Wednesday, March 28, 2012

Difficult Patients


Every nurse will eventually get a difficult patient on their list of responsibilities. These patients can be mentally, physically, and emotionally combative in many different environments. Consequently, care of these patients should be conducted in a manner for personal and self-protection of the nurse.  Some of the key guidelines are as follows:


1.  Never allow yourself to be cornered in a room with the patient positioned between you and the door.
2.  Dont escalate the tension with verbal bantering. Basically, dont argue with the patient or resident.
3.  Ask permission before performing any normal tasks in a patients room whenever possible.
4.  Discuss your concerns with other nursing staff.  Consult the floor supervisor if necessary, especially when safety is an issue.
5.  Get help from other support staff when offering care. Get a witness if you are anticipating abuse of any kind.
6.  Remove yourself from the situation if you are concerned about your personal safety at all times.
7.  If attacked, defend yourself with the force necessary for self-protection and attempt to separate from the patient.
8.  Be aware of the patients medical and mental history prior to entering the patients room.
9.  Dont put yourself in a position to be hurt.

10. Get the necessary help for all transfers, bathing and dressing activities from other staff members for difficult patients.
11. Respect the resident and patients personal property.

12. Get assistance quickly, via the call bell or vocal projection, if a situation becomes violent or abuse.
 13. Immediately seek medical treatment if injured.
14. Fill out an incident report for proper documentation of the occurrence.

15. Protect other patients from abusive behavior.






ECG lecture for download





The Nclex also asks on ECG interpretation, so here is a powerpoint lecture for you to download
hope this helps
ecg powerpoint click here    

Feel free to ask me questions regarding ECG readings

Drug mnemonic


DRUG mnaemonic
Morphine: side-effects MORPHINE:
Myosis
Out of it (sedation)
Respiratory depression
Pneumonia (aspiration)
Hypotension
Infrequency (constipation, urinary retention)
Nausea
Emesis

Tricyclic antidepressants: members worth knowing
"I have to hide, the CIA is after me":
Clomipramine Imipramine Amitrptyline
· If want the next 3 worth knowing, the DNDis also after me:
Desipramine Norrtriptyline Doxepin

Patent ductus arteriosus: treatment
"Come In and Close the door": INdomethacin is used to Close PDA

SIADH-inducing drugs ABCD:
Analgesics: opioids, NSAIDs
Barbiturates
Cyclophosphamide/ Chlorpromazine/ Carbamazepine
Diuretic (thiazide)

Vir-named drugs: use"-vir at start, middle or end means for virus": · Drugs:
Abacavir,
Acyclovir,
Amprenavir,
Cidofovir,
Denavir,
Efavirenz,
Indavir,
Invirase,
Famvir,
Ganciclovir,
Norvir,
Oseltamivir,
Penciclovir,
Ritonavir,
Saquinavir,
Valacyclovir,
Viracept,
Viramune,
Zanamivir,
Zovirax.

Phenobarbitone: side effects
Children are annoying (hyperkinesia, irritability, insomnia, aggression).
Adults are dosy (sedation, dizziness, drowsiness).

Thrombolytic agents USA:
Urokinase Streptokinase Alteplase (tPA)



Narcotic antagonists
The Narcotic Antagonists are NAloxone and NAltrexone. · Important clinically to treat narcotic overdose.


Routes of entry: most rapid ways meds/toxins enter body
"Stick it, Sniff it, Suck it, Soak it":
Stick = Injection
Sniff = inhalation
Suck = ingestion
Soak = absorption

Anticholinergic side effects
"Know the ABCD'S of anticholinergic side effects":
Anorexia
Blurry vision
Constipation/ Confusion
Dry Mouth
Sedation/ Stasis of urine


Atropine use: tachycardia or bradycardia
"A goes with B": Atropine used clinically to treat Bradycardia.


Aspirin: side effects ASPIRIN:
Asthma
Salicyalism
Peptic ulcer disease/ Phosphorylation-oxidation uncoupling/ PPH/ Platelet disaggregation/ Premature closure of PDA
Intestinal blood loss
Reye's syndrome
Idiosyncracy
Noise (tinnitus)


Morphine: effects at mu receptor PEAR:
Physical dependence
Euphoria
Analgesia
Respiratory depression

Beta-1 vs Beta-2 receptor location "You have 1 heart and 2 lungs":
Beta-1 are therefore primarily on heart. Beta-2 primarily on lungs.

SSRIs: side effects SSRI:
Serotonin syndrome
Stimulate CNS
Reproductive disfunctions in male
Insomnia


Warfarin: action, monitoring WePT:
Warfarin works on the extrinsic pathway and is monitored by PT.


