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Final review for Step 2 Ck > Peds > Flashcards

Peds Flashcards

1
Q

A sickle cell patient with an episode of gross blood in urine that resolves is likely due to?

A

Renal papillary necrosis happens in SCA patients due to occlusion of renal vessels and results in gross hematuria after the glomeruli so there is no protein and no WBC and no nitries/leukoesterase

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2
Q

what causes ARDS?

A

Protein leakage from capillary breakage and formation of hylaine membranes – PEEP

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3
Q

When don’t you tap an unkonwn effusion

A

Tap all unknown effusions unless the patient has CHF

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4
Q

what causes Vfib after MI

A

reentrant rhythm cause Vfib after MI

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5
Q

what should you treat with when you hear a S3 in a patient with dyspnea?

A

think CHF and give IV diuretics, do NOT give BB

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6
Q

treatment of ventricular tachycardia

A

treat ventricular tachcyardia (fusion beats), wide complex (stable), with amiodarone

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7
Q

what does acidosis do to K+

A

acid shifts K+ out of cells

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8
Q

What are the GLP agonists

A

exenatide and liraglutide are the GLP1 agnoists

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9
Q

what effect do FLP 1 have

A

GLP1 can cause weight loss

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10
Q

what second line diabetic drug causes weight loss

A

GLP1 eneatide and liraglutide causes weight loss

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11
Q

what are the gliptins

A

the gliptins are DPPIV inhibitors

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12
Q

what do the ligpitins do

A

gliptins are weight neutral and are used in renal insffu

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13
Q

what is used in renal insuff for DM

A

you can use the glipitins (DPPIV) which are weight neutral

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14
Q

what causes weight loss for diabetes

A

for diabetes the GLP agnosits cause weight loss

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15
Q

What are AE of sulnyulrea

A

sulonyule cause hypoglycemia and weight gain

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16
Q

what DM drug causes weight ain

A

sulfnyoluea cause weight gain

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17
Q

what does DPPIV cause

A

weight neutral used in renal failure

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18
Q

GLP1 agonists do what

A

the eneatides are weight los causing seocnd line

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19
Q

Chemically what are key ways to tell DM2 from Dm2 diabetic state

A

DM2 has hyperosmoalr and very high omsliarty but enough insulin to not make ketones and they bicarb is is more than 18 versus les than 18 in DM1

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20
Q

What are key in DKA

A

DKA has ketones and AGMA versus DM2 HHS which has higher osmolarity and and NNORMAL anion gap

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21
Q

DKA what do you look for

A

DKA look for the anion gap right away

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22
Q

Tx first line in HHS

A

HHS jUST GIVE IVF at first they are severely volume down and this helps correct

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23
Q

what is treatment in DKA

A

DKA tx is IVF + insulin versus HHS you only need fluids first

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24
Q

Most important step in HHS

A

the most improtatn step in HHS is IVF first

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25
Q

best way to slow DM nephropathy?

A

BP control is best way to slow DM nephroaphty

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26
Q

BP goal in CKD or Dm

A

below 140

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27
Q

BP goal in older than 60 with no disease

A

150/90

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28
Q

Earliest abnormality in Dm pnehproatphy

A

hyperfiltration and icnreased GFR is earliest abn in DM nephropathy

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29
Q

what happens to GBM in DM

A

the DM GBM THICKENS as first quatnifable chacne

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30
Q

What does A1c control do

A

A1c control reduces MICROvescile disease like nephropathy adn reintopahty

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31
Q

Concenrs of rhizopus

A

coma, cavernous sunis syndrome and coma, get CT to be sure or biopsy and treat with amphotericin B and debridement

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32
Q

What are you looking for in thryotoxicosis

A

in thryoidtoxiciosis there is tremor, high BP, lid lag, afib/fluttera nd Pac and high output failure

