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Medicine > Diabetes Mellitus -2 > Flashcards

Diabetes Mellitus -2 Flashcards

1
Q

DKA - Acute Complication

A

Occurs in type 1 DM or type 2DM who have high levels of anti-insulin caused by intercurrent illness - rare in type 2

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2
Q

Causes of DKA

A

*Missed insulin
*Relative insulin deficiency
stress, steroid therapy, infection
*Tissue damage : trauma, operation, burns, shock, stroke, MI
*Pregnancy, labor & lactation
↑ ketone bodies Formation : as in Starvation, severe exertion or excess fat intake

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3
Q

Clinical Picture of DKA

A

*Symptoms of uncontrolled DM
*Respiratory - Kussmaul respiration which is deep and rapid
*Acetone breath
*Patient becomes unconcious

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4
Q

Systemic symptoms of DKA

A

Cardiovascular symptoms: shock - due to polyuria, peripheral vascular disease, dysrhythmias, Dehydration

Kidney :
Ketonuria + glucosuria, severe polyuria, polydypsia and dehydration (dry inelastic skin, sunken eye, thirst, low BP & low temp)

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5
Q

Systemic symptoms of DKA - GIT, Muscular, End Stage

A

GIT:
Acute abdomen (epigastric pain), Nausea, vomiting, constipation & hematemesis

Muscles:
Generalized weakness & muscle pain due to absence of energy.

End stage:
coma (due to acidosis, ketosis, dehydration & electrolyte imbalance)

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6
Q

Complications of DKA

A

Adult respiratory disorders syndrome (ARDS,)
DIC, arterial and venous thrombosis,
Pancreatitis,
Brain edema

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7
Q

Investigations for DKA

A

Blood
-Blood sugars: Hyperglycemia, ketonemia
- Blood pH : Acidosis (decreased plasma HCO3) dehydration leads to ↑ PCV, ↑ serum creatinine c-T FFA & TG
- Serum K: normal or high despite depletion of body K due to extracellular shift
leucocytosis and ↑ serum amylase (for pancreatitis)
- Full blood count
Euglycemic ketosis: when blood glucose is normal
* Urine: glucosuria, ketonuria (to check Rx response), polyuria
ECG (To check for hypokalemia, tall QRS wave),
chest X-ray

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8
Q

Treatment Aim

A
  • Confirm diagnosis
  • Search for and treat any precipitating cause
  • Assess hydration status and give fluid
  • Give insulin
  • Monitor clinical signs and biochemistry
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9
Q

Fluid replacement

A
  • Hospitalization better in ICU
  • Fluid replacement:
    Amount: guided by CVP - by central venous catheter (10cm H2O ideal)
    *1 L / hour till HR & BP return to normal - monitor blood sugar.
    *Type of fluid:
    At 1st: isotonic saline
    Then: dextrose 5% when blood glucose drops < 14 mmol/l (to avoid hypoglycemia from insulin admin). In KATH if the patient is still hypovolemic 5% dextrosaline is given, then freq. of insulin given is reduced.
    –Hypotonic saline with hypernatremia
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10
Q

Insulin Rx for DKA

A

Insulin
Type: soluble/short acting
Dose: low dose regimen 0.1 U / kg / h. continuous infusion via insulin pump or deep IM.
Follow up: by blood sugar every hour & give further insulin accordingly.

In KATH - Give bolus of insulin - IV 10U soluble + IV 10U subcutaneous. Continue monitoring blood sugar till <14mmol/l, put on dextrose and reduce freq. of insulin.

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11
Q

Treatment of acid base and electrolyte disturbances - DKA

A

Shouldn’t always be done, but if patient has the following: *Metabolic acidosis : -+ NaHCO3.
Indication : in severe case
Clinical : Kussmaul respiration),
Lab.: pH < 7.1 & HC03 <10 mEq
Dose: 1 L of 1/6 molar NaHC03 IV (till PH > 7.2 not reach 7.4 to avoid over correction -> Alkalosis)

*Correct plasma K+ level:
K from the start Hypo K+ : occurs with insulin treatment due to intracellular shift
Dose: Add 10 ml KCL (20 mEq) to each 1 L of fluid given. Oral given after recovery

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12
Q

Care for comatose patient, treat cause and precipitating factors & monitor

A
  • Care of comatose Pt.:
  • Treat cause & precipitating factors
  • Monitoring: state of hydration, urine output, conscious level, plasma glucose, K and ABG
    Blood culture, urine culture and chest xray
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13
Q

Care for comatose patient, treat cause and precipitating factors & monitor

A
  • Care of comatose Pt.:
  • Treat cause & precipitating factors
  • Monitoring: state of hydration, urine output, conscious level, plasma glucose, K and ABG
    Blood culture, urine culture and chest xray
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13
Q

