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Final Flashcards

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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
Lead direction Stemi?
Postive towards lead = positive deflection positive away from lead = negative deflection STEMI - dead tissue cause charge to stay positive
26
CAD Types of anginia
Build up of fatty deposits. Everyone has it Stable - Predicatble Unstable - non predicable Variant - Spontanious... sleep
27
Types of Stents
Rotary Balloon stent
28
Types of infarcs
Subcrainail (1-5 hr) Transmurual (12 hr)
29
Atrial hypertrophy
P mitrale - P wave notched (L enlarge) P pulmaonale - P wave tall (R enlarge)
30
Progression on Angina and biomarkers
Angina MI (Trop I/T) & little necrosis Heart Failues (BNP, but shits already dead) major death BNP and ANP Make you piss
31
Future Direction of heart failure
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
Impairments of Blood Flow for HF
1. Vasodilation (no) 2. Chronic Vasoconstriction (angio up) 3. Lower capillary density.
33
Secondary symptoms of HF
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
Characteristics of fatigue
a. Reduced force b. caused by action c. recoverable @ muscle not brain weak= no recovery
35
Determinate of muscle type
1. Genetics 2. training/detraining 3. blood supply 4. nerve/ innervation 5. disease 6. gender / race
36
Estrogen and HF
Protective NO is controlled by estro Low Fibroblast prolif and coligen synth Worse in diabetic women... reverse cardio protective effects
37
Ischemic preconditioning
Remote = heart and heart Pre condition at distance = limbs Ability dimishes with age. (40/50) Classical window + Second window of protection
38
5 Terms of failure (2 what, 3 why) resp Ventaltory failure central NMT Perifph
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
Bones 1.Function (4) 2. Type (3)
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
Bone Structure (2)
Cortical : Compact outter later Trab: Inner sponge
41
Osteomalacia AKA Rickets
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
Osteoperosis
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
Arthritis
Inflammation. Over active immune. Infection. Abnormal motabolism
44
Osteoarthritis
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
RA
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
Infectious/Septic arthritis
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
Layers of a Muscle
Muscle Muscle Fassicle Muscle Fibre Myofibril Myofilament
48
Actin and Myosin Contain
Actin - Light thin band (I Band, Z line) Myosin - Thick Dark (A Band, H Zone)
49
Normalize Data
1. Remove Bias 2. Rectify 3. Filter 4. Normalize
50
4 MU Firing Rate
Single Twitch Wave Sumation Unfused Tetanus Fused Tetnus
51
Factors effecting EMG
1. Fibre Type 2. Larger MU's closer to the skin 3. Firing Rate 4. Synergistic / Antagonist
52
Fatiuge vs Failure ?
Fatiuge - decrease of force Failure - what ever you set it to be
53
Things that can cause central fatiuge
Decrease in voluntary action MN Firing rate Sensroy efferent pathwys Coritoexcitability
54
Peripferal
1.Impared synaptic transmission along NMJ 2. Slow Ach 3. Poor restore of Na and K 4. ATP down 5. H up
55
Type of muscle
1. Parallel -Flat, Fusiform/spiral**, Strap, Circular, Convergant or radiant. 2. Pennate - Fibres diagnal to the tendon. Slower and smaller movements. More force.
56
Penation Angle
Angle between muscle fibres and line of pull
57
ACSA Vs PCSA
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
PSCA Equation
((Volume / Cos (Pangle) ) / Fibre Length
59
PCSA Vs Force Fibre Length vs Force
Muscle Length = same Longer PSCA = More max tension Same Max Tension. Shorter fibre = max force over shorter period of time
60
3 Componenets of Hill Muscle Model
Nervous System Stim : CC - Contractile component (Myosin / Actin) Muscle Elasticity: SEC - Series Elastic Component (Tendon) PEC - Parallel Elastic Component ( Epi, Peri, Endo)
61
Force Length Relationship Curve
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
Why study mechanics of human tissue?
1. Injury 2. Prevnsion of injury 3. Joint replacement
63
How Injuries occour? Loading Scenario
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
Components of Load Deformation Curve?
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
Strain Equation
Current length - Original length / Origional Length
66
Big 3
Repitition Force Posture
67
2 Types of Stress
Engineering Stress: Force divided by original cross sectional area of tissue True Stress: Force divided by cross sectional area
68
5 Types of loading
Compressive Tension Shear Tension Bending
69
Tendon and Ligament Similaratiries nad Differences
Tendon : Motion and More organized. (Muslce to bone) Ligament : Less organized and stability (Bone to Bone)
70
When load and deformation are normalized they are ___
Stress and straing

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