presentation

1. PRESENTED BY
Mr. Vinay Kumar
M.Sc. Nursing 1st year
HCN, SRHU

2. Anatomy of liver

3. location
Upper right quadrant (Right
hypochondriac region) of
the abdominal cavity.
it rests just below the diaphragm,
to the right of the stomach and
overlies the gallbladder.

4. • Size about 15 cm
• Shape wedge-shaped
• Weight 1.44–1.66 kg (3.2–3.7 lb)
• Colour reddish-brown
• It is both the heaviest internal organ and the
largest gland in the human body.

5. Layers
Covered by visceral peritoneum
layer
Lobe and lobules
• The liver has two lobes larger
right lobe and a smaller left lobe,
divided by the falciform ligament.
falciform ligament

6. • Each lobe is further divided into eight segments.
• Each segment has an estimated 1,0000 lobules, or
small lobes.
• Each of these lobules has a small tube (duct) that
flows toward the common hepatic duct.

7. Ducts

8. The liver is connected to two large blood
vessels: the hepatic artery and the portal
vein.
• The hepatic artery carries oxygen-rich
blood from the aorta,
• And the portal vein carries blood rich in
digested nutrients from the
entire gastrointestinal tract and also from
the spleen and pancreas.
• These blood vessels subdivide into small
capillaries known as liver sinusoids,
hepatic artery
portal vein
BloodSupply

9. hepatic lobules

11. 1. Metabolic Functions
Liver actively participates in carbohydrate metabolism, lipid,
protein, mineral and vitamin metabolisms.
2.Hematological and synthetic functions
Liver participates in formation of blood (particularly in embryo)
• Synthesis of plasma proteins (albumin and prothrombin),and
hormones e.g angiotensinogen, insulin-like growth factor and
triiodothyronine.
• Destruction of erythrocytes (Bilirubin)

12. 3.Protective functions & detoxification
Kuffer cells of liver perform phagocytosis to eliminate foreign
compounds.
4.Storage functions
Glycogen, vitamins A,D and B12
5.Excretory Functions
Bile pigments, bile salts and cholesterol are excreted in bile, into
intestine.

13. 8.Breakdown
The liver is responsible for the breakdown of insulin and
other hormones

14. Cirrhosis of liver

15. • Cirrhosis is a condition in which the liver does not function
properly due to long term damage of liver
• The development of cirrhosis is an insidious, prolonged
course, usually after decades of chronic liver disease.

16. DEFINITION
Cirrhosis of liver is a chronic
progressive disease of liver
characterised destruction and
replacement of normal tissue by
scar tissue.

17. Causes:
• excessive alcohol consumption (40%)
• hepatitis B (30%)
• Hepatitis C (20%)
• Injury

18. • Obesity and diabetic
• Prolonged use of Steroid medication
• Biliary cirrhosis
• New over growth of fibrous connective tissue (alteration in blood
flow)
• Wilson’s disease (excess copper accumulation in liver)

19. Pathophysiology

20. Hepatocyte injury with necrosis fibrosis, regeneration and eventual
degeneration
Diminished parenchymal cell mass causes regeneration of tissue with
nodular areas of proliferating hepatocytes
Hepatocyte respond to injury with deposition of collagen that forms
fibrous connective tissue
This scar tissue and nodular areas of regeneration impaired the intra
hepatic blood flow

21. Ongoing necrosis
Failure of hepatocellular function and portal hypertension occurs
Ascites, severe calcification, scaring, fibrosis, encephalopathy (hepatic
coma) and G.I. bleeding

22. CLINICAL MANIFESTATION

23. Early manifestation:
Usually no symptoms or may be non specific such as-
 headache
 fatigue
 jaundice.
Later manifestation-
• May be severe and result from liver failure and portal hypertension.

24. Hematologic problem:
It include-
• leukopenia
• anaemia
• coagulation disorder
• thrombocytopenia

25. Endocrine problem
• Men show- gynecomastia (benign growth of the glandular tissue of
the male breast)
• Loss of axillary and pubic hair
• Testicular atrophy
 Female show-
• amenorrhea
• Vaginal bleeding (older women)

26. Skin lesion:
Spider angiomas- small dilated blood
vessels with a bright red centre point
and spinder like branches.
Usually occur in neck, nose, cheeks,
upper trunks and shoulder.
• Palmar erythema- is a rare skin
condition where the palms of both
hands become reddish.
• Usually affects the base of the palm
and the area around the bottom of
thumb and little finger

