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Fundamentals 2 > Summative 2 Review > Flashcards

Summative 2 Review Flashcards

1
Q

Where do injuries that cause hemianopia occur?

A

either at (bitemporal hemianopia) or after the optic chiam

anything before optic chiasm is optic nerve problem

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2
Q

Signs of ischemic optic neuropathy

A

Acute vision loss in ONE eye

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3
Q

what is ischemic optic neuropathy?

A

stroke of the optic nerve

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4
Q

signs of retinal detachment

A

Monocular vision loss that occurs gradually

Described as a curtain being drawn down

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5
Q

Optic neuritis vs. ischemic optic neuropathy

A

ischemic optic neuropathy is sudden

optic neuritis is subacute

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6
Q

Occipital stroke vs. ischemic optic neuropathy

A

both occur quickly

occipital stroke happens in both eyes (homonymous hemianopsia)

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7
Q

Retinal artery occlusion vs. ischemic optic neuropathy

A

Both occur quickly and monocularly

retinal artery occlusion has a cherry red spot on macula

ischemic optic neuropathy has swollen optic nerve

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8
Q

Pituitary adenoma

A

compression of optic chiasm

subacute timing

results in bitemporal hemianopsia due to damage of optic chiasm

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9
Q

Th1 response normally targets …

A

intracellular pathogens

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10
Q

Th2 response normally targets …

A

extracellular pathogens (worms)

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11
Q

How do Th1 trigger an immune response?

A

they secrete IFN-y which activates macrophages

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12
Q

Th17 normally targets …

A

extracellular bacteria + fungi

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13
Q

What is the cell type that Th1 targets?

A

macrophages

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14
Q

What is the cell type that Th2 targets?

A

Eosinophils and mast cells

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15
Q

What is the cell type that Th17 targets?

A

neutrophils

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16
Q

Defining cytokines of Th1

A

IFN-y

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17
Q

Defining cytokines of Th2

A

IL-4, IL-5, IL-13

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18
Q

Defining cytokines of Th17

A

IL-17 and IL-22

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19
Q

What is the main function of CD8 cells?

A

works on intracellular pathogens

cytotoxic T-cell

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20
Q

What would defects in TLR-4 result in?

A

defective response to LPS and bacteria

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21
Q

What would defects in CD28 result in?

A

T-cells could not bind B7 on APCs

this would result in an ineffective immune response

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22
Q

STAT-3

A

important transcription factor in differentiation of Th17 cells

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23
Q

Glatiramer acetate

A

MS medication

prevents activation of autoreactive cells by mimicking the self-antigen

called a “myelin” mimic

T-cells will not recognize myelin, they will recognize the mimic

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24
Q

How do cyclosporin and FK506 work?

A

they inhibit calcineurin which then inhibits NFAT

without NFAT (transcription factor), IL-2 will not be produced and T-cell response will dampen

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25
Q

What is activation of NFAT dependent on?

A

calcium activation

you actually dephosphorylate NFAT to activate it

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26
Q

HLA DR2

A

important in the pathophysiology of MS

presents a putative myelin peptide to autoreactive T-cells

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27
Q

Why are MHC alleles important factors of autoimmune disease?

A

because they can present self-peptides needed to activate self-reactive T-cells

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28
Q

Which element does an MRI work on?

A

hydrogen

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29
Q

How does BOTOX work?

A

proteolysis of proteins required for acetylcholine release

prevents excitatory state

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30
Q

What happens when you go from sitting to standing?

A

BP drops

therefore, you want to increase HR, cardiac output and peripheral vascular resistance (all sympathetic stimulation)

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31
Q

Why do we give epinephrine to patient’s in anaphylactic shock?

A

stimulates B2-adrenergic receptors and subsequent bronchodilation

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32
Q

a1-adrenergic receptor bladder

A

constricts the urethra to prevent peeing

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33
Q

What 2 things induce peeing?

