Physiology Flashcards
(38 cards)
How much does a pancreas secrete
Pancreatic secretions are usually 1000-1500ml per 24 hours and have a pH of 8.
Regulation of pancreas
The cephalic and gastric phases (neuronal and physical) are less important in regulating the pancreatic secretions. The effect of digested material in the small bowel stimulates CCK release and ACh which stimulate acinar and ductal cells. Of these CCK is the most potent stimulus. In the case of the ductal cells these are potently stimulated by secretin which is released by the S cells of the duodenum. This results in an increase in bicarbonate.
Normal ICP
<15mmHG
causes of hyponatraemia
carbamazepine, sulfonylureas, SSRIs, tricyclics
Define anatomical dead space
Volume of gas in the respiratory tree not involved in gaseous exchange: mouth, pharynx, trachea, bronchi up to terminal bronchioles
Measured by Fowlers method
Increased by:
Standing, increased size of person, increased lung volume and drugs causing bronchodilatation e.g. Adrenaline
Define Physiological dead space
150 mls, increases in ventilation/perfusion mismatch e.g. PE, COPD, hypotension
Volume of gas in the alveoli and anatomical dead space not involved in gaseous exchange.
Alveolar ventilation is the volume of fresh air entering the alveoli per minute.
Alveolar ventilation = minute ventilation - Dead space volume
Prolactin role
TRH stimulates it - milk production and inhibits gonadal activity
Dopamine inhibits it
Cortisol is predominantly produced by which of the following?
Fasciculata
How does cardiac muscle contract
Cardiomycyte gets depolarised which increases calcium extracellular through T tubules which then attaches to sarcoplasmic reticulum to increase calcium further into cytoplasm. This then attaches to troponin C which uncovers the binding site for myosin head to attach. This is cross bridging to allow contraction. ATP is required for detachment.
Myocytes consist of actin and myosin filaments which is responsible for contraction. Contain myofibrils which are made up of sarcomeres.
Define myocytes
- voltage operated ion channels
- myofibirls made up of sarcomeres
- sarcomeres consist of actin and myosin filaments
- large numbers of mitochondria.
- T-tubles and sarcoplasmic reticulum
Define action potential and how it works in cardio
Electrical signal that travels throughout the cardiac muscle to initiate contraction
Phase 0 when sodium influx happens and it goes above -70. Depolarisation occurs.
Phase 1 When it reaches 20 K channel opens and Na closes -> initial repolarisation
Phase 2 - slow replorasation where calcium channel opens and there is an influx to allow platuea and contraction of muscle. Empty during contraction.
Phase 3 - rapid repolarisation where all channels close and K leaves - heart relax o allow chambers to fill
Phase 4 resting membrane potential of ventricular muscle. SA node and onducting system are constantly depolarising
Role of SA + AV node
right atrium near the entrance of the SVC. Determines heart rate.
AV node -> AV fibrous ring on the right side of the atrial septum.
Define EF
Stroke volume/end diastolic volume
What is first heart sound, second, third + fourth
Closure of AV valves
second - closure of aortic and pulmonary
Third - rapid ventricular filling heard in children
Fourth - stiff ventricle - LVH, heart failure
Cardiac output define
CO = stroke volume x heart rate
Starlings law of heart
greater the stretch of the ventricle in diastole, greater the stroke volume
What affects cardiac output
Causes of increased contractility
stroke volume
- increased contractility
- increased Preload
- reduced Afterload
Contractility
-> increased catecholamine stimulation via B1 receptor
-> decreased beta blocker, HF w systolic dysfunction, acidosis, hypoxia/hypercapnia, calcium channel blockers
Preload -> end diastolic volume depends on venous tone and circuating blood volume. venous vasodilators GTN
Afterload - increased wall tension per Laplace’s law -> increased pressure -> increase afterload.
LV compensates for increased afterload by thickening (hypertrophy) in order to reduce wall stress.
Reduce afterload -> arterial vasodilators, ACEi and ARBs reduce, chronic HTN increase MAP leading to LV hypertrophy
Cardiac oxygen demand
increased -> increased contractility, afterload, HR, diameter of ventricle
Define pulse pressure
Systolic BP - Diastolic BP
MAP
Cardiac output x total peripherla resistance
cerebral blood flow
Factors affecting the cerebral pressure include; systemic carbon dioxide levels, CNS metabolism, CNS trauma, CNS pressure
The PaCO2 is the most potent mediator
Acidosis and hypoxaemia will increase cerebral blood flow but to a lesser degree
Intra cranial pressure may increase in patients with head injuries and this can result in impaired blood flow
Intra cerebral pressure is governed by Monroe-Kelly Doctrine which considers skull as closed box, changes in pressure are offset by loss of CSF. When this is no longer possible ICP rises
causes of hypokalemia with alkalosis
Vomiting
Diuretics
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)
causes of hypokalaemia with acidosis
Diarrhoea
Renal tubular acidosis
Acetazolamide
Partially treated diabetic ketoacidosis
how do we assess upper airway compression
flow volume loop
composition of CSF
Glucose: 50-80mg/dl
Protein: 15-40 mg/dl
Red blood cells: Nil
White blood cells: 0-3 cells/ mm3
approx 150ml