27. AscitesJAUNDICE Hepatomegaly
splenomegalyClubbingof finger

28. • Peripheral neuropathy- Due to dietary deficiency of thymine folic
acid and cobalamin.
• Itching

29. DIAGNOSTIC EVALUATION

30. History collection
present health history
past health history
Physical examination
Skin colour
Enlarge left hepatic lobe
splenomegaly

31. • Gold standard test for diagnosis is liver biopsy through a
percutaneous transjuglar, laparoscopic of fine needle approach

32. • LFT (liver function test)
• RFT (Renal function test)
• Blood investigation for hepatitis b and c
• CBC (complete blood count)
• Ct scan
• MRI
• Ultrasonography

33. MANAGEMENT

34. MEDICAL MANAGEMENT

35. • Fluid build-up in the belly (ascites). It can be deadly if it is
not controlled. Treatment can include:
• Following a low-sodium diet.
• Medicines such as diuretics.
• Removing fluid with a needle(paracentesis)

36. • Bleeding from enlarged veins. Variceal bleeding in the
digestive tract can be treated with:
• Beta-blocker such as carvedilol
• Antibiotic therapy for infection
• Fluid restriction >1000ml/day
• Monitor daily weight and abdominal girth INJ.of vit.k 1amp.iv-
OD for 3 days Analgesic such as

37. Surgical management:

38. • Transjuglar intrahepatic portosystemic shunt (TIPS). by useing
imaging guidance connect the portal vein to the hepatic vein in the
liver.
• A small metal device called a stent is placed to keep the connection
open and allow it to bring blood draining from the bowel back to
the heart while avoiding the liver.

39. .

40. • Liver transplantation

42. 1-Pain related to liver tissue damage as evidence by patient verbalization.
Goal- to reduce pain
Intervention-
Provide comfortable position
Provide calm environment
Administer analgesic medication

43. 2-Imbalanced Nutrition Less Than Body Requirements related to
Inadequate diet as evidence by Weight loss
• Goal: improve the nutritional status
• Intervention
• Measure dietary intake by calorie count
• Encourage patient to eat explain reasons for the types of diet
• Give small, frequent meals
• Provide tube feedings if indicated

44. 3- Increased isotonic fluid retention related to compromised
regulatory mechanisms evidenced by Edema
• Goal: stabilized fluid volume
• Intervention:
• Measure I&O, weigh daily, and note gain of more than 0.5 kg/day.
• abdominal vein distension
• Assess degree of peripheral Edema
• Measure abdominal girth daily

45. 4-Risk for Impaired Skin Integrity related to presence of Edema as
evidence by patient appearance
• Goal : Maintain skin integrity
• Intervention:
• Inspect pressure points and skin surfaces closely and routinely
• Recommend elevating lower extremities
• Keep linens dry and free of wrinkles
• Administer medications as prescribed by

46. COMPLICATION

47. Edema:
As cirrhosis of the liver becomes severe, signals are sent to the kidneys
to retain salt and water in the body.
The excess salt and water first accumulates in the tissue beneath the
skin of the ankles and legs because of the effect of gravity when
standing or sitting.
This accumulation of fluid is called peripheral Edema

48. Ascites:
• As cirrhosis worsens and more salt and water are retained, fluid also
may accumulate in the abdominal cavity between the abdominal wall
and the abdominal organs.
• This accumulation of fluid (called ascites) causes swelling of the
abdomen, abdominal discomfort, and increased weight.

49. Spontaneous bacterial peritonitis (SBP):
• Fluid in the abdominal cavity (ascites) is the perfect place for bacteria
to grow.
• Normally, the abdominal cavity contains a very small amount of fluid
that is able to resist infection well, and bacteria that enter the abdomen
(usually from the intestine) are
• killed or find their way into the portal vein and to the liver where they
killed.

50. • In cirrhosis, the fluid that collects in the abdomen is unable to
resist infection normally. In addition, more bacteria find their way
from the intestine into the ascites.
• Therefore, infection within the abdomen and the ascites, referred
to as spontaneous bacterial peritonitis or SBP, is likely to occur.
SBP is a life- threatening complication.
• Some patients with SBP have no symptoms, while others have no
symptoms,
• while others have fever, chills, abdominal pain and
tenderness, diarrhoea, and worsening ascites.

