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Endocrinology > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

What is the pathophysiology of DM type 1?

A

An autoimmune disease (immune system mediates destruction of pancreatic beta-cells)

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2
Q

Is type 2 DM are pts insulin resistant or insulin dependant?

A

Insulin Resistant - d/t obesity

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3
Q

What are 3 risk factors of type 2 DM?

A
  1. Obesity
  2. Genetics (maternal more so)
  3. Age (insulin production decreases w/ age)
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4
Q

What is the onset, age at onset, body habitus and the chance of ketosis in type 1?

A
  • Onset: Sudden (sometimes appear after an illness)
  • Age: Any age, usually young
  • Body Habitus: usually thin
  • Ketosis: Common (DKA)
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5
Q

What is the onset, age at onset, body habitus and the chance of ketosis in type 2?

A
  • Onset: Gradual
  • Age: Adults (usually)
  • Body Habitus: Obese
  • Ketosis: Rare
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6
Q

What is the dawn phenomenon d/t and is it related to the Somogyi effect?

A
  • D/t an increase in nocturnal secretion of GH

- Independent of the Somogyi effect

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7
Q

What is the Somogyi effect and what occurs when you are sleeping?

A
  • Rebound response to nocturnal hypoglycemia

- Counterrefulatory systems are activated in response to hypoglycemia, leading to nocturnal hyperglycemia.

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8
Q

If pt checks blood glucose at 3 AM and glucose is elevated is it Dawn or Somogyi?

A

Dawn Phenomenon

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9
Q

If pt checks blood glucose at 3 AM and glucose is low is it Dawn or Somogyi?

A

Somogyi Effect

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10
Q

What is the recommended screening for type 2 DM? How often should you repeat screening?

A
  • Adult w/ BMI > 25 and at least one risk factor
  • Age 45 if normal BMI and no risk factors
  • repeat screening q 3 yrs
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11
Q

What is the American Diabetes Association Dx criteria or DM?

A
  • Sxs of DM + random BG [ ] of >200
  • Fasting BG of >126 on 2 separate occasions
  • BG of >200, 2 hrs after a 75g glucose load during OGTT
  • Hgb A1c: >6,5% (repeat test should occur several months as opposed to next day)
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12
Q

What is the range of Hbg A1c in a pt with impaired fasting glucose?

A

5.7% - 6.4%

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13
Q

What are the 3 polys associated with DM?

A
  • Polyuria
  • Polydipsia
  • Polyphagia
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14
Q

What is polyuria and what does it cause?

A

Glucose in renal tubule causes osmotic retention of water causing diuresis

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15
Q

What is polydipsia?

A

A physiologic response to diuresis to maintain plasma volume

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16
Q

What is polyphagia?

A

A physiologic response to the inability for cells to take in and use glucose

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17
Q

Why does fatigue occur in DM?

A

Unknown but likely d/t increased glucose in plasma

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18
Q

What eye problem occurs in pts with DM and what is it d/t?

A

Blurred vision- swelling of lense d/t osmosis

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19
Q

What infections occur in DM pts? and where do the infections most commonly occur?

A

Fungal infxns

- Mouth and vaginal - Candida Albicans

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20
Q

What occurs to the extremities in pts with DM?

A

Neuropathy- Numbness, tingling of hands and feet

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21
Q

What are the causes of mononeuropathy and polyneuropathy?

A
  • Mono: d/t microscopic vasculitis leading to axonal ischemia
  • Poly: multifactorial
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22
Q

When should a pt monitor glucose after meals and why is that important?

A

90-120 min enables the pt to control postprandial hyperglycemia?

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23
Q

How often should you screen a pt for microalbuminuria and how do you tx for postie microalbuminuria?

A
  • Screen 1x per yr w/ eGFR, in DM pts w/ no evidence of nephropathy
  • Tx if positive: ACE or ARB
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24
Q

How often do you order eye screening for DM and who do you refer to Optometrist or Ophthalmologist?

A

Yearly by Ophthalmologist

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25
Q

How often do you check for peripheral neuropathy in DM pts? Who do you refer to and what type of pt would you need to refer?

A

Check feet every visit!

- refer to Podiatrist for high-risk pts (ulcers)

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26
Q

How often do you check Cholesterol? and when should you give statin therapy?

A
  • Once a yr

- Give statin in LDL is > 100

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27
Q

How often do you check B/P and when should medication (ACE or ARB) be considered?

A
  • Check at every visit

- Tx if >130/80

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28
Q

What vaccine should be UTD in all DM pts?

A

Pneumococcal vaccine

29
Q

What should ideally be the only intervention in most type 2 DM pts?

A

Diet and Exercise

30
Q

When diet and exercise fail what is the best initial drug for DM and who is it CI in?

A
  • Metformin

- CI: pts w/ renal failure

31
Q

What is the main microvascular complication of DM pts?

A 
Accelerated Atherosclerosis (main problem)
- pts are at an increased risk of CVA, MI, and HF
32
Q

What is the MCC of death in DM pts? What is one other COD in DM pts?

A
  • MC: Coronary Artery Disease

- Other: silent MI

33
Q

DM Nephropathy is the MCC of what disease? and what is the pathognomonic finding?

A
  • ESRD

- Nodular glomerular sclerosis: deposits of hyaline in one area of the glomerulus

34
Q

What increases the risk of progression of DM nephropathy to ESRD?

