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1
Q

What is cholelithiasis?

A

Precipitate formed by the concentration of cholesterol and/or pigments in the gallbladder.

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2
Q

What is cholecystitis?

A

Inflammation of the gallbladder caused by irritation d/t stasis of concentrated bile.

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3
Q

What is choledocholithiasis?

A

Gallstones located in the common bile duct.

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4
Q

What is cholangitis? What can cause cholangitis?

A

Inflammation of the common bile duct.

May be caused by autoimmune diseases, Crohn’s disease, or ulcerative colitis

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5
Q

What hormone causes contraction of the gallbladder?

A

Cholecystokinin

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6
Q

What makes up the contents of bile?

A

Bile pigment
Cholesterol (5%)
Calcium salts
Water

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7
Q

What is the relationship between calcium salts and gallstones?

A

High [Ca2+] = Bile flows freely

Low [Ca2+] = Bile is viscous and precipitates

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8
Q

What are yellow stones?

A

Precipitate formed d/t high concentrations of cholesterol in the bile. D/t poor lipid metabolism (obesity or pregnancy)

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9
Q

What type of gallstone is most common?

A

Yellow stones (75-80% of all gallstones)

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10
Q

What are black stones?

A

Precipitate formed d/t high concentrations of bilirubin in the bile d/t excessive breakdown of RBC.

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11
Q

What are brown stones?

A

Precipitate formed d/t a mix of high concentrations of cholesterol and pigment in the bile.

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12
Q

Who is most at risk for yellow stones?

A

Women
Multigravida women
First Nations

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13
Q

Who is most at risk for black stones?

A

Patients with:
Sickle cell anemia
Splenomegaly
Hemolytic anemia

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14
Q

Where are brown stones usually located? What can precede the formation of brown stones?

A

In the common bile duct. Associated with infection.

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15
Q

What is the most extreme complication of gallstones?

A

Obstruction of the common bile duct leading to pancreatitis. Causes extreme pain in RUQ d/t highly vascular structure. Enzymes back up and cause degradation of the pancreas.

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16
Q

What are common complications of gallstones?

A

Cholecystitis

Secondary obstruction

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17
Q

What is the pathophysiology of biliary reflux?

A
  1. Gallbladder contracts.
  2. Bile is sent down common bile duct.
  3. Blockage forms in ampulla of Vater; bile cannot enter duodenum.
  4. Bile goes up pancreatic duct.
  5. Bile in pancreas disrupts tissues; digestive enzymes activated.
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18
Q

What is the relationship between cholestasis and intrahepatic biliary disorders? Describe the pathology.

A
  1. Bile flow in the liver slows down
  2. Bile accumulates and forms plugs in the ducts.
  3. Ducts rupture and damage liver cells. AST, ALT, and ALP are released into blood.
  4. Liver is unable to continue processing bilirubin
  5. Increased bile acids in blood and skin (puritus)
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19
Q

What is primary biliary cirrhosis (PBC)?

A

Autoimmune disease causing neutrophils to be present in the intrahepatic bile duct. Neutrophils release inflammatory mediators which cause the gallbladder wall to thicken.

Gallbladder shuts down, bile release decreases, bile backs up into the liver causing liver damage.

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20
Q

Who is most affected by primary biliary cirrhosis?

A

Women 9:1

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21
Q

What are some diseases of the extrahepatic bile ducts?

A 
Bile duct carcinoma
Hodgkin disease, metastatic carcinoma (enlarged lymph nodes)
Sclerosing cholangitis
Post operative stricture of the bile duct
Congenital biliary atresia
Pancreatic carcinoma
Gallstones
Carcinoma of the ampulla of vater
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22
Q

What is primary sclerosing cholangitis?

A

Bile ducts appears beaded with alternating narrow and flared segments. Victims usually have another inflammatory disorder such as ulcerative colitis.

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23
Q

Who is most affected by sclerosing cholangitis?

A

Men are more affected than women 3 to 1.

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24
Q

How is sclerosing cholangitis treated?

A

Treat with long acting anti-inflammatory medication.

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25
Q

Who is most affected by brown stones?

A

People of Asian descent.

26
Q

What is another name for black stones?

A

Polybilirubin stones

27
Q

What is the pathogenesis of cholecystitis?

A

Gallstone is wedged in mucosa, which can cause a decubital ulcer, which leads to secondary infection of the ulcer which can cause a cholecystoenteric ulcer or carcinoma

28
Q

What are the signs and symptoms of secondary obstruction?

A

Jaundice, increased conjugated bilirubin levels

29
Q

What is the pathology of cholecystitis?

A

secondary infection leading to ulcer formation; cholecystoenteric fistula forms, perforation occurs

30
Q

What does the presence of >70 mLs of bile in the gallbladder means?

A

Failure to contract gallbladder or gallstones are present

31
Q

What is the normal volume of the gallbladder?

