Internal medicine Flashcards

Question

Pericardial tamponade

Answer 1

* Tamponade is the physiologic result of rapid accumulation of fluid within the relatively inelastic pericardial sac. Pericardial tamponade impairs cardiac filling and reduces CO * Etiology: pericarditis, trauma, ruptured ventricular wall, aortic dissection, malignancy * Symptoms: becks triad: hypotension, muffled heart sounds, elevated JVP; pulsus paradoxus (sBP decreases by \>10 with inspiratory); narrow pulse pressure * Diagnosis: echo; ECG (alternans); CXR (enlarge heart) * Treatment: pericardiocentesis

Answer 2

* Granulation and scarring of the pericardium secondary to acute pericarditis. CO is reduced * Symptoms: SOB, fatigue, tachy, JVD, LV failure, periperal edema

Answer 3

* Etiology: rheumatic heart disease (most common), congential (rare) * Epidemiology: most cases occur in women * Symptoms are due to the left atrium backing up into the lungs and then the right heart * CHF and right sided failure * Murmur: mid-diastolic with opening snap

Answer 4

* Etiology: MI with papillary rupture, endocarditis, ischemia; rheumatic fever, mitral prolaspe, left ventricular dilation * Symptoms: CHF due to back up from mitral valve to right heart. When LV contracts blood goes both backwards into left atrium and forward into aorta. At first this can be asymptomatic in chronic cases, and then progress as the left ventricle and left atrium dilate and fail and pulmonary artery pressure increases. Dyspnea, weakness, and A fib develop * Murmu: Loud, holosystolic, apical radiating to axilla

Answer 5

* Most common valvular disorder: causes: idopathic, rheumatic heart disease, ischemic heart disease, atrial spetal defect, marfan syndrome, genetic * Mostly asymptomatic but can have chest pain and SOB * Murmur: Mid systolic click, wide splitting of S2

Answer 6

* Etiology: calcification or bicuspid aortic valve * Symptoms: Angina, syncope, CHF * murmur: loud systolic ejection murmur, crescendo-decrescendo * Avoid strenuous activity

Answer 7

* Etiology: Caused by dilation of the aortic root causes the valve not to work (marfans, collagen vascular disease) or a problem with the valve itself (rheumatic, endocarditis, syphilis, marfans, ehler-danlos, turner's syndrome, trauma) * Murmu: high pitched, blowing, decrescondo diastolic murmur, accentuated by leaning forward * Symptoms: SOB, orthopnea, PND, angina

Answer 8

* VF: Disorganized electrical activity of the ventricular myocardium. Because the myocardium depolarize in an irregular, disorganized fasion, regular myocardial contraction does not occur * PVT: organized rapid contraction of myocardium with insufficient filling time and lack of forward flow resuling in loss of pulse. It may degenerate into ventricular fibrillation. Both of these conditions are medical emergencies and require immediate cardioversion and IV amiodarone or lidocane * Causes: MI, prolonged QT, torsades de points, WPW, drugs

Answer 9

* Wide compelx arrhythmia with rotating axis and prolonged QT. Usually degenerated into Vtach * Treatment: magnesium IV, overdrive pacing, beta blockers for prolonged QT syndrome

Answer 10

* Syndrome where there is an accessory pathway that allows the electrical signal to travel from sinus node to ventricle bypassing the AV node and then back up the normal His-Purkinje system. This results in an abnormal ECG and risk of arrhythmia. Antiarrhythmia meds that block the AV node (adenosine, beta blockers, calcium channel blockers, and digoxin) will make it worse * Treatment * Unstable: cardioversion * Stable: procainamide

Answer 11

* A systemic immune process that usually occurs secondary to pharyngeal streptococcal infection * Rheumatic heart disease - the occurence of valvular abnormalities due to immune complex deposition in valve leaflets generated by rheumatic fever

Answer 12

1. 2 or more of * Temp \>38 or \<36 * Heart rate \>90 * RR \>20 * WBC \>12 or \<4 2. SIRS + infection 3. Sepsis + evidence of organ hypoperfusion 4. Severe sepsis + hypotension despite adequate fluid resuscitation

Answer 13

* E. coli \> Staph saprophyticus \> Klebsiella, proteus, pseudomonas, and enterococci \> group B strep

Answer 14

* Normal vaginal flora creates an acidic environment through colonization of loactobacilli. This protects the vagina from pathogenic organisms. When disturbed, infections become possible * Causes: * Bacteria vaginosis - gardnerella * Trichomonas vaginalis * yeast - candida albicans * Symptoms - itch and burning, odous, discharge * BV - fishy * Trich - fishy, strawberry cervix * yeast - cottage cheese like * Treatment * BV - metronidazole * trich - metronidazole * yeast - azole antifungals

Answer 15

* Spread through sexual contact or mucosal abrasion * Organism = treponema pallidum (a spirochete). Once it can entered the body it spreads through most of the organ systems and the disease progresses through 3 stages 1. Painless chancre and region lymphadenopathy 2. macolopapular rash scattered over trunk, palms, soles and genitals * Latent phase - can last for years. Patient is asymptomatic but seropositive 3. develops any time during latent phase. Gummans (rubbery granulomatous lesions in subQ tissues of CNS, heart, and aorita) * Investigations - VDRL and RPR if positive do a FTA-ABS test * Treatment - penicillin G

Answer 16

* Usually caued by gonorrhea or chlamydia * diagnose vis PCR analysis of vaginal or penil swab or urine culture * Treatment * gonorrhea - 125mg ceftriazone IM * chlamydia - 1g azithromycin PO * Always treat chlamydia and gonorrhea concurrently because coinfection is often present

Answer 17

* Inflammation of the prostate due to bacteria ascending the urethra and then passing into the prostate through the prostatic ducts * Causes: E. coli, pseudomonas * Symptoms : perineal and suprapubic pain, dysuira frequency, fever, tender boggy prostate * Investigations: leukcoytosis with neurtrophil predominance; urinalysis shows bacteriuria and pyuria * Treatment- TMP-SMZ or cirpofloxacin for 21 days

