Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Level 4 > Nurs 4000 > Flashcards

Nurs 4000 Flashcards

1
Q

What is diabetic ketoacidosis?

A

acute life threatening complication of diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is DKA characterized by?

A

Hyperglycemia, ketonemia and metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What causes DKA?

A
  1. New onset of DM1
  2. Inadequate insulin therapy
  3. Infection (UTI, pulmonary, pneumonia)
  4. Stress (CVA, ETOH abuse, pancreatitis, trauma)
  5. Drugs (steroids, thiazides, sympathomimetics)
  6. Eating disorders in young DM patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the pathogenesis of DKA?

A

Insulin increases the uptake of glucose in the cell, allowing for ATP formation. It also prevents FFA from entering cells.

W/o insulin, glucose doesn’t enter cell, and FFAs can. FFAs are broken into ketone bodies and ATP.

Ketone bodies are broken down into

  1. acetone - fruity smell
  2. acetoacetate and bHb. These are acidic (lose H+ ions)

Increase of H+ ions causes K+ to be pushed out into the blood. Leads to hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are S&S of hyperglycemia?

A
  • Polydipsia - hyperglycemia and loss of H2O dt polyuria increases osmololatiy of ECF, causing water to move from cells to ECF - causes thirst
  • polyuria - hyperg interferes with reabsorption of H2O
  • fatigue - dt dehyration and hypovolemia, muscle wasting dt protein metabolism
  • weakness -
  • vision changes - hyperg causes dilation of lense, altering focal length
  • recurrent infection
  • numbness in extremities,
  • dehydration
  • polyphagia - weight loss dt dehdration. cells cna’t uptake glucose despite eating, triggers hunger sensors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the early and late presentations of DKA?

A

Early:

  • early onset N&V
  • abdo pain
  • muscle cramps (dt hyperkalemia)

Late:

  • Fruity, sweet breath
  • Kussmaul breathing
  • hypotension
  • stupor
  • coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are normal BS for DKA? HHNS?

A

DKA: 13.9

HHNS: 33.3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is DKA treated?

A
  1. IV fluid
  2. Insulin therapy
  3. Electrolyte abnormalities (infuse K+/Na+)
  4. Tx precipitating cause
  5. Educate pt how to prevent in future
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are potential complications of DKA treatment?

A
  1. Hypoglycemia from sugars dropping too much
  2. Hypokalemia
  3. Cerebral edema - adjusting blood sugars too quickly can produce swelling in the brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is Type 1 DM?

A

AUtoimmune disease characterized by the destruction of pancreatic beta cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the difference between alpha and beta cell?

A

Alpha: produce glucagon (mobilizes sugars from body during fasting from the liver and muscles)

Beta cells: produce insulin

  1. Stimulates liver & muscle to store glucose as glycogen
  2. inhibits liver glycoglucogenesis
  3. Forms fats from FFA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are normal blood sugars?

A

4-7mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the pathogensis of Type 1 DM?

A

Autoimmune destruction of beta cells on islets of langerhands. Loss of all capacity to produce insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the etiology of Type 1 DM?

A
  1. Genetics - family members = more liekly to have
  2. environment - exposure to cow milk - molecularly similar to beta cells
  3. damage - severe pancreatitis (ETOH abuse)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the etiology of hypoglyvemia?

A
  1. too much insulin
  2. not eating enough
  3. excess excercise
  4. illness
  5. insulinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are S&S of hypoglycemia?

A
  • Confusion
  • cold, clammy skin
  • pallow
  • shakiness, lack of coordination
  • irritability
  • abdo pain/ nausea
  • headache
  • fatigue
  • blurred vision and dizziness
  • seizure
  • decrease LOC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is HHSN?

A

Hyperglycemic hyperosmolar nonketotic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is HHNS characterized by?

