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VET 433c > Renal/ Endo pt.1 > Flashcards

Renal/ Endo pt.1 Flashcards

1
Q

Polydipsia

A
  • voluntarily increased water intake
  • n is 50-100 ml/kg-day
  • PD is > 80-100 ml/kg-day
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2
Q

Polyuria

A
  • production of large volumes of dilute, unconcentrated or poorly concentrated urine
  • n is 50ml/kg-day
  • polyuria is > 50ml/kg-day
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3
Q

Consequences of PU/PD (patient)

A
  • urinary incontinence –> urine scald, UTI
  • QoL issues –> stress, accidents, need to be @ water bowl constantly
  • risk for dehydration
  • atonic bladder (uncommon)
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4
Q

Consequences of PU/PD (owner)

A
  • urinary incontinence
  • inappropriate urination
  • time constraints
  • emotional stress for owners
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5
Q

USGs

A
  • dilute (USG < 1.008)
  • isosthenuric (USG < 1.008 - 1.012)
  • concentrated ( USG >1.012)
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6
Q

Confirming PU/PD

A
  • we do not use urine output volume
  • serial USG measurements (first morning collection ideal)
  • pertinent history (drinking/ urinating more, etc)
  • Physical Exam (bladder palpation, rectal, neuro exam, watch p urinate)
  • CBC, Chem, UA
  • Ultrasound/ Rads
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7
Q

Diabetes Insipidus

A

Nephrogenic - 2* to pyometra, hypercalcemia, cushing’s, pyelonephritis, hyperT4)
Central - traumatic, neoplasia, cysts, malformation

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8
Q

Why does Polyuria occur

A
  • glc causing osmotic diuresis
  • damaged kidneys prevent urine concentration
  • incr. [Ca] or other molecules that prevent appropriate response to concentrating urine (ie Ca and ADH)
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9
Q

Polydipsia can be normal w/

A
  • water loss from disease ( diarrhea)

- dogs that are swimming often get transient polydipsia –> polyuria

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10
Q

Loss of medullary concentrating gradient w/

A

IV fluid administration, after treating underlying condition that has caused pu/pd

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11
Q

Kidney Functions

A
  • Excretory: nitrogenous wastes, H2O, K+, Na+, phosph, medications
  • Endocrine: EPO, Vit. D (calcitriol)
  • Regulatory: Fluids, electrolytes, minerals, bp
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12
Q

T/F: whole kidney GFR depends on filtration rate of all functioning glomeruli (proportion of perfused and filtering glomeruli)

A

T

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13
Q

Medullary Interstitium

A
  • semi-solid gel of viscoelestic hyalauron produced by interstitial cells
  • forms matrix between LoH and vasa recta
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14
Q

Pathophys. of CKD

A
  • Permanent damage and loss of nephrons –> once critical mass is lost, hyperperfusion/ filtration of surviving nephrons –> progressive glomerular hypertension –> inflammation –> progressive damage –> CKD
  • inability to ‘hold’ water
  • loss of communication between nephron segments and vasa recta
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15
Q

Chronic Kidney Disease

A
  • any structural of functional abnormality present in the kidney for > 3 months
  • -> 3 months should allow for repair and regen
  • -> irreversible and typically progressive
  • -> CKD exists before azotemia exists
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16
Q

CKD - Diagnosis

A
  • elevations in creatinine w/ inappropriate urine concentration (often isosth.) –> can lose [ ] ability
  • critical evaluation of creatinine (r/o pre-renal azotemia)
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17
Q

T/F: elevation in creat/ BUN requires >75% loss to renal fx

A

T

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18
Q

T/F: Body size has influences Creatinine and GFR reference range.

