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50 Cards in this Set
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Cough
Description Protective respiratory reflex, induced by stimulation of respiratory tree receptors. Symptoms Cough. May be productive or nonproductive (dry). |
Diagnosis
History and physical, chest x-ray (CXR), pulmonary function testing (PFTs), sputum analysis (culture and cytology), upper gastrointesti- nal (UGI) (rule out reflux/aspiration), empiric trial of PPI (proton pump inhibitor) for reflux. • Differential Diagnosis: Asthma, foreign body, congestive heart failure (CHF), chronic aspiration, pneumonia, sinusitis, severe gastroesophageal reflux disease (GERD), malignancies, angiotensin-converting enzyme (ACE) inhibitor related, other pulmonary diseases. |
Treatment Steps
Treatment: Will vary depending on the insulting factor (etiology). Could be as simple as bronchodilators and/or H2 blockers, or as complex as bronchoscopy for foreign body retrieval |
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Hemoptysis
Description Bloody sputum production. Symptoms Ranges from sputum tinged with blood to expectoration of frank blood. May see shortness of breath. |
Diagnosis
History and physical, CXR, bronchoscopy, computed tomographic (CT) scan of chest, pulmonary angiography, labs (prothrombin time [PT], partial thromboplastin time [PTT], complete blood count [CBC]) Pathology A result of carcinoma, bronchitis, tuberculosis (TB), pulmonary em- bolism, coagulation disorder, Goodpasture’s syndrome, mycetomas, bronchiectasis, hemosiderosis, Wegener’s disease, and mitral stenosis |
Treatment Steps
1. Supportive. 2. Control cough (codeine). 3. Intubation. 4. Tamponade or thoracotomy for massive hemorrhage/tumor |
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Epistaxis
Symptoms Nasal bleeding (slight or brisk), hypertension. Anterior Bleed—Often one side only. Posterior Bleed—Both sides, coughing/choking on blood. |
Diagnosis
History and physical examination Pathology Anterior (Kiesselbach’s or Little’s plexus bleeding, trauma, low hu- midity), or posterior sites. Additional etiologies: hypertension, nasal foreign body, tumor, vascular abnormalities/arteriosclerosis, leukemia, bleeding disorders, and infection. |
Treatment Steps
Anterior: 1. Pressure/packing. 2. Cautery. Posterior: 1. Posterior pack/balloon. 2. Artery ligation |
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Dyspnea
Description Air hunger. Symptoms Subjective complaint of uncomfortable shortness of breath, of more than expected severity for activity level. |
Diagnosis
History and physical, cardiac and pulmonary evaluation as guided by the history. Note the patient’s vital signs. Pulse, blood pressure, pulse ox. CBC, SMA-12, electrocardiogram (ECG), CXR, arterial blood gas (ABG), 2-dimensional (2-D) echo, ventilation/perfusion (V/Q) scan, cardiac enzymes (creatine kinase [CK], CK-MB, troponin), PFTs, stress test. Pathology Most frequently pulmonary or cardiac disease, of acute or chronic nature. Deconditioning and psychogenic factors may be present Pulmonary Asthma, pulmonary embolism, chronic obstructive pulmonary disease (COPD) exacerbation, acute bronchitis, pneumonia, aspiration, airway obstruction (due to foreign body or tumor), pleural effusion, cor pulmonale. Cardiac Angina, myocardial infarction (MI), CHF, pericarditis, cardiomyopathy, arrhythmia. Other Anemia (acute or severe and chronic), metabolic disorders (metabolic acidosis due to diabetic ketoacidosis [DKA]), end- stage liver disease with ascites, pregnancy, acute intoxications, panic attacks |
Treatment Steps
Treat primary problem |
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Chest Pain
Symptoms Chest pain. May be pleuritic (pleurisy), exacerbated by chest wall palpation (costochondritis) or exercise (angina), or episodic (spasm?) and atypical (other disorder |
Diagnosis
History and physical, cardiac workup (ECG, 2-D echocardiogram, stress testing, arteriography), CXR. Other studies may include V/Q scan, high-resolution CT scan of chest, ultrasound of aorta, and gas- trointestinal (GI) workup. Pathology Rule out angina pectoris: ischemic cardiac pain. Other etiologies in- clude pleurisy, pericarditis, costochondral disease, GERD, esophageal spasm, neuritis, pulmonary embolism, aortic aneurysm, pulmonary hypertension, valvular disorders, and others. |
