Kirilla ClinMed Flashcards

(64 cards)

1
Q

What does Diabetes Mellitis mean?

A
  • DB => excessive urination
  • Mellitis => sweet as honey
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2
Q

What are the MULTIPLE names for capillary glucose monitoring, including glucose monitoring that occurs in outpatient setting?

A
  1. FSG (Fingerstick glucose)
  2. BSG (Bedside glucose)
  3. Accucheck (MC used monitor)
  4. Outpatient:
    1. HGM (home glucose monitoring)
    2. GSM (glucose self-monitoring)
    3. SBGM (self-blood glucose monitoring
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3
Q

What is the difference between basal insulin & bolus insulin?

A
  • Basal insulin: long-acting insulin used to acheive a more steady state of glucose control (to mimic baseline insulin levels in non-DB)
  • Bolus insulin is adjusted at meal and based on FSG +/- carb count
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4
Q

Signs/Sx of DM (6)

A
  1. Poluria (excessive urination) = large amount, more frequently
  2. Polydipsia (excessive thirst)
  3. Nocturia (waking up to pee)
  4. Blurred vision (depending on blood sugar)
  5. Unintentional WL
  6. Frequent infections, even with tx and clearance
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5
Q

Guidlines for DB Dx

A
    1. Fasting plasma glucose (FPG) > 126 (7.0 mmol/L)
    1. 2-hour plasma glucose value of > 200 mg/dL (11.1 mmol/L) during a 75g OGTT (oral glucose tolerance test)
  • 3. HbA1c > 6.5% (48mmol/mol)
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6
Q

Recommend monitoring for long term chronic care to prevent/detect common complications from DB

A

HbA1C levels (3 month average of blood glucose) –done every 3-4 months to monitor control typically w/ venipuncture.

  • Less than 6.5% is ideal, however, lows can cause syncope/increase risk of falls.
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7
Q

Other names for HbA1C tests?

A
  1. Hemoglobin A1C
  2. HbA1C
  3. GHbA1C
  4. Glycoslylated Hb
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8
Q

Common presenting signs that may be caused by DM

A
  1. AMS
  2. Abdominal pain
  3. Dehydration
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9
Q

Formulate a differential diagnosis for common presenting signs and symptoms that may be caused by DM

AMS

A

“AEIOUTIPS”

  • ​Alcohol
  • Epilepsy + seizures
  • Infection
  • OD
  • Uremia
  • Trauma
  • Insulin (high/low BS)
  • Poisoning/psychosis
  • Stroke
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10
Q

Formulate a differential diagnosis for common presenting signs and symptoms that may be caused by DM

Abdominal Pain

A

BAD GUT PAINS

  • Bowel obstruction
  • Appy/adentitis
  • Divertivulitis, DKA, dysentary/diarrhea drug withdrawal
  • Gastroenteritis (GB disease/stones, obstruction, infection)
  • UTI/obstruction
  • Testicular torsion
  • Pneumonia/pleurisy/pancreatitis/ perforated bowel/peptic ulcer/porphyria
  • Abdominal aneurysm
  • IN (infracted bowel, myocardium (AMI), inflammatory bowel disease)
  • Splenic rupture/infarction/ sicckle cell pain crisis
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11
Q

What are acute complications of DM?

A
  1. DKA
  2. HHS (hyperglycemic hyperosmolar syndrome) aka NKHS (non-ketotic hyperosmolar state) and HNKC (hyperosmolar non-ketotic coma)
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12
Q

What can cause DKA?

A
  1. Inadequate insulin administration
  2. Infection (pneumonia, UTI, gastroentiritis, sepsis)
  3. Infarction (coronary, cerebral, mesenteric, peripheral)
  4. Surgery
  5. Drugs (cocaine)
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13
Q

Initial symptoms of DKA

A
  1. Anorexia
  2. N/V
  3. Poluria
  4. Thirst
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14
Q

===> Progression of symptoms of DKA

A
  1. Abdominal pain
  2. AMS
  3. Coma
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15
Q

What are the clinical signs of DKA?

A
  1. Kussmaul respirations (rapid and deep)
  2. Acetone (fruity) breath
  3. Dry mucuous membranes
  4. Poor skin turgor
  5. Tachycardia
  6. HTN
  7. Fever, abdominal tenderness
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16
Q

What kind of acidosis does DKA cause?

A

High anion-gap metabolic acidosis

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17
Q

DDx for High Anion Gap Acidosis

A

MUDPILES

  1. Methanol
  2. Uremia
  3. DKA
  4. Paraledehyde
  5. Isopropyl alcohol, iron, INH (isoniazid)
  6. Lactic acidosis
  7. Ethylene glycol
  8. Salicylates
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18
Q

How are those with DKA treated?

A

ICU: frequent monitoring of [general status, VS, glucose and other labs]

  1. Acid-base status
  2. Renal fx
  3. K+ & other electrolytes
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19
Q

How should fluid replaced in DKA?