Propranolol and related '-olol' drugs: usage"olol" is just two backwards lower case b's. Backward b's stand for "beta blocker". · Beta blockers include acebutolol, betaxolol, bisoprolol, oxprenolol, propranolol.


Depression: 5 drugs causing it PROMS:
Propranolol
Reserpine
Oral contraceptives
Methyldopa
Steroids

Lead poisoning: presentation ABCDEFG:
Anemia
Basophilic stripping
Colicky pain
Diarrhea
Encephalopathy
Foot drop
Gum (lead line)


Cholinergics (eg organophosphates): effects
If you know these, you will be "LESS DUMB":
Lacrimation
Excitation of nicotinic synapses
Salivation
Sweating
Diarrhea
Urination
Micturition
Bronchoconstriction

Benzodiazepines: actions
"Ben SCAMs Pam into seduction not by brain but by muscle":
Sedation
anti-Convulsant
anti-Anxiety
Muscle relaxant
Not by brain: No antipsychotic activity.


Teratogenic drugs "W/ TERATOgenic":
Warfarin
Thalidomide
Epileptic drugs: phenytoin, valproate, carbamazepine
Retinoid
ACE inhibitor
Third element: lithium
OCP and other hormones (eg danazol)

Gynaecomastia-causing drugs DISCOS:
Digoxin
Isoniazid
Spironolactone
Cimetidine
Oestrogens
Stilboestrol

Osmotic diuretics: members GUM:
Glycerol
Urea
Mannitol


Antibiotics contraindicated during pregnancy MCAT:
Metronidazole
Chloramphenicol
Aminoglycoside
Tetracycline


Lithium: side effects LITH:
Leukocytosis
Insipidus [diabetes insipidus, tied to polyuria]
Tremor/ Teratogenesis
Hypothyroidism

Endocrine system


Pancreas –   Endocrine and Exocrine gland

Hormones produced

Insulin     

  • Decrease blood sugar by
  1. Stimulating active transport of glucose into muscle and adipose tissue
  2. Promoting the conversion of glucose to glycogen for storage
  3. Promoting conversion of fatty acids into fat
  4. Stimulating protein synthesis

          Glucagon

Increases blood sugar by promoting conversion of glycogen to glucose

  • Beta cells of Islets of langerhans
  • Insulin
  1. Transcellular membrane transport of glucose
  2. Inhibits breakdown of fats and protein
  3. Requires Na for transport of glucose
Diabetes Mellitus – is a metabolic disease characterized by elevated levels of  glucose in the blood, resulting from defects in insulin secretion , insulin action or both

Manifestations
1)      Polyuria
2)      Polydypsia
3)      Polyphagia
4)      Weight loss

Diagnostic test

FBS ( Fasting Blood Sugar )  = or > than 126 mg/dl ( 7.0 mmol/L)  on two separate occasion
Normal –  < 100 mg/dl ( < 5.6 mmol/L)
Impaired Fasting Glucose – 100 –125 mg/dl (5.6-6.9 mmol/L)
2 Hours post prandial blood sugar  - Following ingestion of 75 gm of glucose  = or >  200mg/dl
                                                                                                                                        11.1mmol/L
Oral Glucose Tolerance test (OGTT/GTT)
  • Initial urine and blood specimen are collected
  • 150 – 300 g of CHO/p.o.

Series of blood specimen is collected

·        30 min
·        1 hour
·        2 hours – returns to Normal
·        3,4,5 as required

Done when results of FBS/ 2 hours PPBS are borderline ( High normal)
Glycosylated Hgb
  • Most accurate
  • Reflects sugar levels for the past 3 – 4 mos
Normal 4- 6 %
Cause – Unknown

Predisposing factors

  • Stress – Stimulates secretion of epinephrine , norephineprine , glucocorticoids
                 
