Digestion & Metabolism 2: Diabetic Ketoacidosis Flashcards

1
Q

DIABETIC KETOACIDOSIS (DKA)….

is a ____ form of diabetes mellitus

causes EXCESS ___-___ that result in ____ and SEVERE ____ ___ that can even be ____-___

A

COMPLICATED form

causes EXCESS KETO-ACIDS that result in ACIDOSIS and SEVERE ELECTROLYTE ABNORMALITIES that can even be LIFE-THREATENING

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2
Q

DKA tends to develop in ____ animals that are VERY ___

why? (give 5 steps)

A

DIABETIC, SICK

why?
1. CONCURRENT ILLNESS to DIABETES

  1. causes STRESS
  2. release of GCC (counter-regulatory hormone)
  3. causes INSULIN RESISTANCE (persistent hyperglycemia)
  4. without INSULIN, causes KETO-ACID PRODUCTION (no glucose in cells)
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3
Q

5 common CONCURRENT diseases that can cause DKA?

A
  1. HEPATIC LIPIDOSIS
  2. CHRONIC RENAL FAILURE
  3. ACUTE PANCREATITIS
  4. BACTERIAL or VIRAL infections
  5. NEOPLASIA
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4
Q

treatment with ___ may help INCREASE/DECREASE risk of DKA

A

INSULIN, DECREASE risk of DKA

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5
Q

what ketone is detected on URINE DIPSTICK?

what ketone is detected on KETONE METER?

A

URINE DIPSTICK = ACETOACETONE

KETONE METER = D-BETA-HYDROXYBUTYRATE

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6
Q

KETONE BODY SYNTHESIS starts from WHAT molecule?

how is this molecule initially made?

what hormones should be HIGH vs. LOW in regards to BLOOD GLUCOSE?

A

KETONE BODY SYNTHESIS starts from ACETYL-CoA

initially made from FAT BREAKDOWN because NOT ENOUGH GLUCOSE

hormones..
INSULIN = LOW
COUNTER-REGULATORY HORMONES = HIGH

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7
Q

in DIABETES MELLITUS, there is ____ SYNTHESIS of ____-____ due to DECREASED ____ and INCREASED ____ resulting in EXCESS ____ ____ ____

A

EXCESS, ACETYL-CoA, INSULIN GLUCOAGON, FATTY ACID OXIDATION

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8
Q

4 CONTRIBUTING FACTORS to METABOLIC ACIDOSIS?

A
  1. formation of KETO-ACIDS
  2. VOMITING
  3. DEHYDRATION
  4. RENAL HYPOPERFUSION
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9
Q

DKA can include clinical signs that include CHRONIC ____ ___, such as (2)…

DKA predisposed in WHAT cat breed?

A

DIABETES MELLITUS…
1. PU/PD
2. POLYPHAGIA

DKA predisposed in SIAMESE

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10
Q

if we see DKA and ABDOMINAL PAIN, can indicate WHAT SECONDARY CAUSE?

A

PANCREATITIS

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11
Q

TRUE/FALSE

we can see NEUROLOGIC ABNORMALITIES with DKA, such as DULL MENTATION, RECUMBENT & PLANTIGRADE STANCE

A

TRUE

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12
Q

what 3 CBC ABNORMALITIES can we find in DKA?

what is NORMAL in A CERTAIN SPECIES?

A

CBC ABNORMALITIES…
1. ANEMIA –> 50% of dos
2. LEFT SHIFT NEUTROPHILIA
3. THROMBOCYTOSIS in DOGS

CATS can have NORMAL PLATELETS

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13
Q

on CHEMISTRY, DOGS tend to have HIGH ____ IN DKA, while in CATS…

what 2 other values are usually also elevated in DOGS?

what 1 other value is usually elevated in CATS?

A

DOGS TEND TO HAVE HIGH ALP IN DKA, but cats have NORMAL ALP because NO STRESS-INDUCED ALP ISOENZYME

can also have HIGH ALT/AST

cats = AST

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14
Q

3 UA findings in DKA?

A
  1. GLUCOSURIA
  2. KETONURIA –> EMERGENCY
  3. PROTEINURIA possible
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15
Q

4 changes in ELECTROLYTES in DKA?

A
  1. LOW K
  2. LOW Mg
  3. LOW P
  4. LOW Na
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16
Q

why does HYPOKALEMIA occur in DKA?

4 common clinical signs?

what MEDICAL INTERVENTION can WORSEN HYPOKALEMIA?

A

because if ACIDOTIC, can EXCHANGE CELLS TAKING IN H+ for EXCRETING K+ IN URINE

4 common clinical signs?
1. MUSCLE WEAKNESS
2. PARALYSIS
3. RESPIRATORY DEPRESSION
4. CARDIAC ELECTRIC CONDUCTION ABNORMALITIES

can make hypokalemia worse by GIVING FLUIDS

17
Q

3 CAUSES for HYPONATREMIA?

A
  1. activation of Na/H EXCHANGER to CORRECT ACIDIC pH (H+ in, Na excreted out)
  2. OSMOTIC DIURESIS
  3. HYPERLIPIDEMIA
18
Q

2 SIGNIFICANT CLINICAL SIGNS from HYPONATREMIA…

A
  1. CEREBRAL SWELLING
  2. ALTERED MENTAL STATUS
19
Q

2 CAUSES for HYPOMAGNESEMIA? (low Mg)

A
  1. INSUFFICIENT DIETARY INTAKE of Mg
  2. INCREASED RENAL EXCRETION of Mg
20
Q

TREATMENT of DKA…

what is MOST IMPORTANT treatment we can do?

SECOND MOST important treatment?

THIRD MOST important? how must this be done? (2)

A

MOST IMPORTANT = DO IV FLUIDS!

SECOND-MOST important = CORRECT ELECTROLYTE ABNORMALITIES

THIRD MOST important = CORRECTION OF HYPERGLYCEMIA
1. must be done SLOWLY to AVOID EXTREME OSMOTIC SHIFTS
2. give GLUCOSE every 4-6 HOURS

21
Q

ELECTROLYTE ABNORMALITIES in DKA tend to develop WHEN?

A

within FIRST 48 HOURS of TREATMENT

22
Q

once we start administering IV FLUIDS to DKA patient, how will GLUCOSE levels change?

A

will start to LOWER BLOOD GLUCOSE CONCENTRATIONS