Usmle Step 2: Electrolytes Part 2 Qbank (6 -> 27) Flashcards - Cram.com
How to treat lithium-induced nephrogenic DI? salt restriction and discontinuation of lithium severe polyuria, mild hypernatremia, urine osmolality may be lower than the elevated serum osmolality chronic compensated respiratory alkalois due to stimulatory effect of progesterone on the medullary respiratory center used to calculated the expected PCO2 during respiratory compensation for a primary metabolic acidosis mixed metabolic and respiratory acidosis lab values -decreased HCO3 to indicate primary metabolic acidosis -inappropriately nl PaCO2 indicates a primary respiratory acidosis (can be proven using Winter's formula -> PaCO2 should be lower than actual PaCO2) primary polydipsia -> nothing wrong with ADH anion gap metabolic acidosis + osmolar gap acidosis calcium oxalate crystals viewed on U/A -> rectangular envelope-shaped crystals serum osmolality (calculated) = 2Na + glucose/18 + BUN/2.8 primary metabolic acidosis with respiratory compensation type A: poor oxygen delivery to tissues 2/2 CO poisoning and circulatory failure (shock) quickest way to correct hyperkalemia + other ways calcium gluconate: cardiac membrane stabilization bicarb/beta 2 agonist: drive K into cells In chronic alcoholic, what must be done to correct hypokalemia appropriately? treat hypomag as well because this causes refractory hypoK Contraction alkalosis refers to the increase in blood pH that occurs as a result of fluid losses (volume contraction). The change in pH is especially pronounced with acidic fluid losses caused by problems like vomiting. One popular theory is that alkalosis is simply the loss of solvent volume without a proportional loss in bicarbonate concentration or increase in carbon dioxide concentration. vomiting can cause what kind of electrolyte abnormalities gastric conte Continue reading >>
Hyperosmolar Hyperglycemic State (hhs)
By Erika F. Brutsaert, MD, Assistant Professor, Albert Einstein College of Medicine; Attending Physician, Montefiore Medical Center Hyperosmolar hyperglycemic state is a metabolic complication of diabetes mellitus (DM) characterized by severe hyperglycemia, extreme dehydration, hyperosmolar plasma, and altered consciousness. It most often occurs in type 2 DM, often in the setting of physiologic stress. HHS is diagnosed by severe hyperglycemia and plasma hyperosmolality and absence of significant ketosis. Treatment is IV saline solution and insulin. Complications include coma, seizures, and death. Hyperosmolar hyperglycemic state (HHSpreviously referred to as hyperglycemic hyperosmolar nonketotic coma [HHNK] and nonketotic hyperosmolar syndrome) is a complication of type 2 diabetes mellitus and has an estimated mortality rate of up to20%, which is significantly higher than the mortality for diabetic ketoacidosis (currently < 1%). It usually develops after a period of symptomatic hyperglycemia in which fluid intake is inadequate to prevent extreme dehydration due to the hyperglycemia-induced osmotic diuresis. Acute infections and other medical conditions Drugs that impair glucose tolerance (glucocorticoids) or increase fluid loss (diuretics) Serum ketones are not present because the amounts of insulin present in most patients with type 2 DM are adequate to suppress ketogenesis. Because symptoms of acidosis are not present, most patients endure a significantly longer period of osmotic dehydration before presentation, and thus plasma glucose (> 600 mg/dL [> 33.3 mmol/L]) and osmolality (> 320 mOsm/L) are typically much higher than in diabetic ketoacidosis (DKA). The primary symptom of HHS is altered consciousness varying from confusion or disorientation to coma, usually as Continue reading >>
Alcohol Intoxication And Withdrawal
Alcohol consumption is not bad if you know your limits and consume moderately. Number of cases due to alcohol intoxication are always at peak during festival season and it is one of the most frequentlytested topic on board exams. Let's move directly on to the high-yield points that are most likely to be tested on exam. Vitamin B1 (thiamine) is used up in metabolism of ethanol, therefore, there is an increase risk of Wenicke-Korsakoff syndrome.Wernicke is reversible while Korsakoff syndrome is non-reversible. Give thiamine as soon as possible when u suspect Wernicke's encephalopathy (ophthalmoplegia, dementia, ataxia). Korsakoff syndrome is anterograde amnesia with/without aphasia, apraxia, agnosia and deficit of executive function. Alcoholics can develop dehydration (due to excessive diuresis), nutritional deficiency (because they are used up in metabolism of alcohol), electrolyte abnormalities (due