Diabetes

Hypoglycemia vs. ketoacidosis—know the manifestations for each. How do they differ?
Hypoglycemia BLG< 70 mg/dL
Reduced cognition, decreased LOC
Tremors
Diaphoresis
Weakness
Hunger
Headache
Irritability
Seizure
Ketoacidosis pH<7.35 & BLG >200, ketones
FRUITY BREATH
Dry mouth, vomit
Rapid, deep respirations (Kassmaul respirations)
Altered reflexes
Coma/stupor (near unconsciousneaa)
Muscle wasting
Dry, warm , inelastic skin
restlessness
 What is the most common cause of death for these patients?
Myocardial Infarction, cardiovascular risk

What priorities are important to educate patient to pay attention to help decrease their risk for the most
common cause of death?
Blood pressure control is priority to reduce the risk of an MI
Blood glucose MUST be controlled!
 Blood glucose control has been shown to
directly impact mortality outcomes after
an MI and is the immediate priority!!!!!
 What is a HgA1c? Why is this important? What is the range WNL?
A1C measures the amount of glycosylated hemoglobin as a percentage of total hemoglobin
A1C provides a measurement of blood glucose levels over the previous 2 to 3 months,
Normal < 5.7
Pre diabetes 5.7 – 6.4
Diabetes 6.5 >

Type I/Type II: (Adults and children)
o BGL levels; fasting (normal/abnormal)
normal is less than 126 mg/dL but not below 70
o Education; exercise, diet (related to taking medications and what should patients do if BLG is
hyper-- or hypo--)
For low, follow rule of 15.
If less than 70 mg/dL, ingest 15 g of simple fast acting carb.
Recheck in 15 min. if value still less than 70 mg/dL, ingest 15 g more
Recheck in 15 min.
If NO significant improvement after 2 or 3 doses of 15 g of carb, call Dr
 Balance nutrients, expenditure of energy, dose and timing of meds.
 People with type 1 diabetes base their meal planning on usual food intake and preferences balanced
with insulin and exercise patterns.
 The patient coordinates insulin dosing with eating habits and activity pattern in mind.
 Patients using rapid-acting insulin can adjust the dose before each meal based on the current blood
glucose level and the carbohydrate content of the meal
 Minimum of 130 g/day
 Serving size is 15 g
 Fruits, vegetables, whole grains, legumes, low-fat dairy
 All benefit from including dietary fiber
The ADA recommends that people with diabetes engage in at least 150 minutes per week (30 minutes, 5 days
per week) of a moderate-intensity aerobic physical activity.
The ADA also encourages people with type 2 diabetes to perform resistance training three times a week, in the
absence of contraindications.
Exercise decreases insulin resistance and can have a direct effect on lowering blood glucose levels. It also
contributes to weight loss, which decreases insulin resistance.
*** emotional and physical stress can increase the blood glucose level and result in hyperglycemia. Because
stress is unavoidable, certain situations may require more intense management, such as extra insulin and more
frequent blood glucose monitoring, to maintain glycemic goals and avoid hyperglycemia.
o Interventions and Assessment
Acanthosis nigricans is a physical exam finding frequently seen in individuals who are insulin resistant
 Medications: Insulin, OAs, corticosteroids, diuretics, phenytoin
 Recent surgery
 Viral infections, trauma, infection, stress, pregnancy, chronic pancreatitis, Cushing syndrome,
acromegaly, family history of diabetes
 Nutritional-metabolic: obesity; weight loss (type 1), weight gain (type 2); thirst, hunger; nausea and
vomiting; poor healing (especially involving the feet), eating habits in patients with previously
diagnosed diabetes
 Elimination: constipation or diarrhea; frequent urination, frequent bladder infections, nocturia, urinary
incontinence
 Activity-exercise: muscle weakness, fatigue
 Cognitive-perceptual: abdominal pain; headache; blurred vision; numbness or tingling of extremities;
pruritus
 Sexuality-reproductive: impotence; frequent vaginal infections; decreased libido
 Coping–stress tolerance: depression, irritability, apathy
 Value-belief: commitment to lifestyle changes involving diet, medication, and activity patterns
 Sunken eyeballs, history of vitreal hemorrhages, cataracts
 Dry, warm, inelastic skin
 Pigmented skin lesions, ulcers, loss of hair on toes, acanthosis nigricans
 Kussmaul respirations
 Hypotension
 Weak, rapid pulse
 Dry mouth
 Vomiting
 Fruity breath Altered reflexes, restlessness

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Interventions



Confusion, stupor, coma
Muscle wasting
Serum electrolyte abnormalities
Fasting blood glucose level of 126 mg/dL or higher
Oral glucose tolerance test and/or random glucose level exceeding 200 mg/dL
Leukocytosis
↑ Blood urea nitrogen, creatinine
Frequent monitoring of blood glucose
Educate, promote proper nutrition
Foot care, inspect daily , don’t be barefoot, proper footwear
 Ketone testing if glucose level exceeds 240 mg/dL
 Report glucose levels exceeding 300 mg/dL twice or moderate to high ketone levels
 Increase insulin for type 1 diabetes
 Type 2 diabetes may necessitate insulin therapy
o Medications
Insulins: Rapid-acting, Short-acting, Intermediate-acting, Long-acting, Combination or premixed
Oral meds: Biguanides, Sulfonyureas (“ides”), Meglitinides (“glinides”), Alpha-glucosidase inhibitors,
Thiazolidinediones (“glitazones”), DPP-4 Inhibitors (“gliptins”), Selective Sodium Glucose Transporter 2,
Amylin Analogue
education r/t medications
 Symptoms/treatment of hypoglycemia
 How to administer accurately
 Best sites fro injection…
 Diet modifications
 “Sick days” or stressors
 Exercise and risk of hypo
 Testing for blood glucose
 Storage of insulin
 Disposal of used needles and syringes
 DKA: Manifestations—be sure to know what findings WILL BE present in a patient with DKA
Tachycardia, hypotension
Rapid, deep respirations + fruity breath
N/V, abdominal pain, electrolyte imbalances, weight loss,
Dehydration, high temp, poor skin turgor
 Interventions/treatments
 Evaluate BGL levels and K levels that may be present with DKA; nursing interventions and why.
Serum blood glucose more than 200 or 300 (powerpoint says 200, books say 20, 300)
Potassium is normal, elevated with acidosis and low with dehydration
Interventions: monitor vitals, i&o, potassium and glucose. Check for intracranialpressure
F: fruity breath
R: respirations kussmail
U: unbalanced electrolytes
I: insulin low
 T: tachycardiaLess severe form of DKA may be treated on an outpatient basis. But, hospitalize
for severe fluid and electrolyte imbalance, fever, N&V, diarrhea, and altered mental state.
 Ensure patent airway, administer O2. Establish IV access; begin fluid resuscitation
 NaCl 0.45% or 0.9%. Add 5-10% dextrose when blood glucose level approaches 250 mg/dL.
 Continuous regular insulin drip 0.1 U/kg/hr. +Potassium replacement as needed
Chronic Renal Failure:
 Describe the 4 stages of chronic renal failure (CKD) {Stage 1, Stage 2, Stage 3 and Stage 4}
End Stage Renal Disease (ESRD):

What is ESRD?

