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DM Flashcards

1
Q

ENDOCRINE DISORDERS

DIABETES MELLITUS

Characteristics of Type I

A

hyperglycemia – elevated blood sugar

ketosis – ketones build up because the body can’t get the glucose into the cell (r/t not producing insulin); because the glucose is stuck in the bloodstream (where it cannot be used as an energy source at a cellular level) the body breaks down fat to be used an energy source instead; when fat is broken down, ketones are released; in other words: body goes to fat stores for energy since it cannot use glucose r/t no insulin production

usually abrupt in onset

affects 5 – 10% of diagnosed diabetics

primarily in childhood or adolescence, but can occur at any age

thin and underweight – pt eats a lot trying to get energy, but cannot get it from glucose, so the body burns fat

fatigue and malaise

3 p’s:

Polyuria - ( urine output

Glucosuria – renal threshold is usually 180 (some pt’s have higher thresholds); when sugar gets to a certain level in the bloodstream, it will spill over into the urine; glucose pulls water with it – when glucose is high in the bloodstream it causes an ( in osmolarity (thicker blood) which makes the pt feel thirsty: the more the pt drinks the more the pt urinates

Polydipsia - ( thirst; pt can end up with electrolyte imbalances

Polyphagia - ( hunger; since the body cannot use the glucose trapped in the bloodstream and is burning fat stores instead, the body is constantly trying to refuel itself (making pt feel hungry)

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2
Q

ENDOCRINE DISORDERS

DIABETES MELLITUS

Characteristics of Type I

hyperglycemia –

A

elevated blood sugar

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3
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS
Characteristics of Type I
ketosis –

A

ketones build up because the body can’t get the glucose into the cell (r/t not producing insulin); because the glucose is stuck in the bloodstream (where it cannot be used as an energy source at a cellular level) the body breaks down fat to be used an energy source instead; when fat is broken down, ketones are released; in other words: body goes to fat stores for energy since it cannot use glucose r/t no insulin production

usually abrupt in onset

affects 5 – 10% of diagnosed diabetics

primarily in childhood or adolescence, but can occur at any age

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4
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS

Characteristics of Type I
thin and underweight –

A

pt eats a lot trying to get energy, but cannot get it from glucose, so the body burns fat

-fatigue and malaise

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5
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS

Characteristics of Type I
3 p’s:

A

Polyuria -increase urin
Polydipsia -increase thirst
Polyphagia -increase hunger

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6
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS

Characteristics of Type I
3 p’s: Polyuria -

A

👆🏿urine output

-Glucosuria – renal threshold is usually 180 (some pt’s have higher thresholds); when sugar gets to a certain level in the bloodstream, it will spill over into the urine; glucose pulls water with it – when glucose is high in the bloodstream it causes an 👆🏿in osmolarity (thicker blood) which makes the pt feel thirsty: the more the pt drinks the more the pt urinates
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7
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS

Characteristics of Type I

3 p’s: Polydipsia

A
  • 👆🏿thirst; pt can end up with electrolyte imbalances
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8
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS

Characteristics of Type I
3 p’s: Polyphagia -

A

👆🏿hunger; since the body cannot use the glucose trapped in the bloodstream and is burning fat stores instead, the body is constantly trying to refuel itself (making pt feel hungry)

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9
Q

ENDOCRINE DISORDERS

DIABETES MELLITUS

Definition:

A

a metabolic disorder characterized by glucose intolerance, a systemic disease caused by an imbalance between insulin supply and demand (supply and demand between glucose [raises BS] and insulin [lowers BS])

Two types:

Type I  (insulin dependent diabetes, IDDM, juvenile onset diabetes, brittle 
diabetes)
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10
Q

ENDOCRINE DISORDERS

DIABETES MELLITUS
Pathophysiology of Type I

A
  • inflammation of islets of Langerhans (the cells within the pancreas)
  • beta cells (the islets of Langerhans) are destroyed resulting in ⭐️absolute ⭐️insulin deficiency (no insulin production)
  • hyperglycemia occurs when 80 – 90 % of beta cells are destroyed
  • honeymoon phase:
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11
Q

ENDOCRINE DISORDERS

DIABETES MELLITUS
Pathophysiology of Type I
honeymoon phase:

A

happens after diagnosis (up to about 6 mos); pt requires ( amounts or no insulin, but then the last of the beta cells are destroyed causing all insulin production to cease

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12
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS
Type II
Characteristics

A

(non-insulin dependent diabetes mellitus, NIDDM, adult onset DM)

