研究生期末考试专业英语试题

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南通大学

2014

—

2015

学年第

1

学期

消化内科

研究生试卷（

A

）

第

1

页

共

2

页

试题

一

二

三

四

五

六

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得分

分

专业英语试题

liver

pathogenesis of renal dysfunction and sodium retention in cirrhosis is the

disease.

One

of

the

key

events

thought

to

be

critical

in

the

PATHOGENESIS OF ASCITES FORMATION

development

1

．

effective

of

systemic

vasodilatation,

mechanism responsible for these changes in vascular function is unknown

arterial

blood

volume

and

a

which

hyperdynamic

causes

a

decrease

in

hepatic

Portal

Role of portal hypertension

but may involve increased vascular synthesis of nitric oxide, prostacyclin,

cavity.

sinusoids

hypertension

and

favours

increases

transudation

the

hydrostatic

of

fluid

pressure

into

the

within

peritoneal

the

as well as changes in plasma concentrations of glucagon,substance P, or

cirrhosis rarely develop ascites. Thus patients do not develop ascites with

However,

patients

with

presinusoidal

portal

hypertension

without

calcitonin gene related peptide.

isolated chronic extrahepatic portal venous occlusion non-cirrhotic causes

of portal hypertension such as congenital hepatic fibrosis, except following

Bernardi et al have shown marked changes in secretion of atrial natriuretic

However, the haemodynamic changes vary with posture, and studies by

an

peptide

Conversely, acute hepatic vein thrombosis, causing postsinusoidal portal

insult

to

liver

function

such

as

gastrointestinal

haemorrhage.

addition,

with

hypertension,

have been disputed. It is agreed however that under supine conditions and

data

posture, as

showing

a

well

decreased

as

changes

effective

in

systemic haemodynamics.

arterial

volume

in

cirrhosis

In

occurs as a consequence of structural changes within the liver in cirrhosis

is

usually

associated

with

ascites.

Portal

hypertension

in

and increased splanchnic blood flow. Progressive collagen deposition and

vasodilatation.

experimental

animals,

there

is

an

increase

in

cardiac

output

and

formation of nodules alter the normal vascular architecture of the liver and

increase resistance to portal flow. Sinusoids may become less distensible

homeostatic

The

development

with the formation of collagen within the space of Disse. While this may

activation of the renin- angiotensin system to maintain blood pressure during

response

of

involving

renal

vasoconstriction

increased

renal

sympathetic

in

cirrhosis

activity

is

partly

and

a

give

systemic vasodilatation. Decreased renal blood flow decreases glomerular

suggested

the

impression

of

a

static

portal

system,

recent

studies

filtration

sinusoidal tone and thus portal pressure.

that activated

hepatic

stellate

cells

may

dynamically

regulate

have

Cirrhosis is associated with enhanced reabsorption of sodium both at the

rate

and

thus

the

delivery

and

fractional

excretion

of

sodium.

proximal tubule and at the distal tubule. Increased reabsorption of sodium in

which

Sinusoidal

endothelial

cells

form

an

extremely

porous

the

plasma

is

aldosterone.

distal

tubule

50

proteins.

almost

completely

In

contrast,

permeable

splanchnic

to

capillaries

macromolecules,

membrane

have

a

including

concentrations

However,

is

due

some

to

patients

increased

with

circulating

ascites

have

concentrations

normal

of

trans- sinusoidal oncotic pressure gradient in the liver is virtually zero while

–

100 times less than that of hepatic sinusoids. As a consequence, the

pore

size

reabsorption

it is 0.8

sensitivity to aldosterone or to other undefined mechanisms.

in

of

the

aldosterone,

distal

tubule

leading

may

to

be

the

related

suggestion

to

enhanced

that

plasma

sodium

renal

pressure

–

0.9 (80%

effect

gradients

–

90% of maximum) in the splanchnic circulation. Oncotic

at such

extreme ends of

the

spectrum minimise

vasodilatation

In compensated cirrhosis, sodium retention can occur in the absence of

transmicrovascular fluid exchange. Therefore, the old concept that ascites

the

changes

in

plasma

albumin

concentration

may

have

any

on

can

is formed secondary to decreased oncotic pressure is false, and plasma

changes

reduce

albumin

hepatorenal

in

renal

and

effective

the

systemic

blood

flow

hypovolaemia.

Sinusoidal

portal

hypertension

circulation,

even

in

suggesting

the

absence

the

of

existence

haemodynamic

of

a

formation.

concentrations

have

little

severity

and

Portal

hypertension

is

critical

influence

to

the

on

development

the

rate

of

of

ascites,

ascites

abnormalities of sodium handling in cirrhosis

of

liver

reflex.

disease

Similarly,

and

in

portal

addition

pressure

to

systemic

also

contribute

vasodilation,

to

the

the

portal

ascites

portacaval

gradient

rarely

vasodilatation

In compensated cirrhosis, sodium retention can occur in the absence of

ascites.

shunt

of

to

＜

develops

12

decrease

mm

Hg.

in

patients

with

a

wedged

hepatic

venous

portal

Conversely,

pressure

insertion

often

causes

of

a

resolution

side

to

side

of

can

2

．

changes

reduce

renal

and

effective

blood

flow

hypovolaemia.

Sinusoidal

portal

hypertension

hepatorenal

in

the

systemic

circulation,

even

in

suggesting

the

absence

the

of

existence

haemodynamic

of

a

due

The

Pathophysiology of sodium and water retention

severity

features of either “underfill” or “overfill” depending on posture or severity of

to

classical

“underfill”

explanations

or

“overfill”

of

are

sodium

oversimplified.

and

water

Patients

retention

may

occurring

exhibit

abnormalities of sodium handling in cirrhosis.

of

liver

reflex.

disease

Similarly,

and

in

portal

addition

pressure

to

systemic

also

contribute

vasodilation,

to

the

the

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