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Pharm Dr. T > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Thrombogenesis

A

The formation of thrombi

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2
Q

Describe how fibrin and platelets are held together

A

“a fibrin clot holds as kind of a net that traps platelets” (RBCs too)

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3
Q

What is substratum? what does it have?

A

connective tissue
collagen and VBF (von Willebrand)

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4
Q

What happens when collagens are exposed?

A

They interact with glycoproteins that are on the platelets cell surface to set up platelet aggregations and the clotting cascade

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5
Q

Describe the two types of thrombi

A

Red- occur in slow moving vessels (like veins) and have more RBCs trapped in them, long tail
White- No RBCs just fibrin clot and platelets in high pressure areas

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6
Q

What is a major issue of thromboembolism?

A

Downstream ischemia

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7
Q

Important chemical for vasoconstriction

A

serotonin

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8
Q

Another term for platelet plugs

A

thrombocytes

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9
Q

T/F: Thrombocytes are cells

A

False; they are components that broke off a larger cell called the megakarocyte

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10
Q

Where are megakarocytes found?

A

bone marrow

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11
Q

How does initial platelet aggregation lead to additional platelets being activated?

A

Thrombocytes stick to the surface of injury and they degranulate, activating additional platelets

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12
Q

What is coagulation

A

The formation of the fibrin clot

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13
Q

Fibrinolysis

A

breakdown of a clot

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14
Q

What do platelets secrete? What does this encourage?

A

serotonin, ADP, and thromboxane A2
formation of a thrombocyte clot

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15
Q

Blood vessel lining is composed of _______ which normally produce ________ also known as ______

A

endothelial cells, prostaglandin I2, prostacyclin

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16
Q

What is the role of prostacyclin?

A

inhibits platelet aggregation

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17
Q

What are two MOA of NSAIDS?

A

Inhibit prostaglandin synthesis
Inhibit thromboxane A2

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18
Q

Difference between aspirin and NSAIDs?

A

Aspirin inhibits platelet aggregation and NSAIDs encourage it

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19
Q

Where does collagen bind to platelets?
von Willebrand?

A
  1. Glycoprotein 1A receptor
  2. Glycoprotein 1B
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20
Q

Other than causing smooth muscle contraction, what is another role of 5HT?

A

Activate platelets once bound to receptors

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21
Q

How are fibrin molecules produced?

A

Coagulation cascade

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22
Q

Where the intrinsic and extrinsic pathway meet in the coagulation cascade? How does it start?

A

Common pathway
Factor 10 is activated

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23
Q

What is the role of Factor X?

A

Factor X activates prothrombin to its active form- thrombin

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24
Q

What are the roles of thrombin (4)? which is most important?

A
  1. Increase production of more thrombin
  2. Activate platelets
  3. Activate Factor V
  4. Convert fibrinogen into fibrin *
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25
Q

What does fibrin form?

A

A mesh network to cover the platelets and link them together so theyre trapped at the area of injury, preventing us from bleeding out

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26
Q

How is the extrinsic pathway activated?

A

When tissue damage exposes the protein tissue factor

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27
Q

How is the intrinsic pathway activated?

A

When the endothelial lining inside vessels are damaged

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28
Q

Extrinsic pathway:
Tissue factor activates ________ which directly activates ______ and now this is the beginning of the _________ pathway

A

factor VII
factor X
common

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29
Q

Intrinsic pathway:
Damaged endothelial cell lining activates _______ which activates _______ which activates _______

A

Factor XII
Factor XI
Factor IX

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30
Q

What happens once factor X is activated?

A

Prothrombin is converted to fibrin and the fibrin is cross linked through the additional action of factor 13

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31
Q

Another name for prothrombin

A

Factor II

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32
Q

Which proclotting factors does thrombin activate? (5)

A

Factor XIII
Factor V
Factor VIII
Factor XI
Protein C

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33
Q

T/F: factor VIII isn’t needed to convert factor X to factor XA

A

True; but its helpful

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34
Q

Hemophilia typeA patients have what deficiency?

A

Factor VIII

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35
Q

Activated protein C inhibits

A

Factor V and VIII

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36
Q

Where are all of the factors produced?

A

in the liver

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37
Q

Prothrombin has effects on ____

A

factor 10

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38
Q

What is our primary activator?

A

thrombin

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39
Q

DVT starts from 3 factors called _____

A

Virchow’s Triad

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40
Q

What are the components of Virchow’s Triad?

A
  1. Decreased blood flow (stasis)
  2. Endothelial injury
  3. Hypercoagulability
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41
Q

How do veins push blood?

A

Skeletal muscle contraction

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42
Q

White thrombi occur due to ______ due to damage or ______

A

abnormal endothelium
plaque

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43
Q

Protein C and Protein S are both inhibitory to

A

Factor VIII

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44
Q

What is activated protein C resistance?

A

When youre producing a normal amount of protein C that’s being activated, but the factors that are produced are resistant to that protein C.

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45
Q

Sickle cell anemia and activated protein C resistance are both __________ states

A

hypercoagulable

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46
Q

It is recommended to do ________ anytime flying more than _______ hours to prevent ______

A

leg exercises
2-3
DVT

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47
Q

What is DIC?

A

Disseminated coagulation; over coagulation response where clots are forming all over the body and you’re using up all the clotting factors and the risk of bleeding out is significantly higher

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48
Q

What percentage of DIC patient’s die?

A

10-50%

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49
Q

Causes of DIC? (4)

A
  1. Bacterial sepsis usually due to gram (-) bacteria because of the endotoxin it produces
  2. Placental abruption
  3. Cancer
  4. Massive tissue injury
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50
Q

Treatment for DIC?

A

Give platelets, plasma, treat bacteria if applicable, deliver the baby if applicable,

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51
Q

What do protease inhibitors do? Where are they produced?

A

Inactivate the coagulation proteins
liver

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52
Q

Name the 4 protease inhibitors

A

α1-antiprotease
α2-macroglobulin
α2-antiplasmin
Antithrombin

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53
Q

Inherited DVT risk factors (5)

A

Antithrombin III deficiency
Protein C deficiency
Protein S deficiency
Sickle cell anemia
Activated protein C resistance

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54
Q

Acquired DVT risk factors

A

Bedridden
Surgery/trauma
Obesity
Estrogen use
Malignancies
Chronic venous insufficiency

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55
Q

What is anti thrombin’s role?

A

to directly inhibit thrombin

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56
Q

Plasmin is producted by it’s inactive form called ______ through a process known as ________

A

plasminogen
tissue plasminogen activator

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57
Q

What are the two main roles of plasmin?

A
  1. Breaks down fibrin into its fibrin split products
  2. Breaks down fibrinogen
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58
Q

What can be used to detect fibrin split products?