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33
Q

what are labs for secondary hyperthyroid

A

secondary hyperthyroid has high TSH and high T4

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34
Q

what has high TSh and high T4

A

High TSH and high T4 is secondary thryoid

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35
Q

what would you do if TSH and T3 are both high

A

high tsh and high t4 both is secondary hyperthryoid and indciates MRI of pitutiar

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36
Q

what is first step in hyperthyroidism

A

look at Tsh and 4

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37
Q

what is first step with high t4 and low tsh

A

if you have primary hyperthyroidism of high T4 and low TSH you look for s/s of graves, if none you do RAI scan

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38
Q

when do you use RAI scan

A

You USE RAI scan in hyperthryoidism (primary) without s/s of Graves

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39
Q

What would you use in primary hyperthryoidism so low TSH and high T4 without s/s of Graves

A

for primary hyperthryoidism you use RAI scan and then follow up with thyroglubolun if low to tell you exogenous hormone

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40
Q

what does thyroglobulin tell you

A

in primary hyperthryoidism with low uptake you look at thryroglboulin which telss you there was lysis and thyroididits or low and exogenous hormoen exposreu

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41
Q

Hyperthryoid s/s

A

secondary = high TSH and t4 = MRI pit, low TSH and high t4 -primary = look for graves if not do RAI scan and if low then you do exongeous for thryoditisi ersus exogenous expsoure

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42
Q

what else causes low RAI uptake with high thyroglublin

A

idoine toxiciosis, levothyroid OD, truma ovariss, painless thryoiditis, granulmouatusou thyroididt

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43
Q

What do PTU and MthZ both cause

A

Antithyorid drugs cause agrnaulocytosis

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44
Q

s/s of thyroid storm

A

FEVER and lid lag and tremor and hypertension and arrhtyhmi

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45
Q

what sign of thryoid toxicosis might throw you off

A

thryoid toxicosis oten has fever with tremor and hypertension, the fever can make you think that it i sdue to infection as it may present PP need to have high suscpitoina ndt reat with BB

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46
Q

First step in thyroid nodule on PE

A

Pe thyroid nodule is TSH and U/s

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47
Q

what od you do with suspcions U/S findigns on thryoid nodule exam

A

first step with thyroid nodule is U.S and TSH anf U/S is susicipions go ight to FNA

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48
Q

when a thyroid nodule get a FNA

A

get FNA with thyroid nodule if the patients have HIGH tsh (HYPOthyroid) as most cancers are cold

49
Q

what happens in a thyroid nodule with low TSH

A

low TSH is hyperthyroid and means it is not likley to malignant so you do radio123 to se if hot or cold

50
Q

When is RAI C/I

A

RAI can worsens severe graves opth and is C/I with Graves, but you don’t need it in Gaves it is diagnostic anyway

51
Q

what causes graves otpho

A

graves optho is due to retroorbibtal fibroblast sitmluation with the TSH-R stimulating Ab

52
Q

odd presentaiotn of myopathy

A

myopathy can be due to hypothyroidism

53
Q

when do you do TSH with high CK levels

A

do TSH with high CK levels in someoen with s/s of hypothyorid and myopathy

54
Q

what DOES NOT work in thyroid myopathy

A

in thyroid myopathy ANA is no good as hypothyroid patients can have psoitive ANA so you need to do TSH and worse iw muscle bioospy

55
Q

What does hypothyroid do to blood labs

A

hyptohyroid causes hyperlipidiema, hyponatremia and aysx elveations of CK

56
Q

A patient is tired with high CK and muscle pain, low Na and hihg lipids, test?

