Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Test reviews DEDICATED > Sat Aug 1 > Flashcards

Sat Aug 1 Flashcards

1
Q

what phase is the oocyte arrest in until ovulation?

A

prophase I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

At ovulation, an oocyte continues dividing and is arrested in what phase, until fertilization by sperm

A

metaphase II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how does low Cl effect HCO?

A

low Cl- impairs renal excretion of HCO- –> can lead to metabolic alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Total body chloride depletion may lead to…

A

metabolic alkalosis (impaired ability to excrete HCO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What can cause chloride depletion?

A

Severe vomiting - loss of H and Cl

Loop or thiazide overuse – Cl excreted in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

If someone has metabolic alkalosis due to Cl depletion, how do you treat them?

A

Normal saline with Cl repletion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

if someone has metabolic alkalosis, measurement of what substance can help determine the etiology?

A

urine Cl-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what type of genetic material does adenovirus have?

A

DS DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

a patient with diverticulosis presents with painless hematochezia, what is the pathophys of the bleed?

A
  • diverticula tend to form in weak points of the colon, usualyl where the vasa recta penetrate through smooth muscle
  • enlargement of the diverticula can lead to painless hematochezia, as a result of ulceration/rupture of the vasa recta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

is P aeruginosa and B cepacia lactose fermenting?

A

NOOOO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is dialtezam?

A

NON dihydropyridine Ca channel blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

risk factors for calcium oxalate stones?

A
  • hypercalciuria
  • hyperoxaluria
  • hypocitraturia
  • low Ca diet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how can you prevent calcium oxalate stones?

A
  • reduce sodium, protein and oxalate intake
  • increase potassium intake, moderate calcium intake (low Ca diet is actually a risk factor)
  • thiazides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

risk factors for uric acid kidney stones?

A
  • gout

- myeloproliferative disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

why does hypocitruria increase the risk of calcium oxalate stones?

A

-the normal function of citrate in the urine is to bind to Calcium, making it soluble and preventing the formation of calcium oxalate complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what type of drug is abacavir?

A

NRTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Abacavir A/E?

A

delayed hypersensitivty reaction (type IV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

whcih patients are at increased risk for a hypersensitivity reaction when taking abacavir?

A

Those with HLA-B*57-01 allele

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what should be done before starting a patient on abacavir?

A

genetic testing for HLA-B*57-01 allele

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is emtricitabine?

A

NRTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

emtricitabine A/E?

A

hyperpigmented macular rash on palms and soles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

which bacteria has Protein A?

A

S aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

MOA of protein A?

A

binds Fc region of IgG - prevents complement - impaired opsonization and phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

which bacteria secrete igA protease?

A

S pneumonia and N gonorrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are the major risk factors for AAA?

A

Male
>65
SMOKING

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is kussmauls sign?

A

increased JVP on inspiratio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

POST MI TIMEFRAME: right ventricular failure?

A

acute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

POST MI TIMEFRAME: papillary muscle rupture?

A

3-5 days OR acute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

POST MI TIMEFRAME: interventricular septal rupture?

A

3-5 days OR acute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

POST MI TIMEFRAME: left ventricular aneurysm?

A

within several months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what will be seen on ECG of someone with carotid sinus hypersensitivity during a symptomatic episode?

A

A prolonged sinus pause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

When does the early, and late, phase of a type I hyersensitivity occur?

A

Early - immediate

Late- hours later

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Findings of early type I hypersensitivty?

A

Wheal and flare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Pathophys of early type I hypersensitivity?

A

Preformed IgE from previous exposure crosslinks on mast cells and causes release of histmaine and leukotrienes ->vasodilation and increased permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

findings of late type I hypersensitivity?

A

palpable, indurated lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

pathophys of late type I hypersensitivity?

A

IgE also stimulates the late phase – stimulates Th2 helper T cells to release cytokines that activate eosinophils, which release major basic protein and peroxidase –> tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is metolazone?

A

thiazide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

histologic findings of HNSCC?

