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Daily Flashcard Quizzes > 7/20 > Flashcards

7/20 Flashcards

1
Q

what can nitroprusside toxicity present as

A

cyanide poisoning

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2
Q

how can you treat cyanide poisoning

A

binding of cyanide ions:
tydroxycobalamin

induction of methemoglobinemia:
Sodium nitirite

Detoxifying sulfur donors:
sodium thiosulfate

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3
Q

what pts don’t have an upper vagina with variable uterine development? normal ovaries and 2ndary sex characteristics

A

Mayer-Roitansky-Kuster-Hauser syndrome

AKA Mullerian aplasia

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4
Q

where does vasopressin work

A

medullary segment of the collecting duct, which is the deeper part (vs cortical segment)

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5
Q

what is the primary stimulator of respiration in healthy pts

A

PaCO2

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6
Q

what is the primary stimulator of respiration in COPD pts

A

response to PaCO2 is blunted, so hypoxemia becomes the important contributor to respiratory drive

PERIPHERAL CHEMORECEPTORS (AKA CAROTID BODIES) are primarily responsible for sensing arterial PaO2 and can be suppressed if you administer O₂ to a COPD pt

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7
Q

how do central chemoreceptors function

A

they’re in the medulla, and
stimulated by decreased pH in the CSF

CO₂ readily diffuses through the BBB and forms H+ in the CSF, so
increased PaCO2 is the major stimulator of CENTRAL chemoreceptors

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8
Q

what heart abnormality is associated with Turner

A

Bicuspid aortic valve

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9
Q

what protein is released by eosinophils

A

Major Basic Protein

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10
Q

what is major basic protein’s function

A

released by eosinophils to kill helminths

also contributes to epithelial damage sustained by pts with allergic asthma

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11
Q

what types of adenomatous polyps are found in colon

A

tubular, villous, and tubulovillous

according to histologic appearance

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12
Q

how does a villous adenoma in the colon present

A

larger, sessile, and more dysplastic (vs the other tubular adenomas)

they can cause bleeding, secretory diarrhea, and partial intestinal obstruction

can secrete large quantities of watery mucus!!! which leads to secretory diarrhea and electrolyte abnormalities

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13
Q

which type of colon adenoma poses the highest malignant potential

A

VILLOUOS > tubulovillous > tubular

VILLAINS ARE THE WORST

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14
Q

what is the buzzword for cauliflower-like colon projections

A

villous adenoma

they’re large, sessile, and can have velvety or cauliflower-like projections

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15
Q

what does a colon tubular adenoma histology look like

A

dysplastic colonic mucosal cells that
form tube-shaped glands and
tend to be smaller and
pedunculated

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16
Q

what would you see in a hamartomatous polyp

A

disorganized mucosal glands, smooth muscle, and CT

may occur sporadically or with Peutz-Jeghers syndrome or Juvenile polyposis

these polyps can cause bleeding and intussusception, but
not secretory/mucos-y diarrhea

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17
Q

what would a hyperplastic polyp present like

A

well-differentiated mucosal cells that form glands and crypts

the crypts may be large or irregular but NOT dysplastic changes

almost always asymptomatic

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18
Q

what do signet ring cells look like

A

push nucleus to edge of cell with large central clearing

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19
Q

how do you use Hardy-Weinberg equation to calculate auto recessive questions

A

allele frequency = p + q = 1

phenotypic frequency = p^2 + 2pq + q^2 = 1

p^2 = frequency of NORMAL people (~1 in rare diseases)

2pq = CARRIER frequency (~2q in rare diseases)

q^2 = frequency of DISEASED people

when they give you disease prevalence (q^2), you can calculate the mutant allele frequency from the disease.  (q).
take sqrt(disease prevalence) = q

carrier frequency:
this is probability of being a heterozygote
carrier = 2pq
for rare auto recessive disorders, p = 1, so
probability of being a carrier = 2q

so....
P(auto recessive disorder) =
1/4 [P(mom carrier) x P(dad carrier)]
which will come out to be:
1/4[(2q)x(2q)]
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20
Q

what is most likely to bleed in epistaxis

A

nasal septum, containing the
Kiesselbach plexus

anterior ethmoidal, sphenopalatine, and superior labial arteries anastomose this region