Answer 18

* An inflammatory process in the prostate from an unknown etiology. Most common cause of chronic prostatitis * Symptoms: frequency and dysuria, nontender enlarged prostate * Investigations: U/S and urine culture are negative; leukocytes seen in prostatic secretions * Treatment: trial of antibiotics, anti-inflammatories

Answer 19

* Staph aureus: gram + coagulase +. Commonly causes infections of the skin, septic arthritis, catheter infections and endocarditis * Toxic shock syndrome - exotoxin mediates, produced by stains of staph A and some group A strep species. Results in fever, rash, desquamation of skin, nasea, evidence of organ failure * Scalded skin syndrome - most severe form of toxic epidermal necrolysis. Starts as preiorbital or perioral erythematous rash and progresses to limbs. In days the skin sloughs off. Must treat as burn with careful monitoring an aggressive fluid administration. * Streptococcus pyogens - causes soft tissue infections such as cellulitis, impetigo, and necrotizing faciitis. Treat with penicillin

Answer 20

* Nucleoside analog reverse transcriptase inhibitors - act as DNA chain terminator * Non-nucleoside reverse transcriptase inhibitors - bind to reverse transcriptase outside the activity site and cause conformational changes that decrease enzyme activity * Protease inhibitors - inhibitd activity of HIV protease * Fusion inhibitors - prevents HIV binding and entery into cells * Integrase inhibitors - prevents the insertion of viral genome into host DNA

Answer 21

* Transmission - skin contact with spores, inhlalation of spores, GI consumption of undercooked or raw meat or dairy products from infected animals * Symptoms: nonspecific symptoms - fever, cough, malaise, fatigue, myalgias, sweats, chest discomfort. 1-5 days after onset see respiratory distress, high fever, and eventually shock and death * Treatment - cipro, doxy, and amox

Answer 22

* Borrelia burgdorferi * Transmitted by Ixodes scapularis tick * Erythemia chronicum migrans is the pathognomonic skin rash that starts at bite and progresses until there is central clearing * Symptoms * Stage 1 - fever, headache, arthralgias, myalgias * Stage 2- recurring rash, myocarditis with heart block, meningitis, cranial nerve palsy, peripheral neuropathy * Stage 3- migratory or oligoarthritis * Investigations: ELISA + western blot * Treatment: doxy + amox if no cardiac involvement; penicillin or cephalosphorin if cardiac or neuro involvement

Answer 23

* Two types: human monocytic ehrlichiosis and human granulocytic ehrlichiosis * Ehrlichia chaffeensis causes HME - lone star tick * Ehrlichia phagocytophili causes HGE - Ixodes tick * Symptoms: flulike, high fever, headache, malaise, leukopenia and thrombocytopenia * Investigations: serum PCR * Treatment: tetracycline or doxycyline

Answer 24

* Rickettsia richettsii, gram - coccobacillus * Wood tick or dog tick * Symptoms - fever, nausea, headache, vomiting, rash (starts nonpruritic, maculopapular on distal extremitis and porgresses to trunk and face). * Can be fatal if not aggressively treate * Complications - DIC and pneumonia * Treatment: tetracyclines

Answer 25

* Babesia microti - an intra-RBC parasite transmitted by Ixodes tick * Symptoms: fever, chills, myagias, hemolytic anemia * Diagnosis - maltese corss on smears * Treatment - quinine and clindamycin *

Answer 26

* Neurosurgerical emergency. Get emergent MRI. * Most commonly found in elderly, immunosuppressed, IV drug users * Staph. aureus, gram - bacilli, and mycobacterium tuberculosis are most common causes * Symptoms: pain, fever, progressive leg weakness * Treatment: surgery + antibiotics

Answer 27

* Acts on liver to increase gluconeogensis and glyogenolysis * Glucagon 1mg Iv is used to resuscitated hypoglycemic coma if you cant get IV access * Will not work in alcoholics with liver failure. Alcohol will suppress gluconeogensisi and glycogen stores are impaired in severe liver disease * Loss of glucagon response to hypoglycemia occurs ovr time leading to hypoglycemia unawareness * to much glucagon (glucagonoma) will present with new onset diabetes, weight loss, and necrolytic migratory erythema

Answer 28

* The most common pituitary tumor. It can present with galactorrhea or amenorrhea. Women usually present earlier than men. Prolactin levels correlate with tumour size. * Treat with dopamine agonists - bromocriptine

Answer 29

* Second most common. Symptoms include visual changes or slightly elevated prolactin levels due to mass effect, which disrupts the inhibtor signal that dopamine has on prolactin producing cells. * Treat with surgery

Answer 30

* Type of pituitary adenoma (or ectopic GH secretion) - progessive enlargment of peripheral body parts resulting from excess GH production * Progressive enlargment of hands, head, and feet. Progessive and irreversible organomegaly, especially heart leading to CHF, imparied glucose tolerance, hyperphosphatemia. * Diagnosis - lack of GH suppression by glucose load, IGF-I levels

Answer 31

* Central DI: inadequate pituitary release of ADH * Idiopathic, posterior pituitary or hypothalamic damage, systemic (sarcoidosis, encephalitis) * Nephrogenic DI: Lack of renal response of ADH * Familial, CKD, sickle cell, hypokalemia, hypercalcemia, drugs (lithium) * Symptoms: polyuria, thirst, dilute urine * Diagnosis: high plasma osmolality, water deprivation followed by exogenosis (central low urine Osm to high urine osm, nephro low to low, normal high to high) * Treatment: DDAVP central, thiazide diuretics nephorgenic

Answer 32

* Excess production of ADH * Etiology: idiopathy, ectopic production by malignant tuours (SCL or pancreatic), drugs * Symptoms: hyponatremia * Diagnosis - low serum osm, high urinary NA, osm urine \> serum, normal adrenal and thyroid function * Treatment - fluid restriction

