill, and hospitalized
|
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What biochem markers make HypoAC hard to tell from renal failure
|
Azotemia
Increased Ca Increased K |
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What does it mean if the post-ACTH cortisol is higher than the baseline RI, but not w/in the post-ACTH RI
|
Likely HypoAC
Use signs to help guide dx |
|
T/F: In a crisis situation, being therapy for HypoAC before you have test results
|
True
Best to wait to administer gluco/mineralo corticoids until have results, too, but cna use Dex if you have to |
|
Why must you keep hypoAC patients NPO for 24hrs
|
It takes 24hrs for GI motility to normalize again (after the v+ they likely presented w/)
|
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What is the fluid therapy of choice for HypoAC
|
0.9% NaCl
Add 2.5-5% glucose if needed (may be hypoglycemic since no glucocorticoids) |
|
What rate should you give fluids to for a hypoAC patient
|
If shocky, 90 mL/kg/hr
If not, rpelace deficit over 12-24hrs Remember to include losses in calculation if still v+ |
|
How often must hyperkalemia be treated (besides fluids) in HypoAC
|
Rarely
Saline rehydration often improves electrolytes alone |
|
T/F: If giving glucose to a Addison's pt, you should also give insulin
|
False
Unless diabetic, does not need |
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What should you use for initial gluco/mineralo replacement in hospital for HypoAC cases
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Hydrocortisone
CRI preferred, but can give IV q6hrs, too |
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When should you switch fromn parenteral to oral mineralo/gluco replacement in a HypoAC patient
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When they are eating
|
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What happens if you change the sodium concentration too quickly in an Addison's pt
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Nervous system abnormalities
|
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What are the electrolytes like in an Addion's pt
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Increased K+ and Ca2+
Decreased Na+ and Cl- Usually Na:K <27:1 |
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How do you use Fludorcortisone as mineralo replacement
|
qd or BID
Check Na+ and K+ qd for 2-3 days; adjust dose to keep wnl PU/PD may occur |
|
What should you use as oral glucocorticoid replacement, and how
|
Prednisolone
Give qd for 1-2wks, and then taper over 1-2wks May be able to withdraw completely (50% cases) if on fludrocortisone b/c has some gluco activity |
|
How and how often should Addison's pts be monitored post-crisis
|
Weekly for 2-3wks:
Na+, K+, BUN Then, q 3-4mths for a year Then, q 3-6mths after that |
|
What is DOCP
|
Injectable mineralocorticoid replacement
Inject q 25-30d IM or SC Less likely to cause PU/PD BUT: 1. Can't change dose quickly 2. Most still need gluco, too 3. Just as $ as fludrocortisone |
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When should salt supplementation be considered in hypoAC
|
When Na+ low despite normal K+
Add to diet, and recheck serum Na+ |
|
What is the px for Addison's
|
Excellent for normal lifespan
Can decomp if miss meds Can be $ for large dogs |
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T/F: Most cases of feline HAC are d/t ADH
|
False
Most cats have PDH |
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What percentage of HAC cats also have DM
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90-100%!!!
|
|
When should you sample for ACTH testing in cats
|
0, 30, and 60 minutes
(some cats peak at 30, some at 60) |
|
What is the most effective tx for feline PDH
|
Bilateral adrenalectomy
|
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T/F: Trilostane can be used in cats
|
True
|
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Why might you be more likely to question your dx of HypoAC in a cat when treating
|
It takes cats 3-5 days to respond to tx (slower than dogs)
Also, very rare in cats anyways |
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If a dog has iatrogenic HAC, what should the ACTH show (assuming patient had meds D/C for 24-48hrs prior to test, as it should)
|
Should have normal results
|
|
What if:
Signs of HAC ACTH stim: Pre- wnl Post- increased from base, but still low |
1. Iatrogenic HAC causing adrenal gland atrophy
OR 2. Atypical HAC- check other Hs |
|
At what age would you be able to detect congenital pituitary dwarfism
|
3-4mths old
Normal until then |
|
How do you dx congenital pituitary dwarfism
|
R/O other DDx
GH assay (stim w/ GHRH or xylazine) Somatomedin-C (IGF-1) Endogenous ACTH ACTH Stim ** do together** T4 and TSH (if both low, may mean 2' hypothyroidism) |
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T/F: In cases of congenital pituitary dwarfism, you may see signs of 2' hypoAC and/or hypothy
|
True
|
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What are 2 txs for congenital pituitary dwarfism
|
Human GH- hard to get
Progesterone (stimulates GH production from mammary tissue) |
|
What causes feline acromegaly, and who does it affect
|
GH-producing pituitary tumor
Males 8-14 years |
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Why do cats w/ feline acromeglay often not lose wt despite their concurrent insulin-resistant DM
|
GH may actually make them get bigger!