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21
Q

what is the MOA for bisphosphonates

A

similar to pyrophosphate- they attach to hydroxyappetite binding sites and inhibit bone respiration by MATURE osteoclasts

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22
Q

what is the MOA for SERMs

A

they slow the rate of bone loss by inhibiting differentiation and maturation of pre-osteoclasts

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23
Q

what is the MOA for interferons alpha and beta

A

produced in response to viral infections

they help suppress viral replication by halting protein synthesis and promoting apoptosis in infected cells, to limit the virus’s ability to spread

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24
Q

what should you be suspicious of in a middle aged/older pt with iron-deficiency anemia but no “real” symptoms that jump out at you

A

occult blood loss from GI tract

this could even be if the pt denies bloody stools, menorrhagia, or any other sort of bleeding

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25
Q

what do pressure values look like when a pt has an inferior wall MI with complete occlusion of the proximal RCA?

A

this pt has a RV presents with hypotension, elevated JVP, and clear lungs

most often occurs in setting of LV inferior wall MI due to proximal RCA occlusion

present with:
high RA pressure (JVD, high CVP)
high Central venous pressure (RV dysfunction–> backup blood)
low PCWP (blood isn’t making it to the LA)
low cardiac output (LV

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26
Q

what characteristics does a Barr body have

A

it’s an inactivated X chromosome in females’ genetics

it’s compact heterochromatin

heterochromatin is densely packed, heavily methylated DNA in tight association with DE-acetylated histones and a low level of transcriptional activity.

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27
Q

what is reactive arthritis associated with

A

it’s associated with HLA-B27 seronegative (Rh negative) arhtropathies

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28
Q

what lab value is always low in the congenital adrenal hyperplasias?

A

cortisol/glucocorticoids

that’s why they don’t make it in the “arrow” trick

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29
Q

what can sickle cell cause to femoral head most commonly

A

osteonecrosis (avascular necrosis)

2/2 impaired blood supply to that bone segment

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30
Q

what is contraindicated in hereditary angioedema

A

ACE inhibitors

this disease causes activation of bradykinin, C3a, and C5a (2/2 lack of C1 esterase inhibition)
so you have lots of vasodilation and vascular permeability

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31
Q

what is diagnostic of hereditary angioedema

A

low serum levels of C1 esterase inhibitor

normally, the C1 esterase inhibitor suppresses activation of the C1 complement component and therefore the rest of the classic complement pathway

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32
Q

what does the Fas receptor do

A

Fas receptor initiates the extrinsic pathway of apoptosis

mutations of Fas and Fas ligand can prevent apoptosis of auto-reactive lymphocytes, and increase risk of autoimmune disease (like SLE)

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33
Q

which 2 diseases have metaplasia

A

smoking will cause squamous metaplasia in lungs-
normal columnar epithelium is replaced by squamous epithelium

Barrett esophagus will cause esophageal squamous epithelium to be replaced by intestinal columnar epithelium

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34
Q

what holds osteocytes geother

A

they exchange nutrients and wastes with adjacent cell via gap junctions

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35
Q

what is NRTIs MOA

A

binds competitively to reverse transcriptase and is incorporated into viral genome as a thymidine analog

it does not have a 3’-OH group, so 3’-5’ phosphodiester bond formation is impossible

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36
Q

how would you describe the process of aortic aneurysms and dissections

A

myxomatous changes with pooling of proteoglycans in the media layer of arteries

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37
Q

what does follicular lymphoma histology look like

A

diffusely purple slide with tons of cells and thin white circles

38
Q

what is follicular lymphoma’s protein problem

A

over expression of anti-apoptotic BCL-2 protein

39
Q

what protein problem goes with CML

A

BCR-ABL

able to eat Philadelphia cream cheese

40
Q

what is the Burkitt lymphoma protein proglem

A

over expression of c-myc

41
Q

what is over expressed in neuroblastoma and small cell carcinomas of the lung

A

N-myc

42
Q

how do you treat congenital adrenal hyperplasia

A

low doses of exogenous corticosteroids to suppress excessive ACTH secretion to reduce stimulation to the adrenal cortex