Treatment Steps
Treat as per specific etiology. |
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Palpitations
Description Subjective sensation of additional/irregular or strong heartbeats, or chest discomfort related to cardiac rhythm. Symptoms As described. Depending on etiology, may also experience chest pain, anxiety, light-headedness, or syncope. |
Diagnosis
History and physical, ECG (see Figs. 19–1 and 19–2), 2-D echocar- diogram, Holter monitor, CBC, thyroid-stimulating hormone (TSH). Pathology Sensation of abnormal beats (palpitations) may reflect significant cardiac pathology or be of no importance whatsoever. |
Treatment Steps
As per individual condition. |
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Cyanosis
Description Blue color of mucous membranes and/or skin and nail beds. Club- bing (see Section II.C). Symptoms As described. May be associated with other symptoms depending on specific disorder. |
Diagnosis
History and physical, cardiopulmonary evaluation (ABG/ECG/ echo/CXR/cath/PFTs). Newborn with cyanosis: oxygen (100%) will improve hypoxemia with pulmonary disorders, but have negligible effect with intracardiac shunt lesions. Pathology Reduced arterial oxygen concentration from central (cardiac shunt or pulmonary pathology), or peripheral (vasoconstriction) mechanisms. |
Treatment Steps
As per individual condition |
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Hypoxemia
Description Inadequate blood oxygen. Symptoms Lethargy, mental status change, arrhythmia, headache, palpitations, impaired judgment |
Diagnosis
History and physical (cyanosis, tachycardia, etc.), cardiopulmonary evaluation, ABGs, response to oxygen, A-a gradient (see the follow- ing), and hemoglobin. Most specific physical sign of hypoxemia: cyanosis. Pathology Etiologies include V/Q mismatch, right-to-left shunt, diffusion ab- normality, alveolar hypoventilation, and reduced inspiratory oxygen content |
Treatment Steps
As per condition, but oxygen is critical. |
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Shock
Description Inadequate tissue perfusion. Symptoms Hypotension, tachypnea, tachycardia, mental confusion, cyanosis |
Diagnosis
History and physical (weak pulse, reduced urinary output, fever, poor skin color, etc.). Other procedures as indicated (blood cultures, hemodynamic monitoring, etc.) Pathology Primary etiology includes cardiogenic and hypovolemic disorders. Other sources include trauma and sepsis e.g., high CO/low SVR suggests sepsis; low CO/high SVR/high wedge pressure suggests cardiogenic shock; equalization of pressures suggests tamponade; high wedge, your patient could be wet; low wedge, your patient might be intravascularly depleted; high RA/high PAP with pad-wedge > 5 suggests pulmonary hypertension). CO = cardiac output SVR = systemic vascular resistance PAP = pulmonary artery pressure |
Treatment Steps
1. Cardiopulmonary resuscitation (CPR) (including ventilatory sup- port, cardiac monitoring, acid–base management, and fluids/vasopressors). 2. Treatment of primary disorder. |
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Respiratory Failure
Description Inadequate oxygen or carbon dioxide exchange. Symptoms Tachypnea, tachycardia, mental confusion, cyanosis, wheezing/dysp- nea. |
Diagnosis
History and physical, most important test is ABGs; clinical findings of respiratory failure, and CXR may all be helpful. Note vitals— pulse, blood pressure, pulse ox, temperature. Pathology Hypercarbia (PaCO2 > 50) and/or hypoxemia (PaO2 < 60) |
Treatment Steps
1. Oxygen (with or without intubation and mechanical ventilation). 2. Treatment of primary problem (drug overdose, infection, trauma, etc.) |
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Edema
Description Increased tissue fluid, swelling of affected area |
Diagnosis
History and physical, evaluation of cardiac, renal, hepatic, and vascu- lar systems. Commonly CBC, SMA-12, urinalysis (UA), CXR, 2-D echo, lower extremity Dopplers, possible stress test Pathology Interstitial fluid excess. “Third spacing” due to low oncotic pressure: cirrhosis, nephrotic syndrome. Also venous insufficiency, obstruction to venous flow by tumor or DVT (deep vein thrombosis), CHF, med- ications (calcium channel blockers, rofecoxib, thiazolidinediones) |