|
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How can you tx feline acromegaly
|
Palliate: insulin, diuretics (of goes into heart failure)
Radiation to shrink mass |
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What clinical signs might patients w/ feline acromegaly present w/
|
PU/PD
Cardiomegaly, Murmur Enlarged head Signs of DM |
|
What causes CDI
|
Partial or complete ADH deficiency
Renal tubules and CDs are impermeable to H2O |
|
True/False: CDI patients have a 1' PU w/ a 2' PD
|
True
|
|
What is the most common cause(s) of CDI
What are some other causes |
Historically, idiopathic
Currently, neoplasia 66% Head trauma Pituitary malformation Inflammation Congenital (familial) |
|
What are the signs of CDI
|
PU/PD
Perceived incontinence Wt loss V+ water Dehydration if water-restricted Dementia/Stupor/Ataxia/ Blindness/Seizures- if pituitary tumor |
|
What is the USG like in CDI
|
Usually <1.008
Often 1.001-1.002 |
|
What is the CBC/Chem like in CDI
|
CBC-wnl
Chem: Decreased BUN If water-deprived, pre-renal azotemia and increased Na+ |
|
When should you do CT/MRI in cases of CDI
|
Esp. older patients
MRI preferred Only do if owner wants to tx tumor |
|
How do you do Modified Water Deprivation test
|
R/O all but CDI, NDI, PP 1st
Water deprive until lose 5% BW (should be maximally making ADH at that point) Give ADH Check urine osmolality (+= 50-600% increase after ADH); can use USG, but osmolality more accurate |
|
Who is Modified Water Deprivation testing C/I in
|
Azotemic patients
Those you have not R'd/O everything but PP, CDI, NDI |
|
Which test for CDI gives the most info
|
MWD test
But, not always easy to do, and can be dangerous |
|
How do you perform ADH response test
|
Measure drinking for 2-3days
Give DDAVP Measure drinking for 5-7days Check USG qd while getting DDAVP CDI=marked decrease in urine volume and H2O consumption Monitor Na+ for 2-4wks |
|
Why do you monitor the plasma Na+ for 2-4 wks after doing ADH response test
|
If remains normal, likely CDI
If it drops, consider PP, etc. |
|
How do you tx CDI
|
DDAVP (synthetic ADH)
- in conjunctival sac or oral - give BID and monitor (or can wait for PU/PD before redose) Consider radiation if pituitary mass |
|
What is the px for CDI
|
Excellend if idiopathic or congenital (b/c can replace ADH)
Worse if pituitary mass (neuro signs w/in 2wks-5mths) $ of tx is limiting factor |
|
Who does PP mostly occur in
|
Hyperactive, lg breed dogs
|
|
What is often the hx of a patient w/ Psychogenic PD
|
Restriction of exercise or human contact (often, reviously v. active)
|
|
How do you test for PP
|
Modified Water Deprivation test
Should have little or no response to ADH since already making as much as they can |
|
How do you interpret MWD test for PP if USG not >1.030, but dx highly suspected
|
Reinstitute medullay solute via parital water restriction and salt supplementation
Then, test again (likely had medullary washout) |
|
How do you tx PP
|
Gradual water restriction
