Eastern University Sri Lanka

Faculty of health care sciences

2nd year in MBBS course – 2020
Phase 1 (proper) examination (2016/2017/ 12th batch)
ESSAY
Part A
1 1.1
 The heart is supplied by the two coronary arteries and their branches.
 Each coronary artery is the main source of supply to its same side atrium and
ventricle, but also supplies the opposite side chambers to some extent.
Right coronary artery
 Running downwards in the atrioventricular groove the right coronary artery
turns backwards at the inferior border of the heart and runs posteriorly.
 It gives off branches to both atrium and ventricle.
 One of the highest branches is the conus artery which passes upwards and
medially on the front of the conus (infundibulum) of the right ventricle.
 It frequently anastomoses with a similar branch from the left coronary artery to
form an anastomosis around the origin of the pulmonary trunk.
 . At the sharp (acute) inferior border the right marginal artery passes to the left
along the right ventricle, although it often has a much higher origin and passes
obliquely down over the front of the ventricle.
 On the diaphragmatic surface of the heart the posterior interventricular
branch—also called the posterior descending artery—is given off.
 This large vessel passes along the interventricular groove towards the apex of
the heart.
 Having given off one or more left ventricular (right posterolateral) branches, the
remaining and much smaller right coronary artery anastomoses with the
termination of the circumflex branch of the left coronary artery to a varying
extent.
Left coronary artery
 it divides into its two terminal (circumflex and anterior interventricular)
branches .
 The circumflex branch continues round the left margin to the back of the heart
in the atrioventricular groove, giving off various ventricular and atrial branches
and anastomosing variably with the end of the right coronary.
 One large left marginal artery frequently runs down the rounded (obtuse) left
border of the heart.
 The anterior interventricular artery is the cardiac vessel most often affected by
disease.
 It runs down in the interventricular groove to anastomose under the apex with
the posterior interventricular branch of the right coronary.
 Near its origin it gives a conus branch and further towards the left several
ventricular branches.
 One is often large; this diagonal artery may arise separately from the left
coronary trunk, which then ends by trifurcation

1.2 SVC

 This vessel commences at the lower border of the first right costal cartilage by
confluence of the two brachiocephalic veins .
 It passes vertically downwards behind the right border of the sternum and,
piercing the pericardium at the level of the second costal cartilage,
 enters the upper border of the right atrium at the lower border of the third right
costal cartilage.
 Behind the sternal angle it receives the azygos vein, which has arched forwards
over the root of the right lung.
 There are no valves in the superior vena cava, the brachiocephalic veins or the
azygos system of veins.

1.3

inferior margin:

 manubrium
 1st left costal cartilage
 First left rib
 1st thoracic vertibra

Deep:
 Left Visceral parietal pleura

Medially:

 thyroid
 Trachea
 Oesophagus
 Great vessels

Superiorly:

 Left suprapleural membrane

 Posterosuperiorly:

 Neck of left first rib

1.3.2

 By the end of the fourth week,the two primitive ventricles begin to

expand.
 This is accomplished by continuous growth of the myocardium on
the outside and continuous diverticulation and trabecula formation
on the inside
 . The medial walls of the expanding ventricles become apposed and
gradually merge, forming the muscular interventricular septum .
 Sometimes the two walls do not merge completely, and a more or
less deep apical cleft between the two ventricles appears.
 The space between the free rim of the muscular ventricular septum
and the fused endocardial cushions permits communication between
the two ventricles.
 The interventricular foramen, above the muscular portion of the
interventricular septum, shrinks on completion of the conus septum .
 During further development, outgrowth of tissue from the inferior
endocardial cushion along the top of the muscular interventricular
septum closes the foramen .
 This tissue fuses with the abutting parts of the conus septum.
Complete closure of the interventricular foramen forms the
membranous part of the interventricular septum.