Treatment Steps
1. Treat primary condition. 2. Reduce salt and fluids. 3. Diuretics (cardiac causes). |
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Jaundice
Description Yellow skin and mucous membranes, secondary to elevated bilirubin levels. Symptoms Yellow skin/mucosa, may have dark urine, pruritus, light-colored stools, and symptoms of individual etiologic disorder |
Diagnosis
History and physical (look for subungual jaundice and scleral icterus as well as skin discoloration), CBC with smear, lactic dehydrogenase (LDH), liver function tests (LFTs), ultrasound or CT scan of liver/abdomen, HIDA (hepatoiminodiacetic acid) scan, ERCP (endoscopic retrograde cholangiopancreatography), liver biopsy. Pathology Unconjugated—Etiology includes excess bilirubin production (hemolytic disorders), or faulty liver conjugation or uptake (genetic disorders). Conjugated—Reduced liver production (hepatic disease of vari- ous types, including inflammation, infection, and obstruction) |
Treatment Steps
Treat primary condition |
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Clubbing
Description Distal phalanx nail deformity. Symptoms Loss of nail plate-to-finger angle (convex nails), with fingernail thickness greater than distal interphalangeal (DIP) joint thickness |
Diagnosis
Physical examination. Pathology Common to many cardiopulmonary disorders (bronchiectasis, pul- monary hypertension, atrial septal defect, lung cancer, cystic fibrosis, cyanotic congenital heart disease, etc.), possibly secondary to hypox- emia. May also be familial. |
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Pruritus
Symptoms Sensation of itching (via skin nerve-ending stimulation) |
Diagnosis
History and physical, routine lab studies, and evaluation for any un- derlying disease as indicated. Pathology May relate to local factors (dry skin, allergy), medications, or sys- temic pathology (uremia, malignancy, endocrine/thyroid disease, liver disease). |
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Abdominal Pain
Description/Symptoms Pain in the abdominopelvic region (may include signs of peritonitis, referred pain, abdominal rigidity, etc.). |
Diagnosis
History and physical (see Cram Facts). CBC, SMA-12, amylase, lipase, UA, obstruction series, ECG, possibly CT scan of abdomen and pelvis, ultrasound, intravenous pyelography (IVP), bimanual pelvic exam with cultures. Pathology Wide etiology including both acute and chronic events, and both ab- dominal and referred pain (cardiac) (see Fig. 19–3) |
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Infantile Colic
Description Prolonged infant crying/abdominal pain Symptoms Crying episodes, with clenched fists and legs pulled up. |
Diagnosis
Clinical. Pathology Uncertain, but most often resolves by 12 weeks of age |
Treatment Steps
1. Reduce infant stress. 2. Increase parent relaxation/supportive care for parents. 3. Hot water bottle for infant. 4. Simethicone drops (Mylicon). 5. Burping. |
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Hepatomegaly (Enlarged Liver)
Symptoms Asymptomatic, or abdominal mass, right upper quadrant or shoul- der pain. |
Diagnosis
History and physical—may lead you to possible etiology (see Clinical Pearl). Based on clinical scenario: LFTs, CBC, LDH, hepatitis serolo- gies (hepatitis A, B, C), ferritin, ultrasound, CT scan abdomen. Pathology Numerous possible etiologies. |
Treatment Steps
Treat primary condition. |
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Splenomegaly
Symptoms Asymptomatic or abdominal mass, left upper quadrant or shoulder pain. |
Diagnosis
History and physical, ultrasound, CT, and radioisotope scan. Pathology Numerous possible etiologies (hemolytic anemia, portal hyperten- sion and hepatocellular disease, mononucleosis, sarcoid, leukemia/ lymphoma, storage disorders, idiopathic) |
Treatment Steps
Treat primary condition. |
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Ascites
Description Excess peritoneal fluid. Symptoms Enlarging abdomen. May also have nausea, abdominal pain, edema, weight gain, and dyspnea. |
