Symptoms and Signs – Differential Diagnosis of Priapism
Priapism is a urologic emergency characterized by a prolonged, painful erection that is not associated with sexual arousal. This uncommon phenomenon may commence during sleep and resemble a typical erection, although it can persist for several hours or days. It is typically accompanied by a strong, persistent, dull ache in the penis. Notwithstanding the discomfort, the patient may feel too ashamed to pursue medical assistance and might attempt to attain detumescence through ongoing sexual engagement. Priapism transpires when the veins of the corpora cavernosa inadequately drain, leading to sustained engorgement of the tissues. In the absence of timely intervention, penile ischemia and thrombosis may develop. In approximately fifty percent of cases, priapism is idiopathic and arises without discernible underlying conditions. Secondary priapism may arise from a hematological condition, tumor, trauma, or the administration of specific pharmaceuticals.

URGENT INTERVENTIONS
In cases of priapism, apply an ice pack to the penis, administer an anesthetic, and install an indwelling urinary catheter to alleviate urine retention. Interventions to extract blood from the corpora cavernosa, including irrigation and surgical procedures, may be necessary. Medical History and Physical Assessment Inquire about the onset of priapism if the patient's state allows. Is it ongoing or sporadic? Has he experienced a prolonged erection previously? What actions did he take to alleviate it? What was the duration of his detumescence? Does he experience pain or soreness while urination? Has he observed alterations in sexual function?

Examine the patient's medical history. If he reports sickle cell anemia, investigate conditions that may trigger a crisis, including dehydration and infection. Inquire whether he has lately experienced genital injuries and gather a comprehensive drug history. Inquire whether he has undergone penile injections or had items inserted into his penis. Assess the patient's penis, observing its coloration and temperature. Assess for sensory loss and indications of infection, including erythema or exudate. Ultimately, assess his vital signs, with particular emphasis on detecting a fever.

Etiological Factors
Penile carcinoma. Neoplasms that apply pressure on the corpora cavernosa may induce priapism. The initial indication typically manifests as a painless ulcerative lesion or an expanding warty growth on the glans or foreskin, maybe accompanied by localized discomfort, a malodorous discharge from the prepuce, a firm mass adjacent to the glans, and lymphadenopathy. Subsequent results encompass hemorrhage, dysuria, urinary retention, and bladder distension. Phimosis and inadequate cleanliness are associated with the onset of penile cancer.

Sickle cell anemia
Painful priapism may develop unexpectedly in individuals with sickle cell anemia, typically upon awakening. The patient may possess a history of priapism, hindered growth and development, and heightened vulnerability to infections. Associated observations encompass tachycardia, pallor, asthenia, hepatomegaly, dyspnea, arthralgia, bone pain, thoracic discomfort, weariness, cardiac murmurs, leg ulcers, and maybe jaundice and significant hematuria. During a sickle cell crisis, the manifestations of sickle cell anemia may intensify, and additional symptoms, such as stomach pain and a low-grade fever, may emerge.

Spinal cord damage
Patients with spinal cord injury may be oblivious to the onset of priapism. Associated consequences are contingent upon the severity and degree of injury and may encompass autonomic manifestations such as bradycardia.

Cerebrovascular accident
A stroke can induce priapism; however, sensory impairment and aphasia may hinder the patient's ability to recognize or articulate it. Additional results are contingent upon the stroke's location and severity, and may encompass contralateral hemiplegia, seizures, headache, dysarthria, dysphagia, ataxia, apraxia, and agnosia. Visual impairments encompass homonymous hemianopsia, blurriness, reduced acuity, and diplopia. Urinary retention or incontinence, fecal incontinence, constipation, and emesis may also manifest.

Alternative Causes
Pharmaceutical substances.
Priapism may occur due to the administration of a phenothiazine, thioridazine, trazodone, an androgenic steroid, an anticoagulant, or an antihypertensive agent. It may also arise following an intracorporeal injection of papaverine, a prevalent remedy for impotence.

Prepare the patient for blood testing to ascertain the etiology of priapism. If he necessitates surgery, maintain his penis in a flaccid state postoperatively by utilizing a pressure dressing. Inspect the glans for indications of vascular impairment, including coolness or pallor, at least every 30 minutes.

Patient Consultation
Elucidate the fundamental condition and its corresponding treatment. Ensure that the patient with sickle cell anemia is informed to report instances of priapism.

In neonates, priapism may arise from hypoxia but typically resolves with oxygen therapy. Priapism is more prevalent in children with sickle cell disease than to adults with the condition.

Symptoms and Signs – Differential Diagnosis of Polyphagia
Polyphagia denotes voracious or excessive consumption of food. This prevalent symptom may be either persistent or intermittent, primarily arising from endocrine and psychiatric diseases, as well as the use of specific medications. Polyphagia may lead to weight increase, contingent upon the underlying cause.

Medical History and Physical Assessment
Commence your assessment by inquiring about the patient's dietary and fluid intake over the preceding 24 hours. If he readily remembers this information, inquire about his intake over the preceding two days to gain a comprehensive understanding of his food habits. Record the frequency of meals together with the quantity and varieties of food consumed. Determine whether the patient's dietary habits have lately altered. Has he consistently possessed a substantial appetite? Does his binging fluctuate with episodes of anorexia? Inquire about factors that may precipitate overeating, like stress, depression, or menstruation. Does the patient genuinely experience hunger, or does he consume food just due to its availability? Does he have vomiting or headaches subsequent to overeating? Investigate associated indications and symptoms. Has the patient had recent weight increase or loss? Is he experiencing fatigue, anxiety, or excitement? Has he encountered heat intolerance, dizziness, palpitations, diarrhea, or heightened thirst or urination? Acquire a comprehensive pharmacological history, encompassing the utilization of laxatives or enemas. Weigh the patient during the physical checkup. Inform him with his present weight and observe for any signs of disbelief or rage.

