Pathophysiology Exam 4: Gi, Diabetes, Reproductive

Front 1

TRUE OR FALSE
Functions of the GI tract are controlled by extrinsic and intrinsic autonomic nerves (enteric plexus) and intestinal hormones.

Back 1

TRUE

Front 2

TRUE OR FALSE
The vagus nerve stimulates gastric (stomach) secretion and motility.

Back 2

TRUE

Front 3

Describe gastrin and motilin
AND
secretin and cholescystokinin

Back 3

GASTRIN & MOTILIN (intestinal hormones) *INCREASE* contraction by making the threshold potential of muscle nerve fibers less negative.
SECRETIN AND CHOLESCYSTOKININ *INHIBIT* gastric motility and decrease gastric emptying.

Front 4

WALL OF THE GI TRACT?

Back 4

four layers:
mucosa=innermost layer, has lymph nodules
submucosa= glands and ducts
ENTERIC PLEXUS
muscularis= circular and longitudinal
serosa= connective tissue layer

Front 5

Describe the role of intrinsic factor?

Back 5

Mucoprotein produced by the parietal cells, combines with vitamin B12 in the stomach. Failure to absorb vit B12 can lead to pernicious anemia.

Front 6

Parietal Cells?
Chief cells?
G cells?
Enterochromaffin-like cells?
D cells?

Back 6

chief= secrete pepsinogen ( an enzyme precursor thats converted to pepsin in gastric juice)
g cells=release gastrin, stim by the pyloric gland mucosa
ec-like cells= secrete histamine
D cells= secrete somatostatin

Front 7

DESCRIBE THE SMALL INTESTINE?

Back 7

5m long.
has 3 segments: duodenum, jejunum, and ileum.
DIgestion and absorption of all major nutrients and most water occurs here.
The duodenum receives chyme from the stomach thru the pyloric valve.
The presence of chyme stimulates the liver and gallbladder to deliver bile, and the pancreas to deliver dig. enzyme and alkaline secretions.
Bile and enzymes flow thru the sphincter of Oddi.
ENZYMES OF THE SMALL INTESTINE: MALTASE, SUCROSE, LACTASE

Front 8

TRUE OR FALSE
Sugars, amino acids, and fats are absorbed primarily by the duodenum and jejunum; bile salts and VIT B12 absorption requires the presence of intrinsic factor.

Back 8

TRUE

Front 9

BLOOD FLOW TO LIVER?

Back 9

Hepatic Artery supplies to liver.
The portal vein receives blood from the inferior and superior mesenteric veins.

Front 10

HEPATOCYTES?

Back 10

Synthesize 700-1200ml of bile per day, and secrete it into the canaliculi, which are small channels between the hepatocytes.
the bile canaliculi drain bile into the common bile duct, and then into the duodenum thru the sphincter of Oddi.

Front 11

Kupffer Cells?

Back 11

Part of the mononuclear phagocyte system, line the sinusoids (capillaries between the hepatocyes) and destroy microorganisms in sinusoidal blood.

Front 12

Unconjugated bilirubin?
Conjugated bilirubin?

Back 12

Bilirubin is the byproduct of the destruction of RBC'S.
Unconj= In the plasma when bilirubin binds to albumin (fat soluble)
Conjugated=within the hepatocytes, it joins with glucuronic acid to form conj. bilirubin. (water soluble)

Front 13

BILE?

Back 13

Produced in liver. Aids in digestion and emulsification of fats.
Bile acts to some extent as a surfactant, helping to emulsify the fats in the food. Bile salt anions have a hydrophilic side and a hydrophobic side, and therefore tend to aggregate around droplets of fat (triglycerides and phospholipids) to form micelles, with the hydrophobic sides towards the fat and hydrophilic towards the outside.The hydrophilic sides are positively charged due to the lecithin and other phospholipids that compose bile, and this charge prevents fat droplets coated with bile from re-aggregating into larger fat particles.
The cholesterol contained in bile will occasionally accrete into lumps in the gallbladder, forming gallstones. Cholesterol gallstones are generally treated through surgical removal of the gallbladder. However, they can sometimes be dissolved by increasing the concentration of certain naturally occurring bile acids, such as chenodeoxycholic acid and ursodeoxycholic acid.

