Pancreatic Flashcards
1
Q
Hepatic system functions to convert ____ and excrete ____
A
Bilirubin and ammonia
2
Q
Hepatic system is the sole source of what protein?
A
Albumin
3
Q
T/F Hepatic system synthesizes clotting factors and cholesterol.
A
True
4
Q
Hepatic system detoxifies the body of what?
A
Drugs, ETOH, toxins
5
Q
Hepatic system stores what?
A
Glycogen, vitamins, iron
6
Q
Liver receives what % of cardiac output?
A
25%
7
Q
The liver receives blood from what two places?
A
- Portal vein (from organs)
2. Hepatic artery
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
9
Q
What is the functional unit of the liver?
A
Liver lobule
10
Q
S&S of hepatic disease include:
A
- Include GI symptoms - N&V, Diarrhea, Constipation, Heartburn, Abdominal pain, GI bleeding
- Edema/ascites
- Dark Urine
- Light/clay-colored stools
- Right upper quadrant abdominal pain
- Neurologic involvement: Confusion, muscle tremors, sleep disturbances, hyperreactive reflexes
- Hepatic Osteodystrophy (abnormal development of bone)
- Osteoporosis:
- Skin changes: Jaundice, increased bruising
11
Q
Why does hepatic disease cause dark urine?
A
- Yellow-orange breakdown product of hemoglobin
2. Bilirubin accumulates in liver -> moves into blood -> increase in urine -> may suggest liver damage
12
Q
Why does hepatic disease cause Light/clay-colored stools?
A
- Reduced ability of the liver to excrete bilirubin into the gut
13
Q
T/F Jaundice (Icterus) is a symptom, not a disease.
A
True
14
Q
What is jaundice
A
Bilirubin breakdown product of RBC in macrophages
yellow discoloration of the skin, sclerae, and mucous membranes.
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
16
Q
Treatment of jaundice?
A
- Resolve underlying disease
- Return to normal color suggests resolution
- Then activity and exercise can be resumed
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
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
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]
20
Q
What is hepatic osteodystrophy?
A
- Abnormal development of bone/osteoporosis in individuals with chronic liver disease
- Leads to osteopenia and osteoporosis
21
Q
(Decrease/Increase) size and weight of liver with aging.
A
↓ size & weight of liver
22
Q
(Decrease/Increase) processing time of liver with aging.
A
↑ processing time
23
Q
How do blood test values change with aging.
A
Blood test value results remain unchanged [disease vs aging]
24
Q
Describe healing of liver:
A
- Occurs quickly
- Complete parenchymal regeneration or scarring or a combination
- Chronic hepatic injury → fibrosis (cirrhosis)
25
What is cirrhosis of the liver?
- 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
26
Cirrhosis of the liver is typically a result of what two things?
1. Alcoholism
| 2. Hepatitis
27
Significant loss of liver function associated with loss of ___% or more of liver function.
80%
28
Describe the cycle that causes cirrhosis of the liver:
- 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
29
Practice implications of cirrhosis:
- 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
30
What is the portal vein?
- 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
31
T/F The portal vein conducts blood to capillary beds in the liver, i.e. it is not a true vein.
True
32
A portal system by definition does what?
links two capillary beds together
33
Portal hypertension -
as an increase in hepatic sinusoidal blood pressure > 6 mm
34
What contributes to portal hypertension?
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
35
Increased portal pressure will cause what?
- retrograde flow of blood back into the stomach, spleen, large and small intestine, rectum and esophagus
- Result in varices back upstream
36
What is a varice?
- 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
37
Consequences of portal hypertension:
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)
38
Portal hypertension can cause splenomegaly which can lead to what 3 things?
1. Moderate anemia
2. Neutropenia
3. Thrombocytopenia
39
Hepatic Encephalopathy -
- 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
40
How does hepatic encephalopathy occur?
- 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
41
Symptoms of hepatic encephalopathy:
- 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
42
Decorticate posturing vs. decerebrate
Decorticate - flexion of wrist and elbows (upper midbrain damage - corticospinal tracts)
Decerebrate - extension of elbow (upper pontine damage)
43
T/F Symptoms can be reversed if cause is determined.
