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1. AA my internal medicine > 3a. Diabetology > Flashcards

3a. Diabetology Flashcards

1
Q

Classification of diabetes mellitus?

A
  1. Type I IDDM: (5%)
    - This is characterized by a severe deficiency of insulin. Patients require insulin to live.
  2. Type II NIDDM: (90%)
    - Insulin resistance.
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2
Q

Pathogenesis of type I diabetes ?

A

a. An autoimmune disease—The immune system mediates the destruction of β-cells.

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3
Q

Pathogenesis of type II diabetes ?

A

A. Risk factors ( Obesity, genetics, age)
B. Obesity ( plays a major role).
C. Lack of compensation in type II diabetic patients.

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4
Q

What can we observe in Lipid profile of insulin resistance and poorly controlled diabetes?

A

Hypertriglyceridemia with HDL depletion.

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5
Q

Diabetes is diagnosed by who one of the following?

A
  1. Two fasting glucose measurements greater than 126 mg/dL.
  2. Single glucose level of 200 mg/dL with symptoms.
  3. Increased Glucose level on oral glucose tolerance testing (after two hrs of 75g. criteria for DM: glucose >200)
  4. Hg A1c >6.5%.
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6
Q

Insulin versus oral hypoglycemic agents and type II diabetes?

A
  • If the patient has severe hypoglycemia (fasting glucose >300 mg/dL), Insulin typically is the agent of choice. (both types).
  • Oral hypoglycemic agents are affective in type II diabetes with moderate hyperglycemia (fasting glucose 140-300 mg/dL)
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7
Q

sliding scale ?

A

The term “sliding scale” refers to the progressive increase in the pre-meal or nighttime insulin dose, based on pre-defined blood glucose ranges. Sliding scale insulin regimens approximate daily insulin requirements.

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8
Q

Intensive insulin therapy ?

A
  • 4 injections daily:
  • 3 regular insulin given 30-45 mins before each meal.
  • 1 long-acting insulin is given in the evening.
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9
Q

If the patient is unable/unwilling to carry out an intensive insulin program:

A
  • Give 70/30 units Before breakfast and before the evening meal for basal coverage.
  • Give a short acting insulin (regular) for prandial control if necessary.
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10
Q

Metformin ?

  • MOA:
  • Body weight:
  • Risk of hypoglycemia:
  • Side effects:
  • Contraindications:
A
  • MOA: decrease hepatic glucose production, increase insulin sensitivity.
  • Body weight: decrease or no change.
  • Risk of hypoglycemia: –
  • Side effects: GI upset
  • Contraindications: organ failure (Heart, brain, liver, kidneys, respiratory), alcohol abuse.
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11
Q

Sulphonylureas ?

  • MOA:
  • Body weight:
  • Risk of hypoglycemia:
  • Side effects:
  • Contraindications:
A
  • MOA: Increase insulin secretion.
  • Body weight: INCREASE.
  • Risk of hypoglycemia: HIGH (2nd after insulin)
  • Side effects: hypoglycemia, gain weight.
  • Contraindications: heart, liver, kidney failure.
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12
Q

Alpha-glucosides inhibitors

  • MOA:
  • Hypoglycemic effect:
  • Body weight:
  • Risk of hypoglycemia:
  • Side effects:
  • Contraindications:
A
  • MOA: Decreased intestinal polysaccharide breakdown.
  • Hypoglycemic effect: LOW
  • Body weight: –
  • Risk of hypoglycemia: –
  • Side effects: GI (flatulence, diarrhea)
  • Contraindications: GI diseases
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13
Q

GLP-1 receptor agonists

  • MOA:
  • Body weight:
  • Risk of hypoglycemia:
  • Side effects:
  • Contraindications:
A
  • MOA: Increased hyperglycemia mediated insulin secretion, decreased appetite.
  • Body weight: DECREASED
  • Risk of hypoglycemia: –
  • Side effects: GI upset
  • Contraindications: GI neuropaty.
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14
Q

DPP-4 inhibitors

  • MOA:
  • Body weight:
  • Risk of hypoglycemia:
  • Side effects:
  • Contraindications:
A
  • MOA: Increased hyperglycemia mediated insulin secretion.
  • Body weight: –
  • Risk of hypoglycemia: –
  • Side effects: –
  • Contraindications: liver failure.
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15
Q

