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Medicine I > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

Obj: know and understand the clinical features of diabetes mellitus in dogs and cats

A
  • Dogs:
    • PU/PD, polyphagic, weight loss, blindness from cataracts
  • Cats:
    • PU/PD, polyphagic/inappetance, weight loss
    • depressed/lethargic
    • rear limb weakness and platigrade stance
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2
Q

Obj: know and understand the clinical use of insulin in diabetic dogs and cats

A
  • Controls glucose fluctuations
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3
Q

Obj: understand the rationale and routine protocols for monitoring the efficacy of therapy in diabetic dogs and cats

A
  • establish control
  • evaluate patient’s and client’s progress
  • Protocols:
    • Clinical signs - resolve symptoms = control
    • Urine glucose (dogs) - measure several times a day
      • helps understand response to insulin
    • Serum fructosamine - establish if hyperglycemia has been present for 3-4 days vs random event
    • Blood glucose curve - see effectiveness, onset of action, time to peak effect, peak effect, and duration of action
      • snapshot in time (can be severely affected by routine changes)
    • Monitoring Glucodynamics - simpler, can be done at home
      • snapshot in time (can be severely affected by routine changes)
    • Continuous Glucose Monitoring - collects large amount of data over a 2 week period get good idea of patient’s average response
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4
Q

Obj: Know and understand diabetic ketoacidosis as it occurs in diabetic dogs and cats especially emergency management

A
  • Acidosis is caused by the accumulation of ketone compounds - acetone, acetoacetic acid, beta hydroxybutyric acid
    • Ketonuria - diabetic ketosis
    • Acidemia w/hyperglycemia and hyperketonemia = ketoacidosis
  • Regular insulin to manage
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5
Q

What is Diabetes Mellius?

A
  • A disorder of the endocrine pancreas
  • Characterized by severly impaired carbohydrate and lipid metabolism
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6
Q

What are the types of diabetes mellitus?

A
  • Type 1 - Insulinopenia
    • reduced or absent insulin production
  • Type 2 - Insulin resistance
    • reduced or absent insulin action
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7
Q

What type of diabetes affects dogs?

A
  • Insulinopenia (Type 1) is main feature
  • Histology shows islet damage w/ loss of functional mass
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8
Q

What are the potential factors in canine DM athophysiology?

A
  • Genetic susceptibility is present for some breeds
  • Autoimmunity
  • Pancreatitis (40% of dogs w/ DM also have pancreatitis)
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9
Q

What is Feline DM?

A
  • Insulin resistance (Early)
  • Insulinopenia (Later)
  • Histology shows islet amyloid deposition / loss of beta cells
    • same in human type 2 DM
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10
Q

What are the potential factors in feline DM pathophysiology?

A
  • Genetic component suspected in some breeds
  • Others:
    • Pancreatitis
    • endocrinopathy (acromegaly)
    • Diabetogenic medications (glucocorticoids)
    • Diestrus / pregnancy
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11
Q

What is the classical triad of clinical signs associated with DM?

A

Polydipsia, Polyuria, Polyphagia

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12
Q

What are the other signs of DM? (outside Triad)

A
  • Weight loss
  • Cataracts (dogs)
  • Neuropathy (cats)
  • Asymptomatic hyperglycemia
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13
Q

Where does the glucose in DM come from for cats and dogs?

A
  • (Usually) not dietary
  • From the liver - increased hepatic glucose production
    • glycogen, gluconeogenesis, etc
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14
Q

What defines DM?

A

persistent fasting hyperglycemia - (not clinical signs)

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15
Q

What are the challenges of diagnosing DM in the lab?

A
  • Glucose in early or mild DM overlaps with normal range
  • Stress hyperglycemia occurs in dogs and cats
    • glucosuria - rarely present but possible
    • ketonuria - never
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16
Q

What CBC findings are common with DM?

A

variable, no consistent abnormalities

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17
Q

What results are common on a biochemistry panel for DM?

A
  • Hyperglycemia - should be repeatable finding
  • Hyperketonemia
  • Elevated liver enzymes (ALP and ALT)
  • Increased serum triglycerides
  • Increased cholesterol
  • Electrolyte abnormalities (Na, Cl, K, Mg)
    • usually decreased w/ uncomplicated DM
    • Variable in complicated DM
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18
Q

What findings are common on a urinalysis with DM?

