EAVALMONTE

DRUG STUDY/
SIGNS AND NURSING NRSG
DISEASE LAB FINDINGS PATHOPHYSIOLOGY
SYMPTOMS INTERVENTIONS RESPONSIBILIT
IES
ANGINA PECTORIS- 1.
1. Initial Diagnosis atherosclerosis 1.) Enforce CBR Nitroglycerine-
A clinical syndrome symptoms – 1.History taking ↓ 2.) Administer meds 1st dose NTG –
characterized by Levine’s sign – & PE reduced coronary tissue NTG – small doses – give 3 – 5 min
paroxysmal chest pain hand clutching 2. ECG – ST perfusion venodilator 2nd dose NTG – 3
usually relieved by REST of chest segment ↓ Large dose – – 5 min
or NGT 2. Chest pain – depression & T diminished myocardial vasodilator 3rd & last dose –
nitroglycerin, resulting sharp, wave inversion oxygenation 3.) Administer O2 3 – 5 min
from temp myocardial stabbing 3. Stress test – ↓ inhalation Still painful after
ischemia. excruciating treadmill = anaerobic metabolism 4.) Semi-fowler 3rd dose – notify
pain. Location abnormal ECG ↓ 5.) Diet- Decrease doc. MI! Keep in
Predisposing Factor: – substernal 4. Serum increased lactic acid Na and saturated a dry place.
1. sex – male -radiates cholesterol & production fats Avoid moisture &
2. black raise back, uric acid - ↓ 6.) Monitor VS, I&O, heat, may
3. hyperlipidemia shoulders, increase chest pain ECG inactivate the
4. smoking axilla, arms & 5. Cardiac 7.) HT: Discharge drug.
5. HPN jaw muscles catheterization- planning: 2. Monitor S/E:
6. DM -relieve by Provides the a. Avoid orthostatic
7. oral contraceptive rest or NGT MOST precipitating factors hypotension –
prolonged 3. Dyspnea DEFINITIVE – 4 E’s dec bp
8. sedentary lifestyle 4. Tachycardia source of b. Prevent transient
9. obesity 5. Palpitation diagnosis by complications – MI headache
10.hypothyroidism 6.diaphoresis showing the c. Take meds before dizziness
7. Dizziness presence of the physical exertion-to 3. Rise slowly
Precipitating factors and syncope atherosclerotic achieve maximum from sitting
4 E’s lesions therapeutic effect of position
1. Excessive physical drug 4. ASPIRIN
exertion d. Importance of B. Beta
2. Exposure to cold follow-up care. blockers –
environment - propanolol
Vasoconstriction Administer
3. Extreme emotional with foods
 EAVALMONTE

response C. ACE
4. Excessive intake of inhibitors –
food – captopril
D. Ca
antagonist -
nefedipine
DRUG STUDY/
SIGNS AND NURSING NRSG
DISEASE LAB FINDINGS PATHOPHYSIOLOGY
SYMPTOMS INTERVENTIONS RESPONSIBILIT
IES
MYOCARDIAL
INFARCTION – heart 1. chest pain – 1. ECG- the ST Interrupted coronary 1. Narcotic 1. ANALGESIC
attack – terminal stage excruciating, segment is blood flow analgesics – The choice is
of CAD vice like, ELEVATED. T ↓ Morphine SO4 – to MORPHINE
- Characterized by visceral pain wave myocardial ischemia induce vasodilation SULFATE
necrosis & scarring due located inversion, ↓ & decrease levels of It reduces pain
to permanent mal- substernal or ECG tracing – anaerobic myocardial anxiety. and anxiety
occlusion precodial area ST segment metabolism for several 2. Administer O2 Relaxes
(rare) increase, hours inhalation – low bronchioles to
Predisposing factors - radiates widening or ↓ inflow (CHF-increase enhance
1. sex – male back, arm, QRS myocardial death inflow) oxygenation
2. black raise shoulders, complexes – ↓ 3. Enforce CBR 2. Vasodilators
3. hyperlipidemia axilla, jaw & means depressed cardiac without BP 1. NTG
4. smoking abd arrhythmia in function a.) Bedside 2. Isordil
5. HPN muscles. MI indicating ↓ commode - Antiarrythmic
6. DM - not usually PVC triggers autonomic 4. Avoid valsalva 1. LYDOCAINE
7. oral contraceptive relived by rest 2. Myocardial nervous system maneuver blocks release of
prolonged r NTG enzymes- response 5. Semi fowler norepenephrine
8. sedentary lifestyle 2. dyspnea elevated ↓ 6. General liquid to 2. Brithylium
9. obesity 3. erthermia Creatinine further imbalance of soft diet – decrease - Beta-blockers –
10. hypothyroidism 4. initial Phospokinase, myocardial O2 demand Na, saturated fat, lol
11. obesity increase/decre Lactic acid and supply caffeine 1. Propanolol
12. stress ase in dehydrogenase 7. Monitor VS, I&O & (inderal)
BP/tachybrady and Troponin ECG tracings - ACE inhibitors -
5. mild levels 8. Take 20 – 30 pril
restlessness & 3. CBC- may ml/week – wine, Prevents
 EAVALMONTE

apprehensions show elevated brandy/whisky to formation of

6. occasional WBC count induce vasodilation. angiotensin II
findings 4. Test after 9. Assist in surgical; Limits the area of
a.) split S1 & the acute CABAG infarction
S2 stage- Exercise 1. Captopril –
b.) pericardial tolerance test, - Ca – antagonist
friction rub thallium scans, 1. Nifedipine
c.) rales cardiac - Thrombolitics or
/crackles catheterization fibrinolytics– to
d.) S4 (atrial 5. serum dissolve clots/
gallop) cholesterol & thrombus
uric acid -
increase

DISEASE SIGNS AND LAB FINDINGS PATHOPHYSIOLOGY NURSING DRUG STUDY/

SYMPTOMS INTERVENTIONS NRSG
RESPONSIBILIT
IES
CONGESTIVE HEART
FAILURE(LEFT) 1. Dyspnea CXR may reveal LEFT Ventricular pump 1. Administer meds M – morphine
Inability of the heart to 2. Orthopnea cardiomegaly failure 2. Administer O2 SO4 to induce
pump sufficiently (Diff of 2. ECG may ↓ inhalation – high! @ vasodilatation
- Backflow breathing identify Cardiac back up of blood into 3 -4L/min via nasal A–
sitting pos – hypertrophy the pulmonary veins cannula aminophylline &
Predisposing factors: platypnea) 3. ↓ 3. High fowlers decrease anxiety
1.) 90% mitral valve 3. Paroxysmal Echocardiogra increased pulmonary 4. Restrict Na! D – digitalis
stenosis – due RHD, nocturnal m may show capillary pressure 5. Provide (digoxin)
aging dysnea – PNO- hypokinetic ↓ meticulous skin care D - diuretics
RHD affects mitral valve nalulunod heart pulmonary congestion 6. Weigh pt daily. O - oxygen
– streptococcal infection 4. Productive 4. ABG and Assess for pitting G - gases
Dx: - Aso titer – anti cough with Pulse oximetry LEFT ventricular failure edema.
streptolysine O > 300 blood tinged may show ↓ Measure abdominal
total units sputum decreased O2 decreased cardiac girth daily & notify
- Steroids 5. Frothy saturation output MD
- Penicillin salivation 5. PCWP- ↓ 7. Monitor V/S, I&O,
- Aspirin 6. Cyanosis Pulmonary decreased perfusion to breath sounds
 EAVALMONTE

Complication: RS-CHF 7. Rales/ Capillary the brain, kidney and 8. Institute

Aging – degeneration / crackles – Wedge other tissues bloodless
calcification of mitral due to fluid Pressure is ↓ phlebotomy.
valve 8. Bronchial increased in oliguria, dizziness Rotating tourniquet
Ischemic heart disease wheezing LEFT sided CHF or BP cuff rotated
55 and CVP is clockwise q 15 mins
1. CAD 9. PMI – increased in = to promote
2. Valvular heart displaced RIGHT sided decrease venous
diseases lateral – due CHF return
3. Hypertension cardiomegaly 6. ABG – PCO2 9. Diet – decrease
4. MI 10. Pulsus increase, PO2 salt, fats & caffeine
5. Cardiomyopathy alternons – decrease = =
6. Lung diseases weak-strong hypoxemia =
7. Post-partum pulse resp acidosis
8. Pericarditis and 11. shock
cardiac tamponade 12. S3 –
ventricular
gallop
13.cerebralan
oxia
14. Oliguria
DISEASE SIGNS AND LAB FINDINGS PATHOPHYSIOLOGY NURSING DRUG STUDY/
SYMPTOMS INTERVENTIONS NRSG
RESPONSIBILIT
IES
CONGESTIVE HEART
FAILURE(RIGHT) 1. Peripheral Diagnosis: RIGHT ventricular failure 1. Administer meds a.) Cardiac
Inability of the heart dependent, 1. CXR – ↓ 2. Administer O2 glycosides
to pump sufficiently pitting edema cardiomegaly blood pooling in the inhalation – high! @ Increase
- Backflow 2. Weight gain 2. CVP – venous circulation 3 -4L/min via nasal myocardial =
3. Distended measures the ↓ cannula increase CO
Predisposing factor neck vein pressure at R increased hydrostatic 3. High fowlers Digoxin
1. 90% - tricuspid 4. atrium pressure 4. Restrict Na! (Lanoxin).
stenosis hepatomegaly Normal: 4 to 10 ↓ 5. Provide Antidote: digivine
2. COPD 5. Ascites cm of water peripheral edema meticulous skin care Digitoxin:
3. Pulmonary embolism Increase CVP > 6. Weigh pt daily. metabolizes in
 EAVALMONTE