43
Q

how doe males with 17-alpha-hydroxylase deficiency present

A

phenotypically female at birth (but LACK internal female genitalia- like a blind ending vagina) because
absent virilizing androgens in utero

females develop normal internal and external gentility at birth

during puberty, neither sex can undergo synthesis of sex hormones, so no secondary sex characteristics develop

you’ll also have hypertension, hypokalemia, and low renin levels 2/2 excessive mineralocorticoid production but the over-stimulated adrenals

44
Q

what’s the embryology of tetralogy of fallot

A

“deviation of the infundibular septum”

results form anterior and cephalic devotion of the infundibular septum during development, causing a:
PROVe

Pulmonary infundibular stenosis (most important prognosis determinant; this is AKA “RVOT obstruction”)
maligned VSD
overriding aorta
RV outflow tract obstruction (systolic murmur)
RV hypertrophy

45
Q

which pts squat to help with cyanosis and why

A

Tetralogy of Fallot pts squat

it increases peripheral systemic vascular resistance (after load) and decrease R to L shunting across the VSD

46
Q

what does flattening of deltoid muscle mean

A

anterior humerus dislocation, causing axillary nerve injury

47
Q

what are the phases of a pacemaker cell action potential

A

phase 4: slow Na inward (funny current)

phase 0: rapid-ish upstroke with Ca influx

phase 3: repo with K efflux

48
Q

what are the phases of a non-pacemaker cardiac action potential

A

phase 0: rapid depo with Na influx

phase 1: K begins to open to start to bring it down

phase 2: K and Ca offset each other to make a plateau

phase 3: un-opposed K to repo the cell

phase 4: hyperpo by K

49
Q

which tumor cells express CD31, and what is it

A

hepatic angiocarcinoma

CD31 is an endothelial cell marker

50
Q

which cancer is associated with exposure to carcinogens like arsenic, PVC, and thorotrast

A

liver angiosarcoma
“lung cancer”
squamous cell carcinoma on skin

51
Q

What do you call it when a pair of alleles are inherited together in the same gamete (haplotype) more or less often than would be expected given random pairing?

A

linkage disequlibrium

52
Q

which anti fungal decreases ergosterol incorporation into the cell membrane

A

Nystatin and Amphotericin

both bind ergosterol

53
Q

which anti fungal inhibits ergosterol synthesis

A

azoles

54
Q

which anti fungal inhibits cell wall syntehsis

A

caspofungin

55
Q

which anti fungal inhibits DNA and RNA synthesis

A

flucytosine

56
Q

which anti fungal inhibits mitosis

A

Griseofulvin

57
Q

what does alternative splicing do

A

allows a single gene to code for various unique proteins by selectively including or excluding different DNA coding regions (eons) into mature mRNA

58
Q

how does Toxic Shock super antigen work

A

it interacts with MHC molecules on antigen-presenting cells and the variable region of the T lymphocyte receptor, to cause nonspecific, widespread activation of T cells

causes release of IL-2 from T cells and
IL-1 and TNF from macrophages

59
Q

what 2 lab values indicate biliary injury

A

Alk phos and

gamma-glutamyl transpeptidase

60
Q

what are the prognostic factor labs you should look at for cirrhosis

A

serum albumin levels
bilirubin levels
prothrombin time

61
Q

what is the major determinant of the degree of R–>L intracardiac shunting and cyanosis in TOF patients?

A

the degree of RVOT obstruction

62
Q

which drugs can cause coronary steal

A

adenosine
dipyridamole

they’re both selective coronary vasodilators, which will cause coronary steal

63
Q

what are the classic histo findings for Alzheimer

A

amyloid plaques and neurofibrillary angels

Neuritic (senile) plaques composed of amyloid beta core

overproduction of amyloid precursor protein

neurofibrillary tangles- aggregates of hyperphosphorylated tau protein

64
Q

what is the pathology of Klinefelter syndrome

A

destruction and hyalinization of seminiferous tubules

causes damaged sertoli cells, so
low Inhibin
high FSH

damaged Leydig cells, so
low testosterone
high LH

pts can develop gynecomastia 2/2 increased aromatase activity (stimulated by gonadotropin excess)

most Klinefelter pts are azoospermic and infertile

this is PRIMARY HYPOGONADISM- high FSH and LH; low Testosterone

65
Q

what is first line for Rheumatoid arthritis

A

Methotrexate

66
Q

what are methotrexate side effects

A

stomatitis (mouth ulcers)
bone marrow suppression
elevated LFTs

67
Q

which “normal” drug is associated with osteoporosis risk when used chronically

A

omeprazole

68
Q

what is neprilysin

A

a metalloproteinase that cleaves and inactivates peptides like BNP/ANP,

if you inhibit Neprilysin, you get increased levels of these natriuretic peptides, which
promotes diuresis, natriuresis, and vasodilation.
all of these are helpful/beneficial in combatting heart failure

