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Pathophys > Pancreatic > Flashcards

Pancreatic Flashcards

1
Q

Hepatic system functions to convert ____ and excrete ____

A

Bilirubin and ammonia

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2
Q

Hepatic system is the sole source of what protein?

A

Albumin

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3
Q

T/F Hepatic system synthesizes clotting factors and cholesterol.

A

True

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4
Q

Hepatic system detoxifies the body of what?

A

Drugs, ETOH, toxins

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5
Q

Hepatic system stores what?

A

Glycogen, vitamins, iron

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6
Q

Liver receives what % of cardiac output?

A

25%

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7
Q

The liver receives blood from what two places?

A
  1. Portal vein (from organs)

2. Hepatic artery

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8
Q

T/F The portal vein (from organs) provides approximately two-thirds of the blood supply, while the hepatic artery provides the rest.

A

True

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9
Q

What is the functional unit of the liver?

A

Liver lobule

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10
Q

S&S of hepatic disease include:

A
  1. Include GI symptoms - N&V, Diarrhea, Constipation, Heartburn, Abdominal pain, GI bleeding
  2. Edema/ascites
  3. Dark Urine
  4. Light/clay-colored stools
  5. Right upper quadrant abdominal pain
  6. Neurologic involvement: Confusion, muscle tremors, sleep disturbances, hyperreactive reflexes
  7. Hepatic Osteodystrophy (abnormal development of bone)
  8. Osteoporosis:
  9. Skin changes: Jaundice, increased bruising
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11
Q

Why does hepatic disease cause dark urine?

A
  1. Yellow-orange breakdown product of hemoglobin

2. Bilirubin accumulates in liver -> moves into blood -> increase in urine -> may suggest liver damage

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12
Q

Why does hepatic disease cause Light/clay-colored stools?

A
  1. Reduced ability of the liver to excrete bilirubin into the gut
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13
Q

T/F Jaundice (Icterus) is a symptom, not a disease.

A

True

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14
Q

What is jaundice

A

Bilirubin breakdown product of RBC in macrophages

yellow discoloration of the skin, sclerae, and mucous membranes.

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15
Q

How does jaundice occur?

A
  • Cause: Increased bilirubin production or decreased processing of bilirubin
  • Hepatocyte dysfunction (hepatitis, hepatic disease, tumor), bilirubin accumulation
  • Impaired bile flow: caused by mechanical damage due to some obstruction of biliary tree
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16
Q

Treatment of jaundice?

A
  • Resolve underlying disease
  • Return to normal color suggests resolution
  • Then activity and exercise can be resumed
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17
Q

How can hepatic disease cause neurologic involvement?

A
  • Ammonia converted into urea in the liver
  • Ammonia comes from the degradation of amino acids
  • Ammonia is then catabolized by the liver generating urea
  • ↓ urea production leads to ammonia accumulation in the blood and neurological symptoms
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18
Q

What is the most common neurologic abnormality associated with liver failure?

A
  • Flapping tremor elicited by attempted wrist extension while the forearm is fixed
  • Maximal on sustained posture
  • Usually bilateral, though one side can be affected more
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19
Q

Where is MSK location of pain associated with the liver and biliary system?

A

Posterior thoracic pain [inter scapular, R shoulder, R upper trap, R subscapular]

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20
Q

What is hepatic osteodystrophy?

A
  • Abnormal development of bone/osteoporosis in individuals with chronic liver disease
  • Leads to osteopenia and osteoporosis
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21
Q

(Decrease/Increase) size and weight of liver with aging.

A

↓ size & weight of liver

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22
Q

(Decrease/Increase) processing time of liver with aging.

A

↑ processing time

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23
Q

How do blood test values change with aging.

A

Blood test value results remain unchanged [disease vs aging]

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24
Q

Describe healing of liver:

A
  • Occurs quickly
  • Complete parenchymal regeneration or scarring or a combination
  • Chronic hepatic injury → fibrosis (cirrhosis)
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25
Q

What is cirrhosis of the liver?

A
  • Chronic disease of liver marked by degeneration of cells, inflammation, and fibrous thickening of tissue
  • A late stage of scarring (fibrosis) of the liver caused by many forms of liver disease
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26
Q

Cirrhosis of the liver is typically a result of what two things?

