Physio questions on acid base found on moodle .pdf - A 30-year-old man with a 10-year history of chronic alcoholism complains of headache chills nausea

Physio questions on acid base found on moodle .pdf - A...

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Unformatted text preview: A 30-year-old man with a 10-year history of chronic alcoholism complains of headache, chills, nausea, and dizziness, which started 24 hours ago. He says he has been "cooped up" in his oneroom apartment using a gas heater to keep warm. His temperature is 37°C (98.6°F), and findings on physical examination are unremarkable. While in the emergency department, the patient becomes unconscious. What abnormality would most likely be detected if this patient's oxygen-hemoglobin dissociation curve were evaluated? A decrease in binding affinity for oxygen in free binding sites of hemoglobin A decrease in the oxygen-carrying capacity of hemoglobin A decrease in the partial pressure of arterial oxygen A shift to the right in partial pressure of oxygen at which the hemoglobin is 50% saturated An increase in offloading of oxygen in tissues Clinical findings of headache, nausea, and dizziness in the setting of a potential carbon monoxide (CO) exposure (gas heater in a poorly ventilated one-room apartment) are suggestive of CO poisoning. The symptoms and signs of CO poisoning are highly variable and largely nonspecific. Patients often present with constitutional symptoms, including headache (the most common presenting symptom), malaise, nausea, and dizziness. Acute CO poisoning is usually suspected on the basis of a suggestive history; potential sources of CO include poorly functioning heating systems, improperly vented fuel-burning devices (eg, kerosene heaters, charcoal grills, camping stoves, gasoline-powered electrical generators), and motor vehicles operating in poorly ventilated areas. CO binds to the oxygen-binding sites of hemoglobin with an affinity 250 times that of oxygen. This results in both decreased oxyhemoglobin saturation and decreased oxygen-carrying capacity. A basic oxygen-hemoglobin dissociation curve is shown in the image. CO exposure can be diagnosed by measuring the carboxyhemoglobin fraction in blood. Treatment is 100% oxygen or hyperbaric oxygen therapy. The other answer choices do not reflect abnormalities related to CO poisoning: CO increases hemoglobin's affinity for oxygen. The presence of CO will cause a left shift in the oxygen-hemoglobin dissociation curve because CO has a higher affinity for hemoglobin and thus will replace oxygen. A decrease in binding affinity would represent a rightward shift of the oxygen-hemoglobin dissociation curve—typically seen in conditions such as increased temperature, increased 2,3-diphophosphoglycerate (2,3DPG), or decreased pH—and would NOT be seen in the presence of CO. CO binding to hemoglobin is independent of the partial pressure of arterial oxygen (Pao2). Furthermore, Pao2 reflects the amount of oxygen gas dissolved directly in blood, not the amount bound to hemoglobin. Pao2 would be unaffected by the presence of CO. Because CO increases hemoglobin's affinity for oxygen, it shifts the partial pressure of oxygen at which the hemoglobin is 50% saturated (P50) to the left. This means that, in the presence of CO, hemoglobin would be 50% saturated with oxygen at a lower Pao2 than under normal conditions. A rightward shift of P50 would be the opposite and is not seen when CO is present. CO causes a left shift of the oxygen-hemoglobin dissociation curve. There is consequently a decrease in the amount of oxygen offloaded to peripheral tissues. Essentially, the oxygen is "stuck" to the carboxyhemoglobin. Because the hemoglobin cannot unload the oxygen, "cherry-red" blood results, as well as tissue ischemia and hypoxia. A 32-year-old woman with a history of Hashimoto disease comes to her primary care physician because of progressive muscle weakness for the past 6 months. She states that she used to work as yoga teacher but now cannot make it through a class because the repetitive movements become increasingly difficult. The patient also reports that she has lost 10 lb in the past 6 months because she finds chewing food to be tiring, and describes double vision when trying to read at night. Her only medications include combined oral contraceptives and levothyroxine. She does not smoke or drink alcohol. Her family history is significant for a mother with rheumatoid arthritis. On physical examination, vital signs are normal. Muscles are nontender and deep tendon reflexes are intact. Strength in all four extremities is 5/5 on initial testing but her strength decreases throughout the examination. Thyroid stimulating hormone concentration is within normal limits. Which of the following is the most likely mechanism of this patient’s condition? Antibody-mediated damage to presynaptic cells at the neuromuscular junction Cytotoxic hypersensitivity Delayed (type IV) hypersensitivity reaction Endomysial inflammation with CD8+ cells. Hereditary segmental demyelination of distal nerves