Facial Expressions

Disease as expressed in the face and posture.

Facies cardiac (heart): An anxious expression seen in the early stages of chronic valvular disease.

A purple or bluish appearance of the face, especially about the eyes, temples, and ears, with veins showing on the nose and sometimes on the cheeks, intensified by lying down: Caused by high blood pressure and an approaching dangerously plethoric state of the body.

Hepatic face: An earthy appearance; yellow tinge, jaundice.

Hippocratic face: Indicating rapid approach of death--pinched nose; hollow temples; eyes sunken; ears leaden and cold; lips relaxed; skin livid, and if the skin is pinched it returns slowly to the plane from which it was pinched or drawn.

Ovarian face: Features emaciated and sunken; anxious expression; forehead furrowed; eyes hollowed; nostrils open and sharply drawn; lips full and compressed; angles of mouth drawn and wrinkled, puckered but protruding"fish mouth."

The stupid face is that of typhoid.

Gastric face in children: A white line around the mouth, extending up by the side of the nose, shows irritation from improper feeding. Add to this sign pungent breath and vomiting, and the child has gastritis.

Gastric face in adults: Chronic irritation of the stomach in adults is indicated by a dragging-down of the comers of the mouth. Add to this drooling or driveling of saliva, and the indication is of starch poisoning; and if there is a broad, pallid tongue, the evidence is strong for overeating on starch.

Hysteria is marked by staring and an ecstatic expression.

Epilepsy is marked by a stupid face after an attack.

Protruding eyes and expressionless face in Graves' disease.

They lypermaniac has sadness written in his face. In general paralysis the countenance is composed and satisfied. The enebriate has trembling bps and a wandering expression.

The child with enlarged tonsils and adenoid growths has a stupid expression; the mouth is open, the lips hanging; the nose is expressionless.

The red nose, enlarged veins, bluish lips, cyanosed cheeks, and puffiness of face of the drinking man are called the mitral face. Where the aorta is diseased there is intense pallor. In Bright's disease the face is swollen and white.

The signs of croup are well known, but the type of disease is not so easily told. There are coughing and suffocating when a foreign body is in the air-passage.

Expiratory disturbance is marked by flushed face, puffed and bluish; the eyes are suffused, and the veins stand out.

In marasmus the features are drawn, the furrows deepened, the neck hollow; emaciation is marked, and, when profound, the whole appearance is that of the monkey.

The consumptive appearance is that of emaciation; protruding, flushed cheeks; pinched nose, with flaring nostrils; short, quick, jerky breathing; halting speech, and more or less suppressed voice.

When the face looks smaller--shrunken--and the nose is thin, long, and drawn, the bones prominent, the skin pale and covered with cold sweat, and, when drawn or pinched, the fold remains for some time, this is the facies of peritonitis, intestinal obstruction, renal and hepatic colic.

Fainting: The heart stops; the patient turns pale and falls motionless, but there is no distortion of the face; breathing is suspended.

Apoplexy: The patient is motionless and lies on the back; all animation is suspended; only breathing and pulse continue; the breathing is noisy, and gradually grows more stertorous. If the patient does not react and improve, the breathing and heart action gradually decline, the skin becomes drawn, the nose thinner and longer, the eyes dull, partially closed, glassy. The breathing stops, starts and continues, until it finally ends with a slight bodily convulsive movement.

Physical appearance must be noted--all deviations from the normal mean something.

Deformities, such as rickets, shorten the stature and cause the head to appear too large; the spine is incurved, the pelvis is deformed, the limbs are curved, the ribs project forward.

When the muscles become atrophied they cause general deformity.

Alterations of the heart or lungs cause deformities of the chest.

The bowels are often too large and distended from gas, fat, or ascites; in fevers, from tympanitis and inflammations.

Enlargement of the liver or spleen causes a large abdomen in the upper region; in the lower abdomen, enlargement may come from tumors, distended bladder, or a gravid uterus.

A large swelling at the base of the great toe, with the toe pointing outward, indicates a bunion. This deformity usually means that there is a slight rheumatism. Deformity of the third joint of the fingers--nodes of Heberden--means arthritis deformans. The nodes of Bouchard on the second joints of the fingers indicate dilation of the stomach--a disturbed nutrition from overeating of the carbohydrate foods. Joint distortions indicate gout, rheumatism, or injury; not infrequently they mean all of these. Frequently injury is complicated by rheumatism.