A
  1. Alcoholism

2. Hepatitis

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27
Q

Significant loss of liver function associated with loss of ___% or more of liver function.

A

80%

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28
Q

Describe the cycle that causes cirrhosis of the liver:

A
  • Liver inflammation causes tissue damage and necrosis
  • Liver repairs itself
  • Liver is reinjured leading to more tissue damage and necrosis
  • This cycle of inflammation and healing leads to the replacement of liver tissue with bands of connective tissue
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29
Q

Practice implications of cirrhosis:

A
  • Osteoporosis (bone injury)
  • Impaired posture
  • Impaired muscle performance/weakness (electrolyte dysfunction)
  • Loss of balance
  • Deconditioning
  • Ascites/bilateral edema of feet and ankles
  • Blood loss: Bruising/bleeding
  • Rest to reduce metabolic demand on the heart is recommended; rest during treatment sessions and avoid unnecessary fatigue
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30
Q

What is the portal vein?

A
  • a vein conveying blood to the liver from the spleen, stomach, pancreas, gall bladder and intestines
  • Carries about 75% of the blood going to the liver
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31
Q

T/F The portal vein conducts blood to capillary beds in the liver, i.e. it is not a true vein.

A

True

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32
Q

A portal system by definition does what?

A

links two capillary beds together

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33
Q

Portal hypertension -

A

as an increase in hepatic sinusoidal blood pressure > 6 mm

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34
Q

What contributes to portal hypertension?

A

Fibrosis, and abnormal liver architecture combine to form mechanical barriers to blood flow in the liver increasing the resistance and blood pressure in the hepatic portal system

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35
Q

Increased portal pressure will cause what?

A
  • retrograde flow of blood back into the stomach, spleen, large and small intestine, rectum and esophagus
  • Result in varices back upstream
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36
Q

What is a varice?

A
  • Varices: An abnormally dilated vessel with a tortuous course
  • Varicose veins as seen in lower extremities
  • May leak blood or bleed
  • Serious bleeding can quickly result in hypovolemia, shock, and death
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37
Q

Consequences of portal hypertension:

A
  1. Ascites: from increased hydrostatic venous pressure
  2. Splenomegaly: enlargement of the spleen caused by venous congestion in spleen
  3. Hemorrhoids: from venous congestion in the bowel
  4. Varices: Esophagus, stomach, rectum or umbilical area (May rupture and bleed)
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38
Q

Portal hypertension can cause splenomegaly which can lead to what 3 things?

A
  1. Moderate anemia
  2. Neutropenia
  3. Thrombocytopenia
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39
Q

Hepatic Encephalopathy -

A
  • Potentially irreversible, decreased level of consciousness in people with severe liver disease
  • Thought to be caused by elevated blood ammonia and altered neurotransmitter status in the brain
  • Insidious onset; progressive worsening of symptoms as disease progresses
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40
Q

How does hepatic encephalopathy occur?

A
  • Ammonia is created by bacteria in the colon from the metabolism of protein and urea.
  • Ammonia is absorbed into the portal blood system and transported to the liver where it is converted into urea
  • But the diseased liver cannot metabolize the ammonia
  • Blood ammonia levels go up impairing cognitive and motor function at the level of the brain
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41
Q

Symptoms of hepatic encephalopathy:

A
  • Depression, personality changes, impaired attention
  • Drowsiness, sleep disorders, ataxia, asterixis (rapid extension-flexion motion of the head and extremities), slurred speech, hyperreflexia
  • Marked confusion, incoherent speech, muscle rigidity
  • Stupor, decerebrate posturing, positive Bobinski’s, dilated pupils
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42
Q

Decorticate posturing vs. decerebrate

A

Decorticate - flexion of wrist and elbows (upper midbrain damage - corticospinal tracts)
Decerebrate - extension of elbow (upper pontine damage)

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43
Q

T/F Symptoms can be reversed if cause is determined.

