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130 Cards in this Set
- Front
- Back
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pruritic
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Severe itching, often of undamaged skin.
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ecclampsia
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an acute and life-threatening complication of pregnancy, is characterized by the appearance of tonic-clonic seizures in a patient who had developed preeclampsia; rarely does eclampsia occur without preceding preeclamptic symptoms. Hypertensive disorder of pregnancy and toxemia of pregnancy are terms used to encompass both preeclampsia and eclampsia. Seizures and coma that happen during pregnancy but are due to preexisting or organic brain disorders are not eclampsia.
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diaphoretic
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sweating
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atelectasis
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is a collapse of lung tissue affecting part or all of one lung
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respiratory embarassement
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embarrassment is a synonym for distress
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VAP
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ventilator-associated pneumonia (VAP)
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ARDS
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Acute respiratory distress syndrome
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SOB
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shortness of breath
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myelophthisis
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1. Wasting or atrophy of the spinal cord.
2. Replacement of hemopoietic tissue in the bone marrow by abnormal tissue, usually fibrous tissue or malignant tumors. Also called panmyelophthisis. |
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pancytopenia
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anemia, leukopenia, thrombocytopenia
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pericardial tamponade
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is an emergency condition in which fluid accumulates in the pericardium
Beck's triad: drop arterial BP, rise venous BP, suppressed heart sounds |
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Cancer symptoms
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Weight loss
Fatigue Anemia Fever Hypoalbuminemia Hypogammaglobinemia Abnormal Protein Impaired Immunity Hypermetabolism/catabolism Hyperuricemia (uric acid) |
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cachexia
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is loss of weight, muscle atrophy, fatigue, weakness and significant loss of appetite in someone who is not actively trying to lose weight.
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nape of the neck
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back of the neck
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Anaphylactoid
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Reactions to radiocontrast dye are anaphylaCTOID, which means mast cell degranulate but not via IgE mediated mechanisms.
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Anaphylactic
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AnaphylaCTIC means mast cells degranulated because antigens have cross linked cell surface IgE.
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Anaphylaxis
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Massive mast cell degranulation causes systemic anaphylaXIS.
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Anaphylaoxins
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C3a, C4a, and C5a are anaphylaTOXINS, which refers to their ability to interact with specific receptors on mast cells (not via IgE) to induce them to degranulate.
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Patients who have reacted to contrast dye in the past should be pretreated with H1 and H2 antihistamines 15 minutes before the procedure. T/F?
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T: Since the reaction is caused by mast cells, you block most of the problematic immediate symptoms by blocking histamine binding to tissue cell receptors. For maximum efficacy, both H1 and H2 blockers are used since there are some H2 receptors in skin and blood vessels. Patients with troublesome urticaria may also require both H1 and H2 blocking antihistamines to effectively treat their urticaria.
Pretreating patients with antihistamines is only contraindicated in one condition – when doing drug desensitization. On that protocol, you induce a slow controlled anaphylaxis. You need to be able to monitor the effect of the mast cells that you are degranulating and slow down the process as needed. You do not want to risk having the antihistamine effect wear off mid-protocol and have the patient become seriously hypotensive, etc. |
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Desensitization?
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slow, controlled anaphylaxis under medical supervision, used to degranulate mast cells over 4-8 hours so that you can administer a substance to which the patient has type I hypersensitivity. The classical example is desensitizing a patient who is allergic to penicillin so that they can be treated with penicillin because it is the only drug that will cure their serious, life-threatening infection.
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“Immunotherapy” is the term for ....
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“allergy shots” where you are trying to divert the immune response away from IgE.
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characteristic timing for type I reactions
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These occur 5-15 min after contact with the allergen, (occasionally an hour for food if it needs to be digested to cause a reaction). There may be a late phase reaction as part of a type I response. These occur 4-10 hrs after antigen exposure, typically 6-8 hrs. Frequently the immediate reaction occurs without an obvious late phase; however it would be very unusual to have a late phase reaction without any apparent immediate reaction.
