Anki Flashcards

What kinds of infections can lead to reactive arthritis? What will you see on joint aspirates?

Chlamydia or GI illness (salmonella, shigella, etc.) Joint aspirates are STERILE (this is reactive arthritis, NOT septic arthritis)

What is the defect in familial chylomicronemia syndrome? What are some possible symptoms?

Defect: LPL or apoC-II Sx: acute pancreatitis, xanthomas, lipemia retinalis (milky appearing retinal vasculature), "creamy supernatant" from a blood draw

DDx Eosinophilia (CANADA-P)

Collagen vascular diseaseAtopic diseasesNeoplasmsAddison's diseaseDrugsAcute interstitial nephritisParasites (esp. helminths)

Cofactors for pyruvate dehydrogenase (and alpha-ketoglutarate dehydrogenase) TLC For Nobody

Thiamine (B1) Lipoic Acid Cofactor A (B5) FAD (B2) NAD+ (B3)

Wernicke-Korsakoff syndrome CAN'O beer

Confusion Ataxia Nystagmus Ophthalmoplegia

hormones using cAMP FLAT ChAMP (+ others)

FSH LH ACTH TSH CRH hCG ADH (V2 receptor) MSHPTH calcitonin GHRH glucagon

hormones acting on IP3 GOAT HAG

GnRH Oxytocin ADH (V1 receptor) TRH Histamine Angiotensin II Gastrin

hormones using tyrosine kinases no good mnemonic sorry :(

GH PRL Insulin IGF-1PDGFFGF cytokines think growth factors, acidophils (SAM - sommatotrophs, acidophils, mammotrophs), cytokines, and insulin!

hormones using cGMP BAN GraMPa from floppy pants

BNP ANP NO (EDRF) cGMP vasodilators

hormones using steroid (intracellular) receptors PET CAT on TV

Progesterone, Estrogen, Testosterone Cortisol (glucocorticoids) Aldosterone T3/T4 Thyroid hormones Vitamin D

Anterior Pituitary hormones FLAT PiG

FSH LH ACTH TSH Prolactin (intermediate pituitary) --> MSH GH

Cortisol FunctionsCortisol is A BIG FIB

Appetite increased Blood pressure increased (upregulation of a1 receptors) Insulin resistance increased Gluconeogenesis, lipolysis, proteolysis increasedFibroblast activity decreased Inflammation and immune response decreased Bone formation decreased

Features of Cushing Syndrome BAM, CUSHINGOID

Buffalo hump AmenorrheaMoon faciesCrazy (neuro sx: insomnia, agitation, psychosis) Ulcers (peptic) Skin changes (striae, acne, thin skin, easy bruising) Hypertension InfectionsNecrosis of femoral headGlaucoma/cataractsOsteoporosis Immunosuppression Diabetes

What substances are known for causing methemoglobinemia?

NitratesAntimalarial drugs (chloroquine, primaquine) DapsoneSulfonamidesLocal anesthetics (lidocaine) Metoclopramide

Drugs that exacerbate G6PD Deficiency Spleen Purges Nasty Inclusions From Damaged Cells

SulfonamidesPrimaquineNitrofurantoinIsoniazid Fava beans DapsoneChloroquine

Where would you see target cells? The hunter yells HALT at its Target

HbC diseaseAspleniaLiver disease Thalassemia

EPO-producing tumorsPotentially Really High Hematocrit

Pheochromocytoma Renal cell carcinoma Hepatocellular carcinoma Hemangioblastoma (vascular CNS tumor)note: occasionally uterine fibroids (leiomyoma)

Plummer-Vinson syndrome Plumber's DIE

DysphagiaIron deficiency anemia Esophageal webs

Pentad of Thrombotic Thrombocytopenic Purpura (TTP)get The Toilet Paper for the FAT RN

TTP FeverAnemia Thrombocytopenia Renal failure Neurologic symptoms

Triad of HUSthe RAT HUStled me!

Renal failure AnemiaThrombocytopenia

Causes of DIC STOP Making New Thrombi

Sepsis (often gram -) Trauma Obstetric complications Pancreatitis (acute) Malignancy - adenocarcinoma, APML (treat with retinoid acid) Nephrotic syndrome Transfusions

Naked RNA Viruses my Really Heavy Picture of California was Ruined without an envelope

ReovirusHepevirusPicornovirusCalicivirus RNA without an envelope --> naked note: naked viruses can survive harsh environments

Naked DNA Viruses PaPa and Aunt Polly Didn't have an envelope

PapillomavirusParvovirus Adenovirus Polyomavirus DNA didn't have an envelope --> naked note: naked viruses can survive harsh environments

HAPPy HiPPo Dung

Herpesvirus AdenovirusParvovirusPapillomavirusHepadnavirusPolyomavirusPoxvirusDNA

Attenuated Live Vaccines Attention! Please Vaccinate Young Infants with MMR Regularly.