4. Pulmonic stenosis 10 – RIGHT ventricular failure Assess for pitting liver not in
5. Left sided heart hypervolemia ↓ edema. kidneys not
failure Decrease CVP blood pooling Measure abdominal given if with
<4– ↓ girth daily & notify kidney failure.
hypovolemia venous congestion in MD b.) Loop
Flat on bed – the kidney, liver and GIT 7. Monitor V/S, I&O, diuretics: Lasix –
post of pt when breath sounds effect with in 10-
giving CVP 8. Institute 15 min. Max = 6
Position during bloodless hrs
CVP insertion – phlebotomy. c.)
Trendelenburg Rotating tourniquet Bronchodilators:
to prevent or BP cuff rotated Aminophillin
pulmonary clockwise q 15 mins (Theophyllin).
embolism & = to promote Avoid giving
promote decrease venous caffeine
ventricular return d.) Narcotic
filling. 9. Diet – decrease analgesic:
3.Echocardiogr salt, fats & caffeine Morphine SO4 -
aphy – enlarged induce
heart vasodilaton &
chamber / decrease anxiety
cardiomyopath e.) Vasodilators –
y NTG
4.Liver enzyme f.) Anti-
SGPT ( ALT) arrythmics –
Lidocaine

DISEASE SIGNS AND LAB FINDINGS PATHOPHYSIOLOGY NURSING DRUG STUDY/

SYMPTOMS INTERVENTIONS NRSG
RESPONSIBILIT
IES
HYPERTENSION-
A systolic BP greater 1. Headache 1. Health 1. Health history Diuretics
than 140 mmHg and a 2. Visual history and PE and PE Beta blockers
diastolic pressure changes 2. Routine 2. Routine Calcium channel
greater than 90 mmHg 3. chest pain laboratory- laboratory- blockers
 EAVALMONTE

over a sustained period, 4. dizziness urinalysis, ECG, urinalysis, ECG, lipid ACE inhibitors
based on two or more 5. N/V lipid profile, profile, BUN, serum A2 Receptor
BP measurements. 6. Blurring of BUN, serum creatinine , FBS blockers
vision creatinine , FBS 3. Other lab- CXR, Vasodilators
Primary HPN- Idiopathic 7. Epistaxis 3. Other lab- creatinine
Secondary HPN- Due to CXR, creatinine clearance, 24-huour -nadolol(corgard)
other conditions like clearance, 24- urine protein -metoprolol
Pheochromocytoma, huour urine 4. Avoid stress. (lopressor)
renovascular protein 5. Provide -
hypertension, Cushing’s, information about clonidine(catapre
Conn’s , SIADH anti-hypertensive ss)
drugs -hydralazine
Major Risk factors Instruct proper (apresoline)
1. Smoking compliance and not -
2. Hyperlipidemia abrupt cessation of captopril(capoten
3. DM drugs even if pt )
4. Age older than 60 becomes -
5. Gender- Male and asymptomatic/ diltiazem(cardize
post menopausal W improved condition m)
6. Family History 6. Promote Home -
7. Smoking care management nifedipine(calcibl
8. Obesity Instruct regular oc)
9. High salt intake monitoring of BP -verapamil
10. Low potassium Involve family
intake members in care
Instruct regular
follow-up
 EAVALMONTE

DISEASE SIGNS AND LAB FINDINGS PATHOPHYSIOLOGY NURSING DRUG STUDY/

SYMPTOMS INTERVENTIONS NRSG
RESPONSIBILIT
IES
BUERGER DISEASE-
Acute inflammatory 1. Intermittent 1. Oscillometry Cause is 1. Encourage a slow -Pentoxyfylline
disorder affecting small claudication – – decrease UNKNOWN progression of (Trental) reduces
to medium sized leg pain upon peripheral Probably an physical activity blood viscosity
arteries & veins of lower walking - pulse volume. Autoimmune disease a.) Walk 3 -4 x / day and improves
extremities. Male/ feet Relieved by 2. Doppler UTZ b.) Out of bed 2 – 3 supply of O2
rest – decrease Inflammation of the x a / day blood to muscles
Predisposing factors: 2. Cold blood flow to arteries 2. Meds
- Male sensitivity & affected ↓ a.) Analgesic -Cilostazol
- Smokers skin color extremities. thrombus formation b.) Vasodilator (Pletaal) inhibits
changes 3. Angiography ↓ c.) Anticoagulant platelet
White bluish – reveals site & occlusion of the vessels 3. Foot care mgt like aggregation and
Pallor cyanosis extent of mal- DM – increases
red rubor occulsion. a.) Avoid walking vasodilatation
3. Decrease or barefoot
diminished b.) Cut toe nails
peripheral straight
pulses - Post c.) Apply lanolin
tibial, Dorsalis lotion – prevent skin
pedis breakdown
4. Tropic d.) Avoid wearing
changes constrictive
5. Ulcerations garments
6. Gangrene 4. Avoid smoking &
formation exposure to cold
environment
5. Surgery: BKA
(Below the knee
amputation)
6. Stop smoking.
 EAVALMONTE

DISEASE SIGNS AND LAB FINDINGS PATHOPHYSIOLOGY NURSING DRUG STUDY/

SYMPTOMS INTERVENTIONS NRSG
RESPONSIBILIT
IES
BRONCHIAL ASTHMA-
reversible inflammation 1. C – cough – 1. Pulmo 1. CBR – all COPD
lung condition due to non function test – 2. Medsa.)
hyerpsensitivity leading productive to decrease lung Bronchodilator
to narrowing of smaller productive capacity through inhalation
airway. 2. D – dyspnea 2. ABG – PO2 or metered dose
3. W – decrease inhaled / pump.
1. Extrinsic Asthma – wheezing on Give 1 s t before
called Atropic/ allergic expiration corticosteroids
asthma 4. Cyanosis b.) Corticosteroids –
a.) Pallor 5. Mild due inflammatory.
b.) Dust apprehension Given 10 min after
c.) Gases & restlessness adm bronchodilator
d.) Smoke 6. Tachycardia c.) Mucolytic/
64 & palpitation expectorant
e.) Dander 7. Diaphoresis d.) Mucomist – at
f.) Lints bedside put suction
machine.
2. Intrinsic Asthma- e.) Antihistamine
Cause: 2. Force fluid
HeredItary 3. O2 – all COPD low
Drugs – aspirin, inflow to prevent
penicillin, b blockers resp distress
Food additives – nitrites 4. Nebulize &
Foods – seafood, suction
chicken, eggs, 5. Semifowler – all
chocolates, milk COPD except
Physical/ emotional emphysema due
 EAVALMONTE

stress late stage

Sudden change of temp, 6. HT
humidity &air pressure a.) Avoid pred
factors
3. Mixed type b.) Complications:
c.) Adherence to
medications