Answer 33

* exaggerated manifestation of hyperthryoidism with fever, CNS, CV, and GI dysfunction * Etiology: infection, trauma, major surgery, DKA, MI, PE, drugs * Symptoms - fever, tachy, CHF, volume depletion, exhaustion, GI, agitation, coma, jaundice (late) * Treatment: treat manifestationa, ABCs, IV hydration, B blocker (prevent peripheral conversion of T4), acetatminophen and cooling blankets, PTU or methimazole, Iodine (decrease release of preformed thyroid hormone. Don't give until PTU has taken effect), corticosteriods (prevent peripheral conversion of T4)

Answer 34

* Hasimotos thyroiditis - autoimmune disorder that involved CD4 lymphocyte mediated destruction of the thyroid. The lymphocytes are specific for thyroid antigens * Subacute - possible a postviral condition because it usually followed an URTI. Tender, severe neck pain * Silent - usually occurs postpartum and thought to be autoimmune mediated. Painless * suppurative - usually a bacterial infection, but fungi and parasites have also been implaicated. Commonly seen in PCP. Focal tenderness * Riedels - firbrous infiltration of the thyroid of unknown etiology

Answer 35

* Epithelial * Papillary - most common, best prognosis * Follicular - heart mets * Anapastic - rare, worse prognosis * Parafollicular (medullary) * Calcitonin is increased from parafollicular C-cells * Seen in MEN IIa and IIb

Answer 36

* Primary insufficiency (addison's disease) - due to a problem with an adrenal gland itself, in which it does not produce hormones. Hyperkalemia, hyponatremia and metabolic acidosis * Secondary insufficiency - adrenal gland is intact, but the pituitary does not produce ACTH, so that there is no stimulus for the adrenal gland to secrete its hormones. Hypoglycemia. * Teritary insufficiency - due to hypothalamic failure * Aldosterone - increases renal sodium reabsorption. Deficiency results in hyperkalemia and hyponatremia * Cortisol - stimulates gluconeogenesis by protein and fat catabolism and decreasing utilization of glucose and tissue sensitvity to insulin. Deficiency results in impairment of the body's ability to handle stress * Diagnosis: Give test dose of ACTH and measure serum cortisol levels at 0, 30, and 60 min. A peak level \< 18-20ug/dL suggests adrenal insufficiency

Answer 37

* Isolated excess production of aldosterone * Unilateral aldosterone producing adenoma or bilateral hyperplasia of zona glomerulosa * Symptoms: asympotmaic, hypertension, hypokalemia * Treatment: adrenalectomy for tumour, medical management for hyperplasia (spironolactone or ACEi for BP, low NA diet)

Answer 38

* chronic disease of adult bone in which localized areas of bone become hyperactive and the normal bone matrix is replaced by softened and enlarged bone.

Answer 39

* Achalasia - neurogenic disorder of esophageal motility with absence of normal peristalsis and impaired relaxation of lower esophageal sphincter. Bird beak narrowing. Relieved by nitroglycerin * Motility disorder with frequent non-peristaltic contractions. Believed to come from hypoactive inhibitor neurons within auerbachs plexus. Corkscrew appearance. Relieved by nitroglycerin.

Answer 40

Anatomical obstructions, usually presenting with dysphagia to solids * Plummer-winson syndrome - hypopharnygeal webs associated with iron deficiency anemia * Schatzki's ring - a narrow lower esophageal ringlike outgrowth associated with dysphagia Note, dysphagia to solids and liquids often indicated a motility problem (i.e., achalasia an esophageal spasm). Dysphagia only to solids indicates a mehcian obstruction (tumor or rings)

Answer 41

* Secretin stimulation test - secretin, a gastrin inhibitor is delivered perenterally and its effect on gastrin secretion is measured. In ZE there is a paradoxical astronomic rise in serum gastrin.

Answer 42

Depends on the cause * Discontinue NSAIDS, steriods, and smoking * Triple therapy for H pylori - PPI, amox, clarithromycin * Antacid agets - H2 blockers and PPis * If bleeding, endoscopy is done and sucralfate or misprostol is used * Surgery is indicated when ulcer is refractory to 12 weeks of medical treatment or if hemorrhage, obstruction, or perforation is present

Answer 43

GA LAW - predicts mortality risk * Blood **glucose** \> 11.1 mmol/L (\> 200 mg/dL) * **Age** in years \> 55 years * Serum **LDH** \> 350 IU/L * Serum **AST** \> 250 IU/L * **WBC** count \> 16000 cells/mm3

Answer 44

* When indirect bilirubin is much higher than direct bilirubin, it usually means there is an increase bilirubin production by hemolysis. The other common cause is Gilbert's syndrome (harmless, common defect in bilirubin conjugation)

Answer 45

* Chronic hepatic injury assoicated with hepatocellular necrosis, fibrosis, and nodular regeneration. There are many causes of cirrohosis but they all share a common clinical picture. * Symptoms: loss of appetite, N/V, jaundice and pruritis, portal hypertesnion, bleeding, encephalopathy, palmar eythema, dupuytren's contracture, gynecomastia and hypogonadism, elevated LFTs (start they normalize as liver atrophies) * Treatment: alcohol cessation, high protein diet, spironolactone for ascites, lactulose for hepatic encaphalopathy

Answer 46

* A nauroendocrine tumour arising from ectodermal stem cells in the gut, usually the ileum. Makes up 30% of gut neoplasms. * Generally slow growing and causes symptoms by the aberrant secretion of serotonin, bradykinin, and histamine * Symptoms - flushing, diarrhea, wheezing, bowel obstruction, or appendicitis * Carcinoid syndrome - occurs in 5-10% and consists of severe symptoms of flushing, diarrhea, and right sided valvular heart disease * Diangosis - urine levels of 5-HIAA and 5-HT + abdo CT * Treatment - surgery, somatosmatin for symptom management