Increase exercise Get another dog? Increase human contact |
|
Of what age are most patients w/ 1' HyperPTism
|
Older
Dog- avg 11 Cat- avg 13 |
|
In which species are females predisposed to 1' hyperPTism
|
Cats
|
|
What is the most common cause of 1' HyperPTism
|
Adenoma
But, realize there is a fine line b/t adenoma and hyperplasia |
|
What are Ca2+ and P like in 1' HyperPTism
|
Ca2+ high (including iCa2+)
P normal or low |
|
What are the 2 main R/Os for high Ca2+/low P
|
Cancer (LSA)
OR HyperPTism |
|
What 4 body systems does hyperCa2+emia affect cell membrane activity and permeability in
|
Neuromuscular
CV Renal (dysfxn) GI (reduced fxn) |
|
When does ST mineralization occur
|
When Ca2+ x P >60-70
Often, we do not see w/ 1' hyperPTism b/c P gets low |
|
How is hyperPTism most commonly noted
|
Serendipitously on chemistry
|
|
What are the most common signs of 1' HyperPTism in dogs
|
LUT signs d/t calculi
(hemat, pollak, stranguria) PU/PD Weak/Lethargy Poor appetite Wt Loss/Muscle Wasting These are the same signs as in cats, but anorexia and lethargy are most common in cats |
|
How common is rubber jaw in cases of 1' hyperPTism
|
It is an uncommon sign, and occurs when bone is demineralized
|
|
How do you make a dx of 1' HyperPTism
|
Typical chem changes
(CBC usually wnl) R/O cancers Rectal palp Thoracic/Abd rads or U/S LN aspirates THEN Simultaneous plasma PTH, PTH-rp, and iCa2+ Surgical exploration/bx |
|
What dz, besides cancer, is it impt to tell apart from 1' hyperPTism
|
1' Renal Failure
(iCa2+ is usually wnl iin renal failure, but is often high in 1' hyperPTism) |
|
What is the typical USG of a patient w/ 1' hyperPTism
|
<1.028
(dogs usually <1.015) |
|
What is PTH normally like in a 1' hyperPTism patient
|
Most are high or in the upper 1/2 of the RI
This is INAPPROPRIATE b/c high PTH should only be seen w/ low Ca2+ (in an effort to increase it) |
|
What is the iCa2+ usually like in a 1' hyperPTism case
|
High
(vs. wnl for renal failure) |
|
How do you tx 1' hyperPTism
|
Sx to remove abnorm tissue
Monitor Ca2+ and P after |
|
What are 5 reasons for implementing aggressive medical therapy for hyperCa2+emia
|
1. Azotemia
2. Dehydration 3. Signs of hyperCa2+emia 4. Ca x P >70 5. Ca >16 mg/dL |
|
What constitutes aggressive medical therapy for hyperCa2+emia
|
IV 0.9% NaCl
Furosemide- NO THIAZIDES Corticosteroids Calcitonin Pamidronate disodium IV |
|
What three things constitute maintenance therapy for hyperCa2+emia
|
Oral:
Corticosteroids and Furosemide Inj: Calcitonin |
|
What is the px for 1' hyperPTism
|
Good w/ sx for adenoma or hyperplasia (35% have low Ca2+ after sx)
RF worsens px |
|
What is the most common cause of hyperCa2+emia in cats
|
Idiopathic Feline HyperCa2+emia (IFH)
|
|
What is the avg age of a cat w/ idiopathic hyperCa2+emia
|
~10yrs
|
|
T/F: Almost 1/2 of cats w/ idipathic hyperCa2+emia have no clinical signs
|
True
46% |
|
What is confusing about the cause of IFH if CRF is present
|
Which came first?