A

urethra relaxes

detrusor contracts

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34
Q

What channels play a role in neuronal repolarization?

A

both K+ and Na+ channels

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35
Q

nicotinic acetylcholine receptors

A

these can be adrenal/sweat glands or muscles

if at neuromusclar junction (NMJ), you know they are referring to the muscle receptors

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36
Q

Carbamazepine

A

antagonist of Na+ channels

this decreases firing of neurons and controls excitatory state

use in seizures

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37
Q

What is the function of CD4 cells?

A

work on extracellular pathogens

expressed by Helper T-cells and macrophages

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38
Q

Where is the LGN? What does it divide?

A

LGN is located on thalamus

before LGN = optic tract

after LGN = optic radiation

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39
Q

What creates contralateral inferior quadrantanopia?

A

lesion to Baum’s loop

Baum’s loop runs through parietal lobe (superiorly) and synapes on cuneus

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40
Q

What creates contralateral superior quadrantanopia?

A

lesion to Meyer’s loop

Meyer’s loop runs through temporal lobe (inferiorly) and synapes on lingual

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41
Q

Does Myelin decrease capacitance? What is capacitance?

A

Yes

Capacitance is the amount of charge needed to propagate a signal

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42
Q

absolute refractory period

A

Na+ is in inactive state and another potential cannot be fired under any circumstance

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43
Q

relative refractory period

A

period of hyperpolarization

K+ channels are slower to close

leads to increased outward flow of K+ and decreased cellular charge

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44
Q

Which way do sodium and potassium move in action potential?

A

salty bannana

Na+ moves inward (depolarizes the cell)

K+ moves outward (repolarizes the cell)

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45
Q

Inhibitory neurons and which toxin prevents them

A

GABA and glycine

C. tetani

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46
Q

excitatory neurons and which toxin prevents them

A

acetylcholine and glutamate

C. botulinum

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47
Q

What 2 signals do you need for T-cell activation?

A

TCR – MHC

CD28 (T-cells) – B7 (APC)

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48
Q

CTLA-4

A

dampens immune response by binding B7 on APC and blocking it

without B7 you have anergy

cancer upregulates CTLA-4

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49
Q

How do Th1 and Th2 antagonize eachother?

A

Th1 produces IFN-y to activate macrophages.

At the same time, Th2 produces IL-4 to inactive macrophages.

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50
Q

Which works more with intracellular pathogens Th1 or Th2?

A

Th1

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51
Q

Nicotinic receptors

A

acted on by acetylcholine

ex: sympathetic sweat glands, neural, somatic muscle

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52
Q

Adrenergic receptors

A

acted on by norepinephrine

exclusively part of the sympathetic ANS

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53
Q

Sympathetic nervous system origins and ganglia location

A

Origin: T1-L3

Ganglia: paravertebral sympathetic trunk

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54
Q

Parasympathetic nervous system origins and ganglia location

A

Origin: craniosacral distribution

Ganglia: located near target organs

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55
Q

-stigmine drugs

A

prevent acetylcholinerase and therefore lead to increased acetylcholine

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56
Q

B3-adrenergic receptor effect on bladder

A

relaxes the detrusor to prevent peeing

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57
Q

M3 muscarinic receptor effect on bladder

A

constricts detrusor to allow peeing

also relaxes the urethra to allow peeing

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58
Q

what is pyruvate an intermediate of?

A

intermediate of conversion of glucose to fat

also of the Cori Cycle

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59
Q

fructose 2,6 bisphosphate function + location

A

increase PFK-1 activity in glycolysis

only found in the liver!

