Diabetes Flashcards
Diabetes Mellitus
A group of disorders of glucose ______ -
A syndrome charactized by and other disturbances in _____ and ____ metabolism
Homeostasis
Chronic hyperglycemia, carbohydrate and fat metabolism
Plasma Glucose Physiology
Normal glucose homeostasis is tightly regulated by three interrelated processes:
- Gluconeogenesis =
- Glycogen synthesis, Glycogenolysis =
- Insulin mediated =
- Glucose production in the liver (and some by kidneys)
- Glucose storage (skeletal muscle and liver)
- Glucose uptake by peripheral tissue (esp skeletal muscle, fat, and liver)
Normal Fluctuations in Plasma Glucose
Absorptive State = priority is to _____ plasma glucose (prevent marked _____)
Post-Absorptive State = priority is to _____/_____ plasma glucose (prevent marked ____)
decrease (prevent marked elevation) - when we are actively absorbing food that we consume
increase/maintain (prevent marked drop)
Glucose Production Notes
- Glucose production from substances such as ____ acid
- Skeletal muscle - significant amount of glycogen to ____ muscle ______
- Liver - significant (1), so glucose in liver can be broken down and released into bloodstream to maintain levels
- Uptake by specific peripheral tissues bc these tissues can derive energy by other means such as breakdown of (1) -> so regulation in times of low blood glucose, uptake into peripheral tissues can be ______ to save glucose for tissues that can’t use fat for energy ie (1) tissue
- lactic
- drive muscle contraction
- glycogen stores
- adipose tissue, limited, central nervous tissue
Glucose Levels (Notes)
Too high lvls of plasma glucose =
Too low of lvls of plasma glucose =
So we have to keep glucose in a ______ range with normal _____ (times of feeding and in between feeding)
toxic
inadequate support of brain function
therapeutic range - normal fluctuations
Absorptive State
What Happens
- We are consuming food, digesting it, absorbing glucose through GI tract so blood glucose levels are starting to ____
The way our body deals with this (how glucose homeostasis is maintained)
- Blood glucose + amino acids is taken up by skeletal ____
- Storage of that glucose (as intracellular ____ stores) and amino acids (in form of _____)
- _____ takes up blood glucose and stores it in form of (2)
- ______ tissues takes up blood glucose and fats -> both converted to triglycerides and stored
rise
- muscle
- glycogen, proteins
- Liver, glycogen and triglycerides
- Adipose
Post Absorptive State
What happens
- To spare glucose for the _____, uptake of glucose by (3) is b____, alternatively
-
(1): key role in post absorptive state - does 2 things
- Liver will (1) and release into blood
- (1) Take up amino acids, lactic acid, energy substrates in circulation and synthesize glucose then release into blood
- Skeletal muscle, adipose tissue, liver is going to use ____ as energy instead of glucose
-
(1): key role in post absorptive state - does 2 things
- brain, skeletal muscle, fat, and liver is blocked
-
Liver
- Break down its glycogen stores
- Gluconeogenesis
- FAT
-
Liver
Plasma Glucose Physiology
During times of high glucose (after meals “_______ state”)
- _____ in Gluconeogenesis and Glycogenolysis
- Increase in tissue ______ to glucose (esp skeletal muscle and fat, mediated by insulin)
- _____ in glucose storage (_____ synthesis)
- _____ use of fat as primary energy source/_____ fat storage
“absorptive state”
- Decrease Gluconeogenesis and Glycogenolysis
- Increase tissue permeability to glucose
- Increase glucose storage (Glycogen synthesis)
- Limit use of fat as primary energy source/increase fat storage
- We shut off gluconeogenesis and glycogenolysis*
- We turn on glucose storage*
Plasma Glucose Physiology
During the fasting state (“_______ state”)
- Release of glucose from their stores (_______)
- Making new glucose (_______)
- ______ access to glucose to only those tissues that absolutely need it like the _____ (insulin level drops)
- Use of ___ as primary energy source (________)
“Postabsorptive state”
- Glycogenolysis
- Gluconeogenesis
- Limit, CNS
- fat as primary source (lipolysis)
How does glucose get in and out of the cell?
Use of (1) - Focusing on (2)
Glucose enters and exits cells via facilitated _____ (in which a protein transporter is used and concentration gradient is still needed)
Glucose transporters - Glut 1 and Glut 4 transporters
facilitated diffusion
Glut 1 Transporters
Allows glucose entry into the cell - is ______ expressed by ____ cells and is responsible for ___ levels of b_____ glucose uptake required to sustain ____ generation by all cells
(Glut 1 expression is ____ with prolonged fasting and _____ by persistent exposure to excessive glucose)
constitutively expressed by all cells, low levels of basal glucose, sustains energy
increased with fasting, decreased with hyperglycemia
Glut 4 Transporters
Expressed in (3) types of cells, is responsibe for _____ stimulated uptake of glucose
- availability of transporters entirely _____ on insulin
Cardiac, Skeletal muscle, Adipose tissue, insulin
entirely dependent on insulin
Glut 4 Transporters
Located where?
- When insulin binds to insulin receptor - (1) pathway (second messenger system) stimulates _____ of glut 4 vesicles into the plasma ____ of the cell - ___ with plasma membrane to insert themselves into membrane and take up ______
inside cell
- PI-3K Signaling pathway, exocytosis, plasma membrane - fuses with plasma membrane to insert themselves into membrane and take up glucose
Other Insulin-Mediated Effects on Cells
- Other intracellular events stimulated by insulin
- (1) Insulin stimulates enzymes necessary to convert glucose to triglycerides, protein, and glycogen
- (1) Insulin stimulates intracellular processes that consume glucose and allow cells to proliferate and grow through (1) pathway
- Glucose Storage
- Glucose as a Growth Factor, Mitogenic Activated Protein Kinase pathway (MAPK)
Glucose Homeostasis Hormones
(2)
Both produced by ______ portion of pancreas (1) cells
Insulin, Glucagon
endocrine, Islets of Langerhans
Islet of Langherhan Cells
- Beta Cells =
- Alpha Cells =
Two hormones critical for (2) states
- Secrete insulin
- Secrete glucagon
absorptive and post-absorptive state
Actions of Insulin
During times of high glucose (after meals “_____ state”)
- Gluconeogenesis and Glycogenolysis =
- Tissue permeability to glucose (esp skeletal muscle and fat) =
- Glycogen synthesis =
- Lipogenesis =
- Lipolysis =
“absorptive state”
- Decreased gluconeogenesis and glycogenolysis
- Increase tissue permeability to glucose (allows insertion of glut 4 transporters to increase permeability)
- Increase in glycogen synthesis
- Promotes lipogenesis
- Inhibits lipolysis
Shuts off gluconeogenesis and glycogenolysis, increases enzymes necessary for glycogen synthesis and lipogenesis (fat formation), inhibits enzymes for fat breakdown
Actions of Glucagon
During the fasting state (“______ state”)
- (1) Release of glucose from their stores
- (1) Making new glucose
- Limiting _____ to glucose (esp skeletal muscle and fat)
- Lipolysis =
- Lipogenesis =
Insulin and Glucagon are ______ regulated/released
“postabsorptive state”
- Glycogenolysis
- Gluconeogenesis
- Limiting access to glucose
- Promotes Lipolysis
- Inhibits Lipogenesis
Reciprocally - presence of one hormone strongly inhibits presence of the other and opposite sources of stimulation/antagonistic relationship
Classification of Diabetes Mellitus
Most Common Types
(1) B cell destruction, leads to ______ insulin deficiency
- (2) causes
(1) insulin resistance with ______ insulin deficiency
Type 1 DM - absolute insulin deficiency
- Immune mediated
- Idiopathic
Type 2 DM - relative insulin deficiency
Classification of Diabetes Mellitus
Other Types and Causes
(1) Maturity-onset diabetes of the young (1), caused by mutations in several autosomal (sex independent) genes producing defects in insulin production. Several types but tend to act like mild type 1
(1) Chronic pancreatitis, Pancreatectomy, Neoplasia, Cystic fibrosis, etc.
(1) Acromegaly, Cushing Syndrome, Hyperthyroidism, etc. .
Genetic defects of B-cell function (MODY)
Exocrine pacreatic defects
Endocrinopathies
Classification of Diabetes Mellitus
Types and Causes
(1) Cytomegalovirus, Coxsackie virus B, etc
(1) Glucocorticoids, Thyroid hormone, a-interferon, B-adrenergic agonists, Protease inhibitors, Thiazides, etc
(1) Down syndrome, Turner syndrome, Kleinfelter syndrome, etc
(1) Diabetes
Infections
Drugs
Genetic syndromes associated with diabetes
Gestational Diabetes
Classification of Diabetes (Notes)
Type 1: autoimmune _____ of pancreatic cells (sometimes just B cells, sometimes B and A cells) - leads to _____ insulin deficiency
Type 2: insulin _____ + _____ insulin deficiency
- Relative bc they? sometimes very high (measurable amount), but deficiency is insulin levels are not high enough to _____ the resistance (insulin receptors not _____ adequately)
- destruction, absolute
- resistance + relative
- still have insulin, overcome, receptors not responding adequately
Classification of Diabetes (Notes)
- All MODY disorders = _____ defect of B cell destruction
- Cystic fibrosis effects _____ glands throughout the body (mostly the lungs) but also tend to have _____ failure -> lack of insulin and glucagon production)
- Cushings = excess cortisol -> chronic ______ -> acts like type __
- Infections = don’t cause diabetes but getting these infections in early childhood ____ the autoimmunity involved in type 1 (already have genetic predisposition but the infection activates their immune system)
- genetic
- exocrine, pancreatic
- hyperglycemia -> type 2
- triggers the autoimmunity
Classification of Diabetes (Notes)
- Drugs = some tend to _____ blood glucose and act like a type 2
- Genetic abnormalities = the same genes/chromosomes are affected in these disorders hapen to be?
- Gestational diabetes = ______ state, usually an ____ or _____ vulnerability + pregnancy/placental hormones create a diabetic state
- elevate
- same genes that regulate blood glucose
- temporary, genetic or environmental vulnerability
Most Common Types of DM
Type 1
- Relationship with insulin?
- Sometimes referred to _____ Onset, however there are adult versions of type 1
Type 2
- Relationship with insulin?
- We tend to think ____ Onset, but now many children are getting it
Type 1
- Insulin Dependent Diabetes* bc a total lack of insulin
- Juvenile
Type 2
- Non-insulin Dependent but can become insulin depedent bc eventually pancreas gets destroyed
- Adult
“Pre-Diabetic” conditions
(2)
Impaired glucose tolerance (IGT)
Impaired fasting glucose (IFG)
Prediabetic Conditions Notes
More often before Type __, bc have a longer _____ stage compared to Type 1 where you have __% destruction of B cells - clinical onset is abrupt
IGT - oral glucose tolerance test =
- At 30 will be ____, 1 and 2 hrs should be ____ (usually normal at 1 hr)
- If person has DM, peak will be _____ and takes ____ to get back to normal
- If high suspicion of DM?
Prediabetic range for Fasting Blood Glucose =
Type 2, longer pre-clinical, 90%
you come fasting, consume a drink that has a high concentration of glucose (75-100g), then blood drawn is at 30min, 1 and 2 hrs
- higher, dropping
- higher, longer
- not recommended
100-126
Screening Tools
(3)
Oral Glucose Tolerance Test (OGTT)
Fasting Plasma Glucose (FPG)
HbA1C
Fasting Plasma Glucose
Normal =
IFG =
Diabetes Mellitus =
<100
100-126
>126
HbA1C
=
Shows average blood glucose over?
However really show the last ___ weeks so if you were good for 3 months but bad the last 2 will be high
Normal =
IGT =
DM =
% of hemoglobin that is glycosylated (how much hgb has glucose attached to it)
extended period of time ~3 months
2 weeks
<5.7
5.7-6.4
>6.5
Type 1 Diabetes Mellitus
Is characterized by an _____-mediated ____ of pancreatic ____ cells leading to an “______“ insulin deficiency
- Accounts for about ___% of all diabetes mellitus
- An autoimmune disorder in which _____ and _____ are thought to play important roles in pathogenesis
- (2) major types
~______ insulin deficiency and often exceedingly high levels of _______~
immune-mediated, destruction of pancreatic beta cells leading to an “absolute” insulin deficiency
- 10%
- heredity/genetics and environment
- Immune, Idiopathic (thought to be underlying autoimmunity but no clear markers)
Absolute, Glucagon (esp early in disease bc in the absence of insulin, alpha cells will have chronic stimulation to release glucagon, as disease progresses, alpha cells will burn out and eventually stop producing glucagon all together)
Pathogeneis of Type 1 Diabetes
Most commonly develops in ______ and becomes manifest at _______
Can develop/manifest at any age (indcluding ______)
The clinical onset is _______ but the autoimmune attack is ______ and usually starts many years before (classic manifestations occur at >__% B cell destruction)
childhood, puberty (something about the rise in hormones)
Adulthood
abrupt onset, autoimmune attack is chronic, 90%
However there are children as young as 3,4 have fully manifested DM
Pathogenesis for Type 1 Diabetes
Mechanisms for B cell destruction
- ___ cell mediated immune attack against poorly defined B cell antigens
- ______ induced B cell damage (IFN-y, TNF-a, IL1, induced apoptosis)
- ______ against islet cells or insulin (detected in 70-80% of patients), usually accompnied by autoantibodies against b cell antigens
- T cell mediated
- Cytokine induced
- Autoantibodies
Pathogeneis of Type 1 Diabetes
Genetic Susceptibility
- (1) presence of certain MHC II alleles (affects T cell antigen presentation)
- (1) tandem repeat polymorphs of insulin gene (affects negative selection of insulin-reactive T cells)
Environmental Factors
- (1) - certain viral infections (mumps, rubella, etc) are thought to increase likelihood of autoimmune triggering
- The MHC locus
- Non-MHC genes
- Infections
Primary cause is genetic susceptibility but there are certain
Type 2 Diabetes Mellitus
Much more ____ than Type 1
Associated with ______, insulin ______, and a ______ insulin deficiency
Strongly influenced by genetic and environmental/lifestyle factors
- Concordance rate between identical ____ is 50-90% and 20-40% between first degree _____ (compared to 5-7% in general population)
- Environmental/lifestyle factors include: _____ level and ____ habits
The most powerful risk factor in type 2 diabetes is ______** - specifically high _____ adiposity (waist-to-hip ratio of greater than 1), and incrased ______ adiposity
While much has been learned in the recent years regarding the pathogenesis of Type 2 DM, it still remain enigmatic to great extant
common
hyperglycemia, insulin resistance, relative inulin deficiency
- twins, relatives
- activity level and eating habits
OBESITY** - abdominal, visceral
Varying degrees of genetic susceptibility (even if mother earth yoga healthy to max, may develop)
Pathogenesis of Type 2 DM
There is ___ evidence to suggest an autoimmune mechanism (or immune related)
Two metabolic defects characteristic of Type 2 DM:
- Decreased ______ to insulin by peripheral _____ (insulin _____)
- B cell _______ manifested as _______ insulin ______ relative to insulin resistance and hyperglycemia
In most cases, Insulin resistance is the _____ event, while B cell dysfunction is the _____ event (insulin resistance can preceded clinically manifested DM by __-__yrs)
no
- sensitivity, tissues, (insulin resistance)
- dysfunction, inadequate insulin secretion
primary, secondary (10-20)
Pathogenesis of Type 2 Notes
Tend to happen in sequence
- Insulin ______ results in
- Pancreas trying to _______ by producing higher amount of insulin (can do this for a long time) - so a lot of ppl have had insulin resistance for a long time but we’re compensating well
- But eventually increased ____, functional demand leads to _____, cell death, and impaired B cells in pancreas -> then insulin production is not high enough to maintain lvls of BG
- Resistance
- compensate
- stress, inflammation
Pathogenesis of Type 2 DM
Functional studies in individuals with insulin resistance have demonstrated numerous quantitive and qualitative abnormalities of the insulin ______ pathway
Mechanisms of Insulin Resistance
- Down regulation of insulin _____
- Decreased insulin receptor - initiated _____ activity
- Reduced levels of insulin receptor signaling _____ (PI-33K and MAPK)
- Impaired docking and fusion of _____ containing vesicles with the plasma membrane
signaling
- receptors
- kinase
- intermediates
- GLUT4
Pathogenesis of Type 2 DM
The B cell dysfunction in Type 2 DM reflects the inability of these cells to _____ themselves to the long-term demands of _____ insulin resistance (IR)
Initially, insulin secretion is higher at every level of plasma glucose with IR, this _________ state can maintain normal plasma glucose for years
Early B cell failure manifests subtly as:
- Loss of normal pulsatile/______ pattern of insulin secretion
- Loss of “_____ phase” of insulin secretion triggered by elevation of plasma glcuose
- Eventually secretory defects affect ___ phases of insulin release, eventhough some basal secretion persists
Late B cell failure
- Decreased B cell ____
- Islet cell d______
- _____ islet deposition
adapt, demands of peripheral insulin resistance
Hyperinsulinemic
- oscillating
- “rapid phase” (cephalic phase)
- all phases
- mass
- destruction
- amyloid
Metabolic Staging of Type 2 DM
IGT = cephalic phase impairment
DM = all phase impairment
Classic Manifestations of DM
(4)
Hyperglycemia
Glucosuria
Polyuria
Polydipsia
Hyperglycemia causes the -> Glucosuria (when plasma lvsl of glucose get above renal threshold) -> causes osmotic diuresis Polyuria -> Dehydration from water loss then causes the Polydipsia (extremet thirst)
Acute Complications of DM
(4)
Hypoglycemia
Hyperglycemic (hyperosmolar) Coma
Diabetic Ketoacidosis
Hyperosmolar hyperglycemic nonketotic syndrome
Acute Complication of DM (Notes)
- Hypoglycemia = potential complication of _____ (insulin)
- Hyperglycemic (Hyperosmolar) Coma = plasma levels get too high -> plasma _____ gets too high can lead to disturbed _____ function leading to potential coma
- Diabetic Ketoacidois = problem of type ___ or late stage type 2 wher eyou have absolute insulin deficiency
- Hyperosmolar hyperglycemic nontketotic syndrome (HH and K) = hyperglycemia, glucosuria, polyuria, polydipsia MINUS the _____ (version of HHC above in ppl w absolute insulin deficiency)
- treatment
- osmolarity -> disturbed mental function
- Type 1 or late Type 2
- minus ACIDOSIS
Mechanism of Hyperglycemia in Type 2 DM
(4)
Problem with insulin - either insulin is ____ or can’t _____ insulin
- When they consume food (esp carbs) - elevates plasma glucose and insulin sensitive tissues can’t take up the glucose so stays in ______ -
- ______ can’t access that glucose (doesn’t now you’re in an absorptive state) -> assumes you’re still in the ________ state where its breaking down glycogen stores and producing glucose (_______) -> so liver ______ of glucose major mechanism of hypergylcemia of diabets