Examine the skin for signs of dryness or inadequate turgor. Examine the thyroid for hypertrophy.

Etiological Factors
Apprehension
Polyphagia may arise from mild to moderate worry or mental distress. Mild anxiety generally manifests as restlessness, insomnia, impatience, persistent questioning, and an incessant need for attention and reassurance. Moderate anxiety may also result in selective inattention and concentration difficulties. Additional manifestations of anxiety may encompass muscle tension, sweating, gastrointestinal trouble, palpitations, tachycardia, and disruption in urine and sexual functions.

Bulimia nervosa
Bulimia, predominantly observed in women aged 18 to 29, is characterized by episodes of polyphagia interspersed by self-induced vomiting, fasting, or diarrhea. The patient generally exhibits a weight below the normative range, however harbors an intense fear of fat. She exhibits signs of depression, possesses low self-esteem, and hides her overeating behavior.

Diabetes mellitus
Diabetes mellitus is characterized by polyphagia accompanied by weight loss, polydipsia, and polyuria. It is associated with nocturia, weakness, weariness, and indicators of dehydration, including dry mucous membranes and diminished skin turgor.

Premenstrual syndrome (PMS)
Alterations in appetite, characterized by food cravings and binge eating, are prevalent during PMS. Abdominal bloating, the most prevalent related symptom, may manifest alongside behavioral alterations, including sadness and sleeplessness. Headache, paresthesia, and further neurological symptoms may also manifest. Associated findings encompass diarrhea or constipation, edema, transient weight gain, palpitations, back pain, breast swelling and tenderness, oliguria, and increased susceptibility to bruising.

Alternative Causes
Pharmaceutical substances
Corticosteroids, cyproheptadine, and some hormone supplements may enhance hunger, resulting in weight gain.

Provide the patient experiencing polyphagia with emotional support and assist him in comprehending its underlying cause. Refer him and his family for psychological counseling as necessary. Refer the patient for dietary advice and for individual and family counseling. Offer emotional support and assist the patient in comprehending the disease process. In children, polyphagia frequently arises from juvenile diabetes. In infants aged 6 to 18 months, it may arise from a malabsorptive illness, such as celiac disease. Polyphagia may develop normally in a youngster undergoing a fast growth spurt.

Symptoms and Signs – Differential Diagnosis of Pleural Friction Rub
This harsh, coarse, grating, or squeaking sound, often indicative of a pulmonary disease or trauma, may be auscultated over one or both lungs during late inspiration or early expiration. It is most effectively heard across the low axilla or the anterior, lateral, or posterior bases of the lung fields when the patient is in an upright position. Occasionally sporadic, it may mimic crackles or a pericardial friction rub. A pleural friction rub signifies inflammation of the visceral and parietal pleura, resulting in congestion and edema. The resulting fibrinous exudate envelops both pleural surfaces, displacing the fluid typically present between them and forcing the surfaces to frictionally interact.

URGENT INTERVENTIONS
Upon identifying a pleural friction rub, promptly assess for indicators of respiratory distress: diminished or shallow respirations; crowing, wheezing, or stridor; dyspnea; heightened utilization of accessory muscles; intercostal or suprasternal retractions; cyanosis; and nasal flaring. Assess for hypotension, tachycardia, and diminished awareness. Upon detecting indications of distress, establish and sustain an airway. Endotracheal intubation and supplementary oxygen may be required. Establish a large-bore intravenous line for the administration of medications and fluids. Elevate the patient's head by 30 degrees. Continuously monitor his heart condition and frequently assess his vital signs.

Medical History and Physical Assessment
Should the patient not exhibit considerable distress, investigate associated symptoms. Ascertain whether he has experienced chest pain. If so, request that he delineate the area and intensity of the discomfort. Additionally, inquire about the duration of his chest pain. Does the pain extend to his shoulder, neck, or upper abdomen? Does the pain intensify with respiration, motion, coughing, or sneezing? Does the discomfort diminish if he applies a splint to his chest, holds his breath, exerts pressure, or lays on the affected side?

CULTURAL INDICATOR
Pain is subjective and intensified by anxiety; thus, individuals with heightened emotionality may express complaints of pleuritic pain more readily than those who are typically stoic regarding sickness symptoms. Inquire with the patient on a history of rheumatoid arthritis, any respiratory or cardiovascular disorders, recent trauma, exposure to asbestos, or radiation therapy. If he smokes, acquire a history in pack-years. Auscultate the lungs for pleural friction rub while the patient is seated upright, inhaling and exhaling deeply and slowly via the mouth. Is the friction rub unilateral or bilateral in nature? Additionally, observe for the absence or reduction of breath sounds, recording their specific place and timing within the respiratory cycle. Do odd breath noises resolve with coughing? Monitor the patient for clubbing and pedal edema, which may suggest a persistent condition. Subsequently, assess for diminished chest movement and do percussion to identify flatness or dullness.

Etiological Factors
Asbestosis. In addition to a pleural friction rub, asbestosis may result in exertional dyspnea, cough, chest discomfort, and crackles. Clubbing is a delayed indicator.

