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M1 Block 3 > Week 4 > Flashcards

Week 4 Flashcards

1
Q

List the models of treatment

A

Neurologic
Metabolic-Energetic
Biomechanical
Respiratory-Circulatory
Behavioral

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2
Q

Briefly describe the neurologic model of goal of Tx of somatic dysfunction

A

Influence viscero-somatic relationships

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3
Q

Briefly describe the goals of treatment of somatic dysfunction in the behavioral model

A

Relieve pain

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4
Q

Osteopathic treatment is not aimed at “turning the system up or down,” but:

A

But at removing the dysfunctions to allow the body to restore a more appropriate autonomic balance

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5
Q

T/F: You can only have too much parasympathetic overriding sympathetic drive and vice versa

A

False, can have too much Parasympathetic and Sympathetic drive in both systems at the same time

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6
Q

Related to the __________ model, what is sensitization

A

Somatic dysfunction increases the excitability the involved neurons, meaning less of an impulse is needed to cause the action of the nerve to happen

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7
Q

In simplest terms what is spinal facilitation

A
  • Nerve is always firing even when body is at rest
  • In this state there is less afferent stimulation needed to discharge impluses
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8
Q

Define: Somatosomatic reflex

A

Localized somatic stimuli producing patterns of reflex response in segmentally related somatic structures

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9
Q

Define somatovisceral reflex

A

Localized somatic stimuli producing patterns of reflex response in segmentally related visceral structures

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10
Q

Define: viscerosomatic reflex

A

Localized visceral stimuli producing patterns of reflex response in segmentally related somatic structures

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11
Q

What are the two forms of viscerosomatic reflexes

A
  1. Sensory, i.e. referred pain
  2. Motor response, i.e. triggered and maintained visceral activity
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12
Q

Describe the goal metabolic energetic model to treat somatic dysfunction

A

Decrease energy output or expenditure
- Enhance the self-regulatory and self-healing mechanisms to foster energy conservation and enhance function

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13
Q

What is the thoraco-abdominopelvic cylinder?

A
  • Descent of the diaphragm creates a relative negative intra-thoracic pressure, to draw inflow of air and fluid for low pressure venous return & lymphatics
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14
Q

What is the osteopathic model of treatment based on the goal: To improve breathing and blood circulation

A

Respiratory circulatory

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15
Q

What is the osteopathic model of treatment corresponding to the goal of treatment: To decrease facilitation of the phrenic nerve secondary to a spastic diaphragm

A

Neurologic

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16
Q

What is the common compensatory pattern?

A
  • Common fascial distortion and its effect on the respiratory circulatory systems of the body
  • Common somatic dysfunctions throughout the entire population
  • Accounts for “asymptomatic” dysfunctions
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17
Q

What causes the S4 sound? When does it occur?

A

Occurs at the end of ventricular filling (diastole) due to the vibration of the ventricular walls making sound after atrial contraction forces more blood into the ventricles

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18
Q

In cardiac muscle, during which phase is potassium permeability the greatest?

A

Phase 3

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19
Q

What occurs immediately after the QRS wave?

A

Ventricles begin to contract in isovolumic contraction only since electrical events precede mechanical

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20
Q

In cardiac muscle, when is sodium permeability the highest?

A

Phase 1

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21
Q

How long does it take for an action potential to travel from the SA node to the AV node?

A

0.03 seconds

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22
Q

What is the heart rate at the AV node?
What about the Purkinje?

A

AV node: 40-60 BPM
Purkinje: <40 BPM

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23
Q

What is the pressure in the aorta?

A

130/90

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24
Q

What is the pressure in the Left ventricle?

A

130/10

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25
Q

What is the pressure in the pulmonary arteries?

A

25/10

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26
Q

What is the pressure in the R ventricle?

A

25/5

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27
Q

What is the pressure in the left atrium?

A

< 12

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28
Q

What is the pressure in the Right atrium?

A

< 12

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29
Q

What pressure is best approximated using Pulmonary capillary wedge pressure?

A

Left atrial pressure

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30
Q

What is the best index measurement of preload? Why?

A

Left ventricular end diastolic volume because it can be measured clinically using echocardiography

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31
Q

Why is pulmonary wedge pressure not used in mitral stenosis?

A
  • PCWP is a good approximation of L atrial pressure
  • Not a good index in mitral stenosis because of pressure changes upstream and decrease downstream
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32
Q

If preload is increased above physiologic limit, what happens

A

The stroke volume begins to increase
- As preload is increased, the CO is increased until ventricle is too stretched to perform optimal contraction

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33
Q

Frank-Starling Law of the heart compares:

A
  • Compares the stroke volume to ventricular volume at the end of diastole
  • Amount of stretch is equal to volume ejected from ventricles within physiologic limits
  • Stroke volume and cardiac output correlate directly with end diastolic volume with correlates with venous return
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34
Q

What determines R vs L heart coronary dominance?

A
  • Dominant circulation is determined by which vessel gives rise to the posterior descending artery (PDA)
  • If Right dominant, PDA comes from Right coronary artery
  • If Left dominant, PDA comes from Left circumflex artery
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35
Q

What does the 1st half of the P wave mean?
2nd half?

A

1st half is R atrial depolarization
2nd half is Left atrial depolarization

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36
Q

What does STEMI stand for vs NSTEMI?

A

STEMI: ST segment elevation
NSTEMI: ST segment depression

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37
Q

What is the HR for regular R-R interval with 2 large boxes between them?

A

150

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38
Q

What is the HR for regular R-R interval with 3 large boxes between them?

A

100 BPM

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39
Q

What is the HR for regular R-R interval with 4 large boxes between them?

A

75 BPM

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40
Q

What is the HR for regular R-R interval with 1 large boxes between them?

A

300

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41
Q

What is the HR for regular R-R interval with 5 large boxes between them?

A

60 BPM

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42
Q

What is Delta wave associated with?

A
  • Wolff Parkinson White where there is not a dip of the Q wave due to fast conduction from atria to ventricle and bypassing of AV node
  • Can lead to SVT
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43
Q

What type of drug has the fastest absorption rate? Why?

A
  • Inhalation due to large surface area, highly vascularized mucus membrane
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44
Q

TB tests are administered via:

A

TB test administered via intradermal injection

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45
Q

Why are IV drugs not considered absorbable?

A
  • When IV drugs are administered they are going directly into the blood and bypassing the absorption process
  • 100% bioavailable
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46
Q

What type of absorption does IM use?

A

Simple diffusion

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47
Q

Why is insulin administered subcutaneous?

A

It is an unstable drug

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48
Q

Pharmacokinetics: Describe what happens to a weak acid, ___, in an acidic environment

A

Weak acid, HA ↔ H⁺ + A‾
Weak acid will be deionized in an acidic environment since there are many protons available

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49
Q

Pharmacokinetics: Describe what happens to a weak base, ____, in a basic environment

A

Weak base, BH⁺ ↔ B + H⁺
Weak base will be deionized in a basic environment since there are fewer protons available

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50
Q

Pharmacokinetics: Describe what happens to a weak base, _____, in an acidic environment

A

Weak base, BH⁺ ↔ B + H⁺
Drug will become ionized

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51
Q

Pharmacokinetics: Describe what happens to a weak acid, ___, in an acidic environment

A

Weak acid, HA ↔ H⁺ + A‾
Drug will become nonionized in an acidic environment

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52
Q

To allow a drug to move through a tissue, what are the best parameters for passage through cell membrane

A
  • Nonpolar
  • Uncharged
  • Lipophilic
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53
Q

A low pKa indicates:
A high pKa indicates:

A
  1. Low pKa indicates a stronger acid
  2. A higher pKa indicates a stronger base
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54
Q

Describe the treatment of hepatic encephalopathy in the setting of drug administration

A

Hepatic encephalopathy treatment is
with lactulose, a drug that is converted by gut bacteria
into lactic acid (more H+). The acid environment in the
gut converts ammonia (NH3) to ammonium (NH4+).

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55
Q

T/F: Since SL and buccal administered drugs enter the blood stream they are 100% bioavailable

A

False, since they enter orally some, very little, is swallowed & thus susceptible to the first pass effect

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56
Q

Describe the difference between a 1:1 drug ratio vs a 1:2 drug ratio.

A
  • Having to do with the dosing between different forms of a drug
    1. For example, 1:1 would mean say IV drug dosage is the same as oral
    2. 1:2 ratio would mean oral dosage is twice as high as IV drug dosing
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57
Q

Why are oral drugs the safest drug administration?

A

They take the longest to absorb allowing time to implement effects of reversal if needed

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58
Q

What are prodrugs?

A

Prodrugs are drugs that enter the body in the inactive form and only become active when met with enzymes in the body

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59
Q

Which is fast absorption, Buccal or SL?

A

Sublingual is faster but both bypass the 1st pass effect through the liver which makes them highly bioavailable

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60
Q

What is the pH of the stomach?

A

pH stomach is 2

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61
Q

What is the pH of the small intestine?

A

pH of the small intestine is 6

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62
Q

What is the pH of blood?

A

pH of the blood is 7.4

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63
Q

Pharmacokinetics: what would you do to prevent movement of a drug through a cell membrane?

A

Make it more ionized

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64
Q

What do P glycoproteins do?

A
  • Monitor foreign substances and push drugs out of the cell
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65
Q

Define: bioavailability

A
  • The rate and extent to which an administered drug reaches systemic circulation
  • Represented by F
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66
Q

What is the bioavailability, __, of IV administered drugs?

A

F = 100% or 1

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67
Q

Briefly describe the 2 compartment method for absorption of drugs

A
  1. Compartment 1: Route of administration
  2. Compartment 2: Movement into Blood, i.e. IV drugs go straight to compartment 2 since they go straight into the blood
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68
Q

Pharmacokinetics: What is Cmax?