  • Heredity
  • Obesity
  • Viral Infection
  • Autoimmune disorders
 TYPES
 Type I  ( 5%-10 % )
  • IDDM
  • Onset any age ( < 30 yrs)
  • Often have islet cells antibody
  • Absolute Insulin deficiency
  • Prone to DKA
  • Often have antibodies to insulin even before insulin treatment
 Type II ( 90 %- 95%)
·        Onset usually over 30 years
·        Usually obese at diagnosis
·        Causes include obesity, heredity or environmental factors
·        No islet cell antibodies
·        Decrease in endogenous insulin, or increased with insulin resistance
·        Most patients can control blood glucose through weight loss if obese
·        Oral antidiabetic agents may improve blood glucose levels if dietary modification and exercise are unsuccessful
·        May need insulin on a short or long term basis to prevent hyperglycemia
·        Ketosis, rare, except in stress or infection
 ·        Gestational Diabetes
  • Onset during pregnancy, usually in the second or third trimester
  • Due to hormones secreted by the placenta, which inhibit the action of insulin
  • Above-normal risk for perinatal complications, especially macrosomia (abnormally large babies)
  • Treated with diet, if needed, insulin to strictly maintain normal blood glucose levels
  • Occurs in about 2%-5% of all pregnancies
  • Glucose intolerance transitory but may recur:
-         In subsequent pregnancies
-         30%-40% will develop overt diabetes (usually type 2) within 10 years (esp. if obese)
  • Risk factors include obesity, age older than 30 years, family history of diabetes, previous large babies (over 9 lb.)
  • Screening tests (glucose challenge test) should be performed on all pregnant women between 24 and 28 weeks gestation
Causes of Morning Hyperglycemia
1.      Dawn Phenomenon-  characterized by a relatively normal blood glucose level when blood glucose level begins to rise.  The phenomenon is thought to result from nocturnal surges in growth hormone secretion that create a greater need for insulin in the early morning hours in patient with Type 1
2.      Somogyi Effect-  normal or elevated blood glucose at bedtime, a decrease at 2-3 am to hypocglycemic levels and subsequent increase caused by the production of counter regulatory hormones
Medications
A.     OHA (Oral Hypoglycemic Agents)
  
          1.  Sulfonylureas
-   Directly stimulating the pancreas to secrete insulin.  These agents improve insulin action at the cellular level.  The common side effects are GI symptoms and dermatologic reactions
Ex.  1st generation: Acetohexamide, chlorpropamide, tolazamide, tolbutamide
        2nd generation:  glipizide, glyburide, glimeperide

           2.  Biguanides
        -  produces its antidiabetioc effects by facilitating insulin’s action on peripheral receptor sites.  Have no effect on pancreatic beta cells.  Biguamides used with sulfonylurea may enhance the glucose lowering effect more than either medication used alone.
         Ex.  Metformin, glucophage
       3. Apha Glucosidase Inhibitors
  they work by delaying the absorption of glucose in the intestinal system resulting in a lower postprandial blood glucose level. 
         Ex. Acarbose
4. Thiazolidineones
     -  they are indicated for patients with Type 2 diabetes who take insulin injections and whose blood glucose control is inadequate.  Enhance insulin action at the receptor sites without increasing insulin secretions from beta cells.  Women should be informed can cause resumption of ovulation in peri-menopausal, anovulatory women.
      Ex.  Pioglitazone
              Rosiglitazone
5. Meglitinides
     -  lowers the blood glucose level by stimulating insulin release from beta cells. 
      Ex.  Repaglinide
            Nateglinide


.  Insulin
     1.  Rapid-Acting: Clear Insulin
-         Regular
-         Humulin-R
-         Semilente
-         Crystalline zinc
-         Actrapid
-         Onset: 30 mins- 1 hr.
-         Peak: 2-4 hrs.
-         Duration: 6-8 hrs.
    2.  Intermediate-Acting: cloudy
-         NPH
-         Humulin-N
-         Lente
-         Monotard
-         Onset: 1-2 hrs
-         Peak: 6-8 hrs.
-         Duration: 18-24 hrs.
  1. Long-Acting: cloudy
-         PZI
-         Ultralente
-         Onset: 3-4 hrs.
-         Peak: 16-20 hrs.
-         Duration: 30-36 hrs.


 Health Teaching
1.      Foot care:  daily cleanse feet in warm, soapy water; rinse and dry carefully; inspect, don’t break blisters; trim nails to follow natural curve of toe;  always wear breathable shoes such as leather; no crossing of the legs; no cream between toes; inspect visually daily  NCLEX
2.      Injection techniques (intra site rotation)
3.      Dietary management
4.      Quit smoking
Stress management (stress increases blood sugar)

PITUITARY GLAND: HORMONES PRODUCED AND FUNCTIONS

- controlled primarily by the hypothalamus; termed “master gland” as it directly affects the function of other endocrine glands

Anterior Lobe
  1. Adrenocorticotropic hormone (ACTH)- concerned with growth and secretory activity of adrenal cortex, which produces steroids
  2. Thyrotropic hormone (TSH) – for growth and secretory activity of thyroid; controls release rate of thyroxine, which controls rate of most chemical reaction in the body; target is thyroid gland
  3. Somatotropic hormones (STH or GH)-  promote growth of body tissue
  4. Gonadotropic hormones and estrogen secretion; follicle stimulating hormone (FSH)-  stimulate development of ovarian follicles; semeniferous tubules and sperm maturation
  5. Luteinizing hormone (LH)- works with FSH in final maturation of follicles; promotes ovulation and progesterone secretion
  6. Prolactin-  for milk production
  7. Melanocyte stimulating hormone (MSH)- produces the characteristic skin darkening

Posterior Lobe
  1. Vasopressin (ADH)- influnces water absorption by kidney
  2. Oxytocin-influences the menstrual cycle, labor and lactation

