Block 1 Flashcards

1
Q

Vomitting reflex can be activated by either _____ or _____ stimuli

A

Humoral or neuronal

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

Area postrema in the _______ has chemoreceptor trigger zone that can respond to may nerotrnsmitters, drugs, or toxins

A

Fourth ventricle

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

The _________ in the 4th ventricle has chemoreceptor trigger zone that can respond to many neurotransmitters, drugs, or toxins

A

Area postrema

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

The _____ receives information from teh area postrema, gastroinestinal tract via the vagu nerve, vestibular system ,and central nervous system.

A

Nucleus tractus solitarius (NTS)

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

The nucleus tractus solitarius is in what area of the brain

A

Medulla

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

Neurons from the nuclus tractus solitarius project to other medullary nuclei and coordinate the _______ process

A

Vomitng

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

5 major receptors involved in stimulating the vomiting reflex in the area postrema an adjacent vomiting center nuclei are _____, ______, ______, ______, _______

A
M1 muscarinic
D2 dopaminergic
H1 hitaminic
5-HT3 serotonergic
Neurokinin 1 (NK1) receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

5-HT3 receptor antagonists (odansetrno) and dopamine receptor antagonists (metoclopramid) are particularly helpful for ________ induced vomiting.

A

Chemotherapy-induced vomiting

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

When 5-ht3 receptor antagonists and dopamine receptor antagonists do not control symptoms, _____ receptor antagonists can be consdered; they prevent both aute and delayed emesis associated with chemotherapy.

A

Nk1 receptor antagonists (prevent substance P release)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

In galactose metabolism, lactose is first broken down into ______ and _______

A

Galactose and glucose

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

Galactose is phosphorylated to galactose-1-phosphate by the enzyme_______

A

Galactokinase (GALK)

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

Excess galactose from a galactokinase (GALK) deficincy is converted to _______-

A

Galactitol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Excess galactose is converted to galactitol, an osmotic agent that causes _____

A

Cataracts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Excess glactose is converted to galactitol which spills into the urine, causing urine to test positive for a ________substance

A

Reducing

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

Which presents more seriously: a glactokinase (GALK) deficiency or a galactose -1-phosphate uridyl transferaase (GALT) defeciency

A

GALT
(GALK deficiencies may only present as cataracts while GALT deficiencies present in early noenates as lethargy, vomiting, and failure to thrive)

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

The mode of inheritence for glucose 6 phosphate- dehydrogenase (G6PD) deficiency is _____

A

X linked recessive

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

G6PD deficienct causes episodic bouts of hemolysis when red blood cells experience __________

A

Increased oxidative stress

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

How is glucose transported into the cells of most tissues

A

Facilitated diffusion via glucose transporter proteins (GLUT)

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

Transmembrane glucose transporter proteins (GLUT) are steroselectiveand have preference for ___- glucose

A

D

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

There are _____ codons for amino acids but only ____ amino acids

A

61

20

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

More than 1 ________ can code for a particular amino acid

A

Codon

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

The ______ hypothesis sates that the first 2 nucleotide positions on the mRNA codon require tradition base pairing with their complementary nucleotides on tRNA whereas the third “______“nucleotide position may undergo less stringent base pairing

A

Wobble

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

DNA polymerases are the primary enzymes responsible for DNA synthesis, which occurs ____ -> _____ direction

A

5’ –> 3’

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

Prokaryotes such as E. Coli have __ major DNA polymerases

A

3

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

High fidelity DNA replication is accomplished by the _________ proofreading exonucleas activity of all 3 DNA polyermases in prokaryotes

A

3’–>5’

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

High fidelity replication i accomplished by the 3’–>5’ “proofreading” ________ activity of all 3 DNA polymerases in prokaryotes

A

Exonuclease

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

DNA polymerase __ is unique as it is the only prokaryotic polymerase that also has 5’–>3” exonuclease activity

A

I

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

DNA polymerase I is uniqueas it is the onl prokaryotic polymerase that also has ___________ exonuclease activity

A

5’–>3’

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

5’–>3’ exonuclease activity functions by removing the ______ created by RNA primase and repair damaged DNA sequences

A

RNA primer

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

Warfarin is a ______ antagonist that inhibits epoxide reductase in the liver, thereby preventing gamma carboxylation ________ dependent clotting factors

A

Vitamin k

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

Warfarin is a vitamin k antagonist that inhibits _________ in the liver

A

Epoxide reductase

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

Vitamin K dependent clotting factors include:

A

II, VII, IX, X

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

What effect does Warfarin have on INR

A

Prolongs the INR

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

How does change in dietary intake of vitamin K induce risk of subtherapeutirc or supratherapeutic INR while on warfarin therapy?

A

Increase in dietary vit K intake –> increased availible vit K which counters inhibitory effect of warfarin on epoxide reductase –> subtherapeutic INR

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

How to antibiotics alter warfarin activity?

A

The gut flora produces vit K. Gram negative antibiotivs wipe out gut flora –> decreased vit K –> supratherepeutic INR (increases effect of warfarin)

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

Increased cytochrome P450 2C9 activity _______ warfarin activity

A

Decreases

Warfarin is metabolized by cytochrome P450 2C9

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

_______ and ______ drug class are used as antiemetics in motion sickness while ______, ______, and ________ are used as antiemetics in chemotherapy induced emesis

A

Antimuscarinics (anticholiergics) and Antihistamines

Dopamine receptor antagonists, setotonin receptor antagonists, and neurokinin 1 receptor antagonists

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

Chronic lung transplant rejection is marked by _____ ____ ______ in the walls of the small airways

A

Lymphocytic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

_____ lung transplant rejection is marked by submucosal lymphocytic inflammation in the walls of the small aiways

A

Chronic

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

Chronic lung transplant rejection is marked by submucosal lymphocytic inflammaion int he walls of the __________

A

Small airways

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

In chronic lung transplant rejection, ingrowth of granulation tissue into the lumen leads to ______

A

Airway obstruction and obliteration: bronchiolitis obliterans

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

Chronic lung transplant rejection presents ______ after transplant

A

Month - years

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

_______ rejection usually ocurs the first day of transplantation

A

Hyperacute

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

Hyperacute rejection is caused by preformed host antibodies against _________ or ______

A

Donor ABO or human leujocyte antigens (HLA)

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

Histology of hyperacute rejection of lung transplant shows “_________”: fibrinoid necrosis with heorrhage and ischemia

A

White graft reaction

46
Q

_______ rejection to lung transplant usually occurs within 6 months of transplat

A

Acute

47
Q

Acute rejection of lung transplant is typically caused by _____________ to donor human leukcyte antigens

A

Cell mediated immune response

48
Q

Histology of acute rejection of lung transplant generally shows ______________ in small blood vessels of the lung which can expand to include alveolar walls

A

Perivascular mononuclear infiltrates

49
Q

The most important opsonins (coating proteins) are ________ and ______

A

Immunoglobulin G and complement C3b

50
Q

On a table displaying test results and disease status, which axes is disease always on?

A

X axis

51
Q

Equation for positive predictive value

A

PPV = TP/(TP + FP)

52
Q

Equation for negative predictive value

A

TN/ (TN + FN)

53
Q

What study design compares two groups (treatment and a control) in the future for outcome of interest

A

Clinical trial

54
Q

What study design compares 2 groups (one with risk factor and one without the risk factor) in the future for disease incidence

A

Prospective cohort

55
Q

What study desing reviews past records and compares 2 groups (one has risk factor and other does not) on disease incidence

A

Retrospective cohort

56
Q

What study design compares 2 groups (diseased cases and nondiseased controls) in the past to compare risk factor frequency

A

Case-control

57
Q

Which study design looks at 2 groups (one with risk factor and other without risk factor) in the present to compare disease prevelance

A

Cross- sectional

58
Q

Endurance training can cause a systolic murmur due to ______

A

Eccentric left ventricular hypertrophy

59
Q

Strength training can cause what changes to the left ventricle

A

Concentric left ventricular hypertrophy

60
Q

Coronary dominance is determined by the coronary artery that:

A

Supplies blood to the posterior descending artery

61
Q

The PDA originates in most people (right dominant) from the ______ . In left dominant people, the PDA originates from the _______

A

Right coronary artery

Left circumflex artery

62
Q

Involvement of the ________ artery during M.I. Can cause varying degrees of AV block

A

AV nodal artery (most commonly a branch of the right coronaryartery although can also arise from left circumflex in left dominant)

63
Q

What is an atheroma

A

An atherosclerotic plaque

64
Q

What is released from platelets, activated macrophages, and enothelial cells to trigger smooth muscle cell recruitment from the media and proliferation of the intima?

A

Growth factors (platelet derived growth factor (PDGF)

65
Q

Platelet derived growth factor has what effect in the vessels during formation of atherosclerotic plaque

A

Trggers smooth muscle cell recruitment and proliferation in the intima

66
Q

A holosstolic murmur at the apex with radiation to the axilla is consistent with _____

A

Mitral regurge

67
Q

A _______ murmur at the apex with radiation to the _____- is consistent with mitral regugitation

A

Holosystolic

Axilla

68
Q

What extra heart sound is sometimes heard in mitral regurge

A

S3

69
Q

Why is an S3 sometimes heard in mitra regurgitation

A

Blood flowing back into left atria increases left atrial pressure –> more blood reentering let ventricle during systole

70
Q

Amphotericin B binds ______ to exert antiungal effects

A

Ergosterol

71
Q

How does amphotericin B cause toxicity in human tissues

A

It also binds cholesterol to some degree (suppose to bind ergosterol)

72
Q

List 3 important adverse effects of amphotericin B

A

Nephrotoxicity
Hypokalemia
Hypomagnesemia

73
Q

Diptheriae has diptheria toxin which inhibits host cell protein synthesis how?