A
  • sheets of polygonal cells with abundant eosinophilic cytoplasm
  • intercellular bridges and keratin pearls (irregular foci of keratinization)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

location of Kiesselbachs plexus?

A

nasal septum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

frontal bossing is a finding in…

A

rickets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

which organelle is required for heme synthesis?

A

mitochondria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

pathophys of hemoglobin C

A

Mutation on beta chain results in glutamate being replaced by lysine.
-hemoglobin C then forms crystals and promotes red cell dehydration ->mild chronic hemolytic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

why are hemoglobin H and hemoglobin barts innefective at oxygen delivery?

A

they have extreme oxygen affinity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

beta globin tetramers =

A

hemoglobin H

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

gamma globin tetramers =

A

hemoglobin barts

46
Q

what type of bone metastasis does melanoma cause?

A

osteoLYTIC

47
Q

which types of cancers result in mixed (osteoblastic AND osteolytic) bone lesions?

A

breast and GI

48
Q

does total lung capacity change with aging?

A

No - the decreased chest wall compliance and increase lung compliance cancer eachother out

49
Q

attributable risk formula?

A

ARPe = 100 x ((risk of exposued-risk of unexposed)/risk of exposed)

50
Q

if you are given the relative risk, what is the attributable risk formula?

A

ARP = 100 x ((RR - 1)/(RR))

-used the relative risk of the exposed group obviously

51
Q

what is the function of ApoE3 and ApoE4?

A

These are found on chylomicrons and VLDL -they bind to hepatic apolipoprotein receptors and are then taken up by the liver

52
Q

what will mutated ApoEs result in?

A

the liver wont be able to remove chylomicrons and VLDL remnants from the blood, leading to increased circulating triglycerides and cholesterol

53
Q

which familial dyslipedemia has defective ApoE proteins?

A

type III - familial dysbetalipoproteinemia

54
Q

patient symptoms of cataracts

A
  • excessive glare at night
  • halos around bright lights
  • difficulty reading
55
Q

clinical findigns of cataracts?

A
  • loss of red reflex
  • cloudiness of the lens
  • decreased visualization of retinal detail
56
Q

pathogenesis of cataracts?

A

from oxidative damage -> opacification of the lens

57
Q

which drugs increase the risk for cataracts?

A

glucocorticoids

58
Q

what is a normal alveolar pO2?

A

104

59
Q

what is a normal alveolar pCO2?

A

40

60
Q

is blood gass exchange at the lungs usually diffusion or perfusion limitied?

A

Perfusion limited- the gases equilibrate after transversing only one third the lenght of the capillary

61
Q

What findings may indicate diffusion limited gas exchange in the lungs?

A

An increased gradient between alveolar pO2 and pulmonary venous pO2 -enough gas isnt able to diffuse to equillibrate in time

62
Q

Will pCO2 in the venous blood usualyl be affected in diffusion limited gas exchange?

A

No - it equibilrates much faster than O2 so is usually normal

63
Q

What normal condition can result in diffusion limited gas exchange?

A

Exercise — blood very high perfusion rates so that diffusion cant keep up

64
Q

Is a pulmonary vein PO2 of 70 normal?

A

NO - should be closer to 100 - this indicates diffusion limited gas exchange

65
Q

antigenic shift AKA

A

genetic reassortment - reassortment of RNA segments between different strains

66
Q

statins MOA

A

HMG coa reductase inhibitors

67
Q

statins effects

A

-decreased LDL, decreased triglycerides

68
Q

statins S/E

A

hepatotoxicity, muscle toxicity

69
Q

ezitimibe MOA

A

decreased intestinal cholesterol absorbtion

70
Q

ezitimibe effects

A

decreased LDL

71
Q

ezitimibe A/E

A

Increased hepatotoxicity when given with statins

72
Q

bile acid sequesterants MOA

A

prevent reabsorption of bile from intestine

73
Q

bile acid sequesterants effects

A

decreased LDL

74
Q

bile acid sequesterants A/E

A
  • nausea, bloating, cramping

- impaired absorption of drug and fat soluble vitamins

75
Q

niacin MOA

A
  • decreases FA release
  • decreases VLDL synthesis
  • decreases HDL breakdwon
76
Q