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characteristic timing for type II/III reactions
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Type II and III reactions also occur rapidly, usually within minutes to at most a few hours after introduction of the antigen into the body since they also depend on the sensitized subject having circulating antibody at the time he/she is exposed to the antigen. The difference is that type II and III reactions are caused by circulating, complement fixing IgM and IgG antibodies.
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characteristic timing for type IV reactions
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Type IV (delayed-type) reactions become apparent 2 days after antigen exposure; think of when PPDs are read, because you have to wait until the right antigen specific T cell happens to migrate past the site where the antigen is located (e.g. the skin for a PPD)
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In almost all cases, whether the reaction is type I, II, III or IV an allergic reaction represents a secondary response to the antigen. The only exceptions are.....??
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reactions to antigens that, when first incorporated in the body, are very slowly catabolized. For example, one can get serum sickness to the initial dose of horse antitoxin because the antigen is the horse IgG and this protein, like all IgGs, has a 2-3 week half-life. This allows plenty of time to make antibodies to the IgG and experience reactions to it when one’s newly produced anti-horse IgM and IgG antibodies react with the horse immunoglobulin that is still in your body. However, the subsequent times you receive horse serum, your reaction would be faster (if you have IgG or IgM) or very fast (if you had IgE) antibodies specific for horse serum proteins.
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Why do a skin test for immediate hypersensitivity?
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Quest to finding IgE
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A patch test looks for?
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Type IV - the T cells march to the injury - tested for the adhesion molecule deficinecy (LFA-1-ICAM or VLA-4-VCAM)
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Tryptase serum test
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Released histamine is promptly degraded by histaminase but tryptase is not. Consequently one can verify that a patient experienced massive mast cell degranulation several hours previously by measuring serum tryptase.
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Complement tests to differentiate the different pathway inhibitions
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A decrease in the CH50 indicates that one or more of the Complement proteins are low, probably because they have been used up or are otherwise deficient. For example when the alternative pathway is activated by bacterial sepsis, activation starts with the binding of C3 to the microbe. Thus C1, C2 and C4 levels will remain within normal limits but C3 will be depleted. If the classical pathway is activated, C1, C2, C3 and C4 will be consumed. Similarly, if activation is through the mannose binding ligand, C1 will be unaffected, but C2, C3 and C4 will be depleted. To save money and time, one measures only C3 and C4 to discriminate alternative from classical or mannose pathway activation. However, measuring C3 can be tricky. If the disease persists and inflammation goes on for several days, the liver begins to make huge quantities of all the complement proteins. Complement proteins are among the acute phase reactants. So as the disease process persists C3 levels may rise to the normal range or beyond even though it is still being consumed at an accelerated rate.
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unusually high frequency of recurrent/persistent episodes of sinusitis. He also has pulmonary symptoms (cough). Your differential diagnosis would include severe recurrent sinusitis, immunodeficiency (HIV or new onset combined variable immunodeficiency), or Wegeners.
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Urinalysis, renal function tests (BUN, Creatinine) and serum C-ANCA.
Yes. Wegeners includes necrotizing glomerulonephritis which would give him abnormal renal function, (tested by BUN and Creatinine) and abnormal urinalysis (hematuria, casts, etc). cANCA is an autoantibody to a cytoplasmic protein (serine protease) in neutrophils. It is highly associated with Wegeners even though it is not clear how this autoantibody might participate in the pathophysiology of the disease. |
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Treatment with systemic corticosteroids is contraindicated in which of the following diseases?
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Kawasaki’s is perhaps the only one of the major vasculitides where corticosteroids are actually contraindicated because children treated with these had a higher incidence of coronary aneurysms and rarely, coronary artery rupture followed by pericardial tamponade and death. Current best treatment is intravenous immunoglobulin which is pooled from thousands of healthy donors. It is not clear why this helps, but the theory is that the children may actually have some type of infection for which the IVIG contains antibodies. Other theories are that the IVIG may contain antibodies that down regulate autoantibody-producing B cells.
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What is allergy?