A

T
high BW means higher Cr
high BW means lower GFR

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19
Q

SDMA

A
  • functional test of the kidneys
  • excreted almost solely by the kidney and not affected by muscle mass (unlike Cr)
  • high [ ] @ 40% nephron loss
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20
Q

CKD - staging

A
  • based on creatinine

- -> substaging based on proteinuria and blood pressure

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21
Q

CKD - Diagnosis

A
  • r/o causes of reversible dz (pyelonephritis, ureteral obstruction, leptosporosis, nephrotoxin)
  • Acute vs Chronic ( Acute has no weight loss and n to large kidneys) (chronic has NNN anemia and n to small, irregular kidneys)
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22
Q

CKD - clinical signs

A
  • PU/PD
  • weight loss (dec. caloric intake)
  • vomiting/ diarrhea
  • malabsorption
  • uremic ulcers (oral, gastric)
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23
Q

CKD - ensuring proper nutrition)

A
  • low protein, low phosphorus, +/- K sup
  • appropriate renal diet may help to improve life
  • monitor weight to ensure adequate amount
  • feeding tube
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24
Q

CKD - Uremic stomatitis

A
  • Causes: oral urease producing bacteria

- Tx: pain management, oral chlorhexidine rinse, maintain oral health

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25
Q

CKD - Uremic Gastropathy

A
  • Causes: elevated gastrin levels ( dec. renal excretion), dystrophic mineralization
  • Tx: H2 antagonists (famotidine), PPI (omeprazole), Sucralfate
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26
Q

CKD - Vomiting

A
  • Causes: uremic toxins affect CRTZ, gastritis, gut edema

- Tx: anti-emetics (ondansetron, cerenia), pain management, prevent fluid overload

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27
Q

CKD - Dehydration

A
  • Causes: PU/PD, p may be inappetent, progressive dehydration, hypovolemia (dec GFR)
  • Tx: rehydration (IV or SQ fluids)
  • -> should only be used to treat dehydration
  • -> every p w/ CKD does not need fluids
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28
Q

CKD - Anemia

A
  • NNN
  • Causes: deficient EPO production, gi hemorrhage, dec rbc lifespan, inc bleeding tendency, iron deficiency (micro, hypochromic)
  • Tx: treat gastritis, ensure adequate iron load, blood transfusion, EPO stimulants
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29
Q

EPO Stimulants

A
  • Darbepoetin - 85% autologous
  • Epoetin - inc risk of side effects
  • antibody response to EPO –> see a pure red cell aplasia (sudden drop in HCT)
  • monitor for polycythemia, hypertension
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30
Q

CKD - Hypertension

A
  • Consequences: progressive renal damage, sustained afterload and L ven. hypertrophy, retinal detachment
  • Tx: amlodipine and ACE-inhibitors (dilates efferent arteriole)(monitor for progressive azotemia)
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31
Q

CKD - Hypokalemia

A
  • Causes: malnutrition***, renal losses, malabsorption
  • Consequences: weakness, anorexia, progressive renal damage
  • Tx: ensure adequate nutrition, potassium sup (K gluconate)
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32
Q

CKD - Metabolic Acidosis

A
  • Causes: retained metabolic acids, dec bicarb production
  • Consequences: disrupts cellular metabolism, increased bone and protein turnover, progressive anorexia or renal dz
  • Tx: goal serum bicarb ~20, sodium bicarb supplementation (make sure not lactic acidotic)
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33
Q

CKD - Hyperphosphatemia

A
  • Causes: inc phosphorus retention, exacerbated by diet
  • Consequences: metastatic mineralization d/t high PTH and Ph not dropping
  • Tx: Diet**, Phosphate Binders (ensure prescribed dose is ingested )
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34
Q

CKD - Aluminum Hydroxide (AlOH)

A
  • Al forms relatively insoluble complexes w/ P and excreted in feces
  • Formulations: powder or dried gel
  • Complications: constipation, toxicity
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35
Q

CKD - Lanthanum Carbonate

A
  • binds and complexes w/ P in food

- increased cost vs others

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36
Q

CKD - Calcium Salts

A
  • in theory, should bind to P and be pooped out
  • however, can be absorbed and make hyperCa worse
  • Epakitin
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37
Q

CKD - Sevelamer

A
  • polymer bound to counter ions

- exchange resin

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38
Q

CKD - Enteric Dialysis

A
  • some uremic acids synthesized by GIT microbes
  • goal is removal of uremic toxins or precursors from the gut
  • Azodyl: no real evidence that it works
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39
Q

CKD - HyperPTH (causes and pathogenesis)

A
  • Causes: decreased GFR, increased Phosphorus retention (exacerbated by diet)
  • CKD causes phosphorus retention –> increased PTH to remove P –> resulting high P and Ca –> metastatic mineralization
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40
Q

CKD - Effects on Calcitriol

A
  • decreased activation of Vit. D

- decreased calcitriol

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41
Q

T/F: Low dose Vit. D has been shown to slow progression of CKD and increase survival time