|
|
What is iCa2+ and PTH like in cases of IFH
|
PTH in lower 1/2 of RI
High iCa2+ This is APPROPRIATE |
|
T/F: Cats w/ IFH that have no, or only mild signs, may not need to be treated
|
True
|
|
What txs can you employ for a cat w/ IFH
|
Diets to decrease Ca2+, i.e.:
High fiber Diets for RF Diets for preventing CaOx's Corticosteroids (Prednisolone)- 1/2 respond to Bisphosphonates helps some (be careful to not cause esophageal erosion) |
|
What are the two major categories of 1' hypoPTism
|
Iatrogenic
Thyroidectomy in cats PT adenoma removal in dogs Naturally Occurring D: immune destruction and atrophy C: idiopathic atrophy |
|
What is the most common cause of 1' hypoPTism
|
Thyroidectomy in cats
|
|
What clinical manifestations can be expected w/ hypoCa2+emia
|
SIgns relating to NM dysfxn(since Ca2+ needed for NT release, and for STABILIZATION OF NERVE CELL MEMBRANES)
|
|
What are some of the signs of 1' hypoPTism
|
Nervousness/Seizures
Muscle fasciculations/tremors Ataxia/Stiff gait/Weakness Muscle cramp/pain Hyperthermia Lethargy/Anorexia Facial pruritus Aggression-dogs Ptyalism/Dysphagia- cats +/- PU/PD Tachyarrhythmias- dogs Bradycardia (dogs or cats) |
|
What is one feature that can be used to tell 1' hypoPTism from RF
|
Lack of azotemia
(Just high P and low Ca2+) |
|
What is PTH like in 1' hypoPTism
|
Low or low normal
INAPPROPRIATE w/ low Ca2+ |
|
How do you treat hypoCa2+emic tetany
|
IV Ca gluconate to effect
Then CRI or SC q6-8hrs |
|
What is the maintenance tx for 1' hypoPTism
|
Oral vit D (calcitriol)
Oral Ca2+ Low P diets Non-Ca2+ P-binders Check Ca and P qd, q wk, q 1-3mths Monitor for PU/PD |
|
Where would we like to keep Ca2+ when monitoring for tx of 1' hypoPTism
|
Ca2+ 8-10 mg/dL
Ca2+ x P <70 |
|
What is the px for 1' hypoPTism
|
Excellent
(only a small % die during initial crisis) |
|
What are 3 reasons you might see increased Na+ in a case of DKA
|
PU/PD
V+ Hyperglycemia |
|
What is the recommended fluid therapy for DKA if glucose >250
|
0.9% NaCl while glucose >250
(not LRS since lactate metabolized by same mechanism as ketones) If shocky, 90 mL/kg/hr If not, replace deficit over 12hrs for dogs, and 24hrs for cats |
|
When should you add dextrose to fluid therapy for DKA, and how much
|
BG 150-250, add 2.5% dextrose
BG <150, add 5% dextrose |
|
Why should you replace the DKA fluid deficit more slowly in cats
|
If replace too quickly, you can cause cerebral edema
|
|
When is using "twice maintenance" an appropriate course of action for DKA
|
Never
Calculate it out |
|
What is the maximum allowable K+ supplementation rate
|
0.5 mEq K+/kg/hr
Don't exceed this! |
|
T/F: Despite bloodwork results, DKA patients likely have a total body K+ deficit
|
True
|
|
T/F: P decreases w/ insulin and fluid therapy
|
True
Monitor it, along w/ K+, q 12-24hrs |
|
T/F: In cases of DKA low P often causes hemolysis, seizures, and cardiomyopathy
|
False
It must be lower than 1.2 to cause these signs, and rarely gets that low If it does, give 1/4 of the K+ supplementation as K-PO4 |
|
What are the three steps of correcting acid/base imbalance in DKA
|
Stop ketone formation (insulin)
Correct hypovolemia- fluids Bicarb if pH<7.1 or CO2<12 |
|
T/F: You can delay administration of insulin to a DKA cat for a few hours
|
True
It might be good to do so since so hyperosmolar initially |
|
Which spp. has been shown to have low Mg in DKA
|
Cats
Can give MgSO4 |
|
T/F: It is best to place a urinary catheter to measure urine output in DKA
|
False
Use repeated palpation or metabolism cage, instead, since I/C Monitor well b/c at risk for ARF |
|
