Patho: Hepatic and Renal Failure

Question 1

Functions of the Liver

Answer 1

1)Many metabolic and regulatory roles
2)Digestive role: To produce bile for export to the duodenum.
3)Bile acts as a fat emulsifier and makes the fat more accessible to digestive enzymes (From the pancreas)
(Note: Liver sends bile to the gallbladder for storage and then the gall bladder releases bile to help digest fat)

Question 2

Function of Hepatocytes (Liver cells)

Answer 2

1)Produce Bile
2)Process blood-borne nutrients (Glucose Glycogen)
3)Store fat soluble vitamins
4)Detoxify the blood (From alcohol)
If the liver is damaged, there are extensive effects to the body.But, the liver has a good functional reserve and excellent regenerative powers.

Question 3

What is Cirrhosis?

Answer 3

It is a disorder of progressive destruction to the liver tissue that eventually leads to liver failure(80%-90% of the liver has been destroyed)

Cirrhosis is the end result of a number of chronic liver diseases.
About 28000 ppl die qyear in the US, which are alcohol related.
(Cirrhosis doesn’t have to be from alcohol intake, can be from liver disease, etc)

Question 4

What are the different Categories of Cirrhosis?

Answer 4

1) Alcoholic Liver Disease-“Portal Cirrhosis”
- It’s the largest group

2) Biliary Cirrhosis
- Associated with immune disorders and those causing obstruction to bile flow

3) Postnecrotic Cirrhosis
- Linked w/ Chronic hepatitis or long term exposure to toxic materials (Drugs, and hepatitis)

4) Metabolic
- Usually caused by storage disorders such as hemochromatosis.

Question 5

Patho of Cirrhosis

Answer 5

1) The liver will have a lot of fibrosis and loss of lobular organization.
2) Nodules of regenerated hepatocytes may be present, but not functional b/c of the vascular network and biliary ducts are distored and non-functional.
3) Even if the primary cause is removed, damage may continue b/c fibrosis interferes w/ the blood supply to the liver tissues, or the bile may back up leading to ongoing inflammation and damage.
4) Initially, the liver is large. But as fibrosis procees, it starts to shirnk.

5)The progressive changes that happen are directly linked to inflammation w/ the primary condition.
In many cases, cirrhosis is asymptomatic until it’s very advanced. (pt won’t know they have cirrhosis till late stages)

Question 6

Causes of Portal Cirrhosis

Answer 6

In pt’s w/ alcoholic liver disease, there are several stages (3) in the development of hepatocellular damage related to the effects of alcohol.

Alcohol and its metabolites are toxis to the liver cells and alter many metabolic processes in the liver.

Secondary malnutrition may aggravate the damaging effects on liver cells.

Question 7

What are the three stages of Portal Cirrhosis?

Answer 7

1) Fatty Liver
2) Alcoholic Hepatisis
3) End-stage Cirrhosis

Question 8

What is the Fatty Liver stage of portal cirrhosis?

Answer 8

-Initial change is the accumulation of fat in liver cells.

Question 9

S/s of Fatty Liver

Answer 9

Other than hepatomegaly, this stage is asymptomatic.

Question 10

Tx of Fatty Liver

Answer 10

It is reversible if alcohol intake is reduced.

Question 11

What is the Alcoholic Hepatitis stage of portal cirrhosis?

Answer 11

• Inflammation and cell necrosis occur during this stage.
• Fibrous tissues form, an irresersible change.
• Acute inflammation may develop when alcohol intake increases or binge drinking becomes more excessive

***In some patients, after an episode of excessive alcohol intake, there may be sufficient damage to precipitate liver failure, encephalopathy, and death.

Question 12

S/s of Alcoholic Hepatisis

Answer 12

May also be asymptomaticCould manifest:-Mild: Anorexia, nausea, liver tenderness.

Question 13

What is Portal Cirrhosis?

Answer 13

Cirrhosis d/t Alcohol intake

Question 14

What is the End-Stage Cirrhosis stage of portal cirrhosis?

Answer 14

• Occurs when fibrotic non-functional tisue replaces normal tisue. (10-20% heptacytes/ 80-90% scar tissue)
• Liver structure is altered to the point that little function remains.

Question 15

S/s of End-Stage Cirrhosis

Answer 15

Signs of portal hypertension

-ascites or impaired digestion, are the usual early indicators of this stage.

Question 16

What pathophysiological effects evolve to form Cirrhosis?

Answer 16

1) The loss of liver cell funstions.

2) Interference w/ blood and bile flow in the liver (d/t fibrous tissue)

Question 17

What are the functional losses d/t Hepatocyte loss?