A

1-2-3 method

  1. 2 –3 liters NS (0.9% Normal Saline) over first 1-3 hours (5-10 ml/kg/hr)
  2. Then, 1/2 strength saline (0.45%) at 150 ml/hr
  3. When glucose reaches 250 mg/dl, switch to D5 1/2 NS (5% dextrose and 0.45% saline) at 100 –200 ml/hr
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20
Q

What is the fluid deficit in those with DKA?

A

3 -5 L

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21
Q

How should insulin be replaced in DKA?

A
  1. 10 –20 units IV/IM (or 0.15/kg)
  2. Then, 5-10 units/hr continuous IV (or 0.05 –0.1/kg/hr)
  3. If no response in 1-2 hrs => increase (orders can be written with guidelines to titrate)
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22
Q

How can we evaluate for underlying causes of DKA?

A
  1. Cultures
  2. Drug screen
  3. EKG
  4. CXR
  5. Ask pt/family
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23
Q

How to monitor a patient with DKA?

A
  1. BSG/hr
  2. Electrolytes/2-4 hours +/- ABGs
  3. Check clinical status /hr
    1. Vitals (BP, P, RR)
    2. Mental status
    3. Fluid I & O
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24
Q

When should K+ be replaced in DKA?

What should be kept in mind when replacing?

A

If serum K+ is [< 5.5 mEq/L]

