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Cystitis Pyelonephritis Urolithiasis

Inflammation of the Bladder Infection of kidney and renal pelvis Presence of calculi in the Urinary Tract

Assessment: Assessment: Assessment:


Frequency, urgency, dysuria, Low back pain (Acute) Fever, chills, Tachycardia, Tender CVA Renal Colic, Oliguria, Anuria
(Chronic) Hypertension, Inability to conserve Na
Urinalysis: Urinalysis:
Pyuria and Hematuria Urinalysis: Hematuria
Positive Leukocytes Esterase and Nitrite Dipstick Test,
Avoid urinary stasis and fluid intake of 1-3L + WBC and Bacteria Pain Relief
Drug therapy needed first 24-36 hrs when
 Antifungal agents – fungal infections  Antibiotic therapy (ciprofloxacin, gentamicin) – pain is most severe
 Amphotericin B – daily bladder instillation first broad spectrum for 2 weeks  Opioid analgesics – control severe pain
 Ketoconazole (Nizoral) – given orally  Urinary antiseptic drugs (ex. Nitrofurantoin  Morphine (Statex) –given IV
[Macrodantin]) – specific antibiotic after urine and  NSAIDs such as ketorolac (Toradol)
 Antispasmodic drugs – decrease bladder
blood C&S results are known  Spasmolytic drugs such as oxybutynin
spasm, promote complete bladder emptying chloride (Ditropan) and propantheline
 Antibiotic therapy – bacterial UTIs bromide (Pro-banthine, Propanthel)
 3-day course of trimethoprim / Drug Therapy
sulfamethoxazole or Fosfomycin –  Broad spectrum antibiotics
community acquired UTIs in women aminoglycosides (ex. Gentamicin
(Garamycin) and cephalosporin (Keflex,
 7-21 days antibiotic – hospitalized patient
Novo-Lexin)
 Trimethoprim 100 mg daily – long-term
 Acetohydroxamic acid (Lithostat) and
management older patient recurrent UTIs hydroxyurea (Hydrea)
 One low-dose tablet TMP – women  Serum creatinine levels are monitored in
recurrent UTI after intercourse patients receiving acetohydroxide acid,
 Estrogen – intravaginal cream stopped if creatinine levels are above 2
postmenopausal mg/dL.
Immunologic Renal Disorders

GN Chronic GN CKD
Inflammation of Glomeruli in both kidneys Progressive and irreversible kidney injury-
becomes ESKD. Causes- DM and HPN
Assessment:
Fluid overload, S3, SOB/DOB Assessment: Assessment:
Check for crackles, Inc. in BP and weight, S3, Uremia, F&E, A-B imbalance, lethargy,
Asterixis Hypervolemia, Uremic Frost
Urinalysis:
Hematuria and Proteinuria, Inc. BUN and
Antitrypsin-O Titers, Dec. s. Albumin, GFR= 50 Urinalysis: Urinalysis:
ml/min Proteinuria, S.G= diluted, RBC, Low Creatine Excessive CHON, CHO, RBC, WBC, dec. Urine
Clearance, Inc. s. Creatinine and BUN osmolarity
Management of infection
• Antibiotic therapy for 7 to 10 days. • Phosphate binding agents such as calcium
• Penicillin, erythromycin or azithromycin – acetate, calcium bicarbonate, sevelamer
caused by streptococcal infection. hydrochloride (Renagel).
• Calcium and vitamin D supplements
Prevention of Complications
• Diuretics and sodium and water restriction • Antihypertensive drugs and cardiac
are prescribed –patients with fluid overload, medications
hypertension, and edema. • Antiseizure agents such as diazepam,
• Antihypertensive drugs - control phenytoin
hypertension. • Erythropoietin – Epogen IV or given SQ 3 times
a week.
OSA Pleurisy Pleural Effusion Pneumothorax
Breathing disruption that lasts atleast Inflammation of both layers of Collection of fluid in the pleural space Injury that allows air to enter
10 sec and occurs a min. of 5x in an hr. the pleura the pleural space

Pathophysiology: mechanical factors- Pathophysiology: accumulation of fluid


upper airway collapse- obstruction- Pathophysiology: may develop in the pleural space to a point at which it
repetitive apneic episode- hypoxia & in conjunction with pneumonia becomes clinically evident
hypercapnia- Sympathetic response-
risk of HPN, MI Stroke