A

D dimer test

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59
Q

T/F: Where there is a thrombus formation, fibrinogen is degrading all over the body

A

No; it is localized

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60
Q

1 Endogenous substance that breaks down clots and 1 exogenous

A

urokinase and streptokinase

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61
Q

T/F: urokinases can be given exogenously

A

true

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62
Q

Combined streptokinase and its activator are called?

A

anistreplase

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63
Q

What may be given to post op patients that inhibits the plasminogen to plasmin switch?

A

aminocaproic acid
transischemic acid
TXA

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64
Q

What are the four classes of coagulation modified drugs?

A
  1. Anticoagulants
  2. Anti-platelets
  3. Thrombolytics
  4. Hemostatic/Antifibroinic
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65
Q

Examples of indirect thrombin inhibitors? What do they target?

A

heparin, low molecular weight heparin, fondaparinux
Factor Xa- they inactivate the protein that activates thrombin

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66
Q

Examples of oral anticoagulant? How does it work?

A

Warfarin; decreases the synthesis of clotting factor in the liver

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67
Q

Compare unfractioned hepain, low molecular weight hepain and fondaparinux

A
  1. Unfractioned heparin has many different sizes of compound from the intestinal lining of pig
  2. Low molecular weight heparin is more purified and more specific for antithrombin Xa, but less effective
  3. Fondaparinux is a pentasaccharide complex that is even less effective than heparin because it targets antithrombin III
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68
Q

Describe how antithrombin works?

A

Antithrombin inactivates thrombin by binding and activating antithrombin through conformational change and increasing the activity 1000 fold

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69
Q

T/F: Low molecular weight heparin is more specific for thrombin

A

False; its more specific for factor Xa, but less effective in general

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70
Q

Give examples of LMW heparin (3)

A

Enoxaparin (Lovenox)
Dalteparin (Fragmin)
Tinzaparin (Innohep)

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71
Q

What is the biggest toxicity with heparin?

A

we can induce a bleeding response because essentially, we’re inactivating the coagulation cascade by inactivating factor X

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72
Q

What needs to be monitored for heparin?

A

aPTT (activated partial thromboplastin time)
PT (prothrombin time)

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73
Q

Which types of patients are more prone to hemorrhage with heparin?

A

elderly women, patients with renal failure

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74
Q

Problem associated with unfractioned/high molecular weight heparin? why does it happen? typical onset?

A
  1. heparin induced thrombocytopenia
  2. the body makes antibodies against the heparin targeting thrombocytes
  3. 7-10 days after the patient is given heparin
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75
Q

What does the PT test look at?

A

Extrinsic and common pathway; how long does it take to clot

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76
Q

?

A

extrinsic pathway, common pathway, and tissue factor (what’s exposed during tissue damage)

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77
Q

What is INR? What is a normal INR? What level do we want for patients on warfarin?

A
  1. international normalized ratio; compares PT of patient to a normal PT
  2. 1
  3. 2-3
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78
Q

What does the aPTT test look at? What is the usual level?

A
  1. intrinisic pathway and phospholipids which are found in damaged endothelium
  2. 35-45 seconds
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79
Q

What is the reversal for heparin? How does it work?

A

protamine sulfate
it is negatively charged and it binds to positively charged heparin , inactivating it

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80
Q

What is the issue with excess protamine sulfate?

A

it can be an anticoagulant

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81
Q

T/F: Protamine sulfate is the reversal for unfractioned, lmw heparin and fondaparinux

A

False; does not work with fondaparinux

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82
Q

Contraindications for heparin

A

hemophilia, thrombocytopenia, severe hypertension, ICH, infective endocarditis, TB, GI ulcers, advanced hepatic disease

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83
Q

What is the MOA of fondeaparinux? is it endogenous or exogenous?

A

activates antithrombin
synthetic; produced in a lab

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84
Q

Why is fondaparinux not as effective as unfractioned and lmw heparin? Why would it be used?

A

It has no interaction with thrombin;
for patients predisposed to HIT

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85
Q

What is Hirudin?

A

an early direct thrombin inhibitor from leech saliva that keeps clots from forming

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86
Q

Recombinant forms of Hirudin?

A

Lepirudun and Bivalirudin; same compound but produced in the lab vs from leeches

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87
Q

Direct thrombin inhibitors that bind to thrombin active sites (3)

A

Agatroban, Melegatran and Dabigatran

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88
Q

How warfarin was named

A

Wisconsin Alumni Research Foundation

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89
Q

What is the oral bioavailability of warfarin?

A

100%

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90
Q

Due to tight protein binding, what is important in patients when giving warfain?

A

protein and albumin levels

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91
Q

MOA of warfarin

A

blocks the gamma carboxylation of glutamate residues on 4 different Vit K dependent clotting factors

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92
Q

Which 4 clotting factors are produced through gamma carboxylation?

A

2,7,9,10

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93
Q

Describe how a clotting factor becomes carboxylated

A

A carboxyl group is attached to the glutamate residue due to vitamin K

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94
Q

What is the active form of Vitamin K? what does it become after carboxylation?

A

hydroquinone
epoxide form of Vitamin K

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95
Q

The epoxide form of Vitamin K needs to be ________ by the enzyme __________because the clotting proteins are constantly being produced in ______

A

recycled
vitamin k reductase
liver

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96
Q

Describe the two reduction systems of Vitamin K

A

Vit K has to go from the epoxide to the quinone form and from the quinone to the hydroquinone form. And those two reductions are accomplished through vitamin K reductase enzyme

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97
Q

Which enzyme is a target of warfain?

A

Vitamin K reductase

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98
Q

What is the delay of onset of action for warfarin? why?

A

8-12 hours
the clotting factors are already circulating in the blood

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99
Q

Toxicity of warfarin

A

hemmorhagic disorder, fetus birth defects, cutaneous necrosis

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100
Q

Why is there such a wide variety in therapeutic doses for patients on warfarin?

A

it is metabolized differently in different people due to genetic mutations

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101
Q

What is the reversal for warfarin?

A

Stop the drug, give large doses of vitamin K, FFP, or specifically target factors like factor 9

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102
Q

What is a benefit of factor Xa inhibitors?

A

More specific, so have less problems with bleeding out

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103
Q

What is the negative aspect of factor Xa inhibitors?

A

There is no reversal

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104
Q

TPA, urokinase, and streptokinase are examples of

A

fibrinolytics

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105
Q

MOA of fibrinolytics

A

rapidly lyse thrombi and catalyze the formation of serine protease plasmin

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106
Q

T/F: TPA is produced recombinantly

A

True; however it is also produced in the body by the tissue thats damaged

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107
Q

Example of a recombinant TPA? MOA?

A

alteplase; activates plasminogen that is bound to fibrin and combines the fibrinolysis to just that thrombosis

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108
Q

Most common OTC anti-platelet? other uses?

A

aspirin; pain and inflammation

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109
Q

What is the target for aspirin?

A

Cox 1 and thromboxane A2

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110
Q

What are produced by arachadonic acid? These are all pro __________

A

thromboxane, leukotrienes, protaglandins
inflammatory

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111
Q

Why does it take time to see an aspirin effect?

