Overview of the Structures & Functions of Nervous System Central NS PNS ANS Brain & spinal cord 31 spinal & cranial sympathetic NS Parasypathatic NS Somatic NS C- 8 T- 12 L- 5 S- 5 C- 1 ANS (or adrenergic of parasympatholitic response) SNS involved in fight or aggression response Release of norepinephrine (adrenaline – cathecolamine) Adrenal medulla (potent vasoconstrictor) Increases body activities VS = Increase Except GIT – decrease GITmotility * Why GIT is not increased = GIT is not important! Increase blood flow to skeletal muscles, brain & heart. I. SNS: Adrenergic Agents – Epinephrine (adrenaline) Anticholinergic , Sympathomimetic, Parasympatholytic -Atropine sulfate II. PNS: Cholinergics, Beta Adrenergic blockers, Sympatholitic, Parasympathomimetic Beta adrenergic blocking agents (opposite of adrenergic agents) (all end in –‘lol’) - Blocks release of norepinephrine. - Decrease body activities except GIT (diarrhea) Ex. Propanolol, Metopanolol SE: B – broncho spasm (bronchoconstriction) E – elicits a decrease in myocardial contraction T – treats HPN A – AV conduction slows down Given to angina & MI – beta-blockers to rest heart Anti HPN agents: 1. Beta blockers (-lol) 2. Ace inhibitors (-pril) ex ENALAPRIL, CAPTOPRIL 3. Calcium antagonist ex CALCIBLOC or NEFEDIPINE Peripheral nervous system: cholinergic/ vagal or sympatholitic response - Involved in fly or withdrawal response - Release of acetylcholine (ACTH) - Decrease all bodily activities except GIT (diarrhea) I Cholinergic agents ex 1. Mestinon Antidote – anti cholinergic agents Atropine Sulfate – S/E – SNS Effect of PNS: (cholinergic) 1. Meiosis – constriction of pupils 2. Increase salivation 3. BP & HR decreased 4. RR decrease – broncho constriction 5. Diarrhea – increased GI motility 6. Urinary frequency 7. Acetylcholine- neurotransmitter 8. Blood vessels- vasodilated Effects of SNS (anti-cholinergic/adrenergic) 1. Dilate pupil – to aware of surroundings - medriasis 2. Dry mouth 3. BP & HR= increased 4. RR increased- broncho dilation 5. Constipation & urinary retention 6. Nor/Epinephrine- neurotransmitter 7. Blood vessels-vasoconstriction


S/E- of anti-hpn drugs: 1. orthostatic hpn 2. transient headache & dizziness.-Mgt. Rise slowly. Assist in ambulation. CNS (brain & spinal cord) I. Cells – A. neurons Properties and characteristics a. Excitability – ability of neuron to be affected in external environment. b. Conductivity – ability of neuron to transmit a wave of excitation from one cell to another c. Permanent cells – once destroyed, cant regenerate (ex. heart, retina, brain, osteocytes) Regenerative capacity A. Labile – once destroyed cant regenerate - Epidermal cells, GIT cells, resp (lung cells). GUT B. Stable – capable of regeneration BUT limited time only ex salivary gland, pancreas cells cell of liver, kidney cells C. Permanent cells – retina, brain, heart, osteocytes can’t regenerate. 3.) Neuroglia – attached to neurons. Supports neurons. Where brain tumors are found. Types: 1. Astrocyte 2. Oligodendria Astrocytoma – 90 – 95% brain tumor from astrocyte. Most brain tumors are found at astrocyte. Astrocyte – maintains integrity of blood brain barrier (BBB). BBB – semi permeable / selective -Toxic substance that destroys astrocyte & destroy BBB. Toxins that can pass in BBB: 1. Ammonia-liver cirrhosis. 2. 2. Carbon Monoxide – seizure & parkinsons. 3. 3. Bilirubin- jaundice, hepatitis, kernicterus/hyperbilirubenia. 4. 4. Ketones –DM. OLIGODENDRIA – Produces myelin sheath – wraps around a neuron – acts as insulator facilitates rapid nerve impulse transmission. No myelin sheath – degenerates neurons Damage to myelin sheath – demyellenating disorders DEMYELLENATING DSE 1.)ALZHEIMER’S DISEASE– atrophy of brain tissue due to a deficiency of acetylcholine. S&Sx: A – amnesia – loss of memory A – apraxia – unable to determine function & purpose of object A – agnosia – unable to recognize familiar object A – aphasia – - Expressive – brocca’s aphasia – unable to speak - Receptive – wernickes aphasia – unable to understand spoken words Common to Alzheimer – receptive aphasia Drug of choice – ARICEPT (taken at bedtime) & COGNEX. Mgt: Supportive & palliative.

Microglia – stationary cells, engulfs bacteria, engulfs cellular debris. II. Compositions of Cord & Spinal cord 80% - brain mass 10% - CSF 10% - blood MONROE KELLY HYPOTHESIS: The skull is a closed vault. Any increase in one component will increase ICP.


Normal ICP: 0-15mmHg Brain mass Connects R & L cerebral hemisphere - Corpus collusum Rt cerebral hemisphere, Lt cerebral hemisphere Function: 1. Sensory 2. Motor 3. Integrative Lobes 1.) Frontal a. Controls motor activity b. Controls personality development c. Where primitive reflexes are inhibited d. Site of development of sense of umor e. Brocca’s area – speech center Damage - expressive aphasia 2.) Temporal – a. Hearing b. Short term memory c. Wernickes area – gen interpretative or knowing Gnostic area Damage – receptive aphasia 3.) Parietal lobe – appreciation & discrimation of sensory imp - Pain, touch, pressure, heat & cold 4.) Occipital - vision 5.) Insula/island of reil/ Central lobe- controls visceral fx Function: - activities of internal organ 6.) Rhinencephalon/ Limbec - Smell, libido, long-term memory Basal Ganglia – areas of gray matte located deep within a cerebral hemisphere - Extra pyramidal tract - Releases dopamine- Controls gross voluntary unit Decrease dopamine – (Parkinson’s) pin rolling of extremiies & Huntington’s Dse. Decrease acetylcholine – Myasthenia Gravis & Alzheimer’s Increased neurotransmitter = psychiatric disorder Increase dopamine – schizo Increase acetylcholine – bipolar MID BRAIN – relay station for sight & hearing Controls size & reaction of pupil 2 – 3 mm Controls hearing acuity CN 3 – 4 Isocoria – normal size (equal) Anisocoria – uneven size – damage to mid brain PERRLA – normal reaction DIENCEPHALON- between brain Thalamus – acts as a relay station for sensation Hypothalamus – (thermoregulating center of temp, sleep & wakefulness, thirst, appetite/ satiety center, emotional responses, controls pituitary function. BRAIN STEM- a. Pons – or pneumotaxic center – controls respiration Cranial 5 – 8 CNS MEDULLA OBLONGATA- controls heart rate, respiratory rate, swallowing, vomiting, hiccups/ singutus Vasomotor center, spinal decuissation termination, CN 9, 10, 11, 12 CEREBELLUM – lesser brain 1. Cerebrum – largest -


- Controls posture, gait, balance, equilibrium Cerebellar Tests: a.) R – Romberg’s test- needs 2 RNs to assist - Normal anatomical position 5 – 10 min (+) Romberg’s test – (+) ataxia or unsteady gait or drunken like movement with loss of balance. b.) Finger to nose test – (+) To FTNT – dymetria – inability to stop a movement at a desired point c.) Alternate pronation & supination Palm up & down . (+) To alternate pronation & supination or damage to cerebellum – dymentrium Composition of brain - based on Monroe Kellie Hypothesis - Skull is a closed container. Any alteration in 1 of 3 intracranial components = increase in ICP Normal ICP – 0 – 15 mmHg Foramen Magnum C1 – atlas C2 – axis (+) Projectile vomiting = increase ICP Observe for 24 - 48 hrs CSF – cushions the brain, shock absorber Obstruction of flow of CSF = increase ICP Hydrocephalus – posteriorly due to closure of posterior fontanel CVA – partial/ total obstruction of blood supply

INCREASED ICP – increase ICP is due to increase in 1 of the Intra Cranial components.
Predisposing factors: 1.) Head injury 2.) Tumor 3.) Localized abscess 4.) Hemorrhage (stroke) 5.) Cerebral edema 6.) Hydrocephalus 7.) Inflammatory conditions - Meningitis, encephalitis B. S&Sx change in VS = always late symptoms Earliest Sx: a.) Change or decrease LOC – Restlessness to confusion Wide pulse pressure: Increased ICP - Disorientation to lethargy Narrow pp: Cardiac disorder, shock - Stupor to coma Late sign – change in V/S 1. BP increase (systolic increase, diastole- same) 2. Widening pulse pressure Normal adult BP 120/80 120 – 80 = 40 (normal pulse pressure) Increase ICP = BP 140/80 = 140 – 80= 60 PP (wide) 3. RR is decreased (Cheyne-Stokes = bet period of apnea or hyperpnea with periods of apnea) 4. Temp increase Increased ICP: Increase BP Shock – decrease BP – Decrease HR Increase HR CUSHINGS EFFECT Decrease RR Increase RR Increase Temp Decrease temp b.) Headache Projectile vomiting Papilledima (edema of optic disk – outer surface of retina) Decorticate (abnormal flexion) = Damage to cortico spinal tract / Decerebrate (abnormal extension) = Damage to upper brain stem-pons/ c.) Uncal herniation – unilateral dilation of pupil. (Bilateral dilation of pupil – tentorial herniation.) d.) Possible seizure.


Nursing priority: 1.) Maintain patent a/w & adequate ventilation a. Prevention of hypoxia – (decrease tissue oxygenation) & hypercarbia (increase in CO2 retention). Hypoxia – cerebral edema - increase ICP Hypoxia – inadequate tissue oxygenation Late symptoms of hypoxia – B – bradycardia E – extreme restlessness D – dyspnea C – cyanosis Early symptoms – R – restlessness A – agitation T – tachycardia Increase CO2 retention/ hypercarbia – cerebral vasodilatation = increase ICP Most powerful respiratory stimulant increase in CO2 Hyperventilate decrease CO2 – excrete CO2 Respiratory Distress Syndrome (RDS) – decrease Oxygen Suctioning – 10-15 seconds, max 15 seconds. Suction upon removal of suction cap. Ambu bag – pump upon inspiration c. Assist in mechanical ventilation 1. Maintain patent a/w 2. Monitor VS & I&O 3. Elevate head of bed 30 – 45 degrees angle neck in neutral position unless contra indicated to promote venous drainage 4. Limit fluid intake 1,200 – 1,500 ml/day (FORCE FLUID means:Increase fluid intake/day – 2,000 – 3,000 ml/day)- not for inc ICP. 5. Prevent complications of immobility 6. Prevent increase ICP by: a. Maintain quiet & comfy environment b. Avoid use of restraints – lead to fractures c. Siderails up d. Instruct patient to avoid the ff: -Valsalva maneuver or bearing down, avoid straining of stool (give laxatives/ stool softener Dulcolax/ Duphalac) - Excessive cough – antitussive Dextrometorpham -Excessive vomiting – anti emetic (Plasil – Phil only)/ Phenergan - Lifting of heavy objects - Bending & stooping e. Avoid clustering of nursing activities 7. Administer meds as ordered: 1.) Osmotic diuretic – Mannitol./Osmitrol promotes cerebral diuresis by decompressing brain tissue Nursing considerations: Mannitol 1. Monitor BP – SE of hypotension 2. Monitor I&O every hr. report if < 30cc out put 3. Administer via side drip 4. Regulate fast drip – to prevent formation of crystals or precipitate 2.) Loop diuretic - Lasix (Furosemide) Nursing Mgt: Lasix Same as Mannitol except - Lasix is given via IV push (expect urine after 10-15mins) should be in the morning. If given at 7am. Pt will urinate at 7:15 Immediate effect of Lasix within 15 minutes. Max effect – 6 hrs due (7am – 1pm)


S/E of Lasix

Hypokalemia (normal K-3.5 – 5.5 meg/L)
1. 2. 3. S&Sx Weakness & fatigue Constipation (+) “U” wave in ECG tracing

Nursing Mgt: 1.) Administer K supplements – ex Kalium Durule, K chloride Potassium Rich food: ABC’s of K Vegetables Fruits A - asparagus A – apple B – broccoli (highest) B – banana – green C – carrots C – cantalope/ melon O – orange (highest) –for digitalis toxicity also. Vit A – squash, carrots yellow vegetables & fruits, spinach, chesa Iron – raisins, Food appropriate for toddler – spaghetti! Not milk – increase bronchial secretions Don’t give grapes – may choke S/E of Lasix: 1.) Hypokalemia

2.) Hypocalcemia (Normal level Ca = 8.5 – 11mg/100ml) or Tetany:
S&Sx weakness Paresthesia (+) Trousseau sign – pathognomonic – or carpopedal spasm. Put bp cuff on arm=hand spasm. (+) Chevostek’s sign Arrhythmia Laryngospasm Administer – Ca gluconate – IV slowly

Ca gluconate toxicity: Sx – seizure – administer Mg SO4
Mg SO4 toxcicity– administer Ca gluconate B – BP decrease U – urine output decrease R – RR decrease P – patellar reflexes absent

3.) Hyponatremia – Normal Na level = 135 – 145 meg/L
Hypotension Signs of Dehydration: dry skin, poor skin turgor, gen body malaise. Early signs – Adult: thirst and agitation / Child: tachycardia Mgt: force fluid Administer isotonic fluid sol 4.) Hyperglycemia – increase blood sugar level P – polyuria P – polyphagia P – polydipsia Nsg Mgt: a. Monitor FBS (N=80 – 120 mg/dl) 5.) Hyperurecemia – increase serum uric acid. Tophi- urate crystals in joint. S/Sx –



ty arthritis

kidney stones- renal colic (pain)

Cool moist skin Sx joint pain & swelling usually at great toe. Nsg Mgt of Gouty Arthritis a.) Cheese (not sardines, anchovies, organ meat) (Not good if pt taking MAO) b.) Force fluid c.) Administer meds – Allopurinol/ Zyloprim – decrease uric acid production – drug of choice for gout Colchicene – excretes uric acid. Acute gout drug of choice. Kidney stones – renal colic (pain). Cool moist skin Mgt: 1.) Force fluid 2.) Meds – narcotic analgesic Morphine SO4 SE of Morphine SO4 toxicity Respiratory depression (check RR 1st) Antidote for morphine SO4 toxicity –Narcan (NALOXONE) Naloxone toxicity – tremors Increase ICP meds: 3.) Corticosteroids - Dexamethsone – decrease cerebral edema (Decadrone) 4.) Mild analgesic – codeine SO4. For headache. 5.) Anti consultants – Dilantin (Phenytoin) Question: Increase ICP what is the immediate nsg action? a. Administer Mannitol as ordered b. Elevate head 30 – 45 degrees c. Restrict fluid d. Avoid use of restraints Nsg Priority – ABC & safety Pt suffering from epiglotitis. What is nsg priority? a. Administer steroids – least priority b. Assist in ET – temp, a/w c. Assist in tracheotomy – permanent (Answer) d. Apply warm moist pack? Least priority Rationale: Wont need to pass larynx due to larynx is inflamed. ET can’t pass. Need tracheostomy onlyMagic 2’s of drug monitoring Drug D – digoxin L - lithium A – aminophylline D – Dilantin A – acetaminophen N range .5 – 1.5 meq/L .6 – 1.2 meq/L 10 – 19 mg/100ml 10 -19 mg/100 ml 10 – 30 mg/100ml Toxicity 2 2 20 20 200 Classification cardiac glycosides antimanic bronchodilator anticonvulsant narcotic analgesic Indication CHF bipolar COPD seizures osteoarthritis

Digitalis – increase cardiac contraction = increase CO
Nursing Mgt 1. Check PR, HR (if HR below 60bpm, don’t giveDigoxin) Digitalis toxicity – antidote - Digivine a. Anorexia -initial sx. b. n/v GIT c. Diarrhea d. Confusion


e. f.

Photophobia Changes in color perception – yellow spots

(Ok to give to pts with renal failure. Digoxin is metabolized in liver not in kidney.) L – lithium (lithane) decrease levels of norepinephrine, serotonine, acetylcholine
Antimanic agent Lithium toxicity S/Sx Anorexia n/s Diarrhea Dehydration – force fluid, maintain Na intake 4 – 10g daily Hypothyroidism (CRETINISM– the only endocrine disorder that can lead to mental retardation)

a.) b.) c.) d.) e.)

A – aminophyline (theophylline) – dilates bronchioles.
Take bp before giving aminophylline. S/Sx : Aminophylline toxicity: 1. Tachycardia 2. Hyperactivity – restlessness, agitation, tremors a. b. c. d. Question: Avoid giving food with Aminophylline Cheese/butter– food rich in tyramine, avoided only if pt is given MAOI Beer/ wine Hot chocolate & tea – caffeine – CNS stimulant tachycardia Organ meat/ box cereals – anti parkinsonian

MAOI – antidepressant m AR plan n AR dil can lead to CVA or hypertensive crisis p AR nate 3 – 4 weeks - before MAOI will take effect Anti Parkinsonian agents – Vit B6 Pyridoxine reverses effect of Levodopa

D – dilatin (Phenytoin) – anti convulsant/seizure
Nursing Mgt: 1. Mixed with plain NSS or .9 NaCl to prevent formation of crystals or precipitate - Do sandwich method - Give NSS then Dilantin, then NSS! 2. Instruct the pt to avoid alcohol – bec alcohol + dilantin can lead to severe CNS depression Dilantin toxicity: S/Sx: G – gingival hyperplasia – swollen gums i. Oral hygiene – soft toothbrush ii. Massage gums H – hairy tongue A - ataxia N – nystagmus – abnormal movement of eyeballs A – acetaminophen/ Tylenol – non-opoid analgesic & antipyretic – febrile pts Acetaminophen toxicity : 1. Hepato toxicity 2. Monitor liver enzymes SGPT (ALT) – Serum Glutamic Piruvate Tyranase SGOT- Serum Glutamic Acetate Tyranase 3. Monitor BUN (10 – 20) Crea (.8-1) Acetaminophen toxicity can lead to hypoglycemia


T – tremors, Tachycardia I – irritability R – restlessness E – extreme fatigue D – depression (nightmares) , Diaphoresis Antidote for acetaminophen toxicity – Acetylcesteine = causes outporing of secretions. Suction. Prepare suctioning apparatus. Question: The following are symptoms of hypoglycemia except: a. Nightmares b. Extreme thirst – hyperglycemia symptoms c. Weakness d. Diaphoresis

PARKINSONS DSE (parkinsonism) - chronic, progressive disease of CNS char by degeneration of dopamine
producing cells in substancia nigra at mid brain & basal ganglia - Palliative, Supportive Function of dopamine: controls gross voluntary motors. Predisposing Factors: 1. Poisoning (lead & carbon monoxide). Antidote for lead = Calcium EDTA 2. Hypoxia 3. Arteriosclerosis 4. Encephalitis High doses of the ff: a. Reserpine (serpasil) anti HPN, SE – 1.) depression - suicidal 2.) breast cancer b. Methyldopa (aldomet) - promote safety c. Haloperidol (Haldol)- anti psychotic d. Phenothiazide - anti psychotic SE of anti psychotic drugs – Extra Pyramidal Symptom Over meds of anti psychotic drugs – neuroleptic malignant syndrome char by tremors (severe) S/Sx: Parkinsonism – 1. Pill rolling tremors of extremities – early sign 2. Bradykinesia – slow movement 3. Over fatigue 4. Rigidity (cogwheel type) a. Stooped posture b. Shuffling – most common c. Propulsive gait 5. Mask like facial expression with decrease blinking eyes 6. Monotone speech 7. Difficulty rising from sitting position 8. Mood labilety – always depressed – suicide Nsg priority: Promote safety 9. Increase salivation – drooling type 10. Autonomic signs: - Increase sweating - Increase lacrimation - Seborrhea (increase sebaceous gland) - Constipation - Decrease sexual activity Nsg Mgt 1.) Anti parkinsonian agents - Levodopa (L-Dopa), Carbidopa (Sinemet), Amantadine Hcl (Symmetrel) Mechanism of action Increase levels of dopa – relieving tremors & bradykinesia S/E of anti parkinsonian - Anorexia - n/v - Confusion - Orthostatic hypotension


- Hallucination - Arrhythmia Contraindication: 1. Narrow angled closure glaucoma 2. Pt taking MAOI (Parnate, Marplan, Nardil) Nsg Mgt when giving anti-parkinsonian 1. Take with meals – to decrease GIT irritation 2. Inform pt – urine/ stool may be darkened 3. Instruct pt- don’t take food Vit B6 (Pyridoxine) cereals, organ meats, green leafy veg - Cause B6 reverses therapeutic effects of levodopa Give INH (Isoniazide-Isonicotene acid hydrazide.) SE-Peripheral neuritis. 2.) Anti cholinergic agents – relieves tremors Artane mech – inhibits acetylcholine Cogentin action , S/E - SNS 3.) Antihistamine – Diphenhydramine Hcl (Benadryl) – take at bedtime S/E: adult– drowsiness,– avoid driving & operating heavy equipt. Take at bedtime. Child – hyperactivity CNS excitement for kids. 4.) Dopamine agonist Bromotriptine Hcl (Parlodel) – respiratory depression. Monitor RR. Nsg Mgt – Parkinson 1.) Maintain siderails 2.) Prevent complications of immobility - Turn pt every 2h Turn pt every 1 h – elderly 3.) Assist in passive ROM exercises to prevent contractures 4.) Maintain good nutrition CHON – in am CHON – in pm – to induce sleep – due Tryptopan – Amino Acid 5.) Increase fluid in take, high fiber diet to prevent constipation 6.) Assist in surgery – Sterotaxic Thalamotomy Complications in sterotaxic thalmotomy- 1.) Subarachnoid hemorrhage 2.) aneurism 3.) encephalitis

Chronic intermittent disorder of CNS – white patches of demyelenation in brain & spinal cord. - Remission & exacerbation - Common – women, 15 – 35 yo cause – unknown Predisposing factor: 1. Slow growing virus 2. Autoimmune – (supportive & palliative treatment only) Normal Resident Antibodies: Ig G – can pass placenta – passive immunity. Short acting. Ig A – body secretions – saliva, tears, colostrums, sweat Ig M – acute inflammation Ig E – allergic reactions IgD – chronic inflammation S & Sx of MS: (everything down) 1. Visual disturbances a. Blurring of vision b. Diplopia/ double vision c. Scotomas (blind spots) – initial sx 2. Impaired sensation to touch, pain, pressure, heat, cold a. Numbness b. Tingling c. Paresthesia 3. Mood swings – euphoria (sense of elation )


4. Impaired motor function: a. Weakness b. Spasiticity –“ tigas” c. Paralysis –major problem 5. Impaired cerebellar function Triad Sx of MS I – intentional tremors N – nystagmus – abnormal rotation of eyes Charcots triad A – Ataxia & Scanning speech 6. Urinary retention or incontinence 7. Constipation 8. Decrease sexual ability Dx – MS 1. CSF analysis thru lumbar puncture - Reveals increase CHON & IgG 2. MRI – reveals site & extent of demyelination 3. Lhermitte’s response is (+). Introduce electricity at the back. Theres spasm & paralysis at spinal cord. Nsg Mgt MS - Supportive mgt 1.) Meds a. Acute exacerbation ACTH – adenocorticotopic Steroids – to reduce edema at the site of demyelination to prevent paralysis Spinal Cord Injury Administer drug to prevent paralysis due to edema a. Give ACTH – steroids b. Baclopen (Lioresol) or Dantrolene Na (Dantrium) To decrease muscle spasticity c. Interferone – to alter immune response d. Immunosuppresants 2. Maintain siderails 3. Assist passive ROMexercises – promote proper body alignment 4. Prevent complications of immobility 5. Encourage fluid intake & increase fiber diet – to prevent constipation 6. Provide catheterization due urinary retention 7. Give diuretics Urinary incontinence – give Prophantheline bromide (probanthene) Antispasmodic anti cholinergic 8. Give stress reducing activity. Deep breathing exercises, biofeedback, yoga techniques. 9. Provide acid-ash diet – to acidify urine & prevent bacteria multiplication Grape, Cranberry, Orange juice, Vit C

MYASTHENIA GRAVIS (MG) – disturbance in transmission of impulses from nerve to muscle cell at neuro muscular
junction. Common in Women, 20 – 40 yo, unknown cause or idiopathic Autoimmune – release of cholenesterase – enzyme Cholinesterase destroys ACH (acetylcholine) = Decrease acetylcholine Descending muscle weakness (Ascending muscle weakness – Guillain Barre Syndrome) Nsg priority: 1) a/w 2) aspiration 3) immobility S/ Sx:

1.) Ptosis – drooping of upper lid ( initial sign)
Check Palpebral fissure – opening of upper & lower lids = to know if (+) of MG.


