Deck 10_Diabetes Mellitus/Endocrine Flashcards

1
Q

What are the signs and symptoms of hyperglycemia?

A
  • Polyuria
  • Polydipsia
  • Polyphagia
  • Fatigue
  • Weight loss
  • Fruity breath
  • Diabetic ketoacidosis- following stressor
  • Abdominal pain will happen
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2
Q

What is the treatment for hyperglycemia?

A
  • Healthy eating
  • Being active
  • Monitoring
  • Taking meds
  • Problem solving
  • Healthy coping
  • Reducing risks
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3
Q

What are the signs and symptoms of hypoglycemia?

A

Symptoms:

  • Anxiety, nervousness
  • Hunger
  • Palpitations
  • Paresthesia (numbness of lips)
  • Sweating
  • Shaking
  • Blurred/Double VisTachycardia
  • Weakness
  • Slurred Speech

Signs:

  • Difficulty thinking
  • Dizziness
  • Fatigue
  • Sleepiness
  • Slurred speech
  • Weakness/lack of coordination
  • Seizures
  • Coma
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4
Q

What is the treatment for hypoglycemia?

A
  • Follow hypoglycemia protocol if available
  • 15-20 g liquid carbohydrate-able to swallow
  • Glucagon IV push-unable to swallow
  • Repeat blood sugar testing- every 15-20 mins
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5
Q

In general, what are the differences between Type 1 diabetes mellitus (DM) and Type 2 DM?

Characteristics of Type 1 Diabetes

  • Abrupt Onset
  • Non-obese
  • Antigen/patterns/antibodies
  • Polyuria, Polydipsia, polyphagia, Fatigue, weightloss
    Dx: before age 30

Characteristics of Type 2 Diabetes

  • Can have low, normal, or high insulin
  • RF include Metabolic syndrome stuff
  • Some insulin still present
A

Characteristics of Type 1 Diabetes

  • Abrupt Onset
  • Non-obese
  • Antigen/patterns/antibodies
  • Polyuria, Polydipsia, polyphagia, Fatigue, weightloss
    Dx: before age 30

Characteristics of Type 2 Diabetes

  • Can have low, normal, or high insulin
  • RF include Metabolic syndrome stuff
  • Some insulin still present

Type 1 DM: 5-10%

  • Genetic & environmental factors:
    • First degree relatives, autoantibodies, viral triggers
    • Monogenetic Diabetes syndromes
  • Destruction of beta cells
  • Absolute lack of insulin
  • Diagnosed before age 30

Type 2 DM: 90-95%

  • Genetic & environmental:
    • BMI>25 kg/m2
    • CVD, HTN, low HDL, high triglycerides
    • Metabolic syndrome
    • Physical inactivity
    • First degree relative
    • High-risk race/ethnicity (ex. AA, Latino, Native American, Asian American, Pacific islander)
    • Polycystic ovary syndrome
  • Relative insulin deficiency & peripheral insulin resistance:
    • Predominantly insulin resistance with relative insulin deficiency
    • Predominantly an insulin secretory defect with insulin resistance
  • Develops over many years
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6
Q

What tests are used to detect diabetic nephropathy?

A
  • Pain
  • Dysesthesias (burning & tingling)
  • Numbness
  • Screen for DPN-annually:
    • Starting at time of diagnosis with type 2 DM
    • Five years after diagnosis of Type 1 DM
  • Monofilament test & microfilament testing
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7
Q

What are the differences between Diabetic Ketoacidosis (DKA) and Hyperglycemic-hyperosmolar state (HHS)?

