uWorld 44 Flashcards

1
Q

production of what cytokine correlates with severity of giant cell arteritis

A

IL-6

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2
Q

why is TOCILIZUMAB

A

monoclonal antibody to Il-6 that is effective in treating Giant Cell arteritis

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3
Q

what is the measure associated with case-control studies

A

exposure ODDs RATIO

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4
Q

what is the MOA of NITROGLYCERINE

A

VENOdilator (large veins in particular)

cardiac workload is decreased b/c blood collects in the venous system (redistribution) thereby decreasing PRELOAD

decreased preload decreased ventricular wall stress thereby decreased O2 demand

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5
Q

what is Osler-Weber-Rendu

A

hereditary hemorrhages telangiectasia

AD

congenital telangiectasis to the skin and mucous membranes

mucosal involvement may affect the lips, oronasopharynx, respiratory tract, gastrointestinal tract, urinary tract

rupture can cause: EPIStAXIS, GI BLEEDS, HEMATURIA

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6
Q

what is Surge-Weber

A

neurocutaneous disorder
cutaneous facial angiomas (leptomeningeal angiomas)

mental retardation

seizure

hemiplegia

skull radiopacitites

“tram track” calcifications on skull radiograph

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7
Q

what is seen in Tuberous sclerosis

A

kidney, lover, pancreatic cysts

CNS cortical and subependymal hamartomas

AD disorder

cutaneous angiofibromas (adenoma sebaceum), visceral cysts, and a variety of other hamartomas

renal angiomyolipomas

cardiac rhabdomyolipomas

seizure is major complication

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8
Q

when taking sexual history do you ask if they are straight, gay, bi or male/female/both

A

ask male, female, both b/c its less judgmental

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9
Q

what do you use in treatment-resistant schizophrenia (if haloperidol and risperidone have been tried and failed)

A

try CLOZAPINE

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10
Q

what is the order of the adenoma carcinoma sequence

A

APC (progression for normal mucosa to small polyp) then KRAS (increase in size) then p53 and DCC (malignant transformation)

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11
Q

what is injured in fracture of the neck of the fibula

A

common peroneal (fibular) nerve (most commonly injured nerve of the leg)- courses laterally around the neck of the fibula

FOOT DROP

  • loss of DORSIFLEXION (anterior compartment- deep peroneal)
  • loss of EVERSION (lateral compartment- superficial peroneal)

LOSS OF SENSATION of DORSUM of FOOT

  • superficial peroneal does forum
  • deep peroneal does area b/w 1st and 2nd toes
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12
Q

where does the common peroneal come from

A

branches off the sciatic (with he tibial were) posteriorly in the thigh just proximal to the popliteal fossa

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13
Q

what innervates the medial aspect of the leg

A

saphenous nerve (largest pure sensory branch of the femoral nerve)

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14
Q

what does the tibial nerve do

A

TIP
INVERSION and PLANTAR flex (gastroc, soles, tibialis posterior)

toe flexion

sensation to the sole of the foot, posterior calf, lateral foot

TISSUES of KNEE JOINT

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15
Q

dorsiflexion and/or eversion of the ankle can cause what kind of sprain

A

HIGH ANKLE sprain affecting the syndesmotic structures (interosseous membrane and anterior, posterior, and transverse tibiofibular ligaments)

these structures connect the tibia and fibula

unstable ankle joint with tenderness at the distal tibiofibular joint, but no significant swelling

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16
Q

what injury typically causes hemiballismus

A

LACUNAR STROKE (long standing htn or dm) of the SUBTHALAMIC NUCLEUS

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17
Q

what are the stool findings in watery diarrhea (noninflammaroty-ENTEROTOXIN)

A

NO FECAL LEUKOCYTES
NO RED CELLS
MUCUS and some SLOUGHED EPITHELIAL CELLS

vibrio, ETEC, bacillus cereus, staph aureus, some viruses, Giardia, Crypto, Cyclospora, microsporidia

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18
Q

what are the stool findings in dysentery or inflammatory diarrhea (inflammatory- invasion or cytotoxin)

A

fecal PMNs
with or without red cells

Shigella, Salmonella, Campy, EIEC, Yersinia enterocolitica, C diff, entamoeba histolytica

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19
Q

what are the stool findings in enteric fever (penetration and possible disseminate)

A

fecal MONONUCLEAR leukocytes

Salmonella TYPHI

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20
Q

what drugs can cause hyperkalemia

A

nonselective beta blockers (mess w/ beta-2 mediated intracellular uptake)
ACEI
ARBs
potassium sparing diuretics
DIGOXIN
NSAIDS (impaired PGs reduced renin and aldosterone secretion)

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21
Q

in a person with 6-months of progressively worsening impotence and loss of libido with suspected prolactinoma (elevated prolactin and blurring of peripheral vision) what are the levels of GnRH, LH, and Testosterone

A

GnRH: DECREASE (protecting down regulated this)

LH: decreased

Testosterone: decreased

22
Q

what kind of protein is amyloid precursor protein

A

transmembrane glycoprotien

23
Q

leprosy (hansen) disease is a deforming infection primarily of what

A

SKIN and NERVES (like schwann cells), also testicles and eyes

transmitted via respirator trout or prolonged skin-to-skin contact

ARMADILLOS is carrier in US

Tuberculoid: intact Th1 response (intact cell mediated immunity)
-mild skin plaques and are associated with hypo pigmentation, hair follicle loss, and focally decreased sensation

Lepratomous: intact Th2, no Th1 (weak cell mediated immunity)
-diffuse skin thickening, plaque-like hypopigmentation (with hair loss), leonine facies, paresis, regional anesthesia, testicular destruction, and blindness

24
Q

whats the fasted and most direct method for diagnosis of syphilis

A

DARK-FIELD MICROSCOPY of material scraped from the surface of a cutaneous syphalic lesion (MOTILE HELICAL ORGANISM)

can also use serologic testing:

  • nontreponemal tests: VDRL, rapid plasma antigen (RPR)- both for cardiolipin
  • treponemal tests: fluorescent treponema antibody absorption, microhemagglutination assay for T palladium- both detect antibodies to specific treponema antigens (PTS REMAIN POSITIVE ON THESE FOR LIFE- antitreponemal therapy doesn’t get rid of them)
25
Q

shallow, painful genital ulceration with regional lymphadenopathy that grows on a culture with factor X (hematin)

A

CHANCROID from Haemophilus ducreyi

26
Q

describe ataxia telangiectasia

A

AR

CEREBELLAR ATROPHY- leads to ataxia in 1st years of life

OCULOCUTANEOUS TELANGIECTASIA

severe immunodeficiency with REPEATED SINOPULMONARY infections

risk of CANCER in these peeps in increased b/c INEFFICIENT DNA REPAIR (high rate of radiation-induced genetic mutation on cultured cells)

27
Q

what inherited disorder are caused by deficient DNA-repair enzymes

A

Ataxia-telangiectaisa- DNA hypersensitivity to ionizing radiation

Xeroderma pigmentosa- DNA hypersensitivity ot UV radiation

Fanconi anemia- hypersensitivity to DNA cross-linking agents

Bloom Syndrome- generalized chromosomal instability (increased susceptibility to neoplasms)

HNPCC: defect in DNA mismatch-repair enzymes

28
Q

physiologic insulin resistance occurs during 2nd and 3rd trimesters due to shunting of carb metabolism toward supplying glucose and amino acids to the fetus, this is primarily due to what

A

HUMAN PLACENTAL LACTOGEN (hPL aka chorionic somatomammotropin)- a peptide creased and secreted by syncytiotrophoblasts

leads to INCREASED GLUCOSE in MATERNAL circulation (glucose crosses freely into the fetus and is continuously confused for fetal energy

lateral lipolysis and proteolysis is also increased by hPL (fatty acids and ketones provide energy to moms)

29
Q

how does gestational diabetes happen

A

the pancreatic function is not sufficient to overcome the pregnancy-related increase in insulin resistance (hPL STIMULATES PANCREATIC BETA ISLET CELL INSULIN PRODUCTION)

testing is more accurate in 3rd TRIMESTER with ORAL GLUCOSE CHALLENGE and measure serum glucose 1 hour after

30
Q

what is seen in theophylline toxicity

A

acute: nausea/vomiting, abdominal pain, diarrhea, cardiac arrhythmias, seizures

SEIZURES And TACHYARRHYTHMIAS are major concerns

Tx: ACTIVATED CHARCOAL, beta blockers for the heart stuff, benzos for seizures

31
Q

bradycardia, hypotension, and hypoglycemia are seen with what medication toxicity

A

beta blocker

GLUCAGON is the antidote (increased cAMP and cardiac contractility)

32
Q

what are some examples of medications that can cause sideroblastic anemia

A

ISONIAZID (B6 is cofactor for ALAS)
chloramphenicol
linezolid

33
Q

cystathionine synthase is fucked up in what

A

pyridoxine-dependent enzyme that catalyzes the formation of cystathionine from homocysteine

HOMOCYTINURIA happens (AR) that has marfanoid body habitus (BUT EYE IS DOWN AND IN), atherosclerosis, kyphosis, retard, osteoporosis

34
Q

what is seen in pyruvate kinase deficiency

A

AR

hemolytic anemia

normocytic, normochromic anmeia

reticulocytois

elevated indirect bilirubin

35
Q

whats a transtentorial herniation

A

uncal herniation

medial temporal lobe (uncus) herniates through gap b/w crus cerebri and the tentorium