A

Hypothyoridism cause high CK and unexplained myopathy with hyponatremia and elevated lipids in the blodo and sometimes hepatic issues and milkd hepati enzyme elevations

57
Q

Subclinilca hypothyroid

A

mild elevation of TSHa dn normal T3/4 without s/s

58
Q

what is the father of all thyorid cancer

A

papillary is the fatehr and most common of all thyroid cancer

59
Q

hat thryoid cancer is most common

A

papillary (pappa) is the father (MC) of all thriod cancer

60
Q

How does papillary spread

A

papillary spread lympathiccally

61
Q

everything about papillary

A

papillary is LN spread, most common, radiation relate

62
Q

what thyorid cancer is the most common adn also related to histoyr of radiation or cancer

A

thryoid papillary cancer spread via LN and is related to lymphoma (LN) and rdaiation and is the MC

63
Q

Two causes of hypocalcemia that need tob ec onsidered

A

hypocalcmia often follows blood transfusion due to citrate in the blood

64
Q

when does a srugical patinet get hypocalcemia

A

surgical patients often get hypocalcemia as they get citrate infusion with chaltes chalsium

65
Q

Levels for low Mg

A

low Mg affects PTH release and K+ and lowers K+ and Ca. it causes low PO4,low PTH, low calcium and is common in alcholics

66
Q

What can vitamin D toxicity cause

A

vitamin D toxicity can cause high calcium, high PO4 and low PTH

67
Q

describe the algorithm for Cushing dx

A

you start with cortisol and low dose dexa and then you do acth, if acth is low you do adrenal Ct if acth is high you do MRI of pituitary right away then if there is a mass you do dexa suppression to confirm

68
Q

how is dx of cushings confirmed comign from pituatiry

A

i acth is high you do an mir and then you confirm it with the dexa suppression test

69
Q

what if actht is high in cushing sna dyou mri ptiutair and no mass?

A

then you do petrosal sinus smapling

70
Q

When is high dose dexa meth used

A

use high dose dexa meha in acth dependent coritsol secreiotn with a + brain tumor as a confirmation and do inferior petrosal sinus samling if no mass seen

71
Q

When do you see hyponatremia and very high urine osmo

A

pirmary polydipisa has low Na and very high urine osmolaityr

72
Q

Who gest low vitamind D

A

kids breastfed with no prenatal care get vit D def, CF patinets and IBD who have chronic diarrhea and thos ein low sun environments or GI tract resection patinest

73
Q

What are s/s of low vit D

A

gatsric resection, chronic diarrhea, hypocalcemia syx and bone pain with pseudofractures or muscle weakness and bone pain

74
Q

Patients with MEN2A and B need what before surgery

A

MEN2A and B patietns often have pheo and need evaluation for urine to make sure they don’e need alpha block before B block in surgery

75
Q

what type of acidosis is primary AI

A

primary AI (addison’s) is no cortisol and no aldosterone = no HCO3 absorbed = low HCO3 but no foreign body = NON ANION GAP metabolic acidosis

76
Q

Biggest risk for stroke

A

In general HTN is the biggest risk for stroke

77
Q

Young person with s/s of parksinosn, next step

A

s/s of parkinsons you’re thinking wilsons disease do LFT and slit lamp

78
Q

What is the only drug effective in preventing restroke

A

all stroke patients need aspirinunless allergy as aspirin is noly agent fective in reducing risk f earlly recurrnece

79
Q

what prevents stroke recurrent

A

aspirin prevents stroke recurrnts give another antiplatelety if recurrents trokes on aspirin therapy

80
Q

When do you get lacunar strokes

A

lacunar strokes happen in small vessel disease

81
Q

HTN stroke think what

A

HTN is leading increase in cause of alls troke and happens in lacunar small vessle dsiease

82
Q

What dont small vessels trokes cause

A

mslal vessle strokes do not have cortical sgins like aphosa,a gnosia, neglact, apraxia or cahnges in mental statsu

83
Q

HTN and lacunar strokes

A

mild deficits affecting in ternal capulse and pure motor dysfunction

84
Q

common acuse of pure motor dysfunction stroke

A

pure motor dysfunctoin internal capusle and HTN

85
Q

pure sensory stroke?

