Chapter 14.1 Flashcards

(54 cards)

1
Q
  1. State the location and specific cells responsible for the secretion of insulin and glucagon.
A

Location – pancreas
Alpha cells produce GLUCAGON
Beta cells produce INSULIN

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2
Q
  1. State the composition and classification of the insulin molecule
A

It is a large polypeptide of 51 amino acids

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3
Q
  1. List the characteristics of patients with type 1 diabetes regarding age of onset, insulin levels, and response to insulin. (will be on test)
A

Onset – juvenile
Insulin level – low level
Response to insulin – normal response
don’t make insulin - deficiency - You can’t use sugar for energy so the body uses fats causing ketoacidosis. Can also start to remove glycogen out of muscles

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4
Q

Type 2

A

Onset – adults
Insulin level – normal/high levels
Response to insulin – decreased response
do make insulin - make too much or too little

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5
Q
  1. State the percent of all diabetic patients who have type 1 and type 2 diabetes
A

Type 1 – 5-10%

Type 2 – 90-95%

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6
Q
  1. State the routes of administration for insulin and why these routes are used
A

Insulin NOT suitable for oral administration – usually administered through sub-Q injection – automatic glucose sensor – insulin pump
Alternative administration
Inhalation or nasal spray

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7
Q
  1. State how insulin is produced today
A

Produced using cell cultures & recombinant DNA techniques

Biosynthetic techniques to produce insulin analogs

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8
Q
  1. Define insulin analogs
A

It is like insulin but varies by a few amino acids - it alters the amino acids to change how the insulin works

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9
Q
  1. Classify the following insulins as rapid acting: lispro, NPH, and glargine. (will be on test)
A

Lispro

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10
Q

intermediate acting

A

NPH

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11
Q

long acting

A

Glargine

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12
Q
  1. State the rationale for insulin mixtures.
A

Patients will need different activity levels of insulin. For example if pt. is eating and needs it right away they can use rapid acting, while intermediate acting ones can be used to control insulin levels throughout the day.
to put two speeds in at the same tim

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13
Q
  1. State the peak effect and duration of the following insulins: rapid acting (lispro) and long acting (glargine).
    (will be on test)
A

rapid acting (lispro)
peak effect .5 – 1.5 hrs.
long-acting (glargine).
Peak effect 3 – 24 hrs.

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14
Q
  1. List the physiologic actions of insulin.
A

Increase glucose entry & storage in tissue (muscles & liver)

Increase protein synthesis & lipid storage

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15
Q
  1. List the physiologic actions of glucagon.
A

The primary effect of glucagon is to increase blood glucose to maintain normal blood glucose levels and to prevent hypoglycemia.

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16
Q
  1. State the acute problems associated with insulin insufficiency
A

Hyperglycemia followed by hypoglycemia

Shift to fat metabolism/ketones

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17
Q

Chronic problems

A

Repeated prolonged hyperglycemia – small vessel angiopathy - occlusion

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18
Q
  1. State how chronic hyperglycemia causes angiopathy.
A

In repeated high blood sugar (Hyperglycemia), glucose binds to proteins in the vessel wall and makes the walls thick and blood can’t get through & effects tissue

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19
Q
  1. List the microangiopathic clinical outcomes of poorly controlled diabetes mellitus. (will be on test)
A

Amputation – blindness – end stage renal failure & peripheral neuropathy

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20
Q

macroangiopathic

A

Hypertension – MI (heart attack & stroke) – CVA

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21
Q
  1. Define the concepts of intensive insulin therapy .
A

Monitoring blood glucose often & adjusting insulin dosage & food intake to keep insulin level in normal range.

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22
Q

a basal-bolus insulin regimen

A

Using both a basal & bolus dose to help control insulin levels. Basal doses give background level of long or intermediate acting for control over day/night while bolus dose to deal with glucose as a pt. is eating.

