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PT 31 Flashcards

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1
Q

Respiratory Acidosis

A

“Tic tac toe, pH and CO2 on same column”
PaCO2 > 45

Partial Compensation:
HCO3- > 26
pH < 7.35

Full Compensation:
HCO3- > 26
pH between 7.35-7.4

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2
Q

Respiratory Alkalosis

A

“Tic tac toe, pH and CO2 on same column”
PaCO2 < 35

Partial Compensation:
HCO3- < 22
pH > 7.45

Full Compensation:
HCO3- <22
pH between 7.4-7.45

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3
Q

Metabolic Acidosis

A

“Tic tac toe, pH and HCO3- are on same column”
HCO3- < 22

Partially Compensated:
PaCO2 < 35
pH < 7.35

Fully Compensated:
PaCO2 < 35
pH between 7.35-7.4

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4
Q

Metabolic Alkalosis

A

“Tic tac toe, pH and HCO3- are on same column”
HCO3- > 26

Partially Compensated:
PaCO2 > 45
pH > 7.45

Fully Compensated:
PaCO2 > 45
pH between 7.4-7-45

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5
Q

What joint is most mobile?

A

The shoulder joint
The upper limb is responsible for range of movements

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6
Q

What are functional layers of the skin?

A

Epidermis
Epidermal appendages
Dermal papillae
Dermis
Subcutaneous layer

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7
Q

What are 3 main types of scars? Which one/s could heal with little to no scarring?

A

Superficial - just epidermis lost, little to no scarring

Partial thickness - part of epidermis and dermis lost, little to no scarring

Full thickness - complete epidermis and dermis lost, goes into subcutaneous layer

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8
Q

Stages of Wound Healing

A
  1. Bleeding control - haemostasis
    And clot formation - harmatoma
  2. Inflammation (heat and pain)
    - redness = erythema
    - swelling = oedema
  3. Matrix - fibroblast = collagen and elastin
  4. Neovascularisation
  5. Re-epitheliaisation
  6. Wound contraction (reduce in size and could lead to deformities) and remodelling
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9
Q

Muscles that CN X innverate

A

CN X = Accessory N. = motor nerve

Innervates trapezius and sternocleidomastoid

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10
Q

Where does subclavian artery changes its name to another artery?

A

The subclavian artery becomes the axillary artery as it passes lateral margin of rib 1

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11
Q

Brachial Plexus Basics

A

Roots C5 - T1

Lateral cord = Muscuolcutaneous (motor) for coracobrachialis, brachialis and biceps brachii

Lateral + Medial cord = Median - affected by carpal tunnel

Posterior cord = Radial (innervates Triceps brachii)

Medial cord = Ulnar (ie on the medial side)

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12
Q

Shunt muscles of the arm

A

To prevent unwanted inferior movement of arm when lifting

  • Deltoid “over the lateral aspect of shoulder”
  • Short head biceps “medial inside of armpit”
  • Coracobrachialis “off the coracoid process”
  • Long head triceps “lengthy long on posterior arm”
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13
Q

Quadrangle space and Triangular interval neurovasculature

A

Triangular space as well, circumflex scapular artery goes thru there

Teres minor on anterior superior

Teres major on posterior and inferior

Long head of triceps is medial and comes from posterior to teres minor and anterior to teres major

Humerus = lateral border

Quadrangular space = axillary n (which innervates the deltoids it passes thru) and posterior humeral circumflex a (branch from axillary a)

Triangular interval = radial n (tightly to the humerus bone) and profunda brachii a

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14
Q

Why funny bone funny?

A

Ulnar n that runs exposed on the posterior of the medial epicondyle

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15
Q

Path of Median N down arm to forearm

A

Passes straight down from brachialis

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16
Q

Path of Musculocutaneous N down arm to forearm and name change

A

Passes btwn biceps brachii and brachialis

Changes to lateral cutaneous n of forearm as it comes around the lateral border of biceps brachii - now solely cutaneous innervation

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17
Q

Arm and forearm, which side is medial and which is lateral?

A

Thumb is lateral
- ie can feel for radial pulse on lateral side

Little finger digit 5 is medial
- ulnar and nerve and funny bone is on the medical side

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18
Q

Cubital Fossa contents and superficial veins

A

My bloods turns red - Medial to Lateral contents

Anatomical landmark for brachial pulse, venipuncture and IV catheter

Median N
Brachial Artery = brachial pulse
Tendon of biceps (the distal tendon at the elbows level)
Radial N

Superficial veins - veins are superficial to arteries, so in case of injury the arteries are deeper and less likely to pop

Venipuncture = Basilic, Median cubital or Cephalic veins (they run superior medially to laterally inferiorly)

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19
Q

Reduce clotting factors

A

Vitamin K - formation of clotting factors

Warfarin - blocks reduction of vit K so less blood clotting

Glucocorticoids - affects COX1 (thromboxane A2 and 2 (prostaglandins)

Aspirin - COX1

Clopidogrel - no ADP binding

Abciximab - MABs, no fibrin binding to platelets cells

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20
Q

Horner’s syndrome

A

Presentation: ptosis, miosis (constriction of pupil) and anhidrosis (no sweating)

3 neurons
1st order from hypothalamus to C8/ T1 T2 level
2nd order travel from sympathetic chain over the apex of lungs to C3 C5 levels of around bifurcations of common carotid arteries
3rd order travel up the adventitia of int. Carotid artery to the eyes - eye lid muscle, iris muscle and control sweat glands of the face

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21
Q

Why breastfeeding

A

Immune system

Digestive enzymes, and then prebiotics for large bowel - gut

Water content as baby cant concentrate urine yet - kidneys

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22
Q

Afebrile = ?