A

thalamus

86
Q

what is the defect in lacunar stroke

A

HTN and lipyalinotic thickening and lucane causing limited deficitis and pure motor (internal capuse) or pure sensory thalamus

87
Q

what is almost alwaysin volved in HTN heomrrhage

A

putamen is right enxt to to the internal capules and is almost alway sinvovled in HTN strokes

88
Q

HTN strokes caue

A

milkd deficits and affect internal capules and putamine and lead to pure sensory and pure motor commonly or a small mixture

89
Q

Who gest central cord syndrome

A

lederly get central cord syndroem

90
Q

who is predipsoed to central cord syndrome

A

central cord synrome in elely with hyperextention and sponylithiss

91
Q

Elderly person has a nexk hyperextension injru with h/o sponylosisi, what is the cysrndome

A

ecntral cord

92
Q

What is centarl cord syndrome s/s

A

older peron with spondylotlihsis in hyperxetnsion with upper extmiry waekness adn sensation loss

93
Q

how is acute MS treated

A

Acute mS with steroids

94
Q

who si acute MS refractory to steroids treated

A

acute MS refractory to steroids ist reated with plasma exchance

95
Q

when is plamsa exchange used in MS

A

plasma exchage in MS refractory to high does steroids

96
Q

How is acute cluster headache treated

A

acute cluster headache ist reated with 100% O2

97
Q

how is cluster headhce prophylai

A

prophylax cluster headache with verapamil and lithium and erogtamine

98
Q

what else is used acutely with 100% o2in cluster headache

A

can use subcutanoue sumatriptan

99
Q

what are s/s of cluster heada

A

retorbiratl pain adn lcarmination with horners

100
Q

what nerve deficit is commonin cluster headq

A

horner is common in cluster headache

101
Q

MC s/s in IIH

A

headhace and vision loss iwth diploplia and pulsailte tininus and CNVI palsy

102
Q

what ss/a re in IIH

A

headhace with ptinnitus and appilledema and CNVI palsy and vision loss

103
Q

what syx can happen in IIH

A

IIH you get headaceh with vision loss and CNVI palsy and visual defects

104
Q

How is IIH diagnosed

A

often a Normal CT – MRI – then do an LP which high openin pressure

105
Q

Complication of IIH

A

complication of IIH is blindness if the pressure is not treated

106
Q

how can you remmeber the Cx of IIH is blindness

A

remmber th complication of IIH is blindness as many presentwith vision loss and diplopia

107
Q

When you see CSF fluid of 1000 or more what do you suspect

A

CSF fluid of 1000 or more you’re thinking bacterial/TB meningitis

108
Q

what is a big feature on cell count of bacterial/TB meningitis

A

over 1000 cells you’re thinking bacterial/TB meningitis

109
Q

What do you suspect when normal protein and cells >100 for CSF

A

when you have high protein, cells over 100 and less than 100 and normal glucose = viral meningitis

110
Q

what is the distingusiher of bacteiral versus TB meningitis

A

TB meningitis has really really low sugar , botherhave cell counts up to or over 100

111
Q

cell coutns in CDF over a thousand it is?

A

bacterial meningitis is cel lcounts > 1000

112
Q

HOw is GBS treated

A

treat GBS with IvIG and nplasmphoresis

113
Q

what isn’t used in GB tx

A

do NOT use steorids in GBS tx

114
Q

What are s/s of ALS

A

ALS has upper and lower MN

115
Q

what is a odd syx of ALS

A

ALS they get faciculations and weakness along with bulbar syx like dysphagica an dexaggerated DTR

116
Q

oni maging what do you see in vacsular demtnin

A

on imaging you see putamien and white matter changes and internal capusel infarcts (white matter) white matter = axons = descending axons = white matter chagnes in vascualr dementai

117
Q

what does AD need for diagnosis

A

functional impairment

118
Q

what is seen on pathology of AD

A

you se nuerofibirally tangles and amyloid deposition

119
Q

Odd sign in Pciks disease

A

frontotemporal deficit and they often have primary reflexes that return

Final review for Step 2 Ck (12 decks)

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