to vomiting and other factors) and acidosis. Symptoms that are observed with increasing alcohol intake are Sense of warmth and well being > Euphoria > Decreased judgement >In-coordination, decreased reaction time/reflexes > Cerebellar dysfunction (ataxia, slurred speech, nystagmus) > Coma and respiratory depression. Holiday heart syndrome (Patients with acute ethanol intoxication may exhibit "holiday heart," in which dysrhythmias, especially atrial fibrillation, occur following a heavy drinking episode. Ethanol lowers the threshold for developing atrial fibrillation). Cirrhosis, esophageal varices, and erosive gastritis are common in chronic alcoholics. If thepatient have low PH (acidosis), then serum anion gap will narrow down the list of differential diagnosis.Early in the course of intoxication with a toxic alcohol, a patient will have neither an anion gap nor an osmolar Continue reading >>
Usmle Step 3 Nephro Flashcards | Quizlet
b. hematocrit will drop within 2 weeks from loss of erythopoietin production c. calcium levels will drop from the loss of Vit D hydroxylation Prerenal Azotemia -- causes of hypoperfusion a. Hypotension - systolic pressure <90 mm Hg b. Hypovolemia - from dehydration/bloodloss c. Low oncotic pressure - from low albumin d. CHD - can't perfuse kidney if pump doesn't work e. Constrictive pericarditis - can't perfuse kidney if heart cannot fill f. Renal artery stenosis - systemic pressure high but kidney thinks body hypotensive due to blockage a. BUN to creatinine ration of >15:1 and >20:1 c. Fractional excretion of sodium <1percent (basically low urine sodium) Mechanism of Elevation of BUN in Prerenal Azotemia ADH increases urea absorption at the collecting duct. ADH increase activity of the urea transporter. CCS, all renal cases should have following tests: c. Cancer of bladder. prostrate, or cervix d. Neurogenic bladder (atonic or noncontracting due to MS or diabetes) a. Elevated BUN to creatinine ratio >15:1 c. Large volume diuresis with urinary cath d. Bilaternal hydronephrosis on ultrasound Can unilaternal obstruction cause renal failure? No. Obstruction must be bilateral to cause renal failure. That's why people can live with donating one kidney. a. BUN to creatinine ration closer to 10:1 Acute Tubular Necrosis (ATN) can be called by: a. hypoperfusion to point of death of tubular cells Causes of Toxin-Induced Renal Insufficiency No single test to prove one particular toxin caused renal failure. Common causes are: a. Aminoglycosides (gentamicin, tobramycin, amikacin) which cause hypomagnesemia and takes 4-5 days of use to effect damage. d. Contrast agents - urine sodium low (<20) and can happen 12 hours later Mechanim of Rapid Onset of Renal Failure with Contrast Agent Continue reading >>
Hyperalimentation Acidosis Associated With Tpn - Deranged Physiology
Hyperalimentation Acidosis Associated with TPN The two definitions for this are over-feeding, and the use of total parenteral nutrition. Only TPN, however, causes metabolic acidosis. This chapter deals with the metabolic acidosis which results from parenteralsupplementation with amino acid mixtures. Hyperchloraemic metabolic acidosis due to the preservatives in TPN The major role in this is again plaid by the chloride ion . There is the presence of the chloride ion in the hydrochloride preparations of lysine and arginine, which had historically formed a major part of the early TPN mixures. And casein hydrolysate had also contained a large amount of hydrochloride. Furthermore, hydrochloric acid is typically added to TPN amino acid mixtures in order to reduce the pH, and thus avoid the unpleasant Maillard reaction. Let us consider the bag of TPN amino acids. At any given pH, amino acids may either be cationic or anionic. In the TPN bag, where the pH is 5.8, the majority will be cationic. This positive charge is balanced by chloride ions. Now, consider what happens to the TPN mixture once it has been infused into the patient. The cationic amino acids have an exit strategy- they can be metabolised and incorporated into proteins. The chloride, however, persists it is a non-metabolisable anion. As cationic amino acids leave the circulation, only chloride remains. The strong ion difference decreases. Hence the acidosis. Of course, this whole business can be avoided if only acetic acid were used to acidify the TPN mixture. Acetic acid is metabolisable, and will not contribute to the strong ion difference. But what about oral overfeeding? This is a curious beast. Many pages have been devoted in the literature to the metabolic and physiological effects of starvation; however, gl Continue reading >>