  1. Kidney fx
  2. Baseline EKG and continously monitor <3 for changes
  3. Verify urinary output and measure q 1 hour; intially will probably need a indweling folley catheter
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25
**Treatment goals** of DKA
1. **Increase rate of glucose utilization** in insulin-dependent tissue to get glucose to 150-250) 2. **Reverse ketonemia** and **acidosis** 3. **Correct depletion of water** and **electrolytes**
26
In a patient with DKA, when should we transition to **intermediate** or **long-acting insulin**? How should it be done?
1. **When patient can eat** 1. Mental status is improved, no N/V, no abdominal pain 2. **NL anion gap** _- Allow overlap timing of IV with SQ insulin by 30-60 minutes_
27
What causes **NKHS** (non-ketotic hyperosmolar state?
1. Insulin deficiency 2. Inadequate fluid intake 3. Osmotic duiresis due to hyperglycemia
28
What are **preciptitating factors** that can cause NKHS?
1. Sepsis 2. MI 3. Glucocorticoids, phenytoin, thiazide diuiretics 4. Imparied access to water
29
Symptoms of **NKHS**
**1. Polyuria** **2. Thirst** **3. AMS**
30
What symptoms are **ABSENT** in **NKHS** _BUT_ occur in DKA?
1. **Abominal pain, N/V** 2. **Kussmual repirations**
31
What is the **fluid deficit** in NKHS?
**8-10 L**
32
How should **fluids** be replaced in **NKHS**?
1. 2 –3 liters NS (**0.9% Normal Saline)** over first 1-3 hours (5-10 ml/kg/hr) 2. Reverse fluid deficit (often 8-10 L) over next 24 –48 hrs using **1/2 strength saline (0.45%)** 3. When glucose reaches 250 mg/dl, switch to D5 1/2 NS (5% dextrose and 0.45% saline) at 100 –200 ml/hr
33
How should **insulin** be replaced in NKHS?
1. **5 –10 units IV bolus** (or IM) 2. **3 –7 units** continuous infusion 3. Transition to intermediate-long term insulin when pt is eating, like DKA
34
What are the differences in **DKA** and **HHS**?
1. Fluid deficit is **greater** in NKHS 2. **Drugs** can cause NKHS 3. NKHS does **not cause** abdominal pain, N/V, ketoacidosis and kussmaul respirations
35
How are **DKA** and **HHS** both the same?
1. **Insulin deficiency** is absolute or relative 2. **Glucagon excess** is absolute or relative 3. **Volume depletion** 4. **AMS** 5. Both are **CRITICAL** and need **INTENSIVE monitoring**
36
**MC** long-term complication of T2DM
1. **50% = underlying \<3 disease** 2. _20% = retinopathy_ 3. 9% = neuropathy 4. 8% = nephropathy
37
What is the major cause of mortality in T2DM?
CV disease
38
With poor DM control, risk of ________ increases.
**Coronary heart/artery disease**
39
Hb1AC of 6.5% = ____ glcuose
125 mg/dL of glucose 6% = 110; 7% = 140
40
**5% of HbA1C** = ____ glucose **10% of HbA1C** = ____ glucose
**5% of HbA1C** = 80 mg/dL glucose **10% of HbA1C** = 240 mg/dL glucose
41
What is **Diabetic Gastropathy?**
* A form of autonomic neuropathy in the area of the stomach referred to as **gastric pacemaker** that causes **very erratic gastric emptying/ absorption** so sugars are increasingly variable and hard to control
42
How are **insulin requirements** different in **diabetic gastropathy** and **nephropathy**?
* **DB gastropathy** = variable insulin requirements and variable/unpredictable insulin requirements * **DB nephropathy** = declining kidney function = decreasing insulin requirements as Cr clearance rate declines bc insulin is not clearing = sugars are lower
43
What is the EARLIEST measurable sign of DB nephropathy?
* **Random urine [microalbumin/Cr] ratio** * Microalbumin = 30 mg - 300 mg (\> 300 = albuminuria)
44
Why do we not use a **standard urine dipstick** urine sample for protein?
**Not sensitive if proteinuria is \<300 mg/24 hours**
45
Why is a 24 hour urine collection test **NOT** used for DB nephropathy?
Used in more advance cases of kidney dz 1. Hard to remember to save ALL urine 2. Dexterity required to get into container 3. Leaks in containor
46
How is **DB** **monitored** to avoid complications?
* **Quarterly**, evaluate 1. HbA1C 2. Review SGM (self-glucose monitoring log) 3. Inspect foot for ulcers * **Every year,** 1. Dilated eye exam 2. Urine protein screening (microalbumin/Cr ratio) 3. Monofilament test
47
What is one complication you want to avoid if possible?
**Neuropathic arthropathy and ulcers**
48
How can we take care of feet in **DB**, which can be hard for ppl with **dexterity** and **visual problems?**
1. Inspect daily 2. Use plastic mirrors on floor when getting out of bed and family assistance 3. Never go barefoot 4. Moisturize, but NOT in between/under toes 5. Prescription shoes (medicare pays for 1/year) 6. Podiatrist
49
**_DB treatment_** Lifestyle mofications are called \_\_\_\_\_\_
**TLC (therapeutic lifestyle changes)**
50
What is the **SINGLE most additive risk** for vascular disease in **DB** patients?
**Cigarette smoking**
51
Co-morbitiies with DB are \_\_\_\_\_\_.
**Additive:** lipids, HTN
52
**_T1DM_** * Insulin: * Glucagon: * BV? * AMS? * Cause
* Insulin depletion (absolute) * Glucagon excess (absolute) * Volume depletion bc glucose is an osmotic diuretic * AMS * AI (viral)
53
**_T2DM_** * Insulin: * Glucagon: * BV? * AMS? * Cause
* Relative insulin deficiency * Glucagon excess relative to bodies utilization/formation * Volume depletion bc glucose is an osmotic diuretic * AMS * Obesity/inacitivity/lifestyle
54
* FT4: \_\_\_\_\_ * FT3: \_\_\_\_\_\_ * TPO Ab: \_\_\_\_\_\_\_\_ * TSI: \_\_\_\_\_\_\_\_
- FT4**: Free (unbound) Thyroxine** * FT3: **Free (unbound) Tri-iodothyronine** * TPO Ab: **Thyroid Peroxidase Antibody** * TSI: T**hyroid Stimulating Immunoglobulin**
55
What are signs of Hyperthyroidism (HYpo are opposite)
1. Exopthalmos and lid lag 2. Bruits over enlarged thyroid 3. Goiter/nodule 4. HR and rhythm quality 5. Tremor 6. Warm, moist skin 7. Gynecomastia 8. Muscle weakness
56
Distinguish **primary**, **secondary** and **tertiary thyroid disorders**
1. **Primary thyroid disorder** –organ itself is the source of dysfunction 2. **Secondary thyroid disorder** –Pituitary dysfunction 3. **Tertiary (aka Central) thyroid disorder** –Hypothalamus dysfunction
57
**_TSH/FT4 i_**n: 1. Primary hypothyroidism 2. Primary hyperthyroidism 3. TSH-producing tumor 4. Central hypothyroidism
1. **Primary hypothyroidism** * ↑ TSH; ↓ FT4 2. **Primary hyperthyroidism** * ↓ TSH; ↑ FT4 3. **TSH-producing tumor** * ↑TSH; ↑ FT4 4. **Central hypothyroidism** 1. ↓ TSH; ↓ FT4
58
What is **Euthyroid Sick Syndrome?**
Critically ill patient with serum levels of thyroid hormones are **low** in clinically **euthyroid patients** with nonthyroidal systemic illness. Diagnosis is based on excluding hypothyroidism. * Lab results do not fit a pattern for primary, secondary or tertiary dysfx.
59
What are possible causes of **euthryoid sick syndrome?**
1. Protein shifts 2. Protective effect of decreased metabolism 3. Maladaptive prcess
60
What is **Graves disease?**
**MC cause** of **hyperthyroisim**, causing a goiter, exopathalmos, heat intolerance, anxiety, proptosis, dermopathy of shins.
61
Nodule W/U
1. **Solitary/suspcious nodule** 2. **Measure TSH** 1. NL TSH =\> FNA with US guidance 1. 69% are benign and should be monitored with US and possible sx later 2. 17% are nondx and repeat FNA 3. If malignant/suscpisious =\> surgery 2. Low TSH =\> Thyroid scan 1. Hot nodule =\> ablate, resect or rx 2. Cold/indertminate =\> FNA with US guidance (follow b4)
62
When removing a **thyroid nodule**, what should be watched for?
damage to **recurrent laryngeal nerve** damage to **parathyroid glands**
63
**Thyroid gland hormones**
1. Low BMR =\> TRH is relased from hypothamus =\> AP 2. TSH is released from hypophysis 3. TSH travels in blood to thyroid =\> TH (T3/4) is relased 4. T3/4 and increased BMR feedsback from hypothalamus to decrease TRH
64