PCOL - Diabetes Mellitus

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Diabetes Mellitus -

-
Type IA is the most common form
JUVENILE onset
- Genetics and some viruses may
contribute to development
Pancreas
TYPE 2
- Located behind the stomach, at
- More common than Type 1;
upper left abdomen
associated with genetic and
- Surrounded by intestine, liver, and
metabolic defects that impact
spleen
glucose production
4 Hormone-Producing Cells - Progresses slowly  ADULT onset
- Greater than 40 years old and obese
1. Alpha  glucagon and proglucagon
are at high risk
2. Beta  insulin, proinsulin, amylin
(pancreatic hormone) Ketoacidosis
3. Delta  somatostatin (GH-IH)
- Starts when the body starts using
4. F-cell  pancreatic polypeptide
FAT as energy at a greater extent 
 Epsilon cell  Ghrelin (hormone
producing ketone bodies  acidity
that induces hunger)
Type 3
Glucagon
- Peripheral or hepatic insulin
- Opposite of insulin; INCREASES
resistance
blood sugar
- Chronic pancreatitis aka chronic
Amylin aka islet amyloid polypeptide continuing inflammatory process of
the pancreas  irreversible,
- Storage and anabolic hormone of morphological changes
body
Gestational DM
Pancreatic polypeptide
- During pregnancy, the placenta
- Stimulated by exercise, eating, and makes hormones that causes
fasting glucose buildup in the bloodstream
- Can inhibit gall bladder contraction  not enough insulin will cause DM
and pancreatic exocrine excretion - PLACENTAL HORMONES: Human
Placental Growth Hormone, Human
DM Placental Lactogen

- Includes a group of common MODY


metabolic disorders characterized by - Affected people have a 50% chance
fasting hyperglycemia and abnormal to pass along the genetic condition
post-prandial (after meal) glucose - Glucokinase is the most common
management\ mutated gene
TYPE 1 - HNF  hepatocyte nuclear factor \
- TX:
- Caused primarily by T-cell mediated  Sulfonylureas  For MODY
autoimmune response  1,3,4 (GLI- drugs)
DESTROYS B cells
 Injection of Insulin  For MODY - Detects HbA1c  dependent on age
2 and other factors
- 3 months corresponds to the
Acanthosis nigricans average lifespan of RBCs
- TX: identifying and correcting 3. OGTT
hyperglycemia; weight loss - Commonly done in GESTATIONAL
- Common in obese patients DM
4. Random BG
DM induced by BETA CELL TOXINS - Blood glucose levels in normal
people do not generally vary
A. Pyriminil
- Should be <140
- Structural analogue of nicotinamide;
- Prediabetic is 140-199
most commonly used as rodenticide
B. Streptozotocin
- Antibiotic that is found to be effective
against gram (-) bacteria INSULIN
- ZINC stimulates insulin action
Diabetic Hyperosmolar Syndrome Functions:
- The body tries get rid of excess A. Increase:
blood sugar by passing it thru the  Glucose uptake
urine
 Glycogen synthesis
Nephropathy  Glycolysis
 Glucose oxidation
- diabetes can damage kidney filtering
B. Decrease
process
 Glycogenolysis
Diabetic Foot Problem  Gluconeogenesis
 Lipolysis
- nerve damage due to poor blood
flow can increase complications Glucagon
*Diabetes increase the risk of CV dx; e.g., - Has chronotropic and inotropic
angina, HA, stroke, atherosclerosis effects
- Antidote for BB toxicity
*Stillbirth is the death of baby in the womb
of the mother