FIRST SIGN is FIXED and DILATED PUPIL

ipsilateral CN III compression (ipsilateral down and out)

ipsilateral PCA compression (CONTRALATERAL HOMONOMYOUS HEMIANOPSIA w/ MACULAR SPARING)

compression of contralateral cerebral peduncle (crus cerebri) against tentorium (damage to contralateral corticospinal tract leads to IPSILATERAL HEMIPARESIS)

compression of ipsilateral cerebral peducle (CONTRALATERAL HEMIPARESIS)

brainstem hemorrhages (DURET hemorrhages) in the PONS and MIDBRAIN due to stretching and rupture of the basilar artery (usually fatal)

36
Q

subfalcine herniation

A

CINGULATE GYRUS herniates under the fall cerebri, potential compressing the ANTERIOR CEREBRAL ATERY

37
Q

tonsillar herniation

A

cerebellar tonsils displace through formate magnus and compress the medulla

COMA and RESPRIATORY DEPRESSION

38
Q

due to link between hyperthyroidism and depression, TSH is a routine screen for depression. a physician not noticing a high TSH and prescribing antidepressants instead of fixing the thyroid problem is an example of what

A

preventable adverse event which resulted in DELAYED DIAGNOSIS

39
Q

what is a preventable medical error

A

involve harm to the patient by ACT of COMMISSION or OMISSIOn rather than from the underlying disease and are the result of FAILURE to FOLLOW evidence-based BEST PRACTICE GUIDELINES

40
Q

what is malpractice

A

LEGAL TERM- situations where treatment is blow accepted standard of practice and has resulted in injury or death to the patient

NOT A TYPE OF MEICAL ERROR

41
Q

what is a near miss

A

medical error that is RECOGNIZED BEFORE any harm is done to the patient (patient is prescribed lethal doe of medication but the error is caught by pharmacist)

42
Q

what is a NON-PREVENTABLE adverse event

A

complication that cannot be prevented given the current state of medical knowledge (allergic reaction to a medication in a patient with no known history of drug allergies)

43
Q

what is a sentinel event

A

occurrence involving DEATH or SERIOUS PHYSICAL or PSYCHOLOGICAL INJURY (inpatient suicide, death of full-term infant, retained object after surgery) that requires IMMEDIATE INVESTIGATION

44
Q

what will INCREASE the intensity of a hypertrophic cardiomyopathy murmur

A

DECREASE IN PRELOAD (or after load): decrease the separation b/w mitral valve and interventricualr septum, increasing obstruction

VALSALVA (straining phase)

ABRUPT STANDING (from sitting or supine position)

NITROGLYCERINE ADMINSTIRIAON

45
Q

what will DECREASE the intensity of a hypertrophic cardiomyopathy murmur

A

SUSTAINED HANDGRIP (increased after load)

SQUATTING from standing position (increased after load and preload)

Passive leg raise (increased preload)

PHENYLEPHRINE infusion (selective alpha-1 agonist)- increased after load

46
Q

what characterizes leukocytoclastic vasculitis (microscopic polyangitis, microscopic polyarteritis, hypersensitivity vasculitis)

A

segmental fibrinoid necrosis

47
Q

what is rheumatoid arteritis

A

hypersensitivity vasculitis affecting arterioles and arteries of any size

produces VISCERAL INFARCTS after long standing rheumatoid arthritis

48
Q

whats up with the SERMS

A

competitive inhibitor of estrogen binding
mixed agonist/antagonist action

both used to PREVENT BREAST CANCER in high-risk peeps
TAMOXIFEN- adjuvant TX of BREAST CANCER
RALOXIFENE: postmenopausal OSTEOPOROSIS

ADRs: photoflashes, venous thromboembolism
tamoxifen ADRs: endometrial hyperplasia and carcinoma

49
Q

hospitalized patient for MI gets decreased urine flow and muddy brown casts, whats up in the kidneys

A

ISCHEMIC ACUTE TUBULAR NECROSIS due to decreased renal perfusion during cardiac arrest

one of most common causes of kidney injury in hospitalized patients

50
Q

what is seen in acute tubular necrosis

A

due to reduced renal perfusion form severe hypovolemia, shock, or surgery

increased serum creatinine and BUN
normal cratinine/BUN ratio
OLIGURIA

predominately affects RENAL MEDULLA, which has low blood supple under normal conditions

straight portion of PROXIMAL TUBUE and THICK ASCENDING LIMB of HENLE are particularly susceptible to hypoxia, as they participate in the active (ATP-consuming) transport of iOS and have high O2 demand

51
Q

what is seen histolgoically in acute tubular necrosis

A

FATTENING of PROXIMAL TUBULAR EPITHELIAL CELLS with LOSS of BRUSH BORDER

cell necrosis and denudation of the tubular basement membrane

MUDDY BROWN CASTS are variant of GRANULAR PIGMENTED CASTS that are PATHOGNOMONIC for ATN

most cases tubular epithelium REGENERATED and renal function typically returns to baseline acer 3 weeks

52
Q

how does renal papillary necrosis present

A

GROSS HEMATURIA
FLANK PAIN
URINE TISSUE FRAGMENTS

due to urinary tract obstruction/infection, interstitial nephritis due to analgesic injection, or microvascular disease (DM or sickle cell)