Toxin-mediated inhibition of acetylcholine release at the neuromuscular junction Type III hypersensitivity This young woman with a history of autoimmune thyroid disease and progressive weakness, bulbar dysfunction (pain while chewing) and diplopia has a likely diagnosis of Myasthenia gravis (MG), which is caused by a type II hypersensitivity reaction. Cytotoxic (type II)hypersensitivity reactions are caused by the action of IgG autoantibodies against cell surface antigens. In the case of MG, autoantibodies are directed against postsynaptic nicotinic acetylcholine (ACh) receptors at the neuromuscular junction (NMJ), leading to complement-mediated injury to the motor endplate. The illustration shows the pathophysiology of MG. Myasthenia gravis typically manifests in young women in their twenties and thirties and in older men in their sixties through eighties. Symptoms include fluctuating muscle weakness that worsens with use and therefore manifests most severely in the evening. Ocular and bulbar symptoms are also seen. Ocular symptoms include diplopia and ptosis; bulbar symptoms include dysarthria, dysphagia, and difficulty chewing. Although it is no longer performed in clinical practice, improvement of symptoms after the administration of edrophonium (an acetylcholinesterase inhibitor), also referred to as a positive tensilon test, is diagnostic of MG. The preferred diagnostic test of choice for the condition is a positive serology for IgG antibodies against acetylcholine receptors. All patients with MG should also be evaluated with chest imaging (either CT or MRI) for the presence of a possible thymoma, which is commonly associated with anti-ACh autoantibody formation. In the long term, patients with MG are treated with pyridostigmine, an acetylcholinesterase inhibitor. Why incorrect answers are wrong: The presence of autoantibodies to presynaptic voltage-gated calcium channels at the neuromuscular junction is characteristic of Lambert-Eaton syndrome, a paraneoplastic syndrome typically associated with lung cancer. In this condition, muscle weakness improves with use and reflexes are classically decreased. Toxin-mediated prevention of acetylcholine release at the neuromuscular junction can occur with exposure to botulinum toxin. Botulism would result in more rapid-onset descending flaccid paralysis and autonomic dysfunction. The disorder is classically associated with the consumption of canned foods. Delayed (type IV) hypersensitivity reaction against myelin and Schwann cells is characteristic of Guillain-Bàrre syndrome (GBS), which typically occurs after an infection (eg, with Campylobacter jejuni). GBS presents with ascending muscle weakness and decreased-to-absent deep tendon reflexes due to demyelination of spinal motor nerve roots and peripheral nerves. Type III hypersensitivity, as seen in SLE, involves the deposition of immune complexes in unwanted locations and can lead to serum sickness, the arthus reaction, and some symptoms of SLE. Hereditary segmental demyelination of distal nerves due to Charcot-Marie-Tooth disease can lead to progressive muscle weakness. Pes cavus can be seen on physical exam, as well as legs classically described as being in the shape of inverted champagne bottles due to muscle atrophy. Symptoms are gradual in onset and would be present at a younger age. Ocular and bulbar symptoms are not typical. Endomysial inflammation with CD8+ T cells leads to skeletal muscle damage characteristic of polymyositis, which presents with progressive, symmetric proximal muscle weakness and tenderness. A 22-year-old college student presents to the emergency department with sudden-onset severe epigastric pain that radiates to the back. He has a history of heavy alcohol abuse, and lab tests show a markedly elevated amylase level. The organ involved in this patient's pathology plays a key role in normal gastrointestinal physiology. Under normal physiologic conditions, the organ is stimulated by a hormone that increases the secretion of bicarbonate. Which of the following will increase release of this hormone? Acid and fatty acids in the duodenal lumen Fasting state Increased stomach distention The presence of fatty acids, amino acids, and oral glucose in the duodenum and jejunum Vagal stimulation This young man presenting with acute-onset epigastric pain that is radiating to the back has a history of alcoholism. Classically, this clinical picture is consistent with an episode of pancreatitis, which is most commonly caused by gallstones and alcohol. The amylase level is elevated during an episode of acute pancreatitis. Thus the organ of interest is the pancreas. The hormone secretin acts on pancreatic duct cells to stimulate bicarbonate secretion, which facilitates functioning of pancreatic enzymes by neutralizing gastric acid. Secretin is released by duodenal S cells in response to increased acid and fatty acids in the lumen of the duodenum. A fasting state increases release of motilin (from the small intestine) and ghrelin (from the stomach). Stomach distention and vagal stimulation