Answer 47

* Familial polyposis coli - autosomal dominant condition where thousands of adenomatous polyps appear by 25. Most develop CRC by 40. Treatment is prophylatic total colectomy * Hereditary nonpolyposus colon cancer- autosomal dominant condition in which 3 or more relatives of a patient and at least one first degree relative develop colon cancer at an early age * Gardners syndrome - automocal dominat disorder characterized by polyposis coli, supernumerary teeth, osteomas, and fibrous dysplasia of the skull * Peutz-Jeghers - multiple polyposis of small intestine with multiple pigmented melanin macules in oral mucosa. Associated with gynecological cancers

Answer 48

* Enterotoxigenic E. Coli - most common cause of travelers diarrhea * Staph. aureus - quick onset (3-4hrs), mostly vomiiting, toxin mediated, associated with mayonnaise comsuption; patients commonly report having been to a picnic or other similar event. * Bacillus cereus - associated with reheated rice, commonly from day old chinese food * Clostridium perfringens * Vibrio cholera - contaminated water in thrid world countries * Antibioitics (if needed) = cipro; TMP-SMX + flagyl; Pip-tazo

Answer 49

* Campylobacter * Amoeba (E. histolytica) * Shigella * E. Coli * Salmonella

Answer 50

* An autoimmune condition affecting the small bowel, triggered by gluten resulting in malaborsorption and diarrhea * Associated with HLA-DR3 and HLA-DQw2 * Manifestations include vitamin deficiencies, iron deficiency, and malnutrition * Diagnosis - antigliadin IgG/IgA, anti enomysial antibody, small bowel biopsy showing flattened intestinal villi * Treatment: avoidence of gluten, steriods can be given if severe

Answer 51

* A malabsorption disease with flattended villi in jejunum similar to celiac spruce - but likely from an infectious etiology * It typically occurs to people living in the tropics * Symptoms and findings are similar to celiac spruce, but often have megalobasltic anemia due to B12 deficiency * Diangosed by a small bowel biopsy demonstrating flattened intestinal villi * Treatment is vitamin B12 and folate supplementation in addition to tetracycline

Answer 52

* Lactase is required to digest lactose, a carbohydrate found in diary products. Deficiency of lactase results in cramping and diarrhea after ingestion of diary products. * Congential deficiency is rare; a milder late onset form is commonly found in adults at any time * Treat with lactase supplements or avoidance of diary

Answer 53

* A severe illness beginning in the GI tract, but spreading systemically often manifesting with fevers, arthralgias and CNS symptoms (Cranial nerve palses, memory loss, nystagmus) * See severe malabsorption syndrome due to destruction of intestinal lamina propria * Organism = Tropheryma whippelii * Most common in white males * Diagnosis made by PCR testing for T whippelii of saliva, stool, or blood * Biopsy demonstrates the replacement of intestinal lamina propria by PAS-positive macrophages * Treatment - ceptra + TMP-SMX or tetracycline * Fatal if untreated, curable if treated

Answer 54

* Condition where plasma proteins fail to be reaborbed by the gut lumen and are lost in the GI tract, normally they are absorbed by the gut and sent into the portal circulation * This occurs due to mucosal injury (due to IBD or celiac) or increase lympatic pressure (where proteins are normally absorbed) in gut wall (neoplasm or CHF) * Get diarrhea and anasarca from protein loss * Diagnose with alpha-1-antitrypsin levels measured simultaneously in stool and serum * Treatment is to address underlying cause

Answer 55

* Renal losses * Renal tubular acidosis * Medications * GI losses * Diarrhea * Ileostomy

Answer 56

* Methanol * Uremia * DKA * Paraaldehyde * Iron, Isoniazide * Lactate * Ethylene glycol, Ethanol * Salicylates

Answer 57

* Chloride-responsive: Urine chloride \< 20 mEq/L * Vomiting or prolonged NG tube drainage * Pyloric stenosis * Laxative abuse * Diuretics * Post-hypercapnic state * Chloride resistant \> 20mEq/L * Severe Mg or K deficiency * Thiazide or loop diuretics * Increase minarlocortiocisd * Licorice, chewing tobacco * Bartter's dyrome, Gitelmans syndrome, Liddles syndrome

Answer 58

* Hypervolemic: CHF (increase free H2O), nephrotic syndrome (decrease albumin), cirrhosis (decrease albumin) * Sodium and water restriction * Isovolemic: renal failure, SiADH, glucocorticoid deficiency (addisons disease), hypothroidism with myxedema, primary polydipsia, and medications * Hypovolemic: Loss of both sodium and water - renal losses (diuretics, partial urinary tract obstruction, salt wasting nephropathies), extrarenal losses (vomiting, diarrhea, extensive burns, third spacing) * NS infusion to correct volume deficit

Answer 59

* SIADH * Isontonic infusions (glucose, mannitol)

Answer 60

* Hyperglycemia - each 100mg/dl increase in serum glucose above 100 there is a decrease in plasma sodium concentration by 1.6mEq/L. Corrected Na = [serum glocse -100]/100 X 1.6 * Hypertonic infusions - mannitol, glucose

Answer 61

* Confusion, muscle cramps, lethargy, anorexia, nausea * Seizures or coma

Answer 62

* Sometimes termed osmotic demyelination syndrome, occurs as a treatment complication of severe or chronic hyponatremia * A symmetric zone of demyelination occurs in the basis pontis, leading to stupor, lethargy, quiet and confused delirium and quadriparesis * CPM can be avoided by increase serum sodium no faster than 1mEq/L/hr. Some patients treated symptomatically will recovered in 3-4 weeks, however in some damage is irreversible