Ventricular septal defect

 Involving the membranous or muscular portion of the septum are the most common
congenital cardiac malformation
 Most occur in the muscular region of the septum and resolve as the child grows.
 . Although it may be found as an isolated lesion, VSD is often associated with
abnormalities in partitioning of the conotruncal region.
 Depending on the size of the opening,blood carried by the pulmonary artery may be
1.2 to 1.7 times as abundant as that carried by the aorta.
 Occasionally the defect is not restricted to the membranous part but also involves
the muscular part of the septum

(2)

2.1)) Nerve supply of stomach

 Symphathetic fibres(vasomotor) + afferent pain fibers - along with arterial branches-
innervates the stomach

Esophageal plexus in posterior mediastinum

1)Anterior vagal trunk (mainly left vagus)

Lies in contact with esophageal wall1/2 hepatic branches
Several gastric branches to fundus and body
Anterior nerve of lartaget( great anterior gastric nerve) –runs down in
lesser Omentum
subdivided like cow's foot
supply antrum + pylorus
2)Posterior vagal trunk (mainly right vagus)
Not in contact with posterior surface of the esophagus
quotes Coeliac branch
Gastric branches to fundus and body
Greater posterior gastric nerve

Lymph drainage of the stomach

 Divided into 3 areas. Watershed line is parallel to greater curvature.

Aortic nodes

 Area 1 - right 2/3 of stomach to- left and right gastric nodes
 Area 2 - upper 2/3 of left 1/3 of stomach - gastro-epiploic nodes - sub plyloric
nodes
 Area 3 - lower 1/3 of left 1/3 of stomach - splenic nodes - supra pancreatic nodes

 Note that all lymphatics of the stomach ultimately drain to

Coeliac nodes - Intestinal Lymph Trunk - Cisterna Chyli
2.2)
 Feature Jejunum Ileum
Location  Occupies upper & left  Occupies lower & right parts of
parts of intestine the intestine
 Completely suspended by  Completely suspended by
mesentery mesentery (peritoneum)

Walls  Thicker  Thinner

 More vascular  Less vascular

Lumen  Wider  Narrower

 Often empty  Filled

Mesentery  Windows present  Windows absent

 Fat less abundant  Fat more abundant
 Few arterial arcades  More arterial arcades
 Vasa recta longer  Vasa recta shorter
 Vasa recta fewer  Vasa recta more

Circular mucosal  Larger  Smaller

folds  More close to each other  More apart

Villi  More abundant  Less abundant

Lymphoid tissue  Fewer solitary lymph  More solitary lymph follicles

follicles  Peyer’s patches prese
 No Peyer’s patches mesogastrium nt

2.3)
Peritoneal Attachments – Liver is enclosed in peritoneum (Ventral), Except bare area
Ventral part
i. Falciform lig. – Attached to liver & anterior abdominal wall Inferior margin
- Ligamentum teres hepatis (Remnant of L. Umbilical V.)
ii. Right & left triangular ligaments
iii. Coronary ligament – Superior & Inferior layers
Dorsal part
Lesser omentum – arise from inverted ‘L’ attachment
o Vertical limb - Ligamentum venosum (Remnant of Ductus Venosus)
o Horizontal limb - margins of porta hepatis

Anatomical Division

Diaphragmatic surface – Falciform lig.

Visceral surface – Fissure for Ligamentum Venosum + Fissure for Ligamentum Teres

o Right Lobe
 Caudate lobe -Between IVC groove & Fissure for Ligamentum venosum -Caudate process
– Inferior to the right, connecting to the right lobe - Papillary process – Inferior to the left

Quadrate lobe -Between GB fossa & Fissure for Ligamentum Teres

Porta hepatis

-Arrangement (behind forwards)

V – Portal V.

A – Hepatic A.

D – Common Hepatic Duct

o Left Lobe

Tuber Omentale – near the fissure for Ligamentum venosum

Functional Division – According to distribution of BD, HA, PV Oblique plane through the GB
Fossa & IVC groove (Middle hepatic V. lies)

Stability – Ligaments, Hepatic veins, Ab. Muscle tone Relations-5 Surfaces

Anterior Surface

-●Diaphragm

●Pleura

●Anterior Abdominal Wall

● Xiphoid Process

Posterior Surface-

Right Lobe (Bare Area – Area that grows in to the Septum Transversum)

●Diaphragm

● IVC + Hepatic V.