Disorders of Anterior Pituitary


1.  Acromegaly-  hypersecretion of GH that occurs in adulthood; commonly associated with benign pituitary tumors

Manifestations:
a. Enlargement of external extremeties (e.g. nose, jaw, hands, feet)
    NCLEX  - assessment question “ are you buying larger size shoes”
                      One of the earliest manifestation is increase in shoe size
b. Protrusion of the jaw and orbital ridges
c.  Coarse features
d.  Visual problems, blindness
e.  Hyperglycemia, insulin resistance
f.   Hypercalcemia

Treatment


a.  Irradiation of pituitary
b.  Transphenoidal hypophysectomy:  removal of pituitary gland
   1. Assess for signs of increased cranial pressure- signs of adrenal insufficiency,   
        hypothyroidism and temporary diabetes insipidus
   2. Elevate head of bed 30 degrees
1.      Avoid coughing, sneezing, blowing nose
2.      Check for CSF in nasal packing
c.  Bromocriptine (Parlodel) with surgery or radiation

Nursing Interventions

a..  Provide emotional support
b.      Directed toward symptomatic care

2.  Gigantism- hypersecretion of GH that occurs in childhood

Manifestations:
a.  Proportional overgrowth in all body tissue
b.  Overgrowth of long bones: height in childhood may reach 8 or 9 feet
c.  Teaching and nursing responsibilities same with acromegaly

3.  Dwarfism-  hyposecretion of GH during childhood

Manifestations:
a.       Retarded symmetrical physical growth
b.      Premature body aging processes
c.       Slow intellectual development

Treatment

1.  Removal of the causative  factor (for ex. Tumors)
2.      Human growth hormone injections (HGH)

Nursing Responsibilities- same with acromegaly

Disorders of Posterior Pituitary


1.  Diabetes Insipidus-  hyposecretion of ADH, due to a tumor or damage of the posterior lobe of the pituitary; may be idiopathic; may be genetic; very common following neurosurgery or head trauma

Manifestations
a.  Polyuria
b.  Polydipsia
c.  Hypernatremia
d.  Weight loss
e.  Dehydration/dry skin

Treatment

a.  Desmopressin acetate (DDAVP) nasal spray
b.  Vasopressin tannate (Pitressin Tannate) in Oil (IM for chronic severe cases)
c.  Lypressin (diapid) nasal spray

Nursing Interventions

1.  Maintain adequate fluids
2.  Avoid foods with diuretic-type action
3.  Monitor intake and output: report any changes; can sometimes have 800mL output per hour
4.  Daily weights
5.  Specific gravity (should be greater that 1.004)

2.  Syndrome of Inappropriate Antidiuretic Hormone (SIADH)-  inappropriate, continued release of antidiuretic hormone resulting in water intoxication; caused by neoplastic tumors, respiratory disorders, drugs

Manifetstions
a.  Mental confusion/irritability
b.  Lethargy/seizures
c.  Dilutional hyponatremia
d.  Weight gain
e.  Anorexia, nausea and vomiting
f.  Weakness

Treatment
a.  Fluid restriction (less than 500 mL/24 hrs) with hypertonic solutions to treat the hyponatremia
2.  Strict intake and output
3.  Treat underlying cause (surgery, radiation, chemotherapy)
4.  diuretics
5.  Daily weight


Adrenal Gland

Disorders of Adrenal Cortex

  1. Addison’s disease- hyposecretion of adrenal cortex hormones, (insufficiency of cortisol, aldosterone and androgen); discontinuing steroid medication abruptly without weaning off them
Causes
1)     Autoimmune or idiopathic atrophy of the adrenal glands
2)     Surgical removal of Adrenal glands
3)     Infection ( Tuberculosis , Histoplasmosis)
4)     Decreased ACTH

Manifestations
a.  Slow, insidious onset
b.  Malaise and generalized weakness from increased potassium restriction
c.  Hypotension, hypovolemia from increased sodium excretion
d.  Increase pigmentation of the skin- “eternal tan”
e.  Anorexia, nausea, vomiting
f.  Electrolyte imbalance (hyponatremia, hyperkalemia)
g. Weight loss
h. Loss of libido
i.  Hypoglycemia
j.  Personality changes

Treatment

a.  Lifelong steroid replacement; hydrocortisone (Florinef); complications of long-term steroid therapy include osteoporosis
b.  High protein, high carbohydrate diet may increase sodium intake ( low potassium intake)
c.  Monitor fluid and electrolytes routinely
d.      Decrease emotional and physical stress

Nursing Interventions

a.  Observe for Addisonian crisis (sudden extreme weakness; severe abdominal, back and leg pain; hyperpyrexia; coma; death)
b.  Observe for side effects of hormone replacement
c.   Provide emotional support
d.  Teaching (lifelong medications, prompt treatment of infection, illness, stress management)
e.  Monitor fluid and electrolyte balance regularly

NCLEX- Common Complication is Shock

CGFNS – Initial manifestation , Hypotension, Bronze skin.

