medecine part 2
C
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Calcinosis (kal-sin-oh-sis) -
happens when small white calcium lumps form under the skin. This is caused by scleroderma and NOT caused by too much calcium in your diet.
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R
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Raynauds (ray-nodes) Phenomenon
- is a problem of poor blood flow to fingers and toes. Blood flow decreases because blood vessels in these areas become narrow for a short time, in response to cold or to emotional stress.
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E
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Esophageal Dysfunction -
the digestive system includes the mouth, esophagus, stomach, and bowels. Scleroderma can weaken the esophagus and the bowels. It can also build-up of scar tissue in the esophagus, which narrows the tube.
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S
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Sclerodactyly -
(sklare-oh-dack-till-ee) - means "scleroderma of the digits" (fingers and toes). The skin becomes hard and shiny and there is difficulty in bending.
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T
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Telangiectasia -
(tah-lan-jec-tay-shah) - happens when tiny blood vessels near the surface of the skin show through the skin. Small reddish spots appear on fingers, palms, face, lips, and/or tongue.
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elderly:
In elderly men, the gonadotropins are increased because of decreased production of testosterone by Leydig's cells [i.e., luteinizing hormone (LH) is increased] and decreased production of inhibin from Sertoli's cells in the seminiferous tubules [i.e., follicle-stimulating hormone (FSH) is increased].
Hemoglobin drops into adult female ranges , because the testosterone level is decreased, and testosterone normally stimulates erythropoiesis.
The arterial oxygen partial pressure (PaO 2) normally decreases [not increases ] as ventilation and perfusion become less evenly matched in the lungs.
Albumin decreases [not increases ] because of increased protein catabolism and decreased liver synthesis of albumin.
The level of alkaline phosphatase increases [not decreases because of degenerative bone disease (e.g., osteoarthritis) and reactive bone formation.
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Vitamin that may be deficient in an infant receiving goat's milk rather than formula: folate acids
Nutritional deficiency associated with hyperpigmentation in sun-exposed areas in people whose diet primarily consists of corn: niacin deficiency
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Nutritional deficiencies associated with diagnostic changes involving hair or the hair follicle: vit c deficiency
Vitamin associated with inhibition of nitrosamine production in the gastrointestinal tract vit c deficiency
Part 1: A vitamin that may be deficient in an infant receiving goat's milk is folate.
Part 2: Corn is deficient in the essential amino acid tryptophan, which is used in the synthesis of niacin. Niacin deficiency (pellagra) is associated with hyperpigmentation in sun-exposed areas, diarrhea, and dementia.
Part 3: Vitamin A deficiency results in follicular hyperkeratosis (similar to ``goose bumps'') owing to increased keratinization in the hair follicle, whereas vitamin C deficiency (scurvy) has corkscrew hairs and perifollicular hemorrhage from vessel instability.
Part 4: Vitamin C prevents the reduction of nitrites into nitrosamines in the gastrointestinal tract, which reduces the incidence of environmental gastritis (type AB atrophic gastritis) and stomach cancer
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details on shoch will be develop in my surgical chapter , chart is available on my usmle 2 page
Endotoxic shock (septic shock) is commonly secondary to gram-negative septicemia (most commonly Escherichia coli) from a urinary tract abnormality,
such as acute pyelonephritis or urinary tract obstruction. Endotoxin released from the cell walls of gram-negative bacteria produces characteristic hemodynamic findings that significantly differ from those associated with shock caused by hypovolemia (fluid loss),
cardiac dysfunction (cardiogenic shock), and reflex vagal stimulation (neurogenic shock).
Endotoxins activate the complement pathway, resulting in the release of anaphylatoxins C3a and C5a, which cause vasodilation of peripheral vessels, resulting in warm skin.
In addition, increased arteriolar dilatation increases venous return to the heart, with a subsequent increase in cardiac output (high-output failure) .
Endotoxins also stimulate macrophages and monocytes to release tumor necrosis factor-alpha and interleukin-1 (IL-1), which damage endothelial cells and also increase neutrophil adhesion to endothelial cells, thus decreasing the peripheral neutrophil count.
Nitric oxide, a potent dilator, is also released from damaged endothelial cells.
Endothelial damage in the lungs commonly predisposes to adult respiratory distress syndrome and disseminated intravascular coagulation (DIC).
Hypovolemic and cardiogenic shock characteristically are associated with a decreased cardiac output; sinus tachycardia with a weak pulse; and cold,
clammy skin because of peripheral vasoconstriction.
Neurogenic shock is caused by reflex vagal stimulation, with decreased cardiac output, hypotension, and decreased cerebral blood flow, causing the patient to faint
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see also my neuro surgery page
a subgaleal hematoma, which is a result of blood collecting subadjacent to the galea.
It is seen after minor injury, and can be very alarming.
It is not associated with loss of consciousness.
The best treatment for this condition is to leave it alone.