Pulmonary carcinoma
A pleural friction rub may be audible in the affected lung region. Additional effects encompass a cough (perhaps with hemoptysis), dyspnea, thoracic discomfort, weight reduction, anorexia, weariness, digital clubbing, pyrexia, and wheezing.

Pleuritis
A pleural friction rub manifests early in pleurisy. The primary symptom is abrupt, severe chest pain that is typically unilateral and situated in the lower lateral regions of the chest. Deep breathing, coughing, or thoracic movement exacerbates the pain. Reduced breath noises and inspiratory crackles may be audible in the affected region. Additional observations encompass dyspnea, tachypnea, tachycardia, cyanosis, fever, and weariness.

Bacterial pneumonia
A pleural friction rub manifests in bacterial pneumonia, typically commencing with a dry, unpleasant, hacking cough that swiftly evolves into a productive one. Associated effects manifest abruptly; these encompass shaking chills, elevated temperature, cephalalgia, dyspnea, pleuritic thoracic pain, tachypnea, tachycardia, grunting respirations, nasal flaring, dullness upon percussion, and cyanosis. Auscultation indicates diminished breath sounds and subtle crackles. Pulmonary embolism. An embolism may induce a pleural friction rub in the impacted region of the lung. The initial symptom is typically abrupt dyspnea, maybe accompanied by angina or unilateral pleuritic chest discomfort. Additional clinical manifestations encompass a nonproductive cough or one that yields blood-tinged sputum, tachycardia, tachypnea, low-grade fever, restlessness, and diaphoresis. Infrequent manifestations encompass significant hemoptysis, thoracic splinting, lower extremity edema, and, in the presence of a substantial embolus, cyanosis, syncope, and distension of the jugular veins. Crackles, generalized wheezing, diminished breath sounds, and indications of circulatory collapse may also manifest.

Systemic lupus erythematosus (SLE)
Pulmonary involvement may result in pleural friction rub, hemoptysis, dyspnea, pleuritic chest discomfort, and crackles. Prominent manifestations of SLE encompass a butterfly rash, non-deforming arthralgia and rigidity, as well as photosensitivity. Fever, anorexia, weight reduction, and lymphadenopathy may also manifest.

Pulmonary tuberculosis
A pleural friction rub may manifest over the lung region affected by pulmonary tuberculosis. Initial manifestations encompass weight reduction, nocturnal perspiration, afternoon low-grade fever, malaise, dyspnea, anorexia, and increased fatigue. The advancement of the disorder typically results in pleuritic pain, fine crackles in the upper lobes, and a productive cough accompanied by blood-streaked sputum. Advanced tuberculosis can result in chest retraction, tracheal deviation, and diminished resonance upon percussion. Alternative Causes and Therapies. Thoracic surgery and radiation therapy may induce a pleural friction rub.

Persist in observing the patient's breathing condition and vital parameters. Administer an antitussive if the patient's chronic dry, hacking cough exhausts him. Avoid administering an opioid, as it may exacerbate respiratory depression. Administer oxygen and an antibiotic. Prepare the patient for diagnostic examinations, including chest X-rays.

Examine analgesic interventions and delineate the indications and symptoms that necessitate reporting. Auscultate for a pleural friction rub in a child exhibiting grunting respirations, experiencing chest pain, or demonstrating chest protection by clutching it or reclining laterally. A pleural friction rub in a youngster typically indicates the onset of pleurisy. For Geriatric Care

In geriatric patients, the severity of pleuritic chest discomfort may resemble that of cardiac chest pain.

Symptoms and Signs – Differential Diagnosis of Photophobia
Photophobia is a prevalent ailment characterized by an unusual sensitivity to light. In numerous instances, photophobia merely signifies heightened ocular sensitivity absent any underlying illness. For instance, it may arise from the excessive use of contact lenses or the utilization of inadequately fitted lenses. Nonetheless, in some cases, this symptom may arise from a systemic ailment, an ocular condition, trauma, or the administration of specific medications.

Medical History and Physical Assessment
Inquire about the onset and severity of the patient's photophobia. Did it result from ocular trauma, a chemical exposure, or irradiation from a sunlamp? If photophobia is caused by trauma, refrain from manipulating the eyes. Inquire with the patient regarding ocular discomfort and request a description of its location, duration, and intensity. Does he experience the sensation of a foreign body in his eye? Does he exhibit additional signs and symptoms, such as heightened lacrimation and alterations in vision? Subsequently, obtain the patient's vital signs and evaluate his neurological condition.

Evaluate visual acuity, except in cases of chemical burns. Subsequently, do a meticulous eye examination, scrutinizing the exterior structures of the eyes for any anomalies. Assess the conjunctiva and sclera, observing their coloration. Describe the volume and uniformity of any discharge. Subsequently, assess the pupillary response to illumination. Assess extraocular muscle function by examining the six cardinal fields of gaze and evaluate visual acuity in each eye. During your evaluation, remember that while photophobia may coexist with life-threatening meningitis, it is not a primary indicator of meningeal irritation.

Etiological Factors
Burn
A chemical burn may result in photophobia and ocular pain, along with erythema and blistering on the face and eyelids, miosis, generalized conjunctival injection, and alterations in the cornea. The patient has hazy vision and may be unable to maintain eye closure. Ultraviolet radiation burns result in photophobia accompanied by moderate to severe ocular discomfort. These symptoms manifest approximately 12 hours following exposure to the radiation from a welding arc or sun lamp.