Answer 63

* Hypovolemic * Loss of water and soidum (water \>\> sodium) * Renal losses (durietics), GI, resp, skin, adrenal deficiencies * Fluid replacement with normal saline * Isovolemic * Decrease TBW, normal total body sodium, and ECF * Diabetes insipidus, skin losses, reset osmostate * Fluid replacement with half NS. Correct only half in first 24. * Hypervolemic * Increase TBW, markedly increase total body Na, and ECF * Iatrogenic, mineralcorticoid excess, excess salt ingestion * Fluid replacement with half NS. Furosedmide * Symptoms - fatigue, confusion, lethargy, edema

Answer 64

* Always consider hypoalbuminemia. Since large amount of calcium is bound to albumin, patients with hypoalbumineia have low total cacium, but normal ionized levels. * Corrected calcium = measured + (4-measured albumin) X 0.8 * hypoparathyroidism, vit D deficiency, sepsis, pancreatitis, rhabdomyolysis, TLS, severe magnesium deficiency * Symptoms - circumoral paresthesia, muscular tetany, laryngospasm, seziure, confusion, cardiovascular collpase * ECG - prolonged QT and ST

Answer 65

* Thiazides; lithium; colon, lung, breast, and prostate cancer, MM, ZE, hyperparathyroid, acromgeal, addisions * Symptoms: malaise, fatigue, headaches, diffuse aches and pains, dehydration, lethargy and psychosis * ECG - QT shortening, AV block * Treatment - IV fluids +/- lasix, calcitonin, bisphosphonate derivatives

Answer 66

* Acoholism or malnutrition. Also seen in DKA and hyperparathyroidism * Symptoms - mental status change, agitation and muscle weakness. * Severe can result in rhabdomyolysis or seizures * Treatment with phosphate supplementation orally or IV if severe

Answer 67

* Renal failure, TLS, iatrogenic * Treat with oral calcium carbonate as it binds phosphate in the gut and decrease absorption, low phosphate diet, aluminum containing antacids, phosphate binds depending on the level

Answer 68

* Loop diuretics, gentamincin, insulin, hungry bone syndrome * Causes hypoK and hypoCA refractory to replacement - unable to correct until Mg is corrected * ECG changes similar to hypokalemia * Treat with oral or IV supplementation

Answer 69

* Iatrogenic, magnesium containing drugs if given to patients with renal failure * Treatment: IV fluids, caclium if there are ECG changes, dialysis of refractory

Answer 70

* ATN - due to ischemia (after prerenal insult/hypoperfusion), toxcins sych as meds (aminoglycosides, cisplastin, pentamidine, lithium, amophotericin), myoglobin from rhabdomyolysis, IV contrast * Many renal epithelial cells and muddy brown granular casts * Acute allergic interstitial nephritis * Vascular disorder and atheromatous embolic * Glomerular disorder (nephrotic and nephritic syndromes) * Acute glomerulonephritis - RBC casts with hematuria, proteinuria, and low urine specific gravity

Answer 71

* Prerenal: FeNA \<1%; low urine sodium \<15; high urine osmolarility * Intrinsic: FeNA \>2%; high urine sodium \>15; low urine osmolarity, high urinary sediment

Answer 72

* Glomerular lesions causing proteinuria \>3g/day * Indicates a defect in the glomerular filtration barrier * Defind by the triad of proteinuria, hyperlipidemia, and peripheral edema * Pathophy: Onset of glomerular permeability to plasma proteins, resultin in proteinuria and loss of albumin. This causes a reductionin oncotic pressure reuslting in edema and serosal effusions. Can also see hyperlidiemia and hypercoagulability due to loss of protein C, S and antithrombin III

Answer 73

* Type of nephrotic syndrome * Usually idiopathic, seen in children * Electron microscopy shows podocyte foot process fusion, but light microscopy shows no change * Usually responds to steriod therapy, through sometimes cytotoxic therapy is requried, especially in recurrent cases * Recurs frequently * Rarely progresses to chronic renal failure (unlike other causes of nephrotic syndrome)

Answer 74

* Cause of nephrotic syndrome * Glomerular scarring involving limited number of glomeruli * May be primary (idiopathic) or secondary to a known disease (i.e., HIV, HBV, heroin abuse, vesicoureteric reflus, morbid obesity) * Immunoglobulin and complement deposition may be detected by immunofluorescen * Treatment - corticosteriods or cytotic therapy, ACEi

Answer 75

* Cause of nephrotic syndrome * Caused by subepitherlial immune complex deposition * Idiopathic or assoiated with SLE, HBV, or soild tumours * Treated with steroids and cytotxic agents

Answer 76

* Indicates inflammation and glomerular damage * Involved abrupt onset hematuria with RBC casts, mild proteinuria and often includes hypertension, edema, and azotemia * Acute glomerulonephritis is a nephritic syndrome

Answer 77

* Associated with group , beta-hemolytic streptococcus * On immunofluorescence, immune complex deposition with complement in a "lumpy-bumpy" pattern between the glomerular epithelial cells and GBM * Presents 2 weeks after infection with dark urine and edema * Usually reversible but occasionally progresses * Labs - RBC casts, low complement, ASO antibody titers

Answer 78

* Most common glomerulonephritis * Presents as hematuria during a viral infection or after exercise * On immunofluroescence, immune complex deposition of IgA and C3 in mesangial matrix. Mesangial proliferation on light microscopy * Consertive management with ACEi or ARB in patients with normal renal function and minimal proteinuria * Corticosteriods may be useful in severe cases

Answer 79

* Idiopathic, associated with Hep C and cryoglobulinemia, bacteria endocarditis, and autoimmune diseases * On immunoflurorescence, subendothemial immune deposits are seen. Basement membrane proliferation causes basement membrane to look double layered. Also see mesangial proligeration * Labs: nephritis sediment and low complement levels * frequently progresses to renal failure * Treatment: depends on cause: i.e., treat Hep C; plasmaphereis for patients with cryoglobulinemia