A

True
Bleeding, infection, hypovolemia, hypokalemia
Anti-depressants, high dietary protein, diuretics

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44
Q

Implications of hepatic encephalopathy for the PT:

A
  1. Patient safety
  2. Impaired motor and sensory integrity i.e. impaired mobility, balance,
  3. Impaired arousal
  4. Risk for pressure ulcers secondary to malnutrition, immobility, edema
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45
Q

Ascites -

A

Abnormal accumulation of fluid in the peritoneal cavity

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46
Q

Ascites associated with what issues?

A

Associated with cirrhosis/portal hypertension

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47
Q

Ascites can lead to what?

A

Can lead to Wt. gain, abdominal distension, peripheral edema, inappropriate dyspnea

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48
Q

Management of ascites:

A
  1. Paracentesis
  2. albumin consumption
  3. diuretics
  4. sodium and fluid restriction
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49
Q

Implications of ascites:

A
  1. Accompanying impaired cardiac and respiratory function
  2. Lymphedema
  3. Integumentary disorders (peripheral edema, reduced blood flow (congestion), lymphedema
  4. Malnutrition
  5. Muscle degradation
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50
Q

What is a sinusoid and how does it contribute to the fundamental function of the liver i.e. purifying the blood?

A
  • A sinusoid is a discontinuous capillary that receives blood from terminal branches of the hepatic artery and portal vein and delivers it to the central veins (through the liver cells)
  • allows for blood filtration, and regulation of blood flow
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51
Q

Hepatitis -

A
  • Inflammatory (acute or chronic) condition of the liver
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52
Q

What causes hepatitis?

A
  • Infection by one of several viruses with specific affinity for the liver (A, B, C, D, E)
  • Other viruses, but not liver-specific including Epstein-Barr or CMV (cyto-megalovirus)
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53
Q

What causes chronic hepatitis -

A
  • viruses
  • medications
  • metabolic abnormalities
  • autoimmune disorder
  • idiopathic
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54
Q

T/F Most people with chronic hepatitis are asymptomatic and when symptoms appear, they are nonspecific

A

True

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55
Q

How do you diagnose viral hepatitis?

A
  1. Symptoms
  2. Physical Exam
  3. Blood test (specific Ab, liver function tests)
  4. liver biopsy (chronic inflammation, necrosis)
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56
Q

Symptoms of viral hepatitis:

A
  • N & V
  • Poor appetite, Wt. loss
  • Weakness
  • Jaundice, Dark urine
  • Pale or clay-colored stool
  • Fatigue
  • Most people have vague or no symptoms at all
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57
Q

Prognosis of viral hepatitis dependent on what factors?

A
  • Type of hepatitis
  • presence of liver comorbidities
  • development of cirrhosis
  • Occurrence of liver cancer and/or cirrhosis hastens the progression
  • Moderate-to-severe ETOH consumption
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58
Q

Hep A formerly known as what?

A

infectious hepatitis

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59
Q

How is HAV spread?

A

Spread by close personal contact or oral-fecal contamination of water and food, poor hand hygiene, shared use of oral utensils

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60
Q

How contagious is HAV?

A

Highly

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61
Q

Does HAV have a vaccine?

A

Yes, preventable with vaccine

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62
Q

Prognosis of HAV:

A
  • Most persons with acute disease recover with no lasting liver damage
  • rarely fatal
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63
Q

Hep B formerly known as what?

A

Serum Hepatitis

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64
Q

How is HBV spread?

A

Spread by blood transfusions, needle sticks, IV drug use/shared needles, dialysis, sexual contact, exchange of bodily fluid

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65
Q

T/F HBV is considered a STD because it is transmitted via sexual intercourse

A

True

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66
Q

What is incubation period for HBV?

A

90 days

67
Q

Who is at risk of getting HBV?

A

Healthcare workers who come in contact with blood

68
Q

Prognosis of HBV:

A
  • Most persons with acute disease recover with no lasting liver damage; acute illness is rarely fatal
  • 15 -25% of chronically infected persons develop chronic liver disease (can lead to liver failure)
69
Q

T/F Vaccine available for HBV.

A

True

70
Q

Which Hep virus is the leading cause of chronic liver disease?

A

HCV

71
Q

How is HCV transmitted?

A

Transmitted by contact with blood of an infected person, primarily through contaminated needles, sexual contact, needle sticks

72
Q

T/F Acute illness is uncommon in patients with HCV

A

TRUE

73
Q

What % of newly infected HCV persons develop a chronic infection?

A

75-85%

74
Q

What % of newly infected HCV persons develop cirrhosis?

A

5-20%

75
Q

What % of newly infected HCV persons will clear the virus?

A

15-25%

76
Q

T/F There is a vaccine for HCV.

A

False

77
Q

Treatment of HCV?

A
  1. Interferon- stimulates the immune system to attack the virus
  2. Ribavirin- An anti-viral drug (Used in tandem with interferon)
  3. New, direct acting antiviral agents
    - Curative
    - 8-12 week course of oral medication
78
Q

Who should be tested for hepatitis C virus?

A
  • Received an organ transplant before 1992
  • If you have ever injected drugs, even once many years ago
  • If you received blood product used to treat clotting problems that was made before 1987
  • If you were born between 1945 and 1965
  • If you have had long term kidney dialysis
  • Children born to HCV-positive mothers
79
Q

Other types/causes of hepatitis:

A
  • Autoimmune hepatitis (inflammatory condition of the liver)

- Other viral causes of hepatitis (CMV, Epstein-Barr (mono), Yellow fever (yellow fever virus))

80
Q

Drug- and toxin-induced liver disease -

A
  • Dose-related meaning that if enough drug is administered, there will be liver damage
  • Drugs include acetaminophen, tetracycline, anti-neoplastic agents; alcohol
81
Q

Fatty liver -

A
  • Fat accumulates → inflammation → scarring (cirrhosis)

- Associated with ETOH consumption

82
Q

Biliary system -

A
  • Of or relating to bile or the bile duct

- The biliary system creates, moves, stores, and releases bile into the duodenum

83
Q

Bile -

A
  • A dark green to yellowish fluid produced by the liver

- Contains bile salts a surfactant that help to emulsify the lipids in food

84
Q

What is the purpose of bile emulsifying lipids in food?

A

This process greatly increases surface area for the action of the enzyme pancreatic lipase

85
Q

Biliary Obstruction -

A

Prevent the flow of bile to the duodenum resulting in accumulation of bile in the blood and causing jaundice

86
Q

Describe pathway of bile to the hepatic duct:

A

through the right and left hepatic ducts -> join to form the common hepatic duct -> through the cystic duct -> gall bladder

87
Q

Describe pathway of hepatic duct to duodenum:

A
  1. common hepatic duct + cystic duct -> common bile duct

2. common bile duct + pancreatic duct -> ampulla of vater of the duodenum

88
Q

gallbladder -

A
  • Saclike organ attached to the inferior surface of the liver
  • Stores and concentrates bile by absorbing water through the wall of the gallbladder
89
Q

How does bile move to and from gallbladder?

A

via peristaltic action of muscles in the cystic duct

90
Q

Common biliary diseases due to what two things?

A
  1. gallstones (cholelithiasis)

2. inflammation of the gallbladder (cholecysstitis)

91
Q

Cholelithiasis -

A
  • “Gallstone disease”
  • Stones form in the gall bladder form when the composition of the bile changes
  • One of the most common GI diseases in the US and a major reason for abdominal surgery
92
Q

Risk factors of gallstones -

A 
Age
Genetics
Decreased physical activity
Obesity
Poor lipid profile 
RA
TPN [Total Parenteral Nutrition]
Liver disease
Gastric bypass surgery
DM
93
Q

Cholesterol stones are ___% of all gallstones cases?

A

80%

94
Q

Bilirubin stones are ___% of all gallstone cases?

A

20%

95
Q

What % of patients with gallstones are symptomatic?

A

25%
- Stones physically obstruct ducts → distension of bladder while the muscles in the duct wall contract, trying to expel the stone

96
Q

What is the most frequent site of obstruction by gallstones?