How Exactly Does 0.9% Saline Cause Hyperchloremic Metabolic Acidosis? Something To Do With It's Strong Iron Difference But I Can't Quite Grasp It. : Medicalschool
Please keep all topics germane to current medical students. ALL QUESTIONS GERMANE TO PREMEDICAL STUDENTS(for example how many doctors should I shadow to get into Harvard?) should be directed to the PREMED subreddit. Filesharing is prohibited in this subreddit. This includes discussion of filesharing or sources of pirated materials (e.g. anki decks). This subreddit is not a place to spam your blog or solicit business. Should you wish to submit your own content, please consider buying a sponsored link from reddit. Keep memes to a minimum. We welcome personal submissions and well-written concerns or stories, but please present them in a more intelligent fashion. Troll posts will not be tolerated. Previous examples of troll posts involved users seeking "help" on mundane or sensitive personal issues. These posts often include an immature or sophomoric subtext. As with memes, we ask you to please exercise judgement and present your content in a more mature and intelligent fashion. Moderator discretion is used to determine and remove posts of this nature. Please limit posts concerning USMLE Step 1 or 2 to their respective stickied threads. Posts not following this rule will be deleted. AMA-style threads are not allowed without prior moderator approval. Moderation issues related to the IRC channel should be directed at the mods of the respective channel. The moderators of the /r/MedicalSchool subreddit do not officially sanction/endorse any channel or take responsibility for any happenings within any channel. Posts made by accounts with less than 10 comment karma or less than 3 days old will be automatically removed. This is to prevent spam/trolling. For information on rules regarding recruitment for research studies, please see this page. You may not recruit for your research Continue reading >>
Usmle Step 2 Second Edition 072208 Part 2 By Surgisphere - Issuu
CHAPTER CONTENTSBasic Science .....................................................................................................444Hypothalamus-Pituitary Axis ............................................................................446Thyroid Gland....................................................................................................451Parathyroid Gland .............................................................................................458Adrenal Gland ...................................................................................................461Pancreas ............................................................................................................467Metabolic Disorders..........................................................................................472Cancer ...............................................................................................................481Practice Questions ............................................................................................482 MECHANISM OF ACTIONMediates glucose, aminoacid, and potassium intakePromotes glycogen and fattyacid synthesisDecreases proteinolysis,lipolysis, andgluconeogenesis Dangerous hypoglycemic stage inoverdose that can lead to severe braindamage Binds to K+-ATPase on beta cells leading to depolarization andincreased insulin releaseSome sensitization of beta cells to glucose MECHANISM OF ACTIONDecrease insulin resistance, decreasesgluconeogenesis in liver, decreases intestinalglucose absorption, and improves peripheraluptake of glucose through AMP-dependentprotein kinase Lactic acidosis(rare)GI SxStop prior to giving IVcontrast (renalfailure) Reducesmorbidity indiabetes (only agentto do so besidesinsulin) MECHANISM OF ACTIONBind to PPARs to i Continue reading >>
Hyperchloremic Acidosis
Author: Sai-Ching Jim Yeung, MD, PhD, FACP; Chief Editor: Romesh Khardori, MD, PhD, FACP more... This article covers the pathophysiology and causes of hyperchloremic metabolic acidoses , in particular the renal tubular acidoses (RTAs). [ 1 , 2 ] It also addresses approaches to the diagnosis and management of these disorders. A low plasma bicarbonate (HCO3-) concentration represents, by definition, metabolic acidosis, which may be primary or secondary to a respiratory alkalosis. Loss of bicarbonate stores through diarrhea or renal tubular wasting leads to a metabolic acidosis state characterized by increased plasma chloride concentration and decreased plasma bicarbonate concentration. Primary metabolic acidoses that occur as a result of a marked increase in endogenous acid production (eg, lactic or keto acids) or progressive accumulation