oral revalida

EAVALMONTE

DISEASE SIGNS AND SYMPTOMS

LAB FINDINGS PATHOPHYSIOLOGY NURSING INTERVENTIONS

DRUG STUDY/ NRSG RESPONSIBILITIES

ANGINA PECTORIS-

A clinical syndrome characterized by paroxysmal chest pain usually relieved by REST or NGTnitroglycerin, resulting from temp myocardial ischemia.

Predisposing Factor:1. sex – male2. black raise3. hyperlipidemia4. smoking5. HPN6. DM7. oral contraceptive prolonged8. sedentary lifestyle9. obesity10.hypothyroidism

Precipitating factors4 E’s1. Excessive physical exertion2. Exposure to cold environment - Vasoconstriction3. Extreme emotional response4. Excessive intake of food –

1. Initial symptoms – Levine’s sign – hand clutching of chest2. Chest pain – sharp, stabbing excruciating pain. Location – substernal-radiates back, shoulders, axilla, arms & jaw muscles-relieve by rest or NGT3. Dyspnea4. Tachycardia5. Palpitation6.diaphoresis7. Dizziness and syncope

Diagnosis1.History taking & PE2. ECG – ST segment depression & T wave inversion3. Stress test – treadmill = abnormal ECG4. Serum cholesterol & uric acid - increase5. Cardiac catheterization-Provides the MOST DEFINITIVE source of diagnosis by showing the presence of the atherosclerotic lesions

atherosclerosis↓

reduced coronary tissue perfusion

↓diminished myocardial

oxygenation↓

anaerobic metabolism↓

increased lactic acid production

↓chest pain

1.) Enforce CBR2.) Administer medsNTG – small doses – venodilatorLarge dose – vasodilator3.) Administer O2 inhalation4.) Semi-fowler5.) Diet- Decrease Na and saturated fats6.) Monitor VS, I&O, ECG7.) HT: Discharge planning:a. Avoid precipitating factors – 4 E’sb. Prevent complications – MIc. Take meds before physical exertion-to achieve maximum therapeutic effect of drugd. Importance of follow-up care.

1. Nitroglycerine- 1st dose NTG – give 3 – 5 min2nd dose NTG – 3 – 5 min3rd & last dose – 3 – 5 minStill painful after 3rd dose – notify doc. MI! Keep in a dry place. Avoid moisture & heat, may inactivate the drug.2. Monitor S/E:orthostatic hypotension – dec bptransient headachedizziness3. Rise slowly from sitting position4. ASPIRINB. Beta blockers – propanolol Administer with foodsC. ACE inhibitors – captoprilD. Ca antagonist - nefedipine

DISEASE SIGNS AND LAB FINDINGS PATHOPHYSIOLOGY NURSING DRUG STUDY/ NRSG

EAVALMONTE

SYMPTOMS INTERVENTIONS RESPONSIBILITIESMYOCARDIAL INFARCTION – heart attack – terminal stage of CAD- Characterized by necrosis & scarring due to permanent mal-occlusion

Predisposing factors1. sex – male2. black raise3. hyperlipidemia4. smoking5. HPN6. DM7. oral contraceptiveprolonged8. sedentary lifestyle9. obesity10. hypothyroidism11. obesity12. stress

1. chest pain – excruciating, vice like, visceral painlocated substernal or precodial area (rare)- radiates back, arm, shoulders, axilla, jaw & abdmuscles.- not usually relived by rest r NTG2. dyspnea3. erthermia4. initial increase/decrease in BP/tachybrady5. mild restlessness & apprehensions6. occasional findingsa.) split S1 & S2b.) pericardial friction rubc.) rales /cracklesd.) S4 (atrial gallop)

1. ECG- the ST segment is ELEVATED. T wave inversion, ECG tracing – ST segment increase,widening or QRS complexes – meansarrhythmia in MI indicating PVC2. Myocardial enzymes- elevated Creatinine Phospokinase, Lactic acid dehydrogenase and Troponin levels3. CBC- may show elevated WBC count 4. Test after the acute stage- Exercise tolerance test, thallium scans, cardiac catheterization5. serum cholesterol & uric acid - increase

Interrupted coronary blood flow↓

myocardial ischemia↓

anaerobic myocardial metabolism for several hours

↓myocardial death

↓ depressed cardiac function

↓triggers autonomic nervous

system response↓

further imbalance of myocardial O2 demand and

supply

1. Narcotic analgesics – Morphine SO4 – to induce vasodilation & decrease levels of anxiety.2. Administer O2 inhalation – low inflow (CHF-increase inflow)3. Enforce CBR without BPa.) Bedside commode4. Avoid valsalva maneuver5. Semi fowler6. General liquid to soft diet – decrease Na, saturated fat, caffeine7. Monitor VS, I&O & ECG tracings8. Take 20 – 30 ml/week – wine, brandy/whisky to induce vasodilation.9. Assist in surgical; CABAG

1. ANALGESICThe choice is MORPHINE SULFATEIt reduces pain and anxietyRelaxes bronchioles to enhance oxygenation2. Vasodilators1. NTG2. Isordil- Antiarrythmic1. LYDOCAINE blocks release of norepenephrine2. Brithylium- Beta-blockers – lol1. Propanolol (inderal)- ACE inhibitors - prilPrevents formation of angiotensin IILimits the area of infarction1. Captopril –- Ca – antagonist1. Nifedipine- Thrombolitics or fibrinolytics– to dissolve clots/ thrombus


EAVALMONTE

SYMPTOMS INTERVENTIONS RESPONSIBILITIESCONGESTIVE HEART FAILURE(LEFT)Inability of the heart to pump sufficiently- Backflow

Predisposing factors:1.) 90% mitral valve stenosis – due RHD, agingRHD affects mitral valve – streptococcal infectionDx: - Aso titer – anti streptolysine O > 300 total units- Steroids- Penicillin- AspirinComplication: RS-CHFAging – degeneration / calcification of mitral valveIschemic heart disease

1. CAD2. Valvular heart diseases3. Hypertension4. MI5. Cardiomyopathy6. Lung diseases7. Post-partum8. Pericarditis and cardiac tamponade

1. Dyspnea2. Orthopnea (Diff of breathing sitting pos – platypnea)3. Paroxysmal nocturnal dysnea – PNO- nalulunod4. Productive cough with blood tinged sputum5. Frothy salivation 6. Cyanosis7. Rales/ crackles – due to fluid8. Bronchial wheezing559. PMI – displaced lateral – due cardiomegaly10. Pulsus alternons – weak-strong pulse11. shock12. S3 – ventricular gallop13.cerebralanoxia14. Oliguria

CXR may reveal cardiomegaly2. ECG may identify Cardiac hypertrophy3. Echocardiogram may show hypokinetic heart4. ABG and Pulse oximetry may show decreased O2 saturation5. PCWP- Pulmonary Capillary Wedge Pressure is increased in LEFT sided CHF and CVP is increased in RIGHT sided CHF6. ABG – PCO2 increase, PO2 decrease = = hypoxemia = resp acidosis

LEFT Ventricular pump failure↓

back up of blood into the pulmonary veins

↓ increased pulmonary

capillary pressure↓

pulmonary congestion

LEFT ventricular failure↓

decreased cardiac output↓

decreased perfusion to the brain, kidney and other

tissues↓

oliguria, dizziness

1. Administer meds2. Administer O2 inhalation – high! @ 3 -4L/min via nasal cannula3. High fowlers4. Restrict Na!5. Provide meticulous skin care6. Weigh pt daily. Assess for pitting edema.Measure abdominal girth daily & notify MD7. Monitor V/S, I&O, breath sounds8. Institute bloodless phlebotomy. Rotating tourniquet or BP cuff rotated clockwise q 15 mins = to promote decrease venousreturn9. Diet – decrease salt, fats & caffeine