DRUG FOR DM
Diagnosis 1. Insulin
- Usually dispensed as pens or 10 mL
1. FBS
vials
- Normal levels are 70-100 mg/dL
- Insulin pen consists of a cartridge,
- Common side effect of OHAs is
dial for dosage measurement, and
hypoglycemia; managed with 1 tsp
disposable needle
of sugar or candy
- To use the pen: Open the pen 
2. Glycosilated HgB
check for injection site (SQ in thighs,
- Used to check if OHAs are working
abdomen, buttocks), press injection
button and wait 10 seconds; do not - Usually used with short acting rapid
rub the skin onset insulin
- Bedtime insulin is associated with
Based on Source
less weight gain
A. Bovine A. Lente
- From Bos taurus or cow - Insulin-zinc suspension
B. Porcine - Semilente  prompt insulin-zinc
- From Sus scrofa or pig/hog suspension
C. Recombinant Insulin
- Can use yeasts or bacteria
- They have superior level of purity 3. Long Acting
and quality; does not cause - Last for 24 hours
hypersensitivity reactions - Modified: Insulin detemir has added
- NPH  Neutral Protamine FATTY ACID side chain  more
Hagedorn protein bound to albumin  slower
release
Recombinant DNA Technology
- Insulin Glargine  decreased
 Scientists build human insulin in the solubility at neutral pH
laboratory - PZI  contain excess protamine
 They remove a loop of bacterial DNA and onset starts after 2 hours
called plasmid Insulin Delivery Systems
 Insulin plasmid is introduced to the
bacteria - Syringes are usually 0.5 cc
 Plasmid + bacterial DNA  - 100 units/mL is common
recombinant DNA - Insulin pumps are programmed to
 Recombinant DNA is put into a pump individualized basal and bolus
fermentation tank  harvested and replacement doses based on the
purified for medicinal uses blood glucose self-monitoring results
- CSII and devices should be replaced
Based on the DOA after 2-3 days with sterile techniques
1. Short Acting with Rapid Onset Undesirable Effects
A. Regular Insulin
- Cannot be given orally as it would be  Lipodystrophy is the abnormal
destroyed by gastric acid distribution of fat  managed by
- Most common routes are SQ, rotation of injection site
intranasal, and IV  Urticaria or hives are pale, red bumps
- For tight control, supplemental rapid on skin
acting insulin should be taken before
meals (before lunch/dinner)
OHAs
*All should be given before lunch time;
usually 30-60 minutes before meals Insulin Secretagogues
- Increase insulin secretion from
pancreatic beta cells
2. Intermediate Acting 1. Sulfonylureas
- Cover half a day or overnight - 1st line for NON OBESE
- Block K channel by binding to First generation Sulfonylureas
sulfonylurea receptor 1 (SUR1) 
partial depolarization and activation
of calcium channels  Ca influx 
exocytosis or release of insulin
- Goal is to render cell depolarized
- Usually C/I with geriatrics - Can cause WEIGHT LOSS; need to
- Cannot be given to patients with be used with exercise to maximize
hepatic or renal insufficiency weight loss
- Are those with suffix -AMIDE - If creatinine levels fall above 0.15
mmol/L or 150 mg/100mL, stop
Second generation Sulfonylureas
therapy
- With prefix GLI-
- For those with sulfa allergy  4. Thiazolidinediones
disulfiram reactions  hangover, - MOA: Activates peroxisome
throbbing headache, flushing, proliferator-activated receptor
nausea, vomiting, and dizziness gamma (PPAR-y)
- Lowers glucose by improving target
2. Meglitinides cell response to insulin, specifically
- Suffix -GLINIDES in the ADIPOSE TISSUE where the
- Same MOA as sulfonylureas  K drug promotes glucose upake,
ATP channel blocker utilization, modulates synthesis of
- Shorter duration but rapid action lipid hormones and other proteins
- Taken 30 minutes before meals - It acts mainly at adipose tissue
- Rosiglitazone can cause MACULAR
3. Biguanides EDEMA  causing swelling macula
- Only available form is Metformin in (area inside retina for central vision);
the Philippines permanent loss of vision in some
- 1st line therapy for OBESE cases but is easily managed due to
- Does not cause hypoglycemia slow progression
- Phenformin is associated with
LACTIC ACIDOSIS
- MOA is not clearly defined; decrease 5. Alpha Glucosidase Inhibitors
hepatic gluconeogenesis via - MOA; Converts complex CHO to
inhibition of mitochondrial respiratory simpler and more absorbable forms
chain complex  decreased - C/I in inflammatory bowel syndrome
signaling response to glucagon and
synergizes with insulin to promote
glucose uptake 6. Incretins
- AMPK  adenosine - Commonly administered as
monophosphate-activated protein parenteral (SQ)
kinase - DPP IV are taken orally
- PCOS  abnormal sex hormones in
women causing the growth of
ovarian cysts 7. Na Glucose CO-transporter 2
inhibitors (SGLT2)
- Canagliflozin 8. Amylin Analog
- Dapagliflozin - Used to maintain postprandial
- Empagliflozin glucose levels
- Newer drugs that inhibit reabsorption - Does not decrease glucose levels
of glucose and increase urinary alone; should be taken with insulin
excretion of glucose 9. Glucagon
- Action is in kidneys

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