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4. Metals and Non-metals Learning Objectives By the end of the lesson, you will be able to: ☑ distinguish between metals and non-metals ☑ describe the physical and chemical properties of metals and non-metals ☑ list the uses of some metals and non-metals MINERALS AND ORES You have learnt that all materials Here is the exact text from the image:are made up of basic substances called elements, and that elements cannot be split into simpler substances by chemical methods. There are 118 known elements. Sodium, zinc, gold, mercury, iron, lead, barium and tin (metals); and hydrogen, oxygen, carbon, sulphur, chlorine, boron, neon and radon (non-metals) are some examples. Only certain unreactive elements are found free in nature. Others occur in combined states as minerals. A mineral is a solid inorganic substance that is found in nature. A mineral deposit that can be mined and from which an element or compound can be obtained profitably is known as an ore. Elements can be broadly classified into two groups—metals and non-metals. Table 4.1 Some common ores Fig. 4.1 Some common ores a. Bauxite (aluminium) b. Malachite (copper) c. Haematite (iron) d. Galena (lead) e. Apatite (phosphorus) f. Quartz (silicon) -- --- METALS All except 20 of the known elements are metals. Most metals are reactive; they combine with other elements in nature, such as oxygen and sulphur, and occur as oxides, sulphides and carbonates. Only a few unreactive metals like gold, silver and platinum are found as free metals in the Earth's crust. Physical Properties of Metals Metals are solids at room temperature, except mercury, which is a liquid at room temperature (Fig. 4.2(a)). They are generally hard and strong, with a few exceptions such as sodium and potassium, which are soft and can be easily cut with a knife (Fig. 4.2(b)). They have a metallic lustre (shine), especially when freshly cut. They have high melting and boiling points, with a few exceptions like sodium, potassium and mercury. They are good conductors of heat and electricity. Silver and copper are the best conductors of electricity, followed by gold and aluminium. Metals are sonorous. They produce a ringing sound when struck. Most metals have high tensile strength. They can take heavy loads without breaking. They are malleable. Metals, with exceptions like sodium and potassium, can be beaten into thin sheets and foils. They are ductile. Metals, with exception like sodium and potassium, can be drawn into wires. Most metals have high density. However, sodium and potassium have low density and float on water. Fig. 4.2 Special metals a. Mercury b. Sodium --- Chemical Properties of Metals Reaction with oxygen Metals react with oxygen under different conditions to form basic oxides. These basic oxides react with water to form bases. Sodium and potassium react vigorously with oxygen at room temperature. 4Na + O_2 \rightarrow 2Na_2O To prevent this oxidation, sodium and potassium are stored under kerosene. Magnesium reacts with oxygen only when ignited. It burns with a dazzling bright flame and forms a white powder of magnesium oxide. 2Mg + O_2 \rightarrow 2MgO Copper and iron react with oxygen only when heated to a very high temperature. 2Cu + O_2 \rightarrow 2CuO --- --- Reaction with water Metals react with water to form hydroxides or oxides, along with hydrogen. Different metals react at different temperatures. Sodium, potassium, and calcium react with cold water to form hydroxides. 2Na + 2H_2O \rightarrow 2NaOH + H_2 Magnesium Reacts with steam or hot water to form magnesium oxide. Mg + H_2O \rightarrow MgO + H_2 Aluminium Forms an oxide too, but this oxide forms a protective covering over the metal and prevents further reactions. 2Al + 3H_2O \rightarrow Al_2O_3 + 3H_2 Zinc Reacts only with steam. Zn + H_2O \rightarrow ZnO + H_2 Iron Reacts with steam when heated strongly. 2Fe + 3H_2O \rightarrow Fe_3O_4 + 3H_2 Copper, gold, silver, and platinum do not react with water at all. --- Activity 4.1 Teacher Demonstration Aim: To study the reaction of metals with water. [Caution: This activity should be demonstrated by the teacher, and students should stand away from the table.] Materials required: Two 200 mL beakers Pieces of sodium and calcium Forceps Knife Litmus papers Water Method: 1. Fill each beaker with 100 mL of water. 2. Using forceps and a knife, cut a small piece of sodium. 3. Dry it on a tissue paper and drop it into one of the beakers. 4. Repeat the same procedure with calcium. 5. Test the water in both the beakers with red and blue litmus papers. Observations and Conclusions: Sodium reacts vigorously and may explode. A gas is also released. The reaction with calcium is quick, though not as vigorous as that with sodium. In both cases, the red litmus paper turns blue, showing that the solutions are bases. --- Reaction with dilute acids Most metals react with dilute acids to form their salts and liberate hydrogen gas. The reaction with reactive metals like sodium, potassium, and calcium is violent. Magnesium, aluminium, zinc, and iron do not react violently. Mg + 2HCl \rightarrow MgCl_2 + H_2 Copper, silver, gold, and platinum do not react with dilute acids. --- Reaction with bases Only some metals such as aluminium and zinc react with strong bases like sodium hydroxide to liberate hydrogen gas. Zn + 2NaOH \rightarrow Na_2ZnO_2 + H_2 --- Activity 4.2 Aim: To study the reaction of metals with dilute hydrochloric acid. Materials required: Sandpaper Six test tubes Dilute hydrochloric acid Strips of magnesium, zinc, iron, tin, lead, and copper Method: 1. Clean the metal strips with sandpaper. 2. Add dilute hydrochloric acid to the six test tubes. 3. Insert a strip of metal into each test tube. Observe if any bubbles are formed in the test tubes. If no bubbles are seen, warm them gently in a beaker of hot water. 4. Observe the speed at which gas is generated. This gives an idea of the speed of the reaction. 5. Classify the metals in order of their reactivity with dilute hydrochloric acid. [Caution: Acids are corrosive and should be handled carefully.] --- Activity 4.3 Aim: To study the reaction of metals with bases. Materials required: Small piece of zinc Beaker Sodium hydroxide Method: 1. Prepare warm sodium hydroxide or caustic soda solution. 2. Drop the piece of zinc into it. Observations and Conclusions: You will notice that zinc reacts with sodium hydroxide to liberate hydrogen gas. Observations on Metals with Dilute Acids Metals like sodium, potassium, and calcium react violently with dilute acids to liberate hydrogen gas. Magnesium, aluminium, zinc, and iron also displace hydrogen from dilute acids, but the reaction is not violent. Metals such as copper, silver, gold, and platinum do not displace hydrogen from dilute acids. --- Activity Series of Metals The activity series of metals is the arrangement of metals in decreasing order of reactivity. The series in the book shows reactivity decreasing from top to bottom. Potassium is the most reactive metal while gold is the least reactive. --- Displacement of a Metal by Other Metals A more reactive metal displaces a less reactive metal from its compounds in an aqueous solution. Some examples: Mg + CuSO_4 \rightarrow MgSO_4 + Cu Zn + FeSO_4 \rightarrow ZnSO_4 + Fe Iron can displace copper from copper sulphate solution (as shown in Activity 4.4). The solution turns green, and reddish-brown copper deposits on the iron nail. Copper cannot displace iron from iron sulphate solution, showing that copper is less reactive than iron. Cu + FeSO_4 \rightarrow \text{No reaction} Question: What do you think will happen if you place a silver spoon in copper sulphate solution? --- Activity 4.4 - Displacement Reaction Aim: To study a displacement reaction. Materials Required: Test tube Iron nail Copper sulphate solution Method: 1. Fill the test tube with copper sulphate solution (blue in colour). 2. Place the clean iron nail in the solution. Observations and Conclusions: After about an hour, the solution changes to green, and a reddish-brown deposit is formed on the iron nail. --- Corrosion of Metals Corrosion is the destruction or damage of a material due to chemical reaction. Rusting of iron happens when iron is exposed to moist air, forming a reddish-brown layer of rust. Rust is iron oxide, which eventually flakes off, damaging the object. Definition written on the page: "Slow eating of a metal’s surface due to oxidation is called corrosion of metals." --Observations on Metals with Dilute Acids Metals like sodium, potassium, and calcium react violently with dilute acids to liberate hydrogen gas. Magnesium, aluminium, zinc, and iron also displace hydrogen from dilute acids, but the reaction is not violent. Metals such as copper, silver, gold, and platinum do not displace hydrogen from dilute acids. --- Activity Series of Metals The activity series of metals is the arrangement of metals in decreasing order of reactivity. The series in the book shows reactivity decreasing from top to bottom. Potassium is the most reactive metal while gold is the least reactive. --- Displacement of a Metal by Other Metals A more reactive metal displaces a less reactive metal from its compounds in an aqueous solution. Some examples: Mg + CuSO_4 \rightarrow MgSO_4 + Cu Zn + FeSO_4 \rightarrow ZnSO_4 + Fe Iron can displace copper from copper sulphate solution (as shown in Activity 4.4). The solution turns green, and reddish-brown copper deposits on the iron nail. Copper cannot displace iron from iron sulphate solution, showing that copper is less reactive than iron. Cu + FeSO_4 \rightarrow \text{No reaction} Question: What do you think will happen if you place a silver spoon in copper sulphate solution? --- Activity 4.4 - Displacement Reaction Aim: To study a displacement reaction. Materials Required: Test tube Iron nail Copper sulphate solution Method: 1. Fill the test tube with copper sulphate solution (blue in colour). 