Micro notes

Posted by Luck from IP 172.160.198.100 on January 17, 2004 at 05:35:58:
FA:Toxin-induced gastroent. and GIT infections!!
Staphylococcus aureus:
. Incubation period:1-8 hours (rarely, up to 18 )
. Signs and sympt:Nausea and vomiting
. Epidemiology: Staphylococci grow in meats, dairy, and other foods and produce enterotoxin.
. Pathogenesis:
Enterotoxin acts on receptors in the gut that transmit impulse to medullary centers that control vomiting.
. Clinica:Very common, abrupt onset, intense vomiting for up to 24 hours, regular recovery in 24-48 hours.Occurs in persons eating the same food.No treatment usually necessary except to restore fluids and electrolytes.
Bacillus cereus:
, I.P: 2-16 hours
. S and S: Vomiting or diarrhea
. Epid:Reheated fried rice is common vehicle.
. Path:Enterotoxin formed in food or in gut from growth of B cereus.
Clin:With incubation period of 2-8 hours, mainly vomiting.With incubation period of 8-16 hours, mainly diarrhea.
Clostridium perfringens:
. 8-16 hours
. Watery diarrhea
. Clostridia grow in rewarmed meat dishes.Huge numbers ingested.
. Enterotoxin produced during sporulation in gut, causes hypersecretion.
. Abrupt onset of profuse diarrhea; vomiting occasionally.Recovery usual without treatment in 1-4 days.Many clostridia in cultures of food and feces of patients.
Clostridium botulinum:
. 18-24 hours
. Paralysis
. C botulinum grows in anaerobic food and produce toxin.
. Toxin absorbed from gut blocks acetylcholine at neuromuscular junction.
. Diploplia, dysphagia, dysphonia, difficulty breathing.Treatment requires ventilatory support and antitoxin. Diagnosis confirmed by finding toxin in blood or stool.
Escherichia coli (enterogenic;ETEC):
. 24-72 hours
. Watery diarrhea
. Most common cause of 'traveler's diarrhea.'
. ETEC in the gut produce heat-labile (HL) or heat-stable (HS) enterotoxins. Toxins1cause hypersecretion in small intestine.
. Usually abrupt onset of diarrhea; vomiting rare.A serious infection in newborns.In adults, usually self-limiting in 1-3 days.
Escherichia coli (enteroinvasive;EIEC):
. 48-72 hours
. Dysentery
. Occasional outbreaks of dysentery; infrequent cause of sporadic infection. .
. Inflammatory invasion of the colonic mucosa;similar to shigellosis.EIEC are closely related to Shigella.
. Acute bloody diarrhea with malaise, headache, high fever, and abdominal pain.Severe disease in poorly nourished children.WBC present in stool.
Escherichia coli (enterohemorrhagic; EHEC)
. 24-72 hours
. Watery, bloody diarrhea
. Bloody diarrhea associated with undercooked hamburgers in fast-food restaurants.
. EHEC produces vero toxin (Shiga-like toxin).Often serotype O157:H7.
. Causes bloody diarrhea, hemorrhagic colitis, and the majority of causes of hemolytic-uremic syndrome.Culture stool for sorbitol-negative E coli and serotype isolates with antisera for O157:H7.
Escherichia coli (enteropathogenic; EPEC)
. Slow in onset .
. Watery diarrhea
. Common cause of diarrhea in neonates in developing countries. Classically, cause of epidemic diarrhea in newborn nurseries with high mortality rates;less common now in developed countries.
. EPEC attach to mucosal epithelial cells and produce cytoskeletal changes;may invade cells.Different from other E coli that are entero-adherent or enteroaggregative and cause diarrhea.
. Insidious onset over 3-6 days with listlessness, poor feeding, and diarrhea.Usually lasts 5-15 days. Dehydration, electrolytic imbalance, and other complications may cause death.Antimicrobial therapy is important.
Vibrio cholerae:
. 24-72 hours
. Watery diarrhea
. Organisms grow in gut and produce toxin.
.Toxin c auses hypersecretion in small intestine.Infective dose > 105organisms.
. Cholera toxin and E coli heat-labile toxin stimulate adenylyl cyclase activity, increasing cAMP concentration in gut, yielding secretion of chloride and water, and reduced reabsorption of sodium. E coli heat-stable toxin activates intestinal guanylyl cyclase and results in hypersecretion.
. Abrupt onset of liquid diarrhea in endemic area.Needs prompt replacement of fluids and electrolytes IV or orally.Stool cultures positive.
Vibrio parahaemolyticus:
. 6-96 hours
. Watery diarrhea
. Organisms grow in seafood and in gut and produce toxin, or invade.
. Toxin causes hypersecretion;vibrios invade epithelium;stools may be bloody.
. Abrupt onset of diarrhea in groups consuming the same food, especially crabs and other seafood.Recovery is usually complete in 1-3 days.Food and stool cultures are positive.
Shigella species (mild cases):
. 24-72 hours
. Dysentery
. Organisms grow in superficial gut epithelium.. . Organisms invade epithelial cells; blood, mucus, and PMNs in stools. Infective dose < 103organisms.
. Abrupt onset of diarrhea;can have blood and pus in stools, cramps, tenesmus, and lethargy.WBC in stool.Stool cultures are positive. Often mild and self-limiting.Restore fluids.

Shigella dysenteriae type 1 (Shiga's bacillus):
. 24-72 hours
. Dysentery, bloody diarrhea
. Causes outbreaks in developing countries.
. Produces cytotoxin and neurotoxin.
. Severe bloody diarrhea in children in developing countries;high fatality rate. Rare in the United States.
Salmonella species:
. 8-48 hours
. Dysentery
. Organisms grow in gut.Do not produce toxin.. . Superficial infection of gut, little invasion.Infective dose > 105organisms.
. Gradual or abrupt onset of diarrhea and low-grade fever.WBC in stool. Stool cultures are positive.No anti-microbials unless systemic dissemination is suspected.Prolonged carriage is frequent.
Clostridium difficile:
. Days to weeks after antibiotic therapy.
. Dysentery
. Antibiotic-associated pseudo-membranous colitis.
. Makes enterotoxin and cytotoxin, which cause diarrhea and epithelial cell necrosis.
. Abrupt onset of bloody diarrhea and fever.Toxin in stool.Patients typically received antibiotics in previous days to weeks.
Campylobacter jejuni:
. 2-10 days
. Dysentery
. Infection via oral route from food, pets.Organisms grow in small intestine.
. Invasion of mucous membrane. Toxin production uncertain.
. Fever, diarrhea;PMNs, and fresh blood in stool, especially in children. Usually self-limited.Special media needed for culture at 42 °C.Patients usually recovery in 5-8 days.
Rotavirus:
. 48-96 hours
. Watery diarrhea
. Virus is the major cause of diarrheal disease in infants and young children worldwide.
. Induces histopathologic changes in intestinal mucosal cells.
. Fever and vomiting usually precede abdominal distress and diarrhea. Death in infants in developing countries follows dehydration and electrolyte imbalance.Typical course is 3-9 days.Diagnosis by immuno-assay detection of rotavirus antigen in stool.
Giardia lamblia:
. 1-2 weeks
. Watery diarrhea
. Most commonly identified intestinal parasite.Frequent pathogen in outbreaks of water-borne diarrhea.
. Complex and poorly understood interaction of parasite with mucosal cells and patient's immune response.
. Diarrhea self-limited in 1-3 weeks; chronic symptoms of intermittent diarrhea, malabsorption, and weight loss may last 6 months.Diagnosis by finding trophozoites or cysts in stool or duodenal contents, or by immuno-assay detection of Giardia antigen in stool.
Entamoeba histolytica:
.Gradual onset 1-3 weeks
.Dysentery
.Highest prevalence in developing countries;10% of world's population may be infected.
.Invades colonic mucosa and lyses cells, including leukocytes.
.Diarrhea, abdominal pain, weight loss, and fever are common.Can give rise to many complications, including fulminant colitis, perforation, and liver abscess.Diagnosis by finding trophozoites or cysts in stool.
Salmonella typhi (S paratyphi A and B; S choleraesuis ):
. 10-14 days
. Enteric fever
. Humans are the only reservoir for S typhi.
. Invade intestinal mucosa and multiply in macrophages in intestinal lymph follicles;enter mesenteric lymph glands to blood and dissemination.