M – morphine SO4 to induce vasodilatationA – aminophylline & decrease anxietyD – digitalis (digoxin)D - diureticsO - oxygenG - gases


EAVALMONTE

SYMPTOMS INTERVENTIONS RESPONSIBILITIESCONGESTIVE HEART FAILURE(RIGHT)Inability of the heart to pump sufficiently- Backflow

Predisposing factor1. 90% - tricuspid stenosis2. COPD3. Pulmonary embolism4. Pulmonic stenosis5. Left sided heart failure

1. Peripheral dependent, pitting edema2. Weight gain3. Distended neck vein4. hepatomegaly5. Ascites

Diagnosis:1. CXR – cardiomegaly2. CVP – measures the pressure at R atriumNormal: 4 to 10 cm of waterIncrease CVP > 10 – hypervolemiaDecrease CVP < 4 – hypovolemiaFlat on bed – post of pt when giving CVPPosition during CVP insertion – Trendelenburg to prevent pulmonary embolism & promote ventricularfilling.3.Echocardiography – enlarged heart chamber / cardiomyopathy4.Liver enzymeSGPT ( ALT)

RIGHT ventricular failure ↓

blood pooling in the venous circulation

↓ increased hydrostatic

pressure↓

peripheral edema

RIGHT ventricular failure↓

blood pooling↓

venous congestion in the kidney, liver and GIT

1. Administer meds2. Administer O2 inhalation – high! @ 3 -4L/min via nasal cannula3. High fowlers4. Restrict Na!5. Provide meticulous skin care6. Weigh pt daily. Assess for pitting edema.Measure abdominal girth daily & notify MD7. Monitor V/S, I&O, breath sounds8. Institute bloodless phlebotomy. Rotating tourniquet or BP cuff rotated clockwise q 15 mins = to promote decrease venousreturn9. Diet – decrease salt, fats & caffeine

a.) Cardiac glycosidesIncrease myocardial = increase CODigoxin (Lanoxin). Antidote: digivineDigitoxin: metabolizes in liver not in kidneys not given if with kidney failure.b.) Loop diuretics: Lasix – effect with in 10-15 min. Max = 6 hrsc.) Bronchodilators: Aminophillin (Theophyllin). Avoid giving caffeined.) Narcotic analgesic: Morphine SO4 - induce vasodilaton & decrease anxietye.) Vasodilators – NTGf.) Anti-arrythmics – Lidocaine


EAVALMONTE

SYMPTOMS INTERVENTIONS RESPONSIBILITIESHYPERTENSION-A systolic BP greater than 140 mmHg and a diastolic pressure greater than 90 mmHg over a sustained period, based on two or more BP measurements.

Primary HPN- IdiopathicSecondary HPN- Due to other conditions like Pheochromocytoma, renovascular hypertension, Cushing’s, Conn’s , SIADH

Major Risk factors1. Smoking2. Hyperlipidemia3. DM4. Age older than 60 5. Gender- Male and post menopausal W6. Family History7. Smoking8. Obesity9. High salt intake10. Low potassium intake

1. Headache2. Visual changes3. chest pain4. dizziness5. N/V6. Blurring of vision7. Epistaxis

1. Health history and PE2. Routine laboratory- urinalysis, ECG, lipid profile, BUN, serum creatinine , FBS3. Other lab- CXR, creatinine clearance, 24-huour urine protein

1. Health history and PE2. Routine laboratory- urinalysis, ECG, lipid profile, BUN, serum creatinine , FBS3. Other lab- CXR, creatinine clearance, 24-huour urine protein4. Avoid stress.5. Provide information about anti-hypertensive drugsInstruct proper compliance and not abrupt cessation of drugs even if pt becomes asymptomatic/ improved condition6. Promote Home care managementInstruct regular monitoring of BPInvolve family members in careInstruct regular follow-up

DiureticsBeta blockersCalcium channel blockersACE inhibitorsA2 Receptor blockersVasodilators

-nadolol(corgard)-metoprolol(lopressor)-clonidine(catapress)-hydralazine(apresoline)-captopril(capoten)-diltiazem(cardizem)-nifedipine(calcibloc)-verapamil


EAVALMONTE

SYMPTOMS INTERVENTIONS RESPONSIBILITIESBUERGER DISEASE-Acute inflammatory disorder affecting small to medium sized arteries & veins of lower extremities. Male/ feet

Predisposing factors:- Male- Smokers

1. Intermittent claudication – leg pain upon walking - Relieved by rest2. Cold sensitivity & skin color changesWhite bluish Pallor cyanosis red rubor3. Decrease or diminished peripheral pulses - Post tibial, Dorsalis pedis4. Tropic changes5. Ulcerations6. Gangrene formation

1. Oscillometry – decrease peripheral pulse volume.2. Doppler UTZ – decrease blood flow to affected extremities.3. Angiography – reveals site & extent of mal-occulsion.

Cause is UNKNOWNProbably an Autoimmune disease

Inflammation of the arteries↓

thrombus formation↓

occlusion of the vessels

1. Encourage a slow progression of physical activitya.) Walk 3 -4 x / dayb.) Out of bed 2 – 3 x a / day2. Medsa.) Analgesicb.) Vasodilatorc.) Anticoagulant3. Foot care mgt like DM –a.) Avoid walking barefootb.) Cut toe nails straightc.) Apply lanolin lotion – prevent skin breakdownd.) Avoid wearing constrictive garments4. Avoid smoking & exposure to cold environment5. Surgery: BKA (Below the knee amputation)6. Stop smoking.

-Pentoxyfylline (Trental) reduces blood viscosity and improves supply of O2 blood to muscles

-Cilostazol (Pletaal) inhibits platelet aggregation and increases vasodilatation


EAVALMONTE

SYMPTOMS INTERVENTIONS RESPONSIBILITIESBRONCHIAL ASTHMA- reversible inflammation lung condition due to hyerpsensitivity leading to narrowing of smallerairway.

1. Extrinsic Asthma – called Atropic/ allergic asthmaa.) Pallorb.) Dustc.) Gasesd.) Smoke64e.) Danderf.) Lints

2. Intrinsic Asthma-Cause:HeredItaryDrugs – aspirin, penicillin, b blockersFood additives – nitritesFoods – seafood, chicken, eggs, chocolates, milkPhysical/ emotional stressSudden change of temp, humidity &air pressure

3. Mixed type

1. C – cough – non productive to productive2. D – dyspnea3. W – wheezing on expiration4. Cyanosis5. Mild apprehension & restlessness6. Tachycardia & palpitation7. Diaphoresis

1. Pulmo function test – decrease lung capacity2. ABG – PO2 decrease

1. CBR – all COPD2. Medsa.)Bronchodilator through inhalation or metered dose inhaled / pump. Give 1 s t before corticosteroidsb.) Corticosteroids – due inflammatory. Given 10 min after adm bronchodilatorc.) Mucolytic/ expectorantd.) Mucomist – at bedside put suction machine.e.) Antihistamine2. Force fluid3. O2 – all COPD low inflow to prevent resp distress4. Nebulize & suction5. Semifowler – all COPD except emphysema due late stage6. HTa.) Avoid pred factorsb.) Complications:c.) Adherence to medications


EAVALMONTE

SYMPTOMS INTERVENTIONS RESPONSIBILITIESPANCREATITIS- acute or chronic inflammation of pancreas leading to pancreatic edema, hemorrhage & necrosis due to auto digestion.Bleeding of pancreas - Cullen’s sign at umbilicus