DISEASE SIGNS AND LAB FINDINGS PATHOPHYSIOLOGY NURSING DRUG STUDY/

SYMPTOMS INTERVENTIONS NRSG
RESPONSIBILIT
IES
PANCREATITIS-
acute or chronic 1. Severe Lt 1. Serum Autodigestion of 1. Administer meds. a.) Narcotic
inflammation of epigastric pain amylase & pancreatic tissue 2. Withold food & analgesic -
pancreas leading to – radiates lipase – ↓ fluid – aggravates Meperidine Hcl
pancreatic edema, from back increase Hemorrhage, Necrosis pain (Demerol)
hemorrhage & necrosis &flank area 2. Urine lipase – and Inflammation 3. Assist in Total Don’t give
due to auto digestion. - Aggravated increase ↓ Parenteral Nutrition Morphine SO4 –
Bleeding of pancreas - by eating, 3. Serum Ca – KININ ACTIVATION will (TPN) or will cause spasm
Cullen’s sign at with DOB decrease result to increased hyperalimentation of sphincter.
umbilicus 2. N/V 4. WBC permeability Complications of b.) Smooth
3. Tachycardia 5. UTZ ↓ TPN muscle relaxant/
Predisposing factors: 4. Palpitation Loss of Protein-rich fluid 1. Infection anti cholinergic
1. Chronic alcoholism due to pain into the peritoneum 2. Embolism - Ex. Papavarine
2. Hepatobilary disease 5. Dyspepsia – HYPOVOLEMIA 3. Hyperglycemia Hcl
3. Obesity indigestion 4. Institute stress Prophantheline
4. Hyperlipidemia 6. Decrease mgt tech Bromide
5. Hyperparathyroidism bowel sounds a.) DBE (Profanthene)
6. Drugs – Thiazide 72 b.) Biofeedback c.) Vasodilator –
diuretics, pills 7. (+) Cullen’s 5. Comfy position - NTG
Pentamidine HCL sign - Knee chest or fetal d.) Antacid –
(Pentam) ecchymosis of like position Maalox
7. Diet – increase umbilicus 6. If pt can tolerate e.) H2 receptor
saturated fats hemorrhage food, give increase antagonist -
8. (+) Grey CHO, decrease fats, Ranitidin
 EAVALMONTE

Turner’s spots and increase CHON (Zantac) to

– ecchymosis 7. Complications: decrease
of flank area Chronic pancreatic
9. hemorrhagic stimulation
Hypocalcemia pancreatitis f.) Ca – gluconate

DISEASE SIGNS AND LAB FINDINGS PATHOPHYSIOLOGY NURSING DRUG STUDY/

SYMPTOMS INTERVENTIONS NRSG
RESPONSIBILIT
IES
APPENDICITIS-
Inflammation of the 1. Abdominal 1. CBC- reveals Obstruction of lumen 1. Preoperative care
vermiform appendix pain: begins in increased WBC ↓  NPO
the umbilicus count increased pressure  Consent
ETIOLOGY: usually then localizes 2. Ultrasound ↓  Monitor for
fecalith, lymphoid in the RLQ (Mc 3. Abdominal X- decreased blood supply perforation
hyperplasia, foreign Burney’s ray ↓ and signs of
body and helminthic point) bacterial proliferation shock
obstruction 2. Anorexia and mucosal  Monitor bowel
3. Nausea and inflammation sounds, fever
Vomiting ↓ and hydration
4. Fever Ischemia status
5. Rebound ↓
 POSITION of
tenderness Necrosis
Comfort:
and ↓
RIGHT
abdominal rupture
SIDELYING in
rigidity (if
a low
perforated)
FOWLER’S
6.
 Avoid
Constipation
 EAVALMONTE

or diarrhea 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

NURSING DRUG STUDY/

SIGNS AND INTERVENTIONS NRSG
DISEASE LAB FINDINGS PATHOPHYSIOLOGY
SYMPTOMS RESPONSIBILIT
IES
IRON DEFICIENCY
ANEMIA- 1. Pallor of the 1. CBC- Low Decreased stores of iron 1. Provide iron rich- 1. Oral Iron
Results when the skin and levels of Hct, ↓ foods -FeSO4- 325mg
(dietary intake of) iron is mucous Hgb and RBC depletion of hemoglobin -Organ meats (liver) (65mg)
inadequate to produce membrane count synthesis -Beans -Fe Fumarate
hemoglobin 2. Weakness 2. low serum ↓ -Leafy green 325mg (107mg)
and fatigue iron, low ferritin reduced oxygen vegetables -Treatment for 6-
Causes: 3. General 3. Bone marrow carrying capacity -Raisins and 12 mos.
1. Increase demand for malaise aspiration- ↓ molasses  Iron
Iron- rapid growth in 4. Pica MOST definitive tissue hypoxia 2. Administer iron should not
 EAVALMONTE

infancy and 5. Brittle nails 4. Fecalysis w/  Oral be taken

adolescence, 6. Smooth and occult blood preparations with
pregnancy, EPO tx. sore tongue tablets- Fe antacid
2. Increase Iron Loss- 7. Angular fumarate, because it
menstruation, blood cheilosis sulfate and decreases
donation, bleeding gluconate absorption
3. Decrease iron intake  Advise to  Take it
or absorption- Crohn’s take iron ONE with
disease, post- hour before vitamin C
gastrectomy, acute or meals (to  It stains
chronic inflammation optimize teeth
absorption)  Drink it
 1mg iron lost  Practice good with a
daily due to oral hygiene straw
exfoliation of
skin and 2. Treat the
mucous cells cause
 Ave loss in 3. Blood
menstruation Transfusion
is 50ml or
0.7mg/day
 Pregnancy
req. 2-
5mg/day

NURSING DRUG STUDY/

SIGNS AND INTERVENTIONS NRSG
DISEASE LAB FINDINGS PATHOPHYSIOLOGY
SYMPTOMS RESPONSIBILIT
IES
APLASTIC ANEMIA-
A condition 1. Fatigue 1. CBC- Toxins cause a direct 1. Assess for signs 1. Bone marrow
characterized by 2. pallor decreased bone marrow of bleeding and transplantation
decreased number of 3. dyspnea blood cell depression infection 2.
RBC as well as WBC and 4.bruising or numbers ↓ 2. Instruct to avoid Immunosupressa
 EAVALMONTE

platelets bleeding 2. Bone Acellular bone marrow exposure to nt drugs

5. retinal marrow ↓ offending agents 3. Rarely,
Causes: hemorrhages aspiration decreased production of steroids
6. Infection confirms the blood elements 4. Blood
1. Environmental toxins- anemia- ↓ transfusion
pesticides, benzene hypoplastic or PANCYTOPENIA
2. Certain drugs- acellular
Chemotherapeutic marrow
agents, replaced by
chloramphenicol, fats
phenothiazines,
Sulfonamides
3. Heavy metals
4. Radiation
5. Idiopathic

NURSING DRUG STUDY/

SIGNS AND INTERVENTIONS NRSG
DISEASE LAB FINDINGS PATHOPHYSIOLOGY
SYMPTOMS RESPONSIBILIT
IES
SICKLE CELL ANEMIA-
1. Anemia – 1. Anemia – Low O2 1. Manage the pain 1. No safe and
-Results from Hgb 7-10g/dL Hgb 7-10g/dL ↓ -Support and effective tx
 EAVALMONTE

inheritance of sickle hgb 2. Jaundice cause defective elevate acutely 2. BM transplant

gene (HbS) from both 3. Enlarged hemoglobin to acquire a inflamed joint BT in ACS,
parents bones in the rigid, crystal-like C- -Relaxation strokes,
-The RBC change shape, skull and face shaped configuration techniques Pregnancy
upon deoxygenation 4. ↓ Analgesics 3. Hydroxyurea-
because of Tachycardia, Sickled RBCs will adhere 2. Prevent and induces
polymerization of the cardiac to endothelium manage infection production of
abnormal sickle murmurs and ↓ -Monitor status of HgbF
hemoglobin. cardiomegally pile up and plug the patient
-This process damages 5. Thrombosis vessels -Initiate prompt
the red blood cell which may ischemia results antibiotic therapy
membrane causing affect any ↓ 3. Promote coping
sickling or cresent organs pain, swelling and fever skills
shape 6. -Provide accurate
-abN hgb leads to Splenomegaly information
chronic hemolytic 7. schemic -Allow patient to
anemia manifesting at 1 symptoms verbalize her
yr. causing back concerns about
-SC crisis occurs at high and chest medication,
altitude, unpressurized pains prognosis and
planes, strenuous 8. Non-healing future pregnancy
exercise and resp. ulcers 4. Monitor and
infections prevent potential
complications
3 Nsg priority -Provide always
1. a/w – avoid adequate hydration
deoxygenating activities -Avoid cold,
- High altitude is bad temperature that
2. Fluid deficit – may cause
promote hydration vasoconstriction
3. Pain & comfort
 EAVALMONTE

NURSING DRUG STUDY/

SIGNS AND INTERVENTIONS NRSG
DISEASE LAB FINDINGS PATHOPHYSIOLOGY
SYMPTOMS RESPONSIBILIT
IES
FOLIC ACID
DEFICIENCY 1. Easy 1. Blood smear Decreased folic acid 1. Folic acid
(MEGALOBLASTIC fatigability 2. Bone marrow ↓ supplementation
ANEMIA)- 2. Pallor examination impaired DNA synthesis 1 mg/day oral
3. Dyspnea 3. Serum folate in the bone marrow supplementation
-anemias characterized 4. Chest pain <150ng/ml ↓ 2. Dietary
by abnormally large 5. Light 4. Schillings impaired RBC enhancement:
RBC secondary to headedness test normal development, impaired Foods rich in Folate:
impaired DNA synthesis 6.Tachycardia 5. (-) neurologic nuclear maturation but asparagus,broccoli,
due to deficiency of or manifestations CYTOplasmic maturation spinach,
Folic acid and/or vitamin palpitations continues lettuce,banana,liver,
B12 ↓ organ meats,
large size peas,beans and
Causes: nuts