Assessment Assessment
3s- Snoring, Signs of apnea, Sleepiness Decreased or absent breath sounds,
Assessment fremitus, and dull, flat on percussion Assessment
 Modafinil (Attenace, Provigil) - Severe, sharp, knifelike pain Reduced breath sounds,
promoting daytime wakefulness intensified during inhalation,  Thoracentesis hyperresonance, mediastinal
 Protryptilin (Triptil) – given pleuritic pain, pleural friction  Closed chest drainage shift
rub (early) (Thoracostomy tube)
bedtime, increase resp. drive and
 Adm analgesic agents as prescribed  Chest tube
improve upper airway muscle tone Thoracentesis  Thoracentesis, emergency
and as needed
 Medroxyprogesterone Actate thoracotomy, open
(Provera) & Acetazolamide  Analgesic agents thoracotomy
(Diamox) – associated w/ chronic  Indomethacin (Indocin) –  High concentration of oxygen
alveolar hypoventilation NSAIDS  Attached to pulse ox
 Adm low-flow oxygen at night  Intercostal nerve block
Reactive Airway Disorders

Asthma Status asthmaticus COPD


Inflammatory disease of airways causes airway Rapid, onset, does not respond to conventional therapy Airflow obstruction involving airways, pulmonary
hyperresponsiveness. Predisposing factor: Allergy parenchyma, or both
Pathophysiology: Severe mucus plugging-asphyxia-
Pathophysiology: Predisposing factor- airway narrowing of airway Physiology: Exacerbation/Remission- exposure to
inflammation-bronchoconstriction- activated noxious gases- inflammatory response-
inflammatory response- increase blood flow- hypersecretion of mucous- airway narrowing
attraction of white blood cells and mucus
secretion- narrowing of airway
Drug therapy involved the same inhaled and
Assessment: Assessment: systemic drugs as for asthma.
Cough, Dyspnea, Wheezing, Barrel Chest Extreme Labored breathing, Wheezing, Distended Neck 1. Bronchodilators - key symptom management
vein, Use of accessory muscles for breathing 1.a. Beta-adrenergic agents (Long and Short
ABG: Decreased O2 and CO2 acting)
1.b. Cholinergic antagonists (Muscarinic
Laboratory: Elevated igE and dec. FEV1 and FVC Initially: short-acting beta2-adrenergic agonist and antagonist)
systemic corticosteroids - to decrease the intense airway
1. Quick relief medications – relax smooth inflammation and swelling. 2. Methylxanthines
muscle, rescue medication 1.Short- acting inhaled beta2-adrenergic agonists - most 3. Corticosteroids
 SABA – Albuterol, Levalbuterol, Pirbuterol rapid relief from bronchospasm. • Inhaled corticosteroids - frequently prescribed
 Anticholinergics (Ipaprotium) - inhibit • pMDI (Pressured Metered Dose Inhaler) or via a • Long-term treatment in oral corticosteroids is
muscarinic cholinergic receptors, reduce nebulizer. NOT recommended
intrinsic vagal tone of airway 2. Supplemental oxygen and IV fluids for hydration. • Combination long-term beta2-agonists plus
2. Long-acting control medications • High flow supplemental oxygen is best delivered using a corticosteroids in one inhaler may be appropriate
 Corticosteroids (Methylprednisolone, partial or complete non-rebreathing mask. •examples include: Formoterol/Budesonide
Prednisone) – inhaled form • Sedatives are contraindicated. (Symbicort), Vilanterol/Fluticasone furoate (Breo
 Mast cell stabilizer (Cromolyn sodium, 3. Magnesium sulfate – smooth muscle relaxation Ellipta) and Salmeterol/Fluticasone (Advair)
nedocromil)
 C/I acute asthma exacerbations 4. Other medications:
 LABA (Theophylline, Salmeterol, Formoterol)  Alpha1-antitrypsin augmentation therapy
– not indicated immediate relief of symptoms,  Mucolytic agents
used with other medications in long term-  Antibiotics
control of asthma  Antitussive agents
3. Leukotriene modifiers/ antileukotrienes –  Vasodilators
dilate blood vessel and alter permeability,  Narcotic
alternative to inhaled corticosteroids, may be
added to a regimen of inhaled corti in more
severe asthma
 Montelukast (Singulair), zafirlukast (accolate),
Zileuton (zyflo)
4. Immunomodulators
 Omalizumab (Xolair) – patients with allergies
and severe persistent asthma
5. Methylxanthines – when others types of
management are ineffective
 Bronchodilators
 Theophylline, Aminophylline, Oxtriphylline
Emphysema (Pink Puffers) Bronchitis (Blue Bloaters) Atelectasis Pulmonary Edema Pneumonia PTB
Distention of air spaces Inflammation of Bronchi Closure or collapse of the Accumulation of Inflammation of lung Infection of lung
beyond terminal and bronchioles alveoli fluid in the lung parenchyma parenchyma caused by
bronchioles tissue. Frothy Pink because alveoli is mycobacterial invasion
Pathophysiology: Smoke Pathophysiology: Reduced Sputum filled with exudates
Pathophysiology: or environment- mucus ventilation- obstruct
Abnormal distention- plugging- reduce ciliary passage of air- reducing
disruption of the function- bronchial walls alveolar ventilation-
parenchymal tissues- become thickened- atelectasis
increase in dead space- narrowed bronchial
continuous destruction of lumen- altered alveolar
alveolar walls- pulmonary macrophages- more
HPN- dependent edema susceptible to respi
infection