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60
Q

hepatic reciprocal regulation

A

insulin activates F-2,6-BPG to increase glycolysis

in the absence of F-2,6-BPG, FBPase1 is turned on and glycolysis occurs

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61
Q

FBPase-1

A

stimulates hepatic gluconeogenesis

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62
Q

Signs of ketoacidosis

A

nausea / abdominal pain

fruity breath

history of T1DM

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63
Q

Ketoacidosis

A

normally insulin prevents ketogenesis in the liver

with T1DM, there is no insulin to stop the production of ketone bodies

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64
Q

What actions does metformin stimulate and inhibit

A

Stimulates hepatic glycolysis (want more glucose uptake)

Inhibits hepatic gluconeogenesis

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65
Q

What cues you in that something is a beta-lactam?

A

-lin suffix

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66
Q

How does T2DM occur?

A

insulin resistance occurs AND your body cannot produce enough insulin

pancreatic B-cells can not compensate for insulin resistance

not everyone with insulin resistance is diabetic

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67
Q

Two ways you can determine between T1 and T2 DM

A

use a C-peptide (if there is C-peptide, you have T2DM)

Islet cell antibodies mark T1DM (remember T1 is an automimmune disease)

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68
Q

What are 2 important components of glomerular filtration barrier?

A

podocytes

fenestrations

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69
Q

Why are cornea transplants successful?

A

the cornea is largely avascular so immune system cannot target

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70
Q

Function and location of cornea

A

clear layer in front of the aqueous humor that helps provide refractive power

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71
Q

Uvea components

A

iris, ciliary body and choroid

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72
Q

Function of the iris

A

regulate the amount of light reaching the retina

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73
Q

Function of ciliary body

A

make aqueous humor, provide multifocal ability to accomodate

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74
Q

Why do we need reading glasses?

A

the lens hardens and we can no longer accomodate

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75
Q

Where do cataract repairs happen?

A

at the lens

largely avascular

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76
Q

Ganglion layer of retina

A

lies closest to vitreous chamber and contains rods and cones

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77
Q

What is non-proliferative diabetic retinopathy associated with?

A

exudate = yellow spots on retina

exudate precipitates out due to macular edema

macular edema! sign of non-proliferative!

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78
Q

What is proliferative retinopathy associated with?

A

blood in vitreous chamber

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79
Q

Steps of proliferative DM retinopathy (4)

A

Leukocytes attach to small capillaries and capillaries close

Swelling of nerve layer causes the retina to not get enough blood

Retina produces VGEF in attempt to get new capillaries which leads to neovascularization

Neovascularization is not strong and these new vessels break and spill blood into the vitreous chamber

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80
Q

Overall formula of aerobic glycolysis

A

1 glucose => 2 pyruvate + 2 ATP + 2 NADH

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81
Q

Overall formula of anaerobic glycolysis

A

1 glucose => 2 lactate + 2 ATP

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82
Q

What activates PFK-1 in the muscles?

A

ATP/AMP ratio

more AMP stimulates glycolysis

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83
Q

3 starting products of gluconeogenesis

A

Glycerol from fatty acid oxidation

Pyruvate

Amino acids (alanine and glutamine)

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84
Q

Why is glycolysis considered anabolic in the liver?

A

2 pyruvate molecules are converted to acetyl-CoA which then leads to fatty acid synthesis

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85
Q

Which receptor has a lower affinity for glucose? Why?

A

GLUT2

only want to uptake glucose when there is a surplus in liver (storage), pancreatic B-cell (insulin secretion), and intestines (after eating)

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86
Q

General steps of insulin release

A

Glucose enters B-cell through GLUT2

Goes through glycolysis and ATP levels rise

K+ channels close and membrane depolarizes

Ca2+ channels open and insulin is released

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87
Q

Citric Acid Cycle

A

oxidizes acetyl-CoA to FADH2 and NADH to be used by the ETC

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88
Q

Cori Cycle

A

connects anaerobic glycolysis (muscle) and gluconeogenesis (liver)

pyruvate is the intermediate

lactate from anaerobic glycolysis is used as the starting product for gluconeogenesis which then make more glucose for glycolysis

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89
Q

4 hallmarks of metabolic syndrome

A

Obesity, insulin resistance, dyslipidemia, and HTN

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90
Q

Sulfonylurea + meglitinides

A

cause K+ channels to close and trigger insulin release

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91
Q

DPP-4

A

inhibit the breakdown of incretins (GIP / GLP-1)

incretins trigger insulin release

having incretins longer = more insulin release

92
Q

alpha-glucosidase

A

prevent glucose reuptake from the GI tract

can lead to GI side effects

93
Q

SGLT2 inhibitors

A

prevents renal recovery of glucose from filtrate

SGLT2 is a synporter for glucose with Na+

94
Q

Thiazolidinedoines

A

increase insulin sensitivity

associated with transcription via PPAR-y

95
Q

If dietary adjustments correct a problem with excess triglycerides, what does this indicate?

A

there was a problem with chylomicrons

96
Q

lipoprotein lipase

A

breaks down triglycerides in VLDL / chylomicron to deliver FA to tissues

cofactor is C-11

97
Q

What is required for maturation of VLDL into IDL / LDL?

A

offloading of triglycerides

need LPL to accomplish this (break down triglycerides)

98
Q

What 3 enzymes are used in reverse transport?

A

LCAT

CETP

SR-B1

99
Q

LCAT

A

makes cholesterol ester

allows cholesterol to be transported by HDL

100
Q

CETP

A

moves cholesterol ester from HDL to other lipoproteins

101
Q

SR-B1

A

directly transports cholesterol ester to tissue/ liver

see a lot in adrenal gland / sex organs where cholesterol is needed to make hormones

102
Q

What is mutated in familial hypercholesterolemia?

A

LDL receptor

103
Q

Incomplete dominance in familial hypercholesterolemia

A

heterzygotes have milder disease than heterozygotes

autosomal dominant disease

104
Q

Which type of muscle has peripheral nuclei?

A

skeletal muscle

105
Q

Which type of muscle does not have striations?

A

smooth muscle

106
Q

What does collagen often look like?

A

often looks wavy

107
Q

What is an irreversible change in cell damage?

A

mitochondrial fragmentation

108
Q

If someone has jaundice, what labs should you check? Why not AST?

A

check bilirubin

AST is not as specific

109
Q

Why are both PTT and closure time affected by vWD?

A

closure time is affected due to lack of vWF / low platelet aggregation

PTT is affected by vWF’s dual activity to stabilize Factor VIII in the intrinsic pathway

110
Q

Where do thrombus exclusively occur?

A

they exclusively occur in the vascular system

this is different from blood clots which can occur anywhere

111
Q

Where are lines of Zahn?

A

only found in thrombi

not seen in blood clots

112
Q

List all the Vitamin K dependent factors

A

Protein C + S

II, VII, IX and X

113
Q

What type of necrosis forms pus?

A

liquefactive necrosis

114
Q

After an MI, what type of necrosis do cardiac myocytes undergo?

A

coagulative necrosis

115
Q

After an MI, what type of necrosis do cardiac vessels undergo?

A

fibrinoid necrosis

116
Q

What are 3 classic signs of apoptosis?

A

Shrunken

Fragmented nucleus

Apoptotic bodies

117
Q

Bcl-2

A

inhibitor of the apoptotic pathway

Bcl-2 inhibits the recruitment and oligomerization of Bax

Also prevents the release of cytochrome C

118
Q

Bad protein

A

Bad protein normally acts to inhibit the action of Bcl2, allowing more apoptosis

119
Q

Which caspase is unique to intrinsic apoptosis?

A

caspase 9

120
Q

Which caspase is unique to extrinsic apoptosis?

A

caspase 8

121
Q

Where are death ligands found?

A

in the extrinsic apoptosis pathways

122
Q

Where is cytochrome C found?

A

in the intrinsic pathway of apoptosis

123
Q

What is the FAS ligand associated with?

A

the extrinsic pathway of apoptosis

124
Q

How do plaques form?

A

LDL particles are transcytosed acrossed the endothelium and accumulate in the subendothelium

in the subendothelium, the LDL particles are converted into cholesterol crystals

cholesterol crystals (form within the intima) are phagocytosed by macrophages

macrophages stimulate recruitment of T-cells and IFN-y

125
Q

What is characteristic of unstable plaque? What are the 2 parts of a plaque?

A

2 parts: fibrous cap + necrotic center

Unstable: thin fibrous cap

126
Q

Apo A-1

A

found on HDL

activates LCAT

127
Q

Apo B-48

A

found on chylomicrons

128
Q

What binds to the LDL receptor?

A

C-terminal of Apo B-100

129
Q

What binds to the remnant receptor?

A

Apo E

130
Q

Xanthuma

A

cutaneous deposit of cholesterol that can be seen in familial HLD

131
Q

PCSK-9 inhibitors

A

prevent degradation of LDL receptors

more LDL receptors are expressed which lowers serum cholesterol levels

132
Q

List the order that cardiac markers peak after an MI

A

CK-MB

Troponin I (24 hours)

AST (2 days)

LDH (3 days)

133
Q

List the 3 receptors platelets express and what they bind to:

A

Fibrinogen - GpIIb/a
vWF - Gp1B
collagen - a2B1

134
Q

What do activated platelets express?

A

phosphatidylserine

135
Q

Dense granules of platelets contain …

A

ADP and Ca2+

136
Q

Alpha granules of platelets contain:

A

vWF

137
Q

What factors does thrombin activate (positive feedback)?

A

8, 5 , 11, and 13

138
Q

t-Pa

A

converts plasminogen to plasmin to activate fibrinolysis

139
Q

Virchow triad

A

endothelial injury, stasis in blood flow, hypercoagulable state

140
Q

Aspirin

A

NSAID

binds COX1 to prevent Thromboxane A

141
Q

Thromboxane A

A

vasoconstrictor that promotes clotting

142
Q

Heparin

A

combines with antithrombin to inhibit activity of thrombin and factor X

143
Q

Clopidigrel

A

antiplatelet that blocks ADP receptors to inhibit platelet activation

144
Q

Rivaroxaban

A

anticoagulation that directly inhibits factor X (x is in name)

145
Q

Warfarin

A

anticoagulation that inhibits vitamin K-dependent clotting factor synthesis

146
Q

What type of necrosis creates abscesses? How about granulomas?

A

abscesses: liquefactive necrosis

granulomas: caseous necrosis

147
Q

How does necrosis stain?

A

basophilic due to accumulation of calcium lipid salts due to saponification

148
Q

Does atherosclerosis occur in veins?

A

No, only in arteries

149
Q

What are some signals of apoptosis?

A

phosphatidylserine

ADP/UTP

150
Q

Difference between scar tissue and granulation tissue

A

Scar tissue is rich in collagen with little capillaries

granulation tissue has many capillaries

151
Q

When does coagulative necrosis turn into scarring following MI?

A

coagulative necrosis comes first 1-3 days post MI

granulation tissue occurs 10+ days later

152
Q

What is scar tissue abundunant in?

A

myofibroblasts and TGF-beta

153
Q

What does TGF-beta inhibit?

A

inflammation

also inhibits keratinocytes

154
Q

What is hypertrophic scar mostly composed of?

A

type III collagen

155
Q

What is keloid scar mostly composed of?

A

type I and type III collagens

156
Q

How long are platelets stable for?

A

5 days at room temperature

they have the highest rate of infection since they have to be kept at room temp

157
Q

Who is RhoGam given to?

A

all Rh- moms when pregnant

158
Q

Histamine

A

amine that is an early mediator of acute inflammation

leads to vasodilation

159
Q

Serotonin

A

amine that is an early mediator of acute inflammation

vasoconstrictor

160
Q

List the 3 basic steps of leukocyte recruitment and the proteins associated with them

A

Rolling - selectins

Firm adhesion - integrins

Migration - PECAM

161
Q

What leads to formation of an exudate?

