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Diabetes Flashcards

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1
Q

Cells of Islet of Langerhans

A

Beta Cells: Insulin
Alpha Cells: Glucagon
Delta Cells: Somatostatin
PP cells: VIP

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2
Q

Beta Cells

A

Sole source of insulin in the body
- The body’s primary anabolic hormone

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3
Q

Alpha Cells

A

Produce glucagon which induces glycogenolysis in the liver
- Antagonizes B cells

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4
Q

Delta cells

A

Produce Somatostatin
- Suppresses both insulin and glucagon release

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5
Q

PP (Pancreatic Polypeptide) Cells

A

Produce VIP
- Stimulates GI enzymes and slow GI motility

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6
Q

Insulin Functions

A
  • Transport Glucose and AAs
  • Glycogen formation in liver and skeletal muscles
  • Glucose transformation to TG (trigliceride-better E)
  • Nucleic acid synthesis
  • Protein synthesis
  • Decreases degradation of glycogen, lipid and protein
  • Body’s major anabolic hormones
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7
Q

How is insulin derived?

A

Derived from pre-proinsulin and proinsulin by sequential peptidase cleavage
- Gene located on Chromosome 11
- Cleavage and storage occurse in the Golgi

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8
Q

Insulin Released in

A

In 3 phases: Basal, Induced by glucose, prolonged
- T1/2 is about 5 min in blood
- Action opposed by glucagon (released by a-cells in islet)

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9
Q

Tissues depenedent on Insuling for glucose intake

A
  • Striated mucles (including heart)
  • Adipose tissue
  • Liver
  • Fibroblasts

Approximately 70% of body mass

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10
Q

Tissues NOT dependent on insulin for glucose uptake

A
  • Eyes
  • Brain
  • Nerve
  • Kidney
  • Blood vessels

Relay on facilitated transporters

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11
Q

Insulin Action on Target Cells

Important screen shot

A

Insuin => insulin receptor => ATP binding => Tyrosine kinase => Protein kinase => Phosphorylation Dephosphorylation => target enzyme => glucose => Glycogen or Pyruvate

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12
Q

Hyperglycemia

Glucose too high

A

B-cell release Insulin =>
- Increased absorption of glucose into cells
- Increased rate of respiration
- Increased rate of glycogenesis

This lead to Glucose levels to fall to normal

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13
Q

Hypoglycemia

Glucose too low

A

a-cells release glucagon =>
- Increased rate of glycogenolysis and release of glucose from liver
- Increased rate of gluconeogensis
- Increased use of fatty acid in respiration instead of glucose (lead to break down of fatty acids)

This result in Glucose increasing to normal levels

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14
Q

Diabetes Mellitus

Flowing through of suger

A

Genetic/epigenetic disorder characterized by an absolute or relative lack of insulin
- Characterized by hyperglycemia
- Result in an impaired use of carbohydrates => body uses stored or dietary lipids instead
- Altered lipid and protein metabolism
- Accumulation of of acetyl-CoA, acetoacetic acid, β-
hydroxybutyric acid, acetone (ketones)
- Result in acidosis, ketosis, hypercholesterolemia and hyperglycemia
- First recognized metabolic disease: Ancient egyption
- Got a diagnostic biomarker (urine test)
- First successful treatment of a metabolic disease

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15
Q

Acetoacetate

A

Screen Shot

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16
Q

Diabetes Facts

A
  • Incidence Increased in Blacks, Native Indians
  • 80% are Type 2, 10-15% Type 1
  • 6-7th leading cause of death in US

A leading cause of
– cardiovascular disease (MI, stroke, accelerated
atherosclerosis in all diabetics )
– adult onset blindness
– non-traumatic lower-limb amputations
– stocking-and glove’ sensory neuropathy
– end-stage renal disease
– markedly increased susceptibility to infections

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17
Q

Types of Diabetes

A

Non-Reversible:
- Type 1: Insulin dependent
– Type 1A: autoimmune
– Type 1B: no autoimmune
- Type 2(non insulin dependent)

  • Monogenetic Forms: MODY, Syndrome-related

Reversible
- Drug Induced: Vacor, Pentamidine, Phenytoin, Steriods
- Gestational: 5% of pregnancies, Major maternal-fetal complecation, malformation, post-maturity
- Insult related: Trauma, buns, pancreatitis, cancer

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18
Q

Diabetes Diagnostic Criteria

Insurance companies made these #

A

Fasting glucose > 126 mg/dL OR symptoms of DM pluse random plasma of >200 AND/OR plasma glucose >200 after oral loading (OGTT)
- Glycated hemoglobin (HbA1C)>6.5%

Rate of onset is clinically useful:
- Type 1 is rapid
- Type 2 is gradual

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19
Q

Prediabetes Diagnostic Criteria

A
  • Fasting glucose >110<126
  • OGTT >140<200 is pre-diabetes
  • Glycated hemoglobin 5.7%-6.4%