Predisposing factors:1. Chronic alcoholism2. Hepatobilary disease3. Obesity4. Hyperlipidemia5. Hyperparathyroidism6. Drugs – Thiazide diuretics, pills Pentamidine HCL (Pentam)7. Diet – increase saturated fats

1. Severe Lt epigastric pain – radiates from back &flank area- Aggravated by eating, with DOB2. N/V3. Tachycardia4. Palpitation due to pain5. Dyspepsia – indigestion6. Decrease bowel sounds727. (+) Cullen’s sign - ecchymosis of umbilicus hemorrhage8. (+) Grey Turner’s spots – ecchymosis of flank area9. Hypocalcemia

1. Serum amylase & lipase – increase2. Urine lipase – increase3. Serum Ca – decrease4. WBC5. UTZ

Autodigestion of pancreatic tissue

↓Hemorrhage, Necrosis and

Inflammation↓

KININ ACTIVATION will result to increased permeability

↓Loss of Protein-rich fluid into

the peritoneumHYPOVOLEMIA

1. Administer meds.2. Withold food & fluid – aggravates pain3. Assist in Total Parenteral Nutrition (TPN) or hyperalimentationComplications of TPN1. Infection2. Embolism3. Hyperglycemia4. Institute stress mgt techa.) DBEb.) Biofeedback5. Comfy position - Knee chest or fetal like position6. If pt can tolerate food, give increase CHO, decrease fats, and increase CHON7. Complications: Chronic hemorrhagic pancreatitis

a.) Narcotic analgesic - Meperidine Hcl (Demerol)Don’t give Morphine SO4 –will cause spasm of sphincter.b.) Smooth muscle relaxant/ anti cholinergic- Ex. Papavarine HclProphantheline Bromide (Profanthene)c.) Vasodilator – NTGd.) Antacid – Maaloxe.) H2 receptor antagonist - Ranitidin (Zantac) to decrease pancreatic stimulationf.) Ca – gluconate


EAVALMONTE

SYMPTOMS INTERVENTIONS RESPONSIBILITIESAPPENDICITIS-Inflammation of the vermiform appendix

ETIOLOGY: usually fecalith, lymphoid hyperplasia, foreign body and helminthic obstruction

1. Abdominal pain: begins in the umbilicus then localizes in the RLQ (Mc Burney’s point)2. Anorexia3. Nausea and Vomiting4. Fever5. Rebound tenderness and abdominal rigidity (if perforated)6. Constipation or diarrhea

1. CBC- reveals increased WBC count2. Ultrasound3. Abdominal X-ray

Obstruction of lumen↓

increased pressure↓

decreased blood supply↓

bacterial proliferation and mucosal inflammation

↓ Ischemia

↓Necrosis

↓ rupture

1. Preoperative care NPO Consent Monitor for

perforation and signs of shock

Monitor bowel sounds, fever and hydration status

POSITION of Comfort: RIGHT SIDELYING in a low FOWLER’S

Avoid Laxatives, enemas & HEAT APPLICATION

2. Post-operative care Monitor VS and

signs of surgical complications

Maintain NPO until bowel function returns

If rupture occurred, expect drains and IV antibiotics


EAVALMONTE

SYMPTOMS INTERVENTIONS RESPONSIBILITIESIRON DEFICIENCY ANEMIA-Results when the (dietary intake of) iron is inadequate to produce hemoglobin

Causes:1. Increase demand for Iron- rapid growth in infancy and adolescence, pregnancy, EPO tx.2. Increase Iron Loss- menstruation, blood donation, bleeding3. Decrease iron intake or absorption- Crohn’s disease, post-gastrectomy, acute or chronic inflammation

1mg iron lost daily due to exfoliation of skin and mucous cells

Ave loss in menstruation is 50ml or 0.7mg/day

Pregnancy req. 2-5mg/day

1. Pallor of the skin and mucous membrane2. Weakness and fatigue3. General malaise4. Pica5. Brittle nails6. Smooth and sore tongue7. Angular cheilosis

1. CBC- Low levels of Hct, Hgb and RBC count2. low serum iron, low ferritin3. Bone marrow aspiration- MOST definitive4. Fecalysis w/ occult blood

Decreased stores of iron↓

depletion of hemoglobin synthesis

↓reduced oxygen carrying

capacity↓

tissue hypoxia

1. Provide iron rich-foods-Organ meats (liver)-Beans-Leafy green vegetables-Raisins and molasses2. Administer iron

Oral preparations tablets- Fe fumarate, sulfate and gluconate

Advise to take iron ONE hour before meals (to optimize absorption)

Practice good oral hygiene

1. Oral Iron-FeSO4- 325mg (65mg)-Fe Fumarate 325mg (107mg)-Treatment for 6-12 mos.

Iron should not be taken with antacid because it decreases absorption

Take it with vitamin C

It stains teeth

Drink it with a straw

2. Treat the cause3. Blood Transfusion




EAVALMONTE

APLASTIC ANEMIA-A condition characterized by decreased number of RBC as well as WBC and platelets

Causes:

1. Environmental toxins- pesticides, benzene 2. Certain drugs- Chemotherapeutic agents, chloramphenicol, phenothiazines, Sulfonamides 3. Heavy metals 4. Radiation 5. Idiopathic

1. Fatigue2. pallor3. dyspnea4.bruising orbleeding5. retinal hemorrhages6. Infection

1. CBC- decreased blood cell numbers2. Bone marrow aspiration confirms the anemia- hypoplastic or acellular marrow replaced by fats

Toxins cause a direct bone marrow depression

↓Acellular bone marrow

↓decreased production of

blood elements ↓

PANCYTOPENIA

1. Assess for signs of bleeding and infection2. Instruct to avoid exposure to offending agents

1. Bone marrow transplantation2. Immunosupressant drugs3. Rarely, steroids4. Blood transfusion




EAVALMONTE

SICKLE CELL ANEMIA-

-Results from inheritance of sickle hgb gene (HbS) from both parents-The RBC change shape, upon deoxygenation because of polymerization of the abnormal sickle hemoglobin.-This process damages the red blood cell membrane causing sickling or cresent shape-abN hgb leads to chronic hemolytic anemia manifesting at 1 yr.-SC crisis occurs at high altitude, unpressurized planes, strenuous exercise and resp. infections

3 Nsg priority1. a/w – avoid deoxygenating activities- High altitude is bad2. Fluid deficit – promote hydration3. Pain & comfort

1. Anemia – Hgb 7-10g/dL2. Jaundice3. Enlarged bones in the skull and face4. Tachycardia, cardiac murmurs and cardiomegally5. Thrombosis which may affect any organs6. Splenomegaly7. schemic symptoms causing back and chest pains8. Non-healing ulcers

1. Anemia – Hgb 7-10g/dL

Low O2↓

cause defective hemoglobin to acquire a rigid, crystal-like

C-shaped configuration↓

Sickled RBCs will adhere to endothelium

↓pile up and plug the vessels

ischemia results↓

pain, swelling and fever

1. Manage the pain-Support and elevate acutely inflamed joint-Relaxation techniquesAnalgesics2. Prevent and manage infection-Monitor status of patient-Initiate prompt antibiotic therapy3. Promote coping skills-Provide accurate information-Allow patient to verbalize her concerns about medication, prognosis and future pregnancy4. Monitor and prevent potential complications-Provide always adequate hydration-Avoid cold, temperature that may cause vasoconstriction