Diagnosis
History and physical—on history, ask about prior liver disease or cir- rhosis (see Clinical Pearl). On physical exam, look for fluid wave, shifting dullness, bulging flanks. Ultrasound is helpful; paracentesis is essential to determine the cause of ascites Paracentesis: It is essential to ask for cell count with differential, cytology, and albumin. Calculate the SAAG (serum ascites:albumin gradient. SAAG > 1.1 is consistent with ascites due to cirrhosis. Pathology Exudate—Protein > 3 g/100 mL (TB, cancer, and others). Transudate—Cirrhosis and CHF |
Treatment Steps
As per individual condition. For cirrhosis: restrict salt, diuretics (furosemide, aldactone), Le Veen shunt. |
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Dysphagia
Description Difficulty swallowing. Symptoms Difficulty swallowing, weight loss, regurgitation. |
Diagnosis
History and physical, barium swallow or UGI series, endoscopy. Pathology Esophageal constriction may be due to tumor, achalasia, stricture, esophageal ring (Schatzki’s ring may cause intermittent dysphagia), or neuromuscular disorders. |
Treatment Steps
As per individual condition. |
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Nausea and Vomiting
Symptoms Nausea, possibly followed by tachycardia, hypersalivation, and vomit- ing. |
Diagnosis
History and physical, x-ray studies (obstruction series), lab studies, endoscopy. Pathology Gastrointestinal Appendicitis, ileus, small bowel obstruction, gastric or duodenal ulcer, pancreatitis Metabolic Pregnancy, uremia, DKA Psychogenic Bulemia Oncologic Chemotherapeutic agents CNS Vertigo (Ménière’s and acute labyrinthitis), neo- plasm, migraine headache Endocrine Gastroparesis (commonly due to diabetes) Cardiac MI |
Treatment Steps
1. Treat primary condition. 2. Antiemetics include scopolamine, meclizine, and corticosteroid |
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Diarrhea
Description Acute or chronic diarrheal illness (increased stool weight per 24 hours). Symptoms Diarrhea (mild or severe), dehydration, fever if infectious. |
Diagnosis
History and physical, stool studies (fecal white blood count [WBC], ova and parasites, Clostridium difficile antigen and toxin), CBC, SMA- 12, amylase, lipase, stool electrolytes (sodium and potassium), stool osmolarity. Pathology Physiology includes secretory, osmotic, impaired motility, and ab- sorptive disorders. Etiology includes infection, medications, and inflammatory bowel disease. Effect of fasting on diarrhea types—secre- tory, no effect; osmotic, diarrhea stops. |
Treatment Steps
1. Rehydration. 2. Treat primary condition (amebiasis/giardiasis: metronidazole; pseudomembranous colitis: metronidazole). 3. Antidiarrheals (if infection is absent) |
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Fecal Incontinence
Description/Symptoms Inability to maintain stool continence. Termed encopresis in children |
Pathology
Anal sphincter disorder (idiopathic, postsurgical, trauma, Crohn’s, etc.). May also relate to impaction, diabetes, and neuromuscular dis- ease. |
Treatment Steps
1. Anal sphincter exercises (consult physician). 2. Biofeedback. 3. Medication. |
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Anorexia Nervosa
See also Chapter 15. Description Weight loss disorder. Symptoms Weight loss, depression, amenorrhea, distorted self-image. |
Diagnosis
History and physical examination, lab studies (SMA-12, CBC) exami- nation of nails and teeth. Rule out GI disease: GI studies (UGI, en- doscopy, barium enema [BE], etc.). Pathology Typically in adolescent females, with unknown etiology (though fam- ily and social situations/pressures play a role). |
Treatment Steps
1. Psychiatric/psychological care. 2. Medication (cyproheptadine, chlorpromazine). |
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Failure to Thrive in Infancy
Symptoms Insufficient weight gain or growth, lethargy, emotional/behavioral disorders |
Diagnosis
History and physical, laboratory, and other studies as indicated. Pathology Etiology most often includes psychological disorders and depriva- tion/abuse |
Treatment Steps
1. Treat any coexisting medical disorder. 2. Family counseling. 3. Social service intervention. 4. Possible child foster placement |
