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ARCHIVED: Pathophysiology > Exam 4: Diabetes > Flashcards

Exam 4: Diabetes Flashcards

1
Q

Binding of insulin to receptor causes:

A

Phosphorylation of receptor and IRS-1 (insulin receptor substrate)

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2
Q

GLUT4 is:

A

Glucose transporter on somatic cells activated by insulin

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3
Q

Non-glucose substances brought into the cell by insulin’s action:

A

Amino acids
K+
PO4-
Mg++

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4
Q

Insulin’s effects on the nucleus:

A

Synthesis of various enzymes suppressed/induced
Cell growth regulated by IREs (insulin responsive elements); mostly signals ATP/glycogen

Insulin is a strong growth factor!!

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5
Q

Effects of insulin:

A

↓ appetite, glucagon

↑ glucose uptake, glycolysis, glycogen synthesis, TG synthesis, amino acid uptake, protein synthesis

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6
Q

Effects of lacking insulin:

A

↑ appetite, glucagon, blood glucose, gluconeogenesis, lipolysis, protein breakdown, glycogenolysis, ketone body production
↓ glucose uptake, protein synthesis

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7
Q

Effect of insulin on fat:

A

Fat takes up glucose, converts it to more fat for later us

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8
Q

Effect of insulin on muscle:

A

Muscle takes up glucose, stores it mostly as glycogen and triglycerides
Also makes ATP/protein synthesis

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9
Q

Effect of insulin on liver:

A

Liver takes up glucose, makes glycogen, and stores it

Also makes proteins

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10
Q

Effect of low glucose on the pancreas:

A

Pancreas releases glucagon

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11
Q

Effect of glucagon on the liver:

A

Signals liver to break down glycogen, release glucose, and make new glucose (gluconeogenesis)

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12
Q

Effect of glucagon on muscle:

A

Minimal effect, though will tell muscle to break down protein and release amino acids

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13
Q

Effect of glucagon on fat:

A

Fat breakdown, free fatty acids and glycerol into blood

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14
Q

Distribution of exocrine/endocrine functions in the pancreas:

A

Exocrine more in the head (digestive functions)

Endocrine functions more in the tail

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15
Q

In diabetes, when glucose is high, insulin and glucagon are:

A

Both are low

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16
Q

Role of β cells:

A

Insulin production, stimulated by glucose

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17
Q

Role of α cells:

A

Produce glucagon

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18
Q

Effect of insulin secretion on α cells:

A

Inhibits glucagon secretion

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19
Q

Effect of glucose on α cells:

A

None

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20
Q

Role of δ cells:

A

Produce somatostatin

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21
Q

GLUT2 is:

A

Glucose transporter on β cells

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22
Q

Mechanism by which glucose triggers β cell insulin release:

A
  1. Glucose entry via GLUT2 leads to ATP production
  2. ATP-gated K+ channel prohibits K+ outflow and depolarizes cell
  3. Voltage-gated Ca++ channel allows Ca++ influx
  4. Ca++ triggers insulin release from storage vesicles
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23
Q

Blood glucose range where insulin balances glucagon:

A

80-100

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24
Q

Describe MODY:

A

Maturity-Onset Diabetes of Youth; genetic defect in insulin production/release

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25
Q

Tx for MODY:

A

Oral drug for DMII to promote insulin release

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26
Q

Effect of Cushing’s on blood sugar:

A

↑ blood sugar from ↑ cortisol

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27
Q

Effect of acromegaly on blood sugar:

A

Growth hormone ↑ blood sugar

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28
Q

Effect of pheochromocytoma on blood sugar:

A

Epi/NE ↑ blood sugar

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29
Q

Diabetes is usually triggered during a time of:

A

Hormone flux

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30
Q

Mechanism by which insulin secretion ↓ in DM II:

A

Persistent leftover glucose in blood causes toxicity of β cells, which ↓ insulin production and ↑ resting blood sugar

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31
Q

Mechanism by which insulin secretion ↓ in DM II:

A

Persistent leftover glucose in blood causes toxicity of β cells, which ↓ insulin production and ↑ resting blood sugar

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32
Q

Clinically typical DM I patient:

A

Young, normal/skinny, with ↓ blood insulin, anti-islet cell antibodies, and ketoacidosis

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33
Q

Clinically typical DM II patient:

A

Older, obese, ↑ blood insulin, no anti-islet cell antibodies, and not in ketoacidosis

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34
Q

Clinical diagnosis of DM:

A

Fasting BG > 126 or

plasma glucose > 200 after 2 hrs during OGTT

35
Q

Glucose levels in pregnancy are:

A

Normally lower

36
Q

Clinical diagnosis of gestational diabetes:

A

FBG > 95
OGTT 1-hr > 180
OGTT 2-hr > 155
OGTT 3-hr > 140

37
Q

Gestational diabetes typically develops:

A

24-28 weeks gestation

38
Q

Complications seen in babies of mothers with gestational diabetes:

A

Hyperglycemia
HTN
Cardiovascular complications

39
Q

Alternate terms for pre-diabetes:

A

Impaired fasting glucose

Impaired glucose tolerance

40
Q

Clinical diagnosis of IFG:

A

FBG 100-125

41
Q

Clinical diagnosis of IGT:

A

BG 140-199 after 2-hr OGTT

42
Q

Prevention of DM II from pre-diabetes:

A

Walking! Activity, diet

43
Q

Acute complications of diabetes:

A

Hypoglycemia (DM I)
DKA (DM I)
HHNKS (DM II)

44
Q

Describe HHNKS:

A

BG is so high it acts as an osmotic agent and draws water out of cells - coma/death from neuron shrinkage

45
Q

Describe AGEs:

A

Advanced Glycosylation End-Products; glucose sticks to proteins and doesn’t let them work properly

46
Q

Examples of microvascular disease:

A

Diabetic retinopathy
Diabetic nephropathy
Diabetic cardiomyopathy

47
Q

Examples of macrovascular disease:

A

Coronary artery disease
Stroke
PAD

48
Q

Examples of increased activity of polyol/sorbitol pathway:

A

Diabetic neuropathy - Schwann cells become swollen and damage axons
Cataracts

49
Q

Examples of increased activity of polyol/sorbitol pathway:

A

Diabetic neuropathy - Schwann cells become swollen and damage axons
Cataracts

50
Q

S/s of mild hypoglycemia:

A 
Hunger
Shakiness
Paleness
Blurry vision
Sweating
Anxiety
51
Q

S/s of severe hypoglycemia:

A 
Extreme fatigue
Confusion
Dazed appearance
Seizures
Unconsciousness
Coma 
Death
52
Q

Pathogenesis of DKA:

A

↓↓ glucose = ↑↑ glucagon
Uncontrolled fat metabolism → ketone production
Life-threatening hyperglycemia

53
Q

S/s of DKA:

A 
Fruity acetone breath
Kussmaul breathing
Dehydration
N/V, abdominal pain
∆LOC, weakness, parasthesia
54
Q

Lab changes in DKA:

A

↑↑ BG
Electrolyte imbalances
Metabolic acidosis
+ ketones in urine

55
Q

Filtered load =

A

Plasma concentration * GFR

56
Q

Normal GFR:

A

125 ml/min

57
Q

Renal threshold for glucose:

A

300 mg/min

58
Q

1 mM glucose = _____ mg/dL

A

18

59
Q

1 mM glucose = _____ mg/dL

A

18

60
Q

Why is acetyl-CoA converted to ketone bodies?

A

During periods of gluconeogenesis, oxaloacetate is used up and Kreb’s cycle cannot run; acetyl-CoA builds up and is converted into ketone bodies that the brain can use

61
Q

Three example ketone bodies:

A

Acetoacetate
Acetone
β-hydroxybutyrate

62
Q

Organs able to use ketone bodies for energy:

A

Brain
Heart
Kidney
Liver

63
Q

Why is acetyl-CoA converted to ketone bodies in DKA?

A

During periods of gluconeogenesis (since glucose cannot get into the cells), oxaloacetate is used up and Kreb’s cycle cannot run; acetyl-CoA builds up and is converted into ketone bodies that the brain can use

64
Q

Organs able to use ketone bodies for energy:

A

Brain
Heart
Kidney
Liver

65
Q

Only true ketoacid of the ketone bodies:

A

Acetoacetate

66
Q

pH in DKA vs. HHNKS:

A

Lower/worse acidosis in DKA

67
Q

Ketone bodies in DKA vs. HHNKS:

A

Much more ketone bodies in DKA

68
Q

C-peptide in DKA vs. HHNKS:

A

Much higher in HHNKS; indicative of how much insulin is being made

69
Q

Anion gap in DKA vs. HHNKS:

A

Much higher in DKA due to ketoacids

70
Q

Effects (3) of AGEs on proteins:

A

Cross-link polypeptides of the same protein; makes collagen brittle
Traps non-glycosylated proteins
Confers resistance to proteolytic digestion

71
Q

Non-protein effects of AGEs:

A

Induce lipid oxygenation
Inactivate NO
Bind nucleic acids

72
Q

Gestational diabetes is probably caused by:

A

Chorionic somatomammotropin

73
Q

Products of glucose on the way to becoming AGEs:

A

Schiff bases

Amadori products

74
Q

Effects of AGEs binding to RAGEs:

A 
Monocyte emigration
Cytokine/growth factor secretion
Vascular permeability
Procoagulant activity
Cellular proliferation
ECM production

Basically… inflammation

75
Q

HbA1c is:

A

Glycosylated hemoglobin; also an Amadori product; hemoglobin with AGEs stuck to it

76
Q

Pathogenesis of diabetic retinopathy:

A

Arterioles in eye leak fluid into retina and cause degradation

77
Q

Prevalence of diabetic retinopathy:

A

40% in type I

20% in type II

78
Q

Early stage of diabetic retinopathy:

A

Background diabetic retinopathy; small, dot hemorrhages

79
Q

Late stage diabetic retinopathy:

A

Proliferative diabetic retinopathy; ischemic areas in retina, neovascularization, hemorrage of delicate new vessels

80
Q

Effects of diabetic nephropathy on the kidney:

A

Glomerular leakiness → proteinuria
Glomerulosclerosis
Tubulointerstitial fibrosis
Arteriolar sclerosis

81
Q

Changes seen in diabetic nephropathy in the glomerulus:

A

Increased mesangial matrix (2/2 growth factor from macrophages)
Nodular lesions
Microaneurysms → fibrin clots/caps

82
Q

Fastest progression of diabetic nephropathy seen in:

A

Pts with poorly controlled HTN

83
Q

Tx of diabetic nephropathy:

A

ACEIs/ARBs to keep HTN under control; dialysis when needed

84
Q

Negative sequelae of diabetic neuropathy:

A

Unawareness of wounds/infection leading to uncontrolled infection

ARCHIVED: Pathophysiology (18 decks)

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