Aspirating the hematoma would only introduce infection, which could be disastrous.
The parent should be reassured that no treatment is necessary.
An epidural hematoma results from blood collecting within the cranial cavity, and is usually seen after a tear of the middle meningeal artery as it courses on the inner aspect of the temporal bone, in which a fracture line is seen. It is associated with a lucid interval and signs of raised intracranial pressure (i.e., headache, vomiting, loss of consciousness, enlarging pupil on the ipsilateral side, and hemiplegia on the contralateral side).
A subdural hematoma results from intracranial hemorrhage within the subdural space. It may be acute or chronic.
A fracture may be absent.
The patient is comatose from the time of injury, and has evidence of cerebral injury.
The prognosis is poor.
Intraventricular hemorrhage is associated with coma, and may result from trauma.
However, it is more commonly seen after hypertensive intracranial hemorrhage,
in which the bleeding spreads to the ventricular system.
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Pain in the face followed by swelling of the face and respiratory difficulties while sunbathing on the grass is most likely due to anaphylactic reaction caused by a bee sting.
Bee stings are the most common cause of death from venomous animal bites in the United States.
Most systemic reactions to insect stings are type I hypersensitivity reactions that occur in previously sensitized patients who have produced high titers of immunoglobulin E (IgE) antibodies against insect venom.
These antibodies attach to mast cells and basophils and are distributed throughout the body. Reexposure to antigen with the bridging of two subadjacent IgE antibodies by antigen on the surface of mast cells and basophils results in the release of histamine and other mediators that are vasodilators and bronchoconstrictors.
The predominant clinical findings involve the skin and the respiratory and cardiovascular systems.
Clinical findings in mildly sensitized persons include a local wheal-and-flare reaction at the site of the bite, pain, hives, flushing, wheezing, rhinitis, conjunctivitis, and fever.
A severely sensitized patient often presents with hypotension, diffuse urticaria, laryngeal edema, bronchospasm, diarrhea with abdominal cramping, and arrhythmias.
Laryngeal obstruction is the most common cause of death in these patients, followed by cardiovascular collapse.
Initially, anaphylaxis is treated with subcutaneous administration of aqueous epinephrine 1:1000.
The dose is 0.1 mg/kg with a maximum dose of 0.3 to 0.5 ml.
This is repeated every 20 to 30 minutes if necessary.
If there is no response to this therapy, or if the patient is in profound shock, a 1:10,000 dose of aqueous epinephrine is given intravenously
. If orofacial swelling is present, the patient is intubated before laryngeal edema precludes this approach.
Other options in less severe envenomations include the use of diphenhydramine hydrochloride (1 mg/kg) either by mouth or parenterally.
A nebulized b2 agonist, such as albuterol , or intravenous aminophylline is useful in the treatment of bronchospasm.
Intravenous administration of hydrocortisone is sometimes used in moderate to severe envenomations but does not appear to prevent recurrent waves of anaphylaxis.
The sting site should be examined and the stinger removed by scraping it out with a knife rather than using tweezers, which can introduce more venom into the wound.
Patients who have demonstrated exaggerated local cutaneous, respiratory, or cardiovascular reactions to insect stings should be prescribed an emergency epinephrine kit with syringe and should be taught how to use it.
Venom immunotherapy is 95% effective in preventing anaphylaxis on subsequent exposures.
Children with only localized cutaneous reactions are at low risk (< 10%) for developing systemic reactions; therefore, immunotherapy is not recommended in these patients.
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Patients with an acute myocardial infarction (MI) who have reappearance of the creatine kinase (CK) isoenzyme MB after 3 days have reinfarction. After an MI, the CK isoenzyme MB begins to rise within 4 to 8 hours, peaks in 24 hours, and disappears in 36 to 72 hours.
Lactate dehydrogenase (LDH) isoenzymes are composed of tetramers of H and M polypeptides to form five distinct isoenzymes that have different proportions in various tissues.
Normally, the
concentration of LDH2 is greater than that of LDH1,
the concentration of LDH1 is greater than that of LDH3,
and LDH4 and LDH5 concentrations are about equal.
In order of decreasing concentration in tissue, LDH2 is present in red blood cells (RBCs) and heart muscle,
whereas LDH1 is present in RBCs and heart muscle in reverse proportions.
Therefore, myocardial damage results in an LDH 1/ LDH 2 flip because LDH 1 has the higher concentration in cardiac muscle.
The LDH 1/LDH 2 flip has a sensitivity of 80% and a specificity of 95%.
It first is evident in 14 hours, peaks in 2 to 3 days, and disappears in 7 days;
therefore, it is not very useful in documenting myocardial injury within the first 24 hours.
Presence of an LDH 1/LDH 2 flip in this patient is expected on day 4 and does not contribute to the diagnosis of reinfarction.
