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Patho > Diabetes > Flashcards

Diabetes Flashcards

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

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

A

Leonard Thompson
- Survived until 27

22
Q

Type 2 DM

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

A

Screen shot

24
Q

Acute Clinical Complications of Diabetes

A
  • Hypoglycemia
  • Hyperglycemia
  • Diabetic ketoacidosis (DKA)
  • Hyperosmolar coma
25
Q

Hypohlycemia

Info

A

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
Q

Symptoms of Hypoglycemia

A

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
Q

Hyperglycemia

A

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
Q

Important; insufficient insulin diagram

A

Check Screen Shot

29
Q

Diabetic Ketoacidosis (DKA)

A

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
Q

Hyperosmolar Coma

A

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
Q

Chronic Metabolic Impairments

A

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
Q

Formation of Advanced Glycation End Products (AGE) and Receptor Specific Glycation (RAGE) End Products

A

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
Q

Disturbance of Polyol Pathways

A

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
Q

Complications of Chronic Diabetes Mellitus

A

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
Q

Macrovascular Complications

A

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
Q

Microvascular Disease

A
  • 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
Q

Kimmelstiel-Wilson Nodules

A

In kidney (glymerulor)
- Cannon balls
- Diagnostic for diabeties

38
Q

Proliferative Retinopathy

A

Proliferation of blood vessels
- Refract light
- Hazy image

38
Q

Proliferative Retinopathy

A

Proliferation of blood vessels
- Refract light
- Hazy image

39
Q

Nonproliferative Retinopathy

A

Blood vessel weak
- aneurythm and blled in aqueous part of eye
- Cause blindness

40
Q

Glaucoma

A

Too much fluid in eyes

41
Q

Cataracts

A

Lense is crystal
- hydrated
- Light can’t pass through

42
Q

Infection

A
  • 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
Q

Diabetic Foot Ulcers

A

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
Q

Diabetic Neuropathy

A
  • 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
Q

Early Signs/Symptoms of DM

A
  • 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
Q

Signs/Symptoms of Severe DM

A
  • 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
Q

Prevention and Control of DM

A
  • 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
Q

Metabolic Syndrome

A

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

Patho (17 decks)

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