A
  • Glucosuria
  • Ketoneuria
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19
Q

What determines inpatient vs outpatient treatment for DM?

A
  • Stable diabetic - outpatient
    • routine signs, normal appetite, hydrated, unremarkable lab results
  • Sick diabetic - inpatient
    • severe clinical signs, appetite loss, dehydration, electrolyte disturbances
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20
Q

What are the treatment goals for DM?

A
  • Eliminate clinical signs
  • Address concurrent disorders and contributing factors
  • Control hyperglycemia
  • Aoid hypoglycemia
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21
Q

What are the different routes of controlling hyperglycemia?

A
  • Insulin - treatment of choice
  • Diet - not a sole therapy
  • Weight loss / exercise - not a sole therapy
  • Oral hypoglycemic drugs - usually ineffective
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22
Q

What are the different formulations of Insulin used in Vet Med?

A
  • U 40 Insulin
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23
Q

What is the difference between U-100 and U-40 insulins

A
  • U = unit
    • indicates the insulin concentration in units/ml
  • U-100 (100 U/ml)
    • most human insulins - HumulinN (NPH), HumulinR (regular) Lantus, many others
  • U-40 insulins (40 U/ml)
    • only vet products (ProZinc (PZII), Vetsulin (lente
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24
Q

Why is it important to match the syringe type and the insulin type?

A
  • Insulin syringes come in 2 sizes U-100 and U-40
  • IF:
    • syringes match (U-100i +U100u, etc) then dose = 100 units
    • syringe mismatch:
      • U-100i + U40s = OVERDOSE 25 (units)
      • U-40i + U100s = UNDERDOSE (4 units)
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25
Q

What is the important key of dietary management in DM?

A
  • Consistency:
    • diet type and composition - feeding times, amount fed should e consistent
    • Optimal body weight should be goal
    • Diet should not be the sole therapy
26
Q

What should the diet for a canine DM patient be?

A
  • Complete / balanced diet will work for most dogs
  • Dietary fiber - insoluble / soluble fiber may improve glycemic control
  • High fiber commercial diets / supplemental=ed with fibber
  • FFIber sources - canned pumpkin, cooked green bens, commercial supplements
27
Q

What should the diet of feline DM patient be?

A
  • High protein (>40% ME) and low carbohydrate content
  • Canned food preferred - potion control, lower Caloric density, increased water intake
28
Q

What does the Treatment/Monitoring Timeline for animals with DM look like?

A
  • El
29
Q

What are Indirect monitoring methods for animals with DM?

A
  • Subjective:
    • Clinical signs
    • Physical examination
  • Objective
    • Blood hemoglobin A1c
    • Serum fructosamine
    • Urine glucose measurement
30
Q

What are the direct monitoring methods for animals with DM?

A
  • Glucose Curve
  • Continuous Glucose monitoring
  • Spot glucose determination
31
Q

How can clinical signs be utilized as a monitoring technique for patients with DM?

A
  • If clinical signs are not resolved early on the insulin dose is too low
  • If patient is on 1x day and experiences signs (PU/PD) during the evening, dose needs to be changed to 2x day
  • If patient is on a high dose of insulin, and has episodes of hypoglycemia, but still is PU/PD, a lower dose is recommended
32
Q

How can Urine glucose monitoring be utilized as a monitoring technique for patients with DM?

A
  • Dogs Only
  • check urine glucose several times a day
  • If values are high - possible hyperglycemic and needs a dose escalation
  • if values are low/negative - possibly adequate control
    • Monitoring can be diminished to several times a week for the pets life
33
Q

How can serum fructosamine be utilized as a monitoring technique for patients with DM?

A
  • Normal range 195 - 400 mg/dl
    • increases w/ hyperglycemia for longer than 3-4 days
    • cats with stress hyperglycemia will have normal serum fructosamine - unless hyperglycemic for >3-4 days
  • DM - 500+ mg/dl - if clinical signs have been present for >3-4 days
34
Q

What is Serum fructosamine?