●Suprarenal Impression - R. Suprarenal Gland

Left Lobe

●Oesophageal Impression - Oesophagus

●2 Crura
●Aortic Opening

●Celiac Trunk

Inferior Surface

*Right Lobe

● Gall Bladder

●Colic Impression - Hepatic Flexure

●R. Kidney - Renal Impression

* Left Lobe

● Gastric Impression - Stomach

●Fissure For Ligmentum Teres

* Quadrate Lobe

●Pylorus Of Stomach

●Duodenal Impression -1st Part of Duodenum

Superior Surface

●Right & Left Domes of Diaphragm

Right Surface

- ●Upper 1/3-Lung, Pleura, Diaphragm (In Mid Axillary Line)

●Middle 1/3-Pleura, Diaphragm
 PART B
3.Intraplueral pressure during quiet breathing is negative. (less than the atmospheric
pressure. In pneumothorax following chest injury the pressure become positive, the lung
collapse and its volume decreases and the volume of thoracic cage increases.

Explain the mechanism that

3.1 keep the normal intrapleural pressure sub atmospheric.

 The lungs and the chest wall are elastic structures.

 Visceral pleura strictly adheres to the lung surface and parietal pleura strictly adhere
to the chest wall.
 A thin layer of fluid is present between the lungs and the chest wall. (intrapleural
space)
 Lungs slide easily on the chest wall but resist the separation.
 End of the quiet expiration the lungs tend to recoil from the chest wall.
 But it is balanced by the recoil force of the chest wall that act outwards.
 Those 02 forces (recoil force of lungs and recoil force of chest wall) are equal in value
and opposite in directions.
 So those 2 forces in equilibrium and make intrapleural pressure sub atmospheric. (-
2.5 mmHg)
 During inspiration,
o inspiratory muscles contract and increase the intrathoracic volume.
o So, the volume between 2 pleural layers is increased and leads to more
pressure drop. ( -6 mmHg)
o Lungs are pulled in to more expanded position.
 At the end of the inspiration, the lung recoil begins to pull the chest back to the
expiratory position and the recoil pressure of the lungs and chest wall is balanced.
 During the expiration chest wall come to normal position and increase the
intrapleural pressure.
 Strong inspiratory efforts reduce intrapleural pressure to values as low as -30mmHg.
3.2 Make the lung collapse in pneumothorax while increasing the thoracic volume

 A pneumothorax is an abnormal collection of air in the pleural space between the

lung and the chest wall.
 Types of pneumothorax
o Closed pneumothorax – chest wall is intact, rupture of lung or visceral pleura
allows air in to the pleural space
o Open pneumothorax – air is allowed to enter pleural space from outside.
Occurs when there is a large open wound in chest wall.
o Tension pneumothorax – develops when air leak occurs from lung or through
chest wall, creating a one-way valve.
 In tension pneumothorax air continuously accumulate in pleural cavity.
 This buildup of air puts pressure on the lung.

 So, lung can’t expand and lungs are beginning to collapsed.

 Due to lung collapsing, recoil force of thoracic wall that act outward can’t be
balanced.
 So, the thoracic wall begins to expand and increase the thoracic volume.
4) Blood pressure and heart rate were measured during Valsalva maneuver in a healthy
young adult. Blood pressure increased at the beginning followed by a drop in blood
pressure and increased in heart rate.
a) Explain the term “Valsalva maneuver”
Breathing technique that can be used to help diagnose a problem with autonomic
function in cardiac function. It is performed closing mouth and nose while expelling
air.
b) Explain the physiological basis of
i) Initial rise in blood pressure
expelling thoracic volume is decreased

Lung volume is decreased

Blood tends to move out of pulmonary

circulation into left atrium

Stroke volume is increased

Blood pressure is increased

ii) Subsequent fall in blood pressure
Expelling Thoracic pressure is increased

Pressure pump doesn’t function properly to pump blood from

lower part of body to thorax.