1. No safe and effective tx2. BM transplantBT in ACS, strokes, Pregnancy3. Hydroxyurea- induces production of HgbF




EAVALMONTE

FOLIC ACID DEFICIENCY(MEGALOBLASTIC ANEMIA)-

-anemias characterized by abnormally large RBC secondary to impaired DNA synthesis due to deficiency of Folic acid and/or vitamin B12

Causes:

1. Alcoholism2. Malabsorption3. Diet deficient in vegetables, or excessively heated or cooked with large amount of water4. Long term anticonvulsant medication5. Use of antimetabolites6. Increased folate demand states as pregnancy and growth spurts like infancy and adolescence

1. Easy fatigability2. Pallor3. Dyspnea4. Chest pain5. Light headedness6.Tachycardia orpalpitations

1. Blood smear2. Bone marrow examination3. Serum folate <150ng/ml4. Schillings test normal5. (-) neurologic manifestations

Decreased folic acid↓

impaired DNA synthesis in the bone marrow

↓impaired RBC development, impaired nuclear maturation but CYTOplasmic maturation

continues↓

large size

1. Folic acid supplementation1 mg/day oral supplementation2. Dietary enhancement:Foods rich in Folate: asparagus,broccoli, spinach, lettuce,banana,liver, organ meats, peas,beans and nuts

EAVALMONTE




VITAMIN B12 DEFICIENCY(PERNICOUS ANEMIA)

-Vitamin B12 deficiency+ intrinsic factor deficiency= Pernicious Anemia

- megaloblastic, chronic anemia due to deficiency of intrinsic factor leading to Hypochlorhydria – decrease Hcl acid secretion. Lifetime B12 injections. With CNS involvement.

-Intrinsic factor binds with Vit. B12 to promote absorption in the terminal ileum

Causes:

1. Strict vegetarian diet2. Gastrointestinal mal-absorption such as Crohn's disease, Gastrectomy and ileal resection3. Absence of intrinsic factor

1. weakness, fatigue, listlessness2. Neurologic manifestations due to affected neuromyelination. E.g. Paresthesias in the extremities, loss of balance and position sense3. Gastric manifestation: weight loss, anorexia, N/V, diarrhea/constipation,

steatorrhea4. Smooth, sore beefy tongue

1. Peripheral blood smear- shows giant RBCs, WBCs with giant hyper-segmented nuclei2. Very high MCV3. Schilling’s test (shows absorption of tagged B12)4. Intrinsic factor antibody test

↓Intrinsic factor production by the parietal cells of the

stomach↓

↓Vitamin b12 absorption↓

↓RBC production↓

↓DNA Synthesis in maturing RBC↓

Impairment of integrity of cells

(mouth, stomach, anus, vagina,)

1. Enforce CBR2. Diet – high calorie or CHO. Increase CHON, iron & Vit C3. Avoid irritating mouthwashes. Use of soft bristled toothbrush is encouraged.4. Avoid applying electric heating pads – can lead to burns5. Provide assistance in ambulation6. Avoid too much heat and cold

1. Administer B12 injections at monthly intervals for lifetime as ordered. IM- dorsogluteal or ventrogluteal. Not given oral –due pt might have tolerance to drug




EAVALMONTE

POLYCTHEMIA-

-Refers to an INCREASE volume of RBCs-The hematocrit is ELEVATED to more than 55%-The overproduction of red blood cells may be due to a primary process in the BM or it may be a reaction to chronically low O2 level or, rarely, a malignancy-Classified as Primary or Secondary

Causes:

-Secondary polycythemia - caused by either natural or artificial increases in the production of erythrocytes-Physiologic polycythemia occurs in individuals living at high altitudes-Other causes include smoking, renal or liver tumors, or heart or lung diseases that result in hypoxia

1. Skin is ruddy2. Splenomegaly3. headache4. dizziness, blurred vision5. Angina, dyspnea and thrombophlebitis

1. CBC- shows elevated RBC mass2. Normal oxygen saturation3 Elevated WBC and Platelets

Myeloproliferative d/o, hypoxia

↓The stem cells grow

uncontrollably↓

The bone marrow becomes HYPERcellular and all the

blood cells are increased in number

↓-Blood becomes thick and viscous causing sluggish

circulationIncreased blood viscosity causes thromboembolism

-Organ infiltration causes hepato,splenomegaly

-Capillary overdistention causes rupture, then

hemorrjage, then hypovolemia.

1. Primary role of the nurse is EDUCATOR2. Regularly asses for the development of complications3. Assist in weekly phlebotomy4. Advise to have cool or tepid bath for itchiness and use cocoa butter based lotion5. Advice to avoid alcohol intake to decrease risk of bleeding

1. To reduce the high blood cell mass- PHLEBOTOMY2. Hydroxyurea- decrease marrow function3. Allopurinol- decrease uric acid caused by increase in cell turn over4. Dipyridamole/ASA- decrease viscousity of blood5. Chemotherapy to suppress bone marrow

EAVALMONTE




IDIOPATHIC THROMBOCYTOPENIA PURPURA-

-Autoimmune disorder in which IgG is formed that binds the platelet-Platelet with Ab is destroyed as it passes the spleen and by Macrophages-Destruction of platelets result in count less than 100,000/mm3

Causes:

-Exact cause is unknown but sometimes associated with:Viral illness, SLE and pregnancy, sulfa drugs

1. Platelet count less than 20T2. Easy bruising3. Heavy mensesPetechiae and Ecchymoses of skin4. Bleeding from mucous membranes- mouth, GIT and lungsspleen not enlarge

1. Platelet count decreases, mild anemia2. BMA: increase megakaryocytes

Viral illness, Pregnancy, SLE, Sulfa drugs

↓Antibody (Ab) Formation

↓Ab attaches to platelet

↓Platelet destruction by WBC and

Spleen↓

Decrease Platelet↓

Hematoma/ecchymosis/bleeding

1. Prevent bruising2. Protect from infection3. Administer meds orally, rectally or IV rather than IM; hold pressure on site for 5 mins4. Avoid aspirin5. Provide client teaching and discharge planning6. Pad crib and playpen7. Provide soft toys8. Provide protective headgear during toddlerhood9. Use soft toothbrush10. Avoid contact sports

Treatment started when there is bleeding or Platelet count of <10T even w/o bleeding1. Stop the medication that caused ITP2. Immunosuppression- block the binding receptor on macrophages so that platelets are not destroyedPrednisone, Cyclophosphamide, Azathioprine3. Splenectomy- effective only in 50% of patientsIV immunoglobulin- also binds receptors4. Chemotheraphy- (Vincristine) binds receptors




EAVALMONTE

HEMOPHILIA-

-Two clinically indistinguishable disease characterized by bleeding disorder due to genetic defect

-Gene is carried by females and manifest only in males -Frequently dx at birth due to cepalhematoma and bleeding after circumcision

-Hemophilia A-Hemophilia B

1. Bleeding in soft tissues, muscles and weight bearing joints2. Bleeding in any body parts

1. prolonged PTT, decrease Factor VIII or IX level

1. Educate about their condition2. Teach about activity restrictions to decrease episodes of trauma and bleeding3. Avoid medications such as ASA, NSaids, alcohol4. Avoid injections5. Precaution on Dental procedures6. Patients should be encouraged to wear identifications bands7. Warm compress are avoided

BT- FFP, cryoprecipitate, FVIII&IX conc.