2. Place the clean iron nail in the solution. Observations and Conclusions: After about an hour, the solution changes to green, and a reddish-brown deposit is formed on the iron nail. --- Corrosion of Metals Corrosion is the destruction or damage of a material due to chemical reaction. Rusting of iron happens when iron is exposed to moist air, forming a reddish-brown layer of rust. Rust is iron oxide, which eventually flakes off, damaging the object. Definition written on the page: "Slow eating of a metal’s surface due to oxidation is called corrosion of metals." Uses of Metals (Continued) Aluminium Used in high-voltage electric lines. Alloys like duralumin and magnalium are used in aircraft and automobile bodies. Used for making aluminium foil and cooking utensils. Copper Good conductor of electricity → Used in electrical wires, cables, motors, and transformers. Good conductor of heat → Used in the bottoms of stainless steel vessels. Zinc Used to make corrosion-resistant galvanised iron (GI) pipes and sheets. Used as an electrode in dry cells. Other Metals Gold and silver → Used in jewellery. Lead → Used in electrodes of lead storage batteries (used in automobiles and inverters). Chromium → Used for electroplating iron to give a shiny, corrosion-resistant finish. --- Looking Back (True/False Statements) 1. Gold, silver, and platinum are found in the Earth’s crust as free metals. → True 2. Most metals are solids that are soft. → False 3. Metals such as zinc and magnesium react with dilute acids to liberate oxygen. → False 4. A less reactive metal displaces a more reactive metal from its aqueous solution. → False 5. The chemical name of rust is zinc oxide. → False (Rust is Fe₂O₃.xH₂O) 6. Coating zinc objects with iron is called galvanising. → False (Galvanising is coating iron with zinc) Non-Metals Physical Properties of Non-Metals Exist as gases or solids at room temperature (except bromine, which is liquid). Not as hard as metals (except diamond, which is very hard). Low tensile strength and low density. Low melting and boiling points (except graphite). Not sonorous (do not produce a ringing sound). Not malleable or ductile (cannot be beaten into sheets or drawn into wires). Do not have lustre (except iodine and graphite). Bad conductors of heat and electricity (except graphite, and silicon under specific conditions). --Chemical Properties of Non-Metals Reaction with Water Most non-metals do not react with water. Highly reactive non-metals (e.g., phosphorus) catch fire in air, so they are stored in water. Fluorine, chlorine, and bromine react with water to form acids. Reaction with Oxygen Non-metals react with oxygen to form acidic or neutral oxides. Carbon and sulfur react with oxygen to form acidic oxides, which dissolve in water to form acids. Some oxides (e.g., CO, N₂O) are neutral and do not form acids. Examples: Carbon + Oxygen → Carbon Dioxide (CO₂) CO₂ + Water → Carbonic Acid (H₂CO₃) Sulfur + Oxygen → Sulfur Dioxide (SO₂) SO₂ + Water → Sulfurous Acid (H₂SO₃) Reaction with Acids Unlike metals, non-metals do not replace hydrogen in acids. Silicon reacts with hydrofluoric acid (HF). --Uses of Non-Metals Hydrogen Used in the manufacture of ammonia and industrial chemicals. Used in vanaspati (a cooking oil). Oxygen Used in breathing support systems in hospitals. Used with other gases in equipment to weld metals. Sulphur Used in the manufacture of sulphuric acid, sulphur dioxide gas, and other industrial chemicals. Used to make pesticides for agriculture. Used in vulcanising rubber (making it harder) and in gunpowder. Nitrogen Used in the manufacture of ammonia and nitrogenous fertilisers like ammonium nitrate and ammonium sulphate. Used as an inert gas in processed food packaging to prevent rancidity. Silicon Used in making semiconductors for microchips. Silicates (oxides of silicon) are used in making glass. Other Non-Metals Phosphorus: Used in making fertilisers (superphosphates). Chlorine: Used for disinfecting drinking water. Argon: Used in welding stainless steel and filling electric bulbs. Helium: Used in balloons for meteorological observations. Neon: Used in fluorescent lights for advertisement displays
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Please wait outside until I let you in, and put all your stuff at the back just like we've done about 20 times already this semester. Okay? Or this semester and last, and you will be just fine. Now your lecture exam too is 90 marks big. It is 90 multiple choice questions. Okay. It is going to be on cardiovascular disorders, urinary system, fluid balance, Okay. So let's start talking about them. First of all, okay, you need to know the difference between a myocardial infarct, ischemic attack, a congestive heart failure, and angina pectorals. You need to know what a low level inflammatory response that develops over time where the endothelium is damaged due to the aging or prolonged hypertension, where LDLs accumulate, and the endothelium is repaired with collagen is called. That might take you a long time to read. Okay? But it is a good question. Okay? You need to know now be really, really clear on these. Okay? You absolutely need to know the difference between right ventricular hypertrophy and left ventricular hypertrophy and what they cause. Because there's two questions on here, and so far, this one hasn't been done very well. Okay? Make sure you understand what right ventricular hypertrophy leads to and you understand what left ventricular hypertrophy leads to. Now the original term, congestive heart failure, that refers to left ventricular hypertrophy leading to backup in the lungs. K? You need to know what arteries or vessels are used in bypass surgery. You need to know what a mini stroke is. Okay? You need to know the difference between thrombus and ballast occlusion and arthroma. You need to know what is a restriction in blood supply generally due to factors in the blood vessels with resultant damage or dysfunction of tissue. You need to know, what are the consequences of an aging cardiovascular system. And then I I've got a matching question for you. You need to match the basic function of the proximal convoluted tubule, the glomerulus, and the peri colic duct. And then two of my favorite questions. Are you ready? Okay. You have to find out which of the following is the best explanation for why the cells of the proximal convoluted tubule contain so many microclonary. Oh, isn't that lovely? Okay. And then the other one you need to know is you need to find the best explanation for the microvilli on the apical surface of the proximal convoluted tubules. So don't get that one wrong because we've talked about microvilli about a bazillion times. Okay? This picture is gonna be on there, folks. Okay? This is the picture of the of the nephron from your textbook. Okay. You need to label things like glomerulus glomerulus afferent arteriole collecting duct nephron move. Okay. Where do you find the granular cells? Okay. The difference between the medulla and the cortex. Make sure you know all of those things. I'll read you this one. This is a good question too. Hydrostatic pressure is the primary driving force of plasma through the filtration membrane into the capsular space. All the publicly following statements reflects why hydrostatic pressure is so high in the glomerular capillaries. Select the one statement that does not explain the high pressure within the glomerular capillaries. So you need to know why glomerular capillary pressure is higher than the rest of the capillaries in the body. You need to know how or why cells or transport proteins are prevented from moving through how yeah. What drives reabsorption of organic nutrients in the proximal condylated tubule? Who drives thus? You need to know the mechanism that establishes the medullary osmotic gradient the The functional and structural unit of the kidneys is what? The g force pushing the blood and solids out