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It is best to reserve “allergy” for type I and to consider the types II, III, and IV as hypersensitivities.
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"I took a Penicillin capsule and felt sick to my stomach later that night" - is this allergy?
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Not allergic. The timing is too late to be type I and the symptoms do not sound like they are mediated by mast cells.
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“I took some Penicillin for about a week and after a couple of days I got this rash all over my body. It really itched” - allergy?
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Not allergic. You have no idea what really caused their rash. It may of may not have been the penicillin. It could have been a virus, or something else they took in that interval. Without the close timing between the penicillin and the reaction, you can’t be sure and you would not want to label them as allergic strictly based on this history.
True, it could be urticarial vasculitis caused by IgG antibodies that developed to penicillin. These could have reacted with penicillin bound to their serum proteins and the immune complexes could have deposited in the tiny vessels of the skin (type III hypersensitivity). Alternatively the penicillin could have bound to blood vessel walls and the IgG antibodies could have reacted with the bound penicillin. This is sort of a type II reaction, since the antigen is located on the tissue. You would want to describe the patient’s reaction in your history but would not label them as necessarily penicillin allergic. |
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urticaria
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Urticaria (or hives) are a kind of skin rash notable for dark red, raised, itchy bumps. Hives are frequently caused by allergic reactions, however there are many non-allergic causes.
For example, most cases of hives lasting less than 6 weeks (acute urticaria) are the result of an allergic trigger. Chronic urticaria (hives lasting longer than 6 weeks) are rarely due to an allergy. The majority of patients with chronic hives have an unknown (idiopathic) cause. Perhaps as many as 30-40% of patients with chronic idiopathic urticaria will, in fact, have an autoimmune cause. Acute viral infection is another common cause of acute urticaria (viral exanthem). Less common causes of hives include friction, pressure, temperature extremes, exercise, and sunlight. It may be true that hives are more common in those with fair skin. Weals (raised areas surrounded by a red base) from urticaria can appear anywhere on the surface of the skin. Whether the trigger is allergic or non-allergic, there is a complex release of inflammatory mediators, including histamine from cutaneous mast cells, resulting in fluid leakage from superficial blood vessels. Weals may be pinpoint in size, or several inches in diameter. Angioedema is a related condition (also from allergic and non-allergic causes), though fluid leakage is from much deeper blood vessels. Individual hives that are painful, last >24 hours, or leave a bruise as they heal are more likely to be a more serious condition called urticaria pigmentosa. Hives caused by stroking the skin (often linear in appearance) is due to a benign condition called dermatographism. |
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“I got a Penicillin shot and as I was leaving the doctor’s office I got this really intense migraine headache” - allergy ?
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Not allergic. Timing could fit with Type I but the symptoms don't fit. Without additional history compatible with anaphylaxis, you would not label them allergic.
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Arthus reactions
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result when an antigen is injected into the muscle, and IgG antibodies react with the antigen where it is deposited. This causes local immune complex mediated inflammation. When there are circulating IgG antibodies these localized type III reactions may develop within a few hours after the injection. They usually resolve within a day or two.
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When to use Desensitization or Immunotherapy?
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Desensitization: ex: when the risk of dying from endocarditis outweighs the risk of desensitization to the only available antibiotic-penicillin.
Immunotherapy: Immunotherapy can be very effective for allergic rhinitis and you have a candidate antigen identified by skin testing neither: aggressive asthma with corticosteroids, a hypersensitivity reaction to an allergen formed when meta toluenediamine binds to some protein in his body. If you have no idea exactly what the allergenic epitope is, you have no reagent with which to administer immunotherapy |
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priapism
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is a potentially harmful and painful medical condition in which the erect penis does not return to its flaccid state, despite the absence of both physical and psychological stimulation, within four hours. Priapism is considered a medical emergency, which should receive proper treatment by a qualified medical practitioner.