2.) 3.) 4.) 5.) 6.) 7.)

Diplopia – double vision Mask like facial expression Dysphagia – risk for aspiration! Weakening of laryngeal muscles – hoarseness of voice Resp muscle weakness – lead respiratory arrest. Prepare at bedside tracheostomy set Extreme muscle weakness during activity especially in the morning.

Dx test 1. Tensilon test (Edrophonium Hcl) – temporarily strengthens muscles for 5 – 10 mins. Short term- cholinergic. PNS effect. Nsg Mgt 1. Maintain patent a/w & adequate vent by: a.) Assist in mechanical vent – attach to ventilator b.) Monitor pulmonary function test. Decrease vital lung capacity. 2. Monitor VS, I&O neuro check, muscle strength or motor grading scale (4/5, 5/5, etc) 3. Siderails 4. Prevent complications of immobility. Adult-every 2 hrs. Elderly- every 1 hr. 5. NGT feeding Administer meds – a.) Cholinergics or anticholinesterase agents Mestinon (Pyridostigmine) Neostignine (prostigmin) – Long term - Increase acetylcholine s/e – PNS b.) Corticosteroids – to suppress immune resp Decadron (dexamethasone) Monitor for 2 types of Crisis: Myastinic crisis Cholinergic crisis A cause – 1. Under medication Cause: 1 over meds 2. Stress S/Sx - PNS 3. Infection n/v, diarrhea, hypotension, meiosis, facial muscle twitching, B S&Sx 1. Unable to see – Ptosis & abdominal cramps diplopia 2. Dysphagia- unable to swallow. Mgt. adm anti-cholinergic 3. Unable to breath - Atropine SO4 C Mgt – adm cholinergic agents - SNS – dry mouth 7. Assist in surgical proc – thymectomy. Removal of thymus gland. Thymus secretes auto immune antibody. 8. Assist in plasmaparesis – filter blood 9. Prevent complication – respiratory arrest Prepare tracheostomy set at bedside.

GBS – Guillain Barre Syndrome
- Disorder of CNS - Bilateral symmetrical polyneuritis - Ascending paralysis Cause – unknown, idiopathic - Auto immune - r/t antecedent viral infection - Immunizations S&Sx Initial : 1. Clumsiness 2. Ascending muscle weakness – lead to paralysis 3. Dysphagia 4. Decrease or diminished DTR (deep tendon reflexes) - Paralysis 5. Alternate HPN to hypotension – lead to arrhythmia - complication 6. Autonomic changes – increase sweating, increase salivation.


Increase lacrimation Constipation Dx most important: CSF analysis thru lumbar puncture reveals increase in : IgG & CHON (same with MS)

Nsg Mgt 1. Maintain patent a/w & adequate vent a. Assist in mechanical vent b. Monitor pulmonary function test 2. Monitor vs., I&O neuro check, ECG tracing due to arrhythmia 3. Siderails 4. Prevent compl – immobility 5. Assist in passive ROM exercises 6. Institute NGT feeding – due dysphagia 7. Adm meds (GBS) as ordered: – 1. Anti cholinergic – atropine SO4 2. Corticosteroids – to suppress immune response 3. Anti arrhythmic agents a.) Lidocaine /Xylocaine –SE confusion = VTach b.) Bretyllium c.) Quinines/Quinidine – anti malarial agent. Give with meals. - Toxic effect – cinchonism Quinidine toxicity S/E – anorexia, n/v, headache, vertigo, visual disturbances 8. Assist in plasmaparesis (MG. GBS) 9. Prevent comp – arrhythmias, respiratory arrest Prepare tracheostomy set at bedside. INFL CONDITONS OF BRAIN Meninges – 3-fold membrane – cover brain & spinal cord Fx: Protection & support Nourishment Blood supply 3 layers 1. Duramater sub dural space 2. Arachmoid matter 3. Pia matter sub arachnoid space

where CSF flows L3 & L4. Site for lumbar puncture.

MENINGITIS – inflammation of meningitis & spinal cord
Etiology – Meningococcus Pneumococcus Hemophilous influenza – child Streptococcus – adult meningitis MOT – direct transmission via droplet nuclei S&Sx Stiff neck or nuchal rigidity (initial sign) Headache Projectile vomiting – due to increase ICP Photophobia Fever chills, anorexia Gen body malaise Wt loss Decorticate/decerebration – abnormal posturing Possible seizure


Sx of meningeal irritation – nuchal rigidity or stiffness Opisthotonus- rigid arching of back Pathognomonic sign – (+) Kernig’s & Brudzinski sign Leg pain neck pain

Dx: 1. Lumbar puncture – lumbar/ spinal tap – use of hallow spinal needle – sub arachnoid space L3 & L4 or L4 & L5 Aspirate CSF for lumbar puncture. Nsg Mgt for lumbar puncture – invasive 1. Consent / explain procedure to pt - RN – dx procedure (lab) - MD – operation procedure 2. Empty bladder, bowel – promote comfort 3. Arch back – to clearly visualize L3, L4 Nsg Ngt post lumbar 1. Flat on bed – 12 – 24 h to prevent spinal headache & leak of CSF 2. Force fluid 3. Check punctured site for drainage, discoloration & leakage to tissue 4. Assess for movement & sensation of extremeties Result 1. CSF analysis: a. increase CHON & WBC Content of CSF: Chon, wbc, glucose b. Decrease glucose Confirms meningitis c. increase CSF opening pressure N 50 – 160 mmHg d. (+) Culture microorganism 2. Complete blood count CBC – reveals increase WBC Mgt: 1. Adm meds a.) Broad-spectrum antibiotic penicillin S/E 1. GIT irritation – take with food 2. Hepatotoxicity, nephrotoxcicity 3. Allergic reaction 4. Super infection – alteration in normal bacterial flora - N flora throat – streptococcus - N flora intestine – e coli Sx of superinfection of penicillin = diarrhea b.) Antipyretic c.) Mild analgesic 2. Strict resp isolation 24h after start of antibiotic therapy A – Cushing’s synd – reverse isolation - due to increased corticosteroid in body. B – Aplastic anemia – reverse isolation - due to bone marrow depression. C – Cancer anytype – reverse isolation – immunocompromised. D – Post liver transplant – reverse isolation – takes steroids lifetime. E – Prolonged use steroids – reverse isolation F – Meningitis – strict respiratory isolation – safe after 24h of antibiotic therapy G – Asthma – not to be isolated 3. 4. 5. 6. 7. Comfy & dark room – due to photophobia & seizure Prevent complications of immobility Maintain F & E balance Monitor vs, I&O , neuro check Provide client health teaching & discharge plan a. Nutrition – increase cal & CHO, CHON-for tissue repair. Small freq feeding b. Prevent complication hydrocephalus, hearing loss or nerve deafness. 8. Prevent seizure.


Where to bring 2 yo post meningitis - Audiologist due to damage to hearing- post repair myelomeningocele - Urologist -Damage to sacral area – spina bifida – controls urination 9. Rehab for neurological deficit. Can lead to mental retardation or a delay in psychomotor development.

CEREBRO VASCULAR ACCIDENT – stroke, brain attack or cerebral thrombosis, apoplexy
Partial or complete disruption in the brains blood supply 2 largest & common artery in stroke Middle cerebral artery Internal carotid artery Common to male – 2 – 3x high risk

Predisposing factor: 1. Thrombosis – clot (attached) 2. Embolism – dislodged clot – pulmo embolism S/Sx: pulmo embolism Sudden sharp chest pain Unexplained dyspnea, SOB Tachycardia, palpitations, diaphoresis & mild restlessness S/Sx: cerebral embolism Headache, disorientation, confusion & decrease in LOC Femur fracture – complications: fat embolism – most feared complication w/in 24hrs Yellow bone marrow – produces fat cells at meduallary cavity of long bone Red bone marrow – provides WBC, platelets, RBC found at epiphisis 2.) 3.) Hemorrhage Compartment syndrome – compression of nerves/ arteries

Risk factors of CVA: HPN, DM, MI, artherosclerosis, valvular heart dse - Post heart surgery – mitral valve replacement Lifestyle: 1. Smoking – nicotine – potent vasoconstrictor 2. Sedentary lifestyle 3. Hyperlipidemia – genetic 4. Prolonged use of oral contraceptives - Macro pill – has large amt estrogen - Mini pill – has large amt of progestin - Promote lipolysis (breakdown of lipids/fats) – artherosclerosis – HPN - stroke 5. Type A personality a. Deadline driven person b. 2 – 5 things at the same time c. Guilty when not dong anything 6. Diet – increase saturated fats 7. Emotional & physical stress 8. Obesity

S & Sx 1. TIA- warning signs of impending stroke attacks - Headache (initial sx), dizziness/ vertigo, numbness, tinnitus, visual & speech disturbances, paresis or plegia (monoplegia – 1 extreme) Increase ICP 2. Stroke in evolution – progression of S & Sx of stroke 3. Complete stroke – resolution of stroke a.) Headache b.) Cheyne-Stokes Resp c.) Anorexia, n/v d.) Dysphagia


e.) Increase BP f.) (+) Kernig’s & Brudzinski – sx of hemorrhagic stroke g.) Focal & neurological deficit 1. Phlegia 2. Dysarthria – inability to vocalize, articulate words 3. Aphasia 4. Agraphia diff writing 5. Alesia – diff reading 6. Homoninous hemianopsia – loss of half of field of vision Left sided hemianopsia – approach Right side of pt – the unaffected side Dx 1. CT Scan – reveals brain lesion 2. Cerebral arteriography – site & extent of mal occlusion - Invasive procedure due to inject dye - Allergy test All – graphy – invasive due to iodine dye Post 1.) Force fluid – to excrete dye is nephrotoxic 2.) Check peripheral pulses - distal Nsg Mgt 1. Maintain patent a/w & adequate vent - Assist mechanical ventilation - Administer O2 2. Restrict fluids – prevent cerebral edema 3. Elevate head of bed 30-45 degrees angle. Avoid valsalva maneuver. 4. Monitor vs., I&O, neuro check 5. Prevent compl of immobility by: a. Turn client q2h Elderly q1h - To prevent decubitus ulcer - To prevent hypostatic pneumonia – after prolonged immobility. b. Egg crate mattress or H2O bed c. Sand bag or foot board- prevent foot drop 6. NGT feeding – if pt can’t swallow 7. Passive ROM exercise q4h 8. Alternative means of communication - Non-verbal cues - Magic slate. Not paper and pen. Tiring for pt. - (+) To hemianopsia – approach on unaffected side 9. Meds Osmotic diuretics – Mannitol Loop diuretics – Lasix/ Furosemide Corticosteroids – dextamethazone Mild analgesic Thrombolytic/ fibrolitic agents – tunaw clot. SE-Urticaria, pruritus-caused by foreign subs. Streptokinase Urokinase Tissue plasminogen activating Monitor bleeding time Anticoagulants – Heparin & Coumadin” sabay” Coumadin will take effect after 3 days Heparin – monitor PTT partial thromboplastin time if prolonged – bleeding give Protamine SO4- antidote. Coumadin –Long term. monitor PT prothrombin time if prolonged- bleeding give Vit K – Aquamephyton- antidote. Antiplatelet – PASA – aspirin paraanemo aspirin, don’t give to dengue, ulcer, and unknown headache. Health Teaching 1. Avoidance modifiable lifestyle - Diet, smoking 2. Dietary modification


- Avoid caffeine, decrease Na & saturated fats Complications: Subarachnoid hemorrhage Rehab for focal neurological deficit – physical therapy 1. Mental retardation 2. Delay in psychomotor development

CONVULSIVE Disorder (CONVULSIONS)- disorder of the CNS char. by paroxysmal seizures with or without loss of
consciousness, abnormal motor activity, alteration in sensation & perception & change in behavior. Can you outgrow febrile seizure? Febrile seizure Normal if < 5 yo Pathologic if > 5 yo Difference between: Seizure- 1st convulsive attack Epilepsy – 2nd and with history of seizure

Predisposing Factor Head injury due birth trauma Toxicity of carbon monoxide Brain tumor Genetics Nutritional & metabolic deficit Physical stress Sudden withdrawal to anticonvulsants will bring about status epilepticus Status epilepticus – drug of choice: Diazepam & glucose S & Sx I. Generalized Seizure – a.) Grand mal / tonic clonic seizures With or without aura – warning symptoms of impending seizure attack- Epigastric pain- associated with olfactory, tactile, visual, auditory sensory experience - Epileptic cry – fall - Loss of consciousness 3 – 5 min - Tonic clonic contractions - Direct symmetrical extension of extremities-TONIC. Contractions-CLONIC - Post ictal sleep -state of lethargy or drowsiness - unresponding sleep after tonic clonic b.) Petimal seizure – (same as daydreaming!) or absent seizure. - Blank stare - Decrease blinking eye - Twitching of mouth - Loss of consciousness – 5 – 10 secs (quick & short) II. Localized/partial seizure a.) Jacksonian seizure or focal seizure – tingling/jerky movement of index finger/thumb & spreads to shoulder & 1 sideof the body with janksonian march b.) Psychomotor/ focal motor - seizure -Automatism – stereotype repetitive & non-purposive behavior - Clouding of consciousness – not in control with environment - Mild hallucinatory sensory experience

1. 2. 3.

HALLUCINATIONS Auditory – schitzo – paranoid type Visual – korsakoffs psychosis – chronic alcoholism Tactile – addict – substance abuse

III. Status epilecticus – continuous, uninterrupted seizure activity, if untreated, lead to hyperprexia – coma – death Seizure: inc electrical firing in brain=increased metabolic activity in brain=brain using glucose and O2=dec glucose, dec O2. Tx:Diazepam (drug of choice), glucose


Dx-Convulsion- get health history! 1. CT scan – brain lesion 2. EEG electroencephalography - Hyperactivity brain waves Nsg Mgt Priority – Airway & safety 1. Maintain patent a/w & promote safety Before seizure: 1. Remove blunt/sharp objects 2. Loosen clothing 3. Avoid restraints 4. Maintain siderails 5. Turn head to side to prevent aspiration 6. Tongue guard or mouth piece to prevent biting of tongue-BEFORE SEIZURE ONLY! Can use spoon at home. 7. Avoid precipitating stimulus – bright glaring lights & noises 8. Administer meds a. Dilantin (Phenytoin) –( toxicity level – 20 ) SE Ginguial hyperplasia H-hairy tongue A-ataxia N-nystagmus A-acetaminophen- febrile pt Mix with NSS - Don’t give alcohol – lead to CNS depression b. (Tegretol) Carbamasene- given also to Trigeminal Neuralgia. SE: arrythmia c. Phenobarbital (Luminal)- SE: hallucinations 2. Institute seizure & safety precaution. Post seizure: Administer O2. Suction apparatus ready at bedside 3. Monitor onset & duration - Type of seizure - Duration of post ictal sleep. The longer the duration of post ictal sleep, the higher chance of having status epilepticus! 4. Assist in surgical procedure. Cortical resection 5. Complications: Subarachnoid hemorrhage and encephalitis Question: 1 yo grand mal – immediate nursing action = a/w & safety a. Mouthpiece – 1 yr old – little teeth only b. Adm o2 inhalation – post! c. Give pillow – safety (answer) d. Prepare suction Neurological assessment: 1. Comprehensive neuro exam 2. GCS - Glasgow coma scale – obj measurement of LOC or quick neuro check 3 components of ECS M – motor 6 V – verbal resp 5 E – eye opening 4 15 15 – 14 – conscious 13 – 11 – lethargy 10 – 8 – stupor 7 – coma 3 – deep coma – lowest score Survey of mental status & speech (Comprehensice Neuro Exam) 1.) LOC & test of memory


2.) 3.) 4.) 5.) 6.) 7.) 8.)

Levels of orientation CN assessment Motor assessment Sensory assessment Cerebral test – Romhberg, finger to nose DTR Autonomics

Levels of consciousness (LOC) – 1. Conscious (conscious) – awake – levels of wakefulness 2. Lethargy (lethargic) – drowsy, sleepy, obtunded 3. Stupor (stuporous) – awakened by vigorous stimulation Pt has gen body weakness, decrease body reflex 4. Coma (Comatose) light – (+) all forms of painful stimulations Deep – (-) to painful stimulation Question: Describe a conscious pt ? a. Alert – not all pt are alert & oriented to time & place b. Coherent c. Awake- answer d. Aware Different types of pain stimulation - Don’t prick 1. Deep sternal stimulation/ pressure 3x– fist knuckle With response – light coma Without response – deep coma 2. Pressure on great toe – 3x 3. Orbital pressure – pressure on orbits only – below eye 4. Corneal reflex/ blinking reflex Wisp of cotton – used to illicit blinking reflex among conscious patients Instill 1-drop saline solution – unconscious pt if (-) response pt is in deep coma 5. Test of memory – considered educational background a.) Short term memory – - What did you eat for breakfast? Damage to temporal lobe – (+) antero grade amnesia b.) Long term memory (+) Retrograde amnesia – damage to limbic system 6. Levels of orientation Time Place Person Graphesthesia- can identify numbers or letters written on palm with a blunt object. Agraphesthesia – cant identify numbers or letters written on palm with a blunt object.

CN assessment:
I– II – III – IV – V– VI – VII – VIII – IX – X– XI– XII – Olfactory Optic Oculomotor Trocheal Trigeminal Abducens Facial Acustic/auditory Glassopharyngeal Vagus Spinal accessory Hypoglossal s s m m b m b b m m longest CN smallest CN largest CN b s

I. Olfactory – don’t use ammonia, alcohol, cologne irritating to mucosa – use coffee, bar soap, vinegar, cigarette tar - Hyposmia – decrease sensitivity to smell - Diposmia – distorted sense of smell


- Anosmia – absence of sense of smell Either of 3 might indicate head injury – damage to cribriform plate of ethmoid bone where olfactory cells are located or indicate inflammation condition – sinusitis II optic- test of visual acuity – Snellens chart – central or distance vision Snellens E chart – used for illiterate chart N 20/20 vision distance by w/c person can see letters- 20 ft Numerator – distance to snellens chart Denominator – distance the person can see the letters OD – Rt eye 20/20 20/200 – blindness – cant read E – biggest OS – left eye 20/20 OU – both eye 20/20 2. a. b. c. d. Test of peripheral vision/ visual field Superiority Bitemporally Inferiorly Nasally

Common Disorders – see page 85-87 for more info on glaucoma, etc. 1. Glaucoma – Normal 12 – 21 mmHg pressure - Increase IOP - Loss of peripheral vision – “tunnel vision” 2. Cataract – opacity of lens - Loss of central vision, “Blurring or hazy vision” 3. Retinal detachment – curtain veil – like vision & floaters 4. Macular degeneration – black spots III, IV, VI – tested simultaneously - Innervates the movementt of extrinsic ocular muscle 6 cardinal gaze EOM Rt eye IO LR SR 3 – 4 EOM IV – sup oblique VI – lateral rectus Normal response – PERRLA (isocoria – equal pupil) Anisocoria – unequal pupil Oculomotor 1. Raising of eyelid – Ptosis 2. Controls pupil size 2 -3 cm or 1.5 – 2 mm V – Trigeminal – Largest – consists of - ophthalmic, maxillary, mandibular Sensory – controls sensation of the face, mucus membrane; teeth & cornea reflex Unconscious – instill drop of saline solution Motor – controls muscles of chewing/ muscles of mastication Trigeminal neuralgia – diff chewing & swallowing – extreme food temp is not recommended Question: Trigeminal neuralgia, RN should give a. Hot milk, butter, raisins b. Cereals c. Gelatin, toast, potato – all correct but d. Potato, salad, gelatin – salad easier to chew SO S MR E N O left eye


VI Facial: Sensory – controls taste – ant 2/3 of tongue test cotton applicator put sugar. -Put applicator with sugar to tip to tongue. -Start of taste insensitivity: Age group – 40 yrs old Motor- controls muscles of facial expression, smile frown, raise eyebrow Damage – Bells palsy – facial paralysis Cause – bells palsy pedia – R/T forcep delivery Temporary only Most evident clinical sign of facial symmetry: Nasolabial folds VIII Acoustic/ vestibule cochlear (controls hearing) – controls balance (kenesthesia or position sense) - Movement & orientation of body in space - Organ of Corti – for hearing – true sense organ of hearing Outer – tympanic membrane, pinna, oricle (impacted cerumen), cerumen Middle – hammer, anvil, stirrup or melleus, incus, staples. Mid otitis media Eustachean ear Inner ear- meniere dse, sensory hearing loss (research parts! & dse) Remove vestibule – meniere’s dse – disease inner ear


Archimedes law – buoyancy (pregnancy – fetus) Daltons law – partial pressure of gases Inertia – law of motion (dizziness, vertigo) 1.) Pt with multiple stab wound - chest - Movement of air in & out of lungs is carried by what principle? - Diffusion – Dalton’s law 2.) Pregnant – check up – ultrasound reveals fetus is carried by amniotic fluid - Archimedes 3.) Severe vertigo due- Inertia Test for acoustic nerve: - Repeat words uttered IX – Glossopharyngeal – controls taste – posterior 1/3 of tongue X – Vagus – controls gag reflex Test 9 – 10 Pt say ah – check uvula – should be midline Damage cerebral hemisphere is L or R Gag reflex – place tongue depression post part of tongue  Don’t touch uvula XI – Spinal Accessory - controls sternocleidomastoid (neck) & trapezius (shoulders and back) - Shrug shoulders, put pressure. Pt should resist pressure. Paresis or phlegia XII – Hypoglossal – controls movement of tongue – say “ah”. Assess tongue position=midline L or R deviation - Push tongue against cheek - Short frenulum lingue – Tongue tied – “bulol”

ENDOCRINE Fx of endocrine – ductless gland Main gland – Pituitary gland – located at base of brain of Stella Turcica Master gland of body Master clock of body


Anterior pituitary gland – adenohypophysis Posterior pituitary gland – neurohypophysis Posterior pituitary: 1.) Oxytocin – a.) Promotes uterine contraction preventing bleeding/ hemorrhage. - Give after placental delivery to prevent uterine atony. b.) Milk letdown reflex with help of prolactin. 2.) ADH – antidiuretic hormone – (vasopressin) -Prevents urination – conserve H2O

A. DIABETIS INSIPIDUS (DI- dalas ihi) – hyposecretion of ADH
Cause: idiopathic/ unknown Predisposing factor: 1. Pituitary surgery 2. Trauma/ head injury 3. Tumor 4. Inflammation * alcohol inhibits release of ADH S & Sx: 1. Polyuria 2. Sx of dehydration - Excessive thirst (adult) - Agitation - Poor skin turgor - Dry mucus membrane 3. Weakness & fatigue 4. Hypotension – if left untreated 5. Hypovolemic shock Anuria – late sign hypovolemic shock (1st sx of dehydration in children-tachycardia)

Dx Proc: 1. Decrease urine specific gravity- concentrated urine N= 1.015 – 1.035 2. Serum Na = increase (N=135 -145 meq/L) Hypernatremia Mgt: 1. 2. 3. 4. Force fluid 2,000 – 3,000ml/day Administer IV fluid replacement as ordered Monitor VS, I&O Administer meds as ordered a.) Pitresin (vasopressin) IM 5. Prevent complications Most feared complication – Hypovolemic shock

B.) SIADH - Syndrome of Inappropriate Anti-Diuretic Hormone
- Increase ADH - Idiopathic/ unknown Predisposing factor 1. Head injury 2. Related to Bronchogenic cancer or lung canerEarly Sign of Lung Ca - Cough –1. non productive 2. productive 3. Hyperplasia of Pit gland Increase size of organ


S&Sx 1. 2. 3. 4.