Answer 80

* DEcrease renal function (GFR \<60) or evidence of kidney injury for \>3months * Causes: DM, HTN, chronic glomerulonephritis, chronic tubulointerstital disease; polycystic kidney disease * Nephrons are lost and remaining healthy nephrons compensate by increases their GFR. This process damages the healthy nephons causing disease progression * Loss of renal endocrine function: decrease synthesis of activated vitamin D, ammonia and eythropoietin

Answer 81

* Patients are usually asymptomatic until GFR \<30 * Water and sodium balance * Inital: decrease urine concentrating ability, easy dehydration, sodium wasting * Later: volume overload once kidneys are no longer able to excrete dietary sodium * Potassium * Once GFR becomes markedly diminished, the ability to excrete dietary potassium is lost. The distal tubule compensates for the loss of excretory function until there is oliguria * Acid-base balance * tubular excretion of H is impaired secondary to impaired renal productionof ammonia, resulting in AG metabolic acidosis * Caclium and phosphate * Decrease vit D activation cause hypoCA * Secondary PTH * Treatment: ACEi, modest protein restriction, dialysis

Answer 82

* A syndrome associated with CKD that affects multiple organ systems * Appearance - pale complexsion, wasting, purpura, excoriation * Complaints- puruitus, polydispsia, N/V * Urinalysis: isosthernuria, proteinuria, abnormal sediment tubular casts

Answer 83

* defect in renal tubular ability to excrete daily acid load created by the metabolism of protein or to reabsorb filtered bicarb, which results in a metabolic acidosis with normal anion gap * Type 1 - caused by a distal tubule defect in hydrogen secretion cuasing acidosis and hypokalemia. Can be cuased by autoimmune disease, medications. Patients may also get renal stones due to hypercalcemia * Type 2 - caused by defect in proximal bicarb reabosprtion usually in setting of fanconis syndrome. Bicarb loss tends to be self limiting as tubules can absorb some bicarb and reach a new, lower, set point * Type 4 - hypoaldosteronism - caused by defect in aldosterone secretion or aldosteron sensitivity by the renal tubules and amnnonium secretion. Patients have low renin and aldosterone levels and hyperkalemia

Answer 84

* The effusion is an exudate if one or more of the following is present * Ratio of pleural to serum protein \> 0.5 * Ratio of pleural to serum LDH \> 0.6 * Pleural fluid LDH \>2/3 upper normal limit of serum LdH * An effusion is a transudate if none of the above are met * Trasudates: CHF, cirrosis, nephrosis * Exudates: Infection, tumour, trauma

Answer 85

* Obstructive * FVC normal or decreased * FEV1 decreased * FEV1/FVC \< o.7 * Lung volume normal or increased * Restrictive * FVC decreased * FEV1 normal or decreased * FEV1/FVC \> o.7 * Lung volume always decreased

Answer 86

* Hopsitalized for 2 or more days in an acute care facility within previous 90 days * Residence in nursing home or long term care facility * Antibiotic therapy, chemotherapy, or wound care within 30 days of current infection * Hemodialysis treatment at a hospital or clinic * Home infusion therapy or wound care

Answer 87

* Antibiotic therapy within 90 days of infection * Current hospitalizatioN \>5 days * High frequency of antibiotic resistance in the specific hospital unit * Immunosuppressive disease or therapy * Presence of HCAP risk factors for MDR

Answer 88

* Transmission occurs by inhalationof droplet nuclei produced by the cough or sneeze of patient with TB. Particles may remaind suspended in air for several hours. 5% of those infected will develop TB in 2 years, 5% will develop the disease in their lifestime, 90% will remain infected but disease free * Symptoms: productive cough, night sweats, hemoptysis, anorexia, weight loss, fever, chills, fatigue, chest pain * Treatment: 2 months INH, rifampin, pyrazinamide, and ethambutol followed by 4 months of INH/rifampin

Answer 89

* Includes chronic bronchitis and emphysema. COPD is defined by chronic obstruction to expiratory airflow, largely irreversble, as evidenced by a decrease in FEV1. * Chronic bronchitis - chronic productive cough on most days for ≥3 months is each of 2 successive years; may or may not be accompained by chronic expiratory airflow obstruction * Emphysema - permanent enlargement of the air space distl to the terminal bronchioles due to destruction of alveolar septa. A pathological entity wose clinical correlate is a chronic expiratory airflow obstruction with evidence of hyperinflation * Treatment: Supplemental oxygen is the only therapy for COPD proven to extend life. O2 should be given to patients with a resting PaO2 \<55mmHg. Vaccination against influenze and streptococcus pneumoniae. Beta agonists and anticholinergics, inhaled corticosteriods. Antibiotics for COPDe

Answer 90

* Made with sleep study * Defined by 5 or more episodes of apnea and hypopnea per hour of sleep

Answer 91

* Caused by Bordetella pertussis, a gram neg coccobacillus * thought to be a common cause of cough in adults * The classic "whoop" caused by rapid air inspiration against a closed glottis is rarely seen in adults * Was a common cause of infant death before routine immunization * Symptoms * Catarrhal stage - lasts 1-2 weeks. Characterized by mild URI symptoms * Paroxysmal stage - lasts 2-4 weeks. Characterized by prolonged paroxysmal cough. Often worse at night. * Convalescent stage - characterized by gradual improvement of symptoms * Treatment: macrolide antibiotic will reduce severity if stated within 8 days

Answer 92

* Anterior * Thymoma * Teratoma * Thryoid * Terrible lymphoma * Middle * Vascular lesions * Lymph nodes * Posterior * Neurogenic tumour

Answer 93

* A group of diverse disorder involving the parenchyma of the lung that cause alveolitis, interstital inflammation, and fibrosis or a granulomatous response. There are both known (environmental, drugs, radiation, neoplastic) and idipathic (sarcoidosus, amyloidosis), causes. * Symptoms: dysnpea, exercise intolerance, non-productive cough, tachynpea, crackles, clubbing, pulmonary hypertension * Diangosis - usually requires biopsy, CT, CXR (recitular infilatrates, PFT (restrictive) * Treatment - removal of exposure, supplemental O2, steriods, lung tansplant

Answer 94

* SC - central location; sensitive to chemo; surgery NOT indicated; poor prognosis * NSC - includes squamous, large cell, and adenocarcinoma; poor response to chemo; treat with surgery if early; prognosis varies with stage

Answer 95

* Folate and vitamin B12 deficiency * Ethanol and liver disease * Drug - AZT, methortrexate * Thyroid (hypo) * Hemolysis * Myelodysplastic syndrome

Answer 96

* Increases PTT * Affects intrinsic pathway * Acts as a cofactor to antithrombin III, which inhibits factor Xa and thrombin * Safe in pregnancy

Answer 97

* Potential catastrophic complication of heparin therapy causing a paradoxical hypercoagulable state and high risk of blood clots. Diagnosed with the finding of low platelts and positive HIT antibodies. Treated by stopping heparin immediately and anticoagulating with argatroban (a direct thrombin inhibitor). * Suspect this with anyone on heparin and dropping platelets. Assume this diagnosis for anyone on heparin with low platetes and a blood clot.

Answer 98

* Increases PT * Affects extrinsic pathway * Inhibits vitamin K- dependent factors * Primary affects II, VII, IX, X * Teratogenic

Answer 99

* Immune mediated thrombocytopenia of unknown etiology * Development of antibodies against a platate surface antigen. The antibody antigen complexes effectively decrease platelet count by being removed from circulation * Signs - petechiae and purura over trunk and limbs, mucosal bleeding * Diagnosis - throbocytopenia on CBC, absence of other factors to explain (diagnosis of exclusion) * Treatment: corticosteriods acutely, IVIG, platelet transfusion if significant bleeding present (generally dont give), splenectomy electively to decrease recurrence

Answer 100

* Microgangiopathic hemolytic anemia that result from circulation and deposition of abnormal vWF multimers. ADAMTS13 is the protease that normally cleaves these multimers, but is deficient in this condition. Usually caued by an immune process that clears ADAMTS13 * Etiology - infection, malginancy, drugs (antiplatlet, chemo, contraceptives), autoimmune disorders, pregnancy * Symptoms - Fever, anemia, thrombocytopenia, Renal dysfunction, neurological dysfunction * Treatment - plasmaphersis (dont transfuse plateletes)

Answer 101

* Acquired coagulation defect that results in consumption of coagulation factors, including fibrinogen, causing bleeding and thrombosis. * Usually secondary to exposure of blood to procoagulants such as tissue factor and cancer procoagulant resulting in depletion of clotting factors and microangiopathic hemolytic anemia * Etiology - obstetric, sepsis, local tissue damage, extensive trauma, chronic illness * symptoms - diffuse, systemic bleeding * diangosis - decrease fibrinogen, elevated PT, aPTT, and TT, thrombocytopenia, elevated D dimer, schistocytes * Treatment - treat underlying cause, platelets, FFP, cryoprecipitate

Answer 102

* Platelet disorders: TTP, ITP, DIC * Leukemia * Anemia * Trauma * Enlarged spleen * Liver disease * EtoH * Toxins - benzene, heparins, aspirin, chemo * Sepsis

Answer 103

* Genetic disease, most commonly autosomal dominant, characterized by lack of functional defect of vWF * vWF forms adhesive bridge between platelets and endotherlium, bridges adjactent platelets, and acts as a carrier protein for factor VIII * Type 1 - decrease in amount. Autosomal dominant * Type 2 - qualitative defect * Type 3 - essentially absent vWF * Symptoms - heavy menstruation or bleeding with dental procedures * Treatment - mild bleed or procedure = DDAVP; serious bleed or procedure = vWF and fractor 8

Answer 104

* disease in which patients present with a relatively sudden acute illness, which can be manifested by bleeding or extreme weakness or infection. This is in contrast to chronic leukemias, in which the patients can be aymptomatic for months or years, and are often picked up on routine blood tests. * Includes acute lymphocytic leukemia and acute myelocytic leukamia

Answer 105

* More common in adults * Associated with a history of beneze exposure * Treatment * M3 subtype - 15q17. All-trans retinoic acid + chemo. Better prognosis then other types * Other types induction, consolidation and maintenance chemotherapy

Answer 106

* Primarily a disease in children but accounts for 20% of adult leukemia * Philadelphia chromosome (22) arising from 9q22 has poorer prognosis * Treatment is induction, consolidation and maintenance chemo. Lasts about 2 years

Answer 107

* Chronic myelocytic leukemia and chronic lymphocytic leukemia. Differs from acute because patients are often asymptomatic for years before having clinical problems.

Answer 108

* A clonal proliferation of cells in the myeloid lineage * Has 25% risk/year of transforming to acute leukemia * Philadelphia chromosome t(9,22) causes fusion of Bcr and Abl, forming a protein (tyrosine kinase) that constantly sends cell proliferation singals * Blood smear shows immature myeloid cells of varying stages of maturation * Treatment -Imatinib, allogenic bone marrow transplant may still have a role for younger or refractory patients

Answer 109

* Malignant clonal disorder for mature B lymphocytes that can but does not always progress to cause lymphadenoapthy, splenomegaly, and bone marrow failure * Richters transformation is the rare transformation to an aggressive large cell lymphoma that is typically refractory to treatment

Answer 110

* Follicular B cells undergo transformation to malignant cells (Reed-sternberg cells) * Bimodal distribution 30s and 70s * May be associated ith EBV * Symptoms - cervical lymph node enlargement + B symptoms * Good prognosis especially in young patients

Answer 111

* Can arise form B\>\> or T cells * Can be aggressive/high grade or indolent/low grade. * Symptoms - B symptoms, lymphadenopathy, cytopenias from bone marrow involvement