The name comes from the Greek god Priapus, referring to the myth that he was punished by the other gods for attempting to rape a goddess, by being given a huge, but useless, set of wooden genitals. |
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Orthostatic hypotension
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dizzy spells upon getting up- Drop in BP. May be due to hypovolemia or alpha 1 blockers (prohibit constriction)
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angioedema
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Quincke's edema, is the rapid swelling (edema) of the dermis, subcutaneous tissue,[1] mucosa and submucosal tissues. It is very similar to urticaria, but urticaria occurs in the upper dermis.[1]
Cases where angioedema progresses rapidly should be treated as a medical emergency as airway obstruction and suffocation can occur. Epinephrine may be lifesaving when the cause of angioedema is allergic. In the case of hereditary angioedema, treatment with epinephrine has not been shown to be helpful. a side effect of ACE inhibitors. three autosomal dominant inherited forms known, due to mutations in the genes that control the clotting cascade, including the SERPING1 gene, which results in deficiency of the blood protein C1-inhibitor (type I HAE) and the F12 gene, which controls Factor XII (type III HAE). There is an additional type in which C1 levels are normal but C1 function is decreased (type II HAE). All three forms are called hereditary angioedema (HAE) or occasionally by the outdated term "hereditary angioneurotic edema" (HANE). In all forms of HAE, swelling may also occur in the digestive tract and other organs. It is life-threatening when it involves the larynx due to the potential for asphyxiation. |
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Asphyxia
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is a condition of severely deficient supply of oxygen to the body that arises from being unable to breathe normally. An example of asphyxia is choking. Asphyxia causes generalized hypoxia, which primarily affects the tissues and organs.
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syncope
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fainting,
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pindolol
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non-selectively antagonizes beta1- and beta2-adrenergic receptors
Serious Reactions * CHF * heart block * bradycardia, severe * Raynaud's phenomenon * bronchospasm * hypersensitivity rxn Common Reactions * insomnia * muscle aches * dizziness * fatigue * elevated LFTs * nervousness * joint pain * edema * abnormal dreams * dyspnea * nausea * weakness * abdominal discomfort * paresthesias * chest pain Contraindications/Cautions * hypersens. to drug/class/compon. * sinus bradycardia * AV block, 2nd or 3rd degree * heart failure, uncompensated * cardiogenic shock * sick sinus syndrome w/o pacemaker * asthma, bronchial * avoid abrupt withdrawal * caution if peripheral vascular dz * caution if bronchospastic dz * caution if major surgery * caution if diabetes mellitus * caution if thyroid disorder * caution if WPW syndrome * caution if impaired liver fxn * caution if impaired renal fxn * caution if pheochromocytoma * caution in pregnancy, 2nd or 3rd trimester * caution if breastfeeding * caution if myasthenia gravis * caution if severe anaphylactic rxn hx * caution in elderly pts |
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acebutolol
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selectively antagonizes beta1-adrenergic receptors
HTN arrhythmia, ventricular Serious Reactions * CHF * heart block * bradycardia, severe * Raynaud's phenomenon * bronchospasm * hypersensitivity rxn Common Reactions * fatigue * dizziness * headache * constipation * diarrhea * dyspepsia * nausea * dyspnea * insomnia * urinary frequency * chest pain * edema * depression * abnormal dreams * rash * arthralgia/myalgia * abnormal vision Contraindications/Cautions * hypersens. to drug/class/compon. * sinus bradycardia * AV block, 2nd or 3rd degree * heart failure, uncompensated * cardiogenic shock * sick sinus syndrome w/o pacemaker * breastfeeding * avoid abrupt withdrawal * caution if peripheral vascular dz * caution if bronchospastic dz * caution if major surgery * caution if diabetes mellitus * caution if thyroid disorder * caution if WPW syndrome * caution if pheochromocytoma * caution if impaired renal fxn * caution if impaired liver fxn * caution if myasthenia gravis * caution if severe anaphylactic rxn hx * caution in elderly pts |
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atenolol
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selectively antagonizes beta1-adrenergic receptors