Assessment: Assessment: Assessment: Assessment: Assessment: Assessment:


Dyspnea at rest, Tripod position, barrel Dyspnea, cough, cyanosis, Tachycardia, JVD, Productive cough, Afternoon fever,
productive cough, barrel chest, chronic cough, tachypnea, tachycardia, noisy breathing, dyspnea, fever, hemoptysis, weight loss
chest, prolonged cyanosis breathlessness pleuritic friction rub,
expiratory grunt, pursed Hallmarks of severity: rales/ crackles
lip ABG: Tachypnea, dyspnea, mild Oxygen therapy,
Respiratory Acidosis to moderate hypoxemia diuretics  CBR  CBR
ABG: (furosemide),  St  Strict respiratory
PO2 Elevation and CO2 Laboratory: decreased ABG: vasodilators (IV  Broad spectrum isolation
depression- Respi Aci FEV1 Laboratory: Low ox sat nitroglycerin, antibiotics  Adm 02 inhalation
nitroprusside)  Penicillin  DBE and coughing
Laboratory: Decreased Deep breathing exercises,  Anti-pyrectics  Nebu and suction
FVC incentive spirometry,  Mucolytics PRN
coughing – first line  Postural drainage  Short course chemo:
 Bronchodilators measures to improve intensive phase:
 Antimicrobials ventilation  Ethambutol
 Corticosteroids  Isoniazid – 4 mo
 Mucolytics/expectorants  Rifampicin and
 Low inflow O2 admin Pyrazinamide – 2 mo
 INH, PZA, Rifampicin
given simultaneously
prevent development
of resistance
 Standard reg:
Streptomycin inj

CAD- 5E’s Angina MI


Obstructed blood flow through the coronary Paroxysms of pain or pressure in the anterior Occlusion of a coronary artery followed by
arteries chest. May relieve in rest and NTG cessation of blood flow to a part of the
myocardial tissue
Pathophysiology: waxy cholesterol deposits- Pathophysiology: Presences of AHD-
atheroma- protrude into the lumen- necrosis- Myocardial Ischemia- Angina Pathophysiology: change in condition of
obstruct blood flow plaque- activation of platelets- thrombus
Assessment: formation- ischemia- less supply than
Assessment: Pain in the center of the chest that radiates demand- myocardial cell death
Pain, retrosternal squeezing, weakness, to left arm
sweating and clammy skin Assessment:
S3, S4, JVD, High BP, dyspnea, tachypnea,
ECG: ST depression and T wave inversion ECG: ST depression and T wave inversion oliguria, cyanosis

Laboratory: Normal Cardiac Enzymes  Nitrates SL (Nitroglycerin) ECG: St elevation, t wave inversion, abnormal
 Beta-blockers (Metroprolol, Atenolol, q wave, Atrial Fibrillation
 Low dose aspirin therapy Propranolol, Lopressor, Toprol)
 Niacin or nicotinic acid  Calcium channel blockers (Amlodipine,  MONA (morphine, oxygen, nitroglycerin,
 Bile-acid-binding resins Diltiazem, Felodipine, Isradipine, aspirin)
(Cholestyramine) Nifedipine, Nisoldipine)  Morphine sulfate – reduce pain & anxiety
 Cholesterol synthesis inhibitors -  Antiplatelet & anticoagulant (Aspirin,  Aspirin – beta-blocker for dysrhythmia,
STATINS Clopidogrel, Heparin Na, Warfarin Na, low heparin or LMWH
molecular weight heparin)  Stool softener
 Glycoprotein IIb/IIIa (Abciximab,  Analgesic
Eptifibatide)  ACE inhibitors
 Statins (Simvastatin)  EPCI
 ACE inhibitors (Captopril)  Thrombolytics
 Oxygen adm. – non-invasive vent >95%
room air

Drugs

Ampothericin B- bladder instillation /Ketoconazole (Nizoral)

Trimethoprim/Sulfamethoxazole or Fosfomycin – treat uncomplicated community acquired UTI

Imaging Assessment

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