Attenuated live vaccinesPolio (sabin, oral) Varicella (Chicken pox) Yellow fever Influenza (intranasal) MMR Rotavirus

Killed Vaccines RIP Always

'RIP' --> killed RabiesInfluenza (injectable) Polio (Salk) --> salK = Killed A - hepatitis A

Subunit vaccines

HepB, HPV

Egg-based vaccines

Yellow fever and Influenzathink about the yellow yolk (yellow fever) and the snotty white (influenza) note: MMR - egg-allergy is NOT a contraindication

Metastasis to Liver Cancer Sometimes Penetrates Benign Liver

Colon Stomach PancreasBreast Lung

Metastasis to Brain Lots of Bad Stuff Kills Glia

Lung Breast Skin (melanoma) Kidney (renal cell carcinoma) GI tract tumor (esp. colon cancer)

Metastasis to Bone Permanently Relocated Tumors That Like Bones

ProstateRenal cell carcinoma Testes Thyroid Lung Breast

Lytic metastasis to bone LyTiK

Lung Thyroid Kidney (breast is mixed)

Symptoms of Multiple Myeloma CRAB

hyperCalcemia Renal insufficiency Anemia Bone lesions/Back pain

Psammoma bodies: what are they and where are they found? PSaMMoMa bodies

laminated, concentric spherules of dystrophic calcification Papillary thyroid carcinoma Serous cystadenocarcinoma of ovary Malignant Mesothelioma Meningioma

Different RAS mutations and the cancers they are associated with

RAS is an oncogene (requires ONE mutation to become cancerous) K-RAS mutation: colon, lung, pancreatic (Kolon, Koughing, panKreatic) H-RAS mutation: bladder, kidney (hematuria) N-RAS: melanomas, hematologic malignancies, follicular thyroid cancer

Sturge-Weber Syndrome (=encephalotrigemical angiomatosis) STURGE

activating mutation of GNAQSporadic/port-wine Stain (V1/V2 distribution) Tram track calcifications (opposing gyri) Unilateral Retardation Galucoma/GNAQ geneEpilepsy

Tuberous Sclerosis Triad and HAMARTOMAS

"Tumor Central" - tumors everywhere Triad: seizures, intellectual disability, facial angiofibromasHamartomas in CNS and skin Angiofibromas on face Mitral regurgitation Ash-leaf spots cardiac Rhabdomyoma (Tuberous sclerosis) autosomal dOminant Mental retardation renal Angiomyolipomas Seizures/Shagreen patches

How does dactinomycin work and what is it used for? Children ACT WEiRd

Dactinomycin intercalates into DNA Children: working against childhood tumors dACTinomycin Wilms tumorEwing sarcomaRhabdomyosarcoma

Drugs that cause pulmonary fibrosis My Nose Cannot Breathe Bad Air

Methotrexate (Nitrofurantoin) (Carmustine) BleomycinBulsulfanAmiodarone

Drugs that are both nephrotoxic and ototoxic

VancomycinAminoglycosidesLoop Diuretics Cisplatin and Carboplatin

Testicular cancer drug cocktail Eradicate Ball Cancer

EtoposideBleomycin (or ifosfamide)CisplatinThink about how Lance Armstrong didn't want bleomycin because of possibility of pulmonary fibrosis

Drugs that interfere with microtubules

Vincristine, VinblastinePaclitaxel, other taxolsBenzimidazoles: Mebendazole, Albendazole Griseofulvin Colchicine

P450 InhibitorsCRACK AMIGOS

CimetidineRitonarvirAmiodaroneCiprofloxacinKetoconazoleAcute alcohol useMacrolidesIsoniazidGrapefruit juiceOmeprazoleSulfonamides

P450 InducersGuiness, Coronas, and PBRS Induce Chronic Alcoholism

GriseofulvinCarbamazepinePhenytoinBarbituratesRifampin St. Johns WortChronic Alcoholism

High Anion Gap Metabolic Acidosis MUDPILES

M â MethanolU â Uremia (chronic kidney failure)D â Diabetic ketoacidosisP â Propylene glycol I â Isoniazid, Infection, Iron L â Lactic acidosisE â Ethylene glycolS â Salicylates

Differential for ACUTE Chest Pain If you're DUMPT, you're heartbroken

DissectionUnstable anginaMI Pulmonary embolism Tension pneumothorax

Drug-Induced Long QT Some Risky Meds Can Prolong QT

Sotalol (Class III antiarrythmics) Risperidone/Haloperidol (antipsychotics) MacrolidesChloroquineProtease inhibitors Quinidine (Class 1A antiarrhythmics) Thiazides, TCAs

Heart Block Mneumonics

1st Degree: prolonged PR (>200msec) -if R is far from P, then you have first degree2nd Degree: Mobitz I (Wenckebach): progressive lengthening of PR followed by a dropped beat -Longer, longer, longer, DROP, that's a case of Wenckebach Mobitz II: dropped beats (QRS) with no preceding change -If some Ps don't get through, then you have Mobitz II 3rd degree: atria and ventricles beat independently of each other -If Ps and Rs don't agree, then you have 3rd degree

What substances cause vasodilation in skeletal muscle CHALK

CO2H+AdenosineLactate K+

Bacterial Endocarditis Symptoms Bacteria FROM JANE

Fever (MC sx) Roth spots Osler nodes (Ouch, ouch osler --> fingers/toes) Murmur Janeway lesions (Gentle jane --> palms/soles) Anemia Nail-bed hemorrhages Emboli

Culture negative endocarditis

HACEK (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella) Coxiella brunette, Bartonella spp., Brucella spp.