non-hepatically metabolized Serious Reactions * CHF * heart block * bradycardia, severe * arrhythmias * Raynaud's phenomenon * bronchospasm * hypersensitivity rxn Common Reactions * bradycardia * hypotension * fatigue * dizziness * cold extremities * depression * dyspnea * postural hypotension * leg pain * bronchospasm * lightheadedness * lethargy * diarrhea * nausea * vertigo * drowsiness Contraindications/Cautions * hypersens. to drug/class/compon. * sinus bradycardia * AV block, 2nd or 3rd degree * heart failure, uncompensated * cardiogenic shock * sick sinus syndrome w/o pacemaker * pheochromocytoma, untreated * avoid abrupt withdrawal * caution if peripheral vascular dz * caution if bronchospastic dz * caution if major surgery * caution if diabetes mellitus * caution if thyroid disorder * caution if WPW syndrome * caution if impaired renal fxn * caution in pregnancy * caution if breastfeeding * caution if myasthenia gravis * caution if severe anaphylactic rxn hx * caution in elderly pts |
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metaprolol
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beta-1 antagonist selective
HTN, Angina, acute MI, post MI, CHF, Serious Reactions * CHF * heart block * cardiogenic shock (MI pts) * bradycardia, severe * Raynaud's phenomenon * gangrene (rare) * bronchospasm * hepatitis (rare) * hypersensitivity rxn * photosensitivity (rare) Common Reactions * fatigue * dizziness * diarrhea * pruritus * rash * depression * dyspnea * bradycardia |
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Indirect Cholinergic Agonist via?
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Acetyl choline esterase inhibitors
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Edrophonium
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indirect cholinergic agonist: acetylcholine esterase inhibitor
an alcohol; used to test myasthenia gravis Serious Reactions * Brand Discontinued in US Common Reactions * Brand Discontinued in US |
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Pyridostigmine
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indirect cholinergic agonist: acetylcholine esterase inhibitor
a carbamate 15-40 min |
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Neostigmine
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indirect cholinergic agonist: acetylcholine esterase inhibitor
a carbamate 2-4h |
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Physiostigmine
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indirect cholinergic agonist: acetylcholine esterase inhibitor
a carbamate 4-6h |
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Parathion
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indirect cholinergic agonist: acetylcholine esterase inhibitor
an organophosphate - nerve gas long lasting effect |
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Sarin
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indirect cholinergic agonist: acetylcholine esterase inhibitor
an organophosphate, very long effect |
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PAM
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Pralidoxime = PAM
Cholinesterase regenerator; the nerve gas antidote |
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Echothiophate
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=Phospholine Iodide
irreversible indirect cholinergic agonist: acetylcholine esterase inhibitor glaucoma, chronic open-angle esotropia, accomodative erious Reactions * arrhythmias * hyphema * retinal detachment * iritis * uveitis * Iris cysts * conjunctival thickening (prolonged use) * nasolacrimal duct obstruction (prolonged use) * lenticular opacification * elevated IOP Common Reactions * stinging * burning * lacrimation * blepharospasm * conjunctival erythema * ciliary erythema * tolerance * browache * miosis * myopia * blurred vision contraindications: * hypersens. to drug/class/compon. * uveal inflammation, active * glaucoma, angle-closure * caution if myasthenia gravis * caution if uveitis hx * caution if quiescent uveitis * caution if vagotonia * caution if asthma * caution if GI motility disorder * caution if PUD * caution if bradycardia * caution if hypotension * caution if recent MI * caution if epilepsy * caution if Parkinson's dz * caution if retinal detachment hx * caution if insecticide/pesticide exposure |
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Isofluorophosphate
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indirect cholinergic agonist: acetylcholine esterase inhibitor
irreversible |
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methacholine
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direct cholinergic agonist
for: bronchial hyperreactivity diagnosis erious Reactions * bronchoconstriction * respiratory distress, acute Common Reactions * throat irritation * headache * lightheadedness * chest tightness * dyspnea * cough * wheezing * incr. respiratory secretions * pruritus Contraindications/Cautions * hypersens. to drug/class/compon. * asthma * concurrent beta-blocker * FEV 1 < 70% * caution if urinary tract obstruction * caution if cardiovascular dz * caution if epilepsy * caution if PUD * caution if thyroid dz * avoid in pregnancy |
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bethanechol
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=Urecholine
muscarinic Acetylcholine agonist urinary retention Neurogenic bladder, GERD Serious Reactions * bronchospasm * hypotension * tachycardia * seizures Common Reactions * abdominal cramps/discomfort/pain * nausea * belching * borborygmi * diarrhea * urinary urgency * salivation * headache * hypotension * vasomotor response * malaise * flushing * diaphoresis * miosis * lacrimation * bronchospasm Contraindications/Cautions * hypersens. to drug/class/compon. * bladder neck obstruction * bladder surgery, recent * GI obstruction * GI surgery, recent * GI disturbances, spastic * GI lesions, acute inflammatory * PUD * peritonitis * vagotonia, severe * vasomotor instability * CAD * hypotension, severe * bradycardia, severe * hyperthyroidism * asthma * seizure disorder * Parkinson's dz * caution if hypotension |
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pilocarpine
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muscarinic Acetylcholine agonist
alkaloid for xerostomia=dry mouth Serious Reactions * pulmonary edema * visual impairment * impaired fertility * bradycardia * tachycardia * hypotension * HTN * syncope (rare) * AV block, complete (rare) * arrhythmias (rare) * cholecystitis * biliary spasm * shock Common Reactions * sweating * chills * nausea * flushing * rhinitis * dizziness * asthenia * urinary frequency * diarrhea * headache * vomiting * dyspepsia * HTN * edema * amblyopia * tremor * dysphagia * voice changes Contraindications/Cautions * hypersens. to drug/class/compon. * asthma, acute * glaucoma, angle-closure * acute iritis * caution if cardiovascular dz * caution if asthma, COPD * caution if bronchitis, chronic * caution if impaired liver fxn * caution if biliary dz * caution if nephrolithiasis * caution if psychiatric illness |
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side effects of cholinergic agonists
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DUMB BELSS
Diarrhea, Urination, Miosis, Bronchoconstriction, Bradycardia, Excitation (of skeletal muscle & CNS), Lacrimation, Salivation and Sweating |
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atropine
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antimuscarinic
use: organophosphate/carbamate poisoning nerve agent poisoning: give atropine first if also using pralidoxime (2-PAM) Serious Reactions * hallucinations * depression * psychosis, anticholinergic * ataxia * arrhythmias * paralytic ileus * glaucoma, angle-closure * seizures * pulmonary edema * respiratory failure * laryngospasm * anaphylaxis Common Reactions * injection site pain * dry mouth * mydriasis * blurred vision * photophobia * confusion * headache * dizziness * tachycardia * palpitations * flushing * urinary hesitancy/retention * constipation * abdominal distension * nausea/vomiting * anhidrosis * heat intolerance * impaired body temperature regulation * restlessness * tremor * fatigue * motor difficulties * rash * delirium * decreased libido * impotence Contraindications/Cautions * caution if hypersens. to drug/class/component * caution if glaucoma, angle-closure * caution if asthma, COPD * caution if cardiac dz * caution if arrhythmia * caution if recent MI * caution in pediatric pts * caution in elderly pts * caution if GI/GU obstruction * caution if pyloric stenosis * caution if prostatic hypertrophy * caution if ulcerative colitis, severe * caution if impaired renal fxn, severe * caution if high environmental temperature * caution if hyperthyroidism |
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Scopolamine
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antimuscarinic
nausea/vomiting prevention anesthesia adjunct anticholinergic antisialogogue amnesia sedation |
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ipratropium
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=Atrovent HFA
antagonizes acetylcholine at muscarinic receptors (anticholinergic) Serious Reactions * hypersensitivity rxn (rare) * anaphylaxis (rare) * angioedema (rare) * laryngospasm (rare) * bronchospasm, paradoxical (rare) * glaucoma, angle-closure * tachycardia * atrial fibrillation Common Reactions * bronchitis * dyspnea * URI * cough * COPD exacerbation * nausea * dry mouth * influenza-like sx * dizziness * rhinitis * UTI * back pain * headache Contraindications/Cautions * hypersens. to drug/class/compon. * hypersens. to atropine * caution if glaucoma, angle-closure * caution if prostatic hypertrophy * caution if bladder neck obstruction |
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Raynaud's phenomenon
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Raynaud's phenomenon (RP) is a condition resulting in a particular series of discolorations of the fingers and/or the toes after exposure to changes in temperature (cold or hot) or emotional events. Skin discoloration occurs because an abnormal spasm of the blood vessels causes a diminished blood supply to the local tissues. Initially, the digit(s) involved turn white because of the diminished blood supply. The digit(s) then turn blue because of prolonged lack of oxygen. Finally, the blood vessels reopen, causing a local "flushing" phenomenon, which turns the digit(s) red. This three-phase color sequence (white to blue to red), most often upon exposure to cold temperature, is characteristic of RP.
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Xerostomia
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Xerostomia is the medical term for a dry mouth due to a lack of saliva. Xerostomia is sometimes colloquially called pasties, cottonmouth, or doughmouth.
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suppuration
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formation of pus
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ulcer
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loss of epithelium
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transudate
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low protein, few cells
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fibrinous pericarditis
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"bread and butter" pericarditis
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lymphangitis
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inflammation of lymph
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cellulitis
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inflammation of the conective tissue -not localized
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dehiscence
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defective scar / ulceration
cut that opens wound |
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systemic effect of inflammation
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fever (chills, anorexia, somnolence, malaise(discomfort)), leukocytosis (left shift)
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wound strength
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never as strongs as becore the injury - best 70-80%
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keloid formation
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hypertrophic scar
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granulation tissue
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Loose, edematous, highly vascular tissue present in the initial phases of healing
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Granuloma
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Specialized type of chronic inflammation characterized by epithelioid histiocytes
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Adhesion (Hemostasis)
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VWF + gpIb
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Aggregation (Hemostasis)
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fibrinogen + gpIIb-IIIa
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PTT
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Intrinisic (XII, XI, IX, VIII, X, V, II)
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Secretion
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ADP and Calcium
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Extrinsic
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III VII X V, II
PT time |
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from X to clot?
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Factor Xa + Va (+ calcium) convert Prothrombin --> Thrombin
Thrombin converts Fibrinogen --> Fibrin Fibrin polymerizes/cross links (with XIII) to make a fibrin clot |
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plasmin action
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Plasmin attacks the D-E bonds
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XIII crosslinks?
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between D-D
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Disseminated Intravascular Coagulation (DIC):
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Positive D-dimer suggests that clotting has taken place; consumptive coagulopathy, is a pathological activation of coagulation (blood clotting) mechanisms that happens in response to a variety of diseases.
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Inhibitors of clotting
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Antithrombin - inhibits the action of thrombin
Proteins C & S - inhibit Factor Va-VIIIa complex Plasminogen - acts on fibrin(ogen) to dissolve clot |
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anasarca
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systemic edema
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hyperemia vs congestion
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Hyperemia = active process - increased arterial blood flow to an area
Congestion = passive process - decreased venous flow from an area both cause increased hyperstatic pressure |
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nutmeg liver
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chronic congestion of right side of heart - the heart won't pull out from IVC as much
central veins - congestion |
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hyperemia and congestion on the lung
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must see the dialated cappilaries in the alveoli;
chronic: heart failure cells with less edema (they ate it up) |
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hematoma of skin
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small = petechiae, medium = purpura, large = ecchymosis
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most common cause of LHF
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* Hypertension.
* CAD. * MI. * Mitral valve incompetence. * Aortic valve incompetence. |
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RHF
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* Distended neck veins, raised JVP.
* Nutmeg liver. * Enlarged, congested spleen. * Congested kidneys. * Pitting, ankle edema. * Ascites. |
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LHF
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* Pulmonary edema.
* Cyanosis. * Dyspnea. * Paroxysmal nocturnal dyspnea. * Cough. * Frothy sputum. * Fatigue. * Tachycardia. * S3. * Pulsus alterans. * Systemic hypofusion: • Kidneys underperfused. • Muscles underperfused, so weak. • Brain underperfused, so confusion in elderly. |
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cause of RHF
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* LHF.
* COPD [called "cor pulmonale"]. * Tricuspid regurgitation. |
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caissons
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the bends, - gas emboli
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Paradoxical embolus
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thrombus from veins that ends up in the arterial circulation bc there is a hole in the heart
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Amniotic fluid embolus -
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tear in placental membranes and uterine veins (cause of DIC)
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types of infarct?
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Red infarct = hemorrhagic (venous obstruction, organs with double blood flow) (loose spongy tissue and double perfusion)
White/pale infarct = arterial occlusion |
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increased ESR/CRP
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ESR/CRP (acute phase reactants) seen in inflammation
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Desmoplasia
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fibrous stroma in some cancers
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Benign tumors = “root word” + _oma
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Fibroma = benign tumor of fibrous tissue
Adenoma = benign gland-forming tumor Cystadenoma = benign tumor forming cysts Papilloma = benign tumor with “finger-like” projections on surface Polyp = tumor that projects into a lumen, generally benign |
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Hamartoma
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tumor composed of indigenous tissues
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Choristoma
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made of tissues that don’t belong in that site – ectopic tissue
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sarcoma or carcinoma?
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Rhabdomyosarcoma (mesenchymal origin)
Adenocarcinoma (epithelial origin) |
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Ewing sarcoma
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malignant bone tumor
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Wilms tumor
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malignant renal tumor (=nephroblastoma)
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Neuroblastoma
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malignant tumor of primitive neural tissue
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Hepatoma –
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malignant - liver tumor
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lymphoma
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Lymphoma – malignant tumor of lymphoid cells
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Anaplasia =
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Anaplasia = lack of differentiation (undifferentiated)
Pleomorphism Hyperchromasia High nuclear:cytoplasmic (N:C) ratio Prominent nucleoli High mitotic rate, abnormal mitotic figures Tumor giant cells Loss of normal orientation |
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ptosis
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drooping of the eyelid
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tarsal
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superior and inferior eyelid contain the respective smooth muscles - sypathetic chain injured causes ptosis
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Horners syndrome
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levator palpebrae or the smooth muscle part? blockage of the sypathetic chain - the smooth muscle is not recieveing it's innervation.
if it wasn't a partial ptosis - then it would be the nerve for the whole muscle - then it would be CN III |
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chalazion
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Blockage of Tarsal Glands that thicken tears. Noninfectious
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style
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Blockage of Eyelash follicles
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lacrimal apparatus
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Lacrimal gland , lacrimal canaliculi, lacrimal sac, and nasolacrimal duct
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choncha with mucousa
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turbinate
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puncta
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openings of the lacrimal canaliculi
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caruncle
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middle corner of eye
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LR(?)SO?
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(LR)6(SO)4
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intortion
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internal rotation, compared to extortion
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SO goes?
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down and out - -
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connection of all 4 rectus?
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central tendinous ring
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ganglion of the CN III
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ciliary ganglion - the parasympathetics will synapse here - they go to the constrictor of the iris -- though the short ciliary
also the sympathetics come through here - they mostly come from the internal carotid and the ophhalmic (some don't come through the ganglion) (M3 and alpha 1) parasympa come through with CNIII inferior to the CNIII they also both go to the ciliary muscle (M3 and beta 2) |
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what nucleus for the eye reflex?
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pretracheal nucleus;
shining in one eye - both eyes should contstrict bc there is a crossing of the inside branches |
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V1 branches and jobs
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lacrimal, frontal and nasociliary - ALL SENSORY
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which CN are only sensory?
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CN1, 2, V1 V2, 8, (is this right? )
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