A

T

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42
Q

CKD - Hyperkalemia

A
  • Cause: dec. renal excretion
  • Tx: therapeutic diet, increased potassium removal, control factors worsening hyperK, sodium bicarb, low dose furosemide
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43
Q

CKD - Nutritional Management Goals

A
  • alleviate clinical signs (proteins)
  • minimize electrolyte, acid-base, fluid abn
  • slow progression of disease
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44
Q

CKD - Nutritional Management - Protein

A
  • low protein is good for CKD, but is required for PLN (25-50% restriction)
  • protein has no effect in progression or tubulointerstitial dz but is used to control the uremia (better QoL)
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45
Q

CKD - Nutritional Management - Phosphorus

A
  • high serum P = shorter lifespan w/ CKD
  • CKD leads to Renal 2* HyperPTH
  • restriction is protective in CKD but moa not understood
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46
Q

CKD - Nutritional Management - Sodium

A
  • recommendations not clear

- might stimulate RAAS

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47
Q

CKD - Nutritional Management - Potassium

A
  • generally supplemented in diets
  • cats w/ CKD have risk of hypoK
  • some dogs risk hyperK
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48
Q

CKD - Nutritional Management - Omega-3 FA

A
  • no data for treatment efficacy in cats
  • dogs fed fish oil had inc renal fx and dec proteinuria
    (safflower oil dec GFR and inc interstitial fibrosis)
  • no data for veggie based PUFA
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49
Q

CKD - Nutritional Management - how much to feed

A
  • energy requirements must be covered
  • treats can be given at <10% calories
  • stimulate appetite to help them
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50
Q

CKD - Nutritional Management - Transition to New Diet

A
  • diet change slowly over 7-14 days (esp. with cats)
  • avoid stress (don’t do it while hospitalized)
  • promote palatability
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51
Q

ARF

A

Acute Renal Failure

  • accumulation of uremic toxins
  • dysregulation of fluids, electrolytes, acid-base
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52
Q

AKI

A
  • represents a spectrum of disease severity ranging from injury that is clinically non-detectable to sever dysfx and ARF
  • ARF is most severe stage of AKI
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53
Q

Staging/ Grading of AKI (and sub-staging)

A
  • AKI is graded while CKD is staged
  • with AKI, you can move from Grade 3–>1 while you cannot do that in CKD
  • Sub-staging based on:
    1. non-oliguric/ oligoanuric
    2. requirement for renal replacement therapy (dialysis)
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54
Q

Common Causes of AKI

A
  1. pyelonephritis (both)
  2. hemodynamic instability (both)
  3. Acute Pancreatitis (both)
  4. Drugs (both)
    Dogs: Grapes/ raisins, lepto, lyme
    Cats: lily, ureteral obstruction, renal lymphoma, fip
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55
Q

AKI - Causes, Consequences and Treatment - Hyperkalemia

A

Causes: dec renal excretion (worsened by iatrogenic)
Consequences: cardiomyopathy, muscle weakness
Tx: Sodium bicarb (only w/ low bicarb), Insulin w/ dextrose, Calcium gluconate (cardioprotective), Furosemide, hemodialysis

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56
Q

AKI - Causes, Consequences and Treatment - Hydration Status

A
  • Fluids are a prescription medication
  • Monitor – repeated physical exams, u-catheter not mandatory
  • must continually re-assess hydration status
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57
Q

AKI - Causes, Consequences and Treatment - Oliguria/ Anuria

A
  • causes: pre-renal, renal (tubular swelling, altered renal blood flow), post-renal (urinary tract obstruction)
  • Tx: ensure adequate hydration, mannitol, furosemide, hemodialysis, Sx intervention
  • Anuria means no fluids allowed
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58
Q

AKI - Causes, Consequences, and Treatment - Metabolic Acidosis

A
  • Causes: inc. production of uremic acids, dec bicarb production, dehydration –> lactic acidosis
  • Consequences: disrupted metabolism, exacerbate hyperkalemia, inc protein and bone turnover
  • Tx: correct hypovolemia, sodium bicarb, hemodialysis
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59
Q