A

DKA= Type 1 DM

  • Blood glucose> 250mg/dl
  • Arterial pH< 7.30 (Acidosis)
  • Serum bicarbonate <15 mEq/L
  • Ketonuria
  • Polydipsia, Polyuria, Polyphagia
  • Lethargy
  • Blurred vision
  • Abdominal pain
  • Smell of acetone
  • Positive anion gap
  • Management-intensive care
    • Fluid replacement (Rehydration)
    • Insulin administration
    • Correction of electrolyte imbalance

HHS- Type 2 DM or Type 1 DM:

  • Hyperglycemia>600 mg/dl
  • Blood osmolarity> 320 mOsm/L
  • Profound dehydration
  • Bicarb>15 mEq/L
  • Small ketonuria and absent or small ketonemia
  • No ketones
  • Excessive thirst
  • Dry mouth
  • Alteration in LOC
  • Management-intensive care:
    • Rehydration
    • Treat altered mental status
    • Possibly required insulin drip
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8
Q

What is the cause of diabetes insipidus? What are the classic signs and symptoms? What is the treatment?

A

Diabetes insipidus:Decrease or absence of antidiuretic hormone (ADH)

Classification:

  • Central:
    • Decreased secretion of ADH from pituitary gland
    • Idiopathic, brain tumors, intracranial surgery, head trauma
  • Nephrogenic:
    • Kidneys resistant to ADH & unable to concentrate urine
    • Chronic renal insufficiency, hypercalcemia, hypokalemia, interstitial disease of renal tubules

-Clinical manifestations:

  • Depends upon extent of water loss
  • Polyuria:

Dilute urine with low specific gravity

  • Polydipsia
  • Nocturia
  • Hemoconcentration:
    • Increased Na, Hct & osmolarity
  • Hypotension
  • Tachycardia
  • Poor turgor
  • Dry mucous membranes

Management (medical):

  • Maintain adequate hydration
    • Hypotonic fluid relative serum
  • Correct hypernatremia
  • Pharmacologic:
    • Desmopressin (DDAVP)
    • Vasopressin

Management (Nursing)

  • Assess
    • VS, Wt, I&O, serum/urine labs
  • Actions
    • Meds
    • Maintain IV access
    • Provide oral fluids
    • Mouth care
    • Correct Hypernatremia
  • Teaching
    • Disease
    • Medications
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9
Q

What is the cause of Syndrome of Inappropriate Antidiuretic hormone (SIADH)? What are the classic signs and symptoms? What is the treatment?

A

Causes:

  • Vasopressin secreted despite normal/low osmolarity
  • Fluid retention
  • Dilutional hyponatremia
  • Common causes:
    • CNS disorders
    • Pulmonary abnormalities
    • Malignancies
    • Meds
    • Idiopathic

Symptoms:

  • Related to hyponatremia:
  • Anorexia
  • Nausea
  • Coma
  • HF
  • Seizure
  • Malaise
  • Headache
  • Irritability
  • Confusion
  • Weakness
  • Oliguria
  • Increased urine specific gravity
  • Increase urine osmolarity
  • Decreased hematocrit

Management (medical):

  • Treatment of hyponatremia
  • Fluid restrictions < 1000 mL/day
  • Diurectics
  • Demeclocycline

Nursing management:

  • Assess:
    • Neurologic status, I&O, serum/urine labs, skin integrity
  • Actions
    • Meds
    • Fluid Restriction and Diuretic
    • Seizure precautions
    • Neuro Checks
  • Teaching
    • Disease * management
    • Fluid restrictions
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10
Q

What causes adrenal insufficiency (Addison’s disease)? What are the classic signs and symptoms? What is the treatment?

A

Addison’s disease: Adrenal insufficiency (hyperpigmentation):

  • Primary (gradual destruction of adrenal)
    • Addison’s disease
    • Autoimmune disease
  • Secondary (decreased secretion of ACTH)
    • Sudden cessation of glucocorticoids
  • Tertiary (dysfunction of the hypothalamus)

Clinical manifestations:

  • Fatigue
  • Weakness
  • Weight loss
  • Nausea
  • Vomiting
  • Abdominal pain
  • Constipation/diarrhea
  • Hyperpigmentation (Disturbed body image)
  • Emotional lability
  • Irritability
  • Depression
  • Inability to concentrate

Complications:

  • Acute adrenal insufficiency or adrenal crisis
  • Life threatening emergency
  • Severe hypovolemia & hypotension