of the blood across the filtration membrane is what? Okay. The macular densities cells do what? Function in angiotensin two is to do what? What is, specific gravity or density? Okay. If you talk about the specific gravity or density of urine, how is it different from water? You need to actually, this is just one question, but it should be a pretty simple one. Okay? You need to place the following and correct sequence from the formation of a drop of urine to its elimination of the body. And so you have to go through from well, I'll just read it to you. Major calyx, minor calyx, nephron, urethra, ureter, and collecting that. So you need to put those in order from start to finish. Okay? What would happen if the capsular hydrostatic pressure were increased above normal? You need to know what would happen. Reabsorption of bilevels of glucose and amino acids in the filtrate is accomplished. The 44 more. Okay. So you need to match to their definition. All of your hypo and hypers. Make sure you have some under control. Okay? And then you need to match possible causes. So there's possible causes of respiratory alkalosis, metabolic alkalosis, metabolic acidosis, and respiratory acidosis. Respiratory alkalosis, metabolic alkalosis, metabolic acidosis, and respiratory acidosis. There are possible causes for those four things. You need to match the disorder to the cause. Okay? And then you need to know, the body's motor volume is mostly tied to the level of then I have a couple of clinical correlation questions for you, but they are multiple choice this time. So something happened to Jane. You have to tell me what's happening to Jane. Okay? Now whereas sodium is mainly found in the extracellular fluid, most is found in intracellular systems are. Okay. Which of the following is not a likely source of hydrogen ions in blood plasma, so there's a few types in the tablets, so make sure you know which ones are going to produce acids and which ones aren't. And then Annie had something happen to her as well. Across capillary walls is what? Regulation of potassium balance is what? Now Dave Dave did something silly. Okay? Dave ran a marathon. Okay? And then Dave did something even more silly afterwards. I want you to tell me what happened to Dave. And in addition to that, Nancy is having a panic attack. So I want you to tell me what's happening to Nancy in terms of respiratory aesophosis and respiratory aldosterone. Okay. If thyroid and parathyroid glands were surgically removed, which of the following would go out of balance without replacement therapy? Falling arterial blood pressure holds which? An illness, Doug. Doug has severe diarrhea. Okay. And, is accompanying the loss of bicarbonate or secretions. So how is Doug gonna compensate for that for Doug? Okay. You need to know what the medical term for kidney stones is. You need to know what happens, or what could cause the passage of proteins, red blood cells, and white blood cells into the urine. You need to know how to solve prostatic enlargement, and, you need to know what the presence of white blood cells in urine is called and what is causing it. Okay? And then there's a picture of the lymphatic of the lymph node. Okay. You need to label the lymph node picture. And then you there is going to be a matching question on lymphatic structures, so you need to know what happens in the spleen, the lymph nodes, the thoracic duct, the lymph, and the pyre patches. There's a list, a small short list. Okay? So in other words, you're going to need to know what is classified as a lymphoid organ and what does not. Okay? So make sure you know what your lymphoid organs are. You need to know the pathway of lymph. So it starts in lymph capillaries. Where does it end? Make sure you know all the steps along the way. And then you need to know the functions of the spleen. What did what does the spleen do? And that is it for an example
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Vegetables are plants or parts of plants like leaves, fruits, tubers, roots, bulbs, stems, shoots, and flower used in a dish either raw or cooked. Give color, texture and flavor to our meals. They are rich sources of vitamins, minerals, and fiber. Are important sources of many nutrients, including potassium, dietary fiber, folate (folic acid), vitamin A, and vitamin C. Roots these are underground parts of plants which include sweet potato, cassava, carrot, radish, turnip, sugar beets, and purple yam or ube. Tubers these are short, thickened, fleshy parts of an underground stem such as Irish potatoes and Jerusalem artichokes. Seeds these are parts from which a new plant will grow which include legumes or beans such as mungo beans, broad beans, garbanzos or chickpeas, paayap or cowpeas, soybeans, white beans, lima beans, and kidney beans. Bulbs these are underground buds that are made of very short stems covered with layers such as garlic, onion, chives, leeks, and shallots. Leaves these include the onion family such as spring onion, leeks, scallion and a wide variety of leaves such as sili leaves, ampalaya, alugbati, spinach, kangkong or swamp cabbage, kintsay or Filipino celery, celery lettuce or letsugas, mustasa or mustard, petsay or Chinese cabbage. Stems and shoots these are the stalks supporting the leaves, flowers, or fruits. They include the stems of the leaves of kangkong, celery, kintsay, alugbati, lettuce, mustard, and petsay. They also include bamboo shoots or labong and coconut pith o ubod. Fruits these include those cooked as viands such as ampalaya, patola, upo, kalabasa, kamatis, langkang hilaw, bell pepper, and siling pansigang. Flowers these are bulaklak ng kalabasa, bulaklak ng saging, cauliflower, puso ng saging, and katuray or sesban flower. washing, soaking, peeling and cutting Preparing vegetables (3) Chopping done with a straight, downward cutting motion Chiffonade (shredding) making very fine parallel cuts Dicing Producing cube shapes Diamond Thinly slicing and cutting into strips of appropriate width Mincing producing very fine cut usually for onions and garlic Julienne Long rectangular cut Pays anne making curved or uneven cuts of the same thickness Rondelle making cylindrical cut Oblique or roll cuts making diagonal cut by rolling the long cylindrical vegetables. Cereals are usually starchy pods or grains. Cereal grains are the most important group of food crops in the world named after the Roman goddess of harvest, "CERES". Rice, wheat and corn are the three most cultivated cereals in the world Starch Are the second most abundant organic substance on earth. It is found in all forms of leafy green plants, located in the roots, fruits or grains. Thickening agent, binding agent, stabilizing agent, gelling agent, coating or dusting Functions of Starch (5) Gelatinization, viscosity, syneresis Principles of Starch cookery (3) Gelatinization The sum of changes that occur in the first stages of heating starch granules in a moist environment which includes swelling of granules as water is absorbed and disruption of the organized granule structure. Viscosity The resistance to flow; increase in thickness or consistency. When the newly gelatinized starch is stirred, more swollen granules break and starch molecules spill causing increase in viscosity or thickness. Syneresis Oozing of liquid from gel when cut and allowed to stand (e.g. jelly or baked custard). The oozing of liquid from a rigid gel; sometimes called weeping. Pasta a general name for a simple dough mixture made from hard wheat, flour, and water. Al dente refers to the desired texture of cooked pasta in Italian cooking. It literally means "to the tooth." Fettuccine A type of pasta popular in Roman cuisine. It is a flat thick noodle made of egg and flour. Linguine Is a long strand pastamade from durum wheat semolina and eggs. Its name is derived from the Italian word, lingua meaning tongue and it means little tongue Rigatoni a type of pasta that is shaped like short, wide tubes Ziti medium-sized tubular pasta Rotini a type of helix or corkscrew-shaped pasta Alimentary Paste Refers to a family of macaroni products of varying sizes and shapes. The more popular ones are spaghetti, macaroni, vermicelli, egg noodles, and lasagna. These products are made from semolina flour durum wheat can be ground into semolina flour, which can be used to make bread, pasta, and porridge. Noodles are made from rice, soft wheat, soybeans, cassava, and other legumes and root crops. Miki flat yellowish noodles made from wheat flour, lye, salt, water, and fat. this is formed into a dough, flattened, and cut into strips Sotanghon long, thin, round, translucent noodles made from mung bean and cornstarch. It is also called nylon or silk noodles Bihon noodles made from rice and corn. Rice and corn are soaked, ground, drained, then ground again. With the addition of cornstarch, it is made into galapong, kneaded, and passed through an extruding machine to produce long thin strands. Pancit canton a mixture of flour, duck eggs, salt, and soda ash. It is kneaded, then cut and pressed hard, then boiled, flattened, cut washed, and drained. The noodles are then fried in deep fat before packaging Instant noodles Dried noodles with various flavorings