Care for comatose patient, treat cause and precipitating factors & monitor

A
  • Care of comatose Pt.:
  • Treat cause & precipitating factors
  • Monitoring: state of hydration, urine output, conscious level, plasma glucose, K and ABG
    Blood culture, urine culture and chest xray
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14
Q

Othe Rx of DKA

A

Take blood sample, give broad spectrum antibiotic, Prophylactic antibiotic.
* Nasogastric tube: to aspirate gastric content - so it won’t aspirate (pneumonia, pneumonitis)
*Heparin IV in old and dehydrated patients to guard against DIC (Because of dehydration and hypovolemic state)
*Frusemide IV in oliguric patients
*O2 if P02 < 80mmHg

*Continue with Insulin therapy
* Prevent recurrence: Avoid reduction of insulin dose during intercurrent illness (when insulin resistant)

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15
Q

Hyperglycemia hyperosmolar non-ketotic state causes

A

Occurs in old type 2 DM due to (infection. MI). 55mmol/l blood sugar
- Absence of fat reserve or fat mobilization (relative lack of GH or cortisol)
- Insensitive thirst center in old age led to dehydration aggravated by use of diuretics.
Be careful of the amount of insulin you give - you’ll push them into hypo.

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16
Q

Precipitative factors of HHNK state

A

Infection
Infarction

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16
Q

Clinical presentation of HHNK state - PPD + Neuro symptoms

A

Severe polyuria, polydipsia & dehydration

*No or little ketosis
* Prerenal uremia may occur due to dehydration
Neurologic symptoms: convulsions, coma, hemiparesis, stupor

17
Q

Investigations for HHNK

A

Investigations
Blood (Culture):
* severe hyperglycemia often > 55mmol/l
* ↑ PCV, ↑ Na, ↑ plasma osmolality (N. 290 mosm/L)  Urine: glucose without ketone bodies

18
Q

Treatment of HHNK

A

Treatment : Same as DKA but without bicarbonate
Fluids
Type : 1/2 normal saline (1/2 molar) - Give ordinary normal saline.
Amount : IL / hour not faster to avoid cerebral edema
Insulin : smaller amount than ketoacidosis (stat dose)
Heparin : since there is ↑ incidence of DIC

19
Q

Chronic Complications - Macrovascular (Affect brain and heart)

A

Diabetes is a risk factor for developing atherosclerosis.

20
Q

Other Risk Factors for development of macrovascular complications:

A
  • Duration of diabetes
  • Increasing age
  • Systolic hypertension
  • Hyperinsulinaemia due to insulin resistance (type 2)
  • Obesity and syndrome X (metabolic syndrome)
  • Hyperlipidaemia (particularly hypertriglyceridaemia/low HDL
  • Proteinuria (including microalbuminuria) 

21
Q

Heart complication of DM

A

Coronary heart disease

  • Myocardial infarction is three to five times more among diabetic people
  • Women with diabetes lose their premenopausal protection from coronary artery disease.
  • Painless angina and myocardial infarction may be due to neuropathic damage to the autonomic nerves serving the myocardium.
  • Atypical presentation of angina and myocardial infarction (malaise, sweating, dyspnea and syncope which may be confused with hypoglycemia
22
Q

Why is long term mortality from MI increased in diabetes?

A

Due to increased risk of Heart Failure in Diabetes.

23
Q

How is MI managed in a diabetic patient?

A

Management is similar to non- diabetic population with more caution with usage of thromolytic therapy because of the risk of intraocular haemorrhage in the patient with retinopathy.

24
Q

Diabetes and Caardiomyopathy + Main feature

A
  • Diabetes can cause a cardiomyopathy even without coronary artery atheroma.
  • Left ventricular contractility abnormalities detected by echocardiology is the main subclinical feature.
25
Q

Hypertension and Diabetes

A

Hypertension is twice more in diabetes than non-diabetic.
* Closely associated with metabolic syndrome X, insulin resistance or hyperinsulinaemia

26
Q

How does hyperinsulinemia lead to hypertension?

A

Through
* Stimulation of kidney reabsorption of sodium and water.
* Stimulation of calcium and sodium in the vascular smooth muscle which enhance contractility causing hypertrophy of vascular smooth muscle, and stimulation of sympathetic nervous systems.

27
Q

Why is the control of hypertension in diabetes important?

A
  • Hypertension is a major CVS risk factor.

*Hypertension can accelerate microvascular complication as nephropathy and retinopathy.

28
Q

How to investigate hypertension in diabetes?

A

Investigate pt’s for
* Secondary hypertension (Cushing’s, Conn’s disease and Pheochromocytoma)
* Renal damage (proteinuria or microalbuminuria, urine microscopy, serum creatinine and electrolytes)
* CV damage (ECG, chest x-ray for left ventricular hypertrophy)
* Other CV risk factors eg. hyperlipidemia, poor glycemic control

29
Q

Treatment of HPT in Diabetes

A

ACE inhibitors are the first choice because:
1. It delays the progression of diabetic retinopathy and reduces microalbuminuria.
2. A thiazide should be used at low dose to avoid worsening of glycemic control and aggravation of dyslipidemia.
3. Beta-adrenoceptors can aggravate hyperglycemia, dyslipidemia and impotence.

