Final Flashcards

1
Q

ParmO2
PaO2
PAo2
PvO2
Pv(-)02

A

Atmosphere
Arterial (away)
Alveolar
Venous (tovards)
Mixed Venous

(PO2 = % x ATM)

1.5% disolved in blood

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2
Q

Takotsubo

A

-Novel because we have never seen emotion induced heart attack.
-recovery was great.
- Mostly Women
-Broken heart syndrome
-Happens in animals

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3
Q

Normal Ejection Fraction?

A

.6-.7

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4
Q

3 Things For a Graph

A

Dependant(y) vs Independant (x)

Shape

Whats normal?

We manipulate the X and oberve Y

Most Physiology is S shaped

X/Y will always be given in question

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5
Q

Colour of Heem

A

Due to iron.
Different animals have different colour.

Octipuss - copper (blue)
worms have cobolt (green)

Also the deeper you go, the higher your blood has an affinity for o2 because its more scarse. aka the Lugworm vs a duck

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6
Q

Ratio of Heem Cell Types are determined by

A

Age
Disease (anemic adult mimic fetus)
Diet
Medication

AB - Adult 95% Fetus 10%
AG - Adults 3% Fetus 90%

Beta always low .

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7
Q

Myoglobin

A

Singular.
Higher affinity for o2 (minus when stored)

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8
Q

p50

A

50% saturation.

Higher affinity = earlier p50

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9
Q

Hematocrit Vs Heem

A

Hematocrit is % of blood that is red. Measure in cms then figure out a %.

50% + = doping

males 42-52%
females - 37-47%

Anemia = low heem
Polycythemia = high heem

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10
Q

Different anemia

A

Microcytic - Low heem low crit

Macrocytic - cirt normal heem low . Large RBC

Hypochromic - cirt normal heem low. Less iron

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11
Q

How to change the o2 disassociation curve

A

Temp (down) Temp
Po2 (down) Haldane
DPG (down) ** Hypoxia/altitude** Inorganic
PH (up) PHOR

Andrew minisota
ITPP (right is added )

ALL LEFT

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12
Q

Farmingham
Bogalusa

A

1960 = Cigs = HD
02 = obese = HD

Bog = ethic

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13
Q

Cpmpensatory —-> Decompensatory

A

Early AF / HF is okay because body over reacts. Its time that fucks you up

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14
Q

LVAD
Abicor Heart

A

Left Vent Assistance Device
Full blown heart. Robbert tool.

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15
Q

Heart Disease Controlables and Non

A

Smoke. Sedentary. Type 2. Obese. Hypertension

Age. Gender. Type 1. Fam history. Hyperlipidema

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16
Q

3 Cause of heart disease

A

AMI
HBP - silent
Gene mutations

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17
Q

Things that can alter heem isoforms

A

Age
Meds
Diet
Disease

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18
Q

Fetal to Adult Heem

A

AG
AB
D on the rise

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19
Q

HR Class of failutre

A

1- not much
2- Fatiuge hurt, rest okay
3. fatiuge at easier things, rest okay
4. not okay at rest

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20
Q

Types of A Fib
What is it?
Treatment?

A

Paro - young + Lasts a few seconds
Persistant - Med. Donest stop by itself
Perminnant- constant. Meds dont work

Vent contract early. Push not enough blood out
Meds or stop doing the thing.

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21
Q

Heart break down

A

Trabeculae
Compact (95%)
Papulary

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22
Q

What is noticed in EKG?

A

prolong QT … mainly t wave is odd

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23
Q

Order of electrical activity of heart.
Where do rotors start? Why

A

SA
AV ** Passage point
Bundle of his
Purkinje

Outside of heart. AP

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24
Q

Thrombosis

A

Warfrin treats clots ** Odds ratio-higher worse** Heart diseas…warfrin bad.

Theres a golden hour

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25
Q

Lead direction
Stemi?

A

Postive towards lead = positive deflection
positive away from lead = negative deflection
STEMI - dead tissue cause charge to stay positive

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26
Q

CAD

Types of anginia

A

Build up of fatty deposits. Everyone has it

Stable - Predicatble
Unstable - non predicable
Variant - Spontanious… sleep

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27
Q

Types of Stents

A

Rotary
Balloon
stent

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28
Q

Types of infarcs

A

Subcrainail (1-5 hr)
Transmurual (12 hr)

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29
Q

Atrial hypertrophy

A

P mitrale - P wave notched (L enlarge)

P pulmaonale - P wave tall (R enlarge)

30
Q

Progression on Angina and biomarkers

A

Angina
MI (Trop I/T) & little necrosis
Heart Failues (BNP, but shits already dead) major death

BNP and ANP Make you piss

31
Q

Future Direction of heart failure

A
  1. Diet
  2. Gut Biome
  3. Chronotherapy
  4. Regeneration a) fish b)
  5. Sex Diffs
    Fill this out more

Sex diff - F more likley to devlop/not survive.

32
Q

Impairments of Blood Flow for HF

A
  1. Vasodilation (no)
  2. Chronic Vasoconstriction (angio up)
  3. Lower capillary density.
33
Q

Secondary symptoms of HF

A
  1. Apoptosis
  2. Connective tissue
  3. Loss of FXN unit . MHC&CSA \/
  4. Metabolism (Mito and Mck /bdown)
  5. Inflamation @ Limbs (1l6/b/@)
  6. Fibre type shift
  7. Muscle mass down.cachexia
34
Q

Characteristics of fatigue

A

a. Reduced force
b. caused by action
c. recoverable
@ muscle not brain
weak= no recovery

35
Q

Determinate of muscle type

A
  1. Genetics
  2. training/detraining
  3. blood supply
  4. nerve/ innervation
  5. disease
  6. gender / race
36
Q

Estrogen and HF

A

Protective

NO is controlled by estro
Low Fibroblast prolif and coligen synth
Worse in diabetic women… reverse cardio protective effects

37
Q

Ischemic preconditioning

A

Remote = heart and heart
Pre condition at distance = limbs
Ability dimishes with age. (40/50)
Classical window + Second window of protection

38
Q

5 Terms of failure (2 what, 3 why)
resp
Ventaltory failure
central
NMT
Perifph

A

Respiratory - inability to sustain expected level of pressure/force

Vent failure - Aveolar vent, insufficent to achieve Co2 elim -> Hypercapnia

Central - Decrease neural outpout, despite stim.

NMT - transpition of AP across NMJ

Peripheral muscle fatiuge - impared output

39
Q

Bones
1.Function (4)
2. Type (3)

A

FXN:
1. Shape and size
2. Calcium and phosphate stores
3. Support
4. Marrow (makes RBC)

Type:
Within - Blast : Make (Can be effected by genes, horemone etc.)

Clast: Reabsorb + Remove unwanted tissue

Within - Cyte: Maintain Bone

40
Q

Bone Structure (2)

A

Cortical : Compact outter later
Trab: Inner sponge

41
Q

Osteomalacia AKA Rickets

A

How? Issues with Vit D (Receptors or nutrition). Many pregnancies. Liver/Kidney issues

Symp? Bow leg cuz heavy body.

Bulbus head. Soft bone turns to hard deformed bone. 40+. Warm bones due to formation.

42
Q

Osteoperosis

A

AKA Porus Bone . Lower bone density. Increase clast activity.

  1. Primary - Aging (estro/calcium) **Females
  2. Secondary - Medical conditions ** men

Natural loss is .2-.5% a year.
Compression factures.
Effects more women than HA, S, BCancer Combined!

43
Q

Arthritis

A

Inflammation.
Over active immune.
Infection.
Abnormal motabolism

44
Q

Osteoarthritis

A

How? AKA Wear and tear 1:1 m/w

What ? Bone degen. Unilateral. Join space narrow

Risk? Obesity, joint injuries, genetics,

Sign ? Crepidus. Deformity. Aches. Sore even when chillin

Treat? Meds (NISA) Orthotics or ambulatory aids.

45
Q

RA

A

What? Rheumatoid - auto immune. 25-55y/o . Mostly women. Symmetrical. Hands, feet, knee..not so much spine

Signs: Redness. Swole. Stuff. Fatiuge.

Test? Rheumatoid factor in synovial fluid, but everyone has it.

Treat? Rest and moderate activity. Splint

Drugs? NSAID

46
Q

Infectious/Septic arthritis

A

What ? Swelling in single joint

Sign? Red swole. ROM Lacks. Blood borne bacteria

How ? Trauma, surgery, nearby disease or infection . Can be transmitted by tiks

47
Q

Layers of a Muscle

A

Muscle
Muscle Fassicle
Muscle Fibre
Myofibril
Myofilament

48
Q

Actin and Myosin Contain

A

Actin - Light thin band (I Band, Z line)

Myosin - Thick Dark (A Band, H Zone)

49
Q

Normalize Data

A
  1. Remove Bias
  2. Rectify
  3. Filter
  4. Normalize
50
Q

4 MU Firing Rate

A

Single Twitch
Wave Sumation
Unfused Tetanus
Fused Tetnus

51
Q

Factors effecting EMG

A
  1. Fibre Type
  2. Larger MU’s closer to the skin
  3. Firing Rate
  4. Synergistic / Antagonist
52
Q

Fatiuge vs Failure ?

A

Fatiuge - decrease of force

Failure - what ever you set it to be

53
Q

Things that can cause central fatiuge

A

Decrease in voluntary action
MN Firing rate
Sensroy efferent pathwys
Coritoexcitability

54
Q

Peripferal

A

1.Impared synaptic transmission along NMJ
2. Slow Ach
3. Poor restore of Na and K
4. ATP down
5. H up

55
Q

Type of muscle

A
  1. Parallel
    -Flat, Fusiform/spiral**, Strap, Circular, Convergant or radiant.
  2. Pennate
    - Fibres diagnal to the tendon. Slower and smaller movements. More force.
56
Q

Penation Angle

A

Angle between muscle fibres and line of pull

57
Q

ACSA Vs PCSA

A

Anatomical CSA perpendicular to
muscle long axis

Only relevant to that particular slice

Accounts for fibres not oriented in the line of action

Measure area (slice) perpendicular to fibres

Better predictor of muscle force

58
Q

PSCA Equation

A

((Volume / Cos (Pangle) ) / Fibre Length

59
Q

PCSA Vs Force

Fibre Length vs Force

A

Muscle Length = same
Longer PSCA = More max tension

Same Max Tension. Shorter fibre = max force over shorter period of time

60
Q

3 Componenets of Hill Muscle Model

A

Nervous System Stim :
CC - Contractile component (Myosin / Actin)

Muscle Elasticity:
SEC - Series Elastic Component (Tendon)
PEC - Parallel Elastic Component ( Epi, Peri, Endo)

61
Q

Force Length Relationship Curve

A

Iso tension on Y
Length on X

Active Tension Cuves in n shame
SEC and PEC tension grow
Total Tension grows a leg off the n

62
Q

Why study mechanics of human tissue?

A
  1. Injury
  2. Prevnsion of injury
  3. Joint replacement
63
Q

How Injuries occour? Loading Scenario

A
  1. Acute (Constant tolerance)
  2. Constant Load (Decrease tolerance )
  3. Rehab and Re Growth (dynamic Tolerance)

They all have a original load tolerance. Rehab changes this

64
Q

Components of Load Deformation Curve?

A
  1. Elastic Region (can reform)
  2. Yeild Point
  3. Plastic Region (Point of no return)
  4. Ultimate Failure

X - Deformation (m)
Y - Load (N)

Toe Reigion for tendons and ligaments

AUC - Energy stored in tissue

65
Q

Strain Equation

A

Current length - Original length / Origional Length

66
Q

Big 3

A

Repitition
Force
Posture

67
Q

2 Types of Stress

A

Engineering Stress: Force divided by original cross sectional area of tissue

True Stress: Force divided by cross sectional area

68
Q

5 Types of loading

A

Compressive
Tension
Shear
Tension
Bending

69
Q

Tendon and Ligament

Similaratiries nad Differences

A

Tendon : Motion and More organized. (Muslce to bone)

Ligament : Less organized and stability (Bone to Bone)

70
Q

When load and deformation are normalized they are ___

A

Stress and straing