True
Bleeding, infection, hypovolemia, hypokalemia
Anti-depressants, high dietary protein, diuretics
44
Implications of hepatic encephalopathy for the PT:
1. Patient safety
2. Impaired motor and sensory integrity i.e. impaired mobility, balance,
4. Impaired arousal
5. Risk for pressure ulcers secondary to malnutrition, immobility, edema
45
Ascites -
Abnormal accumulation of fluid in the peritoneal cavity
46
Ascites associated with what issues?
Associated with cirrhosis/portal hypertension
47
Ascites can lead to what?
Can lead to Wt. gain, abdominal distension, peripheral edema, inappropriate dyspnea
48
Management of ascites:
1. Paracentesis
2. albumin consumption
3. diuretics
4. sodium and fluid restriction
49
Implications of ascites:
1. Accompanying impaired cardiac and respiratory function
2. Lymphedema
3. Integumentary disorders (peripheral edema, reduced blood flow (congestion), lymphedema
4. Malnutrition
5. Muscle degradation
50
What is a sinusoid and how does it contribute to the fundamental function of the liver i.e. purifying the blood?
- 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
51
Hepatitis -
- Inflammatory (acute or chronic) condition of the liver
52
What causes hepatitis?
- 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)
53
What causes chronic hepatitis -
- viruses
- medications
- metabolic abnormalities
- autoimmune disorder
- idiopathic
54
T/F Most people with chronic hepatitis are asymptomatic and when symptoms appear, they are nonspecific
True
55
How do you diagnose viral hepatitis?
1. Symptoms
2. Physical Exam
3. Blood test (specific Ab, liver function tests)
4. liver biopsy (chronic inflammation, necrosis)
56
Symptoms of viral hepatitis:
- 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
57
Prognosis of viral hepatitis dependent on what factors?
- 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
58
Hep A formerly known as what?
infectious hepatitis
59
How is HAV spread?
Spread by close personal contact or oral-fecal contamination of water and food, poor hand hygiene, shared use of oral utensils
60
How contagious is HAV?
Highly
61
Does HAV have a vaccine?
Yes, preventable with vaccine
62
Prognosis of HAV:
- Most persons with acute disease recover with no lasting liver damage
- rarely fatal
63
Hep B formerly known as what?
Serum Hepatitis
64
How is HBV spread?
Spread by blood transfusions, needle sticks, IV drug use/shared needles, dialysis, sexual contact, exchange of bodily fluid
65
T/F HBV is considered a STD because it is transmitted via sexual intercourse
True
66
What is incubation period for HBV?
90 days
67
Who is at risk of getting HBV?
Healthcare workers who come in contact with blood
68
Prognosis of HBV:
- 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
T/F Vaccine available for HBV.
True
70
Which Hep virus is the leading cause of chronic liver disease?
HCV
71
How is HCV transmitted?
Transmitted by contact with blood of an infected person, primarily through contaminated needles, sexual contact, needle sticks
72
T/F Acute illness is uncommon in patients with HCV
TRUE
73
What % of newly infected HCV persons develop a chronic infection?
75-85%
74
What % of newly infected HCV persons develop cirrhosis?
5-20%
75
What % of newly infected HCV persons will clear the virus?
15-25%
76
T/F There is a vaccine for HCV.
False
77
Treatment of HCV?
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
Who should be tested for hepatitis C virus?
- 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
Other types/causes of hepatitis:
- Autoimmune hepatitis (inflammatory condition of the liver)
| - Other viral causes of hepatitis (CMV, Epstein-Barr (mono), Yellow fever (yellow fever virus))
80
Drug- and toxin-induced liver disease -
- Dose-related meaning that if enough drug is administered, there will be liver damage
- Drugs include acetaminophen, tetracycline, anti-neoplastic agents; alcohol
81
Fatty liver -
- Fat accumulates → inflammation → scarring (cirrhosis)
| - Associated with ETOH consumption
82
Biliary system -
- Of or relating to bile or the bile duct
| - The biliary system creates, moves, stores, and releases bile into the duodenum
83
Bile -
- A dark green to yellowish fluid produced by the liver
| - Contains bile salts a surfactant that help to emulsify the lipids in food
84
What is the purpose of bile emulsifying lipids in food?
This process greatly increases surface area for the action of the enzyme pancreatic lipase
85
Biliary Obstruction -
Prevent the flow of bile to the duodenum resulting in accumulation of bile in the blood and causing jaundice
86
Describe pathway of bile to the hepatic duct:
through the right and left hepatic ducts -> join to form the common hepatic duct -> through the cystic duct -> gall bladder
87
Describe pathway of hepatic duct to duodenum:
1. common hepatic duct + cystic duct -> common bile duct
| 2. common bile duct + pancreatic duct -> ampulla of vater of the duodenum
88
gallbladder -
- Saclike organ attached to the inferior surface of the liver
- Stores and concentrates bile by absorbing water through the wall of the gallbladder
89
How does bile move to and from gallbladder?
via peristaltic action of muscles in the cystic duct
90
Common biliary diseases due to what two things?
1. gallstones (cholelithiasis)
| 2. inflammation of the gallbladder (cholecysstitis)
91
Cholelithiasis -
- “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
Risk factors of gallstones -
```
Age
Genetics
Decreased physical activity
Obesity
Poor lipid profile
RA
TPN [Total Parenteral Nutrition]
Liver disease
Gastric bypass surgery
DM
```
93
Cholesterol stones are ___% of all gallstones cases?
80%
94
Bilirubin stones are ___% of all gallstone cases?
20%
95
What % of patients with gallstones are symptomatic?
25%
- Stones physically obstruct ducts → distension of bladder while the muscles in the duct wall contract, trying to expel the stone
96
What is the most frequent site of obstruction by gallstones?
Cystic duct
97
Symptoms of Cholelithiasis/gallstones:
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
T/F 50% of people with symptomatic cholelithiasis will have a recurrent episode
True
99
Diagnose gallstones:
Ultrasound
100
Treatment of gallstones:
Surgery (cholecystectomy)
101
Special implications for therapist working gallstone patient:
- 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
Choledocholithiasis:
- complication of gallstones
- calculi in the common bile duct
- Can cause pancreatitis
103
How is the pancreas drained?
Pancreatic duct drains the organ, joining with the common bile duct which in turn drains into the duodenum
104
Pancreas as an endocrine gland:
- Ductless glands that secrete their products, hormones, directly into the blood
- Insulin
- Glucagon
105
Insulin -
- 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
Glucagon -
- 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
Pancreas as an exocrine gland:
- 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
What is the regions of the pancreas that contain its endocrine cells?
Islet of Langerhans
109
Islets house 3 types of cells:
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
How is insulin secretion regulated?
by circulating glucose levels
111
Mechanism of insulin:
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
Actions of insulin:
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
Actions of glucagon:
- 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
What molecules does the pancreas secrete into a duct [pancreatic duct] on onto an epithelial surface [duodeneum]?
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
Zymogen granules -
- the specialized organelle in pancreatic acinar cells for digestive enzyme storage
- Have no catalytic activity until they are transformed
116
Proteases -
- Enzyme secreted from pancreas as exocrine function
| - Digest proteins and peptides to single amino acids
117
Pancreatic lipase -
- Enzyme secreted from pancreas as exocrine function
| - Digests triglycerides, monoglyceride and free fatty acids
118
Amylase -
- Enzyme secreted from pancreas as exocrine function
| - Digests Starch and maltose
119
Chymotrypsinogen -
- 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
Acute pancreatitis -
- 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
Causes of Acute pancreatitis:
```
Gallstones (obstruction of the common bile duct)
Chronic ETOH consumption
Idiopathic
Pancreatic cancer
Drugs
```
122
Symptoms of Acute pancreatitis:
- Pain, N&V, anorexia
- Abdominal pain: cardinal symptom of acute pancreatitis; sharp & severe; position changes do not alleviate the pain
123
Difference between acute and chronic pancreatitis?
Acute - inflamed pancreas due to gallstones blocking pancreatic duct
chronic - inflamed pancreas due to gallstones and calcifications in dilated pancreatic duct
124
Acute pancreatitis can be a systemic disease and lead to what things:
```
Hyperglycemia
Hypoxemia, atelectasis
Kidney failure
Hypovolemia (bleed into abdomen) and shock
Jaundice, Portal vein thrombosis
```
125
Treatment for acute pancreatitis:
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
Pt implications for acute pancreatitis:
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
Chronic pancreatitis -
Characterized by the development of irreversible changes in the pancreas secondary to chronic inflammation
128
Causes of chronic pancreatitis -
- Chronic abdominal pain
- opioid abuse
- decreased appetite
- wt. loss
- poor quality of life
129
Where is pain usually in chronic pancreatitis -
Epigastric (upper central region of the abdomen) pain with radiation to the back
130
How is pain relieved in chronic pancreatitis -
Pain relieved by knee to chest or bending forward
131
Pt involvement of chronic pancreatitis:
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
Adenocarcinoma -
Pancreatic cancer
133
Incidence of pancreatic cancer -
> 55 YOA
Head of the pancreas (70%)
More common in blacks than whites
134
Symptoms of pancreatic cancer -
- Wt. loss, pain and jaundice
- Impaired posture
- Impaired muscle performance, ROM
- Intractable back pain
135
T/F Pancreatic cancer usually diagnosed as an advanced disease
True
136
Whipple procedure for pancreatic cancer -
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
Type 1 diabetes accounts for __% of all DM cases
5-10%
138
Type 1A DM -
Autoimmune destruction of B cells resulting in an insulin deficiency
139
Type 1B DM -
Insulin deficiency with no evidence of autoimmune disease
140
T/F Regardless of type (A/B), Type 1 patients are on indefinite insulin therapy
True
141
What complications can arise with Type 1 DM?
1. Diabetic ketoacidosis
2. Hyper- and hypoglycemia
3. Coma induced by hypoglycemia
142
Diabetic ketoacidosis -
- Accelerated degradation of fatty acids→ formation of ketones → lowers blood pH
- A medical emergency
143
Clinical features of DM?
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
Normal fasting glucose levels =
Impaired fasting glucose levels (IFG) =
Provisional fasting glucose levels =
Normal fasting glucose levels = <100
Impaired fasting glucose levels (IFG) = 100-125
Provisional fasting glucose levels (FPG) = >126
145
Hb A1C levels defines what?
Glycosylated hemoglobin
| Measure of glucose control
146
Optimal Hb A1C levels:
Optimal < 7% or 7 g/dl
Normal levels < 6 % or 6 g/dl
Monitored at least biannually
147
With Reduction of Hb A1C levels from 8% to 7%, what changes do you see in mortality/incidence of MI's?
14% decrease
148
Type 2 DM accounts for ___% of DM cases.
80-90%
149
T/F Type 2 DM can reflect an insulin deficiency and/or insulin resistance.
True
150
T/F Patients with type 2 DM may or may not be on insulin therapy
True
151
Components of metabolic syndrome:
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
Diabetic retinopathy -
- 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
Macular degeneration -
loss of vision in middle of view
154
Peripheral degeneration -
blurry peripheral vision
155
Diabetes is the most common cause of what?
- End stage renal disease (approx 40% of all cases)
| - 20-30 % of all diabetics will develop ESRD
156
How can you reduce risk and slow progression of neuropathy for diabetic patient?
Glycemic control and HTN control
157
Diabetic neuropathy -
- Damage to nerves
- Involves sensory (loss, numbness, tingling, burning), motor (foot drop) & autonomic nerves
- Often involves lower extremities but may involve up extremities
158
Diabetic Charcot foot syndrome -
- 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
Peripheral Vascular Disease -
1. Reduced blood flow to the periphery
2. Decreased or absent pedal pulse
3. Decreased nutrient delivery
- Impaired wound repair
- Decreased exertional demand
160
Pathology of Peripheral Vascular Disease -
- Damage to the basement membrane of smaller blood vessels
| - Ischemic insult
161
Cardiovascular Disease -
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
PT and Type 1 DM:
- Manage comorbidities
| - movement and exercise
163
PT and Type 2 DM:
- Manage emerging comorbidities
| - movement and exercise
164
PT and Metabolic syndrome:
- Manage the criteria which define the presence of metabolic syndrome
- movement and exercise