What are the two indications for placement of urinary catheter in DKA
|
Oliguria
Comatose |
|
What are the 3 fxns of insulin
|
1. Decrease glucose
2. Stop ketogenesis 3. Decrease glucagon |
|
T/F: Overcorrecting metabolic acidosis can cause more problems than you had initially in DKA
|
True
|
|
What type of insulin, and by which route, should DKA patients get
|
Short-acting (i.e. Regular)
IV or IM Delay for 2-6hrs in cats until rehydrated somewhat |
|
Explain CRI insulin for DKA
|
Uses pump
2.2 U/kg dogs; 1.1 U/kg cats Put in 250mL 0.9% NaCl Use double-lumen or 2 catheters Adjust rate depending on BG (monitor BG q 2hrs) |
|
What is the therapeutic endpoint for CRI of insulin in DKA
|
No urine ketones
Patient eats |
|
How long does it take DKA patients to decrease their BG to <250
|
dogs- 10 hours avg
cats- 16 hours avg |
|
After BG drops below 250 when using CRI of insulin for DKA, then what
|
Regular insulin SC until nexty morning
Intermediate-acting insulin starting the next morning |
|
Explain Low Dose IM insulin therapy for DKA
|
Give hourly IM injections and monitor BG hourly
0.2 U/kg initially Ten, 0.1 U/kg/hr |
|
What might be the most practical way to give insulin for a DKA patient
|
IM low dose
|
|
What is the therapeutic endpoint for IM low dose insulin therapy in cases of DKA
|
Glucose < 250
|
|
How long does it take most dogs to decrease glucose to <250 when using low dose IM insulin therapy for DKA
|
4hrs avg
(faster than for CRI, so be careful) |
|
When should SC insulin be started in cases of low dose IM insulin therapy for DKA
|
When glucose b/t 150 and 250
|
|
If BG drops too low, and there are still ketones present, what should you do
|
Add glucose to the fluids
You have to give insulin to get rid of ketones, regardless of whether or not BG has resolved |
|
What is the px for DKA
|
25-30% die
BUT: <5% die from the DKA; most die from the inciting cause |
|
What are some potential complications of DKA
|
Cerebral edema
Hypokalemia Hypoglycemia Hypophosphatemia |
|
What is Hyperosmolar Nonketotic DM (HNDM)
|
Severe elevation of BG w/ DM w/o significant ketosis
Made possible via enough insulin-producing capacity remaining despite underlying/2' dz causing abnormal insulin:glucose |
|
What are the signs of HNDM
|
Like DKA
Concurrent renal failure common |
|
How is fluid therapy different for HNDM than for DKA
|
Replace 1/2 of the deficit and maintenance in 1st 12 hrs, then next half over next 24hrs
(since often have RF, too) |
|
As long as urine output is okay, how should K+ be supplemented in cases of HNDM
|
20 mEq/L
|
|
T/F: Insulin therapy should be held off for 4-6hrs in cases of HNDM
|
True
This prevents too rapid of a decrease in glucose and osmolality |
|
How is insulin therapy different in cases of HNDM than for DKA
|
Use only 1/2 of the insulin dose you would use for DKA
|
|
What is the px for HNDM
|
Poor-Grave
|
|
What is Whipple's Triad
|
Qualifications for dx of Insulinoma:
1. Typical signs 2. Hypoglycemia 3. Correction of signs once hypoglycemia is corrected |
|
What are insulinomas tumors of
|
Insulin-secreting islet cells of the pancreas
|
|
What test helps make dx of insulinoma
|
Simultaneous BG and insulin levels
Measure when hypoglycemic If insulin is in upper 1/2 of RI, or higher, w/ simultaneous BG <60 mg/dL, likely insulinoma (if also has signs) |
|
How quickly do most insulinoma patients become hypoglycemic in hospital
|
w/in 10-12hrs
Use overnight fast (normal at home) to kick it off, and then measure BG every hour until low BG, and then do insulin level |
|
What percentage of insulinoma cases have normal insulin
|
25-35%
|
|
What is AIGR?