  • generally slow in onset; insidious (developing so gradually as to be well established before becoming apparent)
  • may go undiagnosed without screening
  • symptoms may be vague
  • 3 p’s when BS is high
  • Visual blurring
  • Poor wound healing
  • Neuropathy- pain in feet
  • 85 – 90% of diabetics have Type II, much more common than Type I
  • usually diagnosed in middle age (over 30) and elderly, but now occurring a lot in children r/t obesity
  • treated with oral agents and/or insulin or diet (for a period of time)wouldn’t die w/o insulin
  • insulin using, not insulin dependent; still have a functioning pancreas

non-ketotic – Type II pts usually have enough insulin to prevent the breakdown of fat (ketones are by-product/waste product of that process)- unlike type 1

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13
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS
Pathophysiology of Type II

3 abnormalities:

A
  • insulin resistance
  • abnormal insulin production
    - hyperinsulinemia
  • inappropriate gluconeogenesis
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14
Q 
ENDOCRINE DISORDERS
DIABETES MELLITUS
Pathophysiology of Type II
3 abnormalities:
insulin resistance =
A

poor utilization of insulin at the cellular level (insulin is used to move glucose into the cells - insulin is the key that unlocks the cell for movement of glucose out of the blood and into the cell)
dependent on pt’s weight: the more obese the pt is the more insulin resistance

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15
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS -Pathophysiology of Type II
3 abnormalities:
abnormal insulin production
- hyperinsulinemia and decreased insulin production

A

hyperinsulinemia = high insulin levels in blood occurring in the early stages of the disease; the beta cells of the pancreas aren’t working properly – they are working overtime trying to send out more insulin to make up for the insulin resistance problem;

  • decreased insulin production – usually occurs later in the disease – the beta cells quit working r/t being overworked because of the insulin resistance; pt may have been controlled by diet, but will now need oral agents or insulin
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16
Q 
ENDOCRINE DISORDERS
DIABETES MELLITUS
Pathophysiology of Type II
3 abnormalities:
inappropriate gluconeogenesis =
A

production of glucose in the liver; in Type II diabetes mellitus the liver does this inappropriately – even when the body doesn’t need the extra glucose the liver pushes glucose out anyway increase BS levels.

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17
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS
Risk factors of Type II

A
  • familial component -increase risk
  • obesity
  • Insulin resistance
  • race/ethnicity
  • polycystic ovarian syndrome
  • acanthosis nigricans (brown, hyperpigmented thickening of the skin)
  • physical inactivity
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18
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS Risk factors of Type II
familial component –

A

-not specifically genetic

👆🏿Your chances of developing DM:

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19
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS Risk factors of Type II
obesity =

A

-BMI (body mass index) of 27 or greater

  • Insulin resistance – especially in certain types of obesity such as “truncal” (body is apple shaped due to excess fat accumulated around the trunk of the body); truncal obesity ( the number of available insulin receptors.
  • increase risk CVD
  • beta cells have impaired ability to release insulin
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20
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS Risk factors of Type II
race/ethnicity –

A

African Americans, Asian Americans, Native Americans and Hispanics have 👆🏿risk of developing Type II

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21
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS Risk factors of Type II
polycystic ovarian syndrome

A

– ovarian cysts; strong correlation between the Type II’s insulin resistance and polycystic ovarian syndrome

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22
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS Risk factors of Type II

acanthosis nigricans (brown, hyperpigmented thickening of the skin) –

A

r/t too much insulin in the bloodstream (hyperinsulinemia); more common in African American and Hispanics; sign of insulin resistance; occurs in skinfolds (neck, knuckles, axilla, etc.) wt loss can prevent

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23
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS -Type II diabetes in children

screening in children:

A
  • diagnosed in increasing numbers in children & adolescents, especially in minority populations
  • obesity (BMI > 85th percentile for age & sex or weight > 120% of ideal weight for height)
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24
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS -Type II diabetes in children
-two or more risk factors:

A
  • family history of Type II DM in first or second degree relative
  • minority ethnicity
  • signs of insulin resistance (acanthosis nigricans; dyslipidemia (high lipid levels: high triglycerides, high LDL; polycystic ovary syndrome)
  • onset of puberty – ages 11-14 years of age
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25
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS -Type II diabetes in children
treatment for kids

A
  • includes use of oral agents (only one kind of med is approved for kids at this time and the kids have to be over the age of 10y),
  • weight reduction,
  • diet
  • and exercise
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26
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS -Prediabetes
(Impaired Glucose Tolerance [IGT] or Impaired Fasting Glucose [IFG]/ old term “Borderline Diabetes”)
Definition:

A

-Fasting (8-12°) glucose > 100 and 140 but

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27
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS
Metabolic Syndrome
(insulin resistance syndrome, Syndrome X)

A

“the silent killer”

  • 1 in 4 Americans have Metabolic Syndrome
  • precursor to DM and cardiovascular disease
  • chronic low grade inflammatory process leading to plaque formation in vessels
28
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS
Metabolic Syndrome
symptoms:

A
  • hyperinsulinemia
  • hypertension
  • hypertriglyceridemia
  • low levels of HDL (good cholesterol)
  • change in LDL (bad cholesterol)
  • abdominal obesity and visceral adiposity - apple shape
  • polycystic ovarian syndrome
29
Q

ENDOCRINE DISORDERS
DIABETES MELLITUS
Type 1 ½
(Latent Autoimmune Diabetes in Adults, LADA, Slow Onset Type I)

A
  • The pt ends up with Type I diabetes, but instead of a quick onset, it
  • happens over a long period of time; the pt’s pancreas continues to
  • produce some insulin for quite a while before shutting down
  • Uncommon type of DM
  • An autoimmune type of diabetes
  • Occurs in adults over the age thirty
  • Pt is usually not overweight / non obese
  • pt usually doesn’t have insulin resistance
  • usually don’t present with ketoacidosis
  • Tx with PO medication
  • Eventually will have to tx with insulin
30
Q

ENDOCRINE DISORDERS

DIABETES MELLITUS -Secondary diabetes

A

– occurs as a result of other diseases

  • pancreatic disease – pancreatitis, pancreatic cancer, cystic fibrosis (involves part of pancreas that produces enzyme to breakdown fat); can become diabetic r/t pancreas itself is diseased
  • treatment with corticosteroids – such as prednisone used to treat acute inflammatory disease (ex. emphysema); pt gets ( BS r/t circulating corticosteroids
31
Q

ENDOCRINE DISORDERS

H. Gestational diabetes –

A
  • diabetes during pregnancy; mother is at risk of developing Type II later in life (usually 5-10 years down the road); thru the maternal blood the fetus also gets increase levels of glucose causing the baby to be large/chubby
32
Q

ENDOCRINE DISORDERS

Diagnosis of DM (either type I or II)

A
  • (normal blood glucose level: 70 –110)
  • Fasting blood glucose level > 126 mg/dl X 2 readings
  • Random blood glucose of > 200 mg/dl with symptoms (polydipsia, polyuria, unexpected weight loss, blurred vision, presence of ketones); if pt on steroids or has an infection – should wait to test again; a normal, non-diabetic will usually not go over 200)
  • Two hour BS > 200 mg/dl during an oral glucose tolerance test (OGTT); 75G glucose test
33
Q

ENDOCRINE DISORDERS

Metabolic Effects of Diabetes

A
  • decreased utilization of glucose – not enough insulin to move glucose into cells = high blood glucose
  • increased fat metabolism
  • body relies on fat for energy when glucose not available
  • fat metabolism results in production of ketones
  • ketones in blood are excreted by kidneys and lungs (when levels are really high the ketones are excreted thru the lungs causing the pt’s breath to smell fruity)
  • increased ketone levels in blood affect pH and leads to acidosis
  • weight loss (when fat being used for energy)
  • increased protein utilization – lack of insulin (which helps push things into cells) causes protein wasting
34
Q

ENDOCRINE DISORDERS
Etiology of Diabetes Mellitus
A. Type I

A
  • Autoimmune (body destroys own cells) disorder in which beta cell destruction in the pancreas occurs in genetically susceptible individual
  • Higher incidence in Caucasian population
  • Environmental factor such as virus or chemical toxin is trigger that leads to destruction of beta cells
  • Genetics load the gun, environment pulls the trigger to start the beta cell destruction
  • Children of Type I diabetics have 1 in 20 to 1 in 50 chance of developing DM
35
Q

ENDOCRINE DISORDERS
Etiology of Diabetes Mellitus
Type II

A
  • Obesity a major factor

- Sedentary life-style that goes along with obesity

36
Q

ENDOCRINE DISORDERS
Etiology of Diabetes Mellitus
Type II
Theories:

A
  • limited beta cell response to hyperglycemia
  • peripheral insulin resistance – don’t use it properly
  • insulin receptor abnormalities
37
Q

