Test + Quiz 1 Flashcards

1
Q

What is pathophysiology

A

The study of functional or physiologic changes in the body that result from disease processes

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2
Q

In what form is glucose stored when not required by the body? where is it stored?

A

Glycogen, polysaccharide glucose molecule in liver and skeletal muscle

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3
Q

What is the term for breaking down stored glucose to make it available for use

A

glycogenolysis

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4
Q

What is the process of making new glucose from fats and proteins called

A

gluconeogenasis

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5
Q

List three functions of insulin

A

Promotes glucose uptake and use by cells. Promotes storage of excess glucose as glycogen in liver. promotes storage of fat. increases protein synthesis.

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6
Q

Name three hormones that oppose the action of insulin

A

epinephrine(raises glucose when its needed during exercise) Growth hormone (when growing) Glucocorticoids (prolonged stress)

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7
Q

Describe Type 1 diabetes

A

Childhood onset. acute onset. autoimmune destruction genetics. low weight and lose weight. low to none plasma insulin levels. treatment is to give insulin

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8
Q

Describe Type 2 diabetes

A

40 age plus onset. slow insidious. etiology= lifestyle, environment, diet, exercise, genetics. higher then normal body weight. Low to normal plasma insulin levels. Treatment is lifestyle changes and occasional medication.

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9
Q

Describe Hypoglycemia?

A

onset is sudden. Blood glucose levels are below 4 mmol/L. Fatigue, weakness, slurred words headache, loss of conciseness. breathing normal to rapid shallow.. hunger and nausea. skin is pale, moist and cool. Tachycardia.

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10
Q

Describe hyperglycemia?

A

onset is gradual(hours or days). BG levels above 11. drowsiness and dim vision. breaths are deep and rapid with the smell of acidosis. Thirst, nausea, vomiting, loss of appetite, increased urination. dry, flushed and warm skin. Tachycardia and week.

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11
Q

What is the normal fasting serum glucose level?

A

more then 4 mmol/L and less then 7 mmol/L

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12
Q

Name 4 test results that would allow for diagnosis of diabetes?

A
  1. Fasting Plasma Glucose (FPG)- 8 hour fast
  2. Random plasma Glucose(RPG)- no fast
  3. Oral Glucose tolerance test (OGTT)- pregnancy
  4. Glycosylated Hemoglobin test (HgbAIC) one shot testing to see how much glucose is bonded to red blood cells.
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13
Q

clients only need to meet 3 but list 5 criteria for a diagnosis of metabolic syndrome

A
  1. abdominal obesity
  2. elevated theyrocids. LDL
  3. hypertension
  4. Low HDL’s (high density lipoprotein, cholesterol)
  5. FBG 5.7- 7.0 mmol/L
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14
Q

58 year old makes insulin int he pancreas but he cells are resistant to its effect. Type 1 or type 2?

A

Type 2

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15
Q

What is the only treatment for type 1 diabetes?

A

insulin

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16
Q

Discuss the reason that clients with diabetes have increased urine outputs

A

Causes diabetic diuresis, when glucose levels are so high that the glucose is exerted int he urine followed by the water content passively.

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17
Q

Define the three polys

A

Polyuria- frequent urination
polydipsia- excessive thirst
polyphagia- excessive hunger

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18
Q

the term that describes the water loss from the kidneys that occurs in diabetes

A

osmotic

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19
Q

how does stress or illness effect diabetes?

A

stress aggravates diabetes, raises blood sugar levels, activates fat cells, increases insulin resistance.

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20
Q

Explain DKA

A

Diabetic ketoacidosis. insulin deficiency leads to inhibition of transfer of glucose into cells. glucose levels are high. affects type 1 diabetes. breakdown of fats. sudden onset. ketones present. Blood pH above 7.3. osmolatrity above 350nmOsmol/L as it increases with dehydration. acidosis is present.

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21
Q

Explain HHNK

A

hyperosmolar hyperglycaemic state. Type two diabetes usually older patients. slow insidious onset. glucose levels are extremely high. no ketone production and no break down of fats. pH is normal. higher rate of mortality.

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22
Q

List 3 treatment interventions for DKA

A

Restore circulatory volume.
Decrease serum glucose levels
correct acidosis
restore electrolytes to normal

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23
Q

List 3 treatment interventions for HHNK

A

Fluid restoration
Correct electrolyte imbalance
Admin of insulin IV

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24
Q

Macroangiopathy

A

obstruction Arteries and arterioles (atherosclerosis) Manifestations incluse CVA, PVD, MI and diabetic ulcers.

