Chapter 33 DIABETES Flashcards

0
Q

Define the term prediabetes

A

prediabetes, meaning they are at relatively high risk for the future development of diabetes as well as cardiovascular disease.

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1
Q

Compare the distinguishing feature of type 1 and type 2 diabetes mellitus, list causes of other specific types of diabetes , and cite the criteria for gestational diabetes

A

type 1 diabetes is resulting from beta cell destruction and an absolute insulin deficiency)
type 2 diabetes due to insulin resistance and a relative insulin deficiency
gestational diabetes mellitus that develops during pregnancy. Referring to any degree of glucose intolerance that begins or first recognize.
Factors that indicate a high risk for GDM include glycosuria, strong family history of type 2 diabetes, severe obesity, polycystic ovary disease, and prior history of GDM or delivery of a previous large for-gestational-age infant.

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2
Q

Relate the physiologic functions of insulin to the manifestation of diabetes mellitus

A

Lack of insulin in people with type 1 diabetes mellitus means that they are particularly prone to the development of ketoacidosis. One of the actions of insulin is the inhibition of lipolysis(fat breakdown) and release of free fatty acids (FFAs) from fat cells.
In the absence of insulin, ketosis develops when these fatty acids are released from fat cells and converted to ketones in the liver. Because of the loss of insulin response, all people with type 1A diabetes require exogenous insulin replacement to reverse the catabolic state, control blood glucose levels, and prevent ketosis.

In Type 2. Insulin resistance can be defined as the failure of target tissues to respond to insulin, leading to decreased uptake of glucose in skeletal muscle and impaired suppression of glucose production by the liver.

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3
Q

Define the term metabolic syndrome and describe its associations

A

Hyperglycemia in these people is frequently associated with intra-abdominal obesity, high levels of plasma triglycerides and low levels of high-density lipoproteins (HDLs), hypertension, systemic inflammation, abnormal fibrinolysis, abnormal function of the vascular endothelium, and macrovascular disease (coronary artery, cerebrovascular, and peripheral arterial disease). This constellation of abnormalities often is referred to as metabolic syndrome

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4
Q

Explain the diagnostic tests that are used to diagnose and monitor diabetes mellitus

A
  • Blood glucose measurements are used in both the diagnosis and management of diabetes.
  • Diagnostic tests include the fasting plasma glucose, casual plasma glucose, the glucose tolerance test, and glycosylated hemoglobin (A1C).
  • Laboratory and capillary or finger-stick glucose tests are used for glucose management in people with diagnosed diabetes.
  • urine test
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5
Q

Describe the cause, progression, and clinical manifestations of diabetic ketoacidosis and their physiologic significance.

A

-Life-threatening complication of DM
Type 1 (usual cause)
-Previously undiagnosed
-Triggered by stress, poor glucose control, etc.

Type 2
-Complicated by major illness

Insulin lack results in breakdown of energy stores (muscle and fat)

Amino acids cause liver to
-Convert glucose for use

  • Mobilize fatty acids which causes ketone production
  • -this requires bicarbonate to maintain pH, which depletes over time

Ketones increase levels of glucagon and counter-regulatory hormones (corticosteroids, epinephrine, GH)

MANIFESTATION
GI : N&V, abdominal pain/tenderness, fruity breath
CVS: Dehydration, hypotension/tachycardia
Resp: Kussmaul breathing
CNS: Confusion, stupor, coma
Note: Cerebral autoregulations not developed in children so at greater risk of being unable to compensate

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6
Q

Describe the pathophysiology and clinical condition resulting from the hyperosmolar hyperglycemia state

A

Insulin deficiency causes hyperglucagonemia
Produced by islets of Langerhans
Glucagon causes glycogenolysis
Breakdown of glycogen to create glucose
Stimulates liver to convert amino acids into glucose (gluconeogenesis)
Significant glycosuria causes ++fluid loss = ++dehydration

Clinical condition - thromboembolism

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7
Q

Describe the clinical manifestations of insulin-induced hypoglycemia and state typical treatment regimes

A
CNS 
Headache
Difficulty problem solving
Confusion, behavioral changes
Coma, seizures

ANS activation
PNS: hunger
SNS: anxiety, tachycardia, sweating, constriction of skin vessels

TREATMENT
Rapid delivery of oral glucose (15 g)
Glucose tablets/solution
Glucose IV (D50W) if emergency
Glucagon IM or s/c if unable to take oral glucose
Won’t be effective if liver’s glycogen stores depleted
-complex carbohydrate to be administer after (CHEESE, PEANUT BUTTER)

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8
Q

Describe alteration in physiologic function that accompany diabetic peripheral neuropathy, retinopathy, and nephropathy,

A

Neuropathy
-Blood supply altered d/t thickening of vessel walls over time
-Demyelination of Schwann cells slows nerve conduction
SOMATIC NEUROPATHY
Diminished perception of vibration, pain, temperature in lower extremities initially
-Diminished proprioception leads to falls
Denervation of foot muscles = “clawing” of toes
Also tendon & connective tissue changes mechanics of foot)
Painful diabetic neuropathy can result in hypersensitivity
Burning, pain on touching, etc.

NEPHROPATHY

-Capillary basement membrane thickening
Allows plasma proteins to escape in the urine
Microalbuminuria is often initial sign**
-Nodular glomerulosclerosis
Nodular lesions in glomerular capillaries resulting in impaired blood flow, eventually failure
-Kidney enlargement, nephron hypertrophy
d/t increased workload from attempting to filter ++ glucose

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