MC cause of Acute bacterial endocarditis

S. aureus

MC cause of subacute bacterial endocarditis

Viridans strep

Beck's Triad for Cardiac Tamponade"Beck wants the 3D's... and a TAMPON. She was supposed to get her period every ALTERNATING month, but for some PARADOXICAL reason, for it today."

Decreased blood pressure --> hypotensionDistant heart soundsDistended neck veins --> increased JVP electrical alternanspulsus paradoxus

Restrictive/Infiltrative Cardiomyopathy Causes You restrict a puppy with its Puppy LEASH

Postradiation fibrosis Loeffler's syndrome (eosinophil infiltrate -> fibrosis) Endocardial fibroelastosis (children!) Amyloidosis Sarcoidosis Hemochromatosis

Kawasaki Disease Symptoms CRASH and Burn your Kawasaki motorcycle

Conjunctivitis Rash (palms/soles --> desquamating) Adenopathy (cervical) Strawberry tongueHand-foot changes (edema, erythema) Fever (burn) **Kawasaki associated with coronary artery aneurysms** --> could cause coronary artery thrombosis or rupture in a young child

The C's of 'WeCener's' (Wegener's granulomatosis)

C shaped distribution: nasopharynx, lungs, kidneys + c-ANCA Tx with Cyclophosphamide

Hypertension treatment for pregnant women Hypertensive Moms Love Nifedipine

HydralazineMethyldopaLabetalol Nifedipine

Manic episode symptoms DIG FAST

Distractibility ImpulsivenessGrandiosity Flight of ideas/racing thoughts Activity increased/psychomotor agitation Sleep (decreased need) Talkativeness/pressured speech (rate of speech)

Depressive episode symptoms SIG E CAPS

Depressed mood*Sleep disturbed Interest lost* Guilt or worthlessness Energy loss and fatigue Concentration problemsAppetite/weight changesPsychomotor retardation or agitationSuicidal ideations

Quad screen for Down Syndrome my BIA has Down Syndrome

Increased B-hCG and Inhibin A

Quad screen for Edwards syndrome Prince Edwards wants to decrease ABE's power

AFP, B-hCG, Estriol are all decreased

Lab values for Patau syndrome

decreased BhCG, decreased PAPP-A

Potter sequence (syndrome) POTTER

Oligohydramnios caused by ARPKD, obstruction (ex. posterior urethral valves), bilateral renal agenesis, chronic placental insufficiency Pulmonary hypoplasia Oligohydramnios (trigger) Twisted skin (wrinkled) Twisted face (everything compressed) Extremity defects Renal failure (in utero)

Concentrations of substances along PCT (from highest concentration to lowest above the [1] line)Plasma Concentrations Increase Unless Cleared by Kidney

PAH CreatinineInulinUreaCl-K+ note: concentration of inulin is increasing, not the amount --> due to water reabsorption

Causes of Potassium shifts OUT OF cell (causing hyperkalemia) hyperkalemia? DO LABSS

Digoxin/Digitalis HyperosmolarityLysis of cells (tumor lysis syndrome, rhabdo, crush injury) Acidosis Beta-blocker high blood Sugar (insulin deficiency) Succinylcholine **give IV Ca2+ to prevent arrhythmias**

Causes of Potassium shifts INTO cell (causing hypokalemia)

Hypoosmolarity Cell proliferation/creationAlkalosis Beta-agonists (increase Na/K ATPase) Insulin (increases Na/K ATPase) "INsulin shifts K+ INto cells"

What are the crescents in RPGN made of?

fibrin and macrophages (inflammatory debris) "I gobbled up (macrophages) ever fiber (fibrin) of that croissant (crescent) RAPIDLY (RPGN)"

Calcium stones

Most common type of kidney stoneMost common kidney stone presentation: hypercalciuria, normocalcemia!!! MC cause: idiopathic hypercalciuria Treat with thiazides

Ammonium magnesium phosphate stones (struvite)

Forms staghorn stone Due to urease positive organisms (Proteus, Klebsiella, Staph. saprophytus) Stones alkalinize the urine Tx: surgical

Uric acid stones

Radiolucent (not seen on x-ray) RFs: decreased urine output, hot/arid climates, acidic pH Strong association with gout, increased cell turnover Tx: alkalization of urine, allopurinol

Cystine stones

Due to hereditary AR condition where cystine cannot be reabsorbed from renal tubules (COLA transporter deficiency) Begins in childhood Can from stag horn calculi Tx: alkalization of urine

Consequences of renal failure MAD HUNGER

Metabolic Acidosis Dyslipidemia Hyperkalemia/Hypocalcemia Uremia (increased BUN --> asterixis/encephalopathy, nausea/anorexia, pericarditis, platelet dysfunction) Na+/H2O retention Growth retardation/delayErythropoietin failure Renal osteodystrophy (osteitis fibrosa cystica, osteomalacia, osteoporosis) MC causes of chronic ESRD: diabetes mellitus, HTN, glomerular disease Shrunken kidneys with cysts (from dialysis)

Renal cell carcinoma "Think of a kidney-shaped red PEAR"

pear is hard (palpable mass), red (hematuria), hurts when thrown at someone (flank pain) PEAR: paraneoplastic syndromes PTHrP EPO ACTH Renin

What paraneoplastic syndromes are associated with RCC?