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25
Q

Retinopathy (micro)

A

Pathological changes occur in the capillaries of the retina. Vision loss develops 10 years after onset of diabetes.

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26
Q

Nephropathy (micro)

A

chronic renal failure of the kidneys. Impaired filtration of blood during urine formation. Kidney failure, 10-15 years after onset for complications to start to appear.

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27
Q

Sensory neuropathy

A

effects both myelinated and non-myelinated nerves. ability to feel strange sensations. feet and hands most effected. Infection falls and injury.

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28
Q

Automatic Neuropathy

A

effects automatic nerve systems. Automatic functions such as heart rate, blood pressure, bowel, bladder and digestion functions.

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29
Q

Explain why diabetic clients are predisposed to infection and poor wound healing

A

Limbs don’t get enough blood flow plus lack of sensation therefor patients don’t feel when they hurt themselves. Lack of blood flow= slower healing rate and microorganisms thrive in high glucose levels.

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30
Q

atherosclerosis

A

Narrowing of large arteries by cholesterol plaque and thrombosis

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31
Q

paresthesia

A

Abnormal sensation of the skin with no apparent physical cause

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32
Q

hyperesthesia

A

when a non-painful stimulus causes the sensation of pain in the area

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33
Q

gastroparesis

A

in which the stomach can not empty its food in a normal fashion

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34
Q

describe Metiformin (glucophage)

A

First line of defense for persons diagnosed with type 2 diabetes. reduces hepatic glucose production and increases insulin sensitivity. no risks. decreases risk of cardio problems. some minor GI symptoms. No alcohol and not to be used during a die test.

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35
Q

why can antihyperglycemic agents not be used in type 1 diabetes?

A

For those agents to work the patients would need to produce some insulin and type 1 patients don’t produce any.

36
Q

which class of diabetic medication is injectable

A

incretin mimetics (G1p1 agonist)

37
Q

which class of medication carries a risk of MI and CVA

A

Thiazolidinediones

38
Q

explain Rapid-acting analogues

A

Apidra, nono-rapid, humalog. onset 10-15 min. peak 1-2 hours. duration 3-5 hours.

39
Q

explain short-acting insulin

A

Humalin R, Toronto. onset 30 min. peak 2-3 hours. duration is 6.5 hours.

40
Q

explain intermediate- acting insulin

A

Humalin N, NPH. 1-3 hours. peak 5-8 hours. duration up to 18 hours.

41
Q

Explain long-acting analogues

A

Lantus, Levemir, tresiba. onset is 90 min. unknown peak and duration up to 24/48 hours.

42
Q

List three actions of insulin

A

Lowers glucose in blood
enhances protein synthesis
promotes lipid synthesis

43
Q

why is it important to rotate insulin injection sites?

A

Lipo-distrophy, adipose tissue starts to break down

44
Q

how long can a open vial of insulin be stored at room temp?

A

30 days

45
Q

what is the most common side effect of insulin?

A

Hypoglycemia

46
Q

After injection of insulin, when is the greatest risk of hypoglycemia?

A

most often occurs when insulin is at it’s peak

47
Q

List 4 common triggers of hypoglycemia in insulin users

A
  1. client doesn’t ingest enough food
  2. drastic increase in physical activity
  3. to much insulin is given in relation to available glucose
  4. greater then the order dose is given
48
Q

How do bacteria develop resistance to antibiotics?

A

They share DNA to other bacteria and develop mutations and pass resistance to future generations

49
Q

What is the connection between C-diff and antibiotic use?

A

Antibiotic may destroy normal flora allowing c-diff to grow.

50
Q

What is the name for a secondary infection that develops due to the killing of microflora by antibiotics?

A

super-infections

51
Q

List signs and symptoms to watch for when monitoring for super infections

A

Prolonged fever or symptoms lasting more then 10-14 days

52
Q

What is MRSA?

A

Methicillin resistant staphylococcus Aureus. Transmitted via physical contact with object that has effected body fluid on it. causes staph infection. persons that are colonized but not infected do not require treatment

53
Q

What is VRE?

A

vancomycin- resistant enterococci. Physical contact with infected body fluids. Causes a entercoccal infection.

54
Q

what is Reyes Syndrome

A

a life threatening metabolic disorder of uncertain cause, but sometimes precipitated by aspirin involving encephalitis and liver failure. don not give aspirin to a child with a virus.

55
Q

list the meds which increase the risk of bleeding when taken with anticoagulant meds.