Blood amount received respectively to left atrium, left

ventricle, right atrium and right ventricle is decreased

Stroke volume is decreased

Cardiac output is decreased

Blood pressure is decreased

 iii) Increase in heart rate
Blood pressure is decreased

Baroreceptors in Aortic arch and carotid sinus are stimulated

Through Depressor
Aortic arch branch of vagus nerve

Medulla oblangata

Carotid sinus Through carotid sinus

nerve of
glossopharyngeal nerve

Cardio acceleratory center

Pacemaker activity is increased

Heart rate is increased

(5)

5.1.1. Patients who are morbidly obese often undergo a surgical procedure which called as
gastrectomy .
Partial gastrectomy means remove part of stomach and rest of stomach is stapledThus
reservior function of stomach is reduced therefore food rapidly comes to small
intestine without storing stomach. Weight loss occur due to this condition
As a result patient must eat frequent small meals. If large meals are eaten because
of rapid absorption of glucose from intestine and results hyperglycemia
Therefore abrupt rise in insulin secretion occur and hypoglycemic symptoms develop
about 2h after meals
Weakness, dizziness, sweating after meals are also part of hypoglycemia. This
condition called as dumping syndrome

5.1.2
Rapid entry of hypertonic meals into the intestine occur due to gastrctomy. Therefore
water move into gut. Before gastrectomy stomach digested most of sugar and
starch. After surgery small intestine has to draw in water from rest of body to
breakdown food.
Much of extra water is taken from blood. Therefore sudden fall in blood pressure.
Dizziness occurs because the intestine sense that the food is too concentrated and
release increased amount of gut hormones

5.2.1
 during overnight fast glucose is synthesized by gluconeogenesis which 90%
occur in liver and remain 10% occur in kidneys
  During prolong fasting kidneys become major glucose producing organ
contributing 40% of total glucose production
 Some tissues such as brain, red blood cells, kidney medulla, lens, cornea of
eye, testes, exercising muscles require continues supply of glucose as
metabolic fuel
 During prolong fast hepatic glycogen stores are depleted and glucose is
formed from noncarbohydrate precursors such as lactate, pyruvate,
glycerol, Alfa keto acids
 If failure of gluconeogenesis causes severe fasting hypoglycemia due to
loss of glucose supply to the tissues
 this process requires both mitochondrial and cytosolic enzymes
Pyruvate

Pyruvate carboxylase

OAA

PEP carboxylase

PEP

Glucose 6-phosphate

Glucose
 First step is the regulatory step and which occurs in mitochondria of liver and
kidney cells
 It has 2 purposes. Those are to provide important substrate for
gluconeogenesis and to provide OAA that can replenish TCA cycle
intermediates
 pyruvate carboxylase requires biotin and ATP and is allosterically activated by
acetyl coA
Liver and kidney are the only organs that release free glucose from glucose 6-
phosphateby glucose 6-phosphatase enzyme.

5.2.2
 Major source of fructose is disaccharide sucrose which cleaved in intestine
 Fructose is found in fruits, honey, high fructose corn syrup

Fructos
Fructokinase
ATP

ADP

Fructose 1-phosphate

Glyceraldehyde dihydroxyacetone phosphate

 Fructokinase and aldolase B enzymes are found in liver, kidney, small

intestinal mucosa
 A deficiency of one of key enzymes can results benign Conditions such as
fructokinase deficiency ( essential fructosuria ) and aldolase B deficiency (
hereditary fructose intolerance- HFI )
 first symptoms of HFI appear when a baby is weaned from milk and begins to
be fed food containing sucrose or fructose
 Fructose 1-phosphate accumulate and resulting in drop in level of inorganic
phosphate and therefore ATP production. then AMP rises.
 AMP is degraded in small intestine

AMP
5´nucleotidase

Adenosine

Adenosine deaminase

Inosine

Hypoxanthine

Xanthin
Uric acid
Finally uric acid Formation occur and it causes hyperuricemia
5.2.3

NADPH is formed via pentose phosphate pathway which is the sole source for red
blood cells. It is required for maintenance of G-SH pool which helps to maintain
reduced states of sulfhydryl groups in haemoglobin. It prevents oxidation of
membrane proteins and formation of heinz bodies. Then it prevents haemolytic
anemia