PPAR-gamma(y) agonist

  • MOA:
  • Body weight:
  • Risk of hypoglycemia:
  • Side effects:
  • Contraindications:
A
  • MOA: Increased insulin sensitivity.
  • Body weight: Increased
  • Risk of hypoglycemia: –
  • Side effects: Fluid retention (edema) , increase body weight, increased risk of long bone fractures.
  • Contraindications: heart or liver failure, bladder cancer.
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16
Q

SGLT-2 inhibitors

  • MOA:
  • Body weight:
  • Risk of hypoglycemia:
  • Side effects:
  • Contraindications:
A
  • MOA: Induction of glucosuria.
  • Body weight: decrease.
  • Risk of hypoglycemia: –
  • Side effects: genital fungal infection, increase thirst.
  • Contraindications: renal failure.
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17
Q

What are the oral anti-diabetic agents that has beneficial cardiovascular effect ?

A
  • GLP-1 receptor agonists.

- SGLT-2 inhibitors.

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18
Q

What are the oral anti-diabetic agents that Increases the body weight?

A
  • Sulphonylureas.

- PPAR-gamma(y) agonist.

19
Q

Chronic Complications of Diabetes Mellitus ?

A

A. Macrovascular complications.

B. Microvascular complications

20
Q

Macrovascular complications ?

A

main problem is accelerated atherosclerosis.

21
Q

What is the most common cause of death in diabetic patients?

A

Coronary artery disease.

22
Q

Microvascular complications ?

A
  1. Diabetic nephropathy.
  2. Diabetic retinopathy.
  3. Diabetic neuropathy.
  4. Diabetic foot.
  5. Increased susceptibility to infection.
23
Q

Microvascular complications ?

A
  1. Diabetic nephropathy.
  2. Diabetic retinopathy.
  3. Diabetic neuropathy.
  4. Diabetic foot.
  5. Increased susceptibility to infection.
24
Q

Definition of Microalbuminuria ?

A
  • 30 to 300 mg/day.
  • Alnumin-creatinine ratio of 0.02 to 0.20.
  • Initiate ACE inhibitors or ARB immediately. These agents are proven to decrease the rate of progression of nephropathy.
25
Q

Diabetic retinopathy ?

A
  • Prevalence is approximately 75% after 20 yr of diabetes. Annual screening
    of all diabetic patients by an ophthalmologist is recommended.
26
Q

Diabetic neuropathy ?

A

A. Peripheral neuropathy (distal symmetric neuropathy):
- Numbness and paresthesias are common.

B. CN complication:
- Most often involves CN III, but may also involve CN VI and IV.

C. Mononeuropathies—secondary to nerve infarction.

D. Autonomic neuropathy.

27
Q

Diabetic 3rd nerve palsy?

A

Eye pain, diplopia, ptosis, inability to adduct the eye: pupils are spared.

28
Q

Autonomic neuropathy in diabetes?

A
  • Impotence in Men. (most common presentation).
  • Neurogenic bladder: retenion, incontinence.
  • Gastroparesis: chronic nausea and vomitingm early satiety.
  • Constipation and diarrhea.
  • Postural hypotension.
29
Q

Progression in diabetic nephropathy ?

A
  • Hypoglycemia -> increase GFR -> Microalbuminuria -»»> Proteinuria -> decrease GFR -> ESRD.
  • once proteinuria develops, glycemic control does little to control the course and will eventually lead to ESRD
30
Q

Diabetic foot ?

A
  • Caused by a combination of artery disease (ischemia) and nerve disease (neuropathy)—can lead to ulcers/infections and may require amputation.
31
Q

Key Features of DKA ?

A
  • Hyperglycemia.
  • Positive serum or urine ketons.
  • Metabolic acidosis.
32
Q

Diabetic ketoacidosis ?

A
  • DKA is an acute, life-threatening medical emergency that can occur in both type I and type II diabetic patients (more common in type I).
33
Q

Pathogenesis of DKA ?

A
  • This is 2ndary to insulin deficiency and glucagons excess, both of which contribute to accelerated severe hyperglycemia and accelerated ketogenesis.
  • Severe hyperglycemia leads to an osmotic diuresis, which causes dehydration and volume depretion.
34
Q

Precipitating factors of DKA ?

A
  • Any type of stress or illness (e.g., infectious process, trauma, myocardial infarc-
    tion, stroke, recent surgery, sepsis, GI bleeding).
  • Inadequate administration of insulin.
35
Q

Clinical features of DKA ?

A
  • Symptoms usually occur rapidly, typically in less than 24 hours.
  • Nausea and vomiting.
  • Kussmaul respiration: rapid, deep breathing.
  • Abdominal pain.
  • Fruity (acetone) breath odor.
  • Marked dehydration, orthostatic hypotension, tachycardia: volume depletion is always present.
  • Polydipsia, polyuria, polyphagia, weakness.
  • Altered consciousness, drowsiness, adn
36
Q

Causes of DKA ?

A

— Interruption or errors of insulin therapy;
— Too late diagnosis of diabetes type 1;
— Alcohol abuse;
— Acute inflammation (e.g., bacterial, viral, and fun-
gal infections);
— Pregnancy;

37
Q

Laboratory criteria of diabetic ketoacidosis ?

A
  1. Blood glucose usually > 250 mg/dL (> 13.9
    mmol/L), ( blood glucose values may be lower in
    patients treated with SGLT-2 inhibitors).
  2. Metabolic acidosis ( PH<7.3 and serum HCO3 <15)
  3. Presence of ketone bodies in urine or serum.
  4. Anion gap: Na (mmol/L) – [Cl (mmol/L) + HCO3
    (mmol/L)] > 12 (measured and not corrected sodium level is used in this formula).
38
Q

Treatment of DKA ?

A

A. Patient hydration:
- Normal saline

B. Correcting hyperglycemia:
- Intravenous insulin therapy (Initial insulin bolus 0.1 unit/kg).

C. Correction of electrolyte disturbances:
- potassium supplementation IV.

D. Bicarbonate administration (consider only if arterial blood pH < 6.9 )

39
Q

Complication of diabetic ketoacidosis ?

A

— Hypovolemic shock;
— Acute renal failure
— Cerebral edema, more commonly in children.

40
Q

Hyperosmolar hyperglycemic nonketotic syndrome ?

A
  • A state of severe hyperglycemia, hyperosmolarity, and dehydration is typically
    seen in elderly type II diabetic patients.
  • Most commonly develops due to a delayed diagnosis or inadequate treatment of diabetes type 2.
41
Q

Hyperosmolar hyperglycemic nonketotic syndrome diagnosis ?

A
    • Blood glucose > 600 mg/dL (> 33.3 mmol/L);
  2. Effective plasma osmolality > 320 mOsm/kg H2O.
  3. pH > 7.30;
  4. Serum bicarbonate level > 15.0 mmol/L;
  5. Hypernatremia.
  6. Serum ketone bodies: absent/trace.
42
Q

Hyperosmolar hyperglycemic nonketotic syndrome treatment ?

A
  • Same as DKA, except for bicarbonate administration.

A. Patient hydration:
- Normal saline
B. Correcting hyperglycemia:
- Intravenous insulin therapy (Initial insulin bolus 0.1 unit/kg).
C. Correction of electrolyte disturbances:
- potassium supplementation IV.

43
Q

Clinical features of HHNS ?

A

a. Thirst, polyuria
b. Signs of extreme dehydration and volume depletion—hypotension, tachycardia
c. CNS findings and focal neurologic signs are common (e.g., seizures)—secondary
to hyperosmolarity.
d. Lethargy and confusion may develop, leading to convulsions and coma.

44
Q

If a patient present with hypoglyxemia of unknown cause, measure ?

A
  • Plasma insulin level.
  • C-peptide (bust the patient coz the exogenous insulin doesn’t increase c-peptide, so it will be normal)
  • Anti-insulin antibodies. (exogenous insulin will also develop anti-insulin antibodies)
  • Plasma and urine sulfonylurea levels.

1. AA my internal medicine (9 decks)

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