Fluid retention Increase BP – HPN Edema Wt gain Danger of H2O intoxication –Complications: 1. cerebral edema – increase ICP – 2. seizure

Dx Proc: 1. Urine specific gravity increase – diluted urine 2. Hyponatremia – Decreased Na

Nsg Mgt: 1. Restrict fluid 2. Administer meds as ordered eg. Diuretics: Loop and Osmotic 3. Monitorstrictly V/S, I&O, neuro check – increase ICP 4. Weigh daily 5. Assess for presence edema 6. Provide meticulous skin care 7. Prevent complications – increase ICP & seizures activity Anterior Pituitary Gland – adeno 1. Growth hormone (GH) (Somatotropic hormone) Fx: Elongation of long bones Decrease GH – dwarfism children Increase GH – gigantism Increase GH – acromegaly – adult Puberty 9 yo – 21 yo Epiphyseal plate closes at 21 yo Square face Square jaw Drug of choice in acromegaly: Ocreotide (Sandostatin) SE dizziness Somatostatin Hormone – antagonizes the release of of GH Melanocytes stimulating hormone - MSH Skin pigmentation 3. Prolactin/luteotrpic hormone/ lactogenic hormone - Promotes development of mammary gland (Oxytocin-Initiates milk letdown reflex) 4. Adrenocorticotropic hormone – ACTH - Development & maturation of adrenal cortex 5. Luteinizing hormone – produces progesterone. 6. FSH- produces estrogen 2. PINEAL GLAND 1. Secretes Melatonin – inhibits lutenizing hormone (LH) secretion THYROID GLAND (TG) Question: Normal physical finding on TG: a. With tenderness – thyroid never tender b. With nodular consistency- answer c. Marked asymmetry – only 1 TG d. Palpable upon swallowing - Normal TG never palpable unless with goiter TG hormones: T3 - Triodothyronine - 3 molecules of iodine

T4 -Tetraiodothyronine/ Tyroxine - 4 molecules of iodine

Thyrocalcitonin FX – antagonizes effects of parathormone


Metabolic hormone Increase metabolism brain –inc cerebration, inc v/s Hypo T3 T4 - lethargy & memory impairment – Hyper T3 T4 - agitation, restlessness, and hallucination 7. Increase VS, increase motility HYPOTHYROIDISM – all decreased except wt & menstruation, loss of appetite but with wt gain menorrhagia – increase in mens HYPERTHYROIDISM - Increase appetite – wt loss, amenorrhea SIMPLE GOITER – enlarged thyroid gland - iodine deficiency Predisposing factors 1. Goiter belt area - Place far from sea – no iodine. Seafood’s rich in iodine 2. Mountainous area – increase intake of goitrogenic foods (US: Midwest, NE, Salt Lake) Cabbage – has progoitrin – an anti thyroid agent with no iodine Example: Turnips (singkamas), radish, peas, strawberries, potato, beans, kamote, cassava (root crops), all nuts. 3. Goitrogenic drugs: Anti thyroid agents :(PTU) prephyl thiupil Lithium carbonate, Aspirin PASA Cobalt, Phenyl butasone Endemic goiter – cause # 1 Sporadic goiter – caused by #2 & 3 S & Sx – enlarged TG Mild restlessness Mild dysphagia Dx Proc. 1. Thyroid scan – reveals enlarged TG 2. Serum TSH – increase (confirmatory) 3. Serum T3, T4 – N or below N Nsg Mgt: 1. Administer meds a.) Iodine solution – Logol’s solution or saturated sol of K iodide SSKI Nsg Mgt Lugol’s sol – violet color 1. use straw – prevent staining teeth 2. Prophylaxis 2 -3 drops Treatment – 5 to 6 drops Use straw – to prevernt staining of teeth 1. Lugol’s sol., 2. tetracycline 3. nitrofurantin (macrodantin)-urinary anticeptic-pyelonephritis. 4. Iron solution. B. Thyroid h / Agents 1. Levothyroxine (Synthroid) 2. Liothyronine (cytomel) 3. Thyroid extract Nsg Mgt: for TH/agents 1. Monitor vs. – HR due tachycardia & palpitation 2. Take it early AM – SE insomnia 3. Monitor s/e Tachycardia, palpitations Signs of insomnia Hyperthyroidism restlessness agitation all v/s down, constipation


Heat intolerance HPN

3. Encourage increase intake iodine – iodine is extracted from seaweeds (!)
Seafood- highest iodine content oysters, clams, crabs, lobster Lowest iodine – shrimps Iodized salt –easily destroyed by heat take it raw not cooked

4. Assist surgery- Sub total thyroidectomyComplication: 1. Tetany 2. laryngeal nerve damage 3.Hemorrhage-feeling of fullness at incision site.Check nape for wet blood. 4.Laryngeal spasm – DOB, SOB – trache set ready at bedside.


HYPOTHYROIDISM – decrease secretion of T3, T4 – can lead to MI / Atherosclerosis

Adult – myxedema Child- cretinism – only endocrine dis lead to mental retardation Predisposing factor: 1. `Iatrogenic causes – caused by surgery 2. Atrophy of TG due to: a. Irradiation b. Trauma c. Tumor, inflammation 3. Iodine def 4. Autoimmune – Hashimoto disease S&Sx everything decreased except wt gain & mens increase) Early signs – weakness and fatigue Loss of appetite – increased lypolysis – breakdown of fats causing atherosclerosis = MI Wt gain Cold intolerance – myxedema - coma Constipation Late Sx – brittle hair/ nails Non pitting edema due increase accumulation of mucopolysacharide in SQ tissue -Myxedema Horseness voice Decrease libido Decrease VS – hypotension bradycardia, bradypnea, and hypothermia Lethargy Memory impairment leading to psychosis-forgetfulness Menorrhagia Dx: 1. 3. Serum T3 T4 decrease RA IU – radio iodine uptake – decrease

2. Serum cholesterol increase – can lead to MI

Nsg Mgt: 1. Monitor strictly V/S. I&O – to determine presence of myxedema coma! Myxedema Coma - Severe form of hypothyroidism Hypotension, hypoventilation, bradycardia, bradypnea, hyponatremia, hypoglycemia, hypothermia Might lead to progressive stupor & coma Impt mgt for Myxedema coma 1. Assist mech vent – priority a/w 2. Adm thyroid hormone 3. Adm IVF replacement – force fluid


Mgt myxedema coma 1. Monitor VS, I&O 2. Provide dietary intake low in calories – due to wt gain 3. Skin care due to dry skin 4. Comfortable & warm environment due to cold intolerance 5. Administer IVF replacements 6. Force fluid 7. Administer meds – take AM – SE insomia. Monitor HR. Thyroid hormones Levothyroxine(Synthroid), Liothyronine (cytomel) Thyroid extracts 8. Health teaching & discharge plan a. Avoidance precipitating factors leading to myxedema coma: 1. Exposure to cold environment 2. Stress 3. Infection 4. Use of sedative, narcotics, anesthetics not allowed – CNS depressants V/S already down Complications: 9. Hypovolemic shock, myxedema coma 10. Hormonal replacement therapy - lifetime 11. Importance of follow up care

HYPERTHYROIDISM - Graves dse or thyrotoxicosis ( everything up except wt and mens)
-Increased T3 & T4 Predisposing factors: 1. Autoimmune disease – release of long acting thyroid stimulator (LATS) Exopthalmos Enopthalmos – severe dehydration depressed eye 2. Excessive iodine intake 3. Hyperplasia of TG S&Sx: 1. Increase in appetite – hyperphagia – wt loss due to increase metabolism 2. Skin is moist - perspiration 3. Heat intolerance 4. Diarrhea – increase motility 5. All VS increase = HPN, tachycardia, tachypnea, hyperthermia 6. CNS changes 8. Irritability & agitation, restlessness, tremors, insomnia, hallucinations 7. Goiter 8. Exopthalmos – pathognomonic sx 9. Amenorrhea Dx: 1. 2. 3. Serum T3 & T4 - increased Radio iodine uptake – increase Thyroid scan – reveals enlarged TG

Nsg Mgt: 1. Monitor VS & I & O – determine presence of thyroid storm or most feared complication: Thyrotoxicosis 2. Administer meds a. Antithyroid agents 1. Prophylthiuracil (PTU) 2. Methymazole (Tapazole) Most toxic s/e agranulocytosis- fever, sore throat, leukocytosis=inc wbc: check cbc and throat swab culture Most feared complication : Thrombosis – stroke CVS 3. Diet – increase calorie – to correct wt loss


4. 5.

7. 8.

Skin care – Comfy & cool environment Maintain siderails- due agitation/restlessness Provide bilateral eye patch – to prevent drying of eyes- exopthalmos Assist in surgery – subtotal thyroidectomy

Nsg Mgt: pre-op Adm Lugol’s solution (SSKI) K iodide 9. To decrease vascularity of TG 10. To prevent bleeding & hemorrhage Mgt post op: Complication: 1. Watch out for signs of thyroid storm or thyrotoxicosis Triad signs of thyroidstorm;

a. Tachycardia /palpitation
b. c. Hyperthermia Agitation 1. 2. 3. Nsg Mgt Thyroid Storm: Monitor VS & neuro check Agitated might decrease LOC Antipyretic – fever Tachycardia - β blockers (-lol) Siderails – agitated

Comp 2. Watch for inadvertent (accidental) removal of parathyroid gland Secretes Para hormone If removed, hypocalcemia - classic sign tetany – 1. .(+) Trousseau sign/ 2. Chvosteck’s sign Nsg Mgt: Adm calcium gluconate slowly – to prevent arrhythmia Ca gluconate toxicity – antidote – MgSO4 3. Laryngeal (voice box) nerve damage (accidental) Sx: hoarseness of voice ***Encourage pt to talk or speak post operatively asap to determine laryngeal nerve damage Notify physician! 4. Signs of bleeding post subtotal thyroidectomy - “Feeling of fullness” at incision site Nsg mgt: Check soiled dressing at nape area 5. Signs of laryngeal spasm a. DOB b. SOB Prepare at bedside tracheostomy 6. Hormonal replacement therapy - lifetime 7. Importance of follow up care (Liver cirrhosis – bedside scissor – if pt complaints of DOB) (Cut cystachean tube to deflate balloon)

Parathyroid gland – pair of small nodules located behind the TG 11. Secrets parathyroid hormone – promotes Ca reabsorption Thyrocalcitonin – antagonises secretion of parathyroid hormone


1. 2.

Hypoparthroidism – decrease of parathyroid hormone Hyperparathroidsm

HYPOPARATHYROIDISM – decreased parathormone
Hypocalcemia (Or tetany) [If Ca decreases, phosphate increases] A. Predisposing, factors: 1. Following subtotal thyroidectomy 2. Atrophy of parathyroid gland due to a. Irradiation b. Trauma S&Sx: 1. Acute tetany a. Tingling sensation b. Paresthesia c. Dysphagia d. Laryngospasm e. Bronchospasm Pathognomonic Sign of tetany: a. (+) Trousseau’s or carpopedial spasm b. (+) Chvosteck’s sign f. Seizure g. Arrhythmia 2. most feared complication Hyperphosphatemia

Chronic tetany a. Loss of tooth enamel b. Photophobia & cataract formation c. GIT changes – anorexia, n/v, general body malaise d. CNS changes – memory impairment, irritability


1. Serum calcium – decrease (N 8.5 – 11 mg/100ml) 2. Serum phosphate increase (N 2.5 – 4.5 mg/100ml)
3. 4. X-ray of long bone – decrease bone density CT Scan – reveals degeneration of basal ganglia

Nsg Mgt: 1. Administration of meds: a.) Acute tetany – Ca gluconate – IV, slowly b.) Chronic tetany 1. Oral Ca supplements Ex. Ca gluconate Ca carbonate Ca lactate Vit D (Cholecalceferol) Drug diet sunlight





7am – 9am

2. Phosphate binder Alumminum DH gel (ampho gel) SE constipation Antacid AAC MAD Aluminum containing acids Aluminum OH gel

Mg containing antacids Ex. Milk or magnesia Diarrhea

Constipation Maalox – magnesium & aluminum - Less s/e 2. Avoid precipitating stimulus such as bright lights & noise: photophobia leading to seizure 3. Diet – increase Ca & decrease phosphorus - Don’t give milk – due to increase phosphorus Good = anchovies – increase Ca, decrease phosphorus + inc uric acid. Tuna & green turnips- Inc Ca. 4. Bedside – tracheostomy set –due to laryngospasm 5. Encourage to breath with paper bag in order to produce mild respiratory acidosis – to promote increase ionized Ca levels 6. Most feared complication : Seizure & arrhythmia 7. Hormonal replacement therapy - lifetime 8. Important fallow up care

HYPERPARATHYROIDISM - increase parathormone. Complication: Renal failure
Hypercalcemia can lead to Hypophosphatemia Bone dse Mineralization Leading to bone fracture Ca – 99% bones 1% serum blood Predisposing Factors: 1. Hyperplasia parathyroid gland (PTG) 2. Over compensation of PTG due to Vit D deficiency Children – Rickets Vit D Adults – Osteomalacia deficiency Sippy’s diet – Vit D diet – not good for pt with ulcer 2 -4 cups of milk & butter Karrel’s diet – Vit D diet – not good for pt with ulcer 6 cups of milk & whole cream Food rich in CHON – eggnog – combination of egg & milk S/Sx: Bone fracture 1. Bone pain (especially at back), bone fracture 2. Kidney stone – a. Renal colic b. Cool moist skin 3. GIT changes – anorexia, n/v, ulcerations 4. CNS involvement– irritability, memory impairment kidney stones


Dx Proc: 1. Serum Ca increase 2. Serum phosphorus decreases 3. X-ray long bones – reveals bone demineralization Nsg Mgt: Kidney Stone Force fluids – 2,000 – 3,000/day or 2-3L/day Isotonic solution Warm sitz bath – for comfort Strain all urine with gauze pad Acid ash diet – cranberry, plum, grapefruit, vit C, calamansi – to acidify urine Adm meds a. Narcotic analgesic – Morphine SO4, Demerol (Meperidine Hcl) S/E – resp depression. Monitor RR) Narcan/ Naloxone – antidote Naloxone toxicity – tremors 7. Siderails 8. Assist in ambulation 9. Diet – low in Ca, increase phosphorus lean meat 10. Prevent complication Most feared – renal failure 11. Assist surgical procedure – parathyroidectomy 12. Impt ff up care 13. Hormonal replacement- lifetime ADRENAL GLAND 12. Atop of @ kidney 13. 2 parts Adrenal cortex – outermost layer Adrenal medulla - innermost layer 14. Secrets cathecolamines a.) Epinephrine / Norephinephrine – potent vasoconstrictor – adrenaline=Increase BP Adrenal Medulla’s only disease: 1. 2. 3. 4. 5. 6.

PHEOCHROMOCYTOMA- presence of tumor at adrenal medulla
-increase nor/epinephrine. HPN with pounding headache. -with HPN and resistant to drugs -drug of choice: beta blockers -complication: HPN crisis = lead to stroke -no valsalva maneuver. Son’t smoke. No caffeine.

Adrenal Cortex –

1. 2.

Zona fasiculata – secrets glucocorticoids. Ex. Cortisol - Controls glucose metabolism (SUGAR) Zona reticularis – secrets traces of glucocorticoids & androgenic hormones M – testosterone F – estrogen & progesterone Fx – promotes development of secondary sexual characteristics

3. Zona glomerulosa - secretes mineralcortisone. Ex. Aldosterone Fx: promotes Na & H2O reabsorption & excretion of potassium (SALT)
ADDISON’S DISEASE – Steroids-lifetime
Decreased adrenocortical hormones leading to: a.) Metabolic disturbances (sugar) b.) F&E imbalances- Na, H2O, K c.) Deficiency of neuromuscular function (salt & sex)


Predisposing Factors: 1. Atrophy of adrenal gland 2. Fungal infections 3. Tubercular infections S/Sx:

1. Decrease sugar – Hypoglycemia – Decreased glucocorticoids - cortisol
T – tremors, tachycardia I - irritability R - restlessness E – extreme fatigue D – diaphoresis, depression

2. Decrease plasma cortisol
Decrease tolerance to stress – lead to Addisonian’s crisis

3. Decrease salt – Hyponatermia – Decreased mineralocorticoids - Aldosterone
Hypovolemia a.) Hypotension b.) Signs of dehydration – extreme thirst, agitation c.) Wt loss 4. Hyperkalemia a.) Irritability b.) Diarrhea c.) Arrhythmia 5. Decrease sexual urge or libido- Decreased Androgen 6. Loss of pubic and axillary hair To Prevent STD Local – practice monogamous relationship CGFNS/NCLEX – condom 7. Pathognomonic sign– bronze like skin pigmentation due to decrease cortisol will stimulate pituitary gland to release melanocyte stimulating hormone. Dx Proc:

1. FBS – decrease FBS (N 80 – 120 mg/dL)


Plasma cortisol – decreased Serum Na – decreased (N 135 – 145 meg/L) Serum K – increased (N 3.5 – 5.5 meg/L)

Nsg Mgt:


Monitor VS, I&O – to determine presence of Addisonian crisis 15. Complication of Addison’s dse : Addisonian crisis 16. Results the acute exacerbation of Addison’s dse characterized by : Hypotension, hypovolemia, hyponatremia, wt loss, arrhythmia 17. Lead to progressive stupor & coma 1. 2. 3. Nsg Mgt Addisonian Crisis (Coma) Assist in mechanical ventilation Adm steroids Force fluids


Administer meds a.) Corticosteroids - (Decadron) or Dexamethazone - Hydrocortisone (cortisone)- Prednisone Nsg Mgt with Steroids 1. Adm 2/3 dose in AM & 1/3 dose in PM in order to mimic the normal diurnal rhythm.


2. Taper the dose (w/draw, gradually from drug) – sudden withdrawal can lead to addisonian crisis 3. Monitor S/E (Cushing’s syndrome S/Sx)
a.) b.) c.) d.) e.) HPN Hirsutism Edema Moon face & buffalo hump Increase susceptibility to infection sue to steroids- reverse isolation

b.) Mineralocorticoids ex. Flourocortisone

3. 4. 5. 6. 7.

Diet – increase calorie or CHO Increase Na, Increase CHON, Decrease K Force fluid Administer isotonic fluid as ordered Meticulous skin care – due to bronze like

HT & discharge planning a) Avoid precipitating factors leading to Addisonian crisis 1. Sudden withdrawal crisis 2. Stress 3. Infection b) Prevent complications Addisonian crisis & Hypovolemic shock

8. 9.

Hormonal replacement therapy – lifetime Important: follow up care

CUSHING’S SYNDROME – increase secretion of adrenocortical hormone
Predisposing Factors: 1. Hyperplasia of adrenal gland 2. Tubercular infection – milliary TB S/Sx 1. Increase sugar – Hyperglycemia 3 P’s 1. Polyuria 2. Polydipsia – increase thirst 3. Polyphagia – increase appetite Classic Sx of DM – 3 P’s & glycosuria + wt loss 2. Increase susceptibility to infection – due to increased corticosteroid 3. Hypernatrermia a. HPN b. Edema c. Wt gain d. Moon face Buffalo hump Obese trunk classic signs Pendulous abdomen Thin extremities 4. Hypokalemia a. Weakness & fatigue b. Constipation c. ECG – (+) “U” wave 5. Hirsutism – increase sex 6. Acne & striae 7. Increase muscularity of female Dx: 1. FBS – increase↑ (N: 80-120mg/dL) 2. Plasma cortisol increase


3. Na – increase (135-145 meq/L) 4. K- decrease (3.5-5.5 meq/L)
Nsg Mgt: 1. Monitor VS, I&O 2. Administer meds a. K- sparing diuretics (Aldactone) Spironolactone - promotes excretion of NA while conserving potassium Not lasix due to S/E hypoK & Hyperglycemia! 3. 4. Restrict Na Provide Dietary intake – low in CHO, low in Na & fats High in CHON & K Weigh pt daily & assess presence of edema- measure abdominal girth- notify doc. Reverse isolation Skin care – due acne & striae Prevent complication - Most feared – arrhythmia & DM (Endocrine disorder lead to MI – Hypothyroidism & DM) Surgical bilateral Adrenolectomy Hormonal replacement therapy – lifetime due to adrenal gland removal- no more corticosteroid!


7. 8.


