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Question 1 of 192

 

A 54 year old lady has her serum calcium measured. Assuming her renal function
is normal, what proportion of calcium filtered at the glomerulus will be reabsorbed
by the renal tubules?

5%

15%
gathered by dr. elbarky

25%

50%

95%

Most filtered calcium is reabsorbed (95%) a rare disorder of familial hypocalcemic


calciurea may affect this proportion.

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Calcium homeostasis

Calcium ions are linked to a wide range of physiological processes. The largest
store of bodily calcium is contained within the skeleton. Calcium levels are
primarily controlled by parathyroid hormone, vitamin D and calcitonin.

Hormonal regulation of calcium

Hormone Actions
Hormone Actions

Parathyroid hormone (PTH) Increase calcium levels and


decrease phosphate levels
Increases bone resorption
Immediate action on osteoblasts to
increase ca2+ in extracellular fluid
Osteoblasts produce a protein
signaling molecule that activate
osteoclasts which cause bone
resorption
Increases renal tubular reabsorption
of calcium
Increases synthesis of 1,25(OH)2D
gathered by dr. elbarky

(active form of vitamin D) in the


kidney which increases bowel
absorption of Ca2+
Decreases renal phosphate
reabsorption

1,25-dihydroxycholecalciferol Increases plasma calcium and


(the active form of vitamin D) plasma phosphate
Increases renal tubular reabsorption
and gut absorption of calcium
Increases osteoclastic activity at
high levels and osteoblasts at low
levels
Increases renal phosphate
reabsorption

Calcitonin Secreted by C cells of thyroid


Inhibits intestinal calcium absorption
Inhibits osteoclast activity
Inhibits renal tubular absorption of
calcium

Both growth hormone and thyroxine also play a small role in calcium metabolism.

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B 10.5%
C 17.1%
D 10.9%
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E 52.8%

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Question 2 of 192

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Which of the following statements is true of glucagon?

Glucagon is produced in response to hyperglycaemia

Released by beta cells

Inhibits gluconeogenesis
gathered by dr. elbarky

Produced in response to an increase of amino acids

Composed of 2 alpha polypeptide chains linked by hydrogen bonds

Glucagon is a protein comprised of a single polypeptide chain.


Produced by alpha cells of pancreatic islets of Langerhans in response to
hypoglycaemia and amino acids.
It increases plasma glucose and ketones.

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Glucagon

Glucagon, the hormonal antagonist to insulin, is released from the alpha cells of
the Islets of Langerhans in the pancreas. It will result in an increased plasma
glucose level.

Stimulation Inhibition

Decreased plasma glucose Somatostatin

Increased catecholamines Insulin

Increased plasma amino acids Increased free fatty acids and keto acids
Sympathetic nervous system Increased urea

Acetylcholine

Cholecystokinin

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A 12%
B 11.7%
C 18.2%
D 33.1%
E 25%

33.1% of users answered this question correctly

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Question 3 of 192

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Which of the following is not caused by cortisol in the stress response?

Anti-inflammatory effects

Hypoglycaemia

Skeletal muscle protein breakdown


gathered by dr. elbarky

Stimulation of lipolysis

Mineralocorticoid effects

An 'anti insulin' effect occurs leading to hyperglycaemia.

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Stress response: Endocrine and metabolic changes

Surgery precipitates hormonal and metabolic changes causing the stress


response.
Stress response is associated with: substrate mobilization, muscle protein
loss, sodium and water retention, suppression of anabolic hormone
secretion, activation of the sympathetic nervous system, immunological and
haematological changes.
The hypothalamic-pituitary axis and the sympathetic nervous systems are
activated and there is a failure of the normal feedback mechanisms of
control of hormone secretion.

A summary of the hormonal changes associated with the stress response:


Increased Decreased No Change

Growth hormone Insulin Thyroid stimulating


hormone

Cortisol Testosterone Luteinizing hormone

Renin Oestrogen Follicle stimulating


hormone

Adrenocorticotrophic hormone
(ACTH)

Aldosterone
gathered by dr. elbarky

Prolactin

Antidiuretic hormone

Glucagon

Sympathetic nervous system


Stimulates catecholamine release
Causes tachycardia and hypertension

Pituitary gland
ACTH and growth hormone (GH) is stimulated by hypothalamic releasing
factors, corticotrophin releasing factor (CRF) and somatotrophin (or growth
hormone releasing factor)
Perioperative increased prolactin secretion occurs by release of inhibitory
control
Secretion of thyroid stimulating hormone (TSH), luteinizing hormone (LH)
and follicle stimulating hormone (FSH) does not change significantly
ACTH stimulates cortisol production within a few minutes of the start of
surgery. More ACTH is produced than needed to produce a maximum
adrenocortical response.

Cortisol
Significant increases within 4-6 hours of surgery (>1000 nmol litre-1).
The usual negative feedback mechanism fails and concentrations of ACTH
and cortisol remain persistently increased.
The magnitude and duration of the increase correlate with the severity of
stress and the response is not abolished by the administration of
corticosteroids.
The metabolic effects of cortisol are enhanced:

Skeletal muscle protein breakdown to provide gluconeogenic precursors and


amino acids for protein synthesis in the liver
Stimulation of lipolysis
'Anti-insulin effect'
Mineralocorticoid effects
Anti-inflammatory effects

Growth hormone
Increased secretion after surgery has a minor role
Most important for preventing muscle protein breakdown and promote
tissue repair by insulin growth factors
gathered by dr. elbarky

Alpha Endorphin
Increased

Antidiuretic hormone
An important vasopressor and enhances haemostasis
Renin is released causing the conversion of angiotensinogen to angiotensin
I
Angiotensin II formed by ACE on angiotensin 1, which causes the secretion
of aldosterone from the adrenal cortex. This increases sodium reabsorption
at the distal convoluted tubule

Insulin
Release inhibited by stress
Occurs via the inhibition of the beta cells in the pancreas by the α2-
adrenergic inhibitory effects of catecholamines
Insulin resistance by target cells occurs later
The perioperative period is characterized by a state of functional insulin
deficiency

Thyroxine (T4) and tri-iodothyronine (T3)


Circulating concentrations are inversely correlated with sympathetic activity
and after surgery there is a reduction in thyroid hormone production, which
normalises over a few days.

Metabolic effect of endocrine response

Carbohydrate metabolism
Hyperglycaemia is a main feature of the metabolic response to surgery
Due to increase in glucose production and a reduction in glucose utilization
Catecholamines and cortisol promote glycogenolysis and gluconeogenesis
Initial failure of insulin secretion followed by insulin resistance affects the
normal responses
The proportion of the hyperglycaemic response reflects the severity of
surgery
Hyperglycaemia impairs wound healing and increase infection rates

Protein metabolism
Initially there is inhibition of protein anabolism, followed later, if the stress
response is severe, by enhanced catabolism
The amount of protein degradation is influenced by the type of surgery and
also by the nutritional status of the patient
Mainly skeletal muscle protein is affected
The amino acids released form acute phase proteins (fibrinogen, C reactive
protein, complement proteins, a2-macroglobulin, amyloid A and
gathered by dr. elbarky

ceruloplasmin) and are used for gluconeogenesis


Nutritional support has little effect on preventing catabolism

Lipid metabolism
Increased catecholamine, cortisol and glucagon secretion, and insulin deficiency,
promotes lipolysis and ketone body production.

Salt and water metabolism


ADH causes water retention, concentrated urine, and potassium loss and
may continue for 3 to 5 days after surgery
Renin causes sodium and water retention

Cytokines
Glycoproteins
Interleukins (IL) 1 to 17, interferons, and tumour necrosis factor
Synthesized by activated macrophages, fibroblasts, endothelial and glial
cells in response to tissue injury from surgery or trauma
IL-6 main cytokine associated with surgery. Peak 12 to 24 h after surgery
and increase by the degree of tissue damage Other effects of cytokines
include fever, granulocytosis, haemostasis, tissue damage limitation and
promotion of healing.

Modifying the response


Opioids suppress hypothalamic and pituitary hormone secretion
At high doses the hormonal response to pelvic and abdominal surgery is
abolished. However, such doses prolong recovery and increase the need for
postoperative ventilatory support
Spinal anaesthesia can reduce the glucose, ACTH, cortisol, GH and
epinephrine changes, although cytokine responses are unaltered
Cytokine release is reduced in less invasive surgery
Nutrition prevents the adverse effects of the stress response. Enteral
feeding improves recovery
Growth hormone and anabolic steroids may improve outcome
Normothermia decreases the metabolic response

References
Deborah Burton, Grainne Nicholson, and George Hall
Endocrine and metabolic response to surgery .

Contin Educ Anaesth Crit Care Pain (2004) 4(5): 144-147 doi:10.1093/bjaceaccp
/mkh040

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D 8%
E 9.6%

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Question 4 of 192

 

Which of the following statements relating to abnormal coagulation is false?

Warfarin affects the synthesis of factor 2,7,9,10

The prothrombin time is prolonged in Haemophilia A

Cholestatic jaundice can cause vitamin K deficiency


gathered by dr. elbarky

Disseminated intravascular coagulation is associated with


thrombocytopenia

Massive transfusion is associated with reduced levels of factor 5 and 8

In haemophilia A the APTT is prolonged and there is reduced levels of factor 8:C.
The bleeding time and PT are normal. Cholestatic jaundice prevents the absorption
of the fat soluble vitamin K. Massive transfusion (>10u blood or equivalent to the
blood volume of a person) puts the patient at risk of thrombocytopaenia, factor 5
and 8 deficiency.

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Abnormal coagulation
Cause Factors affected

Heparin Prevents activation factors 2,9,10,11

Warfarin Affects synthesis of factors 2,7,9,10

DIC Factors 1,2,5,8,11

Liver disease Factors 1,2,5,7,9,10,11

Interpretation blood clotting test results

Disorder APTT PT Bleeding time


gathered by dr. elbarky

Haemophilia Increased Normal Normal

von Willebrand's disease Increased Normal Increased

Vitamin K deficiency Increased Increased Normal

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A 6.4%
B 52.4%
C 12.5%
D 11.3%
E 17.4%

52.4% of users answered this question correctly


Question 5 of 192

 

Which of the following is not classically seen in coning resulting from raised intra
cranial pressure?

Coma

Hypotension
gathered by dr. elbarky

Unreactive mid sized pupils

Cheyne Stokes style respiratory efforts

Bradycardia

Cushings triad
Widening of the pulse pressure
Respiratory changes
Bradycardia

Due to raised ICP systemic hypertension is usually seen. Compression of the


respiratory centre will typically result in Cheyne Stokes style respiration.

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Coning

The cranial vault is a confined cavity apart from infants with a non fused
fontanelle.
Rises in ICP may be accommodated by shifts of CSF.
Once the CSF shifting has reached its capacity ICP will start to rise briskly.
The brain autoregulates its blood supply, as ICP rises the systemic
circulation will display changes to try and meet the perfusion needs of the
brain. Usually this will involve hypertension.
As ICP rises further, the brain will be compressed, cranial nerve palsies may
be seen and compression of essential centres in the brain stem will occur.
When the cardiac centre is involved bradycardia will often develop.

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B 57.6%
C 15.3%
D 11.4%
E 10.2%

57.6% of users answered this question correctly

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Question 6 of 192

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Control of ventilation. Which statement is false?

Peripheral chemoreceptors are located in the bifurcation of the carotid


arteries and arch of the aorta

Central chemoreceptors respond to changes in O2


gathered by dr. elbarky

The respiratory centres control the rate and depth of respiration

Involuntary control of respiration is from the medulla and pons

Irritant receptors cause bronchospasm

- Central chemoreceptors: Respond to increased H+ in BRAIN INTERSTITIAL


FLUID to increase ventilation.

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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 Inspiratory and expiratory neurones. Has ventral group
respiratory centre 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 Upper pons, inhibits inspiration at a certain point. Fine


centre tunes the respiratory rate.

Ventillatory variables
Levels of pCO2 most important in ventilation control
gathered by dr. elbarky

Levels of O2 are less important.


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: 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

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Question 7 of 192

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A 52-year-old woman with a history of gastrectomy reports lethargy and a sore


tongue. Blood tests are reported as follows:

Hb 10.7 g/dl

MCV 121 fl

Plt 177 * 10^9/l


gathered by dr. elbarky

WBC 5.4 * 10^9/l

What is the most likely cause?

Vitamin B12 deficiency

Vitamin C deficiency

Iron deficiency anaemia

Anaemia of chronic disease

Vitamin E deficiency

A history of gastrectomy and a macrocytic anaemia should indicate a diagnosis of


B12 deficiency.

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Vitamin B12 deficiency

Vitamin B12 is mainly used in the body for red blood cell development and also
maintenance of the nervous system. It is absorbed after binding to intrinsic factor
(secreted from parietal cells in the stomach) and is actively absorbed in the
terminal ileum. A small amount of vitamin B12 is passively absorbed without being
bound to intrinsic factor.

Causes of vitamin B12 deficiency


pernicious anaemia
post gastrectomy
poor diet
disorders of terminal ileum (site of absorption): Crohn's, blind-loop etc

Features of vitamin B12 deficiency


macrocytic anaemia
sore tongue and mouth
neurological symptoms: e.g. Ataxia
neuropsychiatric symptoms: e.g. Mood disturbances
gathered by dr. elbarky

Management
if no neurological involvement 1 mg of IM hydroxocobalamin 3 times each
week for 2 weeks, then once every 3 months
if a patient is also deficient in folic acid then it is important to treat the B12
deficiency first to avoid precipitating subacute combined degeneration of
the cord

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D 6.5%
E 5.2%

69.2% of users answered this question correctly


Question 8 of 192

 

Which of the following surgical procedures will have the greatest long term impact
on a patients calcium metabolism?

Distal gastrectomy

Cholecystectomy
gathered by dr. elbarky

Extensive small bowel resection

Sub total colectomy

Gastric banding for obesity

Calcium is mainly absorbed from the small bowel and this will have a direct long
term impact on calcium metabolism and increase the risk of osteoporosis. Gastric
banding and distal gastrectomy may affect a patients dietary choices but any
potential deleterious nutritional intake may be counteracted by administration of
calcium supplements orally. Only 10% of calcium is absorbed from the colon so
that a sub total colectomy will only have a negligible effect.

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Calcium homeostasis

Calcium ions are linked to a wide range of physiological processes. The largest
store of bodily calcium is contained within the skeleton. Calcium levels are
primarily controlled by parathyroid hormone, vitamin D and calcitonin.

Hormonal regulation of calcium

Hormone Actions
Hormone Actions

Parathyroid hormone (PTH) Increase calcium levels and


decrease phosphate levels
Increases bone resorption
Immediate action on osteoblasts to
increase ca2+ in extracellular fluid
Osteoblasts produce a protein
signaling molecule that activate
osteoclasts which cause bone
resorption
Increases renal tubular reabsorption
of calcium
Increases synthesis of 1,25(OH)2D
gathered by dr. elbarky

(active form of vitamin D) in the


kidney which increases bowel
absorption of Ca2+
Decreases renal phosphate
reabsorption

1,25-dihydroxycholecalciferol Increases plasma calcium and


(the active form of vitamin D) plasma phosphate
Increases renal tubular reabsorption
and gut absorption of calcium
Increases osteoclastic activity at
high levels and osteoblasts at low
levels
Increases renal phosphate
reabsorption

Calcitonin Secreted by C cells of thyroid


Inhibits intestinal calcium absorption
Inhibits osteoclast activity
Inhibits renal tubular absorption of
calcium

Both growth hormone and thyroxine also play a small role in calcium metabolism.

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C 60.7%
D 8.7%
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E 7.1%

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Question 9 of 192

 

What is measured to obtain renal plasma flow?

Creatinine

Para-amino hippuric acid (PAH)

Inulin
gathered by dr. elbarky

Glucose

Protein

Renal plasma flow = (amount of PAH in urine per unit time) / (difference in PAH
concentration in the renal artery or vein)

Normal value = 660ml/min

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Renal Physiology

Overview
Each nephron is supplied with blood from an afferent arteriole that opens
onto the glomerular capillary bed.
Blood then flows to an efferent arteriole, supplying the peritubular capillaries
and medullary vasa recta.
The kidney receives up to 25% of resting cardiac output.

Control of blood flow


The kidney is able to autoregulate its blood flow between systolic pressures
of 80- 180mmHg so there is little variation in renal blood flow.
This is achieved by myogenic control of arteriolar tone, both sympathetic
input and hormonal signals (e.g. renin) are responsible.

Glomerular structure and function


Blood inside the glomerulus has considerable hydrostatic pressure.
The basement membrane has pores that will allow free diffusion of smaller
solutes, larger negatively charged molecules such as albumin are unable to
cross.
The glomerular filtration rate (GFR) is equal to the concentration of a solute
in the urine, times the volume of urine produced per minute, divided by the
plasma concentration (assuming that the solute is freely diffused e.g.
inulin).
In clinical practice creatinine is used because it is subjected to very little
proximal tubular secretion.
Although subject to variability, the typical GFR is 125ml per minute.
gathered by dr. elbarky

Glomerular filtration rate = Total volume of plasma per unit time leaving the
capillaries and entering the bowman's capsule
Renal clearance = volume plasma from which a substance is removed per
minute by the kidneys

Substances used to measure GFR have the following features:


1. Inert
2. Free filtration from the plasma at the glomerulus (not protein bound)
3. Not absorbed or secreted at the tubules
4. Plasma concentration constant during urine collection

Examples: inulin, creatinine

GFR = urine concentration (mmol/l) x urine volume (ml/min)


--------------------------------------------------------------------------
plasma concentration (mmol/l)

The clearance of a substance is dependent not only on its diffusivity across


the basement membrane but also subsequent tubular secretion and / or
reabsorption.
So glucose which is freely filtered across the basement membrane is usually
reabsorbed from tubules giving a clearance of zero.

Tubular function
Reabsorption and secretion of substances occurs in the tubules.
In the proximal tubule substrates such as glucose, amino acids and
phosphate are co-transported with sodium across the semi permeable
membrane.
Up to two thirds of filtered water is reabsorbed in the proximal tubules.
This will lead to increase in urea concentration in the distal tubule allowing
for its increased diffusion.
Substances to be secreted into the tubules are taken up from the peritubular
blood by tubular cells.
Solutes such as paraaminohippuric acid are cleared with a single passage
through the kidneys and this is why it is used to measure renal plasma flow.
Ions such as calcium and phosphate will have a tubular reabsorption that is
influenced by plasma PTH levels.
Potassium may be both secreted and re-absorbed and is co-exchanged with
sodium.

Loop of Henle
Approximately 60 litres of water containing 9000mmol sodium enters the
descending limb of the loop of Henle in 24 hours.
Loops from the juxtamedullary nephrons run deep into the medulla.
The osmolarity of fluid changes and is greatest at the tip of the papilla.
The thick ascending limb is impermeable to water, but highly permeable to
sodium and chloride ions.
gathered by dr. elbarky

This loss means that at the beginning of the thick ascending limb the fluid is
hypo osmotic compared with adjacent interstitial fluid.
In the thick ascending limb the reabsorption of sodium and chloride ions
occurs by both facilitated and passive diffusion pathways.
The loops of Henle are co-located with vasa recta, these will have similar
solute compositions to the surrounding extracellular fluid so preventing the
diffusion and subsequent removal of this hypertonic fluid.
The energy dependent reabsorption of sodium and chloride in the thick
ascending limb helps to maintain this osmotic gradient.

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Question 10 of 192

 

Which of the following statements relating to alveolar ventilation is untrue?

Anatomical dead space is measured by helium dilution

Physiological dead space is increased in PE

Alveolar ventilation is defined as the volume of fresh air entering the


gathered by dr. elbarky

alveoli per minute

Anatomical dead space is increased by adrenaline

Type 2 pneumocytes in the alveoli secrete surfactant

Anatomical dead space is measured by Fowlers method.

A patient inhales 100% oxygen to empty the conducting zone gases of nitrogen
and then exhales through a mouthpiece which analyses the nitrogen concentration
at the mouth. Initially the exhaled gases contain no nitrogen as this is dead space
gas; the nitrogen concentration will increase as the alveolar gases are exhaled.
Nitrogen which is measured following the breath of 100% oxygen must then have
come only from gas exchanging areas of the lung and not dead space.

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Alveolar ventilation

Minute ventilation is the total volume of gas ventilated per minute.

MV (ml/min)= tidal volume x Respiratory rate (resps/min).

Dead space ventilation describes the volume of gas not involved in


exchange in the blood.
There are 2 types:

1. Anatomical dead space: 150mls


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

2. Physiological dead space: normal 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
gathered by dr. elbarky

gaseous exchange.

Alveolar ventilation is the volume of fresh air entering the alveoli per minute.

Alveolar ventilation = minute ventilation - Dead space volume

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E 8.3%

30.8% of users answered this question correctly


Question 11 of 192

 

Which of the following is associated with reduced lung compliance?

Older age

Emphysematous type COPD

Decline in pulmonary blood flow


gathered by dr. elbarky

Adopting a vertical posture

Adjusting a ventilator to maintain high lung volumes

Increased lung compliance = Older age, COPD

Lung compliance is a measure of the ease of expansion of the lungs and thorax,
determined by pulmonary volume and elasticity. A high degree of compliance
indicates a loss of elastic recoil of the lungs, as in old age or emphysema. This
increased lung compliance is due to loss of supportive tissue around the airways.
While a normal lung has a high passive elastic recoil, the sick lung has a decreased
elasticity (i.e. decreased transpulmonary pressure) which leads to increased lung
compliance.

Decreased compliance means that a greater change in pressure is needed for a


given change in volume, as in atelectasis, pulmonary fibrosis, pneumonia, or lack
of surfactant.

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Lung volumes

The diagram demonstrates lung volumes and capacities


(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb048b.png)
gathered by dr. elbarky

Image sourced from Wikipedia


(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Lung
/images_eMRCS/swb048b.png)
volumes)

Definitions

Tidal volume (TV) Is the volume of air inspired and expired during
each ventilatory cycle at rest.
It is normally 500mls in males and 340mls in
females.

Inspiratory reserve Is the maximum volume of air that can be forcibly


volume (IRV) inhaled following a normal inspiration. 3000mls.

Expiratory reserve Is the maximum volume of air that can be forcibly


volume (ERV) exhaled following a normal expiration. 1000mls.

Residual volume Is that volume of air remaining in the lungs after a


(RV) maximal expiration.
RV = FRC - ERV. 1500mls.

Functional residual Is the volume of air remaining in the lungs at the


capacity (FRC) end of a normal expiration.
FRC = RV + ERV. 2500mls.

Vital capacity (VC) Is the maximal volume of air that can be forcibly
exhaled after a maximal inspiration.
VC = TV + IRV + ERV. 4500mls in males, 3500mls
in females.
Total lung capacity Is the volume of air in the lungs at the end of a
(TLC) maximal inspiration.
TLC = FRC + TV + IRV = VC + RV. 5500-6000mls.

Forced vital The volume of air that can be maximally


capacity (FVC) forcefully exhaled.

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Question 12 of 192

 

A 43 year old lady presents with urinary incontinence. At which of the following
locations is Onufs nucleus likely to be found?

Medulla oblongata

Anterior horn of L5 nerve roots


gathered by dr. elbarky

Micturition centre in the Pons

Anterior horn of S2 nerve roots

None of the above

Onufs nucleus is located in the anterior horn of S2 and is the origin of neurones to
the external urethral sphincter.

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Urinary incontinence

Involuntary passage of urine. Most cases are female (80%). It has a prevalence of
11% in those aged greater than 65 years. The commonest variants include:
Stress urinary incontinence (50%)
Urge incontinence (15%)
Mixed (35%)

Males
Males may also suffer from incontinence although it is a much rarer condition in
men. A number of anatomical factors contribute to this. Males have 2 powerful
sphincters; one at the bladder neck and the other in the urethra. Damage to the
bladder neck mechanism is a factor in causing retrograde ejaculation following
prostatectomy. The short segment of urethra passing through the urogenital
diaphragm consists of striated muscle fibres (the external urethral sphincter) and
smooth muscle capable of more sustained contraction. It is the latter mechanism
that maintains continence following prostatectomy.

Females
The sphincter complex at the level of bladder neck is poorly developed in females.
As a result the external sphincter complex is functionally more important, its
composition being similar to that of males. Innervation is via the pudendal nerve
and the neuropathy that may accompany obstetric events may compromise this
and lead to stress urinary incontinence.

Innervation
Somatic innervation to the bladder is via the pudendal, hypogastric and pelvic
nerves. Autonomic nerves travel in these nerve fibres too. Bladder filling leads to
gathered by dr. elbarky

detrusor relaxation (sympathetic) coupled with sphincter contraction. The


parasympathetic system causes detrusor contraction and sphincter relaxation.
Overall control of micturition is centrally mediated via centres in the Pons.

Stress urinary incontinence


50% of cases, especially in females.
Damage (often obstetric) to the supporting structures surrounding the
bladder may lead to urethral hypermobility.
Other cases due to sphincter dysfunction, usually from neurological
disorders (e.g. Pudendal neuropathy, multiple sclerosis).

Urethral mobility:
Pressure not transmitted appropriately to the urethra resulting in involuntary
passage of urine during episodes of raised intra-abdominal pressure.

Sphincter dysfunction:
Sphincter fails to adapt to compress urethra resulting in involuntary passage of
urine. When the sphincter completely fails there is often to continuous passage of
urine.

Urge incontinence
In these patients there is sense of urgency followed by incontinence. The detrusor
muscle in these patients is unstable and urodynamic investigation will
demonstrate overactivity of the detrusor muscle at inappropriate times (e.g.
Bladder filling). Urgency may be seen in patients with overt neurological disorders
and those without. The pathophysiology is not well understood but poor central
and peripheral co-ordination of the events surrounding bladder filling are the main
processes.

Assessment
Careful history and examination including vaginal examination for cystocele.
Bladder diary for at least 3 days
Consider flow cystometry if unclear symptomatology or surgery considered and
diagnosis is unclear.
Exclusion of other organic disease (e.g. Stones, UTI, Cancer)

Management
Conservative measures should be tried first; Stress urinary incontinence or mixed
symptoms should undergo 3 months of pelvic floor exercise. Over active bladder
should have 6 weeks of bladder retraining.
Drug therapy for women with overactive bladder should be offered oxybutynin (or
solifenacin if elderly) if conservative measures fail.
In women with detrusor instability who fail non operative therapy a trial of sacral
neuromodulation may be considered, with conversion to permanent implant if
good response. Augmentation cystoplasty is an alternative but will involve long
term intermittent self catheterisation.
In women with stress urinary incontinence a urethral sling type procedure may be
undertaken. Where cystocele is present in association with incontinence it should
gathered by dr. elbarky

be repaired particularly if it lies at the introitus.

NICE guidelines
Initial assessment urinary incontinence should be classified as stress/urge
/mixed.
At least 3/7 bladder diary if unable to classify easily.
Start conservative treatment before urodynamic studies if a diagnosis is
obvious from the history
Urodynamic studies if plans for surgery.
Stress incontinence: Pelvic floor exercises 3/12, if fails consider surgery.
Urge incontinence: Bladder training >6/52, if fails for oxybutynin
(antimuscarinic drugs) then sacral nerve stimulation.
Pelvic floor exercises offered to all women in their 1st pregnancy.

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Question 13 of 192

 

A 67 year old male is admitted to the surgical unit with acute abdominal pain. He is
found to have a right sided pneumonia. The nursing staff put him onto 15L O2 via a
non rebreathe mask. After 30 minutes the patient is found moribund, sweaty and
agitated by the nursing staff. An arterial blood gas reveals:

pH 7.15

pCO2 10.2
gathered by dr. elbarky

pO2 8

Bicarbonate 32

Base excess - 5.2

What is the most likely cause for this patients deterioration?

Acute respiratory alkalosis secondary to hyperventilation

Over administration of oxygen in a COPD patient

Metabolic acidosis secondary to severe pancreatitis

Metabolic alkalosis secondary to hypokalaemia

Acute respiratory acidosis secondary to pneumonia

This patient has an acute respiratory acidosis, however this is on a background of


chronic respiratory acidosis (due to COPD) with a compensatory metabolic
alkalosis (the elevated bicarbonate is the main clue to the chronic nature of the
respiratory acidosis). This blood gas picture is typical in a COPD patient who has
received too much oxygen; these patients lose their hypoxic drive for respiration,
therefore retain CO2 and subsequently hypoventilate leading to respiratory arrest. If
the bicarbonate was normal, then the answer would be acute respiratory acidosis
secondary to pneumonia.

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Arterial blood gas interpretation

In advanced life support training, a 5 step approach to arterial blood gas


interpretation is advocated.

1. How is the patient?

2. Is the patient hypoxaemic?


gathered by dr. elbarky

The Pa02 on air should be 10.0-13.0 kPa

3. Is the patient acidaemic (pH <7.35) or alkalaemic (pH >7.45)

4. What has happened to the PaCO2?


If there is acidaemia, an elevated PaCO2 will account for this

5. What is the bicarbonate level or base excess?


A metabolic acidosis will have a low bicarbonate level and a low base excess (< -2
mmol)
A metabolic alkalosis will have a high bicarbonate and a high base excess (> +2
mmol)

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C 10.3%

Question 14 of 192

 

Which of the following statements relating to low molecular weight heparins is


false?

They act via inhibition of Factor Xa

Large doses may be used prior to commencing cardiopulmonary bypass


gathered by dr. elbarky

They have a highly predictable pharmacokinetic profile

They are derivatives of unfractionated heparin

They have a molecular mass in the range of 3000-10000Da

As they are not easily reversed they are unsuitable for this purpose.

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Heparin

Causes the formation of complexes between antithrombin and activated


thrombin/factors 7,9,10,11 & 12

Advantages of low molecular weight heparin


Better bioavailability
Lower risk of bleeding
Longer half life
Little effect on APTT at prophylactic dosages
Less risk of HIT

Complications
Bleeding
Osteoporosis
Heparin induced thrombocytopenia (HIT): occurs 5-14 days after 1st
exposure
Anaphylaxis

In surgical patients that may need a rapid return to theatre, administration of


unfractionated heparin is preferred; as low molecular weight heparins have a
longer duration of action and are harder to reverse.

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C 15.8%
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Question 15 of 192

 

A 43 year old lady undergoes a day case laparoscopic cholecystectomy. The


operation is more difficult than anticipated and a drain is placed to the operative
site. Whilst in recovery, the patient loses 1800ml of frank blood into the drain.
Which of the following will not occur?

Release of aldosterone via the Bainbridge reflex


gathered by dr. elbarky

Reduced urinary sodium excretion

Increase in sympathetic discharge to ventricular muscle

Fall in parasympathetic discharge to the sino atrial node

Decreased stimulation from atrial pressure receptors

The Bainbridge reflex is the increase in heart rate mediated via atrial stretch
receptors that occurs following a rapid infusion of blood. Note the question asks
which will not occur and that is why it is A and not the other options.

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Cardiac physiology

The heart has four chambers ejecting blood into both low pressure and high
pressure systems.
The pumps generate pressures of between 0-25mmHg on the right side and
0-120 mmHg on the left.
At rest diastole comprises 2/3 of the cardiac cycle.
The product of the frequency of heart rate and stroke volume combine to
give the cardiac output which is typically 5-6L per minute.

Detailed descriptions of the various waveforms are often not a feature of MRCS A
(although they are on the syllabus). However, they are a very popular topic for
surgical physiology in the MRCS B exam.

Electrical properties
Intrinsic myogenic rhythm within cardiac myocytes means that even the
denervated heart is capable of contraction.
In the normal situation the cardiac impulse is generated in the sino atrial
node in the right atrium and conveyed to the ventricles via the
atrioventricular node.
The sino atrial node is also capable of spontaneous discharge and in the
absence of background vagal tone will typically discharge around 100x per
minute. Hence the higher resting heart rate found in cardiac transplant
cases. In the SA and AV nodes the resting membrane potential is lower than
in surrounding cardiac cells and will slowly depolarise from -70mV to around
gathered by dr. elbarky

-50mV at which point an action potential is generated.


Differences in the depolarisation slopes between SA and AV nodes help to
explain why the SA node will depolarise first. The cells have a refractory
period during which they cannot be re-stimulated and this period allows for
adequate ventricular filling. In pathological tachycardic states this time
period is overridden and inadequate ventricular filling may then occur,
cardiac output falls and syncope may ensue.

Parasympathetic fibres project to the heart via the vagus and will release
acetylcholine. Sympathetic fibres release nor adrenaline and circulating adrenaline
comes from the adrenal medulla. Noradrenaline binds to β 1 receptors in the SA
node and increases the rate of pacemaker potential depolarisation.

Cardiac cycle

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb034b.png)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Cardiac
/images_eMRCS/swb034b.png)
cycle)
Mid diastole: AV valves open. Ventricles hold 80% of final volume. Outflow
valves shut. Aortic pressure is high.

Late diastole: Atria contract. Ventricles receive 20% to complete filling.


Typical end diastolic volume 130-160ml.

Early systole: AV valves shut. Ventricular pressure rises. Isovolumetric


ventricular contraction. AV Valves bulge into atria (c-wave). Aortic and
pulmonary pressure exceeded- blood is ejected. Shortening of ventricles
pulls atria downwards and drops intra atrial pressure (x-descent).

Late systole: Ventricular muscles relax and ventricular pressures drop.


gathered by dr. elbarky

Although ventricular pressure drops the aortic pressure remains constant


owing to peripheral vascular resistance and elastic property of the aorta.
Brief period of retrograde flow that occurs in aortic recoil shuts the aortic
valve. Ventricles will contain 60ml end systolic volume. The average stroke
volume is 70ml (i.e. Volume ejected).

Early diastole: All valves are closed. Isovolumetric ventricular relaxation


occurs. Pressure wave associated with closure of the aortic valve increases
aortic pressure. The pressure dip before this rise can be seen on arterial
waveforms and is called the incisura. During systole the atrial pressure
increases such that it is now above zero (v- wave). Eventually atrial pressure
exceed ventricular pressure and AV valves open - atria empty passively into
ventricles and atrial pressure falls (y -descent )

The negative atrial pressures are of clinical importance as they can allow air
embolization to occur if the neck veins are exposed to air. This patient positioning
is important in head and neck surgery to avoid this occurrence if veins are
inadvertently cut, or during CVP line insertion.

Mechanical properties
Preload = end diastolic volume
Afterload = aortic pressure

It is important to understand the principles of Laplace's law in surgery.


It states that for hollow organs with a circular cross section, the total
circumferential wall tension depends upon the circumference of the wall,
multiplied by the thickness of the wall and on the wall tension.
The total luminal pressure depends upon the cross sectional area of the
lumen and the transmural pressure. Transmural pressure is the internal
pressure minus external pressure and at equilibrium the total pressure must
counterbalance each other.
In terms of cardiac physiology the law explains that the rise in ventricular
pressure that occurs during the ejection phase is due to physical change in
heart size. It also explains why a dilated diseased heart will have impaired
systolic function.

Starlings law
Increase in end diastolic volume will produce larger stroke volume.
This occurs up to a point beyond which cardiac fibres are excessively
stretched and stroke volume will fall once more. It is important for the
regulation of cardiac output in cardiac transplant patients who need to
increase their cardiac output.

Baroreceptor reflexes
Baroreceptors located in aortic arch and carotid sinus.
gathered by dr. elbarky

Aortic baroreceptor impulses travel via the vagus and from the carotid via
the glossopharyngeal nerve.
They are stimulated by arterial stretch.
Even at normal blood pressures they are tonically active.
Increase in baroreceptor discharge causes:

*Increased parasympathetic discharge to the SA node.


*Decreased sympathetic discharge to ventricular muscle causing decreased
contractility and fall in stroke volume.
*Decreased sympathetic discharge to venous system causing increased
compliance.
*Decreased peripheral arterial vascular resistance

Atrial stretch receptors


Located in atria at junction between pulmonary veins and vena cava.
Stimulated by atrial stretch and are thus low pressure sensors.
Increased blood volume will cause increased parasympathetic activity.
Very rapid infusion of blood will result in increase in heart rate mediated via
atrial receptors: the Bainbridge reflex.
Decreases in receptor stimulation results in increased sympathetic activity
this will decrease renal blood flow-decreases GFR-decreases urinary sodium
excretion-renin secretion by juxtaglomerular apparatus-Increase in
angiotensin II.
Increased atrial stretch will also result in increased release of atrial
natriuretic peptide.

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C 9%
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Question 16 of 192

 

Which one of the following is least associated with thrombocytopenia?

Heparin therapy

Rheumatoid arthritis

Infectious mononucleosis
gathered by dr. elbarky

Liver disease

Pregnancy

Rheumatoid arthritis, unlike systemic lupus erythematous, is generally associated


with a thrombocytosis. In some cases of Felty's syndrome thrombocytopaenia may
be seen secondary to hypersplenism. This however represents a small percentage
of patients with rheumatoid arthritis.

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Thrombocytopenia

Causes of severe thrombocytopenia


ITP
DIC
TTP
haematological malignancy

Causes of moderate thrombocytopenia


heparin induced thrombocytopenia (HIT)
drug-induced (e.g. quinine, diuretics, sulphonamides, aspirin, thiazides)
alcohol
liver disease
hypersplenism
viral infection (EBV, HIV, hepatitis)
pregnancy
SLE/antiphospholipid syndrome
vitamin B12 deficiency

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Question 17 of 192

 

Which of the following statements relating to the pharmacology of warfarin is


untrue?

Interferes with clotting factors 2,7,9 and 10

It may not be clinically effective for up to 72 hours


gathered by dr. elbarky

The half life of warfarin is 40 hours

Warfarin has a large volume of distribution

It is metabolized in the liver

Factors 2,7,9,10 affected

Warfarin interferes with fibrin formation by affecting carboxylation of glutamic acid


residues in factors 2,7,9 and 10. Factor 2 has the longest half life of approximately
60 hours, therefore it can take up to 3 days for warfarin to be fully effective.
Warfarin has a small volume of distribution as it is protein bound.

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Warfarin

Warfarin is an oral anticoagulant which inhibits the reduction of vitamin K to its


active hydroquinone form, which in turn acts as a cofactor in the formation of
clotting factor II, VII, IX and X (mnemonic = 1972) and protein C

Factors that may potentiate warfarin


Liver disease
P450 enzyme inhibitors, e.g.: amiodarone, ciprofloxacin
Cranberry juice
Drugs which displace warfarin from plasma albumin, e.g. NSAIDs
Inhibit platelet function: NSAIDs

Side-effects
Haemorrhage
Teratogenic
Skin necrosis: when warfarin is first started biosynthesis of protein C is
reduced. This results in a temporary procoagulant state after initially
starting warfarin, normally avoided by concurrent heparin administration.
Thrombosis may occur in venules leading to skin necrosis.

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Question 18 of 192

 

Which of the following drugs is least likely to cause syndrome of inappropriate anti
diuretic hormone release?

Haloperidol

Carbamazepine
gathered by dr. elbarky

Amitriptylline

Cyclophosphamide

Methotrexate

Drugs causing SIADH: ABCD

A nalgesics: opioids, NSAIDs


B arbiturates
C yclophosphamide/ Chlorpromazine/ Carbamazepine
D iuretic (thiazides)

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Hyponatraemia

This is commonly tested in the MRCS (despite most surgeons automatically


seeking medical advice if this occurs!). The most common cause in surgery is the
over administration of 5% dextrose.

Hyponatraemia may be caused by water excess or sodium depletion. Causes of


pseudohyponatraemia include hyperlipidaemia (increase in serum volume) or a
taking blood from a drip arm. Urinary sodium and osmolarity levels aid making a
diagnosis.

Classification

Urinary sodium > 20 Sodium depletion, renal loss Mnemonic:


mmol/l Patient often Syndrome of
hypovolaemic INAPPropriate Anti-
Diuretics (thiazides) Diuretic Hormone:
Addison's In creased
Diuretic stage of renal Na (sodium)
failure PP (urine)
SIADH (serum osmolality
low, urine osmolality high,
gathered by dr. elbarky

urine Na high)
Patient often euvolaemic

Urinary sodium < 20 Sodium depletion, extra-renal


mmol/l loss
Diarrhoea, vomiting,
sweating
Burns, adenoma of
rectum (if villous lesion
and large)

Water excess Secondary


(patient often hyperaldosteronism: CCF,
hypervolaemic and cirrhosis
oedematous) Reduced GFR: renal
failure
IV dextrose, psychogenic
polydipsia

Management

Symptomatic Hyponatremia :

Acute hyponatraemia with Na <120: immediate therapy. Central Pontine


Myelinolisis, may occur from overly rapid correction of serum sodium. Aim to
correct until the Na is > 125 at a rate of 1 mEq/h. Normal saline with frusemide is
an alternative method.

The sodium requirement can be calculated as follows :

(125 - serum sodium) x 0.6 x body weight = required mEq of sodium


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B 14.9%
C 17.4%
D 13.9%
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Question 19 of 192

 

Which of the following substances related to thyroid function has its effects
mediated by a nuclear receptor?

Triiodothyronine

Thyroxine
gathered by dr. elbarky

Thyroglobulin

Thyroid stimulating hormone

Thyroxin binding globulin

T3 binds to a receptor on chromatin to induce protein synthesis.

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Thyroid hormones

Hormones of the thyroid gland

Triiodothyronine Major hormone active in target cells


T3

Thyroxine T4 Most prevalent form in plasma, less biologically active


than T3

Calcitonin Lowers plasma calcium

Synthesis and secretion of thyroid hormones


Thyroid actively concentrates iodide to twenty five times the plasma
concentration.
Iodide is oxidised by peroxidase in the follicular cells to atomic iodine which
then iodinates tyrosine residues contained in thyroglobulin.
Iodinated tyrosine residues in thyroglobulin undergo coupling to either T3 or
T4.
Process is stimulated by TSH, which stimulates secretion of thyroid
hormones.
The normal thyroid has approximately 3 month reserves of thyroid
hormones.

LATS and Graves disease


In Graves disease patients develop IgG antibodies to the TSH receptors on the
thyroid gland. This results in chronic and long term stimulation of the gland with
release of thyroid hormones. The typically situation is raised thyroid hormones and
low TSH. Thyroid receptor autoantibodies should be checked in individuals
gathered by dr. elbarky

presenting with hyperthyroidism as they are present in up to 85% cases.

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Question 20 of 192

 

The blood - brain barrier is not highly permeable to which of the following?

Carbon dioxide

Barbituates

Glucose
gathered by dr. elbarky

Oxygen

Hydrogen ions

The blood brain barrier is relatively impermeable to highly dissociated compounds.

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Cerebrospinal fluid

The CSF fills the space between the arachnoid mater and pia mater (covering
surface of the brain). The total volume of CSF in the brain is approximately 150ml.
Approximately 500 ml is produced by the ependymal cells in the choroid plexus
(70%), or blood vessels (30%). It is reabsorbed via the arachnoid granulations
which project into the venous sinuses.

Circulation
1. Lateral ventricles (via foramen of Munro)
2. 3rd ventricle
3. Cerebral aqueduct (aqueduct of Sylvius)
4. 4th ventricle (via foramina of Magendie and Luschka)
5. Subarachnoid space
6. Reabsorbed into the venous system via arachnoid granulations into superior
sagittal sinus
Composition
Glucose: 50-80mg/dl
Protein: 15-40 mg/dl
Red blood cells: Nil
White blood cells: 0-3 cells/ mm3

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C 14.1%
D 8.9%
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Question 22 of 192

 

Which of the following arterial blood gas results would fit with chronic respiratory
acidosis with a compensatory metabolic alkalosis?

pH 7.36, PaCO2 7.3, PO2 8.9 (FiO2 40%), Bicarbonate 30.2, Base excess
+5.3

pH 7.32, PCO2 3.8, PaO2 22.2 (FiO2 40%), Bicarbonate 19.1, Base excess
gathered by dr. elbarky

-7.9

pH 7.14, PaCO2 7.4, PaO2 8.9 (FiO2 40%), Bicarbonate 14 mmol, Base
excess -10.6

pH 7.57, PaCO2 3.5, Pa O2 24.5 (FiO2 85%), Bicarbonate 23.5, Base excess
+1.8 mmol

pH 7.19, pCO2 10.2, pO2 16 (FiO2 85%), Bicarbonate 23.8, Base excess -2.2
mmol

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Arterial blood gas interpretation

In advanced life support training, a 5 step approach to arterial blood gas


interpretation is advocated.

1. How is the patient?

2. Is the patient hypoxaemic?


The Pa02 on air should be 10.0-13.0 kPa

3. Is the patient acidaemic (pH <7.35) or alkalaemic (pH >7.45)


4. What has happened to the PaCO2?
If there is acidaemia, an elevated PaCO2 will account for this

5. What is the bicarbonate level or base excess?


A metabolic acidosis will have a low bicarbonate level and a low base excess (< -2
mmol)
A metabolic alkalosis will have a high bicarbonate and a high base excess (> +2
mmol)

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D 7.2%
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Question 21 of 192

 

A 73 year old man has an arterial line in situ. On studying the trace the incisura can
be seen. What is the physiological event which accounts for this process?

Atrial repolarisation

Mitral valve closure


gathered by dr. elbarky

Ventricular repolarisation

Elastic recoil of the aorta

Tricuspid valve closure

It is the temporary rise in aortic pressure occurring as a result of elastic recoil. its
the same thing as the dicrotic notch.

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Cardiac physiology

The heart has four chambers ejecting blood into both low pressure and high
pressure systems.
The pumps generate pressures of between 0-25mmHg on the right side and
0-120 mmHg on the left.
At rest diastole comprises 2/3 of the cardiac cycle.
The product of the frequency of heart rate and stroke volume combine to
give the cardiac output which is typically 5-6L per minute.

Detailed descriptions of the various waveforms are often not a feature of MRCS A
(although they are on the syllabus). However, they are a very popular topic for
surgical physiology in the MRCS B exam.
Electrical properties
Intrinsic myogenic rhythm within cardiac myocytes means that even the
denervated heart is capable of contraction.
In the normal situation the cardiac impulse is generated in the sino atrial
node in the right atrium and conveyed to the ventricles via the
atrioventricular node.
The sino atrial node is also capable of spontaneous discharge and in the
absence of background vagal tone will typically discharge around 100x per
minute. Hence the higher resting heart rate found in cardiac transplant
cases. In the SA and AV nodes the resting membrane potential is lower than
in surrounding cardiac cells and will slowly depolarise from -70mV to around
-50mV at which point an action potential is generated.
Differences in the depolarisation slopes between SA and AV nodes help to
explain why the SA node will depolarise first. The cells have a refractory
gathered by dr. elbarky

period during which they cannot be re-stimulated and this period allows for
adequate ventricular filling. In pathological tachycardic states this time
period is overridden and inadequate ventricular filling may then occur,
cardiac output falls and syncope may ensue.

Parasympathetic fibres project to the heart via the vagus and will release
acetylcholine. Sympathetic fibres release nor adrenaline and circulating adrenaline
comes from the adrenal medulla. Noradrenaline binds to β 1 receptors in the SA
node and increases the rate of pacemaker potential depolarisation.

Cardiac cycle

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb034b.png)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Cardiac
/images_eMRCS/swb034b.png)
cycle)

Mid diastole: AV valves open. Ventricles hold 80% of final volume. Outflow
valves shut. Aortic pressure is high.
Late diastole: Atria contract. Ventricles receive 20% to complete filling.
Typical end diastolic volume 130-160ml.

Early systole: AV valves shut. Ventricular pressure rises. Isovolumetric


ventricular contraction. AV Valves bulge into atria (c-wave). Aortic and
pulmonary pressure exceeded- blood is ejected. Shortening of ventricles
pulls atria downwards and drops intra atrial pressure (x-descent).

Late systole: Ventricular muscles relax and ventricular pressures drop.


Although ventricular pressure drops the aortic pressure remains constant
owing to peripheral vascular resistance and elastic property of the aorta.
Brief period of retrograde flow that occurs in aortic recoil shuts the aortic
gathered by dr. elbarky

valve. Ventricles will contain 60ml end systolic volume. The average stroke
volume is 70ml (i.e. Volume ejected).

Early diastole: All valves are closed. Isovolumetric ventricular relaxation


occurs. Pressure wave associated with closure of the aortic valve increases
aortic pressure. The pressure dip before this rise can be seen on arterial
waveforms and is called the incisura. During systole the atrial pressure
increases such that it is now above zero (v- wave). Eventually atrial pressure
exceed ventricular pressure and AV valves open - atria empty passively into
ventricles and atrial pressure falls (y -descent )

The negative atrial pressures are of clinical importance as they can allow air
embolization to occur if the neck veins are exposed to air. This patient positioning
is important in head and neck surgery to avoid this occurrence if veins are
inadvertently cut, or during CVP line insertion.

Mechanical properties
Preload = end diastolic volume
Afterload = aortic pressure

It is important to understand the principles of Laplace's law in surgery.


It states that for hollow organs with a circular cross section, the total
circumferential wall tension depends upon the circumference of the wall,
multiplied by the thickness of the wall and on the wall tension.
The total luminal pressure depends upon the cross sectional area of the
lumen and the transmural pressure. Transmural pressure is the internal
pressure minus external pressure and at equilibrium the total pressure must
counterbalance each other.
In terms of cardiac physiology the law explains that the rise in ventricular
pressure that occurs during the ejection phase is due to physical change in
heart size. It also explains why a dilated diseased heart will have impaired
systolic function.
Starlings law
Increase in end diastolic volume will produce larger stroke volume.
This occurs up to a point beyond which cardiac fibres are excessively
stretched and stroke volume will fall once more. It is important for the
regulation of cardiac output in cardiac transplant patients who need to
increase their cardiac output.

Baroreceptor reflexes
Baroreceptors located in aortic arch and carotid sinus.
Aortic baroreceptor impulses travel via the vagus and from the carotid via
the glossopharyngeal nerve.
They are stimulated by arterial stretch.
Even at normal blood pressures they are tonically active.
gathered by dr. elbarky

Increase in baroreceptor discharge causes:

*Increased parasympathetic discharge to the SA node.


*Decreased sympathetic discharge to ventricular muscle causing decreased
contractility and fall in stroke volume.
*Decreased sympathetic discharge to venous system causing increased
compliance.
*Decreased peripheral arterial vascular resistance

Atrial stretch receptors


Located in atria at junction between pulmonary veins and vena cava.
Stimulated by atrial stretch and are thus low pressure sensors.
Increased blood volume will cause increased parasympathetic activity.
Very rapid infusion of blood will result in increase in heart rate mediated via
atrial receptors: the Bainbridge reflex.
Decreases in receptor stimulation results in increased sympathetic activity
this will decrease renal blood flow-decreases GFR-decreases urinary sodium
excretion-renin secretion by juxtaglomerular apparatus-Increase in
angiotensin II.
Increased atrial stretch will also result in increased release of atrial
natriuretic peptide.

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C 11.8%
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53.2% of users answered this question correctly


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Question 23 of 192

 

A 44 year old man receives a large volume transfusion of whole blood. The whole
blood is two weeks old. Which of the following best describes its handling of
oxygen?

It will have a low affinity for oxygen

Its affinity for oxygen is unchanged


gathered by dr. elbarky

It will more readily release oxygen in metabolically active tissues than


fresh blood

The release of oxygen in metabolically active tissues will be the same as


fresh blood

It will have an increased affinity for oxygen

Stored blood has less 2,3 DPG and therefore has a higher affinity for oxygen, this
reduces its ability to release it at metabolising tissues.

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Oxygen Transport

Oxygen transport
Almost all oxygen is transported within erythrocytes. It has limited solubility and
only 1% is carried as solution. Therefore the amount of oxygen transported will
depend upon haemoglobin concentration and its degree of saturation.

Haemoglobin
Globular protein composed of 4 subunits. Haem consists of a protoporphyrin ring
surrounding an iron atom in its ferrous state. The iron can form two additional
bonds; one with oxygen and the other with a polypeptide chain. There are two
alpha and two beta subunits to this polypeptide chain in an adult and together
these form globin. Globin cannot bind oxygen but is able to bind to carbon dioxide
and hydrogen ions, the beta chains are able to bind to 2,3 diphosphoglycerate. The
oxygenation of haemoglobin is a reversible reaction. The molecular shape of
haemoglobin is such that binding of one oxygen molecule facilitates the binding of
subsequent molecules.