What is occurring or what has occurred to the kidneys? (patho)
medical condition in which a person's kidneys cease functioning on a permanent basis leading to the need for a regular
course of long-term dialysis or a kidney transplant to maintain life
Loss of nephrons and reduction of functional renal mass reaches a certain point, the remaining nephrons begin a
process of irreversible sclerosis that leads to a progressive decline in the GFR. Decreased renal function interferes with
the kidneys' ability to maintain fluid and electrolyte homeostasis. The ability to concentrate urine declines early and is
followed by decreases in ability to excrete excess phosphate, acid, and potassium
 Clinical manifestations
Waste product accumulation
 As GFR ↓, BUN and serum creatinine levels ↑
As CKD progresses patients have increasing fluid retention
 N/V, lethargy, fatigue, impaired thought processes, and headaches occur
Altered carbohydrate metabolism Caused by impaired glucose metabolism From cellular insensitivity to normal
action of insulin
**Patients with uremia develop dyslipidemia, with elevated levels of very-low-density lipoproteins (VLDLs),
normal or decreased levels of low-density lipoproteins (LDLs), and decreased levels of high-density
lipoproteins (HDLs).
The altered lipid metabolism is related to decreased levels of the enzyme lipoprotein lipase, which is important
in the breakdown of lipoproteins
• Hyperkalemia results from the decreased excretion of potassium by the kidneys, the breakdown of
cellular protein, bleeding, and metabolic acidosis. Fatal when more than 7 or 8 meq/L
Because of impaired excretion, sodium along with water is retained
 Calcium and phosphate and Magnesium alterations
 Hypermagnesemia Related to ingestion of magnesium and Can result in absence of reflexes,
decreased mental status, cardiac dysrhythmias, hypotension, respiratory failure
 Metabolic acidosis Results from
 Kidneys’ impaired ability of to excrete excess acid (primary ammonia)
 Defective reabsorption and regeneration of bicarbonate
Anemia due to less erythropoietin from decreased function of renal tubular cells, less stores, folic acid lost
Infection r/t changes in WBC function, altered immune response, hyperglycemia
Most common cause in pt with CKD is CV disease complications r/tElevated lipids and hypertension, arterial
stiffness, PAD, HF, cardiomyopathy, stroke
Hypertension r.t to water/sodium retension and increased renin
Kassmaul respirations and dyspnea
GI affected r/t increased urea,
Neurologic: increased nitrogenous waste, electrolyte imbalaces, metabolic acidosis, Lethargy, apathy Decreased
ability to concentrate, Fatigue, irritability, Altered mental ability, Seizures, Coma, Hypertensive encephalopathy
skin crusts because of urea crystallization, itching
infertility and decreased libido, sexual dysfunction
Assessment & Interventions
Assess the patient's dietary habits and discuss any problems regarding intake. Measure the patient’s height and
weight, and evaluate any recent weight changes.
Assess the patient's support systems. The choice of treatment modality may be related to support systems
available.
Teach patient and caregiver about Diet/Drugs
 Common side effects
 Pill organizer
 Avoid over-the-counter drugs
Take daily BP and Identify signs of fluid overload, electrolyte imbalances
Patients with chronic kidney disease are taught to report weight gain greater than 4 pounds
 Interprofessional interventions: Correction of extracellular fluid volume overload or deficit, Nutritional
therapy, Erythropoietin therapy, Calcium supplementation, phosphate binders, Antihypertensive therapy,
Measures to lower potassium, Adjustment of drug dosages to degree of renal function, Restriction of
high-potassium foods and drugs, IV glucose and insulin, IV 10% calcium gluconate, Weight loss (if
indicated), Therapeutic lifestyle changes, Diet recommendations (DASH Diet), Administration of
antihypertensive drugs, Antihypertensive drugs: ACE inhibitors & ARB agents

When is a patient referred to begin Dialysis treatment? Why? (patho)
Dialysis is needed when you develop end stage kidney failure --usually by the time you lose about 85 to 90 percent of
your kidney function and have a GFR of <15. kidneys filter wastes and excess fluids from your blood, which are then
excreted in your urine. When your kidneys lose their filtering capabilities, dangerous levels of fluid, electrolytes and
wastes can build up in your body.
Dialysis is begun when the patient’s uremia can no longer be adequately treated with conservative medical
management. Generally, this is when the GFR is less than 15 mL/min/1.73 m2. This criterion can vary widely in
different clinical situations. The nephrologist determines when to start dialysis based on the patient’s clinical
status. Certain uremic complications, including encephalopathy, neuropathies, uncontrolled hyperkalemia,
pericarditis, and accelerated hypertension, indicate a need for immediate dialysis.
 What is Dialysis? What is this doing to the blood of the patient? Why do they need this? Can they live
without Dialysis? Why or why not?
Dialysis is the movement of fluid and molecules across a semipermeable membrane from one compartment to
another. Clinically, dialysis is a technique in which substances move from the blood through a semipermeable
membrane and into a dialysis solution (dialysate). It corrects fluid and electrolyte imbalances and removes
waste products in kidney failure. It also can be used to treat drug overdosesSolutes and water move across the
semipermeable membrane from the blood to the dialysate or from the dialysate to the blood per concentration
gradients. The principles of diffusion, osmosis, and ultrafiltration are involved in dialysis. Diffusion is the
movement of solutes from an area of greater concentration to an area of lesser concentration. In kidney failure,
urea, creatinine, uric acid, and electrolytes (potassium, phosphate) move from the blood to the dialysate with the
net effect of lowering their concentration in the blood.
They cannot live without dialysis
 What are different ways that patient receive Dialysis?
o Describe the following:
tunneled dialysis catheter: has two inner channels, one for removing the blood to the machine and the other for
returning blood to the bloodstream. The catheter usually enters the skin below the collar bone (clavicle) and travels
under the skin to enter the jugular vein, with its tip in the very large vein (the vena cava)
fistula: fistula is created by connecting an artery directly to a vein. Once it has matured and grown, a fistula is a natural
part of the body and requires less attention and care than an AV graft. A mature fistula that has grown bigger and
stronger can provide good blood flow for decades
graft: If veins are too small for a fistula or your veins are blocked, an arteriovenous (AV) graft is used. A graft is a manmade tube that is inserted into your arm to connect an artery to a vein. Grafts can usually be used for dialysis within two
to six weeks.
peritoneal dialysis: the peritoneal membrane acts as the semipermeable membrane. D is done by putting dialysis
solution into the peritoneal space. The 3 phases of the PD cycle are inflow (fill), dwell (equilibration), and
drain. Together, the 3 phases are an exchange
Children with Endocrine or Metabolic Alterations:

Nursing care for the infant with congenital hypothyroidism
congenital hypothyroidism is associated with either the congenital absence of a thyroid gland or the inability of the
thyroid gland to secrete thyroid hormone
*levothyroxine and dietary iodine sup
Imbalanced nutrition, deficient knowledge, fatigue r/t impaired metabolic state
Maintain stable weight
Family members/caregivers verbalize correct information given
 Nursing care for the child with Acquired Hypothyroidism
Hashimoto thyroiditis is the most common cause.
Thyroid gland produces an inadequate amount of thyroid hormone. Goiter present
Assessment of the thyroid from an interior or posterior position.
Auscultation of the lobes of the thyroid gland using the diaphragm of the stethoscope if there are abnormalities
palpated.
Assess thyroid gland for firmness (Hashimoto’s) or tenderness (thyroiditis)
Activity intolerance related to fatigue and depressed cognitive process.
Risk for imbalanced body temperature related to cold intolerance.
Constipation related to depressed gastrointestinal function.
Ineffective breathing pattern related to depressed ventilation.
Disturbed thought processes related to depressed metabolism and altered cardiovascular and respiratory statu
 What are indicators of Diabetes Insipidus or SIADH?
 Syndrome of Inappropriate Antidiuretic Hormone
An inability to concentrate urine
Increased urination and nocturia
Increased thirst (polydipsia)
Dehydration
Hypernatremia
Urine specific gravity less than 1.005
Elevated serum osmolality (greater than 300 mOsm/kg)
Decreased urine osmolality
 SIADH is characterized by low serum sodium (less than 125 mEq/L) and high urine specific gravity as
well as decreased serum osmolality and increased urine osmolality.
Seizures may develop with hyponatremia.
Treatment depends on strict fluid restriction to maintain serum sodium in a near-normal range.
Thyroid Disorders
Hyperthyroidism
 Assessment, clinical manifestations, interventions and education
Excessive activity of thyroid gland,
High energy; High metabolism
Enlarged thyroid
High Blood Pressure
 Agitation, Confusion, Restlessness, Exophthalmos, Goiter, Extremely high temperature > 105,
HOT & sweaty skin (diaphoresis), Heat Intolerance, tachycardia 100+, Hypertension 180/100+
Heart palpitations + atrial fibrillation, High GI; diarrhea
PRIORITY!!!!Extreme High—Thyroid Storm
 HIGH calories (4,000-5,000/day), HIGH protein & carbs,‘Frequent” meals & snacks (6-8/day)
 AVOID: high fiber, caffeine (coffee, soda, tea), spicy food

Graves Disease (describe in detail) What has occurred in the body? (patho) (assessment,
Hyperparathyroidism)
Normally, the thyroid gets its production orders through thyroid-stimulating hormone (TSH), released by the
pituitary gland in the brain.
Graves' disease, a malfunction in the body's immune system releases abnormal antibodies that mimic TSH.
Spurred by these false signals to produce, the thyroid's hormone factories work overtime and exceed their
normal quota.
Autoimmune disorder: Antibody in serum causes thyroid cells to hyperfunction
Enlarged thyroid gland (goiter)
Manifestations of hyperthyroidism:Ophthalmopathy, proptosis (bulging, protrusion of an organ/area)
Fatigue, sleep difficulties, hand tremors, changes in menstruation
 Client complaints that would be characteristic of this disorder
Life-threatening event that occurs with uncontrolled hyperthyroidism due to Graves disease
Extreme state of hyperthyroidism with organ changes
Cardio-tachycardia, hypertension, chest pain, CHF, pulmonary edema: SOB
Neuro-agitation, anxiety, confusion, psychotic; seizures
GI-fever, increased vomiting/diarrhea; shock
Untreated hyperthyroidism or stressor/trigger
Rapid increase in metabolic rate
Rapid treatment essential
Hypothyroidism