EPO --> reactive polycythemia ACTH --> Cushing's syndrome PTHrP --> hypercalcemia Renin --> HTN

What disease is RCC associated with?

VHL disease associated with deletion/inactivation of VHL gene on chromosome 3 --> increased IGF1, VEGF, PDGF

RCC vs. Wilms tumor (very basic level)

present similarly (unilateral flank mass with hematuria and flank pain), main difference is age of patient RCC --> adult Wilms tumor --> children

What is the WAGR complex?

A syndrome that is associated with Wilms tumor due to a WT1 deletion Wilms tumor AnhiridiaGenitourinary malformations Retardation

What are risk factors for transitional cell carcinoma (urothelial cell carcinoma)? Associated with problems in your Pee SAC

Phenacetin Smoking (polyaromatic hydrocarbons) Aniline dyes (hairdressers) Cyclophosphamide

Features of acute interstitial nephritis (AIN) FEAR

Fever Eosinophilia Azotemia Rash - maculopapular ***can progress to renal papillary necrosis

Causes of AIN (remember the P's)these drugs cause me P-AIN

Pee (diuretics) Pain-free (NSAIDs) Penicillins and cephalosporins Proton pump inhibitors rifamPin

Renal papillary necrosis Caused be... SAAD papa with papillary necrosis

Sickle cell disease/trait Acute pyelonephritis Analgesics (NSAID, phenacetin) Diabetes mellitus

Mature Ego Defenses include... "Mature adults wear a SASH"

Sublimation Altruism Suppression Humor

What kind of hallucinations are more common with medical illnesses (ex. delirium)?

Visual

What kind of hallucinations are more common with psychiatric illnesses (ex. SCZ)?

Auditory

What kind of hallucinations are more common in narcolepsy?

Hypnagogic and Hypnopompic Usually auditory

What kind of hallucinations often occur as an aura of temporal lobe epilepsy?

Olfactory (burning rubber)

Difference between delusion, hallucination, illusion

Delusion: firm, fixed belief that persists despite the factsHallucination: perception of something with NO external stimuli Illusion: misinterpreting something that is present (do have an external stimuli)

What dopaminergic pathways are affected in SCZ?

Increase in dopamine in mesolithic pathways --> positive symptoms Decrease in dopamine in mesocortical pathways --> negative symptoms

Stages of GriefDABDA

Denial AngerBargainingDepression Acceptance

What is buspirone?

Used for generalized anxiety disorderStimulates 5-HT1a receptors --> does not interact with alcohol (because acting at different place) 1-2 weeks to take effect "I'm always anxious if the BUS will be ON time, so I take BUSpirONe, but once i take my SEAT, i'm HAPPY (stimulated 5-HT1a RECEPTOR (the bus seat is the receptor))"

Collagen Synthesis SHaGG EPiC

1) Synthesis --> alpha-preprocollagen to ER 2) Hydroxylation of prolines and lysines --> requires vitamin C (def. = scurvy) 3) Glycosylation of hydroxylysines AND formation of triple helices (tropocollagen) (Grouping) 4) Exocytosis into extracellular space (through Golgi) 5) Proteolytic cleavage of C- and N-terminal disulfide rich ends 6) Cross-linking between lysines-hydroxylysines to form collagen fibrils note: glycine makes up bulk of collagen

Congenital defects of Down Syndrome"Don't Have A Clue"

Duodenal atresia Hirschsprung disease Annular pancreas Cystic fibrosis

Fetal Erythropoiesis occurs in... Young Liver Synthesizes Blood

Yolk sac (3-8 weeks)Liver (6 weeks - birth) Spleen (10-28 weeks) Bone marrow (18 weeks to adult)

Hemoglobin electrophoresis What is the order of Hb bands (from traveling the farthest to least) A Fat Santa Claus

HbA --> travels the farthest toward the anode (+) HbFHbSHbC --> travels the least

Hemophilias affect which clotting cascade components?

Hemophilia A --> factor VIII ('A sounds like eight') Hemophilia B --> factor IX ('be-nine')

What stabilizes factor VIII?

von Willenbrand Factor (vWF) "volksWagon Factories make gr8 cars"

Pathologic RBC forms (limited list) What are some abnormal 'materials' that can be found in these different pathologic RBC forms? (i.e. what are the abnormal substances in the RBCs made up of) Basophilic stippling Ringed sideroblastHeinz bodiesHowell-Jolly bodies

Basophilic stippling --> residual ribosomes Ringed sideroblast --> excess iron in granules in mitochondria in a nucleated RBC precursor (note: only see ringed sideroblasts in BONE MARROW) Heinz bodies --> Hb precipitation (note: can have many in one cell) Howell-Jolly bodies --> basophilic nuclear remnant (note: can only have one in a cell)

Where can you see echinocytes (burr cells)?

End-stage renal disease, pyruvate kinase deficiency these are uniformly spiky (as opposed to acanthocytes)

Where can you find acanthocytes (spur cells)?

liver disease, abetalipoproteinemia these are irregularly spiky (as opposed to echinocytes)

Lead poisoning LEAD

Lead lines (on gingivae = Bruton lines, and on metaphyses of long bones) Encephalopathy and Erythrocyte basophilic stippling Abdominal colic and sideroblastic Anemia Drops (wrist drop, foot drop) mechanism: 1) lead inhibits ALA dehydratase and ferrochelatase 2) lead inhibits rRNA degradation (basophilic stippling) 1st line treatment: Dimercaperol and EDTA, Succimer for chelation in kids

You got this!!!

You can do this!!!

What is the commonly presenting symptom in sickle cell disease?

presenting sx: dactylitis (swelling of hands and feet)

what is the most common cause of death in sickle cell disease (children vs. adults)?

children: infection with encapsulated organism adult: acute chest syndrome (vasodilation-occlusion in pulmonary microvasculature)

What is the defect in paroxysmal nocturnal hemoglobinuria?

ACQUIRED mutation in GPI anchor for DAF (CD55/59) which normally prevents complement from attacking their own cells affects lots of cells (RBCs, platelets, WBCs, etc.) --> pancytopenia

What are the substrates, enzymes, cofactors, and inhibitors of the first step of the heme synthesis pathway?

Substrates: glycine + succinyl-CoAEnzyme: ALA synthase (RLS!!!) Cofactors: B6Inhibitors: glucose, heme

Vitamine B1 is needed as a cofactor for which enzymes? =Thiamine pyrophosphate (TPP)

Alpha-ketoglutarate dehydrogenase (TCA cycle) Transketolase (HMP shunt) Pyruvate dehydrogenase (links glycolysis to TCA cycle) Branched-chain ketoacid dehydrogenase B1 with the planet, use your ATP to Branch out!

X-linked dominant disorders

Fragile X syndrome Alport syndrome Hypophosphatemic rickets

X-linked recessive disorders Oblivious Female Will Often Give Her Boys Her x-Linked Disorders

Ornithine transcarbamylase deficiency Fabry disease Wiskott-Aldrich syndrome Ocular albinism G6PD deficiency Hunter syndrome Bruton agammaglobinemia Hemophilia A and BLesch-Nyhan syndrome Duchenne (and Becker) muscular dystrophy

Most common causes of neonatal meningitis

Streptococcus agalactiae (most common) Escherichia coliListeria monocytogenes

Muscarinic Effects (Each effects)

Diarrhea Urination Miosis Bronchospasm Bradycardia Excitation of skeletal muscle (because somatic Nm receptors) Lacrimation Salivation Sweating (sympathetic adrenal glands use muscarinic receptors) DUMBBELSS

What 'sequences' does the spliceosome look for to identify an intron

GU at 5' end AG at 3' end

What cell type is the most sensitive to radiation?

Lymphocytes

What kinds of leukemias are associated with Down syndrome?

BEFORE 5 years old: Acute megakaryocytic leukemia (type of AML) due to t(8;21) AFTER 5 years old: ALL

What are some keywords for each type of leukemia? ALL, AML, CLL, CML

ALL: Tdt (DNA polymerase), good prognosis in children, may spread to CNS/testes (need prophylaxis chemo) AML: Auer rods (crystallized MPO) APML: Auer rods, t(15;17) disruption of retinoid acid receptor (Tx with ATRA) Acute monocytes leukemia: infiltrates gums CLL: smudge cells, acute hemolytic anemia, can transform to small cell lymphoma (into LN) and then to diffuse B cell lymphoma CML: Philadelphia chromosome (t(9;22)), basophilia, LAP(-), progresses to AML (80%) or ALL (20%), treat with imatinib

How do you determine the severity of mitral stenosis?

Use the A2-OS interval shorter --> more severe MS

Ruptured GI ulcers will cause hemorrhage from which vessels? Gastric ulcer on lesser curvature of stomach vs. posterior wall duodenal ulcer

Gastric ulcer on lesser curvature of stomach --> L. gastric artery Posterior wall duodenal ulcer --> gastroduodenal artery

What happens to the C-peptide of proinsulin after being cleaved?

Since proinsulin is cleaved to insulin and C-peptide once already packaged in a vesicle, C-peptide is released with insulin in equimolar amounts

LT toxin from ETEC is similar to what other toxin from what other organism?

Cholera toxin they both activate AC to increase cAMP and cause profuse, watery diarrhea

What is the greatest risk factor for completed suicide?

Previous suicide attempt (5-6x more likely) note: access to firearms (3x more likely)

Opioids

What are the 4 phases of a clinical trial?

Phase I: is it Safe? (testing in healthy volunteers) Phase II: does it Work? (testing in small group of patients with disease) Phase III: is it an Improvement? (testing in larger group of patients, comparing to placebo or standard of care) Phase IV: can it stay on the Market? (postmarked surveillance looking for rare or long-term side effects) Can the drug SWIM?

What are the 4 core ethical principles?