A

Cystic duct

97
Q

Symptoms of Cholelithiasis/gallstones:

A
  1. Abdominal pain
    - Distension of the gallbladder
    - Muscles in the duct wall contract trying to expel the stones
  2. R upper quadrant
  3. Just below or slightly to the right of the sternum
  4. Abdominal tenderness & muscle guarding
  5. Pain may radiate shoulder and upper back or mid back and scapula
98
Q

T/F 50% of people with symptomatic cholelithiasis will have a recurrent episode

A

True

99
Q

Diagnose gallstones:

A

Ultrasound

100
Q

Treatment of gallstones:

A

Surgery (cholecystectomy)

101
Q

Special implications for therapist working gallstone patient:

A
  • Physical activity important in prevention of symptomatic gallstone disease “just move”
  • Many experience referred pain to the right shoulder for 24 to 48 hours post surgery.
  • Usual postoperative exercises for any surgical procedure apply:
    1. Breathing
    2. Bed positioning
    3. Couching wound splinting if needed
    4. Compressive stockings and leg exercises
102
Q

Choledocholithiasis:

A
  • complication of gallstones
  • calculi in the common bile duct
  • Can cause pancreatitis
103
Q

How is the pancreas drained?

A

Pancreatic duct drains the organ, joining with the common bile duct which in turn drains into the duodenum

104
Q

Pancreas as an endocrine gland:

A
  • Ductless glands that secrete their products, hormones, directly into the blood
  • Insulin
  • Glucagon
105
Q

Insulin -

A
  • secreted by pancreas
  • Hormone that regulates the metabolism of carbohydrates, fats and protein by promoting the absorption of glucose from the blood into liver, fat and skeletal muscle cells
  • It is calorie conserving
106
Q

Glucagon -

A
  • hormone
  • produced by alpha cells of the pancreas
  • It functions to raise the concentration of glucose and fatty acids in the bloodstream.
  • It favors energy utilization
107
Q

Pancreas as an exocrine gland:

A
  • Glands that secrete substances onto an epithelial surface by way of a duct
  • Secretes HCO3- and a number of digestive enzymes into the pancreatic duct which in turns conducts these molecules to the epithelial lining of duodenum
108
Q

What is the regions of the pancreas that contain its endocrine cells?

A

Islet of Langerhans

109
Q

Islets house 3 types of cells:

A
  1. Alpha cells (A cells): Secrete glucagon
  2. Beta cells (B cells): Secrete insulin
  3. Delta cells (D cells): Secrete somatostatin [growth hormone-inhibiting hormone (GHIH)
110
Q

How is insulin secretion regulated?

A

by circulating glucose levels

111
Q

Mechanism of insulin:

A
  1. High levels of circulating blood glucose levels
  2. Pancreas secretes insulin
  3. Insulin binds to receptors on cells
  4. GLUT-4 increases movement of glucose from the bloodstream into the cells
112
Q

Actions of insulin:

A
  1. Stimulates cellular uptake of glucose - Reduces circulating levels of glucose
  2. Stimulates glycolysis and glycogenolysis - Favors the utilization of available glucose
  3. Inhibits gluconeogenesis and glycogenolysis - Inhibits storage of glucose
  4. Stimulates cellular uptake of amino acids - Is an anabolic hormone
  5. Stimulates the uptake of glucose by fat cells and its conversation into fats
  6. Stimulates cell growth and synthesis of new mRNA’s
113
Q

Actions of glucagon:

A
  • Released from the alpha cells in response to declining insulin levels
  • It works to increase the concentration of glucose and fatty acids in the bloodstream
  • It is a catabolic (degrading) hormone
114
Q

What molecules does the pancreas secrete into a duct [pancreatic duct] on onto an epithelial surface [duodeneum]?

A
  1. Digestive Enzymes - Essential for processing foodstuffs
  2. HCO3: neutralize the acidic pH of the gastric juices
  3. Epithelial surface of the pancreatic duct
115
Q

Zymogen granules -

A
  • the specialized organelle in pancreatic acinar cells for digestive enzyme storage
  • Have no catalytic activity until they are transformed
116
Q

Proteases -

A
  • Enzyme secreted from pancreas as exocrine function

- Digest proteins and peptides to single amino acids

117
Q

Pancreatic lipase -

A
  • Enzyme secreted from pancreas as exocrine function

- Digests triglycerides, monoglyceride and free fatty acids

118
Q

Amylase -

A
  • Enzyme secreted from pancreas as exocrine function

- Digests Starch and maltose

119
Q

Chymotrypsinogen -

A
  • Inactive form of chymotrypsin found in alpha cells
  • Once it reaches the duodeneum, it is activated by trypsin and becomes chymotrypsin
  • digestive enzyme which breaks down proteins in the small intestine
120
Q