Hippocratic fingers (clubbing of finger-tips, with incurving nails) indicate heart or lung disease--scrofulous diathesis.

Mnemonics For Paediatrics Medicine

Croup: symptoms 3 S's:
Stridor
Subglottic swelling
Seal-bark cough

Ataxia-Telangiectasia (AT): common sign AT:
Absent
Thymus

Guthrie card: diseases identified with it "Guthrie Cards Can HelpPredict Bad Metabolism":
Galactosaemia
Cystic fibrosis
Congenital adrenal hyperplasia
Hypothyroidism
Phenylketonuria
Biotidinase deficiency
Maple syrup urine disease

Williams syndrome: features WILLIAMS:
Weight (low at birth, slow to gain)
Iris (stellate iris)
Long philtrum
Large mouth
Increased Ca++
Aortic stenosis (and other stenoses)
Mental retardation
Swelling around eyes (periorbital puffiness)

Russell Silver syndrome: features ABCDEF:
Asymmetric limb (hemihypertrophy)
Bossing (frontal)
Clinodactyly/ Cafe au lait spots
Dwarf (short stature)
Excretion (GU malformation)
Face (triangular face, micrognathia)

Dentition: eruption times of permanent dentition "Mama Is In Pain,Papa Can Make Medicine":
1st Molar: 6 years
1st Incisor: 7 years
2nd Incisor: 8 years
1st Premolar: 9 years
2nd Premolar: 10 years
Canine: 11 years
2nd Molar: 12 years
3rd Molar: 18-25 years

Cyanotic heart diseases: 5 types · Use your five fingers:
1 finger up: Truncus Arteriosus (1 vessel)
2 fingers up: Dextroposition of the Great Arteries (2 vessels transposed)
3 fingers up: Tricuspid Atresia (3=Tri)
4 fingers up: Tetralogy of Fallot (4=Tetra)
5 fingers up: Total Anomalous Pulmonary Venous Return (5=5 words)

Head circumference with age · Remember 3, 9, and multiples of 5:
Newborn 35 cm
3 mos 40 cm
9 mos 45 cm
3 yrs 50 cm
9 yrs 55 cm

Cyanotic congenital heart diseases 5 T's:
Truncus arteriosus
Transposition of the great arteries
Tricuspid atresia
Tetrology of Fallot
Total anomalous pulmonary venous return

Weights of children with age Newborn 3 kg
6 mos 6 kg (2x birth wt at 6 mos)
1 yr 10 kg (3x birth wt at 1 yr)
3 yrs 15 kg (odd yrs, add 5 kg until 11 yrs)
5 yrs 20 kg
7 yrs 25 kg
9 yrs 30 kg
11 yrs 35 kg (add 10 kg thereafter)
13 yrs 45 kg
15 yrs 55 kg
17 yrs 65 kg

Hemolytic-Uremic Syndrome (HUS): components "Remember to decrease the RATE of IV fluids in these patients":
Renal failure
Anemia (microangiopathic, hemolytic)
Thrombocytopenia
Encephalopathy (TTP)

Cough (chronic): differential When cough in nursery, rock the"CRADLE":
Cystic fibrosis
Rings, slings, and airway things (tracheal rings)/ Respiratory infections
Aspiration (swallowing dysfunction, TE fistula, gastroesphageal reflux)
Dyskinetic cilia
Lung, airway, and vascular malformations (tracheomalacia, vocal cord dysfunction)
Edema (heart failure)

Cystic fibrosis: presenting signs CF PANCREAS:
Chronic cough and wheezing
Failure to thrive
Pancreatic insufficiency (symptoms of malabsorption like steatorrhea)
Alkalosis and hypotonic dehydration
Neonatal intestinal obstruction (meconium ileus)/ Nasal polyps
Clubbing of fingers/ Chest radiograph with characteristic changes
Rectal prolapse
Electrolyte elevation in sweat, salty skin
Absence or congenital atresia of vas deferens
Sputum with Staph or Pseudomonas (mucoid)