Answer 17

1) Decr. removal and conjugaton of bilirubin (jaundice)
2) Decr. production of bile (cannot break down fats)
3) Impaired digestion and absorption of nutrients, particularly fats and fats-soluble vitamins
4) Decr. production of blood clotting factors and plasma proteins (decr. albumin –> higher bleeding b/c cannot clot) (also edema b/c decreased capillary colloidal osmotic pressure d/t loss of plasma proteins)
5) Impaired glucose/glycogen metabolism (Decr. BG)
6) Inadequate storage of iron and Vit B12 b/c its stored there. (Anemia)
7) Decreased inactivation of hormones, such as aldosterne and estrogen
8) Decreased removal of toxic substances, such as ammonia and drugs (ammonia from protein metabolism)

Question 18

What are the Functional losses d/t Altered Blood and Bile Flow?

Answer 18

1) Reduction of the amount of bile entering the intestine, impairing digestion and absorption. 2)Backup of bile in the liver, leading to jaundice.
3) Blockage of blood flow through the liver, leading to “Portal Hypertension”
4) Splenomegaly (large spleen) leading to increasing hemolysis b/c the spleen is working too much filtering the blood. (hemolysis)
5) Congestion in intestinal walls and stomach, impairing digestion and absorption.6)Development of esophageal varices.

Question 19

S/s of Portal Cirrhosis

Answer 19

Inital:

• Mild and vague
• Fatigue
• Anorexia
• Weight loss
• Anemia
• Diarrhea
• Dull aching pain may be present in URQ of the abdomen.
• Bruising b/c not clottig well d/t decr. albumin

Advanced:

• Ascites
• Peripheral edema (Both from portal HTN)
• Jaundice
• Encephalopathy
• Esophageal varices
• Alteres reproductive hormone levels
• Persistent infections.

Question 20

Why does Ascites occur?

Answer 20

When cirrhosis develops, the portal vein system cannot filter effectively through the cirrhotic and nodular liver which results in increased pressure of the blood flowing from the digestive system.
This increased pressure forces fluid (made up of water and proteins) out of the blood vessels which collects in the abdominal cavity.
BECAUSE GI stuff gets to the blood system BY the liver!
If liver is full of nonfunctional tissue, then nothing is getting to the blood stream from the GI tract.Then theres increased pressure, then there’s a result of Ascites.

Question 21

Tx of Cirrhosis

Answer 21

• Supportive or symptomatic tx
• Dietary restrictions include restrictions on protein and sodium intake.
• High CHO intake and Vitamin supplements are necessary
• Serum electrolytes may have to be balances, possible requiring the use of diuretics to reduce body fluids
• Liver transplants provide another option.

Question 22

Functions of the Kidney

Answer 22

1) Filter 200L of fluid/day (1.8L/day)
2) Excrete toxins, metabolic wastes and excess electrolytes
3) Regulate volume and metabolic compsition of the blood including water, salt, acid and base balance.Kidneys are the major excretory organ

Question 23

What is Renal Failure?

Answer 23

Failure so the kidneys to work as a result from another condition (Ex: Decr. Co)

Question 24

Patho of Renal Failure

Answer 24

1) Either directly reduced blood flow into the kidney, or
2) inflammation and necrosis of the tubules cause obstruction and back pressue, leading to greatly resuced GFR(Glomerular Filtration Rate- amount of blood that gets filtered out in the glomerulus into the tubule) and oliguria or anuria.
- Both kidneys must be involved to be renal failure.
- The failure is usually reversible if the primary problem is tx’d successfully (more often acute than chronic cases)
- Dialysis may be used to replace the kidney funtion during this period
- In some cases, they kidneys sustain a degree of permenent damage.

Question 25

Etiology of Acute Renal Failure (ARF)

Answer 25

1) Acute bilateral kidney disease (Glomerulonepheritis, which reduces GFR (Immune attacks on tubules)) 2) Severe and prolonged circulatory shock or Heart failure, which results in tubule necrosis (Decr. in blood flow) 3) Nephrotoxins (drugs, chemicals, toxins) which cause tubule necrosis and obstruction of blood flow. - includes sulfa drugs, phenacetin, NSAID's, tylenol, ASA, penicillin.-When pts take these meds, fluid intake must be incr. to reduce the risk of kidney damage from the metabolites. Occasionally, mechanical obstructions (calculi, blood clots, tumours) can block urine flow beyond the kidneys and cause acute renal failure.