1. Alcoholism
2. Malabsorption
3. Diet deficient in
vegetables, or
excessively heated or
cooked with large
amount of water
4. Long term
anticonvulsant
medication
5. Use of
antimetabolites
6. Increased folate
demand states as
pregnancy and growth
spurts like infancy and
adolescence
 EAVALMONTE

NURSING DRUG STUDY/

SIGNS AND LAB INTERVENTIONS NRSG
DISEASE PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
VITAMIN B12
DEFICIENCY 1. weakness, 1. Peripheral ↓Intrinsic factor 1. Enforce CBR 1. Administer
(PERNICOUS fatigue, blood smear- production by the 2. Diet – high B12 injections at
ANEMIA) listlessness shows giant parietal cells of the calorie or CHO. monthly
2. Neurologic RBCs, WBCs stomach Increase CHON, intervals for
-Vitamin B12 manifestations with giant ↓ iron & Vit C lifetime as
deficiency+ intrinsic due to affected hyper- ↓Vitamin b12 3. Avoid irritating ordered. IM-
factor deficiency= neuromyelination segmented absorption mouthwashes. Use dorsogluteal or
. E.g. nuclei ↓ of soft bristled ventrogluteal.
Pernicious Anemia
Paresthesias in 2. Very high ↓RBC production toothbrush is Not given oral –
- megaloblastic, the extremities, MCV ↓ encouraged. due pt might
loss of balance 3. Schilling’s ↓DNA Synthesis in 4. Avoid applying have tolerance
chronic anemia due to
and position test (shows maturing RBC electric heating to drug
deficiency of intrinsic sense absorption of ↓ pads – can lead to
factor leading to 3. Gastric tagged B12) Impairment of integrity burns
Hypochlorhydria – manifestation: 4. Intrinsic of cells 5. Provide
decrease Hcl acid weight loss, factor antibody (mouth, stomach, anus, assistance in
secretion. Lifetime B12 anorexia, N/V, test vagina,) ambulation
injections. With CNS diarrhea/constipa 6. Avoid too much
tion, heat and cold
involvement.
steatorrhea
4. Smooth, sore
 EAVALMONTE

-Intrinsic factor binds beefy tongue

with Vit. B12 to
promote absorption in
the terminal ileum

Causes:

1. Strict vegetarian diet

2. Gastrointestinal mal-
absorption such as
Crohn's disease,
Gastrectomy and ileal
resection
3. Absence of intrinsic
factor
NURSING DRUG STUDY/
SIGNS AND LAB INTERVENTIONS NRSG
DISEASE PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
POLYCTHEMIA-
1. Skin is ruddy 1. CBC- shows Myeloproliferative d/o, 1. Primary role of 1. To reduce the
-Refers to an INCREASE 2. Splenomegaly elevated RBC hypoxia the nurse is high blood cell
volume of RBCs 3. headache mass ↓ EDUCATOR mass-
-The hematocrit is 4. dizziness, 2. Normal The stem cells grow 2. Regularly asses PHLEBOTOMY
ELEVATED to more blurred vision oxygen uncontrollably for the 2. Hydroxyurea-
than 55% 5. Angina, saturation ↓ development of decrease
-The overproduction of dyspnea and 3 Elevated The bone marrow complications marrow function
red blood cells may be thrombophlebitis WBC and becomes HYPERcellular 3. Assist in weekly 3. Allopurinol-
due to a primary Platelets and all the blood cells phlebotomy decrease uric
process in the BM or it are increased in 4. Advise to have acid caused by
may be a reaction to number cool or tepid bath increase in cell
chronically low O2 level ↓ for itchiness and turn over
or, rarely, a -Blood becomes thick use cocoa butter 4.
malignancy and viscous causing based lotion Dipyridamole/AS
-Classified as Primary sluggish circulation 5. Advice to avoid A- decrease
or Secondary Increased blood alcohol intake to viscousity of
 EAVALMONTE

viscosity causes decrease risk of blood

thromboembolism bleeding 5. Chemotherapy
Causes: to suppress bone
-Organ infiltration marrow
-Secondary causes
polycythemia - caused hepato,splenomegaly
by either natural or
artificial increases in -Capillary
the production of overdistention causes
erythrocytes rupture, then
-Physiologic hemorrjage, then
polycythemia occurs in hypovolemia.
individuals living at
high altitudes
-Other causes include
smoking, renal or liver
tumors, or heart or
lung diseases that
result in hypoxia

NURSING DRUG STUDY/

SIGNS AND LAB INTERVENTIONS NRSG
DISEASE PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
IDIOPATHIC
THROMBOCYTOPENI 1. Platelet count 1. Platelet Viral illness, Pregnancy, 1. Prevent bruising Treatment
A PURPURA- less than 20T count SLE, Sulfa drugs 2. Protect from started when
2. Easy bruising decreases, ↓ infection there is bleeding
-Autoimmune disorder 3. Heavy mild anemia Antibody (Ab) Formation 3. Administer meds or Platelet count
in which IgG is menses 2. BMA: ↓ orally, rectally or IV of <10T even
formed that binds the Petechiae and increase Ab attaches to platelet rather than IM; hold w/o bleeding
platelet Ecchymoses of megakaryocyt ↓ pressure on site for 1. Stop the
-Platelet with Ab is skin es Platelet destruction by 5 mins medication that
destroyed as it passes 4. Bleeding from WBC and Spleen 4. Avoid aspirin caused ITP
the spleen and by mucous ↓ 5. Provide client 2.
 EAVALMONTE

Macrophages membranes- Decrease Platelet teaching and Immunosuppress

-Destruction of mouth, GIT and ↓ discharge planning ion- block the
platelets result in lungs Hematoma/ecchymosis/bl 6. Pad crib and binding receptor
count less than spleen not eeding playpen on macrophages
100,000/mm3 enlarge 7. Provide soft toys so that platelets
8. Provide are not
Causes: protective destroyed
headgear during Prednisone,
-Exact cause is toddlerhood Cyclophosphami
unknown but 9. Use soft de, Azathioprine
sometimes associated toothbrush 3. Splenectomy-
with: 10. Avoid contact effective only in
Viral illness, SLE and sports 50% of patients
pregnancy, sulfa IV
drugs immunoglobulin-
also binds
receptors
4.
Chemotheraphy-
(Vincristine)
binds receptors

NURSING DRUG STUDY/

SIGNS AND LAB INTERVENTIONS NRSG
DISEASE PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
HEMOPHILIA-
1. Bleeding in 1. prolonged 1. Educate about BT- FFP,
-Two clinically soft tissues, PTT, decrease their condition cryoprecipitate,
indistinguishable muscles and Factor VIII or 2. Teach about FVIII&IX conc.
disease characterized weight bearing IX level activity restrictions
by bleeding disorder joints to decrease
due to genetic defect 2. Bleeding in episodes of trauma
any body parts and bleeding
 EAVALMONTE

-Gene is carried by 3. Avoid

females and manifest medications such
only in males as ASA, NSaids,
-Frequently dx at birth alcohol
due to 4. Avoid injections
cepalhematoma and 5. Precaution on
bleeding after Dental procedures
circumcision 6. Patients should
be encouraged to
-Hemophilia A wear identifications
-Hemophilia B bands
7. Warm compress
are avoided