AKI - Consequences, and Treatment - Hypertension

A
  • ensure accurate measurement and results (minimize stress, appropriate cuff size)
  • Consequences: retinal detachment, hypertensive encephalopathy, progressive renal damage
  • Tx: prevent/ treat overhydration, amlodipine
  • Tx (refractory): acepromazine, hydralazine, nitroprusside, ACEi
60
Q

AKI - Causes - Pain Management

A
  • Nephritis
  • ureteral obstruction
  • esophagitis
  • uremic stomatitis
  • gi pain
61
Q

AKI - Causes, Consequences, and Treatment - Resp. Disease

A
  • Causes: fluid overload - pulmonary edema (furosemide), pleural edema (tap it), Asp. pneumonia (abx), Lepto Lung (anti-coag. ampi/doxy)
62
Q

AKI - Causes, Consequences, and Treatment - Anemia

A
  • Causes: gi hemorrhage, dec rbc lifespan, inc. bleeding, iatrogenic sampling, dec. EPO
  • Tx: blood transfusion (if indicated), judicious blood sampling, EPO stimulants (darbopoetin)
63
Q

AKI - Consequences and Treatment - Hyperphosphatemia

A
  • Causes: inc phosphate retention, renal 2* hyperPTH

- Tx: renal diet, phosphate binders (if eating) (AlOH)

64
Q

Adrenal Anatomy

A

Cortex:
- glomerulosa (mineralocorticoids –> Aldosterone)
- fasciculata (glucocorticoids –> Cortisol)
- reticularis (sex hormones)
Medulla:
- catecholamines –> epinephrine

65
Q

Hypoadrenocorticism is also known as

A

Addison’s Disease

66
Q

Addison’s (Classificiation)

A

Primary (path of the adrenal gland):
- 2 flavors (Typical and Atypical)
Secondary (path @ pituitary so no ACTH)

67
Q

Primary Addison’s (Typical)

A
  • decreased gluco and mineralo

- decreased mineralo can lead to an ‘Addisonian cirisis’ (severe shock d/t severe electrolyte abn)

68
Q

Primary Addison’s (Atypical)

A
  • decreased gluco (normal mineralo)
  • usually more chronic w/ history of GI
  • progression from atypical to typical is possible
69
Q

Secondary Addison’s

A
  • pathology @ pituitary and so no ACTH production ( only affects gluco d/t ACTH has no effect on mineralo (Aldosterone))
  • looks very similar to atypical addison’s
  • caused by: exogenous steroid administration, hypopituitarism (less common)
70
Q

Addison’s (Signalment)

A
  • typically young adult (~4yrs) female dog

- duration of clinical signs vary (typical vs atypical)

71
Q

Addison’s (Blood Work Findings)

A
  • Anemia (NNN)
  • Lack of a stress leukogram (no neutrophilia, eosinophilia, lumphocytosis)
  • hyperkalemia, hyponatremia (typical Addison’s)
  • hypoglycemia
  • hypocholesterolemia
  • hypercalcemia
  • hypoalbuminemia
72
Q

Addison’s (Testing)

A
  1. Resting Cortisol (useful to rule out dz)
    - >2.0 rules out
    - <2.0 fails to rule out
  2. ACTH stim test (gold standard)
    - >2.0 no Addison’s
    - <2.0 Addison’s
73
Q

Addison’s (Treatment)

A
  1. Supplement deficient hormones
    - glucocorticoid replacement in all cases (prednisone)
    - mineralocorticoids only needed with typical
  2. Monitoring
    - especially for Cushing’s
    - for ‘addisonian’ crisis if forgotten Aldosterone dosing
74
Q

Addison’s (Prognosis)

A

Excellent (>80% respond to treatment)

75
Q

T/F: it is normal for some protein to pass through the normal glomerulus

A

T; this protein is most often small (hemoglobin, myoglobin, bence-Jones protein) and normally is taken up by renal tubular epithelium before any damage is done

76
Q

3 types of proteinuria

A
  1. pre-renal (excessive amount of normal)
  2. Renal (fx-al or pathologic)
  3. Post-renal (protein enters after urine enters renal pelvis)
77
Q

T/F: the persistence and degree of renal proteinuria correlates with chronic kidney disease (CKD)

A

T

78
Q

Consequences of Proteinuria

A
  1. development and progression of renal tubular disease and azotemia (nephrotoxic albumin, hypertension)
  2. Hypoalbuminemia (edema/ ascites, drug metabolism changes)
  3. alteralion in coagulation
  4. hyperlipidemia
  5. Nephrotic Syndrome
79
Q