|
Adjusted Insulin:Glucose Ratio
Useful if normal insulin, but suspect insulinoma AIGR= Insulin x 100/ (glucose-30) Values >30 "positive" Not Sp for insulinoma, though |
|
T/F: Most cases of insulinoma are treated w/ combo of sx and medical tx
|
True
|
|
What % of insulinoma cases have LN or liver mets at time of sx
|
Almost 1/2
(45%) |
|
What are some common insulinoma post-op complications
|
Pancreatitis- 1/3 cases
Continued low BG- 1/4-1/3 Hyperglycemia- 10-15% |
|
What is medical mgmt of insulinoma
|
Multiple small meals
Oral Prednisolone Diazoxide- hard to get (Streptozotocin experimental) May need CRI of dextrose or glucagon while waiting for sx to prevent clinical signs |
|
What is the px for insulinoma
|
Nearly all met despite histological appearance
Avg survival 10-14mths w/ combo sx & medical mgmt 6 1/2 mths if medical alone |
|
How does Diazoxide affect insulinoma px
|
60-65% improve
Avg duration of improvement 6 mths |
|
Who is VUH appropriate for
|
Dogs-
<4mm for females >10# <3mm for males >15# Cats- </= 2mm for females |
|
Who is VUH C/I in
|
Male cats
Urethral obstruction (even partial) Giant breed dogs b/c size Uncontrolled infection Uro sx w/in 2wks |
|
T/F: Patients need to be heavily sedated or anesthetized for VUH
|
True
Need abd to be loose and for sphincter tone to be abolished |
|
What are some possible complications of VUH
|
Hematuria WILL occur (for a few days)
UTI- can put on ABx for few days after procedure Bladder rupture Urethral obstruction |
|
What is the other name for Brushite stones
|
Ca-H-P Dihydrate
|
|
What is the other name for Hydroxyapatite stones
|
Ca-P Apatite
|
|
What is the other name for Carbonate Apatite stones
|
Ca-P Carbonate
|
|
Which stones occur secondary to excessive urinary Ca2+ loss
|
Brushite and Hydroxyapatite
|
|
What are some causes of excessive urinary Ca2+ loss
|
Distal renal tubular acidosis
Hypercalcemia (d/t hypetPT) Decreased crystallization inhibitors HAC Normocalcemic Hypercalciuria (idiopathic) |
|
What is the association b/t calcium phosphate stones and urine pH
|
Acidic- Brushite
Alkaline- Hydroxyapatite and Carbonate Apatite |
|
Which stone type are Ca-H-P Dihydrate stones often seen w/
|
CaOx (acidic urine)
|
|
Which stone type are Ca-P Apatite stones often seen w/
|
Struvite (alkaline)
|
|
What type of stone is Ca-P Carbonate typically seen w/
|
Can see w/ CaOx or MAP
|
|
Which calcium phosphate stone is NEVER 100% pure
|
Carbonate Apatite
|
|
Which calcium phosphate stones can be seen in environments w/ urease producing bacteria
|
Ca-P Apatite
Ca-P Carbonate |
|
What is the typical signalment of calcium phosphate stones
|
Middle-aged
Breeds predisposed to other stones |
|
When should you work calcium phosphate stone patients up for hypercalcemic disorders
|
If they have Ca Apatite or Brushite stones
|
|
T/F: Calcium phophate stones can be a reason for incomplete dissolutionof struvites
|
True
|
|
How do you treat calcium phosphate stones if they are assoc'd w/ struvites and urease-producing bacteria
|
Treat for the bacteria and struvites
|
|
What type of diuretic is indicated in tx of calcium phosphate stones
|
Thiazides to decrease Ca2+ in urine
|
|
Of what pH is urine typically if it has cystine stones
|
Usually acidic
|
|
What are some of the Newfie exceptions w/ Cystine stones
|
Non-sense mutation in gene
Autosomal recessive (carriers not affected) Females often affected Nephroliths common |
|
What is the typical opacity of cystine stones
|
Variable, but more likely opaque if big
|
|
Aside from Newfies, what is the typical signalment of dogs w/ cystine stones
|
Middle-aged
Almost only males |
|
How long does it take to dissolve cystine stones usually
|
3-4mths
|
|
How do you dissolve cystine stones
|
Increase H2O intake
U/D to alkalinize urine and decrease protein/AAs 2MPG or Penicillamine to bind cysteine so can't make cystine |
|