Autonomy Beneficence Nonmaleficence Justice

Who can act as a surrogate decision-maker if no advanced directive was prepared?

Spouse --> adult CHildren --> Parents --> Siblings the Spouse CHiPS in

Exceptions to confidentiality

Suicidal AbuseVictim of harm (warn/prevent harm) Epileptic/other impaired automobile driversDisease is reportable (Schools/employers) The physicians good judgement SAVED the day

Malpractice claim has 4 parts

Duty (physician's duty to provide care to that patient) Breach of Duty Harm (as a result of breach of duty) Damage (physical, emotional, financial)

What is the problem in Lynch syndrome?

aka hereditary nonpolypopsis colorectal cancer (HNPCC) AD mutation in DNA mismatch repair genes (includes MSH1, MLH1) with subsequent microsatellite instability always involves the proximal colon also associated with endometrial, ovarian and skin cancers

What are the causes of microcytic anemia?

Sideroblastic Anemia of chronic disease Lead poisoning ThalassemiasIron deficiency SALTI think about how: hemoglobin = heme (iron + protoporphyrin) + globin -if any part of this is messed up/reduced, a microcytic anemia can result

Pathology: mesothelioma

cuboidal/flattened (epithelium-like) or spindle cells (stromal-like) that are calretinin and cytokeratin (+)

Pathology: silicosis

nodules composed of whorled collagen fibers and dust-laden macrophages, upper lobe predominant

Pathology: small cell lung cancer

neuroendocrine Kulchitsky cells (small round blue cells) that are chromogranin (+)

Pathology: empyema

thick, fibrinous exudate and pus pus accumulates in pleural cavity

Physical exam: genital HSV

multiple painful, superficial vesicles or ulcerations on erythematous base

What is dystrophic calcification?

deposition of calcium in tissues (not bone)Tissues are not normally suppose to accumulate calcium.happens in dying/damaged tissues, calcium can bind to the released fatty acids Serum calcium and serum phosphate levels will be NORMAL

What is metastatic calcification?

When EITHER the serum calcium or serum phosphate is high and calcium can be forced from circulation into tissues and precipitates note: higher pH (more basic) favors calcium deposition -often in kidneys, lungs, gastric mucosa because they lose acid quickly

In what organs would you have a red infarct?

venous occlusion in tissues with multiple blood supplies includes liver, lung, intestines, testes, REPERFUSION INJURY

In what organs would you have a pale infarct?

solid organs with single (end-arterial) blood supply includes heart, kidney, spleen

What is defective in leukocyte adhesion deficiency?

LAD Type 1: defective CD18 integrin --> defective tight binding step LAD Type 2: defective Sialyl-Lewis --> defective margination/rolling

How do free radicals damage cells?

-membrane lipid peroxidation (damages membranes) -protein modification -DNA breakage

What is the main 'feature' of each type of collagen?

Type I: strong (highest tensile strength) Type II: stretchy Type III: slippery Type IV: BM SCAB I --> Skin, bone, tendons, scar tissue, dentin II --> Cartilage, vitreous body, nucleus pulpous III --> Arteries, granulation tissue, uterus, reticular fibers IV --> BM

What type of collagen is found in hypertrophic scars vs. keloids?

Hypertrophic scars --> parallel Type III collagen Keloid --> disorganized Type I and III collagen

What are some common features of different kinds of amyloid?

-Beta-pleated sheet configuration -Congo red staining w/ apple green Birefringence ABC --> amyloid, beta sheet, congo red

SYSTEMIC: KIDNEY is most commonly involved organ -Primary: AL amyloid (Ig light chains) deposit throughout the body, seen with plasma cell disorders (ex. multiple myeloma) -Secondary: AA amyloid (from SAA, an acute phase reactant) deposits in multiple tissues, seen in conditions with chronic inflammation (RA, IBD, Familial Mediterranean fever, etc.) LOCALIZED: -Dialysis-related: Beta-2-microglobulin (not filtered well by the dialysis) deposited in JOINTS (presents as carpal tunnel syndrome) -Heritable: MUTATED transthyretin (TTR) deposits in heart (symptomatic) -Age-related senile: NONMUTATED (wild-type) transthyretin (TTR) deposits in heart (asymptomatic) -Organ-specific --Alzheimer's disease: ABeta-amyloid deposits as amyloid plaques in brain (from APP on Chr. 21) --Diabetes mellitus Type II: IAPP (amylin) deposits in pancreatic islets (pancreas trying to pump out more insulin, IAPP is made by the same cells) --Medullary carcinoma of thyroid: calcitonin deposits in thyroid

Paraneoplastic syndrome: Opsoclonus-myoclonus ataxia syndrome (what is it and what cancers do you see it with?)

"Dancing eyes, dancing feet" Neuroblastoma (children) Small cell lung cancer (adults)

Paraneoplastic syndrome: myasthenia gravis (watt cancers do you see it with?)

Antibodies to post-synaptic ACh receptors at NMJ -weakness gets worse with use Thymoma

How may alleles need to be damaged in oncogenes vs. tumor suppressors to cause cancer?