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1. Hyperemesis Gravidarum/ Pernicious Vomiting Definition: Excessive nausea and vomiting during pregnancy, extending beyond week 12 or causing dehydration, ketonuria, and significant weight loss within the first 12 weeks. Incidence: 1 in 200-300 women Cause: Unknown, but may be associated with increased thyroid function and Helicobacter pylori infection. Signs and Symptoms: • Decreased urine output • Weight loss • Ketonuria • Dry mucous membranes • Poor skin turgor • Elevated hematocrit • Decreased sodium, potassium, and chloride levels • Polyneuritis (in some cases) Assessment: • Hemoglobin: Elevated hematocrit concentration (hemoconcentration) due to inability to retain fluids. • Electrolytes: Decreased sodium, potassium, and chloride levels due to low intake. • Acid-base Balance: Hypokalemic alkalosis (severe vomiting, prolonged period). • Neurological Examination: Polyneuritis due to B vitamin deficiency. Effects (if left untreated): • Intrauterine Growth Restriction (IUGR): Dehydration and inability to provide nutrients for fetal growth. • Preterm birth: Due to complications caused by the condition. • Prolonged hospitalization/home care: Resulting in social isolation. Therapeutic Management: • Fluid and Electrolyte Management: Monitor input and output, blood chemistry to prevent dehydration. • Nutritional Support: Withhold oral food and fluids (usually) and administer total parenteral nutrition (TPN). • Intravenous Fluid Replacement: 3000 ml Ringer's lactate with added vitamin B to increase hydration. • Antiemetic Medication: Metoclopramide (Reglan) to control vomiting. 2. Ectopic Pregnancy Definition: Implantation of a fertilized egg outside the uterine cavity (ovary, cervix, fallopian tube - most common). Incidence: Second most frequent cause of bleeding during the first trimester. Causes: • Obstruction of the fallopian tube: ◦ Adhesions (from previous infection like chronic salpingitis or pelvic inflammatory disease). ◦ Congenital malformations. ◦ Scars from tubal surgery. ◦ Uterine tumor pressing on the proximal end of the tube. ◦ Current use of an intrauterine device (IUD). Signs and Symptoms: • Missed period/amenorrhea. • Positive hCG test. • Sharp, stabbing pain in the lower abdominal quadrants and pelvic pain (at time of rupture). • Scant vaginal spotting/bleeding. • Rigid abdomen (from peritoneal irritation). • Leukocytosis (increased WBC count due to trauma). • Decreased blood pressure and increased pulse rate (signs of shock). • Cullen's sign (bluish tinge around the umbilicus). • Tender mass palpable in the cul-de-sac of Douglas (vaginal exam). • Falling hCG or serum progesterone level (suggesting the pregnancy has ended). • No gestational sac on ultrasound. Therapeutic Management: • Non-ruptured Ectopic Pregnancy: Oral administration of methotrexate followed by leucovorin. • Ruptured Ectopic Pregnancy (emergency): Laparoscopy to ligate bleeding vessels and remove or repair the damaged fallopian tube. 3. Hydatidiform Mole (H-mole)/ Gestational Trophoblastic Disease/ Molar Pregnancy Definition: A gestational anomaly of the placenta consisting of a bunch of clear vesicles resembling grapes. This neoplasm is formed from the swelling of the chorionic villi, resulting from a fertilized egg whose nucleus is lost, and the sperm nucleus duplicates, producing a diploid number 46XX. Incidence: Approximately 1 in every 1500 pregnancies. Risk Factors: • Low socioeconomic group (decreased protein intake). • Women under 18 or over 35 years old. • Women of Asian heritage. • Receiving clomiphene citrate (Clomid) for induced ovulation. Types of Molar Growth: • Complete/Classic H-mole: All trophoblastic villi swell and become cystic. No embryonic or fetal tissue present. High risk for malignancy. • Partial/Incomplete H-mole: Some of the villi form normally. Presence of fetal or embryonic tissue. Low risk for malignancy. Signs and Symptoms: • Uterus expands faster than normal. • No fetal heart sounds heard. • Serum or urine test for hCG strongly positive. • Early signs of preeclampsia. • Vaginal bleeding (dark-brown spotting or profuse fresh flow). • Discharge of fluid-filled vesicles. Diagnosis: • Ultrasound. • Chest x-ray (lung metastasis). • Amniocentesis (no fluid). • Hysteroscopy (via cervix). Management: • Evacuation of the mole: Dilation and curettage (D&C). • Blood transfusion. • Hysterectomy (in some cases). • Monitoring hCG levels: Every 2 weeks until normal. • Contraception: Reliable method for 12 months to prevent confusion with a new pregnancy. 4. Premature Cervical Dilatation/ Incompetent Cervix Definition: Premature dilation of the cervix, usually occurring around week 20, when the fetus is too immature to survive. Incidence: About 1% of pregnancies. Causes: • Increased maternal age. • Congenital structural defects. • Trauma to the cervix (cone biopsy, repeated D&C). Signs and Symptoms: • Painless dilation of the cervix. • Pink-stained vaginal discharge. • Increased pelvic pressure. • Rupture of membranes and discharge of amniotic fluid. Therapeutic Management: • Cervical cerclage: Surgical procedure to prevent loss of the child due to premature dilation. • Bed rest: After cerclage surgery, to decrease pressure on the sutures. 5. Abortion Definition: Termination of pregnancy before the fetus is viable (400-500 grams or 20-24 weeks gestation). Types of Abortion: • Spontaneous Abortion: Pregnancy interruption due to natural causes. ◦ Threatened: Mild cramping, vaginal spotting. ◦ Inevitable/Imminent: Profuse bleeding, uterine contractions, cervical dilation. ◦ Complete: All products of conception expelled spontaneously. ◦ Incomplete: Part of the conceptus expelled, some retained in the uterus. ◦ Missed: Fetus dies in utero but is not expelled. ◦ Habitual: 3 or more consecutive spontaneous abortions. • Induced Abortion: Deliberate termination of pregnancy in a controlled setting. Complications of Abortion: • Hemorrhage. • Infection (endometritis, parametritis, peritonitis, thrombophlebitis, septicemia). Management: • Bed rest. • Emotional support. • Sedation. • D&C: Surgical removal of retained products of conception. • Antibiotics. • Blood transfusion. 6. Placenta Previa Definition: The placenta is implanted in the lower uterine segment, covering the cervical os, obstructing the birth canal. Incidence: 5 per 1000 pregnancies. Signs and Symptoms: • Abrupt, painless vaginal bleeding (bright red). • Bleeding may stop or slow after the initial hemorrhage, but continue as spotting. Types: • Total: Placenta completely obstructs the cervical os. • Partial: Placenta partially obstructs the cervical os. • Marginal: Placenta edge approaches the cervical os. • Low-lying: Placenta implanted in the lower rather than the upper portion of the uterus. Therapeutic Management: • Immediate Care: Bed rest in a side-lying position. • Assessment: Monitor vital signs, bleeding, and fetal heart sounds. • Intravenous Therapy: Fluid replacement with large gauge catheter. • Delivery: Vaginal birth (safe for infant if previa is less than 30%). Cesarean section (safest for both mother and infant if previa is over 30%). 7. Abruptio Placenta/ Premature Separation of Placenta/ Accidental Hemorrhage/ Placental Abruption Definition: Separation of a normally implanted placenta after the 20th week of pregnancy, before birth of the fetus. Incidence: Most frequent cause of perinatal death. Causes: • Unknown. • Predisposing Factors: ◦ High parity. ◦ Advanced maternal age. ◦ Short umbilical cord. ◦ Chronic hypertensive disease. ◦ PIH. ◦ Trauma (automobile accident, intimate partner abuse). ◦ Cocaine or cigarette use. ◦ Thrombophilitic conditions (autoimmune antibodies). Classification: • Total/Complete: Concealed hemorrhage. • Partial: Concealed or apparent hemorrhage. Signs and Symptoms: • Sharp, stabbing pain in the uterine fundus. • Contractions accompanied by pain. • Uterine tenderness on palpation. • Heavy vaginal bleeding (may be concealed). • Signs of shock. • Tense, rigid uterus. • Disseminated Intravascular Coagulation (DIC). Therapeutic Management: • Fluid Replacement: IV fluids. • Oxygen: Limit fetal hypoxia. • Fetal Monitoring: External fetal heart rate monitoring. • Fibrinogen Determination: IV fibrinogen or cryoprecipitate. • Lateral Position: Prevent pressure on the vena cava. • Delivery: CS is the method of choice if birth is not imminent. 