EAVALMONTE

PEPTIC ULCER DISEASE

-Excoriation / erosion of submucosa & mucosal lining due to:a.) Hypercecretion of acid – pepsinb.) Decrease resistance to mucosal barrierCauses:1. Hereditary2. Emotional3. Smoking – vasoconstriction – GIT ischemia4. Alcoholism – stimulates release of histamine = Parietal cell release Hcl acid = ulceration5. Caffeine – tea, soda, chocolate6. Irregular diet/rapid eating7. Ulcerogenic drugs – NSAIDS, aspirin, steroids, indomethacin, ibuprofenIndomethacin - S/E corneal cloudiness. Needs annual eye check up.9. Gastrinoma10. Microbial invasion – helicobacter pylori.

According to location1. Stress ulcer2. Gastric ulcer3. Duodenal ulcer – most common

1. Endoscopic exam2. Stool from occult blood3. Gastric analysis – N – gastricIncrease – duodenal4. GI series – confirms presence of ulceration

Disturbance in acid secretion and mucosal protection

↓Increased acidity or decreased

mucosal resistance↓

erosion and ulceration

Nursing Mgt:1. Diet – bland, non irritating, non spicy2. Avoid caffeine & milk/ milk productsIncrease gastric acid secretion3. Administer meds4. Maintain patent IV line4. VS, I&O & bowel sounds5. Complications:a.) Hemorrhage – hypovolemic shockLate signs – anuriab.) Peritonitisc.) Paralytic ileus – most fearedd.) Hypokalemiae.) Thromobphlebitisf.) Pernicious anemia

1. Antacids2. H2 receptor antagonistEx1. Ranitidine (Zantac)2. Cimetidine (Tagamet)3. Tamotidine (Pepcid)- Avoid smoking – decrease effectiveness of drug

- Administer antacid & H2 receptor antagonist – 1hr apart-Cemetidine decrease antacid absorption & vise versa

Cytoprotective agentsEx1. Sucralfate (Carafate) - Provides a paste like subs that coats mucosal lining of stomach2. Cytotec




EAVALMONTE

LIVER CIRRHOSIS-

-lost of architectural design of liver leading to fat necrosis & scarring

Causes:

1. Chronic alcoholism2. Malnutrition – decreaseVit B, thiamin - main cause3. Virus –4. Toxicity- eg. Carbon tetrachloride5. Use of hepatotoxic agents

Early sign – hepatic encephalopathy1. Asterixis – flapping hand tremorsLate signs – headache, restlessness, disorientation, decrease LOC – hepatic coma.

Early signs:

a.) Weakness, fatigueb.) Anorexia, n/vc.) Stomatitisd.) Urine – tea colorStool – clay colore.) Amenorrheaf.) Decrease sexual urgeg.) Loss of pubic, axilla hairh.) Hepatomegalyi.) Jaundicej.) Pruritus or urticaria

1. Liver enzymes- increaseSGPT (ALT)SGOT (AST)2. Serum cholesterol & ammonia increase3. Indirect bilirubin increase4. CBC - pancytopenia5. PTT – prolonged6. Hepatic ultrasonogram – fat necrosis of liver lobules

Inflammation causes liver parenchymal cell destruction

↓Fibrotic changes causes

obstruction of hepatic blood flow and normal liver function

↓Obstruction causes of hepatic blood flow and normal liver

function↓

Decreased liver function results changes in the body

↓Decreased absorption and

utilization of vit. Adek-ineffective detoxification of

protein wates

1. CBR2. Restrict Na!3. Monitor VS, I&O4. With pt daily & assess pitting edema5. Measure abdominal girth daily – notify MD6. Meticulous skin care717. Diet – increase CHO, vit & minerals. Moderate fats. Decrease CHONWell balanced diet8. Complications:a.) Ascites – fluid in peritoneal cavityNursing Mgt:1. Meds: Loop diuretics – 10 – 15 min effect2. Assist in abdominal paracentesis - aspiration of fluid- Void before paracentesis to prevent accidental puncture of bladder as trochar is inserted




EAVALMONTE

CHOLECYSTITIS/ CHOLELITHIASIS-

- Inflammation of gallbladder with gallstone formation.

Predisposing factor:

1. High risk – women 40 years old2. Post menopausal women – undergoing estrogen therapy3. Obesity4. Sedentary lifestyle5. Hyperlipidemia6. Neoplasm

1. Severe Right abdominal pain (after eating fatty food). Occurring especially at night2. Fatty intolerance3. Anorexia, n/v4. Jaundice5. Pruritus6. Easy bruising7. Tea colored urine8. Steatorrhea

1. Oral cholecystogram (or gallbladder series)- confirms presence of stones

Supersaturated bile, Biliary stasis

↓Stone formation

↓Blockage of Gallbladder

↓Inflammation, Mucosal Damage

and WBC infiltration↓

Less bile in the duodenum↓

Impaired fat digestion and absorption

↓Vitamin ADEK mal-absorption,

STEATORHEA with increased gas formationJaundice

ACHOLIC stools

1. Meds – a.) Narcotic analgesic - Meperdipine Hcl – Demerolb.) Anti cholinergic - Atropine SO4c.) Anti emeticPhenergan – Phenothiazide with anti emetic properties2. Diet – increase CHO, moderate CHON, decrease fats3. Meticulous skin care4. Surgery: CholecystectomyNursing Mgt post cholecystectomy-Maintain patency of T-tube intact & prevent infection

a.) Narcotic analgesic - Meperdipine Hcl – Demerolb.) Anti cholinergic - Atropine SO4c.) Anti emeticPhenergan – Phenothiazide with anti emetic properties




EAVALMONTE

ULCERATIVE COLITIS-

-Ulcerative and inflammatory condition of the GIT usually affecting the large intestine-The colon becomes edematous and develops bleeding ulcerations-Scarring develops overtime with impaired water absorption and loss of elasticity

Causes:

unknown

1. Anorexia2. Weight loss3. Fever4. SEVERE diarrhea with Rectal bleeding5. Anemia6. Dehydration7. Abdominal pain and cramping

1. Sigmoidoscopy- increased mucosal friability, decreased mucosal detail, thick inflammatory exudates, edema, erosion2. Stool specimen- positive for blood and mucus

Inflammation edema of the mucous membrane of the colon

and rectum leads to bleeding and shallow ulcerations

↓Abscess formation causes

bowel-wall shortening, thinning, fragility, hypermotility, and

decreased absorption↓

Mucosal ulcerations begin in the distal end of the colon and ascend the large intestine

1. Maintain NPO during the active phase2. Monitor for complications like severe bleeding, dehydration, electrolyte imbalance3. Monitor bowel sounds, stool and blood studies4. Restrict activities5. Administer IVF, electrolytes and TPN if prescribed6. Instruct the patient to AVOID gas-forming foods, MILK products and foods such as whole grains, nuts, RAW fruits and vegetables especially SPINACH, pepper, alcohol and caffeine7. Diet progression- clear liquid LOW residue, high protein diet8. Administer drugs- anti-inflammatory, antibiotics, steroids, bulk-forming agents and vitamin/iron supplements

Aminosalicylic agents




EAVALMONTE

DISSEMINATED INTRAVASCULAR COAGULATION-

- Acute hemorrhagic syndrome char by wide spread bleeding & thrombosis due to a def of clotting factors (Prothrombin &Fibrinogen

Predisposing factor:1. Rapid BT2. Massive trauma3. Massive burns4. Septicemia5. Hemolytic reaction6. Anaphylaxis7. Neoplasia – growth of new tissue8. Pregnancy

1. Petechiae – widespread & systemic (lungs, lower & upper trunk)2. Ecchymosis – widespread3. Oozing of blood from venipunctured site4. Hemoptysis – cough blood5. Hemorrhage6. Oliguria – late sx

1. CBC – reveals decrease platelets2. Stool for occult blood (+)Specimen – stool3. Opthalmoscopic exam – sub retinal hemorrhage4. ABG analysis – metabolic acidosis

1. Monitor signs of bleeding – hema test + urine, stool, GIT2. Administer isotonic fluid solution to prevent shock.3. Administer O2 inhalation4. Administer meds47a. Vit K aquamephytonb. Pitressin or vasopressin – to conserve water.5. NGT – lavage- Use iced saline lavage6. Monitor NGT output7. Provide heplock8. Prevent complication: hypovolemic shockLate signs of hypovolemic shock : anuria

Vit K aquamephyton

Pitressin or vasopressin – to conserve water.




EAVALMONTE

ADDISON’S DISEASE-

-Steroids-lifetimeDecreased adrenocortical hormones leading to:

-a.) Metabolic disturbances (sugar)b.) F&E imbalances- Na, H2O, Kc.) Deficiency of neuromuscular function (salt & sex)

Predisposing Factors:

1. Atrophy of adrenal gland2. Fungal infections3. Tubercular infections

Complication of Addison’s dse : Addisonian crisis16. Results the acute exacerbation of Addison’s dse characterized by :Hypotension, hypovolemia, hyponatremia, wt loss, arrhythmia

1. T – tremors, tachycardiaI - irritabilityR - restlessnessE – extreme fatigueD – diaphoresis, depression2. Decrease sexual urge or libido- Decreased Androgen3.Loss of pubic and axillary hair4. Pathognomonic sign– bronze like skin pigmentation due to decrease cortisol will stimulate pituitary gland to releasemelanocyte stimulating hormone.

1. FBS – decrease FBS (N 80 – 120 mg/dL)2. Plasma cortisol – decreasedSerum Na – decreased (N 135 – 145 meg/L)3. Serum K – increased (N 3.5 – 5.5 meg/L)

Autoimmune theory: body produces antibodies, resulting in

adrenal hypofunction

Decreased aldosterone causes disturbances in sodium, water,

and potassium metabolism

Decreased cortisol causes abnormal metabolism of fat,

protein, and carbohydrate

1. Monitor VS2. Adm meds3. Diet – increase calorie or CHOIncrease Na, Increase CHON, Decrease K4. Force fluid5. Administer isotonic fluid as ordered6. Meticulous skin care – due to bronze like7. HT & discharge planninga) Avoid precipitating factors leading to Addisonian crisis1. Sudden withdrawal crisis2. Stress3. Infectionb) Prevent complicationsAddisonian crisis & Hypovolemic shock8. Hormonal replacement therapy – lifetime9. Important: follow up care

Administer medsa.) Corticosteroids - (Decadron) or Dexamethazone- Hydrocortisone (cortisone)- Prednisone1. 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 crisis3. Monitor S/E (Cushing’s syndrome S/Sx)a.) HPNb.) Hirsutismc.) Edemad.) Moon face & buffalo humpe.) Increase susceptibility to infection sue to steroids- reverse isolation




EAVALMONTE

CUSHING’S SYNDROME-

-increase secretion of adrenocortical hormone

Predisposing Factors:

1. Hyperplasia of adrenal gland2. Tubercular infection – milliary TB

1. Increase sugar – Hyperglycemia3 P’s1. Polyuria2. Polydipsia – increase thirst3. Polyphagia – increase appetiteClassic Sx of DM – 3 P’s & glycosuria + wt loss2. Increase susceptibility to infection – due to increased corticosteroid3. Hypernatrermiaa. HPNb. Edemac. Wt gaind. Moon faceBuffalo humpHypokalemiaHirsutism – increase sex6. Acne & striae7. Increase muscularity of female

1. FBS – increase↑ (N: 80-120mg/dL)2. Plasma cortisol increase3. Na – increase (135-145 meq/L)4. K- decrease (3.5-5.5 meq/L)

1. Monitor VS, I&O2. Administer meds3. Restrict Na4. Provide Dietary intake – low in CHO, low in Na & fatsHigh in CHON & K5. Weigh pt daily & assess presence of edema- measure abdominal girth- notify doc.6. Reverse isolation7. Skin care – due acne & striae8. Prevent complication- Most feared – arrhythmia & DM(Endocrine disorder lead to MI – Hypothyroidism & DM)9. Surgical bilateral Adrenolectomy10. Hormonal replacement therapy – lifetime due to adrenal gland removal- no more corticosteroid!

a. K- sparing diuretics (Aldactone) Spironolactone- promotes excretion of NA while conserving potassiumNot lasix due to S/E hypoK & Hyperglycemia!


LAB FINDINGS PATHOPHYSIOLOGY NURSING INTERVENTIONS DRUG STUDY/ NRSG RESPONSIBILITIES

EAVALMONTE

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)ExopthalmosEnopthalmos – severe dehydration depressed eye2. Excessive iodine intake3. Hyperplasia of TG

1. Increase in appetite – hyperphagia – wt loss due to increase metabolism2. Skin is moist - perspiration3. Heat intolerance4. Diarrhea – increase motility5. All VS increase = HPN, tachycardia, tachypnea, hyperthermia6. CNS changes8. Irritability & agitation, restlessness, tremors, insomnia, hallucinations7. Goiter8. Exopthalmos – pathognomonic sx9. Amenorrhea

1. Serum T3 & T4 - increased2. Radio iodine uptake – increase3. Thyroid scan – reveals enlarged TG

Increased thyroid hormones↓

Increased metabolic rate, oxygen consumption,

sympathetic activity and cns function, altered protein, fat,

carbohydrate metabolism↓

Changes in the body

1. Monitor VS & I & O – determine presence of thyroid storm or most feared complication: Thyrotoxicosis2. Administer meds3. Diet – increase calorie – to correct wt loss4. Skin care –5. Comfy & cool environment6. Maintain siderails- due agitation/restlessness7. Provide bilateral eye patch – to prevent drying of eyes- exopthalmos8. Assist in surgery – subtotal thyroidectomy

Complication- thyroid storm

1. Prophylthiuracil (PTU)2. Methymazole (Tapazole)Most toxic s/e agranulocytosis- fever, sore throat, leukocytosis=inc wbc: check cbc and throat swab cultureMost feared complication : Thrombosis – stroke CVS




EAVALMONTE

HYPOTHYROIDISM-

-decrease secretion of T3, T4 – can lead to MI / AtherosclerosisAdult – myxedemaChild- cretinism – only endocrine dis lead to mental retardation

Predisposing factor:

1. `Iatrogenic causes – caused by surgery2. Atrophy of TG due to:a. Irradiationb. Traumac. Tumor, inflammation3. Iodine def4. Autoimmune – Hashimoto disease

Early signs – 1. weakness and fatigue2. Loss of appetite – increased lypolysis – breakdown of fats causing 3. atherosclerosis = MIWt gain5. Cold intolerance – myxedema - comaConstipationLate Sx – brittle hair/ nailsNon pitting edema due increase accumulation of mucopolysacharide in SQ tissue -MyxedemaHorseness voiceDecrease libidoDecrease VS – hypotension bradycardia, bradypnea, and hypothermiaLethargyMemory impairment

1. Serum T3 T4 decrease2. Serum cholesterol increase – can lead to MI3. RA IU – radio iodine uptake – decrease

1. Monitor VS. Check for s/sx of cardiovascular disorder.2. Monitor daily weigh.3. Diet, decrease calorie, increase fiber4. Provide warm environment during cold climate.5.