Blood glucose can be elevated transiently by trauma, burns, infections
- This is why the Dx of diabetes require PERSISTENT elevation of blood glucose

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20
Q

Type 1 DM

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A

Result from a failure of self-tolerance in T cells specific for B-cell antigens (eg. preproinsulin, cleavage products): Autoimmune disease
- Account for 5-10% of all cases; usually young
- Clinical signs may be abrupt but death of B-cells begin years earlier
- Must lose 90% of all B-cells for onset of ype 1 DM
- Absolute deficiency of insulin
- Patient ketosis-prone due to activity of glucagon (keto-acidosis is life-threatening)
- Patient in catabolic state-tine/emaciated
- Frequently associated with other autoimmuneities; Partericularly of thyroid

21
Q

The first patient treated with insulin

Study These Flashcards
A

Leonard Thompson
- Survived until 27

22
Q

Type 2 DM

Study These Flashcards
A

Lack of insulin availability or effectiveness
- Failure of target tissue to response (insulin resistance)
- Some insulin present; not ketosis-prone
- Strongly associated with obesity; not being seen in children (centeral obesity is worse)
- Dysregulation of adipokines
- Premissive inflammatory milieu

Can be a result of
- Inadequate production
- Premature destruction
- Release out of phase with food intake
- Decrease insulin receptors or their responsiveness