Management (medical)

  • Cortisol replacement
  • Emergency stabilization:
    • IV fluids & glucose
    • IV hydrovortisone
    • Monitor VS, LOC, serum glucose, Na, K

Management (nursing)

  • Assess
    • I&O, VS, lab results
  • Actions
    • Cortisol Replacement
    • IV Hydrocortisone and Glucose
    • Maintain IV access
    • Cortisol replacement for life​
  • Teaching
    • Disease process & management
    • Taking medication without abrupt discontinuation

Medical ID bracelet

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11
Q

What is the cause of Cushing’s disease? What are the classic signs and symptoms? What is the treatment?

A

Cushing’s disease.

Cause: anterior pituitary or adrenal cortex tumors

  • Tumor on pituitary
  • Too much Cortisol

Clinical manifestations:

General appearance:

  • Fat redistribution
  • Moon face
  • Buffalo hump
  • Truncal obesity
  • Weight gain
  • Striae
  • Increased infection

Cardiovascular:

  • HTN
  • Thromboembolic events
  • Dependent edema
  • Capillary fragility

MSK:

  • Muscle atrophy
  • Osteoporosis

Skin:

  • Thinning skin
  • Striae
  • Increased pigmentation
  • Immune
    • Increased infection
    • Decreased immune function
    • Decresed inflammatory response
    • Decreased production
    • Masked infection/inflammation

Management (nursing):

  • Assess
    • VS, wt, I&O, serum glucose & K, wound healing, skin, fat distribution, muscle mass
  • Actions
    • Turn Q2hrs
    • HOB elevated
    • Meds
      • Reduce Steroids
      • Eliminate Tumor
  • Teaching:
    • Disease process
    • modify salt intakes
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12
Q

What is the cause of hyperthyroidism? What are the classic signs and symptoms? What is the treatment?

A

Causes: Excess thyroid hormone

Hypermetabolism

Grave’s disease: Autoimmune disorder

Clinical manifestations:

  • Heat intolerance
  • Fatigue
  • Palpitations
  • Exothalamus
  • Chest pain
  • Increased systolic BP
  • Tachycardia
  • Dysrhythmias
  • Excessive sweating
  • Thinning of scalp hair
  • Decreased attention
  • Restlessness
  • Irritability
  • Tremors
  • Imsonia
  • Huge appetite but lose weight
  • Amenorrhea
  • Decreased menstrual flow

Tx of Hyperthyroidism

  • Medications
  • Surgery

Nsing interventions

  • Cooling measures
  • Lubricate eyes
  • Diarrhea
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13
Q

What is the cause of hypothyroidism? What are the classic signs and symptoms? What is the treatment?

A

Causes:

  • Hypometabolic state
  • Hashimoto’s thyroiditis
    • Most common
    • Autoimmune disease
  • Tx for hyperthyroidism
    • Thyroid surgery
    • Radioactive iodine therapy
  • Major cause of goiter
  • Women>men

Manifestations:

  • Skin dry, coarse, scaly
  • Thick, brittle hair
  • Decreased Tendon Reflex
  • Apathy
  • Depression Anorexia
  • Weight gain
  • Constipation
  • Decreased metabolic rate
  • Decreased temperature
  • Cold intolerance
  • Impaired memory
  • Inattentiveness
  • Prolonged Menstration
  • Anovulation
  • Impotence in men
  • Decreased libido

Tx for Hypothyroidism

  • Thyroid replacement hormone for life
  • (Levothyroxine in morning)
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14
Q

Why do we “taper” steroid therapy?

A

We taper steroid therapy to make sure we don’t leave the patient with adrenal insufficiency.

Goal of tapering: to prevent adrenal Crisis
(Life threatening hypovolemia and hypotension)
• Hyponatremia
• Hyperglycemia
• Hyperkalemia
• Hypercalcemia

When the patient is using exogenous (synthetic) steroids, the body produces less ACTH and produces less of its own endogenous steroids. You want to taper so the patient starts to make its own steroids more and more.

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