A

Maximum effective drug concentration

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69
Q

What happens if you administer a basic drug with a weak base drug?

A
  • The drug will create a more basic environment to maximize the absorption & decrease lag time
  • Can even increase chance of toxicity
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70
Q

Pharmacokinetics: what is Vd?

A
  • Volume of distribution in body
  • Helps determine where the drug is, i.e. intracellular, plasma, interstitial
  • Volume that would be required to contain all of the drug in the body at the same concentration as plasma
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71
Q

What is total Vd for a 75 kg man?

A

42 L total volume distribution

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72
Q

What is the Vd for extracellular fluid for a 70 kg man?

A

Vd ECF is 14 L

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73
Q

What is the Vd for interstitial fluid for a 70 kg man?

A

Vd interstitial fluid is 10 L

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74
Q

What is Vd for plasma volume for a 70 kg man?

A

Vd for plasma volume is 4 L

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75
Q

What is Vd for intercellular fluid for a 70 kg man?

A

Vd for intercellular fluid is 28 L

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76
Q

What happens to drugs when they are bound to albumin?

A
  • Albumin is the main plasma protein that drugs bind to
  • When drugs bound to albumin they are inactive
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77
Q

What does a high Vd correspond to?
T/F: You can have a higher Vd than total Vd

A
  1. High Vd means more drug moving into extravascular compartment
  2. True, a drug can have a higher Vd than 42 L
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78
Q

When discussing bioavailibility, what 2 parameters are the same for everyone?

A
  • C min & MTC are the same for all people
  • C min is the minimum effective concentration
  • MTC: minimum concentration at which toxicity occurs
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79
Q

What does it mean for a drug to be metabolized?

A

Drug is made inactive
Does not necessarily mean the drug is already gone from the body

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80
Q

List some drug reservoirs:

A
  • Fat
  • Bone, i.e. tetracycline
  • Cellular
  • Plasma proteins
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81
Q

Give an example of a prodrug:
How is it activated?

A
  • Plavix/Clopidogrel is a anti-platelet prodrug
  • Must be metabolically activated via Phase 1 Cyp450 enzyme
  • 1st pass effect is encouraged here
  • Inactive → Active
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82
Q

Compare the activation pathway for drugs vs prodrugs

A

Drugs: active → inactive
Prodrugs: inactive → active

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83
Q

Describe the metabolism of Lithium

A

Lithium is a drug that is ingested and eliminated with no biotransformation
Goes straight through the body

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84
Q

How to calculate Vd

A

Vd = Amount of drug given/ [concentration in blood]

Vd = amount of drug in body/ Cp

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85
Q

What does a high Vd indicate?

A
  • Large Vd indicates most of the drug is in the extraplasmic space
  • Vd high = elimination low
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86
Q

T/F: Even if drugs are lipophilic and very small they cannot cross the blood brain barrier

A

False, the more lipophilic and very small the can cross the blood brain barrier

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87
Q

List 6 CYP inducing drugs

A
  1. Rifampin
  2. Benzopyrenes in cigarette smoke
  3. Chronic ethanol
  4. Barbiturates
  5. Carbamazepine
  6. Phenytoin
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88
Q

Describe how CYP inducers exert their effects on drugs

A

CYP gene, if upregulated, will increase expression of CYP enzymes which act in metabolize drugs
- Can either quicken metabolism by increasing effects of drug metabolic pathway
Drugs: active → inactive
Prodrugs: inactive → active

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89
Q

T/F: One dose of a CYP inducer can exert maximal effects on a drug metabolism

A

False, since CYP inducing drugs effect gene expression, their effects only take place in the setting of repeated dosing over a period of time
I.e. Being prescribed 1 week of Rifampin will cause faster metabolism of oral contraceptives

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90
Q

List 5 CYP inhibitor drugs

A
  1. Cimetidine
  2. Omeprazole
  3. Ketoconazole
  4. Erythromycin
  5. Grapefruit Juice
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91
Q

What is the goal of CYP inhibitor drugs?

A
  • Block metabolism
  • So decrease,
    Drugs: active → inactive
    Prodrugs: inactive → active
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92
Q

In metabolism, very briefly describe phase 1 & 2 goals

A

Metabolism
Phase 1: Convert lipophilic molecules into more polar molecules via reaction
Phase 2: Conjugation to further inactivation by transferring a larger molecule onto a drug so it is more favorable for elimination

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93
Q

What reactions take place metabolism: Phase I

A
  1. Oxidation via CYP most common
  2. Reduction
  3. Hydrolysis
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94
Q

What type of reactions take place in metabolism: Phase 2

A
  1. Glucuronidation
  2. Sulfation
  3. Acetylation
  4. Glycine conjugation
  5. Glutathione conjugation
  6. Methylation
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95
Q

List 5 sites of drug metabolism not including cellular level

A
  1. Liver most common metabolizing site since so many enzymes here
  2. Kidneys
  3. GI tract
  4. Skin
  5. Lungs
    - Note some drugs are metabolized by multiple organs
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96
Q

What is the most common type of Metabolism Phase II reaction?

A

Glucuronidation

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97
Q

All anti-seizure meds are CYP inducers, except:

A

Valproic acid

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98
Q

Name where metabolism occurs in enzymes:

A

Smooth ER (Phase I reaction)
Cytoplasm (Phase II reaction)
Cell membrane of mitochondria

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99
Q

Where are renal drugs excreted?

A

Glomerulus
Proximal Tubular Secretion
Distal Tubular Reabsorption

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100
Q

What does the Glomerulus discriminate against?
What does it filter?

A
  • Discriminates only large molecules size matters!
  • Does not care if non-ionized or ionized or lipophilic or non lipophilic
  • Filtered = *NOT REABSORBED INTO THE BODY**
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101
Q

Where are organic acid transporters and organic base transporters found?

A

PCT

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102
Q

What does PCT discriminate against?

A
  • Depends on OAT & OBT, they filter out acids and basic drugs respectively leading to secretion
  • Largely based on acidity and basicity
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103
Q

What kind of drug is aspirin?
Based on this information, what can you deduce about the movement of aspirin in the PCT?

A
  • Weak acid drug
  • The organic acid transporters will secrete the weak acid, aspirin for excretino
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104
Q

What does the DCT discriminate against?
What happens in the DCT?

A
  • Polarity matters in DCT
  • Nonionized drugs are reabsorbed
  • Ionized drugs are secreted & eliminated
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105
Q

Describe the treatment of weak acid overdose (aspirin) via kidneys

A
  • Weak acid overdose (aspirin) is treated with IV sodium bicarb to alkanize the urine
  • By making the urine more alkaline will make the weak acid in its ionized for secretion from the DCT
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106
Q

Describe the treatment of weak base (amphetamine) overdose via the kidneys

A
  • Weak base overdose (amphetamine) is treated with IV NH4Cl (ammonium chloride) to acidify the urine
  • By making the urine more acid will make the weak base drug more ionized for secretion & elimination in the DCT
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107
Q

How does elimination affect half life?

A
  • Depends on if drug is active or inactive during reabsorption
  • If drug is being eliminated the half life will decrease since it will not be reabsorbed
  • If drug is being reabsorbed and not eliminated the half life will increase since it will go back into the body
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108
Q

What is a common antidote for weak acid drug overdose?

A

Sodium bicarb

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109
Q

What is a common antidote for weak base overdose

A

Ammonium chloride (NH4Cl)

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110
Q

How does the GI tract manage drug excretion?

A

Drugs with MW > 300 are excreted

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111
Q

What does the Pulmonary system excrete?

A

Anesthetic gases
Alcohol

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112
Q

What does breast milk excrete?

A

Lipophilic drugs
i.e. barbituates, salicylates, morphine, steriods, radioactive substancesO

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113
Q

Other than breast milk, what is another form of milk excretion is important?

A
  • Cows can also have residue drugs be excreted through their milk that humans can ingest
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114
Q

How do you calculate renal clearance (CL)

A

CL (L/hr) = Rate of elimination (mg/Hr) / Plasma drug concentration (Cp) (mg/L)

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115
Q

What is 1972?

A
  • Regarding clotting factors
  • Clotting factor 10, 9 , 7, 2 require Vitamin K
  • Thus how Vitamin K deficiency can disallow coagulation
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116
Q

What does Heparin Sulfate bind? What is the result?

A

Heparin sulfate binds Antithrombin III which will inactivate circulating plasma clotting factors including Clotting Factor II, Clotting IX, Clotting X

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117
Q

What is another name for Thrombin

A

Factor II (activated)

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118
Q

What does ANP do?

A

Diuretic, encourage fluid excretion

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119
Q

On cardiac auscultation, a snap followed by a rumbling diastolic murmur is heard over the cardiac apex (mitral area). The snap most likely occurs at which of the following periods?

A

Mitral valve open

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120
Q

Physical examination reveals bounding femoral pulses and carotid pulsations that are accompanied by head bobbing. What is the likely diagnosis

A

Aortic regurgitation

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121
Q

What is the Triangle of Koch

A

IVC, Tricuspid valve, AV node

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122
Q

What does the liver make that contributes to osmotic pressure?

A

Albumin

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123
Q

Which tissues is most likely dependent upon tissue metabolism and not autonomic control?

A

Brain

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124
Q

Atrial fibrillation can cause:
Why?

A
  • Stroke due to embolus
  • The atria are improperly contracting and not pushing all the blood out during atrial contraction
  • This blood can accumulate in the auricle and clot together
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125
Q

Carotid A uses ______________ to reach the NTS efferent via ____________.
_______________ uses vagus both afferent and efferent.

A

Glossopharyngeal

Vaugs

Aorta uses both vagus both afferent and efferent pathway

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126
Q

DIC means what?

A

Loss of clotting factors via due to multiple thrombi throughout the body
leading to deficit of clotting factors

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127
Q

What does protein C inactivate?
What cofactor does protein C need?

A

Protein C inactivates factor inactivates V & VIII

Needs protein S

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128
Q

Which type of hip dislocation is most common anterior or posterior? Why?

A

Posterior more common due to weakness of ischiofemormal ligament

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129
Q

Describe the presentation of posterior hip dislocation

A
  • Deep anterior acetabulum
  • Affected lower extremity appearing shorter, flexed, adducted and medially rotated
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130
Q

Describe the presentation of anterior hip dislocation

A
  • Affected lower extremity is flexed, abducted, laterally rotated
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131
Q

Describe presentation of femoral neck fracture

A
  • affected lower extremity shorted
  • Laterally rotated limb
  • Muscles may be attached to distal fracture fragment
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132
Q

Where along the tibia do compound tibial shaft fractures occur?

A
  • Open fracture at the middle inferior 1/3 of tibial shaft most common
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133
Q

What is a common cause of Transverse tibial stress/march fracture?

A

Common in people who take long hikes prior to being conditioned for the activity

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134
Q

What is a diagonal tibial fracture?

A
  • Severe torsion (typically while skiiing)
  • Causing diagonal fracture at the middle and inferior shaft of tibia and fibula
  • Presenting as limb shortening
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135
Q

What might cause patellofemoral dysfunction?

A
  • Overuse, trauma, muscle imbalance or increased Q angle
  • Leads to mistracking of the patella
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136
Q

What is the difference between prepatellar bursitis and deep infrapetallar bursitis?

A
  • Prepatellar is housemaids knee due to trauma or pressure on prepatellar bursa presenting with pain and swelling of anterior knee
  • DIB: aka Clergyman’s knee due to pressure on infrapatellar bursa presenting with pain below the knee cap exacerbated by kneeling
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137
Q

What causes ACL tear?

A
  • Hyperextension of knee
  • Anterior femoral force of semiflexed knee or lateral twisting
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138
Q

What is the mechanism of injury for the Terrible Triad?

A

Forced flexion and abduction of knee with foot fixed upon group

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139
Q

What mechanism of injury is associated with PCL tear?

A
  • Force to tibial tuberosity when knee flexed
  • Dashboard injuries in MVC
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140
Q

What is injured in a high ankle sprain?

A

Tibiofibular syndesmosis

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141
Q

What is Maisonneuve fracture?

A
  • Unstable ankle injury
  • Caused by disruption of distal tibiofibular syndesmosis
  • Or fx of medial malleolus + spiral fracture of proximal fibula
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142
Q

What tests might be used to screen for thoracic outlet syndrome?

A
  • Adson’s test: assessing subclavian A compression caused by scalenes
  • Roos/Elevated arm stress test: neurovascular compressed
  • Wright’s/Hyperabduction test: Compression of axillary artery and brachial plexus
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143
Q

Where is chest tube inserted? What condition might this be indicated?

A
  1. Chest tube inserted into 2nd & 3rd intercostal space at midclavicular line
  2. Pneumothorax or Hemothorax (different space for this)
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144
Q

Where is the blood located in a hemothorax?

A
  • Blood in pleura space
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145
Q

What is the treatment for hemothroax?

A
  • Chest tube inserted into 5th ICS at midaxillary line
  • Thoracentesis through 8th-10th ICS at midaxillary line into costodiaphragmatic recess
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146
Q

What is the difference between pneumothorax and pleural effusion?

A
  • Pneumothorax is air leaking into pleural space due to collapsed lung
  • Pleural effusion is FLUID in the pleural space
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147
Q

What is empyema?

A

Pus in the pleural space

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148
Q

What is pericarditis? What is it associated with?

A

Pericarditis is inflammation of pericardia
- Identified by distinct pericardial friction rub
- Can lead to pericardial effusion

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149
Q

What is pericardial effusion? What is the treatment?

A
  • Fluid accumulation in fluid of pericardium
  • Can lead to cardiac tamponade
  • Tx: pericardiocentesis through left subcostal angle
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150
Q

When does this murmur occur?
Describe it:
Aortic stenosis

A
  • Systolic murmur
  • Crescendo-decrescen
    do murmur
  • Aortic area (sternal
    border at R 2nd ICS)
    → carotids
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151
Q

When does this murmur occur?
Describe it:
Mitral Regurgitation

A
  • Systolic murmur
  • Holosystolic murmur
  • Mitral area (mid-axillar
    line, L 5th ICS) →
    axilla
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152
Q

When does this murmur occur?
Describe it:
Tricuspid regurgitation

A
  • Holosystolic murmur
  • Tricuspid area (sternal
    border, L 4th ICS)
  • Systolic murmur
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153
Q

When does this murmur occur?
Describe it:
Mitral prolapse

A
  • Midsystolic ejection
    click followed by
    crescendo murmur
  • Mitral area (mid-axillar
    line, L 5th ICS)
  • Can predispose to
    infective endocarditis
  • Systolic murmur
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154
Q

When does this murmur occur?
Describe it:
Hypertrophic cardiomyopathy

A
  • Systolic murmur
  • Crescendo-decrescen
    do murmur
  • Erb’s point (sternal
    border, L 3rd ICS)
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155
Q

When does this murmur occur?
Describe it:
Aortic regurgitation

A
  • Diastolic murmur
  • Descrescendo
    murmur
  • Aortic area (sternal border, 2nd ICS) if aortic root dilation,
    pulmonary area
    (sternal border, L 2nd
    ICS)
  • Can progress to left
    heart failure
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156
Q

When does this murmur occur?
Describe it:
Mitral stenosis

A
  • Diastolic murmur
  • Opening click followed
    by delayed rumbling
  • Opening click
    = valve
    buckling as
    blood flows
    from LA→LV
  • Mitral area (mid-axillar
    line, L 5th ICS)
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157
Q

What is stage 1 hypertension?

A
  • Sytolic 130-139
  • Diastolic 80-89
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158
Q

What is stage 2 hypertension?

A
  • Systolic greater than 140+
  • Diastolic greater than 90+
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159
Q

What is hypertensive crisis parameters?

A

Systolic: 180+
Diastolic: 120+

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160
Q

What is acquisition & mechanism of the transposition of the great arteries

A
  • Acquisition & mechanism: defective migration of neural crest cells → conus
    arteriosus does not develop normally during incorporation of bulbus cordis into
    ventricles → aorticopulmonary septum fails to pursue spiral course → aorta and
    pulmonary artery switching in location → oxygen-poor blood goes back to body,
    oxygen-rich blood goes back to lungs
  • Often associated with other cardiac defects (like ASD or VSD)
  • Common cause of cyanotic heart disease in neonates
  • Infants typically die within few months if not surgically corrected
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161
Q

What is the equation to calaculate blood pressure?

A

BP = CO * TPR

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162
Q

List 3 ways to increase arterial pressure

A
  • Constrict arterioles of the body inducing increase in TPR
  • Constrict large vessels of the circulation to increase venous return & CO
  • Directly increase CO by increasing HR & contractility
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163
Q

What nerves does the carotid sinus reflex use?
What does it increase?

A
  • Carotid sinus reflex uses afferent Hering nerve (branch of Glossopharyngeal AKA CN IX) and efferent Vagus N (CN X_
  • Increases parasympathetic outflow
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164
Q

What condition can predispose a patient to carotid sinus syndrome?

A

Atherosclerosis

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165
Q

T/F: The vasomotor center only directs parasympathetic outflow activity via Vagus and CN IX

A

False, it has a vasoconstrictor area too that maintain partial state of constriction of blood. Also the lateral portion controls heart rate and activity. Can release norepinephrine

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166
Q

What chemoreceptors respond to?

A
  • Low O2
  • Too much CO2
  • H+ excess
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167
Q

Where are chemoreceptors?
When are they activated?

A
  • Located in carotid bodies
  • Activated by chemical changes and stimulated after pressure below 80 mmHg
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168
Q

Carotid sinus baroreceptors respond to pressures between:
The baroreceptor reflex is most sensitive at _____________ mmHg

A
  • Carotid sinus baroreceptors respond to pressures between 60 and 180 mmHg
  • Baroreceptor reflex is most sensitive at pressure of 100 mmHg
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169
Q

What are the effects of the Bainbridge reflex?

A

Increase in atrial pressure/stretch sends signals to Vasomotor center via vagal afferents to increase heart rate and contractility

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170
Q

What is Stokes-Adams syndrome?

A
  • Transient (5-20 sec) lack of blood to brain due to the delay in heart beat leading to syncope
  • Delay in pick up heartbeat
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171
Q

How do you calculate stroke volume?

A

SV = EDV - ESV

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172
Q

What is another name for afterload?

A

Systemic vascular resistance

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173
Q

What is ejection fraction an index of?

A

Index of ventricular function and contractility

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174
Q

How to calculate Ejection fraction?

A

EF = SV/EDV * 100
AKA
EF = ( EDV-ESV / EDV ) * 100

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175
Q

What receptors does epinephrine work on in the heart?

A
  • Acts on β1 receptors to increase heart rate and afterload thus increasing CO
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176
Q

What does Epoxide reductase do?

A
  • Reduces Vitamin K converting it to its active form so that it can activate vitamin K clotting factors along with γ Glutamyl carboxylate
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177
Q

Describe Fibrinolysis

A
  • Proteins on endothelial surface binds with circulating plasminogen to form plasmin that will break down fibrin mesh
  • Releases D-dimer
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178
Q

What is administered in the clinical setting to break up clots?

A
  • Tissue plasminogen activator encourages plasmin formation to breakdown fibin mesh
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179
Q

Describe the hemostasis extrinsic pathway

A
  • Factor III is released by damaged epithelial cells
  • Interaction b/t Factor III & Factor VII activates Factor VII
  • Factor VII activates the common coagulation pathway
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180
Q

What cofactors are required for Factor IX & Factor VIII that will eventually activate Factor X?

A

PF3 & Ca

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181
Q

Along with Factor 8 & 9, What other cofactor is required to activate Factor X?

A

Factor V

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182
Q

Describe the common coagulation factor

A
  1. Factor Xa activates prothrombin activator
  2. Prothrombin activator interacts with circulating Factor II, Thrombin
  3. Thrombin will begin to link molecules of Fibrinogen to Fibrin
  4. Thrombin will interact with Factor XIII to further engage cross linking to create Fibrin mesh
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183
Q

What does Thrombomodulin do?

A
  1. Thrombomodulin binds with Thrombin, Factor II
  2. Factor II activates Protein C
    2a. Protein C requires protein S
  3. Protein C degrades Factor V & Factor VIII
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184
Q

What does Protein C do?

A

Degrades Factor V & VIII thus is a anticoagulation protein

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185
Q

Describe platelet plug formation

A
  1. Start with Von Willebrand Factor binding to platelet receptor, GP1B
  2. Platelets release: ADP, Serotonin, Thromboxane A2 (TXA2) to recruit more platelets
  3. Between the endothelial cells, Fibrinogen binds to receptors, GPIIb & GPIIIa, to form a platelet plug
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186
Q

Contrast the extrinsic prothombin activator extrinsic and intrinsic pathway

A

Extrinsic:
- activated by trauma to vessel wall & adjacent tissue
- Activated within <15 seconds
Intrinsic:
- Trauma to the blood or exposure of the blood to collagen
- Activated within 1-6 minute

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187
Q

What increases levels of circulating t-PA?

A

Catecholamines & bradykinin

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188
Q

What organ(s) produces a large amount of clotting factors?

A

Liver

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189
Q

What does Vitamin B1, thymine deficiency cause?

A

Cardiomyopathy

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190
Q

What can cause vitamin K deficiency?

A
  • Lack of bile production or malnutrition can cause fat malabsorption and thus vitamin K deficiency
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191
Q

Vitamin K is important to what clotting factors?

A

1972: Factor X, Factor IX, Factor VII, Factor II
Protein C

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192
Q

What is Factor II deficiency ?

A
  • Inherited autosomal recessive
  • Results in Dysprothrombinemia & Hypoprothrombinemia
  • Easy bruising, frequent nose bleeds, hemorrhaging after surgery or trauma
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193
Q

What is Dysprothrombinemia

A

Abnormality in the structure in prothrombin

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194
Q

What is Hypoprothrombinemia

A

Inadequate production of prothrombin

195
Q

What is the predominant form of Hemophilia?

A

Hemophilia A

196
Q

What is Hemophilia A a deficiency of?

A

Deficiency of Factor VIII

197
Q

What is Hemophilia B a deficiency of?

A

Deficiency of Factor IX

198
Q

What is Hemophilia C a deficiency of?

A

Deficiency of factor XI

199
Q

Describe the small and large components of Factor VIII Deficiency

A
  • Deficiency of small component causes Hemophilia A, treatable with VIII Replacement
  • Deficiency of large component is von Willebrand disease
200
Q

Describe thrombocytopenia

A
  • Low platelet number
  • Bleeding from small venules or capillaries
  • Petechiae, thrombocytopenic purpura
201
Q

What are the two platelet counts indicating moderate to life threatening thrombocytopenia

A
  • Modest bleeding: < 50,000 platelets
  • Life threatening: <10,000 platelets
202
Q

Where do PE usually occlude?
What is administered for treatment of PE?

A
  • PE arise from deep leg veins that occlude pulmonary arteries
  • tPA is administered to bind to plasminogen to form plasmin that will breakdown fibrin mesh
203
Q

What is disseminated intravascular coagulation?

A
  • Consumptive coagulopathy
  • Occuring in the setting of massive tissue damage or sepsis
  • Widespread coagulation in small vessels
  • Clotting factors have been expended and used up allowing bleeding, low clotting fibers
  • Fibrin degrading products are elevated & increase D dimer
204
Q

What does the anticoagulant Heparin do?

A
  • Potentiates Antithrombin III
  • Clinically useful anticoagulant
  • Works very fast
205
Q

How do coumarins work?

A
  • Inhibit epoxide reductase. This enzyme inactivates Vitamin K so that it cannot be a cofactor for clotting cascade
206
Q

What is the treatment for over-anticoagulation

A

Fresh frozen plasma and Vit K

207
Q

What does PT assess?

A
  • Prothrombin Time assesses extrinsic and common pathway clotting cascades
208
Q

What is factor I

A

Fibrinogen

209
Q

What is the difference between Partial Thromboplastin time and Prothrombin time?

A
  • PTT: Assessing intrinsic & common pathway clotting
    & thus used to monitor heparin therapy
  • PT: assessing extrinsic pathway and common pathway & thus used to monitor warfarin therapy
210
Q

What is normal platelet count?

A

150,000-450,000 platelets

211
Q

What does Fibrin split product analyze?

A

Indicates the cleavage of fibrin or fibrinogen

212
Q

What do platelet aggregation tests analyze?

A

Determine if Glycogen IIb/IIIa protein is working for clotting

213
Q

What is Factor V Leiden?

A

Production of mutant Factor that is resistant to degradation by activated protein C
- can allow DCT, cerebral vein thrombus, recurrent pregnancy loss

214
Q

What is Factor V Leiden?

A

Production of mutant Factor that is resistant to degradation by activated protein C
- can allow DCT, cerebral vein thrombus, recurrent pregnancy loss

215
Q

What is Bernard-Soulier?

A
  • Clotting deficiency disorder
  • Protein that binds platelets to endothelial collagen, Gp1b, does not bind to von Willebrand factor
  • Tested via Ristocetin levels
216
Q

What is Glanzmann thrombasthenia?

A
  • Deficiency of GpIIb/IIIa which disallows platelets to form platelet plugs
  • Platelet disorder
217
Q

What is RISTOCETIN

A

Activator that binds von Willebrand factor to bind to Glycoprotein I b, Gp1b

218
Q

What are vitamin K dependent factors?

A

1972, Protein C & S

219
Q

Which clotting factor has the longest half life?
Shortest half life?

A

Factor VII is shortest half life
Factor II has longest half life

220
Q

Where does immune thrombocytopenia occur?

A

Destruction of platelets in the spleen

221
Q

Hereditary thrombophilias are inherited via:

A

All autosomal dominant inheritance

222
Q

What does prothrombin G20210A hereditary thrombophilia cause?

A
  • Comes from point mutation in 3’ untranslated region of DNA
  • Increased production of prothrombin
  • Hypercoagulable state
223
Q

What are DAMPS?

A

Associated with acute inflammation innate, internal immunity
- Damage associated molecular patterns
- Intracellular molecules that are released from damaged cell & interpreted as antigens

224
Q

What are DAMPs released in response to?

A

DAMPS are released in response to necrosis from ischemia, trauma,
physical or chemical injury

225
Q

What are PAMPS?

A

Associated with acute inflammation, innate external immunity
- PAMPS: Pathogen Associated Molecular patterns
- immune rxn to pathogenic antigens

226
Q

What are signs of inflammation?

A
  • Calor
  • Dolor
  • Rubor
  • Tumor: swelling
  • Functio Laesa: temporary loss of function
227
Q

What is purulent exudate?

A

containing neutrophils, cellular debris & microbes

228
Q

What is transudate?

A
  • Low protein content
  • Few cells overall
229
Q

Describe how extravasation allows WBC to move from blood vessels to interstitial space

A

Endothelial cells contract to create spaces in the capillaries due to histamine, bradykinin, & Leukotrienes which allows fluid and WBC to go into IF

230
Q

Describe how loss of fluid and increased diameter of vessels allows rubor during acute inflammation

A

Loss of fluid and increased diameter of vessels increases Hct that allows for vascular congestion leading to Rubor of tissue

231
Q

What are C₃a & C₅a?

A
  • Histamine complement proteins
  • cause vasodilation and increased vascular permeability
232
Q

What are: Leukotrines

A

produced by Leukocytes cause vasodilation and increased vascular permeability

233
Q

Acute inflammation: what do Interleukin 1 & Tumor Necrosis Factor

A

Fever induced by Interleukin 1 & Tumor Necrosis Factor

234
Q

What induces pain during acute inflammation

A

Pain induced by Prostaglandins, Bradykinin, Neuropeptides

235
Q

What do Lysosomal enzymes & Reactive Oxygen Species (ROS) during acute inflammation

A

Induce tissue damage

236
Q

What type of immunity are marcophages?

A
  • Monocytes turn to macrophages that have phagocyte activity
  • Innate immunity
237
Q

What type of immunity are T & B cells

A
  • Lymphocytes are T & B cells
  • Adaptive Immunity
238
Q

What is Serous Inflammation:

A

Exudate in peritoneum, pleura, pericardium, dermis

239
Q

What is fibrous inflammation?

A
  • activation of coagulation & depositions of fibrin
  • May resolve on its own
  • Plasmin is an enzyme that helps remove fibrous inflammation
  • May not resolve = scarring
240
Q

What is Purulent Inflammation

A
  • Abscesses, exudate containing neutrophils, debris & edema fluid
  • Caused by bacterial infection
241
Q

Define ulcer

A

Localized Shedding of inflamed or necrotic tissue

242
Q

Define scarring:

A

fibroblasts produce collagen distributed to extracellular matrix

243
Q

Where do adult monocytes originate from?

A

Bone marrow

244
Q

Where do embryonic monocytes originate from?

A

Embryologic development occurring in yolk sac resulting in production of Microglia, Kupffer in Liver, Alveolar macrophages

245
Q

Chronic inflammation: What do M1 macrophages secrete?

A
  • Secrete chemokines 1, 6, 12 as pro-inflammation
  • Macrophages secrete lysosomal enzymes, induce nitric oxide all for antimicrobial action
246
Q

What initiates the M1 classic chronic inflammation pathway?

A

Pro-inflammatory & production triggered by T helper cells via INF γ

247
Q

What induces M2 alternative chronic inflammation pathway?

A

Induced by T Helper cells 2 via IL-13 and/or IL-4

248
Q

What is M2 alternative chronic inflammation pathway?

A

Healing, tissue repair, angiogenesis, non-inflammatory component

249
Q

What do T Helper Cells 1 secrete?

A

Produce INF γ which activate M1 macrophages

250
Q

What do T Helper Cells 2 secrete?

A
  • Secrete IL-4, IL-5, IL-13 that activate M2 macrophages
  • Also recruit eosinophils-parasitic infection
251
Q

What do recruits Eosinophils?

A

Eotaxin

252
Q

What do T Helper Cells 7 do?

A

Make IL-17 that recruit neutrophils

253
Q

Where do B cells come from?
What do they do?

A
  • B cells are activated by T cells. T cells came from Lymphocytes
  • Plasma cells are involved in antibody production
254
Q

Define Non-Specific Proliferative chronic inflammation

A

non-specific granulation with infiltration by lymphocytes, macrophages & plasma cells and proliferation of fibroblasts, connective tissue, vessels, & epithelial cells

255
Q

Give 3 examples of Non-specific proliferative chronic inflammation

A
  • nasal/cervical/gastric polyps
  • Organized hematoma
  • Lung abcess
256
Q

Define Granulomatous Inflammation

A
  • has particular granulomas that form due to foreign body or T cell mediated immune response or chronic infection
  • Characterized by being surrounded by lymphocytes to form Langhans/Gaint cells
  • Caseating or Noncaseating
257
Q

Define caseating granulomatous inflammation

A
  • Surround low virulent pathogens, have epithelioid cells, T cells, B cells, macrophages
  • Chronic infection, contain necrotic tissue
258
Q

Give 3 examples of Caseating granulomatous inflammation

A
  1. TB
  2. Syphilis
  3. Cat-Scratch
259
Q

Describe Noncaseating granulomatous inflammation

A
  • Multinucleated giant cells which are fusion of monocytes and macrophages, have B cells to produce antibodies
260
Q

Give 3 examples of noncaseating granulomatous inflammation

A
  1. Leprosy
  2. Sarcoidosis
  3. Chron’s Disease
261
Q

What is normal range of Leukocytes?

A

15,000-20,000

262
Q

What are 3 acute phase proteins made by the liver in chronic inflammation?

A
  • C-Reactive protein to help body recognize foreign: opsonization
    -Fibrinogen
  • Serum Amyloid A protein
263
Q

Liver & lungs are most frequently involved in _____________________
_________________

A

hematogenous dissemination

Hematogenous dissemination is the spread of something through the bloodstream, such as bacteria or cancer cells

264
Q

Describe characteristics of benign tumor

A
  • well defined borders & encapsulated
  • low nuclear cytoplasmic ratio
  • tend to be differentiated
  • low mitotic activity
  • resemble normal tissue
    -never invasive or metastatic
264
Q

What is the difference between Neoplasia & Neoplasm?

A
  • Neoplasia: abnormal and uncontrolled cell growth
  • Neoplasm: an abnormal mass of tissue that forms when cells grow and divide more than they should or do not die when they should
265
Q

What are some benign tumors that form in the epithelium?

A

adenoma, papilloma, fibroadenoma

266
Q

What are some benign tumors the form in the mesenchyme?

A

Fibroma
Lipoma

267
Q

What are some benign tumors that form on the smooth muscle and blood?

A

leiomyoma, rhabdomyoma, mature teratoma

268
Q

What are some characteristics of malignant tumors?

A

poor demarcation
- nuclear pleomorphism (varied size & shape)
- nuclear hyperchromatic (darkly stained nuclei) with prominent nuclei
- increased nuclear to cytoplasmic ratio
- invasive growth pattern
- increased mitotic activity with abnormal mitotic figures

269
Q

What are some malignant tumors that form in the epithelium?

A

carcinoma (adenocarcinoma, papillary carcinoma, & invasive ductal carcinoma)

270
Q

What are some malignant tumors that form in the epithelium?

A

sarcoma including fibrosarcoma & liposarcoma

271
Q

What are some malignant tumors that form in the blood/lymph:

A

leiomyosarcoma, rhabdomyosarcoma, leukemia, lymphoma, immature teratoma

272
Q

Define anaplasia:

A

cellular process that implies dedifferentiation, meaning there is loss of structural and functional differentiation or normal cells during tumorigenesis

273
Q

Define dysplasia:

A
  • presence of abnormal cells within a tissue or organ (with features of malignant neoplasms)
  • noncancerous but has potential to become cancerous
  • occurring in epithelia
274
Q

There is been a decrease in death rate in many cancers except:

A

liver cancer due to increase in Hep C incidence

275
Q

What are the top 3 cancer incidents for men?

A

Prostate (27%), lung (12%), colon & rectum (8%)

276
Q

What are the top 3 cancer incidents for women?

A

Breast (31%), lung (13%), colon and rectum (8%)

277
Q

What are the top 3 cancer incidents for children?

A

Leukemia, brain/CNS cancer, neuroblastoma, non-Hodgkins’s lymphoma

278
Q

These drugs are anticancer drugs but are also carcinogenic agents:

A

aflatoxin & benzopyrene

279
Q

How is overexposure to radiation a carcinogenic agent

A

causing pyrimidine dimers in DNA, UVB is most carcinogenic

280
Q

HTLV-1 causes what cancer

A

HTLV-1 causing Leukemia and Lymphoma (RNA virus

281
Q

What type of cancer does EBV

A

EBV causing Burkitt Lymphoma

282
Q

What type of cancer does HPV cause?

A

Squamous papilloma

283
Q

What type of cancer does HHV-8 cuase?

A

Kaposi sarcoma

284
Q

These carcinogenic chemicals: Chromium & nickel cause what type of cancer?

A

Lung cancer

285
Q

These carcinogenic chemicals: Nitrosamine cause what type of cancer?

A

Gastric cancer

286
Q

These carcinogenic chemicals: Vinyl chloride cause what type of cancer?

A

Angiosarcoma of liver

287
Q

These carcinogenic chemicals: Aromatic amines cause what type of cancer?

A

Hepatocellular carcinoma

288
Q

These carcinogenic chemicals: Benzene cause what type of cancer?

A

Leukemia

289
Q

These carcinogenic chemicals: Alkylating agents cause what type of cancer?

A

Leukemia, lymphoma, skin and bladder cancer (they block DNA replication)

290
Q

What does ERBB2 oncogene do?

A
  • amplifies HER2, growth factor receptor, initiating breast, ovary, lung cancer
  • Cancer management based on grading and markers-estrogen receptor, progesterone receptor, and HER2 for treatment decision making
  • Seen more often in sporadic cancer with double hit
291
Q

ABL oncogene translocating from Cr. 9 to 22 (t9;22) does what?

A

Initiates chronic myeloid leukemia

292
Q

Point mutation of _____________ affecting small G protein leading to:

A

Point mutation of KRAS affecting small G protein leading to lung, pancreas, colon cancer

293
Q

Translocation of MYC gene translocating from Cr _ to __ causes:

A

Translocation of MYC gene translocating from Cr 8 to 14 (t8;14) upregulating transcription factor leading to Burkitt lymphoma

294
Q

Translocation of CCND1 from Cr. __ to ___ causing:

A

Translocation of CCND1 from Cr. 11 to 14 causing Mantle cell lymphoma

295
Q

VHL gene inactivation disallowing ubiquitin E3 ligase causing: ___________________. By what mechanism?

A

Hemangioblastoma (VHL syndrome) and allows HIF to be too active

296
Q

What is HIF?

A

HIF is a transcription factor that plays an essential role in the cellular response to low oxygen, orchestrating a metabolic switch that allows cells to survive in this environment

297
Q

BRCA2 gene mutation disrupts & causes:

A

BRCA2 gene mutation disrupting SS DNA-binding protein/repair causing Hereditary breast cancer

298
Q

___ mutation causing binding and inhibition of ____ causing Retinoblastoma, osteosarcoma

A

RB1 mutation causing binding and inhibition of E2F-DP causing Retinoblastoma, osteosarcoma

299
Q

_____ mutation causing lung, breast, colon (Most common mutation found in cancers)

A

TP53 mutation causing lung, breast, colon

300
Q

______ gene mutation disrupting a __________________ protein causing neurofibromas

A

NF1 gene mutation disrupting a GTPase-activating protein causing neurofibromas

301
Q

BRCA1 mutation disrupts & causes:

A

BRCA1 mutation disrupts double stranded break DNA repair complex causing breast and ovarian cancer

302
Q

What is Warburg effect?

A
  • Deviation of normal cells in cancer where in cancer cells oxidative phosphorylation and mitochondria activity is downregulated and glycolysis is upregulated to use the intermediate products
303
Q

How does metastasis function?

A

Metastasis by disrupting cadherin or upregulating matrix metalloproteinases to allow movement of cell into other tissue

304
Q

What is Cancer cachexia?

A

Loss of body weight

305
Q

Give an example of paraneoplastic syndrome:

A
  • Paraneoplastic Syndrome: secondary/global effects from a specific cancer
  • Ex. lung cancer causing Cushing syndrome or squamous cell carcinoma causing hypercalcemia via overexpression of PTH or Small-Cell carcinoma of the lung causing overexpression of ADH
306
Q

What is the difference between low grade and high grade regarding tumor grading and staging?

A
  • Low grade: well differentiated borders
  • High grade: poorly differentiated borders
307
Q

What does T stand for in TMN cancer staging system

A

T is for size of primary tumor

308
Q

List the meaning for TMN staging
T1
T2
T3
T4

A
  • 1: Small, minimally invasive within primary organ site
  • 2: Larger, more invasive within primary organ site
  • 3: Larger and/or invasive beyond margins of primary organ site
  • 4: Very large and/or very invasive spread to adjacent organs
309
Q

What does N stand for in the TMN cancer staging system?

A

Extent of regional lymph node spread

310
Q

List the meaning for TMN staging
N0
N1
N2
N3

A
  • 0: No lymph node spread
  • 1: Regional lymph node involvement
  • 2: Extensive regional lymph node involvement
  • 3: More distant lymph node involvement
311
Q

What does M stand for in TMN cancer staging system?
What are the M stages?

A
  • M: presence of metastasis
  • 0: No distant metastases
  • 1: Distant metastases present
312
Q

What is a good molecular marker for monitoring breast cancer?

A

Estrogen levels

313
Q

What cancers does intermediate filament make a good marker for?

A

Intermediate Filament is good marker to monitor carcinoma, sarcoma, astrocytoma
- Can indicate where the tumor came from

314
Q

What tissue specific markers are used to monitor Lung cancer?

A
  • NSE
  • CEA
  • TP53
  • Ras mutants
315
Q

What tissue specific markers are used to monitor breast cancer?

A

CA 15-3 & CA27-29

316
Q

What tissue specific markers are used to monitor colon cancer?

A
  • CA 19-9
  • CEA
  • TP53
  • Ras mutants
317
Q

What tissue specific markers are used to monitor prostate cancer?

A

PSA & PAP

318
Q

Observing G6PD isoforms G6PD₅₄₅ & G6PD₅₁₅ are useful for:

A
  • Found more often in women
  • Useful in T cell vs B cell lymphoma
  • Neoplasm: found only 1 isoform
319
Q

What does Kappa Lambda (light chains of antibodies) Ratio in B lymphocytes indicate?

A

Normal K: L ratio is 3:1
Lymphoma: Reversed or increased > 6:1

320
Q

Desmin seen in normal muscle cells but also seen in what type of cancer cells?

A

uterine leiomyoma & rhabdomyosarcoma

321
Q

Vimentin seen in normal mesenchymal cells but also found in what type of cancer?

A

Vimentin seen in normal mesenchymal cells but also found in Sarcoma

322
Q

Desmin seen in normal muscle cells but also seen in what type of cancer?

A

Desmin seen in normal muscle cells but also seen in uterine leiomyoma & rhabdomyosarcoma

323
Q

What are some examples of cellular hypertrophy?

A
  • Increase in uterus size during pregnancy
  • Cardiac muscle
  • Skeletal muscle
  • Pathologic: aortic stenosis & thiamine deficiency
324
Q

Contrast hypertrophy vs hyperplasia

A
  • Hypertrophy is increase in size of cells
  • Hyperplasia is increase in number/quantity of cells
325
Q

What are some examples of hyperplasia:

A
  • Female breasts in puberty (in addition to hypertrophy)
  • Liver
  • Bone marrow
  • Pathologic: endometrial hyperplasia, benign prostatic hyperplasia, skin warts
326
Q

What are some causes of atrophy?

A

Can be caused by decreased workload, loss of innervation, diminished blood supply, inadequate nutrition, decreased hormonal stimulation

327
Q

Why does metaplasia occur?

A

New cell type is better able to withstand stresses

328
Q

T/F: Metaplasia is a reversible process

A

True, if stressing stimulus is removed sometimes reprogramming of stem cells will reverse the metaplasia

329
Q

What type of cell transition occurs in Barret’s esophagus?

A
  • Mucus Secretion diminished in Barret’s esophagus from columnar epithelium to squamous cells
  • Causing decreased ciliary clearance
330
Q

How does the cell respond to prolonged hypoxia?

A
  • Decrease synthesis of ATP causes decreased function of Na+/K+ pumps that allows an influx of Na+ and efflux of K+. This results in cellular swelling and swelling of endoplasmic reticulum
  • The cell will then use anaerobic glycolysis for energy production which decreases cytoplasmic glycogen, increase lactic acid, and decrease pH
  • Clumping of nuclear chromatin
331
Q

What does decreased protein synthesis in the cell do?

A

Decreased protein synthesis causes detachment of ribosomes from the rough ER

332
Q

Unde what circumstances might Plasma-membranes blebs and myelin figures may be seen

A

During tissue hypoxia

333
Q

Cellular swelling is a reversible cell injury, describe what happens & how

A
  • Causes decreased ATP production causing decrease in ionic pump failure and inability to maintain fluid homeostasis
  • Cellular swelling causes hydropic change (containing too much water or fluid) or vacuolar degeneration
334
Q

What is Steatosis?

A

Fatty Change: appearance of lipid vacuoles in cytoplasm (e.g. liver) with accumulation of TAG (triacylglycerols)

335
Q

Myelin figures appear in reversible cell injury, what is another name for them?

A

Zebra bodies

336
Q

What can transform reversible cell injury to irreversible?

A
  • Mass of calcium damage can result in severe membrane damage as well as efflux of intracellular enzymes and proteins into circulation
  • Mitochondria dysfunction causing mitochondrial swelling
  • Rupture of lysosomes
337
Q

What is Karyolysis?

A

Nuclear change
- dissolution of chromatin (specifically in necrosis)

338
Q

What is Karyorrhexis?

A
  • Nuclear change
  • Fragmentation of the nucleus
339
Q

What is Pyknosis?

A
  • Nuclear change
  • Condensation of chromatin
340
Q

Describe characterizing factors of Necrosis:

A
  • Necrosis characterized by swelling, nuclear changes, plasma membrane disruption
  • Inflammation present
  • Usually due to pathology or culmination of irreversible cellular injury
341
Q

Describe characterizing factors of Apoptosis:

A
  • Shrinkage, fragmentation to nucleosome-size fragments, intact plasma membrane with altered structure-especially orientation of lipids, cellular contents are intact, no accompanying inflammation, often physiologic
  • Usually only affects a single cell or small group of cells
  • Stimulus for Apoptosis: Cellular Damage & Extrinsic signals (FasL)
342
Q

List 5 enzymes released indicating cellular damage:

A
  1. AST (liver injury)
  2. ALT (liver injury)
  3. Creatinine kinase (heart injury)
  4. Amylase and lipase (pancreatic injury; amylase rise in salivary gland injury)
343
Q

What does BAX do?

A
  • Related to Apoptosis
  • If BAX binds with Bcl-2 this is anti-apoptotic
344
Q

Describe Intrinsic pathway for Apoptosis

A

Uses: BAX, APAF-1, Caspase 9 & 3
1. Start with cell injury or cell having lack of growth factor, P53 activates BAX
2. BAX dimerizes
3. APAF-1 is activated and initiates the initiator caspase, Caspase 9
4. Initiator Caspase activates the executioner caspase, Caspase 3

345
Q

What do Caspase 8 & 9 have in common? Where do they differ?

A
  • Both initiator Caspases that recruit executioner Caspases
  • Caspase 8 is in the Extrinsic pathway of apoptosis
  • Caspase 9 is in the Intrinsic pathway of apoptosis
346
Q

Describe the _____________ apoptosis TNF pathway

A
  • Extrinsic pathway
    1. TNF2 binds to TNF receptor on cell membrane
    2. Recruits FADD which initiates the initiator caspase, Caspase 8
    3. Initiator caspase recruits executioner caspase, Caspase 3
347
Q

Describe the ____________ apoptosis Fas pathway

A
  1. Fas ligand binds with Fas receptor on cell membrane
  2. Fas receptor recruits FADD
  3. FADD initiates the initiator caspase, Caspase 8
  4. Initiator caspase recruits executioner caspase, Caspase 3
348
Q

What is coagulative necrosis?

A
  • Necrosis due to hypoxia inducing ischemic injury
  • Denaturing proteins in the cytoplasm
  • Loss of nucleus in the cell but cellular shape is preserved
349
Q

Where does coagulative necrosis occur?

A

Heart
Kidney
Liver
NOT IN THE BRAIN

350
Q

What is Liquefactive necrosis and where does it occur?

A
  • Digestion of dead cells by hydrolytic enzymes creating liquid mass
  • Occurring in sites including hypoxic areas of the central nervous system, pancreas, abscesses
351
Q

What is Caseous necrosis?

A
  • Coagulative + liquefactive necrosis appearing as white, crumbly, like cheese.
  • Occurring in granulomas and characteristic of TB
352
Q

What is Fat Necrosis? Where does it occur?

A
  • Action of lipases acting on adipocytes appearing as chalky white
  • Occurring in acute pancreatitis and inflammation of the breast
353
Q

Describe Fibrinoid necrosis:
Where does it occur?

A
  • Antigen-antibody complexes are deposited in the walls of blood vessels along with fibrin
  • Occurring in autoimmune and malignant HTN
354
Q

Describe Gangrenous necrosis:
Where might it occur?

A
  • Occurring in lower limbs, GI tract, testes
  • If ischemia only = dry gangrene due to coagulative necrosis, Example of this is diabetic foot
  • If ischemia and bacterial infection = wet gangrene that will lead to liquefactive necrosis, Example of this is severe burn or frostbite
355
Q

Describe pathologic accumulation: lipid accumulation

A
  • Caused by steatosis (fat buildup in organ) or fatty change
  • Can be seen on CT as decreased liver attenuation
  • Can be seen in alcoholics with fatty liver
356
Q

Describe pathologic protein accumulation:

A
  • May form Russell bodies in plasma cells
  • Cause unfolding of proteins in ER
  • May occur in proximal tubules in kidney
357
Q

What is an example of pathologic exogenous pigment accumulation

A

Exogenous Pigments: Coal dust causing anthracosis

358
Q

Endogenous pigments can be pathologic accumulations, describe:
Lipofuscin

A
  • Lipofuscin (browning pigment due to lipid digestion)
  • Can be seen in heart and liver of aging patients or in malnutrition
  • Residual bodies: cells within the autophagic vacuoles that resist digestion and persist in the cytoplasm and are membrane bound
359
Q

Endogenous pigments can be pathologic accumulations, describe: residual bodies

A

Residual bodies: cells within the autophagic vacuoles that resist digestion and persist in the cytoplasm and are membrane bound

360
Q

Endogenous pigments can be pathologic accumulations, describe: Hemosiderin

A
  • Hemosiderin-pigmentation caused by breakdown of blood cells
  • Found in hemorrhage or bruise due to systemic iron overload
  • Can also be seen in transfusion or hemochromatosis
361
Q

Endogenous pigments can be pathologic accumulations, describe: Dystrophic Calcification

A

Dystrophic Calcification occurring in dying or necrotic tissue including in fat, psammoma bodies or calcific valvular disease of the heart

362
Q

Endogenous pigments can be pathologic accumulations, describe: Metastatic Calcification

A
  • seen in normal tissues due to hypercalcemia
  • Can be seen in hyperparathyroidism
  • Found in interstitial side of stomach, kidneys, lung, systemic arteries, and pulmonary veins
  • Can cause renal injury leading to polyuria
  • Can be seen on XR
363
Q

Hyaline changes can be pathologic, describe intracellular hyaline changes

A

Protein reabsorption droplets in the proximal tubules, include Russell bodies, and alcoholic hyaline

364
Q

Hyaline changes can be pathologic, describe extracellular hyaline changes

A

In patients with long-standing hypertension and diabetes, extravasated plasma proteins or other proteins in the walls of arterioles

365
Q

Cancer genetics can arise from chromosomal instability and microsatellite instability. Differentiate the two:

A
  • Genetic instability: accelerates cancer progression by increasing likelihood of mutation
  • Chromosomal Instability results from defective repair of DNA double stranded breaks
  • Microsatellite Instability: number of repeated units in a microsatellite is different from what was inherited
366
Q

Cancer genetics, describe caretaker genes

A

Caretaker Genes: genes that don’t directly affect cell growth, rather affect ability for cell to maintain integrity of its genome

367
Q

How can proto-oncogenes be turned into oncogenes?

A
  • Point mutation
  • Amplification
  • Chromosomal rearrangement
368
Q

Cancer genetics- what is amplification?

A

Increase in DNA copy number

369
Q

This gene is amplified in cancer neuroblastoma

A

NMYC & LMYC

370
Q

This gene is amplified in agressive breast cancer

A

ERBB2/HER2

371
Q

Point mutation of RET results in proto-oncogene for GDNF resulting in:

A

Multiple Endocrine Neoplasia IIA or IIB

372
Q

Describe Multiple Endocrine Neoplasia IIA:

A
  • causing pheochromocytoma
  • medullary carcinoma and increased PTH due to parathyroid hyperplasia
373
Q

Describe Multiple Endocrine Neoplasia IIB:

A
  • Pheochromocytoma
  • medullary carcinoma
  • normal PTH
374
Q

Chromosomal rearrangement can induce cancer. What causes Chronic myelogenous leukemia and subsequent production of B genes?

A

translocation of ABL gene from Cr. 9 to Cr. 22 induces Chronic myelogenous leukemia and increased production of B cells

375
Q

Chromosomal rearrangement can induce cancer. What causes Mantle cell lymphoma?

A

Translocation of BCL1 gene from Cr. 11 to Cr. 14 induces Mantle cell lymphoma

376
Q

Chromosomal rearrangement can induce cancer. What causes Follicular lymphoma?

A

Translocation of BCL2 gene from chromosome 14 to chromosome 18 induces Follicular Lymphoma and increased production of B cells

377
Q

List 3 cancers that increase production of B cells

A
  • Chronic myelogenous leukemia
  • Follicular lymphoma
  • Burkitt’s lymphoma
378
Q

List 2 cancer translocations that translocate the gene to an IgH enhancer

A
  • Follicular lymphoma
  • Burkitt’s Lymphoma
379
Q

Translocation of ABL gene from Cr. ___ to Cr. ___ induces:

A
  • Chronic myeloid leukemia
  • ABL gene from Cr. 9 to Cr. 22
380
Q

What does P53 control?

A
  • Controls entry into S phase
  • Can allow entry from G1 to S phase or induce apoptosis
381
Q

What does RB control?

A
  • can prevent cell from G1 to S phase by inhibiting the transcription factor, E2F
382
Q

What causes Retinoblastoma: childhood eye tumor inheritance?
What is special about it inheritance?

A
  • Mutation of RB1 gene
  • Follows two hit model theory that must have inherited mutation and somatic mutation
383
Q

What happens to RB gene that causes inactivation and allow upregulation of cell cycle and subsequently proliferation?

A

If CDK phosphorylates RB this will cause inactivation and allow upregulation of cell cycle and subsequently proliferation

384
Q

What type of mutations inactivate tumor suppressor genes?

A
  • Point mutations
  • Deletions
  • Environment
  • Viruses
385
Q

What do point mutations cause?

A

Result in truncated or nonfunctional proteins

386
Q

These familial cancers follow the two hit model theory of cancer genetics

A
  • Familial breast cancer
  • Familial colon cancer
  • Familial melanoma
  • Neurofibromatosis
387
Q

Exposure to Aflatoxin (Mold) causes modification of TP53 which results in:

A

Exposure to Aflatoxin (Mold) causes modification of TP53 which results in hepatocellular carcinoma

388
Q

Exposure to cigarette smoke increases ____________ __________ __________ _________ that induces _________ _______________ which cause throat and lung cancer

A

Exposure to cigarette smoke increases CYP1A1 coding for AAH that induces epoxide hydrocarbons which cause throat and lung cancer

389
Q

HPV will inhibit __ protein which inactivates P53

A

HPV will inhibit E6 protein which inactivates P53

390
Q

HPV will inhibit ___ protein which inactivates Rb gene

A

HPV will inhibit E7 protein which inactivates Rb gene

391
Q

Familial Adenomatous Polyposis is caused by this mutation:

A

Familial Adenomatous Polyposis is caused by a mutation in APC on Chromosome 15q

392
Q

Hereditary Non-Polyposis also known as Lynch Syndrome is caused by a mutation of: ____________ & _______________. These are normally involved in:

A

Hereditary Non-Polyposis also known as Lynch Syndrome is caused by a mutation of hMLH1 & hMSH2 genes that are normally involved in DNA mismatch repair

393
Q

Melanoma caused by:
- Loss of function of this tumor suppressor gene:
- Amplified ____________ proto-oncogene

A

Melanoma caused by:
- Loss of function of this tumor suppressor gene CDK2A
- Amplified CDK2A proto-oncogene

394
Q

What is Von-Hipple Disease?

A

Tumors in multiple organs including hemangioblastomas: tumors occurring in brain spinal cord eye, retinal angiomas

395
Q

What causes Von-Hipple Disease?

A

Caused by mutation of Tumor suppressor gene: VHL where normal ubiquitinating property of the gene & hypoxia inducible factor are lost

396
Q

β thalassemia and Cystic fibrosis are caused by what type of gene mutation?

A

Nonsense mutation

397
Q

What is Vd of ECF for a 70 kg man?

A

Vd of ECF is 14 L

398
Q

What is Vd of interstitial fluid in a 70 kg man?

A

Vd of Interstitial fluid 10 L

399
Q

What is Vd of intracellular fluid for a 70 kg man?

A

Vd intracellular fluid 28 L

400
Q

When are weak base drugs protonated?

A

Protonated and ionized in a acidic environment

401
Q

Describe weak bases in basic environment

A

Weak bases in an basic environment is: B + H +

402
Q

When are weak acid drugs protonated?

A

Protonated in acidic environment

403
Q

Describe weak acid drugs in acidic environments

A

HA, protonated & non-ionized

404
Q

Describe weak acid drugs in basic environments

A

A -
Ionized and nonprotonated

405
Q

Describe weak base drugs in an acidic environment

A

BH +
Protonated and ionized

406
Q

How do you calculate loading dose?

A

LD = (Css * Vd) / F

407
Q

How do you calculate maintance dose?

A

MD = (Css * Clearance Level) / F

408
Q

How do you calculate Vd?

A

Vd = Amount given/ [Concentration in blood/plasma]

409
Q

How do you calculate corrected dose?

A

CD = (Normal dose * Pt clearance dose) / 100 mL/min

410
Q

How do you calculate T i AKA therapeutic index?

A

T i = TD 50 / ED 50

TD 50 : Median toxic dose
ED 50 : Median effective dose

411
Q

What is ED 50 ?

A

ED 50 : Median effective dose
- The dose at which 50% of individuals exhibit the specified quantal effect

412
Q

What is
TD 50 ?

A

TD 50 : median toxic dose
- The dose required to produce a particular toxic effect in 50% of the population

413
Q

The wider the therapeutic index, the:

A

The wider the therapeutic index, the safer the drug

414
Q

How do competitive antagonists exert their effects?

A

Competitive antagonists bind directly with the receptor site to block agonists from being able to bind
They do not exert any direct effects or signaling pathway

415
Q

How do noncompetitive antagonists exert their effects?