Acute and Chronic Complications of DM
ACUTE Complications
-Hypoglycemia
Definition:

A

– LOW blood sugar

-blood glucose

38
Q

Acute and Chronic Complications of DM
ACUTE Complications
-Hypoglycemia
Causes:

A
  • overdose of insulin – taking too much
  • omitting a meal or eating less than necessary
  • overexertion without additional food intake (used up too much glucose)
  • imbalances due to nausea and vomiting (can’t keep food down = decrease BS)
  • alcohol intake (alcohol alone decrease BS, especially fruity drinks and beer)
  • inadequate food absorption – gastroparesis – nerves that innervate the stomach and intestines don’t work very well so food sits in stomach and doesn’t get digested; the person may be eating enough, but the nutrients aren’t getting absorbed which can cause the blood glucose level to drop.
39
Q

Acute and Chronic Complications of DM
ACUTE Complications
-Symptoms of MILD to MODERATE hypoglycemia

A
  • sudden hunger
  • diaphoresis – objective symptom (sweating, moist upper lip)
  • weakness
  • nervousness or shaking – can see their hands shake
  • headache
  • apprehension
  • person aware of symptoms and can do something about it
40
Q

Acute and Chronic Complications of DM
ACUTE Complications
Symptoms of SEVERE hypoglycemia

A

– this pt doesn’t recognize the problem

  • confusion – appears drunk
  • slurred speech – appears drunk
  • behavior changes - combative
  • somnolence - sleepy
  • staring
  • stupor
  • seizures - if BS gets very low
  • coma – if BS gets very low

Symptoms may be masked by beta blockers (cardiac drugs) – pt may not be as aware of symptoms as quickly when on beta blockers

41
Q

Acute and Chronic Complications of DM
ACUTE Complications
-Hypoglycemia at NIGHT

A
  • pt usually wakes up if BS is getting low
  • bizarre nightmares
  • restlessness or sleeplessness
  • confusion
  • difficulty arousing
42
Q

Acute and Chronic Complications of DM
ACUTE Complications
Somogyi Effect (rebound) – occurs with TYPE I

A

-pt gets hypoglycemia during the night; the liver appropriately converts glycogen back to glucose, BUT at the same time stress hormones were also released in response to the low blood sugar so the pt will have a higher BS in the am

43
Q

Acute and Chronic Complications of DM
ACUTE Complications
Dawn Phenomenon – TYPE II;

A

-pt gets hypoglycemia during the night; the liver appropriately converts glycogen back to glucose, BUT because of insulin resistance the BS will be elevated in the am

44
Q

Acute and Chronic Complications of DM
ACUTE Complications
Diabetic ketoacidosis (DKA) (diabetic coma)
Causes

A
  • acidosis caused by high levels of ketones in the blood
  • Occurs in Type I DM when undiagnosed or BS out of control; this might be the piece that gets the DM diagnosed; may be r/t non-compliance (teenager gets sick of dealing with DM and quits taking care of him/herself); may be r/t illness (pt has had N&V/ stress hormones have been released causing BS to be out of control)
  • fat is used as source of energy – give off ketones which lead to metabolic acidosis
  • may have gradual or sudden onset
45
Q

Acute and Chronic Complications of DM
ACUTE Complications
Diabetic ketoacidosis (DKA) (diabetic coma)
Signs and symptoms

A

-blood sugar > 250, as high as 800
-3P’s (polydipsia, polyuria, polyphagia)
-nausea and vomiting
-fruity breath (r/t loss of ketones thru the lungs)
-vague abdominal pain (r/t hypokalemia)
-ketones in the urine
-dry, flushed skin – cheeks fire-red
-signs of dehydration
-hypokalemia (initial level might be high, but later the levels fall)
pH

46
Q

Acute and Chronic Complications of DM
ACUTE Complications
Diabetic ketoacidosis (DKA) (diabetic coma) late signs

A
  • Kussmaul’s respirations – rapidly and deep to get rid of ketones and raise the pH
  • lethargy or coma
  • hypotension r/t dehydration (less volume = low B/P)
47
Q

Acute and Chronic Complications of DM
ACUTE Complications
Diabetic ketoacidosis (DKA) (diabetic coma)
-treatment –

A
  • admit to hospital
  • fluids:
    • isotonic solutions 0.9% NS or 0.45% NS (or hypotonic soln if severely dehydrated); don’t want to give anything with dextrose in it
    • switch to D5W when BS reaches 250 – want to decrease BS slowly
    • reduces blood sugar level
    • prevents vascular collapse – from losing so much fluid
    • 250 to 1000 mL per hour depending on level of dehydration
    • give fluids (to correct dehydration) before starting insulin
48
Q