Conjunctivitis
Moderate to severe conjunctivitis may induce photophobia. Additional prevalent manifestations of conjunctivitis encompass conjunctival injection, heightened lacrimation, a sensation of foreign body presence, a feeling of fullness surrounding the eyes, as well as ocular pain, burning, and pruritus. Allergic conjunctivitis is characterized by a viscous white ocular discharge and a diffuse erythema of the conjunctiva. Bacterial conjunctivitis typically results in abundant, mucopurulent, crusty ocular discharge that may adhere the eyelids together, accompanied by vivid red conjunctiva. Fungal conjunctivitis results in a viscous, purulent discharge, severe erythema, and crusted, adhesive eyelids. Viral conjunctivitis results in excessive tearing with minimal discharge and swelling of the preauricular lymph nodes.

Corneal abrasion
Photophobia is typically associated with corneal abrasion, often accompanied by increased lacrimation, conjunctival hyperemia, observable corneal injury, and a sensation of a foreign body in the eye. Blurred vision and ocular discomfort may also manifest.

Corneal ulceration
A corneal ulcer is a vision-threatening condition that induces intense photophobia and ocular pain exacerbated by blinking. Compromised visual acuity may be associated with blurriness, ocular discharge, and adhesive eyelids. Conjunctival injection may manifest despite the cornea exhibiting a white and opaque appearance. A bacterial ulcer might exhibit an uneven form. A fungal ulcer may have gradually clearer concentric rings.

Acute iritis
Acute iritis may lead to severe photophobia, accompanied by significant conjunctival injection, moderate to severe ocular discomfort, and blurred vision. The pupil may exhibit constriction and demonstrate a diminished response to light.

Interstitial keratitis
Keratitis is an inflammation of the cornea characterized by photophobia, ocular discomfort, impaired vision, significant conjunctival injection, and opacification of the corneas.

Acute bacterial meningitis
Photophobia, a prevalent symptom of meningitis, may accompany with indicators of meningeal irritation, including nuchal stiffness, hyperreflexia, and opisthotonos. Brudzinski's and Kernig's signals may be elicited. A fever, a first symptom, may be followed by chills. Associated signs and symptoms may encompass cephalalgia, emesis, ocular palsies, facial paresis, pupillary irregularities, and auditory impairment. Severe meningitis may result in seizures, stupor, and progression to coma.

Migraine cephalalgia
Photophobia and phonophobia are salient characteristics of a typical migraine. This intense headache may also induce exhaustion, impaired vision, nausea, and vomiting.

Uveitis
Anterior and posterior uveitis may induce photophobia.Typically, anterior uveitis results in moderate to severe ocular pain, pronounced conjunctival injection, and a constricted, nonreactive pupil. Posterior uveitis progresses gradually, resulting in visual floaters, ocular discomfort, pupil irregularity, conjunctival hyperemia, and impaired vision.

Peristaltic Waves, Visible
With intestinal obstruction, peristalsis temporarily increases in strength and
frequency as the intestine contracts to force its contents past the obstruction. As
a result, visible peristaltic waves may roll across the abdomen. Typically, these
waves appear suddenly and vanish quickly because increased peristalsis
overcomes the obstruction or the GI tract becomes atonic. Peristaltic waves are
best detected by stooping at the patient’s side and inspecting his abdominal
contour while he’s in a supine position.
Visible peristaltic waves may also reflect normal stomach and intestinal
contractions in thin patients or in malnourished patients with abdominal muscle
atrophy.
History and Physical Examination
After observing peristaltic waves, collect pertinent history data. Ask about a
history of a pyloric ulcer, stomach cancer, or chronic gastritis, which can lead to
pyloric obstruction. Also, ask about conditions leading to intestinal obstruction,
such as intestinal tumors or polyps, gallstones, chronic constipation, and a
hernia. Has the patient had recent abdominal surgery? Make sure to obtain a
drug history.
Determine if the patient has related symptoms. Spasmodic abdominal pain,
for example, accompanies small-bowel obstruction, whereas colicky pain
accompanies pyloric obstruction. Is the patient experiencing nausea and
vomiting? If he has vomited, ask about the consistency, amount, and color of the
vomitus. Lumpy vomitus may contain undigested food particles; green or brown
vomitus may contain bile or fecal matter.
Next, with the patient in a supine position, inspect the abdomen for
distention, surgical scars and adhesions, or visible loops of bowel. Auscultate for
bowel sounds, noting high-pitched, tinkling sounds. Then, jar the patient’s bed
(or roll the patient from side to side) and auscultate for a succussion splash — a
splashing sound in the stomach from retained secretions due to pyloric
obstruction. Palpate the abdomen for rigidity and tenderness, and percuss for
tympany. Check the skin and mucous membranes for dryness and poor skin
turgor, indicating dehydration. Take the patient’s vital signs, noting especially
tachycardia and hypotension, which indicate hypovolemia.
Medical Causes
Large-bowel obstruction. Visible peristaltic waves in the upper abdomen
are an early sign of large-bowel obstruction. Obstipation, however, may be
the earliest finding. Other characteristic signs and symptoms develop more
slowly than in small-bowel obstruction. These include nausea, colicky
abdominal pain (milder than in small-bowel obstruction), gradual and
eventually marked abdominal distention, and hyperactive bowel sounds.
Pyloric obstruction. Peristaltic waves may be detected in a swollen
epigastrium or in the left upper quadrant, usually beginning near the left rib
margin and rolling from left to right. Related findings include vague
epigastric discomfort or colicky pain after eating, nausea, vomiting,
anorexia, and weight loss. Auscultation reveals a loud succussion splash.
Small-bowel obstruction. Early signs of mechanical obstruction of the
small bowel include peristaltic waves rolling across the upper abdomen and
intermittent, cramping periumbilical pain. Associated signs and symptoms
include nausea, vomiting of bilious or, later, fecal material, and
constipation; in partial obstruction, diarrhea may occur. Hyperactive bowel
sounds and slight abdominal distention also occur early.
Special Considerations
Because visible peristaltic waves are an early sign of intestinal obstruction,
monitor the patient’s status and prepare him for diagnostic evaluation and
treatment. Withhold food and fluids, and explain the purpose and procedure of
abdominal X-rays and barium studies, which can confirm obstruction.
If tests confirm obstruction, nasogastric suctioning may be performed to
decompress the stomach and small bowel. Provide frequent oral hygiene, and
watch for a thick, swollen tongue and dry mucous membranes, indicating
dehydration. Frequently monitor the patient’s vital signs and intake and output.
Patient Counseling
Discuss dietary and fluid requirements. Encourage the use of stool softeners and
increased intake of high-fiber foods for patients with chronic constipation.
Pediatric Pointers
In infants, visible peristaltic waves may indicate pyloric stenosis. In small
children, peristaltic waves may be visible normally because of the protuberant
abdomen, or visible waves may indicate bowel obstruction stemming from
congenital anomalies, volvulus, or swallowing a foreign body.
Geriatric Pointers
In elderly patients who present with visible peristaltic waves, always check for
fecal impaction, which is a common problem among those of this age group.
Also, obtain a detailed drug history; antidepressants and antipsychotics can
predispose patients to constipation and bowel obstruction.