LevothyroxineThyroglobulin




EAVALMONTE

DM TYPE 1-

-“Juvenile “ onset, common in children, non-obese “brittle dse”-Insulin dependent diabetes mellitus

Causes:

1. 90% hereditary – total destruction of pancreatic dells2. Virus3. Toxicity to carbon tetrachloride4. Drugs – Steroids both cause hyperglycemiaLasix - loop diuretics

1.) Polyuria2.) Poydipsia3.) Polyphagia4.) Glycosuria5.) Weight loss6.) Anorexia7.) N/V8.) Blurring of vision9.) Increase susceptibility to infection10.) Delayed/ poor wound healing

1. FBS- > 1262. RBS- >2003. OGTT- > 200

Destruction of BETA cells↓

decreased insulin production↓

uncontrolled glucose production by the liver

↓Hyperglycemia

↓ signs and symptoms

Complication: DKA

1. Insulin Therapy2. Diet3. Exercise4. Regular Glucose Monitoring

InsulinRoute: Subq

-Do not massage site of injection.-Store at room temp or ref.-Shake before using.




EAVALMONTE

DM TYPE 2-

-A type of DM characterized by insulin resistance and impaired insulin production

Causes:

1. Unknown2. Probably genetic and obesity

1. Asymptomatic2. 3 P’s and 1G

1. FBS- > 1262. RBS- >2003. OGTT- > 200

Decreased insulin production↓

diminished insulin action↓

Hyperglycemia↓

signs and symptoms

Complication: HONKCH – hyperO – osmolarN – nonK – ketoticC – coma

1. Diet2. Exercise3. Regular Glucose Monitoring4. Oral Hypoglycemic Agents (OHA)




EAVALMONTE

PLACENTA PREVIA-

-it occurs when the placenta is improperly implanted in the lower uterine segment, sometimes covering thecervical os. Abnormal lower implantation of placenta.- candidate for CS

Causes:

1. Increased parity2. Advanced maternal age3. Past cesarian births4. Past uterine curettage5. Multiple gestations6. Decreased vascularity of upper uterine segment7. Use of cocaine

1. Abrupt, painless , bright red vaginal bleeding.

TYPES:

1. Low-lying – implantation of the placenta in the lower rather than in the upper portion of the uterus2. Marginal – placenta edge approaches that of the cervical os3.partial – implantation that occludes a portion of the cervical os4. Complete ( totalis) – placenta that totally obstructs the cervical os

Ultrasound Fertilized ovum↓

implantation in uterus↓

embryonic stage↓

placenta arise in thropoblast tissues↓

insufficient blood↓

Placenta migrates to where there is sufficient blood supply

↓placenta resides in lower part

↓(low lying, total, partial,

marginal)↓

painless dark red bleeding↓

Profuse bleeding↓

Hypotension↓

Hypovolemic shock↓

Coma↓

death

1. Monitor vital signs & bleeding ( weigh unused perineal pad, then weigh perineal pad soaked in blood, then subtract. The difference is the weight of the blood loss.)2. Monitor fetal heart rate3. Provide strict bed rest to minimize the risk to fetus.4.observe for further bleeding episodes5. Avoid vaginal examinations ( no ie). If ie is indicated, it should be done in a double set-up environment. ( meaning: or/dr) wherein the patient has already signed a consent form, pre-op




EAVALMONTE

ABRUPTIO PLACENTA-

-it is the premature separation of the placenta form the implantation site. It usually occurs after thetwentieth week of pregnancy.

Causes:

1.maternal hypertension ( chronic or pregnacy induced)2. Advanced maternal age3. Grand multiparity – more than 5 pregnancies4. Trauma to the uterus5. Sudden release of amniotic fluid that cause sudden decompression of te uterus.

1. Painful dark red vaginal bleeding in covert type2.painful bright red vaginal bleeding in overt type3.hard, rigid, firm,board-like abdomen caused by accumulation of blood behind the placenta with fetal parts hard to palpate.4. Abnormal tenderness due to distentionof the uterus with blood. 5. Sharp pain over the fundus as the placenta separates.6. Signs of shock & fetal distress as the placenta separates.

Ultrasound 1. Infuse IV, prepare to administer blood2. Type and crossmatch3. Monitor FHR4. Insert Foley5. Measure blood loss; count pads6. Report s/sx of DIC7. Monitor v/s for shock8. Strict I&O




EAVALMONTE

ECLAMPSIA-

-with seizure! Increase BUN – glomerular damage. Provide safety.

Causes:

1.maternal hypertension ( chronic or pregnacy induced)2. Advanced maternal age3. Grand multiparity – more than 5 pregnancies4. Trauma to the uterus5. Sudden release of amniotic fluid that cause sudden decompression of te uterus.

1. All the signs & symptoms of preeclampsia 2. Convulsion followed by coma is the main difference of eclampsia & preeclampsia3. Oliguria4. Pulmonary edema

1. Home management is allowed only if:A. Bp is 140/90 o belowB. There is no proteinuriaC. There is no fetal growth retardationD. The patient is not a young primipara.2. Cbr3. Diet should be high in protein & carbohydrates with moderate sodium restriction.4. Provide detailed instructions about warning signs:A. Epigastric pain –aura to convulsionB. Visual disturbancesC. Severe continuous headache5. A. Rest in left lateral position to promote blood supply to the placenta & the fetus.6. Absence of pattelar reflex is sign of MGSO4 toxicity

1. Hydralazine – ( apresoline )- antihypertensive2. Magnesium sulfate ( mgso4) - drug of choice to treat & prevent convulsions.3. Diuretics are not given & ivf is limited

Actions of mgso4:

Prevent convulsionB. Reduce blood pressureCheck the following first before administering mgso4:Deep tendon reflex present - +2 ( normal)2. Rr should be at least 12 bpm3. Urine output should be at least 30 ml/hr

Antidote- Calcium Gluconate




EAVALMONTE

BURNS-

- direct tissue injury caused by thermal, electric, chemical & smoke inhaled (TECS)Nursing Priority – infection (all kinds of burns)Head burn-priority- a/w2nd priority for 1st & 2nd ° - pain2nd priority for 3rd ° - F&E

Causes:

1. Thermal- direct contact – flames, hot grease, sunburn.

2. Electric, – wires3. Chem. – direct

contact – corrosive materials acids

4. Smoke – gas / fume inhalation

1. BP decrease- Urine output- HR increase- Hct increase- Serum Na decrease- Serum K increase- Met acidosisClass:I. Partial Burn1. 1 s t degree – superficial burns- Affects epidermis- Cause: thermal burn- Painful- Redness (erythema) & blanching upon pressure with no fluid filled vesicles2. 2 nd degree – deep burns- Affects epidermis & dermis- Cause –chem. burns- very painful- Erythema & fluid filled vesicles (blisters)

(cont)II Full thickness Burns1. Third & 4 th 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.

1. Home management is allowed only if:A. Bp is 140/90 o belowB. There is no proteinuriaC. There is no fetal growth retardationD. The patient is not a young primipara.2. Cbr3. Diet should be high in protein & carbohydrates with moderate sodium restriction.4. Provide detailed instructions about warning signs:A. Epigastric pain –aura to convulsionB. Visual disturbancesC. Severe continuous headache5. A. Rest in left lateral position to promote blood supply to the placenta & the fetus.6. Absence of pattelar reflex is sign of MGSO4 toxicity

Mafenide acetateMorphine sulfateLactated RingersD5W




EAVALMONTE

EMPHYSEMA-

-irreversible terminal stage of COPD- Characterized by inelasticity of alveolar wall leading to air trapping, leading to maldistribution of gases.- Body will compensate over distension of thoracic cavity- Barrel chest

- There is progressive and irreversible alveolocapillary destruction with abnormal alveolar enlargement causing alveolar wall destruction. The result is INCREASED lung compliance, DECREASED oxygen diffusion and INCREASED airway resistance!