51. Bleeding from oesophageal varices:
• In the cirrhotic liver, the scar tissue blocks the flow of blood returning to the
heart from the intestines and raises the pressure in the portal vein

52. Portal hypertension.
When pressure in the portal vein becomes high enough, it causes
blood to flow around the liver through veins with lower pressure
to reach the heart.
The most common veins through which blood bypasses the liver
are the veins lining the lower part of the oesophagus and the
upper part of the stomach.
As a result of the increased flow of blood and the resulting
increase in pressure, the veins in the lower oesophagus and upper
stomach expand and then are referred to as oesophageal and
gastric

53. • varices; the higher the portal pressure, the larger the varices and the
more likely a patient is to bleed from the varices into the oesophagus
or stomach. Bleeding from varices usually is severe and, without
immediate treatment, can be fatal.

54. • Symptoms- vomiting blood (the vomitus can be red blood mixed
with clots or "coffee grounds" in appearance, the latter due to the
effect of acid on the blood), passing stool that is black and tarry due
to changes in the blood as it passes through the intestine (melena),
and orthostatic dizziness or fainting (caused by a drop in blood
pressure especially when standing up from a lying position).
• Bleeding also may occur from varices that form elsewhere in the
intestines, for example, the colon, but this is rare.

55. Hepatic encephalopathy:
• Some of the protein in food that escapes digestion and absorption is
used by bacteria that are normally present in the intestine.
• While using the protein for their own purposes, the bacteria make
substances that they release into the intestine.
• These substances then can be absorbed into the body.
Some of these substances, for example, ammonia, can have toxic
effects on the brain.
Ordinarily, these toxic substances are carried from the intestine in the
portal vein to the liver where they are removed from the blood and
detoxified.

56. • liver cells cannot function normally either because they are damaged
or because they have lost their normal relationship with the blood. In
addition, some of the blood in the portal vein bypasses the liver
through other veins.
• The result of these abnormalities is that toxic substances cannot be
removed by the liver cells, and, instead, the toxic substances
accumulate in the blood.
• When the toxic substances accumulate sufficiently in the blood, the
function of the brain is impaired, a condition called hepatic
encephalopathy.

57. • Symptoms: Sleeping during the day rather than at night (reversal of
the normal sleep pattern).
• Other symptoms include irritability, inability to concentrate or
perform calculations, loss of memory, confusion, or depressed levels
of consciousness. Ultimately, severe hepatic encephalopathy
causes coma and death.

58. Hepatorenal syndrome:
• It is a functional problem in the kidneys, meaning there is no physical
damage to the kidneys
• The hepatorenal syndrome is defined as progressive failure of the
kidneys to clear substances from the blood and produce adequate
amounts of urine while other important functions of the kidney, such
as retention of salt, are maintained.
• If liver function improves or a healthy liver is transplanted into a
patient with hepatorenal syndrome, the kidneys usually begin to work
normally again.
• This suggests that the reduced function of the kidneys is the result of
either the accumulation of toxic substances in the blood or abnormal
liver function when the liver fails.

59. Hepatopulmonary syndrome:
• some patients with advanced cirrhosis can develop hepatopulmonary
syndrome. These patients can experience difficulty breathing because
certain hormones released in advanced cirrhosis cause the lungs to
function abnormally.
• The basic problem in the lung is that not enough blood flows through
the small blood vessels in the lungs that are in contact with the alveoli
(air sacs) of the lungs.
• Blood flowing through the lungs is shunted around the alveoli and
cannot pick up enough oxygen from the air in the alveoli.
• As a result the patient experiences shortness of breath
• experiences shortness of breath, particularly with exertion

60. • Hepatopulmonary syndrome:
• Rarely, some patients with advanced cirrhosis can develop
hepatopulmonary syndrome.
• These patients can experience difficulty breathing because certain
hormones released in advanced cirrhosis cause the lungs to function
abnormally.
• The basic problem in the lung is that not enough blood flows through
the small blood vessels in the lungs that are in contact with the alveoli
(air sacs) of the lungs.
• Blood flowing through the lungs is shunted around the alveoli and
cannot pick up enough oxygen from the air in the alveoli.
• As a result, the patient experiences shortness of breath, particularly
with exertion.

61. Hypersplenism:
The spleen normally acts as a filter to remove older red blood cells,
white blood cells, and platelets (small particles that are important for
the clotting of blood).
The blood that drains from the spleen joins the blood in the portal vein
from the intestines.
As the pressure in the portal vein rises in cirrhosis, it increasingly
blocks the flow of blood from the spleen.

62. Liver cancer (hepatocellular carcinoma:
• Cirrhosis due to any cause increases the risk of primary
liver cancer (hepatocellular carcinoma). Primary refers to the fact that
the tumour originates in the liver.
• A secondary liver cancer is one that originates elsewhere in the body
and spreads (metastasizes) to the liver.