. Insidious onset of malaise, anorexia, myalgias, and headache;high remittent fever;may have constipation or diarrhea.Hepatosplenomegaly in about 50% of patients.Diagnosis by culture of S typhi from blood, stool, or other site.Antibiotic therapy is important.
Yersinia enterocolitica:
. 4-7 days
. Enteric fever
. Fecal-oral transmission.Food-borne.Animals infected..
.Gastroenteritis or mesenteric adenitis.Occasional bacteremia. Toxin produced occasionally.
. Severe abdominal pain, diarrhea, fever;PMNs and blood in stool; polyarthritis, erythema nodosum, especially in children.Keep stool specimen at 4 °C before culture.
Source: Jawetz
Complications of MEASLES:
M: Myocarditis
E: Encephalitis ( most feared)
A: Abortion ( if the woman is pregnant)
S: Stillbirth ( intrauterine death of baby)
L: LRTI ( Pneumonia)
E: Eye damage ( after conjungtivitis in the prodrom phase)
S: SSPE ( subacute sclerosing panencephalitis)
complications of MUMPS:
M: Meningoencephalitis
U: Unilateral Deafness
M: Myocarditis
P: Pancreatitis and remember Parotitis here
S: Scrotum ( epidydimorchiotis inside the scrotum)



not sure,is this wat u r looking for?
[ Follow Ups ] [ Post Followup ] [ Step 1 ]

Posted by Hamidi from IP 68.2.101.4 on January 16, 2004 at 07:22:33:
In Reply to: Lamia posted by usmletaker on January 16, 2004 at 03:51:40:
HIGH YIELD * IMPORTANT* STUFF TO
REVIEW JUST BEFORE EXAM
PAT
HOPHSIOLOGY/SIGN SYMPTOMS
THE EYE
SYMPTOMS:
• SUDDEN LOSS of VISION: Potential Causes
o AMAUROSIS FUGAX: Temporary, monocular, ischemic blindness.
Painless
Caused bu ipsilateral Carotid stenosis or embolization of the retinal artery.
o RETINAL DETACHMENT: Flashing lights, floating halos, and blurry vision before the blindness is indicative of retinal detachment.
o UVEITIS: Inflammation of uveal tract -- iris, ciliary body, and choroid.
Always painful
Associated with multiple diseases: connective tissue diseases, histoplasmosis, sarcoidosis, tuberculosis.
• GRADUAL LOSS of VISION: Potential Causes
o CATARACTS: Opacities of the lens, occurring with age.
o GLAUCOMA: Increased intraocular pressure.
It is the most common reason for loss of vision over age 50.
o MACULAR DEGENERATION: Secondary to Diabetes, and expected to cause visual blindness.
Retinopathy.Diabetic
o OPTIC NERVE COMPRESSION: Caused by an intracranial neoplasm, or pituitary adenoma.
o OPTIC NEUROPATHY (Optic Neuritis): Multiple Sclerosis, and drugs such as Ethambutol, Methanol, can all cause optic neuritis and gradual blindness.
o PRESBYOPIA: Gradual loss of ability of Accommodation for near-vision, occurring with age.
o CORTICAL BLINDNESS: Infarct of the Occipital Lobe can lead to cortical blindness. Patient will have binocular blindness, but will retain the pupillary light reflex which is unaffected.
• DIPLOPIA: Double vision.
o Monocular Diplopia: Should suggest corneal or lens problem.
o Binocular Diplopia: Indicative of cranial nerve palsy or ocular muscle problems, or a brainstem problem.
o Myasthenia Gravis (MG): Diplopia without pain is often the presenting complaint in MG.
• EYE PAIN:
o The cornea is innervated by the Ophthalmic Nerve, CN V1.
o Possible causes of eye pain
CNS problems affecting CN V1: Meningitis, cavernous sinus thrombosis, aneurysms, migraine
Adjacent structures: sinus problems
Eye problems / inflammations: Conjunctivitis, stye, chalazion
o Photophobia: Eye pain upon exposure to light, indicative of
• SCOTOMATA: Specific islands or spots of impaired vision; an impaired visual field.
EYELIDS:
• PTOSIS: Droopy eyelids; failure of lids to open fully.
o Caused by failure of levator palpebrae, innervated by CN III, or failure of Tarsal Muscle, innervated by sympathetics.
o Some causes: Horner's Syndrome, Myasthenia Gravis, Encephalitis
• LID LAG: Evidence of white sclera between the iris and upper lid margin. This is normally not found.
o It is a sign of Grave's Disease
• STYE: Small abscess caused by infection of sebaceous glands of Zeis.
• CHALAZION: Acute inflammation of the meibomian gland.
SCLERA:
• SCLERITIS: Inflammation of the sclera, visible as brown / red infiltrates in sclera on gross examination. Found in autoimmune and collagen vascular diseases, such as SLE, RA.
• BLUE SCLERA: Pathognomonic of Osteogenesis Imperfecta.
o Results from very thin sclera in which the choroid shows through.
• BROWN SCLERA: Found in disorder Alkaptonuria (metabolic disorder)
• YELLOW SCLERA: Found in Jaundice. It should raise the question of liver disease or hemolytic anemia.
EXOPHTHALMOS: Eyes jutting out past eyelids. A sign of Grave's disease, acromegaly, and cavernous sinus thrombosis.
CORNEA:
• KERATOCONJUNCTIVITIS (KERATITIS) SICCA: Found in Sjögren's Syndrome, resulting from autoantibodies against salivary glands resulting in no salivary secretion.
o Classic triad of symptoms with Sjögren's Syndrome:
 Keratitis Sicca (dry eyes)
Xerostomia (dry mouth)
Rheumatoid Arthritis
• INTERSTITIAL KERATITIS: A sign of congenital syphilis.
o Hutchinson's Triad: Triad of interstitial keratitis, deafness, and notched teeth is classical evidence for congenital syphilis.
• ARCUS SENILIS: Gray band of opacity around the cornea.
• KAYSER-FLEISCHER RINGS: Copper in Descemet's Membrane.
o Circular bands of brownish pigment on lateral and medial margins of cornea.
o Found in Wilson's Disease
• PINGUECULAE: Small, yellowish elevations of the conjunctivae, which appear brown in Gaucher's disease. It is caused by hyaline degeneration of conjunctival tissue.
• ANISOCORIA: Unequal pupils, caused by miosis or mydriasis of one pupil.
PUPILS:
• MARCUS GUNN PUPIL: A pupil that dilates (rather than constricts) as light swings toward it.
o It indicates either severe macular disease or optic nerve disease in the affected eye.
• PUPILLARY REFLEXES:
o Absent Direct Reflex: Indicates a problem with the afferent branch (Trigeminal V1) of the reflex.
o Absent Consensual Reflex: Indicates a problem with the efferent branch (CN III, Edinger-Westphal Nucleus) of the affected eye.
• CONVERGENCE: Ability of eyes to focus inward and accommodate for near vision.
o Impaired convergence is seen with Grave's Disease.
• ARGYLL ROBERTSON PUPIL: Indicates a form of CNS Syphilis, Tabes Dorsalis.
o Weak or absent direct pupillary reflex.
o Normal response to accommodation.
o Failure of pupillary dilation with painful stimulation or after atropine administration.
• ADIE'S PUPIL: Similar to Argyll Robertson Pupil.
o Weak or absent direct pupillary reflex.
o Impaired or absent accommodation.
o Eye appears larger than the other eye on inspection.
• MYDRIASIS: Abnormal dilation of pupil, can occur in Diabetes.
• MIOSIS: Abnormal constriction of pupil, seen in Horner's syndrome.
o HORNER'S SYNDROME: Lost sympathetics from the Superior Cervical Plexus. Ptosis, Miosis, Anhydrosis.
NYSTAGMUS: Nystagmus is normal when looking in the periphery for extended times. All other nystagmus is abnormal.
• Causes: Labyrinthitis, MS, Wernicke-Korsakoff, Meniere's Disease
EXTRAOCULAR PALSIES:
• Internal Strabismus: Eye points in, due to denervation of the Abducens, CN VI.
• External Strabismus: Eye points out and down, due to denervation of the Oculomotor, CN III.
o Eye points out because of influence of Abducens (CN VI)
o Eye points down because of influence of Trochlear (CN IV) ------> Superior Oblique muscle.
VISUAL FIELD DEFICITS:
• BITEMPORAL HEMIANOPSIA: Loss of peripheral vision; tunnel vision, occurs with Pituitary Tumor.