Recurrent angina is ruled out by the reappearance of CK isoenzyme MB, which documents further injury
Dressler's syndrome is an autoimmune pericarditis that presents with fever, a pericardial friction rub, pleuritis, arthralgias, and neutrophilic leukocytosis in weeks to months following myocardial injury.
It is not associated with the presence of CK isoenzyme MB.
A posteromedial papillary muscle most commonly ruptures when the cardiac muscle is softest, and that occurs approximately day 4 to 7.
The ruptured muscle would present with a murmur of mitral insufficiency.
In addition, it is associated with thrombosis of the right coronary artery, which supplies the posterior part of the heart rather than being associated with the left anterior descending coronary artery, which would be responsible for the anterior MI in this patient.
A pulmonary embolus does not produce an increase in CK isoenzyme MB.
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Upon even slight suspicion of meningitis, it is wise to perform a spinal tap
Features common to most cases of meningitis include headache (often the predominant presenting symptom and, unlike most headaches, is generally more severe when lying down and resting); photophobia; vomiting; giddiness; fever; and stiffness of the neck, spinal muscles, and hamstrings.
The analysis of the spinal fluid indicated that she suffered from aseptic meningitis, most typically induced by a viral infection. In viral meningitis, there are few white blood cells (WBCs), which primarily are mononuclear lymphocytes.
In aseptic meningitis, the spinal fluid glucose level is usually in the low-normal range, and protein levels tend to be elevated.
Although the patient presented with sufficient symptoms to diagnose a case of meningitis, many symptoms were marginal, suggesting that it was not a fulminating case, as is often seen in bacterial meningitis .
Bacterial meningitis is characterized by a greater number of leukocytes, which are primarily polymorphonuclear neutrophils.
The spinal fluid glucose level is generally significantly lower than normal, and protein levels are elevated to a greater degree than in aseptic meningitis (i.e., often above 100 mg/ml).
Cryptococcal meningitis is almost always an opportunistic infection in an immunocompromised host.
Although human immunodeficiency virus (HIV) and herpes simplex virus type 2 infection may cause chronic viral meningitis, her history tends to rule these out as causative agents.
Actinomyces meningitis , although uncommon, might be suspected in this case because the patient had recent dental work, a significant risk factor for infection by this anaerobic class of bacteria.
However, the laboratory results are characteristic of a bacterial infection.
Coccidia immitis meningitis , although relatively rare, might also be suspected because the patient comes from the San Joaquin valley in California.
To make this diagnosis, the glucose level in the spinal fluid should be well below normal.
It is critically important to distinguish between bacterial and viral meningitis.
If bacterial meningitis is not properly managed, the consequences are severe, often resulting in death, whereas viral meningitis is generally self-limited. Viral meningitis caused by herpes and HIV are major exceptions to this rule.
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African-American woman with right upper quadrant pain has calculi present in the gallbladder on ultrasound examination. Physical examination shows mild splenomegaly. Laboratory studies show a mild normocytic anemia with an elevated reticulocyte count. Many of her red blood cells (RBCs) are reported to have no central areas of pallor. Which of the following mechanisms is most likely responsible for her anemia and subsequent gallbladder disease= Extravascular hemolysis
Young patients with gallstones, anemia, and splenomegaly are always suspect for an extravascular hemolytic anemia, particularly congenital spherocytosis.
Gallstones are best recognized by ultrasound (gold standard test), whereas hemolytic anemias are identified by an elevated reticulocyte count reflecting increased marrow turnover of red blood cells (RBCs) in response to the hemolysis.
The patient has congenital spherocytosis, which is an autosomal dominant disease with a deficiency of spectrin in the RBC membrane.
Spectrin deficiency results in the formation of spherocytes that have less membrane than a normal RBC.
This condition renders them extremely susceptible to rupture when placed in hypotonic saline solution, which is the basis for the osmotic fragility test. In the peripheral smear,
spherocytes do not have a central area of pallor, as opposed to normal RBCs, which are biconcave discs (doughnuts without holes) with a central area of pallor where hemoglobin (Hgb) is less concentrated.
In addition, their spheroidal shape causes them to be trapped and destroyed in the splenic sinusoids by macrophages, thus the term extravascular hemolysis.
Macrophages degrade the heme of Hgb into unconjugated bilirubin, which is released into the blood stream, taken up by the hepatocyte, converted into conjugated bilirubin, and excreted in the bile.
The increased bilirubin load in the bile precipitates as jet-black calcium bilirubinate stones (pigment stones), predisposing the patient to cholecystitis. Splenectomy is the treatment of choice.
Iron deficiency and anemia associated with inflammation are not hemolytic anemias and do not predispose to gallstones.
Bile salt deficiency does predispose to gallstones but is not associated with a hemolytic anemia.
Although sickle cell disease, the most common hemoglobinopathy in African Americans, is commonly associated with gallstones, no sickle cells are reported in the peripheral smear, thus excluding that diagnosis. Sickle cell trait does not predispose a person to a hemolytic anemia or stone formation.
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