Assessment, clinical manifestations, interventions, education
Assess:
Cold intolerance
Constipation
Signs of depression
Heart rate
Gland tenderness
Edema
Clinical manifestations below
 DIET:LOW calories, LOW cholesterol & saturated fats, FREQUENT rest periods!!!!
 AVOID: Narcotics ‘painkiller’, Vicodin, Morphine, Dilaudid, Fentanyl, Sedatives ‘anti-anxiety’,
Benzodiazepines: Lorazepam
L: Life Long: Long slow onset; 3-4 weeks till relief, Not a CURE; only treats
E: Early Morning; Empty Stomach;
 1 tablet daily 1 HOUR BEFORE breakfast! (not at night!
 NO doubling doses! If missed, take ASAP
 NEVER abruptly stop taking medication! Can lead to Myxedema Coma!
V: Very Hyper (High HR, BP, Temp.)
 Teach patients to report: ‘agitation/confusion’
 Oh Baby is Fine; Pregnancy safe:
 Myxedema coma (assessment, clinical manifestations, interventions and education for myxedema)
Clinical manif
myxedema, which is the physical appearance of the skin and subcutaneous tissues.
Myxedema is due to the accumulation of hydrophilic mucopolysaccharides in the dermis and other tissues.
This edema causes puffiness, facial and periorbital edema, and a masklike affect.
Individuals with hypothyroidism may describe an altered self-image related to their disabilities and altered
appearance.
The mental sluggishness, drowsiness, and lethargy of hypothyroidism may progress gradually or suddenly to a
notable impairment of consciousness or coma. This situation, termed myxedema coma, is a medical emergency.
Myxedema coma can be precipitated by infection, drugs (especially opioids, tranquilizers, and barbiturates),
exposure to cold, and trauma.
It is characterized by subnormal temperature, hypotension, and hypoventilation.
Cardiovascular collapse can result from hypoventilation, hyponatremia, hypoglycemia, and lactic acidosis.
For the patient to survive a myxedema coma, vital functions must be supported, and IV thyroid hormone
replacement must be administered.
Assess: Lethargy and fatigue, Weakness, muscle aches, paresthesias, Intolerance to cold, Weight gain, Dry
skin and hair, Loss of body hair, Bradycardia, Constipation, Generalized puffiness and edema around the
eyes and face, Forgetfulness and loss of memory, Menstrual disturbances, Cardiac enlargement, tendency to
develop congestive heart failure.
Interventions:
Monitor vital signs, including heart rate and rhythm.
Administer thyroid replacement, levothyroxine sodium (Synthroid) is most commonly prescribed.
Instruct the client about thyroid replacement therapy.
Instruct the client in low-calorie, low-cholesterol, low-saturated-fate diet.
Assess the client for constipation; provide roughage and fluids to prevent constipation.
Provide a warm environment for the client.
Avoid sedatives and narcotics because of increase sensitivity to these medications.
Monitor for overdose of thyroid medications, characterized by tachycardia, restlessness,, nervousness, and
insomnia.
Instruct the client to report episodes of chest pain immediately
Explain all medications, including dosage, potential side effects, and drug interactions. Instruct the patient to check the
pulse at least twice a week and to stop the thyroid supplement and notify the physician if the pulse is greater than 100
Teach the patient about the thyroid gland and hypothyroidism, as well as complications such as heart disease and
edema. Teach the patient that new cardiac or hyperthyroidism symptoms need to be reported immediately. Explain that
the caloric and fiber requirements vary. The patient should report any abnormal weight gain or loss or change in bowel
elimination
Treatments for hyper- and hypothyroidism:
Hyper
Hypo
SSKI methimazole
Hormone replacement
Sodium/potassium iodine
Levothyroxine/synthroid/levothroid
dexamethansone
B blockers
Propythiouracil
Irradation
Thyroidectomy
Radioactive Iodine Update What is the nurse’s role BEFORE and AFTER treatment? Why?
Destroys the Thyroid in 1 dose)
Toxic-patient becomes radioactive
BEFORE:
 Pregnancy Test (negative)
 REMOVE neck jewelry & dentures
 5-7 days before HOLD antithyroid medications
 Pt. is AWAKE; no anesthesia or conscious sedation
 NPO 2-4 hrs. BEFORE and 1-2 hrs AFTER
AFTER
 AVOID EVERYONE!NO pregnant people. NO crowds. NOT same restroom. NOT same food
utensils. NOT same laundry as your family. No cuddling. No kissing. No Sex

Thyroidectomy
o Assessment; priority before
Right patient, right procedure, consent signed, I don’t knowwww
????????
o after surgery
 Airway:
Laryngeal Stridor
Noisy Breathing
Hoarseness
Weak Voice
**PRIORITY**Endotracheal tube set up at bedside!!!
Breathing
Voice strength and quality
Circulation
Assess for bleeding! Neutral Head and Neck Alignment
NOT SUPINE! HOB 30-45 degree
NO flexing or Extending Neck!
Calcium (Below 8.6) Normal 8.6 – 10.2 Hypocalcemia Trousseau Chvostek Sign
Circumoral tingling Check for tingling of toes and fingers and around the mouth
Assessment of palpation of the thyroid gland (review concept in book!)
Glomerulonephritis
Inflammation of the small blood vessels in the kidneys, called glomeruli. These glomeruli are responsible for
removing waste, fluid and electrolytes from the bloodstream in order to transfer them into the urinary system for
excretion. This inflammation can also cause a disturbance in blood pressure. A urineanalysis indicates red cell
casts are present in the urine, and blood levels show increased levels of creatinine and urea
RISK FACTORS THAT PLACE AN INDIVIDUAL AT RISK FOR GLOMERULONEPHRITIS AND
KIDNEY STONES:
Dehydration
Diet, (high protein, high Nacl, high Ca)
Reduced urine volume
High levels of (uric acid, calcium, oxalate)
Infectious diseases such as TB or syphilis
Viral infections like Hep c or HIV
 Possible causes; manifestations of possible causes
Addisons Disease vs Cushings Syndrome:
Addisons: adrenal glans produce too little cortisol
and aldosterone
Cushings: body makes too much cortisol
Added tan: bronze pigmentation
Cushion: trunical obesity+moon face + buffalo hump
Added potassium: hyperkalemia
Unusual hair growth : hirsutism
Decreased weight: water loss = weight loss
Skin: purple striae, butterfly mark
Decreased bp, hair, sugar and energy
High sugar, bp, weight
Sodium loss: less than 135
Addisons cause: autoimmune, diseases like cancer, infections, TB/HIV
Cushings causes : prolonged steroid use, tumor (adrenal or pituitary), small lung cell cancer