NURSING DRUG STUDY/

SIGNS AND LAB INTERVENTIONS NRSG
DISEASE PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
PEPTIC ULCER
DISEASE According to 1. Endoscopic Disturbance in acid Nursing Mgt: 1. Antacids
location exam secretion and mucosal 1. Diet – bland, non 2. H2 receptor
-Excoriation / erosion 1. Stress ulcer 2. Stool from protection irritating, non spicy antagonist
of submucosa & 2. Gastric ulcer occult blood ↓ 2. Avoid caffeine & Ex
mucosal lining due to: 3. Duodenal 3. Gastric Increased acidity or milk/ milk products 1. Ranitidine
a.) Hypercecretion of ulcer – most analysis – N – decreased mucosal Increase gastric (Zantac)
acid – pepsin common gastric resistance acid secretion 2. Cimetidine
 EAVALMONTE

b.) Decrease Increase – ↓ 3. Administer meds (Tagamet)

resistance to mucosal duodenal erosion and ulceration 4. Maintain patent 3. Tamotidine
barrier 4. GI series – IV line (Pepcid)
Causes: confirms 4. VS, I&O & bowel - Avoid smoking
1. Hereditary presence of sounds – decrease
2. Emotional ulceration 5. Complications: effectiveness of
3. Smoking – a.) Hemorrhage – drug
vasoconstriction – GIT hypovolemic shock
ischemia Late signs – anuria - Administer
4. Alcoholism – b.) Peritonitis antacid & H2
stimulates release of c.) Paralytic ileus – receptor
histamine = Parietal most feared antagonist – 1hr
cell release Hcl acid = d.) Hypokalemia apart
ulceration e.) -Cemetidine
5. Caffeine – tea, Thromobphlebitis decrease antacid
soda, chocolate f.) Pernicious absorption &
6. Irregular diet/rapid anemia vise versa
eating
7. Ulcerogenic drugs – Cytoprotective
NSAIDS, aspirin, agents
steroids, Ex
indomethacin, 1. Sucralfate
ibuprofen (Carafate) -
Indomethacin - S/E Provides a paste
corneal cloudiness. like subs that
Needs annual eye coats mucosal
check up. lining of stomach
9. Gastrinoma 2. Cytotec
10. Microbial invasion
– helicobacter pylori.
NURSING DRUG STUDY/
SIGNS AND LAB INTERVENTIONS NRSG
DISEASE PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
LIVER CIRRHOSIS-
Early sign – 1. Liver Inflammation causes liver 1. CBR
 EAVALMONTE

-lost of architectural hepatic enzymes- parenchymal cell 2. Restrict Na!

design of liver leading encephalopathy increase destruction 3. Monitor VS, I&O
to fat necrosis & 1. Asterixis – SGPT (ALT) ↓ 4. With pt daily &
scarring flapping hand SGOT (AST) Fibrotic changes causes assess pitting
tremors 2. Serum obstruction of hepatic edema
Causes: Late signs – cholesterol & blood flow and normal 5. Measure
headache, ammonia liver function abdominal girth
1. Chronic alcoholism restlessness, increase ↓ daily – notify MD
2. Malnutrition – disorientation, 3. Indirect Obstruction causes of 6. Meticulous skin
decreaseVit B, thiamin decrease LOC – bilirubin hepatic blood flow and care
- main cause hepatic coma. increase normal liver function 71
3. Virus – 4. CBC - ↓ 7. Diet – increase
4. Toxicity- eg. Carbon Early signs: pancytopenia Decreased liver function CHO, vit &
tetrachloride 5. PTT – results changes in the minerals. Moderate
5. Use of hepatotoxic a.) Weakness, prolonged body fats. Decrease
agents fatigue 6. Hepatic ↓ CHON
b.) Anorexia, n/v ultrasonogram Decreased absorption and Well balanced diet
c.) Stomatitis – fat necrosis utilization of vit. Adek 8. Complications:
d.) Urine – tea of liver lobules -ineffective detoxification a.) Ascites – fluid in
color of protein wates peritoneal cavity
Stool – clay color Nursing Mgt:
e.) Amenorrhea 1. Meds: Loop
f.) Decrease diuretics – 10 – 15
sexual urge min effect
g.) Loss of 2. Assist in
pubic, axilla hair abdominal
h.) paracentesis -
Hepatomegaly aspiration of fluid
i.) Jaundice - Void before
j.) Pruritus or paracentesis to
urticaria prevent accidental
puncture of
bladder as trochar
is inserted
 EAVALMONTE

NURSING DRUG STUDY/

SIGNS AND LAB INTERVENTIONS NRSG
DISEASE PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
CHOLECYSTITIS/
CHOLELITHIASIS- 1. Severe Right 1. Oral Supersaturated bile, 1. Meds – a.) Narcotic
abdominal pain cholecystogra Biliary stasis a.) Narcotic analgesic -
- Inflammation of (after eating m (or ↓ analgesic - Meperdipine Hcl
gallbladder with fatty food). gallbladder Stone formation Meperdipine Hcl – – Demerol
gallstone formation. Occurring series)- ↓ Demerol b.) Anti
especially at confirms Blockage of Gallbladder b.) Anti cholinergic - cholinergic -
Predisposing night presence of ↓ Atropine SO4 Atropine SO4
factor: 2. Fatty stones Inflammation, Mucosal c.) Anti emetic c.) Anti emetic
intolerance Damage and WBC Phenergan – Phenergan –
1. High risk – women 3. Anorexia, n/v infiltration Phenothiazide with Phenothiazide
40 years old 4. Jaundice ↓ anti emetic with anti emetic
2. Post menopausal 5. Pruritus Less bile in the duodenum properties properties
women – undergoing 6. Easy bruising ↓ 2. Diet – increase
estrogen therapy 7. Tea colored Impaired fat digestion and CHO, moderate
3. Obesity urine absorption CHON, decrease
4. Sedentary lifestyle 8. Steatorrhea ↓ fats
5. Hyperlipidemia Vitamin ADEK mal- 3. Meticulous skin
6. Neoplasm absorption, STEATORHEA care
with increased gas 4. Surgery:
formation Cholecystectomy
Jaundice Nursing Mgt post
ACHOLIC stools cholecystectomy
-Maintain patency
of T-tube intact &
prevent infection
 EAVALMONTE

SIGNS AND LAB NURSING DRUG STUDY/

SYMPTOMS FINDINGS INTERVENTIONS NRSG
DISEASE PATHOPHYSIOLOGY
RESPONSIBILIT
IES
ULCERATIVE
COLITIS- 1. Anorexia 1. Inflammation edema of 1. Maintain NPO Aminosalicylic
2. Weight loss Sigmoidoscop the mucous membrane of during the active agents
-Ulcerative and 3. Fever y- increased the colon and rectum phase
inflammatory 4. SEVERE mucosal leads to bleeding and 2. Monitor for
condition of the GIT diarrhea with friability, shallow ulcerations complications like
usually affecting the Rectal bleeding decreased ↓ severe bleeding,
large intestine 5. Anemia mucosal Abscess formation causes dehydration,
-The colon becomes 6. Dehydration detail, thick bowel-wall shortening, electrolyte
edematous and 7. Abdominal inflammatory thinning, fragility, imbalance
develops bleeding pain and exudates, hypermotility, and 3. Monitor bowel
ulcerations cramping edema, decreased absorption sounds, stool and
-Scarring develops erosion ↓ blood studies
overtime with 2. Stool Mucosal ulcerations begin 4. Restrict activities
impaired water specimen- in the distal end of the 5. Administer IVF,
absorption and loss of positive for colon and ascend the electrolytes and
elasticity blood and large intestine TPN if prescribed
mucus 6. Instruct the
Causes: patient to AVOID
gas-forming foods,
unknown MILK products and
foods such as whole
grains, nuts, RAW
fruits and
vegetables
especially SPINACH,
pepper, alcohol and
caffeine
7. Diet progression-
clear liquid LOW
 EAVALMONTE

residue, high
protein diet
8. Administer drugs-
anti-inflammatory,
antibiotics, steroids,
bulk-forming agents
and vitamin/iron
supplements
DISEASE NURSING DRUG STUDY/
SIGNS AND LAB INTERVENTIONS NRSG
PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
DISSEMINATED
INTRAVASCULAR 1. Petechiae – 1. CBC – 1. Monitor signs of Vit K
COAGULATION- widespread & reveals bleeding – hema aquamephyton
systemic (lungs, decrease test + urine, stool,
- Acute hemorrhagic lower & upper platelets GIT Pitressin or
syndrome char by trunk) 2. Stool for 2. Administer vasopressin – to
wide spread bleeding 2. Ecchymosis – occult blood isotonic fluid conserve water.
& thrombosis due to a widespread (+) solution to prevent
def of clotting factors 3. Oozing of Specimen – shock.
(Prothrombin & blood from stool 3. Administer O2
Fibrinogen venipunctured 3. inhalation
site Opthalmoscopi 4. Administer meds
Predisposing factor: 4. Hemoptysis – c exam – sub 47
1. Rapid BT cough blood retinal a. Vit K
2. Massive trauma 5. Hemorrhage hemorrhage aquamephyton
3. Massive burns 6. Oliguria – late 4. ABG b. Pitressin or
4. Septicemia sx analysis – vasopressin – to
5. Hemolytic reaction metabolic conserve water.
6. Anaphylaxis acidosis 5. NGT – lavage
7. Neoplasia – growth - Use iced saline
of new tissue lavage
8. Pregnancy 6. Monitor NGT
output
7. Provide heplock
 EAVALMONTE