of endogenous acids when excretion is impaired by renal insufficiency are characterized by decreased plasma bicarbonate concentration and increased anion gap without hyperchloremia. The initial differentiation of metabolic acidosis should involve a determination of the anion gap (AG). This is usually defined as AG = (Na+) - [(HCO3- + Cl-)], in which Na+ is plasma sodium concentration, HCO3- is bicarbonate concentration, and Cl- is chloride concentration; all concentrations in this formula are in mmol/L (mM or mEq/L) (see also the Anion Gap calculator). The AG value represents the difference between unmeasured cations and anions, ie, the presence of anions in the plasma that are not routinely measured. An increased AG is associated with renal failure, ketoacidosis, lactic acidosis, and ingestion of certain toxins. It can usually be easily identified by evaluating routine plasma chemistry results and from the clinical picture. A normal AG Continue reading >>
Comments On Nsim Of Dm1 ?
A 20-year-old female is brought to the Emergency Room by her college roommate who states that the patient vomited all night. The patient complains of a sore throat and says she has not eaten for the last two days. She admits to a "sugar problem" and quit taking her medication because she has not been eating. Examination reveals an ill-appearing woman. and respirations are 30/min. The patient's lips and mucous membranes are dry. There is a fruity odor noted to the patient's breath. The lung and cardiac examination are unremarkable except for mild tachypnea and tachycardia. Laboratory analysis shows: Diabetic ketoacidosis (DKA) is a life threatening complication of diabetes mellitus. DKA exists if there is hyperglycemia (glucose >300), ketonemia, acidosis (pH <7.30, HCO3 < 15) with clinical symptoms of diabetes. The mainstay of treatment for DKA is intravenous insulin. Intubation (choice A) is rarely necessary in DKA patients. The patient is alert enough to give some history and appears to be oxygenating well. Intramuscular ceftriaxone (choice C) may be necessary in this case to treat an underlying infection, which may have precipitated this episode of DK A. However, this is certainly not first-line treatment for DKA. Intravenous fluids (choice D) are also vital for DKA patients, as they are severely dehydrated. However, potassium is not initially added to intravenous fluids, especially if the potassium level is greater than 6.0 mEq/L. Mannitol (choice E) is used in suspected cases of cerebral edema, a complication of DKA. Clinical signs include deterioration in mental status, headache, and unequal pupils. The Barbara Davis Center for Childhood Diabetes in Denver, Colorado, has prepared an excellent poster for hospital emergency rooms with the correct treatment procedure Continue reading >>
Questions On First Aid Info On Metabolic Acidosis And Rta
SDN members see fewer ads and full resolution images. Join our non-profit community! Questions on first aid info on metabolic acidosis and RTA In first aid, they gave an mnemnic on normal anion gap: They didn't explain why and I'm not certain. Can someone go over how these cause metabolic acidosis [other than RTA, Acetazolamide] My understanding is hyperalimentation = high organic acid = acidosis, Addison's disease = low aldosterone = acidosis, diarrhea = bicarb loss = acidosis, spirolactone = aldosterone fail = acidosis, can someone confirm if these are the reasons?, And also what are the reasons for saline infusion? It seems to me increased Na flow should increase H+ excretion which should increase pH.. Also for RTA type 1 and 2, what are the reasons for Hypokalemia? especially for type 2. And Ive seen places that said RTA cause sodium wasting.. can someone explain this? Thread continues after this sponsor message. SDN Members do not see this ad. In first aid, they gave an mnemnic on normal anion gap: They didn't explain why and I'm not certain. Can someone go over how these cause metabolic acidosis [other than RTA, Acetazolamide] My understanding is hyperalimentation = high organic acid = acidosis, Addison's disease = low aldosterone = acidosis, diarrhea = bicarb loss = acidosis, spirolactone = aldosterone fail = acidosis, can someone confirm if these are the reasons?, And also what are the reasons for saline infusion? It seems to me increased Na flow should increase H+ excretion which should increase pH.. Also for RTA type 1 and 2, what are the reasons for Hypokalemia? especially for type 2. And Ive seen places that said RTA cause sodium wasting.. can someone explain this? Continue reading >>
Nephron Power: Consult Rounds: Why Does Infusion Of Normal Saline Cause Metabolic Acidosis?