Question 26

S/s of Acute Renal Failure

Answer 26

Acute Renal Failure usually develops rapidly Blood tests show: - Elevated serum Blood urea nitrogen (BUN) - Elecated creatinine - Metabolic Acidosis (to much toxins) - Hyperkalemia (not excreting it)

Question 27

Tx of Acute Renal Failure

Answer 27

Important to reverse the primary problem as quickly as possible to minimize the risk of necrosis and permenent kidney damage. 1) Remove obstruction Ex: Clot, kidney stone 2) Dialysis may be used to normalize body fluids and maintain hemostasis during oliguric stage. Recovery from ARF is shown by increase U/O (diuretic stage) It may take a few months before the epithelium lining the renal tubules recovers totally, so fluid and electrolyte balance may not return to normal for some time.

Question 28

Etiology of Chronic Renal Failure

Answer 28

It's the gradual irreversible destruction of the kidneys over a long period of time. - It may result from Chronic kidney disease, such as bilateral pyelonephritis or congenial polycystic kidney disease, or from systemic disorders such as HTN or DM. - Long term exposure to nephrotoxins is a cause. - The gradual loss of nephrons is asymptomatic until it is well advanced b/c the kidneys normally have considerable reserve function. - Once advanced, the prognosis of Chronic Renal Failure may be slowed, but not stopped, because the scar tissue and loss of funtional organization tend to cause further degenerative changes.

Question 29

Patho of Chronic Renal Failure

Answer 29

Three Stage: 1) Decreased renal reserve 2) Renal insufficiency 3) Uremia (Renal Failure)

Question 30

What is Decreased Renal Reserve?S/s

Answer 30

Around 60% of nephrons are lost-Is a decrease in GFR, - serum creatinine levels that are consistently higher than average but within normal range, - serum urea levels that are normal, and no apparent clinical signs. The remaining nephrons appear to adapt, increasing their capacity for filtration. (Any nephrons left just become better at their job when others die off)

Question 31

What is Renal Insufficiency?S/s

Answer 31

Around 75% of nephrons are lost (60-75%) - Indicated by a change in blood chemistry and manifestation. - At this point, GFR is decreased to approx. 20% of normal, and there is significant retention of nitrogen wastes (urea and creatinine) in the blood - Tubule function is decreased, resulting in failure to concentrate the urine and control the secretion and exchange of acids and eletrolytes. - Osmotic diuresis occurs as the remaining functional nephrons filter an increased solute load. - This stage is marked by excretion of large volumes of dilite urine. - Erythropoiesis is decreased d/t depressed bone marrow. - the pt's BP is elevated. (The cardiovascular system must compensate for these effects)

Question 32

What is Uremia?S/s

Answer 32

More than 90% (75-90% of nephrons are lost.-Occurs when GFR is negligible (no longer clearing/filtering waste) - Fluids/electrolytes/wastes (everything) is retained in the body, and all body systems are affected. - In this stage, marked oliguria or anuria develops. - Regular dialysis or a kidney transplant is required to maintain the pt's life.

Question 33

S/s of Chronic Renal Failure

Answer 33

Early: - polyuria and nocturia - general signs such as anorexia, nausea, anemia, fatigue, unintended weight loss, exercise intolerance. - Bone marrow depression and impaired cell function cause by increased wastes and altered blood chemistry - High BP (cardiac compensation b/c RBC creating is decr.) Late: - Oliguria - Dry, pruritic, hyperpigmented skin, easing bruising d/t decr.platelets - Peripheral neuropathy - imptence and decreased libido in men, menstral irregularities in women. - Encephalopathy (brain damage) - CHF, arrythmias (w/ lack of waste removal and electrolyte imbalance) - Loss of calcium balance. - Systemic infections such as pneumonia d/t poor tissue resistance related to anemia, - fluid retention, and low protein levels.

Question 34

Dx of Chronic Renal Failure

Answer 34

1) Anemia, acidosis, and azotemia (azotemia refers to the presence of nitrogen wastes in the blood, as indicated by elevated serum creatinine and urea levels) are the key indicators of chronic renal failure. 2) Anemia becomes severe 3) Serum electrolyte levels may vary depending on the amount of water retained in the body. - Usually hyponatremia ( b/c too much fluid) and hyperkalemia occur (trying to deal w/ the acid and the SE of hyperkalemia) - Often coupled w/ hypocalcemia and hyperphosphatemia

Question 35

Tx of Chronic Renal Failure

Answer 35

1) Meds to help stimulate erythropoiesis and reduce phosphate levels, and some meds to tx cardiovascular complications 2) Intake of fluids/electrolytes and protein must be restricted b/c the kidneys are limited in their ability to excrete excess wastes and fluid. - Drug dosages need to be carefully considered and adjusted if necessary in pts w/ uremia b/c of the kidneys decr. ability to excrete drugs in a timely manner. - Simple infections can be difficult d/t the increased stress on the excretory system b/c they already immunosupressed.