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MedSurg > Exam #6 > Flashcards

Exam #6 Flashcards

1
Q

What is Diabetes Incipidus?

A

Diabetes Incipidus is a water loss caused by a lack of ADH or an inability of the kidneys to respond to ADH (=Extreme dehydration)

Decreased ADH
Dehydration
Increased urination
Increased serum Sodium
Decreased Specific Gravity 
Decreased Urine Sodium 
Increased Solute (Kool Aid Powder)
Decreased Solution (Water for Kool Aid)
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2
Q

What is ADH (AntiDiuretic Hormone)?

A

AntiDiuretic hormone is Vasopressin

Anticholinergic effects: no pee, no see, no shit, no spit

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3
Q

What are Key assessment findings associated with Diabetes Incipidus?

A

Hypotension, Tachycardia, Weak and thready peripheral pulses, Hemoconcentration, sunken eyeballs
Increased urine output (polyuria); Dilute, specific gravity
Poor Skin turgor, Dry mucous membranes, increased thirst

Decreased Cognition, Ataxia, irritability occur when water is limited and rapid dehydration result!
Do NOT go more than 4 hrs without fluids, will cause SEVERE dehydration (cannot reduce urine output)

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4
Q

What is Nephrogenic Diabetes Insipidus?

A

Nephrogenic Diabetes Insipidus is caused by damage to the loop of Henli. (Kidneys inability to respond to ADH)

Genetically inherited X-linked recessive disorder:

  • AVPR2 gene coding ADH receptor is mutated and only males are affected
  • AQP2 gene mutated affected males and females
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5
Q

What is primary Diabetes Insipidus?

A

Primary diabetes Insipidus is caused by a defect in the hypothalamus gland or posterior pituitary

Can be transient, treated if caught early

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6
Q

What is secondary diabetes Insipidus?

A

Secondary diabetes Insipidus is caused by tumors, head trauma, infection, brain surgery, or metastatic tumor.

Can be transient, treated if caught early

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7
Q

What is Drug-related Diabetes Insipidus?

A

Drug-related Diabetes Insipidus is caused by lithium or demeclocycline.

Can be transient, treated if caught early

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8
Q

What is the diagnostic tool used to diagnose Diabetes Insipidus?

A

24 hour fluid intake and output without restricting food or fluids.

Urine output is GREATER than 4L/day (can vary 4-30 L/day)
-diluted, low SG, and low osmolarity

Urine Specific Gravity < 1.005 and low urine osmolarity (50-200) DILUTE

Labs: Blood
Increased Sodium
Increased H&H
Decreased CVP (preload) (9-13 is Normal)

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9
Q

What is the medication of choice for Diabetes Insipidus?

A

Drug of choice: Desmopressin acetate (DDAVP)

  • synthetic vasopressin given PO or intranasal
  • –intranasal spray is 10 mcg per spray
  • —-Mild DI: 1-2 sprays in 24 HR
  • —-Severe DI: 1-2 sprays 2-3 times per day

For severe dehydration, give ADH IV or IM

Side effects of intranasal spray: ulceration of mucous membranes, allergy, tightness of the chest, and lung inhalation
–if occurs, or upper respiratory infection do NOT use intranasal, use PO or SubQ Vasopressin

Parental Desmopressin is 10 times stronger than the PO or intranasal forms

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10
Q

What are other interventions for Diabetes Insipidus?

A

Focus on early detection of dehydration and maintaining fluids

Accurate measure I/O’s, assess specific gravity
Urge drink fluids in equal amounts of output
IV access, large bore
Life-long drug therapy
DAILY WEIGHTS-same scale, time, clothes
**report weight gain of more than 2.2 lbs and water toxicity (persistent HA, acute confusion)
Wear medical alert bracelet
Assess VS and neuro checks

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11
Q

What is SIADH?

Syndrome of Inappropriate AntiDiuretic Hormone

A

SIADH is excessive production of ADH even when plasma osmolarity is normal or low

Negative feedback loop does not function properly

Increased ADH (vasopressin)
Water Retention
Decreased Urination 
Decreased serum Sodium
Increased urine Sodium
Increased Specific Gravity 
Decreased Solute (Kool Aid powder) 
Increased solution (Water for Kool Aid)
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12
Q

What are key assessment findings associated with SIADH?