Consult Rounds: Why does infusion of normal saline cause metabolic acidosis? Why does infusion of normal saline cause metabolic acidosis? This should be an easyanswer but when you review the literature, the literature is all over theplace( literally!!).Collection of responses I received when I asked few expertsin the field: 1. Thebicarbonate ions are diluted bythe isotonic fluid,and acidosis occursas a result. 2. The fall in serum bicarbonate is dueto the expansion of the extracellular fluid volume withlarge IV fluids 3. The "strong ion difference" (SID) helpsexplain this that in order to maintain electroneutrality. Since there is diluting fluid, water must dissociate, providing excess protons which leads to metabolic acidosis. - via the stewart method of acid base 4. Usually 60% of the filtered bicarbonate load isreabsorbed in euvolemia. When extracellular volume is low the proximaltubular absorption is increased, maybe to 80%,due to changes in oncoticpressure and hydrostatic pressure of peri tubular capillaries and glomerulus.This results in increased reabsorption in setting of volume depletion.When extracellular volume is increased then proximal tubular absorptionof bicarbonate is decreased, thus an acidosis. 5. The ph of normal saline is 5.5, won'tthat also lead to dissociation and use of Hco3 and cause an acidic environment Continue reading >>
Diabetic Ketoacidosis
We are looking for contributors to author, edit, and peer review our vast library of review articles and multiple choice questions. In as little as 2-3 hours you can make a significant contribution to your specialty. In return for a small amount of your time, you will receive free access to all content and you will be published as an author or editor in eBooks, apps, online CME/CE courses, and an online Learning Management System for students, teachers, and program directors that allows access to review materials in over 300 specialties. Improve Content - Become an Author or Editor This is an academic project designed to provide inexpensive peer reviewed Apps, eBooks, and very soon an online CME/CE system to help students identify weaknesses and improve knowledge. We would like you to consider being an author or editor. Please click here to learn more. Thank you for you for your interest, the StatPearls Publishing Editorial Team. The intent of StatPearls is to provide practice questions and explanations to assist you in identifying and resolving knowledge deficits. These questions and explanations are not intended to be a source of the knowledge base of all of medicine, nor is it intended to be a board or certification review of USMLE Step 3. The authors or editors do not warrant the information is complete or accurate. The reader is encouraged to verify each answer and explanation in several references. All drug indications and dosages should be verified before administration. StatPearls offers the most comprehensive database of free multiple-choice questions with explanations and short review chapters ever developed. This system helps physicians, medical students, dentists, nurses, pharmacists, and allied health professionals identify education deficits and learn new Continue reading >>
Acid-base Physiology
8.4.1 Is this the same as normal anion gap acidosis? In hyperchloraemic acidosis, the anion-gap is normal (in most cases). The anion that replaces the titrated bicarbonate is chloride and because this is accounted for in the anion gap formula, the anion gap is normal. There are TWO problems in the definition of this type of metabolic acidosis which can cause confusion. Consider the following: What is the difference between a "hyperchloraemic acidosis" and a "normal anion gap acidosis"? These terms are used here as though they were synonymous. This is mostly true, but if hyponatraemia is present the plasma [Cl-] may be normal despite the presence of a normal anion gap acidosis. This could be considered a 'relative hyperchloraemia'. However, you should be aware that in some cases of normal anion-gap acidosis, there will not be a hyperchloraemia if there is a significant hyponatraemia. In a disorder that typically causes a high anion gap disorder there may sometimes be a normal anion gap! The anion gap may still be within the reference range in lactic acidosis. Now this can be misleading to you when you are trying to diagnose the disorder. Once you note the presence of an anion gap within the reference range in a patient with a metabolic acidosis you naturally tend to concentrate on looking for a renal or GIT cause. 