USG and Proteinuria

A
  • expect more protein in a concentrated specimen

- UPC ratio not affected by concentration

80
Q

T/F: urine culture should always be run before pursuing a workup for proteinuria

A

T

81
Q

T/F: you can have significant glomerular proteinuria without azotemia

A

T

82
Q

Proteinuria (treatment)

A
  • treat underlying cause
  • low/moderate protein diet
  • treat hypertension (amlodipine)
  • ACEi + Angiotensin 2 rec. blocker (can cause progressive azotemia and hyperkalemia)
  • anti-platelet drug (after biopsy)
83
Q

T/F: the treatment for proteinuria is the same regardless of the cause is immune-mediated or not

A

F, you won’t be giving immunosuppressive therapy in non-immune mediated disease

84
Q

What is the primary goal of renal biopsy in proteinuria

A
  1. to underlying if there is immune-mediated disease

2. to help determine underlying causes (amyloidosis)

85
Q

Can a patient with PLN have a normal serum albumin

A

Yes, the liver will ramp up production (ie compensation)

86
Q

Can a patient with PLN be non-azotemic?

A

Yes, as long as the GFR is normal then they won’t be azotemic

87
Q

How can hypoalbuminemia lead to azotemia and tubular damage?

A

albumin will damage the tubular epithelium –> glomerulo-tubular feedback causes kidney to shunt blood away from nephron –> large scale loss of nephrons –> azotemia

88
Q

List the components of nephrotic syndrome.

A
  1. Hyperlipidemia/ cholesterolemia (overexertion of liver to produce albumin causes it to produce other things)
  2. hypoalbuminemia
  3. ascites/ edema
  4. proteinuria
89
Q

What does nephrotic syndrome indicate

A

the patient has a very bad PLN

90
Q

In a patient with nephrotic syndrome, what factors would you need to consider when making a fluid plan?

A

Can be interstitially over-hydrated but intravascularly hypovolemic

91
Q

In most cases, how to albumin and globulins look different in patients with PLN vs PLE?

A

PLN –> hypoalbuminea with n globulins

PLE –> hypoalbuminea and hypoglobuminemia

92
Q

Functional (transient) proteinuria

A

proteinuria due to some underlying condition: fever, seizures, cushing’s, hypertension

  • will resolve once the underlying condition is solved
93
Q

Diabetes Mellitus (Clinical Signs)

A
  • polyphagia
  • weight loss
  • glucosuria
  • PU/PD
94
Q

Diabetes Mellitus (Canine DM)

A
  • immune-mediated destruction of B cells and absolute insulin deficiency
  • insulin-dependent
95
Q

Diabetes Mellitus (Feline DM)

A
  • insulin resistant DM
  • ~75% from B-cell loss and dysfunction combined w/ insulin resistance
  • ~25% from hypersomatotropism (inc GH –> severe insulin resistance –> DM) (inc IGF-1)
96
Q

Diabetes Mellitus (Diagnostics)

A

PE - unremarkable (maybe cataracts)
CBC - +/- hemoconcentration (if dehydrated)
Chem - hyperglc, hypercholesterolemia, high liver enzymes, hyponatremia
UA - glucosuria, ketonuria, bactinuria

97
Q

Diabetes Mellitus (Confirming the Diagnosis)

A
  • fasting hyperglycemia and glucosuria
  • fructosamine (avg. 2-3 week period)
  • HbA1c (monitor for rbc lifespan)
98
Q

Diabetes Mellitus (treatment)

A
  • insulin
  • diet
  • exercise
  • +/- oral hypoglycemics (not very reliable)
99
Q

Diabetes Mellitus (Insulin Sequence)

A

Dogs - Hogs; ok with humans

Cats - Cows; no match with humans

100
Q

Diabetes Mellitus (Insulin Formulations)

A 
Regular Insulin (SQ, IV, IM)
Intermediate Insulin (SQ) - addition of protamine or zinc and injected as a suspension
Long-acting Insulin (SQ) - change aa sequence or addition of f.a. to promote albumin binding
101
Q

Diabetes Mellitus (Insulin for Dogs)

A
  • Vetsulin (intermediate) (0.25-0.33IU/kg)