Symptoms and Signs- Differential Diagnosis of Pericardial Friction Rub
A pericardial friction rub, typically brief, is a scratching, grating, or crunching sound produced when two inflamed layers of the pericardium move against each other. This odd sound, varying from weak to loud, is most audible around the lower left sternal boundary during deep inspiration. This suggests pericarditis, which may arise from an acute infection, a cardiac or renal condition, postpericardiotomy syndrome, or the administration of specific medications. At times, a pericardial friction rub may mimic a murmur or a pleural friction rub. The basic pericardial friction rub comprises three components.

Medical History and Physical Assessment Acquire a comprehensive medical history, with particular emphasis on heart problems. Has the patient recently experienced a myocardial infarction or undergone heart surgery? Has he ever experienced pericarditis or a rheumatic condition, such as rheumatoid arthritis or systemic lupus erythematosus? Does he have chronic kidney disease or an infection? Should the patient report chest pain, inquire about its characteristics and location. What alleviates the discomfort? What exacerbates it? Assess the patient's vital signs, with particular attention to hypotension, tachycardia, an irregular pulse, tachypnea, and fever. Examine for jugular vein distention, edema, ascites, and hepatomegaly. Perform auscultation of the lungs to detect crackles.

EXAMINATION TIP: Pericardial Friction Rub vs Murmur Is the auditory phenomenon a pericardial friction rub or a murmur? This is how to determine. The traditional pericardial friction rub comprises three auditory components, according to the periods of the heart cycle. In certain cases, the presystolic and early diastolic sounds of the rub may be imperceptible, leading to a resemblance to the murmurs associated with mitral insufficiency or aortic stenosis and insufficiency. To differentiate a pericardial friction rub from a murmur in the absence of the traditional three-component sound, re-auscultate and consider the following questions:
WHAT IS THE DEPTH OF THE SOUND?
A pericardial friction rub typically has a surface sound, but a murmur has a deeper resonance in the chest. Does the sound propagate? A pericardial friction rub typically does not radiate, although a murmur may radiate extensively. Does the sound fluctuate with inspiration or alterations in patient position? A pericardial friction rub is typically most pronounced during inhalation and is optimally detected when the patient assumes a forward-leaning position. A murmur fluctuates in timing and duration with both variables.

Etiological Factors
Pericarditis
A pericardial friction rub is the defining characteristic of acute pericarditis. This condition induces acute precordial or retrosternal discomfort that typically radiates to the left shoulder, neck, and back. The pain intensifies when heavy breathing, coughing, lying flat, and potentially while swallowing. It diminishes as he assumes an upright position and leans forward. The patient may additionally have fever, dyspnea, tachycardia, and arrhythmias.

Contrasting Auscultation Results During auscultation, one may identify a pleural friction rub, a pericardial friction rub, or crackles—three aberrant noises frequently conflated. Utilize these pictures to elucidate auscultation findings.

EXAMINATION TIP: Comprehending Pericardial Friction Rubs The basic pericardial friction rub is characterized by three distinct phases. The three auditory components are associated with periods of the cardiac cycle. The presystolic component (A) signifies atrial systole and occurs before to the first heart sound (S1). The systolic component (B), typically the most pronounced, signifies ventricular systole and transpires between the first heart sound (S1) and the second heart sound (S2). The early diastolic component (C) signifies ventricular diastole and occurs subsequent to S2. Occasionally, the early diastolic component coalesces with the presystolic component, resulting in a diphasic to-and-fro sound during auscultation. Auscultation in some patients may reveal only a single component—a monophasic rub, usually occurring during ventricular systole.

Chronic constrictive pericarditis leads to the gradual development of a pericardial friction rub, accompanied by manifestations of reduced cardiac filling and output, including peripheral edema, ascites, Kussmaul's sign (jugular vein distention on inspiration), and hepatomegaly. Dyspnea, orthopnea, paradoxical pulse, and thoracic discomfort may also manifest.

