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Applied Physiology - Coggle Diagram

- - - - Inner adrenal medulla
        
        Chromaffin cells from ectodermal cells from neural crest
      - Outer adrenal cortex
        
        Mesodermal origin
  - - - Outer - Zona Glomerulosa
        
        Produces aldosterone
      - Middle - Zona Fasiculata (largest)
      - Inner - Zona Reticularis
  - - - Gluco & Mineralo are termed C-21 (have 21 carbon chains)
      - Androgens C-19
    - - Activates Gs proteins, increasing cAMP
        
        Cholesterol converted by mitochondria to pregnenolone
        
        Modified @ smooth ER to specific steroid
  - - - CVS - maintenance of catechol response
      - Kindey - weak mineralo activity
      - Liver - protein catabolism
      - Immune - immunosuppression & slow healing
    - - Kidney (DCT) - Na reabsorp, K+ and H+ excretion - expands intravascular volume
  - - - Primary (Conn's)
      - Secondary (Raised renin & aldosterone)
      - Clinical Features
        
        HTN
        
        Hypokalaemia
        
        Metabolic alkalosis
      - Diagnosis
        
        Aldosterone:Renin ratio
        
        400 is consistent with Conns
        
        MRI
        
        Adrenal Scintigraphy with 131I-label or 75SE-label
      - Treatment
        
        Bilateral Hyperplasia
        
        Spironolactone +/- ACE-i
        
        Adrenal adenoma
        
        Surgical
    - - Excess cortisol from adrenals or exogenous
        
        Can be pit adenoma with ACTH release
        
        Ectopic ACTH release
        
        Oat cell carcinoma of lung
      - Clincial Features
        
        Moon face, central obesity, buffalo hump, thin skin, purple striae
        
        OP, muscle wasting, LVH
        
        Impaired glucose tolerence or DM
        
        Hypokalaemia (weak mineralocorticoid effect)
      - Screening
        
        24h urinary free cortisol (normal 450-700)
        
        Short dexamethasone suppression test
        
        Give 1mg Dex orally @ midnight - supress 9am coritsol
      - Finding Cause
        
        Serum ACTH
        
        Raised in Addison's, Cushings, adrenoleukodystrophy, ectopic ACTH
        
        Low in Cushings syndrome related to adrenal tumour, exogenous Cushings and pit insufficiency
        
        MRI
        
        Following biochemical tests that point to pituitary cause
        
        Inferior petrosal venous sampling
      - Treatment
        
        Trans-sphenoidal +/- radiotherapy if pituitary dependent
        
        Adrenal adenoma/carcinoma requires surgery
        
        Metyrapone (inhib cortisol synth) if not ameanable to surgery
    - - Reduced or absent secretion of glucocorticoids
      - Primary hyopadrenalism usually autoantibodies
      - Secondary hypoadrenalism from prolonged steroid therapy or hypopituitarism
      - Clinical Features
        
        Crisis
        
        Abdo pain, vomiting, dehydration, hypotension (esp postural)
        
        Chronic
        
        Fatigue, anorexia, weight loss, pigmentation, hypotension
        
        Hypoglycaemia, hyponatraemia, hyperkalaemia
        
        Autoimmune is associated with pernicious anaemia & Grave's
      - Diagnosis
        
        Short Synacthen Test
        
        Give 20ug tetracosactrin & measure corisol @ 0, 30 & 60min
        
        Low initial with little response suggests diagnosis
        
        Adrenal antibodies and imaging
      - Treatment
        
        Replace steroids
        
        Hydrocortisone 20mg OM, 10mg ON
        
        Fludrocortisone 50-100ug OD
        
        Acute crisis
        
        High dose IV hydrocortisone 200mg + 100mg 6 hourly until oral route
        
        Fluid resuscitation
        
        Dextrose to support blood sugars
  - - - Correct Hypoklaemia + alkalosis preop
      - Hypokalaemia
        
        Prolongs NMB (non depol)
        
        Supprress baroR tone
        
        Rx hypovolaemia aggressively
      - Spironolactone moderates metabolic and electrolyte effects
      - Manipulation of adrenal gland can cause CVS instabolity
        
        Use short acting A-blocker (phentolamine)
      - Replacement steroids
    - - ECG - ?IHD
      - Obseity issues
      - Poorly controlled HTN - check for endo organ damage
      - GORD
    - - Check serum K+ and glucose pre and post-op
      - Give 25mg IV hydrocort @ induction
      - Routine medication
      - If intermediate, give 25mg x 4 in 24h
      - Major - 200mg each 24h & d/w endocrinologist
- - - - Anterior (RCA)
      - Left/posterior (LCA)
  - - - Gives rise to diagonal arteries
    - - Gives rise to obtuse marginal branches
  - - - Especially if intracavity pressure>aortic pressure (AORTIC STENOSIS)
  - - - As diastole is 2/3 (systole 1/3) RCA recieves ~ 50% of blood flow during each
    - - So dangerous as effects RCA perfusion which in turn affects electrical signalling -> arrhythmias
      - As Pul HTN and RVESP increases less blood flows during systole until it is purely diastolic
  - - - Normally around 15-25mmHg -> reduces capillary bed perfusion pressure
        
        Closure of capillaries -> ischaemia
      - Important to maintain good diastolic pressure in these pts
- - - - Can lead to AF...
  - - - Class I - procainamide, flecainide
      - Class 3 - sotalol, amiodarone
- - - - PAO2 = PiO2 - PaCO2/RQ
    - - Size of FRC
        
        Anaesthesia (reduces FRC)
        
        External pressure (pregnancy, obesity, ascities etc)
        
        Posture (less when supine)
        
        Age (lower FRC per unit weight in kids)
      - O2 content
        
        Lung disease (shunt reduces effectiveness)
        
        PaCO2 (increased reduces PAO2 - see alveolar gas equation)
        
        FiO2
    - - Pregnancy
      - Critical illness
      - Thyroxicosis
      - Fasciculations due to suxamethonium
      - Sepsis
      - Childhood - greater consumption per unit weight
    - - Partial pressure of CO2 in lungs starts to rise, conc gradient equilibrates between alveolus and blood -> reduced CO2 into lungs, volume falls (as 80% O2 comes out as CO2 (RQ=0.8)), which passively draws O2 into lungs
- - - - Early (neonates)
        
        Valvular
        
        Subvalvular
        
        Supravalvular
      - Late
        
        Biscupid valve 30s/40s
    - - Senile calcification 70s/80s
      - Rheumatic Heart Disease (immune complex from Group B Strep)
  - - - 50% mortality @ 5yrs
    - - 50% mortality @ 3 years
    - - 50% mortality @ 2 yrs
  - - - Peak transvalvular flow >4m/s
      - Aortic valve area <1cm2 (or <0.6cm2/m2 BSA)
      - Mean transaortic gradient >50mmHg
    - - Jet Velocity 3-4m/s
      - Peak pressure gradient 36-64mmHg
      - Valve area 1.5-1cm2
      - Mean gradient 25-50mmHg
- - - - Acute pulmonary oedema
      - Cardiogenic shock
      - Tachycardia
    - - Exersional breathlessness
      - Angina (less common)
      - Asymptomatic
  - - - Moderate 30-59ml
    - - Moderate 30-49%
    - - Moderate 10-29mm
- - - - Mean PA pressure normally <25mmHg
      - Mild 25-40mmHg
      - Moderate 40-55mmHg
      - Severe >55mmHg
      - PCWP <15mmHg
    - - PCWP >15mmHg
  - - - Lung disease
        
        COPD/ILD/low O2 disease
        
        Rx underlying disease
      - Unclear mechanisms
        
        Sarcoidosis/HbSS/chronic haemolytic anaemia/splenic removal/metabolic disorders (Gauchers)
        
        Rx underlying cause
      - Left heart disease
        
        Coronary artery disease, HTN, age, valvular disease
        
        Rx underlying issues
      - Chronic thromboembolic disease
        
        Due to organised, physical barrier to blood flow
        
        Rx via surgical or pharm removal of clot
      - Pulmonary artery HTN
        
        Genetics/drugs/idiopathic/diseases (CT disease, HIV, Portal HTN)
        
        Rx with medications
- - - - Actin/troponin/tropomyosin
    - - Myosin
  - - - Dihydropyridine R - Voltage gated Ltype Ca2+ channel
      - Ryanodine R - releases large amounts of Ca2+ activated by dihydropyridine R
  - - - Multiple mitochondria, slow sustained contraction, resistant to fatigue
    - - Few mitochondria, lots of glycogen, strong contractions but easily fatigued
- - - - Increased Hb O2 affinity
  - - - Decreased Hb O2 affinity - increased release to tissues
- - - - If cardiac sympathetics involved -> hypotension and bradycardia
    - - Initial flaccid areflexia (D0-1)
      - Gradual return of reflexes (D1-3)
      - Automonic hypereflexia + spasticity (up to 1 yr)
  - - - Adductor spasms - if chronic
      - Neurogenic bladder
      - CVS instability
        
        Reduced venous return to heart
        
        Interuption of sympathetic fibres to the heart (T1-4)
        
        Loss of sympathetic innervation to vessels -> venous pooling
        
        Unopposed parasymp stimulation to heart -> bradycardia
        
        Potential for arrest if vagal stimulation (suctioning etc)
      - Autonomic dysreflexia -> HTN or hypotension, issues with temp control
    - - C1-8 injury
      - Trauma or transverse myelitis, polio or muscular dystrophy
- - - - intestinal cells to reduce iron absorption
      - macrophages to inhibit iron release and iron-restricted erythropoiesis
    - - Inflammation
        
        Means oral iron is ineffective
      - Pro-inflammatory state of ageing
      - Iron overload
    - - Iron deficiency
      - Hypoxia