Acute pancreatitis -

A
  • Occurs when there is an abnormal activation of digestive enzymes within the pancreas
  • Results in the autodigestion of the pancreas
  • Sudden hyper inflammation in the pancreas with accompanying damage
121
Q

Causes of Acute pancreatitis:

A 
Gallstones (obstruction  of the common bile duct)
Chronic ETOH consumption
Idiopathic
Pancreatic cancer
Drugs
122
Q

Symptoms of Acute pancreatitis:

A
  • Pain, N&V, anorexia
  • Abdominal pain: cardinal symptom of acute pancreatitis; sharp & severe; position changes do not alleviate the pain
123
Q

Difference between acute and chronic pancreatitis?

A

Acute - inflamed pancreas due to gallstones blocking pancreatic duct
chronic - inflamed pancreas due to gallstones and calcifications in dilated pancreatic duct

124
Q

Acute pancreatitis can be a systemic disease and lead to what things:

A 
Hyperglycemia
Hypoxemia, atelectasis
Kidney failure
Hypovolemia (bleed into abdomen) and shock
Jaundice, Portal vein thrombosis
125
Q

Treatment for acute pancreatitis:

A
  1. Symptomatic, designed to preserve normal pancreatic function
  2. IV fluids
  3. Analgesics
  4. NPO/Stop feeding the patient to “rest” the pancreas
  5. Severe pancreatitis: Admission to ICU
126
Q

Pt implications for acute pancreatitis:

A
  1. Presents with back pain
  2. Pancreatic scarring may occur and limit trunk extension
  3. Don’t feed the patient if NPO
  4. Bed positioning: side-lying, knee-chest position with a pillow pressed against the chest or sitting with trunk flexed
127
Q

Chronic pancreatitis -

A

Characterized by the development of irreversible changes in the pancreas secondary to chronic inflammation

128
Q

Causes of chronic pancreatitis -

A
  • Chronic abdominal pain
  • opioid abuse
  • decreased appetite
  • wt. loss
  • poor quality of life
129
Q

Where is pain usually in chronic pancreatitis -

A

Epigastric (upper central region of the abdomen) pain with radiation to the back

130
Q

How is pain relieved in chronic pancreatitis -

A

Pain relieved by knee to chest or bending forward

131
Q

Pt involvement of chronic pancreatitis:

A
  1. Back pain: upper thoracic, thoracolumbar area
  2. Diabetes (controlled), neuropathy, osteoporosis
  3. Complications of ETOH: malnutrition, cirrhosis and ascites
  4. Past medical hx. of pancreatitis- Red flag
132
Q

Adenocarcinoma -

A

Pancreatic cancer

133
Q

Incidence of pancreatic cancer -

A

> 55 YOA
Head of the pancreas (70%)
More common in blacks than whites

134
Q

Symptoms of pancreatic cancer -

A
  • Wt. loss, pain and jaundice
  • Impaired posture
  • Impaired muscle performance, ROM
  • Intractable back pain
135
Q

T/F Pancreatic cancer usually diagnosed as an advanced disease

A

True

136
Q

Whipple procedure for pancreatic cancer -

A

Is done to remove a tumor in the head of your pancreas, your ampulla, or the first part of your duodenum (possibly part of stomach)

137
Q

Type 1 diabetes accounts for __% of all DM cases

A

5-10%

138
Q

Type 1A DM -

A

Autoimmune destruction of B cells resulting in an insulin deficiency

139
Q

Type 1B DM -

A

Insulin deficiency with no evidence of autoimmune disease

140
Q

T/F Regardless of type (A/B), Type 1 patients are on indefinite insulin therapy

A

True

141
Q

What complications can arise with Type 1 DM?

A
  1. Diabetic ketoacidosis
  2. Hyper- and hypoglycemia
  3. Coma induced by hypoglycemia
142
Q

Diabetic ketoacidosis -

A
  • Accelerated degradation of fatty acids→ formation of ketones → lowers blood pH
  • A medical emergency
143
Q

Clinical features of DM?