2.  Cushing’s Syndrome-  hypersecretion of the glucocorticoids; overdose of steroid medications

Manifestations

a.  Central-type obesity, moon face, buffalo hump and obese trunk with thin extremities
b.  Mood swings
c.  Malaise and muscular weakness (increase preotein catabolism)
d.  Masculine characteristics in females (hirsutism)
e.  Hypokalemia (may cause arrythmias)
f.  Hyperglycemia (insulin resistant)
g.  Hypertension (edema; may lead to CHF or CVAs)
h.  Acne (striae on chest, abdomen, legs)
i.  Amenorrhea
j.  Osteoporosis; thin skin with ecchymosis
k.  Increased susceptibility to infections
l. Peptic ulcer

Treatment

a.  Adrenalectomy: unilateral or bilateral
b.  Chemotherapy:  bromocriptine (Parlodel) ; mitotane (Lysodren), or aminoglutethimide (Cytadren)
c.  High-protein, low-carbohydrate, low sodium diet with potassium supplement

Nursing Interventions

a.  Protect from infection
b.  Protect from accidents and falls due to osteoporosis
c.  Client education concerning lifelong self-administration of hormone suppression therapy

Steroid replacement (similar to Cushing’s syndrome but in lesser effect)
Purpose:
a.  anti-inflammatory and anti-allergic reaction
b.  Enables one to tolerate high degree of stress

Indications:
a.  Crisis (fro ex. Shock, bronchial obstruction)
b.  Long-term therapy (for ex. Post-adrenalectomy, arthritis, leukemia)

3.  Aldosteronism (Conn’s syndrome)- hypersecretion of aldosterone from adrenal cortex (usually due to tumor)

Manifestations:
a.  Hypokalemia and hypernatremia
b.  Hypertension from hypernatremia
c.  Muscle weakness and cardiac problems related to hypokalemia

Treatment
a.  Surgical removal of tumor/adrenal gland
b.  Potassium replacement
c.  Antihypertensive drugs: spinolactone (Aldactone)

Nursing Interventions
a.  Provide quiet environment
b.  Monitor BP and cardiac activity
c.  Monitor potassium level

Disorders of Adrenal Medulla

1.  Pheochromocytoma- hypersecretion of the hormones of adrenal medulla (exact cause unknown)

Manifestations (sudden onset): seen in young women and men
a.  Hypertension (principal manifestation): very high crisis
b.  Sudden attackes resemble manifestations of overstimulation of sympathetic nervous system
-         Sweating
-         Apprehension
-         Palpitations
-         Nausea
-         Vomiting
-         Orthostatic hypotension
-         Headache
-         Tachycardia
c.  Hyperglycemia

Treatment
a.  Surgical excision of tumor or adrenal gland
b. Symptomatic if surgery not feasible

Nursing Interventions:

a.  Provide high-calorie, nutritious diet (avoid caffeine)
b.  Preoperative:  control hypertension

Thryroid Gland

Disorders of Thyroid Gland

1.  Myxedema: hyposecretion of throid hormone in adulthood; highest incidence between ages 50 & 60; more often in women

Manifestations
a.  Slow rate of metabolism
b.  Personality changes (depression)
c.  “Dull” appearance
d.  Anorexia and constipation
e.  Intolerance to cold
f.  Decreased sweating
g.  Hypersensitivity to barbiturates and narcotics
h.  Generalized interstitial edema
i.  Husky voice from swelling of vocal cords
j.  Coarse, dry skin
k.  Thin hair
l.  Generalized weakness
m.  Goiter
n.  Weight gain
o. puffy appearance (nonpitting)
p. Anemia
q.  Increased cholesterol and lipids
r.  Menstrual disorders in women

Treatment: drug therapy:  Levothyroxine (Synthroid)
a.  Thyroid replacement hormones should be taken on an empty stomach
b.  Monitor heart rate: fewer than 100 beats per minute is desirable; monitor for cardiac symptoms of angina at initiation of therapy

Nursing Interventions
a.  Directed toward manifestations of decreased metabolism
-         provide warm environment
-         Low-calorie, low cholesterol, low saturated fat diet
-         Increase roughage
-         Moderate fluids
-         Avoid sedatives
-         Plan rest periods
-         Weigh client
b.  Observe for overdosage manifestations of thyroid preparations

2.  Cretinism- hyposecretion of thyroid hormones in the fetus or neonate
-         diagnosed shortly after birth thru newborn screening
-         can lead to severe, irreversible mental retardation, if not treated
-         requires lifelong hormone replacement therapy

3.  Hyperthyroidism (Grave’s disease, diffuse toxic goiter)-  hypersecretion of thyroid hormone; over treatment of hypothyroidism

Manifestations
a.  Increased rate of body metabolism
b.  Personality changes
c.  Enlargement of the thyroid gland
d.  Exopthalmos (never goes away)
e.  Cardiac dysrhytmia and hypertension
f.  Increased appetite (but weight loss)
g.  Diaerrhea
h.  Diaphoresis and heat intolerance
i.  Easy fatigability
j.  Anxiety/insomnia
k.  Nervous appearance
l.  Amenorrhea

Treatment
a.  Drug therapy
1.      Methimazole (Tapazole): blocks thyroid hormone production
2.      Propylthiouracil (Propyl-Thyracil): blocks thyroid hormone production
-         can cause agranulocytosis
-         client must have frequent CBCs performed
3.      Iodides: decrease vascularity; inhibit release of thyroid hormones
-         Lugol’s solution ( use is decreasing because this medication is expensive and inactivates thyroid medications in the bowel)
-         Saturated solution of potassium iodide (SSKI); use prior to thyroidectomy

4.      Propanolol (inderal); relief of tachycardia

b.  Radioiodinetherapy: slowly destroys hyperfunctioning thyroid tissue
c.  Thyroidectomy: subtotal or total

Nursing Interventions:
a.  Provide adequate rest
b.  Provide cool, quiet environment
c.  Provide high calorie (4000-5000 cal.day), high protein, carbohydrate, vitamin diet without stimulants, extra fluids
d.  Weigh client daily
e.  Provide emotional support; activities
f.  Provide eye protection: ophthalmic medicine; tape eyes at night; decrease sodium and water
g.  elevate head of bed
h.  Be alert for complications
-         corneal abrasion
-         heart disease
-         Thyroid Storm (usually occurs after thyroid surgery)

Thyroidectomy- removal of the thyroid gland, either total or partial

Nursing Interventions
a.  Semi-Fowler’s position
b.  Check dressing esp. back of neck
c.  Observe for repiratory distress; tracheostomy tray, oxygen and suction apparatus at bedside
d.  Be alert for signs of hemorrhage
e.  Talking limited, note any hoarseness; may indicate injury to laryngeal nerve
f.  Observe for signs of tetany: Chvostek’s sign and Trousseau’s sigh (parathyroid glands may accidentally be removed)
g.  Calcium gluconate IV at bedside
h.  Observe for Thryoid Storm (life threatening)
-         Fever
-         Tachycardia
-         Delirium
-         Irritability
-         Important to assess temperature routinely
-     gradually increase range of motion to neck; support when sitting up


Parathyroid Gland

Disorders of Parathyroid Gland

1.      Hypoparathyroidism- hyposecretion of the parathyroid hormone; accidental removal during thyroid surgery

Manifestations
a.  Hypocalcemia
b.  Acute: increased neuromuscular irritability tetany (positive Chvostek and positive Trousseau)
c.  Chronic:
-         Poor development of tooth enamel
-         Lethargic
-         Thin hair; brittle nails
-         Mental retardation
-         Circumoral paresthesia with numbness and tingling of fingers

Treatment
a.  Acute:  IV Calcium Gluconate
b.  Chronic:
-         oral calcium salts
-         Vitamin D and aluminum hydroxide gel (Amphojel)
-         High calcium, low phosphorous diet

Nursing Interventions
a.  Provide quiet room, no stimulus
b.      Assess for increased signs of neuromuscular irritability

2. Hyperparathyroidism (causes are tumor or renal disease)- hypersecretion of parathyroid hormone

Manifestations (causes loss of calcium from the bones to the serum)
a.  Bone deformities (susceptible to fractures
b.  Calcium deposits in various body organs
c.  Hypercalcemia
d.  Gastric ulcers and GI disturbances
e.  Apathy, fatigue, weakness, depression
f.  Nausea, vomiting, anorexia
g.  Constipation, abdominal pain
h.  Joint and bone pain
i.  Polyuria
j.  Polydipsia
k.  Azotemia
l.  Hypertension

Treatment

a.  Subtotal surgical resection of parathyroid gland
b.  Hydration and diuretics- furosemide (Lasix) excretes excess calcium
c.  Plicamycin (Mithracin) or gallium nitrate (Ganite)

Nursing Interventions
a.  Force fluids
b.  Provide a low-calcium, low Vit. D diet
c.  Prevent constipation and fecal impaction
d.  Strain all urine
e.  Safety measures to prevent breaks
f.  Calcitonin; binds phosphate; in renal failure

