Diabetes 3 Flashcards

1
Q

This is particularly true in obese patients, whose diabetes may be detected only after

A

Glycosuria or hyperglycemia is noted during routine laboratory studies.

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2
Q

Occasionally, type 2 patients may present with evidence of

A

neuropathic or cardiovascular complications because of occult disease present for some time prior to diagnosis.

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3
Q

Generalized pruritus and symptoms of vaginitis are frequently the initial complaints of women.

A

chronic skin conditions

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4
Q

Diabetes should be suspected in women with

A

chronic
Candida vulvovaginitis

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5
Q

may have any variety of fat distribution; however, diabetes seems to be more often associated in both men and women with localization of fat deposits on the upper segment of the body (particularly the abdomen, chest, neck, and face) and relatively less fat on the appendages, which may be quite muscular.

A

Obese diabetics

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6
Q

is often present in obese diabetics

A

mild hypertension

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7
Q

on the flexor surface of the limbs and on the buttocks and Lipemia retinalis due to hyperchylomicronemia can occur in patients with uncontrolled type 2 diabetes who also have a familial form of hypertriglyceridemia.

A

Eruptive xanthomas

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8
Q

Acute Complications of DM

A

Diabetic ketoacidosis
• Hyperosmolar non ketotic coma o Lactic acidosis
• Hypoglycemia

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9
Q

a state of inadequate insulin levels resulting in high blood sugar and accumulation of organic acids and ketones in the blood.
• It is a potentially life-threatening complication in patients with diabetes mellitus.
• It happens predominantly in type 1 diabetes mellitus, but it can also occur in type 2 diabetes mellitus under certain circumstances.

A

DTK

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10
Q

Diabetic ketoacidosis may occur in those previously known to have diabetes mellitus type 2 or in those who on further investigations turn out to have features of type 2 diabetes (e.g. obesity, strong family history);
• This is more common in African, African-American and Hispanic people.

A

“ketosis-prone type 2 diabetes”

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11
Q

DKA results from relative or absolute insulin deficiency combined with counter regulatory hormone excess

A

(Glucagon, Catecholamines, cortisol, and growth hormone).

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12
Q

The decreased ratio of insulin to Glucagon promotes

A

Gluconeogenesis, glycogenolysis, and Ketone body formation in the liver, as well as increases in substrate delivery from fat and muscle (free fatty acids, amino acids) to the liver.

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13
Q

This enzyme is crucial for regulating fatty acid transport into the mitochondria, where beta oxidation and conversion to ketone bodies occur.

A

enzyme carnitine palmitoyl Transferase I.

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14
Q

DKA- Clinical manifestations

A

Nausea and vomiting
• Pronounced thirst
• Excessive urine production and abdominal pain that may be severe.
for the acidosis, he blood carbon
• Hyperglycemia is always present.
•In severe DKA, breathing becomes labored and of a deep, gasping character (a state referred to as “Kussmaul respiration”

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15
Q

is present, this is reflected in an increased respiratory rate.

A

Kussmaul respiration

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16
Q

• If the dehydration is profound enough to cause a decrease in the circulating blood volume,

A

tachycardia (a fast heart rate and low blood pressure may be observed.

17
Q

is usually performed to demonstrate the acidosis

A

Arterial blood gas measurement

18
Q

(measures of kidney function, which may be impaired in DKA as a result of dehydration) and electrolytes.

A

Urea and creatinine estimations

19
Q

confusion, recurrent vomiting or other symptoms, computed tomography may be performed to assess its severity and to exclude other causes such as stroke.

A

• If cerebral edema

20
Q

The amount of fluid depends on the estimated degree of dehydration

A

fluid dehydration

21
Q

administration of fluids is slowed; intravenous Mannitol and hypertonic saline (3%) are used

A

• Cerebral edema-

22
Q

is administered to rapidly improve the acid levels in the blood.

A

• Sodium bicarbonate solution

23
Q

occurs in hypoxic individuals and is due to an excessive production of lactate by peripheral tissues.

A

lactic acidosis

24
Q

caused by excess insulin is the most common complication of insulin therapy, occurring in more than 90% of the patients.
• In normal individuals, hypoglycemia triggers a compensatory secretion of counter regulatory hormones, most notably glucagon and epinephrine, which promote hepatic production of glucose.
However patients with type 1 diabetes also develop a deficiency of glucagon secretion.

A

hypoglycemia

25
Chronic complications can be divided into
vascular and nonvascular complications.
26
The vascular complications of DM are further subdivided into
microvascular and macrovascular
27
Microvascular complications include-
Retinopathy • Neuropathy, and • Nephropathy
28
include -Gastroparesis, infections, and skin changes. Long-standing diabetes may be associated with hearing loss.
nonvascular complications
29
increases glucose metabolism via the Sorbitol pathway. olncreased sorbitol concentration alters redox potential, increases cellular osmolality, generates reactive oxygen species, and likely leads to other types of cellular dysfunction.
hyperglycemia
30
Diabetic retinopathy is classified into two stages:
nonproliferative and proliferative.
31
approximately 6% of persons with diabetes. • It is responsive to the usual therapy for open-angle disease.
Glaucoma
32
The earliest detectable change in the course of diabetic nephropathy is a thickening in the
glomerulus.
33
its effects produce the large vessel diseases.
Atherosclerosis