PANCREAS – behind the stomach, mixed gland – both endocrine and exocrine gland
Acinar cells (exocrine gland) Secrete pancreatic juices at pancreatic ducts. Aids in digestion (in stomach) Islets of Langerhans (endocrine gland ductless) α cells secrets glucagon Fxn: hyperglycemia (high glucose) β Cells Secrets insulin Fxn: hypoglycemia Delta Cells Secrets somatostatin Fxn: antagonizes growth hormone

3 disorders of the Pancreas 1. DM 2. Pancreatic Cancer 3. Pancreatitis

Overview only:


PANCREATITIS (check page 72)– acute inflammation of pancreas leading to pancreatic edema, hemorrhage & necrosis due to
Autodigestion – self-digestion Cause: unknown/idiopathic 18. Or alcoholism Pathognomonic sign- (+) Cullen’s sign - Ecchymosis of umbilicus (bluish color)- pasa (+) Grey turner’s sign – ecchymosis of flank area Both sx means hemorrhage

Predisposing factors - unknown Risk factor: 1. History of hepatobiliary disorder 2. Alcohol 3. Drugs – thiazide diuretics, oral contraceptives, aspirin, penthan 4. Obesity 5. Hyperlipidemia 6. Hyperthyroidism 7. High intake of fatty food – saturated fats

DIABETES MELLITUS - metabolic disorder characterized by non utilization of CHO, CHON,& fat metabolism


Type I DM (IDDM) – “Juvenile “ onset, common in children, non-obese “brittle dse”

-Insulin dependent diabetes mellitus Incidence rate 1.) 10% of population with DM have Type I Predisposing Factor: 1. 90% hereditary – total destruction of pancreatic dells 2. Virus 3. Toxicity to carbon tetrachloride 4. Drugs – Steroids both cause hyperglycemia Lasix - loop diuretics S/Sx: 3 P’S + G 1.) Polyuria 2.) Poydipsia 3.) Polyphagia 4.) Glycosuria 5.) Weight loss 6.) Anorexia 7.) N/V 8.) Blurring of vision 9.) Increase susceptibility to infection 10.) Delayed/ poor wound healing Mgt: 1. Insulin Therapy Diet Exercise Complications – Diabetic Ketoacidosis (DKA) Diabetic Ketoacidosis (DKA) – due to increase fat catabolism or breakdown of fats


DKA –(+) fruity or acetone breath odor Kassmaul’s respiration – rapid, shallow breathing Diabetic coma (needs oxygen)


Type II DM – (NIDDM)

Adult/ maturity onset type – age 40 & above, obese Incidence Rate 1. 90% of pop with DM have Type II Mid 1980’s marked increase in type II because of increase proliferation of fast food chains! Predisposing Factor: 1. Obesity – obese people lack insulin receptors binding site 2. Hereditary S/Sx: 1. 2. Tx: 2. 3. Asymptomatic 3 P’s and 1G

1. Oral Hypoglycemic Agents (OHA)
Diet Exercise

Complication: HONKC H – hyper O – osmolar N – non K – ketotic C – coma III. GESTATIONAL DM – occurs during pregnancy & terminates upon delivery of child Predisposing Factors: 1. Unknown/ idiopathic 2. Influence of maternal hormones S/Sx : Same as type II – 1. Asymptomatic 2. 3 P’s & 1G Type of delivery – CS – due to large baby Sx of hypoglycemia on infant 1. High pitched shrill cry 2. Poor sucking reflex IV. DM ASSOCIATED WITH OTHER DISORDER a.) Pancreatic tumor b.) Cancer c.) Cushing’s syndrome 3 MAIN FOOD GROUPS Anabolism 1. CHON glucose 2. CHON amino acids 3. Fats fatty acids

Catabolism glycogen nitrogen free fatty acids (FFA) – Cholesterol & Ketones

Pancreas → glucose → ATP (Main fuel/energy of cell ) Reserve glucose – glycogen


Liver will undergo – glucogenesis – synthesis of glucagons & Glycogenolysis – breakdown of glucagons & Gluconeogenesis – formation of glucose form CHO sources – CHON & fats Hyperglycemia – pancreas will not release insulin. Glucose can’t go to cell, stays at circulation causing hyperglycemia. increase osmotic diuresis – glycosuria Lead to cellular starvation Lead to wt loss stimulates the appetite/ satiety center (Hypothalamus) Polyphagia Stimulates thirst center (hypothalamus) Polydipsia Increased CHON catabolism Lead to (-) nitrogen balance Tissue wasting (cachexia) polyuria Cellular dehydration

Increase fat catabolism Free fatty acids Cholesterol Atherosclerosis HPN MI stroke ketones DKA coma death

Acute complication of Type I DM due to severe hyperglycemia leading to CNS depression & Coma. Ketones- a CNS depressant

Predisposing factor: 1. Stress – between stress and infection, stress causes DKA more. 2. Hyperglycemia 3. Infection S/Sx: 1. 2. 3. 4. 5. 6. 3 P’s & 1G Polyuria Polydipsia Polyphagia Glycosuria Wt loss Anorexia, N/V (+) Acetone breath odor- fruity odor Kussmaul's resp-rapid shallow respiration CNS depression

7. 8.

pathognomonic DKA


10. Coma Dx Proc: 1. FBS increase, Hct – increase (compensate due to dehydration) N =BUN – 10 -20 mg/100ml --increased due to severe dehydration Crea - .8 – 1 mg/100ml Hct 42% (should be 3x high)-nto hgb Nsg Mgt: 1. Can lead to coma – assist mechanical ventilation 2. Administer .9NaCl – isotonic solution Followed by .45NaCl hypotonic solution To counteract dehydration. 3. Monitor VS, I&O, blood sugar levels 4. Administer meds as ordered: a.) Insulin therapy – IV push Regular Acting Insulin – clear (2-4hrs, peak action) b.) To counteract acidosis – Na HCO3 c.) Antibiotic to prevent infection Insulin Therapy A. Sources: 1. Animal source – beef/ pork-rarely used. Causes severe allergic reaction. 2. Human – has less antigenecity property Cause less allergic reaction. Humulin 3. If kid is allergic to chicken – don’t give measles vaccine due it comes from chicken embryo. Artificially compound

B. Types of Insulin 1. Rapid Acting Insulin - Ex. Regular acting I 2. Intermediate acting I - Ex. NPH (non-protamine Hagedorn I) 3. Long acting I - Ex. Ultra lente Types of Insulin 1. Rapid 2. Intermediate 3. Long acting color & consistency clear cloudy cloudy onset peak duration 2-4h 6-12h 12-24h -

Ex. 5am Hemoglucose test (HGT) 250 mg/dl Adm 5 units of RA I Peak 7-9am – monitor hypoglycemic reaction at this time- TIRED Nsg Mgt: upon injection of insulin: 1.Administer insulin at room temp! – To prevent lipodystrophy = atrophy/ hypertrophy of SQ tissues 2. Insulin is only refrigerated once opened! 3. Gently roll vial bet palms. Avoid shaking to prevent formation of bubbles. 4. Use gauge 25 – 26needle – tuberculin syringe 5. Administer insulin at either 45(for skinny pt) or 90° (taba pt)depending on the client tissue deposit. 6. Don’t aspirate after injection 7. Rotate injection site to prevent lipodystrophy 8. Most accessible site – abdomen 9. When mixing 2 types of insulin, aspirate 1st regular/ clear – before cloudy to prevent contaminating clear insulin & to promote accurate calibration. 10. Monitor signs of complications: a. Allergic reactions – lipodystrophy


b. Somogyi’s phenomenon – hypoglycemia followed by periods of hyperglycemia or rebound effect of insulin. 11. 1ml or cc of tuberculin = 100 units of insulin

- - 1 cc = 100 units - - .5cc = 50 units - - .1 cc = 10 units 6 units RA Most Feared Complication of Type II DM Hyper ↑ osmolarity = severe dehydration Osmolar Non - absence of lipolysis Ketotic - no ketone formation Coma – S/Sx: headache, restlessness, seizure, decrease LOC = coma Nsg Mgt; - same as DKA except don’t give NaHCO3! 1.Can lead to coma – assist mechanical ventilation 2. Administer .9NaCl – isotonic solution Followed by .45NaCl hypotonic solution To counteract dehydration. 3.Monitor VS, I&O, blood sugar levels 4.Administer meds a.) Insulin therapy – IV b.) Antibiotic to prevent infection Tx: O ral H ypoglycemic A gents 19. Stimulates pancreas to secrete insulin Classifications of OHA 1. First generation Sulfonylurear a. Chlorpropamide (diabenase) b. Tolbutamide (orinase) c. Tolazamide (tolinase)

2. 2nd generation sulfonylurear a. Diabeta (Micronase) b. Glipside (Glucotrol)
Nsg Mgt or OHA 1. Administer with meals – to lessen GIT irritation & prevent hypoglycemia 2. Avoid alcohol (alcohol + OHA = severe hypoglycemic reaction=CNS depression=coma) Antabuse-Disufram Dx for DM 1. FBS – N 80 – 120 mg/dl = Increased for 3 consecutive times + 3 P’s & 1G

=confirms DM!!


2. Oral glucose tolerance (OGTT) - Most sensitive test
3. 4. Random blood sugar – increased Alpha Glucosylated Hgb – elevated

Nsg Mgt; 1. Monitor for PEAK action of OHA & insulin Notify Doc 2. Monitor VS, I&O, neurocheck, blood sugar levels. 3. Administer insulin & OHA therapy as ordered. 4. Monitor signs of hyper & hypoglycemia. Pt DM –“ hinimatay” 20. You don’t know if hypo or hyperglycemia. Give simple sugar (Brain can tolerate high sugar, but brain can’t tolerate low sugar!) Cold, clammy skin – hypo – Orange Juice or simple sugar / warm to touch – hyper – adm insulin 5. Provide nutritional intake of diabetic diet: CHO – 50% CHON – 30% Fats – 20% -Or offer alternative food products or beverage. -Glass of orange juice. 6. Exercise – after meals when blood glucose is rising. 7. Monitor complications of DM a. Atherosclerosis – HPN, MI, CVA b. Microangiopathy – small blood vessels Eyes – diabetic retinopathy , premature cataract & blindness Kidneys – recurrent pyelonephritis & Renal Failure (2 common causes of Renal Failure : DM & HPN) c. Gangrene formation d. Peripheral neuropathy 1. Diarrhea/ constipation 2. Sexual impotence e. Shock due to cellular dehydration 8. Foot care mgt a. Avoid waking barefooted b. Cut toe nails straight c. Apply lanolin lotion – prevent skin breakdown d. Avoid wearing constrictive garments 9. Annual eye & kidney exam 10. Monitor urinalysis for presence of ketones Blood or serum – more accurate 11. Assist in surgical wound debridement 12. Monitor signs or DKA & HONKC 13. Assist surgical procedure BKA or above knee amputation

I Blood 55% Plasma, 45% cellular/ formed elements II Blood vessels III Blood forming organs 1. Thymus – removed myasthenia gravis 2. Liver – largest gland 3. Lymph nodes 4. Lymphoid organs – payers patch 5. Bone marrow


6. Spleen – destroys RBC Blood vessels 1. Veins –SVC, IVC, Jugular vein – blood towards the heart 2. Artery – carries blood away from the 21. Aorta, carotid 3. Capillaries
Blood 45% formed elements – 55% plasma – fluid portion of vlood. Yellow color. Serum Plasma CHON’s (Produced in Liver) 1. Albumin- largest, most abundant plasma Maintains osmotic pressure preventing edema FXN: promotes skin integrity 2. Globulins – alpha – transports steroids Hormones & bilirubin β - Transports iron & copper Gamma – transport immunoglobulins or antibodies (Acute or Chronic) 3. Prothrombin and Fibrinogen – clotting factor to prevent bleeding Cellular Elements: 1. RBC (erythrocytes) Spleen life span = 120 days (N) 3 – 6 M/mm3 - Anucleated - Biconcave discs - Has molecules of Hgb (red cell pigment) Transports & carries O2

SICKLE CELL ANEMIA –sickle shaped RBC. Should be round. Impaired circulation of RBC. -immature cells=hemolysis of RBC=decreased hgb
3 Nsg priority 1. AIRWAY (priority) – avoid deoxygenating activities - High altitude is bad 2. Fluid deficit – promote hydration 3. Pain & comfort Hgb ( hemoglobin)- red cell pigment which transport O2 F= 12 – 14 gms % M = 14-16 gms % Hct – 3x hgb 12 x 3 = 36 (hamatocrit) F 36 – 42% 14 x 3 = 42 *Hematocrit is the red cell pigment in whole blood M 42 – 48% *Erythropoietin- stimulate bone marrow to produce RBC Average 42% - Red cell percentage in whole red Substances needed for maturation of RBC a.) Folic acid b.) Iron c.) Vit C d.) Vit B12 (cyanocobalamin) e.) Vit B6 (Pyridoxine) f.) Intrinsic factor Pregnant: 1st trimester- Folic acid – prevent neural tube deficit 3rd tri – iron Life span of rbc – 80 – 120 days. Destroyed at spleen.


WBC – leukocytes 5,000 – 10,000/mm3 GRANULOCYTES 1. Polymorphonuclearneutrophils Most abundant 60-70% WBC - fx – short term phagocytosis For acute inflammation 2. PM Basophils -Involved in Parasitic infection - Release of chemical mediators for inflammation -Serotonin, histamine, prostaglandin, bradykinins 3. PM Eosinophils - Allergic reactions NON-GRANULOCYTES 1. Monocytes (macrophage) - largest WBC - involved in long term phagocytes - For chronic inflammation - Other name macrophage Macrophage in CNS- microglia Macrophage in skin – Histiocytes Macrophage in lungs – alveolar macrophage Macrophage in Kidneys – Kupffer cells 2. Lymphocytes B Cell – L – bone marrow or bursa dependent T cell – dev’t of immunity- target site for HIV NK cell – natural killer cell Have both antiviral & anti-tumor properties immunity

3.Platelets (thrombocytes) N- 150,000 – 450, 000/ mm3 it promotes hemostasis – prevention of blood loss by activating clotting - Consists of immature or baby platelets known as megakaryocytes – target of virus – dengue - Normal lifespan 9 – 12 days Drug of choice for HIV Zidovudine (AZT) or Ritonavir or Retrovir Standard precaution for HIV gloves, gown, goggles & mask Malaria – night biting mosquito Dengue – day biting mosquito Signs of platelet dys function: a.) Petechiae Hemophilia b.) Ecchymoses/ bruises DIC c.) Oozing or blood ON venipuncture site

Iron deficiency Anemia – chronic normocytic, hypochromic (pale), microcytic anemia due to inadequate absorption of iron leading to hypoxemic tissue injury. Incidence rate: 1. Common – developed country – due to high cereal intake Third leading cause of death in the US due to accidents 2. Common – tropical countries – blood sucking parasites 3. Women – 15 – 35yo – reproductive yrs 4. Common among the poor – poor nutritional intake THINGS TO REMEMBER: Suicide - common in teenagers Poisoning – common in children (aspirin) Aspiration – common in infant Accidents – common in adults Choking – common in toddler SIDS – common in infant in US 22. Common in tropical zone – Phil due blood sucks


Predisposing factors: 1. Chronic blood loss a. Trauma b. Mens c. GIT bleeding: i. Hematemesisii. Melena – upper GIT – duodenal cancer iii. Hematochezia – lower GIT – large intestine – fresh blood from rectum 2. Inadequate intake of food rich in iron A. Eggs B. Organ meats, eggs, oatmeals, dried fruits, legumes, raisins 3. Inadequate absorption of iron – due to : a. Chronic diarrhea b. Malabsorption syndrome –celiac disease-gluten free diet. Food for celiac pts- sardines c. High cereal intake with low animal CHON ingestion d. Subtotal gastrectomy- partial removal of the stomach 4. Improper cooking of food S/Sx:

1. Usually asymptomatic
2. 3. 4. Weakness and Fatigue Headache, dizziness, dyspnea, palpitations, cold sensitivity, gen body malaise, pallor Brittle hair, spoon shaped nails (KOILONYCHIA)=Dec O2=hypoxia=atrophy of epidermal cells Atropic glossitis, dysphagia, stomatitis Pica – abnormal craving for non edible food (caused by hypoxia=dec tissue perfusion=psychotic behavior)

5. 6.

Brittle hair, spoon shaped nail – atrophy of epidermal cells N = capillary refill time < 2 secs N = shape nails – biconcave shape, 180° Atrophy of cells “Plummer Vinsons Syndrome” due to cerebral hypoxia 1. Atropic glossiti s– inflammation of tongue due to atrophy of pharyngeal and tongue cells 2. Stomatitis – mouth sores 3. Dysphagia Dx Proc: 1. RBC 2. Hgb 3. Reticulocyte 4. Hct 5. Iron 6. Ferritin Nsg Mgt

1. Monitor signs of bleeding of all hema test including urine & stool, GIT 2. Complete bed rest – don’t overtire pt =weakness and fatigue=activity intolerance
Encourage – iron rich food Raisins, legumes, egg yolk Instruct the pt to avoid taking tea - impairs iron absorption Administer meds a.) Oral iron preparation Ferrous SO4 Fe gluconate Fe Fumarate Nsg Mgt oral iron meds: 1. Administer with meals – to lessen GIT irritation 3. 23. 4. 5.


2. If diluting in iron liquid prep –adm with straw
Straw 1. 2. 3. 4. Lugol’s Tetracycline Oral iron Macrodantine

3. Give Orange juice – for iron absorption
4. a. b. c. d. e. Monitor & inform pts S/E Anorexia n/v Abdominal pain Diarrhea or constipation Melena

If pt can’t tolerate oral iron prep – administer parenteral iron prep example: 1. Iron dextran (IV, IM) 2. Sorbitex (IM) Nsg Mgt parenteral iron prep 1. Administer of use Z tract method to prevent discomfort, discoloration leakage to tissues. 2. Don’t massage injection site. Ambulate to facilitate absorption. 3. Monitor S/E: a.) Pain at injury site b.) Localized abscess (“nana”/ pus formation) c.) Lymphadenopathy d.) Fever/ chills e.) Urticaria – itchiness f.) Hypotension – anaphylactic shock Anaphylactic shock – give epinephrine

PERNICIOUS ANEMIA - megaloblastic, chronic anemia due to deficiency of intrinsic factor leading to
Hypochlorhydria – decrease Hcl acid secretion. Lifetime B12 injections. With CNS involvement. Predisposing factor 1. Subtotal gastrectomy –partial removal stomach 2. Hereditary 3. Inflammatory dse of ileum 4. Autoimmune 5. Strict vegetable diet STOMACH Parietal or argentaffin Oxyntic cells Fxn – produce intrinsic factor For reabsorption of B12 For maturation of RBC 6. Diet high caloric or CHO to correct wt loss S/Sx: 1. Headache dizziness, dyspnea, palpitations, cold sensitivity, gen body malaise, pallor Fxn – secrets Hcl acid Fx aids in digestion


GIT changes a. Red – beefy tongue – PATHOGNOMONIC – mouth sores b. Dyspepsia – indigestion c. Wt loss d. Jaundice 3. CNS – Most dangerous anemia: pernicious due to neuroglogic involvement. a. Tingling sensation b. Paresthesia c. (+) Romberg’s test (Ataxia) d. Psychosis Dx: Schilling’s test—measures reabsorption of Vit B12 Confirmatory: absence of intrinsic factor Nsg Mgt – Pernicious anemia 1. Enforce CBR 2. Administer B12 injections at monthly intervals for lifetime as ordered. IM- dorsogluteal or ventrogluteal. Not given oral – due pt might develop resistance to drug Does not develop toxicity because of it is water soluble therefore it is easily excreted 3. Diet – high calorie or CHO. Increase CHON, iron & Vit C 4. Avoid irritating mouthwashes. Use of soft bristled toothbrush is encouraged. Provide oral care 5. Avoid applying electric heating pads or any heat application – can lead to burns


APLASTIC ANEMIA – stem cell disorder due to bone marrow depression leading to pancytopenia – all RBC are decreased
Decrease RBC Anemia Increase WBC leukocytocystosis Increase RBC polycythemia vera – complication stroke, CVA, thrombosis Predisposing factors leading to Aplastic Anemia 1. Chemicals – Banzene & its derivatives 2. radiation 3. Immunologic injury 4. Drugs – cause bone marrow depression a. Broad spectrum antibiotic - Chloramphenicol - Sulfonamides – bactrim b. Chemo therapeutic agents Methotrexate – alkylating agents Nitrogen mustard – anti metabolic Vincristine – plant alkaloid S/Sx: 1. Anemia: a. Weakness & fatigue b. Headache, dizziness, dyspnea c. cold sensitivity, pallor d. palpitations 2. Leukopenia – increase susceptibility to infection 3. Thrombocytopenia – a. Petecchiae b. Oozing of blood from venipuncture site c. ecchymoses Dx: 1. 2. CBC – pancytopenia Bone marrow biopsy/ aspiration at post iliac crest – reveals fatty streaks in bone marrow decrease WBC leukopenia decrease platelets thrombocytopenia


Nsg Mgt: 1. Removal of underlying cause 2. Blood transfusion as ordered 3. Complete bed rest 4. O2 inhalation 5. Reverse isolation due leukopenia 6. Monitor signs of infection 7. Avoid SQ, IM or any venipuncture site = HEPLOCK 8. Use electric razor when shaving to prevent bleeding 9. Administer meds Immunological injury: give steroids Immunosuppresants: Anti lymphocyte globulin (Alg) given via central venous catheter, 6 days – 3 weeks to achieve max therapeutic effect of drug. BLOOD TRANSFUSION: Objectives: 1. To replace circulating blood volume 2. To increase O2 carrying capacity of blood 3. To combat infection if there’s decrease WBC 4. To prevent bleeding if there’s platelet deficiency Nsg Mgt & principles in Blood Transfusion 1. Proper refrigeration 2. Proper typing & crossmatching Type O – universal donor AB – universal recipient 85% of people are RH (+) 3. Asceptically assemble all materials needed: a.) Filter set b.) Isotonic or PNSS or .9NaCl to prevent Hemolysis Hypotonic sol – swell or burst Hypertonic sol – will shrink or crenate c.) Needle gauge 18 - 19 or large bore needle to prevent hemolysis. d.) Instruct another RN to recheck the following . Pts name, blood typing & cross typing, expiration date, serial number. e.) Check blood unit for presence of bubbles, cloudiness, dark in color & sediments – indicates bacterial contamination. Don’t dispose. Return to blood bank. f.) Never warm blood products – may destroy vital factors in blood. - Warming is done if with warming device – only in EMERGENCY! For multiple BT. - Within 30 mins room temp only! g.) Blood transfusion should be completed < 4hrs because blood that is exposed at room temp for > 2h causes blood deterioration may cause bacterial contamination. h.) Avoid mixing or administering drug at BT line – leads to hemolysis i.) Regulate BT 15-20 gtts/min KVO or 100cc/hr to prevent circulatory overload j.) Monitor VS before, during & after BT especially q15 mins(local board) for 1st hour. NCLEX-q5min for 1st 15min. - Majority of BT reaction occurs within 1h.

BT reactions S/Sx Hemolytic reaction: H – hemolytic Reaction 1. Headache, dizziness, dyspnea, palpitation, lumbar/ sterna/ flank pain, A – allergic Reaction hypotension, flushed skin , (red) port wine urine. P – pyrogenic Reaction C – circulatory overload A – air embolism T - thrombocytopenia C – citrate intoxication – expired blood =hyperkalemia H – hyperkalemia


Nsg Mgt: Hemolytic Reaction: 1. Stop BT 2. Notify Doc 3. Flush with plain NSS 4. Administer isotonic fluid sol – to prevent acute tubular necrosis & conteract shock 5. Send blood unit to blood bank for reexamination 6. Obtain urine & blood samples of pt & send to lab for reexamination 7. Monitor VS & Allergic Rxn

Allergic Reaction:
S/Sx 1. 2. 3. 4. 5. Fever/ chills Urticaria/ pruritus Dyspnea Laryngospasm/ bronchospasm Bronchial wheezing

Nsg Mgt: 1. Stop BT 2. Notify Doc 3. Flush with PNSS 4. Administer antihistamine – diphenhydramine Hcl (Benadryl). Give bedtime.SE-Adult-drowsiness. Child-hyperactive If (+) Hypotension – anaphylactic shock administer – epinephrine 5. Send blood unit to blood bank 6. Obtain urine & blood samples – send to lab 7. Monitor VS & IO 8. Adm antipyretic & antibiotic for pyrogenic Rxn & TSB

Pyrogenic Reaction:

a.) Fever/ chills b.) Headache c.) Dyspnea
Nsg Mgt: 1. 2. 3. 4. 5. 6. 7.

d. tachycardia e. palpitations f. diaphoresis

Sx a. b. c. d.