A
  • a complex of glucose and albumin (or other serum proteins)
  • Form by a non-enzymatic, insulin-independent, amadori reaction in the presence of prolonged hyperglycemia
  • Reflects the mean blood glucose level for the preceeding 1-3 weeks
35
Q

What is Glycalated Hemoglobin?

A
  • a complex of glucose and hemoglobin
  • formed by a non-enzymatic, insulin-independent reaction
  • longer half-life = reflects glycemic control over the previous 5-9 weeks
36
Q

How can Blood glucose curve be utilized as a monitoring technique for patients with DM?

A
  • Gold standard
  • 12 hr curve is adequate for most patients (24hr may be performed)
    • after breakfast & insulin blood glucose is drawn at time of arrival and every 2 hrs after that.
  • Can see insulin effectiveness, onset of action, time to peak effect, peak effect, and duration of action
37
Q

What are some problems of blood glucose curve?

A
  • Cats that are easily stressed in the hospital usually do not have a curve that reflects at home response
  • Some animals may fail to eat in the hospital
  • activity level in the hospital is altered from home
  • there is an expected normal daily variation in any animal’s glucose curve
38
Q

How can monitoring glucodynamics be utilized as a monitoring technique for patients with DM?

A
  • Glucose Curve - BG sampled intermittently
  • Continuous Glucose monitoring
39
Q

How can Continuous glucose monitoring (CGM) be utilized as a monitoring technique for patients with DM?

A
  • Frequent measurement of glucose over an extended time
  • becoming more popular as flash glucose monitoring technology is available
40
Q

What are blood glycated proteins

A
  • Proteins that change in the presence of hyperglycemia
41
Q

Guidelines for Glycated protein test interpretation

A
  • Therapeutic targets are not clearly defined
  • Trends over tie provide the most useful information
  • Tests can distinguish non-diabetic state from diabetic state
  • Unaffected by transient hyperglycemia (stress hyperglycemia)
  • Relatively insensitive to hypoglycemia, especially if episodic
    • Affected by concurrent disorders (hypoalbuminemia, anemia)
42
Q

What is “spot glucose” monitoring

A
  • Blood glucose
  • Urine Glucose
  • Should NOT be used to:
    • infer glycemic status (except hypoglycemic)
    • Adjust insuline dose
43
Q

What is the benefit of blood glucose spot monitoring?

A

useful to detect or confirm hypoglycemia

44
Q

What is the benefit of urine glucose spot monitoring?

A
  • represents accumulation over time
  • May detect large changes in glucosuria or onset of ketonuria
45
Q

What conditions can complicate DM?

A
  • Diabetic Ketosis (DK) / ketoacidosis (DKA)
  • Hyperosmolar Hyperglycemic State (HHS)
46
Q

What is Hyperosmolar hyperglycemic State?

A
  • Results from relative lack of insulin
  • Hyperglycemia induces osmotic diuresis
  • Lack of fluid (water) intake
  • Hyperglycemia and hypernatremia cause Hyperosmolarity (may be severe)
47
Q

What is Diabetic ketoacidosis?

A
  • Results from insulin deficiency
  • Ketones produced by impaired FA metabolism
  • Ketones are metabolic acids
  • Requires insulin for resoution
48
Q

How can complicated diabetes be recognized?

A
  • Insonsistent presentation
  • May not have DM history
  • Non-specific signs
    • PU/PD
    • Lethargy and weakness
    • Inappetence
    • Vomiting (diarrhea)
    • Neurological abnormalities
      • more pronounced in HHS
    • Emaciation
    • Recent illness/drug therapy
    • Acetone Odor (DKA - from ketones)
49
Q

What laboratory findings are common with complicated DM?

A
  • Hyperglycemia / glucosuria
  • Azotemia - pre-renal (common) or renal
  • Electrolyte abnormalities
    • DKA - hyponatremia, hypochloremia, hypokalemia are common
    • HHS - hypernatremia, hyperchloremia
      • hypernatremia especially when glucose >600 mg/dl
    • Hypophosphatemia, hypomagnesemia (common after insulin therapy)
  • Metabolic acidosis (more pronounced with DKA)
    • elevated AG
    • Hypobicarbonemia
    • Hyperketonemia / ketonuria
  • Effective osmolality > 330 mOsm/L
    • depends on electrolytes and glucose but does not include urea
50
Q

What physical exam findings are common with complicated DM

A
  • Dehydration - mild (5%) to severe (15%)
  • Hypo- or hyperthermia
  • Signs of hypovolemia and shock
    • Tachycardia
    • Poor pulse strength
    • Poor perfusion
  • Neurological abnormalities
    • more pronounced in HHS
  • Evidence of diabetes
  • Signs of concurrent disorders
51
Q

What is the overall treatment for complicated DM?