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Headache
Description Head pain. Symptoms Migraine—Throbbing, unilateral, nausea/vomiting, photophobia, phonophobia. Cluster—Periorbital, severe pain, unilateral autonomic signs. Tension—Bilateral, neck muscles tight, tight band feeling. Acute Central Nervous System (CNS)—Acute-onset severe headache, neurologic signs. |
Diagnosis
History and physical examination, lab testing (glucose, CBC), x-ray head/sinuses, electroencephalogram (EEG), CT/magnetic reso- nance imaging (MRI) studies, lumbar puncture (LP). Pathology May include migraine, cluster, tension, CNS disease, exertional, and others (carbon monoxide, nitrites, temporal arteritis, temporo- mandibular joint [TMJ], etc.), as a result of inflammation or alter- ation of pain-sensitive CNS structures |
Treatment Steps
As per individual condition. |
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Delirium
Description Alteration of consciousness. Symptoms Confusion, memory difficulty, disorientation, agitation, perception disturbance. |
Diagnosis
History and physical examination, lab studies CBC, SMA-12, B12, fo- late, rapid plasma reagin (RPR), TSH, urine drug screen, possibly LP, CT of head, EEG. Pathology Etiology includes infection, medication, metabolic disease, cardiac disease, sleep deprivation, and CNS disease. Most frequent in el- derly hospital patients, and resulting from complex and multiple factors. |
Treatment Steps
1. Diagnose and treat the primary condition. 2. Provide orientation for the patient. 3. Nursing support. 4. Discontinue unnecessary medications and avoid anticholinergic and sedative–hypnotic medications. 5. Allow sleep (intensive care unit [ICU] psychosis). 6. Avoid restraints. 7. Medication if necessary, i.e., if patient is very agitated or psychotic (low-dose haloperidol [Haldol], antipsychotics [risperidol]). |
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Coma
Description State of unconsciousness, and unresponsiveness, resulting from meta- bolic, CNS pathology, and other causes. Symptoms Unresponsiveness. |
Diagnosis
History and physical examination, EEG, CT, laboratory studies (SMA-12, CBC, drug screen, PT, PTT, ABGs, thyroid functions), LP. Pathology Only two causes: extensive bilateral cerebral disorder or brain stem disorder. |
• Pupils reactive and
small—narcotics, metabolic, and pontine pathology • Pupils fixed and dilated—anoxia, and scopolamine overdose (OD) • Pupils face hemiparesis side—pontine lesion • Pupils face strong side—unilateral cerebral hemisphere lesion • Other antidotes— benzodiazepines (give flumazenil) |
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Convulsions
Description Seizure, and/or uncontrolled contraction of muscles Symptoms As described for following seizure disorders: Grand Mal—Tonic–clonic, incontinence, postictal lethargy. Petit Mal—Staring/absence spells, patient possibly unaware. Partial—Simple (consciousness not lost), or complex (possible unconsciousness). Both may have sensory and/or motor signs |
Diagnosis
History and physical examination, EEG, CT/MRI, laboratory studies, including blood cultures and toxicology screening. Pathology Convulsions—Wide etiology (epilepsy, poisoning, infection, heat- stroke, etc.). Seizures—Generalized or partial (focal). Wide variety of CNS causes (trauma, metabolic, drugs/drug withdrawal, congenital dis- ease, etc.). |
Treatment Steps
1. Neurologic workup. 2. Medication (see Chapter 11). |
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nsomnia
Symptoms Inability to sleep, disrupted sleep, or perceived poor sleep quality |
Diagnosis
Clinical, psychological evaluation, routine laboratory studies, sleep studies, EEG. Pathology May result from medication, depression, anxiety, and/or alcohol use. Also may be a primary sleep disorder (see Cram Facts). |
Treatment Steps
1. Treat coexisting medical disorders. 2. Psychological evaluation. 3. Progressive relaxation/biofeedback. 4. Sleep hygiene. |
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Syncope
Description Fainting. Symptoms Sudden loss of consciousness asovagal—May have diaphoresis, ringing in the ears, and blurry vision prior to fainting. Orthostatic—Postural-related symptoms. Cardiac—Possibly exercise induced. |
Diagnosis
History and physical, Holter monitor, ECG, EEG, and laboratory studies (rule out hypoglycemia and seizure disorders). Pathology Reduced cerebral blood perfusion, via reduced cardiac output/ve- nous return, or other disorders. |
Treatment Steps
Treat primary disorder. |
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Ataxia
Description Disorder of muscle coordination. Symptoms Balance loss, may have limb, gait, or dysarthric ataxia. |
Diagnosis
History and physical, CT/MRI. MRI is superior to CT in imaging the cerebellum. Pathology Cerebellar or brain stem pathology. Multiple disorders (drugs/alco- hol, B12 deficiency, hypothyroidism, viral infection, etc.). |
Treatment Steps
Treat primary condition |
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Weakness
Description Muscle and/or neurologic disease resulting in reduced muscle strength. Symptoms Weakness (may include reduced deep tendon reflexes, and fascicula- tions). Try to distinguish muscle weakness from generalized fatigue |
Diagnosis
History and physical, laboratory studies (CK, aldolase), CT/MRI, LP, electromyogram (EMG)/nerve conduction velocity (NCV), PFTs. Pathology Neurologic (most often myasthenia gravis, Guillain–Barré syn- drome), infectious, endocrine, psychological, and other conditions (botulism, medication, etc.) |
Treatment Steps
As per individual condition |
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Dysphasia
Description Impaired speech and verbal comprehension. Aphasia––acquired dis- order of language due to brain damage. Symptoms Receptive (Posterior)—Difficulty with comprehension, speech re- mains fluent. Expressive (Anterior)—Difficulty with expression, speech fluency dis- turbed. |
Diagnosis
History and physical/neurologic examination. Pathology Brain pathology (cerebrovascular accident [CVA], trauma, infec- tion), typically of dominant temporal lobe. |
Treatment Steps
1. Treat primary condition. 2. Speech therapy when stable |
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Dyslexia
Description Reading disorder. Symptoms Reading disorder without associated intellectual or visual disability. |
Diagnosis
History and physical, reading tests. Pathology Cortical developmental disorder. |
Treatment Steps
Tutoring |
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Vertigo
Description Sensation of “the room spinning.” Symptoms Inappropriate perception of motion, often of abrupt onset (periph- eral disease) with associated nausea and vomiting. May have nystag- mus (peripheral disease, horizontal; central pathology vertigo, verti- cal nystagmus |
Diagnosis
History and physical, CT/MRI, electronystagmography (ENG), brain stem auditory-evoked responses (BAER), and audiologic test- ing. Pathology Vestibular disorder |
Treatment Steps
1. Medication. 2. Attempt to fatigue response. 3. Surgery |
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Diplopia
Symptoms Double vision; may demonstrate head tilt/compensation (head turns toward weak lateral rectus muscle with sixth nerve lesion). |
Diagnosis
History and physical examination, laboratory studies, CT/MRI. Pathology Loss of eye muscle strength (neurologic disease, infection, tumor, and trauma). |
Treatment Steps
Treat individual condition. |
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Dysuria
Symptoms Pain with urination, possibly associated with other urinary tract signs and symptoms (frequency, urgency). |
Diagnosis
History and physical, UA and culture, cystoscopy, x-rays (KUB, possi- bly renal ultrasound or spinal CT). Pathology Urinary tract inflammation; suggestive of infection, though other etiologies possible (stone, foreign body, tumor, etc.). |
Treatment Steps
1. Treat primary disorder. 2. Antibiotics empirically or as per culture. |
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Pyuria
Description White blood cells in the urine. Symptoms Asymptomatic, or symptoms of infection (urgency, frequency, noc- turia, etc.). In a female, ask about vaginal discharge, sexual history |
Diagnosis
Midstream UA, and culture, KUB (rule out stone and foreign body). Pathology Urinary system inflammation (suggestive of infection), with poly- morphonuclear leukocytes in the urine. |
Treatment Steps
1. Antibiotics as per culture. 2. Treatment of other coexisting disorders. |
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Glycosuria
Description Urine glucose. Symptoms Often asymptomatic. |
Diagnosis
UA, dipstick tests (Clinitest, Testape). Pathology Urinary glucose after renal threshold is exceeded (may indicate dia- betes). Also noted with renal glycosuria: normal serum glucose with disorder of glucose reabsorption (congenital, drug/heavy metal in- duced, or associated with Fanconi syndrome). |
Treatment Steps
Blood glucose control. |
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Hematuria
Description Presence of red blood cells (RBCs) in urine (> 3–5 RBC per hpf). Symptoms Microscopic hematuria is asymptomatic. If associated with kidney stones, may see flank pain and/or dysuria. If due to infections, may see symptoms of urinary tract infection (UTI) (dysuria, frequency, urgency). If severe glomerulonephritis (GN), may see signs of renal failure. |
DDX OF HEMATURIA–
HITTTS Hematologic disorder Infections Tumor Trauma TB Stone Diagnosis UA, microscopic analysis of urine looking for cells, casts, crystals. Urine culture, SMA-7. Pathology Depending on etiology. Need to consider infection (simple UTI, he- morrhagic cystitis, pyelonephritis), nephrolithiasis, bladder or kid- ney malignancy, intrinsic kidney disease (nephritic or nephrotic GN). |
Treatment
Treat the underlying disorder. |
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Azotemia
Description Elevated blood urea nitrogen (BUN) and creatinine. Symptoms Multisystem abnormalities with renal failure (skeletal, metabolic, cardiovascular, hematologic, etc.). (See Chapter 17.) |
Diagnosis
History and physical, UA, urine soduim, urine creatinine, laboratory studies, SMA-12, magnesium, phosphorus, cystoscopy, Foley catheter insertion (may treat and define obstruction), renal ultrasound. Pathology Renal failure may be prerenal (dehydration or decreased blood flow to kidneys), intrinsic renal disease, or postrenal (obstruction). |
Treatment Steps
Prerenal—Fluids. Renal—Treat primary renal injury (e.g., stop offending medica- tion; for rhabdomyolysis, give mannitol). Postrenal—Remove obstruction |
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Proteinuria
Description Elevated urinary protein, indicating renal parenchymal disease. Symptoms Asymptomatic, unless severe (nephrotic syndrome—see below). |
Diagnosis
UA (dipstick method), followed by 24-hour urine protein study (> 400 mg/24 hr is abnormal). Pathology A result of abnormal proteins (Bence Jones), inadequate reabsorp- tion, glomerular permeability disorder, or renal flow dysfunction. |
Treatment Steps
Treat primary condition. |
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Nephrotic Syndrome
Description Syndrome involving glomerular dysfunction with massive loss of pro- tein in the urine. Symptoms Peripheral edema, ascites, occasionally anasarca, pleural effusion, periorbital edema. Also can see hypertension, hyperlipidemia, and hypercoagulability (renal vein thrombosis in particular |
Diagnosis
History and physical, 24-hour urine protein collection (> 3.5 g/day proteinuria), laboratory studies (hypoalbuminemia, hyperlipidemia), UA (casts, oval fat bodies), renal biopsy. Biopsy will delineate the type of GN present and see a secondary etiology. Pathology Wide etiology. More common systematic causes include diabetes mellitus (DM), systemic lupus erythematosus (SLE), intravenous drug use, amyloidosis, hepatitis B, Hodgkin’s disease, human immun- odeficiency virus (HIV). Idiopathic nephrotic syndrome can also oc- cur. The most common type in children is minimal change disease, in blacks focal segmental glomerulosclerosis, and whites membra- nous nephropathy. |
Treatment Steps
Treat underlying etiology if possible. Can use loop diuretics for edema, hydroxymethylglutaryl coenzyme A (HMG CoA) reductase inhibitors for hyperlipidemia, ACE inhibitors for proteinuria and blood pressure control, and anticoagulation if thrombosis is present. |
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Renal Colic
