Endo - Pathology (Diabetes) Flashcards
Pg. 327-328 in First Aid 2014 Sections include: -Diabetes mellitus -Type 1 vs. Type 2 diabetes mellitus -Diabetic ketoacidosis -Insulinoma
What are 4 presenting signs/symptoms of diabetes mellitus? What are 2 conditions associated with diabetes mellitus, and which is type 1 versus type 2 DM?
Polydipsia, polyuria, polyphagia, weight loss; DKA (type 1), Hyperosmolar coma (type 2)
What is a rare cause of diabetes mellitus?
Rarely, can be caused by unopposed secretion of GH and epinephrine
What are the 2 key causes of pathophysiology in diabetes mellitus? What 3 consequences do they have?
Insulin deficiency (and glucagon excess) => Decreased glucose uptake, Increased protein catabolism, & Increased lipolysis
What are 4 effects of decreased glucose uptake in diabetes mellitus?
Decreased glucose uptake => hyperglycemia, glycosuria, osmotic diuresis, electrolyte depletion
What are 2 effects of increased protein catabolism in diabetes mellitus? How do they relate to decreased glucose uptake in diabetes mellitus?
Increased protein catabolism => Increased plasma amino acids, nitrogen los in urine; Can lead to same 4 effects as decreased glucose uptake in diabetes mellitus: hyperglycemia, glycosuria, osmotic diuresis, electrolyte depletion
What are 4 effects of increased lipolysis in diabetes mellitus?
Increased lipolysis => Increased plasma FFAs, Ketogenesis, Ketonuria, Ketonemia
What are 4 general clinical complications that may result from the pathophysiology of diabetes mellitus?
(1) Dehydration (2) Acidosis => (3) Coma (4) Death
Create a diagram demonstrating the pathophysiology and general outcomes of diabetes mellitus.
See p. 327 in First Aid 2014 for visual on left top of page
What are 2 chronic manifestations/processes of diabetes mellitus?
(1) Nonenzymatic glycosylation (2) Osmotic damage
Describe the pathophysiology and effects of nonenzymatic glomerulosclerosis as a chronic manifestation of diabetes mellitus.
(1) Small vessel disease (diffuse thickening of basement membrane) => retinopathy (hemorrhage, exudates, microaneurysms, vessel proliferation), glaucoma, nephropathy (nodular sclerosis, progressive proteinuria, chronic renal failure, ateriolosclerosis leading to hypertension) (2) Large vessel atherosclerosis, CAD, peripheral vascular occlusive disease, and gangrene => limb loss, cerebrovascular disease. MI most common cause of death.
Describe the pathophysiology and effects of osmotic damage as a chronic manifestation of diabetes mellitus.
Osmotic damage (sorbitol accumulation in organs with aldolase reductase and decreased or absent sorbitol dehydrogenase) => (1) Neuropathy (motor, sensory, and autonomic degeneration) (2) Cataracts
What is the most common cause of death in diabetes mellitus patients? What is the pathophysiology behind this?
MI most common cause of death; Nonenzymatic glycosylation => Large vessel atherosclerosis, CAD, peripheral vascular occlusive disease, and gangrene => limb loss, cerebrovascular disease. MI most common cause of death.
What are 3 clinical tests used for diabetes mellitus?
(1) Fasting serum glucose (2) Oral glucose tolerance test (3) HbA1c (reflects average blood glucose over prior 3 months)
What does HbA1c reflect?
HbA1c (reflects average blood glucose over prior 3 months)
What is the mechanism by which retinopathy occurs in diabetes mellitus? What are 2 other conditions/complications that occur this way?
Nonenzymatic glycosylation => Small vessel disease (diffuse thickening of basement membrane) => retinopathy (hemorrhage, exudates, microaneurysms, vessel proliferation), glaucoma, nephropathy (nodular sclerosis, progressive proteinuria, chronic renal failure, ateriolosclerosis leading to hypertension)
What is the mechanism by which limb loss occurs in diabetes mellitus? What are 2 other conditions/complications that occur this way?
Nonenzymatic glycosylation => Large vessel atherosclerosis, CAD, peripheral vascular occlusive disease, and gangrene => limb loss, cerebrovascular disease. MI most common cause of death.
What is the mechanism by which neuropathy occurs in diabetes mellitus? What are is another conditions/complications that occurs this way?