How long should you treat for cystine stones
|
1 mth past resolution
|
|
What is responsible for silica stones
|
Diets high in plant matter
Pica |
|
What normally happens to any silica ingested/absorbed
|
It is readily filtered through the kidney
|
|
What stone type may be seen w/ silicates (d/t epitaxial growth)
|
CaOx
|
|
Which gender are silica stones usually seen in
|
Males
|
|
T/F: Silica stones are not seen on UA
|
True
|
|
What do the silica stones look like (if they are pure)
|
Jackstone shape
|
|
What is the radiographic density of silica stones
|
Opaque (if pure)
|
|
How can you treat/prevent silica stones
|
Feed low plant matter diet
Increase H2O intake Treat for CaOx if present |
|
What is the common denominator, usually, in dogs w/ xanthine stones
|
On Allopurinol for recurrent urates
|
|
What pH of urine do you see xanthine stones in
|
Acidic
|
|
What stone type are xanthines usually compounded w/
|
Urates
|
|
T/F: Xanthines are usually found unexpectedly when analyzing stone of another suspected type
|
True
|
|
What is the radiographc density of xanthine stones
|
Radiolucent to only moderately opaque
|
|
How can you be sure that an animal w/ xanthines (or urates) is actually eating a low protein diet (to prevent them)
|
Low-Low normal BUN
Low norm Alb USG <1.020 Neutral urine pH |
|
If animal is eating low protein diet for urates/xanthines, but pH is not neutral, what can you do
|
Add K Citrate to alkalinize back to neutral
|
|
What are sulfadiazine stones usually d/t
|
Chronic, high dose therapy w/ Sulfadiazine-Trimethoprim
(not done much anymore, anyway, b/c of concern for KCS) |
|
What stone type has crystals that resemble wheat bunches
|
Sulfadiazene
|
|
What are the only three stone types formed in alkaline urine
|
Struvites/MAP
Ca-P Carbonate (Carbonate Apatite) Ca-P Apatite (Hydroxyapatite) |
|
What are 4 types of non-erosive, non-infectious inflammatory jt dz
|
Idiopathic Immune-Mediated Polyarthritis
Chronic Inflammatory-Induced Polyarthritis Plasmacytic-Lymphocytic Synovitis SLE |
|
What are 4 types of erosive, non-infectious inflammatory jt dz
|
RA
Feline Chronic Progressive Polyarthritis Erosive Polyarthritis of Greyhounds Periosteal Proliferative Arthropathy |
|
What is the hallmark of inflammatory arthritis
|
Cyclic, Non-Abx responsive fever
|
|
What is a 1' immune-mediated polyarthritis
|
Abs directed against the jts
|
|
What is reactive polyarthritis
|
Deposition of immune complexes into joints (d/t chronic long-term infection, for example)
|
|
What is the most commonly diagnosed immune-mediated inflammatory jt dz
|
Idiopathic Polyarthritis
|
|
What is the #1 erosive jt dz er see assoc'd w/ polyarthritis
|
RA
|
|
How commonly is bacteria the cause of inflammatory arthritis
|
Rare, except for 2' to trauma or multiple sx procedures
Although, a foci/abscess/endocarditis can cause reactive polyarthritis |
|
Which viruses are thought to have a role in inflamm arthritis
|
Calici
FeLV FIV |
|
Which mycoses are most commonly seen w/ inflamm arthritis
|
Blasto
Coccidio Can also see Crypto, Histo |
|
How does RMSF typically present
|
Acutely in the spring
Patient often systemically ill |
|
What is the most common sign of SLE
|
Polyarthritis
Many signs are present, and not all of them occurring at the same time |
|
Which types of immunological injury are implemented in SLE
|
II- cytotoxic
III- immune complex IV- CMI |
|
What are the major signs of SLE
|
Polyarthritis
Glomerulonephritis (proteinuria) Bullous dermatitis Polymyositis Hemo- pancytopenia |
|
What are the minor signs of SLE
|
FUO
Pleuritis Pericarditis Oral ulcerations Neuro signs Lymphadenopathy |
|
Why might you see inflammatory urine sediment in SLE w/ sterile urine
|
Vasculitis can cause leakage of RBC and WBC
|
|
What is the biggest complicating factor for dx/tx of SLE
|
Renal dz
|
|
How are the Sp and Se for ANA testing
|
Very Se