Oxygen dissociation curve


The oxygen dissociation curve describes the relationship between the
percentage of saturated haemoglobin and partial pressure of oxygen in the
blood. It is not affected by haemoglobin concentration.
Chronic anaemia causes 2, 3 DPG levels to increase, hence shifting the
curve to the right
gathered by dr. elbarky

Haldane effect
Shifts to left = for given oxygen tension there is increased saturation of Hb
with oxygen i.e. Decreased oxygen delivery to tissues

Bohr effect
Shifts to right = for given oxygen tension there is reduced saturation of Hb
with oxygen i.e. Enhanced oxygen delivery to tissues

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb038b.png)
Image sourced from Wikipedia
(http://en.wikipedia.org/wiki/Oxygen (https://d2zgo9qer4wjf4.cloudfront.net
%E2%80%93haemoglobin dissociation /images_eMRCS/swb038b.png)
curve)
Shifts to Left = Lower oxygen delivery Shifts to Right = Raised oxygen
HbF, methaemoglobin, delivery
carboxyhaemoglobin raised [H+] (acidic)
low [H+] (alkali) raised pCO2
low pCO2 raised 2,3-DPG*
low 2,3-DPG raised temperature
low temperature

*2,3-diphosphoglycerate

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Question 24 of 192

 

A 43 year old presents to the urology clinic complaining of impotence. Which of


the following will occur in response to increased penile parasympathetic
stimulation?

Detumescence

Ejaculation
gathered by dr. elbarky

Erection

Vasospasm of the penile branches of the pudendal artery

Contraction of the smooth muscle in the epididymis and vas deferens

Memory aid for erection


p=parasympathetic=points
s=sympathetic=shoots

Parasympathetic stimulation causes erection. Sympathetic stimulation will


produce ejaculation, detumescence and vasospasm of the pudendal artery. It will
also cause contraction of the smooth muscle in the epididymis and vas to convey
the ejaculate.

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Penile erection

Physiology of erection
Autonomic Sympathetic nerves originate from T11-L2 and
parasympathetic nerves from S2-4 join to form pelvic

plexus.
Parasympathetic discharge causes erection, sympathetic
discharge causes ejaculation and detumescence.

Somatic Supplied by dorsal penile and pudendal nerves. Efferent signals


nerves are relayed from Onufs nucleus (S2-4) to innervate
ischiocavernosus and bulbocavernosus muscles.

Autonomic discharge to the penis will trigger the veno-occlusive mechanism which
triggers the flow of arterial blood into the penile sinusoidal spaces. As the inflow
gathered by dr. elbarky

increases the increased volume in this space will secondarily lead to compression
of the subtunical venous plexus with reduced venous return. During the
detumesence phase the arteriolar constriction will reduce arterial inflow and
thereby allow venous return to normalise.

Priapism
Prolonged unwanted erection, in the absence of sexual desire, lasting more than 4
hours.

Classification of priapism

Low flow Due to veno-occlusion (high intracavernosal pressures).


priapism Most common type
Often painful
Often low cavernosal flow
If present for >4 hours requires emergency treatment

High flow Due to unregulated arterial blood flow.


priapism Usually presents as semi rigid painless erection

Recurrent Typically seen in sickle cell disease, most commonly of


priapism high flow type.

Causes
Intracavernosal drug therapies (e.g. for erectile dysfunction>
Blood disorders such as leukaemia and sickle cell disease
Neurogenic disorders such as spinal cord transection
Trauma to penis resulting in arterio-venous malformations

Tests
Exclude sickle cell/ leukaemia
Consider blood sampling from cavernosa to determine whether high or low
flow (low flow is often hypoxic)

Management
Ice packs/ cold showers
If due to low flow then blood may be aspirated from copora or try
intracavernosal alpha adrenergic agonists.
Delayed therapy of low flow priapism may result in erectile dysfunction.

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D 7.6%
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Question 25 of 192

 

A 28 year old man undergoes a completion right hemicolectomy for treatment of a


5cm appendiceal carcinoid. As part of his follow up he is due to undergo 24 hour
urine collection for 5-HIAA. Which of the following causes an elevated 5-HIAA in a
24-hour urine collection?

Naproxen
gathered by dr. elbarky

Oranges

Flucloxacillin

Amiodarone

Beef

It is important to be aware of what can falsely elevate 5-HIAA to avoid diagnosing


carcinoid syndrome incorrectly. These include:

Food: spinach, cheese, wine, caffeine, tomatoes


Drugs: Naproxen, Monoamine oxidase inhibitors
Recent surgery

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Carcinoid syndrome

Carcinoid tumours secrete serotonin


Originate in neuroendocrine cells mainly in the intestine (midgut-distal
ileum/appendix)
Can occur in the rectum, bronchi
Hormonal symptoms mainly occur when disease spreads outside the bowel
Clinical features
Onset: insidious over many years
Flushing face
Palpitations
Pulmonary valve stenosis and tricuspid regurgitation causing dyspnoea
Asthma
Severe diarrhoea (secretory, persists despite fasting)

Investigation
5-HIAA in a 24-hour urine collection
Somatostatin receptor scintigraphy
CT scan
Blood testing for chromogranin A
gathered by dr. elbarky

Treatment
Octreotide
Surgical removal

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C 9.7%
D 24%
E 17.5%

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Question 26 of 192

 

Which is the least likely to cause hyperuricaemia?

Severe psoriasis

Lesch-Nyhan syndrome

Amiodarone
gathered by dr. elbarky

Diabetic ketoacidosis

Alcohol

Mnemonic of the drugs causing hyperuricaemia as a result of reduced


excretion of urate

'Can't leap'

C iclosporin
A lcohol
N icotinic acid
T hiazides

L oop diuretics
E thambutol
A spirin
P yrazinamide

Decreased tubular secretion of urate occurs in patients with acidosis (eg, diabetic
ketoacidosis, ethanol or salicylate intoxication, starvation ketosis). The organic
acids that accumulate in these conditions compete with urate for tubular
secretion.

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Hyperuricaemia

Increased levels of uric acid may be seen secondary to either increased cell
turnover or reduced renal excretion of uric acid. Hyperuricaemia may be
found in asymptomatic patients who have not experienced attacks of gout

Hyperuricaemia may be associated with hyperlipidaemia and hypertension.


It may also be seen in conjunction with the metabolic syndrome

Increased synthesis
gathered by dr. elbarky

Lesch-Nyhan disease
Myeloproliferative disorders
Diet rich in purines
Exercise
Psoriasis
Cytotoxics

Decreased excretion
Drugs: low-dose aspirin, diuretics, pyrazinamide
Pre-eclampsia
Alcohol
Renal failure
Lead

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Question 27 of 192

 

Approximately what proportion of basal salivary secretions are provided by the


submandibular glands?

10%

70%
gathered by dr. elbarky

40%

90%

20%

Although they are small, the submandibular glands provide the bulk of salivary
secretions and contribute 70%, the sublingual glands provide 5% and the remainder
from the parotid. During food consumption the contribution of the parotid
secretions is greater.

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Submandibular gland

Relations of the submandibular gland

Superficial Platysma, deep fascia and mandible


Submandibular lymph nodes
Facial vein (facial artery near mandible)
Marginal mandibular nerve
Cervical branch of the facial nerve
Deep Facial artery (inferior to the mandible)
Mylohyoid muscle
Sub mandibular duct
Hyoglossus muscle
Lingual nerve
Submandibular ganglion
Hypoglossal nerve

Submandibular duct (Wharton's duct)


Opens lateral to the lingual frenulum on the anterior floor of mouth.
5 cm length
Lingual nerve wraps around Wharton's duct. As the duct passes forwards it
crosses medial to the nerve to lie above it and then crosses back, lateral to
gathered by dr. elbarky

it, to reach a position below the nerve.

Innervation
Sympathetic innervation- Derived from superior cervical ganglion
Parasympathetic innervation- Submandibular ganglion via lingual nerve

Arterial supply
Branch of the facial artery. The facial artery passes through the gland to groove its
deep surface. It then emerges onto the face by passing between the gland and the
mandible.

Venous drainage
Anterior facial vein (lies deep to the Marginal Mandibular nerve)

Lymphatic drainage
Deep cervical and jugular chains of nodes

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45.4% of users answered this question correctly
C 17.5%
D 11.5%
E 16.5%
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Question 28 of 192

 

Which of the following changes are not typically seen in established dehydration?

Rising haematocrit

Urinary sodium <20mmol/ litre

Metabolic acidosis
gathered by dr. elbarky

Decreased serum urea to creatinine ratio

Hypernatraemia

Diagnosing dehydration can be complicated, laboratory features include:


Hypernatraemia
Rising haematocrit
Metabolic acidosis
Rising lactate
Increased serum urea to creatinine ratio
Urinary sodium <20 mmol/litre
Urine osmolality approaching 1200mosmol/kg

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Pre operative fluid management

Fluid management has been described in the British Consensus guidelines on IV


fluid therapy for Adult Surgical patients (GIFTASUP) and by NICE (CG174
December 2013 updated May 2017)

The Recommendations include:


Use Ringer's lactate or Hartmann's when a crystalloid is needed for
resuscitation or replacement of fluids. Avoid 0.9% N. Saline (due to risk of
hyperchloraemic acidosis) unless patient vomiting or has gastric drainage.
Use 4%/0.18% dextrose saline or 5% dextrose in maintenance fluids. It
should not be used in resuscitation or as replacement fluids.
Adult maintenance fluid requirements are: Na 50-100 mmol/day and K 40-80
mmol/day in 1.5-2.5L fluid per day.
Patients for elective surgery should NOT be nil by mouth for >2 hours
(unless has disorder of gastric emptying).
Patients for elective surgery should be given carbohydrate rich drinks 2-3h
before. Ideally this should form part of a normal pre op plan to facilitate
recovery.
Avoid mechanical bowel preparation.
If bowel prep is used, simultaneous administration of Hartmann's or Ringer's
lactate should be considered.
Excessive fluid losses from vomiting should be treated with a crystalloid
with potassium replacement. 0.9% N. Saline should be given if there is
gathered by dr. elbarky

hypochloraemia. Otherwise Hartmann's or Ringer lactate should be given for


diarrhoea/ileostomy/ileus/obstruction. Hartmann's should also be given in
sodium losses secondary to diuretics.
High risk patients should receive fluids and inotropes.
An attempt should be made to detect pre or operative hypovolaemia using
flow based measurements. If this is not available, then clinical evaluation is
needed i.e. JVP, pulse volume etc.
In Blood loss or infection causing hypovolaemia should be treated with a
balanced crystalloid or colloid (or until blood available in blood loss). A
critically ill patient is unable to excrete Na or H20 leading to a 5% risk of
interstitial oedema. Therefore 5% dextrose as well as colloid should be
given.
If patients need IV fluid resuscitation, use crystalloids that contain sodium in
the range 130-154 mmol/l, with a bolus of 500 ml over less than 15 minutes
(NICE Guidance CG 174).

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The British Association for Parenteral and Enteral Nutrition


(BAPEN) (http://www.bapen.org.uk/pdfs/bapen_pubs  
/giftasup.pdf)
British Consensus Guidelines on Intravenous Fluid Therapy for Adult Surgical
Patients

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Question 29 of 192

 

Which of the following best accounts for the action of PTH in increasing serum
calcium levels?

Activation of vitamin D to increase absorption of calcium from the small


intestine.

Direct stimulation of osteoclasts to absorb bone with release of calcium.


gathered by dr. elbarky

Stimulation of phosphate absorption at the distal convoluted tubule of the


kidney.

Decreased porosity of the vessels at Bowmans capsule to calcium.

Vasospasm of the afferent renal arteriole thereby reducing GFR and


calcium urinary loss.

PTH increases the activity of 1-α-hydroxylase enzyme, which converts 25-


hydroxycholecalciferol to 1,25-dihydroxycholecalciferol, the active form of vitamin
D.
Osteoclasts do not have a PTH receptor and effects are mediated via osteoblasts.

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Parathyroid hormone

Parathyroid hormone is secreted by the chief cells of the parathyroid glands. It acts
to increase serum calcium concentration by stimulation of the PTH receptors in
the kidney and bone. PTH has a plasma half life of 4 minutes.

Effects of PTH

Bone Binds to osteoblasts which signal to osteoclasts to cause


resorption of bone and release calcium.
Kidney Active reabsorption of calcium and magnesium from the distal
convoluted tubule. Decreases reabsorption of phosphate.

Intestine via Increases intestinal calcium absorption by increasing activated


kidney vitamin D. Activated vitamin D increases calcium absorption.

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Question 30 of 192

 

Which of the following cell types is least likely to be found in a wound 1 week
following injury?

Macrophages

Fibroblasts
gathered by dr. elbarky

Myofibroblasts

Endothelial cells

Neutrophils

Myofibroblasts are differentiated fibroblasts, in which the cytoskeleton contains


actin filaments. These cell types facilitate wound contracture and are the hallmark
of a mature wound. They are almost never found in wounds less than 1 month old.
Remember the question asks about the cell type asks about which cells are least
likely to be found.

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Phases of wound healing

Phase Key features Cells Timeframe

Haemostasis Vasospasm in Erythrocytes and Seconds/


adjacent vessels platelets Minutes
Platelet plug
formation and
generation of fibrin
rich clot
Inflammation Neutrophils migrate Neutrophils, Days
into wound (function fibroblasts and
impaired in diabetes). macrophages
Growth factors
released, including
basic fibroblast
growth factor and
vascular endothelial
growth factor.
Fibroblasts replicate
within the adjacent
matrix and migrate
into wound.
Macrophages and
gathered by dr. elbarky

fibroblasts couple
matrix regeneration
and clot substitution.

Regeneration Platelet derived Fibroblasts, Weeks


growth factor and endothelial cells,
transformation growth macrophages
factors stimulate
fibroblasts and
epithelial cells.
Fibroblasts produce a
collagen network.
Angiogenesis occurs
and wound resembles
granulation tissue.

Remodelling Longest phase of the Myofibroblasts 6 weeks to


healing process and 1 year
may last up to one
year (or longer).
During this phase
fibroblasts become
differentiated
(myofibroblasts) and
these facilitate wound
contraction.
Collagen fibres are
remodelled.
Microvessels regress
leaving a pale scar.
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Question 31 of 192

 

What is the half life of insulin in the circulation of a normal healthy adult?

Less than 30 minutes

Between 1 and 2 hours

Between 2 and 3 hours


gathered by dr. elbarky

Between 4 and 5 hours

Over 6 hours

Insulin is degraded by enzymes in the circulation. It typically has a half life of less
than 30 minutes. Abnormalities of the clearance of insulin may occur in type 2
diabetes.

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Insulin

Insulin is a peptide hormone, produced by beta cells of the pancreas, and is central
to regulating carbohydrate and fat metabolism in the body. Insulin causes cells in
the liver, skeletal muscles, and fat tissue to absorb glucose from the blood. In the
liver and skeletal muscles, glucose is stored as glycogen, and in fat cells
(adipocytes) it is stored as triglycerides.

Structure
The human insulin protein is composed of 51 amino acids, and has a molecular
weight of 5808 Da. It is a dimer of an A-chain and a B-chain, which are linked
together by disulfide bonds.

Synthesis
Pro-insulin is formed by the rough endoplasmic reticulum in pancreatic beta cells.
Then pro-insulin is cleaved to form insulin and C-peptide. Insulin is stored in
secretory granules and released in response to Ca2+.

Function
Secreted in response to hyperglycaemia
Glucose utilisation and glycogen synthesis
Inhibits lipolysis
Reduces muscle protein loss

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Question 32 of 192

 

Which of the following is responsible for the release and synthesis of calcitonin?

Parathyroid glands

Anterior pituitary

Thyroid gland
gathered by dr. elbarky

Posterior pituitary

Adrenal glands

Calcitonin has the opposite effect of PTH and is released from the thyroid gland.

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Calcium homeostasis

Calcium ions are linked to a wide range of physiological processes. The largest
store of bodily calcium is contained within the skeleton. Calcium levels are
primarily controlled by parathyroid hormone, vitamin D and calcitonin.

Hormonal regulation of calcium

Hormone Actions
Hormone Actions

Parathyroid hormone (PTH) Increase calcium levels and


decrease phosphate levels
Increases bone resorption
Immediate action on osteoblasts to
increase ca2+ in extracellular fluid
Osteoblasts produce a protein
signaling molecule that activate
osteoclasts which cause bone
resorption
Increases renal tubular reabsorption
of calcium
Increases synthesis of 1,25(OH)2D
gathered by dr. elbarky

(active form of vitamin D) in the


kidney which increases bowel
absorption of Ca2+
Decreases renal phosphate
reabsorption

1,25-dihydroxycholecalciferol Increases plasma calcium and


(the active form of vitamin D) plasma phosphate
Increases renal tubular reabsorption
and gut absorption of calcium
Increases osteoclastic activity at
high levels and osteoblasts at low
levels
Increases renal phosphate
reabsorption

Calcitonin Secreted by C cells of thyroid


Inhibits intestinal calcium absorption
Inhibits osteoclast activity
Inhibits renal tubular absorption of
calcium

Both growth hormone and thyroxine also play a small role in calcium metabolism.

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Question 33 of 192

 

Which main group of receptors does dobutamine bind to?

α-1

α-2

ß-1
gathered by dr. elbarky

ß-2

D-1

Dobutamine is a sympathomimetic with both alpha- and beta-agonist properties; it


displays a considerable selectivity for beta1-cardiac receptors.

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Inotropes and cardiovascular receptors

Inotropes are a class of drugs which work primarily by increasing cardiac output.
They should be distinguished from vasoconstrictor drugs which are used
specifically when the primary problem is peripheral vasodilatation.

Catecholamine type agents are commonly used and work by increasing cAMP
levels by adenylate cyclase stimulation. This in turn intracellular calcium ion
mobilisation and thus the force of contraction. Adrenaline works as a beta
adrenergic receptor agonist at lower doses and an alpha receptor agonist at higher
doses. Dopamine causes dopamine receptor mediated renal and mesenteric
vascular dilatation and beta 1 receptor agonism at higher doses. This results in
increased cardiac output. Since both heart rate and blood pressure are raised,
there is less overall myocardial ischaemia. Dobutamine is a predominantly beta 1
receptor agonist with weak beta 2 and alpha receptor agonist properties.
Noradrenaline is a catecholamine type agent and predominantly acts as an alpha
receptor agonist and serves as a peripheral vasoconstrictor.

Phosphodiesterase inhibitors such as milrinone act specifically on the cardiac


phosphodiesterase and increase cardiac output.

Inotrope Cardiovascular receptor action

Adrenaline α-1, α-2, β-1, β-2

Noradrenaline α-1,( α-2), (β-1), (β-2)

Dobutamine β-1, (β 2)

Dopamine (α-1), (α-2), (β-1), D-1,D-2


gathered by dr. elbarky

Minor receptor effects in brackets

Effects of receptor binding

α-1, α-2 vasoconstriction

β-1 increased cardiac contractility and HR

β-2 vasodilatation

D-1 renal and spleen vasodilatation

D-2 inhibits release of noradrenaline

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Question 34 of 192

 

A 43 year old man has recurrent episodes of dyspepsia and treatment is


commenced with oral antacids. Which of the substances listed below is released
in response to increased serum gastrin levels and decreases intra gastric pH?

Cholecystokinin

Histamine
gathered by dr. elbarky

Somatostatin

Insulin

Vasoactive intestinal peptide

Remember that a low pH value indicates an acidic solution. Solutions of less


than 7 (i.e. 1) have more free hydrogen ions than solutions of pH 10.

Histamine is released from enterochromaffin cells in the stomach mucosa which


stimulates acid secretion. It is usually released in response to increased serum
gastrin levels. Histamine blockers (e.g. cimetidine) were extremely popular
treatments until the advent of proton pump inhibitors.

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Gastric secretions

A working knowledge of gastric secretions is important for surgery because peptic


ulcers are common, surgeons frequently prescribe anti secretory drugs and
because there are still patients around who will have undergone acid lowering
procedures (Vagotomy) in the past.
Gastric acid
Is produced by the parietal cells in the stomach
pH of gastric acid is around 2 with acidity being maintained by the H+/K+
ATP ase pump. As part of the process bicarbonate ions will be secreted into
the surrounding vessels.
Sodium and chloride ions are actively secreted from the parietal cell into the
canaliculus. This sets up a negative potential across the membrane and as a
result sodium and potassium ions diffuse across into the canaliculus.
Carbonic anhydrase forms carbonic acid which dissociates and the
hydrogen ions formed by dissociation leave the cell via the H+/K+ antiporter
pump. At the same time sodium ions are actively absorbed. This leaves
hydrogen and chloride ions in the canaliculus these mix and are secreted
into the lumen of the oxyntic gland.
gathered by dr. elbarky

This is illustrated diagrammatically below:

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb028b.jpg)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Gastric
/images_eMRCS/swb028b.jpg)
acid)

Phases of gastric acid secretion


There are 3 phases of gastric secretion:
1. Cephalic phase (smell / taste of food)
30% acid produced
Vagal cholinergic stimulation causing secretion of HCL and gastrin release
from G cells

2. Gastric phase (distension of stomach )


60% acid produced
Stomach distension/low H+/peptides causes Gastrin release

3. Intestinal phase (food in duodenum)


10% acid produced
High acidity/distension/hypertonic solutions in the duodenum inhibits
gathered by dr. elbarky

gastric acid secretion via enterogastrones (CCK, secretin) and neural


reflexes.

Regulation of gastric acid production


Factors increasing production include:
Vagal nerve stimulation
Gastrin release
Histamine release (indirectly following gastrin release) from
enterchromaffin like cells

Factors decreasing production include:


Somatostatin (inhibits histamine release)
Cholecystokinin
Secretin

The diagram below illustrates some of the factors involved in regulating gastric
acid secretion and the relevant associated pharmacology

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb029b.jpg)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Gastric
/images_eMRCS/swb029b.jpg)
acid)

Below is a brief summary of the major hormones involved in food digestion:

Source Stimulus Actions

Gastrin G cells in Distension of Increase HCL, pepsinogen


antrum of stomach, and IF secretion, increases
the extrinsic nerves gastric motility, trophic effect
stomach Inhibited by: low on gastric mucosa
antral pH,
gathered by dr. elbarky

somatostatin

CCK I cells in Partially Increases secretion of


upper digested enzyme-rich fluid from
small proteins and pancreas, contraction of
intestine triglycerides gallbladder and relaxation of
sphincter of Oddi, decreases
gastric emptying, trophic
effect on pancreatic acinar
cells, induces satiety

Secretin S cells in Acidic chyme, Increases secretion of


upper fatty acids bicarbonate-rich fluid from
small pancreas and hepatic duct
intestine cells, decreases gastric acid
secretion, trophic effect on
pancreatic acinar cells

VIP Small Neural Stimulates secretion by


intestine, pancreas and intestines,
pancreas inhibits acid and pepsinogen
secretion

Somatostatin D cells in Fat, bile salts Decreases acid and pepsin


the and glucose in secretion, decreases gastrin
pancreas the intestinal secretion, decreases
and lumen pancreatic enzyme secretion,
stomach decreases insulin and
glucagon secretion
inhibits trophic effects of
gastrin, stimulates gastric
mucous production
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Question 35 of 192

 

A 22 year old man suffers a blunt head injury. He is drowsy and has a GCS of 7 on
admission. Which of the following is the major determinant of cerebral blood flow
in this situation?

Systemic blood pressure

Mean arterial pressure


gathered by dr. elbarky

Intra cranial pressure

Hypoxaemia

Acidosis

Hypoxaemia and acidosis may both affect cerebral blood flow. However, in the
traumatic situation increases in intracranial pressure are far more likely to occur
especially when GCS is low. This will adversely affect cerebral blood flow.

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Cerebral blood flow

CNS autoregulates its own blood supply


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 brain as closed box, changes in pressure are offset by loss of CSF.
When this is no longer possible ICP rises
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C 50.4%
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Question 36 of 192

 

A surgeon is considering using lignocaine as local anasthesia for a minor


procedure. Which of the following best accounts for its actions?

Blockade of neuronal acetylcholine receptors

Blockade of neuronal nicotinic receptors


gathered by dr. elbarky

Blockade of neuronal sodium channels

Blockade of neuronal potassium channels

Blockade of neuronal calcium channels

Lignocaine blocks sodium channels. They will typically be activated first, hence the
pain some patients experience on administration.

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Local anaesthetic agents

Lidocaine
An amide
Local anaesthetic and a less commonly used antiarrhythmic (affects Na
channels in the axon)
Hepatic metabolism, protein bound, renally excreted
Toxicity: due to IV or excess administration. Increased risk if liver
dysfunction or low protein states. Note acidosis causes lidocaine to detach
from protein binding.
Drug interactions: Beta blockers, ciprofloxacin, phenytoin
Features of toxicity: Initial CNS over activity then depression as lidocaine
initially blocks inhibitory pathways then blocks both inhibitory and activating
pathways. Cardiac arrhythmias.
Increased doses may be used when combined with adrenaline to limit
systemic absorption.

Cocaine
Pure cocaine is a salt, usually cocaine hydrochloride. It is supplied for local
anaesthetic purposes as a paste.
It is supplied for clinical use in concentrations of 4 and 10%. It may be
applied topically to the nasal mucosa. It has a rapid onset of action and has
the additional advantage of causing marked vasoconstriction.
It is lipophillic and will readily cross the blood brain barrier. Its systemic
effects also include cardiac arrhythmias and tachycardia.
Apart from its limited use in ENT surgery it is otherwise used rarely in
mainstream surgical practice.
gathered by dr. elbarky

Bupivacaine
Bupivacaine binds to the intracellular portion of sodium channels and blocks
sodium influx into nerve cells, which prevents depolarization.
It has a much longer duration of action than lignocaine and this is of use in
that it may be used for topical wound infiltration at the conclusion of
surgical procedures with long duration analgesic effect.
It is cardiotoxic and is therefore contra indicated in regional blockage in
case the tourniquet fails.
Levobupivacaine (Chirocaine) is less cardiotoxic and causes less
vasodilation.

Prilocaine
Similar mechanism of action to other local anaesthetic agents. However, it
is far less cardiotoxic and is therefore the agent of choice for intravenous
regional anaesthesia e.g. Biers Block.

All local anaesthetic agents dissociate in tissues and this contributes to their
therapeutic effect. The dissociation constant shifts in tissues that are acidic e.g.
where an abscess is present, and this reduces the efficacy.

Doses of local anaesthetics

Agent Dose plain Dose with adrenaline

Lignocaine 3mg/Kg 7mg/Kg

Bupivacaine 2mg/Kg 2mg/Kg

Prilocaine 6mg/Kg 9mg/Kg

These are a guide only as actual doses depend on site of administration, tissue
vascularity and co-morbidities.
Maximum total local anaesthetic doses
Lignocaine 1% plain - 3mg/ Kg - 200mg (20ml)
Lignocaine 1% with 1 in 200,000 adrenaline - 7mg/Kg - 500mg (50ml)
Bupivacaine 0.5% - 2mg/kg- 150mg (30ml)
Maximum doses are based on ideal body weight

Effects of adrenaline
Adrenaline may be added to local anaesthetic drugs. It prolongs the duration of
action at the site of injection and permits usage of higher doses (see above). It is
contra indicated in patients taking MAOI's or tricyclic antidepressants. The toxicity
of bupivacaine is related to protein binding and addition of adrenaline to this drug
does not permit increases in the total dose of bupivacaine, in contrast to the
gathered by dr. elbarky

situation with lignocaine.

References
An excellent review is provided by:
French J and Sharp L. Local Anaesthetics. Ann R Coll Surg Engl 2012; 94: 76-80.

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Question 37 of 192

 

A 25 year old man undergoes an appendicetomy for appendicitis. The appendix is


submitted for histopathological evaluation. Which of the following is most likely to
be identified microscopically?

Macrophages

Neutrophils
gathered by dr. elbarky

Fibroblasts

Lymphocytes

Stem cells

Neutrophil polymorphs are the cell type most commonly encountered in acute
inflammation.

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Acute inflammation

Inflammation is the reaction of the tissue elements to injury. Vascular changes


occur, resulting in the generation of a protein rich exudate. So long as the injury
does not totally destroy the existing tissue architecture, the episode may resolve
with restoration of original tissue architecture.

Vascular changes
Vasodilation occurs and persists throughout the inflammatory phase.
Inflammatory cells exit the circulation at the site of injury.
The equilibrium that balances Starlings forces within capillary beds is
disrupted and a protein rich exudate will form as the vessel walls also
become more permeable to proteins.
The high fibrinogen content of the fluid may form a fibrin clot. This has
several important immunomodulatory functions.

Sequelae

Resolution Typically occurs with minimal initial injury


Stimulus removed and normal tissue
architecture results

Organisation Delayed removal of exudate


Tissues undergo organisation and usually
fibrosis

Suppuration Typically formation of an abscess or an


empyema
gathered by dr. elbarky

Sequestration of large quantities of dead


neutrophils

Progression to chronic Coupled inflammatory and reparative


inflammation activities
Usually occurs when initial infection or
suppuration has been inadequately managed

Causes
Infections e.g. Viruses, exotoxins or endotoxins released by bacteria
Chemical agents
Physical agents e.g. Trauma
Hypersensitivity reactions
Tissue necrosis

Presence of neutrophil polymorphs is a histological diagnostic feature of acute


inflammation

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Question 38 of 192

 

A 23 year old man is undergoing an inguinal hernia repair under local anaesthesia.
The surgeon encounters a bleeding site which he manages with diathermy. About
a minute or so later the patient complains that he is able to feel the burning pain of
the heat at the operative site. Which of the following nerve fibres is responsible for
the transmission of this signal?

A α fibres
gathered by dr. elbarky

A β fibres

B fibres

C fibres

None of the above

Slow transmission of mechanothermal stimuli is transmitted via C fibres.


A γ fibres transmit information relating to motor proprioception, A β fibres transmit
touch and pressure and B fibres are autonomic fibres.

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Pain - neuronal transmission

Somatic pain
Peripheral nociceptors are innervated by either small myelinated fibres (A-
delta) fibres or by unmyelinated C fibres.
The A gamma fibres register high intensity mechanical stimuli. The C fibres
usually register high intensity mechanothermal stimuli.

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C 9.3%
D 54.7%
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Question 39 of 192

 

In a 70 Kg male, what proportion of total body fluid will be contributed by plasma?

50%

5%

35%
gathered by dr. elbarky

65%

25%

70 Kg male = 42 L water (60% of total body weight)

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Fluid compartment physiology

Body fluid compartments comprise intracellular and extracellular compartments.


The latter includes interstitial fluid, plasma and transcellular fluid.
Typical figures are based on the 70 Kg male.

Body fluid volumes

Compartment Volume in litres Percentage of total volume

Intracellular 28 L 60-65%

Extracellular 14 L 35-40%
Compartment Volume in litres Percentage of total volume

Plasma 3L 5%

Interstitial 10 L 24%

Transcellular 1L 3%

Figures are approximate

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C 16.1%
D 17.7%
E 16%

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Question 40 of 192

 

Which of the following hormones is mainly responsible for sodium - potassium


exchange in the salivary ducts?

Vasopressin

Angiotensin I
gathered by dr. elbarky

Aldosterone

Somatostatin

Cholecystokinin

Aldosterone is responsible for regulating ion exchange in salivary glands. It acts on


a sodium / potassium ion exchange pump.It is a mineralocorticoid hormone
derived from the zona glomerulosa of the adrenal gland.

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Parotid gland

Anatomy of the parotid gland

Location Overlying the mandibular ramus; anterior and inferior to


the ear.

Salivary duct Crosses the masseter, pierces the buccinator and drains
adjacent to the 2nd upper molar tooth (Stensen's duct).
Structures Facial nerve (Mnemonic: The Zebra Buggered My
passing through Cat; Temporal Zygomatic, Buccal, Mandibular,
the gland Cervical)
External carotid artery

Retromandibular vein
Auriculotemporal nerve

Relations Anterior: masseter, medial pterygoid, superficial


temporal and maxillary artery, facial nerve,
stylomandibular ligament
Posterior: posterior belly digastric muscle,
sternocleidomastoid, stylohyoid, internal carotid
artery, mastoid process, styloid process
gathered by dr. elbarky

Arterial supply Branches of external carotid artery

Venous drainage Retromandibular vein

Lymphatic Deep cervical nodes


drainage

Nerve innervation Parasympathetic-Secretomotor


Sympathetic-Superior cervical ganglion
Sensory- Greater auricular nerve

Parasympathetic stimulation produces a water rich, serous saliva. Sympathetic


stimulation leads to the production of a low volume, enzyme-rich saliva.

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11

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13

Question 41 of 192

 

What are the most likely effects of the release of vasopressin from the pituitary?

Vasoconstriction of the afferent glomerular arteriole

Increased permeability of the mesangial cells to glucose

Reduced permeability of the inner medullary portion of the collecting duct


gathered by dr. elbarky

to urea

Increased secretion of aldosterone from the macula densa

Increased water permeability of the distal tubule cells of the kidney

ADH (vasopressin) results in the insertion of aquaporin channels in apical


membrane of the distal tubule and collecting ducts.

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Renal Physiology

Overview
Each nephron is supplied with blood from an afferent arteriole that opens
onto the glomerular capillary bed.
Blood then flows to an efferent arteriole, supplying the peritubular capillaries
and medullary vasa recta.
The kidney receives up to 25% of resting cardiac output.

Control of blood flow


The kidney is able to autoregulate its blood flow between systolic pressures
of 80- 180mmHg so there is little variation in renal blood flow.
This is achieved by myogenic control of arteriolar tone, both sympathetic
input and hormonal signals (e.g. renin) are responsible.
Glomerular structure and function
Blood inside the glomerulus has considerable hydrostatic pressure.
The basement membrane has pores that will allow free diffusion of smaller
solutes, larger negatively charged molecules such as albumin are unable to
cross.
The glomerular filtration rate (GFR) is equal to the concentration of a solute
in the urine, times the volume of urine produced per minute, divided by the
plasma concentration (assuming that the solute is freely diffused e.g.
inulin).
In clinical practice creatinine is used because it is subjected to very little
proximal tubular secretion.
Although subject to variability, the typical GFR is 125ml per minute.
Glomerular filtration rate = Total volume of plasma per unit time leaving the
gathered by dr. elbarky

capillaries and entering the bowman's capsule


Renal clearance = volume plasma from which a substance is removed per
minute by the kidneys

Substances used to measure GFR have the following features:


1. Inert
2. Free filtration from the plasma at the glomerulus (not protein bound)
3. Not absorbed or secreted at the tubules
4. Plasma concentration constant during urine collection

Examples: inulin, creatinine

GFR = urine concentration (mmol/l) x urine volume (ml/min)


--------------------------------------------------------------------------
plasma concentration (mmol/l)

The clearance of a substance is dependent not only on its diffusivity across


the basement membrane but also subsequent tubular secretion and / or
reabsorption.
So glucose which is freely filtered across the basement membrane is usually
reabsorbed from tubules giving a clearance of zero.

Tubular function
Reabsorption and secretion of substances occurs in the tubules.
In the proximal tubule substrates such as glucose, amino acids and
phosphate are co-transported with sodium across the semi permeable
membrane.
Up to two thirds of filtered water is reabsorbed in the proximal tubules.
This will lead to increase in urea concentration in the distal tubule allowing
for its increased diffusion.
Substances to be secreted into the tubules are taken up from the peritubular
blood by tubular cells.
Solutes such as paraaminohippuric acid are cleared with a single passage
through the kidneys and this is why it is used to measure renal plasma flow.
Ions such as calcium and phosphate will have a tubular reabsorption that is
influenced by plasma PTH levels.
Potassium may be both secreted and re-absorbed and is co-exchanged with
sodium.

Loop of Henle
Approximately 60 litres of water containing 9000mmol sodium enters the
descending limb of the loop of Henle in 24 hours.
Loops from the juxtamedullary nephrons run deep into the medulla.
The osmolarity of fluid changes and is greatest at the tip of the papilla.
The thick ascending limb is impermeable to water, but highly permeable to
sodium and chloride ions.
This loss means that at the beginning of the thick ascending limb the fluid is
gathered by dr. elbarky

hypo osmotic compared with adjacent interstitial fluid.


In the thick ascending limb the reabsorption of sodium and chloride ions
occurs by both facilitated and passive diffusion pathways.
The loops of Henle are co-located with vasa recta, these will have similar
solute compositions to the surrounding extracellular fluid so preventing the
diffusion and subsequent removal of this hypertonic fluid.
The energy dependent reabsorption of sodium and chloride in the thick
ascending limb helps to maintain this osmotic gradient.

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Question 42 of 192

 

A 25 year old man is undergoing respiratory spirometry. He takes a maximal


inspiration and maximally exhales. Which of the following measurements will best
illustrate this process?

Functional residual capacity

Vital capacity
gathered by dr. elbarky

Inspiratory capacity

Maximum voluntary ventilation

Tidal volume

The maximum voluntary ventilation is the maximal ventilation over the course of 1
minute.

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Lung volumes

The diagram demonstrates lung volumes and capacities


(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb048b.png)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
gathered by dr. elbarky

(http://en.wikipedia.org/wiki/Lung
/images_eMRCS/swb048b.png)
volumes)

Definitions

Tidal volume (TV) Is the volume of air inspired and expired during
each ventilatory cycle at rest.
It is normally 500mls in males and 340mls in
females.

Inspiratory reserve Is the maximum volume of air that can be forcibly


volume (IRV) inhaled following a normal inspiration. 3000mls.

Expiratory reserve Is the maximum volume of air that can be forcibly


volume (ERV) exhaled following a normal expiration. 1000mls.

Residual volume Is that volume of air remaining in the lungs after a


(RV) maximal expiration.
RV = FRC - ERV. 1500mls.

Functional residual Is the volume of air remaining in the lungs at the


capacity (FRC) end of a normal expiration.
FRC = RV + ERV. 2500mls.

Vital capacity (VC) Is the maximal volume of air that can be forcibly
exhaled after a maximal inspiration.
VC = TV + IRV + ERV. 4500mls in males, 3500mls
in females.
Total lung capacity Is the volume of air in the lungs at the end of a
(TLC) maximal inspiration.
TLC = FRC + TV + IRV = VC + RV. 5500-6000mls.

Forced vital The volume of air that can be maximally


capacity (FVC) forcefully exhaled.

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Question 43 of 192

 

Which of the following is the main site of dehydroepiandrosterone release?

Posterior pituitary

Zona reticularis of the adrenal gland

Zona glomerulosa of the adrenal gland


gathered by dr. elbarky

Juxtaglomerular apparatus of the kidney

Zona fasciculata of the adrenal gland

Adrenal cortex mnemonic: GFR - ACD

DHEA possesses some androgenic activity and is almost exclusively released from
the adrenal gland.

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Renin-angiotensin-aldosterone system

Adrenal cortex (mnemonic GFR - ACD)


Zona glomerulosa (on outside): mineralocorticoids, mainly aldosterone
Zona fasciculata (middle): glucocorticoids, mainly cortisol
Zona reticularis (on inside): androgens, mainly dehydroepiandrosterone
(DHEA)

Renin
Released by JGA cells in kidney in response to reduced renal perfusion, low
sodium
Hydrolyses angiotensinogen to form angiotensin I

Factors stimulating renin secretion


Low BP
Hyponatraemia
Sympathetic nerve stimulation
Catecholamines
Erect posture

Angiotensin
ACE in lung converts angiotensin I → angiotensin II
Vasoconstriction leads to raised BP
Stimulates thirst
gathered by dr. elbarky

Stimulates aldosterone and ADH release

Aldosterone
Released by the zona glomerulosa in response to raised angiotensin II,
potassium, and ACTH levels
Causes retention of Na+ in exchange for K+/H+ in distal tubule

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb138b.png)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Renin%E2%80
/images_eMRCS/swb138b.png)
%93angiotensin system)

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E 14.8%
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Question 44 of 192

 

A 63 year old female is referred to the surgical clinic with an iron deficiency
anaemia. Her past medical history includes a left hemi colectomy but no other co-
morbidities. At what site is most dietary iron absorbed?

Stomach

Duodenum
gathered by dr. elbarky

Proximal ileum

Distal ileum

Colon

Iron is best absorbed from the proximal small bowel (duodenum and jejunum) in
the Fe 2+ state. Iron is transported across the small bowel mucosa by a divalent
membrane transporter protein (hence the improved absorption of Fe 2+). The
intestinal cells typically store the bound iron as ferritin. Cells requiring iron will
typically then absorb the complex as needed.

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Iron metabolism
Absorption Duodenum and upper jejunum
About 10% of dietary iron absorbed
Fe2+ (ferrous iron) much better absorbed than Fe3+ (ferric
iron)
Ferrous iron is oxidized to form ferric iron, which is
combined with apoferritin to form ferritin
Absorption is regulated according to body's need
Increased by vitamin C, gastric acid

Transport In plasma as Fe3+ bound to transferrin

Distribution
Storage in body
Ferritin (or haemosiderin) in bone marrow
gathered by dr. elbarky

Total body iron 4g


Excretion Lost via intestinal tract following desquamation
Haemoglobin 70%

Ferritin and haemosiderin 25%

Myoglobin 4%

Plasma iron 0.1%

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C 19.8%
D 22.9%
E 8.5%

Question 45 of 192

 

A 56 year old man has long standing chronic pancreatitis and develops pancreatic
insufficiency. Which of the following will be absorbed normally?

Fat

Protein
gathered by dr. elbarky

Folic acid

Vitamin B12

None of the above

Pancreatic lipase is required for digestion of fat, Proteases facilitate protein and
B12 absorption. Folate digestion is independent of the pancreas.

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Pancreas exocrine physiology

Composition of pancreatic secretions


Pancreatic secretions are usually 1000-1500ml per 24 hours and have a pH of 8.
Secretion Source Substances secreted

Trypsinogen
Procarboxylase
Enzymic Acinar cells
Amylase
Elastase
Sodium
Bicarbonate
Water
Ductal and
Aqueous Potassium
Centroacinar cells
Chloride
NB: Sodium and potassium reflect their plasma levels;
chloride and bicarbonate vary with flow rate

Regulation
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.
gathered by dr. elbarky

Enzyme activation
Trypsinogen is converted via enterokinase to active trypsin in the duodenum.
Trypsin then activates the other inactive enzymes

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C 32.1%
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Question 46 of 192

 

Which vitamin is involved in the formation of collagen?

Vitamin A

Vitamin B

Vitamin C
gathered by dr. elbarky

Vitamin D

Vitamin E

Vitamin C is needed for the hydroxylation of proline during collagen synthesis.

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Collagen

Collagen is one of the most important structural proteins within the extracellular
matrix, collagen together with components such as elastin and
glycosaminoglycans determine the properties of all tissues.
Composed of 3 polypeptide strands that are woven into a helix, usually a
combination of glycine with either proline or hydroxyproline plus another
amino acid
Numerous hydrogen bonds exist within molecule to provide additional
strength
Many sub types but commonest sub type is I (90% of bodily collagen),
tissues with increased levels of flexibility have increased levels of type III
collagen
Vitamin c is important in establishing cross links
Synthesised by fibroblasts
Collagen Diseases
Disorders of collagen range from relatively common, acquired defects (typically
aging), through to rarer congenital disorders. The latter are exemplified by
conditions such as osteogenesis imperfecta and Ehlers Danlos syndromes.

Osteogenesis imperfecta:
-8 Subtypes
-Defect of type I collagen
-In type I the collagen is normal quality but insufficient quantity
-Type II- poor quantity and quality
-Type III- Collagen poorly formed, normal quantity
-Type IV- Sufficient quantity but poor quality
Patients have bones which fracture easily, loose joint and multiple other defects
depending upon which sub type they suffer from.
gathered by dr. elbarky

Ehlers Danlos:
-Multiple sub types
-Abnormality of types 1 and 3 collagen
-Patients have features of hypermobility.
-Individuals are prone to joint dislocations and pelvic organ prolapse. In addition to
many other diseases related to connective tissue defects.

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Question 47 of 192

 

A 28 year old man is shot in the abdomen and haemorrhages. Which of the
following substances will produce vasoconstriction in response to this process?

Renin

Angiotensin I
gathered by dr. elbarky

Angiotensin II

Aldosterone

None of the above

Renin does not cause vasoconstriction. Angiotensin I is biologically inactive.


Aldosterone will increase blood pressure but does not have direct vasospastic
effects.

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Shock

Shock occurs when there is insufficient tissue perfusion.


The pathophysiology of shock is an important surgical topic and may be
divided into the following aetiological groups:
Septic
Haemorrhagic
Neurogenic
Cardiogenic
Anaphylactic

Septic shock
Septic shock is a major problem and those patients with severe sepsis have a
mortality rate in excess of 40%. In those who are admitted to intensive care
mortality ranges from 6% with no organ failure to 65% in those with 4 organ failure.

Sepsis is defined as an infection that triggers a particular Systemic Inflammatory


Response Syndrome (SIRS). This is characterised by body temperature outside 36
oC - 38 o C, HR >90 beats/min, respiratory rate >20/min, WBC count >12,000/mm 3

or < 4,000/mm3, altered mental state or hyperglycaemia (in absence of diabetes).

Patients with infections and two or more elements of SIRS meet the diagnostic
criteria for sepsis. Those with organ failure have severe sepsis and those with
refractory hypotension -septic shock.

During the septic process there is marked activation of the immune system with
extensive cytokine release. This may be coupled with or triggered by systemic
gathered by dr. elbarky

circulation of bacterial toxins. These all cause endothelial cell damage and
neutrophil adhesion. The overall hallmarks are thus those of excessive
inflammation, coagulation and fibrinolytic suppression.

The surviving sepsis campaign (2012) highlights the following key areas for
attention:
Prompt administration of antibiotics to cover all likely pathogens coupled
with a rigorous search for the source of infection.
Haemodynamic stabilisation. Many patients are hypovolaemic and require
aggressive fluid administration. Aim for CVP 8-12 cm H2O, MAP >65mmHg.
Modulation of the septic response. This includes manoeuvres to counteract
the changes and includes measures such as tight glycaemic control. The
routine use of steroids is not advised.

In surgical patients, the main groups with septic shock include those with
anastomotic leaks, abscesses and extensive superficial infections such as
necrotising fasciitis. When performing surgery the aim should be to undertake the
minimum necessary to restore physiology. These patients do not fare well with
prolonged surgery. Definitive surgery can be more safely undertaken when
physiology is restored and clotting in particular has been normalised.

Haemorrhagic shock
The average adult blood volume comprises 7% of body weight. Thus in the 70 Kg
adult this will equate to 5 litres. This changes in children (8-9% body weight) and is
slightly lower in the elderly.

The table below outlines the 4 major classes of haemorrhagic shock and their
associated physiological sequelae:

Parameter Class I Class II Class III Class IV

Blood loss ml <750ml 750-1500ml 1500-2000ml >2000ml


Parameter Class I Class II Class III Class IV

Blood loss % <15% 15-30% 30-40% >40%

Pulse rate <100 >100 >120 >140

Blood pressure Normal Normal Decreased Decreased

Respiratory rate 14-20 20-30 30-40 >35

Urine output >30ml 20-30ml 5-15ml <5ml

Symptoms Normal Anxious Confused Lethargic


gathered by dr. elbarky

Decreasing blood pressure during haemorrhagic shock causes organ


hypoperfusion and relative myocardial ischaemia. The cardiac index gives a
numerical value for tissue oxygen delivery and is given by the equation: Cardiac
index= Cardiac output/ body surface area. Where Hb is haemoglobin
concentration in blood and SaO2 the saturation and PaO2 the partial pressure of
oxygen. Detailed knowledge of this equation is required for the MRCS Viva but not
for part A, although you should understand the principle.

In patients suffering from trauma the most likely cause of shock is haemorrhage.
However, the following may also be the cause or occur concomitantly:

Tension pneumothorax
Spinal cord injury
Myocardial contusion
Cardiac tamponade

When assessing trauma patients it is worth remembering that in order to generate


a palpable femoral pulse an arterial pressure of >65mmHg is required.

Once bleeding is controlled and circulating volume normalised the levels of


transfusion should be to maintain a Hb of 7-8 in those with no risk factors for
tissue hypoxia and Hb 10 for those who have such risk factors.

Neurogenic shock
This occurs most often following a spinal cord transection, usually at a high level.
There is resultant interruption of the autonomic nervous system. The result is
either decreased sympathetic tone or increased parasympathetic tone, the effect
of which is a decrease in peripheral vascular resistance mediated by marked
vasodilation.

This results in decreased preload and thus decreased cardiac output (Starlings
law). There is decreased peripheral tissue perfusion and shock is thus produced. In
contrast with many other types of shock peripheral vasoconstrictors are used to
return vascular tone to normal.

Cardiogenic shock
In medical patients the main cause is ischaemic heart disease. In the traumatic
setting direct myocardial trauma or contusion is more likely. Evidence of ECG
changes and overlying sternal fractures or contusions should raise the suspicion
of injury. Treatment is largely supportive and transthoracic echocardiography
should be used to determine evidence of pericardial fluid or direct myocardial
injury. The measurement of troponin levels in trauma patients may be undertaken
but they are less useful in delineating the extent of myocardial trauma than
following MI.

When cardiac injury is of a blunt nature and is associated with cardiogenic shock
the right side of the heart is the most likely site of injury with chamber and or valve
gathered by dr. elbarky

rupture. These patients require surgery to repair these defects and will require
cardiopulmonary bypass to achieve this. Some may require intra aortic balloon
pump as a bridge to surgery.

Anaphylactic shock
Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic
hypersensitivity reaction.

Anaphylaxis is one of the few times when you would not have time to look up the
dose of a medication. The Resuscitation Council guidelines on anaphylaxis have
recently been updated. Adrenaline is by far the most important drug in anaphylaxis
and should be given as soon as possible. The recommended doses for adrenaline,
hydrocortisone and chlorpheniramine are as follows:

Adrenaline Hydrocortisone Chlorpheniramine

< 6 months 150 mcg (0.15ml 1 25 mg 250 mcg/kg


in 1,000)

6 months - 6 150 mcg (0.15ml 1 50 mg 2.5 mg


years in 1,000)

6-12 years 300 mcg (0.3ml 1 in 100 mg 5 mg


1,000)

Adult and child 500 mcg (0.5ml 1 in 200 mg 10 mg


12 years 1,000)

Adrenaline can be repeated every 5 minutes if necessary. The best site for IM
injection is the anterolateral aspect of the middle third of the thigh.

Common identified causes of anaphylaxis


food (e.g. Nuts) - the most common cause in children
drugs
venom (e.g. Wasp sting)

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Question 48 of 192

 

A 73 year old lady is admitted for a laparoscopic cholecystectomy. During her pre-
operative assessment it is noted that she is receiving furosemide for the treatment
of hypertension. Where is the site of action of this diuretic?

Proximal convoluted tubule

Descending limb of the loop of Henle


gathered by dr. elbarky

Ascending limb of the loop of Henle

Distal convoluted tubule

Collecting ducts

Action of furosemide = ascending limb of the loop of Henle

Furosemide and bumetanide are loop diuretics that act by inhibiting the Na-K-Cl
cotransporter in the thick ascending limb of the loop of Henle, reducing the
absorption of NaCl.

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Diuretic agents

The diuretic drugs are divided into three major classes, which are distinguished
according to the site at which they impair sodium reabsorption: loop diuretics in
the thick ascending loop of Henle, thiazide type diuretics in the distal tubule and
connecting segment; and potassium sparing diuretics in the aldosterone -
sensitive principal cells in the cortical collecting tubule.
In the kidney, sodium is reabsorbed through Na+/ K+ ATPase pumps located on the
basolateral membrane. These pumps return reabsorbed sodium to the circulation
and maintain low intracellular sodium levels. This latter effect ensures a constant
concentration gradient.

Physiological effects of commonly used diuretics

Carrier or Percentage of
channel filtered sodium
Site of action Diuretic inhibited excreted

Ascending limb of Frusemide Na+/K+ 2Cl - Up to 25%


loop of Henle carrier

Distal tubule and Thiazides Na+Cl- carrier Between 3 and 5%


connecting
segment
gathered by dr. elbarky

Cortical collecting Spironolactone Na+/K+ ATP Between 1 and 2%


tubule ase pump

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Question 49 of 192

 

Which of the following blood gas results would fit with metabolic acidosis with a
compensatory respiratory alkalosis?

pH 7.36, PaCO2 7.3, PO2 8.9 (FiO2 40%), Bicarbonate 30.2, Base excess
+5.3

pH 7.14, PaCO2 7.4, PaO2 8.9 (FiO2 40%), Bicarbonate 14 mmol, Base
gathered by dr. elbarky

excess -10.6

pH 7.57, PaCO2 3.5, Pa O2 24.5 (FiO2 85%), Bicarbonate 23.5, Base excess
+1.8 mmol

pH 7.32, PCO2 3.8, PaO2 22.2 (FiO2 40%), Bicarbonate 19.1, Base excess
-7.9

pH 7.19, pCO2 10.2, pO2 16 (FiO2 85%), Bicarbonate 23.8, Base excess -2.2
mmol

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Arterial blood gas interpretation

In advanced life support training, a 5 step approach to arterial blood gas


interpretation is advocated.

