MRCS 1 Flashcards
(94 cards)
Control of ventilation
Control of ventilation is coordinated by the respiratory centres, chemoreceptors, lung receptors and muscles
Automatic, involuntary control of respiration occurs from the medulla.
The respiratory centres control the respiratory rate and the depth of respiration.
Respiratory centres
Medullary respiratory centre
Inspiratory and expiratory neurones. Has ventral group which controls forced voluntary expiration and the dorsal group controls inspiration. Depressed by opiates.
Apneustic centre
Lower pons
Stimulates inspiration - activates and prolongs inhalation
Overridden by pneumotaxic control to end inspiration
Pneumotaxic centre
Upper pons, inhibits inspiration at a certain point. Fine tunes the respiratory rate.
Ventillatory variables
Levels of pCO2 most important in ventilation control
Levels of O2 are less important.
Peripheral chemoreceptors location and what do they respond to
Peripheral chemoreceptors: located in the bifurcation of carotid arteries and arch of the aorta. They respond to changes in reduced pO2, increased H+ and increased pCO2 in ARTERIAL BLOOD.
Central chemoreceptors location and what do they respond to
Central chemoreceptors: located in the medulla. Respond to increased H+ in BRAIN INTERSTITIAL FLUID to increase ventilation.
NB the central receptors are NOT influenced by O2 levels.
Lung receptors
include:
Stretch receptors: respond to lung stretching causing a reduced respiratory rate
Irritant receptors: respond to smoke etc causing bronchospasm
J (juxtacapillary) receptors
Hypercalcaemia - main causes?
Malignancy (most common cause in hospital in-patients)
Primary hyperparathyroidism (commonest cause in non hospitalised patients)
Less common
Sarcoidosis (extrarenal synthesis of calcitriol )
Thiazides, lithium
Immobilisation
Pagets disease
Vitamin A/D toxicity
Thyrotoxicosis
MEN
Milk alkali syndrome
Hypercalcaemia Clinical features?
Stones, bones, abdominal groans, and psychic moans
There are clinical features such as bone pain, osteoporosis, fatigue, confusion, memory problems, depression, nausea, vomiting, abdominal pain, weight loss, thirst, polyuria, constipation, abdominal pain, renal colic, or renal impairment. Symptoms and signs are often non-specific, and relate to the severity and rate of onset of hypercalcaemia.
High serum calcium levels result in decreased neuronal excitability. Therefore sluggish reflexes, muscle weakness and constipation may occur.
Myocardial action potential
0 Rapid depolarisation Rapid sodium influx
These channels automatically deactivate after a few ms
1 Early repolarisation Efflux of potassium
2 Plateau Slow influx of calcium
3 Final repolarisation Efflux of potassium
4 Restoration of ionic concentrations Resting potential is restored by Na+/K+ ATPase
There is slow entry of Na+ into the cell decreasing the potential difference until the threshold potential is reached, triggering a new action potential
Conduction velocity
Atrial conduction - Spreads along ordinary atrial myocardial fibres at 1 m/sec
AV node conduction - 0.05 m/sec
Ventricular conduction Purkinje fibres are of large diameter and achieve velocities of 2-4 m/sec (this allows a rapid and coordinated contraction of the ventricles
Large villous adenomas? common electrolyte abnormality
Large villous adenomas of the rectum may have marked secretory activity and result in the development of hypokalaemia as rectal secretions are rich in potassium.
Which medications can cause SIADH
SIADH - drug causes: sulfonylureas SSRIs, tricyclics carbamazepine vincristine cyclophosphamide
Where is the vomiting centre located?
medulla oblongata
Reflex oral expulsion of gastric (and sometimes intestinal) contents - reverse peristalsis and abdominal contraction
The vomiting centre is in part of the medulla oblongata and is triggered by receptors in several locations
Non- GI causes of vomiting
ABC’s of Non- GI causes of vomiting
Acute renal failure DKA Brain (Increased ICP) Cardiac (Inferior MI) Ears (labyrinthitis) Foreign substances (Tylenol, theo, etc) Glaucoma Hyperemesis Gravidarum Infections (pyelonephritis, meningitis)
Where are the receptors which trigger vomiting?
The vomiting centre is in part of the medulla oblongata and is triggered by receptors in several locations
Labyrinthine receptors of ear (motion sickness)
Over distention receptors of duodenum and stomach
Trigger zone of CNS - many drugs (e.g., opiates) act here
Touch receptors in throat
PTH half life?
PTH has a very short half life usually less than 10 minutes
Therefore a demonstrable drop in serum PTH should be identified within 10 minutes of removing the adenoma. This is useful clinically since it is possible to check the serum PTH intraoperatively prior to skin closure and explore the other glands if levels fail to fall.
lung compliance
Lung compliance is defined as change in lung volume per unit change in airway pressure
Causes of increased compliance
age
emphysema - this is due to loss of alveolar walls and associated elastic tissue
Causes of decreased compliance pulmonary oedema pulmonary fibrosis pneumonectomy kyphosis
4 Types of opioid receptor
4 Types of opioid receptor:
δ (located in CNS)- Accounts for analgesic and antidepressant effects
k (mainly CNS)- analgesic and dissociative effects
µ (central and peripheral) - causes analgesia, miosis, decreased gut motility
Nociceptin receptor (CNS)- Affect of appetite and tolerance to µ agonists.
Drugs causing SIADH: ABCD
A nalgesics: opioids, NSAIDs
B arbiturates
C yclophosphamide/ Chlorpromazine/ Carbamazepine
D iuretic (thiazides)
causes of hypercalcaemia
Main causes
Malignancy (most common cause in hospital in-patients)
Primary hyperparathyroidism (commonest cause in non hospitalised patients)
CHIMPANZEES
C alcium supplementation H yperparathyroidism I atrogentic (Drugs: Thiazides) M ilk Alkali syndrome P aget disease of the bone A cromegaly and Addison's Disease N eoplasia Z olinger-Ellison Syndrome (MEN Type I) E xcessive Vitamin D E xcessive Vitamin A S arcoidosis
Obesity hormones
leptin
ghrelin
leptin decreases appetite
ghrelin increases appetite
TI resection may cause malabsorption of bile salts ? management
The question is about high output diarrhoea following terminal ileal resection and the most likely cause is malabsorption of bile salts
he administration of cholestyramine (bile salt binding agent) will counter this
Conns syndrome
Excessive production of aldosterone
Leads to hypokalemia, hypertension/water(Na) retention
pre renal uraemia vs ATN
Prerenal uraemia - kidneys retain sodium to preserve volume
Pre-renal uraemia Acute tubular necrosis Urine sodium < 20 mmol/L > 30 mmol/L Fractional sodium excretion* < 1% > 1% Fractional urea excretion** < 35% >35% Urine:plasma osmolality > 1.5 < 1.1 Urine:plasma urea > 10:1 < 8:1 Specific gravity > 1020 < 1010 Urine 'bland' sediment brown granular casts Response to fluid challenge Yes No