Oncogenes: one allele damaged --> "ONe mutation in ONcogenes" Tumor suppressors: both alleles damaged --> "TUmor suppressors need TWO mutations"

How do most carcinomas vs. sarcomas spread? What are exceptions to this rule?

Carcinomas: spread lymphatically Sarcomas: spread hematogenously Exceptions: 4 carcinomas spread hematogenously -Follicular thyroid carcinoma -Choriocarcinoma -Renal cell carcinoma -Hepatocellular carcinoma "Four Carcinomas Route Hematogenously"

Pathology: deQuervain's Thyroiditis

also called subacute GRANULOMATOUS thyroiditis GRANULOMAS (inflammatory infiltrates with macrophages and giant cells) -diffuse low radioiodine uptake note: self-limited tender thyroid following flu-like illness (ex. viral infection)

Pathology: Hashimoto thyroiditis

Hurthle cells (eosinophilic epithelial cells) and lymphoid aggregates with germinal centers

What bursa is often injured by repetitive anterior motion of the knee?

AKA housemaid's knee Prepatellar bursa

What enzyme converts sugars to their sugar alcohols?

Aldose reductase glucose --> sorbitolgalactose --> galactitol too much sugar alcohols --> cataracts

How can the risk of wrong-site surgery be reduced?

"dual identifiers" (ex. nurse and surgeon) verifying the surgical site INDEPENDENTLY if verified together, there is a chance that the error could be replicated

What is flutamide?

A drug that competes with DHT and testosterone for testosterone receptorsoften used in combination with GnRH agonists (to prevent the initial increase in androgens caused by the agonist action) used for prostate cancer, etc.

Symptoms of Lupus (SLE) RASH OR PAIN

Rash (malaria or discoid) Arthritis (nonerosive) Serositis (pleurites, pericarditis, peritonitis) Hematologic disorders (cytopenias) Oral/nasopharyngeal ulcersRenal disease Photosensitivity Antinuclear antibodies Immunologic disorders (anti-dsDNA, anti-Smith, anti-histone, anti-phospholipid) Neurologic disorders (seizures, psychosis)

What are the functions of the common peroneal vs. tibial nerve? How can each be injured?

Common peroneal nerveFunction: everts and dorsiflexes foot (PED) Injury: compression of lateral aspect of leg, fibular neck fracture (foot dropPED) --> steppage gait Tibial nerveFunction: inverts and plantarflexes (TIPInjury: Baker cyst, tarsal tunnel syndrome (can't walk on TIPtoes)

Features of Osteogenesis Imperfecta

due to defect in Type I collagen synthesis (AD Mutation) Bones (multiple fractures) I (eye) (blue sclerae due to choroidal veins) Teeth (dental imperfections) Ear (hearing loss) Patients can't BITE

Pathology: What are the findings of osteosarcoma on x-ray and on biopsy?

X-ray: Codman's triangle (from elevation of periosteum) and sunburst pattern Biopsy: pleomorphic cells producing osteoid

Pathology: What do you see on histology and x-ray for Ewing sarcoma?

Histology: NEUROECTODERMAL tumor, sheet of small blue cells, possibly with circular groupings of cells with central clearing (Homer-Wright rosettes)X-ray: moth eaten appearance, ONION SKINNING

What is the hallmark of rheumatoid arthritis?

Synovitis leading to formation of pannus (inflammed granulation tissue)Myofibroblasts in the pannus contract and can cause... -fusion of the two bones of the joint (ankylosis) -joint pulling in opposite directions Pannus can cause damage to articular cartilage

Pathology; What are rheumatoid nodules? (seen in rheumatoid arthritis)

fibrinoid necrosis with palisading histiocytes

What is granulation tissue made up of?

blood vessels, fibroblasts, myofibroblasts

Pathology: What are tophi and when do you see them?

White chalky deposits surrounded by fibrosis seen in gout

What do the crystals look like in gout vs. pseudogout?

Gout: monosodium urate crystals, needle shaped, (-) birefringence under polarized light (yellow when parallel to the light) Pseudogout: calcium pyrophosphate crystals, rhomboid shaped, (+) birefringence under polarized light (blue)

Pathology: histology or polymyositis vs. dermatomyositis

polymyositis: endomysial infiltrate with CD8+ T cells dermatomyositis: perimysial infiltrate with CD4+ T cells

What is the difference between albinism and vitiligo?

Albinism: have a normal number of melanocytes, missing an enzyme to convert tyrosine --> melanin (tyrosinase) or to transport tyrosine into the cell Vitiligo: have irregular areas of hypopigmentation due to autoimmune destruction of melanocytes

Pathology: what does psoriasis look like on histology and on physical exam?

histology: -elongation of dermal papillae (acanthosis)-the rest of the epidermis above that is thin, nuclei retained in corneum (parakeratosis) -munro microabscesses (collection of neutrophils within the corneum) physical exam: -parakeratotic silvery scaling-Auspitz sign (when the plaques are scraped off, since the epidermis is so thin, it reveals the blood vessels of the dermis underneath and there is pinpoint bleeding)

Pathology: Lichen planus histology and physical exam

Histology: lymphocytic infiltrate at the dermal-epidermal junction causing a sawtooth-shaped infiltrate Physical exam-6P's: purple, pruritic, polygonal, planar, papules/plaques