A

Diptheria toxin inactivates EF-2 via ribosylation

74
Q

What toxin in Pseudomonas aeruginosa inhibits host cell protein synthesis and how

A

Exotoxin A inactivates EF-2 via ribosylation (same as diptheriae toxin)

75
Q

Staph aureus’ enterotoxin, a superantigen, is responsible for what symptom of staph

A

It acts locall on GI tract to cause vomiting

76
Q

Staph aureus’ TSS toxin, a superantigen, leads to what symptoms

A

TSS toxin stimulates T cells –> wide spread cytokine release and shock

77
Q

C. Dif’s cytoxin B leads to what changes in the intestine

A

Actin depolymerization –> cell death
Necrosis of colonic surfaces
Pseudomembrane formation

78
Q

B pertusis’ pertussis toxin disinhibits adenylate cyclase via ____ , increasing cAMP

A

Gi ADP ribosylation

79
Q

What is the effect of pertussis toxin increasing cAMP production in host cell?

A

Increased histamine sensitivity and phagocyte dysfunction

80
Q

V. Cholerae’s cholera toxin activates adenylate cyclase via ______, increasing cAMP production in host cells

A

Gs ADP ribosylation

81
Q

What is the result of cholera toxin increasing cAMP production in host cells

A

Secretory diarrhea, dehydration, and electrolyte imbalances

82
Q

What is the most common cause of malaria in non african countries

A

Plasmodium vivax

83
Q

How is the latent liver phase of plasmodium vivax treated

A

Primaquine

84
Q

Verrucous, skin colored genital lesion = _________ (anogenital warts)

A

Condylomata acuminatum

85
Q

What virus causes condylomata acuminatum

A

HPV (specifically types6 and 11)

86
Q

HPV infects ___________ cells through small breaks in the skin or mucosal surfaces

A

Basal epithelial cells (specifically stratified squamous epithelium (found in anal canal ,vagina, and cervix)

87
Q

Infants can aquire respiratory papillomatosis via passage through the birth canal of mothers infected with HPV leading to warty growths on _______ which can lead to weak cry, hoarsness, and stridor

A

True vocal cords (only part of respiratory tract with stratisfied squamous epithelium)

88
Q

Positive hepatitis B surface antibody,
Negative hep B surface antigen,
Negative hep B core antibody reflects what in the patient regarding post or present Hep B infection/vaccination?

A

Immunization against hep B with no prior hep B infection

89
Q

CMV is defferentiate from mononucelosis by what negative test result?

A

CMV is heterophile antibody (Monospot) negative

90
Q

How might CMV present in immunocompromised patients with reactivated infection?

A

Severe retinitis , pneumonia, esophagitis, colitis, hepatitis

91
Q

What is the most common indicator of obesity related restrictive lung disease? (On pulmonary function test)

A

Reduction in ERV (expiratory reserve volume: maximum volume of air that can be expired after a normal tidal expiration)

92
Q

What is the ERV on a pulmonary function test

A

Expiratory reserve volume: max volume of ir that can be expired after a normal tidal expiration

93
Q

How does perfusion change as you approach the apex of the lung compared to ventilation?

A

They both decrease but the ventilation only decreases slightly while the perfusion decreases more dramatically –> increased V/Q

94
Q

What is the diagnosis of a patient with a heavy smoking history, exertional dyspnea, and dilated airspaces on CT scan?

A

Centriacinar emphysema

95
Q

Smoking induced emphysema involves oxidative injury to respiratory bronchioles and activation of ____________

A

Resident alveolar macrophages

96
Q

Cigarette smoke ctivates resident alveolar macrophages causing inflammatory recruitment of nutrophils. Nutrophils and activated macrophages release ______ that degrade extracellular matrix

A

Proteases such as elastave but also cathepsins, and metalloproteinases

97
Q

Where does the protease-antiprotease imbalance lead to irreversible airspace dilation in emphysema?

A

Distal to the terminal bronchioles

98
Q

Panacinar emphysema is due to what deficiency?

A

Alpha-1 antitrypsin deficiency

99
Q

Centriacinar emphysema is due to what?

A

Cigarette smoke

100
Q

INR equation

A

INR = (PT test/PT normal) ^ ISI (international sensitivity index)

101
Q

Prothrombin time tests which coagulation pathways

A

Extrinsic pathwa

102
Q

What factors are in the extrinsic coagulation pathway and tested in PT?

A

VII, II, V, X, and fibrinogen

103
Q

Vitamin K gamma carboxylation is required for ativation of what coagulation factors

A

II, VII, IX, X

104
Q

Does aspiring effect INR?

A

No, it causes prolonged bleeding time but does not increase INR

105
Q

Name the phospholipid in surfactant

A

Dipalmitoyl phosphatidylcholine

106
Q

Inferior epigastric artery is a branch of what artery?

A

External iliac artery

107
Q

What stain is used for malaria

A

Giemsa stain

108
Q

How is the measles rash described

A

Maculopapular
Starts on face and descends
Spares palms and feet

109
Q

What virus has a vesicular rash

A

Herpes/chicken pox

110
Q

Why is a HBV infection required for hepatitis D infection

A

HBV provides the surgace antigen for HDV envelope

111
Q

Why are patients not instructed to take nitrates at night?

A

Decreases tolerance

112
Q

How to calculate odds ratio>

A

Set up a 4 x 4 with the disease on x axis

AxD)/BxC