• HOMONYMOUS HEMIANOPSIA: Loss of same visual field in both eyes. Occurs due to lesion in Optic Tract.
• QUADRANT HEMIANOPSIA: Lesion in the optic radiations.
FUNDUSCOPIC INSPECTION:
• RED REFLEX: Its absence indicates a cataract.
• VESSELS:
o The veins are normally slightly bigger than the arteries.
o ARTERIO-VENOUS (AV) NICKING: Hypertension narrows the arteries and creates indentations in the veins, where arteries cross the veins.
• MACULA: Dimmer, darker area in fundoscope, containing the fovea.
• OPTIC DISC: Out of which vessels travel. The brightest area of fundoscope.
• RETINOPATHOLOGIES:
o DIABETIC RETINOPATHY: Shows hard exudates on the retina, which are lipid laden. They are dense, well-defined creamy white spots.
Cotton Wool Exudates are poorer defined and can occur with hypertension.
o PAPILLEDEMA: Swelling of retinal vessels, from impaired venous return in the eye ------> venous distension.
causedPapilledema is by increased intracranial pressure.
Causes: Brain tumors, malignant hypertension, hydrocephalus.
As opposed to Pappilitis, there is no loss of vision.
o HYPERTENSION: Changes in retina are graded 1 thru 4. An abnormally high V/A ratio can be found, indicating venous distension.
Stage I: Arteriolar narrowing but no AV-nicking.
Stage II: Focal spasm, AV-nicking.
Stage III: Hemorrhages and exudates
Stage IV: Papilledema, Optic disc edema (due to ischemia) and hemorrhage, which can lead to retinal detachment
.
THE EAR
TINNITUS: Ringing in ear.
VERTIGO:
• Objective Vertigo: The earth is moving around you.
• Subjective Vertigo: You are moving in space.
RINNE TEST: Test for conductive hearing loss by comparing air conduction to bone conduction.
• First hold tuning fork right near auricle, then place it over the Mastoid Process.
• NORMAL: It should sound louder near the auricle, because air conduction should be better than straight bone conduction.
• ABNORMAL: If it sounds louder over the mastoid process instead, that indicates a conductive hearing loss in the middle ear.
WEBER TEST: Place tuning fork over head. It should be heard equally in both ears.
• ONE EAR IS LOUDER: If one ear is louder, than there is either conductive hearing loss in that ear or sensorineural hearing loss in the other ear.
MENIERE'S DISEASE: Triad of tinnitus, vertigo, and sensorineural hearing loss. May see nausea, vomiting, nystagmus.
BENIGN POSITIONAL VERTIGO: Transient attacks of vertigo, induced by movements of the head and trunk. Symptoms can be induced by having the patient merely think about the movements.
NOSE and THROAT
NOSE:
• EPISTAXIS: Bloody nose.
o Transient Epistaxis: May occur with forceful nose-blowing, sneezing, nose-picking, facial trauma.
o Recurrent Epistaxis: Differential diagnosis = hypertension, coagulopathies, renal failure, cirrhosis, hereditary hemorrhagic telangiectasia.
• RHINOPHYMA: Severe acne rosacea found in association with skin hypertrophy and congestion of subcutaneous tissue, around the nose.
THROAT:
• SOAR THROAT: Infection mononucleosis, strep-throat (streptococcal pharyngitis).
• HOARSENESS: Larynigitis, Laryngeal cancer, hypothyroidism, smoking ------> broncho-genic carcinoma.
ABNORMAL TASTE:
• Hypoguesia: Impaired ability to taste. Seen in URI's, glossitis, stomatitis.
• Dysguesia: Unpleasant taste. Differential diagnosis:
o Medications: metronidazole
o Vitamin and mineral deficiencies: zinc depletion
o Chyronic hypercalcemia, hyperparathyroidism.
o Viral hepatitis
TONGUE:
• MACROGLOSSIA: Large tongue can occur with amyloidosis and acromegaly.
• GLOSSITIS: Inflammation on sides, base, and underside of tongue.
o Vitamin and mineral deficincies
o Medications: metronidazole, phenytoin
o Infections: candidiasis
o Pernicious Anemia
o Cytotoxic drugs, radiotherapy.
MOUTH EXAMINATION:
• ORAL ULCERS: Recurrent oral ulcers differential diagnosis:
o Recurrent aphthous ulcers (canker soars): Common, frequently associated with Inflammatory Bowel Disease.
o Infections: HSV-1, Herpes Zoster, tuberculosis, histoplasmosis, syphillis.
o Trauma
o Cytotoxic drugs
o Rare: Erythema Multiforme, Wegener's Granulomatosis, *******-Johnson Syndrome, Reiter's Syndrome
• SYNDROMES:
o PEUTZ-JEGHER'S SYNDROME: Melanin spots on lips are found.
o OLIVER-WEBER-RENDU SYNDROME: Telangiectasia, vascular lesion formed by dilation of small group of blood vessels.
• KOPLIK'S SPOTS: White spots on the buccal mucosa, indicative of the measles.
• STRAWBERRY TONGUE: Erythema of tongue, occurs with scarlet fever.
RESPIRATORY SYSTEM
PULMONARY SYMPTOMS:
• COUGH:
o Possible Causes of Cough:
Pulmonary / Mechanical causes: Asthma, Irritants, aspiration
Infectious: Tuberculosis, Histoplasmosis, Pneumonia
cold airTemperature: Inhaling
Pulmonary Embolism, pulmonary edema.
ear canal irritation.Non-Pulmonary: external
o Details:
morning and isSmoker's Cough usually occurs in productive.
Asthmatic Cough usually is non-productive.
• SPUTUM: It is always abnormal.
o PRODUCTIVE COUGHS are seen in:
Bronchitis,Chronic Smoker's cough
bronchioles.Bronchiectasis: chronically dilated
Large layers uponvolume of sputum, which separates into two or three standing.
Tumors: Bronchoalveolar Carcinoma
Pneumonia,Infections: tuberculosis, Lung Abscess
Will usually see yellow or green sputum.
Pulmonary Edema
• HEMOPTYSIS:
o CAUSES:
Most common: Bronchitis, Bronchogenic Carcinoma, Pneumococcal Pneumonia
More rare infections:
Tuberculosis: Age over 60, crackles, few other symptoms
 Coccidiomycosis, Histoplasmosis
Other Tumors: Weight loss, cigarettes, anorexia
Rare Immune Disorders: Goodpasture's Syndrome, Wegener's Granulomastosis
Pulmonary Embolism:
ventilation,High V/Q Ratio. Lots of poor perfusion. Excessive dead space.
accentuatedFriction rub, P2.
Pleuritic chest pain.
o MASSIVE HEMOPTYSIS = 600 mL in 24 hrs. Usually associated with bronchiectasis, and may be indicative of lung cancer or pulmonary aspergillosis.
• PLEURITIC CHEST PAIN: Chest pain upon breathing.
o PULMONARY CAUSES: Bronchitis, pneumonia, pulmonary embolism, tuberculosis, lung carcinoma.
o NON-PULMONARY CAUSES:
Tietze's Syndrome (Costochondritis): Superficial chest pain with local tenderness.
 Tracheitis presents with retrosternal chest pain, made worse by coughing.
• DYSPNEA: Difficult, labored breathing.
o Differential Diagnosis: A laundry list of possible causes
Pulmonary Disease: COPD, cancer, asthma, chronic or acute bronchitis, emphysema, pneumonia, pulmonary emboli, pneumothorax
 Cystic Fibrosis: Sweat test
Cardiac causes: CHF, Pulmonary edema, PND
 Hematologic: Anemia, CO-Poisoning
Metabolic: Ketoacidosis
Salicylate poisoning
o Symptoms: Dyspnea may be masked by tachypnea (shallow, rapid breathing).
Hyperpnea is not tachypnea -- it is hyperventilation (not labored breathing) usually caused by metabolic acidosis and is unrelated to dyspnea. Distinguish the two with pulmonary function studies.
• ORTHOPNEA: Dyspnea with onset occurring while lying down, and which is immediately corrected upon restoring upright position.
o Differential Diagnosis: Congestive Heart Failure or COPD
Also bilateral paralysis of diaphragms.
• PAROXYSMAL NOCTURNAL DYSPNEA (PND): Dyspnea at night, created by lying down, but which does not immediately improve upon standing up. Patient feels acutely air-hungry and frequently wakes up at night. Night sweats common.
o Differential Diagnosis: Acute Pulmonary Edema secondary to congestive heart failure.
• WHEEZING: High-pitched musical breath sound usually heard on expiration, but can be heard on inspiration.
o CAUSED by air rushing past a constricted airway, constricted by secretions, mucous, edema, neurogenic, a tumor, or an aspirated foreign body.
o Asthma: Wheezing is characteristic of asthma.
Silent Asthma is asthma without wheezing.
o STRIDOR: High-pitched sound occurring with inspiration.
Stridor portends total airway obstruction, a medical emergency.
o Acute Epiglottitis: H. Influenza infection in kids. Stridor is characteristic. Have a chest-tube nearby before examining epiglottis to prevent (or treat imminent) aspiration.
• CYANOSIS:
o Central Cyanosis: Face, lips, tongue. Results from systemic hypoxia due to poor perfusion or ventilation in the lungs.
o Peripheral Cyanosis: May be found in extremities, ears, cheeks, etc. Can be caused by cold-induced vasoconstriction (Raynaud's Phenomenon) or poor circulation (shock, CHF).
o Differential Diagnosis: Pulmonary hypoventilation, COPD
Cardiac causes: Shunt (Tetralogy of Fallot), pulmonary edema (cor pulmonale)
• RHINORRHEA: Nasal discharge
• CORYZA: Nasal discharge caused by a viral upper respiratory tract infection.
FAMILY / SOCIAL HISTORY:
• Previous Tuberculosis infection, PPD test.
• Poor dental hygiene is a risk for a lung abscess.
• Environmental exposures revealed in social history
o Travel
o Psittacosis: Exposure to birds
o Legionellosis: Exposure to water, air-conditioners
• Tobacco use
EXTRAPULMONARY EXAMINATION:
• HALITOSIS: Some possible causes
o Campylobacter Pylori colonization of stomach
o Lung abscess or bronchiectasis (foul-smelling, fecal breath-odor)
o Necrotic lesions of mouth or throat
o Zenker's Diverticulum
• Clubbing of fingernails:
o Congenital Heart Disease: Chronic hypoxia of VSD or Tetralogy, in kids.
o Adults: Systemic hypoxia, lung cancer, bronchiectasis, mesothelioma.
• Chemosis: Conjunctival edema. Hyperthyroidism or obstruction of SVC.
BREATHING:
• Bradypnea: Slow breathing rate
o Insulin Coma
o Drug-induced respiratory depression
• Tachypnea: Rapid, shallow breathing, caused by pleuritic chest pain or diseases that immobilize the lung.
• Hyperpnea: Rapid, deep breathing; hyperventilation.
o Diabetic ketoacidosis compensation (to lower PCO2)
o KUSSMAUL RESPIRATIONS: Central hyperventilation, deep rapid breaths characteristic of Diabetic hyperglycemic coma.
• CHEYNE-STOKES RESPIRATION: Cyclic alternations between apnea and hyperpnea, in which PCO2 fluctuates and is unstable. It occurs when the respiratory centers of the brain become insensitive to changes in CO2
o ASSOCIATED DISEASES: Congestive Heart Failure (CHF), Uremia, Meningitis, Pneumonia.
• BIOT'S BREATHING: Ataxic breathing; unpredictable and irregular respirations.
o Caused by meningitis or other cerebral dysfunction.
• SLEEP APNEA: Obesity, leading to airway obstruction at night and chronic fatigue during the day. Treat with CPAP.
INSPECTION:
• BACK SIDE:
o Buffalo Hump: Fatty deposit overlying C7, characteristic of Cushing's Syndrome
o Barrel Chest: Chronically inflated lungs characteristic of COPD.
o Kyphosis: Excessive anterior curvature of spine, as in hunchback.
Cause: normal or from aging, osteoporosis.
o Scoliosis: Lateral curvature of spine.
May be detected by patient bending forward and noting uneven paravertebral back muscles.
o Lordosis: Excessive posterior curvature of spine. Bowing of lumbar and cervical spines together.
o Gibbus Deformity: Sharp change of angle of spine instead of gradual change. Characteristic of Pott's Disease, or Vertebral Tuberculosis
• FRONT SIDE
o Pectus Carinatum (Pigeon Chest): Sternum placed forward, increased anteroposterior chest measurement.
Found in Marfan's Syndrome, Rickets
o Pectus Excavatum (Funnel-Chest): Lower end of sternum is depressed inward. May also be found in Marfan's Syndrome or Rickets.
o Flail Chest: Caused by multiple fractures ribs. One side of chest moves paradoxically relative to the other side of the chest.
PALPATION: Assess chest excursion by placing fingers at costovertebral angle and having patient inhale.
• Subcutaneous Emphysema: Air in subcutaneous space. Can occur in tracheostomy patients, or people with ARDS who have an endotracheal tube.
• Oliver's Sign: Tracheal tug when patient lifts his chin up.
o Indicative of Aortic Aneurysm, pulling trachea downward by pressure of left main bronchus.
• Tactile Fremitus: Vibration on lungs when you have patient say "ninety-nine"
o Increased fremitus is found with pulmonary consolidation in pneumonia.
o Fremitus cannot be heard below the level of fluid in emphysema or pleural effusion, because the fluid stops the sound from being transmitted further.
PNEUMOTHORAX: Trachea will shift toward opposite side as the pneumothorax. The side of the pneumothorax acquires positive pressure, thus trachea deviates to the other side.
• Tracheal Deviation: Tracheal deviation can be caused by other things than pneumothorax.
o Pleural Effusion, Emphysema may also cause trachea to deviate to the opposite side.
o Atelectasis of lung may cause trachea to deviate toward same side as diseased lung.
• Tension Pneumothorax: Medical emergency in which air enters the pleural cavity and is trapped during expiration
o Intrathoracic pressure builds to values higher than atmospheric pressure, compresses the lung, and may displace the mediastinum and its structures toward the opposite side, with consequent disadvantageous effects on blood flow.
PERCUSSION:
• Resonance: Normal breath sound
• Hyperresonance: Increased resonance over thorax.
o May be found in Emphysema or Pneumothorax.
• Tympany: Percussion of gastric air-bubble or air-filled bowel. Increased resonance.
• Dullness: Decreased resonance, normally found over liver, spleen, and below lung.
o Causes: Emphysema, Pneumonia with consolidation, pleural effusion.
• Flatness: Extreme dullness with few or no ringing tones.
o Pleural effusions, massive pulmonary consolidations with tumor, pneumonia.
AUSCULTATION:
• General Properties:
o Stethoscope Sounds: Use the bell side to listen to breath sounds.
Press lightly: hear low-pitched sounds.
Press hard: hear high pitched sounds.
o Tracheal Breath Sounds: Loud, harsh, high pitched.
o Bronchial Breath Sounds: Loud, high-pitched with air swishing past.
o Bronchovesicular Sounds: Heard near branching of main bronchi, combination of bronchial and vesicular sounds.
o Vesicular Sounds: Soft, low-pitched, airy, swishing, heard below the level of the bronchi.
• CRACKLES (RALES, CREPITATIONS): Soft, short, high-pitched fine sounds.
o CAUSES: Congestive heart failure, bronchitis, pneumonia, pulmonary edema, bronchiectasis.
• RHONCHUS: Snoring sound, characteristic of Asthma. It indicates fluid or mucus in airways.
• WHEEZE: On expiration, squeaking high pitched sound, often audible to unaided ear.
o Caused by air passing by obstructed airway.
o Characteristic of Asthma, but also found in Emphysema, bronchitis.
• PLEURAL FRICTION RUB: Grating sound heard during breathing that stops when the breath is held. Caused by friction of visceral and parietal pleura.
• PULMONARY CONSOLIDATION: Occurs with late-stage lobar pneumonia.
o BRONCHOPHONY: Increased transmission of sound to the lung periphery. Indicative of pulmonary consolidation.
o WHISPERED PECTORILOQUY: Words being understood better when whispered. Also indicative of pulmonary consolidation.
o EGOPHONY: "E" to "A" sound-changes. Indicative of pulmonary consolidation or pleural effusion.
• HAMMAN'S SIGN: Crunching, crackling sound over chest heard synchronous with the heart beat. Occurs with mediastinal emphysema -- air in the mediastinum.
o CAUSES: Can follow thoracic surgery, trauma.
mediastinum.Boerhaave's Syndrome: Esophageal rupture causing air in Rare.
LUNG DISEASES:
• Asthma
• Atelectasis: Bronchial plug ------> decreased lung volume ------> higher lung density ------> lung mass is pulled toward chest wall by negative pressure
o Tracheal deviation toward affected side
o crackles, maybe
o no breath sounds
• Bronchiectasis: Chronic bronchial dilation.
o Caused by frequent pulmonary infections or pneumonia.
o Large amounts of sputum will be expectorated when patient lies prone hanging toward floor.
• Bronchitis: Acute (infectious) or chronic (smoker's)
• Bronchiolitis: Common in infants and children.
• Lung Cancer
• Cor Pulmonale
• Croup: Kids under 3 years old. Rapid, staccato coughs.
o Differential Diagnosis is between inflammatory Croup or Spasmodic Croup.
• Cystic Fibrosis
• Pleural Effusion: Dullness on percussion. Decreased fremitus. Reduced breath sounds.
• Emphysema
• Epiglottitis: In kiddies, don't inspect the pharynx without a chest tube nearby.
• Pneumonia
CARDIAC
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CARDIAC SYMPTOMS, HISTORY:
• CHEST PAIN
o ANGINA (ISCHEMIC CARDIAC PAIN): Squeezing, crushing, strangling, constricting pain in center of chest. Pain may radiate to left shoulder, left arm, right shoulder, jaw.
Stable (Typical) Angina: Angina upon effort, or angina induced by increased blood pressure or increased heart-rate. Angina is relieved by nitroglycerin, although nitroglycerin is not specific to this type of angina.
PatientLevine's Sign: makes fist and holds it up to his chest, to describe the pain.
Second-wind Phenomenon: If patient repeats same activity after the attack, he may not feel the attack again the second time.
pain subsides asWalk-through Angina: The patient continues the activity.
presentation ofAtypical Angina: Atypical typical angina.
rather thanAtypical Symptoms: Sharp or stabbing pain, crushing pain.
for example,Atypical Causes: Angina with change in position, rather than angina strictly upon effort.
Other symptomsAngina Equivalents: that are caused by myocardial ischemia.
dyspnea.Exertional
Nausea, indigestion.
Dizziness, sweating.
Angina: Angina even at rest,Unstable or angina that has recently gotten worse. It is associated with sharply increased risk for myocardial infarct within 4 months.
Angina Decubitus is a rest.specific term for angina occurring at
Variant Angina (Prinzmetal rest but usually not duringAngina): Paradoxic angina occurring during exercise. It is caused by coronary artery spasm. It can be hard to spot because it can coexist with typical angina.
Characteristic ECG findings can help distinguish variant angina from typical angina.
Nitroglycerin will probably coronary arteries.still relieve pain, as it relaxes
Myocardial Infarct: angina lasting longer than 15 minutes, that isTypical presentation = Unstable not relieved by nitroglycerin.
Silent MI's and MI's with atypical occur.presentation do
o NON-ISCHEMIC CARDIAC PAIN:
Mitral Valve asymptomatic, but may present with an intermittent, sharp,Prolapse: Usually sticking pain over left precordium.
Pericarditis: The patient feels relief by breathing and by sitting up and leaning forward.shallow
Dissecting Sudden, severe tearing pain, radiating to the abdomen, neck, or back,Aneurysm: depending on where the aneurysm is going.
o PLEURITIC (PULMONARY) CHEST PAIN: Also see pulmonary study guide.
Pulmonary Embolism: May be asymptomatic, or patient may feel a dull tightness if the embolus is large enough.the
 Paroxysmal Dyspnea is the most common symptom of pulmonary embolism.
 Pleurisy: Pain upon breathing. May be caused by pulmonary embolism, pneumonia, bronchitis, or pleural effusion.
Pulmonary Hypertension: Dyspnea is a more common symptoms than pleuritic pain.
withPneumothorax: Pain may be confused pain of an MI.
producesMediastinal Emphysema: Free air in the mediastinum chest tightness and dyspnea.
sound heardHamman's Sign: Crunching, rasping synchronous with the heartbeat, indicative of mediastinal emphysema.
o GASTROINTESTINAL CHEST PAIN:
chest pain andEsophageal Spasm: Substernal dysphagia.
Esophageal Reflux (GERD): Chest pain relieved by antacids.
Gallstone Colic: Colicky RUQ pain radiating to back and to right shoulder. Occasionally it may be confused with angina.
o CHEST WALL PAIN:
TIETZE'S SYNDROME (COSTOCHONDRITIS): Inflammation of Costochondral joints. Pain is often localized and can be elicited by palpating the sternum over the involved ribs.
HERPES ZOSTER: Pain may precede the appearance of the rash. Both pain and rash follow dermatomal distribution.
DACOSTA'S SYNDROME: Psychogenic pain usually localized to the cardiac apex. May be associated with anxiety.
May also see palpitations, hyperventilation, dyspnea, weakness, depression, or other signs of anxiety.
Vertebral Column Disease: It may occasionally lead to anterior chest pain.
• DYSPNEA: Air hunger or difficulty breathing may be associated with cardiac diseases.
o EXERTIONAL DYSPNEA: Dyspnea on exertion is a common symptom of mild or severe Congestive Heart Failure.
o DYSPNEA at REST:
Pulmonary causes of dyspnea (PE, COPD, pneumothorax) often occur at rest. With cardiac problems, dyspnea usually does not occur at rest, or it is overshadowed by angina.
Anxiety Dyspnea: Difficulty breathing due to anxiety occurs only at rest.
o ORTHOPNEA: Dyspnea occurring with patient in the supine position. Orthopnea is a sign of Congestive Heart Failure that is more severe than that associated with exertional dyspnea.
CAUSE: Supine position increases pulmonary blood flow ------> exacerbate pulmonary congestion and pulmonary edema. The problem is relieved by resuming a more upright position.
Two-Pillow, Three-Pillow Orthopnea: Terms to describe the severity of the orthopnea. Three pillow is worse than two-pillow.
o PAROXYSMAL NOCTURNAL DYSPNEA (PND): Similar to orthopnea, except it has sudden onset and occurs only after the patient has been lying down at rest for at least an hour.
Unlike orthopnea, It is not relieved immediately by sitting up.
Patient is usually able to return to sleep, eventually.
o PULMONARY EDEMA: Pulmonary edema is usually a manifestation of left-ventricular heart failure. Peripheral edema associated with CHF is a manifestation of right-sided heart failure (Cor Pulmonale).
 SYMPTOMS: Severe symptoms. Extreme anxiety, dyspnea, air hunger, cold sweats, fear of impending death.
SIGNS: Pink, frothy sputum, and bubbly breath sounds.
o VALVULAR HEART DISEASE: Mitral Stenosis is associated with dyspnea.
o CONGENITAL HEART DISEASES:
Tetralogy of Fallot: Exertional dyspnea is common.
Ventricular Septal Defect: Tachypnea and sweating. Late cyanosis.
o CARDIAC -vs- PULMONARY DYSPNEA:
o OTHER CAUSES OF SHORTNESS OF BREATH:
Kussmaul Respiration: Intense hyperventilation (respiratory alkalosis) occurring with Diabetic Ketoacidosis, as a compensatory mechanism to relieve the metabolic acidosis.
• PALPITATIONS: An unpleasant awareness of one's own heart-beat. Often described as fluttering, or skipping a beat.
o Paroxysmal Atrial Tachycardia: May cause palpitations with an instantaneous onset.
o Premature Ventricular Contractions (PVC's): May be experienced as palpitations or a skipped beat. The premature contraction is followed by a compensatory pause, to allow for ventricular filling.
• FATIGUE: Non-specific finding often found with heart disease.
o FATIGUE CAUSED BY HEART DISEASE: It usually occurs later in the day or in the evening. Fatigue early in the morning is usually not associated with heart disease, unless the patient was aroused from REM sleep.
The heart disease gets worse, as the patient experiences onset of fatigue earlier in the day.
o OTHER CAUSES OF FATIGUE: Lots. Chronic illness of many types, anemia, psychological causes.
• SYNCOPE: Fainting, transient loss of consciousness.
o VASOVAGAL EVENTS: Most common cause of syncope, it is caused by excessive stimulation of the Vagus nerve ------> excessive bradycardia and reduced blood-flow to the brain.
Anxiety: It is usually associated with acute anxiety or excessive emotion. The Vagal hyperactivity is thought to be a hypersensitive response to sympathetic outflow.
o CARDIOVASCULAR CAUSES:
Arrhythmias:
SYNDROME:STOKES-ADAMS Syncope caused by reduced cardiac output secondary to an arrhythmia.
