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Block 2 Pathophysiology > endocrine-pancreas > Flashcards

endocrine-pancreas Flashcards

1
Q

Glucose production primarily in the ____ (gluconeogenesis)

A

liver

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2
Q

CNS uses ____ of all blood glucose at rest, 25% of total

A

60%

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3
Q

Skeletal muscle uses glucose for rapid activity, ____ energy from fat at rest

A

85%

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4
Q

RBC require____.

A

glucose

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5
Q

Most tissues can use ____ and___.

A

glucose and fat

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6
Q

β cells secrete___.

A

insulin

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7
Q

α cells secrete ____.

A

glucagon

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8
Q

δ cells secrete _____(inhibits release of gastrin, CCK, secretin)

A

somatostatin

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9
Q

Balance between insulin and glucagon activity normally maintains blood glucose between____, whether in a fasting or postprandial (after eating) state

A

~60 and 140 mg/dL

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10
Q

Insulin is an ______, i.e., it promotes building new tissue and energy storage

A

anabolic hormone

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11
Q

what is insulin secreted by?

A

Secreted by pancreatic β-cells

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12
Q

Insulin release is stimulated by

A 
Glucose (primary stimulus, amino acids to a lesser extent)
Several hormones: 
Gastric inhibitory polypeptide (GIP) 
Glucagon-like peptide-1 (GLP-1) 
Growth hormone (pregnancy, puberty, adolescence)
Estrogens (pregnancy, puberty)
Melatonin
Leptin
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13
Q

Practically speaking, insulin only affects glucose metabolism in what three tissues?

A

Liver
Adipose tissue
Muscle

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14
Q

Insulin Stimulatory Effects in liver

A

Protein, fatty acid and glycogen synthesis

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15
Q

Insulin Stimulatory Effects in adipose tissue

A

Glucose and fatty acid uptake

Triglyceride synthesis and storage

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16
Q

Insulin Stimulatory Effects in muscle

A

Glucose uptake

Protein and glycogen synthesis

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17
Q

Insulin Inhibitory Effects in liver

A

Ketogenesis and gluconeogenesis

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18
Q

Insulin Inhibitory Effects in adipose tissue

A

Lipolysis

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19
Q

Insulin Inhibitory Effects in muscle

A

Proteolysis

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20
Q

______ is a polypeptide secreted by α-cells of the pancreatic islets of Langerhans

A

Glucagon

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21
Q

Glucagon is a _____ hormone which increases blood glucose when glucose is not being absorbed

A

catabolic

22
Q

glucagon secretion is Promoted by ______.

A

hypoglycemia and elevated blood amino acids, gastric inhibitory peptide (GIP)

23
Q

glucagon secretion is inhibited by?

A

high blood glucose, free fatty acids and ketones

24
Q

Suppression of glucagon secretion is blunted with prolonged _______ (diabetes)

A

hyperglycemia

25
Q

Glucagon Stimulatory Effects of liver

A

Gluconeogenesis

Glycogenolysis

26
Q

Glucagon Stimulatory Effects of adipose tissue

A

Lipolysis, free fatty acid release

27
Q

Glucagon Stimulatory Effects of skeletal muscle

A

Protein degradation (supply amino acids for gluconeogenesis by liver)

Glycogenolysis

28
Q

First-phase insulin release is rapidly triggered in response to __________, lasts ~10 minutes (composed of preformed insulin)

A

increased blood glucose levels

29
Q

Second-phase insulin release is composed of ______, continues after first-phase and peaks in 1 to 3 hours (depending on glucose load)

A

newly formed insulin

30
Q

First-phase insulin release inhibits ______ secretion

A

glucagon

31
Q

what may be the earliest detectable beta cell defect predicting onset of type2 diabetes?

A

Reduced first-phase insulin release

32
Q

____ and ____ secretion occur incrementally to maintain blood glucose within narrow limits

A

Insulin and glucagon

33
Q

what are incretins?

A

GI hormones that regulate glucose metabolism by effects on insulin and glucagon secretion, tissue insulin sensitivity, and nutrient absorption rate

34
Q

These hormones are released when food enters the GI tract, referred to as the “incretin effect”

A

incretins

35
Q

Gastric inhibitory polypeptide (GIP) secreted by____ of the proximal duodenum epithelium

A

K cells

36
Q

Gastric inhibitory polypeptide (GIP) Secretion is stimulated by ?

A

food entering from stomach

37
Q

what doesGastric inhibitory polypeptide (GIP) stimulate?

A

Insulin secretion
Insulin sensitivity
Fatty acid synthesis (liver) and triglyceride synthesis (liver, adipose)

38
Q

what does Gastric inhibitory polypeptide (GIP) inhibit?

A

gastric acid secretion

39
Q

what in Gastric inhibitory polypeptide (GIP) Degraded by?

A

dipeptidyl peptidase 4 (DPP-4), a circulating enzyme made by adipose (an “adipokine”)

40
Q

GIP t½ =___ minutes

A

1-2 minutes

41
Q

what is Released from distal ileum and colon L-cells within minutes of oral food intake?

A

Glucagon-like peptide-1 (GLP-1)

42
Q

Glucagon-like peptide-1 (GLP-1) is Released from distal ileum and colon L-cells within minutes of oral food intake, followed by a second response when nutrients contact ____.

A

L-cells

43
Q

Glucagon-like peptide-1 (GLP-1) Secretion stimulated by ____.

A

oral food intake

44
Q

Glucagon-like peptide-1 (GLP-1) Stimulates

2 things

A

Insulin release

Insulin sensitivity

45
Q

Glucagon-like peptide-1 (GLP-1) inhibits (3 things)

A

Glucagon secretion
Hepatic gluconeogenesis
Gastric emptying

46
Q

Glucagon-like peptide-1 is degraded by what?

A

dipeptidyl peptidase 4 (DPP-4)

47
Q

An autoimmune disease characterized by pancreatic β-cell destruction and an absolute deficiency of insulin

A

Type 1 Diabetes Mellitus

48
Q

Type 1 Diabetes Mellitus Genetic factors

A

Susceptibility loci: HLA locus contributes up to 50% of risk:

90-95% of Caucasians with type 1 DM have HLA-DR3 or DR4 haplotype (vs 40% without type 1 DM)

40-50% are combined DR3/DR4 heterozygotes (vs 5% without type 1 DM)

49
Q

Type 1 Diabetes Mellitus Environmental factors

A

Certain viral infections may be involved in triggering islet cell destruction:
Mumps, rubella, coxsackie B, or cytomegalovirus, among others

50
Q

Type 1 Diabetes Mellitus Proposed mechanisms for initial immune response

A
  1. “Bystander” damage: Viral infections induce islet injury and inflammation, leading to the release of “sequestered” β-cell antigens and the activation of autoreactive T cells (e.g., post-traumatic uveitis)
  2. “Molecular mimicry”: Viruses may produce proteins that mimic β-cell antigens, trigger autoimmune response (e.g., rheumatic fever)
51
Q

autoimmune disease associated with the absolute deficiency of insulin

A

Type 1 Diabetes Mellitus

Block 2 Pathophysiology (8 decks)

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