30
Q

Peripheral arterial disease and Diabetes - symptoms

A
  • Asymptomatic
  • Intermittent claudication (calf pain on walking)
  • Buttock pain may occur if iliac vessels are affected
  • Decreasing claudication distance and rest pain denote critical ischemia
  • Unhealed skin wound
31
Q

Peripheral arterial disease and Diabetes - Signs

A
  • Absence of pedal pulse ( 8% dorsalis pedis, 2% posterior tibialis)
  • Cold extremities
  • Pale or bluish color of the skin
  • thin, shiny skin with scanty hair
  • dystrophic toenail
32
Q

Investigations for Peripheral artery disease

A
  • Doppler US
  • Ankle Brachial Index (ABI) : normal value 0.98 - 1.31
  • Angiography
33
Q

Prevention of macrovascular complication

A
  • Early control of blood glucose
  • Strict control of hypertension.
  • Stop smoking
  • Treatment of lipid abnormalities: to the lowest achievable level
  • ACE inhibitors /angiotensin II receptor antagonists: 25–35% lowering of the risk of heart attack, stroke, overt nephropathy or cardiovascular death
  • Low dose aspirin: can reduce macrovascular risk, but is associated with a morbidity and mortality from bleeding.
34
Q

Cerebral stroke and Diabetes (macro)

A
  • Stroke is twice higher in diabetic population than non-diabetics
  • Mortality and disability from stroke are also worse in the diabetic person compared to non- diabetic people (May because of elevation of blood glucose level following stroke)
35
Q

The Danger sites of Microvascular complications - Diabetes Mellitus

A

Retina
Renal Glomerulus
Nerves

36
Q

Classification of Diabetic Neuropathies

A
  • Focal and multifocal neuropathies e.g. mononeuropathy, amyotrophy, radiculopathy, entrapment neuropathy, mononeuritis multiplex.
  • Symmetrical neuropathies e.g. diabetic peripheral neuropathy and autonomic Neuropathy
  • Cranial nerve palsies (III, IV, VI & VII)
37
Q

Mononeuropathies + Peroneal nerve palsy

A

Affect (single nerve) peroneal, median or ulnar nerves. It tends to occur at sites of entrapment (wrist) or external compression.

  • Peroneal nerve palsy is characterized by weakness or paralysis of foot and toe dorsiflexors, foot drop and foot eversion.
  • Impaired sensation over the dorsum of the foot and the lower anterior aspect of the leg.

*The ankle reflex is preserved as is foot inversion.

38
Q

Entrapment neuropathies

A

1-Carpal tunnel syndrome: found in 5.8 % of diabetic patients. It has a less favorable outcome after surgical decompression, as diabetes slows nerve regeneration.

2- Ulnar neuropathy at the elbow affects 2.1% of diabetic patients

3- Peroneal neuropathy at the fibular head affects 1.4–13% of diabetic patients.

4- Lateral cutaneous nerve of the thigh (meralgia paresthetica) affect 0– 1.0% of diabetic patients.

39
Q

Clinical Features of autonomic neuropathy

A
  • Impotence
  • Postural hypotension (giving dizziness and syncope)
  • Resting tachycardia or fixed heart rate
  • Gustatory sweating—sweating after tasting food
  • Dysphagia with delayed gastric emptying, nausea/vomiting
  • Constipation or diarrhea
  • Urinary retention or overflow incontinence
  • absent sweating on the feet (anhidrosis). This increases the risk of ulceration.
  • Abnormal pupillary reflexes
40
Q

Assessments for diabetic neuropathy

A

Annually check the following:
* Lying and standing BP (measure systolic BP 2 minutes after standing; normal is difference <10 mmHg drop, >30 mmHg is abnormal)
* Pupillary responses to light

41
Q

Other less common tests for diabetic neuropathy if the diagnosis is uncertain or in high-risk patients.

A
  • Loss of sinus arrhythmia: Measure inspiratory and expiratory heart rates after 5 seconds of each (<10 beats/min difference is abnormal,>15 are normal).
  • Loss of heart rate response to Valsalva maneuver: Look at the ratio of the shortest R–R interval during forced expiration against a closed glottis compared to the longest R–R interval after it (<1.2 is abnormal).
  • BP response to sustained hand-grip: Diastolic BP prior to the test is compared to diastolic BP after 5 minutes of sustaining a grip equivalent to 30% of maximal grip. A diastolic BP rise >16 mmHg is normal, <10 mmHg is abnormal. A rolled-up BP cuff to achieve the required handgrip may be used.

Medicine (18 decks)

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