Know the differences between the two (assessment, clinical manifestations, interventions, evaluation
and education.
Addisons:
Nursing Assessment, Fatigue, weakness, Weight loss, anorexia, nausea, vomiting, Postural hypotension,
Hypoglycemia, hyponatremia, hyperkalemia, Hyperpigmentation of mucous membranes and skin (only if
primary Addison disease, not seen in secondary Addison disease), Signs of shock, Loss of body hair,
Hypovolemia; (hypotension, tachycardia, fever)
interventions: Take vital signs frequently (q 15 minutes if in crisis), Monitor I & O and weigh dailyInstruct
client to rise slowly because of the possibility of postural hypotension, During Addison crises, administer IV
glucose with parenteral hydrocortisone, a steroid with both mineralocorticoid and glucocorticoid properties;
requires large fluid volume replacement,Monitor serum electrolyte levels, Maintain low-stress environment
(protect patient from noise, light, and temperature extremes because patient cannot physiologically cope with
stress)
teach: Need for lifelong hormone replacement,Need for close medical supervision, Need for Medic Alert
jewelry, Signs and symptoms of overdosage and underdosage of medication
Diet requirements: High sodium, low potassium, and high carbohydrate (complex carbohydrates)
Fluid requirements:Intake of at least 3L/fluid per day. Provide Ulcer prophylaxis
Cushings:
Patient health history Pituitary tumor; adrenal, pancreatic, or pulmonary neoplasms; GI bleeding; frequent
infections
Medications: Corticosteroids
Assess for: Malaise, Weight gain, Anorexia, Polyuria, Prolonged wound healing, Easy bruising, Weakness,
fatigue, Insomnia, poor sleep quality, Headache, Back, joint, bone, and rib pain, Poor concentration and
memory, Negative feelings, Amenorrhea, Impotence, decreased libido, Anxiety, Mood disturbances, Emotional
lability, Psychosis
Truncal obesity, Supraclavicular fat pads, Buffalo hump, Moon facies, Plethora, Hirsutism of body and face
Monitor vital signs, daily weight, glucose level.
Assess for possible infection: Because signs and symptoms of inflammation (e.g., fever, redness) may be
minimal or absent, assess for pain, loss of function, and purulent drainage.
Monitor for signs and symptoms of thromboembolic events such as pulmonary emboli (e.g., sudden chest pain,
Home health nurse
Wear MedicAlert bracelet at all times, Avoid exposure to extremes of temperature, infection, and stress, Teach
how to adjust medication and when to call health care provider, Lifetime replacement therapydyspnea,
tachypnea).
The overall goals are that the patient with Cushing syndrome will: Experience relief of symptoms, Avoid
serious complications, Maintain a positive self-image, Actively participate in the therapeutic plan
Appendicitis: inflammation of vermiform appendix (a wormlike blunt process extending from the cecum. Its
length varies from 7 to 15 cm. and its diameter is about 1 cm.), Affects over 5% of population, Can occur at any
age, but most common in children, Most treatment involves emergency abdominal surgery

Assessment, Clinical Assessment
Health history
 Current manifestations
 Pain; When did it begin? How does it feel? Pain scale
Most recent food or fluid intake
Known allergies, current medications
Chronic diseases
Physical examination
Vital signs
Apparent general health
Abdominal assessment
 Interventions
Promote effective respiratory gas exchange
Encourage client to turn, cough, and deep breathe
Encourage ambulation
Encourage client to splint incision with pillow when coughing
Encourage use of incentive spirometry or bubble blowing
Promote fluid volume balance
Monitor, continue IV infusion
Until bowel function returns
Offer water in small amounts
Offer clear fluids
Monitor for nausea
Monitor intake and output

Education


Pre-op care and education
Managing the patient who has manifestations of appendicitis focuses on preventing fluid volume deficit,
relieving pain, and preventing complications. To ensure the stomach is empty in case surgery is needed,
keep the patient NPO until the HCP evaluates the patient. Monitor vital signs and perform ongoing
assessment to detect any deterioration in condition. Give IV fluids, analgesics, and antiemetics as
ordered. Provide comfort measures.
Postoperative care for the patient who had an appendectomy is similar to the patient after a laparotomy
(see p. 935). Patients are usually discharged within 24 hours after an uncomplicated laparoscopic
appendectomy. Ambulation begins a few hours after surgery, and the diet is advanced as tolerated.
Those who had a perforation usually have a longer length of stay and need IV antibiotic therapy. Most
patients resume normal activities 2 to 3 weeks after surgery
 Pain Management (pre- and post-op)
Strong analgesics withheld preoperative because sudden disappearance of pain indicates perforation
 Assess pain: Administer analgesics as ordered, Assess effectiveness of medication
 30 minutes after administration
 Plan of Care
RN DX:
 Risk for Impaired Gas Exchange
 Risk for Deficient Fluid Volume
 Risk for Infection
 Acute Pain
 Anxiety
 Fear
POC evaluations
 Client demonstrates effective respiratory gas exchange
 Client will not develop secondary infection
 Client's pain is managed effectively
 Client, family verbalize understanding of condition
 Adequate hydration achieved/maintained
 Client experiences decreased fear, anxiety
 Possible Complications for client with appendicitis
If the appendix has ruptured and there is evidence of peritonitis or an abscess, giving parenteral fluids and
antibiotic therapy for 6 to 8 hours before the appendectomy helps prevent dehydration and sepsis.
 What is perforation?
Rupture of appendix: A break or tear in the appendix, usually due to appendicitis. Also called perforation of the
appendix. Rupture of appendix can lead to a periappendiceal abscess (a collection of infected pus) or diffuse
peritonitis (infection of the entire lining of the abdomen and the pelvis)

Perforated appendix: What is the purpose of a post-op drain in a patient who had a perforated appendix
and returns from surgery with a drain in place.
Patients who had appendectomy for complicated appendicitis are more prone to develop post-operative complications
such as peritoneal abscess or wound infection. Sometimes, abdominal drainage is used to reduce these complications.
peritoneal drain seems to reduce overall complication rate, re-intervention rate and readmission rate in patients treated
with perforated appendicitis
Crohn’s DiseaseInflammation of any segment of GI tract from mouth to anus. Usually affects terminal ileum
and ascending colon

Assessment
Past health history: Infection, autoimmune disorders
Medications: Antidiarrheal drugs
Health perception–health management: Family history of ulcerative colitis or Crohn’s disease. Fatigue, malaise
Nutritional-metabolic: Nausea, vomiting; anorexia. Weight loss
Elimination: Diarrhea. Blood, mucus, or pus in stools
Cognitive-perceptual: Lower abdominal pain (worse before defecation), cramping, tenesmus
Intermittent fever, emaciated appearance, fatigue
Integumentary: Pale skin with poor turgor, dry mucous membranes. Skin lesions, anorectal irritation, skin tags,
cutaneous fistulas
Abdominal distention, hyperactive bowel sounds, abdominal cramps
CardiovascularTachycardia, hypotension
Anemia, leukocytosis. Electrolyte imbalance, hypoalbuminemia, vitamin, and trace metal deficiencies. Guaiacpositive stool. Abnormal sigmoidoscopy, colonoscopy, and/or barium enema findings
 Clinical Manifestations
(diarrhea, weight, loss, abdominal pain, fever, and fatigue)
In Crohn's disease, diarrhea and cramping abdominal pain are common symptoms. If the small
intestine is involved, weight loss occurs from inflammation of the small intestine causing malabsorption.
Rectal bleeding sometimes occurs with Crohn's disease, although not as often as with ulcerative colitis.

