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

1
Q

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?

A

Polydipsia, polyuria, polyphagia, weight loss; DKA (type 1), Hyperosmolar coma (type 2)

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2
Q

What is a rare cause of diabetes mellitus?

A

Rarely, can be caused by unopposed secretion of GH and epinephrine

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3
Q

What are the 2 key causes of pathophysiology in diabetes mellitus? What 3 consequences do they have?

A

Insulin deficiency (and glucagon excess) => Decreased glucose uptake, Increased protein catabolism, & Increased lipolysis

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4
Q

What are 4 effects of decreased glucose uptake in diabetes mellitus?

A

Decreased glucose uptake => hyperglycemia, glycosuria, osmotic diuresis, electrolyte depletion

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5
Q

What are 2 effects of increased protein catabolism in diabetes mellitus? How do they relate to decreased glucose uptake in diabetes mellitus?

A

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

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6
Q

What are 4 effects of increased lipolysis in diabetes mellitus?

A

Increased lipolysis => Increased plasma FFAs, Ketogenesis, Ketonuria, Ketonemia

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7
Q

What are 4 general clinical complications that may result from the pathophysiology of diabetes mellitus?

A

(1) Dehydration (2) Acidosis => (3) Coma (4) Death

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8
Q

Create a diagram demonstrating the pathophysiology and general outcomes of diabetes mellitus.

A

See p. 327 in First Aid 2014 for visual on left top of page

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9
Q

What are 2 chronic manifestations/processes of diabetes mellitus?

A

(1) Nonenzymatic glycosylation (2) Osmotic damage

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10
Q

Describe the pathophysiology and effects of nonenzymatic glomerulosclerosis as a chronic manifestation of diabetes mellitus.

A

(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.

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11
Q

Describe the pathophysiology and effects of osmotic damage as a chronic manifestation of diabetes mellitus.

A

Osmotic damage (sorbitol accumulation in organs with aldolase reductase and decreased or absent sorbitol dehydrogenase) => (1) Neuropathy (motor, sensory, and autonomic degeneration) (2) Cataracts

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12
Q

What is the most common cause of death in diabetes mellitus patients? What is the pathophysiology behind this?

A

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.

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13
Q

What are 3 clinical tests used for diabetes mellitus?

A

(1) Fasting serum glucose (2) Oral glucose tolerance test (3) HbA1c (reflects average blood glucose over prior 3 months)

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14
Q

What does HbA1c reflect?

A

HbA1c (reflects average blood glucose over prior 3 months)

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15
Q

What is the mechanism by which retinopathy occurs in diabetes mellitus? What are 2 other conditions/complications that occur this way?

A

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)

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16
Q

What is the mechanism by which limb loss occurs in diabetes mellitus? What are 2 other conditions/complications that occur this way?

A

Nonenzymatic glycosylation => Large vessel atherosclerosis, CAD, peripheral vascular occlusive disease, and gangrene => limb loss, cerebrovascular disease. MI most common cause of death.

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17
Q

What is the mechanism by which neuropathy occurs in diabetes mellitus? What are is another conditions/complications that occurs this way?

A

Osmotic damage (sorbitol accumulation in organs with aldolase reductase and decreased or absent sorbitol dehydrogenase) => (1) Neuropathy (motor, sensory, and autonomic degeneration) (2) Cataracts

18
Q

What is the primary defect for Type 1 versus Type 2 DM?

A

TYPE 1: Autoimmune destruction of Beta cells; TYPE 2: Increased resistance to insulin, progressive pancreatic Beta-cell failure

19
Q

In Type 1 versus Type 2 DM, when is insulin necessary in treatment?

A

TYPE 1: Always; TYPE 2: Sometimes

20
Q

What is the typical age (exceptions commonly occur) associated with Type 1 versus Type 2 DM?

A

TYPE 1: < 30 yr; TYPE 2: > 40 yr

21
Q

Is Type 1 versus Type 2 DM associated with obesity?

A

TYPE 1: No; TYPE 2: Yes

22
Q

Describe the genetic predisposition for Type 1 versus Type 2 DM.

A

TYPE 1: Relatively weak (50% concordance in identical twin), polygenic; TYPE 2: Relatively strong (90% concordance in identical twins), polygenic

23
Q

Is Type 1 versus Type 2 DM associated with the HLA system? If so, via what markers?

A

TYPE 1: Yes (HLA-DR3 and 4); TYPE 2: No

24
Q

What is the level of glucose intolerance in Type 1 versus Type 2 DM?

A

TYPE 1: Severe; TYPE 2: Mild to moderate

25
Q

What is the level of insulin sensitivity in Type 1 versus Type 2 DM?

A

TYPE 1: High; TYPE 2: Low

26
Q

Is ketoacidosis common or rare in Type 1 versus Type 2 DM?

A

TYPE 1: Common; TYPE 2: Rare

27
Q

What are beta-cell numbers in the islets like in Type 1 versus Type 2 DM?

A

TYPE 1: Low; TYPE 2: Variable (with amyloid deposits)

28
Q

What is serum insulin level like in Type 1 versus Type 2 DM?

A

TYPE 1: Low; TYPE 2: Variable

29
Q

What are the classic symptoms of diabetes mellitus? How frequent do they present in Type 1 versus Type 2 DM?

A

Classic symptoms of polyuria, polydipsia, polyphagia, weight loss; TYPE 1: Common; TYPE 2: Sometimes

30
Q

What is a key histologic finding of Type 1 versus Type 2 DM?

A

TYPE 1: Islet leukocytic infiltrate; TYPE 2: Islet amyloid polypeptide (IAPP) deposits

31
Q

What is the clinical relevance of diabetic ketoacidosis? With what type of DM is it usually associated?

A

One of the most important complications of diabetes (usually type 1)

32
Q

What usually causes DKA, and what pathophysiology results?

A

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)

33
Q

What are 6 signs/symptoms of diabetic ketoacidosis?

A

(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)

34
Q

What are 6 lab findings associated with diabetic ketoacidosis? For which of this is there a caveat, and what is that caveat?

A

(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

35
Q

What are 4 treatment options for diabetic ketoacidosis? Where applicable, briefly explain the use.

A

Treatment: IV fluids, IV insulin, and K+ (to replace intracellular stores); glucose if necessary to prevent hypoglycemia

36
Q

What is an insulinoma, and what metabolic effects does it have?

A

Tumor of Beta cells of pancreas => overproduction of insulin => hypoglycemia

37
Q

What is the name of the triad associated with Insulinoma? What are the 3 symptoms, and how do they present?

A

Whipple triad of episodic CNS symptoms: lethargy, syncope, and diplopia.

38
Q

What are 2 key lab findings in symptomatic insulinoma patients?

A

Symptomatic patients have low blood glucose and high C-peptide levels (vs. exogenous insulin use)

39
Q

What is the treatment for insulinoma?

A

Treatment: surgical resection

40
Q

What 4 possible complications of DKA?

A

Life-threatening mucormycosis (usually caused by Rhizopus infection), cerebral edema, cardiac arrhythmias, heart failure