1750: Metabolism 1 EXAM III

FSH, LH, prolactin,*ACTH, *TSH, *GH

Hyper: *Cushing, gigantism, acromegaly

Hypo: dwarfism, panhypopituitarism

*ADH/vasopression, Oxytocin

Hyper: SIADH

Hypo: DI (decreased ADH=large urine output)

Tumors: 95% benign

Surgery: hypophysectomy

Decreased ADH/vasopressin produced = LARGE volumes of dilute urine excreted (>250mL/h)

Specific gravity of urine <1.005

Tx: Desmopressin (DDAVP)

Excessive ADH secretion = holding onto fluids

Restrict fluid intake

Concentrated urine

Monitor I/O

ADdison's Disease: adrenal suppressed d/t exogenous steroid use.

Addisonian crisis: dark pigmentation of skin & mucosa; decreased Na+, increased K+

Dx test: ACTH levels.

• —Risk for FVD: monitor for s/sx of FVD;
• encourage fluids and foods; select foods high in sodium; administer hormone
• replacement as prescribed.

• —Activity intolerance:
• avoid stress and activity until stable, reduce anxiety

Excessive adrenocortical activity or corticosteroid medications

Hyperglycemia w/ *"BUFFALO HUMP", heavy trunk & thin extremities, fragile, muscle wasting,*MOON FACE.

Dx: —Dexamethasone suppression test

• Activity level; self-care
• Skin assessment
• Changes in physical —appearance & patient responses to these changes
• Mental function
• Emotional status
• Medications

—Patient education: refer to Table 52-5

—Timing of doses

• —Need to take as prescribed, TAPER OFF
• required to d/c or reduce therapy

—Potential SFX & measures to reduce SFX.

• Alpha cells:
• —Produce glucagon

—Aids in breakdown of glycogen in liver, formation of CHO in liver, breakdown of lipids

• —Primary function:
• Decrease glucose, oxygenation and increase blood glucose level.

• —Produce insulin:
• aids in movement of glucose across cell membranes; leads to decreased
• serum blood glucose level

—Insulin level increases when BG level increases

• —Somatostatin (NT):
• Inhibits production of glucagon and insulin
• Blood glucose homeostasis

—Transports and metabolizes glucose for energy

—Stimulates storage of glucose in the liver and muscle as glycogen

—Signals the liver to stop the release of glucose

—Enhances storage of fat in adipose tissue

—Accelerates transport of AA into cells

—Inhibits the breakdown of stored glucose, protein, and fat

—Insulin-producing beta cells in the pancreas are destroyed by an autoimmune process

—Requires insulin because little or no insulin is produced

—Onset is acute and usually before 30 years of age

—5% - 10% of persons with diabetes

insulin resistance & impaired beta cell function results in decreased insulin production

—90% - 95% of person with diabetes, onset >30 yo, increasing in children, obesity

—Slow, progressive glucose intolerance

—Treated initially with diet/exercise (more so about the use of sugar)

—Oral hypoglycemic agents initially may need to convert to insulin or use both (*only Type II)

• T1:
• early onset
• genetics
• environment factors

• TII:
• obesity
• age
• previous identified impaired fasting glucose HTN: > or equal to 140/90 mm Hg
• HDL < or = to 35 mg/dL 
• Triglycerides > = to 250 mg/dL
• Hx of gestational diabetes or babies >9 lbs.

Polyuria, Polyphagia, Polydipsia

• Sx:
• fatigue, weakness, vision changes, tingling&numbness, wounds slow to heal, recurrent infections

• Hyperglycemia
• Ketosis (DKA)
• Glucosuria

>126 mg/dL

Hgb A1C: reflects your avg BG level for the past 2-3 months. Specifically, the A1C test measures what % of your Hgb — a protein in RBCs that carries oxygen — is coated with sugar (glycated). The higher your A1C level, the poorer your blood sugar control and the higher your risk of diabetes complications.

• —Intensive control, defined as 3-4 insulin injections per day
• Continuous subQ insulin infusion, insulin pump therapy + frequent blood glucose monitoring,
• Weekly contacts with diabetic educators dramatically decreases development and progression of complications such as retinopathy, nephropathy, and neuropathy.

—Carbs: 50% - 60%; emphasize whole grains

—Fat: 20% - 30%, with >10% from saturated fat and <300 mg cholesterol; protein: 10% to 20%

—Fiber: 25 g/daily; refer to Table 51-2

a diet to eat carb-containing foods that are less likely to cause large increases in BG levels.

It is used to guide food choices.

—Rapid acting-NovoLog (acts in 5 min/lasts 2-4h)

—Short acting-Novolin (acts 1h/lasts 4-6h)

—Intermediate acting-NPH (2-4h/16h)

—Very long acting-Lantus (1 dose/24 hours)

NPH is cloudy.

"air into cloudy, air into clear; draw up clear, draw up cloudy"

Always, draw "clear before cloudy" insulin into the syringe.

—Use and action of insulin

—Sx of hypoglycemia & hyperglycemia

—Required actions

—Blood glucose monitoring

—Self-injection of insulin

—Insulin pump use

—Rise in BG between 4 am - 8 am

—Not a response to hypoglycemia

—Occurs with both TI & TII

—Cause unknown

—Growth hormone?

—Nighttime hypoglycemia with rebound morning hyperglycemia

—Gluconeogenesis and glycogenolysis occurs and decreases peripheral glucose use

—May lead to insulin resistance for 12-48 hours

—Common in type 1 DM

—Insulin reaction

—Intake of alcohol, drugs can cause

—Manifestations

—Compensatory ANS response

—Hypoglycemic unawareness

l-fill-alpha:100.0%'>Insulin pump use

—15 g of rapid-acting sugar

• —Hospitalized if: 
• Blood glucose <50 mg/dL
• —Coma, seizures
• —Altered behaviors
• —Caused by sulfonylurea drug

FBG: 70-110 mg/dL

subQ or IM glucagon (1mg); 25-50 mL 50% DW IV

If 50 mg/dL, then give half cup of soda/juice. If unconscious, give glucagon or IV.

• —Absence or inadequate amount of insulin resulting in abnormal metabolism of
• CHO, protein, and fat.

Hyperglycemia.

• Acetone breath
• dehydration
• ketones in urine/blood
• hyperglycemia
• kussmaul respirations (rapid, deep breathing)
• decreased HCO3-, PCO2, pH, met. acidosis

—Rehydration w/ IV fluid: 8-10 L of 0.9% or 0.45% saline

—IV continuous infusion of regular insulin

—Reverse acidosis and restore electrolyte balance