Exam 3- DKA, HHS, Shock

Question 1

What is Diabetic Keto Acidosis?

Answer 1

A metabolic disorder that occurs suddenly, most often seen in type 1 diabetes and younger (newly diagnosed patients). It is caused by an absence or inadequate amount of insulin.

Question 2

What are the three main clinical features of Diabetic Keto Acidosis?

Answer 2

1. Hyperglycemia
2. Dehydration and electrolyte loss
3. Acidosis and ketones

Question 3

What happens to glucose without insulin?

Answer 3

Glucose is unable to enter the cells, leading to increased gluconeogenesis, which causes hyperglycemia.

Question 4

What is the effect of insulin deficiency on the kidneys?

Answer 4

The kidneys will excrete glucose along with electrolytes and water, leading to water and electrolyte loss.

Question 5

What is lipolysis?

Answer 5

The breakdown of fat into free fatty acids and glycerol, which leads to the production of ketone bodies (which is an acid) the accumulation of ketones leads to metabolic acidosis.

Question 6

What are long-term complications of Diabetic Keto Acidosis?

Answer 6

Microvascular / Macrovascular complications, and neuropathies.

Question 7

What are the causes of Diabetic Keto Acidosis?

Answer 7

1. Decreased or missed insulin
2. Illness or infection
3. Undiagnosed and untreated diabetes

Question 8

What are some clinical manifestations of Diabetic Keto Acidosis?

Answer 8

Polyuria, polydipsia, marked fatigue, blurred vision, weakness, headache, frank hypotension, acetone breath (fruity odor), hyperventilation (Kussmaul respirations), MS changes, abdominal pain.

Question 9

What is the typical blood sugar level in DKA?

Answer 9

BS typically >300 (severity of DKA is not necessarily related to blood glucose levels)

Question 10

What are the bicarbonate and pH levels in ketoacidosis?

Answer 10

Ketoacidosis (bicarbonate 0-15), low pH, and low carbon dioxide (PaCO2 10-30)

Question 11

What are some diagnostic findings in DKA?

Answer 11

Ketones in urine, increased BUN, creatinine, and hyperkalemia

Question 12

What is the treatment for DKA?

Answer 12

Insulin is infused at a slow continuous rate (regular insulin) until bicarbonate level is at least 15-18 and patient can eat.

Question 13

How often are blood sugar levels taken during DKA treatment?

Answer 13

Hourly BS levels are taken.

Question 14

What should be done when blood sugar levels reach 250-300?

Answer 14

IV fluid with concentrations of glucose are given to avoid rapid drop in BS.

Question 15

What should patients do during illnesses to manage blood glucose?

Answer 15

Keep their insulin dosage the same and consume frequent small portions of carbohydrates to avoid hyperglycemia and DKA. They should also hydrate as much as they can, and if they cannot rink water without vomiting or if elevated glucose levels persist then the provider must be contacted.

Question 16

What is the guideline for sick days regarding insulin?

Answer 16

• Take insulin as usual
• Test BS and urine ketones every 3-4 hours
• Take supplemental doses of regular insulin every 3-4 hours if needed
• Take liquids every 1 hour to prevent dehydration
• Report elevated glucose levels or urine ketones
• Report N/V and diarrhea to your provider

Question 17

What should be done if elevated glucose levels or urine ketones are reported?

Answer 17

Report to your provider.

Question 18

What is Hyperglycemic Hyperosmolar Nonketotic Syndrome?

Answer 18

A metabolic disorder that gradually occurs, most often of type 2 diabetes resulting from a relative insulin deficiency initiated by an illness or medications that raise the demand for insulin (thiazides).

Question 19

What are the diagnostic findings of HHS (Hyperglycemic Hyperosmolar Nonketotic Syndrome)?

Answer 19

Assessments and Diagnostic findings
- Blood glucose >600 (Heavy-duty Hyperglycemia)
- Osmolality exceeds 320 (super high)
- No ketoacidosis
- Electrolyte imbalances
- High BUN and Creatine
- MS changes (possible hallucinations)

Question 20

What are some causes of Hyperglycemic Hyperosmolar Nonketotic Syndrome?

Answer 20

Cells not receptive to insulin, severe infection or illness, medications such as thiazides, and dialysis.

Question 21

What are clinical manifestations of HHS?

Answer 21

Hypotension, profound dehydration, tachycardia, alterations in consciousness, seizures, hemiparesis.

Question 22

Medics Management for HHS

Answer 22

• FLUID REPLACEMENT
• Insulin (not as important as it is in DKA)
• Correction of electrolyte imbalances
• Glucose concentrated fluid once BS gets down to 250-300 to prevent hypoglycemia
• Treatment will continue well after metabolic abnormalities have resolved

Question 23

What are the long-term complications of diabetes?

Answer 23

Micro/macrovascular complications and neuropathy

Question 24

What risk factors contribute to diabetic complications?

Answer 24

Hyperglycemia and hypertension

Question 25

Which type of diabetes is more prevalent with microvascular complications?

Answer 25

Type one diabetes

Question 26

What areas of the body are affected by microvascular complications?

Answer 26

Eyes, Kidneys, and Nerves

Question 27

What is diabetic retinopathy?

Answer 27

Damage to the small blood vessels that nourish the retina

Question 28

What are the three stages of diabetic retinopathy?

Answer 28

1. Background, 2. Preproliferative, 3. Proliferative

Question 29

What occurs in the background stage of diabetic retinopathy?

Answer 29

Asymptomatic stage with micro aneurysms that leak fluid causing swelling and deposits. Macular edema that can in some cases distort vision.

Question 30

What happens in the proliferative stage of diabetic retinopathy?

Answer 30

Abnormal growth of new blood vessels on the retina that can rupture. New vessels rupture bleeding into the vitreous blocking vision and causing formation of scar tissue that can eventually cause detachment of retina

Question 31

What are symptoms of hemorrhaging in diabetic retinopathy?

Answer 31

Floaters/cobwebs in visual field, sudden visual changes including spotty or hazy vision or complete loss of vision.

Question 32

What is the leading cause of blindness among people aged 20-74?

Answer 32

Diabetic retinopathy Almost all people with diabetes have some form of diabetic retinopathy after age 20

Question 33

What is Argon Laser Photocoagulation?

Answer 33

Tx used for advanced retinopathy, it is a laser treatment that destroys leaky blood vessels for pts at increased risk of hemorrhage

Question 34

What is panretinal photocoagulation?

Answer 34

more than 1000 laser burns throughout the retina (not macular region) to stop the widespread growth of new vessels and hemorrhaging of damaged vessels.

Question 35

What is vitrectomy used for?

Answer 35

Performed for patients who already have vision loss

Question 36

After retinopathy procedures….

Answer 36

activities can resume the next day, avoid weight bearing and bearing down, Tx does not cause intense pain (may have headache), anesthetic eye drop is all that is needed during the procedure Out pt procedure

Question 37

What is nephropathy?

Answer 37

Nephropathy is a condition where hyperglycemia causes overwork of the kidneys, allowing blood proteins to leak into the urine, thus increasing pressure in the blood vessels of the kidneys.

Question 38

What are the clinical manifestations of nephropathy?

Answer 38

Symptoms of kidney failure along with frequent hypoglycemic episodes.

Question 39

What assessments and diagnostics are used for nephropathy?

Answer 39

Albumin in the urine should be tested annually for microalbuminuria. If greater than 30mg/24hr on two consecutive tests, a 24 hr urine sample should be obtained and tested. Kidney function tests are also performed (such as creatine and BUN) Cardiac tests to assess for complications

Question 40

What is the medical management for nephropathy?

