MRCS 1 Flashcards
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
Normal Gap Acidosis: HARDUP
H - Hyperalimentation/hyperventilation A - Acetazolamide R - Renal tubular acidosis D - Diarrhoea U - Ureteral diversion P - Pancreatic fistula/parenteral saline
Inhibition of insulin release:
Alpha adrenergic drugs
Beta blockers
Sympathetic nerves
carbimazole mechanism of action
Thionamides group.
Carbimazole is a pro-drug as after absorption it is converted to the active form, methimazole.
Inhibits thyroid hormone production via inhibition of thyroid peroxidase → blockade of iodide oxidation, organification, coupling
Potassium iodides - MOA
Lugol’s iodine (oral potassium iodide)
Saturated solution of potassium iodide (SSKI
Inhibit proteolytic cleavage of T3 and T4 from thyroglobulin→ inhibits thyroid hormone release
Also decrease thyroid vascularity and decrease the size of the gland
Glucocorticoids MOA
Glucocorticoids exert their effects by binding intracellular receptors that are then transported to the nucleus where they affect gene transcription.
Glucocorticoids reduce inflammation through a combination of both inhibition & upregulation of gene transcription, including: INHIBITION of genes regulating expression of: COX-2
Corticosteroids - how are they synthesised
Synthesised from cholesterol within the adrenal cortex
Effects of glucocorticoids
Metabolic (generally oppose those of insulin):
- breakdown of protein to amino acids (increased protein catabolism)
- amino acids then converted to glucose (gluconeogenesis)
- storage of glucose as glycogen
- lipolysis: mobilised free fatty acids and glycerol: these are then converted to glucose in the liver
Regulatory actions
- Has a negative feedback action on the hypothalamus causing reduced release of endogenous glucocorticoids
- Within the CVS they cause decreased vasodilation and decreased fluid exudation
- They decrease osteoblastic activity and increase osteoclastic activity
- Decrease acute and chronic inflammation (decrease in influx and activity of leukocytes), decreased clonal expansion of B and T lymphocytes.
ECG features in hypokalemia
U waves Small or absent T waves (occasionally inversion) Prolonged PR interval ST depression Long QT interval
One registered user suggests the following rhyme!
In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT!
Recklinghausen’s disease
Neurofibromatosis 1 (NF1)
autosomal dominant disorder
caused by the mutation of a gene on chromosome 17
NF-1 causes tumors along the nervous system which can grow anywhere on the body
NF1, benign tumors called neurofibromas cover the peripheral nerve and, similarly, may cause pain or specific neurologic symptom
NF1 vs NF2
NF2 is caused by a mutation on chromosome 22 and involves a protein called merlin, which is thought to be involved in cell shape and structure.
NF1 - chromosome 17.
Individuals with NF2 do not have learning disabilities, a complication that is very commonly seen in people with NF1.
In NF2, benign tumors called schwannomas grow on nerves throughout the nervous system and often cause impaired hearing and vision.
NF1, benign tumors called neurofibromas cover the peripheral nerve and, similarly, may cause pain or specific neurologic symptom
Symptoms of NF2 are typically detected between the ages of 18 and 24 years, while NF1 is diagnosed in infancy or early childhood.
Li-Fraumeni syndrome (LFS)
- ALSO KNOWN AS SBLA syndrome (the sarcoma, breast, leukaemia and adrenal gland) .
- AUTOSOMAL DOMINANT
- linked to germline mutations of the p53 tumor suppressor gene
- predisposes carriers to cancer development
- Li–Fraumeni syndrome is diagnosed if these three criteria are met:
The patient has been diagnosed with a sarcoma at a young age (below 45).
A first-degree relative has been diagnosed with any cancer at a young age (below 45).
Another first- or a second-degree relative has been diagnosed with any cancer at a young age (below 45) or with a sarcoma at any age.
Pierre Robin syndrome
- small lower jaw (micrognathia)
- glossoptosis (displacement of the tongue toward the back of the oral cavity)
- can have cleft palate
Kartagener’s syndrome
- AUTOSOMAL RECESSIVE genetic disorder
- ciliary disorder comprising the triad of situs inversus, chronic sinusitis, and bronchiectasis.