1. How is the patient?

2. Is the patient hypoxaemic?


The Pa02 on air should be 10.0-13.0 kPa

3. Is the patient acidaemic (pH <7.35) or alkalaemic (pH >7.45)


4. What has happened to the PaCO2?
If there is acidaemia, an elevated PaCO2 will account for this

5. What is the bicarbonate level or base excess?


A metabolic acidosis will have a low bicarbonate level and a low base excess (< -2
mmol)
A metabolic alkalosis will have a high bicarbonate and a high base excess (> +2
mmol)

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Question 50 of 192

 

Which of the following is not well absorbed following a gastrectomy?

Vitamin c

Zinc

Vitamin B12
gathered by dr. elbarky

Copper

Molybdenum

Vitamin B12. The others are unaffected

Post gastrectomy syndrome


Rapid emptying of food from stomach into the duodenum: diarrhoea,
abdominal pain, hypoglycaemia
Complications: Vitamin B12 and iron malabsorption, osteoporosis
Treatment: High protein, low carbohydrate diet. Replace B12/Fe/Ca

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Gastric emptying
The stomach serves both a mechanical and immunological function. Solid
and liquid are retained in the stomach during which time repeated peristaltic
activity against a closed pyloric sphincter will cause fragmentation of food
bolus material. Contact with gastric acid will help to neutralise any
pathogens present.
The amount of time material spends in the stomach is related to its
composition and volume. For example a glass of water will empty more
quickly than a large meal. The presence of amino acids and fat will all serve
to delay gastric emptying.

Controlling factors
Neuronal stimulation of the stomach is mediated via the vagus and the
parasympathetic nervous system will tend to favor an increase in gastric motility. It
is for this reason that individuals who have undergone truncal vagotomy will tend
gathered by dr. elbarky

to routinely require either a pyloroplasty or gastro-enterostomy as they would


otherwise have delayed gastric emptying.

The following hormonal factors are all involved:

Delay emptying Increase emptying

Gastric inhibitory peptide Gastrin

Cholecystokinin

Enteroglucagon

Diseases affecting gastric emptying


All diseases that affect gastric emptying may result in bacterial overgrowth,
retained food and eventually the formation of bezoars that may occlude the
pylorus and make gastric emptying even worse. Fermentation of food may cause
dyspepsia, reflux and foul smelling belches of gas.

Iatrogenic
Gastric surgery can have profound effects on gastric emptying. As stated above
any procedure that disrupts the vagus can cause delayed emptying. Whilst this is
particularly true of vagotomy, this operation is now rarely performed. Surgeons are
divided on the importance of vagal disruption that occurs during an
oesophagectomy, some will routinely perform a pyloroplasty and others will not.

When a distal gastrectomy is performed, the type of anastomosis performed will


impact on emptying. When a gastro-enterostomy is constructed, a posterior,
retrocolic gastroenterostomy will empty better than an anterior one.

Diabetic gastroparesis
This is predominantly due to neuropathy affecting the vagus nerve. The stomach
empties poorly and patients may have episodes of repeated and protracted
vomiting. Diagnosis is made by upper GI endoscopy and contrast studies, in some
cases a radio nucleotide scan is needed to demonstrate the abnormality more
clearly. In treating these conditions, drugs such as metoclopramide will be less
effective as they exert their effect via the vagus nerve. One of the few prokinetic
drugs that do not work in this way is the antibiotic erythromycin.

Malignancies
Obviously a distal gastric cancer may obstruct the pylorus and delay emptying. In
addition, malignancies of the pancreas may cause extrinsic compression of the
duodenum and delay emptying. Treatment in these cases is by gastric
decompression using a wide bore nasogastric tube and insertion of a stent or, if
that is not possible, by a surgical gastroenterostomy. As a general rule
gathered by dr. elbarky

gastroenterostomies constructed for bypass of malignancy are usually placed on


the anterior wall of the stomach (in spite of the fact that they empty less well). A
Roux en Y bypass may also be undertaken, but the increased number of
anastomoses for this, in malignant disease that is being palliated, is probably not
justified.

Congenital Hypertrophic Pyloric Stenosis


This is typically a disease of infancy. Most babies will present around 6 weeks of
age with projectile non bile stained vomiting. It has an incidence of 2.4 per 1000
live births and is more common in males. Diagnosis is usually made by careful
history and examination and a mass may be palpable in the epigastrium (often
cited seldom felt!). The most important diagnostic test is an ultrasound that
usually demonstrates the hypertrophied pylorus. Blood tests may reveal a
hypochloraemic metabolic alkalosis if the vomiting is long standing. Once the
diagnosis is made the infant is resuscitated and a pyloromyotomy is performed
(either open or laparoscopically). Once treated there are no long term sequelae.

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11

12

13

Question 51 of 192

 

Which of the following best accounts for the mechanism of action of


glucocorticoids?

Binding of cell wall receptors and intracellular tyrosine kinase activation

Binding of intracellular receptors that migrate to the nucleus to then affect


gene transcription
gathered by dr. elbarky

Activation of transmembrane tyrosine kinase systems to affect


intranuclear gene transcription

Induces post translational modification of intracellular proteins

Direct binding of inflammatory cells inducing apoptosis

Glucocorticoids exert their effects by binding intracellular receptors that are then
transported to the nucleus where they affect gene transcription. There are some
questions in the MRCS now that seem to test common pharmacology and so we
have decided to include this. A detailed knowledge of the mechanisms by which
these effects occur is not needed.

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Corticosteroids

Synthesised from cholesterol within the adrenal cortex


Bind to specific intracellular glucocorticoid receptors located on the nucleus

Effects of glucocorticoids
Metabolic
Decreased uptake and utilisation of glucose, increased gluconeogenesis and
hyperglycaemia
Increased protein catabolism
Permissive effect on lipolytic hormones

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.

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Question 52 of 192

 

A healthy man has a blood pressure of 120/80 mmHg and an intra cranial pressure
of 17 mmHg. What is the approximate cerebral perfusion pressure?

103 mmHg

63 mmHg
gathered by dr. elbarky

83 mmHg

91 mmHg

76 mmHg

Cerebral perfusion pressure= Mean arterial pressure - intra cranial pressure

The mean arterial pressure can be calculated as:


MAP= Diastolic pressure+ 0.333(Systolic pressure- Diastolic pressure)
In this situation the MAP = 93.
The ICP is subtracted from this value; 93 - 17 = 76

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Cerebral perfusion pressure

The cerebral perfusion pressure (CPP) is defined as being the net pressure
gradient causing blood flow to the brain. The CPP is tightly autoregulated to
maximise cerebral perfusion. A sharp rise in CPP may result in a rising ICP, a fall in
CPP may result in cerebral ischaemia. It may be calculated by the following
equation:

CPP= Mean arterial pressure - Intra cranial pressure


Following trauma, the CPP has to be carefully controlled and the may require
invasive monitoring of the ICP and MAP.

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Question 53 of 192

 

Which of the following statements related to the coagulation cascade is true?

The intrinsic pathway is the main pathway in coagulation

Heparin inhibits the activation of Factor 8

The activation of factor 8 is the point when the intrinsic and the extrinsic
gathered by dr. elbarky

pathways meet

Tissue factor released by damaged tissue initiates the extrinsic pathway

Thrombin converts plasminogen to plasmin

The extrinsic pathway is the main path of coagulation. Heparin inhibits the
activation of factors 2,9,10,11. The activation of factor 10 is when both pathways
meet. Thrombin converts fibrinogen to fibrin. During fibrinolysis plasminogen is
converted to plasmin to break down fibrin.

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Coagulation cascade
Two pathways lead to fibrin formation

Intrinsic pathway (components already present in the blood)


Minor role in clotting
Subendothelial damage e.g. collagen
Formation of the primary complex on collagen by high-molecular-weight
kininogen (HMWK), prekallikrein, and Factor 12
Prekallikrein is converted to kallikrein and Factor 12 becomes activated
Factor 12 activates Factor 11
Factor 11 activates Factor 9, which with its co-factor Factor 8a form the
tenase complex which activates Factor 10

Extrinsic pathway (needs tissue factor released by damaged tissue)


Tissue damage
gathered by dr. elbarky

Factor 7 binds to Tissue factor


This complex activates Factor 9
Activated Factor 9 works with Factor 8 to activate Factor 10

Common pathway
Activated Factor 10 causes the conversion of prothrombin to thrombin
Thrombin hydrolyses fibrinogen peptide bonds to form fibrin and also
activates factor 13 to form links between fibrin molecules

Fibrinolysis
Plasminogen is converted to plasmin to facilitate clot resorption

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb030b.jpg)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org
/images_eMRCS/swb030b.jpg)
/wiki/Coagulation)
Clotting pathway Clotting parameters affected Factors affected

Intrinsic pathway Increased APTT Factors 8,9,11,12

Extrinsic pathway Increased PT Factor 7

Common pathway Increased APTT & PT Factors 2,5,10

Vitamin K dependent Factors 2,7,9,10

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gathered by dr. elbarky

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D 47.3%
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Question 54 of 192

 

The pressure within the pleural space is negative with respect to atmospheric
pressure, except for which of the following?

At the end of inspiration

When taking a deep breath


gathered by dr. elbarky

If the patient is intubated with an endotracheal tube

During a Valsalva manoeuvre

At the end of expiration

During a Valsalva manoeuvre, the intra pleural pressure rises owing to extrinsic
compression.

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Pleural pressure

Pleural pressure is the pressure surrounding the lung, within the pleural space.
During quiet breathing, the pleural pressure is negative; that is, it is below
atmospheric pressure.

The pleura is a thin membrane which invests the lungs and lines the walls of the
thoracic cavity. During development the lungs grow into the pleural sacs until they
are completely surrounded by them. The side of the pleura that covers the lung is
referred to as the visceral pleura and the side of the pleura which covers the chest
wall is called the parietal pleura. These two sides are continuous and meet at the
hilum of the lung. The two faces of the pleural membranes are directly opposed to
one another, and the entire potential space within the pleura contains only a few
milliliters of serous pleural fluid.
The size of the lung is determined by the difference between the alveolar pressure
and the pleural pressure, or the transpulmonary pressure. The bigger the
difference, the bigger the lung. As a result of gravity, in an upright individual the
pleural pressure at the base of the lung base is greater (less negative) than at its
apex; when the individual lies on his back, the pleural pressure becomes greatest
along his back. Since alveolar pressure is uniform throughout the lung, the top of
the lung generally experiences a greater transpulmonary pressure and is therefore
more expanded and less compliant than the bottom of the lung.

During active expiration, the abdominal muscles are contracted to force up the
diaphragm and the resulting pleural pressure can become positive. Positive pleural
pressure may temporarily collapse the bronchi and cause limitation of air flow.
gathered by dr. elbarky

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Question 55 of 192

 

Which of the blood gas results listed below is most likely to fit with a patient who
has acute respiratory acidosis?

pH 7.57, PaCO2 3.5, Pa O2 24.5 (FiO2 85%), Bicarbonate 23.5, Base excess
+1.8 mmol

pH 7.19, pCO2 10.2, pO2 16 (FiO2 85%), Bicarbonate 23.8, Base excess -2.2
gathered by dr. elbarky

mmol

pH 7.14, PaCO2 7.4, PaO2 8.9 (FiO2 40%), Bicarbonate 14 mmol, Base
excess -10.6

pH 7.36, PaCO2 7.3, PO2 8.9 (FiO2 40%), Bicarbonate 30.2, Base excess 5.3

pH 7.32, PCO2 3.8, PaO2 22.2 (FiO2 40%), Bicarbonate 19.1, Base excess
-7.9

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Arterial blood gas interpretation

In advanced life support training, a 5 step approach to arterial blood gas


interpretation is advocated.

1. How is the patient?

2. Is the patient hypoxaemic?


The Pa02 on air should be 10.0-13.0 kPa

3. Is the patient acidaemic (pH <7.35) or alkalaemic (pH >7.45)

4. What has happened to the PaCO2?


If there is acidaemia, an elevated PaCO2 will account for this

5. What is the bicarbonate level or base excess?


A metabolic acidosis will have a low bicarbonate level and a low base excess (< -2
mmol)
A metabolic alkalosis will have a high bicarbonate and a high base excess (> +2
mmol)

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Question 56 of 192

 

A patient has an arterial blood gas sample taken and the following result is
obtained:
pH 7.48

pO2 10.1

Bicarbonate 30
gathered by dr. elbarky

pCO2 4.5

Chloride 10meq

What is the most likely cause?

Respiratory alkalosis

Metabolic alkalosis

Type 1 respiratory failure

Metabolic acidosis with normal anion gap

Metabolic acidosis with increased anion gap

This would be a typical result of prolonged vomiting.

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Disorders of acid - base balance

Disorders of acid- base balance are often covered in the MRCS part A.

The acid-base normogram below shows how the various disorders may be
categorised
gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb072b.png)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Acid-base
/images_eMRCS/swb072b.png)
homeostasis)

Metabolic acidosis
This is the most common surgical acid - base disorder.
Reduction in plasma bicarbonate levels.
Two mechanisms:

1. Gain of strong acid (e.g. diabetic ketoacidosis)


2. Loss of base (e.g. from bowel in diarrhoea)
- Classified according to the anion gap, this can be calculated by:
(Na+ + K+) - (Cl- + HCO3-).
- If a question supplies the chloride level then this is often a clue that the anion gap
should be calculated. The normal range = 10-18 mmol/L

Normal anion gap ( = hyperchloraemic metabolic acidosis)


Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
Renal tubular acidosis
Drugs: e.g. acetazolamide
Ammonium chloride injection
Addison's disease

Raised anion gap


Lactate: shock, hypoxia
Ketones: diabetic ketoacidosis, alcohol
Urate: renal failure
Acid poisoning: salicylates, methanol

Metabolic acidosis secondary to high lactate levels may be subdivided into two
types:
Lactic acidosis type A: (Perfusion disorders e.g.shock, hypoxia, burns)
Lactic acidosis type B: (Metabolic e.g. metformin toxicity)

Metabolic alkalosis
Usually caused by a rise in plasma bicarbonate levels.
Rise of bicarbonate above 24 mmol/L will typically result in renal excretion
of excess bicarbonate.
Caused by a loss of hydrogen ions or a gain of bicarbonate. It is due mainly
gathered by dr. elbarky

to problems of the kidney or gastrointestinal tract

Causes
Vomiting / aspiration (e.g. Peptic ulcer leading to pyloric stenosis,
nasogastric suction)
Diuretics
Liquorice, carbenoxolone
Hypokalaemia
Primary hyperaldosteronism
Cushing's syndrome
Bartter's syndrome
Congenital adrenal hyperplasia

Mechanism of metabolic alkalosis


Activation of renin-angiotensin II-aldosterone (RAA) system is a key factor
Aldosterone causes reabsorption of Na+ in exchange for H+ in the distal
convoluted tubule
ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA
system → raised aldosterone levels
In hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+
into cells to maintain neutrality

Respiratory acidosis
Rise in carbon dioxide levels usually as a result of alveolar hypoventilation
Renal compensation may occur leading to Compensated respiratory acidosis

Causes
COPD
Decompensation in other respiratory conditions e.g. Life-threatening asthma
/ pulmonary oedema
Sedative drugs: benzodiazepines, opiate overdose

Respiratory alkalosis
Hyperventilation resulting in excess loss of carbon dioxide
This will result in increasing pH

Causes
Psychogenic: anxiety leading to hyperventilation
Hypoxia causing a subsequent hyperventilation: pulmonary embolism, high
altitude
Early salicylate poisoning*
CNS stimulation: stroke, subarachnoid haemorrhage, encephalitis
Pregnancy
gathered by dr. elbarky

*Salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis.


Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst
later the direct acid effects of salicylates (combined with acute renal failure) may
lead to an acidosis

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Question 57 of 192

 

Which of the following substances is released from the sympathetic nervous


system to stimulate the adrenal medulla?

Noradrenaline

Acetyl choline
gathered by dr. elbarky

Substance P

Tyrosine

Arginine

In the autonomic nervous system, noradrenaline is the commonly used


neurotransmitter. However, in the adrenal medulla, Acetylcholine is released to
stimulate adrenaline release.

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Adrenal physiology

Adrenal medulla
The chromaffin cells of the adrenal medulla secrete the catecholamines
noradrenaline and adrenaline. The medulla is innervated by the splanchnic nerves;
the preganglionic sympathetic fibres secrete acetylcholine causing the chromaffin
cells to secrete their contents by exocytosis.
Phaeochromocytomas are derived from these cells and will secrete both
adrenaline and nor adrenaline.

Adrenal cortex
Three histologically distinct zones are recognised:
gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb215b.png)
Image sourced from (https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS
Wikipedia () /swb215b.png)

Zone Location Hormone Secreted

Zona glomerulosa Outer zone Aldosterone

Zona fasiculata Middle zone Glucocorticoids

Zona reticularis Inner zone Androgens

The glucocorticoids and aldosterone are mostly bound to plasma proteins in the
circulation. Glucocorticoids are inactivated and excreted by the liver.

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11

12

13

Question 58 of 192

 

A 65 year old man is admitted for a below knee amputation. He is taking digoxin.
Clinically the patient has an irregularly irregular pulse. What would you expect to
see when you examine the jugular venous pressure?

Absent y waves

Slow y descent
gathered by dr. elbarky

Cannon waves

Steep y descent

Absent a waves

Jugular venous pressure

Absent a waves = Atrial fibrillation


Large a waves = Any cause of right ventricular hypertrophy, tricuspid stenosis
Cannon waves (extra large a waves) = Complete heart block
Prominent v waves = Tricuspid regurgitation
Slow y descent = Tricuspid stenosis, right atrial myxoma
Steep y descent = Right ventricular failure, constrictive pericarditis, tricuspid
regurgitation

This patient has atrial fibrillation and is most likely to have absent a waves.

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Jugular venous pressure

As well as providing information on right atrial pressure, the jugular vein waveform
may provide clues to underlying valvular disease. A non-pulsatile JVP is seen in
superior vena caval obstruction. Kussmaul's sign describes a paradoxical rise in
JVP during inspiration seen in constrictive pericarditis

'a' wave = atrial contraction


large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis,
pulmonary hypertension
absent if in atrial fibrillation

Cannon 'a' waves


caused by atrial contractions against a closed tricuspid valve
are seen in complete heart block, ventricular tachycardia/ectopics, nodal
rhythm, single chamber ventricular pacing
gathered by dr. elbarky

'c' wave
closure of tricuspid valve
not normally visible

'v' wave
due to passive filling of blood into the atrium against a closed tricuspid
valve
giant v waves in tricuspid regurgitation

'x' descent = fall in atrial pressure during ventricular systole

'y' descent = opening of tricuspid valve

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb145b.png)
Image sourced from (https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS
Wikipedia () /swb145b.png)

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Question 59 of 192

 

Which of the following is not secreted by the parietal cells?

Hydrochloric acid

Mucus

Magnesium
gathered by dr. elbarky

Intrinsic factor

Calcium

Chief of Pepsi cola = Chief cells secrete PEPSInogen

Parietal cells: secrete HCl, Ca, Na, Mg and intrinsic factor


Chief cells: secrete pepsinogen
Surface mucosal cells: secrete mucus and bicarbonate

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Gastric secretions

A working knowledge of gastric secretions is important for surgery because peptic


ulcers are common, surgeons frequently prescribe anti secretory drugs and
because there are still patients around who will have undergone acid lowering
procedures (Vagotomy) in the past.

Gastric acid
Is produced by the parietal cells in the stomach
pH of gastric acid is around 2 with acidity being maintained by the H+/K+
ATP ase pump. As part of the process bicarbonate ions will be secreted into
the surrounding vessels.
Sodium and chloride ions are actively secreted from the parietal cell into the
canaliculus. This sets up a negative potential across the membrane and as a
result sodium and potassium ions diffuse across into the canaliculus.
Carbonic anhydrase forms carbonic acid which dissociates and the
hydrogen ions formed by dissociation leave the cell via the H+/K+ antiporter
pump. At the same time sodium ions are actively absorbed. This leaves
hydrogen and chloride ions in the canaliculus these mix and are secreted
into the lumen of the oxyntic gland.

This is illustrated diagrammatically below:


gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb028b.jpg)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Gastric
/images_eMRCS/swb028b.jpg)
acid)

Phases of gastric acid secretion


There are 3 phases of gastric secretion:

1. Cephalic phase (smell / taste of food)


30% acid produced
Vagal cholinergic stimulation causing secretion of HCL and gastrin release
from G cells

2. Gastric phase (distension of stomach )


60% acid produced
Stomach distension/low H+/peptides causes Gastrin release

3. Intestinal phase (food in duodenum)


10% acid produced
High acidity/distension/hypertonic solutions in the duodenum inhibits
gastric acid secretion via enterogastrones (CCK, secretin) and neural
reflexes.

Regulation of gastric acid production


gathered by dr. elbarky

Factors increasing production include:


Vagal nerve stimulation
Gastrin release
Histamine release (indirectly following gastrin release) from
enterchromaffin like cells

Factors decreasing production include:


Somatostatin (inhibits histamine release)
Cholecystokinin
Secretin

The diagram below illustrates some of the factors involved in regulating gastric
acid secretion and the relevant associated pharmacology

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb029b.jpg)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Gastric
/images_eMRCS/swb029b.jpg)
acid)
Below is a brief summary of the major hormones involved in food digestion:

Source Stimulus Actions

Gastrin G cells in Distension of Increase HCL, pepsinogen


antrum of stomach, and IF secretion, increases
the extrinsic nerves gastric motility, trophic effect
stomach Inhibited by: low on gastric mucosa
antral pH,
somatostatin

CCK I cells in Partially Increases secretion of


upper digested enzyme-rich fluid from
gathered by dr. elbarky

small proteins and pancreas, contraction of


intestine triglycerides gallbladder and relaxation of
sphincter of Oddi, decreases
gastric emptying, trophic
effect on pancreatic acinar
cells, induces satiety

Secretin S cells in Acidic chyme, Increases secretion of


upper fatty acids bicarbonate-rich fluid from
small pancreas and hepatic duct
intestine cells, decreases gastric acid
secretion, trophic effect on
pancreatic acinar cells

VIP Small Neural Stimulates secretion by


intestine, pancreas and intestines,
pancreas inhibits acid and pepsinogen
secretion

Somatostatin D cells in Fat, bile salts Decreases acid and pepsin


the and glucose in secretion, decreases gastrin
pancreas the intestinal secretion, decreases
and lumen pancreatic enzyme secretion,
stomach decreases insulin and
glucagon secretion
inhibits trophic effects of
gastrin, stimulates gastric
mucous production

Next question 
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Question 60 of 192

 

Which of the following is not an effect of somatostatin?

It stimulates pancreatic acinar cells to release lipase

It decreases gastric acid secretion

It decreases gastrin release


gathered by dr. elbarky

It decreases pepsin secretion

It decreases glucagon release

It inhibits pancreatic enzyme secretion.

Please rate this question:

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Gastric secretions

A working knowledge of gastric secretions is important for surgery because peptic


ulcers are common, surgeons frequently prescribe anti secretory drugs and
because there are still patients around who will have undergone acid lowering
procedures (Vagotomy) in the past.

Gastric acid
Is produced by the parietal cells in the stomach
pH of gastric acid is around 2 with acidity being maintained by the H+/K+
ATP ase pump. As part of the process bicarbonate ions will be secreted into
the surrounding vessels.
Sodium and chloride ions are actively secreted from the parietal cell into the
canaliculus. This sets up a negative potential across the membrane and as a
result sodium and potassium ions diffuse across into the canaliculus.
Carbonic anhydrase forms carbonic acid which dissociates and the
hydrogen ions formed by dissociation leave the cell via the H+/K+ antiporter
pump. At the same time sodium ions are actively absorbed. This leaves
hydrogen and chloride ions in the canaliculus these mix and are secreted
into the lumen of the oxyntic gland.

This is illustrated diagrammatically below:


gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb028b.jpg)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Gastric
/images_eMRCS/swb028b.jpg)
acid)

Phases of gastric acid secretion


There are 3 phases of gastric secretion:

1. Cephalic phase (smell / taste of food)


30% acid produced
Vagal cholinergic stimulation causing secretion of HCL and gastrin release
from G cells

2. Gastric phase (distension of stomach )


60% acid produced
Stomach distension/low H+/peptides causes Gastrin release
3. Intestinal phase (food in duodenum)
10% acid produced
High acidity/distension/hypertonic solutions in the duodenum inhibits
gastric acid secretion via enterogastrones (CCK, secretin) and neural
reflexes.

Regulation of gastric acid production


Factors increasing production include:
Vagal nerve stimulation
Gastrin release
Histamine release (indirectly following gastrin release) from
enterchromaffin like cells
gathered by dr. elbarky

Factors decreasing production include:


Somatostatin (inhibits histamine release)
Cholecystokinin
Secretin

The diagram below illustrates some of the factors involved in regulating gastric
acid secretion and the relevant associated pharmacology

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb029b.jpg)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Gastric
/images_eMRCS/swb029b.jpg)
acid)

Below is a brief summary of the major hormones involved in food digestion:

Source Stimulus Actions


Source Stimulus Actions

Gastrin G cells in Distension of Increase HCL, pepsinogen


antrum of stomach, and IF secretion, increases
the extrinsic nerves gastric motility, trophic effect
stomach Inhibited by: low on gastric mucosa
antral pH,
somatostatin

CCK I cells in Partially Increases secretion of


upper digested enzyme-rich fluid from
small proteins and pancreas, contraction of
intestine triglycerides gallbladder and relaxation of
sphincter of Oddi, decreases
gathered by dr. elbarky

gastric emptying, trophic


effect on pancreatic acinar
cells, induces satiety

Secretin S cells in Acidic chyme, Increases secretion of


upper fatty acids bicarbonate-rich fluid from
small pancreas and hepatic duct
intestine cells, decreases gastric acid
secretion, trophic effect on
pancreatic acinar cells

VIP Small Neural Stimulates secretion by


intestine, pancreas and intestines,
pancreas inhibits acid and pepsinogen
secretion

Somatostatin D cells in Fat, bile salts Decreases acid and pepsin


the and glucose in secretion, decreases gastrin
pancreas the intestinal secretion, decreases
and lumen pancreatic enzyme secretion,
stomach decreases insulin and
glucagon secretion
inhibits trophic effects of
gastrin, stimulates gastric
mucous production

Next question 

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Question 61 of 192

 

Which of the following is not a feature of normal cerebrospinal fluid?

It has a pressure of between 10 and 15 mmHg.

It usually contains a small amount of glucose.

It may normally contain up to 5 red blood cells per mm3.


gathered by dr. elbarky

It may normally contain up to 3 white blood cells per mm3.

None of the above

It should not contain red blood cells.

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Cerebrospinal fluid

The CSF fills the space between the arachnoid mater and pia mater (covering
surface of the brain). The total volume of CSF in the brain is approximately 150ml.
Approximately 500 ml is produced by the ependymal cells in the choroid plexus
(70%), or blood vessels (30%). It is reabsorbed via the arachnoid granulations
which project into the venous sinuses.

Circulation
1. Lateral ventricles (via foramen of Munro)
2. 3rd ventricle
3. Cerebral aqueduct (aqueduct of Sylvius)
4. 4th ventricle (via foramina of Magendie and Luschka)
5. Subarachnoid space
6. Reabsorbed into the venous system via arachnoid granulations into superior
sagittal sinus
Composition
Glucose: 50-80mg/dl
Protein: 15-40 mg/dl
Red blood cells: Nil
White blood cells: 0-3 cells/ mm3

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Question 62 of 192

 

Which of the following is responsible for the rapid depolarisation phase of the
myocardial action potential?

Rapid sodium influx

Rapid sodium efflux


gathered by dr. elbarky

Slow efflux of calcium

Efflux of potassium

Rapid calcium influx

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Electrical activity of the heart

Myocardial action potential

Phase Description Mechanism

0 Rapid Rapid sodium influx


depolarisation 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


Phase Description Mechanism

4 Restoration of ionic Resting potential is restored by Na+/K+ ATPase


concentrations There is slow entry of Na+ into the cell
decreasing the potential difference until the
threshold potential is reached, triggering a new
action potential

NB cardiac muscle remains contracted 10-15 times longer than skeletal muscle

Conduction velocity

Atrial Spreads along ordinary atrial myocardial fibres at 1 m/sec


gathered by dr. elbarky

conduction

AV node 0.05 m/sec


conduction

Ventricular Purkinje fibres are of large diameter and achieve velocities of


conduction 2-4 m/sec (this allows a rapid and coordinated contraction of
the ventricles

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51.8% of users answered this question correctly


Question 63 of 192

 

Which one of the following cells secretes the majority of tumour necrosis factor in
humans?

Neutrophils

Macrophages
gathered by dr. elbarky

Natural killer cells

Killer-T cells

Helper-T cells

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Tumour necrosis factor

Tumour necrosis factor (TNF) is a pro-inflammatory cytokine with multiple roles in


the immune system

TNF is secreted mainly by macrophages and has a number of effects on the


immune system, acting mainly in a paracrine fashion:
activates macrophages and neutrophils
acts as costimulator for T cell activation
key mediator of bodies response to Gram negative septicaemia
similar properties to IL-1
anti-tumour effect (e.g. phospholipase activation)

TNF-alpha binds to both the p55 and p75 receptor. These receptors can induce
apoptosis. It also cause activation of NFkB
Endothelial effects include increase expression of selectins and increased
production of platelet activating factor, IL-1 and prostaglandins

TNF promotes the proliferation of fibroblasts and their production of protease and
collagenase. It is thought fragments of receptors act as binding points in serum

Systemic effects include pyrexia, increased acute phase proteins and disordered
metabolism leading to cachexia

TNF is important in the pathogenesis of rheumatoid arthritis - TNF blockers (e.g.


infliximab, etanercept) are now licensed for treatment of severe rheumatoid
gathered by dr. elbarky

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Question 64 of 192

 

Where are the arterial baroreceptors located?

Carotid sinus and aortic arch

Carotid sinus only

Superior vena cava


gathered by dr. elbarky

External carotid artery

None of the above

They lie in the carotid sinus and aortic arch.

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Cardiac physiology

The heart has four chambers ejecting blood into both low pressure and high
pressure systems.
The pumps generate pressures of between 0-25mmHg on the right side and
0-120 mmHg on the left.
At rest diastole comprises 2/3 of the cardiac cycle.
The product of the frequency of heart rate and stroke volume combine to
give the cardiac output which is typically 5-6L per minute.

Detailed descriptions of the various waveforms are often not a feature of MRCS A
(although they are on the syllabus). However, they are a very popular topic for
surgical physiology in the MRCS B exam.

Electrical properties
Intrinsic myogenic rhythm within cardiac myocytes means that even the
denervated heart is capable of contraction.
In the normal situation the cardiac impulse is generated in the sino atrial
node in the right atrium and conveyed to the ventricles via the
atrioventricular node.
The sino atrial node is also capable of spontaneous discharge and in the
absence of background vagal tone will typically discharge around 100x per
minute. Hence the higher resting heart rate found in cardiac transplant
cases. In the SA and AV nodes the resting membrane potential is lower than
in surrounding cardiac cells and will slowly depolarise from -70mV to around
-50mV at which point an action potential is generated.
Differences in the depolarisation slopes between SA and AV nodes help to
explain why the SA node will depolarise first. The cells have a refractory
period during which they cannot be re-stimulated and this period allows for
adequate ventricular filling. In pathological tachycardic states this time
gathered by dr. elbarky

period is overridden and inadequate ventricular filling may then occur,


cardiac output falls and syncope may ensue.

Parasympathetic fibres project to the heart via the vagus and will release
acetylcholine. Sympathetic fibres release nor adrenaline and circulating adrenaline
comes from the adrenal medulla. Noradrenaline binds to β 1 receptors in the SA
node and increases the rate of pacemaker potential depolarisation.

Cardiac cycle

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb034b.png)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Cardiac
/images_eMRCS/swb034b.png)
cycle)

Mid diastole: AV valves open. Ventricles hold 80% of final volume. Outflow
valves shut. Aortic pressure is high.

Late diastole: Atria contract. Ventricles receive 20% to complete filling.


Typical end diastolic volume 130-160ml.

Early systole: AV valves shut. Ventricular pressure rises. Isovolumetric


ventricular contraction. AV Valves bulge into atria (c-wave). Aortic and
pulmonary pressure exceeded- blood is ejected. Shortening of ventricles
pulls atria downwards and drops intra atrial pressure (x-descent).

Late systole: Ventricular muscles relax and ventricular pressures drop.


Although ventricular pressure drops the aortic pressure remains constant
owing to peripheral vascular resistance and elastic property of the aorta.
Brief period of retrograde flow that occurs in aortic recoil shuts the aortic
valve. Ventricles will contain 60ml end systolic volume. The average stroke
volume is 70ml (i.e. Volume ejected).
gathered by dr. elbarky

Early diastole: All valves are closed. Isovolumetric ventricular relaxation


occurs. Pressure wave associated with closure of the aortic valve increases
aortic pressure. The pressure dip before this rise can be seen on arterial
waveforms and is called the incisura. During systole the atrial pressure
increases such that it is now above zero (v- wave). Eventually atrial pressure
exceed ventricular pressure and AV valves open - atria empty passively into
ventricles and atrial pressure falls (y -descent )

The negative atrial pressures are of clinical importance as they can allow air
embolization to occur if the neck veins are exposed to air. This patient positioning
is important in head and neck surgery to avoid this occurrence if veins are
inadvertently cut, or during CVP line insertion.

Mechanical properties
Preload = end diastolic volume
Afterload = aortic pressure

It is important to understand the principles of Laplace's law in surgery.


It states that for hollow organs with a circular cross section, the total
circumferential wall tension depends upon the circumference of the wall,
multiplied by the thickness of the wall and on the wall tension.
The total luminal pressure depends upon the cross sectional area of the
lumen and the transmural pressure. Transmural pressure is the internal
pressure minus external pressure and at equilibrium the total pressure must
counterbalance each other.
In terms of cardiac physiology the law explains that the rise in ventricular
pressure that occurs during the ejection phase is due to physical change in
heart size. It also explains why a dilated diseased heart will have impaired
systolic function.

Starlings law
Increase in end diastolic volume will produce larger stroke volume.
This occurs up to a point beyond which cardiac fibres are excessively
stretched and stroke volume will fall once more. It is important for the
regulation of cardiac output in cardiac transplant patients who need to
increase their cardiac output.

Baroreceptor reflexes
Baroreceptors located in aortic arch and carotid sinus.
Aortic baroreceptor impulses travel via the vagus and from the carotid via
the glossopharyngeal nerve.
They are stimulated by arterial stretch.
Even at normal blood pressures they are tonically active.
Increase in baroreceptor discharge causes:
gathered by dr. elbarky

*Increased parasympathetic discharge to the SA node.


*Decreased sympathetic discharge to ventricular muscle causing decreased
contractility and fall in stroke volume.
*Decreased sympathetic discharge to venous system causing increased
compliance.
*Decreased peripheral arterial vascular resistance

Atrial stretch receptors


Located in atria at junction between pulmonary veins and vena cava.
Stimulated by atrial stretch and are thus low pressure sensors.
Increased blood volume will cause increased parasympathetic activity.
Very rapid infusion of blood will result in increase in heart rate mediated via
atrial receptors: the Bainbridge reflex.
Decreases in receptor stimulation results in increased sympathetic activity
this will decrease renal blood flow-decreases GFR-decreases urinary sodium
excretion-renin secretion by juxtaglomerular apparatus-Increase in
angiotensin II.
Increased atrial stretch will also result in increased release of atrial
natriuretic peptide.

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C 5.1%
D 5%
E 5.3%

74% of users answered this question correctly


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Question 65 of 192

 

A 47 year old lady is diagnosed as suffering from a phaeochromocytoma. From


which of the following amino acids are catecholamines primarily derived?

Aspartime

Glutamine
gathered by dr. elbarky

Arginine

Tyrosine

Alanine

Catecholamine hormones are derived from tyrosine, it is modified by a DOPA


decarboxylase enzyme to become dopamine and thereafter via two further
enzymic modifications to noradrenaline and finally adrenaline.

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Adrenal physiology

Adrenal medulla
The chromaffin cells of the adrenal medulla secrete the catecholamines
noradrenaline and adrenaline. The medulla is innervated by the splanchnic nerves;
the preganglionic sympathetic fibres secrete acetylcholine causing the chromaffin
cells to secrete their contents by exocytosis.
Phaeochromocytomas are derived from these cells and will secrete both
adrenaline and nor adrenaline.

Adrenal cortex
Three histologically distinct zones are recognised:
gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb215b.png)
Image sourced from (https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS
Wikipedia () /swb215b.png)

Zone Location Hormone Secreted

Zona glomerulosa Outer zone Aldosterone

Zona fasiculata Middle zone Glucocorticoids

Zona reticularis Inner zone Androgens

The glucocorticoids and aldosterone are mostly bound to plasma proteins in the
circulation. Glucocorticoids are inactivated and excreted by the liver.

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B 14.7%
C 14.8%
D 51.7%
E 12%

51.7% of users answered this question correctly

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11

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13

Question 66 of 192

 

Adult lung volumes. Which statement is false?

In restrictive lung disease the FEV1/FVC ratio is increased

Residual volume is increased in emphysema

Functional residual capacity is measured by helium dilution test


gathered by dr. elbarky

The tidal volume is approximately 340mls in females

The vital capacity is increased in Guillain Barre syndrome

FEV1/FVC is normal or >80% in restrictive lung disease such as pulmonary


fibrosis. The ratio is reduced in obstructive airways disease.

The functional residual capacity, residual volume and the total lung capacity
cannot be measured with spirometry. They can only be measured by helium
dilution.
The vital capacity is reduced in:
1. Pulmonary fibrosis/infiltration/oedema/effusions
2. Weak respiratory muscles e.g. MG, GBS, myopathies
3. Skeletal abnormalities e.g. chest wall abnormalities

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Lung volumes

The diagram demonstrates lung volumes and capacities


(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb048b.png)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
gathered by dr. elbarky

(http://en.wikipedia.org/wiki/Lung
/images_eMRCS/swb048b.png)
volumes)

Definitions

Tidal volume (TV) Is the volume of air inspired and expired during
each ventilatory cycle at rest.
It is normally 500mls in males and 340mls in
females.

Inspiratory reserve Is the maximum volume of air that can be forcibly


volume (IRV) inhaled following a normal inspiration. 3000mls.

Expiratory reserve Is the maximum volume of air that can be forcibly


volume (ERV) exhaled following a normal expiration. 1000mls.

Residual volume Is that volume of air remaining in the lungs after a


(RV) maximal expiration.
RV = FRC - ERV. 1500mls.

Functional residual Is the volume of air remaining in the lungs at the


capacity (FRC) end of a normal expiration.
FRC = RV + ERV. 2500mls.

Vital capacity (VC) Is the maximal volume of air that can be forcibly
exhaled after a maximal inspiration.
VC = TV + IRV + ERV. 4500mls in males, 3500mls
in females.
Total lung capacity Is the volume of air in the lungs at the end of a
(TLC) maximal inspiration.
TLC = FRC + TV + IRV = VC + RV. 5500-6000mls.

Forced vital The volume of air that can be maximally


capacity (FVC) forcefully exhaled.

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gathered by dr. elbarky

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C 18.6%
D 9.7%
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Question 67 of 192

 

What is the most significant event to contribute to wound healing immediately


following injury?

Neutrophil activation

Platelet degranulation
gathered by dr. elbarky

Endothelial cell proliferation

Migration of tissue macrophages

Proliferation of wound bed fibroblasts

Many of these events contribute to healing. However, platelet degranulation is the


earliest phase and results in haemostasis, the main event in then allowing the
release of cytokines to attract other cells types to the wound and co-ordinate
healing.

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Phases of wound healing

Phase Key features Cells Timeframe

Haemostasis Vasospasm in Erythrocytes and Seconds/


adjacent vessels platelets Minutes
Platelet plug
formation and
generation of fibrin
rich clot
Inflammation Neutrophils migrate Neutrophils, Days
into wound (function fibroblasts and
impaired in diabetes). macrophages
Growth factors
released, including
basic fibroblast
growth factor and
vascular endothelial
growth factor.
Fibroblasts replicate
within the adjacent
matrix and migrate
into wound.
Macrophages and
gathered by dr. elbarky

fibroblasts couple
matrix regeneration
and clot substitution.

Regeneration Platelet derived Fibroblasts, Weeks


growth factor and endothelial cells,
transformation growth macrophages
factors stimulate
fibroblasts and
epithelial cells.
Fibroblasts produce a
collagen network.
Angiogenesis occurs
and wound resembles
granulation tissue.

Remodelling Longest phase of the Myofibroblasts 6 weeks to


healing process and 1 year
may last up to one
year (or longer).
During this phase
fibroblasts become
differentiated
(myofibroblasts) and
these facilitate wound
contraction.
Collagen fibres are
remodelled.
Microvessels regress
leaving a pale scar.
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A 24.7%
B 39.9%
C 15%
D 10.5%
E 9.8%

39.9% of users answered this question correctly

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Question 68 of 192

 

Which receptor does noradrenaline mainly bind to?

α 1 receptors

α 2 receptors

β 1 receptors
gathered by dr. elbarky

β 2 receptors

G receptors

Noradrenaline is the precursor of adrenaline. It is a powerful α 1 stimulant


(although it will increase myocardial contractility). Infusions will produce
vasoconstriction and an increase in total peripheral resistance. It is the inotrope of
choice in septic shock.

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Inotropes and cardiovascular receptors

Inotropes are a class of drugs which work primarily by increasing cardiac output.
They should be distinguished from vasoconstrictor drugs which are used
specifically when the primary problem is peripheral vasodilatation.

Catecholamine type agents are commonly used and work by increasing cAMP
levels by adenylate cyclase stimulation. This in turn intracellular calcium ion
mobilisation and thus the force of contraction. Adrenaline works as a beta
adrenergic receptor agonist at lower doses and an alpha receptor agonist at higher
doses. Dopamine causes dopamine receptor mediated renal and mesenteric
vascular dilatation and beta 1 receptor agonism at higher doses. This results in
increased cardiac output. Since both heart rate and blood pressure are raised,
there is less overall myocardial ischaemia. Dobutamine is a predominantly beta 1
receptor agonist with weak beta 2 and alpha receptor agonist properties.
Noradrenaline is a catecholamine type agent and predominantly acts as an alpha
receptor agonist and serves as a peripheral vasoconstrictor.

Phosphodiesterase inhibitors such as milrinone act specifically on the cardiac


phosphodiesterase and increase cardiac output.

Inotrope Cardiovascular receptor action

Adrenaline α-1, α-2, β-1, β-2

Noradrenaline α-1,( α-2), (β-1), (β-2)

Dobutamine β-1, (β 2)
gathered by dr. elbarky

Dopamine (α-1), (α-2), (β-1), D-1,D-2

Minor receptor effects in brackets

Effects of receptor binding

α-1, α-2 vasoconstriction

β-1 increased cardiac contractility and HR

β-2 vasodilatation

D-1 renal and spleen vasodilatation

D-2 inhibits release of noradrenaline

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Question 69 of 192

 

Where does spironolactone act in the kidney?

Glomerulus

Proximal convoluted tubule

Descending limb of the loop of Henle


gathered by dr. elbarky

Ascending limb of the loop of Henle

Distal convoluted tubule

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Potassium sparing diuretics

Potassium-sparing diuretics may be divided into the epithelial sodium channel


blockers (amiloride and triamterene) and aldosterone antagonists (spironolactone
and eplerenone).

{Amiloride} is a weak diuretic which blocks the epithelial sodium channel in the
distal convoluted tubule.

Usually given with thiazides or loop diuretics as an alternative to potassium


supplementation.

{Spironolactone} is an aldosterone antagonist which acts act in the distal


convoluted tubule.

Indications
ascites: patients with cirrhosis develop a secondary hyperaldosteronism.
Relatively large doses such as 100 or 200mg are often used
heart failure
nephrotic syndrome
Conn's syndrome

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D 12.4%
E 59.5%

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Question 70 of 192

 

A man is admitted after a period of prolonged self, induced starvation. Naso


gastric feeding is planned. Which of the following is least likely to occur?

Hypokalaemia

Increased risk of cardiac arrhythmias


gathered by dr. elbarky

His haemoglobin will have decreased affinity for oxygen

Hypophosphataemia

Hypoalbuminaemia

The process of starvation may lower DPG levels, in practice this is unlikely to occur
early as it is generated during glycolysis. Altered metabolism in starvation may be
more acidotic and this would also tend to impair oxygen carriage.

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Nutrition - Refeeding syndrome

Refeeding syndrome describes the metabolic abnormalities which occur on


feeding a person following a period of starvation. The metabolic consequences
include:
Hypophosphataemia
Hypokalaemia
Hypomagnesaemia
Abnormal fluid balance

These abnormalities can lead to organ failure.

Re-feeding problems
If patient not eaten for > 5 days, aim to re-feed at < 50% energy and protein levels
High risk for re-feeding problems
If one or more of the following:
BMI < 16 kg/m2
Unintentional weight loss >15% over 3-6 months
Little nutritional intake > 10 days
Hypokalaemia, Hypophosphataemia or hypomagnesaemia prior to feeding
(unless high)

If two or more of the following:


BMI < 18.5 kg/m2
Unintentional weight loss > 10% over 3-6 months
Little nutritional intake > 5 days
History of: alcohol abuse, drug therapy including insulin, chemotherapy,
gathered by dr. elbarky

diuretics and antacids

Prescription
Start at up to 10 kcal/kg/day increasing to full needs over 4-7 days
Start immediately before and during feeding: oral thiamine 200-300mg/day,
vitamin B co strong 1 tds and supplements
Give K+ (2-4 mmol/kg/day), phosphate (0.3-0.6 mmol/kg/day), magnesium
(0.2-0.4 mmol/kg/day)

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B 9.4%
C 58.2%
D 9.2%
E 11.8%

Question 71 of 192

 

Which of the following statements are not typically true in hypokalaemia?

It may occur as a result of mechanical bowel preparation

Chronic vomiting may increase renal potassium losses

It may be associated with aciduria


gathered by dr. elbarky

It may cause hyponatraemia

It often accompanies acidosis

Potassium depletion occurs either through the gastrointestinal tract or the kidney.
Chronic vomiting in itself is less prone to induce potassium loss than diarrhoea as
gastric secretions contain less potassium than those in the lower GI tract. If
vomiting produces a metabolic alkalosis then renal potassium wasting may occur
as potassium is excreted in preference to hydrogen ions. The converse may occur
in potassium depletion resulting in acid urine.

Hypokalemia is very commonly associated with metabolic alkalosis. This is due to


2 factors: 1) the common causes of metabolic alkalosis (vomiting, diuretics)
directly induce H+ and K loss (via aldosterone) and thus also cause hypokalemia
and 2) hypokalemia is a very important cause of metabolic alkalosis by three
mechanisms. The initial effect is by causing a transcellular shift in which K leaves
and H+ enters the cells, thereby raising the extracellular pH. The second effect is
by causing a transcellular shift in the cells of the proximal tubules resulting in an
intracellular acidosis, which promotes ammonium production and excretion.
Thirdly, in the presence of hypokalemia, hydrogen secretion in the proximal and
distal tubules increases. This leads to further reabsorption of HCO3-. The net
effect is an increase in the net acid excretion.

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Hypokalaemia

Potassium and hydrogen can be thought of as competitors. Hyperkalaemia tends


to be associated with acidosis because as potassium levels rise fewer hydrogen
ions can enter the cells

Hypokalaemia with alkalosis


Vomiting
Diuretics
Cushing's syndrome
Conn's syndrome (primary hyperaldosteronism)

Hypokalaemia with acidosis


Diarrhoea
gathered by dr. elbarky

Renal tubular acidosis


Acetazolamide
Partially treated diabetic ketoacidosis

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Question 72 of 192

 

A 16 year old girl develops pyelonephritis and is admitted in a state of septic


shock. Which of the following is not typically seen in this condition?

Increased cardiac output

Increased systemic vascular resistance


gathered by dr. elbarky

Oliguria may occur

Systemic cytokine release

Tachycardia
Cardiogenic Shock:
e.g. MI, valve abnormality

increased SVR (vasoconstriction in response to low BP)


increased HR (sympathetic response)
decreased cardiac output
decreased blood pressure

Hypovolaemic shock:
blood volume depletion
e.g. haemorrhage, vomiting, diarrhoea, dehydration, third-space losses during
major operations

increased SVR
gathered by dr. elbarky

increased HR
decreased cardiac output
decreased blood pressure

Septic shock:
occurs when the peripheral vascular dilatation causes a fall in SVR
similar response may occur in anaphylactic shock, neurogenic shock

reduced SVR
increased HR
normal/increased cardiac output
decreased blood pressure

The SVR is reduced in sepsis and for this reason a vasopressor such as
noradrenaline may be used if hypotension and oliguria remain a concern despite
administration of adequate amounts of intravenous fluids.

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Shock

Shock occurs when there is insufficient tissue perfusion.


The pathophysiology of shock is an important surgical topic and may be
divided into the following aetiological groups:
Septic
Haemorrhagic
Neurogenic
Cardiogenic
Anaphylactic

Septic shock
Septic shock is a major problem and those patients with severe sepsis have a
mortality rate in excess of 40%. In those who are admitted to intensive care
mortality ranges from 6% with no organ failure to 65% in those with 4 organ failure.

Sepsis is defined as an infection that triggers a particular Systemic Inflammatory


Response Syndrome (SIRS). This is characterised by body temperature outside 36
oC - 38 o C, HR >90 beats/min, respiratory rate >20/min, WBC count >12,000/mm 3

or < 4,000/mm3, altered mental state or hyperglycaemia (in absence of diabetes).


gathered by dr. elbarky

Patients with infections and two or more elements of SIRS meet the diagnostic
criteria for sepsis. Those with organ failure have severe sepsis and those with
refractory hypotension -septic shock.

During the septic process there is marked activation of the immune system with
extensive cytokine release. This may be coupled with or triggered by systemic
circulation of bacterial toxins. These all cause endothelial cell damage and
neutrophil adhesion. The overall hallmarks are thus those of excessive
inflammation, coagulation and fibrinolytic suppression.

The surviving sepsis campaign (2012) highlights the following key areas for
attention:
Prompt administration of antibiotics to cover all likely pathogens coupled
with a rigorous search for the source of infection.
Haemodynamic stabilisation. Many patients are hypovolaemic and require
aggressive fluid administration. Aim for CVP 8-12 cm H2O, MAP >65mmHg.
Modulation of the septic response. This includes manoeuvres to counteract
the changes and includes measures such as tight glycaemic control. The
routine use of steroids is not advised.

In surgical patients, the main groups with septic shock include those with
anastomotic leaks, abscesses and extensive superficial infections such as
necrotising fasciitis. When performing surgery the aim should be to undertake the
minimum necessary to restore physiology. These patients do not fare well with
prolonged surgery. Definitive surgery can be more safely undertaken when
physiology is restored and clotting in particular has been normalised.

Haemorrhagic shock
The average adult blood volume comprises 7% of body weight. Thus in the 70 Kg
adult this will equate to 5 litres. This changes in children (8-9% body weight) and is
slightly lower in the elderly.
The table below outlines the 4 major classes of haemorrhagic shock and their
associated physiological sequelae:

Parameter Class I Class II Class III Class IV

Blood loss ml <750ml 750-1500ml 1500-2000ml >2000ml

Blood loss % <15% 15-30% 30-40% >40%

Pulse rate <100 >100 >120 >140

Blood pressure Normal Normal Decreased Decreased

Respiratory rate 14-20 20-30 30-40 >35


gathered by dr. elbarky

Urine output >30ml 20-30ml 5-15ml <5ml

Symptoms Normal Anxious Confused Lethargic

Decreasing blood pressure during haemorrhagic shock causes organ


hypoperfusion and relative myocardial ischaemia. The cardiac index gives a
numerical value for tissue oxygen delivery and is given by the equation: Cardiac
index= Cardiac output/ body surface area. Where Hb is haemoglobin
concentration in blood and SaO2 the saturation and PaO2 the partial pressure of
oxygen. Detailed knowledge of this equation is required for the MRCS Viva but not
for part A, although you should understand the principle.