Answer 40

Control hypertension (ACE inhibitors, ARBs), prevention and treatment of UTIs, avoidance of nephrotoxic drugs, adjust medications as kidney function changes, low sodium and low protein diet, and treatment for kidney failure. ACE inhibitors and ARBs also help to reduce microalbuminuria CPAAL

Question 41

What is peripheral neuropathy?

Answer 41

Peripheral neuropathy occurs when high glucose damages the nerves, causing pain and sensation loss (paresthesia) and a burning sensation at night. May develop Charcot joints along with a decrease in deep tendon reflexes and vibratory sensations

Question 42

What are the medical management options for peripheral neuropathy? (Include pharm therapy)

Answer 42

Insulin therapy to delay onset or slow progression, and Tx of pain with analgesics, tricyclic antidepressants, or duloxetine. Anticonvulsants (pregabalin or gabapentin) Mexiletine (anti arrhythmic agent) Transcutaneous electrical nerve stimulation.

Question 43

What is autonomic neuropathy?

Answer 43

hypoglycemic unawareness, sudomotor neuropathy (no longer sweating), dryness of the feet increases thus increasing the risk for foot injuries, sexual dysfunction, and delayed gastric emptying. Management is to alleviate symptoms.

Question 44

What are macrovascular complications of diabetes?

Answer 44

Macrovascular complications involve large blood vessels and are more prevalent with type two diabetes, leading to CAD, CVD, PVD, heart attacks, and strokes.

Question 45

What is the risk of myocardial infarction (MI) in diabetics?

Answer 45

MI is twice as common in men with diabetes and three times as likely in women with diabetes compared to those without diabetes.

Question 46

What are the signs of peripheral vascular disease (PVD) in diabetics?

Answer 46

Signs include diminished peripheral pulses and intermittent claudication (pain) of the butt, thigh, or calf during walking.

Question 47

What are the stages of shock?

Answer 47

The stages of shock include 1. Initial/Compensatory 2. Progressive and 3. Refractory.

Question 48

What happens during the initial/compensatory stage of shock?

Answer 48

The cell switches from aerobic to anaerobic metabolism, forming lactic acid due to low cardiac output. The body attempts to correct low BP and cardiac output through biochemical and hormonal responses, leading to increased BP and cardiac output. This stage is reversible, we want to keep the body from going into the third stage of shock

Question 49

What are the signs and symptoms of progressive shock?

Answer 49

Signs include MAP <60 confusion agitation decreased urine output increased BUN and creatinine. pale, cool, and clammy skin weak rapid pulse hypotension

Question 50

What characterizes the refractory stage of shock?

Answer 50

The refractory stage is unmanageable and results in the shutdown of all organs, leading to death.

Question 51

What is the treatment for shock?

Answer 51

Treatment includes addressing the underlying condition, administering IV fluids, blood products, vasopressors, and monitoring vital signs.

Question 52

What are foot and leg problems in diabetics caused by?

Answer 52

Foot and leg problems are caused by neuropathy, peripheral vascular disease, and decreased ability to fight off infections.

Question 53

What is the sequence of events leading to foot problems in diabetics?

Answer 53

1. Soft tissue injury, 2. Formation of callus or fissure, 3. Injury goes unnoticed, 4. Serious infection develops.

Question 54

What is the recommended treatment for diabetic foot problems?

Answer 54

Keep the patient off feet, administer antibiotics, control glucose levels, and encourage daily foot examinations.

Question 55

Preproliferative stage of Diabetic Retinopathy

Answer 55

increases destruction of retinal blood vessels

Question 56

Medical management of Macrovascular complications

Answer 56

- Exercise, nutrition therapy, control of BS - Medications to control hyperlipidemia and hypertension

Question 57

What happens during progressive shock

Answer 57

body systems are failing; body can no longer compensate. Progressing to multiple organ system failure. Complete drop in CO. Cells start to experience hypoxic injury= which increases capillary permeability. Fluids and proteins leave the cells causing loss of BV and massive edema.