Physiology Flashcards
What is the systemic response in vasculature to hypoxia?
Where is this NOT the case?
Hypoxia results in vasodilation in systemic arteries
e.g. brain, kidneys, gut and myocardium
Pulmonary arteries causes vasoconstriction
e.g. in lungs to allow blood to be re-directed within the lung to higher concentrations of O2: allows blood to flow to the most well ventilated parts of the lung = improve O2 delivery
Occurs via increased sympathetic tone
Osmolality =
- Low osmolality
2(Na+ + K+) + glucose + urea
Low = dilution, low solute available
Control of inspiration and expiration
Expiration = ventral medulla oblongata
Inspiration = dorsal medulla oblongata
Anion Gap =
(Na+ + K+) - (Cl- + HCO3-)
Usually 10-16
Causes of raised anion gap
MUDPILES
Methanol
Uraemia
Renal failure
DKA
Lactic Acidosis
Salicylate
Ethylene glycol
Where does bicarbonate buffering occur (2)
Proximal tubules (most)
- H+ coupled with sodium/bicarbonate reabsorption
RBC (minor role)
- bicarbonate exchanged for chloride
How is an acidosis compensated for? (2)
Acute = red blood cell buffering
Chronic = renal bicarbonate
Causes of respiratory alkalosis (5)
Raised ICP
PE
Pneumonia
Anxiety
Pulmonary oedema
Causes of metabolic alkalosis (4)
Vomiting
Hyperaldosteronism
Cushing’s syndrome
Bartter’s syndrome
Hyperchloraemic acidosis
= occurs when there is loss of bicarbonate (rather than increased acid production)
e.g. renal tubular acidosis, acetazolamide
Hypochloraemic Acidosis (3)
Loss of GI fluids
Over treatment with diuretics
Adrenal insufficiency
Expiratory reserve volume
= maximum volume of air that can be forcibly expired in a normal breath
Tidal volume =
approx. 500ml in males
= volume inspired at rest in a normal breath
Inspiratory reserve volume
= maximum volume of air that can be inspired at the end of a normal tidal respiration
Vital Capacity =
= TV + IRV + ERV
Inspiratory capacity =
= tidal volume + inspiratory reserve volume
VQ Ratio
- what does it mean if it is high?
Volume of air entering alveoli/blood flow through lungs
High = poor perfusion, wasted ventilation
Low = poor ventilation, wasted perfusion
Production of pulmonary surfactant
Type II pneumocytes
Types of resistance in work of breathing (2)
Static resistance - elastic recoil of lungs
Dynamic resistance - airways obstruction
Transfer factor =
= rate at which gas will difuse from alveoli into the blood
Effects of inspiration and expiration on the heart
Inspiration = increased RV filling and output increases
Expiration = increased LV filling and output
What is the most important factor in the control of breathing?
pCO2 due to pH effect - central chemoreceptors respond to changes in H+
Cardiac pacemaker potential
Slow Na+ in
Rapid Calcium in
Rapid K+ out
Hering Bruer Reflex
= distension of lung slows rate of breathing
Phases of Cardiac Action Potential
4,0,1,2,3,4
4 - plateau
0 = Na+ in, rapid depolarisation
1 = K+ out
2 = Ca2+ in/K+ out in balance
3 = K+ out
Cardiac output =
= heart rate x stroke volume
Cardiac contractility
- term
- positive
- negative
= inotropy
Positive inotropes = sympathetics, decrease in intracellular Na+, digoxin
Negative inotropes = B-blockers, heart failure, hypoxia, acidosis
Preload =
= ventricular end diastolic volume, increased with increased venous return
Afterload =
= total peripheral resistance
Altered by increasing/altering vessel calibre
Blood pressure =
= cardiac output x peripheral resistance
Trigger for release of insulin by vesicles
= influx of calcium
Inhibition of insulin secretion (3)
Sympathetics
A-blockers
B-blockers
Gastrin
- where released
- action
G cells in antrum of stomach
= increased gastric acid production and emptying
Secretin
- where released
- action
S cells of duodenum/jejunum
Action = inhibits gastric acid
CCK
- where released
- action
I cells of duodenum/jejunum
Actions = gallbladder contraction, sphincter of oddi relaxation, satiety
Somatostatin
- where released
- action
D cells of pancreas/stomach
Action = decreases acid secretion, decreases gastrin, insulin and glucagon secretion
VIP
- where released
- action
Small intestine
Action = stimulates pancreatic secretions, inhibits acid secretion
What do parietal cells produce (2)?
HCl
Intrinsic Factor
What do chief cells produce?
Pepsinogen (precursor of pepsin)
Pancreatic acinar cells produce…
Enzymes
What do the parafollicular cells produce?
Calcitonin
What does calcitonin do?
Reduces blood calcium levels
What does the zona glomerulosa produce?
Mineralocorticoids
Anterior Pituitary
- hormones secreted from basophils
LH and FSH
TSH
ACTH
MSH
Anterior Pituitary
- hormones secreted from acidophils
GH
Prolactin
Where is ADH synthesised?
Where is ADH released from?
Synthesis = supraoptic and paraventricular nuclei of hypothalamus
Release from posterior pituitary
Causes of SIADH (8)
Vincristine
TB
Ectopic focus e.g. small cell lung cancer
Pleural effusion
Stroke
Head Injury
Carbamazepine
Encephalitis
Where is most sodium and potassium reabsorbed?
Proximal tubule
Distal tubule
- secretion
- reabsorption
Secretion = H+ and K+ under influence of aldosterone
Reabsorption = Na+ and bicarbonate
Carbonic anhydrase inhibitors act on…
Na+/H+ channel in proximal tubule of kidney
Loop Diuretics act on…
Na+/Cl-/2K+ channel in ascending loop
= NKCC2 channel
Where is BNP released from?
Ventricular myocytes = natriuresis
Hypervolaemic Hyponatraemia
- causes (3)
- biochemical findings
Low serum osmolality = dilution
- Cirrhosis
- Heart Failure
Low urine sodium
(kidney trying to reabsorb sodium to try and increase sodium levels) - Nephrotic Syndrome
High urine sodium - unable to reabsorb
Euvolaemic Hyponatraemia
- cause
- biochemical findings
Usually SIADH
= increased ADH, promotes water retention (lower levels of aldosterone/RAAS as increased ANP/BNP to try and counter water retention)
Low serum osmolality
High urine sodium
(less reabsorption of sodium mediated by aldosterone)
Hypovolaemic Hyponatraemia
- causes (4)
- biochemical findings
- Diuretics
- Vomiting
- Adrenal Insufficiency
High urine Na+ - less reabsorption by aldosterone - Burns