A

Platelets circulate for about 9 days

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112
Q

How long should one stop aspirin before surgery?

A

one week

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113
Q

How do clopidogrel and ticlopidine work?

A

by inhibiting ADP receptors
(ADP is released by platelets that activates more platelets)

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114
Q

What are the 3 soluble mediators in the coagulation cascade? How do they activate more platelets?

A

ADP
thromboxane A2
Serotonin 5HT
There are receptors on the platelets for each

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115
Q

What happens after ADP, thromboxane A2 and 5HT bind to receptors on platelets?

A

The platelet becomes activated to degranulate and release additional ADP, TA2, and 5HT

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116
Q

Essay question:
Describe platelet aggregation

A

The endothelial cells which make up the blood vessel lining normally produce protaglandin I2 which inhibits platelet aggregation. Damage to the cell lining exposes collagen and von Willebrand factor. The collagen binds to platelets at the glycoprotein 1A receptor and VWB binds to glygoprotein 1B. Both set up signaling to activates soluble mediators (ADP, TA2, 5HT) which bind to platelets and activate additional platelets though degranulation

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117
Q

Essay question: Describe the coagulation cascade

A
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118
Q

T/F: Aspirin reduces ischemic events 8.7% more than plavix

A

False; Plavix does

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119
Q

What is a drug eluting stent?

A

A metal stent that releases a drug such as plavix to prevent platelet aggregation

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120
Q

What mab is used to prevent platelet aggregation? Where does it work?

A

Abciximab; targets 2B and 3A glycoproteins.

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121
Q

Vitamin K is ________ soluble and can be found in _______

A

fat
leafy green vegetables

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122
Q

What produces endogenous Vit K? Where is it transmitted?

A

gut bacteria
the liver

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123
Q

What clotting factors are affected by Vitamin K? Which is primary?

A

prothrombin*
Factor 7,9,10

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124
Q

What increases factor VIII activity? What disease processes is it used for?

A

Desmopressin acetate
mild hemophilia A, von Willebrand disease

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125
Q

When would plasma fractions be indicated? Are they naturally derived or recombant?

A
  1. different types of hemophilia, antitrypsin deficiency
  2. Both
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126
Q

MOA of Aminocaproic acid

A

Competitively inhibits plasminogen activation

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127
Q

Clinical indications for aminocaproic acid? (4)

A
  1. Adjuctive hemophilia therapy
  2. Bleeding from fibrinolytic therapy
  3. Intracranial aneurysms
  4. Surgical bleeding
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128
Q

MOA and Clinical indications for tranexamic acid (TXA)?

A
  1. bleeding from trauma
  2. heavy menstrual bleeding
  3. postpartum bleeding
  4. epitaxis

It is an antifibrinolytic

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129
Q

Describe an endocrine disorder

A

Involves tissues that release secretions into the bloodstream

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130
Q

Describe exocrine organs

A

Release secretions onto a surface

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131
Q

Is the pancreas an endocrine or exocrine organ?

A

Both

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132
Q

What is the exocrine function of the pancreas?

A

Release digestive enzymes into the duodenum to help with protein, lipid and cab digestion

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133
Q

T/F: The endocrine portion of the pancreas is the largest portion

A

False

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134
Q

What are the pancreatic cells called? how many cell types are there? What are the names?

A

pancreatic islets
5
alpha(A), beta (B), Delta (D), G, F (PP)

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135
Q

What are the two most common Islet of langerhans cells? Which is most associated with pancreatic function? Why?

A

Alpha and beta
Beta; they release insulin

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136
Q

What do beta cells secrete?

A

insulin, c-peptide, proinsulin, amylin

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137
Q

What do alpha cells secrete?

A

Glucagon, proglucagon

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138
Q

What is the function of amylin?

A

suppresses the production of glucagon

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139
Q

What is released when out blood glucose gets too low?

A

Glucagon

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140
Q

What percent of islet mass is in the beta cell?

A

75

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141
Q

What do D pancreatic cells secrete? What is the function of this compound? When is it released?

A
  1. somatostatin;
  2. bocks the release of both insulin and somatostatin
  3. Right after we eat to prevent an insulin spike
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142
Q

What would happen if we did not release somatostatin after eating?

A

Alot of our glucose would end up in the liver, because it tries to draw in as much as possible and we wouldn’t get as much to our peripheral cells
it basicallly allows the glucose in our bloodstream to circulate throughout the body

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143
Q

Essay question
Describe the process of insulin release and binding

A

Insulin is released from the pancreatic cells and binds to insulin receptors. The receptors are tyrosine kinases that dimerize and set up a series of signals within the cell including translocating glucose transporters from the cytoplasm to the surface. Glucose in the bloodstream is now able to be transported used in cells

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144
Q

What is a normal blood glucose level?

A

90 mg/dl

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145
Q

How does the liver store glucose?

A

As a long chain of glucose called glycogen that can be cleaved off if needed for glucose

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146
Q

Glucagon receptors are ________ and cause the breakdown of ________ in the liver in a process known as ____________.

A

GPCRs
glycogen
glycogenesis

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147
Q

What is an insulin secretagogue? What is an example?

A

something that causes the secretion of insulin; glucose

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148
Q

Something that causes a decrease in glucose levels is considered a ________

A

Glucagon secretagogue

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149
Q

How does our body respond when blood sugar is 60-70 mg/dl?

A

Release glucagon

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150
Q

T/F: We have zero insulin release in between meals

A

False

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151
Q

What is the renal threshold? What is the level?

A

The point where glucose is not reabsorbed into the PCT by SGLT
160 mg/dl

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152
Q

What are the signs and symptoms of diabetes insipidus?

A

polyurina, polydipsia, polyphagia

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153
Q

Mellitus means

A

sugar

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154
Q

How many types of diabetes mellitus are there? Name/briefly describe them

A

four
DM type I- insulin dependent
DM type II- non insulin dependent
DM type III- anything that causes elevated glucose levels (usually temporary)
DM type IV- gestational diabetes

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155
Q

Describe type I DM. What causes it?

A
  1. Destruction of the pancreatic islet cells; insulin dependent diabetes. The patient has 20% or less of insulin
  2. Most common is immune but oftentimes is idiopathic
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156
Q

Clinical manifestations of DM type I

A

hyperglycemia, polydipsia, polyuria, polyphagia, weight loss, fatigue

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157
Q

What causes and describe diabetic ketoacidosis. What is the by product?

A

Glucose cannot be absorbed because there is no insulin and the body switches over to fatty acid metabolism. Keto acids will be in the bloodstream

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158
Q

What is the goal for type II DM?

A

control with diet and oral medications to avoid needing injectable insulin

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159
Q

Why is DM II considered a metabolic syndrome?

A

It is associated with things like obesity, high BP. cardiovascular disease

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160
Q

T/F: Type II diabetics can convert to type I diabetics

A

true

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161
Q

Generally, what is the cause for DM type II?