WAGR syndrome: components WAGR:
Wilm's tumor
Aniridia
Gential abnormalities
Mental Retardation

Haematuria: differential in children ABCDEFGHIJK:
Anatomy (cysts, etc)
Bladder (cystitis)
Cancer (Wilm's tumour)
Drug related (cyclophosphamide)
Exercise induced
Factitious (Munchausen by proxy)
Glomerulonephritis
Haematology (bleeding disorder, sickle cell)
Infection (UTI)
In Jury (trauma)
Kidney stones (hypercalciuria)

Vitamin Toxicity:

Excess vitamin A: Anomalies (teratogenic)
Excess vitamin E: Enterocolitis (necrotizing enterocolitis)
Excess vitamin K: Kernicterus (hemolysis)

Pediatric milestones in development 1 year:
-single words
2 years:
-2 word sentences
-understands 2 step commands
3 years:
-3 word combos
-repeats 3 digits
-rides tricycle
4 years:
-draws square
-counts 4 objects

Breast feeding: contraindicated drugs BREAST:
Bromocriptine/ Benzodiazepines
Radioactive isotopes/ Rizatriptan
Ergotamine/ Ethosuximide
Amiodarone/ Amphetamines
Stimulant laxatives/ Sex hormones
Tetracycline/ Tretinoin

Paediatric history taking · Begin with standard things: patient name, presenting complaint, history of presenting complaint and past medical history.
· Then ask BIFIDA:
Birth details and problems
Immunisations
Feeding
Infection, exposure to
Development, normality of
Allergies
· End by customary review of the rest of the standard things: medications, family history and social history.

Neonatal resuscitation: successive steps "Do What Pediatricians SayTo, Or Be Inviting Costly Malpractice":
Drying
Warming
Positioning
Suctioning
Tactile stimulation
Oxygen
Bagging
Intubate endotracheally
Chest compressions
Medications

Pruritus and Systemic Disease

Pruritus, or itch, is defined as an unpleasant sensation that provokes the desire to scratch. Certain systemic diseases have long been known to cause pruritus that ranges in intensity from a mild annoyance to an intractable, disabling condition. Generalized pruritus may be classified into the following categories on the basis of the underlying causative disease: renal pruritus, cholestatic pruritus, hematologic pruritus, endocrine pruritus, pruritus related to malignancy, and idiopathic generalized pruritus.

Pathophysiology

The sensation of pruritus is transmitted through slow-conducting unmyelinated C-polymodal and possibly type A delta nociceptive neurons with free nerve endings located near the dermoepidermal junction or in the epidermis. These neurons appear to be located more superficially and are more sensitive to pruritogenic substances than pain receptors. Activators of these nerves include histamine, neuropeptide substance P,serotonin, bradykinin, proteases (eg, mast cell tryptase), and endothelin (which stimulates the release of nitric oxide). Impulses are transmitted from the dorsal root ganglion to the spinothalamic tract.

Opioids are known to modulate the sensation of pruritus, both peripherally and centrally. Stimulation of opioid mu receptors accentuates pruritus, while stimulation of kappa receptors and blockage of mu receptors suppress pruritus.

In the mouse model that mimics atopic dermatitis in humans, the histamine (H4) receptor mediates both TH-2 inflammation and pruritus.

Renal pruritus

Renal pruritus can occur in patients with chronic renal failure (CRF) and is most often seen in patients receiving hemodialysis (HD). This term is synonymous with uremic pruritus; however, the condition is not due to elevated serum urea levels. The actual pruritogenic substance has yet to be identified. Pruritus is relatively absent in persons with acute renal failure; therefore, serum mediators other than urea and creatinine are implicated.

Other theories include elevated levels of circulating histamine in patients receiving HD. Researchers have found increased numbers of mast cells in various organ systems. However, antihistamines are, at best, marginal in the treatment of renal pruritus, suggesting other causative factors.

Parathyroid hormone (PTH) levels are commonly elevated in persons with CRF.Dramatic relief of renal pruritus after subtotal parathyroidectomy has been described, and findings from 1 study confirmed previous case reports. However, other studies have shown no correlation between circulating PTH levels and the intensity of pruritus. Of note, a patient with a PTH-producing bronchogenic carcinoma was reported to have intractable pruritus as the presenting symptom.

