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101 Cards in this Set
- Front
- Back
Congenital cardiac defect associations
22q11 syndromes |
Truncus arteriosus
Tetralogy of Fallot |
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Congenital cardiac defect associations
Down Syndrome |
ASD, VSD
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Congenital cardiac defect associations
Congenital Rubella |
Septal Defects, PDA
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Congenital cardiac defect associations
Turner's Syndrome |
Coarctation of Aorta
Bicuspid Aortic Valve (predisposed to A.S.) |
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Congenital cardiac defect associations
Marfan's Syndrome |
Aortic Insufficiency due to cystic medial necrosis (no media in vessel)
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Congenital cardiac defect associations
Offspring of diabetic mother |
Transposition of Great Vessels
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Reaction of hyperlipidemia medication is rash, itchiness, GI upset
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Niacin
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Pericarditis:
Viral Infection SLE RA Uremia |
Serous Pericarditis
if there is an increased JVD on INSPIRATION --> Kussmaul sign --> Constrictive Pericarditis --> Compromised CO |
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Pericarditis:
Uremia MI Rheumatic fever |
Fibrinous Pericarditis
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Pericarditis:
Tb Malignancy |
Hemorrhagic Pericarditis
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Pressure in all four chambers of the heart are equal. Total arterial BP is decreased. Pulsus paradoxus is present (dec. in BP less than 10 mmHg during inspiration)
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Cardiac Tamponade
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Temporal arteritis is associated with what condition? Hint: pain and stiffness in shoulders and hips associated with fever, malaise, wt loss and increased ESR
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Polymyalgia rheumatica
Rx: prednisone |
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C-ANCA
Small-medium vessels Lungs --> Cystic lesions on CT Renal: C-ANCA associated RPGN Do not treat with methotrexate |
Wegener's Granulomatosis
***similar in presentation to Goodpasture's syndrome*** Tx with cyclophophamide and steroids. Methotrexate is nephrotoxic |
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Wide Splitting S2
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Pulmonary Stenosis
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Fixed Splitting S2
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ASD (no widening that is expected on inspiration)
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Parodoxical Splitting S2
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P2 --> A2
Aortic Stenosis |
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During which phase of myocardial AP is the muscle contraction?
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Phase 2: Calcium spark
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What are the two leak currents in myocardial cells
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K out
Ca in |
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What is one of the most common congenital LQT syndromes presenting with syncope, Torsades de pointes and deafness
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Jervell & Lange-Nielson Syndrome
A.R. |
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What causes Tetralogy of Fallot?
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Anterosuperior displacement of infundibular septum
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Why is the abdominal aorta the most vulnerable to atherosclerosis and aneurysms?
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No vaso vasorum below renal artery so easily ischemic and damaged.
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Why are infarcts to the lung liver and intestines red?
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Hemorrhage
Loose Tissues Lots of collateral circulation On reperfusion, the increases PO2 causes increases reactive oxygen species because conc. of O2 is too high and forms radicals. |
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When is someone at risk for ventricular aneurysm post-MI?
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~ 7 days (scar formation complete)
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6 days after an MI someone presents to the ER and you can barely hear the heart sounds plus pulsus paradoxus is present. What is your dx?
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Free wall rupture leading to cardiac tamponade.
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4 days after an MI someone presents to the ER with pain in their chest and upon auscultation you notice a friction rub. What is your dx?
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Fibrinous Pericarditis
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Major causes of restrictive/obliterative cardiomyopathy?
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Sarcoidosis
Amyloidosis Postradiation Fibrosis Endocardial Fibroelastosis Endomyocardial fibrosis (Loeffler's --> ass with cancer) Hemochromatosis |
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How would you differentiate between right and left sided murmurs?
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If it's worse on inspiration, it's most likely on the right side of heart (increased venous return)
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Focal interstitial myocardial inflammation with fragmented collagen and FIBRINOID material
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Aschoff bodies in Rheum heart diseaes
Autoimmune destruction = Fibrinoid necrosis |
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Dobutamine
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B-adrenergic agonist (b1 mostly)
used in CHF associated with decreased myocardial contractility (cardiogenic shock) Increased cAMP (Gs) 1. inc contractility -> increase CO, decreased ventricular filling pressures 2. Inc HR and myocardial O2 consumption (less so than giving pure dopamine) 3. Increased conduction velocity --> Arrhythmias |
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Child presents with hypertension, hypokalemia, and an enlarged clitoris. She was born with ambigious genitalia. Her labia are fused. What is the most likely diagnosis?
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11 beta hydroxylase deficiency.
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Where is the mutation for the following deficiency?
autosomal dominant or recessive? |
CYP11B1 gene
AR |
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How would you treat this patient?
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Dexamethasone or hydrocortisone (replace where the patient isn't making)
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Child presents with hypotension, hyperkalemia, and an enlarged clitoris. She was born with ambigious genitalia. Her labia are fused. What is the most likely diagnosis?
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21 beta hydroxylase deficiency
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What will this patient's renin levels be?
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increased because there are no mineralocorticoids being produced.