8. Prevent
complication:
hypovolemic shock
Late signs of
hypovolemic
shock : anuria

DISEASE NURSING DRUG STUDY/

SIGNS AND LAB INTERVENTIONS NRSG
PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
ADDISON’S
DISEASE- 1. T – tremors, 1. FBS – Autoimmune theory: body 1. Monitor VS Administer meds
tachycardia decrease FBS produces antibodies, 2. Adm meds a.)
-Steroids-lifetime I - irritability (N 80 – 120 resulting in adrenal 3. Diet – increase Corticosteroids -
Decreased R - restlessness mg/dL) hypofunction calorie or CHO (Decadron) or
adrenocortical E – extreme 2. Plasma Increase Na, Dexamethazone
hormones leading to: fatigue cortisol – Decreased aldosterone Increase CHON, - Hydrocortisone
D – diaphoresis, decreased causes disturbances in Decrease K (cortisone)-
-a.) Metabolic depression Serum Na – sodium, water, and 4. Force fluid Prednisone
disturbances (sugar) 2. Decrease decreased (N potassium metabolism 5. Administer 1. Adm 2/3 dose
b.) F&E imbalances- sexual urge or 135 – 145 isotonic fluid as in AM & 1/3 dose
Na, H2O, K libido- meg/L) Decreased cortisol causes ordered in PM in order to
c.) Deficiency of Decreased 3. Serum K – abnormal metabolism of 6. Meticulous skin mimic the
neuromuscular Androgen increased (N fat, protein, and care – due to normal diurnal
function (salt & sex) 3.Loss of pubic 3.5 – 5.5 carbohydrate bronze like rhythm.
and axillary hair meg/L) 7. HT & discharge 2. Taper the
Predisposing 4. planning dose (w/draw,
Factors: Pathognomonic a) Avoid gradually from
sign– bronze like precipitating factors drug) – sudden
1. Atrophy of adrenal skin leading to withdrawal can
gland pigmentation Addisonian crisis lead to
2. Fungal infections due to decrease 1. Sudden addisonian crisis
3. Tubercular cortisol will withdrawal crisis 3. Monitor S/E
 EAVALMONTE

infections stimulate 2. Stress (Cushing’s

pituitary gland 3. Infection syndrome S/Sx)
Complication of to release b) Prevent a.) HPN
Addison’s dse : melanocyte complications b.) Hirsutism
Addisonian crisis stimulating Addisonian crisis & c.) Edema
16. Results the acute hormone. Hypovolemic shock d.) Moon face &
exacerbation of 8. Hormonal buffalo hump
Addison’s dse replacement e.) Increase
characterized by : therapy – lifetime susceptibility to
Hypotension, 9. Important: follow infection sue to
hypovolemia, up care steroids- reverse
hyponatremia, wt isolation
loss, arrhythmia
DISEASE NURSING DRUG STUDY/
SIGNS AND LAB INTERVENTIONS NRSG
PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
CUSHING’S
SYNDROME- 1. Increase 1. FBS – 1. Monitor VS, I&O a. K- sparing
sugar – increase↑ (N: 2. Administer meds diuretics
-increase secretion of Hyperglycemia 80-120mg/dL) 3. Restrict Na (Aldactone)
adrenocortical 3 P’s 2. Plasma 4. Provide Dietary Spironolactone
hormone 1. Polyuria cortisol intake – low in CHO, - promotes
2. Polydipsia – increase low in Na & fats excretion of NA
Predisposing increase thirst 3. Na – High in CHON & K while conserving
Factors: 3. Polyphagia – increase (135- 5. Weigh pt daily & potassium
increase 145 meq/L) assess presence of Not lasix due to
1. Hyperplasia of appetite 4. K- decrease edema- measure S/E hypoK &
adrenal gland Classic Sx of DM (3.5-5.5 abdominal girth- Hyperglycemia!
2. Tubercular – 3 P’s & meq/L) notify doc.
infection – milliary glycosuria + wt 6. Reverse isolation
TB loss 7. Skin care – due
2. Increase acne & striae
susceptibility to 8. Prevent
infection – due complication
to increased - Most feared –
 EAVALMONTE

corticosteroid arrhythmia & DM

3. (Endocrine disorder
Hypernatrermia lead to MI –
a. HPN Hypothyroidism &
b. Edema DM)
c. Wt gain 9. Surgical bilateral
d. Moon face Adrenolectomy
Buffalo hump 10. Hormonal
Hypokalemia replacement
Hirsutism – therapy – lifetime
increase sex due to adrenal
6. Acne & striae gland removal- no
7. Increase more corticosteroid!
muscularity of
female

DISEASE NURSING DRUG STUDY/

SIGNS AND LAB INTERVENTIONS NRSG
PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
HYPERTHYROIDISM
1. Increase in 1. Serum T3 Increased thyroid 1. Monitor VS & I & O – 1.
-Graves dse or appetite – & T4 - hormones determine presence of Prophylthiuracil
thyrotoxicosis hyperphagia – increased ↓ thyroid storm or most (PTU)
( everything up wt loss due to 2. Radio Increased metabolic feared complication: 2. Methymazole
except wt and mens) increase iodine uptake rate, oxygen Thyrotoxicosis (Tapazole)
-Increased T3 & T4 metabolism – increase consumption, 2. Administer meds Most toxic s/e
2. Skin is moist 3. Thyroid sympathetic activity and 3. Diet – increase agranulocytosis-
Predisposing - perspiration scan – cns function, altered calorie – to correct wt fever, sore
factors: 3. Heat reveals protein, fat, loss throat,
intolerance enlarged TG carbohydrate 4. Skin care – leukocytosis=inc
1. Autoimmune 4. Diarrhea – metabolism 5. Comfy & cool wbc: check cbc
disease – release of increase ↓ environment and throat swab
long acting thyroid motility Changes in the body 6. Maintain siderails- culture
stimulator (LATS) 5. All VS due Most feared
 EAVALMONTE

Exopthalmos increase = HPN, agitation/restlessness complication :

Enopthalmos – tachycardia, 7. Provide bilateral eye Thrombosis –
severe dehydration tachypnea, patch – to prevent stroke CVS
depressed eye hyperthermia drying of eyes-
2. Excessive iodine 6. CNS changes exopthalmos
intake 8. Irritability & 8. Assist in surgery –
3. Hyperplasia of TG agitation, subtotal thyroidectomy
restlessness,
tremors, Complication- thyroid
insomnia, storm
hallucinations
7. Goiter
8. Exopthalmos
–
pathognomonic
sx
9. Amenorrhea

DISEASE NURSING DRUG STUDY/

SIGNS AND LAB INTERVENTIONS NRSG
PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
HYPOTHYROIDISM-
Early signs – 1. Serum T3 1. Monitor VS. Levothyroxine
-decrease secretion of 1. weakness and T4 decrease Check for s/sx of Thyroglobulin
T3, T4 – can lead to MI fatigue 2. Serum cardiovascular
/ Atherosclerosis 2. Loss of cholesterol disorder.
Adult – myxedema appetite – increase – can 2. Monitor daily
Child- cretinism – only increased lead to MI weigh.
endocrine dis lead to lypolysis – 3. RA IU – 3. Diet, decrease
mental retardation breakdown of radio iodine calorie, increase
fats causing uptake – fiber
Predisposing 3. decrease 4. Provide warm
factor: atherosclerosis environment during
 EAVALMONTE

= MI cold climate.
1. `Iatrogenic causes Wt gain 5.
– caused by surgery 5. Cold
2. Atrophy of TG due intolerance –
to: myxedema -
a. Irradiation coma
b. Trauma Constipation
c. Tumor, Late Sx – brittle
inflammation hair/ nails
3. Iodine def Non pitting
4. Autoimmune – edema due
Hashimoto disease increase
accumulation of
mucopolysachar
ide in SQ tissue
-Myxedema
Horseness voice
Decrease libido
Decrease VS –
hypotension
bradycardia,
bradypnea, and
hypothermia
Lethargy
Memory
impairment
DISEASE NURSING DRUG STUDY/
SIGNS AND LAB INTERVENTIONS NRSG
PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
DM TYPE 1-
1.) Polyuria 1. FBS- > 126 Destruction of BETA cells 1. Insulin Therapy Insulin
-“Juvenile “ onset, 2.) Poydipsia 2. RBS- >200 ↓ 2. Diet Route: Subq
common in children, 3.) Polyphagia 3. OGTT- > decreased insulin 3. Exercise
non-obese “brittle 4.) Glycosuria 200 production 4. Regular Glucose -Do not massage
dse” 5.) Weight loss ↓ Monitoring site of injection.
 EAVALMONTE

-Insulin dependent 6.) Anorexia uncontrolled glucose -Store at room

diabetes mellitus 7.) N/V production by the liver temp or ref.
8.) Blurring of ↓ -Shake before
Causes: vision Hyperglycemia using.
9.) Increase ↓
1. 90% hereditary – susceptibility to signs and symptoms
total destruction of infection
pancreatic dells 10.) Delayed/ Complication: DKA
2. Virus poor wound
3. Toxicity to carbon healing
tetrachloride
4. Drugs – Steroids
both cause
hyperglycemia
Lasix - loop diuretics

DISEASE NURSING DRUG STUDY/

SIGNS AND LAB INTERVENTIONS NRSG
PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
DM TYPE 2-
1. 1. FBS- > 126 Decreased insulin 1. Diet
-A type of DM Asymptomatic 2. RBS- >200 production 2. Exercise
characterized by 2. 3 P’s and 1G 3. OGTT- > ↓ 3. Regular Glucose
 EAVALMONTE

insulin resistance and 200 diminished insulin action Monitoring

impaired insulin ↓ 4. Oral
production Hyperglycemia Hypoglycemic
↓ Agents (OHA)
Causes: signs and symptoms

1. Unknown Complication: HONKC

2. Probably genetic H – hyper
and obesity O – osmolar
N – non
K – ketotic
C – coma

DISEASE NURSING DRUG STUDY/

SIGNS AND LAB INTERVENTIONS NRSG
PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
PLACENTA PREVIA-
1. Abrupt, Ultrasound Fertilized ovum 1. Monitor vital
-it occurs when the painless , bright ↓ signs & bleeding
 EAVALMONTE

placenta is improperly red vaginal implantation in uterus ( weigh unused

implanted in the lower bleeding. ↓ perineal pad, then
uterine segment, embryonic stage weigh perineal pad
sometimes covering TYPES: ↓ soaked in blood,
the placenta arise in then subtract. The
cervical os. Abnormal 1. Low-lying – thropoblast tissues difference is the
lower implantation of implantation of ↓ weight of the blood
placenta. the placenta in insufficient blood loss.)
- candidate for CS the lower rather ↓ 2. Monitor fetal
than in the Placenta migrates to heart rate
Causes: upper portion of where there is sufficient 3. Provide strict bed
the uterus blood supply rest to minimize the
1. Increased parity 2. Marginal – ↓ risk to fetus.
2. Advanced maternal placenta edge placenta resides in lower 4.observe for
age approaches that part further bleeding
3. Past cesarian births of the cervical ↓ episodes
4. Past uterine os (low lying, total, partial, 5. Avoid vaginal
curettage 3.partial – marginal) examinations ( no
5. Multiple gestations implantation ↓ ie). If ie is indicated,
6. Decreased that occludes a painless dark red bleeding it should be done in
vascularity of upper portion of the ↓ a double set-up
uterine segment cervical os Profuse bleeding environment.
7. Use of cocaine 4. Complete ↓ ( meaning: or/dr)
( totalis) – Hypotension wherein the patient
placenta that ↓ has already signed
totally obstructs Hypovolemic shock a consent form, pre-
the cervical os ↓ op
Coma
↓
death

DISEASE SIGNS AND LAB PATHOPHYSIOLOGY NURSING DRUG STUDY/

SYMPTOMS FINDINGS INTERVENTIONS NRSG
 EAVALMONTE

RESPONSIBILIT
IES
ABRUPTIO
PLACENTA- 1. Painful dark Ultrasound 1. Infuse IV, prepare
red vaginal to administer blood
-it is the premature bleeding in 2. Type and
separation of the covert type crossmatch
placenta form the 2.painful bright 3. Monitor FHR
implantation site. It red vaginal 4. Insert Foley
usually occurs after bleeding in 5. Measure blood
the overt type loss; count pads
twentieth week of 3.hard, rigid, 6. Report s/sx of
pregnancy. firm,board-like DIC
abdomen 7. Monitor v/s for
Causes: caused by shock
accumulation of 8. Strict I&O
1.maternal blood behind
hypertension ( chronic the placenta
or pregnacy induced) with fetal parts
2. Advanced maternal hard to palpate.
age 4. Abnormal
3. Grand multiparity – tenderness due
more than 5 to distentionof
pregnancies the uterus with
4. Trauma to the blood.
uterus 5. Sharp pain
5. Sudden release of over the fundus
amniotic fluid that as the placenta
cause sudden separates.
decompression of te 6. Signs of
uterus. shock & fetal
distress as the
placenta
separates.
 EAVALMONTE

DISEASE NURSING DRUG STUDY/

SIGNS AND LAB INTERVENTIONS NRSG
PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
ECLAMPSIA-
1. All the signs 1. Home 1. Hydralazine –
-with seizure! Increase & symptoms of management is ( apresoline )
BUN – glomerular preeclampsia allowed only if: -
damage. Provide 2. Convulsion A. Bp is 140/90 o antihypertensive
safety. followed by below 2. Magnesium
coma is the B. There is no sulfate ( mgso4)
Causes: main difference proteinuria - drug of choice
of eclampsia & C. There is no fetal to treat &
1.maternal preeclampsia growth retardation prevent
hypertension ( chronic 3. Oliguria D. The patient is not convulsions.
or pregnacy induced) 4. Pulmonary a young primipara. 3. Diuretics are
2. Advanced maternal edema 2. Cbr not given & ivf
age 3. Diet should be is limited
3. Grand multiparity – high in protein &
more than 5 carbohydrates with Actions of
pregnancies moderate sodium mgso4:
4. Trauma to the restriction.
uterus 4. Provide detailed Prevent
5. Sudden release of instructions about convulsion
amniotic fluid that warning signs: B. Reduce blood
cause sudden A. Epigastric pain – pressure
decompression of te aura to convulsion Check the
uterus. B. Visual following first
disturbances before
C. Severe administering
continuous mgso4:
 EAVALMONTE

headache Deep tendon

5. A. Rest in left reflex present -
lateral position to +2 ( normal)
promote blood 2. Rr should be
supply to the at least 12 bpm
placenta & the 3. Urine output
fetus. should be at
6. Absence of least 30 ml/hr
pattelar reflex is
sign of MGSO4 Antidote-
toxicity Calcium
Gluconate
DISEASE NURSING DRUG STUDY/
SIGNS AND LAB INTERVENTIONS NRSG
PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
BURNS-
1. BP decrease (cont) 1. Home Mafenide
- direct tissue injury - Urine output II Full management is acetate
caused by thermal, - HR increase thickness allowed only if: Morphine sulfate
electric, chemical & - Hct increase Burns A. Bp is 140/90 o Lactated Ringers
smoke inhaled (TECS) - Serum Na 1. Third & 4 th below D5W
Nursing Priority – decrease degrees burn B. There is no
infection (all kinds of - Serum K - Affects all proteinuria
burns) increase layers of skin, C. There is no fetal
Head burn-priority- - Met acidosis muscles, growth retardation
a/w Class: bones D. The patient is not
2nd priority for 1st & I. Partial Burn - Cause – a young primipara.
2nd ° - pain 1. 1 s t degree – electrical 2. Cbr
2nd priority for 3rd ° - superficial burns - Less painful 3. Diet should be
F&E - Affects - Dry, thick, high in protein &
epidermis leathery carbohydrates with
Causes: - Cause: thermal wound surface moderate sodium
burn – known as restriction.
1. Thermal- direct - Painful ESCHAR – 4. Provide detailed
contact – - Redness devitalized or instructions about
 EAVALMONTE

flames, hot (erythema) & necrotic warning signs:

grease, blanching upon tissue. A. Epigastric pain –
sunburn. pressure with no aura to convulsion
2. Electric, – wires fluid filled B. Visual
3. Chem. – direct vesicles disturbances
contact – 2. 2 nd degree – C. Severe
corrosive deep burns continuous
materials acids - Affects headache
4. Smoke – gas / epidermis & 5. A. Rest in left
fume inhalation dermis lateral position to
- Cause –chem. promote blood
burns supply to the
- very painful placenta & the
- Erythema & fetus.
fluid filled 6. Absence of
vesicles pattelar reflex is
(blisters) sign of MGSO4
toxicity
DISEASE NURSING DRUG STUDY/
SIGNS AND LAB INTERVENTIONS NRSG
PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
EMPHYSEMA-
1. Productive 1. Pulmonary Smoking 1. CBR Aminophylline
-irreversible terminal cough function test – ↓ 2. Meds Theophylline
stage of COPD 2. Dyspnea at decrease vital Particle deposition in 3. O2 – Low inflow
- Characterized by rest – due lung capacity airways 4. Force fluids Ventolin
inelasticity of alveolar terminal 2. ABG – ↓ 5. High fowlers Salbutamol
wall leading to air 3. Anorexia & a.) low level inflammatory 6. Neb & suction
trapping, leading to gen body Panlobular / response 7. Institute Bricanyl
maldistribution of malaise centrolobular due to aging P – posture Terbutaline
gases. 4. Rales/ rhonchi emphysema ↓ E – end
- Body will 5. Bronchial pCO2 increase Disequilibrium between E – expiratory to Alupent
compensate over wheezing pO2 decrease elastase and antielastase prevent collapse of
distension of thoracic 6. Decrease – hypoxema ↓ alveoli
cavity tactile fremitus resp acidosis Destruction of elastic P – pressure
 EAVALMONTE