A

Non-feverish

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23
Q

Carpal tunnel

A

Pain as compresses on the Median N that runs btwn FDS and FDP through the carpal tunnel

Flexor retinaculum = deep fascia on the anterior medial 2/3 of wrist
From scaphoid (likely fractured bone of carpals on the lateral side x thumb)
To pisiform and hamate on the medial side

Pressure build up and cause pain as impinges on softer structures

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24
Q

FDS Vs FDP

Study These Flashcards
A

Flexor digitorium superficialis = insert on middle phalanxes of the medial 4 phalanges
- can flex the proximal inter-phalangeal joint without flexing the distal inter-phalangeal joint

Flexor digitorium profundus v insert on distal phalanxes of the medial 4 phalanges
I.e it flexs the DIP joint

25
FPL
Flexor pollicis longus = powerful flexor of thumb = lateral side, anterior to radius
26
Landmark of the anterior and posterior compartment of the forearm
Radial N = posterior compartment Everything medial to it = anterior compartment
27
Scaphoid and avascular necrosis
Scaphoid - most commonly fractured carpal bones Blood supply = 70-80% from dorsal branch of radial artery = palmer scaphoid branch from the superficial palmer branch of the radial artery - Supplies distal head of scaphoid process, and oxygen and nutrients diffuse to proximal end - I.e if fracture occurs, proximal end of scaphoid can die by avascular necrosis
28
ST elevation and areas of MI (think positions of the leads)
Myocardial infarction = heart attack = cardiac myocytes die because of no blood flow to heart Anterior: V1-4 Lateral: lead I, V5-6, aVL Inferior: Leads II and III, and aVF
29
Correspondence between ST elevation and depression on particular leads
An elevation in eg I and aVL typically = depression in III
30
Characteristic Pericarditis on ECG
Saddle back ST elevation on most leads except on leads aVR and V1 is the exact reverse saddle A Presentation of chest pain
31
Presentation with chest pain and potential causes
MI Pericarditis Pneumonia, pneumothorax, pulmonary embolism, pleurisy Aortic dissection Oesophageal spasm - random contractions, no longer regular peristalsis Costochondritis
32
ST depression
Myocardial Ischemia
33
Myocardial Ischemia and Myocardial Infarction
Ischemia = blocked blood flow MI = myocytes die due to lack of blood supply bc of ischemia which could be caused by atherosclerosis (build up of plaques)
34
First degree AV block
Longer PR interval, sinus Rarely cause symptoms or require treatment
35
Second degree AV block type 1
Progressively elongated PR intervals until a missing QRS complex meaning missed a beat, then cycle repeats all over again with each P wave longer than before until missing a beat Aka blocked P wave or Dropped QRS complex Symptoms are mild and no treatment indicated
36
Second degree AV Block Type 2
P wave is normal but conduction doesn’t generate ventricular depolarisations Pacemaker recommended treatment as dangerous and could lead to cardiac arrest = heart stops functioning
37
Ratio of heart blocks
Eg 4:3 heart blocks 4 P waves with 3 QRS, might be second degree AV block type 1 when periodically the number of QRS is always one fewer than P waves 3:1 heart block Ie 3 P waves per 1 QRS, could be in seen second degree AV block type 2 that have a pattern for every 3 P waves a ventricular depol could be seen A 3:1 ratio could also be seen in Atrial flutter if atrium (often R atrium) keeps depol by re-entrant, the AV blocks the fast depols so ventricles only depol once every three atrial depols (which are v fast in this case)
38
Third degree AV block
Complete heart block. None if electrical activity in atria reach ventricles, ventricles don’t get the notice to contract So ventricles generate their own rhythm = escape rhythm - regular and normal size P waves - Regular WRS complexes but are unusually slow snd not always after P waves Could be lead to by second degree AV block type II Patients high risk of cardiac arrest, immediate treatment and pacemaker implant
39
PAC VS PVC
PAC = non compensatory PP interval, looks like irregular interval btwn P waves of ectopic beats as an ectopic site might be close to AV node which could depol SA node to start a whole depol all over again causing this delay in time PVC = compensatory PP interval, seen as regular PO intervals between ectopic beats as ectopic site isn’t affecting atrial depol Premature atrial contraction - ectopic site of atrial origins (ie diff to PVCs which are ventricular in origin) - might not notice anything and might not need any at treatment BUT UNDERLYING CONDITIONS MUST THEN BE TREATED FOR PVC Premature ventricular contraction - very common - Few symptoms including skipped heart beats or palpitations - ectopic site in ventricles ie there is no P wave before the QRS Ie wider = longer lasting QRS as initiated by cardiac myocytes snd spread through ventricles more slowly - can be taller or reverse depending on location of ectopic site to lead II - a P wave following this ectopic beat might not have a QRS following as ventricles might still be in its refractory period = compensatory P Potential Causes of PVC ONE - intracellular Ca2+ overload = increase automaticity (the likelihood that cardiac myocytes can depolarise themselves and initiate a PVC) - Excess catecholamines eg adrenaline - drugs eg digoxin - hypokalemia or hypomagnesemia TWO heart muscle damage leading to re-entry circuit - damaged tissue conduct more slowly and form a conducting loop cuz it’s just bit slow to depol all at the same time and yet triggers new round of depol THREE beats triggered by early or delayed after-polarisations Early after-depolarisations can be due to long QT syndrome, hypokalemia, potassium channel blocker drugs Delayed after-depolarisations can be due to digoxin excess causing toxicity or excess catecholamines eg adnrelaine
40
Digoxin mechanism
Blocks Na/K ATPase, keeps Na in and K out So Na Ca exchanger doesn’t work, intracellular Ca increases which increases cardiac mycocyte contratility
41
Atrial fibrillation
No Atrium contractions bc all fibrillates so no P waves Irregular heart beats cuz dunno which one of these atrial fibrillations becomes a ventricular contraction
42
AV re-entrant atrial rhythm
Re-entrant fast depol loop stimulating AV node which causes ventricular depol everything so see QRS after every P and at very high frequency ie heart beat b fast
43
Ventricular rhythms
Lethal Ventricular tachycardia - structural heart problem Premature and irregular ventricular depols ECG looking like QRS after QRS and are wider as the electrical impulse is spread from cardiac myocyte to cardiac myocyte, not along fast purkingjie fibres of the cardiac electrical conduction system - no P waves - sustained V Tach longer than 30 seconds need to be treated to prevent cardiac arrest - can lead to V Fib (see below) Ventricular fibrillation - multiple, unsynchronised, weak quivers from ventricular ectopic sites, causing ventricles to quiver (fibrillate) rather than contract - can quickly lead to - random ECG waves of random amplitude and wavelength, no identifiable waves such as no P, QRS or ST - amplitude decreases from initial V Fib to final V fib to flat line……
44
What are two classes of moecules that regulate the Na+/K+ ATPase?
Hormones and catecholamines
45
Hypokalemia and cardiac myocytes
Increase hyperpolarisation means higher gradiant for the funny currents Purkinjie fibres and esp sensitive which could lead to PVC v tach and v fib
46
Range of K+ in blood
3.5 mmol/L - 5 mmol/L Regulate by kidney excetion Intake of K Intracellular shifts of K
47
Cancer tumour cells surviving the immune system
CD80 from tumour cells block CTLA4 on T cellls And PD-L1 blocked PD1
48
Cancer progression (rough stages)
1. Acquire cancer abilities of replication 2. Invade neighbouring cells cia basement membrane 3. Angiogenesis and get in blood stream 4. Secondary site, metastasis
49
CA 125
Cancer antigen marker for breast cancer
50
Angiotensin II
Works in body to constrict arteioles and conserve BP by conserving the floods Causes secretion of aldosterone Aldosterone causes excretion of K Spironolactone blocks bind of aldosterone Amiloride is K sparing diuretic that blocks ENaC
51
ENaC
Reasorbs Na+ Ie water follows to conserve osmolaltiy Water is conserved
52
Beta adrenoceptor agonists for asthma
Generates cAMP which inhibits contraction of muscles hence the contraction of airways Opens K channels so body muscle cells hyperpols so harder to make contractions happen
53
SABA VS LABA
Salbutamol VS Salmeterol SABA - faster onset but shorter durability Shorter side chain = more Water soluble, gets there fast but washes away fast Difference due to lipid solubility LABA - longer side chain so more lipid soluble Takes longer to diffuse to beta receptors but sits in the lipid membrane for longer Formoterol = intermediate as it has an intermediate length side chain
54
Paracetamol poison
N-acetylcysteine
55
Methylxanthines and asthma
PDE inhibitors ie accumulation of cAMP so decreases contraction Side effects nausea and tachycardia Theophylline and aminophylline
56
Muscarinic antagonists and asthma
Blocks ACh binding to sm muscles so no ACh to cause contraction Also inhibits mucus pd Ipratopium Tiotropium
57
Glucocorticoids and asthma
Used in late stage to dampen inflammation And use to reduce likelihood of asthma Have relevance to COPD
58
Glucocorticoids and COPD
Glucocorticoids turns of inflammatory molecule transcription by activating histone deacetylase which removes acetyl groups which turns off gene transcriptions So works for asthma patients but not COPD patients as irreversible change in COPD means glucocorticoids can’t really do anything

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