A
  • Fluid replacement
  • Restore Euglycemia
  • Correct Metabolic Imbalances
  • Systemic support
    • Address any concurrent disorders
    • Monitor
52
Q

Describe the fluid replacement treatment for complicated DM

A
  • Volume Replacement - Replace deficit over 6-12 hours
    • Replace deficit due to volume loss/dehydration
    • Replace ongoing losses
  • Isotonic fluid - 0.9% NaCl or Lactated Ringers Solution (LRS)
    • Hypovolemic shock
      • Need to restore BP
      • May need shock fluid dose
    • Moderate to severe dehydration
      • replace deficit
      • Meet maintenance + losses
53
Q

How is Fluid Replacement for Hyperosmotic Hyperglycaemic State (HHS) approached?

A
  • HHS - monitor the sodium level
    • Hypernatremia usually associated with hyperosmolality
    • Judicious use of fluids so that sodium is lowered slowly
    • Monitor neurologic status
54
Q

Describe how to restore euglycemia in complicated DM?

A
  • Diuresis promotes renal glucose loss
  • Insulin promotes glucose uptake
    • Always use short-acting insulin preparation
      • target Glucose is <250 mg/dl
    • Use CRI or intermittent therapy
      • CRI for regular and ultrafast insulin types
      • intermittent therapy using regular insulin is suitable
55
Q

What are the goals of insulin therapy?

A
  • Control hyperglycemia
  • Stop ketogenesis
56
Q

How are metabolic imbalances corrected in complicated DM?

A
  • Metabolic imbalances:
    • Electrolyte correction
    • Acid / Base correction
  • Na- and Cl- - replaced with NaCl-containing fluids
  • K+ - add KCl supplement to crystalloid
  • Other Electrolytes
    • Phosphorous - important after insulin therapy begins
      • signs when phos. < 1.0 mg/dL ⇢ weakness, hemolysis
      • supplementation needed when Phos. < 2 mg/dL
    • Magnesium -
      • signs: cardiac, neuromuscular, and electrolyte disturbances
      • Supplement when total Mg2+ falls below 1.0 mg/dL
    • Bicarbonate - treatment of acidosis (not usually needed)
      • Use if severe acidemia (pH < 7.1) persists after volume
  • Glucose supplementation:
    • rationale - support blood glucose during insulin therapy
    • Not usually needed
    • If used: 2.5 - 5% glucose CRI to maintain BG
    • Continue CRI insulin until ketones resolve
57
Q

How are metabolic imbalances corrected in Diabetic Ketoacidosis?

A

Isotonic fluid (Lactated Ringers Solution or 0.9% NaCl) is used to replace volume deficit and Na+ and CL-

58
Q

How are Metabolic imbalances corrected in a Hyperosmolar Hyperglycaemic State (HHS)?

A
  • Isotonic fluid is used to replace volume deficit
  • If hypernatremia persists following initial volume replacement, hypotonic fluid (0.45% NaCl or 5% Dextrose (D5W) is used to replace free water
59
Q

What systemic support can be needed for complicated DM cases?

A
  • Systemic Support
    • Body temperature (warming)
    • Oxygen support
    • Nutritional support
60
Q

What concurrent disorders may need to be addressed in complicated cases of DM?

A
  • Pancreatitis
  • Bacterial infection (UTI, pneumonia)
  • Other endocrinopathy
61
Q

What should be monitored in complicated cases of DM?

A
  • Clinical parameters: body weight, urine output, blood pressure
  • Serum glucose concentration
  • Urine Ketone level
  • Electrolytes
    • Na and K are frequently monitored, monitoring of Phos and Mg
    • Monitoring is essential when electrolytes are being supplemented

Medicine I (43 decks)

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