Elevated levels of divalent ions, such as calcium, magnesium, and phosphate, are thought to play a role. Marked improvement of pruritus resulting from low dialysate calcium and magnesium concentrations has been reported. Increased amounts of these ions are also seen in the skin of pruritic patients.

Decreased transepidermal elimination of pruritogenic substances, xerosis, elevated levels of serum bile acids, and increased epidermal vitamin A levels all may contribute to the condition. Elevated serum levels of serotonin are seen in patients with CRF. Serotonin is important in the transmission of pain and may be a contributing factor.

Pruritus in CRF also may be a possible manifestation of peripheral neuropathy.

Proliferation of nonspecific enolase-positive sensory nerves in the epidermis has been documented in patients with uremia and may contribute; however, these results must be confirmed.

Opioid accumulation may contribute to itching in persons with CRF and overexpression and activation of opioid mu receptors. Mixed results with the use of opioid antagonists in the treatment of renal pruritus have led to conflicting opinions about the role of opioids.

An immune hypothesis has also been suggested. In patients with CRF, a systemic inflammatory response involving overexpression of activated type 1 helper T lymphocytes (which secrete interleukin 2) may induce pruritus. UV-B, thalidomide, and tacrolimus all target mediators of this inflammation. Elevated ferritin and low transferrin and albumin levels have been correlated with the severity of pruritus

Cholestatic pruritus

Cholestasis, or a decrease or arrest in the flow of bile, is associated with pruritus. The deposition of bile salts in the skin was thought to directly cause a pruritogenic effect, but this theory has been proven incorrect. In addition, indirect hyperbilirubinemia does not induce pruritus.

Other theories implicate elevated venous histamine levels, retention of pruritogenic intermediates in bile salt synthesis, and high hepatic concentrations of bile salts resulting in hepatic injury and release of a pruritogenic substance. In support of the last point, rifampin and ursodeoxycholic acid decrease intrahepatic concentrations of bile salts and provide some relief of cholestatic pruritus.

The accumulation of endogenous opioids, which modulate pruritus and increase opioidergic tone in the brain, is of recent interest because opioid antagonists have been shown to partially relieve cholestatic pruritus. In support of this theory, treatment with opioid antagonists may induce an opioid withdrawal–like syndrome.

Perhaps some combination of the pruritogenic substances mentioned above (ie, bile salts, histamine, opioids) induces cholestatic pruritus.

Hematologic pruritus

Iron is a critical factor in many enzymatic reactions. Although iron deficiency has not been proved to be a cause of pruritus, it may contribute to pruritus through a variety of metabolic paths. Patients with pruritus and iron deficiency may not be anemic; this observation suggests that pruritus may be related to iron and not hemoglobin.

Patients with polycythemia vera have increased numbers of circulating basophils and skin mast cells, which have been correlated with itching. The itch typically occurs during cooling after a hot shower. Mast cell prostaglandins and increased platelet degranulation, which lead to the release of serotonin and prostanoids, are thought to be important mediators of itching, along with iron deficiency, which may be a contributing factor.

Endocrine pruritus

Hyperthyroidism has been associated with pruritus. Excess thyroid hormone may activate kinins from increased tissue metabolism or may reduce the itch threshold as a result of warmth and vasodilation.

Hypothyroidism is also implicated because pruritus is likely secondary to xerosis.

Diabetes mellitus is another possible cause, but cause and effect remain unproven. Metabolic abnormalities, autonomic dysfunction, anhydrosis, and diabetic neuropathy all may contribute.

Pruritus and malignancy

Numerous reports have linked pruritus to almost every type of malignancy. Release of toxins and the immune system have been suggested to play roles in malignancy-related pruritus.

In patients with Hodgkin disease, leukopeptidase and bradykinin appear to be the pruritogenic mediators released as an autoimmune response is mounted against malignant lymphoid cells.

Carcinoid syndrome may be associated with pruritus triggered by serotonin.

Epidemiology

Frequency

United States

Pruritus occurs in approximately 20% of adults. It is present in approximately 25% of patients with jaundice and in 50% of patients receiving renal dialysis.

