Renal and Liver diseases

Question 1

The area of the kidneys which contain the glomeruli is the

Answer 1

Cortex

Question 2

Urea

Answer 2

catabolism of amino acids

Question 3

Azotemia

Answer 3

elevation of BUN leves

Question 4

Uremia

Answer 4

disease state of kidney

Question 5

Proteinuria

Answer 5

protein in the urine

Question 6

Glycosuria

Answer 6

glucose/sugar in the urine

Question 7

Hematuria

Answer 7

blood in the urine

Question 8

Pyuria

Answer 8

white blood cells in the urine

Question 9

Oliguria

Answer 9

decreased urine production

Question 10

BUN

Answer 10

blood urea nitrogen

Question 11

Glomerulonephritis

Answer 11

• Immunological
• Antibody-antigen complex
o Causes compliment activation and degranulation
 Leads to scarring
• Circulating
o AB/AG complex stuck in basement membrane, causes inflammatory cell activity
 Granular
o Similar to Type 3 hypersensitivity (antibody-antigen)
• In-situ
o AG reacts toward AB in basement membrane
 Linear
o Similar to Type 2 hypersensitivity (tissue specific)

Question 12

Rapidly progressive GN

Answer 12

•	treatable
•	Loss of function (rapid)
•	GFR decreased
•	Typically post-infection
o	Systemic lupus
•	Crescentic scarring
•	Proteinuria

Question 13

Acute diffuse GN

Answer 13

•	Treatable
•	Post-strep GN/staph/pneumococcal 
•	6-10 years of age, 7-28 days
•	Many inflammatory cells
•	Antigen stuck in glomerular basement membrane, antibody attacks
o	In-situ
•	No scarring
•	Inflammatory cells in Bowman’s space

Question 14

Chronic GN

Answer 14

• Most frequent cause of renal failure
• Necrosisscarring=cobblestone texture
• Untreatable because of too much scarring

Question 15

Clinical manifestations of glomerulonephritis

Answer 15

• Decreased GFR (oliguria)
• Proteinuria
• Hematuria (rbcs in urine)
• Pyuria (wbcs in urine)
• Tissue edema because water follows salts

Question 16

Nephrosclerosis

Answer 16

 Scarring of nephron
 Diabetics, chronic hypertension
 Arteriolosclerosis of hyaline arteries near nephron, causes nephrons to look like donuts

Question 17

Clinical symptoms of nephrosclerosis

Answer 17

• Proteinuria
• Focal ischemia of kidneys
o Necrosis (coagulative)
• Decreased blood protein serum

Question 18

Types of acute renal failure

Answer 18

Pre-renal
Parenchymal
Post-renal

Question 19

Pre-renal ARF

Answer 19

hemorrhagic shock
drop in blood pressure, block of blood flow to the kidneys
usually in aorta

Question 20

Parenchymal (Inrarenal) ARF

Answer 20

Direct damage to the kidneys
glomerulonephritis, pyelonephritis, acute tubular necrosis
inflammation in kidneys

Question 21

Post-Renal ARF

Answer 21

obstruction of urine flow
enlarged prostate, kidney stones, tumor, injury
Hematogenous-problem in blood moves to kidney, ends up in bladder, ureter
Ascending-problem in outer environment, moves backwards to kidney

Question 22

Etiological causes of ARF

Answer 22

Infection (pyelonephritis)
Acute tubular necrosis (common cause, nephrons last to get blood, first concern in ischemic attack)
-ischemic, toxic
Shock

Question 23

Pyelonephritis

Answer 23

Bacterial-caused inflammation (renal pelvis, parenchyma, renal calyces)
contributing factors
-gender
-Vesicoureteric reflux
-UT obstruction
-Diabetes
-Congenital abnormalities

Question 24

Reflux nephropathy

Answer 24

form of chronic pyelonephritis
induces scarring
UTI, vasico-ureteral reflux

Question 25

Bilirubin

Answer 25

breakdown of red blood cells

Question 26

Jaundice

Answer 26

unconjugated bilirubin in body (bilirubin normally binds to albumin) hyperbilirubinemia

Question 27

Cholestasis

Answer 27

decrease in bile flow common in liver failure or liver cancer painful use biliary catheter

Question 28

Portal hypertension

Answer 28

high bp in portal veins | common with damage to liver

Question 29

Coagulopathy

Answer 29

liver makes most coagulation factors in body (besides factor H) if liver compromised, bleed easily

Question 30

Hypoalbuminemia

Answer 30

not enough albumin | coloid osmotic pressure decreased, decreased blood volume

Question 31

Ascites

Answer 31

portal hypertension liver disfunction->hypoalbuminemia renin released to conserve water bloated belly, using albumin for protein

Question 32

Steatosis

Answer 32

 Earliest stage  Fatty liver  Reversible • Hepatocytes regenerate

Question 33

Alcoholic hepatits

Answer 33

```  Reversible  Necrosis  Imflammation  Mallory bodies • Early scar formation ```

Question 34

Cirrhosis

Answer 34

```  Final stage  Scarring of liver  Can be from steatosis, hepatitis, or both  Non-reversible  Can be fatal • Liver failure  Non-fatty • Shrunken liver ```

Question 35

Risk factors for cirrhosis

Answer 35

```  Genetics  Risky use • Males o Less than five drinks per occasion o Less than 14 drinks per week • Females o Less than 4 per occasion o Less than 7 drinks per week  “Negative consequences” • Hangover • Blacking out • Fights • Injuries ```

Question 36

Pathogenesis of Steatosis

Answer 36

EtOH + NAD+-> acetylaldehyde+NADH ->acetate • Acetylaldehyde is a hepatotoxin, which damages the liver • NADH encourages liver to store lipids (lipogensis) instead of breaking it down

Question 37

Clinical manifestations of steatosis

Answer 37

``` Enlarged liver (hepatomegaly) Increased bilirubin (yellow liver) ```

Question 38

Pathogenesis of alcoholic hepatitis

Answer 38

Acetaldehyde->inflammationnecrosis Inflammation->white blood cells o TNF-alpha from Kuppfer cells->damage o Stellate cells activated->matrix proteins->fibrosis

Question 39

Clinical manifestations of alcoholic hepatitis

Answer 39

Anorexia Jaundice Malaise (general weakness) Tender liver

Question 40

Pathogenesis of cirrhosis

Answer 40

Repeat stellate cell activation | Fibrosis

Question 41

Clinical manifestation of cirrhosis

Answer 41

Severe jaundice Portal hypertensionascites (fluid buildup in peritoneal cavity) edema