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A 40 yo patient presents with weakness, orthostatic hypotension, hyperpigmented skin, low bicarbonate, low sodium levels, high potassium levels and low cortisol. What is the most likely diagnosis?
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Addison's Disease.
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What is the most likely etiology?
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Autoimmune/idiopathic
Also DIC Waterhouse-Fridrichson Syndrome (post meningococcal infection) Tb (miliary -> most common in developing countries) HIV |
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What is conn's syndrome?
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primary hyperaldosteronism
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What is the likely etiology of conn's syndrome?
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#1 - adenoma of zona granulosa
#2 - bilateral hyperplasia of zona glomerulosa |
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What will hypokalemia (secondary to increased aldosterone prod in conn's) present with on an EKG?
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prominent U waves
flattened T waves ST segment depression |
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How would you treat conn's syndrome?
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Spironolactone or Epotereone (latter does not have anti-andronergic effects)
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What is the treatment for cushing's syndrome?
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1. Ketoconazole - inhibits desmolase
2. Metyrapone 3. Aminoglutethimide |
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What if cushing's syndrome is cause by a neoplasia?
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Surgery
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A new patient is dx with Type I D.M. with high glucose levels. Why not give rapid insulin therapy?
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Cerebral edema secondary to decreased EC osmolality and influx of water into neurons
Hypokalemia (insulin drives K+ into cells) Hypoglycemia |
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What are the two treatments for chronic gout?
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Probenecid --> inhibits renal reabsorption of uric acid
Allopurinol --> inhibits xanthine oxidase (contraindicated in patients taking mercaptopurine, thiazide diuretics) |
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WHat are the common causes of hypercalcemia? (MISHAP)
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Malignancy
Intox of Vit D Sarcoidosis Hyperparathyroidism (painful bones, stones, groans, moans) Alkali syndrome Paget's Disease of Bone |
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A biopsy of the thyroid shows nests of cells in AMYLOID stroma. What is your diagnosis?
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Medullary ca of the thyroid (MEN II and II --> RET --> AD)
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What is pseudohypoparathyroidism?
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The kidney doesn't respond to PTH.
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What is the genetic cause of this?
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mutated G_s-alpha_1 protein of adenylyl cyclase
Associated with Albright's Hereditary Osteodrystrophy (some patients have GHRH resistance) |
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What are common causes of hypothyroidism?
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Alcohol
Autoimmune (hashimoto's) Drugs (amiodarone, lithium) infection |
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Ascaris Lumbricoides
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Southern U.S., Tropical Climates
Most common worldwide 1.) Eat eggs 2.) Larvae in SI 3.) Move to alveoli 4.) Cough and swallow 5.) GI (again!) as adults 6.) Go to bile ducts and pancreas Test: Stool --> Eggs are knobby rough surface Rx: Mebendazole, Pyrantel Palmoate |
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45 degree branched hyphae
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Aspergillus
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What would a CXR look like of someone infected with this and is immunocompromised?
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"Fungus ball" in preexisting lung lesions --> aspergilloma
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How would you treat aspergillosis?
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Amphotericin B (binds to ergo)
AE: Kidney prob, arrhythmias, fever, chills, hypotension |
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What is invasive aspergillosis?
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Can go to kidneys and pericardium causing oliguria and chest pain
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Pork Tapeworm
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T. solium
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T. solium
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Cysticercosis
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How do you get cysticercosis?
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1. Eat undercooked pork
2. Larvae in GI and mature 3. Release Eggs in feces THEN 4. Fecal --> Oral (eat your feces) 5. Eat EGGS (not larvae like initially) that go to GI tract 6. Egg hatch into onchospheres 7. Penetrate GI wall 8. Migrate to eye (blindness), brain (seizures) and muscle |
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What would you see on head CT of someone who has cysticercosis?
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Calcified lesions
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What is the treatment?
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Praziquantal or albendazole + steroids or anticonvulsants for neurocysticercosis
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Wuchereria bancrofti
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Elephantitis
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How do you get this?
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Bite of a mosquito
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What happens then?
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Larvae go to lymphatics and block them by maturing
1 year later --> adult worms in LYMPH NODES causes inflamm response and repeated bouts of inflammation cause fibrosis which blocks lymph nodes |
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How would you dx elephantitis?
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draw blood in evening (larvae = microfilariae)
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How would you treat this?
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diethylcarbamzine to kill larvae
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What causes ITP?
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Autoimmune in which the body makes Ab against platelets
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What do you need for a diagnosis?
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low platelets
coomb's test positive petechiae and purpura of mucus membranes |
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What happens to the control of blood flow to the kidney when giving NSAIDs?
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NSAIDS inhibit prod of PGE2 which is the primary regulator of afferent arterioles. Therefore the only control on renal blood blow is the potent vasoconstrictor.
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What is that vasoconstrictor?
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AT II --> Increases risk of ischemic damage to medulla
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Fusion of podocytes =
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Sign of nephrotic syndrome
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Mutations to different genes cause similar phenotypes
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Genetic heterogeneity
Ex: Marfans (fibrillin 1 gene) and Homocystinuria both have marfanoid like body habitus and lens dyslocation |
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Genetic Heterogeneity
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Mutations to different genes cause similar phenotypes
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Alleleic Heterogeneity
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different mutations on same locus cause same phenotype
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Phenotypic heterogeneity
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mutations on SAME gene cause different phenotype
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What happens to Type I and II errors and power if the study's statistical significance is changed from 0.05 to 0.01?
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Type I (alpha) will decrease
(you will have less chance of rejecting the null hypothesis when it is actually true) Type II (beta) error will increase Power will decrease (P = 1 - beta) |
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Bacterial antibiotic efflux pumps (resistance to Ab()
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Need energy
1.) proton gradient 2.) sodium gradient 3.) ATP |
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Catecholamine degradation
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1. MAO -> oxid. deamination (MITOCHONDRIA = MAO)
2. COMT -> methylation (CYTOSOL) Yields Vanillymandelic acid (VMA) |
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Mutations on Chr 7
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Cystic Fibrosis
Ehlers Danlos Syndrome Osteogenesis imperfecta |
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Mutations on Chr 16
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Adult PKD
Tuberous Sclerosis |
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Paget's disease of bone places someone at increased risk of...
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Osteosarcoma (DUH)
mixed radiolucent and radiodense areas on the bone CODMAN's TRIANGLE SUNBURST |
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Viruses in the paramyxoviridae family
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Mumps
Measles (3 C's) RSV (bronciolitis in < 2 y.o, Tx: Ribavirin) Parainfluenza (Croup) |
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Acute Intermittent Porphyria
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Auto Dom
No Uroporphyrinogen I synthetase AKA HMB synthase S/S: episodes of stomach pain with neuro symptoms after exposure to offending agent Urine from patients will turn dark upon standing NO NO NO NO NO NO photosensitivity (those are later in the Heme pathway) |
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DNA laddering (fragments of DNA on southern blot)
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Apoptosis (Karyohexis?)
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AE of cyclosporine
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Renal Injury (you can't ride your bike through the kidney)
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What if someone is drinking grapefruit juice and taking cyclosporine?
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Worse renal injury because GF juice is an inhibitor of P450 (which is not only in the liver but also in the GI tract supposedly)
This is a pharmacokinetic interaction) |
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Analgesic abuse + acetominaphen in kidneys
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Thickened vasa recta capillaries
Intermittent tubular necrosis Eventually PAPILLARY NECROSIS FOCAL/SEGMENTAL GLOMERULOSCLEROSIS Interstitial infiltration/fibrosis |
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X-linked disease
Trinucleotide repeat Bulbospinal muscular atrophy leading to difficult swallowing, facial and tongue fasciculations |
Kennedy Disease (yeah, I know, I never heard of it either but apparently it exists)
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Calcium dependent adhesion molecules that help muscle and epi cells bind together
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Cadherins (in desmosomes and adeherens)
Not in hemidesmosomes |
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Lets play a game:
You remove on kidney. What happens to GFR? After 1 week? After 6 weeks? |
Immediately it will decrease by 50% (DUH)
1 week later --> Increase to 65-70% 4-6 Weeks later --> 80% How? remaining kidney hypertrophies and hyperfiltrates |
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What is the most common organism in endometriosis post-partum?
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Bacteroides and mixed flora
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What are the components of the inguinal canal?
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Deep inguinal ring (defect in transversalis fascia_)
Posterior wall (conjoint tendon of transversus abdominus and internal oblique mm) Superficial inguinal ring --> defect in external oblique mm aponeurosis |
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Child with rash on legs and buttocks, increased IgA levels, knee and ankle stiffness plus stomach pain. What is the most likely dx?
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HSP
small vessel vasculitis etiology: usually idiopathic but follows an URI in children. IgA deposition in blood vessels cause leaking leading to purpura and petechiae. |
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What renal pathology is similar to HSP's pathophys?
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IgA (berger's) nephropathy
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HIV, Heroin --> Nephrotic Syndrome
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Focal Segmental Glomerulosclerosis
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What can this lead to?
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Collapsing glomerulopathy where there is collapse and sclerosis of the whole glomerular tuft.
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What are the most common causes of hypokalemia?
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1. decreased intake (rare)
2. Increased loss 3. Increased movement into cells |
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How can you lose too much K?
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GI (vomiting, diarrhea, laxatives) or urinary (diuretics, primary aldosteronism, loss of gastric secretions, metabolic acidosis or polyuria)
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How would metabolic acidosis lead to hypokalemia?
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H ions go into cell pushing out K ions. This increases serum levels of K+ but ultimately results in increased K excretion in kidney
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How is hypokalemia cause dby increased movement into cells?
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Alkalosis, Beta-adrenergic stim, hypothermia
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Why is hypocitraturia associated with renal calculi?
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Citrate is a potent inhibitor of stone formation because it's a great chelator of calcium.
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How do you calculate serum osmolality?
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2*Na + glucose/18 + BUN/2.8
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How does demeclocycline help SIADH?
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It poisons the collecting tubule making it unresponsive to ADH
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