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Physiology Exam 2 > Endo 5 > Flashcards

Endo 5 Flashcards

1
Q

What do the alpha cells in the pacreas make?

A

insulin

Glucagon? - Molly

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2
Q

What do the beta cells in the pancreas make?

A

insulin?

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3
Q

What do delta cells in the pancreas make?

A

somatostatin

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4
Q

What does somatostatin do in the pancreas?

A

inhibit the secretion of insulin and glucagon

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5
Q

How much of the pancreas is for endocrine function?

A

1%

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6
Q

What are the islet of langerhans?

A

groups of cells in the pancreas that are made of alpha, beta, and delta cells

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7
Q

What is insulin secretion associated with?

A

energy abundance

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8
Q

What is insulin composed up>

A

two amino acid chains, connected by disulfide bonds

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9
Q

How does insulin circulate?

A

mostly unbound
-relatively short half life

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10
Q

What digestive hormones work to stimulate insulin?

A

incretin

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11
Q

What is the sulfonylurea receptor?

A

a potassium transport channel that moves K out of the cell that closes when glucose enters the cell to help release insulin

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12
Q

What are the steps of insulin release?

A

-glucose enters the cell
-the glucose is metabolized and ATP is made
-ATP sensitive K channels close (sulfoynurea)
-the cell depolarized
-Ca channels open
-there is an exocytosis of insulin

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13
Q

What is ozempic?

A

GLP-1 agonist
-causes increased secretion of insulin

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14
Q

What are insulin and glucaogon?

A

antagonists

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15
Q

Is insulin stored prior to being needed?

A

yes
-however after the storage runs out, the body makes more insulin

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16
Q

When blood glucose increases, what hormone increases?

A

insulin

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17
Q

What is normal fasting blood glucose?

A

80-90 mg/100ml

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18
Q

When blood glucose decreases, what hormone increase?

A

glucagon

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19
Q

What type of receptors does insulin bind to on the receptor/

A

tyrosine kinase receptors

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20
Q

What is the fast response of insulin?

A

increase glucose uptake, especially by muscle cells and adipocytes due to translocation of vesicles containing GLUT-4 to the membrane

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21
Q

What does the movement of GLUT-4 to the membrane cause?

A

cause the membrane to become more permeable to amino acids, potassium, and phosphate ions

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22
Q

What is the slower response of insulin binding to the tyrosine kinase receptors?

A

change in enzyme activity leading to changes in metabolism
-the enzyme activity caused by the phosphorylation

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23
Q

What is the slowest response of insulin binding to tyrosine kinase receptors?

A

changes in gene expression and growth
-allow the cell to make more protiens

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24
Q

What are the effects of insulin in muscles?

A

Overall- promotes muscle glucose uptake and metabolism-anabolic effect
- insulin increases movement of glucose into the cell
-increases glycogen storage in muscle
-increase protein synthesis and inhibit protein degradation

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25
Q

What are the effects of insulin on protein metabolism and growth?

A

Overall- promote protein synthesis and storage inhibits protein degradation
- insulin and GH work synergistically to promote growth

26
Q

What are the effects of insulin on the liver?

A

Overall- insulin promotes the uptake and storage of glucose as glycogen in the liver
-increase glucose uptake
-increase glycogen synthase
-decrease breakdown of glycogen by inhibiting liver phosphorylase
-promote conversion of excess glucose into free fatty acids

27
Q

What are the effects of insulin on fat metabolism?

A

overall- promote fat synthesis and storage
-glucose enters the adipocyte
-activate lipoprotein lipase
-splitting triglycerides into fatty acids to enter the cell
-become triglycerides to be stored

28
Q

What does a lack of insulin do to fat?

A

increase lipolysis
-release free fatty acids that will lead to ketoacidosis

29
Q

What happens in the plasma when there is insulin?

A

decrease glucose
decrease free fatty acid
decrease ketoacids
decrease amino acids

30
Q

What increases insulin secretion?

A

-increased blood glucose
-increase blood FFA
-increase blood AA
-GI hormones (incretin)
-glucagon, GH, cortisol
-PNS stimulation
-SNS
insulin resistance
-sulfonylurea

31
Q

What decreases insulin secretion?

A

-decrease blood glucose
-fasting
-somatostatin
-alpha adernergic activity
-leptin

32
Q

What is glucagon?