niacin effects

A

decreased LDL

increased HDL

77
Q

niacin A/E

A
  • flushing and pruritis
  • gout/hyperuricemia
  • hepatoxicity
78
Q

fibrates MOA

A
  • activate PPAR-alpha

- decrease VLDL synthesis

79
Q

fibrates effects

A
  • decreased triglycerides

- increased HDL

80
Q

fibrates A/E

A
  • muscle toxicity

- gallstones

81
Q

fish oil MOA

A
  • decrease VLDL synthes

- decrease apolipoprotien B synthesis

82
Q

fish oil effects

A
  • decrease triglycerides

- increase HDL

83
Q

clinical manifestations of congenital hypothyroidism?

A
  • initially normal at birth
  • enlarged fontanelle
  • protruding tongue
  • umbilical hernia
  • poor feeding
  • constipation
  • dry skin
  • jaundice
84
Q

why are babies with congenital hypothyroidism normal at first?

A

they have maternal T4

85
Q

inheritance of vWF disease?

A

AD

86
Q

what causes a decreased maternal alpha fetoprotein?

A

Aneuploides - trisomy 18, 21, etc.

87
Q

What causes an increased maternal alpha fetoprotein?

A
  • open neural tube defects
  • abdominal wall defects
  • multiple gestations
88
Q

does the maternal quadrupel screening test detect fetal alcohol syndrome?

A

NOOO

89
Q

what does adalimumab bind?

A

TNF-alpha

90
Q

chronic lymphadema is a risk factor for which cancer?

A

cutaneous angiosarcoma

91
Q

what is stewart treves syndrome

A

the development of angiosarcoma in the presence of lymphadema - often after radical masectomy

92
Q

pharmacological treatment of restless leg syndrome?

A

Dopamine agonists

Gabapentin/pregabalin

93
Q

pramipexole moa?

A

dopamine agonist (DR3)

94
Q

lacy, reticular rash =

A

parvovirus

95
Q

what is the purpose of carnitine acyltransferase?

A

shuttles fatty acids into the mitochondria for beta oxidation

96
Q

what substance inhibits carnitine acyltransferase?

A

malonyl-coa

97
Q

in what state is there increased malonyl-coa?

A

well-fed state

98
Q

explain trastuzomab cardiotoxicity?

A

it causes a decrease in cardiac contractility but does not cause any cardiomyocyte destruction or fibrosis. Often results after cessation of treatment

99
Q

antidote to serotonin toxicity?

A

cyproheptidine

100
Q

which drugs may cause a significant first dose hypotension?

A

ACE inhibitors -should start with low doses

in the presence of preexisiting volume depletion

101
Q

what is dystonia?

A

sustained, involuntary muscle contraction

102
Q

what is myoclonus?

A

sudden, brief, muscle contraction

103
Q

phenylalanine is converted into waht?

A

tyrosine

104
Q

what enzyme converts phenylalaline to tyrosine?

A

phenylalaline hydroxylase

105
Q

what is the cofactor for phenylalaline hydroxylase?

A

BH4

106
Q

what is the precursor to serotonin?

A

tryptophan

107
Q

what is the cofactor of tryphtophan hydroxylase?

A

BH4

108
Q

Neurologic manifestations of PKU?

A

developmental delay, hypotonia, dystonia and seizures

109
Q

the superior thryoid artery runs along with which nerve?

A

external branch of the superior laryngeal nerve

110
Q

what muscle is innervated by the external branch of the superior laryngeal nerve?

A

cricothyroid

111
Q

all laryngeal muscles except for the cricothryoid are innervated by what nerve?

A

reccurent laryngeal nerves

112
Q

the recurrent laryngeal nerves are at risk during ligation of which artery?

A

the inferior thyroid artery

Test reviews DEDICATED (70 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions