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Medicine 1 VCS860 > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

Insulin

A

Polypeptide containing 2 peptide chains that are linked by disulfide bridges

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2
Q

Glucagon-like Peptide

A

derived from proglucagon in the L-cells of the intestinal mucosa, which is cleaved to produce GLP-1 and GLP-2, not glucagon.

GLP-1 strongly augments glucose-stimulated insulin release, decreases glucagon secretion, and inhibits gastric motility and acid secretion

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3
Q

Glucagon

A

Produced by alpha cells of the isltes and released by vagal stimulation.

Glucagon directly stimulates insulin release.

Raise blood glucose levels by activation of hepatic gluconeogenesis and accelerated glycogenolysis.

Inhibited by insulin and somatostatin

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4
Q

Somatostatin

A

inhibitory peptide.

Released from delta cells, inhibits glucagon and insulin release.

inhibits voltage dependent calcium channels.

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5
Q

Miscellaneous Peptide

A

Gastric Inhibitory Peptide (GIP), vasoactive intestinal peptide,

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6
Q

Physiologic Action of Insulin

A

Facilitates the entry of glucose into cells by increasing the number of glucose transporters in the cell membrane. The only cells that do not need insulin for glucose uptake are liver, red blood cells, and brain.

Increases uptake of amino acids and potassium inot insulin-sensitive cells

Stimulates protein synthesis

Inhibits protein degradation

Activates glycogen synthetase and glycolytic enzymes

Inhibits phophorylase and gluconeogenic enzymes

Incrases mRNAs for lipogenic enzymes, which promotes lipogenesis

Inhibits Hormone-sensitive lipase, which inhibits lypolysis

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7
Q

Canine Diabetes

A

Type 1 Human Diabetes mellitus (Insulin dependent diabetes mellitus)

Insulin Deficient

NO change in serum insulin level after glucagon or glucose challenge test.

Dogs require insulin to control hyperglycemia form the time of DM diagnosis

Prone to develop Ketosis as a result of isulin deficiency and a proportion of cases present in a state of diabetic Ketoacidosis

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8
Q

Feline Diabetes

A

Type 2 Human DM

Insulin resistance and a relative insulin deficiency are pathological characteristics of human Type 2 DM.

Plasma insulin level may actually be increased, but not enought o control hyperglycemia

Obese cats have insulin Resistance, abnormal insulin secretory response to glucose challenges, and increased islet amylin depostition but the natural progession form obese non-diabetic to diabetic is not well documented.

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9
Q

Transient Diabetes Mellitus or “DM remission”

A

20% of cats diagnosed with diabetes mellitus

Term misnomer since it is actually the insulin requirement that resolves in these cats, while the underlying pathology that led to the development of clinically diabetic may persist.

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10
Q

Miscellaneous causes of diabetes in dogs and cats

A

can result form pathologies that are uncommon and distinct form the etiologies of typical diabetes as discussed above

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11
Q

Juvenile Diabetes

A

Uncommon but occasionally encountered in puppies and kittens.

Potential causes include any variety of congenital pancreatic anomalies

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12
Q

Secondary Diabetes mellitus

A

Can develop secondary to another pathology

Pancreatitis, pancreatic neoplasia.

Hyperadrenocorticism and acromegaly.

Administration of Glucocorticoids and progestin compounds

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13
Q

Gestational Diabetes

A

Precipitated by physiologic changes that occur during pregnancy has been reported in small numbers of dogs in scandinavia.

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14
Q

Diabetes Mellitius

A

Chronic syndrome of impaired carbohydrate, protein, and fat metabolism due to relative or absolute deficiency of insulin secretion

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15
Q

Ketoacidosis

A

Acidosis caused by the accumulation of ketone compounds

Three important ketones are:

acetone

acetoacetic acid

beta-hydroxybutyric acid

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16
Q

Glucosuria

A

Presence of glucose in the urine

Glucose appears in the urine only after the renal threshold for glucose reabsorption is exceeded.

Renal threshold is 180-220 mg/dL (dog) and 260-280mg/dL (cat)

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17
Q

Criteria needed to make diagnosis of DM

A

Appropriate clinical sings

Persistent hyperglycemia

Glycosuria

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18
Q

Diagnostic Work-up

A

CBC

Serum biochemistry profile

Urinalysis

Urine culture

Serum Fructosamine or hemoglobin A1c test

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19
Q

Treatment Goals

A

eliminate clinical sings

control glucose fluctuation

prevent hypoglycemia

Make therapy convenient

20
Q

Treatment

Components

A

Insulin

Diet optimization

Exercise and weight loss

Optional oral hypoglycemia agents in cats

21
Q

Regular Insulin

A

has no zinc crystals mixed with it and can be administered IV, IM, SQ

Most potent insulin available and has a rapid onset of action and a short duration of action

Short term action = poor sole therapy for management

22
Q

NPH insulin

A

intermediate acting form of insulin and is the insulin of choice for initiating therapy in dogs

Absorption is delayed by the addition of the fish protein protamine and zinc crystals.

ONLY SQ

onset action 0.5-3 hours, peak action 2-10 hours, duration 4-24 hrs.

23
Q

Lente Insulin

A

ultralente and semilente insulin

Semilene is short acting, causes rapid onset.

ultralente is a long acting insulin

ONLY SQ

24
Q

PZI insulin

A

long acting form of insulin

Absorption is slowed by the addition of protamine and zinc

ONLY SQ

PZI is good for long-acting treatment in cats

25
Q

Glargine Insulin

A

Long acting

Synthetic insulin with modifications to its amino acid structure that slows its absorption from the SQ space and prolongs its effects

Slow onset

when used in cats produces an encouraging result

26
Q

Detemir Insulin

A

Long acting

increases insulin binding to lipid membranes.

27
Q

Monitoring therapy effectiveness

Clinical signs

A

are not resolved early in treatment, insulin dose is too low.

28
Q

Monitoring therapy effectiveness

Urine glucose monitoring

A

DOGS ONLY

may be beneficial to have owner check the urine glucose level 2-4 times daily early on in the course.

Don’t allow owner to change insulin dose based on these values.

29
Q

Monitoring Therapy Effectiveness

Serum Fructosamine

A

complex of glucose and albumin, non-enzymatic insulin-independent hyperglycemia

Fructosamine levels should drop with successful therapy.

30
Q

Monitoring Therapy Effectiveness

Blood Glucose Curve

A

GOLD STANDARD for evaluating a paitients response to insulin

Pt is given his normal meal, and insulin dose at home. Shortly there after they are brought to the hospital, blood is drawn at arrival and every 2 hours after. 12 hour curves are best, but 24 hour curves can be performed

31
Q

Monitoring Therapy Effectiveness

Continuous Glucose monitoring (CGM)

A

frequent measurment of glucose over an extended period of time.

Flask glucose monitoring technology.

Sensor attached to the patient, wirelessly transfers data to a separate reader, stored for evaluation after two weeks.

32
Q

Adjustment in insulin dose

A

made based on presence or absence of clinical signs, development of chronic complications, serum fructosamine levels, and blood glucose curve

if nadir > 150mg/dl the dose can be increased

if nadir <80mg/dl the dose should be decreased

33
Q

Important components of diabetic control

A

dietary therapy

exercise

weight loss

34
Q

Complication of insulin therapy

Recurrence of clinical signs

A

poor owner technique, or a problem with the insulin type, dose, frequenct

35
Q

Complications of insulin therapy

Hypoglycemia

A

Severe and potentially life-threatening complication of diabetes treatment

can precipitate hypoglycemia, promote hypophosphotemia, hypokalemia, and hypovolemia

36
Q

Compliacation of Insulin Therapy

Somogyi phenomenon

A

normal physiologic response to impending hypoglycemia.

Should be considered when morning glucose is greater than 400-450, continued PU/PD, polyphagia, and weight loss, and the insulin does is near 2U/kg.

Poorly documented in dogs and cats

37
Q

Complications of Insulin Therapy

Hypophosphotemia

A

develops after treatment has begun, and is caused by rapid insulin-mediated cellular uptake of phosphorous

if severe can cause hemolysis, which can be life threatening

38
Q

Complications of Insulin Therapy

Hypokalemia / hypomagnesemia

A

may be noted at diagnosis or develop during treatment of ketoacidosis.

39
Q

Insulin Resistance

A

Pre-receptor: increased insulin degradation or metabolism at the site of injection or presence of anti-insulin antibodies - NOT TRUE INSULIN RESISTANCE

Receptor: Altered affinity and concentration of receptors or the presence of blocking antibodies

Post-receptor: altered response to binding of insulin to receptor, senn with obesity, hyperadrenocorticism, acromegaly, diestrus, hyperthyroidism

40
Q

Chronic Complication of Diabetes

Persistent Hyperglycemia

A

due to ineffective insulin therapy

Places patient at risk for glucose toxicity and othere chronic diabetie complications.

Fix compliance, type of insulin, dose rate

41
Q

Chronic Complications of Diabetes

Cataracts

A

most common compliaction of diabetes mellitus in dogs.

During hyerglycemia, glucose freely enters the lens, but cannot be converted to lactic acid and enters the sorbitol and fructose pathways.

Sorbitol and fructose cannot be removed from the lens where they draw in water.

42
Q

Chronic Complications of Diabetes

Diabetic Retinopathy

A

Uncommon,

results form retinal ischemia

43
Q

Chronic Complications of Diabetes

Diabetic nephropathy

A

uncommonly diagnosed

44
Q

Chronic complications from Diabetes

Peripheral Neuropathy

A

Distal symmetrical polyneuropatht has been described in dogs and cats.

pelvic limbs more commonly affected.

Pelvic limb weakness, abnormal postural reactions, depressed tendon reflexes

45
Q

Chronic Complications of diabetes

Susceptibility to infection

A

evidence that diabetes can cause immune suppression in dogs and cats.

Risk factor for bacterial and fungal urinary tract infections.

Emphysematous cystitis caused by infection with gas forming bacteria occurs more often in dogs.

Medicine 1 VCS860 (13 decks)

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