In patients suffering from trauma the most likely cause of shock is haemorrhage.
However, the following may also be the cause or occur concomitantly:

Tension pneumothorax
Spinal cord injury
Myocardial contusion
Cardiac tamponade

When assessing trauma patients it is worth remembering that in order to generate


a palpable femoral pulse an arterial pressure of >65mmHg is required.

Once bleeding is controlled and circulating volume normalised the levels of


transfusion should be to maintain a Hb of 7-8 in those with no risk factors for
tissue hypoxia and Hb 10 for those who have such risk factors.

Neurogenic shock
This occurs most often following a spinal cord transection, usually at a high level.
There is resultant interruption of the autonomic nervous system. The result is
either decreased sympathetic tone or increased parasympathetic tone, the effect
of which is a decrease in peripheral vascular resistance mediated by marked
vasodilation.

This results in decreased preload and thus decreased cardiac output (Starlings
law). There is decreased peripheral tissue perfusion and shock is thus produced. In
contrast with many other types of shock peripheral vasoconstrictors are used to
return vascular tone to normal.

Cardiogenic shock
In medical patients the main cause is ischaemic heart disease. In the traumatic
setting direct myocardial trauma or contusion is more likely. Evidence of ECG
changes and overlying sternal fractures or contusions should raise the suspicion
of injury. Treatment is largely supportive and transthoracic echocardiography
should be used to determine evidence of pericardial fluid or direct myocardial
gathered by dr. elbarky

injury. The measurement of troponin levels in trauma patients may be undertaken


but they are less useful in delineating the extent of myocardial trauma than
following MI.

When cardiac injury is of a blunt nature and is associated with cardiogenic shock
the right side of the heart is the most likely site of injury with chamber and or valve
rupture. These patients require surgery to repair these defects and will require
cardiopulmonary bypass to achieve this. Some may require intra aortic balloon
pump as a bridge to surgery.

Anaphylactic shock
Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic
hypersensitivity reaction.

Anaphylaxis is one of the few times when you would not have time to look up the
dose of a medication. The Resuscitation Council guidelines on anaphylaxis have
recently been updated. Adrenaline is by far the most important drug in anaphylaxis
and should be given as soon as possible. The recommended doses for adrenaline,
hydrocortisone and chlorpheniramine are as follows:

Adrenaline Hydrocortisone Chlorpheniramine

< 6 months 150 mcg (0.15ml 1 25 mg 250 mcg/kg


in 1,000)

6 months - 6 150 mcg (0.15ml 1 50 mg 2.5 mg


years in 1,000)

6-12 years 300 mcg (0.3ml 1 in 100 mg 5 mg


1,000)

Adult and child 500 mcg (0.5ml 1 in 200 mg 10 mg


12 years 1,000)
Adrenaline can be repeated every 5 minutes if necessary. The best site for IM
injection is the anterolateral aspect of the middle third of the thigh.

Common identified causes of anaphylaxis


food (e.g. Nuts) - the most common cause in children
drugs
venom (e.g. Wasp sting)

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Question 73 of 192

 

A 45 year old man is undergoing a small bowel resection. The anaesthetist decides
to administer an intravenous fluid which is electrolyte rich. Which of the following
most closely matches this requirement?

Dextrose / Saline

Pentastarch
gathered by dr. elbarky

Gelofusine

Hartmans

5% Dextrose with added potassium 20mmol/ L

Hartmans solution is the most electrolyte rich. However, both pentastarch and
gelofusine have more macromolecules.

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Intra operative fluid management


Composition of commonly used intravenous fluids mmol-1

Na K Cl Bicarbonate Lactate

Plasma 137-147 4-5.5 95-105 22-25 -

0.9% Saline 153 - 153 - -

Dextrose / saline 30.6 - 30.6 - -

Hartmans 130 4 110 - 28

Recommendations for intra operative fluid management


gathered by dr. elbarky

The latest set of NICE guidelines produced in 2013 relating to intravenous fluids
did not specifically address the requirements of intra operative fluid
administration. The reason for this is that administration of fluids in this specific
situation does not lend itself to rigid algorithms.
With the introduction of enhanced recovery programmes 10 years ago there was
an increasing emphasis of the concept of fluid restriction. Historically, patients
received very large volumes of saline rich solutions peri-operatively. Clearing the
sodium load of a single litre of saline may take up to 36 hours or more. This can
have deleterious effects on the tissues including the development of oedema. This
results in poor perfusion, increased risk of ileus and wound breakdown. A tailored
approach to fluid administration is now practiced and far greater usage is made of
cardiac output monitors in providing goal directed fluid therapy.

References
British Consensus Guidelines on Intravenous Fluid Therapy for Adult Surgical
Patients
GIFTASUP (2009) Revised May 2011.

Frost P. Intravenous fluid therapy in adult inpatients. BMJ 2015 (350): 31-34.

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Question 74 of 192

 

A 17 year old lady with long standing anorexia nervosa is due to undergo excision
of a lipoma. Which of the following nutritional deficiencies is most likely to be
implicated in poor collagen formation as the wound heals?

Deficiency of copper

Deficiency of iron
gathered by dr. elbarky

Deficiency of ascorbic acid

Deficiency of phosphate

None of the above

Vitamin C is involved in the cross linkage of collagen and impaired wound healing
is well described in cases of vitamin C deficiency.

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Collagen

Collagen is one of the most important structural proteins within the extracellular
matrix, collagen together with components such as elastin and
glycosaminoglycans determine the properties of all tissues.
Composed of 3 polypeptide strands that are woven into a helix, usually a
combination of glycine with either proline or hydroxyproline plus another
amino acid
Numerous hydrogen bonds exist within molecule to provide additional
strength
Many sub types but commonest sub type is I (90% of bodily collagen),
tissues with increased levels of flexibility have increased levels of type III
collagen
Vitamin c is important in establishing cross links
Synthesised by fibroblasts

Collagen Diseases
Disorders of collagen range from relatively common, acquired defects (typically
aging), through to rarer congenital disorders. The latter are exemplified by
conditions such as osteogenesis imperfecta and Ehlers Danlos syndromes.

Osteogenesis imperfecta:
-8 Subtypes
-Defect of type I collagen
-In type I the collagen is normal quality but insufficient quantity
-Type II- poor quantity and quality
-Type III- Collagen poorly formed, normal quantity
-Type IV- Sufficient quantity but poor quality
gathered by dr. elbarky

Patients have bones which fracture easily, loose joint and multiple other defects
depending upon which sub type they suffer from.

Ehlers Danlos:
-Multiple sub types
-Abnormality of types 1 and 3 collagen
-Patients have features of hypermobility.
-Individuals are prone to joint dislocations and pelvic organ prolapse. In addition to
many other diseases related to connective tissue defects.

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Question 75 of 192

 

A 69 year old man has been living in sheltered accommodation for many months,
with inadequate nutrition notices that his night vision is becoming impaired.
Deficiency of which vitamin is responsible?

Vitamin B3

Vitamin A
gathered by dr. elbarky

Vitamin C

Vitamin B12

Vitamin E

Loss of vitamin A will result in impair rhodopsin synthesis and results in poor night
vision.

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Vitamin deficiency

Vitamin Effect of deficiency

A Night blindness
Epithelial atrophy
Infections

B1 Beriberi

B2 Dermatitis and photosensitivity

B3 Pellagra
B12 Pernicious anaemia

C Poor wound healing


Impaired collagen synthesis

D Rickets (Children)
Osteomalacia (Adults)

K Clotting disorders

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Question 76 of 192

 

Which of the following statements relating the fluid physiology of a physiologically


normal 70 Kg adult male is false?

He will have more water per unit of body weight than a female of similar
weight

Plasma will comprise 25% of his body weight


gathered by dr. elbarky

Interstitial fluid will account for up to 24% of body water

Approximately 65% of total body water is intracellular

60% of his body weight is composed of water

The 60-40-20 rule:


60% total body weight is water
40% of total body weight is intracellular fluids
20% of body weight is extracellular fluids

Plasma typically accounts for 4-6% of body weight in healthy individuals.


Males typically have more water per unit weight than females, as females have a
higher fat content.

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Fluid compartment physiology

Body fluid compartments comprise intracellular and extracellular compartments.


The latter includes interstitial fluid, plasma and transcellular fluid.
Typical figures are based on the 70 Kg male.
Body fluid volumes

Compartment Volume in litres Percentage of total volume

Intracellular 28 L 60-65%

Extracellular 14 L 35-40%

Plasma 3L 5%

Interstitial 10 L 24%

Transcellular 1L 3%

Figures are approximate


gathered by dr. elbarky

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Question 77 of 192

 

Which of the following statements relating to blood transfusions in surgical


patients is false?

Packed red cells typically have a haematocrit of between 55 and 75%

Clotting factor activity in whole blood decreases in samples stored for


longer than 7 days
gathered by dr. elbarky

After 3 weeks of storage blood has a pH of 6.9

Gamma irradiated blood products are not required routinely

Patients should be transfused to achieve a target haemoglobin of 10 g/dl


and a haematocrit of 30%

Patients can generally be managed without transfusion as long as the Hb is 7 or


greater. The exact level depends upon patient factors such as co-morbidities. Old
blood functions less effectively and should not be used during massive
transfusions.

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Blood products

Whole blood fractions

Fraction Key points

Packed red cells Used for transfusion in chronic anaemia and cases where
infusion of large volumes of fluid may result in
cardiovascular compromise. Product obtained by
centrifugation of whole blood.
Platelet rich Usually administered to patients who are
plasma thrombocytopaenic and are bleeding or require surgery. It is
obtained by low speed centrifugation.

Platelet Prepared by high speed centrifugation and administered to


concentrate patients with thrombocytopaenia.

Fresh frozen Prepared from single units of blood.


plasma Contains clotting factors, albumin and
immunoglobulin.
Unit is usually 200 to 250ml.
Usually used in correcting clotting deficiencies in
patients with hepatic synthetic failure who are due to
undergo surgery.
gathered by dr. elbarky

Usual dose is 12-15ml/Kg-1.


It should not be used as first line therapy for
hypovolaemia.

Cryoprecipitate Formed from supernatant of FFP.


Rich source of Factor VIII and fibrinogen.
Allows large concentration of factor VIII to be
administered in small volume.

SAG-Mannitol Removal of all plasma from a blood unit and substitution


Blood with:
Sodium chloride
Adenine
Anhydrous glucose
Mannitol

Up to 4 units of SAG M Blood may be administered.


Thereafter whole blood is preferred. After 8 units, clotting
factors and platelets should be considered.

Cell saver devices


These collect patients own blood lost during surgery and then re-infuse it. There
are two main types:
Those which wash the blood cells prior to re-infusion. These are more
expensive to purchase and more complicated to operate. However, they
reduce the risk of re-infusing contaminated blood back into the patient.
Those which do not wash the blood prior to re-infusion.

Their main advantage is that they avoid the use of infusion of blood from donors
into patients and this may reduce risk of blood borne infection. It may be
acceptable to Jehovah's witnesses. It is contraindicated in malignant disease for
risk of facilitating disease dissemination.
Blood products used in warfarin reversal
In some surgical patients the use of warfarin can pose specific problems and may
require the use of specialised blood products

Immediate or urgent surgery in patients taking warfarin(1) (2):

1. Stop warfarin

2. Vitamin K (reversal within 4-24 hours)


-IV takes 4-6h to work (at least 5mg)
-Oral can take 24 hours to be clinically effective

3. Fresh frozen plasma


Used less commonly now as 1st line warfarin reversal
-30ml/kg-1
gathered by dr. elbarky

-Need to give at least 1L fluid in 70kg person (therefore not appropriate in fluid
overload)
-Need blood group
-Only use if human prothrombin complex is not available

4. Human Prothrombin Complex (reversal within 1 hour)


-Bereplex 50 u/kg
-Rapid action but factor 6 short half life, therefore give with vitamin K

References
1. Dentali, F., C. Marchesi, et al. (2011). 'Safety of prothrombin complex
concentrates for rapid anticoagulation reversal of vitamin K antagonists. A meta-
analysis.' Thromb Haemost 106(3): 429-438.

2. http://www.transfusionguidelines.org/docs/pdfs/bbt-03warfarin-reversal-
flowchart-2006.pdf

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Question 79 of 192

 

The acute phase response to injury does not typically include:

Pyrexia

Decreased albumin

Hepatic sequestration of cations


gathered by dr. elbarky

Increased transferrin

Increased serum amyloid A

The acute phase response includes:

Acute phase proteins


Reduction of transport proteins (albumin, transferrin)
Hepatic sequestration cations
Pyrexia
Neutrophil leucocytosis
Increased muscle proteolysis
Changes in vascular permeability

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Stress response: Endocrine and metabolic changes

Surgery precipitates hormonal and metabolic changes causing the stress


response.
Stress response is associated with: substrate mobilization, muscle protein
loss, sodium and water retention, suppression of anabolic hormone
secretion, activation of the sympathetic nervous system, immunological and
haematological changes.
The hypothalamic-pituitary axis and the sympathetic nervous systems are
activated and there is a failure of the normal feedback mechanisms of
control of hormone secretion.

A summary of the hormonal changes associated with the stress response:

Increased Decreased No Change

Growth hormone Insulin Thyroid stimulating


hormone

Cortisol Testosterone Luteinizing hormone

Renin Oestrogen Follicle stimulating


gathered by dr. elbarky

hormone

Adrenocorticotrophic hormone
(ACTH)

Aldosterone

Prolactin

Antidiuretic hormone

Glucagon

Sympathetic nervous system


Stimulates catecholamine release
Causes tachycardia and hypertension

Pituitary gland
ACTH and growth hormone (GH) is stimulated by hypothalamic releasing
factors, corticotrophin releasing factor (CRF) and somatotrophin (or growth
hormone releasing factor)
Perioperative increased prolactin secretion occurs by release of inhibitory
control
Secretion of thyroid stimulating hormone (TSH), luteinizing hormone (LH)
and follicle stimulating hormone (FSH) does not change significantly
ACTH stimulates cortisol production within a few minutes of the start of
surgery. More ACTH is produced than needed to produce a maximum
adrenocortical response.

Cortisol
Significant increases within 4-6 hours of surgery (>1000 nmol litre-1).
The usual negative feedback mechanism fails and concentrations of ACTH
and cortisol remain persistently increased.
The magnitude and duration of the increase correlate with the severity of
stress and the response is not abolished by the administration of
corticosteroids.
The metabolic effects of cortisol are enhanced:

Skeletal muscle protein breakdown to provide gluconeogenic precursors and


amino acids for protein synthesis in the liver
Stimulation of lipolysis
'Anti-insulin effect'
Mineralocorticoid effects
Anti-inflammatory effects
gathered by dr. elbarky

Growth hormone
Increased secretion after surgery has a minor role
Most important for preventing muscle protein breakdown and promote
tissue repair by insulin growth factors

Alpha Endorphin
Increased

Antidiuretic hormone
An important vasopressor and enhances haemostasis
Renin is released causing the conversion of angiotensinogen to angiotensin
I
Angiotensin II formed by ACE on angiotensin 1, which causes the secretion
of aldosterone from the adrenal cortex. This increases sodium reabsorption
at the distal convoluted tubule

Insulin
Release inhibited by stress
Occurs via the inhibition of the beta cells in the pancreas by the α2-
adrenergic inhibitory effects of catecholamines
Insulin resistance by target cells occurs later
The perioperative period is characterized by a state of functional insulin
deficiency

Thyroxine (T4) and tri-iodothyronine (T3)


Circulating concentrations are inversely correlated with sympathetic activity
and after surgery there is a reduction in thyroid hormone production, which
normalises over a few days.
Metabolic effect of endocrine response

Carbohydrate metabolism
Hyperglycaemia is a main feature of the metabolic response to surgery
Due to increase in glucose production and a reduction in glucose utilization
Catecholamines and cortisol promote glycogenolysis and gluconeogenesis
Initial failure of insulin secretion followed by insulin resistance affects the
normal responses
The proportion of the hyperglycaemic response reflects the severity of
surgery
Hyperglycaemia impairs wound healing and increase infection rates

Protein metabolism
Initially there is inhibition of protein anabolism, followed later, if the stress
gathered by dr. elbarky

response is severe, by enhanced catabolism


The amount of protein degradation is influenced by the type of surgery and
also by the nutritional status of the patient
Mainly skeletal muscle protein is affected
The amino acids released form acute phase proteins (fibrinogen, C reactive
protein, complement proteins, a2-macroglobulin, amyloid A and
ceruloplasmin) and are used for gluconeogenesis
Nutritional support has little effect on preventing catabolism

Lipid metabolism
Increased catecholamine, cortisol and glucagon secretion, and insulin deficiency,
promotes lipolysis and ketone body production.

Salt and water metabolism


ADH causes water retention, concentrated urine, and potassium loss and
may continue for 3 to 5 days after surgery
Renin causes sodium and water retention

Cytokines
Glycoproteins
Interleukins (IL) 1 to 17, interferons, and tumour necrosis factor
Synthesized by activated macrophages, fibroblasts, endothelial and glial
cells in response to tissue injury from surgery or trauma
IL-6 main cytokine associated with surgery. Peak 12 to 24 h after surgery
and increase by the degree of tissue damage Other effects of cytokines
include fever, granulocytosis, haemostasis, tissue damage limitation and
promotion of healing.

Modifying the response


Opioids suppress hypothalamic and pituitary hormone secretion
At high doses the hormonal response to pelvic and abdominal surgery is
abolished. However, such doses prolong recovery and increase the need for
postoperative ventilatory support
Spinal anaesthesia can reduce the glucose, ACTH, cortisol, GH and
epinephrine changes, although cytokine responses are unaltered
Cytokine release is reduced in less invasive surgery
Nutrition prevents the adverse effects of the stress response. Enteral
feeding improves recovery
Growth hormone and anabolic steroids may improve outcome
Normothermia decreases the metabolic response

References
Deborah Burton, Grainne Nicholson, and George Hall
Endocrine and metabolic response to surgery .
gathered by dr. elbarky

Contin Educ Anaesth Crit Care Pain (2004) 4(5): 144-147 doi:10.1093/bjaceaccp
/mkh040

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Question 80 of 192

 

Which of the following mechanisms best accounts for the release of adrenaline?

Release from the adrenal medulla in response to increased angiotensin 1


levels

Release from the zona fasiculata from the adrenal gland in response to
increased sympathetic discharge
gathered by dr. elbarky

Release from the adrenal medulla in response to increased noradrenaline


levels

Release from the adrenal medulla in response to sympathetic stimulation


from the splanchnic nerves

None of the above

The adrenal gland releases adrenaline in response to increased sympathetic


discharge from preganglionic sympathetic fibres of the splanchnic nerves. These
cause the chromafin cells of the medulla to release adrenaline (which is
preformed) by exocytosis.

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Adrenaline

Fight or Flight response

- Catecholamine (phenylalanine and tyrosine)


- Neurotransmitter and hormone
- Released by the adrenal glands
- Effects on α 1 and 2, β 1 and 2 receptors
- Effect on β 2 receptors in skeletal muscle vessels-causing vasodilation
- Increase cardiac output and total peripheral resistance
- Vasoconstriction in the skin and kidneys causing a narrow pulse pressure
Actions
α adrenergic receptors:
Inhibits insulin secretion by the pancreas
Stimulates glycogenolysis in the liver and muscle
Stimulates glycolysis in muscle

β adrenergic receptors:
Stimulates glucagon secretion in the pancreas
Stimulates ACTH
Stimulates lipolysis by adipose tissue

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Question 81 of 192

 

A 43 year old lady is admitted with cholestasis secondary to a stone impacted at


the level of the ampulla of vater. Which of the following tests is most likely to be
predictive of bleeding diathesis at the time of ERCP in this particular case?

Bleeding time

Prothrombin time
gathered by dr. elbarky

APTT

Platelet count

Factor I levels

PT: Vitamin K dependent factors 2, 7, 9, 10


APTT: Factors 8, 9, 11, 12

Jaundice will impair the production of vitamin K dependent clotting factors. This is
most accurately tested by measuring the prothrombin time. APTT can be affected
by vitamin K deficiency (due to factor 9 deficiency), however this occurs to a lesser
extent and is normally associated with severe liver disease. The bleeding time is a
measure of platelet function.

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Abnormal coagulation

Cause Factors affected

Heparin Prevents activation factors 2,9,10,11


Cause Factors affected

Warfarin Affects synthesis of factors 2,7,9,10

DIC Factors 1,2,5,8,11

Liver disease Factors 1,2,5,7,9,10,11

Interpretation blood clotting test results

Disorder APTT PT Bleeding time

Haemophilia Increased Normal Normal


gathered by dr. elbarky

von Willebrand's disease Increased Normal Increased

Vitamin K deficiency Increased Increased Normal

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Question 82 of 192

 

Which of the following hormonal agents will increase secretions of water and
electrolytes in pancreatic juice?

Secretin

Aldosterone
gathered by dr. elbarky

Somatostatin

Cholecystokinin

Adrenaline

Secretin causes secretion of water and electrolytes


Cholecystokinin causes enzyme secretion

While secretin will typically increase electrolyte and water volume of secretions,
the enzyme content is increased by cholecystokinin. Somatostatin will decrease
the volume of secretions. Aldosterone will tend to conserve electrolytes.

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Pancreas exocrine physiology

Composition of pancreatic secretions


Pancreatic secretions are usually 1000-1500ml per 24 hours and have a pH of 8.
Secretion Source Substances secreted
Trypsinogen
Procarboxylase
Enzymic Acinar cells
Amylase
Elastase

Sodium
Bicarbonate
Water
Ductal and
Aqueous Potassium
Centroacinar cells
Chloride
NB: Sodium and potassium reflect their plasma levels;
chloride and bicarbonate vary with flow rate

Regulation
The cephalic and gastric phases (neuronal and physical) are less important in
regulating the pancreatic secretions. The effect of digested material in the small
gathered by dr. elbarky

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.

Enzyme activation
Trypsinogen is converted via enterokinase to active trypsin in the duodenum.
Trypsin then activates the other inactive enzymes

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Question stats
A 49.7%
B 9.5%
C 10.2%
D 24.9%
E 5.8%

49.7% of users answered this question correctly

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gathered by dr. elbarky

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Question 83 of 192

 

A 73 year old lady is diagnosed with hyperaldosteronism. From which of the


following structures is aldosterone released?

Zona fasciculata of the adrenal gland

Juxtaglomerular apparatus of the kidney


gathered by dr. elbarky

Zona reticularis of the adrenal gland

Adrenal medulla

Zona glomerulosa of the adrenal cortex

Aldosterone serves to conserve sodium and water. It is produced in the zona


glomerulosa of the adrenal cortex.

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Aldosterone

Aldosterone is secreted by the zona glomerulosa of the adrenal cortex. It is a


mineralocorticoid hormone. Secretion is regulated by the renin- angiotensin
system, and by plasma levels of sodium and potassium. Aldosterone conserves
sodium by stimulating the reabsorption of sodium in the distal nephron in
exchange for potassium. Lack of aldosterone release will result in hyperkalaemia
and hyponatraemia.

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A 12.3%
B 6.9%
C 9.1%
gathered by dr. elbarky

D 6.2%
E 65.5%

65.5% of users answered this question correctly

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Question 84 of 192

 

Which of the following inhibits gastric acid secretion?

Histamine

Nausea

Calcium
gathered by dr. elbarky

Parasympathetic vagal stimulation

Gastrin

Nausea inhibits gastric secretion via higher cerebral activity and sympathetic
innervation.

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Gastric secretions

A working knowledge of gastric secretions is important for surgery because peptic


ulcers are common, surgeons frequently prescribe anti secretory drugs and
because there are still patients around who will have undergone acid lowering
procedures (Vagotomy) in the past.

Gastric acid
Is produced by the parietal cells in the stomach
pH of gastric acid is around 2 with acidity being maintained by the H+/K+
ATP ase pump. As part of the process bicarbonate ions will be secreted into
the surrounding vessels.
Sodium and chloride ions are actively secreted from the parietal cell into the
canaliculus. This sets up a negative potential across the membrane and as a
result sodium and potassium ions diffuse across into the canaliculus.
Carbonic anhydrase forms carbonic acid which dissociates and the
hydrogen ions formed by dissociation leave the cell via the H+/K+ antiporter
pump. At the same time sodium ions are actively absorbed. This leaves
hydrogen and chloride ions in the canaliculus these mix and are secreted
into the lumen of the oxyntic gland.

This is illustrated diagrammatically below:


gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb028b.jpg)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Gastric
/images_eMRCS/swb028b.jpg)
acid)

Phases of gastric acid secretion


There are 3 phases of gastric secretion:

1. Cephalic phase (smell / taste of food)


30% acid produced
Vagal cholinergic stimulation causing secretion of HCL and gastrin release
from G cells

2. Gastric phase (distension of stomach )


60% acid produced
Stomach distension/low H+/peptides causes Gastrin release
3. Intestinal phase (food in duodenum)
10% acid produced
High acidity/distension/hypertonic solutions in the duodenum inhibits
gastric acid secretion via enterogastrones (CCK, secretin) and neural
reflexes.

Regulation of gastric acid production


Factors increasing production include:
Vagal nerve stimulation
Gastrin release
Histamine release (indirectly following gastrin release) from
enterchromaffin like cells
gathered by dr. elbarky

Factors decreasing production include:


Somatostatin (inhibits histamine release)
Cholecystokinin
Secretin

The diagram below illustrates some of the factors involved in regulating gastric
acid secretion and the relevant associated pharmacology

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb029b.jpg)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Gastric
/images_eMRCS/swb029b.jpg)
acid)

Below is a brief summary of the major hormones involved in food digestion:

Source Stimulus Actions


Source Stimulus Actions

Gastrin G cells in Distension of Increase HCL, pepsinogen


antrum of stomach, and IF secretion, increases
the extrinsic nerves gastric motility, trophic effect
stomach Inhibited by: low on gastric mucosa
antral pH,
somatostatin

CCK I cells in Partially Increases secretion of


upper digested enzyme-rich fluid from
small proteins and pancreas, contraction of
intestine triglycerides gallbladder and relaxation of
sphincter of Oddi, decreases
gathered by dr. elbarky

gastric emptying, trophic


effect on pancreatic acinar
cells, induces satiety

Secretin S cells in Acidic chyme, Increases secretion of


upper fatty acids bicarbonate-rich fluid from
small pancreas and hepatic duct
intestine cells, decreases gastric acid
secretion, trophic effect on
pancreatic acinar cells

VIP Small Neural Stimulates secretion by


intestine, pancreas and intestines,
pancreas inhibits acid and pepsinogen
secretion

Somatostatin D cells in Fat, bile salts Decreases acid and pepsin


the and glucose in secretion, decreases gastrin
pancreas the intestinal secretion, decreases
and lumen pancreatic enzyme secretion,
stomach decreases insulin and
glucagon secretion
inhibits trophic effects of
gastrin, stimulates gastric
mucous production

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A 10.3%
B 42.2%
C 21.4%
D 14.4%
gathered by dr. elbarky

E 11.8%

42.2% of users answered this question correctly

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Question 85 of 192

 

A 22 year old man is undergoing a daycase excision of a sebaceous cyst. He is


needle phobic and as the surgeon approaches with the needle the patient begins
to hyperventilate. He soon develops circumoral parasthesia and muscular
twitching. Which of the following is the most likely explanation for this event?

Temporal lobe epilepsy


gathered by dr. elbarky

Reduction in ionised calcium levels

Increase in ionised calcium levels

Fall in serum PTH levels

Rise in serum PTH levels

50% of plasma calcium is ionised. Hyperventilation will induce a state of alkalosis


which will lower ionised plasma calcium levels.

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Calcium homeostasis

Calcium ions are linked to a wide range of physiological processes. The largest
store of bodily calcium is contained within the skeleton. Calcium levels are
primarily controlled by parathyroid hormone, vitamin D and calcitonin.

Hormonal regulation of calcium

Hormone Actions
Hormone Actions

Parathyroid hormone (PTH) Increase calcium levels and


decrease phosphate levels
Increases bone resorption
Immediate action on osteoblasts to
increase ca2+ in extracellular fluid
Osteoblasts produce a protein
signaling molecule that activate
osteoclasts which cause bone
resorption
Increases renal tubular reabsorption
of calcium
Increases synthesis of 1,25(OH)2D
gathered by dr. elbarky

(active form of vitamin D) in the


kidney which increases bowel
absorption of Ca2+
Decreases renal phosphate
reabsorption

1,25-dihydroxycholecalciferol Increases plasma calcium and


(the active form of vitamin D) plasma phosphate
Increases renal tubular reabsorption
and gut absorption of calcium
Increases osteoclastic activity at
high levels and osteoblasts at low
levels
Increases renal phosphate
reabsorption

Calcitonin Secreted by C cells of thyroid


Inhibits intestinal calcium absorption
Inhibits osteoclast activity
Inhibits renal tubular absorption of
calcium

Both growth hormone and thyroxine also play a small role in calcium metabolism.

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A 7.7%
B 59%
C 20.9%
D 6.6%
gathered by dr. elbarky

E 5.8%

59% of users answered this question correctly

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Question 86 of 192

 

Which of the following statements relating to gastric acid secretions are untrue?

In parietal cells carbonic anhydrase generates hydrogen ions which are


then actively secreted

The cephalic phase is abolished following truncal vagotomy


gathered by dr. elbarky

The intestinal phase accounts for 60% of gastric acid produced

Histamine acts in a paracrine manner on H2 receptors

H2 receptor antagonists will not completely abolish gastric acid


production

The intestinal phase of gastric acid secretion accounts for only 10% of gastric acid
produced.

Please rate this question:

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Gastric secretions

A working knowledge of gastric secretions is important for surgery because peptic


ulcers are common, surgeons frequently prescribe anti secretory drugs and
because there are still patients around who will have undergone acid lowering
procedures (Vagotomy) in the past.

Gastric acid
Is produced by the parietal cells in the stomach
pH of gastric acid is around 2 with acidity being maintained by the H+/K+
ATP ase pump. As part of the process bicarbonate ions will be secreted into
the surrounding vessels.
Sodium and chloride ions are actively secreted from the parietal cell into the
canaliculus. This sets up a negative potential across the membrane and as a
result sodium and potassium ions diffuse across into the canaliculus.
Carbonic anhydrase forms carbonic acid which dissociates and the
hydrogen ions formed by dissociation leave the cell via the H+/K+ antiporter
pump. At the same time sodium ions are actively absorbed. This leaves
hydrogen and chloride ions in the canaliculus these mix and are secreted
into the lumen of the oxyntic gland.

This is illustrated diagrammatically below:


gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb028b.jpg)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Gastric
/images_eMRCS/swb028b.jpg)
acid)

Phases of gastric acid secretion


There are 3 phases of gastric secretion:

1. Cephalic phase (smell / taste of food)


30% acid produced
Vagal cholinergic stimulation causing secretion of HCL and gastrin release
from G cells

2. Gastric phase (distension of stomach )


60% acid produced
Stomach distension/low H+/peptides causes Gastrin release

3. Intestinal phase (food in duodenum)


10% acid produced
High acidity/distension/hypertonic solutions in the duodenum inhibits
gastric acid secretion via enterogastrones (CCK, secretin) and neural
reflexes.

Regulation of gastric acid production


Factors increasing production include:
Vagal nerve stimulation
Gastrin release
gathered by dr. elbarky

Histamine release (indirectly following gastrin release) from


enterchromaffin like cells

Factors decreasing production include:


Somatostatin (inhibits histamine release)
Cholecystokinin
Secretin

The diagram below illustrates some of the factors involved in regulating gastric
acid secretion and the relevant associated pharmacology

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb029b.jpg)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Gastric
/images_eMRCS/swb029b.jpg)
acid)

Below is a brief summary of the major hormones involved in food digestion:


Source Stimulus Actions

Gastrin G cells in Distension of Increase HCL, pepsinogen


antrum of stomach, and IF secretion, increases
the extrinsic nerves gastric motility, trophic effect
stomach Inhibited by: low on gastric mucosa
antral pH,
somatostatin

CCK I cells in Partially Increases secretion of


upper digested enzyme-rich fluid from
small proteins and pancreas, contraction of
intestine triglycerides gallbladder and relaxation of
sphincter of Oddi, decreases
gathered by dr. elbarky

gastric emptying, trophic


effect on pancreatic acinar
cells, induces satiety

Secretin S cells in Acidic chyme, Increases secretion of


upper fatty acids bicarbonate-rich fluid from
small pancreas and hepatic duct
intestine cells, decreases gastric acid
secretion, trophic effect on
pancreatic acinar cells

VIP Small Neural Stimulates secretion by


intestine, pancreas and intestines,
pancreas inhibits acid and pepsinogen
secretion

Somatostatin D cells in Fat, bile salts Decreases acid and pepsin


the and glucose in secretion, decreases gastrin
pancreas the intestinal secretion, decreases
and lumen pancreatic enzyme secretion,
stomach decreases insulin and
glucagon secretion
inhibits trophic effects of
gastrin, stimulates gastric
mucous production

Next question 

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Question stats

A 10.7%
B 17%
C 50.7%
D 10.4%
gathered by dr. elbarky

E 11.2%

50.7% of users answered this question correctly

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Question 87 of 192

 

Which of the following stimulates gastric acid secretion?

Cholecystokinin

Gastric inhibitory peptide

Secretin
gathered by dr. elbarky

Histamine

Somatostatin

Gastrin: From G cells: stimulates gastric acid production

Pepsin: Digestion of protein, secretion occurs simultaneously with gastrin

Secretin: From mucosal cells in the duodenum and jejunum: inhibits gastric acid,
stimulates bile and pancreatic juice production

Gastric inhibitory peptide: (produced in response to fatty acids) inhibits gastrin


release and acid secretion from parietal cells

Cholecystokinin: From mucosal cells in the duodenum and jejunum (produced in


response to fatty acids) inhibits acid secretion from parietal cells, causes
gallbladder contraction and relaxation of sphincter of Oddi

Somatostatin: From D cells

Please rate this question:

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Hormonal control of gastric acid secretion


Source Stimulus Actions

Gastrin G cells in Distension of Increase HCL, pepsinogen


antrum of stomach, and IF secretion, increases
the extrinsic nerves Next
gastric motility, question
trophic 
effect
stomach Inhibited by: low on gastric mucosa
antral pH,
somatostatin
Display my notes on this topic
CCK I cells in Partially Increases secretion of
   upper
  digested
   enzyme-rich
 fluid from
 
small proteins and pancreas, contraction of
intestine triglycerides gallbladder and relaxation of
sphincter of Oddi, decreases
gathered by dr. elbarky

Save my notes gastric emptying, trophic


effect on pancreatic acinar
Question stats cells, induces satiety

Secretin S cells in Acidic chyme, Increases secretion of


A upper 11.5%
fatty acids bicarbonate-rich fluid from
B small 5.4% pancreas and hepatic duct
intestine cells, decreases gastric acid
C 19.2%
secretion, trophic effect on
D 58.7% pancreatic acinar cells
E 5.3%
VIP Small Neural Stimulates secretion by
intestine, pancreas and intestines,
58.7% of users answered this question correctly
pancreas inhibits acid and pepsinogen
secretion

Somatostatin D cells in Search


Fat, eMRCS
bile salts Decreases acid and pepsin
the and glucose in secretion, decreases gastrin
pancreas the intestinal secretion, decreases
Search term Go
and lumen pancreatic enzyme secretion,
stomach decreases insulin and
glucagon secretion
 Open MRCS Part A textbook (../review/textbook.php) inhibits trophic effects of
gastrin, stimulates gastric
mucous production

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Question 88 of 192

 

A 34 year old lady develops septic shock and features of the systemic
inflammatory response syndrome as a complication of cholangitis. Which of the
following is not a typical feature of this condition?

Body temperature less than 36oC or greater than 38oC

Respiratory rate >20


gathered by dr. elbarky

Lactate <4 mmol/L

High levels of tumour necrosis factor α

WCC >12,000 mm3

Septic shock will typically result in end organ hypoperfusion and as a result lactate
levels will often be high. In the surviving sepsis campaign it is suggested that
elevated lactate levels are an independent indicator for vasopressor support in
patient with sepsis. The WCC may be paradoxically low in severe sepsis, although
it is most often elevated.

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Shock

Shock occurs when there is insufficient tissue perfusion.


The pathophysiology of shock is an important surgical topic and may be
divided into the following aetiological groups:
Septic
Haemorrhagic
Neurogenic
Cardiogenic
Anaphylactic
Septic shock
Septic shock is a major problem and those patients with severe sepsis have a
mortality rate in excess of 40%. In those who are admitted to intensive care
mortality ranges from 6% with no organ failure to 65% in those with 4 organ failure.

Sepsis is defined as an infection that triggers a particular Systemic Inflammatory


Response Syndrome (SIRS). This is characterised by body temperature outside 36
oC - 38 o C, HR >90 beats/min, respiratory rate >20/min, WBC count >12,000/mm 3

or < 4,000/mm3, altered mental state or hyperglycaemia (in absence of diabetes).

Patients with infections and two or more elements of SIRS meet the diagnostic
criteria for sepsis. Those with organ failure have severe sepsis and those with
refractory hypotension -septic shock.
gathered by dr. elbarky

During the septic process there is marked activation of the immune system with
extensive cytokine release. This may be coupled with or triggered by systemic
circulation of bacterial toxins. These all cause endothelial cell damage and
neutrophil adhesion. The overall hallmarks are thus those of excessive
inflammation, coagulation and fibrinolytic suppression.

The surviving sepsis campaign (2012) highlights the following key areas for
attention:
Prompt administration of antibiotics to cover all likely pathogens coupled
with a rigorous search for the source of infection.
Haemodynamic stabilisation. Many patients are hypovolaemic and require
aggressive fluid administration. Aim for CVP 8-12 cm H2O, MAP >65mmHg.
Modulation of the septic response. This includes manoeuvres to counteract
the changes and includes measures such as tight glycaemic control. The
routine use of steroids is not advised.

In surgical patients, the main groups with septic shock include those with
anastomotic leaks, abscesses and extensive superficial infections such as
necrotising fasciitis. When performing surgery the aim should be to undertake the
minimum necessary to restore physiology. These patients do not fare well with
prolonged surgery. Definitive surgery can be more safely undertaken when
physiology is restored and clotting in particular has been normalised.

Haemorrhagic shock
The average adult blood volume comprises 7% of body weight. Thus in the 70 Kg
adult this will equate to 5 litres. This changes in children (8-9% body weight) and is
slightly lower in the elderly.

The table below outlines the 4 major classes of haemorrhagic shock and their
associated physiological sequelae:
Parameter Class I Class II Class III Class IV

Blood loss ml <750ml 750-1500ml 1500-2000ml >2000ml

Blood loss % <15% 15-30% 30-40% >40%

Pulse rate <100 >100 >120 >140

Blood pressure Normal Normal Decreased Decreased

Respiratory rate 14-20 20-30 30-40 >35

Urine output >30ml 20-30ml 5-15ml <5ml

Symptoms Normal Anxious Confused Lethargic


gathered by dr. elbarky

Decreasing blood pressure during haemorrhagic shock causes organ


hypoperfusion and relative myocardial ischaemia. The cardiac index gives a
numerical value for tissue oxygen delivery and is given by the equation: Cardiac
index= Cardiac output/ body surface area. Where Hb is haemoglobin
concentration in blood and SaO2 the saturation and PaO2 the partial pressure of
oxygen. Detailed knowledge of this equation is required for the MRCS Viva but not
for part A, although you should understand the principle.

In patients suffering from trauma the most likely cause of shock is haemorrhage.
However, the following may also be the cause or occur concomitantly:

Tension pneumothorax
Spinal cord injury
Myocardial contusion
Cardiac tamponade

When assessing trauma patients it is worth remembering that in order to generate


a palpable femoral pulse an arterial pressure of >65mmHg is required.

Once bleeding is controlled and circulating volume normalised the levels of


transfusion should be to maintain a Hb of 7-8 in those with no risk factors for
tissue hypoxia and Hb 10 for those who have such risk factors.

Neurogenic shock
This occurs most often following a spinal cord transection, usually at a high level.
There is resultant interruption of the autonomic nervous system. The result is
either decreased sympathetic tone or increased parasympathetic tone, the effect
of which is a decrease in peripheral vascular resistance mediated by marked
vasodilation.

This results in decreased preload and thus decreased cardiac output (Starlings
law). There is decreased peripheral tissue perfusion and shock is thus produced. In
contrast with many other types of shock peripheral vasoconstrictors are used to
return vascular tone to normal.

Cardiogenic shock
In medical patients the main cause is ischaemic heart disease. In the traumatic
setting direct myocardial trauma or contusion is more likely. Evidence of ECG
changes and overlying sternal fractures or contusions should raise the suspicion
of injury. Treatment is largely supportive and transthoracic echocardiography
should be used to determine evidence of pericardial fluid or direct myocardial
injury. The measurement of troponin levels in trauma patients may be undertaken
but they are less useful in delineating the extent of myocardial trauma than
following MI.
gathered by dr. elbarky

When cardiac injury is of a blunt nature and is associated with cardiogenic shock
the right side of the heart is the most likely site of injury with chamber and or valve
rupture. These patients require surgery to repair these defects and will require
cardiopulmonary bypass to achieve this. Some may require intra aortic balloon
pump as a bridge to surgery.

Anaphylactic shock
Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic
hypersensitivity reaction.

Anaphylaxis is one of the few times when you would not have time to look up the
dose of a medication. The Resuscitation Council guidelines on anaphylaxis have
recently been updated. Adrenaline is by far the most important drug in anaphylaxis
and should be given as soon as possible. The recommended doses for adrenaline,
hydrocortisone and chlorpheniramine are as follows:

Adrenaline Hydrocortisone Chlorpheniramine

< 6 months 150 mcg (0.15ml 1 25 mg 250 mcg/kg


in 1,000)

6 months - 6 150 mcg (0.15ml 1 50 mg 2.5 mg


years in 1,000)

6-12 years 300 mcg (0.3ml 1 in 100 mg 5 mg


1,000)

Adult and child 500 mcg (0.5ml 1 in 200 mg 10 mg


12 years 1,000)

Adrenaline can be repeated every 5 minutes if necessary. The best site for IM
injection is the anterolateral aspect of the middle third of the thigh.
Common identified causes of anaphylaxis
food (e.g. Nuts) - the most common cause in children
drugs
venom (e.g. Wasp sting)

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B 5.5%
C 56.4%
D 26.1%
E 5.4%

56.4% of users answered this question correctly

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Question 89 of 192

 

Release of somatostatin from the pancreas will result in which of the following?

Decrease in pancreatic exocrine secretions

Contraction of the gallbladder

Increase in the rate of gastric emptying


gathered by dr. elbarky

Increased synthesis of growth hormone

Increased insulin release

Octreotide reduces exocrine pancreatic secretions so is used to treat high output


pancreatic fistulae (though parenteral feeding is most effective). Other uses
include variceal bleeding and treatment of acromegaly.
Inhibits growth hormone and insulin release (when released from pancreas).
Somatostatin is also released by the hypothalamus causing a negative feedback
response on growth hormone.

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Somatostatin

Somatostatin is produced in the D cells of the pancreatic islets. It is also produced


in the gut (enterochromaffin cells) and is found in brain tissue. Those substances
that stimulate insulin release will also induce somatostatin secretion. It is an
inhibitor of growth hormone, it also delays gastric emptying and reduces gastrin
secretion.
It reduces pancreatic exocrine secretions and may be used therapeutically to treat
pancreatic fistulae.

Somatostatinomas are rare pancreatic endocrine tumours and will result in the
clinical manifestations of diabetes mellitus, gallstones and steatorrhoea.
Next question 

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Question stats
gathered by dr. elbarky

A 49.1%
B 14.6%
C 17.6%
D 8.9%
E 9.8%

49.1% of users answered this question correctly

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Question 90 of 192

 

Which of the following is least likely to be associated with hypercalcaemia?

Thiazides

Antacids

Coeliac disease
gathered by dr. elbarky

Sarcoidosis

Zolinger-Ellison syndrome

Mnemonic for the causes of hypercalcaemia:

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

Patients with coeliac disease tend to develop hypocalcaemia due to malabsorption


of calcium by the bowel.

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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
gathered by dr. elbarky

MEN
Milk alkali syndrome

Clinical features
Stones, bones, abdominal groans, and psychic moans
High serum calcium levels result in decreased neuronal excitability. Therefore
sluggish reflexes, muscle weakness and constipation may occur.

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Question 91 of 192

 

Which one of the following would cause a rise in the carbon monoxide transfer
factor (TLCO)?

Emphysema

Pulmonary embolism
gathered by dr. elbarky

Pulmonary haemorrhage

Pneumonia

Pulmonary fibrosis

Transfer factor
raised: asthma, haemorrhage, left-to-right shunts, polycythaemia
low: everything else

Where alveolar haemorrhage occurs the TLCO tends to increase due to the
enhanced uptake of carbon monoxide by intra-alveolar haemoglobin.

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Transfer factor

The transfer factor describes the rate at which a gas will diffuse from alveoli into
blood. Carbon monoxide is used to test the rate of diffusion. Results may be given
as the total gas transfer (TLCO) or that corrected for lung volume (transfer
coefficient, KCO)
Causes of a raised TLCO Causes of a lower TLCO
asthma pulmonary
pulmonary haemorrhage (Wegener's, fibrosis
Goodpasture's) pneumonia
left-to-right cardiac shunts pulmonary emboli
polycythaemia pulmonary
hyperkinetic states oedema
male gender, exercise emphysema
anaemia
low cardiac
output
gathered by dr. elbarky

KCO also tends to increase with age. Some conditions may cause an increased
KCO with a normal or reduced TLCO
pneumonectomy/lobectomy
scoliosis/kyphosis
neuromuscular weakness
ankylosis of costovertebral joints e.g. ankylosing spondylitis

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B 14.8%
C 33.9%
D 7.6%
E 14.4%

33.9% of users answered this question correctly


Question 92 of 192

 

Which of the following does not cause a normal anion gap acidosis?

Pancreatic fistula

Acetazolamide

Uraemia
gathered by dr. elbarky

Ureteric diversion

Renal tubular acidosis

Normal Gap Acidosis: HARDUP

H - Hyperalimentation/hyperventilation
A - Acetazolamide
R - Renal tubular acidosis
D - Diarrhoea
U - Ureteral diversion
P - Pancreatic fistula/parenteral saline

Uraemia will typically cause a high anion gap acidosis. It is one of the unmeasured
anions.

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Disorders of acid - base balance

Disorders of acid- base balance are often covered in the MRCS part A.

The acid-base normogram below shows how the various disorders may be
categorised
gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb072b.png)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Acid-base
/images_eMRCS/swb072b.png)
homeostasis)

Metabolic acidosis
This is the most common surgical acid - base disorder.
Reduction in plasma bicarbonate levels.
Two mechanisms:

1. Gain of strong acid (e.g. diabetic ketoacidosis)


2. Loss of base (e.g. from bowel in diarrhoea)
- Classified according to the anion gap, this can be calculated by:
(Na+ + K+) - (Cl- + HCO3-).
- If a question supplies the chloride level then this is often a clue that the anion gap
should be calculated. The normal range = 10-18 mmol/L

Normal anion gap ( = hyperchloraemic metabolic acidosis)


Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
Renal tubular acidosis
Drugs: e.g. acetazolamide
Ammonium chloride injection
Addison's disease

Raised anion gap


Lactate: shock, hypoxia
Ketones: diabetic ketoacidosis, alcohol
Urate: renal failure
Acid poisoning: salicylates, methanol

Metabolic acidosis secondary to high lactate levels may be subdivided into two
types:
Lactic acidosis type A: (Perfusion disorders e.g.shock, hypoxia, burns)
Lactic acidosis type B: (Metabolic e.g. metformin toxicity)

Metabolic alkalosis
Usually caused by a rise in plasma bicarbonate levels.
Rise of bicarbonate above 24 mmol/L will typically result in renal excretion
of excess bicarbonate.
gathered by dr. elbarky

Caused by a loss of hydrogen ions or a gain of bicarbonate. It is due mainly


to problems of the kidney or gastrointestinal tract

Causes
Vomiting / aspiration (e.g. Peptic ulcer leading to pyloric stenosis,
nasogastric suction)
Diuretics
Liquorice, carbenoxolone
Hypokalaemia
Primary hyperaldosteronism
Cushing's syndrome
Bartter's syndrome
Congenital adrenal hyperplasia

Mechanism of metabolic alkalosis


Activation of renin-angiotensin II-aldosterone (RAA) system is a key factor
Aldosterone causes reabsorption of Na+ in exchange for H+ in the distal
convoluted tubule
ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA
system → raised aldosterone levels
In hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+
into cells to maintain neutrality

Respiratory acidosis
Rise in carbon dioxide levels usually as a result of alveolar hypoventilation
Renal compensation may occur leading to Compensated respiratory acidosis

Causes
COPD
Decompensation in other respiratory conditions e.g. Life-threatening asthma
/ pulmonary oedema
Sedative drugs: benzodiazepines, opiate overdose

Respiratory alkalosis
Hyperventilation resulting in excess loss of carbon dioxide
This will result in increasing pH

Causes
Psychogenic: anxiety leading to hyperventilation
Hypoxia causing a subsequent hyperventilation: pulmonary embolism, high
altitude
Early salicylate poisoning*
CNS stimulation: stroke, subarachnoid haemorrhage, encephalitis
gathered by dr. elbarky

Pregnancy

*Salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis.


Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst
later the direct acid effects of salicylates (combined with acute renal failure) may
lead to an acidosis

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Question 93 of 192

 

An arterial blood gas sample is taken and the following results obtained;
PaO2 8kPa

PaCO2 4kPa

pH 7.4

With which of the following are these values most consistent?


gathered by dr. elbarky

Compensated metabolic alkalosis

Pulmonary atelectasis

Alveolar hypoventilation

Residing at 4500M for 48 hours

LAD occlusion

The patient has low oxygen tension and low carbon dioxide. The pH is normal so
there is compensation for a long standing condition in which oxygenation is
reduced. There is neither alkalosis, nor hypoventilation as the carbon dioxide is
low. At very high altitude, the low oxygen tension can exceed the anaerobic
threshold and carbon dioxide levels increase.

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Arterial blood gas interpretation

In advanced life support training, a 5 step approach to arterial blood gas


interpretation is advocated.

1. How is the patient?


2. Is the patient hypoxaemic?
The Pa02 on air should be 10.0-13.0 kPa

3. Is the patient acidaemic (pH <7.35) or alkalaemic (pH >7.45)

4. What has happened to the PaCO2?


If there is acidaemia, an elevated PaCO2 will account for this

5. What is the bicarbonate level or base excess?


A metabolic acidosis will have a low bicarbonate level and a low base excess (< -2
mmol)
A metabolic alkalosis will have a high bicarbonate and a high base excess (> +2
mmol)
gathered by dr. elbarky

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Question 94 of 192

 

Which of the following is not a characteristic of the proximal convoluted tubule in


the kidney?

Up to 95% of filtered amino acids will be reabsorbed at this site

It is a risk of damage in a patient with compartment syndrome due to a


tibial fracture
gathered by dr. elbarky

It is responsible for absorbing more than 50% of filtered water

Its secretory function is most effective at low systolic blood pressures


(typically less than 100mmHg)

Glucose is reabsorbed by a process of facilitated diffusion

The proximal convoluted tubule may undergo necrosis in situations such as


compartment syndrome. It is responsible for reabsorbing up to two thirds of
filtered water. Low systolic blood pressures (below the renal autoregulatory range)
are a risk factor for acute tubular necrosis. Within the autoregulatory range the
absolute value of systolic BP has little effect.

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Renal Physiology

Overview
Each nephron is supplied with blood from an afferent arteriole that opens
onto the glomerular capillary bed.
Blood then flows to an efferent arteriole, supplying the peritubular capillaries
and medullary vasa recta.
The kidney receives up to 25% of resting cardiac output.
Control of blood flow
The kidney is able to autoregulate its blood flow between systolic pressures
of 80- 180mmHg so there is little variation in renal blood flow.
This is achieved by myogenic control of arteriolar tone, both sympathetic
input and hormonal signals (e.g. renin) are responsible.