A

chronically high glucose levels in the body cause the body cells to stop responding to insulin and stop producing receptors for it

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162
Q

First medication for type II DM is usually

A

metformin

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163
Q

T/F: During Nonketotic hyperosmolar syndrome, there are deficient amounts of insulin in the body?

A

False; excess insulin

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164
Q

Severe effect wtih ketotic hyperosmolar coma? why?

A

Dehydration; the excess sugar will cause an increase in osmolarity, causing excess urination

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165
Q

Clinical manefistations of Hyperosmolar Ketonic Coma

A

infection, vision problems, neuropathy

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166
Q

Desribe glycosylation? Which cells are seen most commonly with this?

A

Protein throughout the body are randomly being glycosylated, or glucose molecules are attaching to them because the levels are so high;
Hemoglobin A

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167
Q

What is a Hgb A1c? What is normal? What is the goal for diabetics?

A

The percent of hemoglobin glycosylated. Nondiabetics have levels around 4%. Goal is below 7% for diabetics

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168
Q

What is the cause of issues like diabetic blindess and neuropathy?

A

If glucose is too high, it gets converted into fructose and sorbitol which is a sugar alcohol. It enters the cell as glucose, gets converted into sorbitol, increasing osmolality, but it cannot exit the cell. Eventually the cell bursts

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169
Q

Disease states associated with diabetes

A

retinopathy, blindess, diabetic neuropathy, kidney disease

170
Q

Special indications for diabetic neuropathy

A

Take special care of the feet, because they might have an injury and not feel it which can lead to chronic infection and amputation

171
Q

What is the cause of type IV diabetes

A

pregnancy hormones cause insulin resistance, and they end up with a lot more glucose in the bloodstream

172
Q

Describe a glucose tolerance test

A

After fasting overnight, the patient is given a very large amount of glucose and 1-3 hours later, their glucose levels are checked

173
Q

Compare POC to HgbA1c?

A

a moment in time vs over the past 90-120 days

174
Q

Describe the molecular structure of insulin

A

a peptide hormone (long string of amino acids)

175
Q

T/F: Insulin is a protein. Why or why not?

A

False; even though proteins are made up of long string of amino acids, proteins have a primary, secondary and tertiary structure, or a three dimensional structure. This molecule does not have a three dimensional structure, therefore referred to as a peptide instead of a protein

176
Q

What are the parts of the insulin peptide chain?

A

alpha and beta chain held together by disulfide linkages

177
Q

The alpha and beta chain in an insulin model are the ______ form and they are activated in the granules _______ being released into the blood stream or ______

A

active
before
shortly after

178
Q

What does the pro form of insulin contain? What happens to it? What’s it’s function?

A

C peptide
It is cleaved off and released into the bloodstream.
It doesn’t seem to have a function

179
Q

What is the importance of measuring C peptide?

A

A C peptide level will give an indication if the insulin dependent patient’s beta cells are producing insulin since the pharmacologic version does not have this

180
Q

The closest insulin to humans is ________ except for ________. What is a potential issue of utilizing this insulin?

A

porcine
threonine, alanine switch
immune reaction

181
Q

What does an insulin secretagogue do? Which is the primary one? Name 4 others that are endogenous

A
  1. Increase the release of insulin;
  2. glucose;
  3. amino acids, leptin (fatty acids), hormones, incretin
182
Q

How does glucose get transported into the pancreatic beta cell?

A

Glut-2 transporter

183
Q

T/F: The glut-2 transporter has a low affinity for glucose

A

True

184
Q

Essay question
Describe how insulin is released from the pancreas

A

Glut-2 transports glucose to the beta cell when there is a large amount of glucose in the blood. Through glycolysis, the glucose is metabolized to produce ATP. The ATP binds to the inward rectifying potassium channels that normally pump potassium into the cell and causes the channels to close. This causes the membrane to depolarize, causing voltage gated calcium channels to open. The Ca binds to a vesicle complex that has stored insulin and the vesicle fuses with the cell membrane, releasing insulin.

185
Q

What is interesting about amino acids? (as in eating protein)

A

They cause the release of insulin and glucagon

186
Q

Where are leptins secreted from?

A

fatty tissues

187
Q

Drugs that are insulin secretagogues

A
  1. Sulfonylureas
  2. Isoproterenol
188
Q

How long does insulin stay in the bloodstream?

A

6 min

189
Q

Essay question
Describe the process of insulin binding

A

The insulin receptor is a dimer with tyrosine kinase domains. So we have dimerization of the units, the insulin molecule binding to it, and the beta units are setting up the signaling within. so the beta units inside the tyrosine kinase receptor become activated, they become phosphorylated, and that sets up a cascade of additional elements within the cell, referred to as insulin response substrates. Whenever the insulin receptor is activated, these insulin response substrates are also activated. Some of them work through the MAP kinase or IP3 pathways. The main effect we talked about already, it’s the movement of the glucose transporter from inside the cell to the cell surface, but can have other effects

190
Q

Describe GLUT4 tranporters

A

Glute four are the majority of the receptors we see most places in the body, like the muscle and the adipose tissue. That’s an intermediate affinity, and it causes that uptake of glucose from the bloodstream because of that insulin.

191
Q

A high Km means?

A

low affinity

192
Q

T/F: Glut3 transporters in the brain have a high Km

A

False

193
Q

What are the 3 main endocrine effects of insulin?

A
  1. inhibits glycogenolysis (the breakdown of glycogen)
  2. Inhibits the conversion of fatty acids and amino acids to keto acids
  3. promotes glucose storage as glycogen
194
Q

What is an inhibitor of insulin secretion? Why?
Name

A

insulin; its a negative feedback mechanism

195
Q

What is the role of leptin?

A

it is a hormone produced by adipocytes that tells us were satiated and decreases insulin secretion

196
Q

Drugs that can decrease insulin secretion (4)

A
  1. Phenytoin
  2. Diazoxide
  3. Vinblastine
  4. Colchicine
197
Q

Insuline preparation classes (4)

A
  1. Rapid
  2. Short
  3. intermediate
  4. Long
198
Q

Name 3 rapid acting insulins

A

Lispro, aspart, glulisine

199
Q

List 2 short acting insulins

A

Normal (Novolin and Humilin)

200
Q

Name an intermediate acting insulin

A

Protamine aspart

201
Q

Name 3 long acting insulins

A

detemir, glargine, Tresiba

202
Q

What is a benefit of 70/30 insulin? Which insulins are usually used? Does it give tight control?

A

Only injecting twice a day vs 4-5
Protamine hagedorn mixed with regular or short acting
No

203
Q

Which form of insulin injection will give the tightest control?

A

Insulin pump

204
Q

One unit of rapid acting insulin disposes _______ g of carbs

A

12-15

205
Q

Eating a meal with 75 carbs would require approx. how many units of rapid acting insulin?