Pathology: distinguish between pemphigus vulgarisms and bullous pemphigoid

Pemphigus vulgaris: -IgG Ab against desmoglein (desmosomes) -Flaccid bullae that rupture easily (thin layer of epidermis above the blister) -INVOLVES oral mucosa -histology: tombstoning (basal keratinocytes still attached to BM look like tombstones) -IF: net-like pattern (IgG Ab surrounding the spinosum keratinocytes -Nikolsky sign (+): can easily separate epidermis by stroking skin Bullous pemphigoid: -IgG Ab against hemidesmosomes -Tense bullae that do not rupture easily (full thickness of epidermis above the blister) -SPARES oral mucosa -histology: full thickness of epidermis lifted off of BM -IF: linear pattern (IgG Ab lined up along the basement membrane) -Nikolsky sign (-)

Pathology: dermatitis herpetiformis

IgA depositing at the tips of the dermal papillae, causing small vesicles to form at those tips --> looks like herpes

Pathology: erythema multiformeHow does this compare to SJS-TEN

targetoid lesions, commonly associated with HSV SJS-TEN usually result from adverse drug reactions, etc. SJS: erythema multiforme with mucosal involvement and fever, skin sloughing off at dermal-epidermal junction TEN: when SJS expands to >30% of body

Pathology: basal cell carcinoma, squamous cell carcinoma, melanoma

Basal cell carcinoma: nodules of basal cells with palisading nuclei Squamous cell carcinoma: keratin pearls Melanoma: nests of melanocytes, different patterns of growth -have a radial growth phase (more horizontal) and a vertical growth phase (spreads down into dermis) --> different growth patterns have differing timing/predominance of these two phases

Patterns of Melanoma growth

1) letingo maligna: stays at dermal-epidermal junction, does not grow down (no vertical phase) --> good prognosis 2) superficial spreading: MC subtype, early radial growth phase, little vertical growth, stays superficial --> good prognosis 3) nodular: early vertical phase, as it grows down it pushes dermis up to create a nodule on the surface of the skin --> poor prognosis 4) arcuate letiginous: on palms and soles, more in dark-skinned people, NOT associated with UV radiation

What is chronic mesenteric ischemia?*What other disease process is it similar too?

-Chronic mesenteric ischemia occurs when there is diminished blood flow to the gut. -There can be atherosclerotic build up in the mesenteric vessels (celiac, SMA, IMA).-Postprandial epigastric pain ('intestinal angina') is present since the intestines need more blood flow when digesting food, but cannot get increased blood flow due to the ischemia. -May also present with food aversion/weight loss. This process is similar to angina (atherosclerosis in coronary vessels) and other atherosclerotic disease processes

How does Cystic Fibrosis affect the sweat glands vs. other organs in the body? What electrolyte lab values would you see in CF?

Sweat glands: defective CFTR prevents Chloride (and hence Na+ and water) from entering the cell --> sodium stays in sweat and sweat tastes salty Other organs (ex. lung, pancreas): defective CFTR prevents chloride (and hence Na+ and water) from exiting the cell and going into secretions to thin them out --> thick secretions that block everything up --> bronchiectasis, chronic pancreatitis, bilateral absence of the vas deferens (infertility) Labs: hypochloremic, hyponatremic (losing Cl- and Na+ through sweat)

COPD exacerbations are often caused by what organisms?

common upper respiratory tract pathogens: H. flu, S. pneumoniae, Moraxella, rhinovirus severe COPD: opportunistic infections (ex. pseudomonas) Allergens can also trigger a COPD exacerbation (eosinophilic inflammation or airway)

Histology of Ewings sarcoma?

sheet of small blue cells with scant cytoplasm with fibrous septae and hemorrhage/necrosis

Cerebral ischemia --> loss of cerebral blood supply How long until a person loses consciousness? How long until there is permanent damage? Why does damage to neurons occur so quickly

Lose consciousness: 5-10 seconds Permanent damage: 4-5 minutes Damage occurs quickly because neurons do not store glycogen --> highly sensitive to ischemia note: profound global cerebral ischemia (ex. in the setting of shock) can lead to ischemic-hypoxic encephalopathy

What amino acid is used to produce Nitric Oxide?

ArginineProduced using nitric oxide synthase

How can levothyroxine lead to cardiac complications? What are those cardiac complications?

Too much endogenous OR exogenous thyroid hormone will lead to over expression of beta-adrenergic receptors This leads to high output heart failure, atrial fibrillation-leads to angina (due to increased myocardial oxygen demand) -high output heart failure because increases CO (increased Beta-1) AND decreases SVR (increased beta-2)

What is Zellweger syndrome?

Disorder in which there is defective peroxisome biogenesis -peroxisomes are needed to oxidize very-long-chain-fatty-acids (VLCFAs) and some branched chain amino acids because they cannot be processed through mitochondria -without peroxisomes, these substances build up in neuronal tissues and lead to neurologic deficits (hypotonia, developmental delay); and other tissues (craniofacial abnormalities, hepatosplenomegaly, etc.)

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