Stop BT Notify Doc Flush with PNSS Administer antipyretics, antibiotics Send blood unit to blood bank Obtain urine & blood samples – send to lab Monitor VS & IO Tepid sponge bath – offer hypothermic blanket

Circulatory Overload:
Dyspnea Orthopnea Rales or crackles Exertional discomfort

Nsg Mgt: 1. Stop BT 2. Notify Doc. Don’t flush due pt has circulatory overload. 3. Administer diuretics –Loop (Furosemide) Priority cases: Hemolytic Rxn – 1st due to hypotension – 1st priority – attend to destruction of Hgb – O2 brain damage


Allergic Pyrogenic Circulatory Hemolytic Anaphylitic

3rd 4th 2nd 2nd 1st priority


24. Acute hemorrhagic syndrome char by wide spread bleeding & thrombosis due to a defiency of clotting factors (Prothrombin
& Fibrinogen). Predisposing factor: 1. Rapid BT 2. Massive trauma 3. Massive burns 4. Septicemia 5. Hemolytic reaction 6. Anaphylaxis 7. Neoplasia – growth of new tissue 8. Pregnancy S/Sx




Petechiae – widespread & systemic (lungs, lower & upper trunk) Ecchymoses – widespread Oozing of blood from venipunctured site

4. 5.


Hemoptysis – cough blood Hemorrhage Oliguria – late sx

Dx Proc– 1. CBC – reveals decrease platelets 2. Stool for occult blood (+) Specimen – stool 3. Opthalmoscopic exam – sub retinal hemorrhage 4. ABG analysis – metabolic acidosis pH pH ph ph ph HCO3 PCO2 PCO2 HCO3 HCO3


respiratory alkalosis respiratory acidosis metabolic alkalosis metabolic acidosis

Diarrhea – met acidosis Vomitting – met alk Pyloric stenosis – met alkalosis – vomiting Ileostomy or intestinal tubing – met acidosis Cushing’s – met alk DM met acid Chronic bronchitis – resp acid – with hypoxemia, cyanosis Nsg Mgt DIC 1. 3. 4. a. Monitor signs of bleeding – hema test + urine, stool, GIT

2. Administer isotonic fluid solution to prevent shock.
Administer O2 inhalation Administer meds Vit K aquamephyton b. Pitressin or vasopressin – to conserve water 5. NGT – lavage - Use iced saline lavage- for decompensation, iced saline is used 6. Monitor NGT output 7. Provide heplock 8. Prevent complication: hypovolemic shock Late signs of hypovolemic shock: anuria Oncologic Nsg: Oncology – study of neoplasia –new growth Benign (tumor) Diff - well differentiated Encapulation – (+) Metastasis – (-) Prognosis – good Therapeutic modality surgery Malignancy (cancer) poorly or undifferentiated (-) (+) poor 1. Chemotherapy plenty S/E 2. Radiation 3. Surgery most preferred treatment 4. Bone marrow transplant - Leukemia only

Predisposing factors: (carcinogenesis) G – genetic factors I – immunologic factors V – viral factors a. Human papiloma virus – causing warts b. Epstein barr virus E – environmental Factors 90% a. Physical – irradiation, UV rays, nuclear explosion, chronic irritation, direct trauma b. Chemical factors – - Food additives (nitrates - Hydrocarbon vesicants, alkalies - Drugs (stillbestrol) - Uraehane - Hormones - Smoking Male 3.) Prostate cancer - common 40 & above (middle age & above) BPH – 50 & above 1.) Lung cancer 2.) Liver cancer


Female 1. Breast cancer – 40 yrs old & up – mammography 15 – 20 mins (SBE – 7 days after mens) 2. Cervical cancer – 90% multi sexual partners 5% early pregnancy 3. Ovarian cancer Classes of cancer Tissue typing 1. Carcinoma – arises from surface epithelium & glandular tissues 2. Sarcoma- from connective tissue or bones 3. Multiple myeloma – from bone marrow Pathological fracture of ribs & back pain 4. Lymphoma – from lymph glands 5. Leukemia – from blood Warning / Danger Sx of CA C – change in bowel /bladder habits A – a sore that doesn’t heal U – unusual bleeding/ Discharge T – thickening of lump – breast or elsewhere I – indigestion? Dysphagia O – obvious change in wart/ mole N – nagging cough/ hoarseness U – unexplained anemia A - anemia S – sudden wt loss L – loss of wt Therapeutic Modality:

1. Chemotherapy – use various chemotherapeutic agents that kills cancer cells & kills normal rapidly producing cells – GIT,
bone marrow, and hair follicle. Classification: a.) Alkylating agents – b.) Plant alkaloids – vincristine c.) Anti metabolites – nitrogen mustard d.) Hormones – DES Steroids e.) Antineoplastic antibiotics S/E & mgt GIT - -Nausea & vomiting Nsg Mgt: 1. Administer anti emetic 4 – 6h before start of chemo Plasil 2. Withhold food/ fluid before start of chemo 3. Provide bland diet post chemo 25. Non irritating / non spicy - Diarrhea 1. Administer anti diarrheal 4 – 6h before start of chemo 2. Monitor urine, I&O qh - Stomatitis/ mouth sores 1. Oral care – offer ice chips/ popsickles 2. Inform pt – hair loss – temporary alopecia Hair will grow back after 4 – 6 months post chemo. -Bone marrow depression – anemia 1. Enforce CBR 2. O2 inhalation 3. Reverse isolation 4. Monitor signs of bleeding Repro organ – sterility 1. Do sperm banking before start of chemo Renal system – increase uric acid 1. Administer allopurinol/ xyloprin (gout) 26. Inhibits uric acid 27. Acute gout – colchicines 28. Increase secretion of uric acid Neurological changes – peristalsis – paralytic ileus Most feared complication ff any abdominal surgery Vincristine – plant alkaloid causes peripheral neuropathy

2. Radiation therapy – involves use of ionizing radiation that kills cancer cells & inhibit their growth & kill N rapidly producing
cells. Types of energy emitted 1. Alpha rays – rarely used – doesn’t penetrate skin tissues 2. Beta rays – internal radiation – more penetration 3. Gamma ray – external radiation – penetrates deeper underlying tissues


Methods of delivery 1. External radiation- involves electro magnetic waves Ex. cobalt therapy 2. Internal radiation – injection/ implantation of radioisotopes proximal to CA site for a specific period of time. 2 types: a.) Sealed implant – radioisotope with a container & doesn’t contaminate body fluid. b.) Unsealed implant – radioisotope without a container & contaminates body fluid. Ex. Phosphorus 32 3 Factors affecting exposure: A.) Half life – time period required for half of radioisotopes to decay. - At end of half life – less exposure B.) Distance – the farther the distance – lesser exposure C. ) Time – the shorter the time, the lesser exposure D.) Shielding – rays can be shielded or blocked by using rubber gloves – α & β gamma – use thick lead on concrete. S/E & Mgt: a.) Skin errythema, redness, sloughing 1. Assist in battling pt 2. Force fluid – 2,000 – 3,000 ml/day 3. Avoid lotion or talcum powder – skin irritation 4. Apply cornstarch or olive oil b.) GIT –nausea / vomiting 1. Administer antiemetic 4 – 6h before start of chemo - Plasil 2 Withhold food/ fluid before start of chemo 3. Provide bland diet post chemo Non irritating / non spicy Dysglusia – decrease taste sensitivity -When atrophy papilla (taste buds) – 40 yo Stomatitis c.) Bone marrow depression 1. Enforce CBR 2. O2 inhalation 3. Reverse isolation 4. Monitor signs of bleeding

Overview of function & structure of the heart
HEART - Muscular, pumping organ of the body - Left mediastinum - Weigh 300 – 400 grams - Resembles a closed fist - Covered by serous membrane – pericardium Pericardium Parietal layer (outer) Layer 1. 2. 3. Pericardial Fluid – to prevent Friction rub (10-20 cc) Visceral layer (inner)

Epicardium – outermost Myocardium – inner – responsible for pumping action/ most dangerous layer - cardiogenic shock - may lead to myocarditis, which may lead to RHD Endocardium – innermost layer

Chambers 1. Upper – collecting/ receiving chamber - Atria 2. Lower – pumping/ contracting chamber - Ventricles Valves 1. Atrioventricular valves - Tricuspid & mitral valve Closure of AV valves – gives rise to 1st heart sound or S1 or “lub” 2. Semi lunar valve a.) Pulmonic b.) Aortic Closure of semilunar valve – gives rise to 2nd heart sound or S2 or “dub” Extra heart Sound S3 – ventricular Gallop – CHF S4 – atrial gallop – MI, HPN Coronary Arteries- arise from base of the aorta Right main coronary artery Supply the Left main coronary artery myocardium Heart conduction system 1. Sino atrial node (SA node) (or Keith-Flock node)


2. 3.


Loc – junction of SVC & Rt atrium Fx- primary pace maker of heart -Initiates electric impulse of 60 – 100 bpm Atrioventicular node (AV node or Tawara node) Loc – inter atrial septum Delay of electric impulse to allow ventricular filling (for about ,08millisecond) Bundle of His – location interventricular septum Rt main Bundle Branch Lt main Bundle Branch Purkinje Fibers Loc- walls of ventricles leading to Ventricular contractions

SA node

Purkenjie Fibers Bundle of His Complete heart block or the bundle block – insertion of pacemaker at Bundle Branch is needed Metal – Pace Maker – change q3 – 5 yo Prolonged PR – atrial fib ST segment depression – angina ST – elev – MI T wave inversion – MI widening QRS – arrhythmia

CAD – coronary artery dse or Ischemic Heart Dse (IHD) ==Nsg Mgt: decrease myocardial workload Stages: 1. Atherosclerosis – Myocrdial injury 2. Angina Pectoris – Myocardial ischemia 3. MI- myocardial necrosis

- Narrowing of artery due to fat - lipid deposits at tunica intima. Artery – tunica adventitia – outer - Tunica intima – innermost - Tunica media – middle ATHEROSCLEROSIS Predisposing Factor 1. Sex – male 2. Black race 3. Hyperlipidemia, increase in saturated fats 4. Smoking 5. HPN 6. DM 7. Oral contraceptive- prolonged use 8. Sedentary lifestyle 9. Obesity 10. Hypothyroidism 11. Stress Signs & Symptoms 1. Chest pain 2. Dyspnea 3. Tachycardia 4. Palpitations 5. Diaphoresis Treatment P – percutaneous T – tansluminar C – coronary A – angioplasty

- Hardening or artery due to calcium & CHON deposits at tunica media.

For single occluded vessels


Obj: 1. 2. 3. To revascularize the myocardium To prevent angina Increase survival rate

PTCA – done to pt with single occluded vessel . Multiple occluded vessels C – coronary A – arterial for 2 or more occluded vessels B – bypass A –and G – graft surgery Nsg Mgt Before CABAG 1. Deep breathing cough exercises 2. Use of incentive spirometer 3. Leg exercises

ANGINA PECTORIS- A clinical syndrome characterized by paroxysmal chest pain usually relieved by REST or NGT
nitroglycerin, resulting fr temp myocardial ischemia. Predisposing Factor: (same with CAD) 1. sex – male 2. black race 3. hyperlipidemia 4. smoking 5. HPN 6. DM 7. oral contraceptive prolonged 8. sedentary lifestyle 9. obesity 10. hypothyroidism Precipitating factors 4 E’s 1. Excessive physical exertion 2. Exposure to cold environment - Vasoconstriction 3. Extreme emotional response 4. Excessive intake of food – saturated fats Signs & Symptoms 1. Initial symptoms – Levine’s sign – hand clutching of chest 2. Chest pain – sharp, stabbing excruciating pain. Location – substernal -radiates back, shoulders, axilla, arms & jaw muscles -relieve by rest or NGT 3. Dyspnea 4. Tachycardia 5. Palpitation 6. diaphoresis Diagnosis 1. History taking & PE 2. ECG – ST segment depression 3. Stress test – treadmill = abnormal ECG 4. Serum cholesterol & uric acid - increase Nursing Management 1.) Enforce CBR 2.) Administer meds as ordered NTG – small doses – venodilator Large dose – vasodilator 1st dose NTG – give 3 – 5 min 2nd dose NTG – 3 – 5 min 3rd & last dose – 3 – 5 min Still painful after 3rd dose – notify doc. MI! 55 yrs old with chest pain: 1st question to ask pt: what did you do before you had chest pain. 2nd question: does pain radiate? If chest pain radiates – heart in nature. If not radiate – pulmonary origin (PTB, Pneumonia, Emphysema) Nitroglycerin- act as Venodilator (if given in small doses)– dilate veins of lower ext – increase venous pooling lead to decrease venous return. Large doses- vasodilators Meds:


A. NTG- Nsg Mgt: 1. Keep in a dry place. 2. Avoid moisture & heat, sunlight may inactivate the drug. 3. Monitor S/E: orthostatic hypotension – dec bp transient headache dizziness 4. Rise slowly from sitting position 5. Assist in ambulation. 6. If giving NTG via patch: i. avoid placing it near hairy areas-will dec drug absorption (SHAVE AREA) ii. avoid rotating transdermal patches- will dec drug absorption iii. avoid placing near microwave oven or during defibrillation-will burn pt due aluminum foil in patch B. Beta blockers – PROPANOLOL (inderal) C. ACE inhibitors – CAPTOPRIL D. Ca antagonist - NIFEDIPINE Administer O2 inhalation Semi-fowler Diet- Decrease Na and saturated fats, caffeine Monitor VS, I&O, ECG HT: Discharge planning: a. Avoid precipitating factors – 4 E’s b. Prevent complications – MI c. Take meds before physical exertion-to achieve maximum therapeutic effect of drug d. Importance of follow-up care.

3.) 4.) 5.) 6.) 7.)

MI – MYOCARDIAL INFARCTION – heart attack – terminal stage of CVD characterized by malocclusion leading to
necrosis and scarring Types: A. According to Location

1. Trasmural MI – most dangerous MI – Mal-occlusion of both R&L coronary artery 2. Sub-endocardial MI – mal-occlusion of either R & L coronary artery
Most critical period upon dx of MI – 48 to 72h—most dangerous hours: first 6-8 hours (majority of arrythmias occur, PVCs) - Majority of pt suffers from PVC premature ventricular contraction. B. According to mortality Killip I – 15-20% chance of mortality (75-80% survival) Killip II – 30-35% mortality Killip III- 45-50% mortality Killip IV- 65-70% mortality—spiritual support is needed, pt chronically ill characterized by cardiogenic shock Predisposing factors 1. sex – male 2. black raise 3. hyperlipidemia 4. smoking 5. HPN 6. DM 7. oral contraceptive prolonged 8. sedentary lifestyle 9. obesity 10. hypothyroidism Signs & symptoms 1. chest pain – excruciating, visceral pain located substernal or precodial area (rare) - radiates back, arm, shoulders, axilla, jaw & abd muscles (abdominal ischemia). - not usually relived by rest or NTG 2. dyspnea 3. Hyperthermia 4. initial increase in BP 5. mild restlessness & apprehensions 6. cool, moist ashen skin 7. occasional findings a.) split S1 & S2 b.) pericordial friction rub c.) rales /crackles d.) S4 (atrial gallop) –(MI and Hypertension) Diagnostic Exam 1. cardiac enzymes a.) CPK – MB – Creatinine Phosphokinase (1224H)--increased b.) LDH – lactic acid dehydrogenase--increased c.) SGPT – (ALT) – Serum Glutanic Pyruvate Transaminase- increased d.) SGOT (AST) – Serum Glutamic Oxaloacetic - increased 2. Troponin test – increase 3. ECG tracing – ST segment increase/elevation, T wave inversion, widening or QRS complexes – means arrhythmia in MI indicating PVC 4. serum cholesterol & uric acid - increase 5. CBC – increase WBC

Nursing Management 1. Narcotic analgesics – Morphine SO4 – to induce vasodilation & decrease levels of anxiety. 2. Administer O2 inhalation – low inflow (CHF-increase inflow)—2-3L/min (high inflow may lead to respiratory arrest) 3. Enforce CBR without BRP a.) use Bedside commode 4. Avoid Valsalva maneuver (give laxatives) 5. Semi fowler 6. Provide a general liquid to soft diet that is low in saturated fats, Na, caffeine 7. Monitor VS, I&O & ECG tracings 8. Take 20 – 30 ml/week – wine, brandy, or whisky to induce vasodilation. 9. Assist in surgical; CABAG Complications: 1. Pneumonia


2. Thrombophlebitis 3. Infarction 10. Provide pt HT a.) Avoid modifiable risk factors (diet, lifestyle) b.) Prevent complications: 1. Arrhythmias – PVC 2. Shock – cardiogenic shock. Late signs of cardiogenic shock in MI – oliguria 3. Thrombophlebitis - deep vein thrombosis 4. CHF – left sided 5. Dressler’s syndrome – post MI syndrome -Resistant to medications -Administer 150,000 – 450,000 units of streptokinase c.) Strict compliance to meds - Vasodilators 1. NTG 2. ISOSURBIDE DINITRATE (Isordil) - Antiarrythmic 1. Lydocaine blocks release of norepinephrine 2. Bretylium - Beta-blockers – “lol” 1. PROPANOLOL (Inderal) - ACE inhibitors - pril 1. CAPTOPRIL– (Enalapril) - Ca – antagonist 1. NIFEDIPINE - Thrombolytics or fibrinolytics– to dissolve clots/ thrombus

S/E allergic reactions/ uticaria 1. Streptokinase—S/E: allergic reaction (urticaria or pruritus)—bec Streptokinase is a foreign protein substance 2. Urokinase 3. Tissue plasminogen activating factor—S/E: chest pain Monitor for bleeding: - Anticoagulants 1. Heparin (short acting) PTT If prolonged bleeding Antidote Protamine sulfate - Anti platelet PASA (aspirin)—anti-thrombotic properties C/I: Dengue, vasoconstrictors, unknown cause of headache

2. Coumadin (Warfarin) – delayed reaction takes 2 – 3 days to take effect PT prolonged bleeding antidote Vit K

d.) Resume ADL – sex/ activity – 4 to 6 weeks Post-cardiac rehab 1.)Sex as an appetizer rather then dessert – Before meals not after, due after meals increase metabolism – heart is pumping hard after meals. 2.) Position – non-weight bearing position. When to resume sex/ act: When pt can already use staircase, then he can resume sex. e.) Diet – decrease Na, Saturated fats, and caffeine f.) Teach importance of follow up care.

CHF – CONGESTIVE HEART FAILURE - Inability of heart to pump blood towards systemic circulation.
- Backflow 1.) Left sided heart failure: Predisposing factors: 1.) 90% mitral valve stenosis – due RHD, aging RHD affects mitral valve – streptococcal infection Dx: - Aso titer – anti streptolysine O > 300 total units Drugs given - Steroids - Penicillin - Aspirin Complication: RS-CHF Aging – degeneration / calcification of mitral valve Ischemic heart disease HPN, MI, Aortic stenosis S/Sx Pulmonary congestion/ Edema 1. Dyspnea 2. Orthopnea (Diff of breathing- put patient on sitting pos – platypnea)—2-3 pillows or high fowlers 3. Paroxysmal nocturnal dysnea – PNO- nalulunod (DOB at night)


4. 6. 7. 8. 9.

Productive cough with blood tinged sputum

5. Frothy saliva (from lungs)
Cyanosis Rales/ crackles – due to fluid Bronchial wheezing PMI – displaced lateral – due cardiomegaly 10. Pulsus alternons – weak- pulse followed by alternating strong bounding pulse 11. Anorexia & general body malaise 12. S3 – ventricular gallop

Dx 1. CXR – cardiomegaly PCWP – Pulmonary CapillaryWedge Pressure PAP – measures pressure of R ventricle. Indicates cardiac status. PCWP – measures end systolic/ diastolic pressure PAP & PCWP: Swan – Ganz catheterization – cardiac catheterization is done at bedside at ICU Operating room: laryngeal/throat cancer- tracheostomy set (Trachesostomy – bedside) - Done 5 – 20 mins – scalpel & trachesostomy set CVP – indicates fluid or hydration status (N: 4-10cm of H2O) Increase CVP – decrease flow rate of IV Decrease CVP – increase flow rate of IV Echocardiography – reveals enlarged heart chamber or cardiomyopathy ABG – PCO2 increase, PO2 decrease = = hypoxemia = resp acidosis

2. PAP – Pulmonary Arterial Pressure

3. 4.

2.) Right sided HF Predisposing factor 1. 90% - tricuspid stenosis 2. COPD 3. Pulmonary embolism 4. Pulmonic stenosis 5. Left sided heart failure S/Sx Venous congestion - Neck or jugular vein distension - Pitting edema - Ascites - Wt gain - Hepatomegalo/ splenomegaly - Jaundice - Pruritus - Esophageal varies - Anorexia, gen body malaise Diagnosis: 1. 2. CXR – cardiomegaly CVP – measures the pressure at R atrium Normal: 4 to 10 cm of water Increase CVP > 10 – hypervolemia – give loop diuretics Decrease CVP < 4 – hypovolemia (fluid challenge by inc IVF rate) Flat on bed – post of pt when giving CVP Position during CVP insertion – Trendelenburg to prevent pulmonary embolism & promote ventricular filling.

3. Echocardiography – enlarged heart chamber / cardiomyopathy 4.Liver enzyme elevation SGPT ( ALT) SGOT AST Nsg mgt: Increase force of myocardial contraction = increase cardiac output 3 – 6L of CO enforce CBR 1. Administer meds: Tx for LSHF: M – morphine SO4 to induce vasodilatation A – aminophylline & decrease anxiety D – digitalis (digoxin) D - diuretics O - oxygen G - gases a.) Cardiac glycosides Increase myocardial = increase CO


Digoxin (Lanoxin). Antidote: digivine Digitoxin: metabolizes in liver not in kidneys not given if with kidney failure. b.) Loop diuretics: Lasix – effect with in 10-15 min. Max = 6 hrs c.) Bronchodilators: Aminophyline (Theophyline). Avoid giving caffeine d.) Narcotic analgesic: Morphine SO4 - induces vasodilaton & decrease anxiety e.) Vasodilators – NTG f.) Anti-arrythmics – Lidocaine Ethacrynic acid- Thiazide diuretics 2. Administer O2 inhalation – high! @ 3 -4L/min via nasal cannula 3. High fowlers 4. Restrict Na! 5. Provide meticulous skin care 6. Weigh pt daily. Assess for pitting edema. Measure abdominal girth daily & notify MD 7. Monitor V/S, I&O, breath sounds, EKG tracings 8. Institute bloodless phlebotomy. Rotating tourniquet or BP cuff rotated clockwise q 15 mins = to promote decrease venous return 9. Diet – decrease salt, fats & caffeine 10. HT: a) Complications :shock Arrhythmia Thrombophlebitis MI Cor Pulmonale – RT ventricular hypertrophy b.) Dietary modifications c.) Adherence to meds

PERIPHERAL MUSCULAR DISEASE Arterial ulcers 1. Thromboangitis Obliterans (Buergers)– male/ feet 2. Reynauds – female/ hands venous ulcer 1. Varicose veins 2. Thrombophlebitis

1.) Thromboangitis obliterates/ BUERGERS arteries & veins of lower extremities. Male/ feet Predisposing factors: - Males greater than 30yo (high risk group) - Smokers

DISEASE- Acute inflammatory disorder affecting small to medium sized

S/Sx 1. Intermittent claudication – leg pain upon walking - Relieved by rest 2. Cold sensitivity & skin color changes White Pallor bluish cyanosis red rubor

3. Decrease or diminished peripheral pulses - Post tibial, Dorsalis pedis 4. Trophic changes 5. Ulcerations 6. Gangrene formation Dx: 1. 2.