A

5

206
Q

One unit of insulin drops glucose levels _______

A

50 mg/dl

207
Q

T/F: Diabetics need more insulin when they are sick. Why or why not?

A

true; metabolic rate is up

208
Q

S/S of hypoglycemia

A

anxiety, headache, sweating

209
Q

The most common oral drug treatment for NIDD? MOA?

A

Biguanines; slows down glucose production in the liver

210
Q

What is gluconeogenesis?

A

The process of making glucose in the liver as needed out of glycerol or breaking down amino acids

211
Q

Would an insulin dependent diabetic benefit from taking an insulin secretagoue in conjunction with insulin? why or why not?

A

No; their insuline secreting cells are destroyed and not producing insulin

212
Q

What is the primary drug class for insulin secretagogues? MOA?

A

Sulfonylureas; bind to and block the potassium channel, cause depolarization, voltage gated calcium channels open, causing the release of insulin

213
Q

What is an alternative to sulfonylureas? When it this an option? What is the downside?

A

Meglitidine; patients who have sulfa drug allergies; much more shorter acting

214
Q

What is the major difference between first gen and second gen sulfonylureas?

A

1st gen require a higher dose

215
Q

Sulfonylureas have a black box warning for

A

increased cardiovascular mortality

216
Q

T/F: Meglitinides are safer than sulfonylureas

A

true

217
Q

Mechanism of action of TZDs

A

Drug binds to receptors through the peroxisome proliterator activated receptor pathway and increasing the likelihood that the cell is going to respond better to insulin;
decrease insulin resistance

218
Q

T/F: Type II DM produce more insulin over time

A

true

219
Q

Why are alpha glucosidase inhibitors not very popular in the US?

A

Our diet is not primarily carbohydrates

220
Q

MOA alpha glucosidase inhibitors? Give an example

A

Prevent disaccarides from working (the enzyme in the lumen of the intestine that breaks down sucrose into glucose and fructose)
Acarbose

221
Q

MOA of bile acid binding resins

A

A resin in powder form that prevents glucose from being absorbed by essentially surrounding and blocking it

222
Q

BABRs can also help treat? Common side effect?

A

hypercholesterolemia and obesity; GI upset

223
Q

MOA amylin analogs

A

Promote amylin, the compound released by beta cells thats suppresses glucagon release

224
Q

Where are incretins normally produced? What is their effect?

A

The intestine; stimulates insulin release and inhibits glucagon release

225
Q

What are the 2 types of incretin based therapies and give drug examples

A
  1. GLP-1 agonists- Trulicity, semaglutide, ozempic, wegovy, robelsis
    DPP4
  2. DPP4 inhibitors- Januvia
226
Q

MOA of DPP4 inhibitors

A

dipeptidyl peptidase 4 is the enzyme that breaks down GLP1; theese inhibitors block this enzyme

227
Q

What is the target for Glifozins and MOA? What is an additional benefit?

A
  1. SGLT2 transporters;
  2. block glucose reuptake in the PCT causing it to be excreted in the urine
  3. can work as an osmotic diuretic, helping lower BP
228
Q

root word for SGLT2 inhibitors

A

-flozin

229
Q

serious potential Side effect of Glifozins

A

necrosis in the genital region

230
Q

The SGLT-1 transporter is located in the _________ and the SGLT-2 transporter is located in the _______

A

loop of henle
PCT

231
Q

What is the biggest problem with dyslipidemia?

A

can lead to atherosclerosis

232
Q

What is the role of LDL cholesterol and where is it produced?

A

cholesterol carrying molecule that distributes cholesterol throughout the body; produced in the liver

233
Q

What happens if we have too much LDL?

A

It ges sequestered underneath the intima of the arteries

234
Q

Essay question
Describe the process of plaque formation

A

Excess LDL cholesterol is deposited in connective tissue causing WBCs to come to the area, differentiate into
pro inflammatory macrophages and phagocytose the cholesterol. This causes them to release superoxides and hydrogen peroxide that lead to oxidation of that LDL molecules. The oxidized LDL can go back into the bloodstream, further causing an immune response. Macrophages continue to try to phagocytose the cholesterol and it builds up to more and more inside the cell (known as foam cells). Cholesterol crystallizes over time and the foam cells eventually rupture, becomes necrotic, and form a calcified plaque in the area causing more inflammation…

235
Q

T/F: Cholesterol is broken down by enzymes

A

False; cholesterol cannot be appreciably broken down

236
Q

Describe a triglyceride

A

A glycerol molecule attached to 3 fatty acids

237
Q

What kind of molecule is cholesterol? Describe it

A

a steroid molecule; 3 six ring carbons and a 5 ring carbon

238
Q

What are some roles of cholesterol?

A

precursor for hormones such as estrogen, testosterone, formation of cell membranes

239
Q

Steroids are produced through which 2 main pathways?

A
  1. Dietary intake (either animal or plant based)
  2. De novo synthesis (made by the liver)
240
Q

Why is the liver producing cholesterol problematic?

A

If the body has become accustomed to high levels of cholesterol and suddenly adjusts their diet to lower cholesterol, the liver will make up for the lower intake by producing more

241
Q

Describe the pathway for cholesterol synthesis

A

HMG COA is converted to mevalonate by the enzyme HMG COA reductase. Mevalonate produces cholesterol through a series of additional steps

242
Q

What is the target for statins? MOA?

A

HMG COA reductase; competitive inhibitor of the enzyme that prevents cholesterol synthesis

243
Q

What is the role of lipoproteins?

A

Circulate in the bloodstream to carry cholesterol and triglycerols and all other lipids in a shell since lipids are not soluble in blood.

244
Q

What is the outer protein coat of lipoproteins? What does it help?

A

apolipoprotein; lipids become more blood soluble

245
Q

What is chylomicron and where is it formed?

A

A lipoprotein formed in the intestine that carries the triacyglycerols and cholesterol molecules ingested and circulates them throughout the body without going through the hepatic portal system.

246
Q

What is VLDL and where is it formed?

A

very low density lipoprotein; secreted from the liver then converted into intermediate and low density lipoprotein

247
Q

What is HDL and where is it produced?

A

high density lipoprotein produced in the liver; it takes the excess LDL from the body back to the liver to be put out into the bile

248
Q

What is an average LDL/HDL risk ratio?

A

Around 3

249
Q

What is the LDL/HDL risk ratio if HDL is 75 and LDL is 250?

A

3.3

250
Q

What is a normal total cholesterol?

A

<200 mg/dl

251
Q

What are hyperlipoproteinemias? Most common kind?

A

Genetic condition where patients have elevated LDLs. Most common in familial hypercholesterolemia

252
Q

Some secondary causes for hypercholesterolemia?

A

DM, estrogen therapy, acromegaly, anorexia nervosa

253
Q

What is the first goal is trying to regulate cholesterol levels?