A
  1. hyperglycemia - >33.3 mmol
  2. Hyperoslmolality - dt polyuria. May lead to hyponatremia
  3. Dehydration - no sweating (not enough fluid to sweat) dt polyuria
  4. Minimal ketoacidosis - there is enough insulin to prevent ketoacidosis, but not enough to prevent hyperglycemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are S&S of hyponatremia?

A
  • Seizures
  • N&V
  • Muscle weakness, spasms
  • afib
  • headache
  • restlessness & irritability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are risk factors of HHNS?

A
  • >60yrs
  • Type 2 DM
  • Chronic illness
  • infection
  • stress
  • Corticosteroids, diuretics, anti seizure
21
Q

What are lab tests which can diagnose HHNS?

A

Blood sugar level

A1C gylcated hemoglobin

presence of ketons in urine

BUN and Cr to test kidney function

Na + K

22
Q

How is HHNS treated?

A
  1. IV fluids
  2. Insulin to lower blood sugars
  3. Fluid and E7 replacement
23
Q

How can HHNS be prevented?

A
  • Know the S&S of hyperglycemia
  • Follow a regular meal plan
  • Monitor blood sugars regularly
  • Take medications as ordered
  • exercise regularly
  • coping strategies for stress
24
Q

What is the clinical pathway for HHNS?

A
  1. Hyperglycemia
  2. Increased hyperosmolarity of blood
  3. Fluid shift from cells to blod
  4. Kidneys excrete Na+ to compensate
  5. Causes Na+ and fluid loss
  6. Dehydratoin occurs
  7. Results in hypovolemia
  8. Causes hypotension
  9. Activates the renin-angiotensin-aldosterone system)
  10. Oliguria and renal failure
  11. coma / death
25
Q

What is the pathophysiology of Type 2 diabetes?

A
  1. Insulin resistance
  2. Irregular secretion of insulin by beta cells
  3. Increased glucose production by liver
26
Q

What factors increase insulin resistance in type 2 diabetes?

A
  1. Genetic predisposition (family hx increases risk)
  2. Free fatty acids concentration dt obesity

FFAs inhibit glucose uptake peripherally, increase stored triglycerides, increases gluconeogenesis, reduces hepatic insulin sensitivity

  3. Adiponectin is secreted by adipocytes. Less = insulin resistance
27
Q

How does irregular secretion of insulin result in hyperglycmeia?

A
  1. Hyperglycemia (dt family hx, mild insulin resistence)
  2. Increases stimulation of beta cells
  3. Causes beta cell exhaustion from chronic elevations
  4. Causes a less efficient response to future blood glucose elevatoins
  5. Desensitization of beta cells
  6. Hyperglcemia
28
Q

What is glycogenesis vs glycogenolysis va gluconeogenesis?

A

Glycogenesis - store excess glucose as glycogen

glycogenolysis - converts stored glycogen to glucose

gluconeogenesis - break down of fats and proteins for energy

29
Q

What are risk factors of Type 2 diabetes?

A
  • Genetics
  • Race (Native, african, hispanic)
  • family hxx
  • sedentary lifestype
  • diet
  • obesity
30
Q

How is diabetes diagnosed?

A

Two of the following tests must be positive

:FPG, random PG, 2hPG, A1C

31
Q

What is the FPG? Advantages and disadvantages

A

fasting plasma glucose. > 7mmol

BG level after no caloric intake for at least 8 hrs

Educate pt re: S&S of hypoglycemia

  • Advantage: established standard. Fast and easy, reqs simple sample, predicts microvascular complicatoins
  • Disadvantage: sample not stable, varies day to day, inconvenient. only reflects at a single point of time
32
Q

What is random plasma glucose?

A

> 11mmol, blood glucose level at any time of day without regard to time since last meal

33
Q

What is 2h PG in a 75g OGTT? Advantages vs disadvantages

A

> 11.1 mmol

Blood glucose level after fasting at least 8 hrs then taking 75g of anhydrous glucose dissolved in water

measures carb metabolisms after the ingestion of a challenge dose of glucose

Educate pt S&S of hyperglycemia. Drink lots of H2O

  • Advantage: established standard, predicts microvascular complications
  • Dis: sample not stable, inconvenient, inpalatable, cost
34
Q

What is A1C? Advantages vs disadvantages?