Acute and Chronic Complications of DM
ACUTE Complications
Diabetic ketoacidosis (DKA) (diabetic coma)
insulin

A
  • IV drip of Regular insulin at 5-10 units per hour – the ONLY kind that can be given IV (mixed with NS)
  • Test BS every hour and titrate drip every hour to BS – titrating depending on how quickly the pt’s BS is coming down
  • lower blood sugar no faster than 75 mg/dl per hour (so if start at 700, in the next hour we don’t want to go below 625)
49
Q

Acute and Chronic Complications of DM
ACUTE Complications
Diabetic ketoacidosis (DKA) (diabetic coma)

Electrolytes

A

-Potassium
lost in diuresis – glucose gets expelled from kidneys and pulls water with it (also pulls K+)
-treatment:
-with insulin drives K+ from bloodstream back into the cell – want to get it back into the bloodstream
-supplement with K+ and monitor closely

  • Phosphate, Magnesium, Calcium
    • phosphate & magnesium plummet after therapy begins this leads to decreased calcium
    • monitor and treat
50
Q

Acute and Chronic Complications of DM
ACUTE Complications
Diabetic ketoacidosis (DKA) (diabetic coma)
patient monitoring

A
  • Hourly glucose and urine ketones – want to see less and less ketones expelled
  • Arterial blood gases to check pH – want to see acidosis corrected
  • Electrolytes q 1-4 hrs.
  • EKG – K+ can cause cardiac issues
  • vital signs
  • I&O – want to see less diuresing and more dilute urine (peeing more r/t polydipsia, and urine is concentrated r/t dehydration)
  • neuro status assessment
  • cardiac monitoring
51
Q

Diagnostic of DM

Hgb A1c

A 
normal range-
-4-6%
increase risk for future DM
-5.7-6.4
Diabetes
-greater than 6.5
52
Q

Diagnostic of DM

two hour BS during an oral glucose test

A

grater than 200mg/Dl

53
Q

Diagnostic of DM

random Blood glucose of

A

grater than 200mg/dl with symptoms 3 P’s, weight loss, blurred vision, ketones

54
Q

Diagnostic of DM

fasting blood glucose

A

greater than 126mg/dl 2 X readings

55
Q

Normal Blood Glucose level

A

70-110mg/dl

56
Q
  1. Hyperosmolar hyperglycemic syndrome or state (HHS) hyperglycemic hyperosmolar nonketotic syndrome (HHNK)
    - causes and triggers:
A
  • occurs in Type II DM (not ketotic),
  • usually older and obese
  • frequently with impaired renal function
  • noncompliance (with diet or insulin administration) or undiagnosed
  • triggers: stress to the body such as infection, MI, stroke, surgery, medications
  • takes days or weeks to develop, insidious onset
57
Q

Hyperosmolar hyperglycemic syndrome or state (HHS)

-symptoms

A

– pt is hyperglycemic

  • BS > 600 mg/dl, can exceed 1000 mg/dl
  • no symptoms until BS is dangerously high
  • polydipsia - thirst
  • tachycardia r/t dehydration
  • polyuria
  • weight loss
  • decreased skin turgor r/t dehydration
  • blurred vision – r/t vls in eyes swelling
  • altered mental status (lethargy to coma)
  • severe dehydration (even worse than what we see in DKA) -r/t long onset
  • dry, flushed skin
  • hypotension
  • rapid, shallow respirations (not deep like we see in DKA trying to rid the ketones)
58
Q

Hyperosmolar hyperglycemic syndrome or state (HHS)

-differances from DKA

A
  • HHS or HHNK has more severe hyperglycemia r/t being allowed to climb for a long period of time
  • more pronounced dehydration
  • neurological symptoms more severe r/t high glucose levels in the brain and the high dehydration in the brain -no acidosis
  • no abdominal pain
  • no acetone breath
  • no Kussmaul’s respirations
  • no ketosis, no ketones in urine
59
Q

HHS or HHNK is a Type II rather than Type I issue

Treatment

A

– treated in ICU

  • Same as DKA with following differences:
  • Fluid given more rapidly; 1-3 liters over 2 hrs. – to correct the severe dehydration
  • May need assistance with ventilation and an NG tube to prevent aspiration if mental status greatly compromised
  • Patient monitoring: Same as DKA
60
Q
  1. Hyperglycemia
A

-common with DKA (type1) and HHS (type2)
– acute complication, but not as urgent as hypoglycemic
-may have no symptoms, not usually emergent situation
-problem when prolonged, very high blood sugars
or when consistently high BS result in complications

61
Q
  1. Hyperglycemia

symptoms:

A
  • pt can usually tell if BS are really high – many not feel it if 150 or so; problems occur when BS are high for a long time or are severely high
    • same symptoms we list for diabetes
  • increased urination
  • thirst
  • dehydration (dry mouth, itchy skin)
  • hunger
  • fatigue
  • vision changes
  • mood changes; irritable (most common)
  • difficulty concentrating
  • increased number of infections
  • poor wound healing
62
Q

CHRONIC Complications – in Type II,

A

pancreas doesn’t function well causing surges of insulin to be released into the bloodstream which damages vessels

  1. Macrovascular complications –
    - Cardiovascular disease
  2. Microvascular Complications – small vessels such as those of the eye and kidneys
  3. Infections –
    - r/t increase BS = more susceptible to infection

4.Sexual dysfunction

63
Q

CHRONIC Complications – in Type II,

1. Macrovascular complications

A

– large vessels; heart and peripheral
-Cardiovascular disease – large vessels get a blockage causing HA, MI, angina (blockage of coronary vessel); diabetics have 2-4 times greater chance of getting cardiovascular disease r/t lipid buildup

 - Atherosclerosis (lipid buildup) at a younger age which is more severe; correlate with how well diabetes is controlled, especially triglycerides (increase BS = increase triglycerides); lipid levels show abnormal levels with uncontrolled diabetes; lipid levels may be normal with controlled diabetes;     - disease is more diffuse – involves even small vessels    - greater rate of restenosis (narrowing again) after angioplasty (opening of a vessel)    - leading cause of death in diabetics – cardiovascular disease (CVA)
- higher mortality rate after MI (compared to a MI pt without diabetes)
- “silent MI” – don’t feel it r/t the neuropathy - Peripheral vascular disease- usually very large vessel in the leg
- atherosclerotic blood vessel changes
- occlusion (blockage) of arteries, especially those in legs
- can result in gangrene and need for amputation - Cerebrovascular disease – large vessels of brain
 - decrease circulation to the brain; causes strokes
64
Q

CHRONIC Complications – in Type II,

2.Microvascular Complications

A

– small vessels such as those of the eye and kidneys

  • Eye disease – diabetic is 25x more likely to have legal blindness
    - Diabetic Retinopathy -(major cause of legal blindness)– retina is damaged from damage to small microvessels around the retina; small vessels get blocked and degenerate and hemorrhage; can lead to retinal detachment
    • Macular Degeneration – permanent blurry area in center area of vision
    • Cataracts – clouded vision
  • Neuropathy – nerve damage; can accentuate the pain or numbness
    • Peripheral – nerves in toes and feet; pt cannot feel feet and toes/ numbness, or feel burning sensation and pain; can lead to tissue damage – sore doesn’t heal, which leads to amputation
    • Autonomic neuropathy– comes off CNS; affects organs (heart, lungs, GI, kidneys) fixed heart rate that results in:
      • Postural Hypotension and Syncope – B/P drops with position changes
      • Neurogenic bladder – unaware bladder is full; UTI’s can develop; pt doesn’t recover from the infections well

GI:

  - Vomiting – damaged nerves to the stomach
  - Constipation 
   - Diarrhea – nerve damage to small intestine 
    - Gastroparesis – nerve damage to stomach – slows down function of stomach, gives pt a full feeling after a small meal. tx: hemodialysis or transplant
65
Q

Chronic Complications of DM

. Nephropathy

A

– microvascular (capillary) damage in kidneys; occurs in 40% of Type I and in 10% of Type II; occurs within 15-20 years of onset if it is going to occur

Microalbuminuria: is the earliest symptom of nephropathy; albumin in present in urine – kidneys are supposed to keep this from filtering thru, but kidney damage causes them to malfunction; will eventually result in end stage renal disease

66
Q

CHRONIC Complications – in Type II, –

3.infections

A
  • r/t increase BS = more susceptible to infection
  • more difficult to treat; pt doesn’t heal as well r/t to poor circulation
  • yeast infections
67
Q

CHRONIC Complications – in Type II,

4.Sexual dysfunction

A
  • retrograde ejaculation – backward flow of ejaculate into bladder
  • erectile dysfunction (impotence) – r/t nerve damage

155 (7 decks)

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