increase release of gastrin (from the antrum of the stomach and duodenum). Fatty acids, amino acids, and oral glucose reaching the duodenum and jejunum increase release of glucose-dependent insulinotropic peptide (GIP) from duodenal and jejunal K cells. None of these hormones increase bicarbonate secretion from the pancreas. The image provides an overview of the locations of gastrointestinal secretory cells. A 64-year-old man is brought to the emergency department by his wife after she noticed slurring of his speech during dinner 30 minutes ago. He has a history of hypertension and diabetes, for which he takes metoprolol and metformin. On physical examination, his temperature is 36.4°C (97.5°F), heart rate is 90/min, blood pressure is 130/88 mm Hg, and respiratory rate is 18/min. He has 3/5 strength in his right upper and lower extremities. A picture of his face is shown below. He is unable to express himself verbally but is able to follow commands appropriately. A computed tomographic (CT) scan of the head shows no sign of hemorrhage. A medication is administered intravenously. What is the mechanism of action of the medication most likely used to treat this patient? Activates antithrombin III Catalyzes conversion of plasminogen to plasmin Direct inhibitor of thrombin Monoclonal antibody against GPIIb/IIIa Phosphodiesterase III inhibitor his patient presents with acute onset of weakness, facial drooping, and expressive aphasia, which are strong indications that he has had an ischemic stroke. A CT scan is important in differentiating between ischemic and hemorrhagic strokes. If a patient who has had an ischemic stroke presents within 3 hours and has no contraindications, the standard treatment is tissue plasminogen activator (tPA). As shown in the diagram, tissue plasminogen activator is secreted by endothelial cells and is the enzyme most directly responsible for degrading the fibrin matrix. Recombinant tPA (alteplase) and streptokinase are similar medications that are used to treat diseases in which fibrin clots prevent adequate blood flow to tissue, such as stroke, pulmonary embolus, and myocardial infarction. Activation of antithrombin III is the mechanism of action of heparin, which is used as an anticoagulant in acute situations such as pulmonary embolisms or DVTs and acute coronary syndromes. Phosphodiesterase III inhibitors, such as dipyridamole and cilostazol, are antiplatelet medications commonly used to treat claudication. Direct thrombin inhibitors, such as lepirudin and bivalirudin, are oral medications that can be used in the event of heparin-induced thrombocytopenia. A monoclonal antibody to GPIIb/IIIa (abciximab) inhibits platelet aggregation and is used in treatment of acute coronary syndromes. Heparin works by binding to and activating the enzyme antithrombin III. Binding of heparin to antithrombin III increases binding of the protease to factors II and X. Heparin is used for immediate anticoagulation in cases of pulmonary embolisms, myocardial infarction, and deep venous thrombosis. Given this patient’s presentation, a different medication was used to treat his condition. Lepirudin and bivalirudin are anticoagulant medications that work via direct inhibition of thrombin. They are used as an alternative to heparin if the patient is at risk for heparin-induced thrombocytopenia. These drugs would not be administered to this patient, given his clinical presentation. Abciximab is a monoclonal antibody against the GPIIb/IIIa receptor on platelets. Binding of fibrinogen to GPIIb/IIIa receptors joins adjacent platelets during platelet aggregation. Abciximab is used in the treatment of acute coronary syndromes and would not have a role in the treatment of this patient. The antiplatelet drugs dipyridamole and cilostazol act via inhibition of phosphodiesterase III. Inhibition of phosphodiesterase III causes increased concentrations of cyclic adenosine monophosphate within platelets, which leads to impaired platelet aggregation. These medications are used to treat claudication. Fibrinolysis begins in endothelial cells with the secretion of tissue plasminogen activator (tPA). This catalyzes the conversion of plasminogen to plasmin. Coagulation and kinin pathways Coagulation cascade components Procoagulation Vitamin K deficiency: synthesis of factors II, VII, I X , X, protein C, protein S. Warfarin inhibits vitamin K epoxide reductase. Vitamin K administration can potentially reverse inhibitory effect of warfarin on clotting factor synthesis. FFP or PCC administration reverses action of warfarin immediately and can be given with vitamin K in cases of severe bleeding. Neonates lack enteric bacteria, which produce vitamin K. Early administration of vitamin K overcomes neonatal deficiency/coagulopathy. Factor VII—Shortest half life. Factor II—Longest half life. vWF carries/protects factor V I I I ; volksWagen F actories make gr8 cars. Anticoagulation Antithrombin inhibits activated forms of factors II, VII, I X , X, XI, XII. Heparin enhances the activity of antithrombin. Principal targets of antithrombin: thrombin and factor Xa. Factor V Leiden mutation produces a factor V resistant to inhibition by activated protein C. tPA is used clinically as a thrombolytic. Thrombogenesis Formation of insoluble fibrin mesh. Aspirin irreversibly inhibits cyclooxygenase, thereby inhibiting T X A 2 synthesis. Clopidogrel, prasugrel, and ticlopidine inhibit ADP-induced expression of GpIIb/IIIa by irreversibly blocking P2Y12 receptor. Abciximab, eptifibatide, and tirofiban inhibit GpIIb/IIIa directly. Ristocetin activates vWF to bind GpIb. Failure of aggregation with ristocetin assay occurs in von Willebrand disease and Bernard-Soulier syndrome. A healthy 21-year-old woman with no history of significant illness comes to the physician requesting combination oral contraceptives. She is sexually active and always uses condoms as contraception. She does not have a history of migraines and no personal or family history of clotting disorders. Blood pressure is 123/76 mm Hg, height is 172 cm (5', 8"), weight is 68 kg (150 lb), and BMI is 23 kg/m2. No abnormalities are noted on physical examination. Urine βHCG results are negative. The physician decides to prescribe combination oral contraceptives to the patient, which will decrease the amount of endogenous follicle-stimulating hormone (FSH) produced. Which of the following events will most likely be affected immediately? Blastocyst implantation Fertilization of ovum Follicular phase estradiol concentration Mid-cycle surge of luteinizing hormone (LH) Ovulation This patient is a 21-year-old healthy woman who is sexually active and desires oral contraceptives (OCPs). She has no contraindications (relative or absolute) to combination OCPs (no personal or family history of thromboembolic disease, normal blood pressure, nonsmoker). After having a conversation with her physician about all forms of contraception, the patient decides that she should be prescribed OCPs if she desires. To understand the mechanism of action of OCPs, it is helpful to understand the hormonal changes that occur in the normal menstrual cycle, which is shown in the image above. The normal menstrual cycle consists of the follicular phase (usually ~14-21 days) and the luteal phase (14 days). The follicular phase begins after the onset of menstruation and is characterized by folliclestimulating hormone (FSH)-stimulated growth of one or more dominant follicles that release estrogen. Estrogen causes the uterine endometrium to enter the follicular phase, which is characterized by a thickened endometrium with an increased number of glands. For most of the follicular phase, estrogen also works to exert negative feedback on FSH and luteinizing hormone (LH) production, but late in the follicular phase, high serum estrogen begins to have a positive feedback effect on LH production, leading to the LH surge (a 10-fold increase in serum LH concentrations). The LH surge characterizes the start of the luteal phase and subsequent ovulation.The oocyte of the dominant follicle completes its first meiotic division and is released from the follicle ~36 hours after the LH surge. The remnant follicle becomes the corpus luteum, which releases progesterone in the mid- to late-luteal phase. Progesterone causes the endometrium to cease thickening and causes glands to “organize” (“secretory endometrium”). The corpus luteum begins to resolve in the late-luteal phase, which occurs when LH release declines via negative feedback mechanisms from the rising serum progesterone concentrations. As the corpus luteum resolves, serum concentrations of progesterone and estrogen decrease, resulting in loss of endometrial blood supply, endometrial sloughing, and the onset of menses. Standard combined OCPs consist of progesterone and estrogen. Progesterone provides negative feedback to decrease the release of GnRH from the hypothalamus, which then decreases the secretion of FSH and LH by the anterior pituitary. The immediate effect of decreased FSH is to inhibit follicular development and to prevent the increase in estrogen concentration during the follicular phase. Without the end-follicular peak in estrogen concentration, positive feedback with LH release cannot occur, and thus the LH surge cannot happen. Without the LH surge, ovulation cannot occur. ,The incorrect answers are wrong for the following reasons: Though the decreased concentrations of FSH lead to the downstream effect of ovulation inhibition, ovulation is not the process that is most immediately and directly affected by the decrease in FSH concentrations. Decreased FSH concentrations lead to decreased follicular-phase estrogen concentrations, which subsequently prevents the LH surge and subsequent ovulation. It is only by way of decreased estrogen concentrations that decreased FSH concentrations serve to prevent the LH surge. Specifically, decreased FSH concentrations lead to decreased follicular-phase estrogen concentrations, which subsequently prevents the LH s...
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  • Spring '16
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