Oscillometry – decrease peripheral pulse volume. Doppler UTZ – decrease blood flow to affected extremities. Angiography – reveals site & extent of malocculsion.

Nsg Mgt: 1. Encourage a slow progression of physical activity a.) Walk 3 -4 x / day b.) Out of bed 2 – 3 x a / day 2. Meds a.) Analgesic b.) Vasodilator c.) Anticoagulant 3. Foot care mgt like DM – a.) Avoid walking barefoot b.) Cut toe nails straight c.) Apply lanolin lotion – prevent skin breakdown d.) Avoid wearing constrictive garments



Avoid smoking & exposure to cold environment

5. Assist patient in surgery: BKA (Below the knee amputation)
2.)REYNAUD’S Predisposing factors: 1. 2. 3. Female, 40 yrs Smoking Collagen dse a.) SLE – pathognomonic sign – butterfly rash on face Chipmunk face – bulimia nervosa Cherry red skin – carbon monoxide Spider angioma – liver cirrhosis Caput medusae – leg & trunk Lion face – leprosy b.) Rheumatoid arthritis – Direct hand trauma – piano playing, excessive typing, operating chainsaw 1. 2. Intermittent claudication - leg pain upon walking - Relieved by rest Cold sensitivity

PHENOMENON – acute episodes of arterial spasm affecting digits of hands & fingers

poisoning umbilicus- Liver cirrhosis

4. S/Sx:

Nsg Mgt: a. Analgesics b. Vasodilators c. Encourage to wear gloves especially when opening a refrigerator. d. Avoid smoking & exposure to cold environment VENOUS ULCERS 1. VARICOSITIES / Varicose veins - Abnormal dilation of veins – lower ext & trunk - Due to: a.) Incompetent valves leading to b.) Increase venous pooling & stasis leading to c.) Decrease venous return Predisposing factors: a. Hereditary b. Congenital weakness of veins c. Thrombophlebitis d. Heart dse e. Pregnancy f. Obesity g. Prolonged immobility - Prolonged standing S/Sx: 1. Pain especially after prolonged standing 2. Dilated tortuous skin veins 3. Warm to touch 4. Heaviness in legs Dx: 1. Venography Trendelenberg’s test – vein distend quickly < 35 secs


Nsg Mgt: 1. Elevate legs above heart level – to promote venous return – 1 to 2 pillows 2. Measure circumference of leg muscles to determine if swollen. 3. Wear anti embolic or knee high stockings. Women – panty hose 4. Meds: Analgesics 5. Surgery: vein sweeping & ligation Sclerotherapy – spider web varicosities S/E thrombosis

THROMBOPHLEBITIS (deep vein thrombosis) - Inflammation of veins with thrombus formation
Predisposing factors: 1. Smoking 2. Obesity 2. Hyperlipedemia 4. Prolonged use of oral contraceptives 5. Chronic anemia 6. DM 7. MI 8. CHF 9. Postop complications 10. Post cannulation – insertion of various cardiac catheters


S/Sx: 1. 2. 3. Dx:

Pain at affected extremities Cyanosis (+) Homan’s sign - Pain at leg muscles upon dorsiflexion of foot.

1. Angiography 2. Doppler UTZ Nsg Mgt: 1. Elevate legs above heart level. 2. Apply warm, moist packs to decrease lymphatic congestion. 3. Measure circumference of leg muscles to detect if swollen. 4. Use anti embolic stockings. 5. Meds: Analgesics. Anticoagulant: Heparin 6. Complication:

Pulmonary Embolism:
- Sudden sharp chest pain - Dyspnea - Tachycardia - Palpitation - Diaphoresis - Mild restlessness OVERVIEW OF RESPIRATORY SYSTEM: I. Upper respiratory tract: Fx: 1. Filtering of air 2. Warming & moistening 3. Humidification a. Nose – cartilage - Parts: Rt nostril separated by septum Lt nostril Consists of anastomosis of capillaries – Liessel – Bach Plexus – site of epistaxis b. Pharynx (throat) – muscular passageway for air& food Branches: 1. Oropharynx 2. Nasopharynx 3. Layngopharynx c. Larynx – voice box Fx: -

1. For phonation- voice or speech production
2. Cough reflex Made up of framework: a. epiglottis b. hyoid bone c. thyroid & crichoid cartilage Glottis – opening of larynx Opens to allow passage of air Closes to allow passage of food -Inability to cough, complete obstruction of airway II. Lower Respiratory tract – Fx for gas exchange d. Trachea – windpipe - has cartillagenous rings - site for permanent/ artificial a/w – tracheostomy b. Bronchus – R & L main bronchus c. Lungs – R – 3 lobes = 10 segments L – 2 lobes – 8 segments Post pneumonectomy - position affected side to promote expansion of lungs==Semi Fowlers Post segmental lobectomy – position unaffected side to promote drainage Serous membrane Pleura Parietal Pleural Fluid Pleural Friction Rub ches pain- pain upon inspiration Pneumonia Pleurisy Visceral


Pleural Effusion Lungs – covered by pleural cavity, parietal lobe & visceral lobe Alveoli – acinar cells - site of gas exchange (O2 & CO2)-diffusion - diffusion: Daltons law of partial pressure of gases - basic living units Powerful stimulating stimulant—increase CO2 COPD – decrease O2 stimulant Ventilation – movement of air in & out of lungs Respiration – movement of air into cells Type II cells of alveoli – secretes surfactant, lipoprotein in nature Surfactant - decrease surface tension of alveoli—prevents collapse of lungs also known as atelectasis Lecithin & spinogomyelin L/S ratio 2:1 – indicator of lung maturity If 1:2 – adm O2 - < 40% Concentration to prevent atelectasis & retinopathy or blindness. Retrolental Fibroplasia-retinopathy/blindness in prematurity

I. PNEUMONIA – inflammation of lung parenchyma leading to pulmonary consolidation as alveoli is filled with exudates. Etiologic agents: 1. Streptococcus pneumoniae (pnemococcal pneumonia) 2. Haemophilus pneumoniae(Bronchopneumonia) in children 3. Escherichia coli 4. Klebsiella P. 5. Diplococcus P. High risk: elderly & children below 5 yo bec of low resistance Predisposing factors: 1. Smoking 2. Air pollution 3. Immuno-compromised patients a. AIDS – PLP b. Bronchogenic CA - Non-productive to productive cough-- CXR 4. Prolonged immobility – CVA- hypostatic pneumonia 5. Aspiration of food 6. Over fatigue S/Sx:

1. Productive cough – pathognomonic: greenish to rusty sputum
2. 3. 4. 5. 6. 7. Dyspnea with prolonged respiratory grunt Fever, chills, anorexia, gen body malaise Wt loss Pleuritic friction rub Rales/ crackles Cyanosis Abdominal distension leading to paralytic ileus (absence of peristalsis)


Sputum exam – could confirm presence of TB & pneumonia Dx:

1. 2. 3. 4.

Sputum GSCS- gram staining & culture sensitivity - Reveals (+) culture microorganism. CXR – pulmonary consolidation CBC – increase WBC and inc Erythrocyte sedimentation rate ABG – PO2 decrease, hypoxemia

Nsg Mgt: 1. 2. 3. Enforce CBR Strict respiratory isolation Meds: a.) Broad spectrum antibiotics Penicillin or tetracycline Macrolides – ex azythromycin (zythromax) b.) Anti pyretics c.) Mucolytics or expectorants Force fluids – 2 to 3 L/day Institute pulmonary toileta.) Deep breathing exercise b.) Coughing exercise

4. 5.


c.) Chest physiotherapy – cupping d.) Turning & reposition - Promote expectoration of secretions 6. Semi-fowler 7. Nebulize & suction as necessary, O2 inhalation 8. Comfy & humid environment 9. Diet: increase CHO or calories, CHON & Vit C 10. Postural drainage - To drain secretions using gravity Mgt for postural drainage: a.) Best done before meals (breakfast) or 2 – 4 hrs after meals to prevent Gastroesophageal Reflux b.) Monitor VS & breath sounds Normal breath sound – bronchovesicular c.) Deep breathing exercises d.) Adm bronchodilators 15 – 30 min before procedure e.) Stop if pt can’t tolerate procedure f.) Provide oral care – it may alter taste sensation g.) C/I – pt with unstable VS & hemoptysis, increase ICP, increase IOP (glaucoma) Normal IOP – 12 – 21 mmHg 11. HT: a.) Avoidance of precipitating factors (smoking) b.) Complication: Atelectacies & meningitis c.) Compliance to meds

PULMONARY TUBERCULOSIS (KOCH’S DSE) - Inflammation of lung tissue caused by invasion of mycobacterium TB
or tubercle bacilli or acid fast bacilli – gram (+) aerobic, motile & easily destroyed by heat or sunlight. Predisposing factors: 1. Malnutrition 2. Overcrowding 3. Alcoholism 4. Ingestion of infected cattle (mycobacterium BOVIS) 5. Virulence 6. Over fatigue or stress S/Sx: 1. 3. 4. Productive cough – yellowish Night sweats Dyspnea Anorexia, generalized body malaise, wt loss Chest/ back pain Hempotysis ==Airborne transmission, droplet nuclei infection

2. Low grade afternoon fever 5.
6. 7.

Diagnosis: 1. Skin test – Mantoux test – infection of Purified Protein Derivative PPD DOH – 8-10 mm induration WHO – 10-14 mm induration Result within 48 – 72h (+) Mantoux test – previous exposure to tubercle bacilli Mode of transmission – droplet infection 2. Sputum AFB – (+) to cultured microorganism 3. CXR – pulmonary infiltrate caseous necrosis 4. CBC – increase WBC Nursing Mgt: 1. CBR 2. Strict resp isolation 3. O2 inhalation 4. Semi fowler 5. Force fluid to liquefy secretions 6. Deep breathing and cough exercises 7. Nebulize & suction if necessary 8. Provide comfortable & humid environment 9. Diet – increase CHO & calories, CHON, Vit, minerals 10. Short course chemotherapy: Intensive phase 1. INH – isoniazid 2. Rifampicin - both given before meals for absorption - both given within 4 months, given simultaneously to prevent resistance -S/E: peripheral neutitis – vit B6 (cereals, green leafy vegetables, organ meat) Rifampicin -All body secretions turn to red orange color urine, stool, saliva, sweat & tears.

3. PZA – Pyrazinamide – given 2 mos/ after meals. S/E: allergic rxn, nephrotoxicity & hepatoxicity


PZA may be replaced by ETHAMBUTOL (S/E: optic neuritis) Standard regimen 1. Injection of streptomycin – Aminoglycosides Ex. Kanamycin, gentamycin, neomycin S/E: a.) Ototoxicity – damage CN # 8 – tinnitus (ringing in the ears), dizziness, vertigo b.) Nephrotoxicicity – monitor BUN (10-20) & Creatinine (.8-1) HT:

a.) Avoid predisposing factors like alcoholism, crowded places
b.) Provide the dietary intake of increased CHO,calories, CHONm and Vitamin C c.) Avoid complications: 1.) Atelectasis 2.) Miliary TB – spread of Tb to other system b.) Strict compliance to meds (if one misses a dose, continue taking the meds) - Religiously take meds e) Know the importance of follow up care

HISTOPLASMOSIS- acute fungal infection caused by inhalation of contaminated dust with Histoplasma Capsulatum
transmitted from bird’s manure. S/Sx: Same as pneumonia & PTB – like 1. Productive cough 2. Dyspnea 3. Chest & joint pains 4. Cyanosis 5. Anorexia, gen body malaise, wt loss 6. Hemoptysis 7. Fever and chills Dx:

1. Histoplasmin skin test = (+) Histoplasma Capsulatum
2. ABG – pO2 decrease Nsg Mgt: 1. CBR 2. Meds:

a.) Antifungal agents
Amphotericin B (Fungizone) S/E:

a.) Nephrotoxcicity check BUN and Creatinine
b.) Hypokalemia b.)Corticosteroids c.) Mucolytic/ or Expectorants 3. Administer O2, force fluids 4. Encourage deep breathing and coughing exercises 5. Nebulize, suction 6. Complications: a.) Atelectasis b.) Bronchiectasis COPD 7. Prevent spread of histoplasmosis: a.) Spray breading places or kill the bird.

COPD – Chronic Obstructive Pulmonary Disease
1. 2. 3. 4. Chronic bronchitis Bronchial asthma Bronchiectasis Pulmonary emphysema – terminal stage

CHRONIC BRONCHITIS - called BLUE BLOATERS inflammation of bronchus due to hypertrophy or hyperplasia of goblet
mucus producing cells leading to narrowing of smaller airways. Predisposing factors: 1. Smoking – all COPD types 2. Air pollution S/Sx: 1. Productive cough 2. Dyspnea on exertion 3. Prolonged expiratory grunt 4. Scattered rales/ rhonchi 5. Cyanosis 6. Pulmonary HPN – a.) Leading to peripheral edema b.) Cor pulmonale – right ventricular hypertrophy --respiratory in origin 7. Anorexia, gen body malaise Dx: 1. ABG




Resp acidosis

Hypoxemia – causing cyanosis - Complications: Emphysema and Pleurisy Nsg Mgt: (Same as emphysema) 2.) BRONCHIAL ASTHMA- reversible inflammation lung condition due to hyerpsensitivity to allergens leading to narrowing of smaller airways. Predisposing factor: 1. Extrinsic Asthma – called Atopic/ allergic asthma a.) Pollen b.) Dust c.) Gases d.) Smoke/fumes e.) Dander f.) Lints g.) Viral infection

2. Intrinsic Asthma- called Non-Atopic, non-allergic asthma
Cause: Hereditary Drugs – aspirin, penicillin, β blockers (beta blockers are bronchoconstrictors) Food additives – nitrites Foods – seafood, chicken, eggs, chocolates, milk Physical/ emotional stress Sudden change of temp, humidity &air pressure 3. mixed type: combination of both extrinsic & intrinsic Asthma 90% cause of asthma S/Sx: 1. C – cough – non productive to productive 2. D – dyspnea 3. W – wheezing on expiration 4. Cyanosis 5. Mild apprehension & restlessness 6. Tachycardia & palpitation 7. Diaphoresis Dx: 1. Pulmo function test – decrease vital lung capacity 2. ABG – PO2 decrease, PCO2 increase- hypoxemia, Ph decreased Respiratory Acidosis Nsg Mgt: 1. CBR – all COPD 2. Medsa.) Bronchodilator through inhalation or metered dose inhaled / pump. Given 1st before corticosteroids to facilitate absorption b.) Corticosteroids – due inflammatory. Given 10 min after adm bronchodilator c.) Mucolytic/ expectorant d.) Mucomist (Acetylcysteine) – at bedside put suction machine. e.) Antihistamine 2. Force fluids 3. Institute pulmonary toilet 4. O2 – all COPD low inflow to prevent resp distress 5. Nebulize & suction client PRN 6. Diet: increase CHO, CHON 7. Semifowler – all COPD except emphysema due late stage 8. HT a.) Avoid predisposing factors (dust, pollen, etc), provide a comfortable environment b.) Complications: • Status astmaticus- give epinephrine & bronchodilators - Emphysema c.) Adherence to meds to prevent status asmaticus d.) Teach the importance of follow up care

BRONCHIECTASIS – abnormal permanent dilation of bronchus resulting to destruction of muscular & elastic tissues of alveoli.
Predisposing factors: 1. Recurrent upper & lower respiratory tract infections 2. Congenital anomalies 3. Lung Tumors 4. Chest Trauma S/Sx: 1. Productive cough 2. Dyspnea 3. Anorexia, generalized body malaise- all energy are used to increase respiration.


4. 5. Dx: 1.

Cyanosis Hemoptisis


ABG – PO2 decrease Bronchoscopy – direct visualization of bronchus using fiberscope. Chest xray Nsg Mgt: before bronchoscopy 1. Consent, explain procedure – MD/ lab explain RN 2. NPO 3. Monitor VS 1. 2. 3. 4. Feeding after return of gag reflex Instruct client to avoid talking, smoking or coughing Monitor signs of frank or gross bleeding Monitor of laryngeal spasm DOB Prepare at bedside tracheostomy set

Nsg Mgt after bronchoscopy

Mgt: same as emphysema except Surgery Pneumonectomy – removal of affected lung – lie on affected side Segmental lobectomy – position of pt – unaffected side to promote drainage

PULMONARY EMPHYSEMA – irreversible terminal stage of COPD - Characterized by inelasticity of alveolar walls leading to air trapping, leading to maldistribution of gases.
- Body will compensate over distension of thoracic cavity - Barrel chest Predisposing factor: 1. Smoking 2. Allergy 3. Air pollution 4. High risk – elderly (above 65yo) 5. Hereditary - α 1 anti trypsin to release elastase for recoil of alveoli. S/Sx:

1. Consistent productive cough 2. Dyspnea at rest with prolonged expiratory grunt – due terminal 3. Anorexia & generalized body malaise
4. 5. 6. Barrel chest Rales/ rhonchi Bronchial wheezing Decrease tactile fremitus (should have vibration) – palpation – “99”. Decreased - with air or fluid Resonance to hyperresonance – percussion Decreased or diminished breath sounds on affected lungs Pathognomonic: barrel chest – increase post/ anterior diameter of chest Pursed lip breathing – to eliminated CO2 Flaring of alai nares/ ala nasi


9. 10. 11. 12.

Diagnosis: 1. Pulmonary function test – decrease vital lung capacity 2. ABG – a.) Panlobular / centri lobular emphysema pCO2 increase pO2 decrease – hypoxema resp acidosis Blue bloaters – Chronic bronchitis b.) Panacinar/ Centriacinar pCO2 decrease pO2 increase – hyperaxemia resp alkalosis Pink puffers Nursing Mgt: 1. CBR 2. Meds – a.) Bronchodilators b.) Corticosteroids- prone to infection c.) Antimicrobial agents d.) Mucolytics/ expectorants e.) Antipyretics PRN --Patient is prone to develop an infection

3. O2 – Low inflow – to avoid rsp arrest
4. 5.


Force fluids High fowlers Nebilize & suction Institute P – posture E – end E – expiratory to prevent collapse of alveoli


P – pressure HT a.) Avoid smoking b.) Prevent complications 1.) Cor pulmonale – R ventricular hypertrophy 2.) CO2 narcosis – lead to coma 3.) Atelectasis 4.) Pneumothorax – air in pleural space 9. Adherence to meds 10. Encourage deep breathing and coughing exercises 11. Diet: increase CHO, DHON, vitamins and minerals 12. Importance of follow up care 8.

RESTRICTIVE LUNG DISORDER PNEUMOTHORAX – partial / or complete collapse of lungs due to entry or air in pleural space. Types: 1. Spontaneous pneumothorax – entry of air in pleural space without obvious cause. eg. Rupture of bleb (alveoli filled sacs) in pt with inflammed lung conditions 2. Open pneumothorax – air enters pleural space through an opening in chest wall -Stab/ gun shot wound 3. Tension Pneumothorax – air enters plural space with @ inspiration & can’t escape leading to over distension of thoracic cavity resulting to shifting of mediastinum content to unaffected side. Eg. Flail chest – “paradoxical breathing pattern” Predisposing factors: 1. Chest trauma 2. Inflammatory lung conditions 3. Tumor S/Sx: 1. Sudden sharp chest pain 2. unexplained Dyspnea or SOB 3. Cyanosis 4. Diminished or decreased breath sound of affected lung 5. Cool moist skin- initial sign of shock 6. Mild restlessness/ apprehension, anxiety 7. Resonance to hyperresonance 8. decreased tactile fremitus Diagnosis: 1. ABG – pO2 decrease – 2. CXR – confirms pneumothorax/ collapse of lung Nursing Mgt: 1. Assist in endotracheal intubation 2. Assist in thoracenthesis 3. Administer meds – Morphine SO4 – due to pain - Anti microbial agents- due to bacteria 4. Assist in test tube thoracotomy attached to H2O sealed drainage system Purpose of H2O sealed drainage 1. Restablish (-) pressure in the lungs- lung 6-12mm Hg 2. Promote reexpansion of the lungs 3. Drain fluid, blood and air 4. To prevent reflux of blood fluid and air Nursing Mgt if pt is on CPT attached to H2O drainage 1. Maintain strict aseptic technique 2. DBE 3. At bedside a.) Petroleum gauze pad if dislodged Hemostat b.) If with air leakage – clamp c.) Extra bottle 4. Meds – Morphine SO4 Antimicrobial 5. Monitor & assess for oscillation fluctuations or bubbling a.) If (+) to intermittent bubbling means normal or intact - H2O rises upon inspiration - H2o goes down upon expiration b.) If (+) to continuous, remittent bubbling 1. Check for air leakage 2. Clamp towards chest tube 3. Notify MD c.) If (-) to bubbling 1. Check for loop, clots, and kink 2. Milk towards H2O seal 3. Indicates re-expansion of lungs 4. Auscultate for breath sounds, Xrays


5. Removal of CTT When will MD remove chest tube? 1. If (-) fluctuations 2. (+) Breath sounds 3. CXR – full expansion of lungs Nursing Mgt of removal of chest tube 1. Encourage DBE 2. Instruct to perform Valsalva maneuver for easy removal, to prevent entry of air in pleural space. 3. Apply vaselinated air occlusive dressing - Maintain dressing dry & intact 4. Prepare: Extra bottle, excellent clamp, petroleum gauze GIT I. Upper alimentary canal - function for digestion a. Mouth b. Pharynx (throat) c. Esophagus d. Stomach- site of digestion e. 1st half of duodenum II. Middle Alimentary canal – Function: for absorption - Complete absorption – large intestine a. 2nd half of duodenum for absorption b. Jejunum c. Ileum d. 1st half of ascending colon III. Lower Alimentary Canal – Function: elimination a. 2nd half of ascending colon for elimination b. Transverse for complete absorption— L I c. Descending colon d. Sigmoid e. Rectum IV. Accessory Organ a. Salivary gland b. Verniform appendix c. Liver d. Pancreas – auto digestion e. Gallbladder – storage of bile I. Salivary Glands 1. Parotid – below & front of ear 2. Sublingual 3. Submaxillary -


Produces saliva – for mechanical digestion 1,200 -1,500 ml/day - saliva produced Lacrimal gland- depression on the frontal bone Lacrimal duct- outer canthus

PAROTITIS – “mumps” – inflammation of parotid gland
-Paramyxovirus S/Sx:

1. Fever, chills anorexia, generalized body malaise
2. 3. 4. enlarged parotid gland Swelling of parotid gland Dysphagia Earache – otalgia


Mode of transmission: Direct transmission & droplet nuclei Incubation period: 14 – 21 days Period of communicability – 1 week before swelling & immediately when swelling begins. Nursing Mgt: 1. CBR 2. Institute a strict respiratory isolation 3. Meds: analgesic Antipyretic Antibiotics – to prevent 2° complications 4. Alternate warm & cold compress at affected part (vinegar promotes cooling) 5. General liquid to soft diet 6. Complications Women – cervicitis, vaginitis, oophoritis Both sexes – meningitis & encephalitis/ reason why antibiotics is needed Men – orchitis might lead to sterility if it occurs during / after puberty.