A

diet*

254
Q

Indications for statin therapy

A

High LDL:HDL ratio, high cholesterol >220, previous MI or heart disease

255
Q

What are the (6) drug classes for hyperlipidemia

A
  1. statins
  2. niacin
  3. fibrates
  4. binding resins
  5. absorption inhibitors
  6. monoclonal antibodies
256
Q

How do statins cause excess LDL receptors on cells?

A

Since the liver is not producing enough cholesterol for the cells, additional LDL receptors pop up and pull excess LDL out of the blood

257
Q

When does cholesterol synethesis occur?

A

overnight

258
Q

What type of patient should not take statins?

A

pregnant or breastfeeding women; children

259
Q

Toxicity with stains? Which is usually a reason to stop statin therapy?

A

increased liver enzymes and increased creatinine kinases causing muscle pain*

260
Q

MOA of niacin?

A

a megadose of vitamin b3 will block the movement of cholesterol into VLDL molecules decreasing VLDL and increasing HDL

261
Q

Most common problem associated with niacin at very high levels?

A

flushing reaction due to dilation of facial arteries

262
Q

MOA of fibrates? Name 2

A

decrease VLDL production in the liver and increase lipolysis; Gemofibrozil and fenofibrate

263
Q

T/F: Bile acids are a form of cholesterol that can be put into the intestine by the gallbladder

A

true

264
Q

Colestipol and cholestyramine are examples of

A

BABRs

265
Q

Typically _____% of our stool is lipid but will raise to _____% with BABRs

A

5
20-30

266
Q

What should and should not be taken with BABRs?

A

Taken with food, not with medications

267
Q

What is the target of the drug Ezetimibe (Zetia)

A

NPC1 light transporter

268
Q

Essay question?
Describe how the NPC1 light transporter works

A

Bile acids and dietary cholesterol form luminary cholesterols referred to as micelles. The micellar cholesterol are absorbed through the NC1L1 and it transports it in its free form. The cholesterol becomes esterified by an enzyme and packs it into chylomicron

269
Q

PCSK9 inhibitors are ________ and are given with ______

A

monoclonal antibodies
statins

270
Q

Describe MOA of PCSK9 inhibitors

A

Block PCSK9 molecules from binding to LDL receptors. (PCSK9 binds to LDL receptors and destroys them, leading to more LDL in the bloodstream and less in the cells)

271
Q

Essay question
Describe how LDL receptors are recycled

A

Cholesterol binds to LDL receptors and it forms a clathrin coated pit. The cholesterol and receptor goes inside the cell and merge with a lysosome that strips the cholesterol from the receptor. The receptor is recycled and the cholesterol is degraded to be used for steroid hormones or cell membranes.

272
Q

Together with statins, PCSK9 inhibitors can lower LDL levels by ______%

A

65

273
Q

Risks of hypocholesterolemia (<25mg/dl)

A

cancer, hemorrhagic stroke, depression, anxiety, preterm birth, low birth weight, delayed wound healing

274
Q

Differentiate between acute and chronic inflammation

A

Acute response is beneficial: blood cells, oxygen and nutrients go to the area and clear out infectious particles;
Chronic inflammation leads to destruction of cell membranes

275
Q

WBC released mediators (4)

A
  1. Interleukins
  2. GM-CSF (granulocyte monocyte colony stimulating factor
  3. Tumor necrosis factor
  4. Interferons
  5. Platelet derived growth factor
276
Q

Arachadonic acid is the precursor to which 2 pathways?

A

LOX and COX

277
Q

Describe an eicosanoid molecule

A

fatty acid molecule with 20 carbons

278
Q

Phospholipids can be broken down into (3)

A

IP3
diacyglycerol
arachadonic acids

279
Q

What enzyme helps produce arachadonic acids?

A

phospholipase

280
Q

The Lox pathways produces _______ which is associated with _________

A

leukotrienes
inflammation

281
Q

What is the role of leukotriene B4?

A

Bring in more WBCs

282
Q

What is produced in the cyclooxygenase?

A

Prostaglandins, thromboxane A2, and prostacyclin

283
Q

_________ prevents platelet aggregation while ________ encourages platelet aggregation

A

protacyclin
thromboxane A2

284
Q

Describe the two main Cox isoforms

A

Cox 1 is constituitive and Cox 2 is only expressed when there is inflammation

285
Q

Homeostatic functions of Cox 1

A

acid production in stomach, keep kidney blood vessels open, macrophage differentiation

286
Q

What three drug classes can be given to inhibit the Cox 2 pathway?

A

NSAIDS, glucocorticoids, and Slow acting anti rheumatic drugs (DMARDs)

287
Q

Cox 1 inhibitors are typcially not given but can be given in low dose if

A

the patient has history or blood clotting disorders or platelet aggregation disorders

288
Q

DMARDs are given for? Why are they considered “disease modifying”?

A

rheumatoid arthritis or osteoarthritis; can reverse signs and symptoms of RA

289
Q

NSAIDs suppress (4)

A
  1. s/s inflammation
  2. prostaglandin synthesis
  3. fever
  4. pain
290
Q

By decreasing sensitivity of vessels to bradykinin histamine, CNS. vessels are no longer ______

A

leaky and swollen

291
Q

Which Cox pathway affects platelet aggregation?

A

1

292
Q

Essay question
Describe the process of aspirin binding to platelet cell membranes

A

Platelets have a double enzyme complex on their surface. Arachadonic acid is produced inside and it goes up to the enzymatic site of Cox 1 where it can break down into prostaglandins. When we give aspirin, through acetylation, it binds to serine 529, preventing arachidonic acid from going up into the catalytic site.

293
Q

Why does it take 8-10 for aspirin to wear off?

A

It is irrevesible and affects circulating platelets that have a life cycle of that amount of time

294
Q

T/F: Aspirin and other NSAIDs work by acetylation, which prevents arachidonic acid from going into the enzymatic pore of platelets

A

False; only aspirin has an acetyl group

295
Q

Compare aspirin to Sulindac and Piroxicam?

A

all affect Cox 1 > 2 but aspirin is irreversible

296
Q

Which 3 NSAIDs have about an equal effect on Cox 1 and 2?

A

ibuprofen, Meclofenamate, Toradol

297
Q

Which is the only drug on the US market that affects Cox 2 > 1

A

Celebrex

298
Q

Which 2 drugs inhibit Cox and Lox pathways?

A

Indomethacin and Diclofenac

299
Q

How does aspirin affect peripheral vessels? How?

A

vasodilation; inhibiting PG synthesis in the hypothalamus causing vasodilation to dissipate heat and lower body temp

300
Q

Aspirin overdose can cause ______ and tylenol overdose can cause ______

A

salicylate poisoning
liver failure

301
Q

Why do we not give aspirin to children?

A

Risk of Reye syndrome that causes encephalopathy

302
Q

Black Box warning for all NSAIDs?

A

pregnant women should not take due to prostaglandin inhibition preventing normal kidney development

303
Q

s/s of aspirin overdose?

