The follicle is the functional unit of the thyroid gland. The follicular cells surround the follicle which is filled with colloid. Suspended within the colloid is the is a pro-hormone complex thyroglobulin.

The synthesis and storage of thyroid hormones is done by follicular cells and the thyroglobulin within the colloid.

Iodide ions (I−) are actively transported against a concentration gradient into the follicular cell under the influence of thyroid stimulating hormone (TSH). It then undergoes oxidation to active iodine catalysed by thyroid peroxidase (TPO). The synthesis of thyroglobulin is in the follicular cells and it contains up to 140 tyrosine residues. The tyrosine residues of thyroglobulin and active iodine are merged to form mono- and di-iodotyrosines (MIT and DIT). The iodinated thyroglobulin is then taken up into the colloid where it is stored and dimerised. Two DIT molecules are joined to produce thyroxine (T4) while one MIT and one DIT molecule are joined to produce tri-iodotyrosine (T3) by a process catalysed by TPO.

Thyroglobulin droplets are taken up as vesicles into follicular cells by pinocytosis. This process is stimulated by TSH. When these vesicles fuse with lysosomes, hydrolysis of the thyroglobulin molecules and subsequent release of T4 and T3 into the circulation occurs.

The hindgut is from the distal third of the transverse colon down to the upper one-third of the anal canal. The inferior mesenteric artery supplies the hindgut.

The inferior mesenteric artery arises from the aorta behind the inferior border of the third part of the duodenum 3–4 cm above the aortic bifurcation, at the third lumbar vertebra level.

The important landmarks of vessels arising from the abdominal aorta at different levels of vertebrae are:

T12 – Coeliac trunk

L1 – Left renal artery

L2 – Testicular or ovarian arteries

L3 – Inferior mesenteric artery

L4 – Bifurcation of the abdominal aorta

The walls of the anterior nasal passage are supplied by the anterior ethmoidal branch of the nasociliary nerve, and the floor is innervated by the superior dental nerve (not the sphenopalatine nerves).

The walls and floor of the posterior nasal passage are innervated by the long and short sphenopalatine nerves and the great palatine nerve (not the superior dental nerves and the nasociliary nerve).

The vestibule is innervated by small branches of the infraorbital branch of the maxillary nerve.

The nasopharynx is innervated by the sensory branches of the trigeminal nerve (not the great palatine nerve).

The major action of ADH is to increase reabsorption of osmotically unencumbered water from the glomerular filtrate and decreases the volume of urine passed. The osmolarity of urine is increased to a maximum of four times that of plasma (approx. 1200 mOsm/kg) by Increasing water reabsorption.

Chronic water loading, Lithium, potassium deficiency, cortisol and calcium excess, all blunt the action of ADH. This leads to nephrogenic diabetes insipidus.

ADH’s primary site of action is the distal tubule and collecting duct.

Peak expiratory flow rate (PEFR) is the maximum speed of air flow generated during a single forced exhaled breath. It is most useful when expressed as a percentage of the best value obtained from the patient.

Forced expiratory volume over 1 second (FEV1) is a lung parameter measured using spirometry. It is the amount of air forced out of the lung in one exhaled breath. It is a more accurate measure of lung obstructions as it doesn’t rely on effort like PEFR

PEFR and FEV1 are usually similar, but become more different in asthmatic patients as airflow becomes increasingly obstructed.

Acute severe asthma is most often diagnosed on history taking and examinations:

Respiratory rate: >25 breaths/min
Heart rate: >110 beats/min
PEFR: 33 – 50% predicted (<200L/min)
Patient state: Unable to complete a sentence in a single breath.

A chest x-ray is not routinely required, and is only indicated in specific circumstances, which are:

If a pneumomediastinum or pneumothorax is suspected
Possible life threatening asthma
Possible consolidation
Unresponsive asthma
If ventilation is required.

An echocardiograph (ECG) is not necessary in this case

Routine haematological and biochemical investigations are not urgent in this case as any abnormalities they detect will be secondary to the patient’s presentation.

An arterial blood gas (ABG) will only be indicated if SPO2 was <92% or if patient presented with life threatening symptoms.

Mesenteric ischemia is ischemia of the blood vessels of the intestines. It can be life-threatening, especially if the small intestine is involved.

The inferior mesenteric artery originates 3-4 cm above the bifurcation of the abdominal aorta.
The left colic artery branches off the inferior mesenteric artery to supply the following:
– distal 1/3 of the transverse colon
– descending colon

At approximately the left colic flexure (splenic flexure), a transition occurs in the blood supply of the GI tract. The SMA supplies the proximal part to the flexure, and the IMA supplies the part distal to the flexure. This is why the left colic flexure is a watershed area and is prone to ischemia exacerbated by atherosclerotic changes or hypotension. The dominant arterial supply of the splenic flexure is usually from the left colic artery, but it may also get collaterals from the left branch of the middle colic artery.

The AMA and PMA do not exist.
The splenic artery directly supplies the spleen and has branches that supply the stomach and the pancreas.
The proximal two-thirds of the transverse colon is supplied by the middle colic artery, a branch of the SMA.

Calcium channel blocker (CCB) blocks L-type of voltage-gated calcium channels present in blood vessels and the heart. By inhibiting the calcium channels, these agents decrease the frequency of opening of calcium channels activity of the heart, decrease heart rate, AV conduction, and contractility.

Three groups of CCBs include
1) Phenylalkylamines: Verapamil, Norverapamil
2) Benzothiazepines : Diltiazem
3) Dihydropyridine : Nifedipine, Nicardipine, Nimodipine, Nislodipine, Nitrendipine, Isradipine, Lacidipine, Felodipine and Amlodipine.

Even though verapamil as good absorption from GIT, its oral bioavailability is low due to high first-pass metabolism.

Nimodipine is a Cerebro-selective CCB, used to reverse the compensatory vasoconstriction after sub-arachnoid haemorrhage and is more lipid soluble analogue of nifedipine

Calcium channel antagonist can potentiate the effect of non-depolarising muscle relaxants.

The posterior tibial artery originates from the popliteal artery in the popliteal fossa. It passes posterior to the popliteus muscle to pierce the soleus muscle. It descends between the tibialis posterior and flexor digitorum longus muscles.

The posterior tibial artery supplies blood to the posterior compartment of the lower limb. The artery can be palpated posterior to the medial malleolus.

There are 4 main pulse points for the lower limb:

1. Femoral pulse 2-3 cm below the mid-inguinal point
2. Popliteal partially flexed knee to loosen the popliteal fascia
3. Posterior tibial behind and below the medial ankle
4. Dorsal pedis dorsum of the foot over the navicular bone

Decreased stroke volume causes decreased ejection fraction which results in diastolic dysfunction.
Ejection fraction is not a useful measure in someone with diastolic dysfunction because stroke volume may be reduced whilst end-diastolic volume may be reduced.
Diastolic dysfunction may arise with reduced heart compliance.

Ejection fraction measures of the proportion of blood leaving the ventricles with each beat and is calculated as follows:
Stroke volume / end-diastolic volume.

A healthy ejection fraction is usually taken as 60% (based on a stroke volume of 70ml and end-diastolic volume of 120ml).

Respiratory inspiration causes a decreased pressure in the thoracic cavity, which in turn causes more blood to flow into the atrium.

Sitting up decreases venous because of the action of gravity on blood in the venous system.
Hypotension also decreases venous return.
A less compliant aorta, like in aortic stenosis increases end systolic left ventricular volume which decreases stroke volume.

Systemic vascular resistance = mean arterial pressure / cardiac output.
Increased vascular resistance impedes the flow of blood back to the heart.

Increased venous return increases end diastolic LV volume as there is more blood returning to the ventricles.

Number needed to treat is a measure of the impact of a treatment or intervention that is often used to communicate results to patients, clinicians, the public and policymakers. It states how many patients need to be treated for one additional patient to experience an adverse outcome (e.g. a death).

It is calculated as the inverse of the absolute risk reduction and is rounded to the next highest whole number.

The absolute risk reduction is 8% (16% – 8%). 100/8 = 12.5, so rounding up the next integer this gives at NNT of 13. i.e. you would need to give the new drug to 13 people to ensure that you prevented one death.