A

HTN

- control B/P aggressively (ACE or ARB)

35
Q

How many yr does it take for microalbuminuria to advance to fill-blown proteinuria? and What can slow this progression?

A
  • Takes 1-5 yrs

- Tx, ACE or ARBs can help slow this progression

36
Q

What are the albumin levels that indicate microalbuminuria?

A

30-300 mg per 24 hrs and urine dipstick become trace positive at 300mg of protein per 24 hrs

37
Q

What is the leading cause of blindness/reversible blindness in the US? What is the leading cause of visual loss in DM pts?

A
  • Blindness: Diabetic retinopathy

- Vision loss: Macular Edema

38
Q

What exam is done to look for diabetic retinopathy? and what is seen?

A
  • Funduscopic examinations

- Hemorrhages, exudates, microaneurysm, cotton wool spots, and venous dilation

39
Q

What is the tx or diabetic retinopathy?

A

Laser photocoagulation

40
Q

Peripheral neuropathy (AKA distal symmetric neuropathy) usually affects sensory nerves in what pattern? and what are the common sxs?

A
  • Stocking/glove pattern

- Numbness and paresthesias

41
Q

Where does peripheral neuropathy usually begin?

A

Beings in the feet and later involved the hands

42
Q

What are sxs of painful diabetic neuropathy?

A
  • Hypersensitivity to light touch

- Severe “burning pain” esp. at night

43
Q

What are the txs for painful diabetic neuropathy?

A
  • Pregabalin
  • Gabapentin
  • Duloxetine
  • TCAs
44
Q

What is the MC cranial nerve that is involved in microvascular complications?

A

CN III: Oculomotor

- may also involve CN IV and VI (Trochlear and Abducens)

45
Q

What are sxs of diabetic nerve palsy?

A
  • Eye pain
  • Diplopia
  • Ptosis
  • Inability to adduct the eye
  • Pupils are spared
46
Q

What is the MC presentation of autonomic neuropathy?

A

Impotence in men

47
Q

What is Gastroparesis, a cause of autonomic neuropathy?

A

Chronic N/V, early satiety

48
Q

During a diabetic foot exam, what are you as the PA looking for? (DIABETICS)

A 
D: Deformity
I: Infection
A: Atrophic nails
B: Breakdown of skin
E: Edema
T: Temperature of skin
I: Ischemia
C: Callous and corns
S: Skin color
49
Q

What is Wagner stage 0?

A

Skin is intact, but the “foot is at risk”

50
Q

What is Wagner stage 1?

A

Superficial diabetic ulcer that is localized

51
Q

What is Wagner stage 2?

A

Deep ulcer and Extention

  • Involved ligament, tendons, joint, capsule or facia
  • NO abscess or osteomyelitis
52
Q

What is Wagner stage 3?

A

Deep ulcer w/ abscess or osteomyelitis

53
Q

What is Wagner stage 4?

A

Gangrene to portion of the forefoot

54
Q

What is Wagner stage 5?

A

Extensive gangrene to entire foot

55
Q

What is the pathogeniesis of DKA?

A

Insulin deficiency and glucagon excess resulting in severe hyperglycemia and accelerated ketogenesis
- leads to osmotic diuresis causing dehydration and volume depletion

56
Q

What are the “5 I’s” that precipitate DKA?

A
  • Infection
  • Ischemia (cardiac, mesenteric)
  • Infarction
  • Ignorance (poor control)
  • Intoxication
57
Q

What are the clinical manifestations of DKA?

A
  • N/V
  • Kussmaul respirations - rapid, deep breathing
  • Abdominal pain (more common in children)
  • Fruity (acetone) odor on breath
58
Q

What may occur when DKA is accompanied by circulatory collapse?

A

Serum and urine may be falsely negative for ketones

59
Q

What is required for diagnosis of DKA?

A

Ketonemia and metabolic acidosis

60
Q

What electrolytes are disturbed d/t DKA?

A

Potassium

- hyperkalemia may be present initially although total body potassium is low.

61
Q

As inulin is given what occurs to the potassium?

A

It causes a shift of potassium into cells resulting in hypokalemia (can happen very rapidly)

62
Q

What medication is given immediately after the diagnosis of DKA is established? and what should you be certain of before giving this medication

A
  • Insulin

- Be certain pt is no hypokalemic before giving the insulin

63
Q

What fluid replacement is given for a pt whos been diagnosed with DKA?

A

Normal Saline

- give immediately after dx is established

64
Q

What should be given to prevent hypoglycemia in a DKA?

A

Add 5% glucose once the BG reaches 250mg/dl to prevent hypoglycemia

65
Q

Aside from insulin and fluid replacement what else should be given to manage DKA? and when should it be given? and what should be monitored during this tx?

A
  • Replace potassium prophylactically w/ IV fluids.
  • Initiate within 1-2 hrs after starting insulin
  • Ensure adequate renal fx (urine output) prior and monitor potassium, magnesium, and phosphate levels very closely and replace as necessary
66
Q

In general, what is hyperosmolar hyperglycemic nonketotic syndrome (HHNS)?

A

A state of severe hyperglycemia, hyperosmolarity, and dehydration. Typically seen in elderly type 2 DM pts.

67
Q

What clinical features are common in HHNS?

A

CNS findings and focal neurologic signs

- seizures occurring secondary to hyperosmolarity

68
Q

What is the most important tx for HHNS?

A

Fluid replacement

- 1 L in the first hr and another L in the next 2 hrs

Endocrinology (18 decks)

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