Answer 112

* Clonal proliferation of plasma cells characterized by the presence of monoclonal immunoglobulin or immunoglobulin fragments in the serum and urine * Other manifestations include bone destruction (lytic) and hypercalcemia * Diagnosis - bence jones proteins, lytic lesions of ray

Answer 113

* Fever in the setting of clinically significant neutropenia (\<500) * Start antibioitc empically (cefepime +/- aminoglycoside); add vanco if person has hypotension, history of MRSA or infusaport. If Vanco was not initially added, add at 3 day if not improved. Att antifungal on day 5 if no improvement

Answer 114

* Cell breakdown causes relase of intracellular ions (phostassium and phosphorus) and DNA breakdown causes hyperuricemia. Also see hypocalcemia due to binding to phosporus * Seen in leukemias, lymphomas and after chemo in bulky tumours * Urice acid can cause acute renal failure and gout * Treament: IV fluids and allopurinol

Answer 115

* Disk herniation is a common cause of chronic lower back pain * L4-L5 are L5-S1 are the most common sites affected * Herniation occurs when the nucleus pulposus prolapses through the annulus fibrosis * More common in men and overweight individuals * Signs - pain worse with valsalva and spinal flexion, pain and paresthesia with a dermatomal distribution. Specific signs depend on nerve root involved * Treatment - NSAIDs, epidural injection for symptomatic relief. Surgery only for refractory pain or neurological deficits

Answer 116

1. Sensory loss/pain of anterior thigh; impaired dorsiflexsion and inversion at the ankle 2. Sensory loss/pain of lateral calf and first web space; impaired big toe extension 3. Sensory loss/pain of lateral and plantar aspect of the foot; impaired foot plantar flexion and eversion

Answer 117

* 1-4 must be present for \>6 weeks. At least four must be present for diagnosis 1. Morning stiffness \> 1 hour 2. Arthritis of 3+ joints 3. Arthritits of hand joints 4. symmetric arthritits 5. rheumatoid nodules 6. + serum RF 7. Radiographic changes - soft tissue swelling, juxta-articular osteopenia, subluxation, erosion * RF is positive in 80% and anti-CCP has 90-95 specificity. Also see elevated ESR

Answer 118

* Chronic inflammatory disease that can affect virtually every organ system. Associated with HLA-DR2 and HLA-DR3. Must have 4 or more of the following: 1. Malar rash 2. Discoid rash 3. Serositis 4. Oral ulcers 5. Arthritis - systemic 6. Photosensitivity 7. Blood disorders 8. Renal disorders 9. ANA 10. Immunologic disorder 11. Neurologic disorders * Antibodies - ANA, Anti-Smith, Anti-dsDNA * Treatment - NSAIDS, antimalarial (chloroquines) for skin rash and arthritis), glucocorticoids for end organ damage

Answer 119

* Splenomegaly * RA * Leukopenia

Answer 120

* An autoimmune disorder characterized by widespread small vessel fibrosis secondary to overproduction of collagen and other extracellular matrix proteins * Symptoms - Calcinosis, Raynauds phenomenon, Esophageal dysmotility, Sclerodactyly, Telangiectasias

Answer 121

* A systemic illness with no known cause, primaryly affecting the lungs. Characterized by noncaseating granulomas * Symptoms - erythema nodosum, hypercalciuria, uveritis, cardiac conduction defects, bell plasy * Diagnosis requried transbronchial biopsy

Answer 122

* A lymphocytic infiltrate in salivery and lacrimal glands, causing decrease section. Usually in association with other rheumatological diseas. * Symptoms - dry mouth and eyes * Treat with artifical tears and sialogogues (i.e., sucking candies that increase saliva production)

Answer 123

* Connective tissue disease causing proximal muscle weakness. Associated with HLA-DR3 * Dermatomyositis has similar manifestations to polymyositis plus skin involvement * Symptoms - weakness first in the legs, dysphagia, dysphonia, abnormal ECG * Dermatomyositis - purple-red papular/scaly photosensitive rash on face and neck, erythmia, scaling on extensor surfaces of joins (Gottrons papules) * Criteria - Muscle weakness, elevated CK, muscle biospy showing T cell infiltrated with myonecrosis, EMG shows myopathy

Answer 124

* Ankylosing spondylitis, psoriatic arthritis, ulcerative colitis, and Reiters Syndrome * Many associated with HLA-B26 genotype. * Unlike SLE, RA, and scleroderma, these have asymmetric arthritis and often have spinal involvement

Answer 125

* An HLA-B27 associated syndrome involving the MSK, genitourinary and ocular systemics. Occurs in 2 forms * sexually transmitted - 1-2 weeks after exposure * post-dysentery - salmonella, shigella, persinia, and campylobacter * symptoms - conjunctivity, urethrirts, arthritis, oral ulcers, balanitis

Answer 126

* Systemic necrotizing vasculitis of small and medium sized muscular arteries * Symptoms - fever, weight loss, malaise, glomerulonephritis, arthritis, mononeuritis multiplex \ * treatment = prednisome, cyclophosphamide

Answer 127

* Medium-vessel arteritis, also known as allergic angiits and granulomatosis; it is very similar to PAN except that the pulmonary findings predominate * symptoms - bronchospams, eosinohilia, fever, erythematous macluopapular rashes, red casts in urine * Treat with steriods

Answer 128

* Chronically relapsing small-artery vasculitis of upper and lower respiratory tracts and glomerulonephritis * Symptoms - glomerulonephritis, hemoptysis, sinusitis, arthritis, fever, weight loss * Diangosis - granulomatous vasculitis on lung biospy

Answer 129

* An arteritis of unknown etiology that is seen commonly in young people of Asian decent. Affects medium and large arterieis. * Symptoms - loss of pulses in arms and carotides bilaterally, Raynauds phenomenon, signs of transient brain ischemia, abdo pain, atypical chest pain

Internal medicine Flashcards

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