A
  1. Polyuria - Excessive urination/clear the excess glucose
  2. Polydipsia (excessive thirst)
  3. Polyphagia - Excessive appetite or desire to eat
  4. Weight loss - Excessive fat catabolism
  5. Ketoacidosis - Secondary to increased fat catabolism
144
Q

Normal fasting glucose levels =
Impaired fasting glucose levels (IFG) =
Provisional fasting glucose levels =

A

Normal fasting glucose levels = <100
Impaired fasting glucose levels (IFG) = 100-125
Provisional fasting glucose levels (FPG) = >126

145
Q

Hb A1C levels defines what?

A

Glycosylated hemoglobin

Measure of glucose control

146
Q

Optimal Hb A1C levels:

A

Optimal < 7% or 7 g/dl
Normal levels < 6 % or 6 g/dl
Monitored at least biannually

147
Q

With Reduction of Hb A1C levels from 8% to 7%, what changes do you see in mortality/incidence of MI’s?

A

14% decrease

148
Q

Type 2 DM accounts for ___% of DM cases.

A

80-90%

149
Q

T/F Type 2 DM can reflect an insulin deficiency and/or insulin resistance.

A

True

150
Q

T/F Patients with type 2 DM may or may not be on insulin therapy

A

True

151
Q

Components of metabolic syndrome:

A
  1. A cluster of conditions that increase the risk of heart disease, stroke, and diabetes
    - Dyslipdemia (abnormal lipids in blood)
    - Hypertension (Increased Na retention)
    - Abdominal obesity
    - Insulin resistance (elevated glucose levels, impaired glucose tolerance)
    - Proinflammatory state
    - Prothromboic state
    - A large waist is 35 inches or more in a woman and 40 inches or more in a man.
152
Q

Diabetic retinopathy -

A
  • damage to the blood vessels of the light-sensitive tissue at the back of the eye
  • 5-20 years to appear
  • After 20 yrs. 60% of type II’s will have retinopathies
  • Progression can be slowed with appropriate glycemic control
153
Q

Macular degeneration -

A

loss of vision in middle of view

154
Q

Peripheral degeneration -

A

blurry peripheral vision

155
Q

Diabetes is the most common cause of what?

A
  • End stage renal disease (approx 40% of all cases)

- 20-30 % of all diabetics will develop ESRD

156
Q

How can you reduce risk and slow progression of neuropathy for diabetic patient?

A

Glycemic control and HTN control

157
Q

Diabetic neuropathy -

A
  • Damage to nerves
  • Involves sensory (loss, numbness, tingling, burning), motor (foot drop) & autonomic nerves
  • Often involves lower extremities but may involve up extremities
158
Q

Diabetic Charcot foot syndrome -

A
  • an inflammatory syndrome
  • characterized by varying degrees of bone and joint disorganization secondary to underlying neuropathy, trauma, and perturbations of bone metabolism
  • typical appearance of a later-stage Charcot foot with a rocker-bottom deformity
159
Q

Peripheral Vascular Disease -

A
  1. Reduced blood flow to the periphery
  2. Decreased or absent pedal pulse
  3. Decreased nutrient delivery
    - Impaired wound repair
    - Decreased exertional demand
160
Q

Pathology of Peripheral Vascular Disease -

A
  • Damage to the basement membrane of smaller blood vessels

- Ischemic insult

161
Q

Cardiovascular Disease -

A
  1. The major cause of mortality for persons with diabetes
  2. Diabetes is an independent risk factor for CAD
  3. Direct effect of:
    - Glycylation of cardiac proteins
    - Altered cardiac metabolism
  4. Secondary to the effects of diabetes on:
    - HTN
    - Dyslipidemia
    - Obesity
    - Autonomic neuropathy
162
Q

PT and Type 1 DM:

A
  • Manage comorbidities

- movement and exercise

163
Q

PT and Type 2 DM:

A
  • Manage emerging comorbidities

- movement and exercise

164
Q

PT and Metabolic syndrome:

A
  • Manage the criteria which define the presence of metabolic syndrome
  • movement and exercise

Pathophys (16 decks)

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