A

contraction of endothelial cells which leads to increased vascular permeability

162
Q

What leads to formation of transudate?

A

changes in hydrostatic or oncotic pressure

163
Q

How does Factor V leiden prolong the bleeding time?

A

It only has 2 binding sites so it is activated for longer

164
Q

If you have an arterial clot, what type of clot is it?

A

a white clot

165
Q

If both PT and PTT are prolonged, what are you thinking about?

A

problem with fibrinogen or vitamin K production

166
Q

Difference between ITP and vWD?

A

vWD has normal platelet count

167
Q

If you have pancytopenia, what should you be worried about / what do you need to do?

A

worried about leukemia

need to check a bone marrow biopsy

168
Q

What 3 organs does GvHD affect?

A

skin, intestine and liver

169
Q

What risk is increased and which risk is decreased with syngeneic transplant?

A

risk of GvHD is decreased

risk of relapse is increased

170
Q

How can you tell the difference in symptoms between extravascular and intravascular hemolysis?

A

in extravascular hemolysis, there will be no mention of dark urine

in extravascular hemolysis, there is also hepatosplenomegaly that you do not see in intravascular

171
Q

Hypersegmented neutrophils indicate ….

A

vitamin B12 or folate deficiency

can differentiate by checking neuro symptoms

172
Q

Laminin

A

component of basement membrane that you want to dowregulate during epidermis migration under eschar

173
Q

When does fibrosis vs. scarring occur

A

Fibrosis = chronic inflammation

Scarring = acute injury

174
Q

Primary vs. secondary provisional matrix

A

primary = formation of fibrin clot

secondary = granulation tissue

175
Q

Which layer of skin has tight junctions?

A

stratum granulosum

176
Q

What type of tissue makes up dermis?

A

dense irregular connective tissue

177
Q

Dystrophic vs. metastatic calcification

A

Dystrophic is fairly normal Ca2+ deposition on vessel (stains basophilic)

Metastatic is Ca2+ deposition with abnormal growth

178
Q

Sclerosis

A

excess deposit of extracellular matrix

179
Q

Forward typing / direct Coombs

A

patient’s RBCs are tested against commercial antibody

180
Q

Reverse typing / indirect Coombs

A

patient’s serum are tested against known antigens

181
Q

Why does acute hemolytic transfusion reaction occur?

A

mismatched blood triggers IgG antibody response

incorrect blood type given

182
Q

2 forms of prep for stem cell transplant

A

myeloablative

immunosuppresants

183
Q

2 general causes of aplastic anemia

A

DNA damage (treat with transplant)

autoimmune disease (treat with immunosuppresion)

184
Q

GvHD vs. Graft Failure

A

GvHD is when donor-derived cells attack the patient’s self-cells

Graft failure is when body attacks the donor cells

185
Q

What is the cause of acute spherocytes?

A

autoimmune hemolytic anemia (can be intracellular or extracellular)

186
Q

5 hypoproliferative anemias

A

anemia of inflammation, B12+folate deficiency, lead toxicity, aplastic anemia, iron deficiency anemia

these will all have a low retic

187
Q

Anemia of inflammation vs. iron def. anemia

A

anemia of inflammation will have low TIBC in addition to low iron

188
Q

When does megaloblastic anemia occur?

A

during vitamin B12 def.

189
Q

Aplastic anemia vs. ITP

A

ITP only platelet count is low

aplastic anemia there is pancytopenia

190
Q

What does the suffix -cytosis mean?

A

high count

ex: leukocytosis = high WBC

191
Q

Can you do a platelet transfusion to cure ITP?

A

No, the antibodies will continue to degrade the new platelets

need to do immunosuppresion or splenectomy to treat ITP

192
Q

How to tell the difference between primary and secondary hemostasis?

A

primary: mucosal bleeding

secondary: deep / joint bleeding

193
Q

What should you check in secondary hemostasis?