(6)

6.1.1 ketone bodies

6.1.2
Brain use ketone bodies which spare glucose and it is important during prolonged
fasting

During fasting liver is flooded with fatty acid mobilized from adipose tissue
As a result elevated hepatic acetyl coA produced by fatty acid oxidation inhibits
pyruvate dehydrogenase and activate pyruvate carboxylase

OAA produced is used by liver for gluconeogenesis rather than for TCA cycle.
Therefore acetyl coA is channelled into ketone body synthesis
HMG coA synthase is the rate limiting step in synthesis of ketone bodies

Ketone bodies are acetoacetate, 3-hydroxy butyrate, acetone

Acetoacetate and 3-hydroxy butyrate are transported into peripheral tissues by blood

Acetone is volatile, biologically nonmetabolized compound which is released in

breath
6.2.3
Ketone bodies are produced by the liver mitochondria which are soluble in aqueous
solution therefore do not need to be incorporated into lipoproteins. They are
transported into brain
3- Hydroxyl butyrate is oxidized to acetoacetate by 3-hydroxybutyrate
dehydrogenase producing NADH
Acetoacetate is then provided with a coA molecule taken from succinyl coA by
succinyl coA : acetoacetste coA transferase (thiophorase)
This reaction is reversible, but acetoacetyl coA is actively removed by its conversion
to two acetyl coAs. This pulls reaction forward.
 Brain efficiently oxidize acetoacetate and 3-htdroxybutyrate
4) Briefly explain the following stating the biochemical basis
I. Hepatic metabolism of glucose increases after a meal containing carbohydrate.
Meal containing carbohydrate leads to increased blood glucose concentration in portal
circulation. That much of glucose shouldn’t be entered into systemic circulation directly. So,
liver has to decrease the glucose amount, that enters to blood. For that liver has many
mechanisms.

 Increased intake of glucose

 Increased glycolysis
 Increased glycogenosis
 Increased pentose phosphate pathway
Increased intake of glucose

Liver expresses the glucose transporter GLUT-2. It is insulin independent glucose

transporter. It enters such a big amount of glucose.
Increased glycolysis

In liver parenchymal cells and beta cells of pancreas contain glucokinase enzyme (hexokinase
D), which phosphorylates glucose.

glucokinase hexokinase
Found in liver Found in most tissues
Lower km Higher km
Higher affinity Lower affinity
Lower glucose concentration is needed for Higher glucose concentration is needed for
half saturation half saturation
Lower Vmax Higher Vmax

So glucokinase enzyme phosphorylates more amount of glucose than hexokinase.

Furthermore, high insulin to glucagon ratio increases

 conversion of glucose into acetyl Co. A

 enzymatic reactions of PK and PDH
acetyl Co. A is the building block of Fatty acids. As much as acetyl Co. A is used, glycolysis
also increases
Increased glycogenesis

By activation of glycogen synthase. It can be done by dephosphorylation and increased

availability of glucose-6-phosphate. Glucose-6-phosphate is an allosteric activator.
 Increased pentose phosphate pathway

Increases availability of glucose-6-phosphate and increased demand for NADPH for

lipogenesis increases pentose phosphate pathway.
II. Orotic aciduria
Orotate phosphoribosyl transferase and OMP decarboxylase are separate domains of a single
polypeptide- UMP synthase
Low activity of orotidine phosphate decarboxylases and orotate phosphoribosyl transferase
result in poor growth, megaloblastic anemia, and the excretion of large amounts of orotate in
the urine

Administration of uridine results in improvement of the anemia and decreased excretion of

orotate
III. Albinism
Defect in tyrosinase metabolism.
Deficiency in the production of melanin
Melanin can be partially or fully absent from skin, hair and eyes.

The characteristics are

 Hypopigmentation
 Vision defect
 Photophobia
 Increased risk for skin cancer
It can be inherited as

 autosomal recessive/ primary mode

 Autosomal dominant
 X- linked
Complete albinism or tyrosinase negative oculocutaneous albinism results from deficiency of
Cu requiring tyrosinase, characterized by total absence of melanin