Both output, leading tosevere tachycardia and bradycardia can reduce cardiac syncope. Severe tachycardia reduces cardiac output by reducing ventricular filling time.
Cardiac Outflow Tract Obstruction:
 Aortic Stenosis may lead to syncope.
cause outflowMyxomas, benign myocardial tumors, may obstruction and lead to syncope.
associated withTetralogy of Fallot is fainting attacks.
Myocardial Ischemia
Syncope:Carotid Sinus Hypersensitivity of the Carotid Sinus in elderly men is common cause of syncope.
Impaired Vasomotor Reflexes: Impairment of Baroreceptors. Syncope is associated with orthostatic hypotension.
Decreased Blood Volume
o FLUID REMOVAL:
Micturition Syncope: Syncope occurring with micturition but at no other time. Associated with removal of fluid from the body.
o POST-TUSSIVE SYNCOPE: Syncope after a bout of coughing, or after the Valsalva maneuver, may occur in patients with COPD.
• HEMOPTYSIS: Mitral Valve Stenosis is a cardiac disease that may cause hemoptysis. Mitral Stenosis ------> pulmonary venous congestion ------> may lead to hemoptysis.
• EDEMA:
o Pitting Edema is a common sign of Congestive Heart Failure.
o Presacral Edema may be found in bed-ridden patients, and may lead to decubitus ulcers.
o Anasarca: Severe generalized edema and ascites, as seen in severe CHF, liver cirrhosis, or nephrotic syndrome.
o Lymphedema may be caused Filariasis or a tumor obstructing a lymphatic vessel.
• CYANOSIS: Presence of excessive deoxygenated hemoglobin in the blood. It becomes visible when the concentration of deoxygenated hemoglobin exceeds 5 g / dL -- a higher rate of desaturation than is found in the venous blood of normal people.
o Central Cyanosis: Visible in the lips, face, conjunctivae, tongue. It is caused by primary systemic hypoxia due to impaired oxygenation of blood. EXAMPLES:
 Tetralogy of Fallot or the late stages of other congenital heart defects
 Venoarterial shunt
o Peripheral Cyanosis (Acrocyanosis): Visible in the fingers and toes, earlobes, nose. It is caused by localized hypoxia due to poor circulation, reduced blood-flow, CHF, shock.
GENERAL PHYSICAL EXAM: Many congenital disorders are associated with various heart defects. See Table 4-5, page 150 for complete list. Also see Table of Physical Findings for a complete list of physical findings.
• THE FACE:
• THE EYES:
• THE MOUTH:
• THE SKIN:
o Rheumatic Fever: Characteristically you will see Erythema Marginatum and Subcutaneous Nodules.
• THE THORAX:
• THE ABDOMEN:
• THE EXTREMITIES:
o Clubbing of fingers and toes is a classic finding of Cyanosis. May also be seen with infective endocarditis or other conditions.
BLOOD PRESSURE:
• PALPATION:
• AUSCULTATION (Korotkoff Sounds):
o Phase 1: Clear tapping sounds representing systolic pressure.
o Phase 2: Softer tones
o Phase 3: Louder once again.
o Phase 4: Muffled Tones.
o Phase 5: Tones cease. Diastolic Pressure. Diastolic pressure may actually be higher than estimated by auscultation.
• INTERPRETATION:
o Auscultatory Gap: Period of silence that may occur between Phase 1 and Phase 2. The beginning and end of the Auscultatory Gap may be mistaken for Diastolic or Systolic blood pressure, respectively.
CAUSES: Venous distension or severe Aortic Stenosis.
o Orthostatic Hypotension: Upon standing, normal decrease in systolic blood pressure is 5-15 mm Hg; anything more is Orthostatic Hypotension. Diastolic pressure normally remains constant or increases slightly.
o Obese Patient: Use a large cuff.
o Hypertension:
Coarctation of the Aorta will result in a systolic pressure that is quite high in the arm, but much lower in the leg.
JUGULAR VENOUS PULSES:
• Central Venous Pressure (CVP): Use the right Internal Jugular to estimate CVP because it is straighter.
o MEASUREMENT:
With patient sitting up, clavicles are 10 cm above right atrium, thus CVP = jugular venous distension above clavicles + 10 cm.
With patient elevated 30, sternal Angle of Louis is normally about 5 cm above right atrium, and Internal Jugular should be visible about 3 cm directly vertical (use a ruler), above the sternal Angle of Louis.
o RESPIRATION: CVP should decrease with inspiration and increase with expiration.
KUSSMAUL'S SIGN: Paradoxical change in CVP during inspiration (and increase instead of decrease), caused by a restriction in filling of the right ventricle, such as pericardial effusion.
HEPATOJUGULAR REFLEX: Normally, it should only show a transient increase in CVP. With Cor Pulmonale, the increased CVP is maintained throughout.
• JUGULAR VENOUS WAVES:
o a-Wave: Right atrial contraction, corresponding to peak filling of the jugular vein.
A large a-wave is characteristic of pulmonary hypertension.
A giant a-wave is characteristic of a total heart block.
No a-wave is characteristic of atrial fibrillation.
o x-Descent: Follows a-wave, as atrium relaxes. Decreased jugular vein filling.
First heart sound is heard during the
o c-Wave: Occurs with contraction of the ventricles. Usually not visible at bedside.
 CAROTID PULSE occurs during this, which is right after the a-wave and also during the x-descent.
o v-Wave: Passive phase of atrial filling during ventricular systole.
o y-Descent: Brief decreases in jugular vein pressure after the Tricuspid valve opens (beginning of Systole).
ARTERIAL PULSES:
• Normal Pulses: Radial, Brachial, Carotid, Femoral, Popliteal, Posterior Tibial, Dorsalis Pedis.
• Rhythm Abnormalities:
o Sinus Arrhythmia: The pulse accelerates with inspiration.
o Premature Contractions:
Atrial Premature Contractions (APC): Normally do not disturb the cycle.
 Ventricular Premature Contractions (PVC): They are followed by a compensatory pause, and a new rhythm is established.
o Pulse Deficit: With Atrial Fibrillation + Tachycardia, the radial pulse may not be equal to the cardiac apical pulse. Two rapid beats in a row may not allow sufficient ventricular filling for the systole to be transmitted to the periphery. The lapse between apical and radial pulse is the pulse deficit.
o Bigeminal Pulse: Two consecutive heartbeats closely coupled, with subsequent pause before the next beat.
• Volume Abnormalities:
o Hyperkinetic Pulse: Quick up stroke and full volume, seen with hypertension, anxiety.
o Corrigan's Pulse: A brisk pulse with large volume, or "Collapsing" pulse, seen in Aortic Regurgitation.
Duroziez Murmur should be heard across the femoral artery simultaneous with the collapsing pulse.
o Quincke's Pulse: Visible capillary pulsations in the nail-bed. Another sign of Aortic Insufficiency.
o Pulsus Bisferiens: Bifid pulse. Two distinct impulses with each heartbeat. Seen in:
Aortic Regurgitation
Hypertrophic Cardiomyopathy.
o Pulsus Alterans: One pulse feels large, the next one small. Due to decreased cardiac contractility and carries a poor prognosis.
o Pulsus Paradoxus: Weakening of the pulse with inspiration more than normal.
Systolic pressure normally decreases by less than 10 mm Hg. Paradoxical pulse occurs when decrease is greater than 10 mm Hg.
Indicative of constrictive cardiac disease: Pericardial effusion, constrictive pericarditis.
• Grading Pulses: Scale of 0 to 4
o Scale:
0 = no pulse
3 = normal pulse
4 = bounding pulse
o Intermittent Claudication: Temporary weakening of lower extremities due to arterial insufficiency.
o Leriche's Syndrome: Atherosclerosis of abdominal Aorta, reducing flow to lower extremities and leading to impotence.
o Takayasu's Disease: Pulseless disease -- no pulse in arms, due to progressive obliterative arteritis.
THE PRECORDIUM:
• Aortic Valve: Second right interspace (upper right -- on the opposite side because the Aorta bends over toward the right side).
• Pulmonic Valve: Second left interspace (upper left -- on opposite side because the Pulmonary arteries bifurcate behind the Aorta.)
• Tricuspid Valve: Lower parasternum (centrally located)
• Mitral Valve: Apex
• Erb's Point: Place to listen to right-sided pathologies, at the third left interspace.
PALPATION / PERCUSSION:
• Point of Maximal Impulse (PMI): Should be at the apex.
o If it is located more centrally and down, that is indicative of COPD due to barrel chest and constantly inflated lungs, displacing the heart centrally (right-sided shift).
o Right Ventricular Hypertrophy can shift the PMI posteriorly, as the right-ventricular mass masks the left-ventricular PMI, making it difficult to palpate.
• Shock: An impulse of a heart sound transmitted to the examining hand.
• Heave / Lift: Forceful, systolic thrust that moves the palpating hand up a little.
• Thrill: A palpable murmur. A palpable vibration that by definition is accompanied by an audible murmur.
STETHOSCOPE: Get a good one. The shorter the tube, the better. Double-barreled tubes are better than single-barrel.
• DIAPHRAGM: High-pitched (primarily systolic) sounds, and press firmly.
• BELL: Low-pitched (primarily diastolic) sounds, and press lightly.
HEART SOUNDS:
• NORMAL HEART SOUNDS: Normal order of events = M1, T1, A2, P2
o S1: Closing of Mitral (M1) and Tricuspid (T1) valves.
theS1 is loudest near apex.
exercise,LOUD S1: Occurs with higher cardiac output, such as fever, thyrotoxicosis.
contraction, CHF,SOFT S1: Occurs with impaired myocardial mitral regurgitation.
o S2: Closing of Aortic (A2) and Pulmonic (P2) valves.
due to higherSPLITTING: Normally, Aortic closes before Pulmonic, pressure in Aorta.
increases theWide Splitting: INSPIRATION normally interval between A2 and P2, which is attributed to increased pulmonary blood flow, and decreased pulmonary vascular resistance.
INTENSITY: A loud S2 usually is attributed to the Aortic valve (A2), and often occurs with hypertension.
• THIRD HEART SOUND (S3): Considered normal in infants and children.
o CAUSE: Slowing of velocity of blood, or vibrations from turbulent blood-flow during ventricular filling, especially at the beginning.
o POSITION: Patient should be in left lateral decubitus position for maximal auscultation of S3.
o Gallop: S3 sound plus tachycardia, giving the sound of a galloping horse.
o ETIOLOGIES: Cardiac disease which causes increased ventricular volume, such as:
Mitral and Tricuspid Regurgitation
Congestive Heart Failure
o Opening Snap (OS): Brief click heard when mitral valve opens at the beginning of diastole (around S3). Associated with Mitral Stenosis
o Kentucky: S1, S2, S3 together have this approximate rhythm.
• FOURTH HEART SOUND (S4): Always pathological.
o CAUSE: Contraction of the atria at the end of diastole ------> turbulent blood flow which is audible as S4.
Decreased ventricular compliance is the most common etiology of S4 sound.
o ETIOLOGIES:
hypertension,Left-Sided: aortic stenosis, angina pectoris.
hypertension,Right-Sided: pulmonary pulmonic stenosis.
o Tennessee: S4, S1, S2 sounds together have this approximate rhythm.
• SUMMATION GALLOP: S3 + S4 + Tachycardia, as seen in chronic hypertension leading to CHF.
• SYSTOLIC SOUNDS and CLICKS:
o Ejection Sounds: Can be innocent, or caused by abnormal Aortic valves or a dilated Aorta.
o Mitral Valve Prolapse (MVP): Will result in a mid or late systolic click, as the mitral leaflet protrudes back into the atrium during ventricular contraction.
• NON-VALVULAR SOUNDS:
o Precordial Knock: Results from constrictive pericarditis and can be heard over the internal jugular at the base of the neck.
CAUSE: thickened pericardium limits expansion of ventricles during rapid filling phase of diastole, resulting in backup of blood.
o Pericardial Friction Rub: Caused by pericardial effusion, and can be heard over a limited area in left parasternal space.
More extensive pericardial effusion may eliminate the rub, as the pericardium gets completely separated from the epicardium.,
HEART MURMURS: General Properties
• Timing
• Location
• Configuration: Crescendo / Decrescendo
• Intensity:
o Grade I: Barely audible by an expert.
o Grade III: Moderately loud with palpable thrill.
o Grade VI: So loud it can be heard without the stethoscope making complete contact with the skin.
• Frequency
• Quality
• TRANSMISSION: Where does the sound transmit to? This is characteristic for certain pathologies and can be diagnostic.
SYSTOLIC MURMURS: Cardiac disorders and their associated findings.
• AORTIC STENOSIS: Diamond-shaped systolic ejection murmur.
o Location: Over the Aortic valve, at the second right intercostal space.
o Transmission: to the carotids bilaterally.
• PULMONIC STENOSIS: Diamond-shaped systolic ejection murmur.
o Location: Second or third left parasternal interspace.
• HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY: Diamond-shaped midsystolic murmur.
o PATHOLOGY of DISEASE:
Septal region of left ventricle is thickened ------> Left Ventricular Hypertrophy.
ofDuring systole, anterior leaflet mitral valve is abnormal.
duringImpaired relaxation of the left ventricle diastole.
o SOUND: Similar to Aortic Stenosis, but it does not transmit to the Carotids.
o EXAMINATION TECHNIQUES: The murmur becomes louder as left ventricular volume is reduced. This is paradoxic behavior as compared to most murmurs
Handgrip ------> increase in left ventricular volume ------> decreased murmur. This occurs because the septal obstruction is relatively less significant.
the late-stage ofValsalva Maneuver: Murmur becomes louder in the Valsalva Maneuver, rather than softer as in most murmurs.
Murmur becomes behavior.quieter when the patient squats -- also paradoxical
• MITRAL VALVE PROLAPSE: If it occurs with mitral regurgitation, a late systolic murmur will be heard after the midsystolic click.
o Examination Technique: Like cardiomyopathy, reduce left ventricular volume ------> louder murmur (and an earlier click).
• HOLOSYSTOLIC MURMURS: They indicate that blood is flowing down a pressure gradient when it shouldn't be, as in insufficiencies.
o CAUSES: Mitral regurgitation, Tricuspid regurgitation, Ventricular septal defect.
• MITRAL REGURGITATION: The most common cause for Holosystolic Murmur.
o Causes: Anything that makes the mitral valve incompetent, or mitral leaflets damage:
Vegetations
dysfunctionpapillary muscle
shortened chordae tendineae
o Concurrent features of Mitral Regurgitation:
Left Ventricular Hypertrophy ------> Shifted PMI
gallopS3
• VENTRICULAR SEPTAL DEFECT: Best heard at lower left parasternal border (Erb's point)
• TRICUSPID REGURGITATION: Holosystolic murmur
o May result from IV drug use ------> endocarditis, or Rheumatic valvular disease.
• OTHER MURMURS:
o STRAIGHT BACK SYNDROME: Systolic ejection murmur.
o Innocent Murmurs
o Venous Hum: Heard above the clavicles in normal individuals.
o Mammary Souffle: High pitched continuous flow heard over base of heart in pregnancy.
DIASTOLIC MURMURS: Cardiac disorders and associated findings.
• AORTIC INSUFFICIENCY: Blowing or Decrescendo diastolic murmur.
o Many causes: infectious, rheumatic, dissecting aortic aneurysm.
o CHF makes the murmur softer.
o Associated findings:
Corrigan's Water Hammer Pulse: Collapsing pulse, with little up stroke or downstroke.
de Musset's Sign: to heartbeat.and fro head movement synchronous with the
Quincke's Pulse: capillary pulsation of fingertips.
Duroziez's Sign: Femoral artery systolic and diastolic bruits.
Blood pressure in the legs beingHill's Sign: higher than it is in the arms.
difference = 20 mm HgNormal
Aortic Insufficiency = 40-60 mm Hg.
• PULMONIC INSUFFICIENCY: Decrescendo diastolic murmur.
o GRAHAM STEELL'S MURMUR: Pulmonary Hypertension as the cause of pulmonic hypertension (due to dilation of pulmonic leaflets).
Prominent murmur.a-wave is found concurrent with the
Paradoxical Splitting also occurs.
• MITRAL STENOSIS: Middiastolic murmur
o CAUSE: Chronic Rheumatic Heart Disease is most common cause.
• TRICUSPID STENOSIS: Middiastolic murmur
• RHEUMATIC FEVER:
o Carey Coombs Murmur is the characteristic murmur occurring during the acute stage of Rheumatic Fever. It is a blubbering middiastolic murmur heard at apex. The murmur disappears after acute disease has subsided.
o Middiastolic murmur of mitral stenosis might then remain as a sequel.
