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Small Animal Medicine Exam 3 (Spring 2016) > L29: KADM (Cooke) > Flashcards

L29: KADM (Cooke) Flashcards

1
Q

Effect of insulin on ketogenesis

A
  • inhibits release of FFAs by lipolysis and therefore formation of ketones
  • uncontrolled lipolysis occurs in the absence of insulin
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2
Q

Diabetogenic hormones

A

(enhance lipolysis and production of FFAs and ketones) Stress results in:

  • catecholamines
  • cortisol
  • growth hormone
  • dopamine
  • thyroxine
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3
Q

Effect of anorexia and dehydration on lipolysis

A
  • anorexia causes body to enhance lipolysis for energy production
  • dehydration decreases GFR, which takes away mech. For clearing ketones
  • osmotic diuresis results from glucosuria and ketonuria
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4
Q

Ketogenesis is controlled by 2 main things

A

1) availability of FFA

2) efficiency of the TCA cycle

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5
Q

Presenting complaint

A

Lethargy, vomiting, severe weakness, PU/PD, wt. loss, normal to increased appetite

If a known diabetic, did initial CS resume?

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6
Q

PE findings

A 
Hypothermia
Tachycardia, weak pulses
Tacky mm
Tachypneic
Prolonged CRT, skin tent
\+/- acetone breath
\+/- cranial abdominal pain (if pancreatitis)
\+/- bladder pain (if UTI)

Muscle wasting
Depressed/obtunded if severe

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7
Q

Diagnosis of DM is based on:**

A

Presence of CS (PU/PD, polyphagia, wt. loss), as well as persistent fasting hyperglycemia and glucosuria

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8
Q

Dx of diabetic ketoacidosis is confirmed by:**

A

Concurrent finding of ketonuria and metabolic acidosis

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9
Q

Steps of diagnostic evaluation:

A

1) PCV/TP (assess hydration)

2) blood glucose (if >500, suggests significant dehydration leading to decreased GFR)
3) Azostix/BUN (assess azotemia)
4) USG (will be concentrated if very dehydrated)
5) Urine dipstick (glucose, ketones, etc.)
6) Electrolytes
7) acid/base status
8) calculated osmolality

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10
Q

Typical electrolyte abnormalities with KADM

A

Hyponatremia (2ary to diuresis, v/d) OR
Hypernatremia (2ary to hyperosmolar hyperglycemic syndrome)

K: low, normal, or high even if body is depleted
Hypophosphatemia

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11
Q

2 biggest components of osmolality

A

Na and K

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12
Q

Purpose of calculating osmolality

A

Can give you clue about whether the patient is hyperglycemic hyperosmolalic (which requires modification of fluid plan)

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13
Q

Next steps after initial diagnostic eval in KADM patient

A

Place IV catheter/central line
Collect for full CBC/Chem
Urine culture
Replacement fluids +/- K (but avoid hypokalemia and fluid overload!)

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14
Q

One of the most common causes for a diabetic patient to become dysregulated

A

UTI

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15
Q

Hypophosphatemia –>

A

Problems with hemolysis

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16
Q

Good insulin to start DKA cat that’s not eating on

A 
Regular insulin (rapid onset, short acting)
-goal is NOT to regulate the diabetes, it's to stop making ketones!
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17
Q

Why are KADM patients often azotemic?

A

Usually pre-renal (dehydration) but can also be renal.

-elevations in serum ketones can artifactually increase creatinine!

18
Q

Why perform a USG in KADM patient?

A

Determine if azotemia has a renal component

19
Q

Progression of hypokalemia in KADM patient

A
  • may appear normokalemic at first because most of K is intracellular, and as K is lost intracellular moves into extracellular space to replace it.
  • K is also lost with metabolic acidosis and lack of insulin also cause K to shift into the extracellular (IV) space
  • after treatment with insulin, K returns to the intracellular space and hypokalemia becomes apparent
20
Q

Fluid therapy guidelines

A
  • do BEFORE giving insulin
  • restoring GFR allows for reduction of ketones AND blood sugar
  • K and P usually don’t have to added (monitor closely)
  • rarely have to add bicarb
21
Q

Monitoring during tx guidelines

A
  • check glucose q1-2 hrs

- use dextrose supplemented fluids once BG

22
Q

Most common complication assoc. with treating DKA?

A

Hypoglycemia

23
Q

Possible predisposing causes of KADM

A 
Pancreatitis
UTI
Pyometra
Prostatitis
Urolithiasis
Etc.
24
Q

Complications of tx for KADM

A
  • hypoglycemia (most common)
  • hypokalemia
  • hypophosphatemia
  • CNS signs (cerebral edema)
25
Q

See vomiting flow chart

A

:)

26
Q

Getting them out of the hospital

A
  • wean off fluids and switch to non-dextrose containing fluid once eating
  • switch to longer acting insulin, but start with conservative dose unless previously well regulated on a certain dose
27
Q

Hyperosmolar NON-ketotic DM

A
  • an uncommon complication of DM
  • similar to DKA except NO ketonuria
  • often have underlying renal or cardiac dz
  • glucosuria –> osmotic diuresis –> water loss
  • underlying dz –> dec. fluid intake –> dehydration –> dec. GFR –> dec. renal glucose excretion
28
Q

Hyperosmolar nonketotic DM is characterized by (4):

A
  • severe hyperglycemia
  • hyperosmolarity
  • severe dehydration
  • absence of ketosis
29
Q

Why is there no ketonuria in Hyperosmolar nonketotic DM?

A
  • patient may still be producing small amount of insulin

- may be producing b-hydroxybutyrate ketones, but these aren’t detected in dip stick

30
Q

CS of Hyperosmolar nonketotic DM

A
  • historical PU/PD, wt. loss
  • profound dehydration
  • lethargic/obtunded
  • hypothermia
  • prolonged CRT
31
Q

Lab findings in Hyperosmolar nonketotic DM

A

-hyperglycemia
-hyper (more common) or hyponatremia
-hypokalemia (may not see on BW)
-hyperosmolality
+/- metabolic acidosis (usually lactic acidosis)
-azotemia

32
Q

Fluid therapy in Hyperosmolar nonketotic DM1

A
  • GO SLOW
  • use isotonic crystalloid (0.9% saline best because has Na to correct hypernatremia imbalance in the blood)
  • replace 50% + maintenance over 12 hrs
  • reassess urine output, CRT, HR, mentation
  • monitor and supplement electrolytes PRN
  • shouldn’t decrease Na more than 0.5 mEq/L/hr
33
Q

Maximum decrease of BG during tx of hyperosmolality

A

50 mg/dL/hr

34
Q

Dogs –> NPH

Cats –> glargine, PZI

A

:)

35
Q

Ideal peak glucose

A

200-300 mg/dL

36
Q

Ideal nadir glucose:

A

100-150

37
Q

Fructosamine won’t help detect Somogyi effect

A

T

38
Q

Level of fructosamine if glucose well controlled?

A

350-450

39
Q

How much fluids to give to DKA patient**

A

Deficit + maintenance + ongoing losses:

-give 1/4 to 1/2 of this over first 4-6 hours, then the remainder over the next 18-20 hours

40
Q

KETOGENESIS

A

1) Fat undergoes lipolysis to FFA, which is taken up by liver
2) FFA either forms triglycerides, enters TCA cycle as acetyl CoA, or manufactures ketones
3) if ketones in abundance, body tries to get rid of them in urine (as acetoacetate and beta-hydroxybutyrate), lungs (as acetone), or brain/muscle

Small Animal Medicine Exam 3 (Spring 2016) (9 decks)

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