International

An underlying systemic disease is reported in 10-50% of patients who seek medical attention for pruritus.

The incidence of renal pruritus appears to be decreasing among patients receiving HD, most likely because of improvements in HD technique. Although previous data showed that as many as 85% of patients on HD are affected, new reports suggest the rate is 22-66%. Pruritus appears to affect up to 30% of patients with severe chronic renal insufficiency who are not undergoing dialysis.

The incidence of cholestatic pruritus depends on the underlying etiology. Approximately 60% of patients with primary biliary cirrhosis present with pruritus, and almost all develop pruritus at some point during the course of their disease.

Among patients with polycythemia vera, 48-70% of patients have aquagenic pruritus. Pruritus associated with iron deficiency is uncommon. Hyperthyroidism is the most common cause of endocrine pruritus. The rate is 4-11%, and the condition is especially prevalent in patients with untreated Graves disease. Pruritus is rare in patients with diabetes mellitus and hypothyroidism.

The rate of malignancy in patients presenting with generalized pruritus is less than 1-8%. Pruritus is commonly associated with Hodgkin disease and was once considered a B symptom of the disease. Approximately 35% of patients with Hodgkin disease have pruritus during their clinical course, whereas only approximately 10% have pruritus associated with non-Hodgkin lymphoma. Pruritus is a rare symptom of leukemia.

Mortality/Morbidity

Pruritus causes significant morbidity. Some conditions that cause systemic pruritus appear to be associated with an increased mortality rate. In patients receiving HD, renal pruritus is an independent marker for mortality at 3 years. Patients with severe, generalized pruritus associated with Hodgkin disease have significantly shorter survival than those with mild or no pruritus.

Sex

The sex of the patient does not seem to be associated with pruritus in systemic diseases.

Certain causes of cholestasis are more common in women than in men. These include primary biliary cirrhosis (90% of patients are women) and cholestasis of pregnancy. Primary biliary cirrhosis is thought to be an autoimmune disease that causes destruction of the small and medium bile ducts, leading to cholestasis. It most often occurs in women in the fourth or fifth decade of life, but it can occur in women as young as 20 years. Most patients initially present with fatigue and pruritus, and any women presenting with these symptoms should be suspected to have primary biliary cirrhosis. A positive antimitochondrial antibody finding has 98% specificity for the disease.

When an older man presents with generalized pruritus and iron deficiency but not anemia, the physician should consider the possibility of cancer, and routine screening tests (eg, fecal occult blood test, serum ferritin test, and urinalysis) may assist in diagnosing the cancer.

Age

Pruritus is more common in elderly people. Age is not related to the development of pruritus in systemic disease.

Causes of night sweat

In some cases, night sweats may be triggered by something as straightforward as too many blankets on your bed or certain medications. Many women have night sweats when they go through menopause. Sometimes night sweats can be caused by a medical disorder. Infection, cancer, problems in your nervous system or in your body's hormone-producing glands (endocrine system) can all trigger night sweats.

Medications that can cause night sweats
Night sweats are a common side effect of many medications, such as:

• Antidepressants
• Antipyrectics — medications that lower your body's temperature
• Hormone therapy — medications that regulate the amount of hormones in your body
• Hypoglycemic agents — medications that decrease the level of sugar (glucose) in your blood

Medical conditions that can cause night sweats
Diseases and conditions that can cause night sweats include:

• Autonomic neuropathy     (damage to your autonomic nerves)
• Brucellosis    (a bacterial infection)
• Carcinoid syndrome     (a syndrome resulting from a certain type of cancerous tumor)
• Endocarditis     (an infection of your heart lining)
• HIV/AIDS
• Hodgkin's lymphoma (Hodgkin's disease)
• Hyperthyroidism (overactive thyroid)
• Leukemia
• Menopause
• Myelofibrosis     (a bone marrow disorder)
• Non-Hodgkin's lymphoma
• Osteomyelitis     (a bone infection)
• Pheochromocytoma     (a rare adrenal gland tumor)
• Pyogenic abscess (a pus-filled cavity caused by an infection)
• Stroke
• Syringomyelia (a fluid-filled cyst in the spinal cord)
• Tuberculosis

Transient ischemic attack

A transient ischemic attack (TIA) is when blood flow to a part of the brain stops for a brief period of time. A person will have stroke-like symptoms for up to 1-2 hours.