A

mild- n/v, diziness
mod- tinnitus, hyperventilation, tachycardia, fever
severe- delirium, hallucination, coma, respiratory arrest

304
Q

treatment for aspirin overdose

A

activated charcoal, IV fluids, HD

305
Q

Why would a coxib (Celebrex) be prescribed? Risk?

A

avoid GI distress
increased risk of CV events

306
Q

Medication similar to celebrex, though not technically a coxib

A

Mobic

307
Q

Synthetic protaglandin

A

misoprostol

308
Q

MOA of Indomethacin

A

Potent COX 1 and 2 inhibitor and has an effect on phospholipase A and C which prevents turning phospholipids to arachadonic acid

309
Q

Clinical indications of Indomethacin?

A

RA, gout, patent ductus arteriosus

310
Q

In regards to patent ductus arteriosus, why would giving a prostaglandin inhibitor help?

A

prostaglandins at a high level are keeping the ductus arteriosus open

311
Q

Why is tylenol not an NSAID even though it works in the Cox 2 pathway

A

Its more central nervous system Cox 2 selective therefore not an antiinflammatory

312
Q

NSAIDs with highest association of toxicity (3)

A

Indomethacin, tolmetin and meclefenamate

313
Q

Effects of gluccocorticoids

A

suppress inflammation, mobilize energy stores, improve cognitive function, salt and water retention

314
Q

Chronic stress leads to

A

salt and water retention, high blood pressure, obesity, diabetes, depression

315
Q

What is the role of phospholipase A2

A

convert phospholipids to arachadonic acid and inbibits leukocytes from migrating

316
Q

A steroid nucleus is common for cholesterol and _____

A

corticosteroids

317
Q

T/F: Glucocorticoids enhance activity of NFkB

A

False; inhibit (they are proinflammatory)

318
Q

MOA of glucocorticoids?

A

inhibit immune response by blocking transcription/translation

319
Q

Why are glucocorticoids indicated in treatment for Addison’s disease?

A

They are not producing adrenal corticosteroids

320
Q

Describe Cushing’s disease. Treatment?

A

Producing too much corticosteroid; s/s of overdose
Removal of the adrenal glands

321
Q

Blood tests that measure inflammation

A

CRP, RBC sed rate, rheumatoid factor

322
Q

List nonbiologic DMARDs

A

Cyclophosphamide – B&T cell suppression
Cyclosporine – Inhibition of interleukins
Methotrexate – blocks production of folic acid

“CCM”

323
Q

List biologic DMARDs

A

Abatacept (Orencia) – Blocks T-cell activation
Adalimumab (Humira) – anti-TNF-α
Rituximab (Rituxan) – Depletes B-lymphocytes

“AAR”

324
Q

Chronic inflammation is a risk factor for ______

A

cancer

325
Q

Which two elements cause mutations in epithelial cells?

A

ROS- reactive oxygen species
RNI-reactive nitrogen intermediates

326
Q

Endogenous ligands for pain modulation

A

Endorphins, enkaphalins, and dynorphins

327
Q

Excitatory neurons release

A

glutamate

328
Q

inhibitory neurotransmitters

A

GABA and glycine

329
Q

What are circuit neurons?

A

neurons that circle back after receiving an excitatory potential and cause an inhibitory response to shut down the signaling

330
Q

Axoaxotic reactions occur directly at ______

A

the axon

331
Q

How are diffuse systems different than pain signaling pathways?

A

non hierarchial; neurotransmitter is being released into csf and floating around leading to essentially all areas of the brain being activated through lightly myelinated neurons

332
Q

What system is monoamine transmission?

A

diffuse

333
Q

two main dopaminergic nuclei? Where do they have entensions?

A

substantia nigra
ventral tegmental areas
throughout the brain, cerebral cortex, and corpus callosum

334
Q

Where does NE come from?

A

Locus coeruleus

335
Q

The serotonin system is diffused primarily through______

A

Rafe nuclei in the brainstem

336
Q

Ach is a _______ system and is associated with _________ and ________

A

diffuse
learning
memory

337
Q

GABA, glycine and glutamate are all ______ system

A

hierarchal

338
Q

3 receptors for endogenous opiods

A

mu, delta, kappa

339
Q

Two components of pain

A

emotional and sensory

340
Q

stimuli for pain

A

noxious chemicals, thermal or heat/cold, mechanical pain

341
Q

what are nociceptors

A

pain receptors

342
Q

What kinds of receptors are on free nerve endings (4)

A

prostaglandin, leukotriene, bradykinins, vanilloid

343
Q

where is pain interpreted

A

somatosensory cortex

344
Q

3 main fibers for sensation into the CNS? which are myelinated?

A

*A -beta
*A- delta
C

345
Q

What type of pain is sensed through A beta fibers

A

non noxious mechanical stimuli

346
Q

What type of pain is sensed through A delta fibers

A

noxious heat, mechanical stimuli

347
Q

Gate control theory of pain

A

We can shut down pain signaling with endogenous opioids in the periaqueductal grey

348
Q

Fibers can overpower each other, it just depends on

A

the strength of the singal and how often the neuron is firing

349
Q

Primary pain pathway? where does it terminate?

A

spinothalamic; somatosensory cortex

350
Q

Emotional path pathway? where does it terminate?

A

spinoreticular; somatosensory cortex

351
Q

3rd pain pathway? where does it terminate?

A

spinomesencephalic; periaqueductal gray

352
Q

The PAG has alot of _______ and alot of _______ are released here

A

opioid receptors
endorphins

353
Q

Most opioids target the ____ receptor though there is some overlap. Name 2 full agonists

A

Mu
morphine and fentanyl

354
Q

Name 2 partial agonists for the Mu opioid receptor

A

codeine and oxycodone

355
Q

Name the 3 endogenous opiods peptide in order of affinity to the mu receptor

A
  1. endorphins
    2., enkephalins
  2. dynorphins
356
Q

T/F: There are opioid receptors in the gastrointestinal tract.

A

true; cause constipation

357
Q

Psychomimetic effects associated with opioids are primary through which receptors?

A

kappa

358
Q

Describe the relationship between opioids and the first pass effect?

A

up to 90% can be metabolized and inactivated by the liver

359
Q

Why does codeine have a lower first pass effect?

A

Codeine is a prodrug and accumulates in highly perfused tissues. The skeletal muscle can even act as a reservoir to slowly release the drug

360
Q

MOA of opioids

A

Bind to receptors, modulate pain response, reduce neurotransmitter release, shut down excitatory postsynaptic potentials and even hyperpolarize postsynaptic neurons

361
Q

T/F: Opioids can decrease cAMP

A

true

362
Q

Describe the 3 locations of Mu opioid receptors in a neuron and how they suppress pain

A
  1. Directly in the pain terminal where the neuron receives the initial signal- suppresses signal by decreasing cAMP
  2. Terminal end of the neuron - prevent calcium from entering the cell, preventing the release of neurotransmitters
  3. Next neuron signal- suppresses K so the cell is hyperpolarized
363
Q

Side effects of opioids that a tolerance cannot be developed (2)

A

meiosis, constipation

364
Q

the only opioid that can cause tachycardia?