Glomerular structure and function


Blood inside the glomerulus has considerable hydrostatic pressure.
The basement membrane has pores that will allow free diffusion of smaller
solutes, larger negatively charged molecules such as albumin are unable to
cross.
The glomerular filtration rate (GFR) is equal to the concentration of a solute
in the urine, times the volume of urine produced per minute, divided by the
plasma concentration (assuming that the solute is freely diffused e.g.
gathered by dr. elbarky

inulin).
In clinical practice creatinine is used because it is subjected to very little
proximal tubular secretion.
Although subject to variability, the typical GFR is 125ml per minute.
Glomerular filtration rate = Total volume of plasma per unit time leaving the
capillaries and entering the bowman's capsule
Renal clearance = volume plasma from which a substance is removed per
minute by the kidneys

Substances used to measure GFR have the following features:


1. Inert
2. Free filtration from the plasma at the glomerulus (not protein bound)
3. Not absorbed or secreted at the tubules
4. Plasma concentration constant during urine collection

Examples: inulin, creatinine

GFR = urine concentration (mmol/l) x urine volume (ml/min)


--------------------------------------------------------------------------
plasma concentration (mmol/l)

The clearance of a substance is dependent not only on its diffusivity across


the basement membrane but also subsequent tubular secretion and / or
reabsorption.
So glucose which is freely filtered across the basement membrane is usually
reabsorbed from tubules giving a clearance of zero.

Tubular function
Reabsorption and secretion of substances occurs in the tubules.
In the proximal tubule substrates such as glucose, amino acids and
phosphate are co-transported with sodium across the semi permeable
membrane.
Up to two thirds of filtered water is reabsorbed in the proximal tubules.
This will lead to increase in urea concentration in the distal tubule allowing
for its increased diffusion.
Substances to be secreted into the tubules are taken up from the peritubular
blood by tubular cells.
Solutes such as paraaminohippuric acid are cleared with a single passage
through the kidneys and this is why it is used to measure renal plasma flow.
Ions such as calcium and phosphate will have a tubular reabsorption that is
influenced by plasma PTH levels.
Potassium may be both secreted and re-absorbed and is co-exchanged with
sodium.

Loop of Henle
Approximately 60 litres of water containing 9000mmol sodium enters the
descending limb of the loop of Henle in 24 hours.
gathered by dr. elbarky

Loops from the juxtamedullary nephrons run deep into the medulla.
The osmolarity of fluid changes and is greatest at the tip of the papilla.
The thick ascending limb is impermeable to water, but highly permeable to
sodium and chloride ions.
This loss means that at the beginning of the thick ascending limb the fluid is
hypo osmotic compared with adjacent interstitial fluid.
In the thick ascending limb the reabsorption of sodium and chloride ions
occurs by both facilitated and passive diffusion pathways.
The loops of Henle are co-located with vasa recta, these will have similar
solute compositions to the surrounding extracellular fluid so preventing the
diffusion and subsequent removal of this hypertonic fluid.
The energy dependent reabsorption of sodium and chloride in the thick
ascending limb helps to maintain this osmotic gradient.

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Question 95 of 192

 

At which of the following sites is the most water absorbed?

Right colon

Left colon

Stomach
gathered by dr. elbarky

Jejunum

Duodenum

Water absorption in the gastrointestinal tract predominantly occurs in the small


bowel (jejunum and ileum). The colon is an important site of water absorption,
however, its overall contribution is relatively small. The importance of the colonic
component to water absorption may increase following extensive small bowel
resections.

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Water absorption

During a 24 hours period the average person will ingest up to 2000ml of liquid
orally. In addition a further 8000ml of fluid will enter the small bowel as
gastrointestinal secretions. Intestinal water absorption is a passive process and is
related to solute load. In the jejunum the active absorption of glucose and amino
acids will create a concentration gradient that water will flow across. In the ileum
most water is absorbed by a process of facilitated diffusion (with sodium).
Approximately 150ml of water enters the colon daily, most is absorbed, the colon
can adapt to, and increase this amount following resection.
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Question 96 of 192

 

A 39 year old lady has recurrent attacks of biliary colic. What is the approximate
volume of bile to enter the duodenum per 24 hours?

500 mL

50 mL
gathered by dr. elbarky

100 mL

2000 mL

150 mL

Between 500 mL and 1.5 L of bile enters the small bowel daily. Most bile salts are
recycled by the enterohepatic circulation. When the gallbladder contracts the
lumenal pressure is approximately 25cm water, which is why biliary colic may be
so painful.

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Bile

Bile is produced at a rate of between 500ml and 1500mL per day. Bile is composed
of bile salts, bicarbonate, cholesterol, steroids and water. There are three main
factors regulating bile flow; hepatic secretion, gall bladder contraction and
sphincter of oddi resistance. Bile salts are absorbed in the terminal ileum (and
recycled to the liver). Over 90% of all bile salts are recycled in this way, such that
the total pool of bile salts is recycled up to six times a day.

Primary bile salts


Cholate and chenodeoxycholate.

Secondary bile salts


Formed by bacterial action on primary bile salts. These are deoxycholate and
lithocholate. Of these deoxycholate is reabsorbed, whilst lithocholate is insoluble
and excreted.

Pathophysiology of gallstones
Bile salts have a detergent action. They aggregate to form micelles and these have
a lipid centre in which fats may be transported. Excessive quantities of cholesterol
cannot be transported in this way and will tend to precipitate, resulting in the
formation of cholesterol rich gallstones.

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Question 97 of 192

 

A 24 year old man is involved in a road traffic accident. His right leg is trapped for
6 hours whilst he is moved. On examination his foot is insensate and a dorsalis
pedis pulse is only weakly felt. Which of the biochemical abnormalities listed
below is most likely to be present?

Alkalosis
gathered by dr. elbarky

Hypercalcaemia

Hypocalcaemia

Hyperkalaemia

Hyponatraemia

In this scenario the patient will have a compartment syndrome, delayed diagnosis
and muscle death. The effect of muscle death will result in the release of
potassium. It is also highly likely that there will be a degree of renal impairment,
the result of which is that the serum potassium is likely to be high.

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Hyperkalaemia

Plasma potassium levels are regulated by a number of factors including


aldosterone, acid-base balance and insulin levels.
Metabolic acidosis is associated with hyperkalaemia as hydrogen and
potassium ions compete with each other for exchange with sodium ions
across cell membranes and in the distal tubule.
ECG changes seen in hyperkalaemia include tall-tented T waves, small P
waves, widened QRS leading to a sinusoidal pattern and asystole
Causes of hyperkalaemia
Acute renal failure
Drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor
blockers, spironolactone, ciclosporin, heparin**
Metabolic acidosis
Addison's
Tissue necrosis/rhabdomylosis: burns, trauma
Massive blood transfusion

Foods that are high in potassium


Salt substitutes (i.e. Contain potassium rather than sodium)
Bananas, oranges, kiwi fruit, avocado, spinach, tomatoes
gathered by dr. elbarky

*beta-blockers interfere with potassium transport into cells and can potentially
cause hyperkalaemia in renal failure patients - remember beta-agonists, e.g.
Salbutamol, are sometimes used as emergency treatment

**both unfractionated and low-molecular weight heparin can cause hyperkalaemia.


This is thought to be caused by inhibition of aldosterone secretion

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Question 98 of 192

 

A 55-year-old man with a history of type 2 diabetes mellitus, bipolar disorder and
chronic obstructive pulmonary disease has bloods taken during a pre operative
assessment of an inguinal hernia repair:

Na+ 125 mmol/l

K+ 3.8 mmol/l
gathered by dr. elbarky

Bicarbonate 24 mmol/l

Urea 3.7 mmol/l

Creatinine 92 µmol/l

Due to his smoking history a chest x-ray is ordered which is reported as normal.
The Consultant asks you what is the most likely cause for the hyponatraemia?

Metformin

Lithium

Carbamazepine

Sodium valproate

Pioglitazone

SIADH - drug causes: carbamazepine, sulfonylureas, SSRIs, tricyclics

Lithium can cause diabetes insipidus but this is generally associated with a high
sodium. Lithium only tends to cause raised antidiuretic hormone levels following a
severe overdosage.

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syndrome of inappropriate antidiuretic hormone (SIADH):


causes

Malignancy
especially small cell lung cancer
also: pancreas, prostate

Neurological
stroke
subarachnoid haemorrhage
gathered by dr. elbarky

subdural haemorrhage
meningitis/encephalitis/abscess

Infections
tuberculosis
pneumonia

Drugs
sulfonylureas
SSRIs, tricyclics
carbamazepine
vincristine
cyclophosphamide

Other causes
positive end-expiratory pressure (PEEP)
porphyrias

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Question 99 of 192

 

A 45 year old man sustains a closed head injury. He is initially alert, however, his
level of consciousness deteriorates on arrival at hospital. An intra cranial pressure
monitor is inserted. What is the normal intracranial pressure?

35 - 45mm Hg

45 - 55mm Hg
gathered by dr. elbarky

<15mm Hg

25 - 35mm Hg

25 - 30 mm Hg

The normal intracranial pressure is between 7 and 15 mm Hg. The brain can
accommodate increases up to 24 mm Hg, thereafter clinical features will become
evident.

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Applied neurophysiology

Pressure within the cranium is governed by the Monroe-Kelly doctrine. This


considers the skull as a closed box. Increases in mass can be
accommodated by loss of CSF. Once a critical point is reached (usually 100-
120ml of CSF lost) there can be no further compensation and ICP rises
sharply. The next step is that pressure will begin to equate with MAP and
neuronal death will occur. Herniation will also accompany this process.
The CNS can autoregulate its own blood supply. Vaso constriction and
dilatation of the cerebral blood vessels is the primary method by which this
occurs. Extremes of blood pressure can exceed this capacity resulting in
risk of stroke. Other metabolic factors such as hypercapnia will also cause
vasodilation, which is of importance in ventilating head injured patients.
The brain can only metabolise glucose, when glucose levels fall,
consciousness will be impaired.

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Question 78 of 192

 

A 73 year old man presents to pre operative clinic for an elective total hip
replacement. He is on furosemide for hypertension. His investigations reveal to the
following results:
Na 120

Urine Na 10 (low)

Serum osmolality 280 (normal)


gathered by dr. elbarky

What is the most likely cause?

Hypotonic hypovolaemic hyponatraemia

Hypertonic hypovolaemic hyponatraemia

Syndrome of inappropriate ADH secretion

Over administration of 5% dextrose

Glomerulonephritis

The blood results reflect extra-renal sodium loss. The body is trying to preserve the
sodium by not allowing any sodium into the urine (hence the low Na in the urine).
Note with renal sodium loss the Urinary sodium is high.

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Hyponatraemia

This is commonly tested in the MRCS (despite most surgeons automatically


seeking medical advice if this occurs!). The most common cause in surgery is the
over administration of 5% dextrose.

Hyponatraemia may be caused by water excess or sodium depletion. Causes of


pseudohyponatraemia include hyperlipidaemia (increase in serum volume) or a
taking blood from a drip arm. Urinary sodium and osmolarity levels aid making a
diagnosis.

Classification

Urinary sodium > 20 Sodium depletion, renal loss Mnemonic:


mmol/l Patient often Syndrome of
hypovolaemic INAPPropriate Anti-
Diuretics (thiazides) Diuretic Hormone:
Addison's In creased
Diuretic stage of renal Na (sodium)
failure PP (urine)
SIADH (serum osmolality
gathered by dr. elbarky

low, urine osmolality high,


urine Na high)
Patient often euvolaemic

Urinary sodium < 20 Sodium depletion, extra-renal


mmol/l loss
Diarrhoea, vomiting,
sweating
Burns, adenoma of
rectum (if villous lesion
and large)

Water excess Secondary


(patient often hyperaldosteronism: CCF,
hypervolaemic and cirrhosis
oedematous) Reduced GFR: renal
failure
IV dextrose, psychogenic
polydipsia

Management

Symptomatic Hyponatremia :

Acute hyponatraemia with Na <120: immediate therapy. Central Pontine


Myelinolisis, may occur from overly rapid correction of serum sodium. Aim to
correct until the Na is > 125 at a rate of 1 mEq/h. Normal saline with frusemide is
an alternative method.

The sodium requirement can be calculated as follows :


(125 - serum sodium) x 0.6 x body weight = required mEq of sodium

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Question 100 of 192

 

Which substance can be used to achieve the most accurate measurement of the
glomerular filtration rate?

Glucose

Protein
gathered by dr. elbarky

Inulin

Creatinine

Para-amino hippuric acid

Creatinine declines with age due to decline in renal function and muscle mass.
Glucose, protein (amino acids) and PAH are reabsorbed by the kidney.

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Renal Physiology

Overview
Each nephron is supplied with blood from an afferent arteriole that opens
onto the glomerular capillary bed.
Blood then flows to an efferent arteriole, supplying the peritubular capillaries
and medullary vasa recta.
The kidney receives up to 25% of resting cardiac output.

Control of blood flow


The kidney is able to autoregulate its blood flow between systolic pressures
of 80- 180mmHg so there is little variation in renal blood flow.
This is achieved by myogenic control of arteriolar tone, both sympathetic
input and hormonal signals (e.g. renin) are responsible.
Glomerular structure and function
Blood inside the glomerulus has considerable hydrostatic pressure.
The basement membrane has pores that will allow free diffusion of smaller
solutes, larger negatively charged molecules such as albumin are unable to
cross.
The glomerular filtration rate (GFR) is equal to the concentration of a solute
in the urine, times the volume of urine produced per minute, divided by the
plasma concentration (assuming that the solute is freely diffused e.g.
inulin).
In clinical practice creatinine is used because it is subjected to very little
proximal tubular secretion.
Although subject to variability, the typical GFR is 125ml per minute.
Glomerular filtration rate = Total volume of plasma per unit time leaving the
gathered by dr. elbarky

capillaries and entering the bowman's capsule


Renal clearance = volume plasma from which a substance is removed per
minute by the kidneys

Substances used to measure GFR have the following features:


1. Inert
2. Free filtration from the plasma at the glomerulus (not protein bound)
3. Not absorbed or secreted at the tubules
4. Plasma concentration constant during urine collection

Examples: inulin, creatinine

GFR = urine concentration (mmol/l) x urine volume (ml/min)


--------------------------------------------------------------------------
plasma concentration (mmol/l)

The clearance of a substance is dependent not only on its diffusivity across


the basement membrane but also subsequent tubular secretion and / or
reabsorption.
So glucose which is freely filtered across the basement membrane is usually
reabsorbed from tubules giving a clearance of zero.

Tubular function
Reabsorption and secretion of substances occurs in the tubules.
In the proximal tubule substrates such as glucose, amino acids and
phosphate are co-transported with sodium across the semi permeable
membrane.
Up to two thirds of filtered water is reabsorbed in the proximal tubules.
This will lead to increase in urea concentration in the distal tubule allowing
for its increased diffusion.
Substances to be secreted into the tubules are taken up from the peritubular
blood by tubular cells.
Solutes such as paraaminohippuric acid are cleared with a single passage
through the kidneys and this is why it is used to measure renal plasma flow.
Ions such as calcium and phosphate will have a tubular reabsorption that is
influenced by plasma PTH levels.
Potassium may be both secreted and re-absorbed and is co-exchanged with
sodium.

Loop of Henle
Approximately 60 litres of water containing 9000mmol sodium enters the
descending limb of the loop of Henle in 24 hours.
Loops from the juxtamedullary nephrons run deep into the medulla.
The osmolarity of fluid changes and is greatest at the tip of the papilla.
The thick ascending limb is impermeable to water, but highly permeable to
sodium and chloride ions.
This loss means that at the beginning of the thick ascending limb the fluid is
gathered by dr. elbarky

hypo osmotic compared with adjacent interstitial fluid.


In the thick ascending limb the reabsorption of sodium and chloride ions
occurs by both facilitated and passive diffusion pathways.
The loops of Henle are co-located with vasa recta, these will have similar
solute compositions to the surrounding extracellular fluid so preventing the
diffusion and subsequent removal of this hypertonic fluid.
The energy dependent reabsorption of sodium and chloride in the thick
ascending limb helps to maintain this osmotic gradient.

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E 17.3%

Question 101 of 192

 

Which of the following statements relating to cerebrospinal fluid is untrue?

The choroid plexus is only present in the lateral ventricles

Total CSF volume is 100-150ml

CSF pressure is usually 10-15mmHg


gathered by dr. elbarky

The cerebral aqueduct connects the third and fourth ventricles

The foramen of Luschka are paired and lie laterally in the fourth ventricle

The choroid plexus lies in all ventricles.

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Cerebrospinal fluid

The CSF fills the space between the arachnoid mater and pia mater (covering
surface of the brain). The total volume of CSF in the brain is approximately 150ml.
Approximately 500 ml is produced by the ependymal cells in the choroid plexus
(70%), or blood vessels (30%). It is reabsorbed via the arachnoid granulations
which project into the venous sinuses.

Circulation
1. Lateral ventricles (via foramen of Munro)
2. 3rd ventricle
3. Cerebral aqueduct (aqueduct of Sylvius)
4. 4th ventricle (via foramina of Magendie and Luschka)
5. Subarachnoid space
6. Reabsorbed into the venous system via arachnoid granulations into superior
sagittal sinus
Composition
Glucose: 50-80mg/dl
Protein: 15-40 mg/dl
Red blood cells: Nil
White blood cells: 0-3 cells/ mm3

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Question 102 of 192

 

A 74-year-old woman with thyroid cancer is admitted due to shortness of breath.


What is the best investigation to assess for possible compression of the upper
airways?

Arterial blood gases

Forced vital capacity


gathered by dr. elbarky

Transfer factor

Peak expiratory flow rate

Flow volume loop

Flow volume loop is the investigation of choice for upper airway compression.

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Flow volume loop

A normal flow volume loop is often described as a 'triangle on top of a semi circle'

Flow volume loops are the most suitable way of assessing compression of the
upper airway

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A 10.1%
B 13.7%
C 8.2%
D 29.8%
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E 38.3%

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Question 103 of 192

 

Which of the following drugs does not cause pseudohaematuria?

Rifampicin

Quinine

Noradrenaline
gathered by dr. elbarky

Levodopa

Phenytoin

Rifampicin, phenytoin, levodopa, methyldopa, and quinine all cause


pseudohaematuria.

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Haematuria

Causes of haematuria

Trauma Injury to renal tract


Renal trauma commonly due to blunt injury
(others penetrating injuries)
Ureter trauma rare: iatrogenic
Bladder trauma: due to RTA or pelvic fractures

Infection Remember TB
Malignancy Renal cell carcinoma (remember paraneoplastic
syndromes): painful or painless

Urothelial malignancies: 90% are transitional cell


carcinoma, can occur anywhere along the urinary
tract. Painless haematuria.
Squamous cell carcinoma and adenocarcinoma:
rare bladder tumours
Prostate cancer
Penile cancers: SCC

Renal disease Glomerulonephritis

Stones Microscopic haematuria common


gathered by dr. elbarky

Structural Benign prostatic hyperplasia (BPH) causes


abnormalities haematuria due to hypervascularity of the
prostate gland
Cystic renal lesions e.g. polycystic kidney disease
Vascular malformations
Renal vein thrombosis due to renal cell carcinoma

Coagulopathy Causes bleeding of underlying lesions

Drugs Cause tubular necrosis or interstitial nephritis:


aminoglycosides, chemotherapy
Interstitial nephritis: penicillin, sulphonamides,
and NSAIDs
Anticoagulants

Benign Exercise

Gynaecological Endometriosis: flank pain, dysuria, and


haematuria that is cyclical

Iatrogenic Catheterisation
Radiotherapy; cystitis, severe haemorrhage,
bladder necrosis

Pseudohaematuria For example following consumption of beetroot

References
Http://bestpractice.bmj.com/best-practice/monograph/316/overview
/aetiology.html

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C 61.6%
D 12.6%
E 9.8%

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Question 104 of 192

 

A 19 year old man is attacked outside a club and beaten with a baseball bat. He
sustains a blow to the right side of his head. He is brought to the emergency
department and a policy of observation is adopted. His glasgow coma score
deteriorates and he becomes comatose. Which of the following haemodynamic
parameters is most likely to be present?

Hypertension and bradycardia


gathered by dr. elbarky

Hypotension and tachycardia

Hypotension and bradycardia

Hypertension and tachycardia

Normotension and bradycardia

Hypertension and bradycardia are seen prior to coning. The brain autoregulates its
blood supply by controlling systemic blood pressure.

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Head injury

Patients who suffer head injuries should be managed according to ATLS principles
and extra cranial injuries should be managed alongside cranial trauma. Inadequate
cardiac output will compromise CNS perfusion irrespective of the nature of the
cranial injury.

Types of traumatic brain injury


Bleeding into the space between the dura mater and the skull. Often
results from acceleration-deceleration trauma or a blow to the side of the
head. The majority of extradural haematomas occur in the temporal
region where skull fractures cause a rupture of the middle meningeal
Extradural artery.
haematoma
Features
Raised intracranial pressure
Some patients may exhibit a lucid interval

Bleeding into the outermost meningeal layer. Most commonly occur


around the frontal and parietal lobes. May be either acute or chronic.
Subdural
haematoma Risk factors include old age and alcoholism.

Slower onset of symptoms than a extradural haematoma.


gathered by dr. elbarky

Usually occurs spontaneously in the context of a ruptured cerebral


Subarachnoid
aneurysm, but may be seen in association with other injuries when a
haemorrhage
patient has sustained a traumatic brain injury.

Pathophysiology
Primary brain injury may be focal (contusion/ haematoma) or diffuse
(diffuse axonal injury)
Diffuse axonal injury occurs as a result of mechanical shearing following
deceleration, causing disruption and tearing of axons
Intra-cranial haematomas can be extradural, subdural or intracerebral, while
contusions may occur adjacent to (coup) or contralateral (contre-coup) to
the side of impact
Secondary brain injury occurs when cerebral oedema, ischaemia, infection,
tonsillar or tentorial herniation exacerbates the original injury. The normal
cerebral auto regulatory processes are disrupted following trauma rendering
the brain more susceptible to blood flow changes and hypoxia
The Cushings reflex (hypertension and bradycardia) often occurs late and is
usually a pre terminal event

Management
Where there is life threatening rising ICP such as in extra dural haematoma
and whilst theatre is prepared or transfer arranged use of IV mannitol/
frusemide may be required.
Diffuse cerebral oedema may require decompressive craniotomy
Exploratory Burr Holes have little management in modern practice except
where scanning may be unavailable and to thus facilitate creation of formal
craniotomy flap
Depressed skull fractures that are open require formal surgical reduction
and debridement, closed injuries may be managed non operatively if there is
minimal displacement.
ICP monitoring is appropriate in those who have GCS 3-8 and normal CT
scan.
ICP monitoring is mandatory in those who have GCS 3-8 and abnormal CT
scan.
Hyponatraemia is most likely to be due to syndrome of inappropriate ADH
secretion.
Minimum of cerebral perfusion pressure of 70mmHg in adults.
Minimum cerebral perfusion pressure of between 40 and 70 mmHg in
children.

Interpretation of pupillary findings in head injuries

Pupil size Light response Interpretation

Unilaterally Sluggish or fixed 3rd nerve compression secondary to


dilated tentorial herniation

Bilaterally dilated Sluggish or fixed Poor CNS perfusion


gathered by dr. elbarky

Bilateral 3rd nerve palsy

Unilaterally Cross reactive Optic nerve injury


dilated or equal (Marcus - Gunn)

Bilaterally May be difficult to Opiates


constricted assess Pontine lesions
Metabolic encephalopathy

Unilaterally Preserved Sympathetic pathway disruption


constricted

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C 11.5%

Question 105 of 192

 

An elderly lady who presented with weight loss and malabsorption was found to
have amyloid of the small bowel. On presentation she was found to have
osteomalacia and was hypocalcaemic. Over the past seven days she has received
total parenteral nutrition with adequate calcium replacement. Despite this she
remained hypocalcaemic. Deficiency of which of the following electrolytes is most
likely to account for this process?
gathered by dr. elbarky

Magnesium

Potassium

Sodium

Phosphate

None of the above

Patients with malabsorption may develop magnesium deficiency, although her


TPN feeds may have contained magnesium it may not have been sufficient to
correct her losses. Sodium, phosphate and potassium would not have this effect
on serum calcium.

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Combined deficiency of magnesium and calcium

Magnesium is required for both PTH secretion and its action on target tissues.
Hypomagnesaemia may both cause hypocalcaemia and render patients
unresponsive to treatment with calcium and vitamin D supplementation.

Magnesium is the fourth most abundant cation in the body. The body contains
1000mmol, with half contained in bone and the remainder in muscle, soft tissues
and extracellular fluid. There is no one specific hormonal control of magnesium
and various hormones including PTH and aldosterone affect the renal handling of
magnesium.

Magnesium and calcium interact at a cellular level also and as a result decreased
magnesium will tend to affect the permeability of cellular membranes to calcium,
resulting in hyperexcitability.

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A 55.6%
B 6.7%
C 5.4%
D 26.8%
E 5.5%

55.6% of users answered this question correctly

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Question 106 of 192

 

Which of the following drugs does not interfere with the laboratory analysis of
serum cortisol levels?

Dexamethasone

Prednisolone
gathered by dr. elbarky

Hydrocortisone IV

Hydrocortisone PO

Hydrocortisone IM

Prednisolone and it's metabolites can chemically mimic cortisol in radio-


immunoassay techniques of laboratory analysis.

Dexamethasone can be given as glucorticoid replacement during testing for


addisons or adrenal insufficiency as it does not interfere with cortisol levels. For
example, if you have a patient with polymyalgia rheumatica and they are on long
term prednisolone, you can replace the prednisolone with dexamethasone to
undertake a short synacthen test.

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Cortisol
Glucocorticoid
Released by zona fasiculata of the adrenal gland
90% protein bound; 10% active
Circadian rhythm: High in the mornings
Negative feedback via ACTH

Actions
Glycogenolysis
Gluconeogenesis
Protein catabolism
Lipolysis
Stress response
Anti-inflammatory
Decrease protein in bones
gathered by dr. elbarky

Increase gastric acid


Increases neutrophils/platelets/red blood cells
Inhibits fibroblastic activity

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B 20%
C 7.7%
D 16.7%
E 12.5%

43% of users answered this question correctly

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Question 107 of 192

 

A 55 year old male is diagnosed with carcinoma of the head of the pancreas. He
reports that his stool sticks to the commode and will not flush away. Loss of which
of the following enzymes is most likely to be responsible for this problem?

Lipase

Amylase
gathered by dr. elbarky

Trypsin

Elastase

None of the above

Loss of lipase is one of the key features in the development of steatorrhoea which
typically consists of pale and offensive stools that are difficult to flush away.

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Pancreatic cancer

Adenocarcinoma
Risk factors: Smoking, diabetes, adenoma, familial adenomatous polyposis
Mainly occur in the head of the pancreas (70%)
Spread locally and metastasizes to the liver
Carcinoma of the pancreas should be differentiated from other
periampullary tumours with better prognosis

Clinical features
Weight loss
Painless jaundice
Epigastric discomfort (pain usually due to invasion of the coeliac plexus is a
late feature)
Pancreatitis
Trousseau's sign: migratory superficial thrombophlebitis

Investigations
USS: May miss small lesions
CT Scanning (pancreatic protocol). If unresectable on CT then no further
staging needed
PET/CT for those with operable disease on CT alone
ERCP/ MRI for bile duct assessment
Staging laparoscopy to exclude peritoneal disease

Management
gathered by dr. elbarky

Head of pancreas: Whipple's resection (SE dumping and ulcers). Newer


techniques include pylorus preservation and SMA/ SMV resection
Carcinoma body and tail: poor prognosis, distal pancreatectomy, if operable
Usually adjuvent chemotherapy for resectable disease
ERCP and stent for jaundice and palliation
Surgical bypass may be needed for duodenal obstruction

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E 6%

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Question 108 of 192

 

Which of the following substances related to thyroid function has its secretion
inhibited by increased plasma T3 and T4?

T3

T4
gathered by dr. elbarky

Thyroglobulin

Thyroxin binding globulin

Thyroid stimulating hormone

TSH release is inhibited by negative feedback.

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Thyroid hormones

Hormones of the thyroid gland

Triiodothyronine Major hormone active in target cells


T3

Thyroxine T4 Most prevalent form in plasma, less biologically active


than T3

Calcitonin Lowers plasma calcium

Synthesis and secretion of thyroid hormones


Thyroid actively concentrates iodide to twenty five times the plasma
concentration.
Iodide is oxidised by peroxidase in the follicular cells to atomic iodine which
then iodinates tyrosine residues contained in thyroglobulin.
Iodinated tyrosine residues in thyroglobulin undergo coupling to either T3 or
T4.
Process is stimulated by TSH, which stimulates secretion of thyroid
hormones.
The normal thyroid has approximately 3 month reserves of thyroid
hormones.

LATS and Graves disease


In Graves disease patients develop IgG antibodies to the TSH receptors on the
thyroid gland. This results in chronic and long term stimulation of the gland with
release of thyroid hormones. The typically situation is raised thyroid hormones and
low TSH. Thyroid receptor autoantibodies should be checked in individuals
gathered by dr. elbarky

presenting with hyperthyroidism as they are present in up to 85% cases.

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B 4.6%
C 6.6%
D 5.5%
E 78.4%

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Question 110 of 192

 

Which one of the following is associated with increased lung compliance?

Kyphosis

Pulmonary oedema

Emphysema
gathered by dr. elbarky

Pulmonary fibrosis

Pneumonectomy

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Respiratory physiology: 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 alveolar walls and associated elastic tissue

Causes of decreased compliance


pulmonary oedema
pulmonary fibrosis
pneumonectomy
kyphosis

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B 6.2%
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C 65%
D 10%
E 9.8%

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Question 109 of 192

 

Which of the following areas is predominantly concerned with thermoregulation?

Hypothalamus

Anterior pituitary

Cerebellum
gathered by dr. elbarky

Brain stem

Temporal lobe

The hypothalamus is primarily concerned with thermoregulation. It may relay to the


cerebral cortex to induce behavioural adaptation to facilitate the thermoregulatory
process.

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Thermoregulation

The hypothalamus is the main centre for thermoregulation. Peripheral and


central thermoreceptors relay to this region.
Central thermoreceptors play the main role in maintenance of core
temperature.
Hypothalamus may initiate involuntary motor responses to raise body
temperature (e.g.shivering). It will also stimulate the sympathetic nervous
system to produce peripheral vasoconstriction and release of adrenaline
from the adrenal medulla.
Heat loss is governed by behavioural responses and by autonomic
responses including peripheral vasodilation.
Heat loss can be maintained within the thermoneutral zone (25 to 30
degrees) although the absolute value depends upon atmospheric humidity.
Sepsis results in the release of cytokines that reset the thermoregulatory
centre resulting in fever.

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Question 111 of 192

 

Which of the following is not a major function of the spleen in adults?

Iron reutilisation

Storage of platelets

Storage of monocytes
gathered by dr. elbarky

Haematopoeisis in haematological disorders

Storage red blood cells

The reservoir function of the spleen is less marked in humans than other animals
(e.g. pigs) and in normal individuals it can sequester between 5 and 10% of the red
cell mass. The other stated processes are major splenic functions and this
accounts for the answer provided.

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Spleen

The spleen is located in the left upper quadrant of the abdomen and its size can
vary depending upon the amount of blood it contains. The typical adult spleen is
12.5cm long and 7.5cm wide. The usual weight of the adult spleen is 150g.
The exact position of the spleen can vary with respiratory activity, posture and the
state of surrounding viscera. It usually lies obliquely with its long axis aligned to
the 9th, 10th and 11th ribs. It is separated from these ribs by both diaphragm and
pleural cavity. The normal spleen is not palpable.

The shape of the spleen is influenced by the state of the colon and stomach.
Gastric distension will cause the spleen to resemble the shape of an orange
segment. Colonic distension will cause it to become more tetrahedral.
The spleen is almost entirely covered by peritoneum, which adheres firmly to its
capsule. Recesses of the greater sac separate it from the stomach and kidney. It
develops from the upper dorsal mesogastrium, remaining connected to the
posterior abdominal wall and stomach by two folds of peritoneum; the lienorenal
ligament and gastrosplenic ligament. The lienorenal ligament is derived from
peritoneum where the wall of the general peritoneum meets the omental bursa
between the left kidney and spleen; the splenic vessels lie in its layers. The
gastrosplenic ligament also has two layers, formed by the meeting of the walls of
the greater sac and omental bursa between spleen and stomach, the short gastric
and left gastroepiploic branches of the splenic artery pass in its layers. Laterally,
the spleen is in contact with the phrenicocolic ligament.

Relations
gathered by dr. elbarky

Superiorly Diaphragm

Anteriorly Gastric impression

Posteriorly Kidney

Inferiorly Colon

Tail of pancreas and splenic vessels (splenic artery divides here, branches pass
Hilum
to the white pulp transporting plasma)

Contents
White Immune function. Contains central trabecular artery. The germinal centres are
pulp supplied by arterioles called penicilliary radicles.

Red
Filters abnormal red blood cells.
pulp

Function
Filtration of abnormal blood cells and foreign bodies such as bacteria.
Immunity: IgM. Production of properdin, and tuftsin which help target fungi
and bacteria for phagocytosis.
Haematopoiesis: up to 5th month gestation or in haematological disorders.
Pooling: storage of 40% platelets.
Iron reutilisation
Storage monocytes

Disorders of the spleen


Massive splenomegaly
Myelofibrosis
Chronic myeloid leukaemia
Visceral leishmaniasis (kala-azar)
Malaria
Gaucher's syndrome
Other causes (as above plus)
Portal hypertension e.g. secondary to cirrhosis
Lymphoproliferative disease e.g. CLL, Hodgkin's
Haemolytic anaemia
Infection: hepatitis, glandular fever
Infective endocarditis
Sickle-cell*, thalassaemia
Rheumatoid arthritis (Felty's syndrome)

*the majority of adult patients with sickle-cell will have an atrophied spleen due to
repeated infarction
gathered by dr. elbarky

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26

27

28

29

30

31

32

33

34
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35

36

37

38

39

40

41

42

43

44

45

46

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48

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52

53

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55

Question 112 of 192

 

A 55 year old man undergoes a laparotomy and repair of incisional hernia. Which
of the following hormones is least likely to be released in increased quantities
following the procedure?

Insulin

ACTH
gathered by dr. elbarky

Glucocorticoids

Aldosterone

Growth hormone

Insulin and thyroxine are often have reduced levels of secretion in the post
operative period. This, coupled with increased glucocorticoid release may cause
difficulty in management of diabetes in individuals with insulin resistance.

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Stress response: Endocrine and metabolic changes

Surgery precipitates hormonal and metabolic changes causing the stress


response.
Stress response is associated with: substrate mobilization, muscle protein
loss, sodium and water retention, suppression of anabolic hormone
secretion, activation of the sympathetic nervous system, immunological and
haematological changes.
The hypothalamic-pituitary axis and the sympathetic nervous systems are
activated and there is a failure of the normal feedback mechanisms of
control of hormone secretion.
A summary of the hormonal changes associated with the stress response:

Increased Decreased No Change

Growth hormone Insulin Thyroid stimulating


hormone

Cortisol Testosterone Luteinizing hormone

Renin Oestrogen Follicle stimulating


hormone

Adrenocorticotrophic hormone
(ACTH)
gathered by dr. elbarky

Aldosterone

Prolactin

Antidiuretic hormone

Glucagon

Sympathetic nervous system


Stimulates catecholamine release
Causes tachycardia and hypertension

Pituitary gland
ACTH and growth hormone (GH) is stimulated by hypothalamic releasing
factors, corticotrophin releasing factor (CRF) and somatotrophin (or growth
hormone releasing factor)
Perioperative increased prolactin secretion occurs by release of inhibitory
control
Secretion of thyroid stimulating hormone (TSH), luteinizing hormone (LH)
and follicle stimulating hormone (FSH) does not change significantly
ACTH stimulates cortisol production within a few minutes of the start of
surgery. More ACTH is produced than needed to produce a maximum
adrenocortical response.

Cortisol
Significant increases within 4-6 hours of surgery (>1000 nmol litre-1).
The usual negative feedback mechanism fails and concentrations of ACTH
and cortisol remain persistently increased.
The magnitude and duration of the increase correlate with the severity of
stress and the response is not abolished by the administration of
corticosteroids.
The metabolic effects of cortisol are enhanced:

Skeletal muscle protein breakdown to provide gluconeogenic precursors and


amino acids for protein synthesis in the liver
Stimulation of lipolysis
'Anti-insulin effect'
Mineralocorticoid effects
Anti-inflammatory effects

Growth hormone
gathered by dr. elbarky

Increased secretion after surgery has a minor role


Most important for preventing muscle protein breakdown and promote
tissue repair by insulin growth factors

Alpha Endorphin
Increased

Antidiuretic hormone
An important vasopressor and enhances haemostasis
Renin is released causing the conversion of angiotensinogen to angiotensin
I
Angiotensin II formed by ACE on angiotensin 1, which causes the secretion
of aldosterone from the adrenal cortex. This increases sodium reabsorption
at the distal convoluted tubule

Insulin
Release inhibited by stress
Occurs via the inhibition of the beta cells in the pancreas by the α2-
adrenergic inhibitory effects of catecholamines
Insulin resistance by target cells occurs later
The perioperative period is characterized by a state of functional insulin
deficiency

Thyroxine (T4) and tri-iodothyronine (T3)


Circulating concentrations are inversely correlated with sympathetic activity
and after surgery there is a reduction in thyroid hormone production, which
normalises over a few days.

Metabolic effect of endocrine response

Carbohydrate metabolism
Hyperglycaemia is a main feature of the metabolic response to surgery
Due to increase in glucose production and a reduction in glucose utilization
Catecholamines and cortisol promote glycogenolysis and gluconeogenesis
Initial failure of insulin secretion followed by insulin resistance affects the
normal responses
The proportion of the hyperglycaemic response reflects the severity of
surgery
Hyperglycaemia impairs wound healing and increase infection rates

Protein metabolism
Initially there is inhibition of protein anabolism, followed later, if the stress
response is severe, by enhanced catabolism
The amount of protein degradation is influenced by the type of surgery and
also by the nutritional status of the patient
gathered by dr. elbarky

Mainly skeletal muscle protein is affected


The amino acids released form acute phase proteins (fibrinogen, C reactive
protein, complement proteins, a2-macroglobulin, amyloid A and
ceruloplasmin) and are used for gluconeogenesis
Nutritional support has little effect on preventing catabolism

Lipid metabolism
Increased catecholamine, cortisol and glucagon secretion, and insulin deficiency,
promotes lipolysis and ketone body production.

Salt and water metabolism


ADH causes water retention, concentrated urine, and potassium loss and
may continue for 3 to 5 days after surgery
Renin causes sodium and water retention

Cytokines
Glycoproteins
Interleukins (IL) 1 to 17, interferons, and tumour necrosis factor
Synthesized by activated macrophages, fibroblasts, endothelial and glial
cells in response to tissue injury from surgery or trauma
IL-6 main cytokine associated with surgery. Peak 12 to 24 h after surgery
and increase by the degree of tissue damage Other effects of cytokines
include fever, granulocytosis, haemostasis, tissue damage limitation and
promotion of healing.

Modifying the response


Opioids suppress hypothalamic and pituitary hormone secretion
At high doses the hormonal response to pelvic and abdominal surgery is
abolished. However, such doses prolong recovery and increase the need for
postoperative ventilatory support
Spinal anaesthesia can reduce the glucose, ACTH, cortisol, GH and
epinephrine changes, although cytokine responses are unaltered
Cytokine release is reduced in less invasive surgery
Nutrition prevents the adverse effects of the stress response. Enteral
feeding improves recovery
Growth hormone and anabolic steroids may improve outcome
Normothermia decreases the metabolic response

References
Deborah Burton, Grainne Nicholson, and George Hall
Endocrine and metabolic response to surgery .

Contin Educ Anaesth Crit Care Pain (2004) 4(5): 144-147 doi:10.1093/bjaceaccp
/mkh040
gathered by dr. elbarky

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Question 113 of 192

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Which of the following stimulates prolactin release or action?

Leutinising hormone

Dopamine

Thyrotropin releasing hormone


gathered by dr. elbarky

Oestrogen

Follicle stimulating hormone

TRH stimulates prolactin release. Dopamine suppresses the release of prolactin.

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Prolactin

Prolactin is a peptide hormone released from the anterior pituitary. It is under tonic
dopamine inhibition, thyrotropin releasing hormone has a stimulatory effect on
release. Prolactin release stimulates milk production but also reduces gonadal
activity. It decreases GnRH pulsatility at the hypothalamic level and to a lesser
extent, blocks the action of LH on the ovary or testis.

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E 8.9%
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Question 114 of 192

 

Which one of the following reduces the secretion of renin?

Erect posture

Adrenaline

Hyponatraemia
gathered by dr. elbarky

Hypotension

Beta-blockers

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Renin

Renin is secreted by juxtaglomerular cells and hydrolyses angiotensinogen to


produce angiotensin I

Factors stimulating renin secretion


Hypotension causing reduced renal perfusion
Hyponatraemia
Sympathetic nerve stimulation
Catecholamines
Erect posture

Factors reducing renin secretion


Drugs: beta-blockers, NSAIDs

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C 11.4%
D 7.3%
E 46.4%

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Question 115 of 192

 

A 22 year old lady receives intravenous morphine for acute abdominal pain. Which
of the following best accounts for its analgesic properties?

Binding to δ opioid receptors in the brainstem

Binding to δ opioid receptors at peripheral nerve sites


gathered by dr. elbarky

Binding to β opioid receptors within the CNS

Binding to α opioid receptors within the CNS

Binding to µ opioid receptors within the CNS

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.

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Morphine

Strong opiate analgesic. It is a pro- type narcotic drug and its effects mediated via
the 4 types of opioid receptor. Its clinical effects stem from binding to these
receptor sites within the CNS and gastrointestinal tract. Unwanted side effects
include nausea, constipation, respiratory depression and, if used long term,
addiction .
It may be administered orally or intravenously. It can be reversed with naloxone.

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gathered by dr. elbarky

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Question 116 of 192

 

A 77 year old man presents to pre operative clinic for a total knee replacement. He
is on furosemide for hypertension. He is known to have multiple myeloma. He is
found to have the following test results:
Na 120

Serum osmolality 280 (normal)

Urine osmolality normal


gathered by dr. elbarky

Urine Na normal

What is the most likely cause?

Pseudohyponatraemia

Syndrome of inappropriate ADH secretion (SIADH)

Hypotonic hypovolaemic hyponatraemia

Psychogenic polydipsia

Hypertonic hypovolaemic hyponatraemia

Hyperlipidaemia and multiple myeloma are known to cause a


pseudohyponatraemia, this is due to raised protein.

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Hyponatraemia

This is commonly tested in the MRCS (despite most surgeons automatically


seeking medical advice if this occurs!). The most common cause in surgery is the
over administration of 5% dextrose.
Hyponatraemia may be caused by water excess or sodium depletion. Causes of
pseudohyponatraemia include hyperlipidaemia (increase in serum volume) or a
taking blood from a drip arm. Urinary sodium and osmolarity levels aid making a
diagnosis.

Classification

Urinary sodium > 20 Sodium depletion, renal loss Mnemonic:


mmol/l Patient often Syndrome of
hypovolaemic INAPPropriate Anti-
Diuretics (thiazides) Diuretic Hormone:
Addison's In creased
Diuretic stage of renal Na (sodium)
gathered by dr. elbarky

failure PP (urine)
SIADH (serum osmolality
low, urine osmolality high,
urine Na high)
Patient often euvolaemic

Urinary sodium < 20 Sodium depletion, extra-renal


mmol/l loss
Diarrhoea, vomiting,
sweating
Burns, adenoma of
rectum (if villous lesion
and large)

Water excess Secondary


(patient often hyperaldosteronism: CCF,
hypervolaemic and cirrhosis
oedematous) Reduced GFR: renal
failure
IV dextrose, psychogenic
polydipsia

Management

Symptomatic Hyponatremia :

Acute hyponatraemia with Na <120: immediate therapy. Central Pontine


Myelinolisis, may occur from overly rapid correction of serum sodium. Aim to
correct until the Na is > 125 at a rate of 1 mEq/h. Normal saline with frusemide is
an alternative method.
The sodium requirement can be calculated as follows :

(125 - serum sodium) x 0.6 x body weight = required mEq of sodium

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Question 117 of 192

 

A homeless 42 year old male had an emergency inguinal hernia repair 24 hours
previously. He has a BMI of 15. He has been put on a feeding regime of 35
kcal/kg/day with no additional medications. The nursing staff contact you as he
has become confused and unsteady. On examination the patient is disorientated
to place, has diplopia and nystagmus. What is the most likely diagnosis?

Cerebellar stroke
gathered by dr. elbarky

Acute dystonic reaction

Cerebrovascular accident

Parkinsonism

Wernickes encephalopathy

Triad of Wernicke encephalopathy:


Acute confusion
Ataxia
Ophthalmoplegia

This patient has received a carbohydrate rich diet without any thiamine or vitamin
B co strong replacement. This has led to Wernickes encephalopathy, which
classically presents with confusion, ataxia and ophthalmoplegia. Characteristically
it is associated with chronic alcoholism, however it is also known to occur post
bariatric surgery.

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Nutrition - Refeeding syndrome


Refeeding syndrome describes the metabolic abnormalities which occur on
feeding a person following a period of starvation. The metabolic consequences
include:
Hypophosphataemia
Hypokalaemia
Hypomagnesaemia
Abnormal fluid balance

These abnormalities can lead to organ failure.

Re-feeding problems
If patient not eaten for > 5 days, aim to re-feed at < 50% energy and protein levels

High risk for re-feeding problems


If one or more of the following:
gathered by dr. elbarky

BMI < 16 kg/m2


Unintentional weight loss >15% over 3-6 months
Little nutritional intake > 10 days
Hypokalaemia, Hypophosphataemia or hypomagnesaemia prior to feeding
(unless high)

If two or more of the following:


BMI < 18.5 kg/m2
Unintentional weight loss > 10% over 3-6 months
Little nutritional intake > 5 days
History of: alcohol abuse, drug therapy including insulin, chemotherapy,
diuretics and antacids

Prescription
Start at up to 10 kcal/kg/day increasing to full needs over 4-7 days
Start immediately before and during feeding: oral thiamine 200-300mg/day,
vitamin B co strong 1 tds and supplements
Give K+ (2-4 mmol/kg/day), phosphate (0.3-0.6 mmol/kg/day), magnesium
(0.2-0.4 mmol/kg/day)

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Question 118 of 192

 

A patient has an arterial blood gas sample which provides the following result:
pH 7.20

pO2 7.5

Bicarbonate 22

pCO2 8.1
gathered by dr. elbarky

Chloride 10meq

What is the most likely cause?

Type II respiratory failure

Metabolic acidosis with increased anion gap

Metabolic alkalosis

Type I respiratory failure

Respiratory alkalosis

This is a sign of acute type 2 respiratory failure (non compensated). This is the
result of carbon dioxide retention.

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Disorders of acid - base balance

Disorders of acid- base balance are often covered in the MRCS part A.

The acid-base normogram below shows how the various disorders may be
categorised
gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb072b.png)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Acid-base
/images_eMRCS/swb072b.png)
homeostasis)

Metabolic acidosis
This is the most common surgical acid - base disorder.
Reduction in plasma bicarbonate levels.
Two mechanisms:

1. Gain of strong acid (e.g. diabetic ketoacidosis)


2. Loss of base (e.g. from bowel in diarrhoea)
- Classified according to the anion gap, this can be calculated by:
(Na+ + K+) - (Cl- + HCO3-).
- If a question supplies the chloride level then this is often a clue that the anion gap
should be calculated. The normal range = 10-18 mmol/L

Normal anion gap ( = hyperchloraemic metabolic acidosis)


Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
Renal tubular acidosis
Drugs: e.g. acetazolamide
Ammonium chloride injection
Addison's disease

Raised anion gap


Lactate: shock, hypoxia
Ketones: diabetic ketoacidosis, alcohol
Urate: renal failure
Acid poisoning: salicylates, methanol

Metabolic acidosis secondary to high lactate levels may be subdivided into two
types:
Lactic acidosis type A: (Perfusion disorders e.g.shock, hypoxia, burns)
Lactic acidosis type B: (Metabolic e.g. metformin toxicity)

Metabolic alkalosis
Usually caused by a rise in plasma bicarbonate levels.
Rise of bicarbonate above 24 mmol/L will typically result in renal excretion
of excess bicarbonate.
Caused by a loss of hydrogen ions or a gain of bicarbonate. It is due mainly
gathered by dr. elbarky

to problems of the kidney or gastrointestinal tract

Causes
Vomiting / aspiration (e.g. Peptic ulcer leading to pyloric stenosis,
nasogastric suction)
Diuretics
Liquorice, carbenoxolone
Hypokalaemia
Primary hyperaldosteronism
Cushing's syndrome
Bartter's syndrome
Congenital adrenal hyperplasia

Mechanism of metabolic alkalosis


Activation of renin-angiotensin II-aldosterone (RAA) system is a key factor
Aldosterone causes reabsorption of Na+ in exchange for H+ in the distal
convoluted tubule
ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA
system → raised aldosterone levels
In hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+
into cells to maintain neutrality

Respiratory acidosis
Rise in carbon dioxide levels usually as a result of alveolar hypoventilation
Renal compensation may occur leading to Compensated respiratory acidosis

Causes
COPD
Decompensation in other respiratory conditions e.g. Life-threatening asthma
/ pulmonary oedema
Sedative drugs: benzodiazepines, opiate overdose

Respiratory alkalosis
Hyperventilation resulting in excess loss of carbon dioxide
This will result in increasing pH

Causes
Psychogenic: anxiety leading to hyperventilation
Hypoxia causing a subsequent hyperventilation: pulmonary embolism, high
altitude
Early salicylate poisoning*
CNS stimulation: stroke, subarachnoid haemorrhage, encephalitis
Pregnancy
gathered by dr. elbarky

*Salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis.


Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst
later the direct acid effects of salicylates (combined with acute renal failure) may
lead to an acidosis

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Question 119 of 192

 

The oxygen-haemoglobin dissociation curve is shifted to the left in:

With decreased 2,3-DPG in transfused red cells

Respiratory acidosis

Sudden move to high altitude


gathered by dr. elbarky

Pyrexia

Haemolytic anaemia

S shaped curve

The curve is shifted to the left when there is a decreased oxygen requirement by
the tissue. This includes:
1. Hypothermia
2. Alkalosis
3. Reduced levels of DPG:
DPG is found in erythrocytes and is reduced in non exercising muscles, i.e.
when there is reduced glycolysis.

4. Polycythaemia

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Oxygen Transport

Oxygen transport
Almost all oxygen is transported within erythrocytes. It has limited solubility and
only 1% is carried as solution. Therefore the amount of oxygen transported will
depend upon haemoglobin concentration and its degree of saturation.

Haemoglobin
Globular protein composed of 4 subunits. Haem consists of a protoporphyrin ring
surrounding an iron atom in its ferrous state. The iron can form two additional
bonds; one with oxygen and the other with a polypeptide chain. There are two
alpha and two beta subunits to this polypeptide chain in an adult and together
these form globin. Globin cannot bind oxygen but is able to bind to carbon dioxide
and hydrogen ions, the beta chains are able to bind to 2,3 diphosphoglycerate. The
oxygenation of haemoglobin is a reversible reaction. The molecular shape of
haemoglobin is such that binding of one oxygen molecule facilitates the binding of
subsequent molecules.
gathered by dr. elbarky

Oxygen dissociation curve


The oxygen dissociation curve describes the relationship between the
percentage of saturated haemoglobin and partial pressure of oxygen in the
blood. It is not affected by haemoglobin concentration.
Chronic anaemia causes 2, 3 DPG levels to increase, hence shifting the
curve to the right

Haldane effect
Shifts to left = for given oxygen tension there is increased saturation of Hb
with oxygen i.e. Decreased oxygen delivery to tissues

Bohr effect
Shifts to right = for given oxygen tension there is reduced saturation of Hb
with oxygen i.e. Enhanced oxygen delivery to tissues
gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb038b.png)
Image sourced from Wikipedia
(http://en.wikipedia.org/wiki/Oxygen (https://d2zgo9qer4wjf4.cloudfront.net
%E2%80%93haemoglobin dissociation /images_eMRCS/swb038b.png)
curve)

Shifts to Left = Lower oxygen delivery Shifts to Right = Raised oxygen


HbF, methaemoglobin, delivery
carboxyhaemoglobin raised [H+] (acidic)
low [H+] (alkali) raised pCO2
low pCO2 raised 2,3-DPG*
low 2,3-DPG raised temperature
low temperature

*2,3-diphosphoglycerate

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Question 120 of 192

 

A 72-year-old woman is admitted to the acute surgical unit with profuse vomiting.
Admission bloods show the following:

Na+ 131 mmol/l

K+ 2.2 mmol/l

Urea 3.1 mmol/l


gathered by dr. elbarky

Creatinine 56 micro mol/l

Glucose 4.3 mmol/l

Which one of the following ECG features is most likely to be seen?

Short PR interval

Short QT interval

Flattened P waves

J waves

U waves

Hypokalaemia - U waves on ECG

J waves are seen in hypothermia whilst delta waves are associated with Wolff
Parkinson White syndrome.

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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!
gathered by dr. elbarky

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Question 121 of 192

 

A 23 year old man has a routine ECG performed. Which part of the tracing obtained
represents atrial repolarisation?

P wave

T wave
gathered by dr. elbarky

Q-T Interval

P-R interval

None of the above

The process of atrial repolarisation is generally not visible on the ECG strip. It
occurs during the QRS complex.

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The normal ECG


gathered by dr. elbarky

Image sourced from Wikipedia (https://d2zgo9qer4wjf4.cloudfront.net


P wave
(http://en.wikipedia.org/wiki/ECG) /images_eMRCS/swb110b.png)
Represents the wave of depolarization that spreads from the SA node
throughout the atria
Lasts 0.08 to 0.1 seconds (80-100 ms)
The isoelectric period after the P wave represents the time in which the
impulse is traveling within the AV node

P-R interval
Time from the onset of the P wave to the beginning of the QRS complex
Ranges from 0.12 to 0.20 seconds in duration
Represents the time between the onset of atrial depolarization and the
onset of ventricular depolarization

QRS complex
Represents ventricular depolarization
Duration of the QRS complex is normally 0.06 to 0.1 seconds

ST segment
Isoelectric period following the QRS
Represents period which the entire ventricle is depolarized and roughly
corresponds to the plateau phase of the ventricular action potential

T wave
Represents ventricular repolarization and is longer in duration than
depolarization
A small positive U wave may follow the T wave which represents the last
remnants of ventricular repolarization.

Q-T interval
Represents the time for both ventricular depolarization and repolarization to
occur, and therefore roughly estimates the duration of an average ventricular
action potential.
Interval ranges from 0.2 to 0.4 seconds depending upon heart rate.
At high heart rates, ventricular action potentials shorten in duration, which
decreases the Q-T interval. Therefore the Q-T interval is expressed as a
'corrected Q-T (QTc)' by taking the Q-T interval and dividing it by the square
root of the R-R interval (interval between ventricular depolarizations). This
allows an assessment of the Q-T interval that is independent of heart rate.
gathered by dr. elbarky

Normal corrected Q-Tc interval is less than 0.44 seconds.

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Question 122 of 192

 

Which one of the following serum proteins is most likely to increase in a patient
with severe sepsis?

Transferrin

Transthyretin
gathered by dr. elbarky

Ferritin

Albumin

Cortisol binding protein

Ferritin can be markedly increased during acute illness. The other parameters tend
to decrease during an acute phase response.

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Acute phase proteins

Acute phase proteins


CRP
procalcitonin
ferritin
fibrinogen
alpha-1 antitrypsin
caeruloplasmin
serum amyloid A
haptoglobin
complement

During the acute phase response the liver decreases the production of other
proteins (sometimes referred to as negative acute phase proteins). Examples
include:
albumin
transthyretin (formerly known as prealbumin)
transferrin
retinol binding protein
cortisol binding protein

Levels of CRP are commonly measured in acutely unwell patients. CRP is a protein
synthesised in the liver and binds to phosphocholine in bacterial cells and on those
cells undergoing apoptosis. In binding to these cells it is then able to activate the
complement system. CRP levels are known to rise in patients following surgery.
However, levels of greater than 150 at 48 hours post operatively are suggestive of
evolving complications.
gathered by dr. elbarky

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Question 123 of 192

 

Which part of the jugular venous waveform is associated with the closure of the
tricuspid valve?

a wave

c wave
gathered by dr. elbarky

x descent

y descent

v wave

JVP: C wave - closure of the tricuspid valve

The c wave of the jugular venous waveform is associated with the closure of the
tricuspid valve.

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Jugular venous pressure


As well as providing information on right atrial pressure, the jugular vein waveform
may provide clues to underlying valvular disease. A non-pulsatile JVP is seen in
superior vena caval obstruction. Kussmaul's sign describes a paradoxical rise in
JVP during inspiration seen in constrictive pericarditis

'a' wave = atrial contraction


large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis,
pulmonary hypertension
absent if in atrial fibrillation

Cannon 'a' waves


caused by atrial contractions against a closed tricuspid valve
are seen in complete heart block, ventricular tachycardia/ectopics, nodal
rhythm, single chamber ventricular pacing
gathered by dr. elbarky

'c' wave
closure of tricuspid valve
not normally visible

'v' wave
due to passive filling of blood into the atrium against a closed tricuspid
valve
giant v waves in tricuspid regurgitation

'x' descent = fall in atrial pressure during ventricular systole

'y' descent = opening of tricuspid valve

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb145b.png)
Image sourced from (https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS
Wikipedia () /swb145b.png)

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C 10.8%
D 15.3%
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Question 124 of 192

 

Which of the following is not an effect of cholecystokinin?

It causes gallbladder contraction

It increases the rate of gastric emptying

It relaxes the sphincter of oddi


gathered by dr. elbarky

It stimulates pancreatic acinar cells

It has a trophic effect on pancreatic acinar cells

It decreases the rate of gastric emptying.

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Gastric secretions

A working knowledge of gastric secretions is important for surgery because peptic


ulcers are common, surgeons frequently prescribe anti secretory drugs and
because there are still patients around who will have undergone acid lowering
procedures (Vagotomy) in the past.

Gastric acid
Is produced by the parietal cells in the stomach
pH of gastric acid is around 2 with acidity being maintained by the H+/K+
ATP ase pump. As part of the process bicarbonate ions will be secreted into
the surrounding vessels.
Sodium and chloride ions are actively secreted from the parietal cell into the
canaliculus. This sets up a negative potential across the membrane and as a
result sodium and potassium ions diffuse across into the canaliculus.
Carbonic anhydrase forms carbonic acid which dissociates and the
hydrogen ions formed by dissociation leave the cell via the H+/K+ antiporter
pump. At the same time sodium ions are actively absorbed. This leaves
hydrogen and chloride ions in the canaliculus these mix and are secreted
into the lumen of the oxyntic gland.

This is illustrated diagrammatically below:


gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb028b.jpg)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Gastric
/images_eMRCS/swb028b.jpg)
acid)

Phases of gastric acid secretion


There are 3 phases of gastric secretion:

1. Cephalic phase (smell / taste of food)


30% acid produced
Vagal cholinergic stimulation causing secretion of HCL and gastrin release
from G cells

2. Gastric phase (distension of stomach )


60% acid produced
Stomach distension/low H+/peptides causes Gastrin release
3. Intestinal phase (food in duodenum)
10% acid produced
High acidity/distension/hypertonic solutions in the duodenum inhibits
gastric acid secretion via enterogastrones (CCK, secretin) and neural
reflexes.

Regulation of gastric acid production


Factors increasing production include:
Vagal nerve stimulation
Gastrin release
Histamine release (indirectly following gastrin release) from
enterchromaffin like cells
gathered by dr. elbarky

Factors decreasing production include:


Somatostatin (inhibits histamine release)
Cholecystokinin
Secretin

The diagram below illustrates some of the factors involved in regulating gastric
acid secretion and the relevant associated pharmacology

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb029b.jpg)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Gastric
/images_eMRCS/swb029b.jpg)
acid)

Below is a brief summary of the major hormones involved in food digestion:

Source Stimulus Actions


Source Stimulus Actions

Gastrin G cells in Distension of Increase HCL, pepsinogen


antrum of stomach, and IF secretion, increases
the extrinsic nerves gastric motility, trophic effect
stomach Inhibited by: low on gastric mucosa
antral pH,
somatostatin

CCK I cells in Partially Increases secretion of


upper digested enzyme-rich fluid from
small proteins and pancreas, contraction of
intestine triglycerides gallbladder and relaxation of
sphincter of Oddi, decreases
gathered by dr. elbarky

gastric emptying, trophic


effect on pancreatic acinar
cells, induces satiety

Secretin S cells in Acidic chyme, Increases secretion of


upper fatty acids bicarbonate-rich fluid from
small pancreas and hepatic duct
intestine cells, decreases gastric acid
secretion, trophic effect on
pancreatic acinar cells

VIP Small Neural Stimulates secretion by


intestine, pancreas and intestines,
pancreas inhibits acid and pepsinogen
secretion

Somatostatin D cells in Fat, bile salts Decreases acid and pepsin


the and glucose in secretion, decreases gastrin
pancreas the intestinal secretion, decreases
and lumen pancreatic enzyme secretion,
stomach decreases insulin and
glucagon secretion
inhibits trophic effects of
gastrin, stimulates gastric
mucous production

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B 48.7%
C 8.1%
D 10.1%
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Question 125 of 192

 

A 24 year old man is injured in a road traffic accident. He becomes oliguric and his
renal function deteriorates. Which of the options below would favor acute tubular
necrosis over pre renal uraemia?

No response to intravenous fluids

Urinary sodium < 20mmol/L


gathered by dr. elbarky

Bland coloured urinary sediment

Increased urine specific gravity

None of the above

In acute tubular necrosis there is no response to intravenous fluids because the


damage occurs from within the renal system rather than as a result of volume
depletion.

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Acute renal failure: Pre renal failure vs. acute tubular necrosis

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%


Pre-renal uraemia Acute tubular necrosis

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

*fractional sodium excretion = (urine sodium/plasma sodium) / (urine


gathered by dr. elbarky

creatinine/plasma creatinine) x 100

**fractional urea excretion = (urine urea /blood urea ) / (urine creatinine/plasma


creatinine) x 100

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C 11.5%
D 16.7%
E 6.4%

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Question 126 of 192

 

Which statement about peristalsis is true?

Longitudinal smooth muscle propels the food bolus through the


oesophagus

Secondary peristalsis occurs when there is no food bolus in the


oesophagus
gathered by dr. elbarky

Food transfer from the oesophagus to the stomach is 4 seconds

Circular smooth muscle is not involved in peristalsis

Peristalsis only occurs in the oesophagus

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Peristalsis

Circular smooth muscle contracts behind the food bolus and longitudinal
smooth muscle propels the food through the oesophagus
Primary peristalsis spontaneously moves the food from the oesophagus
into the stomach (9 seconds)
Secondary peristalsis occurs when food, which doesn't enter the stomach,
stimulates stretch receptors to cause peristalsis
In the small intestine each peristalsis waves slows to a few seconds and
causes mixture of chyme
In the colon three main types of peristaltic activity are recognised (see
below)

Colonic peristalsis
Segmentation Localised contractions in which the bolus is
contractions subjected to local forces to maximise mucosal
absorption

Antiperistaltic Localised reverse peristaltic waves to slow entry


contractions towards into colon and maximise absorption
ileum

Mass movements Waves migratory peristaltic waves along the entire


colon to empty the organ prior to the next ingestion
of food bolus

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B 17.9%
C 16.5%
D 7.3%
E 6.8%

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Question 127 of 192

 

What is the main component of colloid in the thyroid gland?

T3

Thyroglobulin

T4
gathered by dr. elbarky

Thyroxin binding globulin

TSH

It is a high molecular weight protein that acts as a storage form of thyroid


hormones.

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Thyroid hormones

Hormones of the thyroid gland

Triiodothyronine Major hormone active in target cells


T3

Thyroxine T4 Most prevalent form in plasma, less biologically active


than T3

Calcitonin Lowers plasma calcium

Synthesis and secretion of thyroid hormones


Thyroid actively concentrates iodide to twenty five times the plasma
concentration.
Iodide is oxidised by peroxidase in the follicular cells to atomic iodine which
then iodinates tyrosine residues contained in thyroglobulin.
Iodinated tyrosine residues in thyroglobulin undergo coupling to either T3 or
T4.
Process is stimulated by TSH, which stimulates secretion of thyroid
hormones.
The normal thyroid has approximately 3 month reserves of thyroid
hormones.

LATS and Graves disease


In Graves disease patients develop IgG antibodies to the TSH receptors on the
thyroid gland. This results in chronic and long term stimulation of the gland with
release of thyroid hormones. The typically situation is raised thyroid hormones and
low TSH. Thyroid receptor autoantibodies should be checked in individuals
gathered by dr. elbarky

presenting with hyperthyroidism as they are present in up to 85% cases.

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C 9%
D 11.2%
E 5.1%

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Question 128 of 192

 

Which of the following is least likely to cause a prolonged prothrombin time?

Cholestatic jaundice

Disseminated intravascular coagulation

Prolonged antibiotic treatment


gathered by dr. elbarky

Liver disease

Acquired factor 12 deficiency

Vitamin K deficiency results from cholestatic jaundice and prolonged antibiotic


therapy. Acquired factor 12 deficiency causes prolonged APTT.

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Abnormal coagulation

Cause Factors affected

Heparin Prevents activation factors 2,9,10,11

Warfarin Affects synthesis of factors 2,7,9,10

DIC Factors 1,2,5,8,11

Liver disease Factors 1,2,5,7,9,10,11

Interpretation blood clotting test results


Disorder APTT PT Bleeding time

Haemophilia Increased Normal Normal

von Willebrand's disease Increased Normal Increased

Vitamin K deficiency Increased Increased Normal

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A 10.3%
B 11.2%
C 27.6%
D 9.8%
E 41%

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Question 129 of 192

 

A 73 year old female is referred to the surgical clinic with an iron deficiency
anaemia. As part of the diagnostic work up the doctor requests a serum ferritin
level. Which of the conditions listed is most likely to lead to a falsely elevated
result?

Locally perforated sigmoid colonic adenocarcinoma


gathered by dr. elbarky

Colonic angiodysplasia

Dieulafoy lesion of the stomach

Transitional cell carcinoma of the bladder

Endometrial adenocarcinoma

A locally perforated colonic tumour will typically cause an intense inflammatory


response and if peritonitis is not present clinically then at the very least a localised
abscess. This inflammatory process is the most likely (from the list) to falsely
raise the serum ferritin level. Angiodysplasia and dieulafoy lesions are mucosal
arteriovenous malformations and unlikely to result in considerable inflammatory
activity.

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Ferritin

Ferritin is an intracellular protein that binds iron and stores it to be released in a


controlled fashion at sites where iron is required. Because iron and ferritin are
bound the total body ferritin levels may be decreased in cases of iron deficiency
anaemia. Measurement of serum ferritin levels can be useful in determining
whether an apparently low haemoglobin and microcytosis is truly caused by an
iron deficiency state.
Ferritin is an acute phase protein and may be synthesised in increased quantities
in situations where inflammatory activity is ongoing. Falsely elevated results may
therefore be encountered clinically and need to be taken in context of the clinical
picture and full blood count results.

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C 25.4%
D 9.3%
E 9%

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Question 130 of 192

 

A 48 year old man undergoes a right hemicolectomy for a large caecal polyp. In the
immediate post operative period which of the physiological processes described
below is least likely to occur?

Glycogenolysis

Increased production of acute phase proteins


gathered by dr. elbarky

Increased cortisol production

Bronchoconstriction

Release of nitric oxide by vessels

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Response to surgery

Sympathetic nervous system


Noradrenaline from sympathetic nerves and adrenaline from adrenal
medulla
Blood diverted from skin and visceral organs; bronchodilatation, reduced
intestinal motility, increased glucagon and glycogenolysis, insulin reduced
Heart rate and myocardial contractility are increased

Acute phase response


TNF-α, IL-1, IL-2, IL-6, interferon and prostaglandins are released
Excess cytokines may cause SIRS
Cytokines increase the release of acute phase proteins

Endocrine response
Hypothalamus, pituitary, adrenal axis
Increases ACTH and cortisol production:

increases protein breakdown


increases blood glucose levels
Aldosterone increases sodium re-absorption
Vasopressin increases water re-absorption and causes vasoconstriction

Vascular endothelium
Nitric oxide produces vasodilatation
Platelet activating factor enhances the cytokine response
Prostaglandins produce vasodilatation and induce platelet aggregation
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C 8.9%
D 55.9%
E 16.8%

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Question 131 of 192

 

Which of the following is the equivalent of cardiac preload?

End diastolic volume

Stroke volume

Systemic vascular resistance


gathered by dr. elbarky

Mean arterial pressure

Peak systolic arterial pressure

Preload is the same as end diastolic volume. When it is increased slightly there is
an associated increase in cardiac output (Frank Starling principle). When it is
markedly increased e.g. over 250ml then cardiac output falls.

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Cardiac physiology

The heart has four chambers ejecting blood into both low pressure and high
pressure systems.
The pumps generate pressures of between 0-25mmHg on the right side and
0-120 mmHg on the left.
At rest diastole comprises 2/3 of the cardiac cycle.
The product of the frequency of heart rate and stroke volume combine to
give the cardiac output which is typically 5-6L per minute.

Detailed descriptions of the various waveforms are often not a feature of MRCS A
(although they are on the syllabus). However, they are a very popular topic for
surgical physiology in the MRCS B exam.
Electrical properties
Intrinsic myogenic rhythm within cardiac myocytes means that even the
denervated heart is capable of contraction.
In the normal situation the cardiac impulse is generated in the sino atrial
node in the right atrium and conveyed to the ventricles via the
atrioventricular node.
The sino atrial node is also capable of spontaneous discharge and in the
absence of background vagal tone will typically discharge around 100x per
minute. Hence the higher resting heart rate found in cardiac transplant
cases. In the SA and AV nodes the resting membrane potential is lower than
in surrounding cardiac cells and will slowly depolarise from -70mV to around
-50mV at which point an action potential is generated.
Differences in the depolarisation slopes between SA and AV nodes help to
explain why the SA node will depolarise first. The cells have a refractory
gathered by dr. elbarky

period during which they cannot be re-stimulated and this period allows for
adequate ventricular filling. In pathological tachycardic states this time
period is overridden and inadequate ventricular filling may then occur,
cardiac output falls and syncope may ensue.

Parasympathetic fibres project to the heart via the vagus and will release
acetylcholine. Sympathetic fibres release nor adrenaline and circulating adrenaline
comes from the adrenal medulla. Noradrenaline binds to β 1 receptors in the SA
node and increases the rate of pacemaker potential depolarisation.

Cardiac cycle

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb034b.png)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Cardiac
/images_eMRCS/swb034b.png)
cycle)

Mid diastole: AV valves open. Ventricles hold 80% of final volume. Outflow
valves shut. Aortic pressure is high.
Late diastole: Atria contract. Ventricles receive 20% to complete filling.
Typical end diastolic volume 130-160ml.

Early systole: AV valves shut. Ventricular pressure rises. Isovolumetric


ventricular contraction. AV Valves bulge into atria (c-wave). Aortic and
pulmonary pressure exceeded- blood is ejected. Shortening of ventricles
pulls atria downwards and drops intra atrial pressure (x-descent).

Late systole: Ventricular muscles relax and ventricular pressures drop.


Although ventricular pressure drops the aortic pressure remains constant
owing to peripheral vascular resistance and elastic property of the aorta.
Brief period of retrograde flow that occurs in aortic recoil shuts the aortic
gathered by dr. elbarky

valve. Ventricles will contain 60ml end systolic volume. The average stroke
volume is 70ml (i.e. Volume ejected).

Early diastole: All valves are closed. Isovolumetric ventricular relaxation


occurs. Pressure wave associated with closure of the aortic valve increases
aortic pressure. The pressure dip before this rise can be seen on arterial
waveforms and is called the incisura. During systole the atrial pressure
increases such that it is now above zero (v- wave). Eventually atrial pressure
exceed ventricular pressure and AV valves open - atria empty passively into
ventricles and atrial pressure falls (y -descent )

The negative atrial pressures are of clinical importance as they can allow air
embolization to occur if the neck veins are exposed to air. This patient positioning
is important in head and neck surgery to avoid this occurrence if veins are
inadvertently cut, or during CVP line insertion.

Mechanical properties
Preload = end diastolic volume
Afterload = aortic pressure

It is important to understand the principles of Laplace's law in surgery.


It states that for hollow organs with a circular cross section, the total
circumferential wall tension depends upon the circumference of the wall,
multiplied by the thickness of the wall and on the wall tension.
The total luminal pressure depends upon the cross sectional area of the
lumen and the transmural pressure. Transmural pressure is the internal
pressure minus external pressure and at equilibrium the total pressure must
counterbalance each other.
In terms of cardiac physiology the law explains that the rise in ventricular
pressure that occurs during the ejection phase is due to physical change in
heart size. It also explains why a dilated diseased heart will have impaired
systolic function.
Starlings law
Increase in end diastolic volume will produce larger stroke volume.
This occurs up to a point beyond which cardiac fibres are excessively
stretched and stroke volume will fall once more. It is important for the
regulation of cardiac output in cardiac transplant patients who need to
increase their cardiac output.

Baroreceptor reflexes
Baroreceptors located in aortic arch and carotid sinus.
Aortic baroreceptor impulses travel via the vagus and from the carotid via
the glossopharyngeal nerve.
They are stimulated by arterial stretch.
Even at normal blood pressures they are tonically active.
gathered by dr. elbarky

Increase in baroreceptor discharge causes:

*Increased parasympathetic discharge to the SA node.


*Decreased sympathetic discharge to ventricular muscle causing decreased
contractility and fall in stroke volume.
*Decreased sympathetic discharge to venous system causing increased
compliance.
*Decreased peripheral arterial vascular resistance

Atrial stretch receptors


Located in atria at junction between pulmonary veins and vena cava.
Stimulated by atrial stretch and are thus low pressure sensors.
Increased blood volume will cause increased parasympathetic activity.
Very rapid infusion of blood will result in increase in heart rate mediated via
atrial receptors: the Bainbridge reflex.
Decreases in receptor stimulation results in increased sympathetic activity
this will decrease renal blood flow-decreases GFR-decreases urinary sodium
excretion-renin secretion by juxtaglomerular apparatus-Increase in
angiotensin II.
Increased atrial stretch will also result in increased release of atrial
natriuretic peptide.

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Question 132 of 192

 

A 33 year old female is admitted for varicose vein surgery. She is fit and well. After
the procedure she is persistently bleeding. She is known to have menorrhagia.
Investigations show a prolonged bleeding time and increased APTT. She has a
normal PT and platelet count. What is the most likely cause?

Anti phospholipid syndrome


gathered by dr. elbarky

Haemophilia

Factor V Leiden deficiency

von Willebrands disease

Protein C and S deficiency

Bleeding post operatively, epistaxis and menorrhagia may indicate a diagnosis of


vWD. Haemoarthroses are rare. The bleeding time is usually normal in haemophilia
(X-linked) and vitamin K deficiency.

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von Willebrands disease

Most common inherited bleeding disorder


All vWD is caused by mutations in the gene for von Willebrand factor. von
Willebrand factor is an adhesive glycoprotein that is secreted by
endothelium and megakaryocytes
von Willebrand factor promotes platelet adhesion to damaged endothelium
and other platelets. It is also involved in the transport and stabilization of
factor VIII
There are 7 subtypes of von Willebrand disease. The commonest is type I
(autosomal dominant) which accounts for 80% of cases, type 2vWD
(autosomal dominant or recessive) accounts for 15% of cases
There is a significant spectrum of severity ranging from spontaneous
bleeding and epistaxis through to troublesome excessive bleeding following
minor procedures
The test that is most typically diagnostic is the bleeding time
Treatments include administration of tranexamic acid for minor cases
undergoing minor procedures. More significant bleeding or more significant
procedures respond well to DDAVP. This is most effective in type I, less
effective in type 2 and contraindicated in type 2B. Patients with type 3
disease do not respond to DDAVP as they lack the ability to secrete vWF
Individuals who cannot have DDAVP or in whom it is contra indicated usually
receive factor VIII concentrates containing vWF

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D 49.3%
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Question 133 of 192

 

A 43 year old man has a nasogastric tube inserted. The nurse takes a small
aspirate of the fluid from the stomach and tests the pH of the aspirate. What is the
normal intragastric pH?

0.5

2
gathered by dr. elbarky

The intragastric pH is usually 2. Administration of proton pump inhibitors can


result in almost complete abolition of acidity

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Gastric secretions

A working knowledge of gastric secretions is important for surgery because peptic


ulcers are common, surgeons frequently prescribe anti secretory drugs and
because there are still patients around who will have undergone acid lowering
procedures (Vagotomy) in the past.

Gastric acid
Is produced by the parietal cells in the stomach
pH of gastric acid is around 2 with acidity being maintained by the H+/K+
ATP ase pump. As part of the process bicarbonate ions will be secreted into
the surrounding vessels.
Sodium and chloride ions are actively secreted from the parietal cell into the
canaliculus. This sets up a negative potential across the membrane and as a
result sodium and potassium ions diffuse across into the canaliculus.
Carbonic anhydrase forms carbonic acid which dissociates and the
hydrogen ions formed by dissociation leave the cell via the H+/K+ antiporter
pump. At the same time sodium ions are actively absorbed. This leaves
hydrogen and chloride ions in the canaliculus these mix and are secreted
into the lumen of the oxyntic gland.

This is illustrated diagrammatically below:


gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb028b.jpg)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Gastric
/images_eMRCS/swb028b.jpg)
acid)

Phases of gastric acid secretion


There are 3 phases of gastric secretion:

1. Cephalic phase (smell / taste of food)


30% acid produced
Vagal cholinergic stimulation causing secretion of HCL and gastrin release
from G cells

2. Gastric phase (distension of stomach )


60% acid produced
Stomach distension/low H+/peptides causes Gastrin release

3. Intestinal phase (food in duodenum)


10% acid produced
High acidity/distension/hypertonic solutions in the duodenum inhibits
gastric acid secretion via enterogastrones (CCK, secretin) and neural
reflexes.

Regulation of gastric acid production


Factors increasing production include:
Vagal nerve stimulation
Gastrin release
gathered by dr. elbarky

Histamine release (indirectly following gastrin release) from


enterchromaffin like cells

Factors decreasing production include:


Somatostatin (inhibits histamine release)
Cholecystokinin
Secretin

The diagram below illustrates some of the factors involved in regulating gastric
acid secretion and the relevant associated pharmacology

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb029b.jpg)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Gastric
/images_eMRCS/swb029b.jpg)
acid)

Below is a brief summary of the major hormones involved in food digestion:


Source Stimulus Actions

Gastrin G cells in Distension of Increase HCL, pepsinogen


antrum of stomach, and IF secretion, increases
the extrinsic nerves gastric motility, trophic effect
stomach Inhibited by: low on gastric mucosa
antral pH,
somatostatin

CCK I cells in Partially Increases secretion of


upper digested enzyme-rich fluid from
small proteins and pancreas, contraction of
intestine triglycerides gallbladder and relaxation of
sphincter of Oddi, decreases
gathered by dr. elbarky

gastric emptying, trophic


effect on pancreatic acinar
cells, induces satiety

Secretin S cells in Acidic chyme, Increases secretion of


upper fatty acids bicarbonate-rich fluid from
small pancreas and hepatic duct
intestine cells, decreases gastric acid
secretion, trophic effect on
pancreatic acinar cells

VIP Small Neural Stimulates secretion by


intestine, pancreas and intestines,
pancreas inhibits acid and pepsinogen
secretion

Somatostatin D cells in Fat, bile salts Decreases acid and pepsin


the and glucose in secretion, decreases gastrin
pancreas the intestinal secretion, decreases
and lumen pancreatic enzyme secretion,
stomach decreases insulin and
glucagon secretion
inhibits trophic effects of
gastrin, stimulates gastric
mucous production

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Question 134 of 192

 

A 54-year-old woman is admitted to the Surgical Admissions Unit with abdominal


pain. Blood tests taken on admission show the following:

Magnesium 0.40 mmol/l (normal value 0.7-1.0 mmol/l)

Which one of the following factors is most likely to be responsible for this result?
gathered by dr. elbarky

Excessive resuscitation with intravenous saline

Digoxin therapy

Diarrhoea

Hypothermia

Rhabdomyolysis

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Hypomagnasaemia

Cause of low magnesium


Diuretics
Total parenteral nutrition
Diarrhoea
Alcohol
Hypokalaemia, hypocalcaemia

Features
Paraesthesia
Tetany
Seizures
Arrhythmias
Decreased PTH secretion → hypocalcaemia
ECG features similar to those of hypokalaemia
Exacerbates digoxin toxicity

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D 5.8%
E 7.9%

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Question 135 of 192

 

Which of the following is not linked to excess glucocorticoids?

Osteonecrosis

Osteoporosis

Hypokalaemia
gathered by dr. elbarky

Hyponatraemia

Growth retardation in children

There are many adverse effects associated with excess glucocorticoids. Thinning
of the skin, osteonecrosis and osteoporosis are all common. Steroids are
associated with retention of sodium and water. Potassium loss may occur and
hypokalaemic alkalosis has been reported.

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Cortisol

Glucocorticoid
Released by zona fasiculata of the adrenal gland
90% protein bound; 10% active
Circadian rhythm: High in the mornings
Negative feedback via ACTH

Actions
Glycogenolysis
Gluconeogenesis
Protein catabolism
Lipolysis
Stress response
Anti-inflammatory
Decrease protein in bones
Increase gastric acid
Increases neutrophils/platelets/red blood cells
Inhibits fibroblastic activity

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Question 136 of 192

 

A 25-year-old man who has been morbidly obese for the past five years is reviewed
in the surgical bariatric clinic. In this patient, release of which of the following
hormones would increase appetite?

Leptin

Thyroxine
gathered by dr. elbarky

Adiponectin

Ghrelin

Serotonin

Obesity hormones
leptin decreases appetite
ghrelin increases appetite

Whilst thyroxine can increase appetite it does not fit with the clinical picture being
described.

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Obesity: physiology

Leptin
Leptin is thought to play a key role in the regulation of body weight. It is produced
by adipose tissue and acts on satiety centres in the hypothalamus and decreases
appetite. More adipose tissue (e.g. in obesity) results in high leptin levels.

Leptin stimulates the release of melanocyte-stimulating hormone (MSH) and


corticotrophin-releasing hormone (CRH). Low levels of leptin stimulates the
release of neuropeptide Y (NPY)

Ghrelin
Where as leptin induces satiety, ghrelin stimulates hunger. It is produced mainly by
the fundus of the stomach and the pancreas. Ghrelin levels increase before meals
and decrease after meals

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C 7%
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E 8.1%

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Question 137 of 192

 

Which of the following drugs causes hyperkalaemia?

Heparin

Ciprofloxacin

Salbutamol
gathered by dr. elbarky

Levothyroxine

Codeine phosphate

Both unfractionated and low-molecular weight heparin can cause hyperkalaemia.


This is thought to be caused by inhibition of aldosterone secretion. Salbutamol is a
recognised treatment for hyperkalaemia.

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Hyperkalaemia

Plasma potassium levels are regulated by a number of factors including


aldosterone, acid-base balance and insulin levels.
Metabolic acidosis is associated with hyperkalaemia as hydrogen and
potassium ions compete with each other for exchange with sodium ions
across cell membranes and in the distal tubule.
ECG changes seen in hyperkalaemia include tall-tented T waves, small P
waves, widened QRS leading to a sinusoidal pattern and asystole

Causes of hyperkalaemia
Acute renal failure
Drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor
blockers, spironolactone, ciclosporin, heparin**
Metabolic acidosis
Addison's
Tissue necrosis/rhabdomylosis: burns, trauma
Massive blood transfusion

Foods that are high in potassium


Salt substitutes (i.e. Contain potassium rather than sodium)
Bananas, oranges, kiwi fruit, avocado, spinach, tomatoes

*beta-blockers interfere with potassium transport into cells and can potentially
cause hyperkalaemia in renal failure patients - remember beta-agonists, e.g.
Salbutamol, are sometimes used as emergency treatment
gathered by dr. elbarky

**both unfractionated and low-molecular weight heparin can cause hyperkalaemia.


This is thought to be caused by inhibition of aldosterone secretion

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Question 138 of 192

 

A 39 year old lady undergoes a laparoscopic cholecystectomy as a daycase. The


operation is more difficult than anticipated and the surgeon places a drain to the
liver bed. In recovery 1.5 litres of blood is seen to enter the drain. Which of the
following substances is the first to be released in this situation?

Angiotensinogen
gathered by dr. elbarky

Renin

Angiotensin I

Angiotensin II

Aldosterone

The decrease in blood pressure will be sensed by the juxtaglomerular cells in the
kidney. This will cause renin secretion.

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Shock

Shock occurs when there is insufficient tissue perfusion.


The pathophysiology of shock is an important surgical topic and may be
divided into the following aetiological groups:
Septic
Haemorrhagic
Neurogenic
Cardiogenic
Anaphylactic

Septic shock
Septic shock is a major problem and those patients with severe sepsis have a
mortality rate in excess of 40%. In those who are admitted to intensive care
mortality ranges from 6% with no organ failure to 65% in those with 4 organ failure.

Sepsis is defined as an infection that triggers a particular Systemic Inflammatory


Response Syndrome (SIRS). This is characterised by body temperature outside 36
oC - 38 o C, HR >90 beats/min, respiratory rate >20/min, WBC count >12,000/mm 3

or < 4,000/mm3, altered mental state or hyperglycaemia (in absence of diabetes).

Patients with infections and two or more elements of SIRS meet the diagnostic
criteria for sepsis. Those with organ failure have severe sepsis and those with
refractory hypotension -septic shock.

During the septic process there is marked activation of the immune system with
gathered by dr. elbarky

extensive cytokine release. This may be coupled with or triggered by systemic


circulation of bacterial toxins. These all cause endothelial cell damage and
neutrophil adhesion. The overall hallmarks are thus those of excessive
inflammation, coagulation and fibrinolytic suppression.

The surviving sepsis campaign (2012) highlights the following key areas for
attention:
Prompt administration of antibiotics to cover all likely pathogens coupled
with a rigorous search for the source of infection.
Haemodynamic stabilisation. Many patients are hypovolaemic and require
aggressive fluid administration. Aim for CVP 8-12 cm H2O, MAP >65mmHg.
Modulation of the septic response. This includes manoeuvres to counteract
the changes and includes measures such as tight glycaemic control. The
routine use of steroids is not advised.

In surgical patients, the main groups with septic shock include those with
anastomotic leaks, abscesses and extensive superficial infections such as
necrotising fasciitis. When performing surgery the aim should be to undertake the
minimum necessary to restore physiology. These patients do not fare well with
prolonged surgery. Definitive surgery can be more safely undertaken when
physiology is restored and clotting in particular has been normalised.

Haemorrhagic shock
The average adult blood volume comprises 7% of body weight. Thus in the 70 Kg
adult this will equate to 5 litres. This changes in children (8-9% body weight) and is
slightly lower in the elderly.

The table below outlines the 4 major classes of haemorrhagic shock and their
associated physiological sequelae:

Parameter Class I Class II Class III Class IV


Parameter Class I Class II Class III Class IV

Blood loss ml <750ml 750-1500ml 1500-2000ml >2000ml

Blood loss % <15% 15-30% 30-40% >40%

Pulse rate <100 >100 >120 >140

Blood pressure Normal Normal Decreased Decreased

Respiratory rate 14-20 20-30 30-40 >35

Urine output >30ml 20-30ml 5-15ml <5ml

Symptoms Normal Anxious Confused Lethargic


gathered by dr. elbarky

Decreasing blood pressure during haemorrhagic shock causes organ


hypoperfusion and relative myocardial ischaemia. The cardiac index gives a
numerical value for tissue oxygen delivery and is given by the equation: Cardiac
index= Cardiac output/ body surface area. Where Hb is haemoglobin
concentration in blood and SaO2 the saturation and PaO2 the partial pressure of
oxygen. Detailed knowledge of this equation is required for the MRCS Viva but not
for part A, although you should understand the principle.

In patients suffering from trauma the most likely cause of shock is haemorrhage.
However, the following may also be the cause or occur concomitantly:

Tension pneumothorax
Spinal cord injury
Myocardial contusion
Cardiac tamponade

When assessing trauma patients it is worth remembering that in order to generate


a palpable femoral pulse an arterial pressure of >65mmHg is required.

Once bleeding is controlled and circulating volume normalised the levels of


transfusion should be to maintain a Hb of 7-8 in those with no risk factors for
tissue hypoxia and Hb 10 for those who have such risk factors.

Neurogenic shock
This occurs most often following a spinal cord transection, usually at a high level.
There is resultant interruption of the autonomic nervous system. The result is
either decreased sympathetic tone or increased parasympathetic tone, the effect
of which is a decrease in peripheral vascular resistance mediated by marked
vasodilation.

This results in decreased preload and thus decreased cardiac output (Starlings
law). There is decreased peripheral tissue perfusion and shock is thus produced. In
contrast with many other types of shock peripheral vasoconstrictors are used to
return vascular tone to normal.

Cardiogenic shock
In medical patients the main cause is ischaemic heart disease. In the traumatic
setting direct myocardial trauma or contusion is more likely. Evidence of ECG
changes and overlying sternal fractures or contusions should raise the suspicion
of injury. Treatment is largely supportive and transthoracic echocardiography
should be used to determine evidence of pericardial fluid or direct myocardial
injury. The measurement of troponin levels in trauma patients may be undertaken
but they are less useful in delineating the extent of myocardial trauma than
following MI.
gathered by dr. elbarky

When cardiac injury is of a blunt nature and is associated with cardiogenic shock
the right side of the heart is the most likely site of injury with chamber and or valve
rupture. These patients require surgery to repair these defects and will require
cardiopulmonary bypass to achieve this. Some may require intra aortic balloon
pump as a bridge to surgery.

Anaphylactic shock
Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic
hypersensitivity reaction.

Anaphylaxis is one of the few times when you would not have time to look up the
dose of a medication. The Resuscitation Council guidelines on anaphylaxis have
recently been updated. Adrenaline is by far the most important drug in anaphylaxis
and should be given as soon as possible. The recommended doses for adrenaline,
hydrocortisone and chlorpheniramine are as follows:

Adrenaline Hydrocortisone Chlorpheniramine

< 6 months 150 mcg (0.15ml 1 25 mg 250 mcg/kg


in 1,000)

6 months - 6 150 mcg (0.15ml 1 50 mg 2.5 mg


years in 1,000)

6-12 years 300 mcg (0.3ml 1 in 100 mg 5 mg


1,000)

Adult and child 500 mcg (0.5ml 1 in 200 mg 10 mg


12 years 1,000)

Adrenaline can be repeated every 5 minutes if necessary. The best site for IM
injection is the anterolateral aspect of the middle third of the thigh.
Common identified causes of anaphylaxis
food (e.g. Nuts) - the most common cause in children
drugs
venom (e.g. Wasp sting)

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Question 139 of 192

 

Which of the following statements relating to the regulation of renal blood flow is
untrue?

In a healthy 70Kg male, the glomerular filtration rate will be the same at a
systolic blood pressure of 120mmHg as a systolic blood pressure of 95
mmHg
gathered by dr. elbarky

Over 90% of the blood supply to the kidney is distributed to the cortex

The kidney receives approximately 25% of the total cardiac output at rest

A decrease in renal perfusion pressure will cause the juxtaglomerular cells


to secrete renin

Systolic blood pressures of less than 65mmHg will cause the mesangial
cells to secrete aldosterone

The kidney autoregulates its blood supply over a range of systolic blood pressures.
Drop in arterial pressure is sensed by the juxtaglomerular cells and renin is
released leading to the activation of the renin-angiontensin system. Mesangial
cells are contractile cells that are located in the tubule and have no direct
endocrine function.

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Renal Physiology

Overview
Each nephron is supplied with blood from an afferent arteriole that opens
onto the glomerular capillary bed.
Blood then flows to an efferent arteriole, supplying the peritubular capillaries
and medullary vasa recta.
The kidney receives up to 25% of resting cardiac output.
Control of blood flow
The kidney is able to autoregulate its blood flow between systolic pressures
of 80- 180mmHg so there is little variation in renal blood flow.
This is achieved by myogenic control of arteriolar tone, both sympathetic
input and hormonal signals (e.g. renin) are responsible.

Glomerular structure and function


Blood inside the glomerulus has considerable hydrostatic pressure.
The basement membrane has pores that will allow free diffusion of smaller
solutes, larger negatively charged molecules such as albumin are unable to
cross.
The glomerular filtration rate (GFR) is equal to the concentration of a solute
in the urine, times the volume of urine produced per minute, divided by the
gathered by dr. elbarky

plasma concentration (assuming that the solute is freely diffused e.g.


inulin).
In clinical practice creatinine is used because it is subjected to very little
proximal tubular secretion.
Although subject to variability, the typical GFR is 125ml per minute.
Glomerular filtration rate = Total volume of plasma per unit time leaving the
capillaries and entering the bowman's capsule
Renal clearance = volume plasma from which a substance is removed per
minute by the kidneys

Substances used to measure GFR have the following features:


1. Inert
2. Free filtration from the plasma at the glomerulus (not protein bound)
3. Not absorbed or secreted at the tubules
4. Plasma concentration constant during urine collection

Examples: inulin, creatinine

GFR = urine concentration (mmol/l) x urine volume (ml/min)


--------------------------------------------------------------------------
plasma concentration (mmol/l)

The clearance of a substance is dependent not only on its diffusivity across


the basement membrane but also subsequent tubular secretion and / or
reabsorption.
So glucose which is freely filtered across the basement membrane is usually
reabsorbed from tubules giving a clearance of zero.

Tubular function
Reabsorption and secretion of substances occurs in the tubules.
In the proximal tubule substrates such as glucose, amino acids and
phosphate are co-transported with sodium across the semi permeable
membrane.
Up to two thirds of filtered water is reabsorbed in the proximal tubules.
This will lead to increase in urea concentration in the distal tubule allowing
for its increased diffusion.
Substances to be secreted into the tubules are taken up from the peritubular
blood by tubular cells.
Solutes such as paraaminohippuric acid are cleared with a single passage
through the kidneys and this is why it is used to measure renal plasma flow.
Ions such as calcium and phosphate will have a tubular reabsorption that is
influenced by plasma PTH levels.
Potassium may be both secreted and re-absorbed and is co-exchanged with
sodium.

Loop of Henle
Approximately 60 litres of water containing 9000mmol sodium enters the
gathered by dr. elbarky

descending limb of the loop of Henle in 24 hours.


Loops from the juxtamedullary nephrons run deep into the medulla.
The osmolarity of fluid changes and is greatest at the tip of the papilla.
The thick ascending limb is impermeable to water, but highly permeable to
sodium and chloride ions.
This loss means that at the beginning of the thick ascending limb the fluid is
hypo osmotic compared with adjacent interstitial fluid.
In the thick ascending limb the reabsorption of sodium and chloride ions
occurs by both facilitated and passive diffusion pathways.
The loops of Henle are co-located with vasa recta, these will have similar
solute compositions to the surrounding extracellular fluid so preventing the
diffusion and subsequent removal of this hypertonic fluid.
The energy dependent reabsorption of sodium and chloride in the thick
ascending limb helps to maintain this osmotic gradient.

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Question 140 of 192

 

Which of the following features does not put a patient at risk of refeeding
syndrome?

BMI < 16 kg/m2

Alcohol abuse
gathered by dr. elbarky

Thyrotoxicosis

Chemotherapy

Diuretics

Diuretics increase the risk of re-feeding syndrome through a process of increasing


the risk of depletion of key electrolytes.

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Nutrition - Refeeding syndrome

Refeeding syndrome describes the metabolic abnormalities which occur on


feeding a person following a period of starvation. The metabolic consequences
include:
Hypophosphataemia
Hypokalaemia
Hypomagnesaemia
Abnormal fluid balance

These abnormalities can lead to organ failure.

Re-feeding problems
If patient not eaten for > 5 days, aim to re-feed at < 50% energy and protein levels
High risk for re-feeding problems
If one or more of the following:
BMI < 16 kg/m2
Unintentional weight loss >15% over 3-6 months
Little nutritional intake > 10 days
Hypokalaemia, Hypophosphataemia or hypomagnesaemia prior to feeding
(unless high)

If two or more of the following:


BMI < 18.5 kg/m2
Unintentional weight loss > 10% over 3-6 months
Little nutritional intake > 5 days
History of: alcohol abuse, drug therapy including insulin, chemotherapy,
diuretics and antacids
gathered by dr. elbarky

Prescription
Start at up to 10 kcal/kg/day increasing to full needs over 4-7 days
Start immediately before and during feeding: oral thiamine 200-300mg/day,
vitamin B co strong 1 tds and supplements
Give K+ (2-4 mmol/kg/day), phosphate (0.3-0.6 mmol/kg/day), magnesium
(0.2-0.4 mmol/kg/day)

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Question 146 of 192

 

A 34 year old man presents with a peptic ulcer. Which of the following is
responsible for the release of gastric acid?

Chief cells

Parietal cells
gathered by dr. elbarky

Brunners Glands

G Cells

None of the above

Parietal cells are responsible for the release of gastric acid. Brunners glands are
found in the duodenum.

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Gastric secretions

A working knowledge of gastric secretions is important for surgery because peptic


ulcers are common, surgeons frequently prescribe anti secretory drugs and
because there are still patients around who will have undergone acid lowering
procedures (Vagotomy) in the past.

Gastric acid
Is produced by the parietal cells in the stomach
pH of gastric acid is around 2 with acidity being maintained by the H+/K+
ATP ase pump. As part of the process bicarbonate ions will be secreted into
the surrounding vessels.
Sodium and chloride ions are actively secreted from the parietal cell into the
canaliculus. This sets up a negative potential across the membrane and as a
result sodium and potassium ions diffuse across into the canaliculus.
Carbonic anhydrase forms carbonic acid which dissociates and the
hydrogen ions formed by dissociation leave the cell via the H+/K+ antiporter
pump. At the same time sodium ions are actively absorbed. This leaves
hydrogen and chloride ions in the canaliculus these mix and are secreted
into the lumen of the oxyntic gland.

This is illustrated diagrammatically below:


gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb028b.jpg)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Gastric
/images_eMRCS/swb028b.jpg)
acid)

Phases of gastric acid secretion


There are 3 phases of gastric secretion:

1. Cephalic phase (smell / taste of food)


30% acid produced
Vagal cholinergic stimulation causing secretion of HCL and gastrin release
from G cells

2. Gastric phase (distension of stomach )


60% acid produced
Stomach distension/low H+/peptides causes Gastrin release

3. Intestinal phase (food in duodenum)


10% acid produced
High acidity/distension/hypertonic solutions in the duodenum inhibits
gastric acid secretion via enterogastrones (CCK, secretin) and neural
reflexes.

Regulation of gastric acid production


Factors increasing production include:
Vagal nerve stimulation
Gastrin release
Histamine release (indirectly following gastrin release) from
gathered by dr. elbarky

enterchromaffin like cells

Factors decreasing production include:


Somatostatin (inhibits histamine release)
Cholecystokinin
Secretin

The diagram below illustrates some of the factors involved in regulating gastric
acid secretion and the relevant associated pharmacology

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb029b.jpg)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Gastric
/images_eMRCS/swb029b.jpg)
acid)

Below is a brief summary of the major hormones involved in food digestion:


Source Stimulus Actions

Gastrin G cells in Distension of Increase HCL, pepsinogen


antrum of stomach, and IF secretion, increases
the extrinsic nerves gastric motility, trophic effect
stomach Inhibited by: low on gastric mucosa
antral pH,
somatostatin

CCK I cells in Partially Increases secretion of


upper digested enzyme-rich fluid from
small proteins and pancreas, contraction of
intestine triglycerides gallbladder and relaxation of
sphincter of Oddi, decreases
gathered by dr. elbarky

gastric emptying, trophic


effect on pancreatic acinar
cells, induces satiety

Secretin S cells in Acidic chyme, Increases secretion of


upper fatty acids bicarbonate-rich fluid from
small pancreas and hepatic duct
intestine cells, decreases gastric acid
secretion, trophic effect on
pancreatic acinar cells

VIP Small Neural Stimulates secretion by


intestine, pancreas and intestines,
pancreas inhibits acid and pepsinogen
secretion

Somatostatin D cells in Fat, bile salts Decreases acid and pepsin


the and glucose in secretion, decreases gastrin
pancreas the intestinal secretion, decreases
and lumen pancreatic enzyme secretion,
stomach decreases insulin and
glucagon secretion
inhibits trophic effects of
gastrin, stimulates gastric
mucous production

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C 5.3%
D 12.3%
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Question 141 of 192

 

Intra cranial pressure is governed by the principles of the Monroe-Kellie doctrine.


To which of the following does this concept not apply?

A 2 month old child

A 2 year old child


gathered by dr. elbarky

A 5 year old child

A 10 year old child

An adult

The Monroe-Kelly Doctrine assumes that the cranial cavity is a rigid box. In children
with non fused fontanells this is not the case.

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Applied neurophysiology

Pressure within the cranium is governed by the Monroe-Kelly doctrine. This


considers the skull as a closed box. Increases in mass can be
accommodated by loss of CSF. Once a critical point is reached (usually 100-
120ml of CSF lost) there can be no further compensation and ICP rises
sharply. The next step is that pressure will begin to equate with MAP and
neuronal death will occur. Herniation will also accompany this process.
The CNS can autoregulate its own blood supply. Vaso constriction and
dilatation of the cerebral blood vessels is the primary method by which this
occurs. Extremes of blood pressure can exceed this capacity resulting in
risk of stroke. Other metabolic factors such as hypercapnia will also cause
vasodilation, which is of importance in ventilating head injured patients.
The brain can only metabolise glucose, when glucose levels fall,
consciousness will be impaired.
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A 73.3%
B 6.4%
C 4.8%
D 5.6%
E 9.9%

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Question 142 of 192

 

A 52 year old man develops septic shock following a Hartmans procedure for
perforated diverticular disease. He is started on an adrenaline infusion. Which of
the following is least likely to occur?

Peripheral vasoconstriction

Coronary artery vasospasm


gathered by dr. elbarky

Gluconeogenesis

Lipolysis

Tachycardia

It's cardiac effects are mediated via β 1 receptors. The coronary arteries which
have β 2 receptors are unaffected.

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Adrenaline

Fight or Flight response

- Catecholamine (phenylalanine and tyrosine)


- Neurotransmitter and hormone
- Released by the adrenal glands
- Effects on α 1 and 2, β 1 and 2 receptors
- Effect on β 2 receptors in skeletal muscle vessels-causing vasodilation
- Increase cardiac output and total peripheral resistance
- Vasoconstriction in the skin and kidneys causing a narrow pulse pressure

Actions
α adrenergic receptors:
Inhibits insulin secretion by the pancreas
Stimulates glycogenolysis in the liver and muscle
Stimulates glycolysis in muscle

β adrenergic receptors:
Stimulates glucagon secretion in the pancreas
Stimulates ACTH
Stimulates lipolysis by adipose tissue

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B 46.9%
C 20%
D 15.1%
E 6.7%

46.9% of users answered this question correctly

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Question 143 of 192

 

Which of the following does not cause hyperkalaemia?

Haemolysis

Burns

Familial periodic paralysis


gathered by dr. elbarky

Type 4 renal tubular acidosis

Severe malnutrition

'Machine' - Causes of Increased Serum K+

M - Medications - ACE inhibitors, NSAIDS


A - Acidosis - Metabolic and respiratory
C - Cellular destruction - Burns, traumatic injury
H - Hypoaldosteronism, haemolysis
I - Intake - Excessive
N - Nephrons, renal failure
E - Excretion - Impaired

Familial periodic paralysis has subtypes associated with hyper and hypokalaemia.

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Hyperkalaemia

Plasma potassium levels are regulated by a number of factors including


aldosterone, acid-base balance and insulin levels.
Metabolic acidosis is associated with hyperkalaemia as hydrogen and
potassium ions compete with each other for exchange with sodium ions
across cell membranes and in the distal tubule.
ECG changes seen in hyperkalaemia include tall-tented T waves, small P
waves, widened QRS leading to a sinusoidal pattern and asystole

Causes of hyperkalaemia
Acute renal failure
Drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor
blockers, spironolactone, ciclosporin, heparin**
Metabolic acidosis
Addison's
Tissue necrosis/rhabdomylosis: burns, trauma
Massive blood transfusion
gathered by dr. elbarky

Foods that are high in potassium


Salt substitutes (i.e. Contain potassium rather than sodium)
Bananas, oranges, kiwi fruit, avocado, spinach, tomatoes

*beta-blockers interfere with potassium transport into cells and can potentially
cause hyperkalaemia in renal failure patients - remember beta-agonists, e.g.
Salbutamol, are sometimes used as emergency treatment

**both unfractionated and low-molecular weight heparin can cause hyperkalaemia.


This is thought to be caused by inhibition of aldosterone secretion

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B 8.3%
C 21%
D 13.3%
E 50.5%

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Question 144 of 192

 

Which of these substances is not released from the islets of Langerhans?