Osmotic damage (sorbitol accumulation in organs with aldolase reductase and decreased or absent sorbitol dehydrogenase) => (1) Neuropathy (motor, sensory, and autonomic degeneration) (2) Cataracts
What is the primary defect for Type 1 versus Type 2 DM?
TYPE 1: Autoimmune destruction of Beta cells; TYPE 2: Increased resistance to insulin, progressive pancreatic Beta-cell failure
In Type 1 versus Type 2 DM, when is insulin necessary in treatment?
TYPE 1: Always; TYPE 2: Sometimes
What is the typical age (exceptions commonly occur) associated with Type 1 versus Type 2 DM?
TYPE 1: < 30 yr; TYPE 2: > 40 yr
Is Type 1 versus Type 2 DM associated with obesity?
TYPE 1: No; TYPE 2: Yes
Describe the genetic predisposition for Type 1 versus Type 2 DM.
TYPE 1: Relatively weak (50% concordance in identical twin), polygenic; TYPE 2: Relatively strong (90% concordance in identical twins), polygenic
Is Type 1 versus Type 2 DM associated with the HLA system? If so, via what markers?
TYPE 1: Yes (HLA-DR3 and 4); TYPE 2: No
What is the level of glucose intolerance in Type 1 versus Type 2 DM?
TYPE 1: Severe; TYPE 2: Mild to moderate
What is the level of insulin sensitivity in Type 1 versus Type 2 DM?
TYPE 1: High; TYPE 2: Low
Is ketoacidosis common or rare in Type 1 versus Type 2 DM?
TYPE 1: Common; TYPE 2: Rare
What are beta-cell numbers in the islets like in Type 1 versus Type 2 DM?
TYPE 1: Low; TYPE 2: Variable (with amyloid deposits)
What is serum insulin level like in Type 1 versus Type 2 DM?
TYPE 1: Low; TYPE 2: Variable
What are the classic symptoms of diabetes mellitus? How frequent do they present in Type 1 versus Type 2 DM?
Classic symptoms of polyuria, polydipsia, polyphagia, weight loss; TYPE 1: Common; TYPE 2: Sometimes
What is a key histologic finding of Type 1 versus Type 2 DM?
TYPE 1: Islet leukocytic infiltrate; TYPE 2: Islet amyloid polypeptide (IAPP) deposits
What is the clinical relevance of diabetic ketoacidosis? With what type of DM is it usually associated?
One of the most important complications of diabetes (usually type 1)
What usually causes DKA, and what pathophysiology results?
Usually due to increased insulin requirements from stress (e.g., infection). Excess fat breakdown and increased ketogenesis from increased free fatty acids, which are then made into ketone bodies (Beta-hydroxybutarate > acetoacetate)
What are 6 signs/symptoms of diabetic ketoacidosis?
(1) Kussmaul respirations (rapid/deep breathing) (2) Nausea/vomiting (3) Abdominal pain (4) Psychosis/delirium (5) Dehydration. (6) Fruity breath odor (due to exhaled acetone)
What are 6 lab findings associated with diabetic ketoacidosis? For which of this is there a caveat, and what is that caveat?
(1) Hyperglycemia (2) High H+ (3) Low HCO3- (anion gap metabolic acidosis) (4) High blood ketone levels (5) Leukocytosis (6) Hyperkalemia, BUT depleted intracellular K+ due to transcellular shift from decreased insulin
What are 4 treatment options for diabetic ketoacidosis? Where applicable, briefly explain the use.
Treatment: IV fluids, IV insulin, and K+ (to replace intracellular stores); glucose if necessary to prevent hypoglycemia
What is an insulinoma, and what metabolic effects does it have?
Tumor of Beta cells of pancreas => overproduction of insulin => hypoglycemia
What is the name of the triad associated with Insulinoma? What are the 3 symptoms, and how do they present?
Whipple triad of episodic CNS symptoms: lethargy, syncope, and diplopia.
What are 2 key lab findings in symptomatic insulinoma patients?
Symptomatic patients have low blood glucose and high C-peptide levels (vs. exogenous insulin use)
What is the treatment for insulinoma?
Treatment: surgical resection
What 4 possible complications of DKA?
Life-threatening mucormycosis (usually caused by Rhizopus infection), cerebral edema, cardiac arrhythmias, heart failure
