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ARCHIVED: Pathophysiology > Exam 4: Diabetes > Flashcards

Exam 4: Diabetes Flashcards

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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
Tx for MODY:
Oral drug for DMII to promote insulin release
26
Effect of Cushing's on blood sugar:
↑ blood sugar from ↑ cortisol
27
Effect of acromegaly on blood sugar:
Growth hormone ↑ blood sugar
28
Effect of pheochromocytoma on blood sugar:
Epi/NE ↑ blood sugar
29
Diabetes is usually triggered during a time of:
Hormone flux
30
Mechanism by which insulin secretion ↓ in DM II:
Persistent leftover glucose in blood causes toxicity of β cells, which ↓ insulin production and ↑ resting blood sugar
31
Mechanism by which insulin secretion ↓ in DM II:
Persistent leftover glucose in blood causes toxicity of β cells, which ↓ insulin production and ↑ resting blood sugar
32
Clinically typical DM I patient:
Young, normal/skinny, with ↓ blood insulin, anti-islet cell antibodies, and ketoacidosis
33
Clinically typical DM II patient:
Older, obese, ↑ blood insulin, no anti-islet cell antibodies, and not in ketoacidosis
34
Clinical diagnosis of DM:
Fasting BG > 126 or | plasma glucose > 200 after 2 hrs during OGTT
35
Glucose levels in pregnancy are:
Normally lower
36
Clinical diagnosis of gestational diabetes:
FBG > 95 OGTT 1-hr > 180 OGTT 2-hr > 155 OGTT 3-hr > 140
37
Gestational diabetes typically develops:
24-28 weeks gestation
38
Complications seen in babies of mothers with gestational diabetes:
Hyperglycemia HTN Cardiovascular complications
39
Alternate terms for pre-diabetes:
Impaired fasting glucose | Impaired glucose tolerance
40
Clinical diagnosis of IFG:
FBG 100-125
41
Clinical diagnosis of IGT:
BG 140-199 after 2-hr OGTT
42
Prevention of DM II from pre-diabetes:
Walking! Activity, diet
43
Acute complications of diabetes:
Hypoglycemia (DM I) DKA (DM I) HHNKS (DM II)
44
Describe HHNKS:
BG is so high it acts as an osmotic agent and draws water out of cells - coma/death from neuron shrinkage
45
Describe AGEs:
Advanced Glycosylation End-Products; glucose sticks to proteins and doesn't let them work properly
46
Examples of microvascular disease:
Diabetic retinopathy Diabetic nephropathy Diabetic cardiomyopathy
47
Examples of macrovascular disease:
Coronary artery disease Stroke PAD
48
Examples of increased activity of polyol/sorbitol pathway:
Diabetic neuropathy - Schwann cells become swollen and damage axons Cataracts
49
Examples of increased activity of polyol/sorbitol pathway:
Diabetic neuropathy - Schwann cells become swollen and damage axons Cataracts
50
S/s of mild hypoglycemia:
``` Hunger Shakiness Paleness Blurry vision Sweating Anxiety ```
51
S/s of severe hypoglycemia:
``` Extreme fatigue Confusion Dazed appearance Seizures Unconsciousness Coma Death ```
52
Pathogenesis of DKA:
↓↓ glucose = ↑↑ glucagon Uncontrolled fat metabolism → ketone production Life-threatening hyperglycemia
53
S/s of DKA:
``` Fruity acetone breath Kussmaul breathing Dehydration N/V, abdominal pain ∆LOC, weakness, parasthesia ```
54
Lab changes in DKA:
↑↑ BG Electrolyte imbalances Metabolic acidosis + ketones in urine
55
Filtered load =
Plasma concentration * GFR
56
Normal GFR:
125 ml/min
57
Renal threshold for glucose:
300 mg/min
58
1 mM glucose = _____ mg/dL
18
59
1 mM glucose = _____ mg/dL
18
60
Why is acetyl-CoA converted to ketone bodies?
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
Three example ketone bodies:
Acetoacetate Acetone β-hydroxybutyrate
62
Organs able to use ketone bodies for energy:
Brain Heart Kidney Liver
63
Why is acetyl-CoA converted to ketone bodies in DKA?
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
Organs able to use ketone bodies for energy:
Brain Heart Kidney Liver
65
Only true ketoacid of the ketone bodies:
Acetoacetate
66
pH in DKA vs. HHNKS:
Lower/worse acidosis in DKA
67
Ketone bodies in DKA vs. HHNKS:
Much more ketone bodies in DKA
68
C-peptide in DKA vs. HHNKS:
Much higher in HHNKS; indicative of how much insulin is being made
69
Anion gap in DKA vs. HHNKS:
Much higher in DKA due to ketoacids
70
Effects (3) of AGEs on proteins:
Cross-link polypeptides of the same protein; makes collagen brittle Traps non-glycosylated proteins Confers resistance to proteolytic digestion
71
Non-protein effects of AGEs:
Induce lipid oxygenation Inactivate NO Bind nucleic acids
72
Gestational diabetes is probably caused by:
Chorionic somatomammotropin
73
Products of glucose on the way to becoming AGEs:
Schiff bases | Amadori products
74
Effects of AGEs binding to RAGEs:
``` Monocyte emigration Cytokine/growth factor secretion Vascular permeability Procoagulant activity Cellular proliferation ECM production ``` Basically... inflammation
75
HbA1c is:
Glycosylated hemoglobin; also an Amadori product; hemoglobin with AGEs stuck to it
76
Pathogenesis of diabetic retinopathy:
Arterioles in eye leak fluid into retina and cause degradation
77
Prevalence of diabetic retinopathy:
40% in type I | 20% in type II
78
Early stage of diabetic retinopathy:
Background diabetic retinopathy; small, dot hemorrhages
79
Late stage diabetic retinopathy:
Proliferative diabetic retinopathy; ischemic areas in retina, neovascularization, hemorrage of delicate new vessels
80
Effects of diabetic nephropathy on the kidney:
Glomerular leakiness → proteinuria Glomerulosclerosis Tubulointerstitial fibrosis Arteriolar sclerosis
81
Changes seen in diabetic nephropathy in the glomerulus:
Increased mesangial matrix (2/2 growth factor from macrophages) Nodular lesions Microaneurysms → fibrin clots/caps
82
Fastest progression of diabetic nephropathy seen in:
Pts with poorly controlled HTN
83
Tx of diabetic nephropathy:
ACEIs/ARBs to keep HTN under control; dialysis when needed
84
Negative sequelae of diabetic neuropathy:
Unawareness of wounds/infection leading to uncontrolled infection

ARCHIVED: Pathophysiology (18 decks)

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