A

demerol (meperedine)

365
Q

Side effects (2) that a tolerance can be built

A

sedation, analgesia

366
Q

Opioid used to treat diarrhea? Does it cross into the CNS?

A

looperamide; no but if given with quinidine it can

367
Q

indications for opioids in infants?

A

renal or biliary colic

368
Q

MONA

A

morphine, oxygen, nitroglycerin, aspririn
(acute coronary syndrome)

369
Q

Toxicity of opioids

A

dysphoric reactions, restlessness, tremor, respiratory depression, n&v, increased ICP, postural hypotension, constipation, urinary retention, itch

370
Q

T/F: Opiods can cause mast cell degranulation

A

true

371
Q

Compare tolerance and dependence

A

tolerance is associated with the receptor itself and dependence is a physical necessity to continue the drug

372
Q

T/F: Tolerance to narcan and naltrexone can be developed at high enough doses

A

False

373
Q

What is opioid induced hyperalgesia

A

Happens to about 30% of patients who are chronically using opioids; due to changes in Mu opioid receptors. A splicfe varient produces an alternative Mu receptor 1k that increases cAMP instead of decreasing

374
Q

3 structures of the 3 different classes of opioids

A
  1. Phenanthrenes
  2. Phenylheptylamines
  3. Phenylpiperidines
375
Q

Which drugs are phenanthrenes? strong and moderate agonists

A

strong agonsits: morphine, dilaudid

moderate agonists: codeine, oxycodone, percocet (oxy + acetaminophen), percodan (oxy + aspirin)

376
Q

What drug is in the phenylhelptylamine class

A

methadone

377
Q

strongest agonist in the phenylpiperidine? Name two moderate agonists

A

fentanyl
demerol and tramadol

378
Q

Methadone is used for the treatment of?

A

opioid overdose

379
Q

Demerol is used for? What effects does it have? (2)

A

post op shivering
antimuscarinic and negative inotrope

380
Q

opioid Medication that can induce seizures if the patient is predisposed to them?

A

demerol

381
Q

Why would we want to decrease post op shivering?

A

shivering uses up alot of oxygen

382
Q

Dextromethorphan is a

A

very weak opioid agonist used for cough
(phenylpiperidines)

383
Q

Butophanol

A

partial opioid agonist for post op shivering

384
Q

Partial opioid agonist used for opioid abuse withdrawal

A

Buprenorphine

385
Q

Opioid antagonist used to increase movement along the digestive tract when you’re taking an opioid

A

Naloxegol

386
Q

Naloxone and Naltrexone are ______

A

opioid antagonists

387
Q

The first antibiotic

A

penicillan

388
Q

T/F: Antivirals come from living organisms

A

False; viruses are not living

389
Q

Two main classes of bacteria? What is the difference?

A

gram positive and gram negative
Gram (+) stain purple - have a very thick peptidoglycan layer
Gram (-) stain pink - very thin peptidoglycan layer and 2 plasma membranes

390
Q

Why are gram - bacterias more harmful when they’re being destroyed? How can this be avoided?

A

They release more endotoxins
slow the growth to allow the immune system to destroy them

391
Q

What is selective toxicity?

A

toxic to bacteria, tend not to hurt human cells

392
Q

Most broad spectrum of antibiotics

A

tetracyclines

393
Q

5 modes of action of antibiotics

A
  1. Cell wall inhibition
  2. Cell membrane (inner or outer)
  3. Inhibition of DNA and RNA
  4. Inhibit folic acid synthesis
  5. Protein synthesis inhibitors
394
Q

Cell wall inhibitors MOA; give examples and what kind of bacteria are these for?

A
  1. block the synthesis and repair of the pepridoglycan layer
  2. Penicillins, carbapenams, vanco
  3. Gram (+)
395
Q

Antibiotics that target the cell membrane are more beneficial against what type of bacteria? Give an example

A

Gram (-)
polymixins

396
Q

What is gyrase? Which drug targets this?
Name one

A
  1. a bacterial enzyme that unwinds DNA so it can be replicated
  2. quinolones
  3. Cipro
397
Q

Drug that inhibits RNA polymerase

A

rifamycin

398
Q

Human vs bacteria folic acid?

A

humans do not make it themselves but bacteria do from a percursor PABA

399
Q

Drugs that inhibit production folic acid

A

sulfonamindes or trimethoprim

400
Q

Most broad spectrum group of antibiotics? MOA?

A

protein synthesis inhibitors; block ribosomes found only on bacteria

401
Q

Give 3 examples of protein synthesis inhibitors

A

erythromycin, gentamicin, tetracycline

402
Q

Red structure? what is the difference between the 2?

A

beta lactam ring
penicillan- five ring structure
cephalosporin- 6 ring structure

403
Q

What does the beta lactam ring do?

A

Binds to the enzyme in bacteria that produces the peptidoglycan cell wall and prevents it from functioning

404
Q

Number 1 common drug allergy

A

penicillin

405
Q

T/F: Sensitivity to penicillin can cross over to cephalosporins

A

true

406
Q

Enzyme that breaks down beta lactam rings?

A

beta lactamase

407
Q

If a bacteria has beta lactamase, it is considered _________. _____________ are resistant to that enzyme

A

penicillan resistant;
carbapenems

408
Q

Drug of “last resort”

A

vanco

409
Q

T/F: Vanco is susceptible to beta lactamase

A

False

410
Q

Toxicity in vanco

A

irritating to tissues, fever, chills, ototoxicity, nephrotoxicity, red neck syndrome (inflammation in the neurons)

411
Q

Largest group of antibiotics and most broad spectrum

A

Inhibition of protein synthesis

412
Q

Polymyxins target ___________ by forming ________ in them without destroying it

A

cell membranes
pores

413
Q

What are the problems associated with tetracyclines?

A

wipe out gut bacteria, n&v, diarrhea, bone disorders, discoloration of bone, neurotoxicity, nephro and ototocixity

414
Q

Examples of macrolides? Are they broad spectrum?

A

Erythromycin, clarithromycin, azithromycin; yes - they belong to the protein synthesis inhibitors

415
Q

3 types of organisms

A

highly sensitive, intermediate, highly resistant

416
Q

Lamisil

A

topical antifungal

417
Q

Niclosamide

A

treatment for tape worms

418
Q
A
419
Q

Why are NSAIDs gastic irritants?

A

They block the protective prostaglandins that help the stomach produce mucus

420
Q

Side effects of Acarbose

A

gas, bloating, diarrhea due to excess sucrose in the large intestine

421
Q

What activates plasminogen?

A

TPA

Pharm Dr. T (3 decks)

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