Week 3- Endocrine Disorders Flashcards

1
Q

islets of Langerhans have four types of hormone-secreting cells:

A
  1. alpha cells (secrete glucago)
  2. beta cells (secrete insulin and amylin)
  3. delta cells (secrete gastrin and somatostatin)
  4. F (or PP) cells (secrete pancreatic polypeptide that stimulates gastric secretion and antagonizes cholecystokinin)
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2
Q

beta cells of the pancreas synthesize

A

insulin from the precursor proinsulin

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3
Q

does insulin circulate freely

A

yes, it is unbound

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4
Q

_______facilitates the rate of glucose uptake into many cells within the body

A

Insulin

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5
Q

insulin binding cascade

A

-insulin binds with an enzyme-linked plasma membrane receptor that contains tyrosine kinase on the cytosolic surface
-Insulin binding sends signals to activate glucose transporters (GLUT) for entry of glucose into the cell

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6
Q

glucagon is produced by

A

alpha cells of pancrease

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7
Q

______ glucose levels cause glucagon release to be inhibited;______ glucose levels and sympathetic stimulation promote glucagon release

A

High

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8
Q

insulin lowers blood sugar
glucagon raises blood sugar

A

insulin lowers blood sugar
glucagon raises blood sugar`

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9
Q

stimulates lipolysis, which has a ketogenic effect caused by the metabolism of free fatty acids in the liver

A

glucagon

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10
Q

result of a loss of beta cells in the pancreatic islets.

A

type 1 diabetes

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11
Q

autoimmune type 1 diabets

A

-environmental and genetic factors trigger cell-mediated destruction of pancreatic beta cells
- Autoimmune type 1 diabetes is called type 1A.

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12
Q

non immune type 1 diabets

A

-less common
-secondary to other diseases (pancreatitis)
t-ype 1B diabetes
-occurs mostly in people of Asian or African descent

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13
Q

type 1 diabetse onset

A

long preclinical period with gradual destruction of beta cells

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14
Q

With insulin deficiency, lipolysis is enhanced and there is an increase in the amount of nonesterified fatty acids delivered to the liver. The consequence is increased gluconeogenesis contributing to hyperglycemia

A

With insulin deficiency, lipolysis is enhanced and there is an increase in the amount of nonesterified fatty acids delivered to the liver. The consequence is increased gluconeogenesis contributing to hyperglycemia

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15
Q

-potentially life-threatening sequelae of Type I DM
-caused by increased levels of circulating ketones in the absence of the antilipolytic effect of insulin

A

diabetic ketoacidosis

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16
Q

diabetic ketoacidosis sxs

A

unintentional weight loss, vomiting, weakness, and cognition changes. Dehydration and metabolic abnormalities worsen with progressive uncontrolled osmolar stress, which can lead to lethargy, May even cause respiratory failure, coma, and death.
Abdominal pain is also a common complaint in DKA
-breath with sweet fruity odor

17
Q

are diagnosis for type 1 and type 2 diabetes the same?

A

yes
-HbA1c, 2 hour OGTT, fasting insulin

18
Q

type 1 DM treatment

A

-Avoidance of cow’s milk
-gluten-free diet
-omega-3 fatty acids and vitamin D
-injecting insulin and momnintor blood sugar

19
Q

insulin resistance and decreased insulin secretion by beta cells

A

type 2 diabetes

20
Q

insulin resistance and decreased insulin secretion by beta cells

A

type 2 diabetes

21
Q

constellation of disorders (central obesity, dyslipidemia, prehypertension, and an elevated fasting blood glucose level) that together confer a high risk of developing type 2 diabetes and associated cardiovascular complications.

A

mystabollic syndrome

22
Q

a suboptimal response of insulin-sensitive tissues (especially liver, muscle, and adipose tissue) to insulin.

A

insulin resistance

23
Q

hormones produced in adipose tissue

A

Adipokines

24
Q

Adipokines in obese individuals

A

-increased serum levels of leptin (leptin resistance) and resistin
-decreased levels of adiponectin

25
Q

Obesity is correlated with hyperinsulinemia and__________ insulin receptor density

A

decreased

26
Q

_________ decreases insulin synthesis in the beta cell

A

leptin

27
Q

In type II DM, pancreatic alpha cells are less responsive to glucose inhibition, resulting in increased_________- secretion

A

glucagon

28
Q

type 2 diabetes sxs

A

-polyuria and polydipsia may present
-nonspecific symptoms: fatigue, pruritus, recurrent infections, visual changes, or symptoms of neuropathy (paresthesias or weakness).

29
Q

normal non-enzymatic process that involves the reversible attachment of glucose to proteins, lipids, and nucleic acids without the action of enzymes

A

Glycation

30
Q

With persistent hyperglycemia, glucose becomes ______________ bound to collagen and other proteins in red blood cells

A

irreversibly bound

31
Q

in type 2 diabetes Chronic hyperglycemia, insulin resistance, hyperinsulinemia, and dyslipidemia contribute to the production of

A

reactive oxygen species (ROS)

32
Q

leading
cause of blindness, end-stage renal failure, and various neuropathies in DM type 2

A

Diabetic microvascular complications (disease in capillaries)

33
Q

____________- is a leading cause of blindness

A

Diabetic retinopathy

34
Q

nephropathy and diabetes mellitus

A

-early phases of nephropathy are asymptomatic
-develop after 10 years with type 1 diabetes -after 5-8 years with type 2

35
Q

diabetic nephropathy details

A

-glomeruli are injured by protein denaturation
-hyperglycemia with high renal blood flow (hyperfiltration)
-intraglomerular hypertension exacerbated by systemic hypertension.

36
Q

first sign of KD dysfunction with DM2

A

Microalbuminuria