VERNIFORM APPENDIX – Rt iliac or Rt inguinal area - Function – lymphatic organ – produces WBC during fetal life - ceases to function upon birth of baby

APENDICITIS – inflamation of verniform appendix
Predisposing factor: 1. Microbial infection 2. Feacalith – undigested food particles – tomato seeds, guava seeds 3. Intestinal obstruction S/Sx:

1. Pathognomonic sign: (+) rebound tenderness

3. 4. 5.

Low grade fever, anorexia, n/v Diarrhea &/ or constipation Pain at Rt iliac region-- MCBURNEY’S point – site of surgical incision Late sign due pain – tachycardia

Diagnosis: 1. CBC – mild leukocytosis – increase WBC 2. PE – (+) rebound tenderness (flex Rt leg, palpate Rt iliac area – rebound) 3. Urinalysis—(+) acetone in urine Treatment: - appendectomy 24 – 45° Nursing Mgt: 1. Secure consent 2. Routinary nursing measures: a.) Skin prep b.) NPO c.) Avoid enema – lead to rupture of appendix 3. Meds: Antipyretic Antibiotics *Don’t give analgesic – will mask pain - Presence of pain means appendix has not ruptured. 4. Avoid heat application – will rupture appendix. 5. Monitor VS, I&O bowel sound 6. Maintain a patent IV line Complications: Peritonitis, Septicemia Nursing Mgt: post op 1. If (+) to Penrose drain – indicates rupture of appendix Position- affected side to drain 2. Meds: analgesic due post op pain Antibiotics, Antipyretics PRN 3. Monitor VS, I&O, bowel sound- N- borborygmy sound 4. Maintain patent IV line 5. Complications- peritonitis, septicemia Liver – largest gland - Occupies most of right hypochondriac region - Color: scarlet red, brown shiny and transparent - Covered by a fibrous capsule – Glisson’s capsule - Functional unit – liver lobules Function: 1. Produces bile Bile – emulsifies fats—H2O and bile salts= cholesterol Right sided pain: Cholelithiasis- easy bruising Left sided pain: Pancreatitis - Composed of H2O & bile salts -Gives color to urine – urobilin Stool color – stechobilin Detoxifies drugs Promotes synthesis of vit A, D, E, K - fat soluble vitamins (needs fat for absorption)



Hypervitaminosis – vit D & K Vit A – retinol Def Vit A – night blindness Vit D – cholecalciferon - Helps calcium - Rickets, osteoarthritis 4. It destroys excess estrogen hormone 5. for metabolism A. CHO – 1. Glycogenesis – synthesis of glycogens


2. Glycogenolysis – breakdown of glycogen 3. Gluconeogenesis – formation of glucose from CHO sources B. CHON1. Promotes synthesis of albumin & globulin Liver Cirrhosis – decrease albumin; ascites and edema Albumin – maintains osmotic pressure, prevents edema 2. Promotes synthesis of prothrombin & fibrinogen 3. Promotes conversion of ammonia to urea. Ammonia like breath – fetor hepaticus C. FATS – promotes synthesis of cholesterol to neutral fats – called triglycerides

LIVER CIRRHOSIS - lost of architectural design of liver leading to fat necrosis & scarring
Laennac Cirrhosis- loss of architectural design of the liver leading to fat necrosis and scarring Early sign – hepatic encephalopathy 1. Asterixis – flapping hand tremors Late signs – headache, restlessness, disorientation, decrease LOC – hepatic coma. Nursing priority – assist in mechanical ventilation Predisposing factor: Decrease Laennac’s cirrhosis – caused by alcoholism 1. Chronic alcoholism- major cause 2. Malnutrition – decreaseVit B, thiamin - primary cause 3. Virus – 4. Toxicity- eg. Carbon tetrachloride (CCL4) 5. Use of hepatotoxic agents S/Sx: Early signs: a.) Weakness, fatigue b.) Anorexia, n/v c.) Stomatitis d.) Urine – tea color Stool – clay color e.) Amenorrhea f.) Decrease sexual urge g.) Loss of pubic, axilla hair h.) Hepatomegaly i.) Jaundice j.) Pruritus or urticaria k.) Decrease bowel sounds 2. Late signs a.) Hematological changes – all blood cells decrease Leukopenia- decrease Thrombocytopenia- bleeding tendencies Anemia- decrease b.) Endocrine changes Spider angiomas, Gynecomastia Caput medusae, Palmar errythema, loss of tortousity of the umbilicus c.) GIT changes Ascites, bleeding esophageal varices – due to portal HPN d.) Neurological changes: hepatic encephalopathy Hepatic encephalopathy - ammonia (cerebral toxin) Late signs: Early signs: Headache and dizziness asterexis Fetor hepaticus (flapping hand tremors) Confusion Restlessness Decrease LOC Hepatic coma Diagnosis: 1. Liver enzymes- increase SGPT (ALT) SGOT (AST) Serum cholesterol & ammonia increase Indirect or conjugated bilirubin increase CBC - pancytopenia PTT – prolonged bleeding Hepatic ultrasonogram – fat necrosis of liver globules



5. 6.
Nursing Mgt 1. CBR


2. 3.

5. 6. 7.


Restrict Na! Monitor VS, I&O Weigh pt daily & assess pitting edema Measure abdominal girth daily – notify MD Meticulous skin care Diet – increase CHO, vit & minerals. Moderate fats. Decrease CHON Well balanced diet Complications of liver cirrhosis: a.) Ascites – fluid in peritoneal cavity Nursing Mgt: 1. Meds: Loop diuretics – 10 – 15 min effect 2. Assist in abdominal paracentesis - aspiration of fluid - Void before paracentesis to prevent accidental puncture of bladder as trochar is inserted b.) Bleeding esophageal varices - Dilation of esophageal veins 1. Meds: Vit K Pitressin or Vasopressin (IM) 2. NGT decompression- lavage - Give before lavage – ice or cold saline solution - Monitor NGT output 3. Assist in mechanical decompression - Insertion of Sengstaken-Blackemore tube- to decompress veins of esophagus-to prevent esophageal varices - 3 lumen typed catheter - Scissors at bedside to deflate/decompress balloon. Prep scissors when pt complains of DOB c.) Hepatic encephalopathy – 1. Assist in mechanical ventilation – due coma 2. Monitor VS, neuro check 3. Siderails – due restless 4. Meds – Laxatives – to excrete ammonia (Lactulose)

HEPATITIS- jaundice (icteric sclera)
Bilirubin Kernicterus/ hyperbilirubinia Irreversible brain damage Pancreas – mixed gland (exocrine & endocrine gland); found behind the stomach

PANCREATITIS – acute or chronic inflammation of pancreas leading to pancreatic edema, hemorrhage & necrosis due to auto
digestion (self-digestion). Bleeding of pancreas - Cullen’s sign on umbilical area Predisposing factors: 1. Chronic alcoholism 2. Hepatobilary disease 3. Obesity 4. Hyperlipidemia 5. Hyperparathyroidism 6. Drugs – Thiazide diuretics,aspirin, pills, Pentamidine HCL (Pentam) for clients with AIDS, 7. Diet – increase saturated fats S/Sx: 1. Severe Lt epigastric pain – radiates from back &flank area (left upper quadrant) - Aggravated by eating, accompanied by DOB 2. N/V 3. Tachycardia 4. Palpitation due to pain 5. Dyspepsia /indigestion 6. Decrease bowel sounds 7. (+) Cullen’s sign - ecchymosis of umbilicus hemorrhage 8. (+) Grey Turner’s spots – ecchymosis of flank area 9. Hypocalcemia Diagnosis: 1. Serum amylase & lipase – increase 2. Urine lipase – increase 3. Serum Ca – decrease Nursing Mgt: 1. Meds a.) Narcotic analgesic - Meperidine Hcl (Demerol) Don’t give Morphine SO4 –will cause spasm of sphincter. b.) Smooth muscle relaxant/ anti cholinergic - Ex. Papavarine Hcl Prophantheline Bromide (Profanthene)


c.) Vasodilator – NTG d.) Antacid – Maalox e.) H2 receptor antagonist - Ranitidin (Zantac) f.) Ca – gluconate

to decrease pancreatic stimulation

2. Withold food & fluid – aggravates pain 3. Assist in Total Parenteral Nutrition (TPN) or hyperalimentation Complications of TPN 1. Infection—maintain a strict aseptic technique 2. Pulmonary Embolism—check all connection to system 3. Hyperglycemia 4. Hyperkalemia 4. Institute stress mgt tech a.) DBE b.) Biofeedback 5. Comfy position - Knee chest or fetal lie position 6. If pt can tolerate food, give increase CHO, decrease fats, and moderate CHON 7. Complications: Chronic hemorrhagic pancreatitis, Peritonitis, Septicemia, Shock

GALLBLADDER – storage of bile – made up of cholesterol. CHOLECYSTITIS/ CHOLELITHIASIS – inflammation of gallbladder with gallstone formation. Predisposing factor: 1. High risk – women 40 years old 2. Post menopausal women – undergoing estrogen therapy 3. Obesity 4. Sedentary lifestyle, prolonged immobility 5. Hyperlipidemia 6. Neoplasm 7. Obstruction S/Sx: 1. Severe Right abdominal pain (after eating fatty food). Occurring especially at night = epigastric or right abdominal quadrant after eating a heavy meal 2. Fat intolerance 3. Anorexia, n/v, feeling of fullness 4. Jaundice 5. Pruritus 6. Easy bruising 7. Tea colored urine 8. Steatorrhea Diagnosis: 1. Oral cholecystogram (or gallbladder series)- confirms presence of gall stones 2. Increased indirect bilirubin 3. Increased alkaline phosphatase 4. increased serum and amylase Nursing Mgt: 1. Meds – a.) Narcotic analgesic - Meperdipine Hcl – Demerol b.) Anti cholinergic/Anti-spasmodic - Atropine SO4 c.) Anti emetic Phenergan – Phenothiazide with anti emetic properties d) Broad spectrum antibiotics 2. Diet – increase CHO, moderate CHON, decrease fats 3. Meticulous skin care 4. Surgery: Cholecystectomy Nursing Mgt post cholecystectomy -Maintain patency of T-tube intact & prevent infection Stomach – widest section of alimentary canal - J shaped structures 1. Anthrum 2. Pylorus 3. Fundus Valves – prevent GERD 1. 1.cardiac sphincter valve 2. Pyloric sphincter valve- stomach and first half of duodenum Cells 1. Chief/ Zymogenic cells – secrets a.) Gastric amylase - digest CHO/ sugars




b.) Gastric lipase – digest fats c.) Pepsin – CHON d.) Rennin – digests milk products Parietal / Argentaffin / oxyntic cells Function: a.) Produces intrinsic factor – promotes reabsorption of vit B12 cyanocobalamin – promotes maturation of RBC b.) Secrets Hcl acid – aids in digestion Endocrine cells - Secretes gastrin – increase Hcl acid secretion

Function of the stomach 1.Mechanical digestion 2.Chem. 3.Storage of food -CHO, CHON- stored 1 -2 hrs. Fats – stored 2 – 3 hrs

PEPTIC ULCER DISEASE – (PUD) – excoriation / erosion of submucosa & mucosal lining due to:
a.) Hypercecretion of acid – pepsin b.) Decrease resistance to mucosal barrier Incidence Rate: 1. Men – 40 – 55 yrs old 2. Aggressive persons/ type A personality 3. Hereditary 4. Emotional Stress Predisposing factors: 1. Hereditary 2. Emotional 3. Smoking – vasoconstriction – GIT ischemia 4. Alcoholism – stimulates release of histamine = Parietal cell release Hcl acid = ulceration 5. Caffeine – tea, soda, chocolate 6. Irregular diet 7. Rapid eating 8. Ulcerogenic drugs – NSAIDS, aspirin, steroids, indomethacin, ibuprofen Indomethacin - S/E corneal cloudiness. Needs annual eye check up. NSAID and steroids= gastropathy

9. Gastrin producing tumor or gastrinoma – Zollinger Ellisons syndrome 10. Microbial invasion – helicobacter pylori. Metronidazole (Flagyl)
Types of ulcers Ascending to severity 1. Acute – affects submucosal lining 2. Chronic – affects underlying tissues – heals & forms a scar, deeper

According to location 1. Stress ulcer 2. Gastric ulcer 3. Duodenal ulcer – most common Stress ulcers – common among eritically ill clients 2 types 1. Curling’s ulcer – cause: trauma & Burns Hypovolemia GIT schemia Decrease resistance of mucosal barriers to Hcl acid Ulcerations 2. Cushing’s ulcer – cause – stroke/CVA/ head injury Increase vagal stimulation Hyperacidity Ulcerations Treatment: Vagotomy- done to prevent hemorrhage and shock prior to surgery on the stomach GASTRIC ULCER Antrum or lesser curvature -30 min – 1 hr after eating - epigastrium DUODENAL ULCER Duodenal bulb -2-3 hrs after eating - mid epigastrium



- gaseous & burning - cramping & burning pain - not usually relieved by food & - usually relieved by food & antacid antacid - 12 MN – 3am pain HYPERSECRETION Normal gastric acid secretion Increased gastric acid secretion VOMITING common Not common HEMORRHAGE hematemesis Melena WT Wt loss Wt gain COMPLICATIONS a. stomach cancer a. perforation b. hemorrhage HIGH RISK 60 years old and above 20 years old and above 90-95% are cases ofduodenal ulcers- less bicarbonate ions, decrease so increase incidence Diagnosis: 1. Endoscopic exam 2. Stool from occult blood (+) 3. Gastric analysis – Gastric Ulcer: normal gastric acid secretion Duodenal: increased gastric acid secretion 4. GI series – confirms presence of ulceration Nursing Mgt: 1. Diet – bland, non irritating, non spicy 2. Avoid caffeine & milk/ milk products Increase gastric acid secretion 3. Administer meds a.) Antacids AAC Aluminum containing antacids Ex. aluminum hydroxide gel (Amphogel) S/E constipation Magnesium containing antacids ex. milk of magnesia S/E diarrhea

Maalox (fever S/E) b.) H2 receptor antagonist Ex 1. Ranitidine (Zantac) SE: fever 2. Cimetidine (Tagamet)—hastens the effect of oral anticoagulants 3. Famotidine (Pepcid) SE: fever - Avoid smoking – decrease effectiveness of drug Nursing Mgt:

1. Administer antacid & H2 receptor antagonist (Cimetidine) – 1hr apart
-Cemetidine decrease antacid absorption & vise versa c.) Cytoprotective agents Ex 1. Sucralfate (Carafate) - Provides a paste like subs that coats mucosal lining of stomach 2. Misoprostol (Cytotec) –SE: menstrual spotting d.) Sedatives/ Tranquilizers - Valium, lithium e.)Anticholinergics / Antispasmodic 1. Atropine SO4 2. Prophantheline Bromide (Profanthene) (Pt has history of hpn crisis with peptic ulcer disease. Rn should not administer alka seltzer- has large amount of Na.

3. Surgery: subtotal gastrectomy - Partial removal of stomach
Billroth I (Gastroduodenostomy) -Removal of ½ of stomach & anastomoses of gastric stump to the duodenum. Billroth II (Gastrojejunostomy) - Removal of ½ -3/4 of stomach & duodenal bulb & anastomostoses of gastric stump to jejunum.

Before surgery for BI or BII - Do vagotomy (severing of vagus nerve) & pyloroplasty (drainage) first. Nursing Mgt: 1. Monitor NGT output or drainage immediately post op- bright red a.) Immediately post op should be bright red b.) Within 36- 48h – output is yellow green c.) After 48h – output is dark red due to HCl acid 2. Administer meds: a.) Analgesic b.) Antibiotic c.) Antiemetics 3. Maintain patent IV line 4. VS, I&O & bowel sounds 5. Complications: a.) Hemorrhage – hypovolemic shock Late signs – anuria


b.) Peritonitis c.) Paralytic ileus – most feared d.) Hypokalemia e.) Thromobphlebitis f.) Pernicious anemia g.) Septicemia 7.)Dumping syndrome – common complication – rapid gastric emptying of hypertonic food solutions – CHYME leading to hypovolemia. Sx of Dumping syndrome: 1. Dizziness 2. Diaphoresis 3. Diarrhea 4. Palpitations Nursing mgt: 1. Avoid fluids in chilled solutions, sweets (fluids must be taken after meals) 2. Small frequent feedings-6 equally divided feedings 3. Diet – decrease CHO, moderate fats & CHON 4. Flat on bed 15 -30 minutes after q feeding

1. 2. 3. A. Diverticulum- an outpouching of the intestinal mucosa particularly the sigmoid colon Diverticulosis- multiple diverticulum Diverticulitis- inflammation of diverticula Predisposing Factors 1. High Risk Groups- men (40-45yo) 2. Congenital weakness of muscle fibers of the intestine. 3. low roughage and fiber in the diet 1. 2. 3. Dx: 1. Barium enema—reveals inflammatory process 2. CBC reveals: decreased hematocrit and hemoglobin Nsg Mgt: 1. Administer meds as ordered: a. antibiotics b. bulk laxatives c. stool softeners d. anti spasmodic agents 2. Instruct clients to take foods high in fiber if there is diverticulosis 3. Monitor for signs of infection Feared complications: Peritonitis 4. Assists in surgical procedure Resection of the diseased bowel and creation of a colostomy Intermittent lower left abdominal quadrant pain, particularly in the rectosigmoid area tenderness alternating bouts of constipation or diarrhea with blood or mucous


BURNS – direct tissue injury caused by thermal, electric, chemical & smoke inhaled (TECS)
Nursing Priority – infection (all kinds of burns) Head burn-priority- a/w 2nd priority for 1st & 2nd ° - pain 2nd priority for 3rd ° - F&E Thermal- direct contact – flames, hot grease, sunburn. Electric, – wires Chem. – direct contact – corrosive materials acids Smoke – gas / fume inhalation Stages:

1. Emergent phase – Removal of pt from cause of burn. Determine source or loc or burn 2. Shock phase – 48 - 72°. Characterized by shifting of fluids from intravascular to interstitial space
=Hypovolemia S/Sx: BP decrease Urine output HR increase Hct increase Serum Na decrease Serum K increase Met acidosis

3. Diuretic/ Fluid remobilization phase - 3 to 5 days. Return of fluid from interstitial to intravascular space 4. Recovery/ convalescent phase – complete diuresis. Wound healing starts immediately after tissue injury. Class: I. Partial Burn 1. 1st degree – superficial burns


- Affects epidermis - Cause: thermal burn - Painful - Redness (erythema) & blanching upon pressure with no fluid filled vesicles 2. 2nd degree – deep burns - Affects epidermis & dermis - Cause –chem. burns - very painful - Erythema & fluid filled vesicles (blisters) II Full thickness Burns 1. Third & 4th degrees burn - Affects all layers of skin, muscles, bones - Cause – electrical - Less painful - Dry, thick, leathery wound surface – known as ESCHAR – devitalized or necrotic tissue. Assessment findings Rule of nines Head & neck = 9% Ant chest = 18% Post chest = 18% @ Arm 9+9 = 18% @ leg 18+18 = 18% Genitalia/ perineum= 1% Total 100% Nursing Mgt 1. Meds a.) Tetanus toxoid- burn surface area is source of anaerobic growth – Claustridium tetany Tetany Tetanolysin Hemolysis tetanospasmin muscle spasm

b.) Morphine SO4 c.) Systemic antibiotics 1. Ampicillin 2. Cephalosporin 3. Tetracyclin 4. Topical antibiotic : 1. Silver Sulfadiazene (silvadene) 2. Sulfamylon 3. Silver nitrate 4. Povidone iodine (betadine) 2. Administer isotonic fluid sol & CHON replacements 3. Strict aseptic technique 4. Diet – increase CHO, increase CHON, increase Vit C, and increase K- orange 5. If (+) to burns on head, neck, face - Assist in intubation 6. Assist in hydrotherapy 7. Assist in surgical wound debridement. Administer analgesic 15 – 30 minutes before debridement 8. Complications: a.) Infection b.) Shock c.) Paralytic ileus - due to hypovolemia & hypokalemia d.) Curling’s ulcer – H2 receptor antagonist e.) Septicemia blood poisoning f.) Surgery: skin grafting GUT – genito-urinary tract Function: 1. Promote excretion of nitrogenous waste products 2. Maintain F&E & acid base balance 1. Kidneys – pair of bean shaped organ - Located retroperitonially (back of peritoneum) on either side of vertebral column. Encased in Bowmans’s capsule. Parts: 1. 2. 3. Renal pelvis – pyelonephritis – inflammation of the renal pelvis Cortex Medulla

Nephrons – basic living unit of the kidneys consisting of glomerulus Glomerulus – filters blood going to kidneys Function of kidneys: 1. Urine formation



Regulation of BP

Urine formation – 25% of total CO (Cardiac Output) is received by kidneys (3,000-6,000 ml.) 125ml/ min filtered by the glomerulus > Glomerular filtration rate 1. Filtration 2. Tubular Reabsorption—124ml of ultra filtered are reabsorbed in the blood 3. Tubular Secretion- 1 ml is excreted in the urine Filtration – Normal GFR/ min is 125 ml of blood Tubular reabsorption – 124ml of ultra infiltrates (H2O & electrolytes is for reabsorption) Tubular secretion – 1 ml is excreted in urine Causes of CRF: 1. HPN 2. DM

Regulation of BP: Predisposing factor: Ex CS – hypovolemia – decrease BP going to kidneys Activation of RAAS Release of Renin (hydrolytic enzyme) at juxtaglomerular apparatus Angiotensin I mild vasoconstrictor Angiotensin II vasoconstrictor Adrenal cortex Aldosterone Increase BP Increase Na & H2O reabsorption Hypervolemia Ureters – 25 – 35 cm long, passageway of urine to bladder Bladder – loc behind symphisis pubis. Muscular & elastic tissue that is distensible - Function – reservoir of urine 1200 – 1800 ml – Normal adult can hold 200 – 500 ml – needed to initiate micturition reflex Color – amber Odor – aromatic Consistency – clear or slightly turbid pH – 4.5 – 8 Specific gravity – 1.015 – 1.030 WBC/ RBC – (-) Albumin – (-) E coli – (-) Mucus thread – few Amorphous urate (-) Urethra – extends to external surface of body. Passage of urine, seminal & vaginal fluids. - Women 3 – 5 cm or 1 to 1 ½ “ - Male – 20cm or 8” increase CO increase PR

UTI CYSTITIS – inflammation of bladder
Predisposing factors: 1. Microbial invasion – E. coli 2. High risk – women 3. Obstruction 4. Urinary retention 5. Increase estrogen levels 6. Sexual intercourse S/Sx: 1. Pain – flank area 2. Urinary frequency & urgency 3. Burning upon urination 4. Dysuria & hematuria


5. 6.