Front 14

UNCONJUGATED HYPERBILIRUBINEMIA?

Back 14

Heme is broken down into unconj. bilirubin in spleen.
unconj. is not water soluble, so bound to albumin and sent to liver.
CHF, SICKLE CELL ANEMIA, JAUNDICE, ABO INCOMPATIBILITY, THALESSEMIA.

Front 15

CONJUGATED HYPERBILIRUBINEMIA?

Back 15

In the liver, bilirubin is conjugated with glucuronic acid, making it water soluble, it is then excreted into bile, and out into sm. intestine.
ALCOHOLIC CIRRHOSIS, PRIMARY BILIARY CIRRHOSIS, ACUTE FATTY LIVER, BILE STONES,
HEPATITIS

Front 16

CIRRHOSIS?

Back 16

-A consequence of chronic liver disease characterized by replacement of liver tissue by fibrosis, scar tissue and regenerative nodules (lumps that occur as a result of a process in which damaged tissue is regenerated),leading to loss of liver function. Cirrhosis is most commonly caused by alcoholism, hepatitis B and C, and fatty liver disease.
can result in ASCITES, HEPATIC ENCEPHALOPATHY, AND ESOPHAGEAL VARICES.
ELEVATED ALT/AST
ELEVATED ALKALINE PHOSPHATASE.
DEC. ALBUMIN.
INCREASED PT.
HYPONATREMIA.

Front 17

HEPATITIS?
ACUTE VS CHRONIC?

Back 17

Inflammation of liver w inflammatory cells.
Can progress to fibrosis and cirrhosis. Often leads to jaundice, anorexia, malaise.
acute=flu like symptoms.N/V/D.
may be asymp. but can dev. acute liver failure w hep. encephalopathy.
Chronic= malaise, tiredness, weakness. Cirrhosis leads to wt. loss and periph. edema, ascites.

Front 18

BILIARY TRACT DZ?

Back 18

Blockages of biliary tract w gallstones.
may present w RUQ Pain, nausea, dark urine, jaundice.

Front 19

PORTAL HYPERTENSION?

Back 19

HTN in portal vein. Causes can be divided into prehepatic, intrahepatic, and posthepatic. Intrahepatic causes include liver cirrhosis, and hepatic fibrosis (e.g. due to Wilson's disease, hemochromatosis, or congenital fibrosis). Prehepatic causes include portal vein thrombosis or congenital atresia. Posthepatic obstruction occurs at any level between liver and right heart, including hepatic vein thrombosis, inferior vena cava thrombosis, inferior vena cava congenital malformation, and constrictive pericarditis.

Front 20

HHNKS VS DKA?

Back 20

DKA- blood sugar > 300-600.
INC. anion gap.
c-peptide decreased. usu. type 1. kussmaul resp.metab. acidosis. fruity breath, abd. pain, N/V, hyponatremia, impaired LOC.
HHNKS- blood sugar > 600.
usu. type 2. usu. brought on by illness of infection.
extreme thirst, loss of vision,
hallucinations, fever.

Front 21

TYPE 1 DM?
TYPE 2 DM?

Back 21

1-autoimmune. type IV, imm. sys. kills pancreatic b cells. can be hyper or hypoglycemic.
2-hyperglycemia, can't get glucose into cells. Progressive loss of insulin sensitivity.

Front 22

TRUE OR FALSE?
When glucagon is high, insulin is low, when Insulin rises, has neg. fb effect on glucagon. (Dec glucagon prod)

Back 22

TRUE

Front 23

Effects of Insulin?

Back 23

Decreased appetite
Decreased glucagon
Inc. glycolysis
Inc. triglycerides
Inc. amino acids
Inc. Protein synthesis

Front 24

Effects of lack of insulin?

Back 24

Inc. appetite
Inc. glucagon
Dec. glucose uptake by cells
Dec. protein synthesis
Inc. glyocgenolysis
Inc. Ketone bodies

Front 25

GLUT 2?

Back 25

a transmembrane carrier protein that enables passive glucose movement across cell membranes. It is the principal transporter for transfer of glucose between liver and blood, and for renal glucose reabsorption
Found on cells that always express glut2, always in cell membrane. Found in liver, pancreas, hypothalamus, sm. intestine.

Front 26

GLUT4?

Back 26

GLUT4 is the insulin-regulated glucose transporter found in adipose tissues and striated muscle (skeletal and cardiac) that is responsible for insulin-regulated glucose translocation into the cell. This protein is expressed primarily in muscle and fat cells, the major tissues in the body that respond to insulin
when insulin low, sequestered in intracellular vesicles in muscle and fat cells, as vesicles fuse, glut4 are inserted and transport glucose.

Front 27

Pancreatitis?

Back 27

Inflammation of pancreas. Occurs when pancreatic enzymes (trypsin) that digest food are activated in the pancreas rather than sm. int.
S/S sever upper abdominal pain radiating to back, nausea, vomiting worsened w eating.
80% caused by alcohol and gallstones.
elevated amylase and lipase.

Front 28

HPG AXIS?

Back 28

This axis controls development, reproduction, and aging in animals. The hypothalamus produces gonadotropin-releasing hormone (GnRH). The anterior portion of the pituitary gland produces luteinizing hormone (LH) and follicle-stimulating hormone (FSH), and the gonads produce estrogen and testosterone.
In females FSH and LH act primarily to activate the ovaries to produce estrogen and inhibin and to regulate the menstrual cycle and ovarian cycle. Estrogen forms a negative feedback loop by inhibiting the production of GnRH in the hypothalamus
In males LH stimulates the interstitial cells located in the testes to produce testosterone, and FSH plays a role in spermatogenesis

Front 29

LH?

Back 29

Leutinizing hormone. A rise in LH stimulates ovulation, and the development of the corpus luteum.
In males, LH stimulates the leydig cells to produce testosterone.

Front 30

ALPHA CELLS?
BETA CELLS?

Back 30

alpha cell release glucagon
beta cells release insulin (have glut2 transporter)

Front 31

TRUE OR FALSE
Insulin secretion is stimulated by glucose?

Back 31

true

Front 32

Describe the atp/ca channel in regards to blood glucose?

Back 32

If high levels of BG, and high glucose into cell, more ATP, raise ATP/ADP ratio, ATP sensitive K channel, K leaves, polarizes cell, ATP Blocks the channel preventing K from leaving. Voltage gated Ca channels open so Ca comes in, secretes insulin, goes out to dec. BG levels.

Front 33

type 1 characteristics?
type 2 characteristics?

Back 33

1- onset <20 yo
normal weight
dec. bld insulin
keto-acidosis
hla-d linked
anti-islet cell ab
marked atrophy and fibrosis of islet cells
muscle wasting
diabetic coma
2- onset > 30 yo
obese
inc. bld. insulin
no ab
90% concord. in twins
no hla assoc
insulin resistance
no insulitis, focal atrophy and amyloid deposits

Front 34

AGE'S?

Back 34

chronic problem related to hyperglycemia.
shiff base-amadori product
cross-link polypeptides of same protein
collagen
trap ldl
induce pro-inflammatory response
HgbA1c
Inc. vasc. permeability
procoag. activity

Front 35

nephrosclerosis?

Back 35

granular surface of kidney, dec. GFR, membrane leaks,
proteinuria, thick wall and narrow lumen.

Front 36

Diabetic nephropathy?

Back 36

Inc. mesangeal matrix, microaneurysms, nodular lesions.
lose filtering capacity of glomerulus.
best prevention is ACE inhibitors

Front 37

true or false?
In the presence of the Y chromosome, anti-wallerian hormone is secreted, deg. mallerian ducts into wolfian ducts, which become epidydymis and vas deferens.
In females the mallerian ducts become the fallopian tubes and uterus.

Back 37

TRUE

Front 38

Seminiferous tubules?

Back 38

in the testes,
sertoli cells
spermatogonia (stem cells)

Front 39

Interstitial?

Back 39

Leydig cells
sit betw. semin. tubules
prod. testosterone