- Levemir (Long acting) (0.1IU/kg)

102
Q

Diabetes Mellitus (Insulin for Cats)

A
  • Prozinc (intermediate) (FDA approved)
  • Lantus (long acting)
  • Levemir (long acting)
103
Q

Diabetes Mellitus (Diet)

A
  • goal: stable weight at ideal BCS
  • Dogs are less sensitive than cats to dietary treatment
    • Cats –> high protein, low carb diet
    • Dogs –> high fiber and complex carbs
104
Q

Diabetes Mellitus (Exercise)

A
  • increases sensitivity to insulin

- weight loss improves sensitivity to insulin

105
Q

Diabetes Mellitus (Monitoring - hypoglycemia )

A

Primarily looking for hypoglycemia

  • -> weakness, disorientation, ataxia
  • -> may progress to seizures
  • -> cats often no clinical signs until severe

Use Glc curves, clinical signs , fructosamine, HbA1c, or continuous GLC monitoring

106
Q

Glucose Curves (4 questions)

A
  • does insulin lower bg
  • how low is nadir
  • how long does insulin last
  • how would you adjust therapy
107
Q

What causes variations in bg curves

A
  • changes in injection site
  • injection technique
  • dose inaccuracies
  • insulin absorption
  • stress
  • activity level
108
Q

Diabetic remission

A
  • cats w/ insulin and diet can go into remission
  • usually transient (wks - months) but may be permanent
  • rare in dogs
109
Q

Diabetes Mellitus (cataracts)

A
  • ~75% of dogs w/ diabetes will develop them
110
Q

Diabetes Mellitus (2 Monitoring Options)

A
  1. Don’t measure BG and use CS, fructosamine, HbA1c
    - -> goals to decrease clinical signs, curb weight loss, prevent DKA, avoid hypoglycemia
  2. continuous bg monitoring over several days
    - -> uses: adjust dose of newly diagnosed diabetic, assess for hypoglycemia, DKA patients in hospital
111
Q

What is the function of PTH

A
  • responds to low Ca in the body and:
  • -> inc vit. D (inc Ca and PO4)
  • -> inc renal reabsorption (lose PO4)
  • -> inc release from bone
112
Q

What is PTHrp and what does it do

A
  • homologous w/ N-terminal of PTH (activates PTH receptors)
  • secreted normally from many adult cells (autocrine an dparacrine), from fetal cells (endocrine), and cancer cells (Lymphoma, Anal Gland Adenocarcinoma, Multiple myeloma)
113
Q

Hypercalcemia (Clinical Signs)

A
  • often none

- PU/PD, muscle weakness, dec. appetite

114
Q

Hypercalcemia (ddx and what you might look at aside from Ca)

A 
H - HyperPTH (PO4)
A - Addison's dz (Na, K, Cholesterol, cortisol)
R - renal dz (BUN, Cr, USG)
D - Vitamin D tox (Hx, PO4)
Y - young
I - Idiopathic
S - spurious 
N - Neoplasia (PE, imaging, FNAs)
O - osteolytic (PE, imaging)
G - granulomatous (PE, imaging)
115
Q

Primary hyperPTH

A
  • usually a single adenoma
  • middle-older dogs (avg. 10yrs)
    • CS: none
    • CBC: n
    • Chem: high Ca, low-normal Ph, BUN/Cr wnl
    • UA: USG < 1.020
  • often high iCa w/ n PTH
116
Q

Hypercalcemia in cats (causes)

A
  • idiopathic (most common)
  • renal dz, neoplasia (#2)
  • hyperPTH, Addison’s (#3)
117
Q

Hypercalcemia in cats (idiopathic hypercalcemia)

A
  • young-middle aged cats
  • mild-moderate high Ca (iCA and total)
  • CS: only in 50% and vomiting, weight loss, dec appetite
  • high iCa w/ low PTH
  • Treatment: high fiber diet, corticosteroids, Aldrenote (bisphosphonate)
118
Q

Hypocalcemia (CS)

A
  • muscle tremors, twitching, fasciculations
  • facial rubbing
  • muscle cramping/ stiff gait
  • behaviour changes
  • seizures
  • arrhythmias
119
Q

Hypocalcemia (DDX)

