Diabetes Patho

Question 1

Diabetes mellitus

Answer 1

Metabolic ex char by inc blood sugar from insulin secretion problem, insulin action problem, or both; occurs from relative or absolute insulin deficiency; assoc with long-term damage to multiple systems when uncontrolled

Question 2

Where carbs are broken down primarily

Answer 2

Duodenum and proximal jejunum

Question 3

Blood glucose level pattern in normal people

Answer 3

Increase when carbs taken in, then decrease

Question 4

Liver’s role in blood sugar

Answer 4

Liver extracts glucose from blood, synthesizes it into glycogen and can break down glycogen in glycogenolysis if needed; peripheral fat and muscle extracts glucose if needed

Question 5

Pancreas role

Answer 5

Produces insulin and controls blood sugar with the liver

Question 6

Exocrine function of pancreas (UNIMPORTANT)

Answer 6

Secrete directly into ducts (not blood)

Question 7

Endocrine function of pancreas and location

Answer 7

Cells secrete insulin directly into blood; occurs in islet of langerhans (cell island in pancreas with several types of cells)

Question 8

Alpha cells

Answer 8

Part of islet of langerhans; secrete glucagon in response to low blood sugar

Question 9

Glucagon

Answer 9

Stimulates liver to release stored glucose (glycogen) into blood

Question 10

Beta cells

Answer 10

Located in islet of langerhans; make insulin which decreases glucose levels by stimulating the movement of glucose into body tissue

Question 11

Insulin

Answer 11

Stimulates uptake, use and storage of glucose by acting like a key to open cells in the liver so they can store glucose as glycogen; ultimately decreases blood plasma concentrations of glucose (Dec blood sugar)

Question 12

Hormones that increase blood glucose levels

Answer 12

Glucagon, epinephrine, glucocorticoids, growth hormone

Question 13

Normal Insulin and lipid metabolism

Answer 13

Promotes synthesis of fatty acids in the liver after the liver has been saturated with glycogen; inhibits metabolism of fat in adipose tissue—build up of TGs in fat cells; fat-sparing effect in healthy people—drives carbs to use carbs instead for energy

Question 14

What happens if you lack insulin?

Answer 14

Can’t b/d carbs well, decrease glucose use by the cells, rapid increase of blood glucose—hyperglycemia, cells use fatty acids instead

Question 15

Insulin deficiency causes…

Answer 15

Dec glucose uptake by the cells (Hyperglycemia), Proteolysis (protein b/d), lipolysis (fat b/d)

Question 16

Impaired fat metabolism

Answer 16

Occurs from insulin deficiency; causes increased lipolysis (fat breakdown) and decreased lipogenesis (fat synthesis) which causes free fatty acids (FFA) in the blood

Question 17

Free fatty acid use

Answer 17

Converted to cholesterol and phospholipids in the blood; breaks down into acetyl-CoA (used by the liver to make acetic acid, which can turn into KETONE BODIES)

Question 18

Short-term effect of ketone bodies

Answer 18

Causes KETOSIS; short-term increase in serum ketones in the blood and urine that can cause severe metabolic ACIDOSIS and COMA

Question 19

Long-term effects of ketone bodies

Answer 19

Increased risk of atherosclerosis bc high serum lipid levels

Question 20

Impaired protein metabolism

Answer 20

Body can’t store protein well and begins to b/d protein and stop pro synthesis, causing muscle b/d, atrophy, and inc amino acids circulating in the blood which cells use as an alternate energy source (bad bc its not normal); lead to gluconeogenesis and more glucose release by the liver

Question 21

Results of abnormal protein catabolism

Answer 21

Muscle wasting, multiple organ dysfunction, aminoacidemia, inc BUN (urea nitrogen)

Question 22

Effect of insulin deficiency on fluid/electrolytes

Answer 22

Inc serum glucose levels—>increased plasma oncotic pressure—>fluid shifts intravascularly to balance out the high glucose levels—>intracellularly dehydration and increased peeing

Question 23

Glycosuria and when does it occur?

Answer 23

Peeing out sugar; occurs when hyperglycemia increases beyond what the kidneys can absorb, causing increased acetones in the urine (can use a urine dipstick to test—rare now)

Question 24

3 Ps of diabetes—more common in Type 1

Answer 24

Polyphagia (excess hunger), polydipsia (excess thirst), polyuria (excess urination)

Question 25

Why does polyphagia occur?

Answer 25

B/d of fat and protein—cell starvation

Question 26

Why does polydipsia occur?

Answer 26

B/c increase serum osmolality; glucose is very concentration in blood so fluid moves out of cells and into space to balance it out

Question 27

Why does polyuria occur?