A 
Dilutional Hyponatermia and Hypervolemia 
Hypertension
Weight Gain (with little edema)
Bounding Rapid Pulse 
Increased urine specific gravity 
JVD
Decreased deep tendon reflexes

GI disturbances: loss of appetite, N, V occur first

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13
Q

What are conditions responsible for causing SIADH?

A

Malignancies:
Small cell lung cancer, Pancreatic/duodenal/GU carcinoma, Thymoma, Hodgkin’s lymphoma, Non-Hodgkin’s lymphoma

Pulmonary Disorders:
Viral/bacterial PNA, lung abscesses, active TB, Pneumothorax, Chronic lung disease, mycoses, positive pressure ventilation

CNS disorders:
Trauma, infection, tumors, stroke, porphyria, SLE (lupus)

Drugs:
Exogenous agents, Chlopropamide, Vincristine, Cyclophophamide, Carbamazepine, opioids, TCAs, general anesthesia, fluoroquinolones ABX

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14
Q

What are interventions used to treat SIADH?

A

Focus on Fluid restriction, promote excretion of water, replace sodium loss, interfere with action of ADH.

Fluid Restriction: 500-1000 mL/24hr

Use saline NOT water

Measure I/O’s, and DAILY WT; wt gain of 2.2 lbs (1kg) = 1000mL (1L) of fluids

Frequent Oral Rinses

Monitor for fluid overload q2 HR (bounding pulses, JVD, crackles in lungs, increased peripheral edema, reduced urine output)

SAFETY, safe environment critical for Na < 120.

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15
Q

What are medications used to treat SIADH?

A

Tolvaptan (Samsca)- Given PO

  • black box warning for increasing Na to rapidly (>12 in 24hr causes CNS demyelination)
  • High doses or prolonged use >30 days significant risk for liver failure or death

Conivaptan (Vaprisol) - Given IV

Both are Vasopressin Antagonists, used to promote water excretion
GIVEN ONLY IN THE HOSPITAL- to monitor Na levels closely

Diuretics are used when Na levels are near normal and HR failure present

Mild SIADH- demeclocycline (Declomycin) oral ABX to correct fluid and electrolyte imbalance

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16
Q

What type of IV fluids are used with SIADH?

A

Saline based solution for routine IV fluids

Hypertonic Saline (3% sodium chloride) used for very low Na levels

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17
Q

Who is at greater risk for developing SIADH?

A

Elderly

Cardiac, kidney, pulmonary, liver problems are at greater risk.

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18
Q 
Question: Which urine properties indicate to the nurse that the client with SIADH is responding to interventions? 
A. Urine output increased, SG increased
B. Urine output increased, SG decreased 
C. Urine output decreased, SG increased
D. Urine output decreased, SG decreased
A

B. Urine output increased, Specific gravity decreased

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19
Q

What is Adrenal Gland hypofunction?

A
  • adrenocortical steroids decrerase from inadequate secretion of ACTH
  • Dysfunction of hypothalamic-pituitary
  • Dysfunction of adrenal tissue

Addisonian Crisis vs Addison’s Crisis

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20
Q

What is Addison’s Disease? What are S/Sx you will see? And what is the treatment for Addison’s disease?

A

Chronic adrenocortical insufficiency, Can live with and treat!

S/Sx: 
Progressive weakness, psychosis 
Decreased BP (postural hypotension)
Decreased Blood sugar (hypoglycemia)
Decreased Na and Increased K+ 
Confusion, Apathy
GI disturbances, weight loss
Bronze pigmentation of the skin
Vascular collapse 
Changes in distribution of body hair

Tx: lifelong corticosteroid replacement therapy
-Wear a medic-alert bracelet

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21
Q

What are Primary and Secondary causes of Addison’s Disease?

A

Primary causes:
-AIDS, hemorrhage, TB, metastatic cancer, autoimmune disease

Secondary causes:
-Sudden cessation of long-term high-dose glucocorticoid therapy

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22
Q

What is an Addisonian Crisis? What are key assessment findings associated with Addisonian Crisis?

A

Addisonian Crisis is a sudden, severe acute adrenocortical insufficiency

    • need cortisol and aldosterone
    • usually response to a stressful event
S/Sx: 
Muscle weakness, fatigue, 
GI disturbance (N/V/D/C, abd pain, salt craving, wt loss) 
Hyper pigmentation 
Anemia
Hypotension
Arrhythmias
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23
Q

What are lab tests and Diagnostic tests for an Addisonian Crisis? What are treatments available for an Addisonian Crisis?

A

Labs:
Decreased Na Increased K
Decreased Blood sugar Increased Ca
Decreased serum Cortisol Increased BUN

Diagnostic tests:
X-ray, CT, MRI

Treatments:
Decrease K+ with Insulin and D50. (Or Kayexulate in K+ <7.5)
Monitor Blood Sugar

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24
Q

What are Emergency Care interventions for an Acute Adrenal Insufficiency (Addisonian crisis)?

A

Hormone replacement:

  • rapid infuse NS or D5NS
  • initial dose hydrocortisone (Solu-Cortef) 100-300mg or dexamethasone 4-12 mg IV bolus
  • –additional hydrocortisone 100mg dose over 8hr
  • –give hydrocortisone 50 mg IM q12hr
  • H2 histamine blocker (Rantidine) IV for ulcer prevention

Hyperkalemia Management:

  • Insulin 20-50 units With Dextrose 20-50 mg in NS
  • Admin K excreting resin (Kayexalate)
  • Loop or thiazides diuretics, avoid K sparing
  • K restriction and I/O’s
  • Monitor VS and EKG

Hypoglycemia management:

  • Admin IV glucose
  • Admin IV glucagon
  • Maintain IV access
  • Monitor Blood sugar HOURLY
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25
Q

What are the normal lab ranges for Na, K, glucose, Ca, HCO3, BUN, and Cortisol?

A 
Na                135-145
K                   3.5-5.0
Glucose       70-110
Ca.                9-10.5 
HCO3.          23-30
BUN.             10-20
Cortisol.        6a-8a: 5-23.  4p-6p: 3-13
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26
Q

Identify the labs values for ADDISON’s DISEASE, by increased or decreased, for Na, K, HCO, Ca, BUN, glucose, and cortisol:

A 
Na                         Decreased
K.                           Increased
Glucose                Normal or decreased 
Ca.                        Increased
HCO3.                  Increased 
BUN.                    Increased 
Cortisol.               Decreased
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27
Q

Identify the labs values for CUSHING’s DISEASE, by increased or decreased, for Na, K, HCO, Ca, BUN, glucose, and cortisol:

A

Na. Increased
K. Decreased
Glucose. Normal or Increased
Ca. Decreased
HCO3. Decreased
BUN. Normal
Cortisol. Increased

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28
Q

What are medications are used to treat Addison’s disease?

Hypofunction ing adrenal

A

Cortisone:
25-50 mg PO daily, take with snack or meal, can cause GI upset

Hydrocortisone (Solu-Cortef)
25-50 mg PO daily; report S/Sx of excess drug: rapid wt gain, round face, fluid retention; Cushing’s syndrome indicates need for dosage adjustment

Prednisone (Winpred)
5-10 mg PO daily; instruct to report illness- severe Diarrhea, vomiting, fever. Need for dose changes.

Fludrocortisone (Florinef)
0.05-0.2 mg PO daily; monitor BP, report wt gain or edema; Hypertension is side effect, fluid retention is possible.

REMEMBER TO TAPER ALL STEROIDS

***Caution sound a-like prednisone and prednisolone—- prednisolone is several times MORE potent

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29
Q

What is Cushing’s Disease?

A

Cushing’s Disease is an adrenal HYPER-secretion by the adrenal cortex, results in hyoercortisolism and excess androgen production

Excess secretion of Cortisol from the adrenal cortex, can be a problem with the adrenal cortex, anterior pituitary, or hypothalamus.

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30
Q

What are the key assessment findings associated with Cushing’s Syndrome?

A

Truncal obesity: Moon (round) face or Buffalo hump (caused by fat redistribution) WT GAIN

Hypertension, frequent dependent edema

Striae (stretch marks)

Decreased muscle mass and strength, thin skin, fragile capillaries (caused by tissue protein breakdown)

Bone density loss (Osteoporosis) and thinning of extremities

Hirsutism (increased body hair growth), acne, and clitoral hyper trophy , Oligomenorrhea (scant or infrequent menses)

Bruises or petechiae, increased r/f infection

Personality changes, CNS irritability

Increased Blood sugar

Gynecomastia

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31
Q

What is the etiology of Cushing’s Syndrome? what is the incidence or prevalence of Cushing’s disease?

A

Etiology:
Excess secretion of cortisol, commonly caused by a pituitary adenoma;—The anterior pituitary over secretes ACTH (andrenocorticotropic hormone) causing excess hormones secreted by the adrenal cortex.

Incidence/prevalence:
More common in women
Cushing’s syndrome more common than Cushing’s disease

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32
Q

What are lab tests associated with Cushing’s Disease?

A

Cortisol levels: either blood, urine, salivary

24 hour urine collection: for Ca, K, glucose

Dexamethasone Suppression test: glucose, Na, Ca

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33
Q

What is the difference between Pituitary Cushing’s Disease, Adrenal Cushing’s Disease, and Cushing’s syndrome?

A

Pituitary Cushing’s Disease is caused by a pituitary disorder

Adrenal Cushing’s Disease is caused by a problem with the adrenal cortex

Cushing’s syndrome results from drug therapy (glucocorticoids)

34
Q

What are conditions that cause Increased cortisol secretions in Cushing’s disease?
(Box on p 1277)

A

Endogenous Secretion:

Bilateral adrenal hyperplasia
Pituitary Adenoma causing increased ACTH (Pituitary Cushing’s)
Malignancies: carcinomas of lung, GI, pancreas
Adrenal Adenomas or carcinomas

35
Q

What conditions can cause increased Cortisol secretions in Cushing’s SYNDROME?

A

Exogenous (external) administration:

Therapeutic use of ACTH or glucocorticoids– used to Tx:

  • Asthma
  • Autoimmune disorders
  • Organ transplant
  • Chemotherapy
  • Allergic responses
  • Chronic Fibrosis
36
Q

What are Diagnostic imaging for Cushing’s Disease?

A

X-ray
CT
MRI

37
Q

What are some safety precautions to prevent injury for Cushing’s Disease? What are ways to prevent infection?

A

Safety:
-Prevent fluid overload, Assess q2hr
(indicators of fluid overload: bounding pulse, JVD, crackles in lungs, peripheral edema, reduced urine output)

-Skin integrity:
assess skin &Turn and reposition q2h, assess for pressure sores often,
use moisturizing lotion, soft tooth brush, electric razor, dry completely after washing, use tape sparingly

-bleeding precautions: apply pressure after puncture, give Antacids and H2 receptor antagonists (cimetidine, rantidine, famotidine, nizatidine) and PPI (Omeprazole and esomeprazole), caution NSAIDs and ASA

Infection prevention:

  • hand washing and aseptic technique
  • pt with Upper Resp Tract Infection must wear mask when entering room
  • if immunosuppressive, may have low grade fever without pus present
  • monitor labs
  • Assess VS q4 hours
  • temp increase by 1 degree above baseline is significant
  • daily bathing and good hygiene
38
Q

What are medications used to treat Cushing’s Disease?

A

Medications that interfere with ACTH (produced in the anterior pituitary) production:
Cypoheptadine (Periactin)

Medications that interfere with cortisol production:
Metyraprone (Metopirone), aminoglutethiamide (Elipten, Cytadren), Ketoconazole

Mitotane (Lysodren) is an adrenal cytotoxic agent used for inoperable tumors

Mifepristone (Korlym) used for patients with DM2, synthetic steroid that blocks glucocorticoid receptors.**cannot be used with pregnancy because it blocks progesterone receptors and would terminate the pregnancy.

New Drug: Pasireotide (Signifor) used for hypercortisolism from a pituitary adenoma- binds to somatostatin receptors to inhibit tumor producing corticotropins.

Monitor Wt loss and urine outputDont stop corticosteroids suddenly if taking more than 1 week, gradually tapper***

additional meds: Antacids and H2 receptor antagonists (cimetidine, rantidine, famotidine, nizatidine) and PPI (Omeprazole and esomeprazole) Avoid NSAIDs and ASA.

39
Q

What are surgical managements for Cushing’s Disease?

A

Hypophysectomy - removal of the pituitary gland

Adrenalectomy - removal of the adrenal gland

Need for life-long supplement therapy

40
Q

What are Pre-Op cares related to Cushing’s disease? What are Post-Op cares?

A 
Pre-Op: 
Monitor Labs (K, Na, Cl) and cardiac function- glucose need to be controlled before surgery

Prevent infections and fractures- Handwashing and aseptic tech. Use side rails and offer assistance getting out of bed

Nutrition- High calorie and Protein diet

Glucocorticoid therapy- before and during to prevent adrenal crisis

Post-Op:
ICU (Assess for Shock q 15 mins)
Monitor Labs
Hormone replacement Therapy: life-long for bilateral adrenalectomy and up to 2 yrs for unilateral adrenalectomy

41
Q

What are Nutrition interventions for Cushing’s Disease? What are things you will monitor in a patient with Cushing’s Disease?

A

Nutrition:

  • Fluid and Sodium restriction: 2-4 g/day of Na
  • High calorie diet, increased Calcium and Vitamin D (yogurt, milk, cheese, green leafy veggies, and root veggies to promote bone density)
  • Avoid caffeine and alcohol

Monitor:

  • daily wt
  • I/O’s
  • Urine Specific gravity (below 1.005 indicates fluid overload)
  • VS
  • Labs

Educate:

  • Avoid crowds
  • get vaccines and flu shot
  • daily wt
  • follow ups
  • Medic-alert bracelet
  • IM injections
  • High protein, high calorie diet
  • infection prevention
  • Bleeding/injury precautions`
42
Q

What is patient education related to Cortisol Replacement Therapy?

A
  • take med in divided doses, first dose in morning and then between 4-6pm
  • take meds with meal or snack
  • Daily wt, and keep a record for your PCP; notify PCP of wt gain of >3lbs/wk or 2lbs in 24 HR
  • Increase dose as directed for increased physical/emotional stress
  • Never skip a dose, if V/N and can’t take dose for 24-36 HR-call PCP ASAP, if cannot reach got o ER
  • Wear medic-alert bracelet
  • Regular follow-ups
  • Learn how to give IM injection of hydrocortisone
43
Q 
Question: The nurse is caring for a patient diagnosed with small cell lung cancer, The nurse understands the patient may also present with which endocrine disorder? 
A. Adrenal Crisis 
B. Cushing's Syndrome
C. DI
D. SIADH
A

D. SIADH

– produces ADH hormone

44
Q

Question: Which priority question should the nurse ask a patient with a pituitary tumor?
A. “Have you had an unexpected wt loss”
B. “have you noticed a change in your libido”
C. “Do you have any changes in your visual acuity?”
D. “Have you experienced a change in growth of your facial hair?”

A

C. “Do you have any changes in your visual acuity?”

– it’s pushing on the optic nerve I the brain

45
Q 
Question: Th nurse knows which patient with Cushing's disease is at greatest risk for developing heart failure?
A. 60 yr with PNA
B. 59 yr with Hx of HTN
C. 32 yr with Hx of Hep B
D. 42 yr with serum Cr 3.7
A

D. 42 yr old with a serum creatinine level of 3.7

–indicates actual kidney damage

46
Q

What is DKA?

A

DKA is a deficiency of insulin and increased hormone release, leading to Increased glucose production and decreased glucose use

Characterized by Uncontrolled hyperglycemia, metabolic acidosis, and increased production of ketones

Most common in Type 1 Diabetes Mellitus and younger patients

47
Q

What is the most common precipitating factor of DKA?

A

INFECTION, death occurs in up to 10% of these cases

48
Q

What are key assessment findings associated with DKA?

A

SUDDEN ONSET, Type 1 DM, younger population
Fruity breath, ketones in urine
Polyuria, Polydipsia, Polyphagia
Nausea/Vomiting , Abdominal Pain
Dehydration, thirst
Weakness, lethargy, Confusion
Shock, Coma
Kussmaul Respirations, tachycardia, hypotension
Metabolic Acidosis, Respiratory Alkalosis
Dry skin, sunken eyes
Blood Glucose >300
Hemoconcentration, hyperviscosity, hypoxia

49
Q

What are priority interventions to provide when caring for a patient with DKA?
(Hi…E)

A

First assess airway! - ABCs always first

Hydrate- Slowly
Insulin- decrease by 50-75 per hour, Regular insulin
Electrolyte Replacement- replace K when level is 5.0

Assess VS q15 minutes until stable, then q4 hr
Assess CVP q30 minutes
Assess BS q 1 hr
Assess K+ q 2 hr

Assess for signs of dehydration or fluid volume excess

50
Q

How do you want to replace fluid volume and maintain perfusion for DKA?

A

REPLACE FLUIDS SLOWLY
Initial infusion: NS @ 15-20ml/kg/hr for the first hour.
then give:
Hypotonic fluids 1/2NS (0.45%) at 4-14ml/kg/hr

When glucose reaches 250:
Dextrose 5% in 1/2NS (D5, 1/2NS)-prevents hypoglycemia and cerebral edema

May give 6-10 Liters of fluids in the first 24Hr.

51
Q

How much insulin do you give to correct DKA? What kind of insulin and what route?

A

Give Regular Insulin IV

Initial Bolus: 0.1 unit/kg

Continued infusion: 0.1 unit/kg/hr

52
Q

When id DKA considered to have resolved?

A

DKA is considered to have resolved when:

  • Glucose < 200
  • HCO3 > 18
  • pH > 7.3
  • ion gap < 12
53
Q

What is a normal Anion Gap? What value indicates Metabolic Acidosis?

A

Anion gap 7-9

> 10-12 indicates Metabolic Acidosis

54
Q

Who is a patient’s Potassium (K+) affected by DKA? When do you begin replacement therapy?
What do you need to assess prior to giving K+?

A

Initially K+ will be HIGH

When insulin therapy is started, the K+ will get LOW

Begin replacement therapy for K+ when lab value reaches 5.0

Assess urine output prior to giving K+, must be at least 30mL per hr

55
Q

What are manifestations of hypokalemia associated with DKA?

A 
Fatigue 
Weakness
Confusion
Muscle Weakness
Shallow Resp
Abdominal Distention
Paralytic ileus 
Hypotension 
Weak Pulse
56
Q

When do you give bicarb (HCO3) for DKA?

A

Give HCO3 for severe acidosis.

Given when pH is < 7.0 -OR- HCO3 < 5.0
Given by slow IV infusion

57
Q

What are lab findings associated with DKA?

A 
Glucose > 300
Osmolarity Variable 
Ketones Positive (1:2 dilution) 
pH < 7.35 
HCO3 < 15 
Na Low, Normal, High 
BUN > 30 (caused by dehydration) 
Cr > 1.5 (caused by dehydration)
Urine Ketones Positive
58
Q

What are normal signs of dehydration?

A 
Acute Wt loss 
Thirst 
Decreased Skin turgor 
Dry mucous membranes 
Oliguria 
weak, rapid pulse 
Flattened neck vein
Increased temp
Decreased CVP
Muscle Weakness 
Postural hypotension 
Cool, clammy, pale skin
59
Q

What are signs of fluid volume excess?

A 
Acute wt gain 
Full, bounding pulse
Distended neck veins 
Pulmonary crackles 
Peripheral Edema 
Elevated CVP
Acute pulmonary edema 
Hypertension
60
Q

What education do you want to provide to a patient with DKA?

A

Check glucose q 4-6 HR when anorexia, N/V present or glucose >250

Check urine ketones when glucose >300

Prevent dehydration, drink at least 2L fluids daily

Increase fluids when infection

If nausea, consume fluids with glucose and electrolytes (soda, diluted fruit juice, sport drinks)

When vomiting and glucose is normal or elevated, consume 8-12 ounces of calorie free, caffeine free liquids q 1 HR to prevent dehydration.

Diabetics unable to eat solid foods: carb containing liquids, at least 150 g of carb daily to reduce r/f starvation ketosis.

Do NOT omit insulin when illness. May need to increase frequency of glucose checks when Ill.

61
Q

What are clinical manifestations of HHS?

A

Gradual ONSET

Precipitated by infection, stress, or poor fluid intake

Altered CNS, confusion to coma

Dehydration

Seizures or reversible paralysis

62
Q

What are lab findings associated with HHS?

A

Glucose > 600

Osmolarity >320

Ketones NEGATIVE

PH >7.4

HCO3 >20

Na Normal or low

BUN elevated

Cr Elevated

Urine ketones NEGATIVE

63
Q

When do you instruct a patient with DKA to contact their Health care provider?

A

Blood glucose exceeds 250

Ketones in urine last for more than 24 hours

The patient cannot take food or fluids

Illness lasts more than 1-2 days.

64
Q

What are the SICK DAY rules?

A

Notify HCP of illness

Monitor glucose q 4 hours

Test you urine for ketones if glucose > 240

Take insulin or oral anti diabetic meds

Prevent dehydration, drink 8-12 ounces of sugar free liquids q hour while awake. If below target, drink fluid with sugar

Continue eating at regular times

If unable to eat because of nausea, drink carb containing liquids

Call HCP if: persistent N/V, moderate or large ketones, glucose elevation after 2 doses of insulin, high temp or fever >24 HR.

Treat symptoms as directed by HCP

Plenty of REST

65
Q

What is HHS?

A

Hyperglycemia-Hyperosmolar State: is a hyperosmolar state caused by hyperglycemia and dehydration- results from sustained diuresis.

TYPE 2 DM and older adults

NO ketones

BS > 600

Osmolarity > 320

The patient excretes enough insulin to prevent ketoacidosis but not enough to prevent hyperglycemia – more severe that DKA, leading to extreme diuresis with severe dehydration and electrolyte loss.

66
Q

Wha are considerations pertaining to older adults with HHS?

A

Older adults with DM2 more likely- mortality rate 40-70%

SLOW onset

> r/f dehydration, altered thirst perception, poor urine-concentrating abilities, and diuretic use.

MAINTAIN HYDRATION is important

67
Q

What is the normal range for osmolarity?

A

275-295

68
Q

What are some causes of HHS?

A

Infection, stress, environment, MI, sepsis, pancreatitis, stroke, medications

–Pt not excreting enough insulin to prevent ketoacidosis but NOT hyperglycemia.

High BSD levels lead to extreme diuresis, severe, dehydration, and electrolyte loss.

69
Q

What are interventions related to HHS?

A

Shock/hypovolemia:
NS 1 L/HR until CVP and BP rise and adequate urine output

Insulin Bolus:
0.15 unit/kg

Continuous infusion: 0.1 unit/kg/HR until glucose 200

Monitor for hypokalemia, may need supplemental K+

Continuous Cardiac monitor, airway, neuro checks, safety

70
Q 
Question: Which complications of DM are considered emergencies? Select all that apply
A. DKA
B. Hypoglycemia
C. Diabetic retinopathy
D. HHS
E. Diabetic neuropathy
A

A. DKA
B. Hypoglycemia
D. HHS

71
Q 
Question: When caring for a patient having a hypoglycemic episode, the nurse knows which symptoms require immediate intervention? 
A. Hunger
B. Confusion
C. HA
D. Tachycardia
A

B. Confusion

— Neuro change is significant cause for concern

72
Q

Question: Before supplementing with potassium, how much hourly urine output should the patient be producing?

A

30mL/HR

73
Q

Question: The critical care nurse is caring for an older patient admitted with HHS. What is the first priority in caring for this patient?
A. Slowly decreasing glucose
B. Fluid replacement to increase blood volume
C. K+ replacement to prevent hypokalemia
D. Diuretic therapy to maintain kidney function

A

B. Fluid replacement to increase blood volume

74
Q

Question: Calculate the anion gap:
Na 136
Cl 102
HCO3 7

A

Add Cl and HCO3 and subtract from Na….

Answer 27= Metabolic acidosis

75
Q 
Question: Identify the acid/base disturbance. Explain teh values. 
PH 7.03
PaO2 88
PaCO2 12 
HCO3 9
A

PH decreased
PaO2 WNL
PaCO2 decreased
HCO3 decreased

Indicates METABOLIC ACIDOSIS AND RESPIRATORY ALKALOSIS
Caused by fat (ketone) breakdown- causing anaerobic respirations

76
Q

A coma can occur when the he osmolarity is greater than what? In patients with HHS…

A

Coma can occur when osmolarity is > 350

77
Q

What is the priority interventions related to HHS?

A

Rehydrate the patient and restore glucose levels within 36-72 hours

78
Q

What is the first priority for HHS? And how is this done?

A

Increase blood volume

Shock or severe hypotension:
NS

Otherwise, use:
1/2 NS (0.45% NS)

Infuse:
1 liter per hour until CVP begins to rise, BP increases, and urine output adequate.
Then, reduce rate to 100-200mL/HR.

HALF the fluid is replaced within 12 hours, then rest is given over 36 hours.

79
Q

What are signs of cerebral edema?

A

ABRUPT change in mental status

Abnormal Neuro signs

Coma

80
Q

In relation to HHS, what do you want to immediately report to the physician?

A

Change in LOC

Change in pupil size, shape, reaction, or seizures.

81
Q

What is the idea HgbA1C?

A

6.5% or below

MedSurg (6 decks)

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