But, not very Sp (treatments can affect, too) |
|
How Sp is LE Prep for SLE (if use jt fluid for test)
|
Very Specific
|
|
T/F: Previous tx can affect results of LE Prep
|
True
|
|
What is the tx/px for SLE
|
Tx:
Immunosuppression w/ Pred; Cyclophosphamide and/or Azathioprine if Pred alone does not work; Life-long Address renal dz! Px-poor |
|
How do the ages for Idiopathic Polyarthritis and Chronic Reactive Polyarthritis compare
|
Idiopathic usually younger
|
|
Which breeds are known to have breed-specific polyarthropathies
|
Akitas
boxers Y-Mars Bernese GSD Beagle Shar-Pei |
|
Which diagnostics should always be done in cases of suspected idiopathic polyarthritis
|
CBC/Chem/UA
Cytology of jt fluid Serology- 4DX, ANA, RA, FeLV/FIV Urine culture |
|
How many joints should be tapped when trying to dx idiopathic polyarthritis
|
At least 3, even if no evidence of effusion or pain
(as long as multiple joints known to be affected) |
|
If get jt fluid, which order should tests be done on it
|
1. Slide/Cytology
2, Purple top (EDTA)- cell ct 3. Red top- Mucin clot 4. Culture (1:9 w/ broth) |
|
Why is the mucin clot reduced in cases of idiopathic polyarthritis
|
Inflammation decreases hyaluronate, which decreases mucin clot
|
|
What is the cell makeup for purulent inflammation
|
>75% neutros
|
|
What is the cell makeup for chronic active inflammation
|
Lymphos and Macrophages
But, also neutros |
|
What is the normal cell count in joint fluid
|
<3000/uL
|
|
What cell count can you expect for degenerative/traumatic jt fluid
|
3,000-5,000/uL
|
|
What cell count is suggestive of immune-mediated jt dz
|
10,000/uL+
The higher it is, though, the more you should suspect infectious component |
|
What are the clinical signs of idiopathic polyarthritis
|
Intermittent shifting leg lameness
Smaller, distal jts more affected (i.e. tarsus) Spinal pain in some CS wax and wane |
|
Explain the Latex Agglutination RA test
|
IgG against IgM Abs
Test joint fluid or serum for RA factor |
|
T/F: Rads can be used to help dx RA
|
True
RA is erosive |
|
What radiographic changes might you see in a case of RA
|
Radiolucent lesions in subchondral bone
Irregular erosions Narrowed jt spaces Fibrous ankylosis |
|
T/F: In cases of RA, you may need to give Abx and steroids concurrently
|
True
If there is an infectious underlying cause, you may need Abx to resolve infection, but also steroids to decrease immune response |
|
How should you recheck patients w/ RA after starting on tx of Abx and steroids (for infectious underlying cause)
|
Re-tap the joints you originally tapped 2-4 wks after starting therapy
Do not wean meds until cell count <2000/uL |
|
What immunosuppressive drugs can be used as tx for RA
|
Prednisolone
Cyclophosphamide Azathioprine- for dogs only Methotrexate Gold salts Leflunomide |
|
What dz is Levamisole used for
|
SLE only
It is an immune stimulant at low doses |
|
What are some complications of RA
|
Renal dz
Cytopenias (check CBCs, esp. w/ drugs aside from Pred) Infxn- skin and UTI most common Cushing's 2' Hypertension |
|
T/F: Culture urine in all cases of RA on immunosuppressives, regardless of clinical signs
|
True
You are inhibiting the ability of the patient to show any signs by suppressing the IR |
|
Explain the pathogenesis of RA
|
Rheumatoid factors are produced against IgG and form complexes that cause:
Joint inflammation Synovial membrane thickening Proteolytic enzyme erosion of articular cartilage and subchondral bone |
|
T/F: Hyperproteinemia and Proteinuria are common in RA
|
True
|
|
What is the most prominent sign of reactive polyarthritis
|
Often, is a sign of the underlying dz process
Arthritis is NOT usually the most prominent sign |
|
T/F: Tx for reactive arthritis is often of long duration
|
False
Usually only need short-term tx b/c not usually any flare-ups like with other dzs (if you tx the underlying problem, too) |