23
Q

Compare 1 & 2

Screen shot

24
Q

Acute Clinical Complications of Diabetes

Study These Flashcards
A
  • Hypoglycemia
  • Hyperglycemia
  • Diabetic ketoacidosis (DKA)
  • Hyperosmolar coma
25
Hypohlycemia | Info
Most common in Type; treatment complication of Type 1 and 2 - May occure when counter-regulatory hormones are stimulated (fasting, exercise, stress) or uncoordinated administration of insulin - Blood glucose <50 mg/dL - May be difficult to detect in children and elderly - Rapidly reversible with glucose/sucrose
26
Symptoms of Hypoglycemia
Secondary to catecholamine release (adrenergic): - Sweating, Shakiness, Anxiety, Hunger, Faintness, Tachycardia,.... Secondary to CNS dysfunction (neuroglucopenic): - Confusion, headaches, weakness, coma, Diplopia,... Nocturnal Hypoglycemia (usually due to excessive insulin therapy) - Morning headaches, Night sweats, Loud respiration, Difficulty in awakening, Psychologic changes
27
Hyperglycemia
Blood glucose of 126+mg/dL usually 160 - 3 polys: Polyuria (frequent urination), Polydipsia (drink a lot), Polyphagia (eats a lot) -- Osmotic dehydration (driving thirst) -- Lower activity of hypothalamic satiety center (huner) -- Increase of plasma osmolality (osmotic diuresis; a lot of hypotonic urine) - Sever weight loss (type 1)
28
Important; insufficient insulin diagram
Check Screen Shot
29
Diabetic Ketoacidosis (DKA)
Increased ketogenesis with loss of insulin activity - Most common in Type I but occures (uncommonly) in elderly Type 2 patients following stress (trauma, infection,..) - Ketone bodies are strong acids => lower pH - pH<7.2 associated with kussmaul breathing; loss of bicarbonate buffering - Sever dehydration, electrolyte loss, arrhythmias - Increased FFA and ketones due to lipase activation - Blood glucose >250mg/dL, usually 500-700 range - Can be life-threatening - Fruity smell of breath
30
Hyperosmolar Coma
Mostly in Type 2 DM patients - Precipitated by low fluid intake (illness, eg. flu) - Sufficient insulin present to prevent ketogenesis => Hyperosmolar, hyperglycemic, nonketotic coma - Late presentation, high glucose level >600+, may reach 3000-4000 mg/dL - Significant mortality, difficult to treat during rehydration
31
Chronic Metabolic Impairments
Formation of advanced glycation end product (AGEs) - Non enzymatic reaction between glucose-derived cellular elements and amino groups on protein - Proliferation of smooth muscle and matrix; increased ROS, release of cytokines, and growth factors Disturbance of polyol pathways in non-insulin dependent tissues: - Osmotic effects, increases extracellular matrix Activation of protein kinase C - Increased ROS, Osmotic injury, pro-angiogenic molecules, activation of multiple signal transduction pathway
32
Formation of Advanced Glycation End Products (AGE) and Receptor Specific Glycation (RAGE) End Products
Non-enzymatic reactions of glucose-derived precursors with protein amino groups or receptors 1) Cross-link extracellular matrix protein (eg., collagen). trapping protein and lipid within cell 2) Bind to membrane receptors 3) Enchances proliferation of smooth muscle cell and extracellular matrix 4) Release pro-inflammatory cytokines from intima and induces ROS 5) Induces state of pro-coagulant activity
33
Disturbance of Polyol Pathways
Occurs in tissues not dependent on insulin - lens, nerve, kidney, blood vessels, with consequent sorbitol increases In case of elevated intracellular glycose: Overhydration - Glucose go into cell => Soribitol act on it => fructose -- (Aldose reductase), (sorbitol dehydration) - These enzymes reaction depete NADPH required for GSH => compromising ROS protection - Increased osmolarity, => influx of water (underlying pathology in diabetic cataracts) - Inhibitation of aldose reductase => protect against cataracts and diabetic neuropathy - Sorbitol inhibit ion pump
34
Complications of Chronic Diabetes Mellitus
Microvascular disease - Retinopathy - Nephropathy Macrovascular disease - Coronary artery disease (major cause of death) - Cerebrovascular disease - Peripheral vascular disease Neuropathic disease - Peripheral symmetric polyneuropathy - Autonomic neuropathies - Mononeuropathies Foot ulcers Infections
35
Macrovascular Complications
Atherosclerosis (with increased acetyl-CoA) - 75% of DM patients <40 years have sever atherosclerosis; - M=F Setting clinicaly - Hypertriglyceridemia - Hyperglycemia - Alteration of lipoprotein composition - Procoagulant state - Hyperinsulinemia in Type 2
36
Microvascular Disease
- Basement membrane thickening in small blood vessel - Advanced glycation end products (AGE-RAGE) - Protein kinase C activation - Polyol pathway - Retinopathy >60% of Type I, 20% of Type 2 - Nephropathy: 75% end stage disease after 20 years
37
Kimmelstiel-Wilson Nodules
In kidney (glymerulor) - Cannon balls - Diagnostic for diabeties
38
Proliferative Retinopathy
Proliferation of blood vessels - Refract light - Hazy image
38
Proliferative Retinopathy
Proliferation of blood vessels - Refract light - Hazy image
39
Nonproliferative Retinopathy
Blood vessel weak - aneurythm and blled in aqueous part of eye - Cause blindness
40
Glaucoma
Too much fluid in eyes
41
Cataracts
Lense is crystal - hydrated - Light can't pass through
42
Infection
- Defective neutrophil chemotaxis and phagocytosis - CMI abnormalities - Complicated by hyperglycemia, glycosuria, Ketoacidosis, vascular disease Bacteria and fungal infection is common: - skin, UTIs, pyelonephritis, vulvo-vaginitis, opportunists (Tb) - Responsible for ~5% diabetes-related deaths - Superimposed on trauma and other deficits
43
Diabetic Foot Ulcers
Symmetric polyneuropathy - A leading cause of (periphral) ischemia and amputation - 3 year mortality following amputation 50% - Microvascular disease + neuropathy + impaired immunity + trauma + infections + defective repair + etc. (all these cause damage in the foot) - Not reversible; amputation only slow it doen FOOT CARE IS ABSOLUTELY ESSENTIAL
44
Diabetic Neuropathy
- Distal, symmetrical sensory polyneuropathy - ‘Stocking and Glove’ distribution - Fixed, resting tachycardia and orthostatic hypertension (lose BP when standing) - Impotence - Incontinence - Anhidrosis (no sweating) in lower limbs - Gustatory sweating - Mononeuropathy - Abrupt, painful loss of nerve function - ‘Foot slap’ Can't feel it at all; sometimes keep looking at feet to know where feet at
45
Early Signs/Symptoms of DM
- Skin rashes (non responsive to cream) - Poor skin healing - Skin ulcers/abscesses - Fungal infections - Tingling of foot (sensory nerves die) - Numbness - UTIs - Blurred vision - Weight change - Absent periods - Erectile dysfunction - Drowsiness - Elevated HbA1C
46
Signs/Symptoms of Severe DM
- Three P’s - Bed wetting in children - Severe vision change - Myalgia (pain in muscles) - Weakness - Acne (30% of cases) - Irritability - Cardiovascular issues - Sexual dysfunction - Absent menstrual periods - Persistent fungal infections, particularly Candida and Mucor - Fatigue, often severe - Headaches - Weight loss with polyphagia should point to DM
47
Prevention and Control of DM
- Control weight and diet!!! - Exercise!! - Rigorous control of blood glucose!! - These control factors can delay the onset of major morbidity and mortality. However, even with control, the complications of DM will occur with variable severity in ALL patients - Most common cause of death is MI; 2nd is renal failure
48
Metabolic Syndrome
Clustering of 3 of the following conditions: - Abdominal obesity - High blood pressure and elevated heart rate - High blood sugar - High serum triglycerides - Low serum HDL - Unclear etiology-insulin resistance Vs obesity - Increased TNF from adipocytes - Diagnosis associated with increased risk of MI, stroke, clinical diabetes Type 2, atherosclerosis

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