A
  • Drugs that bind allosterically or to the receptor (irreversibly)
  • Such a strong binding that even if maximal agonist is added the receptors will not kick of agonsts
416
Q

What type of antagonists drugs can be overcome?

A

Competitive antagonists can be overcome by adding agonists that kick off antagonists from their receptors

417
Q

___________ __________________ activate the receptor signal, same as the endogenous ligand.

A

Agonists/Full agonsits

418
Q

What do allosteric agonists require for them to work?

A

Allosteric agonists require the endogenous ligand
Allosteric agonists require smaller doses due to potentiation of endogenous ligands

419
Q

What is the associated dermatome at the level of T10?

A

Umbilicus

420
Q

What is the dermatome associated with L1?

A

Nerve root has sensation in the anterior thigh below the inguinal ligament

421
Q

What dermatome is associated with L2?

A

Middle and anterior thigh below

422
Q

What muscle would be used to treat ribs 3-5?

A

Pectoralis minor

423
Q

What muscle would treat ribs 6-9?

A

Serratus anterior

424
Q

What muscle would treat ribs 6-9?

A

Serratus anterior

425
Q

What muscle is used to treat ribs 10-11?

A

Latissimus dorsi

426
Q

Define spondylosis

A

Degenerative changes within the intervertebral disc and ankylosing of adjacent vertebral bodies

427
Q

Define spondylosis

A

Degenerative changes within the intervertebral disc and ankylosing of adjacent vertebral bodies

428
Q

Define spondylolysis

A
  • Defect usually of the pars interarticularis without anterior displacement of the vertebral body
  • Oblique XR view will identify fracture of pars interarticularis
429
Q

Define spondylolysis

A
  • Defect usually of the pars interarticularis without anterior displacement of the vertebral body
  • Oblique XR view will identify fracture of pars interarticularis
430
Q

Define spondylolisthesis

A
  • Anterior displacement of one vertebrae in relation to the one below
  • Often occurring at L4 or L5
431
Q

Define spondylolisthesis

A
  • Anterior displacement of one vertebrae in relation to the one below
  • Often occurring at L4 or L5
432
Q

Which ribs are primarily pump handle?

A

Ribs 1-5

433
Q

Which ribs are primarily pump handle?

A

Ribs 1-5

434
Q

Which ribs are primarily bucket-handle motion?

A

Ribs 6-10

435
Q

What is the vertebral level of the angle of Louis?

A

T4

436
Q

What is the main motion of the lumbar spine?

A

Flexion and extension

437
Q

What causes cauda equina syndrome?
List some symptoms

A
  • Compression of the thecal sac of the spinal cord
  • Reduced deep tendon reflexes in lower extremities bilaterally
  • Decreased rectal tone
438
Q

Why do walking and standing worsen spinal stenosis symptoms?

A

Standing and walking exacerbates the narrowed spinal canal and neural foament

439
Q

What vertebrae are associated with Psoas syndrome?

A

L1 or L2

440
Q

Describe the diagnosis of the vertebrae in Psoas syndrome

A

L1 or L2 vertebrae is commonly flexed and rotated to the affected side

441
Q

How to test L4 nerve root integrity

A
  • Patellar deep tendon reflexes
  • Ankle dorsiflexion
  • Sensation along the medial leg and malleolus
442
Q

What is a manifesting heterozygote?

A
  • A manifesting heterozygote refers to a heterozygous female who expresses
    an X-linked recessive mutation due to random X-inactivation.
  • A manifesting heterozygote may occur in females who carry an X-linked recessive mutation such as loss-of-function mutations in factor VIII, factor IX, OTC, GLA, or G6PD gene.
443
Q

Describe a pedigree for Autosomal dominant inheritance

A

The pedigree shows 3 features:
1) occurring in in multiple
generations
2) no skipped generation
3) equal incidence in males and females.

444
Q

Any child born to a person affected with an AD trait or disorder has a ____________ chance of inheriting it and being similarly affected

A

1 in 2 (50%)

445
Q

The risk of being a carrier of an autosomal recessive trait would be _____ if the
child (already born) were not affected but the parents were carriers.

A

The risk of being a carrier of an autosomal recessive trait would be 67% if the
child (already born) were not affected but the parents were carriers.

446
Q

The risk of the next child of the parents to be a carrier would be ____ in an autosomal recessive disorder.

A

50%

447
Q

Hemophilia A is an _______________________________ inherited disorder. Explain how a female could have mild expression of this disease if she is a heterozygous carrier

A
  • X Linked Recessive disorder
  • A high proportion of the X chromosomes carrying the mutation are
    active in this woman.
  • This woman is a manifesting heterozygote. Normal females have
    two copies of the X chromosome, so they usually require two copies of the mutation to express the disease. However, because X inactivation is a random process, a
    heterozygous female will occasionally express an X-linked recessive mutation because, by random chance, most of the X chromosomes carrying the normal allele have been
    inactivated
448
Q

Define the founder effect

A

The founder effect is a genetic phenomenon that occurs when a small group of individuals from a larger population establishes a new population, resulting in a loss of
genetic variation

449
Q

What causes Fragile X syndrome?

A

It is caused by expansion of CGG repeats in the 5’-UTR of FMR-1 gene
- Triplet repeat expansion

450
Q

What causes Angelman syndrome?

A
  • Microdeletion in an autosome
  • Around 70 to 75% of cases arise from maternal
    deletion within chromosome 15q11-q13, containing the UBE3A gene
451
Q

What does UBE3A codes for?

A
  • UBE3A codes for ubiquitin and appears to be preferentially or exclusively expressed from the maternally
    derived chromosome 15 in the brain
452
Q
A
453
Q

What type of inheritance is Wiskott-Aldrich syndrome?

A

Wiskott-Aldrich syndrome is an X-linked recessive disorder

454
Q

Describe in vivo gene therapy for Hemophelia B

A
  • caused by factor IX deficiency
  • Factor IX is produced in the liver. Liver-related diseases are amenable to in vivo gene therapy.
  • Other organs that in vivo gene therapy may apply to include eye, brain, and skeletal muscle
455
Q

What does alpha-L-iduronidase indicate?

A

Lysosomal storage disease

456
Q

What therapy is used to treat lymphomas and leukemias?

A

T cells to generate CAR T-cell therapy

457
Q

What treatment is used for SCID and lysosomal storage disease?

A

Hematopoietic stem cell

458
Q

What type of cells do Mesenchymal stem cells differentiate into?

A
  • Mesenchymal stem cells (MSCs) are multipotent stromal cells that can differentiate into a variety of cell types, including osteoblasts, chondrocytes, and
    adipocytes
  • It is unclear whether and how efficient MSCs can be used to differentiate into blood cells
459
Q

What are side effects of axicabtagne?
What type of therapy is it and what does it treat?

A
  • CAR T-cell therapy that is used to treat follicular lymphoma
  • fever, low white blood cells, increase risk of recurrent infection), and low red blood cells (increase risk of anemia)
460
Q

What does Dinucleotide instability refer to?

A
  • Example of microsatellite instability
  • Microsatellite DNA refers to a short segment of DNA, usually one to 6 base pairs in length that is repeated multiple times
461
Q

Overactivation of ______________________ leads to von Hippel-Lindau disease

A

Overactivation of HIF (or defective VHL) leads to von Hippel-Lindau disease

462
Q

Overactivation of ___________________ leads to melanomas.

A

CDK4 (or defective CDKN2A)

463
Q

Defective ____ leads to Li-Fraumeni syndrome

A

P53

464
Q

Defective ____ leads to VHL disease by what mechanism?

A

Defective VHL leads to increased HIF activity
- HIF Activity is synonymous with increased cancer to help survival and growth

465
Q

Defective ____________________ leads to HNPCC

A

Defective MLH1 or MSH2 leads to HNPCC

466
Q

What are the gatekeeper genes for G2 to M cell cycle transition?

A

MLH1
MSH2

467
Q

List 4 ways to inactivate a tumor suppressor gene

A

1) genetic mutation (point mutation or deletion)
2) epigenetic (methylation)
3) environmental factors.
4.) Hypermethylation of a promoter region, enhancer region or coding region can contribute to silencing of a TSG.

468
Q

____________ __________________ lead to familial adenomatous polyposis, a type of colon cancer

A

APC mutations

469
Q

__________________ mutations lead to HNPCC (or Lynch syndrome)

A

MLH1

470
Q

What is Pompe disease?

A

Glycogen storage disease
- Intracellular accumulation of glycogen

471
Q

What is Lynch syndrome?

A

Hereditary nonpolyposis colorectal cancer

  • Associated with colon cancer, endometrial cancer, ovary, stomach, small intestine, hepatobillary tract, URI, brain and skin
472
Q

What does loss of NF1 gene allow?

A

Allows for persistent activation of the Ras gene

473
Q

Why does coronary ischemia cause increased end systolic volume?

A

The heart does not have enough blood flow to contract properly so not enough volume is being ejected

474
Q

OPC: What is the sympathetic innervation of the heart?

A

T1-T5

475
Q

OPC: What is the sympathetic innervation for the lungs?

A

T1-T6(7)

476
Q

OPC: What is the sympathetic innervation for the lungs?

A

T1-T6(7)

477
Q

OPC: what is the sympathetic innervation of the upper extremity?

A

T1-T6

478
Q

OPC: what is the sympathetic innervation of the upper extremity?

A

T1-T6

479
Q

OPC: What is the sympathetic innervation of the lower extremities?

A

T10-L2

480
Q

What is cisterna chyli?

A

Lymphatic vessels that collect lymph from the abdomen, pelvis, and lower extremities located just below the diaphragm

481
Q

Describe OA in CCP

A

OA is rotated Left

482
Q

Describe OA in CCP

A

OA is rotated Left

M1 Block 3 (6 decks)

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