A TIA is felt to be a warning sign that a true stroke may happen in the future if something is not done to prevent it.

Causes, incidence, and risk factors

A TIA is different than a stroke. After a TIA, the blockage breaks up quickly and dissolves. Unlike a stroke, a TIA does not cause brain tissue to die.

The loss of blood flow to an area of the brain can be caused by:

• A blood clot in an artery of the brain
• A blood clot that travels to the brain from somewhere else in the body (for example, from the heart)
• An injury to blood vessels
• Narrowing of a blood vessel in the brain or leading to the brain

High blood pressure is the number one risk for TIAs and stroke. The other major risk factors are:

• Atrial fibrillation
• Diabetes
• Family history of stroke
• High cholesterol
• Increasing age, especially after age 55
• Race (African Americans are more likely to die from stroke)

People who have heart disease or poor blood flow in their legs caused by narrowed arteries are also more likely to have a TIA or stroke.

Symptoms

Symptoms begin suddenly, last only a short time (from a few minutes to 1 - 2 hours), and go away completely. They may occur again at a later time.

The symptoms of TIA are the same as the symptoms of a stroke and include sudden:

• Abnormal feeling of movement (vertigo) or dizziness
• Change in alertness (sleepiness, less responsive, unconscious, or in a coma)
• Changes in feeling, including touch, pain, temperature, pressure, hearing, and taste
• Confusion or loss of memory
• Difficulty swallowing
• Difficulty writing or reading
• Inability to recognize objects or people
• Lack of control over the bladder or bowels
• Lack of coordination and balance, clumsiness, or trouble walking
• Muscle weakness of the face, arm, or leg (usually only on one side of the body)
• Numbness or tingling on one side of the body
• Personality, mood, or emotional changes
• Problems with eyesight (double vision, loss of all or part of vision)
• Trouble speaking or understanding others who are speaking

Signs and tests

Almost always, the symptoms and signs of a TIA will have gone away by the time you get to the hospital. A TIA diagnosis may be made based on your medical history alone.

The health care provider will do a complete physical exam to check for heart and blood vessel problems, as well as for problems with nerves and muscles.

Yourblood pressure may be high. The doctor will use a stethoscope to listen to your heart and arteries. An abnormal sound called a bruit may be heard when listening to the carotid artery in the neck or other artery. A bruit is caused by irregular blood flow.

Tests will be done to rule out a stroke or other disorders that may cause the symptoms.

• You will almost always have a head CT scan or brain MRI. A stroke will show changes on these tests, but TIAs will not.
• You will have an angiogram, CT angiogram, or MR angiogram to see which blood vessel is blocked or bleeding.
• You may have an echocardiogram if your doctor thinks you may have a blood clot from the heart.
• Carotid duplex (ultrasound) can show if the carotid arteries in your neck have narrowed.
• You may have EKG and heart rhythm monitoring tests to check for irregular heartbeat.

Your doctor may do other tests to check high blood pressure, heart disease, diabetes, high cholesterol, and other causes of and risk factors for TIAs or stroke.

Treatment

The goal is to prevent a stroke.

If you have had a TIA within the last 48 hours, you will likely be admitted to the hospital so that doctors can search for the cause and observe you.

High blood pressure, heart disease, diabetes, and blood disorders should be treated as needed.

You may receive blood thinners, such as aspirin, to reduce blood clotting. Other options include dipyridamole, clopidogrel, Aggrenox or heparin, Coumadin, or similar medications. You may be treated for a long period of time.

Some people who have clogged neck arteries may need surgery (carotid endarterectomy).

Expectations (prognosis)

TIAs do not cause lasting damage to the brain.

However, they are a warning sign that you may have a true stroke someday. More than 10% of people who have a TIA will have a stroke within 3 months. Half of these strokes happen during the 48 hours after a TIA. The stroke may occur that same day or at a later time. Some people have only a single episode, and some have more than one episode.

You can reduce your chances of a future stroke by following-up with your health care provider to manage your risk factors.