A

hormone of starvation

33
Q

What is the primary target tissue for glucagon?:

A

liver
-want to increase blood glucose by
* stimulating glycogenolysis
* stimulate gluconeogenesis
* increase blood fatty acids and ketoacid levels

34
Q

What is diabetes mellitus?

A

metabolic disorder characterized by hyperglycemia due to insufficient insulin or cellular resistance to insulin or both

35
Q

What is hypoinsulinemia?

A

type I diabetes

36
Q

What is hyperinsulinemia?

A

type II diabetes

37
Q

What are symptoms of diabetes mellitus?

A

-polyuria
-polydipsia
-polyphagia
-extreme fatigue
-blurry vision
-cuts/bruises slow to heal
-weight loss even though you are eating more (type I)
-tingling, pain, or numbness in hands/feet (type II)

38
Q

What is the normal fasting glucose?

A

100 mg/dl

39
Q

What is the fasting glucose of prediabetes?

A

100-125 mg/dl

40
Q

What is the fasting glucose of diabetes?

A

126 mg/dl or above

41
Q

What is the 2-h PG of a healthy person?

A

140 mhg/dl

42
Q

What is the 2-h PG of prediabetes?

A

140-199 mg/dl

43
Q

What is the 2-h PG of diabetes?

A

over 200 mg/dl

44
Q

What is the A1C of a healthy person?

A

less than 5.6%

45
Q

What is the A1C of a prediabetic person?

A

5.7-6.4%

46
Q

What is the A1C of someone with diabetes?

A

above 6.5%

47
Q

What is the pathophysiology of DM type I?

A

-autoimmune destruction of pancreatic beta cells
-5-10% of DM cases
-formerly called juvenileonset diabetes or insulin dependent diabetes

48
Q

What are the risk factors of DM type I?

A

-genetic predisposition-increases susecptibility
-environmental triggers stimulate autoimmune response
-usually develop younger than the 40 years old

49
Q

What does hyperglycemia lead to?

A

-polyuria
-polydipsia
-polyphagia
-glucosuria
-weight loss
-malaise and fatigue
-hyperkalemia

50
Q

What does insulin do to Na/K pump?

A

increase the activity

51
Q

What causes ketoacidosis?

A

-increased lipolysis to fatty acids
-infection
-pregnancy
-pheochromocytoma
-cushings syndrome
-major trauma
-surgery

52
Q

What is DKA a response to?

A

cellular starvation brought on by relative insulin deficiency

53
Q

What is the pathophysiology of DKA?

A

-osmotic diuresis
-dehydration
-metabolic acidosis
-fluid and electrolyte imbalances

54
Q

Signs and symptoms of DKA?

A

-fruity breath
-nausea/abdominal pain
-dehydration
-tachycardia (increase SNS)
-lethargy
-coma
-polydipsia, polyuria, polyphagia
-kussmaul respirations (blow off CO2 to reverse acidosis)

55
Q

What does acidosis do to neuronal activity?

A

decreases neuronal function
-blocks inward current of Na and Ca

56
Q

What are risk factors of DM type II?

A

-history of diabetes in family
-obesity
-physical inactivity
-race/ethnicity
-women
-patients with hypertension

57
Q

What is the pathophysiology of Type 2 DM?

A

hyperinsulinemia due to insulin resistance (early)
-beta cell dysfunction due to possible exhaustion (late)
-down regulation of inulin receptors in target tissue and insulin resistance

58
Q

Examples of metabolic syndromes:

A

-obesity
-insulin resistance
-fasting hyperglycemia
-lipid abnormalities
-hypertension

59
Q

What are chronic complication of DM?

A

-retinopathy
-nephropathy
-neuropathy
-vascular disease
-myopathies

60
Q

What are oral manifestations of DM?

A

-periodontal disease
-salivary and taste dysfunction
-oral bacterial and fungal infections
-oral mucosa lesions
-diminished salivary flow and burning mouth syndrome
-delayed mucosa wound healing
-xerostomia in patients on oral hypoglycemia agents

61
Q

What does periodontal disease do to diabetes?

A

periodontal disease exacerbates diabetic complications
-poor glycemic control
-cardiovascular complications

Physiology Exam 2 (6 decks)

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