1. One possibility is the increase in anions may be too low to push the anion gap out of the reference range. In lactic acidosis, the clinical disorder can be severe but the lactate may not be grossly high (eg lactate of 6mmol/l) and the change in the anion gap may still leave it in the reference range. So the causes of high anion gap acidosis should be considered in patients with hyperchloraemic acidosis if the cause of the acidosis is otherwise not apparent. Continue reading >>
Acid-base Differential Diagnosis
This patient's elevated blood pH and decrease in PaCO2 is consistent with acute respiratory alkalosis. Respiratory acid-base disorders are caused by primary changes in PaCO2, whereas metabolic acid-base disorders are due to primary changes in the concentration of HCO3-. A primary rise in PaCO2 or a fall in plasma HCO3- reduces the pH (acidemia), whereas the opposite increase the pH (alkalemia). Patients suffering from pneumonia can have tachypnea due to hypoxia. Increased minute ventilation reduces arterial CO2, an acid, resulting in alkalosis. A slight decrease in bicarbonate level may be seen due to early renal compensation. Answer 1: Normal pH range is 7.35-7.45. This patient's pH is outside this range, which indicates an acid-base disturbance. Answer 2: A decreased pH and an decrease in HCO3- would be consistent with metabolic acidosis. Answer 3: An elevated pH and an increase in HCO3- would be consistent with metabolic alkalosis. Answer 4: Respiratory acidosis results from decreased alveolar ventilation, which causes increased arterial CO2 levels. Continue reading >>
Renal (usmle First Aid)
primitive kidney, degenerates after 4 weeks interim kidney in 1st trimester, contributes to male GU system permanent structure, appears 5th week, nephrogenesis continues derived from caudal mesonephric duct, gives rise to ureter, pelvises, calyces, collecting ducts Metanephric mesenchyme/blastema characteristics/function interaction with ureteric bud induces glomerulus-DCT formation effects of aberrant interaction between ureteric bud and metanephric mesenchyme when is the ureteric bud fully canalized? last to canalize, most common site of obstruction oligohydramnios causes fetal compression, pulmonary hypoplasia Potter sequence (syndrome) clinical presentation low set ears, retrognathia, flat nose, pulmonary hypoplasia, renal failure Potter sequence (syndrome) etiology (risk factors) ARPKD, obstructive uropathy, b/l renal agenesis, chronic placental insufficiency fusion of inferior poles of kidneys during ascention from pelvis, trapped under IMA ureteric bud bifurcationb efore it enters metanephric blastema, creastes bifid ureter VUR, ureteral obstruction, recurrent UTIs posterior ruetthra membrane remnant in males hydronephrosis, dilated/thick walled bladder, bladder outlet obstruction which kidney is typically used as the donor for transplantation and why? renal A>segmental A>interlobar A>arcuate A>interlobular>efferent arteriole>glomerulus>afferent arteriole Location of ureters relative to uterine artery/vas deferens Cautions of gynecologic procedures with respect to ureters ligation of uterine/ovarian vessels may damage ureters identify the clinical finding and associated pathology*** dilates afferent arteriole, increases GFR, RPF constrict efferent arteriole, increases GFR, filtration fraction, decreases RPF afferent arteriole constriction effect on GFR, RPF and Continue reading >>