Answer 27

B/c osmotic diuretics; excreting water and electrolytes

Question 28

Diabetes diagnosis

Answer 28

6.5% A1C (3 month average of diabetes), fasting glucose of 126 or above, OGTT 200+

Question 29

Prediabetic diagnosis

Answer 29

A1C 5.7-6.4%, 100-125 fasting average, 140-199 OGTT

Question 30

Why use OGTT for pregnant?

Answer 30

Don’t want preg women to fast, 3 month average is too long for 9 month preg period

Question 31

Type 1 DM

Answer 31

Autoimmune disease triggered by genetic predisposition and environmental trigger; slowly progressive T-cell mediated disease that destroys beta cells after autoantigens form on the beta cells and T cells attack; causes a complete lack of endogenous insulin

Question 32

DM1 the numbers

Answer 32

5-10% cases in US; usually diagnosed around age 12

Question 33

Clinical manifestations of type 1 diabetes

Answer 33

Often kids 11-13; long preclinical period of sx until almost no insulin produced; hyperglycemia and 3Ps with weight loss, recurrent infection, fatigue; other same diagnostics as Type 2

Question 34

DM type 2

Answer 34

Insulin resistance and some decreased insulin secretion; receptors lose sensitivity so insulin stops working as the key to let glucose into the cell; genetic and environmental combo

Question 35

Nonmodifiable risk factors for diabetes

Answer 35

Family, age over 45, race, history of gestational diabetes

Question 36

Modifiable risk factors for diabetes

Answer 36

Physical inactivity, high body fat and weight, high BP, high cholesterol

Question 37

Sx of DM2

Answer 37

Blurry vision, tired, dry skin, reoccurring infection, prolonged infection, feel ill, loss of feeling in feet

Question 38

Metabolic complications associated with DM2

Answer 38

Impaired insulin secretion (B-cells exhausted), peripheral insulin resistance (inc visceral fat), inc hepatic glucose production, altered production of hormones and cytokines by adipose tissue

Question 39

Why does hepatic glucose production occur?

Answer 39

Impaired suppression of gluconeogenesis in the liver (which results from proteolysis); body thinks it is hungry so it releases more glucose when really it needs more insulin; releases glucose instead of storing it

Question 40

Diabetic ketoacidosis (DKA)

Answer 40

Acute complication of diabetes (especially in Type 1) where you get super high sugar (400, 500, 600) and get hyperglycemia, acidosis, ketonuria; often end up in ER and can end up in coma and die

Question 41

Hyperosmolar hyperglycemic syndrome (HHNS)

Answer 41

Acute complication of type 2 (bc you need some insulin to cause it) where you get sugar in the 600, 700, 800s and big problems with osmolality where blood becomes so concentrated that body begins to shut down (fluid shifting problems)

Question 42

Hypoglycemia

Answer 42

Rapid onset, blood sugar below 55-60; usually related to meds (excess insulin); can be symptomatic of this with a higher blood sugar if your normal blood sugar is higher (like 150); symptoms pallor, tachy, palpitation, hunger, restless, tremor, convulse, coma

Question 43

Chronic complications

Answer 43

Poorly controlled diabetes; insulin resistance/deficit, chronic hyperglycemia, accumulation advance glucagon end products, activate metabolic pathway that cause tissue damage; microvascular and macrovascular

Question 44

Microvascular complications

Answer 44

Damaged capillaries, retinopathies, nephropathies, neuropathies caused by lesions whose frequency and severity are proportional to duration of disease; hypoxia and ischemia in eyes, kidneys, nerves and microangiopathy (small vessel disease with capillary membrane thickening)

Question 45

Diabetic neuropathy

Answer 45

Most common complication of diabetes; ischemia and demyelination of nerves causing neural changes and delayed conduction; loss of pain, temperature, vibratic sensation; results in ulcer, infection, amputation

Question 46

Diabetic retinopathy

Answer 46

Leading cause of blindness; hypoxemia, damage to retinal BVs, RBC aggregation and HTN; small vessel infarction and death

Question 47

Nephropathy

Answer 47

CKD and ESKD very common in diabetes; glomerular basement thinking and hardening; doesn’t work as well; half of people with diabetes get kidney disease

Question 48

Macrovascular complications

Answer 48

Damage to big vessels causing atherosclerosis and coronary artery disease, PVD, stroke, inc risk of infection; caused by oxidative stress and stuff

Question 49

Diabetes and infection

Answer 49

Diabetics have decreased warning signs of infection bc less feeling, get tissue hypoxia and impaired skin, rapid proliferation of pathogens that feed on excess glucose and less circulation of WBCs (also are less effective and abnormal); more fungal, yeast infection, UTI, gangrene