A

Aspirin and ibuprofen

56
Q

What are the advantages and risks of using selective COX 2 inhibitors instead of general NSAIDs

A

Risks: mI, CVA
Adv: reduce risk of GI problems and bleeding. Block COX 2 with minimal effect on COX 1

57
Q

List 10 manifestations of Cushing’s syndrome which may occur with glucocorticoid use.

A

mood swings, insomnia, loss of libido, clavical fat pud, buffalo hump, loss of muscles in extremities, gain fat in abdomen, thin and fragile skin, thinning hair, moon face and impaired wound healing.

58
Q

Why should glucocorticoid meds not be discontinued abruptly but rather tapered slowly?

A

abrupt withdrawal can result in acute lack of adrenal function

59
Q

Ideal time for collection of c and s specimens.

A

Prior to the administration of antibiotic therapy

60
Q

methods of monitoring effectiveness of therapy

A

white blood cells should be decreased. symptoms decreasing. fever lowering

61
Q

manifestations of antibiotic allergy

A

patchy rash(hives) itchy. Anaphylactic shock

62
Q

How do prostaglandins effect inflammation, pain and fever

A

they cause vasodialation, pain, capillary permeability.

63
Q

what is the max dose for acetaminophen for a 24 hour time period?

A

4000 mg per day

64
Q

signs and symptoms of acetaminophen over dose?

A

tinnitus acid base and electrolyte disturbance. hyperthermia, dehydration, vertigo, headache, confusion, vomiting, diarrhea, hyperventilation

65
Q

Describe acetaminophen

A

Tylenol. for pain or fever. can not use if you have liver issues. side effects include, anemia, HTN, Jaundice, GI pain and ademia. produces analgesia, inhibits prostiglandon that subdues pain receptors.

66
Q

Describe aspirin

A

Mainly for heart-attacks.inhibits prostiglandon and subdue pain receptors. cant use with hepatic impairment. Helps inflammation, pain, fever, acute MI and reduces risk of TIA.

67
Q

describe ibuprofen

A

Advil, Motrin. Pain for migraines and arthritis. do not use if you have angeodemia (swelling of the heart). anti-inflammatory, analgesia components and inhibits prostigladon.

68
Q

List and describe the four stages of fever

A
  1. Prodromal: nonspecific symptoms
    2: chill stage: shivering
  2. plateau: skin warm and flushed Pt too hot
    4: defervescence: sweating. fever breaks body temp returns to normal
69
Q

describe neutrophils

A

predominant phagocyte in early inflammation. they arrive first, short lived. remove debris and become pus

70
Q

describe macrophages

A

begin as monocytes (immature macrophages) arrive later. live longer and able to divide and reproduce. able to fuse into larger cells to capture big targets

71
Q

degranulation

A

the process of releasing pre-formed granules

72
Q

chemotaxis

A

components of inflammation are attracted to the site of injury

73
Q

margination

A

sticking of phagocytes to a vessel wall

74
Q

diapedesis

A

emigration of a phagocyte through a vessel wall

75
Q

migration

A

movement of a phagocyte to the site of injury

76
Q

describe the complement system

A

cell lysis- cells punching holes in bacteria

77
Q

describe the coagulation cascade

A

clotting system formation of a fibrin clot

78
Q

describe the kinin system

A

vasodialation vascular perm-ability and pain

79
Q

order the seven stages in the acute inflammatory response

A
  1. tissue injury
  2. transient vasoconstriction
  3. histamine release
  4. vasodilation
  5. diapesis
  6. neutrophils
  7. macrophages
80
Q

6 factors for the development of pressure injuries

A

mechanical load, immobility, inadequate nutrition, incontinence, advanced age, excessive body heat

81
Q

difference between arterial ulcer and venous ulcer

A

arterial- when blood cant get to leg, distal leg and foot, shiny skin, pain when walking
venous- when blood cant get pumped back, shallow and moist, lower third of leg, edema of the leg. pain decreased when leg is elevated

82
Q

which wound reconstruction step helps give strength to a wound

A

collagen deposition

83
Q

describe modes of wound healing

A

primary intention- limited scars like surgery
secondary intention- wound that became complicated and needs longer healing time
tertiary intention- large tissue loss

84
Q

Angiogenesis

A

angiogenic capillary sprouts invade fibrin rich wound clot and within day organize into a micro-vascular network

85
Q

Granulation

A

new collective tissue and blood vessels that form from the base up and fill in the wound

86
Q

Epitheliazation

A

process by which the skin and mucous membranes replace superficial epithelial cells damaged or lost in cells