23
Q
  1. List the symptoms of hypoglycemia.
A

Headache – shaking – sweating – tired – weakness – hunger

24
Q
  1. State reasons that a patient on an insulin regimen might experience hypoglycemia.
A

Dose too high – delayed/missed meal – strenuous exercise

25
19. State the glucose level defining hypoglycemia. will be on test)
BG < 70 mg/dl
26
20. List common sources of 15 grams of carbohydrate used to treat hypoglycemia. (will be on test)
``` Glucose tablet (usually like 3 tablets) – gel tub – 4 oz (1/2) of juice or regular soda – 1 TBSP of sugar, honey, corn syrup – 8 oz nonfat or 1% milk hard candies – jelly beans, or gum drops every 15 min until back to normal range ```
27
21. Outline a management plan for a patient having a hypoglycemic episode during a physical therapy session.
Consume 15-20 g of glucose – monitor symptoms & check glucose in 15 minutes. Repeat is needed – once they are back to normal levels eat a small snack.
28
22. State the location of incretins and what stimulates their release.
Location – released from GI tract after eating a meal
29
23. List the actions of the following two incretins: glucagon-like peptide-1 (GLP-1)
Regulate glucose metabolism by stimulating insulin release
30
glucose-dependent insulinotropic polypeptide (GIP)
Inhibits glucagon activity – reduces appetite – increased beta cell mass & differentiation – promotes weight loss
31
24. State the mechanism of action and physiological effects of the following drugs used to manage type 2 diabetes: sulfonylureas
Increases insulin release (direct effect) – decreases hepatic glucose production (indirectly) – variable efficacy/effects tend to diminish with time.
32
meglitinides
Act like sulfonylureas – increase insulin release from pancreatic beta cells
33
GLP-1 agonists
Stimulate insulin release – inhibit glucagon production – enhance beta cell mass & differentiation
34
DPP4 inhibitors
Inhibit dipeptidyl peptidase 4 (enzyme that breaks down incretins) Prolong effects of GLP-1 & GIP
35
biguanides
Acts directly on liver to decrease hepatic glucose production/increase peripheral sensitivity to insulin; metformin
36
glitazones
Increase tissue sensitivity to insulin – Decrease hepatic glucose production; facilitate activity
37
α-glucosidase inhibitor
inhibit glucose absorption from GI Tract
38
sodium-glucose co-transporter-2 (SGLT-2) inhibitors (gliflozins).
Decrease glucose reabsorption in kidneys; glucose is lost in urine
39
25. State the most common adverse effect of the following medications or medication classifications used to manage diabetes: insulin
Dramatic fall in blood glucose levels because insulin lower blood glucose
40
sulfonylureas
Hypoglycemia – GI disturbances - Headaches
41
GLP-1 agonists
GI problems – pancreatitis – mild hypoglycemia
42
metformin
GI problems – lactic acidosis
43
26. Match the following drugs with their therapeutic category: lispro (Humalog®)
Rapid acting insulin
44
NPH (Humulin N®)
Intermediate acting insulin
45
glargine (Lantus®)
Long-acting insulin
46
glipizide (Glucotrol®) glyburide (DiaBeta®)
Sulfonylureas
47
repaglinide (Prandin®)
Meglitinides
48
exenatide (Byetta®) liraglutide (Victoza®)
GLP-1 agonists
49
sitagliptin (Januvia®)
DPP4 inhibitors
50
metformin (Glucophage®)
Biguanides
51
pioglitazone (Actos®)
Glitazones
52
acarbose (Precose®)
α-glucosidase inhibitors
53
empagliflozin (Jardiance®)
sodium-glucose co-transporter-2 (SGLT-2) inhibitors (gliflozins)
54
27. State the considerations of a physical therapist working with patients who are being treated for diabetes mellitus.
Insulin absorption can be effect by physical agents – massage – recognize & deal w/ hypoglycemia – encourage & supervise non drug managements (diet & exercise