8. Premature Rupture of Membranes Definition: Rupture of the fetal membranes with loss of amniotic fluid during pregnancy before 37 weeks. Incidence: 5%-10% of pregnancies. Causes: • Unknown. • Associated with: Infection of the membranes (chorioamnionitis), vaginal infections (gonorrhea, streptococcus B, Chlamydia). Signs and Symptoms: • Sudden gush of clear fluid from the vagina with continued minimal leakage. • Nitrazine paper test: Amniotic fluid turns the paper blue (alkaline), urine remains yellow (acidic). • Microscopic examination: Amniotic fluid shows ferning, urine does not. • Ultrasound: Assess amniotic fluid index. • Signs of infection (increased WBC count, C-reactive protein, temperature, tenderness, odorous vaginal discharge). Therapeutic Management: • Bed Rest: To prevent further leakage and risk of infection. • Corticosteroids: To hasten fetal lung maturity. • Prophylactic Antibiotics: To reduce risk of infection. • Intravenous Penicillin/Ampicillin: If (+) for streptococcus B. • Induction of Labor: If fetus is mature and labor does not begin within 24 hours. 9. Pregnancy-Induced Hypertension (PIH)/ Toxemia Definition: Vasospasm occurring in both small and large arteries during pregnancy, causing elevated blood pressure, proteinuria, and edema. Incidence: Rarely occurs before 20 weeks of pregnancy. Risk Factors: • Multiple pregnancy. • Primiparas younger than 20 or older than 40. • Low socioeconomic background. • Five or more pregnancies. • Hydramnios. • Underlying diseases (heart disease, diabetes). • Rh incompatibility. • History of H-mole. Categories: • Gestational Hypertension: Blood pressure 140/90 or greater, without proteinuria or edema. • Preeclampsia: Blood pressure 140/90 or greater, with proteinuria and edema. • Eclampsia: Seizures or coma accompanied by preeclampsia. Therapeutic Management: • Preeclampsia: Bed rest, balanced diet, left lateral position. • Severe Preeclampsia: Hospitalization, diazepam, hydralazine, magnesium sulfate. • Eclampsia: Magnesium sulfate, diazepam, oxygen therapy, left lateral position
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Primary adrenal insufficiency = problem at level of adrenal glands Causes? Addison’s disease Pathophys? Autoimmune destruction of the adrenal glands Associated with hyperpigmentation POMC is precursor to both ACTH and MSH PAI → lack of negative feedback → high ACTH Lab findings? ACTH high Aldosterone low Destruction of zona glomerulosa Renin high Hypotension → RAAS activation Electrolytes Na+ low, K+ high CBC Eosinophils high Pathophys? Glucocorticoids → eosinophil apoptosis. Lack of glucocorticoids cause eosinophilia. Dx? Cosyntropin testing → no rise in cortisol Adrenal glands aren’t working, so no response to ACTH. Tx? prednisone/hydrocortisone/dexamethasone + fludrocortisone (mineralocorticoid) Stress-dose steroids for surgery, serious illness, etc. Secondary adrenal insufficiency = problem at level of pituitary, reduced ACTH release Causes? MC is prolonged steroid use → ACTH suppression Sheehan’s syndrome (infarction of pituitary) pregnancy Pituitary tumors (ACTH-producing tumor) Lab findings? ACTH low Anterior pituitary is being inhibited Aldosterone normal Zona glomerulosa under control of RAAS system Renin normal Electrolytes Na+ & K+ unaffected (Aldosterone levels are normal) CBC Neutrophilia due to demargination (if pt was recently taking steroids) Dx? Cosyntropin testing → rise in cortisol Adrenal gland is functional Tx? Glucocorticoids Do not need to replace mineralocorticoids since adrenals are functional and aldosterone is under RAAS control Stress-dose steroids for surgery, serious illness, etc. AI with a history of nuchal rigidity and purpuric skin lesions → Waterhouse-Friedrichson syndrome Pathophys? AI 2/2 hemorrhagic infarction of the adrenal glands in the context of Neisseria meningitidis infection Adrenal synthesis enzymes If the enzyme starts with 1 → HTN (high mineralocorticoids) and hypokalemia If the second # is 1 → virilization (high androgens) E.g. 11-beta hydroxylase deficiency → HTN & virilization E.g. 21 hydroxylase deficiency → virilization only E.g. 17-alpha hydroxylase deficiency → HTN only B12 deficiency Where does B12 come from? Animal products VS folic from plants Physiology R factor in saliva binds to B12 and protects it from acidity in the stomach. R factor protector -B12 travels to the duodenum. Parietal cells produce intrinsic factor, which travels to the duodenum. Pancreatic enzymes cleave B12 from R factor and B12 then binds IF. B12-IF complex is reabsorbed in the terminal ileum Reabsorption where? Terminal ileum Causes of B12 deficiency Extreme vegan Pernicious anemia Pancreatic enzyme deficiency Cystic Fibrosis Can’t cleave B12 from R factor Crohn’s Affects terminal ileum Lab markers Homocysteine HIGH MethlyManoicAcid HIGH Presentation? Megaloblastic anemia Subacute combined degeneration (of dorsal columns + lateral corticospinal tract) Peripheral neuropathy Dx of pernicious anemia? anti-IF Ab Folate deficiency Where does folate come from? Leafy things Causes of folate deficiency Poor diet (e.g. alcoholics, elderly) Phenytoin Lab markers Homocysteine HIGH MMA normal Presentation? Megaloblastic anemia Prophylaxis in HIV+ patients CD4 < 200 → PCP TMP-SMX, inhaled pentamidine, dapsone, atovaquone CD4 < 100 → Toxoplasm Treat: TMP-SMX CD4 < 50 → MAC Treat: Azithromycin If live in endemic area, CD4 < 250 → Coccidioides Immitis E.g. Arizona, Nevada, Texas, California Treat: Itraconazole If live in endemic area, CD4 < 150 → Histoplasma Capsulatum E.g. Kentucky, Ohio, Missouri Treat: Itraconazole Diabetes insipidus Dx? Water deprivation test Measure serum osmolality & urine osmolality Deprive pt of water Remeasure serum osmolality & urine osmolality If urine osmolality doesn’t go up → suspect DI Central DI → deficiency of ADH Pathophys? Supraoptic nucleus not making enough ADH Dx? Give desmopressin → urine osmolality increases significantly Nephrogenic DI → kidneys are not responding to ADH Dx? Give desmopressin → urine osmolality doesn’t change much Tx? Hydrochlorothiazide Unless 2/2 lithium, use amiloride or triametere Causes? Lithium SSRIs Carbamazepine Demeclocycline Tx of normovolemic hypernatremia? D5W to correct free water deficit Divine says NS, but most other resources I found said correct free water deficit Tx of hypovolemic hypernatremia? Give NS first until normal volume, then give D5W Consequence of correcting hypernatremia too rapidly? Cerebral edema Osteoarthritis Presentation? Old person with joint pain that gets worse throughout the day Risk Factr? Obesity vs decreases osteoporosis Imaging findings? Joint space narrowing Subchondral sclerosis Subchondral cysts Osteophytes Arthrocentesis findings? <2000 cells Tx? 1st line acetaminophen 2nd line NSAID (e.g. naproxen) 3rd line joint replacement surgery Returned from a business conference 1 week ago + Fever + Nonproductive cough + Abdominal pain + Hyponatremia → Legionella Dx? Urine antigen Tx? FQ or macrolide MaCroLide mnemonic = Mycoplasma, Chlamydia, Legionella What are the common causes of atypical PNA? Mycoplasma, Legionella, Chlamydia MC cause? Mycoplasma CXR findings? Interstitial infiltrates HY associations C. Psittaci → birds C. Burnetii → cows, goats, sheet Mycoplasma → college student w/ walking pneumonia Midsystolic click heard best at the apex. → mitral valve prolapse “Stenosnap & Proclick” Risk Factor? Connective tissue disease Marfarn Ehlers-Danlos ADPKD bilateral renal masses Classic demographic? Young woman psychiatric Pathophys? Myxomatous degeneration MVP vs aortic dissection: cystic medial necrosis Exam maneuvers Anything that increase amount of blood in LV → murmur softer Increase preload Increase afterload Anything that decreases amount of blood in LV → murmur louder Dx? Echo Scaly, itchy skin with yellowish crusting in the winter. → seborrheic dermatitis Tx? Topical antifungals e.g. ketoconazole or selenium sulfide shampoo Classic disease distribution? Hair → e.g. cradle cap Eyebrows Episodic/intermittent HTN + HA → pheochromocytoma Genetic disease associations MEN2A MEN2B VHL in brain (hemangioma) NF-1 growth in skin Pathophys? Catecholamine-secreting tumor Location? Adrenal medulla Posterior mediastinum Organ of Zuckerkandl (chromaffin cells along the aorta) Dx? 1st step: urine metanephrines If elevated → CT abdomen If nothing found on CT → MIBG scan Tx? Alpha blocker (e.g. phenoxybenzamine, phenotaline) THEN beta blocker Most common cause of a Lower GI Bleed in the elderly → diverticulosis Dx? Colonoscopy or barium enema Recall that you acutely do a CT scan for diverticulitis, then 6 weeks later colonoscopy to r/o cancer Ppx? Eat fiber Megaloblastic anemias Blood smear findings? Hypersegmented neutrophils MCV > 100 Classic patient demographic with folate deficiency? Alcoholics Elderly person with poor nutrition Folate synthesis inhibitors Pt with molar pregnancy → methotrexate Pulmonary issue? Pulmonary fibrosis HIV+ pt with ring-enhancing lesions → pyrimethamine-sulfadiazine Pyrimethamine inhibits DHFR AIDS pt on ppx for toxo → TMP-SMX TMP inhibits DHFR Use of leucovorin? Rescue bone marrow in setting of methotrexate toxicity Mechanism? Folinic acid analog CMV presentations Esophagitis → linear ulcers Colitis → post-transplant pt Retinitis → HIV pt with CD4 < 50 Congenital CMV → periventricular calcifications + hearing loss calcifications elsewhere → toxo Histology? Owl’s eye intranuclear inclusions Tx? Gancicyclovir Resistance? UL97 kinase mutation Tx for resistance? foscarnet CD4 < 200 + severe peripheral edema + frothy urine. → FSGS in HIV pt Variant classic in HIV+ pts? Collapsing variant Tx? Steroids + cyclophosphamide + ACE-I Indinavir AE? Kidney stones triad of fever, rash, and eosinophiluria → acute interstitial nephritis Drugs cause? Penicillins Tx? Stop the drug! Can add steroids if severe Vitamin D metabolism Liver converts Vit D to calcidiol (25OH-Vit D). Calcidiol goes to kidney. Alpha-1 hydroxylase converts calcidiol to calcitriol (1,25-OH Vit D). Common causes of Vitamin D deficiency CKD → 1-alpha hydroxyalse deficiency Liver disease → can’t make calcidiol CF → malabsorption Crohn’s → malabsorption Osteomalacia vs Rickets Osteomalacia in adults Rickets in kids Tx? Calcium + vit D Lab findings? Ca++ low Phos low Low in liver disease High in kidney disease (kidneys can’t get rid of phos) PTH high (2ary hyperpara) vs liver dx PTH low Alk phos Aspiration pneumonia Risk Factor? Alcoholism Dementia Neuromuscular problems (e.g. MG, ALS) Bugs? Anaerobes foul smelling Bacteroides FUsobacterium Peptostreptococcus Klebsiella → currant jelly sputum alcoholic Tx? Clindamycin CURB-65 criteria Purpose? Who to admit Cutoff? 2+ → hospitalize C = confusion U = uremia (BUN > 20) R = RR > 30 B = BP < 90/60 Age > 65 Drugs commonly used in PNA treatment Ceftriaxone Levofloxacin fluoroquinolone Macrolides - great for atypical PNA Pharmacological management of pulmonary arterial HTN Endothelin antagonists Bosentan ambrisentan PDE-5 inhibitors Sildenafil Tadalafil Prostacyclin analogs Iloprost Epoprostenol Treprostinil Causes? Young female → idiopathic PAH Mutation? BMPR2 55 yo F presents with a 5 week history of a rash on her forehead. PE reveals scaly macules with a sandpaper texture. → actinic keratosis Risk Factor? Sun exposure Tx? Topical 5-FU Possible dangerous sequelae? Squamous cell carcinoma Most likely disease sequelae? Resolution 1ary hyperparathyroidism 2ary hyperparathyroidism 3ary hyperparathyroidism Autonomous PTH production Causes? Adenoma Parathyroid hyperplasia PTH high Ca++ high Phos low Low Ca++ → PTH production Causes? CKD PTH high Ca++ low Phos high PTH production despite normalized of Ca++ levels Causes? CKD s/p transplant PTH high Ca++ high Phos low Tx? Parathyroidectomy (remove 3.5 glands) Cinacalcet (CSR modulator) Hypercalcemia Presentation? bones, stones, groans, psychic overtones Tx? 1st step: Normal Saline Hypercalcemia of malignancy → bisphosphonates EKG finding? Shortened QT Periumbilical pain that migrates to the right lower quadrant. → appendicitis PE findings? McBurney’s point tenderness Psoas sign (flex hip pain) Obturator sign (pain with internal rotation of hip) Rovsing’s sign (palpation of LLQ → pain in RLQ) Dx? CT scan Pregnant → US Kid → US Tx? Surgery Classic drug and viral causes of aplastic anemia. Drugs? Carbamazepine Chloramphenicol Viral? Parvovirus B19 (single stranded DNA virus) Fanconi anemia Pathophys? Problems with DNA repair Fanconi anemia vs Fanconi syndrome Fanconi anemia → cytopenias + thumb anomalies + short stature + cafe-au-lait spots Fanconi syndrome → type 2 RTA (proximal) CD4 count of 94 + MRI revealing ring enhancing lesions in the cortex → toxoplasmosis Tx? Pyrimethamine-sulfadiazine Rescue agent for pt who becomes leukopenic with treatment? leucovorin Who should get steroids? Increased ICP For PCP pneumonia: O2 sat < 92 PaO2 < 70 A-a gradient > 35 Ppx? TMP-SMX for CD4 < 100 Congenital toxo Hydrocephalus Chorioretinitis Intracranial calcifications Classic methods of transmission? handling cat litter Lupus nephritis Associated autoantibody? anti-dsDNA Classic “immunologic” description? “Full house” pattern Tx? Steroids + cyclophosphamide Osteoporosis Screening population? women > 65 Screening modality? DEXA scan Dx? T-score < -2.5 Risk Factor? Postmenopauseal Low BMI Smoking Alcohol Preventive strategies? Weight bearing exercise Smoking cessation Reduce alcohol consumption Tx? 1st line: bisphosphonates + Ca/Vit D supplementation Raloxifene (SERM) Agonist in bone Blocker Antagonist in breast Classic locations of osteoporotic fractures Vertebral compression fracture Hip fracture Name the PNA Red currant jelly sputum. → Klebsiella Rust colored sputum. → Strep pneumo PNA in an alcoholic. → Klebsiella Post viral PNA with a cavitary CXR lesion. → Staph aureus PNA in a patient that has chronically been on a ventilator. → Pseudomonas MC cause of Community Acquired Pneumonia. → Strep pneumo Pharmacological management of MRSA. Vancomycin Clindamycin Linezolid Ceftaroline (5th gen cephalosporin) Tigecycline, tertracycline Pharmacological management of Pseudomonas. Ceftazidime (only 3rd gen cephalosporin) Cefepime (4th gen cephalosporin) Pip-tazo Fluoroquinolones Carbapenems Aztreonam Aminoglycosides JVD and exercise intolerance in a patient with a recent history of an URI. → dilated cardiomyopathy 2/2 viral myocarditis MC cause? Coxsackie B VS Coxsackie A: Hand foot mouth dx Drug causes myocarditis Clozapine Anthracyclines Prevention? Dexrazoxane (iron chelator) Trastuzumab reversible tx for breast cancer Classic cause in a patient with recent history of travel to S. America? Chagas T. Cruzi Potential sequelae? Achalasia Dilated cardiomyopathy Megacolon (2/2 degeneration of myenteric plexus) Massive skin sloughing (45% BSA) in a patient that was recently started on a gout medication? TEN Dx? <10% BSA → SJS >30% BSA → TEN Tx? STOP the drug IVF Topical abx to prevention infection Tetany and a prolonged QT interval in a patient with recent surgical treatment of follicular thyroid carcinoma. → hypocalcemia due to removal of parathyroids Recurrent viral infections + QT prolongation + tetany → DiGeorge syndrome Pathophys? Failure of development of 3rd/4th pharyngeal pouches Trousseau and Chvostek signs. Trousseau → inflation of BP cuff causes carpopedal spasm Chvostek → taping on cheek causes facial muscle spasm Hypocalcemia that is refractory to repletion → consider hypomagnesemia Electrolyte/drug causes of prolonged QT intervals Electrolytes? Hypocalcemia Hypomagnesemia Hypokalemia Drugs? Macrolides FloroQunlones Haloperidol Ondensatron Methadone Hypoalbuminemia and Ca balance Hypoalbumenia → decrease in total body Ca++, no change in ionized Ca++ Drop of 1 in albumin → add 0.8 to Ca++ Abdominal pain radiating to the back → acute pancreatitis Causes? #1 = Gallstones #2 = Alcohol Hypertriglyceridemia Hypercalcemia Scorpion sting Handlebar injuries Lab markers? Lipase - most sensitive Amylase Physical exam signs in pancreatitis. Cullen’s sign = periumbilical ecchymosis Grey Turner sign = flank ecchymosis Tx? NPO + IVF + pain control Meperidine is a good agent because it doesn’t cause sphincter of Oddi spasms Management of gallstone pancreatitis Dx? US then ERCP Tx? DELAYED cholecystectomy What if the patient becomes severely hypoxic with a CXR revealing a “white out” lung? ARDS noncardiogenic pulm edema PCWP? <18 mmHg NORMAL 20 yo M with red urine in the morning + hepatic vein thrombosis + CBC findings of hemolytic anemia. → paroxysmal nocturnal hemoglobinuria Pathophys? Defect in GPI anchors, which attach CD55 and CD59 to cell (they prevent complement from destroying RBC) Sleep → hypoventilation → mild respiratory acidosis → activation of complement cascade Gene mutation? PIGA Dx? Flow cytometry Tx? Eculizumab (terminal complement inhibitor) Vaccine required? pnemococal Neisseria meningitidis Chronic diarrhea and malabsorption in a HIV+ patient + detection of acid fast oocysts in stool. → cryptosporidium parvum Acid-fast organisms Cryptosporidium TB MAC Nocardia Dx? Stool O&P Tx? Nitazoxanide Route of transmission? Contaminated water Muddy brown casts on urinalysis in a patient with recent CT contrast administration (or Gentamicin administration for a life threatening gram -ve infection) → Acute Tubular Necrosis Woman with morning joint stiffness > 1 hr → Rhematoid Arthritis. Antibodies? Rheum Factor (IgM against IgG) anti-CCP - more specific HLA? DR4 Pathophys? IgM constant region activates complement → inflammation → formation of pannus (hypertrophied synovium) → damage to cartilage and bone Caplan syndrome = RA + pneumoconiosis Felty syndrome = RA + neutropenia + splenomegaly (“RANS”) Classic hand/finger findings/distribution? MCP & PIP joints of hands (DIP joints spared) Imaging findings? Symmetric joint space narrowing Tx? Methotrexate (DMARDs) If no response → TNF alpha inhibitor (e.g. infliximab) Required testing prior to starting methotrexate? PFTs Required testing prior to starting infliximab? TB Hep B/Hep C Differentiating Strep pharyngitis from Infectious Mononucleosis LND distribution Anterior cervical → Strep Posterior cervical → Mono Disease onset Acute → Strep Over weeks → Mono Organ involvement Splenomegaly → Mono Pt with sore throat takes amoxicillin and gets rash → mono NOT allergic rxn! CENTOR criteria C = absence of Cough E = tonsillar Exudates N = nodes/anterior cervical lymphadenopathy T = temp (fever) OR <15 → +1 >=45 → -1 Using CENTOR score 0/1 → don’t test, don’t treat 2/3 → rapid antigen test Positive → treat Negative → throat culture 4/5 → treat empirically Tx of Strep pharyngitis? Amoxillcin If PCN allergic → azithromycin Potential sequelae of Strep pharyngitis RF - preventable with abx PSGN Endocarditis MC cause of endocarditis? IVDU Bug? Staph aureus Valve? tricuspid Prosthetic valve endocarditis Bug? Staph epidermidis Endocarditis after dental procedure? Viridans group streptococci Strep viridans, Strep mitis, Strep mutans, Strep sanguineous Patient with malar rash and echo showing vegetations on both sides of the mitral valve → Libman-Sacks endocarditis Presentation? Fever + night sweats + new murmur Splinter hemorrhages Roth spots (retinal hemorrhages) Painless Janeway lesions + painful Osler nodes (immune phenomenon) Dx? 1st step: blood cultures TEE Tx? Abx that include Staph aureus coverage (e.g. vancomycin) for WEEKS Bugs implicated in culture negative endocarditis HACEK H = haemophilus A = actinobacillus C = cardiobacterium E = eikenella K = kingella Coxiella burnetii Blood cultures in a patient with endocarditis reveal S. Bovis (or S. Gallolyticus bacteremia). NBS? Colonoscopy Who needs antibiotic prophylaxis? Hx endocarditis Prosthetic valve Unrepaired cyanotic congenital dz Heart transplant with valve dysfunction Erythematous salmon colored patch with silvery scale on the elbows and knees. → psoriasis Tx? Topical steroids If this patient presents with joint pain (especially in the fingers)? Psoriatic arthritis Imaging? Pencil-and-cup deformity Tx? NSAIDs T of 104 + tachycardia + new onset Afib in a patient with a history of Graves disease. → thyroid storm Lab findings? TSH low T3/T4 high Tx? 1st step: propranolol 2nd step: PTU Then: Prednisone Potassium iodide (Lugul’s solution) Wolff-Chaikoff effect → large amounts of iodine inhibit thyroid hormone synthesis Biopsy revealing tennis racket shaped structures in cells of immune origin. → Langerhans cell histiocytosis Electron microscopy? Birbeck granules (tennis rackets) Marker? S100 Small bowel obstruction in a HIV patient with purple macules on the face, arms, and lower extremities. → Kaposi’s sarcoma Bug? HHV8 Tx? HAART Pathophys of vascular lesions? Overexpression of VEGF Fever + rash + eosinophiluria 10 days after a patient started an antistaphylococcal penicillin. → acute interstitial nephritis Tx? STOP drug + steroids SLE SOAP BRAIN MD S = serositis O = oral ulcers A = arthritis P = photosensitivity B = blood disorders (cytopenias) R = renal A = ANA/anti-dsDNA I = immunologic N = neurologic findings M = malar rash D = discoid rash Type 2 vs 3 HSRs in lupus Type 2 → cytopenias Type 3 → all other manifestations Lupus Ab? ANA anti-dsDNA anti-Smith Lupus nephritis → full house pattern on IF Antiphospholipid antibody syndrome → recurrent pregnancy losses Pathophys? Thrombosis of the uteroplacental arteries. MC cause of death in lupus patients? What I’ve read recently: CV disease Per Divine: Treated → infection Untreated → renal dz Also 40x risk MI Endocarditis in lupus pt? Libman-Sacks endocarditis Neonatal 3rd degree heart block → neonatal lupus Maternal autoimmune dz? Sjogren’s SLE Ab? anti-SSA/anti-Ro anti-SSB/anti-La Tx? Steroids Cyclophosphamide Hydroxychloroquine → good for skin lesions Pulmonary abscesses Bugs? Staph Anaerobes Klebsiella RF? Alcoholism Elderly Post-viral pneumonia MC location of aspiration pneumonia? Superior segment of RLL Chest pain worsened by deep inspiration and relieved by sitting up in a patient with a recent MI or elevated creatinine or URI or RA/SLE. → pericarditis EKG findings? Diffuse ST elevations + PR depression PE finding? Friction rub (“scratchy sound on auscultation”) A few days after MI → fibrinous pericarditis Weeks after MI → Dressler’s Tx? NSAIDS Consider adding on colchicine Cardiac tamponade Beck’s triad = hypotension + JVD + muffled heart sounds EKG findings? Electrical alternans Type of shock? Obstructive cardiogenic (Amboss) CO low SVR high PCWP high Tx? Pericardiocentesis or pericardial Pearly lesion with telangiectasias on the ear in a farmer. → Basal Cell Carcinoma MC type skin cancer Location? Upper lip Dx? Biopsy Tx? Mohs surgery Cold intolerance in a 35 yo white F → hypothyroidism MC cause? Hashimoto’s Histology? lymphoid follicles w/ active germinal centers Lab findings? TSH high T3/T4 low Ab? anti-TPO Anti-thyroglobulin HLA? DR3/DR5 Tx? Levothyroxine Future complication? thyroid lymphoma Massive hematemesis in a patient with a history of chronic liver disease. → ruptured varices Pathophys? L gastric vein has anastomosis with azygos veins. Increased portal pressure → backward flow from L gastric veins to azygous vein (which empties into SVC). Acute tx? IVF + octreotide + ceftriaxone/cipro + EGD w/ ligation/banding Do NOT give a beta blocker for acute tx Prophalaxsis? Beta blocker + spironolactone Other manifestations of elevated portal pressures Caput medusa Internal hemorrhoids Tx for cirrhotic coagulopathies? FFP If uremia → give desmopressin Note: Desmopressin = ADH analog → so, it can cause AE of hyponatremia 2/2 SIADH Hemophilia A Pathophys? deficiency of factor 8 Inheritance? XLR Coag labs? Bleeding time normal PTT HIGH b/c clotting problem PT normal Hemophilia B Pathophys? deficiency of factor 9 Inheritance? XLR Coag labs? Bleeding time normal PTT HIGH PT normal Hemophilia C Pathophys? deficiency of factor 11 Inheritance? AR Coag labs? Bleeding time normal PTT HIGH PT normal Bernard Soulier Syndrome Pathophys? Deficiency of GpIb Coag labs? Bleeding time HIGH PTT normal PT normal Glanzmann Thrombasthenia Pathophys? Deficiency of GpIIbIIIa Coag labs? Bleeding time HIGH PTT normal PT normal Von Willebrand’s disease Pathophys? Deficiency of vWF Inheritance? AD Coag labs? Bleeding time HIGH PTT HIGH vWF is a protecting group for factor 8 PT normal ITP Pathophys? Ab against GpIIbIIIa Classic pt? Pt with SLE Tx? Observation Steroids IVIG Splenectomy TTP Pathophys? Deficiency in ADAMTS13 enzyme → cannot cleave vWF multimers → activation of platelets → thrombosis → thrombocytopenia Presentation? microangiopathic hemolytic anemia + thrombocytopenia + renal failure + fever + neurologic problems Tx? Plasma exchange transfusion****** HUS Bugs? Shigella or E. coli O157:H7 Presentation? Fever+ microangiopathic hemolytic anemia + thrombocytopenia + renal failure + neurologic Platelet deficiency vs coagulation factor bleeds Platelet deficiency → mucosal bleeds, petechiae, heavy menses Coag factor deficiency bleeds → hemarthrosis Why do patients with CKD develop coagulopathy? Uremia → platelet dysfunction Tx? Desmopressin Note: Desmopressin = ADH analog → so, it can cause AE of hyponatremia 2/2 SIADH Exercising caution with transfusion in patients with Bernard Soulier syndrome Do NOT give transfusion that includes platelets They can have an anaphylactic rxn to GpIb (since they don’t have GpIb) Oropharyngeal candidiasis. RF? HIV Chronic ICS use TNF inhibitor Micro finding? Germ tubes at 37 C Tx oral candidiasis? Nystatin swish-and-swallow Tx invasive candidiasis? Amphotericin B Prevention of Amphotericin B toxicity? Liposomal formulation Pleural effusions Light’s criteria (must meet all 3 to be considered transudative!) LDH < 2/3 ULN LOW Pleural LDH/serum LDH < 0.6 LOW Pleural protein/serum protein < 0.5 LOW Causes of transudative effusion CHF Cirrhosis Nephrotic syndrome Note: Per UW 2021: Mechanism of transudate effusion? Decreased pulmonary artery oncotic pressure, e.g. hypoalbuminemia in nephrotic syndrome Increased pulmonary capillary hydrostatic pressure, e.g. volume overload in heart failure Causes of exudative effusion Malignancy Cancer Parapneumonic effusion Tb Note: Per UW 2021: Mechanism of exudate effusion? Inflammatory increased in vascular permeability of membrane (increased flow of interstitial edema into pleural space) Unique cause of both transudative & exudative effusions? PE Classic Pleural Effusion findings? Decreased breath sounds Dullness to percussion Decreased tactile fremitus Tx? Chest tube Chylothorax = lymph in the pleural space Pathophys? Obstruction of thoracic duct or injury to the thoracic duct Pleural fluid findings? High Triglycerides Holosystolic murmur heard best at the apex with radiation to the axilla in a patient with a recent MI. → mitral regurg 2/2 papillary muscle rupture Dx? Echo Why widely split S2? Aortic valve is closing earlier (LV is emptying into both aorta & LA) Maneuvers that increase intensity Increase preload (putting more blood in that can be regurgitated) Increase afterload Decubitus ulcers RF? Elderly Paraplegic Fecal/urinary incontinence Poor nutrition Staging Stage 1 = non-blanchable erythema