PITUITARY GLAND: HORMONES PRODUCED AND FUNCTIONS

- controlled primarily by the hypothalamus; termed “master gland” as it directly affects the function of other endocrine glands

Anterior Lobe
  1. Adrenocorticotropic hormone (ACTH)- concerned with growth and secretory activity of adrenal cortex, which produces steroids
  2. Thyrotropic hormone (TSH) – for growth and secretory activity of thyroid; controls release rate of thyroxine, which controls rate of most chemical reaction in the body; target is thyroid gland
  3. Somatotropic hormones (STH or GH)-  promote growth of body tissue
  4. Gonadotropic hormones and estrogen secretion; follicle stimulating hormone (FSH)-  stimulate development of ovarian follicles; semeniferous tubules and sperm maturation
  5. Luteinizing hormone (LH)- works with FSH in final maturation of follicles; promotes ovulation and progesterone secretion
  6. Prolactin-  for milk production
  7. Melanocyte stimulating hormone (MSH)- produces the characteristic skin darkening

Posterior Lobe
  1. Vasopressin (ADH)- influnces water absorption by kidney
  2. Oxytocin-influences the menstrual cycle, labor and lactation



Neurologic diseases review


Basic Concepts in Normal Neurologic Function

 Oxygen supply:  The brain requires 20% of the O2 in the body
  • Glucose supply:  The brain requires 65 to 70% of the glucose in the body
  • Blood supply:  The brain requires 1/3 of the cardiac output
  • Acid-base balance

            Acidosis
1.      Cerebral vasodilation
2.      CNS depressant    ® coma

           Alkalosis
1.      Cerebral vasocontriction
2.      CNS stimulant     ®  seizures

§        Blood-brain barrier:  Protects the brain from certain drugs, chemicals and microorganism.  It a layer of least semi-permeable capillaries
§        CSF volume:  CSF cushions the brain; it nourishes the brain and determines the ICP.  The choroids plexus in the lateral ventricles primarily produces CSF.  The normal CSF volume is 100 to 150 mls at a time, an average of 120 mls.

Neurologic Assessment

 1.  Mental Status
  • Orientation to three spheres :  people, time and place
  • Memory:  Immediate recall, recent memory, remote memory
a.       Immediate recall:  Ask the client to repeat your question
b.      Recent memory:  Ask client about recent events that occurred few minutes, few hours
c.       Remote memory:  Ask the client about events in the remote past, or historical events that can be answered by the general population

2.  Level of consciousness (LOC)
-         It is the most sensitive indicator of the changes in the neurologic status of the client
-         The center for wakefulness is the ascending reticular activating system ARAS/reticular formation

-         Assess both wakefulness and content of thought
-         Levels of consciousness:
§         Level I- conscious, coherent, cognitive (3 Cs)
§         Level II- confused, drowsy,  lethargic, obtunded, somnolent
§         Level III- stuporous; responds only to noxious, strong or intense stimuli. e.g.  sternal pressure, trapezius pinch, pressure at the base of the nail or supraorbital area, very strong light or very loud sound
§         Level IV
1.  Light coma; response is only by grimace or withdrawing limb from pain; primitve and disorganized response to painful stimuli

2.  Deep Coma; absence of response to even the most painful stimuli

 GLASGOW COMA SCALE (GCS) is an objective measure to describe LOC.  It is based on the client’s response in three areas :  eye opening, motor response, verbal response

Normal 8-15; 7 or less indicates coma

    1. Best eye-opening response
a.  Spontaneously                                                           = 4
b.  To speech                                                                 = 3
c.  To painful stimuli                                                        = 2
d.  No opening                                                                = 1

    1. Best Motor Response
a. Obeys verbal command                                       = 6
b.      Localizes painful stimuli                                     = 5
c. Flexion: withdrawal to pain                                   = 4
d.      Flexion: abnormal (decorticate                          = 3
e. Extension:abonormal(decerebrate)                       =2
f.  No response to pain on any limb                          = 1

      3. Best Verbal Response
                    a.  Oriented to time, place, person                             = 5
                     b. Engages in conversation, confused in content        = 4
                     c.  Words spoken but conversation not sustained      = 3
                     d.  Groans on evoked pain                                       = 2
                     e.  No response                                                                   = 1


                                                             CVA, Stroke
1.  Anterior cerebral stroke: lower extr emity more involved than upper extremity,
contralateral hemiparesis and sensory deficits
2.  Posterior cerebral stroke: contralateral sensory loss, transient contralateral
hemiparesis

Middle cerebral artery stroke: upper extremity more involved than the lower
extremity, contralateral sensory loss

Risk Factors
1. Diabetes
2.   Atherosclerosis
3.   Hypertension
4. Cardiac disease
5.  Transient ischemic attacks