Impaired insulin secretion
Increased basal hepatic glucose production
Carb absorption
Decreased insulin stimulated glucose uptake
resistant or can’t produce insulin
- bloodstream
- Liver can’t access -> assumes still in postabsorptive state -> gluconeogenesis - liver production of glucose major mechanism of hyperglycemia of diabetes
Hypogylcemia
A ____ in blood glucose below what is normal for a___/s___
Most common acute complication in type __ diabetes
Can occur in type 2 pts being _____ with insulin
drop, age/sex
Type 1
Type 2 being treated w insulin
Hypoglycemia (Notes)
Adults < ___
Neonates/Baby range is
- Usually a _______ of timing or dose of tx compared to timing of meals
- (1) takes up more gluocose, you don’t need as much insulin
- (1) you need more insulin bc stress/infection tends to elevate blood glucose
- So even if you have a routine down pat with food and insulin, things can ______ that relationship
<70
<40
- miscalculation
- Exercise
- Sick
- complicate
Symptoms of Hypoglycemia
Autonomic
- Adrenergic: T______/shakiness, Anx____, Palpitations/t_______
- Cholinergic: Sw_____, Hu_____
Neurologic
- Weak/fatigued/dr______, head____, b______ change, con______, Dip_____, difficulty speaking, se_____, coma
- Tremors, Anxiety, tachycardia
- Sweating, Hunger
- drowsy, headache, behavior change, confusion, diplopia, seizure, coma
Autonomic Response
In ______ stages, like when you haven’t eaten in a while, tachycardia, palpitations, anxiety, hungry, start to sweat
- Whenever your SNS turns on, it releases catecholamines like (1) which will elevate BG a bit (along w release of glucagon)
- Purpose of Autonomic response: acts as a _____: feelings make you ____ that you are becoming hypoglycemic to _____ you to go ____ something (HANGRY)
early
- epi, norepi
- bridge, makes you aware -> triggers you to go eat
Hypoglycemia Unawareness
Like any other stimulus, with more episodes your body ____ and eventually the next time you’re hypoglycemic, you’re body may ____ have any of these ______ responses and the first manifestations you’ll experience is ________ (can be embarrassing)
adapts, may not have autonoimc responses, neurologic
Glucose Counter-regulation
Part of autonomic response is a rise in ______ which gives you a little boost of glucose before you can consume food
- For ppl with abslolute insulin deficiency they hav a period of time where their glucagon can be very ____, but at some point their glucagon system can ____ out and alpha cells can no longer _____ and produce glucagon
- For these pts, whether they have repeated experiences of hypoglycemia or not - Hypoglycemia can be very ______ very ______ bc they no longer have glucagon response
Takeaway: for diabetics, hypoglycemia not only a complication of tx but is something that is easy to do bc body doesn’t have all the _______ responses in place
glucagon
- high, burn out, can no longer respond
- severa very quickly
Compensatory
Diabetic Ketoacidosis
Develops when there is an _____ insulin deficiency of insulin or an increase in (1) hormone like (2)
Under these circumstances, ____ metabolism increases and there is an increased production of keto_____
Occurs with increased frequency of i_____, trauma, surgery or myocardial infarction, or increased ____ from other sources
Clinical Manifestations
- Fairly __specific
- Can include ______ respirations (hyperventilation in attempt to compensate for ____), postural d______, CNS ______, ___uria, abdominal _____, poly____, poly____
Absolute, counter regulatory hormone like catecholamines or glucagon
fat metabolism, ketoacids
infection, stress
- nonspecific
- kussmauls, compensate for acidosis, dizziness, CNS depression, ketonuria, pain, polydipsia, polyuria
Diabetic Ketoacidosis (Notes)
Bc normally, any amount of insulin in the body really does what?
But bc of absolut insulin deficiency -> _____ fat breakdown -> acute buildup of _____ -> causes a _____ acidosis
- CNS depression, Nausea, abdominal pain, dizziness (all from altered plasma ___)
Ketoacidosis happens more commonly under stress responses (trauma, infection) - so children at home that have type 1 that stay home from school bc of sick, often have to do what?
preserves fat stores
accelerated fat breakdown -> acute buildup of ketoacids -> metabolic acidosis
- plasma pH
often have to check urine for ketones a lot bc normal insulin regiment may not be enough to prevent ketoacidosis from stress of infection
DKA Chart
Why do you usually NOT see DKA with Type 2DM?
What happens
- Breakdown of ____
- Lack of glucose _______
- Liver thinks your ______ bc doesn’t get insulin signal so breaks down stored glycogen -> gluco_____ -> puts out alot of glucose -> osmotic _____ -> de_____ -> __ may crash dt dehydration
- Accerlated fat breakdwon causes buildup of ____ -> metabolic ____ that effects ____ function -> _____ breathing (compensation for acidosis), appears ____kalemic (from acidosis) but paradoxical bc body has pushed it out of the cells and peeing it out
- So when giving insulin, can rapidly become hypo_____
Bc not an insulin deficiency they have insulin to prevent accelerated fat breakdown
- fat
- uptake
- starving, gluconeogenesis, diuresis, dehydration -> BP may crash
- ketones -> metabolic acidosis, brain -> kussmaul breathing, hyperkalemic
- hypokalemic
Hyperosmolar Hyperglycemic Nonketotic Syndrome
Usually seen in Type __ DM
A complication with insulin resistance and a “_____“ insulin deficiency
A constellation of signs and symptoms that reflect a _____ but ____ state
Insulin levels are high enough to suppress ______ but not high enough to facilitate glucose ____ into (2)
Clinical Manifestations (4)
Type 2
“relative”
hyperglycemic but nonketotic
lipolysis, entry into muscle and fat tissue
Hyperglycema, Glucosuria, Polyuria, Polydipsia
HHK (Notes)
Basically the left part of the diagram (minus the ____ _____)
(1) bc glucose very high
Difference btween HHK and DKA
- Both have (2) but in DKA -> will happen at a ____ plasma glucose lvl than HHK
- Bc in DKA coma and depression from hyperosmolar plasma AND _____ vs.
- HHK just the _____ and hyperosmolar plasma
- Ex) Someone in Type 2 DM you see coma in ____mg/dL vs DKA can be in a coma at ____ mg/dL
metabolic acidosis
hyperosmolar
- CNS depression and Coma, lower
- Acidosis vs.
- just hyperglycemia
- 700 vs. 400
Chronic Complications of Diabetes Mellitus
(3) (2) (2)
There is extreme variability among patients in the time of onset (severity, and organs involved) of chronic complications
Macrovascular Disease
Microvascular Disease
Diabetic Nephropathy, Diabetic Retinopathy
Neuropathy
Autonomic Neuropathy, Sensory Neuropathy
Chronic Complications (Notes)
All due to TOXIC NATURE OF HYPERGLYCEMIA on _____ and ____ TISSUE
- Macrovascular disease: Injury to large blood vessels such as _____ artery disease, _____ disease, _____ vascular disease -> all can lead to ______ throughout the body (whether in ____, ____, or ____)
- Microvascular: injury to microcirculation -> Thickens basement _____ in connective tissue -> impedes delivery of _____ -> poor perfusion to issues like in (2) a lot of microvascular in kidneys and eyes
-
Neuropathy: injury to nervous system esp _____ nervous system (not rly CNS)
- Autonomic neuropathy: damage to autonomic nerve that regulates things like (2)
- Manifestation (1)
- Autonomic neuropathy: damage to autonomic nerve that regulates things like (2)
NERVOUS AND VASCULAR
- coronary, cerebrovascular, peripheral -> atherosclerosis (brain, heart, periphery)
- membrane -> oxygen -> diabetic nephropathy and retinopathy
-
Autonomic
- BP and perfusion
- Orthostatic hypotension