69
Q

what do hypersegmented neutrophils indicate

A

megaloblastic anemia

70
Q

which part of the spine does rheumatoid arthritis attack

A

cervical spine

71
Q

how can you test for H pylori

A

urease test-
gastric mucosa is added to a urea solution

urease will convert urea to CO₂ and NH3 to cause a pH increase and color change, indicating
alkalinization of the solution

could also use a breath test

72
Q

what presents with nosebleeds, telangectasias on oral and nasal mucosa, face, and arms?

A

Osler-Weber-Rendu syndrome
AKA hereditary hemorrhagic telangiectasia

rupture of the telangectasias may cause epistaxis, GI bleeds, and hematuria

73
Q

what does a pt have with neurofibromas, optic nerve gliomas, Lisch nodules, and cafe au late spots

A

Von Recklinghausen’s

or NF1

74
Q

what does a pt have with multiple meningiomas and bilateral CN8 schwannomas

A

NF2

75
Q

what does a pt have with congenital cutaneous facial angiomas, leptomeningeal angiomas, mental retardation, seizures, hemiplegia, and skull radiopacities

A

Sturge Weber syndrome

AKA encephalotrigeminal angiomatosis

76
Q

what disease has characteristic “tram track” on skull XR

A

Sturge Weber Syndrome

77
Q

which embryologic derive do melanocytes (and therefore melanoma) come from

A

neural crest cells

78
Q

what is the serious drug effect you have to look out for when treating hypothyroidism

A

agranulocytosis!

present with sudden onset fever and erythematous pharynx

with drugs like methimazole or propylthiouracil

79
Q

what is pulsus paradoxes and when is it seen

A

drop in systolic pressure during inspiration

commonly seen in pts with cardiac tamponade

80
Q

what should you check before starting a TNF-alpha inhibitor

A

for latent TB

81
Q

what is ataxia telangiectasia

A

ineffective DNA damage repair- DNA has hypersensitivity to ionizing radiation, so you get
CELLEBAR ATROPHY

leads to ataxia
severe immunodeficiency, with recurrent sinopulmonary infections

82
Q

what is dystrophic calcification

A

a hallmark of cell death and injury, occurring in all types of cellular necrosis

83
Q

what is the primary course of morbidity in a strep pyo infection

A

you get acute rheumatic fever, then

heart failure from severe pancarditis!

84
Q

what is Henoch Schonlein purpura’s pathogenesis

A

IgA immune complex mediated vasculitis!!

with PALPABLE PURPURA ON BUTTOCKS

generally following a URI

85
Q

what is the most common congenital heart defect in Down Syndrome pts

A

a complete AV canal defect:

ASD
VSD
common AV valve

86
Q

how do you increase preload and/or afterload on a pt’s heart

A

squatting
sustained hand grip
passive leg raise

87
Q

how do you decrease preload on a pt’s heart

A

sudden standing
valsalva (Straining)
nitroglycerin

88
Q

how do you make a pt with HCM have a louder murmur

A

they will have asymmetric ventricular septal hypertrophy

25% of these pts will have a dynamic LVOT obstruction, which causes
harsh systolic ejection-type murmur

the degree of LVOT obstruction (and murmur intensity) depend on LVEDV, or the preload.

decreasing preload/venous return or after load decrease the LV chamber size, which
decreases the separation between the mitral valve and inter ventricular septum,
increasing obstruction

to make this murmur louder, you should DECREASE PRELOAD to cause a smaller LV space, and a bigger obstruction

89
Q

What presents with onion-like concentric thickening of arteriolar walls in the renal vasculature and elsewhere

A

hyperplastic arteriolosclerosis in renal arterioles, which can perpetuate malignant HTN

90
Q

what are the IF deposits in PSGN

A

IgG, IgM, and C3

91
Q

what disease do you see Fibrin deposits in the glomeruli

A

RPGN

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