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Pathophysiology and Pharmacology 2 > Diabetes > Flashcards

Diabetes Flashcards

FML

1
Q

Pancreas Components

A

exocrine (80) acini glands

endocrine (20) islets of langerhans

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2
Q

Islets of Langerhans components/secretions

A

alpha cells: glucagon
beta cells: insulin
delta cells: somastatin
f cells: pancreatic polypeptide

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3
Q

Insulin primary FX

A

synthesis of glycogen/protein in liver/muscle
suppression of gluconeogenesis/glycogenlysis/lipolysis
glycolysis/glucose transport

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4
Q

Insulin Release Process

A

BG increases –> insulin released –> BG lowers

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5
Q

Glucagon Release Process

A

BG decreases –> glucagon released –> BG raises

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6
Q

Endocrine Hormones Fueling Metabolism

A 
Glucagon
cortisol
growth hormone
epinephrine
norepinephrine
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7
Q

Post-absorptive (fasting) State

A

provides glucose for brain/nervous tissue
higher ratio of glucagon to insulin
hepatic glycogenolysis/gluconeogenesis
muscle oxidizes ffa

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8
Q

Absorptive State

A

insulin levels rise
stimulates glucose uptake into tissues
excess glucose stored as glycogen

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9
Q

Starvation State

A

glucagon levels elevated
hepatic gluconeogenesis
brain oxidizes ketones for energy

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10
Q

Type 1 Diabetes DKA

A

increased mobilization of free fatty acids –> increased hepatic synthesis of ketones
diabetic ketoacidosis

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11
Q

Type 2 Diabetes DKA

A

ketone bodies not sufficient for DKA

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12
Q

Type 2 Diabetes

A

can’t produce/respond to insulin

can’t use energy in food as well

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13
Q

Type 1 Diabetes

A

lack of insulin secretion (total or partial)
auto-immune (pancreatic beta cells destroyed)
no oral meds

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14
Q

Hyperglycemia acute symptoms

A

increased thirst/urination

weight loss

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15
Q

Monogenic DM

A

neonatal diabetes

maturity-onset diabetes of oung

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16
Q

Gestation DM onset/TX

A

during pregnancy
dietary TX, oral meds, exogenous insulin
hyperglycemia can lead to fetal/maternal complications

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17
Q

Prediabetes DX

A

impaired fasting glucose (100-125)
impaired glucose intolerance (144-199)
increased hemoglobine

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18
Q

Diabetes (nonpregnant) DX

A

Hemoglobin >6.5% increase
random serum glucose >200
FAsting serum glucose >126

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19
Q

Most common Type 1 DM

A

T-cell mediated autoimmune against beta cells

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20
Q

Type 1 DM etiology

A

childhood disease
genetic predisposition
viruses
cow’s milk proteins

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21
Q

Type 1 DM pathogeneisis

A

environmental triggers immune response
autobodies develop (honeymoon period)
insulin production ceases

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22
Q

Type 1 DM s/s

A 
hyperglycemia (fasting BG >126 x2)
polyuria
polyphagia (hunger)
polydipsia
glucosuria
weight loss
fatigue
n/v
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23
Q

Insulin aspart

onset/peak/lasts/admin

A

rapid acting
(15 min onset) (1-3 hr peak) (lasts 3-5 hrs)
SQ 5-10 min AC
must eat within onset

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24
Q

Insulin regular

onset/peak/lasts/admin

A

short-acting
(30-60 min onset)(2-5 hr peak)(lasts 5-8 hr)
SQ 30-60 min AC
Iv for DKA (only IVP)