A

PT / PTT and mixing studies

194
Q

What should you check in primary hemostasis?

A

vWF and ITP

(platelets normal in vWF)

195
Q

What type of cells are seen in G6PD?

A

Heinz bodies and bite cells

196
Q

When are schistocytes seen?

A

HUS

197
Q

When is basophilic stipling seen?

A

iron and lead toxicity

198
Q

What type of cell has bilobed nucleus?

A

eosinophil

199
Q

What type of cell has a large, sometimes odd-shaped nucleus?

A

monocyte

200
Q

How do neutrophils appear on smear?

A

multilobed

201
Q

When is agglutination seen?

A

autoimmune hemolytic anemia

202
Q

C. diff route of transmission

A

fecal oral transmission

hand washing prevents transmission

203
Q

What types of organisms does endogenous acquisition normally occur with?

A

gram negative bacteria

C. Diff

204
Q

What can the non-treponemal syphilis screen show?

A

can distinguish active (high titer) from old/cured infection

RPR is non-treponemal syphilis screen

205
Q

What is an example of a treponemal syphilis screen? What can this tell you?

A

IgM/IgG screen

Tells you that the patient was infected at some point. Cannot distinguish between active and cured infection

206
Q

Can non-treponemal (RPR) testing tell you primary vs. secondary syphilis?

A

no!

207
Q

What is the preferred first line treatment for HIV?

A

integrase inhibitor

nucleoside reverse transcriptase inhibitor (NRTI)

208
Q

What leads to chronic inflammation in HIV?

A

dysbiosis (imbalance in gut) and microbial translocation due to permanent loss of Gut Associated Lymphoid Tissue

209
Q

Signs of candida

A

yeast cells with pseudohyphae

budding yeast

white patches in mouth (if oral thrush)

210
Q

What do you use to treat HCV?

A

NS5B polymerase ingibitors

211
Q

What do you use to treat influenza?

A

neuraminidase inhibitors

212
Q

What is the only mold we have learned?

A

aspergillus

213
Q

What do we use to treat cryptococcus?

A

amphotericin + flucytosine

214
Q

Patients on anti-TNF inhibitors / immunosuppressants are at risk for what infection?

A

TB

need TNF-a to form granuloma in order to control the infection

215
Q

How does TB transmission normally occur?

A

airborne

aerosol droplet typically by cough from someone with active TV

216
Q

What is more specific TST or IGRA?

A

IGRA since this can tell the difference between old infection and BCG vaccine which the TST (PPD) test cannot

217
Q

Rifampin MOA

A

inhibition of DNA-dependent RNA polymerase

218
Q

Ethambutol MOA

A

interferes with arabinosyl transferase to prevent polymerization of cell wall

219
Q

Isoniazid MOA

A

inhibits mycolic acid synthesis pathways

220
Q

Why do plasma cells have large cytoplasm?

A

need lots of ER to generate antibodies

221
Q

How can you describe N. gonorrhea ?

A

gram negative diplococci

222
Q

Cervical lymphadenopathy in toddlers indicates …

A

MAC

223
Q

3 genes of HIV and what each encodes

A

Env gene: gp120 and gp41

Gag gene: p24 core antigen and p17

Pol gene: reverse transcriptase, integrase and protease

224
Q

Testing order for HIV

A

fourth generation screening

if positive, HIV 1/2 differentiation assay

then, NAAT testing

225
Q

Difference between NNRTI and NRTI

A

NRTI = DNA analog that competes with the host DNA to block reverse transcriptase (actually DNA)

NNRTI = non-competitive inhibitor of reverse transcriptase that binds directly to reverse transcriptase

226
Q

What is another example of a budding yeast ?

A

cryptococcus (also candida)

227
Q

Sodium potassium pump

A

works against concentration gradient

3 Na+ out and 2 K+ in

Fundamentals 2 (30 decks)

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