Aneurysm Precautions
1.  Avoid rectal temperatures
2. Limit visitors
3.  Avoid Valsalva’s maneuver
4.  Head of bed should be between 30-45 degrees
Valsalva’s maneuver – occurs when attempting to forcibly exhale with the glottis,
mouth and nose closed.  It causes an increase in intrathoracic pressure with an
accompanying collapse of the vein of the chest wall. The following may result:
1.  Slowing of the pulse
2.  Decreased return of blood to the heart
3.  Increased intrathoracic pressure

Elevated Intracranial Pressure
In most cases you should do the following:
1.  Maintain proper fluid volumes
2.  Set-up quiet environment for minimal sensory stimulation
3.  Elevate HOB (head of bed) to approximately 30 degrees
4.  Limit suctioning performed

Horner’s Syndrome
- Sympathetic innervation to the face is interrupted by a lesion
in the brain stem resulting in pupillary constriction, dry and red face with no
sweat, ptosis-Mueller’s muscle, problem located in sympathetic ascending fibers
Autonomic Dysreflexia
- caused by a lesion in the high thoracic or cervical cord.
Severe hypertension, sweating and headaches noted.  May occur with a
blockage in a urine catheter


Parkinson’s Disease
-a degenerative disease with pr imary involvement of the
basal ganglia; characterized by the following:
Signs/Symptoms
1. Bradykinesia
2. Resting tremor
3.  Impaired postural reflexes
4. Rigidity
5.  Loss of inhibitory dopamine
6.  Mask like affect
7. Emotional lability

Multiple Sclerosis
–progressive demyelinating disease of the central nervous
system affecting mostly young adults
Cause unknown, most likely viral.
1. Fluctuating exacerbations
2. Demyelinating lesions limit neural transmission
3.  Confirmed with lumbar puncture, elevated gamma globulin, CT/MRI,
myelogram, EEG.
4.  Mild to moderate impaired cognition common
5. Sensory Deficits
6. Bowel and Bladder Deficits
7. Spasticity common
8. Ataxic gait



Myasthenia gravis
- neuromuscular disease characterized by fatigue of skeletal
muscles and muscular weakness.
**
Key point
-Review the differentiation between MG and a cholinergic crisis, using
the Tensilon Test. A cholinergic crisis may have hypotension, bradycardia vs.
myasthenia gravis.
Signs/Symptoms
1. Progressive involvement
2. Decreased muscle membrane acetylcholine receptors
3.  Severe weakness (proximal more than distal muscles)
4.  Facial, ocular and bulbar weakness
5. Possible life-threatening respiratory muscle weakness
6.  Probable use of anticholinesterase drugs for treatment

Guillain-Barre’ Syndrome
-polyneuropathy with progressive muscular weakness
Signs/Symptoms
1.  Demyelination of peripheral and cranial nerves
2.  Motor paralysis in an ascending pattern
3.  3% Mortality – respiratory failure
4. Autonomic dysfunction-arrhythmias, blood pressure changes, tachycardia

Amyotrophic lateral sclerosis
(Lou Gehrig’s disease) – degenerative disease
affecting upper and lower motor neurons
Signs/Symptoms
1.  Death typically in 2-5 yrs.
2. Spasticity, hyperreflexia
3. Dysarthria, Dysphagia
4.  Autonomic Dysfunction in approximately 1/3 of patients
5.  Cognition is normal
Post-polio Syndrome
- slowly progressive muscle weakness that occurs in
patients with a history of acute poliomyelitis, after a stable period
Sign/Symptoms
1. New Weakness
2. Pain/Myalgia
3. Abnormal fatigue
Seizures
Epilepsy-recurrent seizures due to excessive and sudden discharge of cerebral
cortical neurons.
Tonic-clonic (Grand Mal) –Pt. confused and drowsy about the seizures, 2-5 min
generally
Absence seizures  (Petit Mal)- Brief, no convulsive contractions, may be up to
100X day
Simple Seizures- no loss of consciousness
Complex Seizures, brief loss of consciousness with psychomotor changes
**
Key Point
- When a patient has a seizure during most interventions, do not use
a tongue blade and allow free movement in a safe environment
Meningitis-inflammation of the meninges of the spinal cord and brain caused by
bacteria.
The most common bacteria are the following:
Neisseria meningitidis, Diploc occus
pneumoniae,
and
Haemophilus influenzae



Signs/Symptoms
1.  Brudzinski’s sign
2.  Kernig’s sign
3. Stiff/Tight neck
4. Fever
5. Confused
Anterior Cord Syndrome – damage is mainly in anterior cord resulting in loss of
motor function and pain and temperature with preservation of light touch,
proprioception and position sense
Brown-Sequard Syndrome – hemisection of SC resulting in ipsilateral weakness
and loss of position and vibration sense below the level of lesion