• PATENT DUCTUS ARTERIOSUS:
o Continuous Murmurs: Murmurs occurring throughout the cardiac cycle, caused by blood continually flowing from higher pressure to lower pressure. Can be heard with Patent Ductus Arteriosus.
TECHNIQUES FOR ENHANCING AUSCULTATION:
• INSPIRATION: Normally you should see splitting of S2 with inspiration. P2 occurs later and moves further away from A2.
o Paradoxic Splitting: S2 splitting is decreased instead of increased with inspiration.
Left Bundle-Branch Block causes condition, under normal circumstances, A2 alreadyparadoxic splitting. In this occurs after P2 (instead of before), because of the left-sided heart-block. Thus, with inspiration, P2 actually moves closer to A2 and you see paradoxic splitting.
• EXHALATION: Can be used to evaluate right-sided heart murmurs.
o The intensity of most right-sided heart murmurs will decrease with exhalation, while left-sided murmurs remain unchanged.
• MÜLLER'S MANEUVER: Have patient pinch the nostrils shut with one hand and suck hard on a finger with the other.
o MECHANISM: This creates prolonged negative intrathoracic pressure. That shift blood from the systemic to the pulmonary circulation, which amplifies and prolongs the murmurs found with inspiration. It makes it easier to hear inspiratory murmurs.
• VALSALVA MANEUVER: Have patient hold breath and bear down for 20 seconds. Can be used to evaluate left-sided heart murmurs.
o MECHANISM: This creates a prolonged positive intrathoracic pressure. That shifts blood from the pulmonary to the systemic circulation -- the exact opposite as Müller's Maneuver.
o TIME COURSE: Most left-side murmurs first grow louder, and then grow softer.
First 10-15 seconds: Initially, cardiac output increases, and the intensity of left-sided murmurs increase accordingly.
 After 10-15 seconds: Cardiac then begins to decrease, as venous return from the lungs decreases. Most left-sided murmurs then grow softer again.
o EXCEPTIONS: Two conditions show different characteristics than above:
 Hypertrophic Obstructive Cardiomyopathy: Left-ventricular hypertrophy and resultant cardiomyopathy, due to hypertension. With this condition, the late-phase of the murmur actually increases or may be heard for the first time.
thanMitral Valve Prolapse: Late-phase murmur usually increases rather decreases, and may be heard for the first time.
• STANDING to SQUATTING: Have patient squat down and breathe normally, and then stand. Squatting increases stroke volume, and standing decreases it again.
o Hypertrophic Obstructive Cardiomyopathy: As patient squats, this murmur should be decreased.
o Mitral Regurgitation: Occasionally decreases.
• SQUATTING to STANDING:
o Hypertrophic Obstructive Cardiomyopathy: As the patient stands back, this murmur should increase.
o Mitral Regurgitation: Occasionally increases.
• PASSIVE LEG ELEVATION:
o Hypertrophic Obstructive Cardiomyopathy: Murmur should decrease, as left ventricular volume increases and the left ventricle enlarges.
• ISOMETRIC HANDGRIP: Using a handgrip for 1 minutes increases peripheral vascular resistance.
o DECREASED INTENSITY: Hypertrophic Obstructive Cardiomyopathy, Aortic Stenosis (about 30% of cases).
o INCREASED INTENSITY: Ventricular Septal Defect, Aortic Regurgitation, Mitral Regurgitation.
o CONTRAINDICATIONS: Do not do this test on people with myocardial ischemia, ventricular arrhythmias, or unstable angina!
• TRANSIENT ARTERIAL OCCLUSION: Place blood pressure cuff on both arms and occlude blood-flow for 20 seconds.
o INCREASED INTENSITY: Mitral Regurgitation, Ventricular Septal Defect. Most other murmurs are unaffected.
• AMYL NITRATE: Have patient inhale amyl nitrate ------> decreased TPR. Auscultate sounds 15-30 seconds later.
o DECREASED INTENSITY: Mitral Regurgitation, Ventricular Septal Defect.
o INCREASED INTENSITY: Right-sided murmurs, aortic stenosis, hypertrophic obstructive cardiomyopathy.
ABDOMEN
HISTORY TAKING:
• ABDOMINAL PAIN
o CHARACTER OF PAIN
PUD: Burning back.or gnawing pain, epigastric, may radiate to the
Precipitated by long periods of no food or skipping meals.
feel pain early in morning,Often which is relieved by intake of food or antacids.
GERD: Burning, epigastric or retrosternum.xiphisternal. Radiates to the
Precipitated by over-eating, reclined position.bending over, or being in a
o LOCATION OF PAIN:
o RADIATION OF PAIN
Colic often radiates to the groin.Renal
Gallbladder scapula, or right shoulder.pain often radiates to back,
Splenic pain often radiates to back.
Pancreatic pain often radiates to back.
o FACTORS PRECIPITATING AND RELIEVING THE PAIN
o PATIENT ASSESSMENT OF PAIN SEVERITY: Scale of 0 to 10.
o COMPARISON WITH OTHER TYPES OF PAIN
• ANOREXIA:
o Differential diagnosis:
Neoplasms
Chronic Renal Failure
Psychiatric: nervosa, depressionAnorexia
Infections: Hepatitis, many chronic infections.
o Polyphagia: Seen in hyperthyroidism, malabsorption syndromes, especially pancreatic insufficiency.
• NAUSEA AND VOMITING:
o Delayed Gastric Emptying: It is a common cause of nausea. Possible causes of delayed gastric emptying:
Pyloric Outlet Obstruction: Ulcers, pyloric stenosis, Disease, neoplasms.Crohn's
Neuromuscular: Scleroderma, vagotomy, diseases (MS), Poliodemyelinating
Metabolic: Diabetic gastroparesis, hypothyroidism.
Drugs: Anti-cholinergics, ganglionic blockers, opiates
 Psychiatric: Anorexia Nervosa
o Projectile Vomiting: Special vomiting that can signify increased intracranial pressure (ICP).
o Regurgitation: Vomiting without nasea. Causes:
Overeating.
Achalasia.
Delayed gastric emptying
Esophageal rings and webs.
• DYSPHAGIA:
o Odnyophagia: Painful difficulty swallowing.
o Common Causes:
CVA, stroke
 Parkinson's
Reflux Esophagitis
Esophageal rings and webs
 Achalasia
Esophageal Tumors
Candidiasis
• DIARRHEA: Excretion of more than 300 g of stool per day.
o Acute Diarrhea:
Infectious Gastroenteritis: Shigella, Salmonella, Campylobacter, invasive E. Coli
 Symptom Cluster: Fever, myalgia, chills, nausea, vomiting, diarrhea, cramping abdominal pain.
Lactose Intolerance
Antibiotic-associated (loss of normal flora)
Inflammatory bowel
o Stool Incontinence: Recurrent defecation in pants is not diarrhea and has a very limited differential diagnosis, all relating to anal sphincter dysfunction:
Diabetes Mellitus
Previous rectal or perirectal surgery.
aErrant episiotomy from traumatic childbirth.
o Chronic diarrhea:
Dietary habits (coffee)
 Parasitic infection: giardiasis, amebiasis.
Inflammatory bowel disease
• CONSTIPATION: 2 bowel movements per week is normal in some people.
o Acute Constipation: Recent change in bowel habits. Causes:
Drugs: anticholinergics, psycho-active drugs, many others.
Hypothyroidism
 Hyperparathyroidism
Decreased food intake, decreased fluid intake.
 Chronic debilitating disease (post-stroke).
o Hirschsprung's Disease: Aganglionic Megacolon
Lifelong constipation
Ocassional passage of enormous stools
Absence or marked dimunition of ganglion cells in rectal tissue
Marked colonic distension.
o Idiopathic Chronic Constipation may be caused by a defect in the pelvis floor in women, in which they contract the anal sphincter, rather than relax it, when defecating.
• HEMATEMESIS
o Possible Causes:
PUD or erosive Gastritis
Mallory-Weiss Tear of esophagus
Esophageal varices, portal hypertension
• HEMATOCHEZIA and MELENA
o HEMATOCHEZIA: Occult blood in stool.
Possible Causes
 Colorectal carcinoma
Infectious enteritis: Shigella, Salmonella, Campylobacter, invasive E. Coli may all cause hematochezia.
 Hemorrhoids
Chronic diverticular disease
o MELENA: Passage of black or very dark stool, reflecting heme breakdown products in stool.
Other causes