A

Concentration of blood glucose level in a RBC span. tests the % of Hbf. average blood glucose level over 3 mos (RBC lifespan)

>6.5%

  • advntages: convenient, single smaple, predicts microvascular complications, predicts macrovascular complications, low variability, long term glucose concentration
  • Disadvantages: can be misleading in medical conditions affecting RBCs, altered by ethnicity and aging, requires standardization
35
Q

What are the most common tests used to diagnose diabetes?

A

FPG & A1C

36
Q

What are other tests that can be done to test if pt is symptomatic?

A
  1. Glycosylated albumin level
  2. connecting peptide level
  3. ketonuria
  4. proteinuria
37
Q

What categories should a diabetic patient be taught about?

A
  1. Diet
  2. Proper insulin management
  3. Importance of exercise
  4. Stress management
  5. Smoking cessation
38
Q

What is microvascular disease?

A

aka microangiopathy

Changes which occur in the retinal, renal and peripheral capillaries in DM

39
Q

What is the pathogenesis of microvascular disease? How can the body compensate?

A
  1. Increased blood sugar causes increased blood viscosity
  2. Increases BP, damages basement membrane
  3. Basement membrane thickens, making it more difficult for O2 and nutrients to diffuse across
  4. Decreased blood perfusion leads to ischemia

To compensate, the body grows new capillaries. However, the new vessels are weak and can easily ruptures

40
Q

What are the three types of chronic retinopathy?

A
  1. Non proliferative - early states. Characterized by microaneruism ( dot and blot hemorrhages). May have some vision loss
  2. Preproliferative - progression of hemorrhages and can cause vision loss
  3. Proliferative - new vessels are formed dt ruptures or leaks in old vessels
41
Q

Why does retinopathy occur?

A

Retuba consumes the most amount of O2 after the brain. When O2 is decreased, damage occurs.

42
Q

What is nephropathy? What are S&S?

A

Thickening of the basement membrane causes a decreased supply of O2 to glomeruli which can lead to renal failure

S&S:

  • Initial increase GFR dt increased viscosity
  • proteinuria in early cases (dt leakage of basement membrane)
  • arteriosclerosis = decreased urine output
43
Q

What are S&S of neuropathy?

A
  • Numbness
  • pain
  • tingling
  • pins & needles
  • impaired sensation
  • itching
44
Q

What are risk factorsfor microvascular disease?

A
  • hyperglycemia
  • age
  • smoking
  • insulin tx
  • dyslipidemia
  • HTN
  • pregnancy
  • chronic diabetes
45
Q

What is peripheral arterial disease?

A

atheriosclerosis of non cardiac vessels where demand is greater than the supply

46
Q

What is the pathophysiology of PAD?

A
  1. Peripheral arteries are occluded by plaques and tissues are slowly starved
  2. Body tries to compensate with vasodilatoin and anerobic pathways
  3. Not enough, arterial stenosis and occlusion occurs
47
Q

What are S&S of PAD?

A
  1. Intermittant claudication - (angina for legs) dt requirement of O2 being greater than supply- unsteady gait
  2. Rest pain - occurs at night, when supine. Deep dull pain of toess/ forefoot
  3. Decreased peripheral pulse
  4. Delayed wound healing - O2 and nutrients not getting to site
48
Q

How is PAD managed?

A
  1. promote arterial flow by decreasaing blood viscosity
  2. Reverse trendelenberg to promote blood flow to extremities
  3. Stop smoking (smoking = vasoconstriction)
  4. Control comorbid disease (HTN, obesisty, lipid)
  5. Control diabetes
  6. ExerciseP
  7. prevent foot injury
49
Q
A

Level 4 (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions