Dysfunctions Of The Parathyroid & Pancreas: Ch. 21 Mccance

Front 1

Hyperparathyroidism may be primary, secondary, or tertiary and is characterized by

Back 1

greater than normal secretion of PTH.

Front 2

Primary hyperparathyroidism is usually caused by a

Back 2

parathyroid adenoma, with interruption of the normal mechanisms that regulate calcium and PTH levels.

Front 3

Manifestations include

Back 3

chronic hypercalcemia, increased bone resorption, and hypercalciuria.

Front 4

Secondary hyperparathyroidism is a compensatory response to

Back 4

hypocalcemia and often occurs with chronic renal failure or chronic vitamin D deficiency.

Front 5

Tertiary hyperparathyroidism is

Back 5

excessive secretion of PTH and hypercalcemia that occurs after long-standing second¬ary hyperparathyroidism.

Front 6

pseudohypoparathyroidism,

Back 6

it is an inherited condition where there is resistance to PTH action

Front 7

familial hypocalciuric hypercalcemia mimics

Back 7

hyperparathyroidism, with failure of calcium sensing by the parathyroid gland.

Front 8

Hypoparathyroidism, defined by abnormally low PTH lev¬els, is caused by

Back 8

thyroid surgery, autoimmunity, or genetic mechanisms.

Front 9

The lack of circulating PTH in hypoparathyroidism causes

Back 9

depressed serum calcium levels, increased serum phos¬phate levels, decreased bone resorption, and eventual hypocalciuria.

Front 10

Diabetes mellitus is a group of diseases characterized by hyperglycemia resulting from defects in

Back 10

insulin secretion, insulin action, or both.

Front 11

A diagnosis of diabetes mellitus is based on

Back 11

glycosylated hemoglobin (HbA1c) levels, fasting plasma glucose (FPG) levels, and 2-hour plasma glucose levels during oral glucose tolerance testing (OGTT).

Front 12

Type 1 diabetes mellitus includes what types?

Back 12

autoimmune (most common) and a nonimmune type.

Front 13

The immune type (type 1A) is associated with genetic susceptibility, environmental factors, and

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autoantibody, T-cell, and macrophage destruc¬tion of pancreatic beta cells with loss of insulin production and a relative excess of glucagon.

Front 14

Antibodies also can be formed against

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glutamic acid decarboxylase and insulin. Nonimmune type diabetes (type 1B) occurs secondary to other disease.

Front 15

A diagnosis of diabetes mellitus is based on

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elevated plasma glucose concentrations and classic signs and symptoms.

Front 16

Type 2 diabetes mellitus is caused by

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genetic susceptibility triggered by environmental factors.

Front 17

The most compelling environmental risk factor is

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obesity.

Front 18

Insulin production continues but the weight and number of

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beta cells decrease.

Front 19

Several mechanisms of insulin resistance (hyperinsulinemia) cause

Back 19

reduced glucose uptake and metabolism in type 2 diabetes.

Front 20

These mechanisms include alteration in the production of adipokines by adipose tissue, also known as

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(leptin resistance),

Front 21

These mechanisms include elevated levels of 1 and 2, release of 3 from adipose tissue, reduced insulin-stimulated 4 activity, and 5-associated insulin resistance.

Back 21

1 serum free fatty acids, 2 intracellular lipid deposits, 3 inflammatory cytokines, 4 mitochondrial, 5 obesity

Front 22

In type 2 diabetes, what deficiency results in increased glucagon secretion and hyperglycemia?

Back 22

Amylin

Front 23

Deposition of amyloid in the pancreas contributes to

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beta cell loss.

Front 24

Decreased ghrelin levels have been associated with what two things in type 2 diabetes?

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insulin resistance and hyperleptinemia

Front 25

MODY is associated with

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autosomal dominant gene mutations,

Front 26

gestational diabetes is associated with

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onset of glucose intolerance during pregnancy.

Front 27

Acute complications of diabetes mellitus include

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hypogly¬cemia, DKA, HHNKS, the Somogyi effect, and the dawn phenomenon.

Front 28

Hypoglycemia is a lowered blood glucose level that may be related to

Back 28

exogenous (e.g., insulin shock or insulin reac¬tion), endogenous, or functional causes.

Front 29

adrenergic symptoms of hypoglycemia are caused by

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activation of the sympathetic nervous system

Front 30

neuroglycopenic symptoms reflect

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defective central nervous system metabolism resulting from impaired energy generation.

Front 31

DKA develops when there is an absolute or relative deficiency of what and an increase in the amounts of what?

Back 31

Insulin and insulin counterregulatory hormones of catecholamines, cortisol, glucagon, and GH, increased lipolysis, and accelerated gluconeogenesis and ketogenesis.

Front 32

It is most common in

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type 1 diabetes, but also occurs in type 2.

Front 33

HHNKS is pathophysiologically similar to DKA, although levels of what are lower in HHNKS and lack of what indicates that some level of insulin is present.

Back 33

FFAs, ketosis The hyperosmolar state can cause osmotic diuresis and profound dehydration, causing coma.

Front 34

The Somogyi effect is a combination of

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hypoglycemia with rebound hyperglycemia caused by the effects of counterregulatory hormones.

Front 35

It is most common in persons with

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type 1 diabetes mellitus and in children.

Front 36

The dawn phenomenon is an early morning rise in glucose levels caused by

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nocturnal elevations of GH concentration.

Front 37

Chronic complications of diabetes mellitus are related to chronic hyperglycemia and include

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microvascular disease (e.g., retinopathy, nephropathy, and neuropathy), macrovascular disease (e.g., CAD, stroke, and peripheral vascular disease), and infection.

Front 38

Metabolic changes contributing to complications include

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oxidative stress, shunting of glucose to the polyol pathway, activation of protein kinase C, formation of AGEs, and accumulation of hexosamines.

Front 39

Microvascular complications are associated with vascular alterations in the

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endothelium and the basement membrane, as well as thrombosis.

Front 40

Diabetic retinopathy is caused by several mechanisms, including microvascular changes and thrombosis that lead to

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microvascular occlusion, retinal ischemia, increased vascular permeability, microaneurysm formation, hemorrhages, and neovascularization, with loss of vision.

Front 41

Diabetic nephropathy is related to hyperglycemia, hyperperfusion, oxidative stress, and inflammation with glomerular enlargement and glomerular basement membrane thicken¬ing,

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diffuse intercapillary glomerulosclerosis, expansion of the mesangial matrix, and progressive renal failure.

Front 42

Diabetic neuropathies may be caused by vascular and metabolic mechanisms or by a combination of both, with

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axonal and Schwann cell degeneration, abnormalities in sensory and motor nerve conduction velocity, and involvement of the autonomic nervous system.

Front 43

Macrovascular disease associated with diabetes mellitus is associated with

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hyperglycemia, hyperlipidemia, inflammation, and altered endothelial function.

Front 44

CAD and stroke in diabetes are a consequence of

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accelerated atherosclerosis, hypertension, and increased risk for thrombus formation.

Front 45

Peripheral vascular disease is a consequence of neuropathy and occlusion of large and small arteries with an increased risk of

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ischemia, necrosis, and amputation.

Front 46

Individuals with diabetes are at risk for a variety of infections related to sensory impairment, vascular complications, rapid proliferation of pathogens, delayed wound healing and

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impaired white blood cells and suppressed immunity