32
Q

What is the normal color of the gallbladder? What color is it with cholesterol deposits? What color is it with pigmentary gallstones?

A
  1. Normal: green
  2. Yellow
  3. Pink - no bile, only mucous
33
Q

Where are the kidneys located?

A

Retroperitoneal

T12 to L3 level

34
Q

What is the mass and volume of each kidney?

A

160g each

About the size of a bar of soap (12x6x3 cm)

35
Q

What structures hold the kidneys in place?

A

The adipose capsule and the renal faschia.

36
Q

What is the adipose capsule?

A

Pararenal fat that cushions the kidney and holds it in place.

37
Q

What is the renal capsule?

A

A cellophane-like membrane that encloses the kidney.

38
Q

How are the kidneys damaged in anorexic individuals?

A

The renal artery usually lines up at the L1 level. The adipose capsule and the renal faschia usually hold the kidneys in place. In anorexic individuals, the fat cushioning may degrade and the kidneys descend. The renal artery buckles and renal tissue necrosis occurs

39
Q

What are the functions of the kidneys?

A
  1. Filters blood plasma
  2. Eliminates waste: urea excretion and creatinine metabolism
  3. Returns useful substances to blood
  4. Regulates blood volume & pressure
  5. Regulates osmolarity of body fluids
  6. Secretes renin (which activates angiotensin I –> II –> aldosterone pathway)
  7. Controls BP & electrolyte balance
  8. Secretes erythropoietin
  9. Regulates acid base balance (secretes H+ or retains HCO3- to buffer acid)
  10. Detoxifies free radicals and drugs
40
Q

What percentage of body mass do the kidneys have? What percentage of cardiac output do the kidneys receive.

A
  1. 0.4%
  2. 22%

The kidneys receive 55 times the amount of blood they are entitled to by virtue of their body mass.

41
Q

How is urea excreted by the kidneys?

A

Proteins –> amino acids –> NH2 removed –> forms ammonia, liver converts to urea –> urea excreted in urine

42
Q

What is the relationship between creatinine and kidney function?

A

creatine phosphate is converted to creatinine (an amino acid) at the cells. Creatinine is excreted by the kidneys. In kidney failure, circulating creatinine rises.

43
Q

How is urine formed?

A
  1. Glomerular filtration creates a plasmalike filtrate of the blood.
  2. Tubular reabsorption removes useful solutes from the filtrate, returns them to the blood and tubular secretion removes additional wastes from the blood, adds them to the filtrate.
  3. Water conservation removes water from the urine and returns it to blood, concentrates wastes.
44
Q

What is blood hydrostatic pressure relative to the capillaries in the renal corpuscle?

45
Q

What is colloid osmotic pressure relative to the capillaries in the renal corpuscle?

46
Q

What is the capsular pressure relative to the capillaries in the renal corpuscle?

47
Q

What is the net filtration pressure relative to the capillaries in the renal corpuscle?

A

10 mmHg out

48
Q

What disorders affect glomerular filtration rate?

A

Hypotension, liver failure, stenosis of afferent or efferent arteriole, kidney stones

49
Q

What is GFR for males?

A

125 mL/min, 180 L/day

50
Q

What is GFR for females?

A

105 mL/min, 150 L/day

51
Q

How much of filtrate is reabsorbed? How much urine is produced per day?

A

99%; 1-2L excreted/day

52
Q

What happens if GFR rises abnormally?

A

Increased GFR, urine output rises, leading to dehydration and electrolyte depletion

53
Q

What happens if GFR decreases abnormally?

A

Decreased GFR, wastes are reabsorbed (azotemia possible), leading to possible hepatic encephalopathy

54
Q

How is GFR controlled?

A

GFR is controlled by adjusting glomerular blood pressure via:

  1. autoregulation
  2. sympathetic control
  3. hormonal mechanisms
55
Q

What is normal blood volume?

56
Q

What is the purpose of the juxtaglomerular apparatus?

A

Plays a role in the autoregulation of GFR. Juxtaglomerular cells monitor BP at teh afferent arteriole leading to vasomotion. The macula densa at the distal tubule monitors salinity and content of the filtrate.

57
Q

What is the relationship between blood pressure and GFR in the autoregulation of GFR?

A

If BP increases, GFR increases, there is a rapid flow of filtrate in the renal tubules which is sensed by the macula densa. Adenosine is secreted by paracrine cells leading to constriction of the afferent arteriole. GFR decreases.

58
Q

What blood pressure range can the autoregulation of GFR compensate for?

A

The autoregulation of GFR is stable for BP ranges of 80 to 170 mmHg (systolic).

Cannot compensate for extreme BP.

59
Q

Where is angiotensin I activated?

A

Angiotensin I is converted to angiotensin II at the lungs by angiotensin-converting enzyme

60
Q

What are the effects of angiotensin II?

Patho 2 (1 decks)

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