Interventions
Observe and record stool frequency, characteristics, amount, and precipitating factors.
Observe for presence of associated factors, such as fever, chills, abdominal pain,cramping, bloody stools, emotional
upset, physical exertion and so forth.
Promote bedrest, provide bedside commode.
Observe for fever, tachycardia, lethargy, leukocytosis, decreased serum protein, anxiety, and prostration.
 Education (Why do these patients have chronic UTI’s)Fistula (patho & education)
Fistulas are abnormal connections between the intestines and adjacent organs or skin. When a fistula develops
between the intestine and the bladder or ureter, the result is frequent urinary tract infections and sometimes air
in the urine. Medications can be used to close certain fistulas. However, when there is a fistula from the
intestine to the bladder, surgery may be needed
Ulcerative Colitis:
 Assessment
Past health history: Infection, autoimmune disorders
Medications: Antidiarrheal drugs
Health perception–health management: Family history of ulcerative colitis or Crohn’s disease. Fatigue, malaise
Nutritional-metabolic: Nausea, vomiting; anorexia. Weight loss
Elimination: Diarrhea. Blood, mucus, or pus in stools
Cognitive-perceptual: Lower abdominal pain (worse before defecation), cramping, tenesmus
Intermittent fever, emaciated appearance, fatigue
Integumentary: Pale skin with poor turgor, dry mucous membranes. Skin lesions, anorectal irritation, skin tags,
cutaneous fistulas
Abdominal distention, hyperactive bowel sounds, abdominal cramps
CardiovascularTachycardia, hypotension
Anemia, leukocytosis. Electrolyte imbalance, hypoalbuminemia, vitamin, and trace metal deficiencies. Guaiacpositive stool. Abnormal sigmoidoscopy, colonoscopy, and/or barium enema findings
 clinical manifestations
In ulcerative colitis, the primary manifestations are bloody diarrhea and abdominal pain. Pain may
vary from the mild lower abdominal cramping associated with diarrhea to severe, constant pain associated with
acute perforations. With mild disease, diarrhea may consist of no more than four semi-formed stools daily that
contain small amounts of blood. The patient may have no other manifestations.
In moderate disease, the patient has increased stool output (up to 10 stools/day), increased
bleeding, and systemic symptoms (fever, malaise, mild anemia, anorexia).
In severe disease, diarrhea is bloody, contains mucus, and occurs 10 to 20 times a day.
In addition, fever, rapid weight loss greater than 10% of total body weight, anemia, tachycardia,
and dehydration are present.
 Interventions:
focus your attention on hemodynamic stability, pain control, fluid and electrolyte balance, and nutritional
support. Maintain accurate intake and output records. Monitor the number and appearance of stools. Assess
for the presence of blood in stools and emesis. Give IV fluids, electrolytes, analgesics, and antiinflammatory
drugs as prescribed. Monitor serum electrolytes, CBC, and vital signs, being alert for changes related to
diarrhea and dehydration. If the patient has orthostatic hypotension, teach the patient to change position
slowly and use safety precautions.Help the patient stay clean, dry, and free of odor until the diarrhea is
under control. Place a deodorizer in the room. Meticulous perianal skin care using plain water (no harsh
soap) with a moisturizing skin barrier cream prevents skin breakdown. Dibucaine, witch hazel, sitz baths,
and other soothing compresses or ointments may reduce perianal irritation and pain.
Calculate the adequacy of the daily calorie intake. Obtain a daily weight. Assess the abdomen, including
bowel sounds, as needed.
 Education
Crohn’s disease: High fiber and fruit intake associated with ↓ risk
Oral contraceptives and NSAIDS exacerbate symptoms
Ulcerative colitis: High vegetable intake associated with ↓ risk

What do you teach a patient about ‘allowing the bowel to rest?”
allows for an inflamed bowel to rest and heal. “It will reduce bowel movements, reduce the bulk to allow the
colon to rest, which can be a relief to some who may go to the toilet 20 to 30 times daily
nvolves giving your digestive system a break from eating any food by mouth, according to the Crohn's & Colitis
Foundation (CCFA). The idea is similar to staying off your foot to give a sprained ankle time to heal,
Know the differences between Crohn’s Disease and Ulcerative Colitis.
Ostomies:
 What is a colostomy?
surgical operation in which a piece of the colon is diverted to an artificial opening in the abdominal wall so as to
bypass a damaged part of the colon
 What is an ostomy?
Ostomy-surgically created opening between the intestine and the abdominal wall that allows the passage of
fecal material
 Why are these created in patients?
Infection of the abdomen, such as perforated diverticulitis or an abscess.
Injury to the colon or rectum (for example, a gunshot wound).
Partial or complete blockage of the large bowel (intestinal obstruction).
Rectal or colon cancer.
Wounds or fistulas in the perineum
 What should an ostomy look like on assessment? Beefy red. stoma should be rosy pink to red and mildly
swollen. A dusky blue stoma indicates ischemia; a brown-black stoma indicates necrosis
 What does the stool output look like, depending on their placement?
Ascending will be liquid. Transverse will be more formed and descending should be formed
 Can a patient with an ostomy swim? Why or why not?
Ostomy.org
pouching system is resistant to water and with a proper fit, it is designed not to leak.

Education for a patient who is being discharged home with an ostomy?

What would you include in the plan of care?
NG tubes:


Describe how to insert an NG tube? What position will you place your patient in?
What is the RN’s scope of practice in managing NG tubes?Assessment of placement; how does the RN
assess for correct placement?
1. Verify dr orders.Perform hand hygiene.
2. Gather the necessary equipment and supplies.
3. Provide for the patient’s privacy.Introduce yourself to the patient and family, if present.
4. Identify the patient using two identifiers,
5. Explain the procedure to the patient
6. Position the patient upright in the high Fowler’s position, unless contraindicated. If the patient is
comatose, raise the head of the bed, as tolerated, into the semi-Fowler’s position. If necessary,
have NAP help with the positioning of confused or comatose patients. If the patient must lie
supine, place him or her in the reverse Trendelenburg position.
7. Apply the pulse oximeter, and measure the patient’s vital signs.Assess the patency of each nare.
8. To determine the length of the tube to be inserted, measure the distance from the tip of the nose to the
earlobe, and then from the earlobe to the xiphoid process of the sternum.
a. Adults: Add 10 cm (4 inches) to ensure gastric placement. Mark the required tube length with
tape or indelible ink.
b. Children: Add half the distance from the xiphoid process to the umbilicus to this measurement to
place the tube more distally in the stomach. Mark the required tube length with tape or indelible
ink.
9. Apply clean gloves.
10. Prepare the NG or nasoenteric tube for intubation:
a. Using a 30-mL to 60-mL catheter-tip syringe, inject 10 mL of water into the tube. If you are
using a stylet, make certain it is securely positioned within the tube.
11. Explain the procedure to the patient, and then gently insert the tube through one nostril to the back of the
throat (posterior nasopharynx), aiming back and down toward the ear. The patient may gag.
12. As the tube passes the nasopharynx, have the patient bend his or her head toward the chest.
13. If drinking water is not contraindicated and the patient prefers, provide small sips of water along with
encouragement to swallow as the tube is inserted and advanced. Advance the tube as the patient
swallows. Emphasize that the patient needs to mouth breathe and swallow throughout the procedure.
14. When the tip of the tube is approximately 25 cm to 30 cm (10 inches to 12 inches), assess for air coming
out of the tubing. If the tube entered the trachea instead of the esophagus, air exchange may be heard. If
air is present, withdraw the tube and start again. If there is no air, continue to advance the tube to the
distance marker.
15. Check the tube position at the back of the patient’s throat with a penlight and tongue blade. Ensure the
tube is not coiled in the posterior pharynx.
16. Anchor the tube to the patient’s cheek with tape.Clamp the tube.
17. Once the placement of the NG tube has been verified, secure it to the patient’s face. Anchor the tube to
the patient’s nose, avoiding pressure on the nares. Mark the exit site on the tube with tape or indelible
ink. Select one of the following options for anchoring:
18. Obtain a chest or abdominal x-ray to verify placement.
19. Apply clean gloves, and administer oral hygiene. Clean the tubing at the nostril with a washcloth
dampened in mild soap and water.
20. Dispose of used supplies.
21. Remove and dispose of used gloves. Perform hand hygiene.
22. Help the patient into a comfortable position, and place toiletries and personal items within reach.
23. Place the call light within easy reach, and make sure the patient knows how to use it to summon
assistance.
 (what are you able to do that falls within the RN scope of practice)
Observe the patient to determine his or her response to intubation. Have the patient speak.
Check the patient’s vital signs and oxygen saturation.
Confirm the x-ray results.
Remove the stylet, if used, after x-ray verification of the correct placement of the tube.
Routinely assess the location of the external exit site marking or tape on the tube. If the tube is dislodged or
must be repositioned, assess and obtain radiologic confirmation before restarting feedings.
Once initial placement has been verified, confirm correct tube placement at least once each shift and before
administering any fluid or medication into the tube.7
Routinely assess the color and pH of fluid withdrawn from the tube.
Routinely assess the condition of the naris and mucosa for skin breakdown, inflammation, and excoriation.
Wound Healing:
 Education to family/clients
Because patients are being discharged earlier after surgery and many have surgery as outpatients, it is important
that the patient and caregiver know how to care for the wound and perform dressing changes. Wound healing
may not be complete for 4 to 6 weeks or longer.
Drug-specific side effects and adverse effects, as well as methods to prevent side effects, should be reviewed
with the patient.
Awareness of the necessity to continue the drugs (i.e., antibiotics) for the specified time is an important point to
teach the patient.
 What promotes wound healing?
Wound healing is facilitated by protein, carbohydrates, and B vitamins.
Calcium, and zinc also encourage healing
Vitamins A, B and C
Snacks made from milk, eggs, sugar and vanilla
Custard, cottage cheese, peaches, yogurt

What factors delay wound healing?
Infection, Age of Patient. There are many overall changes in healing capacity that are related to age. ... Type
of Wound. The characteristics of a wound can affect the speed of wound healing. Infection. Chronic
Diseases. Poor Nutrition. Lack of Hydration. Poor Blood Circulation. Edema.


Describe different types of inflammatory exudate
Serous




o Thin, watery drainage seen in the early stages of inflammation (ie; skin blisters)
Sanguinous
o Fresh blood that is prevalent among deep wounds of full and partial thickness
o During the inflammatory stage, a small amount of this bloody leakage is natural
Serosanguineous
o Midpoint in healing; frequently seen post-operatively. composed of RBCs and serous fluid;
semi-clear pink and may have red streaks
Hemorrhagic
o Bloody drainage
Purulent (pus)
o Consists of WBCs, liquefied dead cells, microorganisms and other debris that signal an infection
 Primary intention
Wound edges are stapled or sutured, and healing occurs until the contraction of the healing area closes the
defect and brings the skin edges closer together to from a mature scar
 Initial phase
 Granulation phase
 Maturation phase and scar contraction
 Secondary intention
Wound is left open and heals from the edges inward and from the bottom up
Extensive wound with tissue loss
Edges that cannot/should not be approximated
Wounds (NOT infected) are open and heal by granulation
 Tertiary intention
The contaminated wound is left open and closed after the infection is controlled
Occurs with an open ragged-edged wound in which the secondary healing became infected
Wound left open for 3–5 days then sometimes, are closed
Allows edema, infection to resolve, wound to drain
Also heals by granulation
 What are some possible complications to wound healing?
Shape and location of wound determine how well wound will heal
Adhesions, Contractions, Dehiscence, Evisceration, Fistula Formation, Infection, Hemorrhage, Hypertrophic
Scars, Keloid Formation
Excess Granulation tissue complications
 What is ‘Dehiscence?’
Splitting or bursting open. Obesity is a risk factor. Vomiting and coughing. These increase the intraabdominal
pressure. During granulation phase, Wound is pink and vascular; the wound is friable and at risk for dehiscence.
 Education to post-op patients to reduce the risk of dehiscence?
Limit activity, proper wound care. infection causing an inflammatory process
• Granulation tissue not strong enough to withstand forces imposed on wound
• Obesity, because adipose tissue has less blood supply and may slow healing
• Pocket of fluid (seroma, hematoma) developing between tissue layers and preventing the edges of the wound
from coming together
 Dehisced wounds (assessment, {measurement, what does it look like? Drainage? Odor? Redness?}
Wound measurements are made in centimeters. The first measurement is oriented from head to toe, the
second is from side to side, and the third is the depth (if any). If there is any tunneling (when cottontipped applicator is placed in wound, there is movement) or undermining (when cotton-tipped applicator
is placed in wound, there is a “lip” around the wound), this is charted in respect to a clock, with 12
o’clock being toward the patient’s head.
 Wound drainage devices:What is a Jackson-Pratt drainage system?
Sometimes drains are inserted into the wound to facilitate removal of fluid. The Jackson-Pratt drain is a suction
drainage device consisting of a flexible plastic bulb connected to an internal plastic drainage tube.