Predisposing factor:1. Smoking2. Allergy3. Air pollution4. High risk – elderly5. Hereditary

1. Productive cough2. Dyspnea at rest – due terminal3. Anorexia & gen body malaise4. Rales/ rhonchi5. Bronchial wheezing6. Decrease tactile fremitus (should have vibration)– palpation – “99”. Decreased - with air or fluid7. Resonance to hyperresonance – percussion8. Decreased or diminished breath sounds9. Pathognomonic: barrel chest – increase post/ anterior diameter of chest10. Purse lip breathing – to eliminated PCO211. Flaring of alai nares

1. Pulmonary function test – decrease vital lung capacity2. ABG –a.) Panlobular / centrolobular emphysemapCO2 increasepO2 decrease – hypoxema resp acidosis Blue bloatersb.) Panacinar/ CentracinarpCO2 decreasepO2 increase – hyperaxemia resp alkalosis Pink puffers

Smoking ↓

Particle deposition in airways↓

low level inflammatory responsedue to aging

↓Disequilibrium between elastase

and antielastase↓

Destruction of elastic recoil↓

Overdistention of alveoli↓

Retention of CO2↓

Hypoxia and resp acidosis

Complication: Pneumothorax – air in pleural space

1. CBR2. Meds3. O2 – Low inflow4. Force fluids5. High fowlers6. Neb & suction7. InstituteP – postureE – endE – expiratory to prevent collapse of alveoliP – pressure8. HTa.) Avoid smoking

AminophyllineTheophylline

VentolinSalbutamol

BricanylTerbutaline

Alupent




EAVALMONTE

PLEURAL EFFUSION-

-referred to as ‘water on the lungs’ is the build up of excess fluid between the layers of the pleura of the lungs. The pleura are thin membranes that line the lungs and the inside chest cavity and act to lubricate and facilitate breathing. It is normally filled with 5-10 milliliters of serous fluid.

Types: 1. Transudative- caused by leaking into pleural space. This is caused by elevated pressure in or low protein content in the bld vessels/ CHF is a common cause.

2. Exudative- results from leaky blood vessels caused by inflammation. Often caused by lung disease, tb, pneumonia, drug reaction.

1. Dyspnea, dullness over affected area upon percussion, absent or decreased breath sounds over affected area, pleural pain, dry cough, pleural friction rub2. Pallor, fatigue, fever, and night sweats (with empyema)

a. Chest x-ray positive if greater than 250 cc pleural fluidb. Pleural biopsy may reveal bronchogenic carcinomac. Thoracentesis may contain blood if cause is cancer, pulmonary infarction, or tuberculosis; positive for specific organism in empyema.

Inflammation of airways↓

Bronchial edema, increased mucus production,

bronchoconstriction, bronchial spasm

↓worsening of obstruction

↓accumulation of fluids caused by

oversecretion↓

multiplication of growth of microorganism

↓Inflammation in the epithelial

wall↓

fluid filled alveoli↓

rupture of inflamed endothelial cells

excess fluid accumulate in the pericardial space

↓Pleural effusion

1. Assist with repeated thoracentesis.2. Administer narcotics/sedatives as ordered to decrease pain.3. Assist with instillation of medication into pleural space (reposition client every 15 minutes to distribute the drug within the pleurae).4. Place client in high-Fowler’s position to promote ventilation.5. O26. ABG

a. Antibiotics: either systemic or inserted directly into pleural spaceb. Fibrinolytic enzymes: trypsin, streptokinase-. streptodornase to decrease thickness of pus and dissolve fibrin clots




EAVALMONTE

CROUP-

-group of respiratory disease that often affects infants, and children under age 6, characterized by barking cough, whistling, stridor as the child breathes in, and hoarseness in the larynx.

Types:

1. Larnygotracheobronchitis- acute viral infection of the larynx, bronchi, which causes obstruction below vocal cords.

2. Spasmodic laryngitis- sudden onset, occurring mainly at night and characterized by laryngeal obstruction at the level of vocal cord

Causes: flu virus, adenovirus, rhinovirus, enterovirus, coxsacklevirus, measles virus, reovirus

1. Colds2. low grade fever3. stridor4. seal bark cough5. cyanosis6. use of accessory muscles to breath7. agitation8. muffled voice9. spontaneous cough

1. Chest xray- difference between croup and epiglottis2. Throat culture- reveals identifies infectious agent and sensitivity to specific antimicrobial therapy3. ABG- reveals hypoxemia state that require oxygen therapy, decreased PH and changes and co2 levels indicating respiratory acidosis or failure in severe cases.

Viral infection↓

affects larynx and trachea↓

subglottic edema↓

airflow obstruction↓

croup

1. Airway2. Assess resp status3. NPO status4. Immunization (haemophilus type B)5. Facilitate hygiene6. Proper hygiene7. Administer meds

1. Antipyretic: Acetaminophen to reduce fever2. Bronchodilator to relax respiratory smooth muscle and relieve stridor3. Corticosteroids- to reduce inflammation and edema around vocal cords4. Antibiotics




EAVALMONTE

TETRALOGY OF FALLOT-

-group of congenital heart conditions including pulmonic stenosis, ventricular hypertrophy, overriding aorta and ventricular septic defect.

Causes:

1. Unknown2. Fetal alcohol syndrome

1. Rt ventricular hypertrophy2. high degree of cyanosis3. polycythemia4. severe dyspnea – squatting position – relief , inhibit venous return facilitate lung expansion.5. growth retardation – due no O26. tet spell or blue spells- short episodes of hypoxia7. syncope8. clubbing of fingernails – due to chronic tissue hypoxia9. mental retardation – due decreased O2 in brain10. boot shaped heart – x-ray

1. Chest X-ray- decreased pulmonary vascular, enlarged right ventricle, a boot shape cardiac silhouette3. Electrocardiography4. diminished o2 saturation

atherosclerosis↓

reduced coronary tissue perfusion

↓diminished myocardial

oxygenation↓

anaerobic metabolism↓

increased lactic acid production

↓chest pain

1. O22. no valsalva maneuver , fiber diet laxative3. morphine – hypoxia4. propranolol – decrease heart spasms5. palliative repair –BLT blalock taussig procedureBrock procedure – complete procedure

MorphinePropranolol




EAVALMONTE

RHEUMATIC HEART DISEASE-

-inflammation disease ff an infection acquired by group A Beta hemolytic strepto coccus-Affected body – cardiac muscles and valves , musculoskeletal , CNS, IntegumentarySorethroat before RHD-Aschoff – rounded nodules with nucleated cells and fibroblasts – stays and occludes mitral valve

Major Minor1. polyarthritis – multi joint pain 1. arthralgia – joint pain2. chorea – sydenhamms chores orst. vetaus dance-purposeless involuntary hand and shoulder withgrimace2. low grade fever3. carditis – tachycardiaerythema marginatum - macular rashesSQ nodules3. all lab resultsincrease antibody“ C reactive protein“ erythrocyte sedimentationrate“ anti streptolysin

1. CBR2. throat swab – culture and sensitivity3. antibiotic mgt – to prevent recurrence4. aspirin – anti-inflammatory. Low grade fever – don’t give aspirin.S/E of aspirin:- Reyes syndrome – encephalopathy- fatty infiltration of organs such as liver and brain

aspirin – anti-inflammatory. Low grade fever – don’t give aspirin.S/E of aspirin:- Reyes syndrome – encephalopathy- fatty infiltration of organs such as liver and brain

oral revalida

Documents

weigh pt daily

serum cholesterol

congestive heart failure

nursing interventions 1

radiates back

black raise 3

high fowlers 4

sex male 2