- Barrel chest (should have Blue bloaters recoil 8. HT

vibration)– b.) Panacinar/ ↓ a.) Avoid smoking
- There is progressive palpation – Centracinar Overdistention of alveoli
and irreversible “99”. Decreased pCO2 ↓
alveolocapillary - with air or fluid decrease Retention of CO2
destruction with 7. Resonance to pO2 increase – ↓
abnormal alveolar hyperresonance hyperaxemia Hypoxia and resp acidosis
enlargement causing – percussion resp alkalosis
alveolar wall 8. Decreased or Pink puffers Complication:
destruction. The result diminished Pneumothorax – air in
is INCREASED lung breath sounds pleural space
compliance, 9.
DECREASED oxygen Pathognomonic:
diffusion and barrel chest –
INCREASED airway increase post/
resistance! anterior
diameter of
Predisposing factor: chest
1. Smoking 10. Purse lip
2. Allergy breathing – to
3. Air pollution eliminated PCO2
4. High risk – elderly 11. Flaring of
5. Hereditary alai nares
DISEASE NURSING DRUG STUDY/
SIGNS AND LAB INTERVENTIONS NRSG
PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
PLEURAL
EFFUSION- 1. Dyspnea, a. Chest x-ray Inflammation of airways 1. Assist with a. Antibiotics:
dullness over positive if ↓ repeated either systemic
-referred to as ‘water affected area greater than Bronchial edema, thoracentesis. or inserted
on the lungs’ is the upon 250 cc pleural increased mucus 2. Administer directly into
build up of excess percussion, fluid production, narcotics/sedatives pleural space
fluid between the absent or b. Pleural bronchoconstriction, as ordered to b. Fibrinolytic
layers of the pleura of decreased biopsy may bronchial spasm decrease pain. enzymes:
the lungs. The pleura breath sounds reveal ↓ 3. Assist with trypsin,
 EAVALMONTE

are thin membranes over affected bronchogenic worsening of obstruction instillation of streptokinase-.
that line the lungs and area, pleural carcinoma ↓ medication into streptodornase
the inside chest cavity pain, dry cough, c. accumulation of fluids pleural space to decrease
and act to lubricate pleural friction Thoracentesis caused by oversecretion (reposition client thickness of pus
and facilitate rub may contain ↓ every 15 minutes to and dissolve
breathing. It is 2. Pallor, blood if cause multiplication of growth of distribute the drug fibrin clots
normally filled with 5- fatigue, fever, is cancer, microorganism within the pleurae).
10 milliliters of serous and night pulmonary ↓ 4. Place client in
fluid. sweats (with infarction, or Inflammation in the high-Fowler’s
empyema) tuberculosis; epithelial wall position to promote
Types: positive for ↓ ventilation.
1. Transudative- specific fluid filled alveoli 5. O2
caused by leaking into organism in ↓ 6. ABG
pleural space. This is empyema. rupture of inflamed
caused by elevated endothelial cells
pressure in or low excess fluid accumulate in
protein content in the the pericardial space
bld vessels/ CHF is a ↓
common cause. Pleural effusion

2. Exudative- results
from leaky blood
vessels caused by
inflammation. Often
caused by lung
disease, tb,
pneumonia, drug
reaction.
DISEASE NURSING DRUG STUDY/
SIGNS AND LAB INTERVENTIONS NRSG
PATHOPHYSIOLOGY
SYMPTOMS FINDINGS RESPONSIBILIT
IES
CROUP-
1. Colds 1. Chest xray- Viral infection 1. Airway 1. Antipyretic:
-group of respiratory 2. low grade difference ↓ 2. Assess resp Acetaminophen
disease that often fever between croup affects larynx and trachea status to reduce fever
 EAVALMONTE

affects infants, and 3. stridor and epiglottis ↓ 3. NPO status 2. Bronchodilator

children under age 6, 4. seal bark 2. Throat subglottic edema 4. Immunization to relax
characterized by cough culture- ↓ (haemophilus type respiratory
barking cough, 5. cyanosis reveals airflow obstruction B) smooth muscle
whistling, stridor as 6. use of identifies ↓ 5. Facilitate hygiene and relieve
the child breathes in, accessory infectious croup 6. Proper hygiene stridor
and hoarseness in the muscles to agent and 7. Administer meds 3.
larynx. breath sensitivity to Corticosteroids-
7. agitation specific to reduce
Types: 8. muffled voice antimicrobial inflammation
9. spontaneous therapy and edema
1. cough 3. ABG- around vocal
Larnygotracheobronch reveals cords
itis- acute viral hypoxemia 4. Antibiotics
infection of the larynx, state that
bronchi, which causes require
obstruction below oxygen
vocal cords. therapy,
decreased PH
2. Spasmodic and changes
laryngitis- sudden and co2 levels
onset, occurring indicating
mainly at night and respiratory
characterized by acidosis or
laryngeal obstruction failure in
at the level of vocal severe cases.
cord

Causes: flu virus,

adenovirus,
rhinovirus,
enterovirus,
coxsacklevirus,
measles virus,
reovirus
 EAVALMONTE

DRUG STUDY/
SIGNS AND NURSING NRSG
DISEASE LAB FINDINGS PATHOPHYSIOLOGY
SYMPTOMS INTERVENTIONS RESPONSIBILIT
IES
TETRALOGY OF
FALLOT- 1. Rt 1. Chest X-ray- atherosclerosis 1. O2 Morphine
ventricular decreased ↓ 2. no valsalva Propranolol
-group of congenital hypertrophy pulmonary reduced coronary tissue maneuver , fiber
heart conditions 2. high degree vascular, perfusion diet laxative
including pulmonic of cyanosis enlarged right ↓ 3. morphine –
stenosis, ventricular 3. ventricle, a diminished myocardial hypoxia
hypertrophy, overriding polycythemia boot shape oxygenation 4. propranolol –
aorta and ventricular 4. severe cardiac ↓ decrease heart
septic defect. dyspnea – silhouette anaerobic metabolism spasms
squatting 3. Electrocardio ↓ 5. palliative repair –
Causes: position – graphy increased lactic acid BLT blalock taussig
relief , inhibit 4. diminished production procedure
1. Unknown venous return o2 saturation ↓ Brock procedure –
2. Fetal alcohol facilitate lung chest pain complete procedure
syndrome expansion.
5. growth
retardation –
due no O2
6. tet spell or
blue spells-
short episodes
of hypoxia
7. syncope
8. clubbing of
fingernails –
due to chronic
tissue hypoxia
9. mental
retardation –
due decreased
O2 in brain
 EAVALMONTE

10. boot
shaped heart
– x-ray

DRUG STUDY/
SIGNS AND NURSING NRSG
DISEASE LAB FINDINGS PATHOPHYSIOLOGY
SYMPTOMS INTERVENTIONS RESPONSIBILIT
IES
RHEUMATIC HEART
DISEASE- Major Minor 1. CBR aspirin – anti-
1. polyarthritis 2. throat swab – inflammatory.
-inflammation disease ff – multi joint culture and Low grade fever
an infection acquired by pain 1. sensitivity – don’t give
group A Beta hemolytic arthralgia – 3. antibiotic mgt – to aspirin.
strepto coccus joint pain prevent recurrence S/E of aspirin:
-Affected body – cardiac 2. chorea – 4. aspirin – anti- - Reyes
muscles and valves , sydenhamms inflammatory. Low syndrome –
musculoskeletal , CNS, chores or grade fever – don’t encephalopathy-
Integumentary st. vetaus give aspirin. fatty infiltration
Sorethroat before RHD dance- S/E of aspirin: of organs such as
-Aschoff – rounded purposeless - Reyes syndrome – liver and brain
nodules with nucleated involuntary encephalopathy-
cells and fibroblasts – hand and fatty infiltration of
stays and occludes shoulder with organs such as liver
mitral valve grimace and brain
2. low grade
fever
3. carditis –
tachycardia
erythema
marginatum -
macular
rashes
SQ nodules
3. all lab
 EAVALMONTE

results
increase
antibody
“ C reactive
protein
“ erythrocyte
sedimentation
rate
“ anti
streptolysin