Description Ureteral spasm and pain, most commonly due to kidney stone. Symptoms Flank or Testicle Pain—Upper ureter stone. Flank/Abdomen Pain, Nausea/Vomiting—Pelvic brim–level stone. Groin Pain—Distal ureter stone. Dysuria/Urgency—Vesical stone. Also chills, fever, muscle spasm, and signs of bladder irritation |
Diagnosis
History and physical, x-ray (KUB, IVP), UA, ultrasound, CT scan. Pathology Obstructive ureteral pain secondary to hyperperistalsis (etiology in- cluding infection, metabolic and renal disorders) |
Treatment Steps
1. Hydration and analgesia. 2. When stone will not pass, stone removal or lithotripsy. 3. Metabolic workup for the etiology of the stone. |
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Urinary Incontinence
Description Loss of urinary retention control. Symptoms Atonic Bladder—Urinary retention and overflow incontinence. Spastic Neuropathic Bladder—Incontinence. Infection––Incontinence, symptoms of infection. Stress Incontinence—Incontinence with exertion and straining |
Diagnosis
History and physical, UA and culture, urodynamic evaluation (cys- tometry, uroflowmetry), and x-ray studies (excretory urography, CT, ultrasound, etc.). Pathology Causes of incontinence: Neurologic, stress incontinence, outlet ob- struction with overflow incontinence, inflammation, medications, trauma, dementia, and infectious etiology |
Treatment Steps
As per individual condition (includes medication, surgery, catheteri- zation, etc.). |
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Urinary Retention
Description Loss of ability to fully empty the bladder. Symptoms Abdominal pain, urgency (without results), nocturia, bladder spasm. |
Diagnosis
History and physical, UA and culture, postvoid residual (after pa- tient voids, insert catheter and record amount of residual urine) urodynamic evaluation, x-ray studies (retrograde urethrography), ul- trasound, and obtain laboratory studies (BUN, creatinine, elec- trolytes, and glucose). Pathology A result of medication (anticholinergics and sympathomimetics), obstruction (cancer, benign prostatic hypertrophy [BPH], stone, valves), or neurologic disease |
Treatment Steps
1. Remove obstruction. 2. Dilate stricture. 3. Stop offending medication |
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Oliguria
Description Reduced urine production. Symptoms As described, urine volume 100–400 mL/day, may cause renal failure (lethargy, hypertension, hematuria, and/or proteinuria), in- creased BUN/creatinine |
Diagnosis
History and physical, UA, laboratory studies (BUN, creatinine, cal- cium, electrolytes, ABGs, urinary osmolality/electrolytes, etc.). Pathology Typically secondary to prerenal pathology (hypovolemia, CHF, burns, etc.), renal pathology (renal failure/disease), or obstruction. |
Treatment Steps
Always start with a fluid challenge. May need diuretics, dialysis |
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Fever of Unknown Origin
Description Fever > 101°F for more than 3 weeks or unexplained even after a 1- week hospital evaluation or three outpatient visits. Symptoms May be nonspecific (lethargy, hot/cold flashes, sweating), or symp- toms associated with the primary disorder. |
Diagnosis
History and physical. Further testing as history and/or physical find- ings dictate (culture blood/urine/sputum/stool, chest/gallbladder x-rays, laboratory testing: CBC, heterophile, RPR, HIV, etc.), bone scan, CT scan of chest/abdomen, and others. Pathology Fever induced by very wide variety of disorders (infection, fungal, medication, tumor, connective tissue, viral, psychogenic, metabolic disorders, etc.) |
Treatment Steps
Treat individual disorder. |
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Lymphadenopathy
Description Enlarged lymph nodes. Symptoms Asymptomatic or local tenderness. May demonstrate signs/symp- toms of associated disorder. |
Diagnosis
History and physical, laboratory studies as indicated (heterophile an- tibodies, HIV, blood culture, serologic testing, etc.), biopsy is diag- nostic. Pathology Infection (localized or widespread) or tumor (lymphoma or metastatic) can cause lymphadenopathy. Examples include dissemi- nated HIV, mononucleosis, cat-scratch disease. Other etiologies in- clude sarcoidosis, phenytoin sodium |
Treatment Steps
Treat specific disorder |