Tx? Repositioning q2hrs Stage 2 = loss of epidermis + partial loss of dermis Tx? Occlusive dressing superficial Stage 3 = involves entire dermis, extending to subQ fat Does NOT extend past fascia Tx? Surgical debridement Stage 4 = muscle/tendon/bose exposed Tx? Surgical debridement General tx strategies? Repositioning + good nutritional support Marjolin’s ulcer = non-healing wound that is actually squamous cell carcinoma T1DM Pathophys? Autoimmune destruction of pancreas Ab? anti-GAD 65 (glutamic acid decarboxylase) anti-IA2 (islet tyrosine phosphatase 2) Islet cell autoantibodies Insulin autoantibodies Dx? A1c > 6.5% (twice) Fasting BG >= 126 (twice) Oral glucose tolerance test >= 200 (twice) Sxs of DM + random glucose > 200 Tx? Long-acting insulin + mealtime insulin Long-acting Glargine Detemir Rapid-acting Lispro Aspart Glulisine 3 HY complications Nephropathy Retinopathy & cataracts Neuropathy Chronic DM care A1c q3 months Foot exam annually Eye exam annually Microalbumin:Cr ratio annually Nephroprotection in DM? ACE-I GI bleed algorithm 1st step: ABCs + 2 large-bore IVs + IVFs 2nd step: NG lavage Clear fluid → go deeper Blood → UGIB → upper endoscopy Bilious fluid → have ruled out UGIB → proceed to colonoscopy See source → intervene as needed See nothing → CT angiography for large bleed Tagged RBC scan for smaller bleed Antiplatelet Pharmacology Aspirin Mechanism? Irreversibly inhibits COX-1 and COX-2 Clopidogrel/ticlopidine = P2Y12 (ADP receptor) blockers Mechanism? Inhibit platelet activation Abciximab/eptifibatide/tirofiban = GpIIbIIIa receptor blockers Mechanism? Inhibit platelet aggregation Ristocetin cofactor assay Issues with adhesion step → abnormal result Abnormal ristocetin cofactor assays: Von Willebrand disease Bernard Soulier disease Normal ristocetin cofactor assay: Glanzmann Thrombasthenia Von Willebrand disease effects on PTT? Increased Pathophys? vWF is a protecting group for Factor 8. Treatment of VWD? Desmopressin Mechanism? Increases release of vWF from Weibel-Palade bodies of endothelial cells Note: Desmopressin = ADH analog → so, it can cause AE of hyponatremia 2/2 SIADH HSV1 vs HSV2. Oral herpes → HSV1 Genital herpes → HSV2 Dx? PCR (most up-to-date) Tzanck smear (outdated, not very sensitive, nonspecific) → intranuclear inclusions Brain area affected by HSV encephalitis? Temporal lobes CSF findings in HSV encephalitis? RBCs******* Tx herpes encephalitis? Acyclovir AE? Crystal nephropathy Can’t see, can’t pee, can’t climb a tree. → reactive arthritis HLA? B27 Classic bug? Chlamydia Tx? steroids Need abx? Only if ongoing infection Can’t see, can’t pee, can’t hear a bee → Alport syndrome Inheritance? X-linked dominant Tx of NG & CT NG → treat empirically for both → ceftriaxone + azithro/doxy CT → azithro/doxy Hypovolemic Septic Neurogenic Cardiogenic CO low PCWP low SVR high*** CO high PCWP normal SVR low Tx? norepi CO low SVR low CO low PCWP high*** SVR high*** Tx anaphylactic shock? epinephrine Melanomas ABCDE A = asymmetry B = irregular borders C = color variation D = diameter > 6 mm E = evolving Dx? Full-thickness biopsy Excisional for small lesions Punch for larger lesions Most important prognostic factor → Breslow depth DM pharmacology Lactic acidosis → metformin Decreases hepatic gluconeogenesis → metformin Hold before CT w/ contrast → metformin Weight gain → sulfonylureas & TZDs (-glitizones) Diarrhea → acarbose & migliton Inhibits disaccharidases (can’t reabsorb disaccharides) Recurrent UTIs → SGLT-2 inhibitors Weight loss → GLP-1 agonists (e.g. liraglutide, exenatide) & DPP4 inhibitors (-gliptins) Contraindicated in pt with HF → TZDs PPAR-gamma receptor found in kidney → water retention Contraindication in pt with MTC → GLP-1 agonists Biggest risk of hypoglycemia? Sulfonylureas RF esophageal adenocarcinoma Barrett’s esophagus RF esophageal squamous cell carcinoma Smoking Drinking Achalasia Location esophageal adenocarcinoma? Lower 1/3 Location esophageal squamous cell carcinoma? Upper 2/3 MC US? Adenocarcinoma MC worldwide? Squamous cell carcinoma Presentation? Dysphagia to solids → dysphagia to liquids Dx? EGD Staging? CT scan or esophageal US Factor V Leiden Pathophys? Resistance to protein C Dx? Activated Protein C resistance assay Patient needs super large doses of heparin to record any changes in PTT → AT-III deficiency Recall that heparin is a AT-III activator 35 yo with a hypercoagulable disorder that does not correct with mixing studies. → antiphospholipid antibody disorder Anaphylaxis in a patient with a long history of Hemophilia A → Ab against factor 8 that cause type 1 HSR with transfusion Hx of hemophilia, diagnosed 5 years ago. Before you would give them factor 8 concentrate and PTT would normalize. Now they’re requirizing larger doses of factor 8 to normalize PTT. → inhibitor formation (antibodies against clotting factors) Skin necrosis with Warfarin → protein C/S deficiency Prothrombin G20210 mutation → overproduction of factor II Rash in dermatomal distribution → VZV infection Contraindications to VZV vaccination? Pregnant woman Kid < 1 year Severe immunosuppression (e.g. HIV with CD4 < 200) Tx? Acyclovir If resistant, foscarnet Tzanck smear findings? Intranuclear inclusions Shingles vaccination guidelines? Adults over 60 #1 cause of ESRD in the US → DM nephropathy Histology? Kimmelsteil-Wilson nodules #2 cause of ESRD in the US → hypertensive nephropathy Pt with BP 240/150. How fast should you lower BP? 25% in first 24 hrs Drugs for hypertensive emergencies? Nicardipine Clevidipine Nitroprusside AE? Cyanide poisoning Tx? Amyl nitrate + thiosulfate OR hydroxocobalamin Labelol Renal protective medications in patients with DKD or hypertensive nephropathy? ACE-I Anemia + Cranial Nerve deficits + Thick bones + Carbonic Anhydrase 2 deficiency + Increased TRAP + Increased Alkaline Phosphatase. → osteopetrosis Pathophys? Carbonic anhydrase is defective → osteoclasts cannot produce acid to resorb bone Tx? IFN-gamma Osteoclasts are a specialized macrophage IFN-gamma is an activator of macrophages Clinical diagnostic criteria for Chronic Bronchitis Diagnostic criteria? 2 years 3 months/year of chronic cough PFT findings FEV1 low FEV1/FVC ratio low RV high TLC high Which PFT market can differentiate CB from emphysema? DLCO DLCO normal → CB DLCO low → emphysema ****** Tx acute exacerbation? Abx + bronchodilators + corticosteroids (“ABCs”) Prevention? Stop smoking! Afib #1 RF? Mitral stenosis #1 RF MS? Rheumatic fever #1 RF CAD and AAA: smoking #1 RF stroke and aortic dissection: HTN MC arrhythmia in hyperthyroidism → Afib MC site of ectopic foci in Afib → pulmonary veins EKG findings? “Irregularly irregular” + no P waves Location of emboli formation? LA appendage Who should be cardioverted back to sinus rhythm? New onset (<48 hrs) Afib Anticoagulated for 3 weeks + TEE negative for clot Afib that’s refractory to medical therapy Afib & HDUS Q on T phenomenon? Depolarization during T wave (repolarization) can cause QT prolongation → Torsades → death Prevention? SYNCHRONIZED cardioversion Tx? Rate control Beta blockers ND-CCB (e.g. verapamil, diltiazem) Rhythmic control Amiodarone Reducing stroke risk in Afib? Anticoagulation for CHA2DS2VASc score >= 2 Anticoagulation options Valvular cause (e.g. MS) → warfarin Any other cause → warfarin or NOAC (apixiban) Reversal of AC Warfarin → Vit K, four-factor PCC Heparin → protamine sulfate Dabigatran → idarucizumab Crusty, scaly, ulcerating lesion with heaped up borders → squamous cell carcinoma Classic location? Below Lower lip Precursor lesion? Actinic keratosis What if it arises in a scar or chronic wound? Marjolin ulcer Hypothermia + hypercapnia + non pitting edema + hyponatremia + HR of 35 + hypotension in a patient with a history of papillary thyroid cancer → myxedema coma Tx? Levothyroxine + steroids Lab findings? TSH high T3/T4 low LDL high Acute onset “dermatologic” breakout in a patient with a recent history of weight loss and epigastric pain. → Leser–Trélat sign associated with visceral malignancy pancreatic cancer Lymph node associations Supraclavicular → Virchow’s node Periumbilical → Sister Mary Joseph What are mets to the ovaries called? Kruckenberg tumor Classic bug associated with gastric cancer? H. pylori (MALToma) Classic histological finding in the diffuse type of gastric cancer? Signet ring cells RBCs without central pallor + elevated MCHC + anemia. → hereditary spherocytosis Inheritance? AD Pathophys? Deficiency of spectrin, ankyrin, or band 3.2 Intravascular or extravascular hemolysis? Extravascular (RBCs bound by IgG, attacked by splenic macrophages) Dx? Osmotic fragility test Eosin-5-maleimide Acidified glycerol lysis test Tx? Splenectomy Post-splenectomy preventative care? Strep pneumo Hinflue vaccine Neisseria Septic shock Hemodynamic parameters CO high SVR low PCWP normal MvO2 high Tx? IVF + norepi + broad-spectrum abx (cover MRSA + Pseudomonas) E.g. vanc + pip-tazo E.g
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