Pancreatic polypeptide

Glucagon

Secretin
gathered by dr. elbarky

Somatostatin

Insulin

Secretin is released from mucosal cells in the duodenum and jejunum.

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Pancreas endocrine physiology

Hormones released from the islets of Langerhans

Beta cells Insulin (70% of total secretions)

Alpha cells Glucagon

Delta cells Somatostatin

F cells Pancreatic polypeptide

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A 14.8%
B 11%
C 45.6%
gathered by dr. elbarky

D 19.5%
E 9.1%

45.6% of users answered this question correctly

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Question 145 of 192

 

Which of the following does not lead to relaxation of the lower oesophageal
sphincter?

Metoclopramide

Botulinum toxin type A


gathered by dr. elbarky

Nicotine

Alcohol

Theophylline

Metoclopramide acts directly on the smooth muscle of the LOS to cause it to


contract.
Theophylline is a phosphodiesterase inhibitor (mimics action of prostaglandin E1)
which causes relaxation of the LOS.

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Peristalsis

Circular smooth muscle contracts behind the food bolus and longitudinal
smooth muscle propels the food through the oesophagus
Primary peristalsis spontaneously moves the food from the oesophagus
into the stomach (9 seconds)
Secondary peristalsis occurs when food, which doesn't enter the stomach,
stimulates stretch receptors to cause peristalsis
In the small intestine each peristalsis waves slows to a few seconds and
causes mixture of chyme
In the colon three main types of peristaltic activity are recognised (see
below)
Colonic peristalsis

Segmentation Localised contractions in which the bolus is


contractions subjected to local forces to maximise mucosal
absorption

Antiperistaltic Localised reverse peristaltic waves to slow entry


contractions towards into colon and maximise absorption
ileum

Mass movements Waves migratory peristaltic waves along the entire


colon to empty the organ prior to the next ingestion
of food bolus
gathered by dr. elbarky

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B 13.5%
C 12.9%
D 11.2%
E 15.3%

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Question 151 of 192

 

Which of the following will increase the volume of pancreatic exocrine secretions?

Octreotide

Cholecystokinin

Aldosterone
gathered by dr. elbarky

Adrenaline

None of the above

Cholecystokinin will often increase the volume of pancreatic secretions.

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Pancreas exocrine physiology

Composition of pancreatic secretions


Pancreatic secretions are usually 1000-1500ml per 24 hours and have a pH of 8.
Secretion Source Substances secreted

Trypsinogen
Procarboxylase
Enzymic Acinar cells
Amylase
Elastase

Sodium
Bicarbonate
Water
Ductal and
Aqueous Potassium
Centroacinar cells
Chloride
NB: Sodium and potassium reflect their plasma levels;
chloride and bicarbonate vary with flow rate
Regulation
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.

Enzyme activation
Trypsinogen is converted via enterokinase to active trypsin in the duodenum.
Trypsin then activates the other inactive enzymes
gathered by dr. elbarky

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B 62.8%
C 8.8%
D 7.7%
E 7.6%

62.8% of users answered this question correctly

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Question 147 of 192

 

A 43 year old lady is diagnosed with primary hyperparathyroidism. Her serum PTH
levels are elevated. An endocrine surgeon performs a parathyroidectomy. How
long will it take for the serum PTH levels to fall if the functioning adenoma has
been successfully removed?

6 hours
gathered by dr. elbarky

24 hours

2 hours

1 hour

10 minutes

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.

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Calcium homeostasis

Calcium ions are linked to a wide range of physiological processes. The largest
store of bodily calcium is contained within the skeleton. Calcium levels are
primarily controlled by parathyroid hormone, vitamin D and calcitonin.

Hormonal regulation of calcium

Hormone Actions
Hormone Actions

Parathyroid hormone (PTH) Increase calcium levels and


decrease phosphate levels
Increases bone resorption
Immediate action on osteoblasts to
increase ca2+ in extracellular fluid
Osteoblasts produce a protein
signaling molecule that activate
osteoclasts which cause bone
resorption
Increases renal tubular reabsorption
of calcium
Increases synthesis of 1,25(OH)2D
gathered by dr. elbarky

(active form of vitamin D) in the


kidney which increases bowel
absorption of Ca2+
Decreases renal phosphate
reabsorption

1,25-dihydroxycholecalciferol Increases plasma calcium and


(the active form of vitamin D) plasma phosphate
Increases renal tubular reabsorption
and gut absorption of calcium
Increases osteoclastic activity at
high levels and osteoblasts at low
levels
Increases renal phosphate
reabsorption

Calcitonin Secreted by C cells of thyroid


Inhibits intestinal calcium absorption
Inhibits osteoclast activity
Inhibits renal tubular absorption of
calcium

Both growth hormone and thyroxine also play a small role in calcium metabolism.

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A 21.7%
B 13.7%
C 9.7%
D 10.8%
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E 44.2%

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Question 148 of 192

 

Which of the following inhibits the secretion of insulin?

Adrenaline

Lipids

Gastrin
gathered by dr. elbarky

Arginine

Vagal cholinergic activity

Inhibition of insulin release:

Alpha adrenergic drugs


Beta blockers
Sympathetic nerves

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Insulin

Insulin is a peptide hormone, produced by beta cells of the pancreas, and is central
to regulating carbohydrate and fat metabolism in the body. Insulin causes cells in
the liver, skeletal muscles, and fat tissue to absorb glucose from the blood. In the
liver and skeletal muscles, glucose is stored as glycogen, and in fat cells
(adipocytes) it is stored as triglycerides.

Structure
The human insulin protein is composed of 51 amino acids, and has a molecular
weight of 5808 Da. It is a dimer of an A-chain and a B-chain, which are linked
together by disulfide bonds.
Synthesis
Pro-insulin is formed by the rough endoplasmic reticulum in pancreatic beta cells.
Then pro-insulin is cleaved to form insulin and C-peptide. Insulin is stored in
secretory granules and released in response to Ca2+.

Function
Secreted in response to hyperglycaemia
Glucose utilisation and glycogen synthesis
Inhibits lipolysis
Reduces muscle protein loss

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B 17.1%
C 12.8%
D 8.7%
E 11.9%

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Question 149 of 192

 

Which opioid receptor does morphine attach to?

mu

alpha

sigma
gathered by dr. elbarky

beta

kappa

Pethidine and other conventional opioids attach to this receptor.

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Opioids

- Combine to specific opiate receptors in the CNS (periaqueductal grey matter,


limbic system, substantia gelatinosa)

- Morphine attaches to mu1 receptors

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A 68.9%
B 8.1%
C 7.3%
D 7.1%
E 8.7%
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Question 150 of 192

 

Where is the majority of iron found in the body?

Bone

Haemoglobin

Ferritin and haemosiderin


gathered by dr. elbarky

Myoglobin

Plasma iron

Approximately 70% of body iron is found bound to haemoglobin.

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Iron metabolism

Absorption Duodenum and upper jejunum


About 10% of dietary iron absorbed
Fe2+ (ferrous iron) much better absorbed than Fe3+ (ferric
iron)
Ferrous iron is oxidized to form ferric iron, which is
combined with apoferritin to form ferritin
Absorption is regulated according to body's need
Increased by vitamin C, gastric acid
Decreased by proton pump inhibitors, tetracycline, gastric
achlorhydria, tannin (found in tea)

Transport In plasma as Fe3+ bound to transferrin


Storage Ferritin (or haemosiderin) in bone marrow

Excretion Lost via intestinal tract following desquamation

Distribution in body

Total body iron 4g

Haemoglobin 70%

Ferritin and haemosiderin 25%

Myoglobin 4%
gathered by dr. elbarky

Plasma iron 0.1%

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B 53%
C 22.7%
D 11%
E 6.5%

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Question 152 of 192

 

Which of the following does not cause an increased anion gap acidosis?

Uraemia

Paraldehyde

Diabetic ketoacidosis
gathered by dr. elbarky

Ethylene glycol

Acetazolamide

Causes of increased anion acidosis: MUDPILES

M - Methanol
U - Uraemia
D - DKA/AKA
P - Paraldehyde/phenformin
I - Iron/INH
L - Lactic acidosis
E - Ethylene glycol
S - Salicylates

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Disorders of acid - base balance

Disorders of acid- base balance are often covered in the MRCS part A.

The acid-base normogram below shows how the various disorders may be
categorised
gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb072b.png)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Acid-base
/images_eMRCS/swb072b.png)
homeostasis)

Metabolic acidosis
This is the most common surgical acid - base disorder.
Reduction in plasma bicarbonate levels.
Two mechanisms:

1. Gain of strong acid (e.g. diabetic ketoacidosis)


2. Loss of base (e.g. from bowel in diarrhoea)
- Classified according to the anion gap, this can be calculated by:
(Na+ + K+) - (Cl- + HCO3-).
- If a question supplies the chloride level then this is often a clue that the anion gap
should be calculated. The normal range = 10-18 mmol/L

Normal anion gap ( = hyperchloraemic metabolic acidosis)


Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
Renal tubular acidosis
Drugs: e.g. acetazolamide
Ammonium chloride injection
Addison's disease

Raised anion gap


Lactate: shock, hypoxia
Ketones: diabetic ketoacidosis, alcohol
Urate: renal failure
Acid poisoning: salicylates, methanol

Metabolic acidosis secondary to high lactate levels may be subdivided into two
types:
Lactic acidosis type A: (Perfusion disorders e.g.shock, hypoxia, burns)
Lactic acidosis type B: (Metabolic e.g. metformin toxicity)

Metabolic alkalosis
Usually caused by a rise in plasma bicarbonate levels.
Rise of bicarbonate above 24 mmol/L will typically result in renal excretion
of excess bicarbonate.
gathered by dr. elbarky

Caused by a loss of hydrogen ions or a gain of bicarbonate. It is due mainly


to problems of the kidney or gastrointestinal tract

Causes
Vomiting / aspiration (e.g. Peptic ulcer leading to pyloric stenosis,
nasogastric suction)
Diuretics
Liquorice, carbenoxolone
Hypokalaemia
Primary hyperaldosteronism
Cushing's syndrome
Bartter's syndrome
Congenital adrenal hyperplasia

Mechanism of metabolic alkalosis


Activation of renin-angiotensin II-aldosterone (RAA) system is a key factor
Aldosterone causes reabsorption of Na+ in exchange for H+ in the distal
convoluted tubule
ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA
system → raised aldosterone levels
In hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+
into cells to maintain neutrality

Respiratory acidosis
Rise in carbon dioxide levels usually as a result of alveolar hypoventilation
Renal compensation may occur leading to Compensated respiratory acidosis

Causes
COPD
Decompensation in other respiratory conditions e.g. Life-threatening asthma
/ pulmonary oedema
Sedative drugs: benzodiazepines, opiate overdose

Respiratory alkalosis
Hyperventilation resulting in excess loss of carbon dioxide
This will result in increasing pH

Causes
Psychogenic: anxiety leading to hyperventilation
Hypoxia causing a subsequent hyperventilation: pulmonary embolism, high
altitude
Early salicylate poisoning*
CNS stimulation: stroke, subarachnoid haemorrhage, encephalitis
gathered by dr. elbarky

Pregnancy

*Salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis.


Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst
later the direct acid effects of salicylates (combined with acute renal failure) may
lead to an acidosis

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D 13.1%
E 44%

44% of users answered this question correctly


Question 153 of 192

 

Which of the following statements about blood clotting is untrue?

Platelet adhesion to disrupted endothelium is dependent upon von


Willebrand factor

Protein C is a vitamin K dependent substance


gathered by dr. elbarky

The bleeding time provides an assessment of platelet function

The prothrombin time tests the extrinsic system

Administration of aprotinin during liver transplantation surgery prolongs


survival

Although aprotinin reduces fibrinolysis and thus bleeding, it is associated with


increased risk of death and was withdrawn in 2007. Protein C is dependent upon
vitamin K and this may paradoxically increase the risk of thrombosis during the
early phases of warfarin treatment.

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Coagulation cascade

Two pathways lead to fibrin formation

Intrinsic pathway (components already present in the blood)


Minor role in clotting
Subendothelial damage e.g. collagen
Formation of the primary complex on collagen by high-molecular-weight
kininogen (HMWK), prekallikrein, and Factor 12
Prekallikrein is converted to kallikrein and Factor 12 becomes activated
Factor 12 activates Factor 11
Factor 11 activates Factor 9, which with its co-factor Factor 8a form the
tenase complex which activates Factor 10

Extrinsic pathway (needs tissue factor released by damaged tissue)


Tissue damage
Factor 7 binds to Tissue factor
This complex activates Factor 9
Activated Factor 9 works with Factor 8 to activate Factor 10

Common pathway
Activated Factor 10 causes the conversion of prothrombin to thrombin
Thrombin hydrolyses fibrinogen peptide bonds to form fibrin and also
activates factor 13 to form links between fibrin molecules
gathered by dr. elbarky

Fibrinolysis
Plasminogen is converted to plasmin to facilitate clot resorption

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb030b.jpg)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org
/images_eMRCS/swb030b.jpg)
/wiki/Coagulation)

Clotting pathway Clotting parameters affected Factors affected

Intrinsic pathway Increased APTT Factors 8,9,11,12

Extrinsic pathway Increased PT Factor 7

Common pathway Increased APTT & PT Factors 2,5,10

Vitamin K dependent Factors 2,7,9,10


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B 18.4%
C 14.1%
D 17.7%
E 38.2%

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Question 154 of 192

 

Which of the substances below is derived primarily from the zona reticularis of the
adrenal gland?

Mineralocorticoid hormones

Glucocorticoid hormones
gathered by dr. elbarky

Sex hormones

FSH

Vasopressin

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Adrenal physiology

Adrenal medulla
The chromaffin cells of the adrenal medulla secrete the catecholamines
noradrenaline and adrenaline. The medulla is innervated by the splanchnic nerves;
the preganglionic sympathetic fibres secrete acetylcholine causing the chromaffin
cells to secrete their contents by exocytosis.
Phaeochromocytomas are derived from these cells and will secrete both
adrenaline and nor adrenaline.

Adrenal cortex
Three histologically distinct zones are recognised:
gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb215b.png)
Image sourced from (https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS
Wikipedia () /swb215b.png)

Zone Location Hormone Secreted

Zona glomerulosa Outer zone Aldosterone

Zona fasiculata Middle zone Glucocorticoids

Zona reticularis Inner zone Androgens

The glucocorticoids and aldosterone are mostly bound to plasma proteins in the
circulation. Glucocorticoids are inactivated and excreted by the liver.

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B 10.8%
C 67.1%
D 5.5%
E 6.4%

67.1% of users answered this question correctly

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Question 155 of 192

 

A patient is seen in clinic complaining of abdominal pain. Routine bloods show:

Na+ 142 mmol/l

K+ 4.0 mmol/l

Chloride 104 mmol/l


gathered by dr. elbarky

Bicarbonate 19 mmol/l

Urea 7.0 mmol/l

Creatinine 112 µmol/l

What is the anion gap?

4 mmol/L

14 mmol/L

20 mmol/L

21 mmol/L

23 mmol/L

The anion gap may be calculated by using (sodium + potassium) - (bicarbonate +


chloride)

= (142 + 4.0) - (104 + 19) = 23 mmol/L

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Anion gap
The anion gap is calculated by:

(sodium + potassium) - (bicarbonate + chloride)

A normal anion gap is 8-14 mmol/L

It is useful to consider in patients with a metabolic acidosis:

Causes of a normal anion gap or hyperchloraemic metabolic acidosis


gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison's disease
gathered by dr. elbarky

Causes of a raised anion gap metabolic acidosis


lactate: shock, hypoxia
ketones: diabetic ketoacidosis, alcohol
urate: renal failure
acid poisoning: salicylates, methanol

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Question 156 of 192

 

A 48 year old woman suffers blunt trauma to the head and develops respiratory
compromise. As a result she develops hypercapnia. Which of the following effects
is most likely to ensue?

Cerebral vasoconstriction

Cerebral vasodilation
gathered by dr. elbarky

Cerebral blood flow will remain unchanged

Shunting of blood to peripheral tissues will occur in preference to CNS


perfusion

None of the above

Hypercapnia will tend to produce cerebral vasodilation. This is of considerable


importance in patients with cranial trauma as it may increase intracranial pressure.

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Applied neurophysiology

Pressure within the cranium is governed by the Monroe-Kelly doctrine. This


considers the skull as a closed box. Increases in mass can be
accommodated by loss of CSF. Once a critical point is reached (usually 100-
120ml of CSF lost) there can be no further compensation and ICP rises
sharply. The next step is that pressure will begin to equate with MAP and
neuronal death will occur. Herniation will also accompany this process.
The CNS can autoregulate its own blood supply. Vaso constriction and
dilatation of the cerebral blood vessels is the primary method by which this
occurs. Extremes of blood pressure can exceed this capacity resulting in
risk of stroke. Other metabolic factors such as hypercapnia will also cause
vasodilation, which is of importance in ventilating head injured patients.
The brain can only metabolise glucose, when glucose levels fall,
consciousness will be impaired.

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B 53.9%
C 11.8%
D 8.6%
E 6%

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Question 157 of 192

 

The Cori cycle is important in lactate metabolism in the septic surgical patient. It is
used to describe a pathway in which glucose is metabolised anaerobically to
lactate in one tissue and the lactate is converted back to glucose in another. Which
one of the following relies on this cycle to meet all of its energy needs?

Hepatocyte
gathered by dr. elbarky

Leucocyte

Erythrocyte

Pneumocyte

Goblet cells

Erythrocytes lack a mitochondria and therefore they generate energy via glycolytic
pathways only. All the other cell types have mitochondria and will therefore use the
Krebs cycle unless true anaerobic conditions prevail.

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Cellular metabolism

Circulating glucose enters the cell, subsequently a glycolytic process results


in the generation of ATP and pyruvate
In the presence of oxygen, the pyruvate from the glycolytic process then
enters the Krebs cycle
When oxygen is limited or absent, pyruvate enters an anaerobic pathway. In
these reactions, pyruvate can be converted into lactic acid. In addition to
generating an additional ATP, this pathway serves to keep the pyruvate
concentration low so glycolysis continues, and it oxidizes NADH into the
NAD+ needed by glycolysis. In this reaction, lactic acid replaces oxygen as
the final electron acceptor. Anaerobic respiration occurs in most cells of the
body when oxygen is limited or mitochondria are absent or nonfunctional.
For example, because erythrocytes (red blood cells) lack mitochondria, they
must produce their ATP from anaerobic respiration. This is an effective
pathway of ATP production for short periods of time, ranging from seconds
to a few minutes. The lactic acid produced diffuses into the plasma and is
carried to the liver, where it is converted back into pyruvate or glucose via
the Cori cycle
In the presence of oxygen, pyruvate can enter the Krebs cycle where
additional energy is extracted as electrons are transferred from the pyruvate
to the receptors NAD+, GDP, and FAD, with carbon dioxide being a by
product. The NADH and FADH2 pass electrons on to the electron transport
chain, which uses the transferred energy to produce ATP. As the terminal
step in the electron transport chain, oxygen is the terminal electron acceptor
and creates water inside the mitochondria.
gathered by dr. elbarky

The oxidative pathways eventually yield a total of 36 ATP molecules and are
therefore far better at generating energy than anaerobic pathways.

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C 45.3%
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Question 158 of 192

 

A 53 year old man is on the intensive care unit following an emergency abdominal
aortic aneurysm repair. He develops abdominal pain and diarrhoea and is
profoundly unwell. His abdomen has no features of peritonism. Which of the
following arterial blood gas pictures is most likely to be present?

pH 7.45, pO2 10.1, pCO2 3.2, Base excess 0, Lactate 0


gathered by dr. elbarky

pH 7.35, pO2 8.0, pCO2 5.2, Base excess 2, Lactate 1

pH 7.20, pO2 9.0, pCO2 3.5, Base excess -10, Lactate 8

pH 7.29, pO2 8.9, pCO2 5.9, Base excess -4, Lactate 3

pH 7.30, pO2 9.2 pCO2 4.8, Base excess -2, lactate 1

This man is likely to have a metabolic acidosis secondary to a mesenteric infarct.

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Disorders of acid - base balance

Disorders of acid- base balance are often covered in the MRCS part A.

The acid-base normogram below shows how the various disorders may be
categorised
gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb072b.png)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Acid-base
/images_eMRCS/swb072b.png)
homeostasis)

Metabolic acidosis
This is the most common surgical acid - base disorder.
Reduction in plasma bicarbonate levels.
Two mechanisms:

1. Gain of strong acid (e.g. diabetic ketoacidosis)


2. Loss of base (e.g. from bowel in diarrhoea)
- Classified according to the anion gap, this can be calculated by:
(Na+ + K+) - (Cl- + HCO3-).
- If a question supplies the chloride level then this is often a clue that the anion gap
should be calculated. The normal range = 10-18 mmol/L

Normal anion gap ( = hyperchloraemic metabolic acidosis)


Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
Renal tubular acidosis
Drugs: e.g. acetazolamide
Ammonium chloride injection
Addison's disease

Raised anion gap


Lactate: shock, hypoxia
Ketones: diabetic ketoacidosis, alcohol
Urate: renal failure
Acid poisoning: salicylates, methanol
Metabolic acidosis secondary to high lactate levels may be subdivided into two
types:
Lactic acidosis type A: (Perfusion disorders e.g.shock, hypoxia, burns)
Lactic acidosis type B: (Metabolic e.g. metformin toxicity)

Metabolic alkalosis
Usually caused by a rise in plasma bicarbonate levels.
Rise of bicarbonate above 24 mmol/L will typically result in renal excretion
of excess bicarbonate.
Caused by a loss of hydrogen ions or a gain of bicarbonate. It is due mainly
to problems of the kidney or gastrointestinal tract
gathered by dr. elbarky

Causes
Vomiting / aspiration (e.g. Peptic ulcer leading to pyloric stenosis,
nasogastric suction)
Diuretics
Liquorice, carbenoxolone
Hypokalaemia
Primary hyperaldosteronism
Cushing's syndrome
Bartter's syndrome
Congenital adrenal hyperplasia

Mechanism of metabolic alkalosis


Activation of renin-angiotensin II-aldosterone (RAA) system is a key factor
Aldosterone causes reabsorption of Na+ in exchange for H+ in the distal
convoluted tubule
ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA
system → raised aldosterone levels
In hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+
into cells to maintain neutrality

Respiratory acidosis
Rise in carbon dioxide levels usually as a result of alveolar hypoventilation
Renal compensation may occur leading to Compensated respiratory acidosis

Causes
COPD
Decompensation in other respiratory conditions e.g. Life-threatening asthma
/ pulmonary oedema
Sedative drugs: benzodiazepines, opiate overdose
Respiratory alkalosis
Hyperventilation resulting in excess loss of carbon dioxide
This will result in increasing pH

Causes
Psychogenic: anxiety leading to hyperventilation
Hypoxia causing a subsequent hyperventilation: pulmonary embolism, high
altitude
Early salicylate poisoning*
CNS stimulation: stroke, subarachnoid haemorrhage, encephalitis
Pregnancy
gathered by dr. elbarky

*Salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis.


Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst
later the direct acid effects of salicylates (combined with acute renal failure) may
lead to an acidosis

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C 57.3%
D 15.1%
E 9%

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Question 159 of 192

 

Which of these fluids is not an intravenous colloid?

Gelofusine

Dextran 40

Human albumin solution


gathered by dr. elbarky

Hydroxyethyl starch

Bicarbonate 8.4%

Bicarbonate is a crystalloid.

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Pre operative fluid management

Fluid management has been described in the British Consensus guidelines on IV


fluid therapy for Adult Surgical patients (GIFTASUP) and by NICE (CG174
December 2013 updated May 2017)

The Recommendations include:


Use Ringer's lactate or Hartmann's when a crystalloid is needed for
resuscitation or replacement of fluids. Avoid 0.9% N. Saline (due to risk of
hyperchloraemic acidosis) unless patient vomiting or has gastric drainage.
Use 4%/0.18% dextrose saline or 5% dextrose in maintenance fluids. It
should not be used in resuscitation or as replacement fluids.
Adult maintenance fluid requirements are: Na 50-100 mmol/day and K 40-80
mmol/day in 1.5-2.5L fluid per day.
Patients for elective surgery should NOT be nil by mouth for >2 hours
(unless has disorder of gastric emptying).
Patients for elective surgery should be given carbohydrate rich drinks 2-3h
before. Ideally this should form part of a normal pre op plan to facilitate
recovery.
Avoid mechanical bowel preparation.
If bowel prep is used, simultaneous administration of Hartmann's or Ringer's
lactate should be considered.
Excessive fluid losses from vomiting should be treated with a crystalloid
with potassium replacement. 0.9% N. Saline should be given if there is
hypochloraemia. Otherwise Hartmann's or Ringer lactate should be given for
diarrhoea/ileostomy/ileus/obstruction. Hartmann's should also be given in
sodium losses secondary to diuretics.
High risk patients should receive fluids and inotropes.
An attempt should be made to detect pre or operative hypovolaemia using
flow based measurements. If this is not available, then clinical evaluation is
needed i.e. JVP, pulse volume etc.
gathered by dr. elbarky

In Blood loss or infection causing hypovolaemia should be treated with a


balanced crystalloid or colloid (or until blood available in blood loss). A
critically ill patient is unable to excrete Na or H20 leading to a 5% risk of
interstitial oedema. Therefore 5% dextrose as well as colloid should be
given.
If patients need IV fluid resuscitation, use crystalloids that contain sodium in
the range 130-154 mmol/l, with a bolus of 500 ml over less than 15 minutes
(NICE Guidance CG 174).

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B 11.7%
C 8.9%
D 7.9%
E 63.6%

63.6% of users answered this question correctly


Question 160 of 192

 

Cortisol is predominantly produced by which of the following?

Zona fasciculata of the adrenal

Zona glomerulosa of the adrenal

Zona reticularis of the adrenal


gathered by dr. elbarky

Adrenal medulla

Posterior lobe of the pituitary

Relative Glucocorticoid activity:

Hydrocortisone = 1
Prednisolone = 4
Dexamethasone = 25

Cortisol is produced by the zona fasciculata of the adrenal gland.

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Cortisol

Glucocorticoid
Released by zona fasiculata of the adrenal gland
90% protein bound; 10% active
Circadian rhythm: High in the mornings
Negative feedback via ACTH
Actions
Glycogenolysis
Gluconeogenesis
Protein catabolism
Lipolysis
Stress response
Anti-inflammatory
Decrease protein in bones
Increase gastric acid
Increases neutrophils/platelets/red blood cells
Inhibits fibroblastic activity
gathered by dr. elbarky

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B 17.1%
C 9.7%
D 7.6%
E 4.8%

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Question 161 of 192

 

A 34 year old male donates a unit of blood. It is stored at 4 oC. After 72 hours
which of the following clotting factors will be most affected?

Factor IV

Factor II
gathered by dr. elbarky

Factor VIII

Factor IX

Factor XI

Factors V and VIII are sensitive to temperature which is the reason why FFP is
frozen soon after collection.

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Blood products

Whole blood fractions

Fraction Key points

Packed red cells Used for transfusion in chronic anaemia and cases where
infusion of large volumes of fluid may result in
cardiovascular compromise. Product obtained by
centrifugation of whole blood.

Platelet rich Usually administered to patients who are


plasma thrombocytopaenic and are bleeding or require surgery. It is
obtained by low speed centrifugation.
Platelet Prepared by high speed centrifugation and administered to
concentrate patients with thrombocytopaenia.

Fresh frozen Prepared from single units of blood.


plasma Contains clotting factors, albumin and
immunoglobulin.
Unit is usually 200 to 250ml.
Usually used in correcting clotting deficiencies in
patients with hepatic synthetic failure who are due to
undergo surgery.
Usual dose is 12-15ml/Kg-1.
It should not be used as first line therapy for
hypovolaemia.
gathered by dr. elbarky

Cryoprecipitate Formed from supernatant of FFP.


Rich source of Factor VIII and fibrinogen.
Allows large concentration of factor VIII to be
administered in small volume.

SAG-Mannitol Removal of all plasma from a blood unit and substitution


Blood with:
Sodium chloride
Adenine
Anhydrous glucose
Mannitol

Up to 4 units of SAG M Blood may be administered.


Thereafter whole blood is preferred. After 8 units, clotting
factors and platelets should be considered.

Cell saver devices


These collect patients own blood lost during surgery and then re-infuse it. There
are two main types:
Those which wash the blood cells prior to re-infusion. These are more
expensive to purchase and more complicated to operate. However, they
reduce the risk of re-infusing contaminated blood back into the patient.
Those which do not wash the blood prior to re-infusion.

Their main advantage is that they avoid the use of infusion of blood from donors
into patients and this may reduce risk of blood borne infection. It may be
acceptable to Jehovah's witnesses. It is contraindicated in malignant disease for
risk of facilitating disease dissemination.

Blood products used in warfarin reversal


In some surgical patients the use of warfarin can pose specific problems and may
require the use of specialised blood products
Immediate or urgent surgery in patients taking warfarin(1) (2):

1. Stop warfarin

2. Vitamin K (reversal within 4-24 hours)


-IV takes 4-6h to work (at least 5mg)
-Oral can take 24 hours to be clinically effective

3. Fresh frozen plasma


Used less commonly now as 1st line warfarin reversal
-30ml/kg-1
-Need to give at least 1L fluid in 70kg person (therefore not appropriate in fluid
overload)
-Need blood group
gathered by dr. elbarky

-Only use if human prothrombin complex is not available

4. Human Prothrombin Complex (reversal within 1 hour)


-Bereplex 50 u/kg
-Rapid action but factor 6 short half life, therefore give with vitamin K

References
1. Dentali, F., C. Marchesi, et al. (2011). 'Safety of prothrombin complex
concentrates for rapid anticoagulation reversal of vitamin K antagonists. A meta-
analysis.' Thromb Haemost 106(3): 429-438.

2. http://www.transfusionguidelines.org/docs/pdfs/bbt-03warfarin-reversal-
flowchart-2006.pdf

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Question 162 of 192

 

A 23 year old man presents with blunt abdominal trauma and a splenic bleed is
suspected. He is commenced on an infusion of tranexamic acid. Which of the
following best describes its mechanism of action?

Inhibition of plasmin

Inhibition of thrombin
gathered by dr. elbarky

Inhibition of factor II

Inhibition of factor Xa

Activation of factor VIII

Tranexamic acid inhibits plasmin and this prevents fibrin degradation.

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Tranexamic acid

Tranexamic acid is a synthetic derivative of lysine. Its primary mode of action is as


an anti fibrinolytic that competitively inhibits the conversion of plasminogen to
plasmin. Plasmin degrades fibrin and therefore rendering plasmin inactive slows
this process.
The role of tranexamic acid in trauma was investigated in the CRASH 2 trial and
has been shown to be of benefit in bleeding trauma when administered in the first
3 hours.

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B 20.1%
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C 7.1%
D 11.8%
E 17.2%

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Question 163 of 192

 

A 44 year old lady presents with jaundice. Following a minor ward based surgical
procedure she develops troublesome and persistent bleeding. Deficiency of which
of the vitamins listed below is responsible?

Vitamin C

Vitamin K
gathered by dr. elbarky

Vitamin D

Vitamin B

Vitamin A

Patients who are jaundiced usually have impaired absorption of vitamin K. This
can result in loss of the vitamin K dependent clotting factors and troublesome
bleeding.

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Vitamin deficiency

Vitamin Effect of deficiency

A Night blindness
Epithelial atrophy
Infections

B1 Beriberi

B2 Dermatitis and photosensitivity


B3 Pellagra

B12 Pernicious anaemia

C Poor wound healing


Impaired collagen synthesis

D Rickets (Children)
Osteomalacia (Adults)

K Clotting disorders

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gathered by dr. elbarky

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A 7.6%
B 77.5%
C 5.2%
D 5.3%
E 4.4%

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Question 164 of 192

 

A 34 year old lady has just undergone a parathyroidectomy for primary


hyperparathyroidism. The operation is difficult and all 4 glands were explored. The
wound was clean and dry at the conclusion of the procedure and a suction drain
inserted. On the ward she becomes irritable and develops stridor. On examination,
her neck is soft and the drain empty. Which of the following treatments should be
tried initially?
gathered by dr. elbarky

Administration of intravenous calcium gluconate

Administration of intravenous lorazepam

Removal of the skin closure on the ward

Direct laryngoscopy

Administration of calcichew D3 orally

Exploration of the parathyroid glands may result in impairment of the blood supply.
Serum PTH levels can fall quickly and features of hypocalcaemia may ensue, these
include neuromuscular irritability and laryngospasm. Prompt administration of
intravenous calcium gluconate can be lifesaving. The absence of any neck swelling
and no blood in the drain would go against a contained haematoma in the neck
(which should be managed by removal of skin closure).

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Calcium homeostasis

Calcium ions are linked to a wide range of physiological processes. The largest
store of bodily calcium is contained within the skeleton. Calcium levels are
primarily controlled by parathyroid hormone, vitamin D and calcitonin.

Hormonal regulation of calcium


Hormone Actions

Parathyroid hormone (PTH) Increase calcium levels and


decrease phosphate levels
Increases bone resorption
Immediate action on osteoblasts to
increase ca2+ in extracellular fluid
Osteoblasts produce a protein
signaling molecule that activate
osteoclasts which cause bone
resorption
Increases renal tubular reabsorption
of calcium
Increases synthesis of 1,25(OH)2D
gathered by dr. elbarky

(active form of vitamin D) in the


kidney which increases bowel
absorption of Ca2+
Decreases renal phosphate
reabsorption

1,25-dihydroxycholecalciferol Increases plasma calcium and


(the active form of vitamin D) plasma phosphate
Increases renal tubular reabsorption
and gut absorption of calcium
Increases osteoclastic activity at
high levels and osteoblasts at low
levels
Increases renal phosphate
reabsorption

Calcitonin Secreted by C cells of thyroid


Inhibits intestinal calcium absorption
Inhibits osteoclast activity
Inhibits renal tubular absorption of
calcium

Both growth hormone and thyroxine also play a small role in calcium metabolism.

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A 49.6%
B 6.2%
C 23.3%
D 14.6%
gathered by dr. elbarky

E 6.3%

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Question 165 of 192

 

What is the approximate volume of pancreatic secretions in a 24 hour period?

100ml

200ml

500ml
gathered by dr. elbarky

1500ml

3000ml

Typically the pancreas secretes between 1000 and 1500ml per day.

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Pancreas exocrine physiology

Composition of pancreatic secretions


Pancreatic secretions are usually 1000-1500ml per 24 hours and have a pH of 8.
Secretion Source Substances secreted

Trypsinogen
Procarboxylase
Enzymic Acinar cells
Amylase
Elastase

Sodium
Bicarbonate
Water
Ductal and
Aqueous Potassium
Centroacinar cells
Chloride
NB: Sodium and potassium reflect their plasma levels;
chloride and bicarbonate vary with flow rate
Regulation
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.

Enzyme activation
Trypsinogen is converted via enterokinase to active trypsin in the duodenum.
Trypsin then activates the other inactive enzymes
gathered by dr. elbarky

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D 54.8%
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Question 166 of 192

 

A patient loses 1.6L of fresh blood from their abdominal drain. Which of the
following will not decrease?

Cardiac output

Renin secretion
gathered by dr. elbarky

Firing of carotid baroreceptors

Firing of aortic baroreceptors

Blood pressure

Renin secretion will increase as systemic hypotension will cause impairment of


renal blood flow. Although the kidney can autoregulate its own blood flow over a
range of systemic blood pressures a loss of 1.6 L will usually produce an increase
in renin secretion.

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Shock

Shock occurs when there is insufficient tissue perfusion.


The pathophysiology of shock is an important surgical topic and may be
divided into the following aetiological groups:
Septic
Haemorrhagic
Neurogenic
Cardiogenic
Anaphylactic

Septic shock
Septic shock is a major problem and those patients with severe sepsis have a
mortality rate in excess of 40%. In those who are admitted to intensive care
mortality ranges from 6% with no organ failure to 65% in those with 4 organ failure.

Sepsis is defined as an infection that triggers a particular Systemic Inflammatory


Response Syndrome (SIRS). This is characterised by body temperature outside 36
oC - 38 o C, HR >90 beats/min, respiratory rate >20/min, WBC count >12,000/mm 3

or < 4,000/mm3, altered mental state or hyperglycaemia (in absence of diabetes).

Patients with infections and two or more elements of SIRS meet the diagnostic
criteria for sepsis. Those with organ failure have severe sepsis and those with
refractory hypotension -septic shock.

During the septic process there is marked activation of the immune system with
gathered by dr. elbarky

extensive cytokine release. This may be coupled with or triggered by systemic


circulation of bacterial toxins. These all cause endothelial cell damage and
neutrophil adhesion. The overall hallmarks are thus those of excessive
inflammation, coagulation and fibrinolytic suppression.

The surviving sepsis campaign (2012) highlights the following key areas for
attention:
Prompt administration of antibiotics to cover all likely pathogens coupled
with a rigorous search for the source of infection.
Haemodynamic stabilisation. Many patients are hypovolaemic and require
aggressive fluid administration. Aim for CVP 8-12 cm H2O, MAP >65mmHg.
Modulation of the septic response. This includes manoeuvres to counteract
the changes and includes measures such as tight glycaemic control. The
routine use of steroids is not advised.

In surgical patients, the main groups with septic shock include those with
anastomotic leaks, abscesses and extensive superficial infections such as
necrotising fasciitis. When performing surgery the aim should be to undertake the
minimum necessary to restore physiology. These patients do not fare well with
prolonged surgery. Definitive surgery can be more safely undertaken when
physiology is restored and clotting in particular has been normalised.

Haemorrhagic shock
The average adult blood volume comprises 7% of body weight. Thus in the 70 Kg
adult this will equate to 5 litres. This changes in children (8-9% body weight) and is
slightly lower in the elderly.

The table below outlines the 4 major classes of haemorrhagic shock and their
associated physiological sequelae:

Parameter Class I Class II Class III Class IV


Parameter Class I Class II Class III Class IV

Blood loss ml <750ml 750-1500ml 1500-2000ml >2000ml

Blood loss % <15% 15-30% 30-40% >40%

Pulse rate <100 >100 >120 >140

Blood pressure Normal Normal Decreased Decreased

Respiratory rate 14-20 20-30 30-40 >35

Urine output >30ml 20-30ml 5-15ml <5ml

Symptoms Normal Anxious Confused Lethargic


gathered by dr. elbarky

Decreasing blood pressure during haemorrhagic shock causes organ


hypoperfusion and relative myocardial ischaemia. The cardiac index gives a
numerical value for tissue oxygen delivery and is given by the equation: Cardiac
index= Cardiac output/ body surface area. Where Hb is haemoglobin
concentration in blood and SaO2 the saturation and PaO2 the partial pressure of
oxygen. Detailed knowledge of this equation is required for the MRCS Viva but not
for part A, although you should understand the principle.

In patients suffering from trauma the most likely cause of shock is haemorrhage.
However, the following may also be the cause or occur concomitantly:

Tension pneumothorax
Spinal cord injury
Myocardial contusion
Cardiac tamponade

When assessing trauma patients it is worth remembering that in order to generate


a palpable femoral pulse an arterial pressure of >65mmHg is required.

Once bleeding is controlled and circulating volume normalised the levels of


transfusion should be to maintain a Hb of 7-8 in those with no risk factors for
tissue hypoxia and Hb 10 for those who have such risk factors.

Neurogenic shock
This occurs most often following a spinal cord transection, usually at a high level.
There is resultant interruption of the autonomic nervous system. The result is
either decreased sympathetic tone or increased parasympathetic tone, the effect
of which is a decrease in peripheral vascular resistance mediated by marked
vasodilation.

This results in decreased preload and thus decreased cardiac output (Starlings
law). There is decreased peripheral tissue perfusion and shock is thus produced. In
contrast with many other types of shock peripheral vasoconstrictors are used to
return vascular tone to normal.

Cardiogenic shock
In medical patients the main cause is ischaemic heart disease. In the traumatic
setting direct myocardial trauma or contusion is more likely. Evidence of ECG
changes and overlying sternal fractures or contusions should raise the suspicion
of injury. Treatment is largely supportive and transthoracic echocardiography
should be used to determine evidence of pericardial fluid or direct myocardial
injury. The measurement of troponin levels in trauma patients may be undertaken
but they are less useful in delineating the extent of myocardial trauma than
following MI.
gathered by dr. elbarky

When cardiac injury is of a blunt nature and is associated with cardiogenic shock
the right side of the heart is the most likely site of injury with chamber and or valve
rupture. These patients require surgery to repair these defects and will require
cardiopulmonary bypass to achieve this. Some may require intra aortic balloon
pump as a bridge to surgery.

Anaphylactic shock
Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic
hypersensitivity reaction.

Anaphylaxis is one of the few times when you would not have time to look up the
dose of a medication. The Resuscitation Council guidelines on anaphylaxis have
recently been updated. Adrenaline is by far the most important drug in anaphylaxis
and should be given as soon as possible. The recommended doses for adrenaline,
hydrocortisone and chlorpheniramine are as follows:

Adrenaline Hydrocortisone Chlorpheniramine

< 6 months 150 mcg (0.15ml 1 25 mg 250 mcg/kg


in 1,000)

6 months - 6 150 mcg (0.15ml 1 50 mg 2.5 mg


years in 1,000)

6-12 years 300 mcg (0.3ml 1 in 100 mg 5 mg


1,000)

Adult and child 500 mcg (0.5ml 1 in 200 mg 10 mg


12 years 1,000)

Adrenaline can be repeated every 5 minutes if necessary. The best site for IM
injection is the anterolateral aspect of the middle third of the thigh.
Common identified causes of anaphylaxis
food (e.g. Nuts) - the most common cause in children
drugs
venom (e.g. Wasp sting)

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Question 167 of 192

 

What is the typical stroke volume in a resting 70 Kg man?

10ml

150ml

125ml
gathered by dr. elbarky

45ml

70ml

Stroke volumes range from 55-100ml.

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Stroke volume-Cardiac physiology

The stroke volume equates to the volume of blood ejected from the ventricle
during each cycle of cardiac contraction. The volumes for both ventricles are
typically equal and equate roughly to 70ml for a 70Kg man. It is calculated by
subtracting the end systolic volume from the end diastolic volume.

Factors affecting stroke volume


Cardiac size
Contractility
Preload
Afterload

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C 19.6%
D 7.5%
E 50.7%

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Question 168 of 192

 

Secretions from which of the following will contain the highest levels of
potassium?

Rectum

Small bowel
gathered by dr. elbarky

Gallbladder

Pancreas

Stomach

The rectum has the potential to generate secretions rich in potassium. This is the
rationale behind administration of resins for hyperkalaemia and the development
of hypokalaemia in patients with villous adenoma of the rectum.

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Potassium secretion -GI tract

Potassium secretions

Salivary glands Variable may be up to 60mmol/L

Stomach 10 mmol/L

Bile 5 mmol/L

Pancreas 4-5 mmol/L

Small bowel 10 mmol/L


Rectum 30 mmol/L

The above table provides average figures only and the exact composition varies
depending upon the existence of disease, serum aldosterone levels and serum pH.

A key point to remember for the exam is that gastric potassium secretions are low.
Hypokalaemia may occur in vomiting, usually as a result of renal wasting of
potassium, not because of potassium loss in vomit.

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gathered by dr. elbarky

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Question 169 of 192

 

Which of the following does not decrease the functional residual capacity?

Obesity

Pulmonary fibrosis

Muscle relaxants
gathered by dr. elbarky

Laparoscopic surgery

Upright position

Increased FRC:
Erect position
Emphysema
Asthma

Decreased FRC:
Pulmonary fibrosis
Laparoscopic surgery
Obesity
Abdominal swelling
Muscle relaxants

When the patient is upright the diaphragm and abdominal organs put less pressure
on the lung bases, allowing for an increase in the functional residual capacity
(FRC). Other causes of increased FRC include:
Emphysema
Asthma

In addition to those listed above, causes of reduced FRC include:


Abdominal swelling
Pulmonary oedema
Reduced muscle tone of the diaphragm
Age
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Lung volumes

The diagram demonstrates lung volumes and capacities


gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb048b.png)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Lung
/images_eMRCS/swb048b.png)
volumes)

Definitions

Tidal volume (TV) Is the volume of air inspired and expired during
each ventilatory cycle at rest.
It is normally 500mls in males and 340mls in
females.

Inspiratory reserve Is the maximum volume of air that can be forcibly


volume (IRV) inhaled following a normal inspiration. 3000mls.

Expiratory reserve Is the maximum volume of air that can be forcibly


volume (ERV) exhaled following a normal expiration. 1000mls.

Residual volume Is that volume of air remaining in the lungs after a


(RV) maximal expiration.
RV = FRC - ERV. 1500mls.
Functional residual Is the volume of air remaining in the lungs at the
capacity (FRC) end of a normal expiration.
FRC = RV + ERV. 2500mls.

Vital capacity (VC) Is the maximal volume of air that can be forcibly
exhaled after a maximal inspiration.
VC = TV + IRV + ERV. 4500mls in males, 3500mls
in females.

Total lung capacity Is the volume of air in the lungs at the end of a
(TLC) maximal inspiration.
TLC = FRC + TV + IRV = VC + RV. 5500-6000mls.
gathered by dr. elbarky

Forced vital The volume of air that can be maximally


capacity (FVC) forcefully exhaled.

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Question 170 of 192

 

An otherwise fit 30 year old male donates 500ml of blood. Which of the processes
outlined below is most likely to occur?

Oliguria

Activation of the renin angiotensin system


gathered by dr. elbarky

Sweating

Fall in mean arterial pressure

Tachypnoea

The loss of 500ml (assuming a 70 Kg male) will usually be sufficient to activate


the renin angiotensin system. It is unlikely that it would cause any other
physiological disturbance.

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Bleeding

The initial response to bleeding, even if of relatively small volume is generalised


splanchnic vasoconstriction mediated by activation of the sympathetic nervous
system. This process of vasoconstriction is usually sufficient to maintain renal
perfusion and cardiac output if the volume of blood lost is small. Over the
following hours the circulating fluid volume is restored and normal
haemodynamics resume. Loss of greater volumes of blood will typically result in
activation in the renin angiotensin system (see diagram below).
(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb138b.png)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Renin%E2%80
/images_eMRCS/swb138b.png)
gathered by dr. elbarky

%93angiotensin system)

Where the source of bleeding ceases these physiological measures will restore
circulating volume. Ongoing bleeding will result in haemorrhagic shock.
Blood loss is typically quantified by the degree of shock produced as outlined
below:

Parameter Class I Class II Class III Class IV

Blood loss ml <750ml 750-1500ml 1500-2000ml >2000ml

Blood loss % <15% 15-30% 30-40% >40%

Pulse rate <100 >100 >120 >140

Blood pressure Normal Normal Decreased Decreased

Respiratory rate 14-20 20-30 30-40 >35

Urine output >30ml 20-30ml 5-15ml <5ml

Symptoms Normal Anxious Confused Lethargic

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E 8.4%

65% of users answered this question correctly


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Question 171 of 192

 

Which of the following haemodynamic changes is not seen in hypovolaemic


shock?

Decreased cardiac output

Increased heart rate


gathered by dr. elbarky

Reduced left ventricle filling pressures

Reduced blood pressure

Reduced systemic vascular resistance


Cardiogenic Shock:
e.g. MI, valve abnormality

increased SVR (vasoconstriction in response to low BP)


increased HR (sympathetic response)
decreased cardiac output
decreased blood pressure

Hypovolaemic shock:
blood volume depletion
e.g. haemorrhage, vomiting, diarrhoea, dehydration, third-space losses during
major operations

increased SVR
gathered by dr. elbarky

increased HR
decreased cardiac output
decreased blood pressure

Septic shock:
occurs when the peripheral vascular dilatation causes a fall in SVR
similar response may occur in anaphylactic shock, neurogenic shock

reduced SVR
increased HR
normal/increased cardiac output
decreased blood pressure

SVR will typically increase

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Shock

Shock occurs when there is insufficient tissue perfusion.


The pathophysiology of shock is an important surgical topic and may be
divided into the following aetiological groups:
Septic
Haemorrhagic
Neurogenic
Cardiogenic
Anaphylactic

Septic shock
Septic shock is a major problem and those patients with severe sepsis have a
mortality rate in excess of 40%. In those who are admitted to intensive care
mortality ranges from 6% with no organ failure to 65% in those with 4 organ failure.

Sepsis is defined as an infection that triggers a particular Systemic Inflammatory


Response Syndrome (SIRS). This is characterised by body temperature outside 36
oC - 38 o C, HR >90 beats/min, respiratory rate >20/min, WBC count >12,000/mm 3

or < 4,000/mm3, altered mental state or hyperglycaemia (in absence of diabetes).

Patients with infections and two or more elements of SIRS meet the diagnostic
gathered by dr. elbarky

criteria for sepsis. Those with organ failure have severe sepsis and those with
refractory hypotension -septic shock.

During the septic process there is marked activation of the immune system with
extensive cytokine release. This may be coupled with or triggered by systemic
circulation of bacterial toxins. These all cause endothelial cell damage and
neutrophil adhesion. The overall hallmarks are thus those of excessive
inflammation, coagulation and fibrinolytic suppression.

The surviving sepsis campaign (2012) highlights the following key areas for
attention:
Prompt administration of antibiotics to cover all likely pathogens coupled
with a rigorous search for the source of infection.
Haemodynamic stabilisation. Many patients are hypovolaemic and require
aggressive fluid administration. Aim for CVP 8-12 cm H2O, MAP >65mmHg.
Modulation of the septic response. This includes manoeuvres to counteract
the changes and includes measures such as tight glycaemic control. The
routine use of steroids is not advised.

In surgical patients, the main groups with septic shock include those with
anastomotic leaks, abscesses and extensive superficial infections such as
necrotising fasciitis. When performing surgery the aim should be to undertake the
minimum necessary to restore physiology. These patients do not fare well with
prolonged surgery. Definitive surgery can be more safely undertaken when
physiology is restored and clotting in particular has been normalised.

Haemorrhagic shock
The average adult blood volume comprises 7% of body weight. Thus in the 70 Kg
adult this will equate to 5 litres. This changes in children (8-9% body weight) and is
slightly lower in the elderly.

The table below outlines the 4 major classes of haemorrhagic shock and their
associated physiological sequelae:

Parameter Class I Class II Class III Class IV

Blood loss ml <750ml 750-1500ml 1500-2000ml >2000ml

Blood loss % <15% 15-30% 30-40% >40%

Pulse rate <100 >100 >120 >140

Blood pressure Normal Normal Decreased Decreased

Respiratory rate 14-20 20-30 30-40 >35

Urine output >30ml 20-30ml 5-15ml <5ml


gathered by dr. elbarky

Symptoms Normal Anxious Confused Lethargic

Decreasing blood pressure during haemorrhagic shock causes organ


hypoperfusion and relative myocardial ischaemia. The cardiac index gives a
numerical value for tissue oxygen delivery and is given by the equation: Cardiac
index= Cardiac output/ body surface area. Where Hb is haemoglobin
concentration in blood and SaO2 the saturation and PaO2 the partial pressure of
oxygen. Detailed knowledge of this equation is required for the MRCS Viva but not
for part A, although you should understand the principle.

In patients suffering from trauma the most likely cause of shock is haemorrhage.
However, the following may also be the cause or occur concomitantly:

Tension pneumothorax
Spinal cord injury
Myocardial contusion
Cardiac tamponade

When assessing trauma patients it is worth remembering that in order to generate


a palpable femoral pulse an arterial pressure of >65mmHg is required.

Once bleeding is controlled and circulating volume normalised the levels of


transfusion should be to maintain a Hb of 7-8 in those with no risk factors for
tissue hypoxia and Hb 10 for those who have such risk factors.

Neurogenic shock
This occurs most often following a spinal cord transection, usually at a high level.
There is resultant interruption of the autonomic nervous system. The result is
either decreased sympathetic tone or increased parasympathetic tone, the effect
of which is a decrease in peripheral vascular resistance mediated by marked
vasodilation.
This results in decreased preload and thus decreased cardiac output (Starlings
law). There is decreased peripheral tissue perfusion and shock is thus produced. In
contrast with many other types of shock peripheral vasoconstrictors are used to
return vascular tone to normal.

Cardiogenic shock
In medical patients the main cause is ischaemic heart disease. In the traumatic
setting direct myocardial trauma or contusion is more likely. Evidence of ECG
changes and overlying sternal fractures or contusions should raise the suspicion
of injury. Treatment is largely supportive and transthoracic echocardiography
should be used to determine evidence of pericardial fluid or direct myocardial
injury. The measurement of troponin levels in trauma patients may be undertaken
but they are less useful in delineating the extent of myocardial trauma than
gathered by dr. elbarky

following MI.

When cardiac injury is of a blunt nature and is associated with cardiogenic shock
the right side of the heart is the most likely site of injury with chamber and or valve
rupture. These patients require surgery to repair these defects and will require
cardiopulmonary bypass to achieve this. Some may require intra aortic balloon
pump as a bridge to surgery.

Anaphylactic shock
Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic
hypersensitivity reaction.

Anaphylaxis is one of the few times when you would not have time to look up the
dose of a medication. The Resuscitation Council guidelines on anaphylaxis have
recently been updated. Adrenaline is by far the most important drug in anaphylaxis
and should be given as soon as possible. The recommended doses for adrenaline,
hydrocortisone and chlorpheniramine are as follows:

Adrenaline Hydrocortisone Chlorpheniramine

< 6 months 150 mcg (0.15ml 1 25 mg 250 mcg/kg


in 1,000)

6 months - 6 150 mcg (0.15ml 1 50 mg 2.5 mg


years in 1,000)

6-12 years 300 mcg (0.3ml 1 in 100 mg 5 mg


1,000)

Adult and child 500 mcg (0.5ml 1 in 200 mg 10 mg


12 years 1,000)

Adrenaline can be repeated every 5 minutes if necessary. The best site for IM
injection is the anterolateral aspect of the middle third of the thigh.

Common identified causes of anaphylaxis


food (e.g. Nuts) - the most common cause in children
drugs
venom (e.g. Wasp sting)

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Question 172 of 192

 

Which of the following does not stimulate insulin release?

Gastrin

Atenolol

Protein
gathered by dr. elbarky

Secretin

Vagal cholinergic action

Beta blockers inhibit the release of insulin.

Stimulation of insulin release:

Glucose
Amino acid
Vagal cholinergic
Secretin/Gastrin/CCK
Fatty acids
Beta adrenergic drugs

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Insulin

Insulin is a peptide hormone, produced by beta cells of the pancreas, and is central
to regulating carbohydrate and fat metabolism in the body. Insulin causes cells in
the liver, skeletal muscles, and fat tissue to absorb glucose from the blood. In the
liver and skeletal muscles, glucose is stored as glycogen, and in fat cells
(adipocytes) it is stored as triglycerides.
Structure
The human insulin protein is composed of 51 amino acids, and has a molecular
weight of 5808 Da. It is a dimer of an A-chain and a B-chain, which are linked
together by disulfide bonds.

Synthesis
Pro-insulin is formed by the rough endoplasmic reticulum in pancreatic beta cells.
Then pro-insulin is cleaved to form insulin and C-peptide. Insulin is stored in
secretory granules and released in response to Ca2+.

Function
Secreted in response to hyperglycaemia
Glucose utilisation and glycogen synthesis
Inhibits lipolysis
gathered by dr. elbarky

Reduces muscle protein loss

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Question 173 of 192

 

A 32 year old man has a glomerular filtration rate of 110ml / minute at a systolic
blood pressure of 120/80. If his blood pressure were to fall to 100/70 what would
glomerular filtration rate be?

110ml / minute

100ml/ minute
gathered by dr. elbarky

55ml/ minute

25ml/ minute

75ml/ minute

The proposed drop in blood pressure falls within the range within which the kidney
autoregulates its blood supply. GFR will therefore remain unchanged.

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Renal Physiology

Overview
Each nephron is supplied with blood from an afferent arteriole that opens
onto the glomerular capillary bed.
Blood then flows to an efferent arteriole, supplying the peritubular capillaries
and medullary vasa recta.
The kidney receives up to 25% of resting cardiac output.

Control of blood flow


The kidney is able to autoregulate its blood flow between systolic pressures
of 80- 180mmHg so there is little variation in renal blood flow.
This is achieved by myogenic control of arteriolar tone, both sympathetic
input and hormonal signals (e.g. renin) are responsible.

Glomerular structure and function


Blood inside the glomerulus has considerable hydrostatic pressure.
The basement membrane has pores that will allow free diffusion of smaller
solutes, larger negatively charged molecules such as albumin are unable to
cross.
The glomerular filtration rate (GFR) is equal to the concentration of a solute
in the urine, times the volume of urine produced per minute, divided by the
plasma concentration (assuming that the solute is freely diffused e.g.
inulin).
In clinical practice creatinine is used because it is subjected to very little
proximal tubular secretion.
Although subject to variability, the typical GFR is 125ml per minute.
gathered by dr. elbarky

Glomerular filtration rate = Total volume of plasma per unit time leaving the
capillaries and entering the bowman's capsule
Renal clearance = volume plasma from which a substance is removed per
minute by the kidneys

Substances used to measure GFR have the following features:


1. Inert
2. Free filtration from the plasma at the glomerulus (not protein bound)
3. Not absorbed or secreted at the tubules
4. Plasma concentration constant during urine collection

Examples: inulin, creatinine

GFR = urine concentration (mmol/l) x urine volume (ml/min)


--------------------------------------------------------------------------
plasma concentration (mmol/l)

The clearance of a substance is dependent not only on its diffusivity across


the basement membrane but also subsequent tubular secretion and / or
reabsorption.
So glucose which is freely filtered across the basement membrane is usually
reabsorbed from tubules giving a clearance of zero.

Tubular function
Reabsorption and secretion of substances occurs in the tubules.
In the proximal tubule substrates such as glucose, amino acids and
phosphate are co-transported with sodium across the semi permeable
membrane.
Up to two thirds of filtered water is reabsorbed in the proximal tubules.
This will lead to increase in urea concentration in the distal tubule allowing
for its increased diffusion.
Substances to be secreted into the tubules are taken up from the peritubular
blood by tubular cells.
Solutes such as paraaminohippuric acid are cleared with a single passage
through the kidneys and this is why it is used to measure renal plasma flow.
Ions such as calcium and phosphate will have a tubular reabsorption that is
influenced by plasma PTH levels.
Potassium may be both secreted and re-absorbed and is co-exchanged with
sodium.

Loop of Henle
Approximately 60 litres of water containing 9000mmol sodium enters the
descending limb of the loop of Henle in 24 hours.
Loops from the juxtamedullary nephrons run deep into the medulla.
The osmolarity of fluid changes and is greatest at the tip of the papilla.
The thick ascending limb is impermeable to water, but highly permeable to
sodium and chloride ions.
gathered by dr. elbarky

This loss means that at the beginning of the thick ascending limb the fluid is
hypo osmotic compared with adjacent interstitial fluid.
In the thick ascending limb the reabsorption of sodium and chloride ions
occurs by both facilitated and passive diffusion pathways.
The loops of Henle are co-located with vasa recta, these will have similar
solute compositions to the surrounding extracellular fluid so preventing the
diffusion and subsequent removal of this hypertonic fluid.
The energy dependent reabsorption of sodium and chloride in the thick
ascending limb helps to maintain this osmotic gradient.

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Question 174 of 192

 

A 23 year old man has taken an opiate overdose. Of the following structures, which
will be most affected by opiates to produce a reduction in respiratory rate?

Carotid chemoreceptors

Central chemoreceptors
gathered by dr. elbarky

Medullary respiratory centre

Pneumotaxic centre

Juxtacapillary (J) receptors

Opiates typically affect the medullary respiratory centre to depress respiratory


activity.

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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 Inspiratory and expiratory neurones. Has ventral group


respiratory centre 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 Upper pons, inhibits inspiration at a certain point. Fine


centre tunes the respiratory rate.

Ventillatory variables
Levels of pCO2 most important in ventilation control
Levels of O2 are less important.
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.
gathered by dr. elbarky

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

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Question 175 of 192

 

What is the substrate of renin?

Aldosterone

Angiotensinogen

Angiotensin converting enzyme


gathered by dr. elbarky

Angiotensin I

Angiotensin II

Renin hydrolyses angiotensinogen to form angiotensin I.


gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb160b.png)
Image sourced from (https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS
Wikipedia () /swb160b.png)

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Renin

Renin is secreted by juxtaglomerular cells and hydrolyses angiotensinogen to


produce angiotensin I

Factors stimulating renin secretion


Hypotension causing reduced renal perfusion
Hyponatraemia
Sympathetic nerve stimulation
Catecholamines
Erect posture

Factors reducing renin secretion


Drugs: beta-blockers, NSAIDs

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Question 176 of 192

 

Which of the following physiological changes do not occur following


tracheostomy?

Alveolar ventilation is increased.

Anatomical dead space is reduced by 50%.


gathered by dr. elbarky

Work of breathing is increased.

Proportion of ciliated epithelial cells in the trachea may decrease.

Splinting of the larynx may lead to swallowing difficulties.

Work of breathing is decreased which is one of the reasons it is a popular option


for weaning ventilated patients. Humidified air in this setting helps to reduce the
viscosity of mucous that forms.

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Trachea

Trachea

Location C6 vertebra to the upper border of T5 vertebra


(bifurcation)

Arterial and venous Inferior thyroid arteries and the thyroid venous
supply plexus.

Nerve Branches of vagus, sympathetic and the recurrent


nerves
Relations in the neck

Anterior(Superior to Isthmus of the thyroid gland


inferior) Inferior thyroid veins
Arteria thyroidea ima (when that vessel
exists)
Sternothyroid
Sternohyoid
Cervical fascia
Anastomosing branches between the
anterior jugular veins

Posterior Oesophagus.

Laterally Common carotid arteries


gathered by dr. elbarky

Right and left lobes of the thyroid gland


Inferior thyroid arteries
Recurrent laryngeal nerves

Relations in the thorax

Anterior
Manubrium, the remains of the thymus, the aortic arch, left common carotid
arteries, and the deep cardiac plexus

Lateral
In the superior mediastinum, on the right side is the pleura and right vagus;
on its left side are the left recurrent nerve, the aortic arch, and the left
common carotid and subclavian arteries.

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Question 177 of 192

 

A 45 year old man undergoes a sub total colectomy and formation of end
ileostomy. What is the most likely sodium content per litre of ileostomy fluid?

120 mmol

60 mmol
gathered by dr. elbarky

20 mmol

210 mmol

180 mmol

Investigators in the 1960's dehydrated and measured the sodium content of


ileostomy effluent and determined this concentration. Not an experiment many
would care to repeat!

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Gastrointestinal secretions

Up to 7 litres of gastrointestinal secretions enter the lumen of the GI tract in a 24


hour period. The absorptive function of the small bowel is such that by the time a
formed stool is created, it will contain, on average 200ml water.
The common secretions together with their approximate volumes are
demonstrated below:

Origin of Volume in ml / Na + K+ Cl-


secretion 24 hour period mmol/L mmol/L mmol/L HCO3

Salivary glands 1500 10 26 10 30


Origin of Volume in ml / Na + K+ Cl-
secretion 24 hour period mmol/L mmol/L mmol/L HCO3

Stomach 1500 60 10 130

Duodenum 100-2000 140 80 80

Pancreas 1000 140 5 70 115

Bile 50-800 145 5 100 35

Jejunum/ileum 3000 140 10 104 30

Colon 100 60 30 40
gathered by dr. elbarky

The regulation of these secretions is dependent upon location. In the salivary


glands a complex interaction of flow rate governed by the autonomic nervous
system. The exact composition of sodium and potassium is regulated by
aldosterone. In the stomach hormones such as gastrin play a role and feedback is
both endocrine and neurologically mediated (vagus). In the duodenum CCK is
released in response to duodenal distension and this causes contraction of the
gallbladder and release of bile.

Pancreatic secretions are affected by somatostatin. The secretions in the small


bowel are affected by the osmolality of the lumenal contents. This is in part due to
the tightness of cellular junctions and in this regard the jejunum is more permeable
than the ileum. The practical implication of this is that if an individual has an
extensive intestinal resection and a high output, proximally sited stoma then
administration of hypotonic rather than isotonic solutions will result in worsening
of electrolyte disturbances as electrolyte rich secretions will enter the jejunum.

In some individuals a colectomy or similar procedure results in formation of an end


or loop ileostomy. Ileostomies typically lose between 500 and 1000ml over a 24
hour period and patients with high output ileostomies can rapidly become
dehydrated. Ileostomy effluent typically contains 126mmol/L of sodium and
22mmol/L of potassium. Knowledge of this fluid composition should guide fluid
prescribing in replacing losses.

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Question 178 of 192

 

The oxygen-haemoglobin dissociation curve is shifted to the right in which of the


following scenarios?

Hypothermia

Respiratory alkalosis
gathered by dr. elbarky

Low altitude

Decreased 2,3-DPG in transfused red cells

Chronic iron deficiency anaemia

Mnemonic to remember causes of right shift of the oxygen dissociation


curve:

CADET face RIGHT

C O2
A cidosis
2,3-DPG
E xercise
T emperature

The curve is shifted to the right when there is an increased oxygen requirement by
the tissue. This includes:
Increased temperature
Acidosis
Increased DPG:

DPG is found in erythrocytes and is increased during glycolysis. It binds to the Hb


molecule, thereby releasing oxygen to tissues. DPG is increased in conditions
associated with poor oxygen delivery to tissues, such as anaemia and high
altitude.

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Oxygen Transport

Oxygen transport
Almost all oxygen is transported within erythrocytes. It has limited solubility and
only 1% is carried as solution. Therefore the amount of oxygen transported will
depend upon haemoglobin concentration and its degree of saturation.

Haemoglobin
gathered by dr. elbarky

Globular protein composed of 4 subunits. Haem consists of a protoporphyrin ring


surrounding an iron atom in its ferrous state. The iron can form two additional
bonds; one with oxygen and the other with a polypeptide chain. There are two
alpha and two beta subunits to this polypeptide chain in an adult and together
these form globin. Globin cannot bind oxygen but is able to bind to carbon dioxide
and hydrogen ions, the beta chains are able to bind to 2,3 diphosphoglycerate. The
oxygenation of haemoglobin is a reversible reaction. The molecular shape of
haemoglobin is such that binding of one oxygen molecule facilitates the binding of
subsequent molecules.

Oxygen dissociation curve


The oxygen dissociation curve describes the relationship between the
percentage of saturated haemoglobin and partial pressure of oxygen in the
blood. It is not affected by haemoglobin concentration.
Chronic anaemia causes 2, 3 DPG levels to increase, hence shifting the
curve to the right

Haldane effect
Shifts to left = for given oxygen tension there is increased saturation of Hb
with oxygen i.e. Decreased oxygen delivery to tissues

Bohr effect
Shifts to right = for given oxygen tension there is reduced saturation of Hb
with oxygen i.e. Enhanced oxygen delivery to tissues
gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb038b.png)
Image sourced from Wikipedia
(http://en.wikipedia.org/wiki/Oxygen (https://d2zgo9qer4wjf4.cloudfront.net
%E2%80%93haemoglobin dissociation /images_eMRCS/swb038b.png)
curve)

Shifts to Left = Lower oxygen delivery Shifts to Right = Raised oxygen


HbF, methaemoglobin, delivery
carboxyhaemoglobin raised [H+] (acidic)
low [H+] (alkali) raised pCO2
low pCO2 raised 2,3-DPG*
low 2,3-DPG raised temperature
low temperature

*2,3-diphosphoglycerate

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Question 179 of 192

 

An over enthusiastic medical student decides to ask you questions about ECGs.
Rather than admitting your dwindling knowledge on this topic, you bravely attempt
to answer her questions! One question is what component of the ECG represents
ventricular repolarization?

QRS complex
gathered by dr. elbarky

Q-T interval

P wave

T wave

S-T segment

The T wave represents ventricular repolarization. The common sense approach to


remembering this, is to acknowledge that ventricular repolarization is the last
phase of cardiac contraction and should therefore correspond the the last part of
the QRS complex.

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The normal ECG


gathered by dr. elbarky

Image sourced from Wikipedia (https://d2zgo9qer4wjf4.cloudfront.net


P wave
(http://en.wikipedia.org/wiki/ECG) /images_eMRCS/swb110b.png)
Represents the wave of depolarization that spreads from the SA node
throughout the atria
Lasts 0.08 to 0.1 seconds (80-100 ms)
The isoelectric period after the P wave represents the time in which the
impulse is traveling within the AV node

P-R interval
Time from the onset of the P wave to the beginning of the QRS complex
Ranges from 0.12 to 0.20 seconds in duration
Represents the time between the onset of atrial depolarization and the
onset of ventricular depolarization

QRS complex
Represents ventricular depolarization
Duration of the QRS complex is normally 0.06 to 0.1 seconds

ST segment
Isoelectric period following the QRS
Represents period which the entire ventricle is depolarized and roughly
corresponds to the plateau phase of the ventricular action potential

T wave
Represents ventricular repolarization and is longer in duration than
depolarization
A small positive U wave may follow the T wave which represents the last
remnants of ventricular repolarization.

Q-T interval
Represents the time for both ventricular depolarization and repolarization to
occur, and therefore roughly estimates the duration of an average ventricular
action potential.
Interval ranges from 0.2 to 0.4 seconds depending upon heart rate.
At high heart rates, ventricular action potentials shorten in duration, which
decreases the Q-T interval. Therefore the Q-T interval is expressed as a
'corrected Q-T (QTc)' by taking the Q-T interval and dividing it by the square
root of the R-R interval (interval between ventricular depolarizations). This
allows an assessment of the Q-T interval that is independent of heart rate.
gathered by dr. elbarky

Normal corrected Q-Tc interval is less than 0.44 seconds.

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Question 180 of 192

 

A 56 year old male presents to the acute surgical take with severe abdominal pain.
He is normally fit and well. He has no malignancy. The biochemistry laboratory
contacts the ward urgently, his corrected calcium result is 3.6 mmol/l. What is the
medication of choice to treat this abnormality?

IV Pamidronate
gathered by dr. elbarky

Oral Alendronate

Dexamethasone

Vitamin D

Resonium salts

IV Pamidronate is the drug of choice as it most effective and has long lasting
effects. Calcitonin would need to be given with another agent, to ensure that the
hypercalcaemia is treated once its short term effects wear off. IV zoledronate is
preferred in scenarios associated with malignancy.

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Management of hypercalcaemia

Free Ca is affected by pH (increased in acidosis) and plasma albumin


concentration
ECG changes include: Shortening of QTc interval
Urgent management is indicated if:

Calcium > 3.5 mmol/l


Reduced consciousness

Severe abdominal pain

Pre renal failure

Management:
Airway Breathing Circulation
Intravenous fluid resuscitation with 3-6L of 0.9% Normal saline in 24 hours
Concurrent administration of calcitonin will also help lower calcium levels
Medical therapy (usually if Corrected calcium >3.0mmol/l)

Bisphosphonates
Analogues of pryrophosphate
gathered by dr. elbarky

Prevent osteoclast attachment to bone matrix and interfere with osteoclast


activity
Inhibit bone resorption.

Agents

Drug Side effects Notes

IV
pyrexia, leucopaenia Most potent agent
Pamidronate

response lasts 30 Used for malignancy associated


IV Zoledronate
days hypercalcaemia

Calcitonin
Quickest onset of action however short duration (tachyphylaxis) therefore
only given with a second agent.

Prednisolone
May be given in hypercalcaemia related to sarcoidosis, myeloma or vitamin
D intoxication.

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Question 181 of 192

 

Which of the conditions listed below is most likely to account for the following
arterial blood gas result:
pH 7.49

pO2 8.5

Bicarbonate 22
gathered by dr. elbarky

pCO2 2.4

Chloride 12meq

Respiratory alkalosis

Metabolic alkalosis

Metabolic acidosis

Type II respiratory failure

Metabolic acidosis with increased anion gap

The hyperventilation results in decreased carbon dioxide levels, causing a


respiratory alkalosis (non compensated).

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Disorders of acid - base balance

Disorders of acid- base balance are often covered in the MRCS part A.

The acid-base normogram below shows how the various disorders may be
categorised
gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb072b.png)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Acid-base
/images_eMRCS/swb072b.png)
homeostasis)

Metabolic acidosis
This is the most common surgical acid - base disorder.
Reduction in plasma bicarbonate levels.
Two mechanisms:

1. Gain of strong acid (e.g. diabetic ketoacidosis)


2. Loss of base (e.g. from bowel in diarrhoea)
- Classified according to the anion gap, this can be calculated by:
(Na+ + K+) - (Cl- + HCO3-).
- If a question supplies the chloride level then this is often a clue that the anion gap
should be calculated. The normal range = 10-18 mmol/L

Normal anion gap ( = hyperchloraemic metabolic acidosis)


Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
Renal tubular acidosis
Drugs: e.g. acetazolamide
Ammonium chloride injection
Addison's disease

Raised anion gap


Lactate: shock, hypoxia
Ketones: diabetic ketoacidosis, alcohol
Urate: renal failure
Acid poisoning: salicylates, methanol

Metabolic acidosis secondary to high lactate levels may be subdivided into two
types:
Lactic acidosis type A: (Perfusion disorders e.g.shock, hypoxia, burns)
Lactic acidosis type B: (Metabolic e.g. metformin toxicity)

Metabolic alkalosis
Usually caused by a rise in plasma bicarbonate levels.
Rise of bicarbonate above 24 mmol/L will typically result in renal excretion
of excess bicarbonate.
Caused by a loss of hydrogen ions or a gain of bicarbonate. It is due mainly
gathered by dr. elbarky

to problems of the kidney or gastrointestinal tract

Causes
Vomiting / aspiration (e.g. Peptic ulcer leading to pyloric stenosis,
nasogastric suction)
Diuretics
Liquorice, carbenoxolone
Hypokalaemia
Primary hyperaldosteronism
Cushing's syndrome
Bartter's syndrome
Congenital adrenal hyperplasia

Mechanism of metabolic alkalosis


Activation of renin-angiotensin II-aldosterone (RAA) system is a key factor
Aldosterone causes reabsorption of Na+ in exchange for H+ in the distal
convoluted tubule
ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA
system → raised aldosterone levels
In hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+
into cells to maintain neutrality

Respiratory acidosis
Rise in carbon dioxide levels usually as a result of alveolar hypoventilation
Renal compensation may occur leading to Compensated respiratory acidosis

Causes
COPD
Decompensation in other respiratory conditions e.g. Life-threatening asthma
/ pulmonary oedema
Sedative drugs: benzodiazepines, opiate overdose

Respiratory alkalosis
Hyperventilation resulting in excess loss of carbon dioxide
This will result in increasing pH

Causes
Psychogenic: anxiety leading to hyperventilation
Hypoxia causing a subsequent hyperventilation: pulmonary embolism, high
altitude
Early salicylate poisoning*
CNS stimulation: stroke, subarachnoid haemorrhage, encephalitis
Pregnancy
gathered by dr. elbarky

*Salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis.


Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst
later the direct acid effects of salicylates (combined with acute renal failure) may
lead to an acidosis

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Question 182 of 192

 

A 34 year old man receives morphine following an appendicectomy. He develops


constipation as a result. Which of the following best accounts for this process?

Stimulation of DOPA receptors

Inhibition of DOPA receptors


gathered by dr. elbarky

Stimulation of Mu receptors

Stimulation of serotonin release

Inhibition of serotonin release

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.

Constipation is a common side effect of morphine treatment and stimulation of


Mu receptors accounts for this process.

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Morphine

Strong opiate analgesic. It is a pro- type narcotic drug and its effects mediated via
the 4 types of opioid receptor. Its clinical effects stem from binding to these
receptor sites within the CNS and gastrointestinal tract. Unwanted side effects
include nausea, constipation, respiratory depression and, if used long term,
addiction .
It may be administered orally or intravenously. It can be reversed with naloxone.

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Question 183 of 192

 

A 28 year old man undergoes an ileocaecal resection to treat terminal ileal Crohns
disease. Post operatively he attends the clinic and complains of diarrhoea. His
CRP is within normal limits and small bowel enteroclysis shows no focal changes.
Which of the following interventions is most likely to be beneficial?

5 ASA drugs
gathered by dr. elbarky

Azathioprine

Pulsed methylprednisolone

Infliximab

Oral cholestyramine

The question is about high output diarrhoea following terminal ileal resection
and the most likely cause is malabsorption of bile salts. The administration of
cholestyramine (bile salt binding agent) will counter this and thats why its the
correct answer.

Malabsorption of bile salts is a common cause of diarrhoea following ileal


resection. A normal small bowel study and CRP effectively excludes active Crohns
disease and therefore immunomodulator drugs are not appropriate.

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Ileum

Anatomical overview
The terminal ileum comprises 20% of the ileum and has a diameter that is smaller
than that of the jejunum (typically 2cm at the ileocaecal valve). The ileum is
attached to the abdominal wall by a mesentery that contains more fat than that of
the jejunum. The blood supply of the ileum is derived from branches of the
superior mesenteric artery, the vascular arcades of the ileum are more densely
packed than those of the jejunum. The wall of the ileum contains Peyers patches
which are aggregations of lymphoid tissue.

Function
The main function of the terminal ileum is absorption of vitamin B12 and bile salts.
The neuroendocrine cells in the wall of the ileum may secrete hormones. In
surgical patients, resection of the terminal ileum is a common procedure for
conditions such as terminal ileal Crohns disease. Where a significant proportion of
the ileum is removed, patients are at increased risk of bile salt malabsorption with
the development of bile salt diarrhoea and increased risk of gallstones. The lack of
vitamin B12 may pre-dispose to macrocytic anaemia.
gathered by dr. elbarky

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Question 184 of 192

 

What is the main event involved in the neovascularization of the immature wound
bed following surgery?

Endothelial cell proliferation

Fibroblast proliferation
gathered by dr. elbarky

Macrophage migration

Neutrophil accumulation

Granulocyte degradation

Angiogenesis is a key event in wound healing and occurs as a result of endothelial


cell proliferation.

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Phases of wound healing

Phase Key features Cells Timeframe

Haemostasis Vasospasm in Erythrocytes and Seconds/


adjacent vessels platelets Minutes
Platelet plug
formation and
generation of fibrin
rich clot
Inflammation Neutrophils migrate Neutrophils, Days
into wound (function fibroblasts and
macrophages
impaired in diabetes).
Growth factors
released, including
basic fibroblast
growth factor and
vascular endothelial
growth factor.
Fibroblasts replicate
within the adjacent
matrix and migrate
into wound.
gathered by dr. elbarky

Macrophages and
fibroblasts couple
matrix regeneration
and clot substitution.

Regeneration Platelet derived Fibroblasts, Weeks


growth factor and endothelial cells,
transformation growth macrophages
factors stimulate
fibroblasts and
epithelial cells.
Fibroblasts produce a
collagen network.
Angiogenesis occurs
and wound resembles
granulation tissue.

Remodelling Longest phase of the Myofibroblasts 6 weeks to


healing process and 1 year
may last up to one
year (or longer).
During this phase
fibroblasts become
differentiated
(myofibroblasts) and
these facilitate wound
contraction.
Collagen fibres are
remodelled.
Microvessels regress
leaving a pale scar.
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Question 185 of 192

 

There is decreased secretion of which one of the following hormones in response


to major surgery:

Insulin

Cortisol
gathered by dr. elbarky

Renin

Anti diuretic hormone

Prolactin

Endocrine parameters reduced in stress response:


Insulin
Testosterone
Oestrogen

Insulin is often released in decreased quantities following surgery.

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Stress response: Endocrine and metabolic changes

Surgery precipitates hormonal and metabolic changes causing the stress


response.
Stress response is associated with: substrate mobilization, muscle protein
loss, sodium and water retention, suppression of anabolic hormone
secretion, activation of the sympathetic nervous system, immunological and
haematological changes.
The hypothalamic-pituitary axis and the sympathetic nervous systems are
activated and there is a failure of the normal feedback mechanisms of
control of hormone secretion.

A summary of the hormonal changes associated with the stress response:

Increased Decreased No Change

Growth hormone Insulin Thyroid stimulating


hormone

Cortisol Testosterone Luteinizing hormone

Renin Oestrogen Follicle stimulating


gathered by dr. elbarky

hormone

Adrenocorticotrophic hormone
(ACTH)

Aldosterone

Prolactin

Antidiuretic hormone

Glucagon

Sympathetic nervous system


Stimulates catecholamine release
Causes tachycardia and hypertension

Pituitary gland
ACTH and growth hormone (GH) is stimulated by hypothalamic releasing
factors, corticotrophin releasing factor (CRF) and somatotrophin (or growth
hormone releasing factor)
Perioperative increased prolactin secretion occurs by release of inhibitory
control
Secretion of thyroid stimulating hormone (TSH), luteinizing hormone (LH)
and follicle stimulating hormone (FSH) does not change significantly
ACTH stimulates cortisol production within a few minutes of the start of
surgery. More ACTH is produced than needed to produce a maximum
adrenocortical response.

Cortisol
Significant increases within 4-6 hours of surgery (>1000 nmol litre-1).
The usual negative feedback mechanism fails and concentrations of ACTH
and cortisol remain persistently increased.
The magnitude and duration of the increase correlate with the severity of
stress and the response is not abolished by the administration of
corticosteroids.
The metabolic effects of cortisol are enhanced:

Skeletal muscle protein breakdown to provide gluconeogenic precursors and


amino acids for protein synthesis in the liver
Stimulation of lipolysis
'Anti-insulin effect'
Mineralocorticoid effects
Anti-inflammatory effects
gathered by dr. elbarky

Growth hormone
Increased secretion after surgery has a minor role
Most important for preventing muscle protein breakdown and promote
tissue repair by insulin growth factors

Alpha Endorphin
Increased

Antidiuretic hormone
An important vasopressor and enhances haemostasis
Renin is released causing the conversion of angiotensinogen to angiotensin
I
Angiotensin II formed by ACE on angiotensin 1, which causes the secretion
of aldosterone from the adrenal cortex. This increases sodium reabsorption
at the distal convoluted tubule

Insulin
Release inhibited by stress
Occurs via the inhibition of the beta cells in the pancreas by the α2-
adrenergic inhibitory effects of catecholamines
Insulin resistance by target cells occurs later
The perioperative period is characterized by a state of functional insulin
deficiency

Thyroxine (T4) and tri-iodothyronine (T3)


Circulating concentrations are inversely correlated with sympathetic activity
and after surgery there is a reduction in thyroid hormone production, which
normalises over a few days.
Metabolic effect of endocrine response

Carbohydrate metabolism
Hyperglycaemia is a main feature of the metabolic response to surgery
Due to increase in glucose production and a reduction in glucose utilization
Catecholamines and cortisol promote glycogenolysis and gluconeogenesis
Initial failure of insulin secretion followed by insulin resistance affects the
normal responses
The proportion of the hyperglycaemic response reflects the severity of
surgery
Hyperglycaemia impairs wound healing and increase infection rates

Protein metabolism
Initially there is inhibition of protein anabolism, followed later, if the stress
gathered by dr. elbarky

response is severe, by enhanced catabolism


The amount of protein degradation is influenced by the type of surgery and
also by the nutritional status of the patient
Mainly skeletal muscle protein is affected
The amino acids released form acute phase proteins (fibrinogen, C reactive
protein, complement proteins, a2-macroglobulin, amyloid A and
ceruloplasmin) and are used for gluconeogenesis
Nutritional support has little effect on preventing catabolism

Lipid metabolism
Increased catecholamine, cortisol and glucagon secretion, and insulin deficiency,
promotes lipolysis and ketone body production.

Salt and water metabolism


ADH causes water retention, concentrated urine, and potassium loss and
may continue for 3 to 5 days after surgery
Renin causes sodium and water retention

Cytokines
Glycoproteins
Interleukins (IL) 1 to 17, interferons, and tumour necrosis factor
Synthesized by activated macrophages, fibroblasts, endothelial and glial
cells in response to tissue injury from surgery or trauma
IL-6 main cytokine associated with surgery. Peak 12 to 24 h after surgery
and increase by the degree of tissue damage Other effects of cytokines
include fever, granulocytosis, haemostasis, tissue damage limitation and
promotion of healing.

Modifying the response


Opioids suppress hypothalamic and pituitary hormone secretion
At high doses the hormonal response to pelvic and abdominal surgery is
abolished. However, such doses prolong recovery and increase the need for
postoperative ventilatory support
Spinal anaesthesia can reduce the glucose, ACTH, cortisol, GH and
epinephrine changes, although cytokine responses are unaltered
Cytokine release is reduced in less invasive surgery
Nutrition prevents the adverse effects of the stress response. Enteral
feeding improves recovery
Growth hormone and anabolic steroids may improve outcome
Normothermia decreases the metabolic response

References
Deborah Burton, Grainne Nicholson, and George Hall
Endocrine and metabolic response to surgery .
gathered by dr. elbarky

Contin Educ Anaesth Crit Care Pain (2004) 4(5): 144-147 doi:10.1093/bjaceaccp
/mkh040

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Question 186 of 192

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A 23 year old is stabbed in the groin and develops hypovolaemic shock. What is
the most likely finding on analysis of his urine?

Decreased specific gravity

Increased specific gravity


gathered by dr. elbarky

Increased urinary glucose

Increased urinary protein

Increased red blood cells in the urine

Hypovolaemic shock is likely to compromise renal blood flow especially if blood


pressure falls below the range at which the kidney is able to autoregulate its blood
flow. The result of this will be an increase of the specific gravity as water retention
occurs in an attempt to maintain circulating volume.

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Renal Physiology

Overview
Each nephron is supplied with blood from an afferent arteriole that opens
onto the glomerular capillary bed.
Blood then flows to an efferent arteriole, supplying the peritubular capillaries
and medullary vasa recta.
The kidney receives up to 25% of resting cardiac output.

Control of blood flow


The kidney is able to autoregulate its blood flow between systolic pressures
of 80- 180mmHg so there is little variation in renal blood flow.
This is achieved by myogenic control of arteriolar tone, both sympathetic
input and hormonal signals (e.g. renin) are responsible.

Glomerular structure and function


Blood inside the glomerulus has considerable hydrostatic pressure.
The basement membrane has pores that will allow free diffusion of smaller
solutes, larger negatively charged molecules such as albumin are unable to
cross.
The glomerular filtration rate (GFR) is equal to the concentration of a solute
in the urine, times the volume of urine produced per minute, divided by the
plasma concentration (assuming that the solute is freely diffused e.g.
inulin).
In clinical practice creatinine is used because it is subjected to very little
proximal tubular secretion.
gathered by dr. elbarky

Although subject to variability, the typical GFR is 125ml per minute.


Glomerular filtration rate = Total volume of plasma per unit time leaving the
capillaries and entering the bowman's capsule
Renal clearance = volume plasma from which a substance is removed per
minute by the kidneys

Substances used to measure GFR have the following features:


1. Inert
2. Free filtration from the plasma at the glomerulus (not protein bound)
3. Not absorbed or secreted at the tubules
4. Plasma concentration constant during urine collection

Examples: inulin, creatinine

GFR = urine concentration (mmol/l) x urine volume (ml/min)


--------------------------------------------------------------------------
plasma concentration (mmol/l)

The clearance of a substance is dependent not only on its diffusivity across


the basement membrane but also subsequent tubular secretion and / or
reabsorption.
So glucose which is freely filtered across the basement membrane is usually
reabsorbed from tubules giving a clearance of zero.

Tubular function
Reabsorption and secretion of substances occurs in the tubules.
In the proximal tubule substrates such as glucose, amino acids and
phosphate are co-transported with sodium across the semi permeable
membrane.
Up to two thirds of filtered water is reabsorbed in the proximal tubules.
This will lead to increase in urea concentration in the distal tubule allowing
for its increased diffusion.
Substances to be secreted into the tubules are taken up from the peritubular
blood by tubular cells.
Solutes such as paraaminohippuric acid are cleared with a single passage
through the kidneys and this is why it is used to measure renal plasma flow.
Ions such as calcium and phosphate will have a tubular reabsorption that is
influenced by plasma PTH levels.
Potassium may be both secreted and re-absorbed and is co-exchanged with
sodium.

Loop of Henle
Approximately 60 litres of water containing 9000mmol sodium enters the
descending limb of the loop of Henle in 24 hours.
Loops from the juxtamedullary nephrons run deep into the medulla.
The osmolarity of fluid changes and is greatest at the tip of the papilla.
The thick ascending limb is impermeable to water, but highly permeable to
gathered by dr. elbarky

sodium and chloride ions.


This loss means that at the beginning of the thick ascending limb the fluid is
hypo osmotic compared with adjacent interstitial fluid.
In the thick ascending limb the reabsorption of sodium and chloride ions
occurs by both facilitated and passive diffusion pathways.
The loops of Henle are co-located with vasa recta, these will have similar
solute compositions to the surrounding extracellular fluid so preventing the
diffusion and subsequent removal of this hypertonic fluid.
The energy dependent reabsorption of sodium and chloride in the thick
ascending limb helps to maintain this osmotic gradient.

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Question 187 of 192

 

A 43 year old lady is recovering on the intensive care unit following a Whipples
procedure. She has a central venous line in situ. Which of the following will lead to
the y descent on the waveform trace ?

Ventricular contraction

Emptying of the right atrium


gathered by dr. elbarky

Emptying of the right ventricle

Opening of the pulmonary valve

Cardiac tamponade

JVP
3 Upward deflections and 2 downward deflections

Upward deflections
a wave = atrial contraction
c wave = ventricular contraction
v wave = atrial venous filling

Downward deflections
x wave = atrium relaxes and tricuspid valve moves down
y wave = ventricular filling

The y descent represents the emptying of the atrium and the filling of the right
ventricle.

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Cardiac physiology

The heart has four chambers ejecting blood into both low pressure and high
pressure systems.
The pumps generate pressures of between 0-25mmHg on the right side and
0-120 mmHg on the left.
At rest diastole comprises 2/3 of the cardiac cycle.
The product of the frequency of heart rate and stroke volume combine to
give the cardiac output which is typically 5-6L per minute.

Detailed descriptions of the various waveforms are often not a feature of MRCS A
(although they are on the syllabus). However, they are a very popular topic for
surgical physiology in the MRCS B exam.
gathered by dr. elbarky

Electrical properties
Intrinsic myogenic rhythm within cardiac myocytes means that even the
denervated heart is capable of contraction.
In the normal situation the cardiac impulse is generated in the sino atrial
node in the right atrium and conveyed to the ventricles via the
atrioventricular node.
The sino atrial node is also capable of spontaneous discharge and in the
absence of background vagal tone will typically discharge around 100x per
minute. Hence the higher resting heart rate found in cardiac transplant
cases. In the SA and AV nodes the resting membrane potential is lower than
in surrounding cardiac cells and will slowly depolarise from -70mV to around
-50mV at which point an action potential is generated.
Differences in the depolarisation slopes between SA and AV nodes help to
explain why the SA node will depolarise first. The cells have a refractory
period during which they cannot be re-stimulated and this period allows for
adequate ventricular filling. In pathological tachycardic states this time
period is overridden and inadequate ventricular filling may then occur,
cardiac output falls and syncope may ensue.

Parasympathetic fibres project to the heart via the vagus and will release
acetylcholine. Sympathetic fibres release nor adrenaline and circulating adrenaline
comes from the adrenal medulla. Noradrenaline binds to β 1 receptors in the SA
node and increases the rate of pacemaker potential depolarisation.

Cardiac cycle
gathered by dr. elbarky

(https://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb034b.png)
Image sourced from Wikipedia
(https://d2zgo9qer4wjf4.cloudfront.net
(http://en.wikipedia.org/wiki/Cardiac
/images_eMRCS/swb034b.png)
cycle)

Mid diastole: AV valves open. Ventricles hold 80% of final volume. Outflow
valves shut. Aortic pressure is high.

Late diastole: Atria contract. Ventricles receive 20% to complete filling.


Typical end diastolic volume 130-160ml.

Early systole: AV valves shut. Ventricular pressure rises. Isovolumetric


ventricular contraction. AV Valves bulge into atria (c-wave). Aortic and
pulmonary pressure exceeded- blood is ejected. Shortening of ventricles
pulls atria downwards and drops intra atrial pressure (x-descent).

Late systole: Ventricular muscles relax and ventricular pressures drop.


Although ventricular pressure drops the aortic pressure remains constant
owing to peripheral vascular resistance and elastic property of the aorta.
Brief period of retrograde flow that occurs in aortic recoil shuts the aortic
valve. Ventricles will contain 60ml end systolic volume. The average stroke
volume is 70ml (i.e. Volume ejected).

Early diastole: All valves are closed. Isovolumetric ventricular relaxation


occurs. Pressure wave associated with closure of the aortic valve increases
aortic pressure. The pressure dip before this rise can be seen on arterial
waveforms and is called the incisura. During systole the atrial pressure
increases such that it is now above zero (v- wave). Eventually atrial pressure
exceed ventricular pressure and AV valves open - atria empty passively into
ventricles and atrial pressure falls (y -descent )
The negative atrial pressures are of clinical importance as they can allow air
embolization to occur if the neck veins are exposed to air. This patient positioning
is important in head and neck surgery to avoid this occurrence if veins are
inadvertently cut, or during CVP line insertion.

Mechanical properties
Preload = end diastolic volume
Afterload = aortic pressure

It is important to understand the principles of Laplace's law in surgery.


It states that for hollow organs with a circular cross section, the total
circumferential wall tension depends upon the circumference of the wall,
multiplied by the thickness of the wall and on the wall tension.
The total luminal pressure depends upon the cross sectional area of the
gathered by dr. elbarky

lumen and the transmural pressure. Transmural pressure is the internal


pressure minus external pressure and at equilibrium the total pressure must
counterbalance each other.
In terms of cardiac physiology the law explains that the rise in ventricular
pressure that occurs during the ejection phase is due to physical change in
heart size. It also explains why a dilated diseased heart will have impaired
systolic function.

Starlings law
Increase in end diastolic volume will produce larger stroke volume.
This occurs up to a point beyond which cardiac fibres are excessively
stretched and stroke volume will fall once more. It is important for the
regulation of cardiac output in cardiac transplant patients who need to
increase their cardiac output.

Baroreceptor reflexes
Baroreceptors located in aortic arch and carotid sinus.
Aortic baroreceptor impulses travel via the vagus and from the carotid via
the glossopharyngeal nerve.
They are stimulated by arterial stretch.
Even at normal blood pressures they are tonically active.
Increase in baroreceptor discharge causes:

*Increased parasympathetic discharge to the SA node.


*Decreased sympathetic discharge to ventricular muscle causing decreased
contractility and fall in stroke volume.
*Decreased sympathetic discharge to venous system causing increased
compliance.
*Decreased peripheral arterial vascular resistance

Atrial stretch receptors


Located in atria at junction between pulmonary veins and vena cava.
Stimulated by atrial stretch and are thus low pressure sensors.
Increased blood volume will cause increased parasympathetic activity.
Very rapid infusion of blood will result in increase in heart rate mediated via
atrial receptors: the Bainbridge reflex.
Decreases in receptor stimulation results in increased sympathetic activity
this will decrease renal blood flow-decreases GFR-decreases urinary sodium
excretion-renin secretion by juxtaglomerular apparatus-Increase in
angiotensin II.
Increased atrial stretch will also result in increased release of atrial
natriuretic peptide.

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Question 188 of 192

 

A 45 year old male has alcoholic cirrhosis and decompensated liver failure, which
of the following clotting factors is least likely to be affected?

Factor V

Factor VII
gathered by dr. elbarky

Factor IX

Factor VIII

Factor XI

Factor VIII is synthesised in the endothelial cells of the liver rather than the liver
itself and therefore is less prone to the effects of hepatic dysfunction.

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Abnormal coagulation

Cause Factors affected

Heparin Prevents activation factors 2,9,10,11

Warfarin Affects synthesis of factors 2,7,9,10

DIC Factors 1,2,5,8,11

Liver disease Factors 1,2,5,7,9,10,11

Interpretation blood clotting test results


Disorder APTT PT Bleeding time

Haemophilia Increased Normal Normal

von Willebrand's disease Increased Normal Increased

Vitamin K deficiency Increased Increased Normal

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E 12.8%

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Question 189 of 192

 

Which part of the ECG represents atrial depolarization?

P wave

Q wave

T wave
gathered by dr. elbarky

QRS complex

P-R interval

The P wave represents atrial depolarization. Note that atrial repolarization is


obscured within the QRS complex.

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The normal ECG


gathered by dr. elbarky

Image sourced from Wikipedia (https://d2zgo9qer4wjf4.cloudfront.net


P wave
(http://en.wikipedia.org/wiki/ECG) /images_eMRCS/swb110b.png)
Represents the wave of depolarization that spreads from the SA node
throughout the atria
Lasts 0.08 to 0.1 seconds (80-100 ms)
The isoelectric period after the P wave represents the time in which the
impulse is traveling within the AV node

P-R interval
Time from the onset of the P wave to the beginning of the QRS complex
Ranges from 0.12 to 0.20 seconds in duration
Represents the time between the onset of atrial depolarization and the
onset of ventricular depolarization

QRS complex
Represents ventricular depolarization
Duration of the QRS complex is normally 0.06 to 0.1 seconds

ST segment
Isoelectric period following the QRS
Represents period which the entire ventricle is depolarized and roughly
corresponds to the plateau phase of the ventricular action potential

T wave
Represents ventricular repolarization and is longer in duration than
depolarization
A small positive U wave may follow the T wave which represents the last
remnants of ventricular repolarization.

Q-T interval
Represents the time for both ventricular depolarization and repolarization to
occur, and therefore roughly estimates the duration of an average ventricular
action potential.
Interval ranges from 0.2 to 0.4 seconds depending upon heart rate.
At high heart rates, ventricular action potentials shorten in duration, which
decreases the Q-T interval. Therefore the Q-T interval is expressed as a
'corrected Q-T (QTc)' by taking the Q-T interval and dividing it by the square
root of the R-R interval (interval between ventricular depolarizations). This
allows an assessment of the Q-T interval that is independent of heart rate.
gathered by dr. elbarky

Normal corrected Q-Tc interval is less than 0.44 seconds.

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Question 190 of 192

 

von Willebrand factor is involved in the stabilization of which of the clotting factors
listed below?

Factor VII

Factor VIII
gathered by dr. elbarky

Factor V

Anti thrombin III

Factor Xa

vWF stabilizes factor VIII

If you answered this incorrectly check you did not select factor VII by mistake!

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von Willebrands disease

Most common inherited bleeding disorder


All vWD is caused by mutations in the gene for von Willebrand factor. von
Willebrand factor is an adhesive glycoprotein that is secreted by
endothelium and megakaryocytes
von Willebrand factor promotes platelet adhesion to damaged endothelium
and other platelets. It is also involved in the transport and stabilization of
factor VIII
There are 7 subtypes of von Willebrand disease. The commonest is type I
(autosomal dominant) which accounts for 80% of cases, type 2vWD
(autosomal dominant or recessive) accounts for 15% of cases
There is a significant spectrum of severity ranging from spontaneous
bleeding and epistaxis through to troublesome excessive bleeding following
minor procedures
The test that is most typically diagnostic is the bleeding time
Treatments include administration of tranexamic acid for minor cases
undergoing minor procedures. More significant bleeding or more significant
procedures respond well to DDAVP. This is most effective in type I, less
effective in type 2 and contraindicated in type 2B. Patients with type 3
disease do not respond to DDAVP as they lack the ability to secrete vWF
Individuals who cannot have DDAVP or in whom it is contra indicated usually
receive factor VIII concentrates containing vWF

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Question 191 of 192

 

Deficiency of which vitamin is most likely to explain the presentation of a 3 year


old child with Rickets?

Vitamin C

Vitamin B3
gathered by dr. elbarky

Vitamin D

Vitamin A

Vitamin E

Vitamin D is needed to help mineralise bone. When this is deficient, mineralisation


is inadequate and deformities may result.

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Vitamin deficiency

Vitamin Effect of deficiency

A Night blindness
Epithelial atrophy
Infections

B1 Beriberi

B2 Dermatitis and photosensitivity

B3 Pellagra
B12 Pernicious anaemia

C Poor wound healing


Impaired collagen synthesis

D Rickets (Children)
Osteomalacia (Adults)

K Clotting disorders

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Question 192 of 192

Which of the following drugs increases the rate of gastric emptying in the
vagotomised stomach?

Ondansetron

Metoclopramide
gathered by dr. elbarky

Cyclizine

Erythromycin

Chloramphenicol

Vagotomy seriously compromises gastric emptying which is why either a


pyloroplasty or gastro-enterostomy is routinely performed at the same time.

Chloramphenicol has no effect on gastric emptying. Ondansetron slows gastric


emptying slightly. Metoclopramide increases the rate of gastric emptying but its
effects are mediated via the vagus nerve. Erythromycin enhances gastric emptying
by acting via the motilin receptor in the gut.

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Gastric emptying

The stomach serves both a mechanical and immunological function. Solid


and liquid are retained in the stomach during which time repeated peristaltic
activity against a closed pyloric sphincter will cause fragmentation of food
bolus material. Contact with gastric acid will help to neutralise any
pathogens present.
The amount of time material spends in the stomach is related to its
composition and volume. For example a glass of water will empty more
quickly than a large meal. The presence of amino acids and fat will all serve
to delay gastric emptying.

Controlling factors
Neuronal stimulation of the stomach is mediated via the vagus and the
parasympathetic nervous system will tend to favor an increase in gastric motility. It
is for this reason that individuals who have undergone truncal vagotomy will tend
to routinely require either a pyloroplasty or gastro-enterostomy as they would
otherwise have delayed gastric emptying.

The following hormonal factors are all involved:

Delay emptying Increase emptying

Gastric inhibitory peptide Gastrin


gathered by dr. elbarky

Cholecystokinin

Enteroglucagon

Diseases affecting gastric emptying


All diseases that affect gastric emptying may result in bacterial overgrowth,
retained food and eventually the formation of bezoars that may occlude the
pylorus and make gastric emptying even worse. Fermentation of food may cause
dyspepsia, reflux and foul smelling belches of gas.

Iatrogenic
Gastric surgery can have profound effects on gastric emptying. As stated above
any procedure that disrupts the vagus can cause delayed emptying. Whilst this is
particularly true of vagotomy, this operation is now rarely performed. Surgeons are
divided on the importance of vagal disruption that occurs during an
oesophagectomy, some will routinely perform a pyloroplasty and others will not.

When a distal gastrectomy is performed, the type of anastomosis performed will


impact on emptying. When a gastro-enterostomy is constructed, a posterior,
retrocolic gastroenterostomy will empty better than an anterior one.

Diabetic gastroparesis
This is predominantly due to neuropathy affecting the vagus nerve. The stomach
empties poorly and patients may have episodes of repeated and protracted
vomiting. Diagnosis is made by upper GI endoscopy and contrast studies, in some
cases a radio nucleotide scan is needed to demonstrate the abnormality more
clearly. In treating these conditions, drugs such as metoclopramide will be less
effective as they exert their effect via the vagus nerve. One of the few prokinetic
drugs that do not work in this way is the antibiotic erythromycin.
Malignancies
Obviously a distal gastric cancer may obstruct the pylorus and delay emptying. In
addition, malignancies of the pancreas may cause extrinsic compression of the
duodenum and delay emptying. Treatment in these cases is by gastric
decompression using a wide bore nasogastric tube and insertion of a stent or, if
that is not possible, by a surgical gastroenterostomy. As a general rule
gastroenterostomies constructed for bypass of malignancy are usually placed on
the anterior wall of the stomach (in spite of the fact that they empty less well). A
Roux en Y bypass may also be undertaken, but the increased number of
anastomoses for this, in malignant disease that is being palliated, is probably not
justified.

Congenital Hypertrophic Pyloric Stenosis


This is typically a disease of infancy. Most babies will present around 6 weeks of
gathered by dr. elbarky

age with projectile non bile stained vomiting. It has an incidence of 2.4 per 1000
live births and is more common in males. Diagnosis is usually made by careful
history and examination and a mass may be palpable in the epigastrium (often
cited seldom felt!). The most important diagnostic test is an ultrasound that
usually demonstrates the hypertrophied pylorus. Blood tests may reveal a
hypochloraemic metabolic alkalosis if the vomiting is long standing. Once the
diagnosis is made the infant is resuscitated and a pyloromyotomy is performed
(either open or laparoscopically). Once treated there are no long term sequelae.

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