Additional Factors: Substances. Procainamide and chemotherapy agents may induce pericarditis.

Persist in observing the patient's cardiovascular condition. Should the pericardial friction rub cease, remain vigilant for indications of cardiac tamponade: pallor; cool, clammy skin; hypotension; tachycardia; tachypnea; paradoxical pulse; and heightened jugular vein distention. Should these indications manifest, prepare the patient for pericardiocentesis to avert cardiovascular collapse. Ensure the patient receives sufficient rest.

Administer an anti-inflammatory, antiarrhythmic, diuretic, or antibiotic to address the underlying etiology. If required, ready him for a pericardiectomy to facilitate optimal heart filling and contraction.

Elucidate the fundamental problem, its therapeutic interventions, and the measures the patient might undertake to alleviate his symptoms. Pediatric Guidelines Bacterial pericarditis can manifest within the initial two decades of life, typically prior to the age of 6. A pericardial friction rub may manifest, although additional signs and symptoms—such as fever, tachycardia, dyspnea, chest discomfort, jugular vein distention, and hepatomegaly—more consistently signify this life-threatening condition. A pericardial friction rub may also manifest following surgery to rectify congenital heart abnormalities. Nevertheless, it typically dissipates without the onset of pericarditis.

Symptoms and Signs – Differential Diagnosis of Peau d'orange
Peau d’orange, characterized by edematous thickening and pitting of breast skin, is typically a late manifestation of breast cancer. This gradually emerging symptom may also manifest in cases of breast or axillary lymphadenitis, erysipelas, or Graves' disease. The pronounced orange peel look results from lymphatic edema surrounding the recessed hair follicles.

Medical History and Physical Assessment Inquire with the patient regarding the initial observation of peau d’orange. Has she observed lumps, discomfort, or other alterations in her breasts? Does she exhibit associated signs and symptoms, including malaise, myalgia, and weight loss? Is she now lactating, or has she recently weaned her child? Has she undergone prior axillary surgery that may have compromised lymphatic drainage of a breast?

Acknowledging Peau d'orange In peau d’orange, the skin exhibits a pitted appearance. This condition typically signifies advanced breast cancer. In a well-illuminated examination room, assess the patient's breasts. Assess the magnitude of the peau d’orange and evaluate for erythema. Evaluate the nipples for exudate, misalignment, retraction, indentation, and fissuring. Carefully examine the peau d’orange region, observing for warmth or induration. Subsequently, palpate the entire breast, observing for fixed or movable masses, and examine the axillary lymph nodes for any enlargement. Ultimately, measure the patient's temperature.

Etiological Factors
Breast abscess
Typically impacting nursing mothers with milk stasis, breast abscess results in peau d’orange, malaise, breast discomfort, erythema, and an abrupt fever perhaps accompanied by rigors. A fissured nipple may yield a purulent exudate, and an indurated or discernible soft mass may be evident.

Breast carcinoma
Advanced breast cancer is the predominant etiology of peau d’orange, typically initiating in the inferior region of the breast or the areola. Palpation generally uncovers a solid, fixed mass that is attached to the skin over the region exhibiting peau d’orange. Breast inspection may disclose alterations in contour, size, or symmetry. Examination of the nipples may disclose deviation, erosion, retraction, and a thin, watery, bloody, or purulent discharge. The patient may have a burning and itchy sensation in the nipples, along with a feeling of warmth in the breast.

Breast pain may manifest; however, it is not a dependable predictor of malignancy. Given that peau d’orange typically indicates advanced breast cancer, offer emotional support to the patient. Urge her to articulate her apprehensions and anxieties. Explicitly delineate anticipated diagnostic procedures, including mammography and breast biopsy.

Detail the necessary diagnostic tests for the patient and instruct her on performing monthly breast self-examinations. Identify the signs and symptoms that require her reporting.

Symptoms and Signs -Differential Diagnosis of Paroxysmal Nocturnal Dyspnea
This indication, often dramatic and frightening for the patient, indicates an episode of dyspnea that suddenly rouses the individual from sleep. Typical observations encompass diaphoresis, coughing, wheezing, and chest discomfort. The episode diminishes if the patient sits up or stands for several minutes, but may reoccur every 2 to 3 hours.

Paroxysmal nocturnal dyspnea indicates left-sided heart failure. This may arise from diminished respiratory drive, compromised left ventricular function, augmented reabsorption of interstitial fluid, or elevated thoracic blood volume. All of these pathophysiological pathways exacerbate dyspnea when the patient assumes a supine position.

Medical History and Physical Assessment
Commence by investigating the patient's report of dyspnea. Does he experience dyspneic bouts exclusively at night, or do they occur at other times, such as post-exertion or while seated? What specific action provokes the attack? Does he exhibit coughing, wheezing, weariness, or weakness during an episode? Determine whether he has a history of lower extremity edema or jugular vein distention.

Inquire whether he sleeps with his head up, and if so, the number of pillows used, or if he sleeps in a reclined chair. Acquire a cardiopulmonary medical history. Does the patient or a family member have a history of myocardial infarction, coronary artery disease, hypertension, chronic bronchitis, emphysema, or asthma? Has the patient undergone cardiac surgery? Subsequently, conduct a physical examination. Commence by assessing the patient's vital signs and developing a comprehensive image of his look. Is he visibly cyanotic or edematous? Examine the lungs for crackles and wheezing, and assess the heart for gallops and arrhythmias.

Etiological Factors
Left ventricular heart failure
Dyspnea—during activity, when sleeping, and ultimately at rest—is an initial indicator of left-sided heart failure. This symptom is typically associated with Cheyne-Stokes respirations, diaphoresis, weakness, wheezing, and a chronic nonproductive cough or a cough that yields clear or blood-tinged sputum. As the patient's condition deteriorates, he exhibits tachycardia, tachypnea, an alternating pulse (often triggered by a premature beat), a ventricular gallop, crackles, and peripheral edema.

In late left-sided heart failure, the patient may present with pronounced orthopnea, cyanosis, clubbing, hemoptysis, and cardiac arrhythmias, alongside manifestations of shock, including hypotension, a weak pulse, and cold, clammy skin.

Prepare the patient for diagnostic evaluations, including a chest X-ray, echocardiography, exercise electrocardiography, and cardiac blood pool imaging. Should the hospitalized patient exhibit paroxysmal nocturnal dyspnea, assist him into a sitting position or facilitate ambulation within the room.

Administer supplementary oxygen if required. Attempt to soothe him, as anxiety may intensify dyspnea. Elucidate the signs and symptoms necessitating urgent medical intervention, and examine nutritional and fluid limitations. Investigate postures that may facilitate respiration, and provide instruction on required pharmacological treatments. In a child, paroxysmal nocturnal dyspnea typically arises from a congenital cardiac abnormality that leads to heart failure. Alleviate the child's dyspnea by raising his head and soothing him.

Symptoms and Signs – Differential Diagnosis of Paresthesia

Paresthesia refers to an atypical sensation or amalgamation of sensations—often characterized as numbness, prickling, or tingling—experienced via peripheral nerve pathways; these sensations are often non-painful. Unpleasant or unpleasant feelings are referred to as dysesthesias.

Paresthesia can manifest abruptly or progressively and may be either transitory or persistent. Paresthesia, a prevalent symptom of various neurological illnesses, may also arise from a systemic condition or specific medication. This may indicate damage or irritation to the parietal lobe, thalamus, spinothalamic tract, or spinal or peripheral nerves, which are integral to the neuronal circuit responsible for transmitting and interpreting sensory stimuli.

Medical History and Physical Assessment
Initially, investigate the paresthesia. When did the odd sensations commence? Request the patient to elucidate their characteristics and distribution. Additionally, inquire about concomitant signs and symptoms, including sensory deficits and paresis or paralysis. Subsequently, obtain a medical history encompassing neurological, cardiovascular, metabolic, renal, and chronic inflammatory conditions, including arthritis and lupus. Has the patient lately experienced a traumatic injury, undergone surgery, or had an invasive procedure that could have compromised peripheral nerves? Concentrate the physical examination on the patient's neurological condition. Evaluate his state of consciousness (LOC) and cranial nerve functionality. Evaluate muscle strength and deep tendon reflexes (DTRs) in limbs exhibiting paresthesia.

Conduct a systematic assessment of light touch, nociception, thermoreception, vibratory sensation, and proprioception. Additionally, observe skin pigmentation and warmth, and assess pulse palpation.

Etiological Factors
Acute arterial occlusion
Acute artery occlusion may result in abrupt paresthesia and coldness in one or both legs due to a saddle embolus. Paresis, intermittent claudication, and resting discomfort are also indicative. The extremities exhibits mottling with a delineation of temperature and color at the site of occlusion. Pulses are nonexistent beneath the occlusion, and the capillary refill time is prolonged.

Obliterative arteriosclerosis
Arteriosclerosis obliterans results in paresthesia, intermittent claudication (the most prevalent symptom), reduced or nonexistent popliteal and pedal pulses, pallor, paresis, and coldness in the affected limb.

Arthritis
Rheumatoid or osteoarthritic alterations in the cervical spine may induce paresthesia in the neck, shoulders, and arms. The lumbar spine may be impacted, resulting in paresthesia in one or both legs and feet.

Neoplasm of the brain
Neoplasms impacting the sensory cortex in the parietal lobe can lead to increasing contralateral paresthesia, along with agnosia, apraxia, agraphia, homonymous hemianopsia, and diminished proprioception.

Buerger's disease
Buerger’s disease, an inflammatory occlusive illness associated with smoking, causes the feet to become cold, cyanotic, and numb upon exposure to cold; subsequently, they redden, warm, and experience tingling sensations. Intermittent claudication, exacerbated by physical activity and alleviated by rest, is also prevalent. Additional findings encompass diminished peripheral pulses, migrating superficial thrombophlebitis, followed by ulceration, muscular atrophy, and gangrene.

Diabetes mellitus
Diabetic neuropathy may induce paresthesia characterized by a burning feeling in the extremities. Additional findings encompass gradual, irreversible anosmia, weariness, polyuria, polydipsia, weight reduction, and polyphagia.

Guillain-Barré syndrome
In Guillain-Barré syndrome, transitory paresthesia may occur prior to the onset of muscle weakness, which often initiates in the legs and progresses to the arms and facial nerves. Weakness may advance to complete paralysis. Additional abnormalities encompass dysarthria, dysphagia, nasal speech, orthostatic hypotension, bladder and bowel incontinence, diaphoresis, tachycardia, and potentially, indications of life-threatening respiratory muscle paralysis.

Cerebral injury
Paresthesia, whether unilateral or bilateral, may arise after head trauma resulting in a concussion or contusion; still, sensory loss is more prevalent. Additional observations encompass varying paresis or paralysis, diminished level of consciousness, headache, blurred or double vision, nausea and vomiting, dizziness, and seizures.

Intervertebral disc herniation
Herniation of a lumbar or cervical disc may result in an immediate or gradual onset of paresthesia along the distribution paths of the afflicted spinal nerves. Additional neuromuscular symptoms encompass intense pain, muscle spasms, and weakness that may advance to atrophy if herniation is not alleviated.

Herpes zoster
Paresthesia, an initial symptom of herpes zoster, manifests in the dermatome innervated by the impacted spinal nerve. Within a few days, this dermatome exhibits a pruritic, erythematous, vesicular rash accompanied by acute, shooting, or scorching pain.

Hyperventilation syndrome
Hyperventilation syndrome, typically induced by severe anxiety, can result in temporary paresthesia in the hands, feet, and perioral region, along with agitation, vertigo, syncope, pallor, muscle twitching and weakening, carpopedal spasm, and cardiac arrhythmias.

Migraine cephalalgia
Paresthesia in the hands, face, and perioral region may indicate an approaching migraine headache. Additional prodromal symptoms encompass scotomas, hemiparesis, disorientation, dizziness, and photophobia. These symptoms may endure throughout the typical pulsating headache and stay even after its resolution.

Multiple sclerosis (MS)
Demyelination of the sensory cortex or spinothalamic tract in multiple sclerosis may result in paresthesia, often one of the initial symptoms. Paresthesia, like to other manifestations of MS, typically fluctuates until the latter stages, at which point it may become permanent. Related results encompass muscular weakness, spasticity, and hyperreflexia. Injury to peripheral nerves. Damage to a significant peripheral nerve can result in paresthesia, sometimes manifesting as dysesthesia, in the region innervated by that nerve. Paresthesia occurs promptly upon trauma and may be enduring.

Additional findings include flaccid paralysis or paresis, hyporeflexia, and varied sensory loss.

Peripheral neuropathy
Peripheral neuropathy may induce increasing paresthesia in all extremities. The patient frequently exhibits muscle weakness, potentially resulting in flaccid paralysis and atrophy, loss of vibration feeling, reduced or absent deep tendon reflexes, neuralgia, and dermatological alterations, including glossy, erythematous skin and anhidrosis.

Rabies
Paresthesia, coldness, and pruritus at the location of an animal bite signify the prodromal phase of rabies. Additional prodromal signs and symptoms include fever, headache, photophobia, hyperesthesia, tachycardia, shallow respirations, and excessive salivation, lacrimation, and perspiration.

Raynaud's phenomenon
Exposure to cold or stress causes the fingers to become pale, chilly, and cyanotic; upon rewarming, they turn red and exhibit paresthesia. Ulceration may manifest in chronic cases.

Epileptic disorders
Seizures originating in the parietal lobe typically induce paresthesia in the lips, fingers, and toes. Paresthesia may serve as auras that precede tonic-clonic seizures.

Spinal cord damage
Paresthesia may manifest following partial spinal cord transection, subsequent to the resolution of spinal shock. It might be unilateral or bilateral, manifesting at or below the lesion level. The associated sensory and motor loss is inconsistent.. Spinal cord abnormalities may be linked to paresthesia during head flexion (Lhermitte’s sign).

Neoplasms of the spinal cord
Tumors of this nature lead to paresthesia, paresis, pain, and sensory loss along the nerve pathways innervated by the impacted spinal cord segment. Paresis may ultimately lead to spastic paralysis accompanied by hyperactive deep tendon reflexes, except when the tumor is located in the cauda equina, which results in hyporeflexia, and potentially causes bladder and bowel incontinence.

Cerebrovascular accident
While contralateral paresthesia can manifest in stroke, sensory loss is more prevalent. Accompanying characteristics differ based on the afflicted artery and may encompass contralateral hemiplegia, diminished level of consciousness, and homonymous hemianopsia.

Systemic lupus erythematosus (SLE)
SLE may induce paresthesia; nevertheless, its principal signs and symptoms encompass nondeforming arthritis (often affecting the hands, feet, and major joints), photosensitivity, and a "butterfly rash" that manifests over the nose and cheeks. Tabes dorsalis. Paresthesia, particularly in the legs, is a prevalent yet late manifestation of tabes dorsalis. Additional findings encompass ataxia, impaired proprioception, altered pain and temperature sensitivity, absent deep tendon reflexes, Charcot's joints, Argyll Robertson pupils, incontinence, and impotence.

Transient ischemic attack (TIA)
Paresthesia generally manifests suddenly during a TIA and is confined to one arm or a specific region of the body. It often endures for approximately 10 minutes and is associated with paralysis or paresis. Related symptoms encompass diminished level of consciousness, vertigo, unilateral visual impairment, nystagmus, aphasia, dysarthria, tinnitus, facial paresis, dysphagia, and ataxic gait.
Additional Causes: Substances. Phenytoin, chemotherapeutic medicines (including vincristine, vinblastine, and procarbazine), isoniazid, nitrofurantoin, chloroquine, and parenteral gold therapy may induce transitory paresthesia that resolves upon cessation of the drug. Radiation treatment. Prolonged radiation therapy may ultimately induce peripheral nerve damage, leading to paresthesia.

Due to the frequent association of paresthesia with localized sensory deficits, instruct the patient on safety precautions. Instruct him to measure the bathwater temperature using a thermometer.

Elucidate safety protocols and inform the patient of the indications and symptoms that necessitate reporting.

While children may have paresthesia due to the same etiologies as adults, many are unable to articulate this symptom. Nonetheless, genetic polyneuropathies are typically initially identified during childhood.