Fever, chills, anorexia, gen body malaise Nocturia

Diagnosis: Urine culture & sensitivity - 80% of the cases are (+) to E. coli Nursing Mgt: 1. Force fluid – 2000 ml= to prevent bacterial multiplication 2. Warm sitz bath – to promote comfort 3. Monitor & assess for gross hematuria 4. Monitor and assess urine for color, odor, and bleeding N pH: 4.8 5. Acid ash diet – cranberry, vit C -OJ to acidify urine & prevent bacterial multiplication 6. Meds: systemic antibiotics Ampicillin Cephalosporin Sulfonamides – cotrimoxazole (Bactrim) - Gantrism (ganthanol) Aminoglycosides: Gentamycin Urinary antiseptics – Nitrofurantoin (Macrodantin) Urinary analgesic- Pyridum 6. Ht a.) Importance of Hydration b.) Void after sex (male and female) c.) Female – avoids cleaning back & front Bubble bath, Tissue paper, Powder, perfume d.) Complications: Pyelonephritis

PYELONEPHRITIS – acute/ chronic infl of 1 or 2 renal pelvis of kidneys leading to tubular destruction, interstitial abscess
formation. - Lead to Renal Failure Predisposing factor: 1. Microbial invasion (Bacterial) a.) E. Coli b.) Streptococcus 2. Urinary retention /obstruction 3. Pregnancy 4. DM 5. Exposure to renal toxins or nephrotoxic agents S/Sx: Acute pyelonephritis a.) Costovertibral angle pain, tenderness b.) Fever, anorexia, gen body malaise c.) Urinary frequency, urgency d.) Nocturia, dysuria, hematuria e.) Burning upon urination Chronic Pyelonephritis a.) Fatigue, wt loss, weakness b.) Polyuria, polydypsia c.) HPN Diagnosis: 1. Urine culture & sensitivity – (+) E. coli & streptococcus 2. Urinalysis (+) WBC, (+)RBC, (+) Pus cells 3. Cystoscopic exam – urinary obstruction Nursing Mgt: 1. Provide CBR – especially during acute phase 2. Force fluid 3. Acid ash diet 4. Provide a warm sitz bath for comfort 5. Meds: a.) Urinary antiseptic – nitrofurantoin (macrodantin) SE: peripheral neuropathy GI irritation Hemolytic anemia Staining of teeth b.) Urinary analgesic – Pyridium Complication- Renal Failure oxalate, uric acid


NEPHROLITHIASIS/ UROLITHIASIS- formation of stones at urinary tract
- calcium ,



cabbage cranberries nuts tea chocolates

anchovies organ meat nuts sardines

Predisposing factors: 1. Diet – increase Ca & oxalate 2. Hereditary – gout 3. Obesity 4. Sedentary lifestyle 5. Hyperparathyroidism S/Sx: 1. Renal colic 2. Cool moist skin (shock) 3. Burning upon urination 4. Hematuria 5. Anorexia, n/v Diagnosis: 1. IVP – intravenous pyelography. Reveals location of stone 2. KUB – reveals location of stone 3. Cytoscopic exam- urinary obstruction 4. Stone analysis – composition & type of stone 5. Urinalysis – increase EBC, increase CHON Nursing Mgt: 1.Force fluid 2.Strain urine using gauze pad 3.Warm sitz bath – for comfort 4.Alternate warm compress at flank area 5. a.) Narcotic analgesic- Morphine SO4 b.) Allopurinol (Zyeoprim) c.) Patent IV line d.) Diet – if + Ca stones – acid ash diet If + oxalate stone – alkaline ash diet - (Ex milk/ milk products) If + uric acid stones – decrease organ meat / anchovies sardines 6. Surgery a.) Nephectomy – removal of affected kidney Litholapoxy – removal of 1/3 of stones- Stones will recur. Not advised for pt with big stones b.) Extracorporeal shock wave lithotripsy - Non - invasive - Dissolve stones by shock wave 7. Complications: Renal Failure

BENIGN PROSTATIC HYPERTROPHY - enlarged prostate gland leading to
a.) Hydro ureters – dilation of ureters b.) Hydronephrosis – dilation of renal pelvis c.) Kidney stones Stone formation-- Renal failure d.) Renal failure encircles the neck of the bladder decreased form of urinary stream Caurse is unknown

  

Predisposing factor: 1. High risk – 50 years old & above 60 – 70 – (3 to 4 x at risk) Prostate cancer: 40 years old & above 2. Influence of male hormone S/Sx: 1.Decrease force of and amount of urinary stream 2.Dysuria 3.Hematuria 4.Burning upon urination 5.Terminal dribbling—early sign of BPH 6.Backache 7.Sciatica 8. Hesitancy Diagnosis: 1. Digital rectal exam – enlarged prostate gland 2. KUB – urinary obstruction 3. Cystoscopic exam – obstruction 4. Urinalysis – increase WBC, CHON, RBC Nursing Mgt: 1. Prostatic message – promotes evacuation of prostatic fluid 2. Limit fluid intake 3. Provide catheterization 4. Provide a warm sitz bath for comfort 5. Meds:


a. Terazozine (hytrin) - Relaxes bladder sphincter, relaxes the smooth muscle of urinary sphincter
S/E: HA, hypotension b. Fenasteride (Proscar) - Atrophy of Prostate Gland (given after meals) S/E: N&V, Anorexia 5. Surgery: Prostatectomy – TURP- Transurethral resection of Prostate- No incision Without incision: for debilitated clients -Assist in cystoclysis or continuous bladder irrigation. Complication: 1. Hemorrhage 2. Urinary obstruction 3. Penile dysfunction Nursing mgt:

c. Monitor signs and symptoms of infection d. Monitor symptoms gross/ frank bleeding. Normal bleeding within 24h.
3. Maintain irrigation or tube patent to flush out clots - to prevent bladder spasm & distention

ACUTE RENAL FAILURE – sudden immobility of kidneys to excrete nitrogenous waste products & maintain F&E balance
due to a decrease in GFR. (N 125 ml/min) Predisposing factors: Pre renal cause- decrease blood flow Causes: 1. Septic shock 2. Hypovolemia 3. Hypotension 4. CHF 5. Hemorrhage 6. Dehydration (chronic diarrhea)

decrease flow to kidneys

Intra-renal cause – involves renal pathology= kidney problem 1. Acute tubular necrosis 2. Pyelonephritis Post renal cause – involves mechanical obstruction Causes: 1. Urinary strictures 2. Urolithiasis 3. BPH 4. Presence of tumors Stages: **I. OLIGURIC STAGE (1-2 weeks) - involves passage of urine < 400ml/day - S/S: a. Hyperkalemia- arrhythmia b. Hypernatremia c. Hyperphosphatemia d. Hypocalcemia e. High BUN 10-20 and creatinine .8-1 f. Metabolic acidosis 1-2wks II. DIURETIC PHASE 2-3 weeks --increased amount of urine -S/S: a. Hypokalemia b. Hyponatremia c. Metabolic Acidosis d. Increased Creatinine and BUN III. CONVALESCENT/RECOVERY PHASE—9-12 months



HPN Acute Glumerulonephritis

CHRONIC RF – irreversible loss of kidney function
Predisposing factors: 1. DM 2. HPN 3. Recurrent UTI/ nephritis/ pyelonephritis 4. Exposure to renal toxins Stages of CRF 1. Diminished Reserve Volume – asymptomatic Normal BUN & Crea, GFR < 10 – 30% 2. Renal Insufficiency 3. End Stage Renal disease S/Sx: 1.) Urinary System a.) polyuria 2.) Metabolic disturbances a.) azotemia (increase BUN & Crea)


b.) nocturia b.) hyperglycemia c.) hematuria c.) hyperinulinemia d.) Dysuria e.) oliguria 3.) CNS 4.) GIT a.) headache a.) n/v b.) lethargy b.) stomatitis c.) disorientation c.) uremic breath d.) restlessness d.) diarrhea/ constipation e.) memory impairment 5.) Respiratory 6.) hematological a.) Kassmaul’s resp a.) Normocytic anemia b.) decrease cough bleeding tendencies reflex 7.) Fluid & Electrolytes 8.) Integumentary a.) hyperkalemia a.) itchiness/ pruritus b.) hypernatermia b.) uremic frost c.) hypermagnesemia 9.) Cardiovascular changes d.) hyperposphatemia a. HPN e.) hypocalcemia b. CHF f.) met acidosis c. Pericarditis Nursing Mgt: 1. Enforce CBR, reverse isolation 2. Monitor strictly VS, I&O, neurocheck, monitor for signs of hypocalcemia 3. Meticulous skin care. Uremic frost – assist in bathing pt 4. Meds: a.) Na HCO3 – due Hyperkalemia b.) Kayexelate enema c.) Anti HPN – Hydralazine (Apresoline) d.) Vit & minerals (Multivitamins) e.) Phosphate binder (Amphogel) Al OH gel - S/E constipation f.) Decrease Ca – Ca gluconate 5. Assist in hemodialysis 1.) Consent/ explain procedure 2.) Weigh patient 3.) Obtain baseline data & monitor VS before and during q30mins, I&O, wt, blood exam 4.) Encourage patient to void 5.) Strict aseptic technique 6.) Monitor for signs of complications: B – bleeding (due to heparin) E – embolism D – disequilibrium syndrome S – septicemia S – shock – decrease in tissue perfusion Disequilibrium syndrome – from rapid removal of urea & nitrogenous waste prod leading to: a.) n/v b.) HPN c.) Leg cramps d.) Disorientation e.) Paresthesia

2. Avoid BP taking, blood extraction, IV, at side of shunt or fistula. Can lead to compression of fistula.
Maintain patency of shunt by: i. Palpate for thrills & auscultate for bruits if (+) patent shunt! ii. Bedside- bulldog clip - If with accidental removal of fistula to prevent embolism. - Infersole (diastole) – common dialisate used 7. Complication - Peritonitis (most feared) - Shock Inflow time: 10-20mins Indwelling time: 30-45 mins 8. Assist in surgery: Renal transplantation : Complication – rejection (feared complication). Reverse isolation Rejection time in Acute—6mos to 1 year Rejection time in Chronic—5-10 years 3.

External parts 1. Orbital cavity – made up of connective tissue protects eye form trauma. 2. EOM – extrinsic ocular muscles – involuntary muscles of eye needed for gazing movement. 3. Eyelashes/ eyebrows – esthetic purposes 4. Eyelids – palpebral fissure – opening upper & lower lid. Protects eye from direct sunlight Meibomean gland – secrets a lubricating fluid inside eyelid b.) Stye/ sty or Hordeolum- inflamed Meibomean gland


5. 6.

Conjunctiva Lacrimal apparatus – tears

Process of grieving a. Denial b. Anger c. Bargaining d. Depression e. Acceptance 2. Intrinsic coat I. sclerotic coat – outer most a.) Sclera – white. Occupies ¾ post of eye. Refracts light rays b.) Canal of schlera – site of aqueous humor drainage c.) Cornea – transparent structure of eye II/ Uveal tract – nutritive care Uveitis – infl of uveal tract Consist of: a.) Iris – colored muscular ring of eye 2 muscles of iris: 1. Circular smooth muscle fiber - Constricts the pupil 2.radial smooth muscle fiber - Dilates the pupil

2 chambers of the eye 1. Anterior a.) Vitereous Humor – maintains spherical shape of the eye b.) Aqueous Humor – maintains intrinsic ocular pressure Normal IOP= 12-21 mmHg II. Retina (innermost layer) i. Optic discs or blind spot – nerve fibers only No auto receptors cones (daylight/ colored vision) phototopic vision rods – night twilight vision “scotopic vision” = vit A deficiency – rods insufficient ii. Maculla lutea – yellow spot center of retina iii. Fovea centralis – area with highest visual acuity oracute vision Physiology of vision 4 Physiological processes for vision to occur: 1. Refraction of light rays – bending of light rays 2. Accommodation of lens 3. Constriction & dilation of pupils 4. Convergence of eyes Unit of measurements of refraction – diopters Normal eye refraction – emmetropia ERROR of refraction 1. Myopia – near sightedness – Treatment: biconcave lens 2. Hyperopia/ or farsightedness – Treatment: biconvex lens 3. Astigmatisim – distorted vision – Treatment: cylindrical 4. Prebyopia – “old slight” – inelasticity of lens due to aging – Treatment: bifocal lens or double vista Accommodation of lenses – based on thelmholtz theory of accommodation Near vision = Ciliary muscle contracts= Lens bulges Convergence of the eye: Error: 1. Exotropia – 1 eye normal 2. Esophoria – 3. Strabismus- squint eye 4. Amblyopia – prolong squinting far vision= ciliary muscle dilates / relaxes= lens is flat

corrected by corrective eye surgery

GLAUCOMA – increase IOP – if untreated, atrophy of optic nerve disc – blindness
Predisposing factors: 1. High risk group – 40 & above 2. HPN 3. DM 4. Hereditary


5. 6. Type: 1. 2. 3. S/Sx:

Obesity Recent eye trauma, infl, surgery Chronic – (open angle G.) – most common type Obstruct in flow of aqueous humor at trabecular meshwork of canal of schlema Acute (close angle G.) – Most dangerous type Forward displacement of iris to cornea leading to blindness. Chronic (closed – angle) - Precipitated by acute attack 1. 2. 3. 4. 5. 6. 7. Loss of peripheral vision – tunnel vision Halos around lights Headache n/v Steamy cornea Eye discomfort If untreated – gradual loss of central vision – blindness

Diagnosis: 1. Tonometry – increase IOP >12- 21 mmHg 2. Perimetry – decrease peripheral vision 3. Gonioscopy – abstruction in anterior chamber Nursing mgt: 1. Enforce CBR 2. Maintain siderails 3. Administer meds a.) Miotics – lifetime - contracts ciliary muscles & constricts pupil. Ex Pilocarpine Na (Carbachol) b.) Epinephrine eye drops – decrease secretion of aqueous humor c.) Carbonic anhydrase inhibitors. Ex. acetapolamide (Diamox) - Promotes increase out flow of aquaeous humor d.) Temoptics (Timolol maleate)- Increase outflow of aquaous humor 2. Surgery: Invasive: a.) Trabeculectomy – eyetrephining – removal of trabelar meshwork of canal or schlera to drain aqueous humor b.) Peripheral Iridectomy – portion of iris is excised to drain aqueous humor Non-invasive: Trabeculoctomy (eye laser surgery)

Nursing Mgt pre op- all types surgery 1. Apply eye patch on unaffected eye to force weaker eye to become stronger. Nursing Mgt post op – all types of surgery 1. Position unaffected/ unoperated side - to prevent tension on suture line. 2. Avoid valsalva maneuver 3. Monitor symptoms of IOP a.) Headache b.) n/v c.) Eye discomfort d.) Tachycardia 2. Eye patch – both eyes - post op

CATARACT – partial/ complete opacity of lens
Predisposing factor: 1. 90-95% - aging (degenerative/ senile cataract) 2. Congenital 3. Prolonged exposure to UV rays 4. DMS/Sx:

1. Loss of central vision - “Hazy or blurring of vision”
2. 3. 4. Painless Milky white appearance at center of pupil Decrease perception of colors

Diagnosis: Opthalmoscopic exam – (+) opacity of lens Nsg Mgt: 1. Reorient pt to environment – due opacity 2. Siderails 3. Meds – a.) Mydriatics – dilate pupil – not lifetime Ex. Mydriacyl c.) Cyslopegics – paralyzes ciliary muscle. Ex. Cyclogye




E – extra C - capsular C – cataract L - lens E – extraction I - intra C - capsular C – cataract L - lens E – extraction Nursing Mgt:

partial removal of lens

total removal of lens & surrounding capsules

1.Position unaffected/ unoperated side - to prevent tension on suture line. 2.Avoid valsalva maneuver 3.Monitor symptoms of IOP a.) Headache b.) n/v c.) Eye discomfort d.) Tachycardia 4.Eye patch – both eyes - post op

RETINAL DETACHMENT- separation of 2 layers of retina
Predisposing factors: 1. 2. 3. 4. 5. S/Sx: 1. 2. 3. 4. 5. Severe myopia – nearsightedness Diabetic Retinopathy Trauma Following lens extraction HPN

“Curtain –veil” like vision Flashes of lights Floaters Gradual decrease in central vision Headache

Diagnosis- opthaloscopic exam Nursing Mgt: 1. Siderails (all visual disease) 2. Surgery: a.) Cryosurgery b.) Scleral buckling EAR – 1. Hearing 2. Balance (Kinesthesia or position sense) Parts: 1. Outera.) Pinna/ auricle – protects ear from direct trauma b.) Ext. auditory meatus – has ceruminous gland. Cerumen c.) Tympanic membrane – transmits sound waves to middle ear

Disorders of outer ear
Entry of insects – put flashlight to give route of exit Foreign objects – beans (bring to MD) H2O - drain 2. Middle ear a.) Ear osssicle 1. Hammer 2. Anvil -Incus 3. Stirrups -malleus for bone conduction -stapes disorder conductive hearing loss


b. Eustachian tube - Opens to allow equalization of pressure on both ears - Yawn, chew, and swallow Children – straight, wide, short c.) Otitis media Adult – long, narrow & slanted c. Muscles 1. Stapedius 2. Tensor tympani 3. Inner ear a. Bony labyrinth – for balance, vestibule Utricle & succule Otolithe or ear stone – has Ca carbonate Movement of head = Righting reflex = Kinesthesia b. Membranous Labyrinth 1. Cochlea – ( function for hearing) has organ of corti 2. Endolymph & perilymph – for static equilibrium 3. Mastoid air cells – air filled spaces in temporal bone in skull Complications of Mastoditis – meningitis Types of hearing loss: 1. Conductive hearing loss – transmission hearing loss Causes: a.) Impacted cerumen – tinnitus & conduction hearing loss- assist in ear irrigaton b.) Immobility of stapes – OTOSCLEROSIS d.) Middle ear disease char by formation of spongy bone in the inner ear causing fixation or immobility of stapes e.) Stapes can’t transmit sound waves Surgery Stapedectomy – removal of stapes, spongy bone & implantation of graft/ ear prosthesis Predisposing factor: 1. Familiar tendency 2. Ear trauma & surgery S/Sx: 1. 2. Tinnitus Conductive hearing loss

Diagnosis: 1. Audiometry – various sound stimulates (+) conductive hearing loss 2. Weber’s test – Normal AC> BC result BC > AC Stapedectomy Nursing Mgt post op 1. Position pt unaffected side 2. DBE No coughing & blowing of nose - Night lead to removal of graft 3. Meds: a.) Analgesic b.) Antiemetic c.) Antimotion sickness agent. Ex. meclesine Hcl (Bonamine) 4. Assess – motor function – facial nerve - (Smile, frown, raise eyebrow) 5. Avoid shampoo hair for 1 to 2 weeks. Use shower cap

Cause: 1. Tumor on cocheal 2. Loud noises (gun shot) 3. Presbycusis – bilateral progressive hearing loss especially at high frequencies – elderly Face elderly to promote lip reading 4. Meniere’s disease – endolymphatic hydrops f.) Inner ear disease char by dilation of endo – lympathic system leading to increase volume of endolin Predisposing factor of MENIERE’S DISEASE Smoking Hyperlipidemia 30 years old Obesity – (+) chosesteatoma Allergy


Ear trauma & infection S/Sx: 1. TRIAD symptoms of Meniere’s disease a.) Tinnitus b.) Vertigo c.) Sensory neural hearing loss Nystagmus n/v Mild apprehension, anxiety Tachycardia Palpitations Diaphoresis

2. 3. 4. 5. 6. 7.

Diagnosis: 1. Audiometry – (+) sensory hearing loss 1. 2. 3. 4. Nursing mgt: Comfy & darkened environment Siderails Emetic basin Meds: a.) Diuretics –to remove endolymph b.) Vasodilator c.) Antihistamine d.) Antiemetic e.) Antimotion sickness agent f.) Sedatives/ tranquilizers Restrict Na Limit fluid intake Avoid smoking Surgery – endolymphatic sac decompression- Shunt

5. 6. 7. 8.

Clindamycin, KCl===NOT for IV push—it may cause arrhythmia Chloramphenicol===NOT for IM Procaine, Penicillin, Benzatine, Pen G, Vancomycin HCl, Acyclovir (Zovirax) ===NOT for IV Opened bottles must be used in 8 hours Hep Lock- flush with NSS KCl < 80meq/L Epinephrine 1:10,000 Lidocaine- 4 mg /ml (1g/250ml) COMPATIBLE WITH PNSS ONLY Phenytoin Vit K Vit B6 Vit C Hydralazine Furosemide COMPATIBLE WITH D5W ONLY Epinephrine Norepinephrine Ephedrine Nitroprusside NaHCO3

Dopamine Dobutamine Not to be diluted in LR Penicillin G Ampicillin Cephalosporin NaHCO3 PRBC—to be infused within 2-4hours FFP—1-1.5 hours Platelet concentrate—infuse immediately and quickly Pathognomonic sign: Pernicious Anemia- red beefy tongue Carbon monoxide poisoning- cherry red face Addison’s Disease- bronze pigmentation of skin Cushing’s syndrome- buffalo hump Bulimia Nervosa- chipmunk face Liver Cirrhosis- spider angioma & Caput medusae Leprosy- lion face SLE- butterfly rash on face Emphysema- barrel chest Parkinson’s – pill rolling tremors Myasthenia Gravis- ptosis & Descending paralysis


GBS- Ascending paralysis- clumsiness Meningitis- nuchal rigidity. Kernig’s & Brudzinskis sign Hypoparathyroidism- Trousseau sign & Chvosteck sign Pancreatitis- Cullen’s sign & Grey Turner’s sign DKA- Acetone breath odor & Kussmaul’s respiration Angina Pectoris- Levine’s sign Pneumonia- rusty sputum Chronic bronchitis- Blue bloaters Asthma- Pink puffers Appendicitis- rebound tenderness Glaucoma-loss of peripheral vision- Tunnel vision Cataract- Loss of central vision Retinal detachment-Curtain-veil like vision Decreased dopamine- Parkinson’s disease Increased dopamine- Schizophrenia Decreased acetylcholine- Myasthenia Gravis / Alzheimer Increased acetylcholine- Bipolar Autoimmune diseases Multiple Sclerosis Myasthenia Gravis GBS Hypothyroidism Hyperthyroidism Pernicious Anemia Acute Glomerulonephritis

Apparatus needed at bedside: Acetaminophen toxicity- Acetylcisteine. Prepare suction apparatus-acetylcysteine causes outpouring of secretions. Myasthenia Gravis- tracheostomy set. For respiratory arrest. Hemodyalisis- bulldog clip Senkstaken tube- scissors to deflate balloon. Guillain Barre Syndrome- tracheostomy set. For respiratory arrest. Convulsion- suction apparatus. Increased secretions. Hyperthyroidism- tracheostomy set. For laryngeal spasm post subtotal thyroidectomy complication. Goiter- tracheostomy set. For laryngeal spasm post subtotal thyroidectomy complication. Hypoparathyroidism- tracheostomy set. For laryngeal spasm. Isolation precautions: Cushing’s synd – reverse isolation - due to increased corticosteroid in body. Aplastic anemia – reverse isolation - due to bone marrow depression. Cancer any type – reverse isolation – immunocompromised. Post liver transplant – reverse isolation – takes steroids lifetime. Prolonged use steroids – reverse isolation Meningitis – strict respiratory isolation – safe after 24h of antibiotic therapy TB- strict respiratory isolation


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