A
  • primary hypoPTH
  • renal failure
  • hypoalbumin
  • pancreattitis
  • eclampsia
  • spurious
  • chelation
  • malabsorption
  • hypomagnesemia
120
Q

Hypocalcemia (Primary Hypoparathyroidism)

A
  • immune-mediaetd destruction (rare)
  • iatrogenic (post-op parathyroid-ectomy)
  • -> Tx: Calcium (IV if emergency), Vit. D (Calcitriol)
121
Q

3 causes of hyperlipidemia

A
  1. Post-prandial hyperlipidemia
  2. Primary hyperlipidemia (genetic)
  3. Secondary Hyperlipidemia (Hypothyroidism, Cushing’s, DM)
122
Q

Hyperlipidemia (CS)

A
  • vomiting, diarrhea, abd pain
  • pancreatitis (common in dogs)
  • cutaneous xanthoma
  • lipema retinalis
  • neuro signs
123
Q

Hyperlipidemia (diagnosis)

A
  • fasted sample
124
Q

Hyperlipidemia (treatment + monitor)

A
  • only really for severe hyperlipidemia ( >1000)
  • often lifelong therapy (dietary restriction)
  • monitor w/in 4wks
125
Q

T/F: in the absence of concurrent disease, diabetes patients can be kept on the same diet

A

T

126
Q

Do cats have a CHO requirement

A

no

127
Q

Do carbs cause obesity in cats

A

no

128
Q

Do carbs cause DM in cats

A

probably not,

chronic consumption –> insulin resistance or beta cell exhaustion and relative insulin deficiency

129
Q

What is the main ER treatment for Addison’s (Addisonian Crissi)

A

IV Fluid Therapy

130
Q

T/F: the classic lab work findings for Addison’s is a low Na/K ratio and a boring leukogram

A

T

Na/K ratio below 28 is required and is often below 23

131
Q

Addisonian Crisis (Hypovolemic Shock Treatment)

A
  • shock dose is 80-90mL/kg
  • we want to give 1/4 of that over 15 minutes so 20mL/kg over 10-15 minutes
  • any isotonic crystalloid will do
132
Q

Addisonian Crisis (Treating Hyperkalemai)

A

IV fluid therapy
Calcium Gluconate
Dextrose +/- Insulin (only give in normoglc animals)

133
Q

Addisonian Crisis (Steroid Replacement)

A
  • dexamethasone (does not interfere with cortisol assay)

- Hydrocortisone after ACTH

134
Q

Hypoglycemia in the ER

A
  • low glucose –> seizures, shock, weakness
135
Q

T/F: high HCT can lead to artifactual hypoglycemia in whole blood measurement

A

T

136
Q

Treating Hypoglycemia (ER)

A
  • IV dextrose (0.25-0.5g/kg) or (0.5-1ml/kg of 50% solution) then change to 2.5-5%
  • oral corn syrup but takes ~30minutes
137
Q

DKA (the basics)

A
  • most common er complication of DM
  • main treatments: Fluids and Insulin
  • heralded by a combination of hyperglycemia and high AG metabolic acidosis
138
Q

DKA (pathophys)

A
  • requires DM and a concurrent pro-inflammatory condition
139
Q

What are the three ketoacids produced during DKA

A
  • B-hydroxybuterate
  • Acetoacetate
  • Acetone
140
Q

DKA Treatment Priorities

A
  1. Fluids (balanced crystalloids such as plasmalyte)

2. Insulin Therapy

141
Q

DKA (advantage of plasmalyte over LRS)

A
  • DKA means your missing K, Mg, and PO4

- plasmalyte has some K and Mg (still need to sup PO4)

142
Q

T/F: Insulin given early offers a huge treatment advantage vs when it’s given late

A

T

Insulin serves to stop keto-genesis

143
Q

Should sodium bicarb be used to treat DKA?

A
  • only rarely if the acidemia is really bad
144
Q

ER Hypocalcemia (4 Causes)

A
  1. Eclampsia
  2. CKD
  3. Pancreatitis
  4. Iatrogenic
145
Q

ER Hypocalcemia (clinical signs)

A
  • none if mild
  • moderate - facial rubbing, muscle tremors, tetany
  • severe - seizures
146
Q

ER Hypocalcemia (treatment)

A
  • IV calcium (Ca Gluconate or Chloride)

- monitor ECG

VET 433c (6 decks)

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