Assessment of the drain and the fluid? (site, skin care, color of fluid?
Pressure Ulcers:Risk factors


Assessment,
Assess pressure ulcer risk on admission and at periodic intervals based on the patient’s condition
o Thorough head-to-toe on admission
o Periodic reassessment
o Inspect
o Palpate
o Document
o Location
o Size, presence of undermining
o Stage
o Color of wound bed, location of necrosis or eschar
o Condition of wound margins
 clinical manifestations,
 interventions and evaluation
Overall Goals
No deterioration of the ulcer
Reduce contributing factors
Not develop an infection
Have healing
Have no recurrence
Use devices to reduce pressure and shearing force (e.g., low-air-loss mattresses, foam mattresses, wheelchair
cushions, padded commode seats, boots [foam, air], lift sheets) as appropriate
 Remove excessive moisture
 Avoid massage over bony prominences
 Use lift sheets




Education for prevention of pressure ulcers
Providing nutrition
Maintaining skin hygiene
Avoiding skin trauma
o Crumb free sheets/bed
o Smooth, firm, wrinkle-free foundation
o Frequent shifts in position
 Correct positioning, transfer, turning
 At least every 2 hours when client confined to bed
o Proper lifting

Define and list the assessment and clinical manifestations and what is expected for the skin to look like
in: Stage I, Stage II and Stage III
1. Pressure Injury stage 1: Non-Blanchable Erythema of Intact Skin
Intact skin with a localized area of non-blanchable erythema, which may appear differently in dark skin.
Blanchable erythema or changes in sensation, temperature, or firmness may precede visual changes.
2. Pressure Injury stage 2 : Partial-Thickness Skin Loss With Exposed Dermis
Partial-thickness loss of skin with exposed dermis. The wound bed is viable, pink or red, and moist. May
present as an intact or ruptured serum-filled blister. Adipose and deeper tissues are not visible. Often
result from adverse microclimate and shear in the skin over the pelvis and shear in the heel.
3. Pressure Injury stage 3: Full-Thickness Skin Loss
Full-thickness loss of skin, in which adipose is visible in the injury. Granulation tissue and epibole
(rolled wound edges) are often present. Slough and/or eschar (types of dead tissue) may be visible. The
depth of tissue damage varies by anatomical location; areas of significant adiposity can develop deep
wounds. Undermining and tunneling may occur.


Treatments and manifestations for Stage I, Stage II, Stage III pressure ulcers
Select the appropriate pressure-relieving technique (e.g., pad, overlay, mattress, specialty bed) to relieve
pressure and keep the patient off of the pressure ulcer.
 Whenever possible, do not turn the patient onto a body surface that is still reddened.
 Massage is contraindicated in the presence of acute inflammation and where there is the possibility of
damaged blood vessels or fragile skin.
 A pressure ulcer that has necrotic tissue or eschar (except for dry, stable necrotic feet or heels) must
have the tissue removed by surgical, mechanical, enzymatic, or autolytic debridement methods.
 Clean pressure ulcers with noncytotoxic solutions (e.g., normal saline) that do not kill or damage cells,
especially fibroblasts. Solutions such as Dakin’s solution (sodium hypochlorite solution), acetic acid,
povidone-iodine, and hydrogen peroxide (H2O2) are cytotoxic and therefore should not be used to clean
pressure ulcers.
 Keep a pressure ulcer slightly moist, rather than dry, to enhance re-epithelialization.
It is important to use enough irrigation pressure to adequately clean the pressure ulcer (4 to 15 psi) without
causing trauma or damage to the wound. To obtain this pressure, a 30-mL syringe and a 19-gauge needle can be
used
 Stage I
 Skin prep, granules
 Hydrocolloid dressing
 Transparent dressing
 Stage II
 Transparent dressing
 Hydrocolloid dressing
 Stage III
 Wet-to dry gauze dressing with sterile NS
 *Dry gauze will stick to the new granulation tissue, causing more damage.
 Hydrocolloid dressing
 Proteolytic enzymes
 Stage IV
 Wet-to dry gauze dressing with sterile NS
 Vacuum-assisted closure (VAC)

Signs of healing in pressure ulcers (assessment of patient, assessment of skin, size of ulcer)
For wounds healing by primary intention, key assessment factors include the approximation of wound margins (the
edges of the wound fit together snugly), drainage (a closed incision should not have any drainage), evidence of infection
and the presence of a palpable healing ridge along the incision by the fifth postoperative day. This confirms that
granulation tissue is forming, which is necessary for wound healing.
For open wounds healing by secondary intention, key assessment factors include the location, dimension and
depth of tunneling, the appearance of the wound base and the status of surrounding tissue. The approximation of
the wound edges are an important factor to evaluate as well.
Continue the wound assessment by describing the condition, color and temperature. Use correct terminology to
describe your findings, such as ecchymosed (bruised), erythematous (red), indurated (firm), edematous (swollen).
Note the amount, color and consistency of wound drainage (exudate).
Drainage can be serous (clear), serosanguinous (blood-tinged) or sanguinous (bloody). Drainage from heavily
colonized wound may have a tan or milky appearance.
Odor in wounds is a significant diagnostic tool. Blue-green drainage combined with a musty odor usually
indicates presence of Pseudomonas in the wound.
The sore will get smaller. Pinkish tissue usually starts forming along the edges of the sore and moves toward the
center; you may notice either smooth or bumpy surfaces of new tissue. Some bleeding may be present. This
shows that there is good blood circulation to the area, which helps healing.
 Education to family/client about home care (importance of ongoing dressing changes and wound care
Repositioning is the primary method of reducing the risk for pressure injury. Pressure relief schedules should be
developed. Pressure-reducing devices (e.g., foam mattress, padded commode, wheelchair seats) may be used
but are not be a substitute for repositioning. In addition, develop a nutrition care plan based on the patient’s
nutritional and hydration needs, feeding route, and care goals.
Clinician Expertise. You know patients with pressure injury should be repositioned at least every 2 hours while
in bed and every hour when in a chair.