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25
``` Insulin isophane (NPH) onset/peak/lasts/admin ```
intermediate acting (onset 1-2 hr)(peak 4-12 hrs)(lasts 12-18 h) SQ 30 min before 1st/last meals NEVER IVP
26
insulin detemir | onset/lasts/admin
long-acting gradual onset over 24 hr (lasts 24 hrs) SQ HS
27
Insulin glargine | onset/lasts
long acting gradual over 24 begining at 1 H lasts 24 hrs
28
Use of combination insulin
long-acting+short-acting use body's natural levels to enhance control should not cause hypoglycemia
29
Insulin that can't be mixed
glargine
30
Hyperglycemia Med Induced
corticosteroids NSAIDS diuretics
31
Hyperglycemia ICU PT Targets
140-180
32
Hyperglycemia non-ICU PT Targets
<140 fasting | <180 random
33
Metabolic Syndrome
``` adipose tissue is an endocrine organ that produces hormones insulin resistance ab obesity increased LDL/BP/artery disease Waste circumference >35/40 Lifestyle changes ```
34
Type 2 DM insulin resistance physiology
unresponsive to insulin (b/c of receptors) --> blood glucose ^ --> pancrease secretes more insulin (hypersecretion) = beta cell exhaustion/death
35
Type 2 DM TX
``` lifestyle change antidiabetic drugs (lower BG) insulin ```
36
Type 2 TX goals
pre-prandial BG <110 | HBA1C <6.5
37
Biguanides action/pro
decreases hepatic production of glucose/reduces insulin resistance does not cause hypoglycemia 1st line med METFORMIN
38
Biguanides Side effects
minor, GI-related lactic acidosis increased risk for renal disease/liver disease/severe infection/shoc/hypoxemia
39
Sulfonylureas MOA/ex/SE
glyburide/glipizide/glimepiride stimulate release of insulin from pancreatic islet cells/increase receptors hypoglycemia
40
Alpha-Glucosidase Inhibitors (ex/MoA/SE)
ACARBOSE/MIGLITOL block enzymes in small intestines from breaking down CHO (delayed digestion) GI SE most common No hypoglycemia (unless w/ Insulin/sulfonylurea)
41
Meglitinides (ex/MoA/Duration/SE/Cont)
``` NATEGLINIDE/REPAGLINIDE) stimulates insulin from pancreatic islet cells short duration (2-4 hrs) well-tolerated hypoglycemia hepatic/renal disease ```
42
Thiazolidinediones (ex/MoA/optimal BG)
PIOGLITAZONE, ROSIGLITAZONE decrease insulin resistance/inhibit hepatic gluconeogenesis 3-4 months
43
Thiazolidineiones SE/Contra
Fluid Retention/headache/weight gain CHF, pulmonary edema, bladder cancer NO hypoglycemia
44
Incretin Enhancers (MoA)
mimic hormones released in response to food (signal insulin secretion/stop glucagon production) reduce food intake (feeling of fullness) protect beta cells from injury
45
Incretin Enhancers (agonists/inhibitors)
(-glutides, -enatide) | -gliptins
46
Hypoglycemia Medical Emergency Levels
<60
47
Hypoglycemia s/s
hunger, sweating, palpitations, tremors, anxious, difficulty speaking, visual disturbances, atypical behavior, confusion, ,seizures
48
Hypoglycemia TX
``` glucose fast-acting simple CHO (juice,) glucagon (to convert glycogen to glucose) (5% Dextrose) (50% Dextrose if unconscious) ```
49
Somogyi Phenomenon
Hypoglycemia @ night (undetected) | Hyperglycemia in the morning
50
Somogyi Phenomenon s/s
night sweats, headaches, nightmares
51
Somogyi Phenomenon DX
BG 0200, 0200, 0600
52
Somogyi PHenomenon TX
complex carbs @ bedtime | may need to change insulin
53
Dawn Phenomenon and DX
Hyperglycemia in AM Most common in Adolescents/YA Testing @ HS, 0200, 0400, fasting
54
Dawn Phenomenon TX
based on testing if below 60 = reduce insulin if above 120 increase insulin snack @ bedtime
55
DKA patho
can be first sign of DM absolute/relative insulin deficiency (most common with Type1) not enough insulin = hyperglycemia = polyuruia, polydipsia, polyphagia = acidosis (fat breakdown)
56
DKA causes
``` infection skipping insulin new onset T1DM surgery trauma pregnancy ```
57
DKA TX
supportive, IV insulin, IV fluids, IV electrolyte replacements
58
DKA progression
hyperglycemia > dehydration > hemoconcentration > peripheral circulation failure > shock > hypotension > anuria > coma/death
59
Hyperglycemia Hyperosmolar Syndrome Patho
severe hperglycemia and coma DKA - ketosis/acidosis/Kussmaul's breathing just enough insulin
60
Hyperglycemia Hyperosmolar Syndrome Etiology
T2 DM | excessive unreplaced fluid losses w/hyperglycemia
61
Hyperglycemia Hyperosmolar Syndrome s/s
r/t hyperglycemia, dehydration, hyperosmolality neuro vascular thromobosis
62
Hyperglycemic Hyperosmolar Syndrome DX
``` glucose >600 osmolality >320 profound dehydration alteration in consciousness Bicarbonate >18 pH >7.3 ```
63
Hyperglycemic Hyperosmolar Syndrome TX
Support IV Insulin IV Fluids IV Electrolytes
64
DKA DX
usually younger BG >250 Serum Ketones Bicarbonate <18
65
Diabetic Neuropathy Pathogenesis
incrreased polyol pathway --> NA retention > edema > myelin swelling > nerve degneration
66
Diabetic Neuropathy s/s
``` GI disturbances Nerve disturbances diarrhea neurogenic bladder impotence distal polyneuropathy ```
67
Diabetic Neuropathy TX
depends | Gabapentin can help

Pathophysiology and Pharmacology 2 (27 decks)

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